FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Shiani, A
Narayanan, S
Pena, L
Friedman, M
AF Shiani, Ashok
Narayanan, Shreya
Pena, Luis
Friedman, Mark
TI The Role of Diagnosis and Treatment of Underlying Liver Disease for the
Prognosis of Primary Liver Cancer
SO CANCER CONTROL
LA English
DT Review
DE liver disease; hepatocellular carcinoma; and cirrhosis
ID CHRONIC HEPATITIS-B; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
ALPHA-1-ANTITRYPSIN DEFICIENCY; NONALCOHOLIC STEATOHEPATITIS; ANTIVIRAL
THERAPY; VIRUS-INFECTION; UNITED-STATES; RISK; MANAGEMENT
AB Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. Underlying chronic liver disease has been associated with an increased risk of developing HCC. This study is a review of the current literature regarding the diagnosis, prognostic significance, and role of treating underlying liver disease in patients who are at risk of primary liver cancer. Relevant peer review of the English literature between 1980 and 2017 within PubMed and the Cochrane library was conducted for scientific content on current advances in managing chronic liver diseases and the development of hepatocellular carcinoma. Hepatitis C virus, hepatitis B virus (HBV), nonalcoholic steatohepatitis, autoimmune hepatitis, hereditary hemochromatosis, Wilson disease, primary biliary cirrhosis, alpha 1-antitrypsin deficiency, and certain drugs lead to an increased risk of developing HCC. Patients with underlying liver disease have an increased incidence of HCC. Hepatitis C virus, HBV, and hemochromatosis can directly lead to HCC without the presence of cirrhosis, while HCC related to other underlying liver diseases occurs in patients with cirrhosis. Treating the underlying liver disease and reducing the progression to cirrhosis should lead to a decreased incidence of HCC.
C1 [Shiani, Ashok; Narayanan, Shreya] Univ S Florida, Morsani Coll Med, Dept Internal Med, Tampa, FL USA.
[Pena, Luis; Friedman, Mark] H Lee Moffitt Canc Ctr & Res Inst, Gastrointestinal Oncol Program, Dept Gastroenterol, 12902 Magnolia Dr,FOB 2 GI PROG, Tampa, FL 33612 USA.
C3 State University System of Florida; University of South Florida; H Lee
Moffitt Cancer Center & Research Institute
RP Friedman, M (corresponding author), H Lee Moffitt Canc Ctr & Res Inst, Gastrointestinal Oncol Program, Dept Gastroenterol, 12902 Magnolia Dr,FOB 2 GI PROG, Tampa, FL 33612 USA.
EM mark.friedman@moffitt.org
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NR 39
TC 80
Z9 87
U1 0
U2 14
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-2748
J9 CANCER CONTROL
JI Cancer Control
PD SEP
PY 2017
VL 24
IS 3
DI 10.1177/1073274817729240
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FW3QY
UT WOS:000425225300003
PM 28975833
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Lleo, A
de Boer, YS
Liberal, R
Colombo, M
AF Lleo, Ana
de Boer, Ynto S.
Liberal, Rodrigo
Colombo, Massimo
TI The risk of liver cancer in autoimmune liver diseases
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE autoimmune hepatitis; autoimmune liver diseases; cholangiocarcinoma;
hepatic cancer; hepatocellular carcinoma; primary biliary cholangitis;
primary sclerosing cholangitis
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY-CIRRHOSIS;
HEPATOCELLULAR-CARCINOMA; INTRAHEPATIC CHOLANGIOCARCINOMA; FOLLOW-UP;
HEPATITIS; COHORT; MANAGEMENT; DIAGNOSIS; CHILDREN
AB Hepatocellular carcinoma (HCC), the dominant primary malignancy of the liver, has almost invariably a fatal outcome that can be averted only by early diagnosis and treatment. While the close association of HCC with chronic viral hepatitis and alcohol abuse has impacted favourably on screening and treatment of this deadly tumour, at the same time it has long obscured the etiologic role of autoimmune liver diseases. Recently, a systematic analysis of 25 published cohorts disclosed a 3.1 x 1000 patients/year incidence of HCC in autoimmune hepatitis patients that tripled in those with cirrhosis. HCC is also a sequela of primary biliary cholangitis, where the incidence is more relevant in males, those with advanced liver disease and nonresponders to ursodeoxycholic acid therapy. Cholangiocarcinoma (CCA), the second ranking primary cancer of the liver, is also on the rise with its intrahepatic pattern, in part reflecting an association with chronic liver diseases of diverse aetiology. In the USA and northern Europe, perihilar CCA is a frequent complication of primary sclerosing cholangitis, a cholestatic disorder thought to be immune mediated. International Guidelines clearly recommend HCC screening with abdominal ultrasonography every 6 months in autoimmune cirrhotic patients. While surveillance of patients with autoimmune liver disorders who are at risk of HCC affects both early diagnosis and radical therapy of this tumour, this is not the case for CCA, where early diagnosis is challenged by the lack of sensitive and accurate tests for screening.
C1 [Lleo, Ana] Humanitas Univ, Div Internal Med & Hepatol, Humanitas Clin & Res Ctr IRCCS, Dept Biomed Sci,Dept Gastroenterol, Via A Manzoni 56, I-20089 Rozzano, MI, Italy.
[de Boer, Ynto S.] Vrije Univ Amsterdam, Amsterdam Univ, Med Ctr, Dept Gastroenterol & Hepatol, Amsterdam, Netherlands.
[Liberal, Rodrigo] Kings Coll London, Inst Liver Studies, London, England.
[Colombo, Massimo] IRCCS, Humanitas Clin & Res Ctr, Rozzano, Italy.
C3 IRCCS Humanitas Research Hospital; Humanitas University; Vrije
Universiteit Amsterdam; University of Amsterdam; University of London;
King's College London; IRCCS Humanitas Research Hospital
RP Lleo, A (corresponding author), Humanitas Univ, Div Internal Med & Hepatol, Humanitas Clin & Res Ctr IRCCS, Dept Biomed Sci,Dept Gastroenterol, Via A Manzoni 56, I-20089 Rozzano, MI, Italy.
EM ana.lleo@humanitas.it
RI LLEO, Ana/AAA-5759-2019; de Boer, Ynto/D-9242-2013
OI LLEO, Ana/0000-0002-0561-7902; de Boer, Ynto/0000-0002-4066-7593
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NR 59
TC 28
Z9 30
U1 1
U2 10
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PD JUL
PY 2019
VL 11
AR 1758835919861914
DI 10.1177/1758835919861914
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IN4TW
UT WOS:000478670400001
PM 31320937
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Rigopoulou, EI
Dalekos, GN
AF Rigopoulou, Eirini I.
Dalekos, George N.
TI Current Trends and Characteristics of Hepatocellular Carcinoma in
Patients with Autoimmune Liver Diseases
SO CANCERS
LA English
DT Review
DE autoimmune liver diseases; hepatocellular carcinoma; autoimmune
hepatitis; hepatic; primary biliary cholangitis; primary sclerosing
cholangitis
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
CLINICAL-PRACTICE GUIDELINES; RISK-FACTORS; HEPATITIS-C; CANCER-RISK;
FOLLOW-UP; PREDICTIVE FACTORS; COST-EFFECTIVENESS; GENDER DISPARITY
AB Simple Summary
While hepatocellular carcinoma (HCC) is inextricably linked to underlying cirrhosis due to chronic viral hepatitis, alcohol consumption, and non-alcoholic fatty liver disease, the role of autoimmune liver diseases (AILDs) as risk factor has been disputed. In this review we present data showing AILDs to confer increased risk for HCC development, albeit lower than other hepatic diseases. We also highlight several risk factors that indicate patients with autoimmune hepatitis and primary biliary cholangitis at high and moderate risk for HCC development, including cirrhosis, older age, male sex, and co-existing factors, such as alcohol consumption and treatment response. As surveillance is of utmost importance for early diagnosis and subsequent effective treatment, we suggest refinement of screening strategies according to prevailing risk factors in patients with AILDs.
Hepatocellular carcinoma (HCC), the commonest among liver cancers, is one of the leading causes of mortality among malignancies worldwide. Several reports demonstrate autoimmune liver diseases (AILDs), including autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC) to confer increased risk of hepatobiliary malignancies, albeit at lower frequencies compared to other liver diseases. Several parameters have been recognized as risk factors for HCC development in AIH and PBC, including demographics such as older age and male sex, clinical features, the most decisive being cirrhosis and other co-existing factors, such as alcohol consumption. Moreover, biochemical activity and treatment response have been increasingly recognized as prognostic factors for HCC development in AIH and PBC. As available treatment modalities are effective only when HCC diagnosis is established early, surveillance has been proven essential for HCC prognosis. Considering that the risk for HCC is not uniform between and within disease groups, refinement of screening strategies according to prevailing demographic, clinical, and molecular risk factors is mandated in AILDs patients, as personalized HCC risk prediction will offer significant advantage in patients at high and/or medium risk. Furthermore, future investigations should draw attention to whether modification of immunosuppression could benefit AIH patients after HCC diagnosis.
C1 [Rigopoulou, Eirini I.; Dalekos, George N.] Gen Univ Hosp Larissa, Dept Med, Natl Expertise Ctr Greece Autoimmune Liver Dis, Larisa 41110, Greece.
[Rigopoulou, Eirini I.] Gen Univ Hosp Larissa, Res Lab Internal Med, Natl Expertise Ctr Greece Autoimmune Liver Dis, Larisa 41110, Greece.
C3 General University Hospital of Larissa; General University Hospital of
Larissa
RP Dalekos, GN (corresponding author), Gen Univ Hosp Larissa, Dept Med, Natl Expertise Ctr Greece Autoimmune Liver Dis, Larisa 41110, Greece.
EM eirigopoulou@med.uth.gr; dalekos@med.uth.gr
OI Rigopoulou, Eirini/0000-0003-1978-4602
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NR 148
TC 22
Z9 23
U1 0
U2 24
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2021
VL 13
IS 5
AR 1023
DI 10.3390/cancers13051023
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QV5EG
UT WOS:000627994100001
PM 33804480
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Hemminki, K
Sundquist, K
Sundquist, J
Försti, A
Liska, V
Hemminki, A
Li, XJ
AF Hemminki, Kari
Sundquist, Kristina
Sundquist, Jan
Foersti, Asta
Liska, Vaclav
Hemminki, Akseli
Li, Xinjun
TI Personal comorbidities and their subsequent risks for liver, gallbladder
and bile duct cancers
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE alcohol; comorbidity; familial risk; hepatocellular carcinoma; risk
factor; smoking
ID HEPATOCELLULAR-CARCINOMA; VIRUS-INFECTION; INFLAMMATION; DISEASE; TRENDS
AB Many environmental risk factors for hepatobiliary cancers are known but whether they are associated with specific cancer types is unclear. We present here a novel approach of assessing standardized incidence ratios (SIRs) of previously diagnosed comorbidities for hepatocellular carcinoma (HCC), gallbladder cancer (GBC), cholangiocarcinoma (CCA) and ampullary cancer. The 13 comorbidities included alcohol and nonalcohol related liver disease, chronic obstructive pulmonary disease, gallstone disease, viral and other kinds of hepatitis, infection of bile ducts, hepatic and other autoimmune diseases, obesity and diabetes. Patients were identified from the Swedish Inpatient Register from 1987 to 2018, and their cancers were followed from 1997 onwards. SIRs for HCC were 80 to 100 in men and women diagnosed with hepatitis C virus and they were also >10 in patients diagnosed with hepatitis B virus, other kind of hepatitis, hepatic autoimmune disease and nonalcohol related liver disease. Many of these risks, as well as alcohol related liver disease, were either specific to HCC or were shared with intrahepatic CCA. For GBC, CCA and ampullary cancer infection of bile ducts was the main risk factor. Gallstone disease, nonhepatic autoimmune diseases and diabetes were associated with all hepatobiliary cancers. The limitations of the study include inability to cover some rare risk factors and limited follow-up time. Many of the considered comorbidities are characterized by chronic inflammation and/or overt immune disturbance in autoimmune diseases. The results suggest that local chronic inflammation and a related immune disturbance is the carcinogenic trigger for all these cancers.
C1 [Hemminki, Kari; Liska, Vaclav] Charles Univ Prague, Fac Med, Plzen 30605, Czech Republic.
[Hemminki, Kari; Liska, Vaclav] Charles Univ Prague, Biomed Ctr Pilsen, Biomed Ctr, Plzen 30605, Czech Republic.
[Hemminki, Kari] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Hemminki, Kari; Sundquist, Kristina; Sundquist, Jan; Foersti, Asta; Li, Xinjun] Lund Univ, Ctr Primary Hlth Care Res, Malmo, Sweden.
[Sundquist, Kristina; Sundquist, Jan] Icahn Sch Med Mt Sinai, Dept Family Med & Community Hlth, Mt Sinai, NY USA.
[Sundquist, Kristina; Sundquist, Jan] Icahn Sch Med Mt Sinai, Dept Populat Hlth Sci & Policy, Mt Sinai, NY USA.
[Sundquist, Kristina; Sundquist, Jan] Shimane Univ, Ctr Community Based Healthcare Res & Educ CoHRE, Sch Med, Dept Funct Pathol, Matsue, Shimane, Japan.
[Foersti, Asta] Hopp Childrens Canc Ctr KiTZ, Heidelberg, Germany.
[Foersti, Asta] German Canc Res Ctr, Div Pediat Neurooncol, German Canc Consortium DKTK, Heidelberg, Germany.
[Liska, Vaclav] Univ Hosp, Sch Med Pilsen, Dept Surg, Plzen, Czech Republic.
[Hemminki, Akseli] Univ Helsinki, Translat Immunol Res Program, Canc Gene Therapy Grp, Helsinki, Finland.
[Hemminki, Akseli] Helsinki Univ Hosp, Comprehens Canc Ctr, Helsinki, Finland.
C3 Charles University Prague; Charles University Prague; Helmholtz
Association; German Cancer Research Center (DKFZ); Lund University;
Icahn School of Medicine at Mount Sinai; Icahn School of Medicine at
Mount Sinai; Shimane University; Helmholtz Association; German Cancer
Research Center (DKFZ); University Hospital Plzen; University of
Helsinki; University of Helsinki; Helsinki University Central Hospital
RP Hemminki, K (corresponding author), Charles Univ Prague, Fac Med, Plzen 30605, Czech Republic.; Hemminki, K (corresponding author), Charles Univ Prague, Biomed Ctr Pilsen, Biomed Ctr, Plzen 30605, Czech Republic.
EM k.hemminki@dkfz.de
RI ; Liska, Vaclav/Q-4402-2017
OI Hemminki, Kari/0000-0002-2769-3316; Hemminki,
Akseli/0000-0001-7103-8530; Liska, Vaclav/0000-0002-5226-0280
FU European Union's Horizon 2020 Research and Innovation Program [856620];
Swedish Research Council; Jane and Aatos Erkko Foundation; Finnish
Cancer Organizations; University of Helsinki; Helsinki University
Central Hospital; Novo Nordisk Foundation; Paivikki and Sakari Sohlberg
Foundation; Sigrid Juselius Foundation; National Institute for Cancer
Research-NICR - European Union-Next Generation EU [LX22NPO5102];
research area SURG
FX Supported by the European Union's Horizon 2020 Research and Innovation
Program, No. 856620, The Swedish Research Council, Jane and Aatos Erkko
Foundation, Finnish Cancer Organizations, University of Helsinki,
Helsinki University Central Hospital, Novo Nordisk Foundation, Paivikki
and Sakari Sohlberg Foundation, Sigrid Juselius Foundation, the
Cooperation Program, research area SURG and National Institute for
Cancer Research-NICR (Program EXCELES, ID Project No. LX22NPO5102),
funded by the European Union-Next Generation EU.
CR Abdel-Rahman Omar, 2017, J Evid Based Med, V10, P245, DOI 10.1111/jebm.12270
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Baumeister SE, 2019, JNCI-J NATL CANCER I, V111, P1142, DOI 10.1093/jnci/djz111
Castro FA, 2014, CLIN GASTROENTEROL H, V12, P1038, DOI 10.1016/j.cgh.2013.11.007
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Henriksson M, 2020, BJS OPEN, V4, P109, DOI 10.1002/bjs5.50226
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2012, IARC Monogr Eval Carcinog Risks Hum, V100, P9
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Leone V, 2021, TRENDS CANCER, V7, P606, DOI 10.1016/j.trecan.2021.01.012
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Villanueva A, 2019, NEW ENGL J MED, V380, P1450, DOI 10.1056/NEJMra1713263
Yi MS, 2022, EUR J CLIN PHARMACOL, V78, P647, DOI 10.1007/s00228-021-03247-1
NR 37
TC 10
Z9 11
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD MAR 15
PY 2023
VL 152
IS 6
BP 1107
EP 1114
DI 10.1002/ijc.34308
EA OCT 2022
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8C1XU
UT WOS:000865465500001
PM 36196489
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Lee, CW
Chen, HY
Tsai, PH
Lee, WC
Wang, CC
Yu, MC
Chen, CW
Lin, PT
Chen, BH
Wang, SF
Chai, PM
Tsai, HI
AF Lee, Chao-Wei
Chen, Hsing-Yu
Tsai, Ping-Han
Lee, Wei-Chen
Wang, Chih-Chi
Yu, Ming-Chin
Chen, Chun-Wei
Lin, Po-Ting
Chen, Bo-Huan
Wang, Sheng-Fu
Chai, Pei-Mei
Tsai, Hsin-I.
TI Does autoimmune disease impair the survival of hepatocellular carcinoma
patients undergoing liver resection? A multi-institutional observational
study
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Autoimmune disease; Chang Gung Research Database; Hepatocellular
carcinoma; Liver resection
ID CANCER; DERMATOMYOSITIS; POLYMYOSITIS; RISK
AB BackgroundPatients with autoimmune diseases (AD) generally carry an increased risk of developing cancer. However, the effect of AD in hepatocellular carcinoma (HCC) patients receiving surgical treatment is uncertain. The present study aimed to investigate the potential influence of AD on the survival of HCC patients undergoing hepatectomies.MethodsOperated HCC patients were identified from the Chang Gung Research Database, and the survival outcomes of HCC patients with or without AD were analyzed ad compared. Cox regression model was performed to identify significant risk factors associated with disease recurrence and mortality.ResultsFrom 2002 to 2018, a total of 5532 patients underwent hepatectomy for their HCC. Among them, 229 patients were identified to have AD and 5303 were not. After excluding cases who died within 30 days of surgery, the estimated median overall survival (OS) was 43.8 months in the AD (+) group and 47.4 months in the AD (-) group (P = 0.367). The median liver-specific survival and disease-free survival (DFS) were also comparable between the two groups. After Cox regression multivariate analysis, the presence of AD did not lead to a higher risk of all-cause mortality, liver-specific mortality, or disease recurrence.ConclusionOur study demonstrated that autoimmune disease does not impair the OS and DFS of HCC patients undergoing liver resections. AD itself is not a risk factor for tumor recurrence after surgery. Patients eligible for liver resections, as a result, should be considered for surgery irrespective of the presence of AD. Further studies are mandatory to validate our findings.
C1 [Lee, Chao-Wei; Lee, Wei-Chen] Linkou Chang Gung Mem Hosp, Dept Surg, Div Gen Surg, Taoyuan, Taiwan.
[Lee, Chao-Wei; Chen, Hsing-Yu; Lee, Wei-Chen; Yu, Ming-Chin; Chen, Chun-Wei; Lin, Po-Ting; Chen, Bo-Huan; Wang, Sheng-Fu; Tsai, Hsin-I.] Chang Gung Univ, Coll Med, Taoyuan, Taiwan.
[Lee, Chao-Wei; Yu, Ming-Chin; Tsai, Hsin-I.] Chang Gung Univ, Grad Inst Clin Med Sci, Taoyuan, Taiwan.
[Chen, Hsing-Yu] Taoyuan Chang Gung Mem Hosp, Ctr Tradit Chinese Med, Div Chinese Internal Med, Taoyuan, Taiwan.
[Chen, Hsing-Yu] Chang Gung Univ, Coll Med, Sch Tradit Chinese Med, Taoyuan, Taiwan.
[Tsai, Ping-Han] New Taipei Municipal Tucheng Hosp, Dept Internal Med, Div Rheumatol Allergy & Immunol, New Taipei, Taiwan.
[Wang, Chih-Chi] Kaohsiung Chang Gung Mem Hosp, Dept Surg, Div Gen Surg, Kaohsiung, Taiwan.
[Yu, Ming-Chin] New Taipei Municipal Tu Cheng Hosp, Built & Operated Chang Gung Med Fdn, Dept Surg, New Taipei, Taiwan.
[Chen, Chun-Wei; Lin, Po-Ting; Chen, Bo-Huan; Wang, Sheng-Fu] Linkou Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, Taoyuan, Taiwan.
[Chai, Pei-Mei] Linkou Chang Gung Mem Hosp, Dept Nursing, Taoyuan, Taiwan.
[Tsai, Hsin-I.] Linkou Chang Gung Mem Hosp, Dept Anesthesiol, 5 Fuxing St, Taoyuan 33305, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; Chang Gung
University; Chang Gung Memorial Hospital; Chang Gung University; Chang
Gung Memorial Hospital; Chang Gung Memorial Hospital; Chang Gung
Memorial Hospital; Chang Gung Memorial Hospital
RP Tsai, HI (corresponding author), Chang Gung Univ, Coll Med, Taoyuan, Taiwan.; Tsai, HI (corresponding author), Chang Gung Univ, Grad Inst Clin Med Sci, Taoyuan, Taiwan.; Tsai, HI (corresponding author), Linkou Chang Gung Mem Hosp, Dept Anesthesiol, 5 Fuxing St, Taoyuan 33305, Taiwan.
EM alanchaoweilee@hotmail.com; b8705016@gmail.com; s001033@gmail.com;
weichen@cgmh.org.tw; ufel4996@ms26.hinet.net; mingchin2000@gmail.com;
8902088@cgmh.org.tw; linpoting0101@gmail.com; spring03258@gmail.com;
shanelily@msn.com; p22015@cgmh.org.tw; tsaic@hotmail.com
RI Huang, James/ADK-6342-2022; Li, Chen/GPX-2756-2022; Chen,
Hsing-yu/C-3979-2011; Chen, Chi/F-4649-2012; 陈, 雨薇/HKF-1175-2023
OI Chen, Hsing-Yu/0000-0001-7897-9851; Tsai, Ping-Han/0000-0002-8134-9022
FU Chang Gung Memorial Hospital, Linkou; Kaohsiung Chang Gung Memorial
Hospitals; Department of Cancer Center, Linkou Chang Gung Memorial
Hospital, and Graduate Institute of Clinical Medical Sciences, Chang
Gung University
FX We are grateful to all our colleagues in the Division of General
Surgery, Department of Surgery, Linkou, Keelung, Chiayi, and Kaohsiung
Chang Gung Memorial Hospitals for patient care and data maintenance. We
also appreciate the support from Department of Cancer Center, Linkou
Chang Gung Memorial Hospital, and Graduate Institute of Clinical Medical
Sciences, Chang Gung University for their technical assistance.
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NR 57
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD JUL 20
PY 2024
VL 150
IS 7
AR 354
DI 10.1007/s00432-024-05885-1
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZC7W7
UT WOS:001273168100002
PM 39031214
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Wong, RJ
Gish, R
Frederick, T
Bzowej, N
Frenette, C
AF Wong, Robert J.
Gish, Robert
Frederick, Todd
Bzowej, Natalie
Frenette, Catherine
TI Development of Hepatocellular Carcinoma in Autoimmune Hepatitis
Patients: A Case Series
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Hepatocellular carcinoma screening; Liver cancer surveillance;
Autoimmune hepatitis with cirrhosis; Autoimmune hepatitis epidemiology
ID PRIMARY BILIARY-CIRRHOSIS; VIRUS-RELATED CIRRHOSIS; C VIRUS; B-VIRUS;
CANCER-RISK; FOLLOW-UP; HEMOCHROMATOSIS; MANAGEMENT; PROGNOSIS; COHORT
AB The risk of hepatocellular carcinoma (HCC) among patients with autoimmune hepatitis (AIH) is believed to be low compared with other chronic liver diseases, and uncertainty exists over the need to perform HCC surveillance. If surveillance is initiated, the optimal timing is also not yet defined.
The aim of the study was to investigate the prevalence of HCC among AIH patients.
This was a retrospective study analyzing patient data from 1999 to 2009 in a large tertiary-care community hospital to assess the prevalence of HCC among AIH patients.
Among 322 AIH cases, cancer screening identified six patients that developed HCC (prevalence: 459 per 100,000 patient-years). All six patients were extracted from the subset of AIH patients with cirrhosis (n = 50), resulting in a prevalence of 1,920 per 100,000 patient-years. In the AIH with HCC cohort, mean age of AIH diagnosis was 51.8 years (range, 24-70) and mean age of HCC diagnosis was 60.0 years (range, 37-71). The mean interval between diagnosis of AIH and HCC was 10.0 years. Three patients had AJCC stage a parts per thousand yen2 cancer at diagnosis, and two had BCLC stage B or C.
The risk of HCC among AIH patients with cirrhosis is 1.9% per year. This is comparable to HCC risk among patients with cirrhosis secondary to HBV, HCV, hemochromatosis, or alcohol-related liver disease. Although this data needs to be confirmed in prospective studies, routine cancer screening and surveillance among this cohort for early detection and treatment should be conducted.
C1 [Wong, Robert J.] Calif Pacific Med Ctr, Dept Med, San Francisco, CA 94115 USA.
[Gish, Robert; Frederick, Todd; Bzowej, Natalie; Frenette, Catherine] Calif Pacific Med Ctr, Dept Liver Dis & Transplant Hepatol, San Francisco, CA 94115 USA.
C3 California Pacific Medical Center; California Pacific Medical Center
RP Wong, RJ (corresponding author), Calif Pacific Med Ctr, Dept Med, 2351 Clay St,Suite 380, San Francisco, CA 94115 USA.
EM RobertWong123@gmail.com
RI Frederick, Todd/KDP-1717-2024; Gish, Robert/B-3605-2018
OI Frenette, Catherine/0000-0002-2245-8173; Gish,
Robert/0000-0001-6306-3189; Wong, Robert/0000-0002-8923-2806; Frederick,
R. Todd/0000-0002-2153-3194
CR Al-Chalabi T, 2008, J HEPATOL, V48, P140, DOI 10.1016/j.jhep.2007.08.013
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[Anonymous], MMWR
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NR 33
TC 51
Z9 51
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD FEB
PY 2011
VL 56
IS 2
BP 578
EP 585
DI 10.1007/s10620-010-1444-6
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 712KF
UT WOS:000286664900041
PM 21046244
DA 2025-01-07
ER
PT J
AU Watanabe, T
Soga, K
Hirono, H
Hasegawa, K
Shibasaki, K
Kawai, H
Aoyagi, Y
AF Watanabe, Takuya
Soga, Kenji
Hirono, Haruka
Hasegawa, Katsuhiko
Shibasaki, Koichi
Kawai, Hirokazu
Aoyagi, Yutaka
TI Features of hepatocellular carcinoma in cases with autoimmune hepatitis
and primary biliary cirrhosis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune hepatitis; Autoimmune liver disease; Hepatocellular
carcinoma; Literature review; Primary biliary cirrhosis
ID C VIRUS; CANCER; INFECTION; SURVIVAL; JAPAN
AB AIM: To characterize the clinical features of hepatocellular carcinoma (HCC) associated with autoimmune liver disease, we critically evaluated the literature on HCC associated with autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC).
METHODS: A systematic review of the literature was conducted using the Japana Centra Revuo Medicina database which produced 38 cases of HCC with AIH (AIH-series) and 50 cases of HCC with PBC (PBC-series). We compared the clinical features of these two sets of patients with the general Japanese HCC population.
RESULTS: On average, HCC was more common in men than in women with AIH or PBC. While many patients underwent chemolipiodolization (CL) or transcatheter arterial embolization (TAE) (AIH-series: P = 0.048 (vs operation), P = 0.018 (vs RFA, PEIT); PBC-series: P = 0.027 (vs RFA, PEIT), others refused therapeutic interventions [AIH-series: P = 0.038 (vs RFA, PEIT); PBC-series: P = 0.003 (vs RFA, PEIT)]. Liver failure was the primary cause of death among patients in this study, followed by tumor rupture. The survival interval between diagnosis and death was fairly short, averaging 14 +/- 12 mo in AIH patients and 8.4 +/- 14 mo in PBC patients.
CONCLUSION: We demonstrated common clinical features among Japanese cases of HCC arising from AIH and PBC. (c) 2009 The WIG Press and Baishideng. All rights reserved.
C1 [Watanabe, Takuya; Soga, Kenji; Hirono, Haruka; Hasegawa, Katsuhiko; Shibasaki, Koichi] Nippon Dent Univ, Sch Life Dent Niigata, Hosp Med, Dept Internal Med & Gastroenterol,Chuo Ku, Niigata 9518580, Japan.
[Kawai, Hirokazu; Aoyagi, Yutaka] Niigata Univ, Grad Sch Med & Dent Sci, Dept Gastroenterol, Chou Ku, Niigata 9518510, Japan.
C3 Nippon Dental University; Niigata University
RP Watanabe, T (corresponding author), Nippon Dent Univ, Sch Life Dent Niigata, Hosp Med, Dept Internal Med & Gastroenterol,Chuo Ku, 1-8 Hamauracho, Niigata 9518580, Japan.
EM nabetaku@dia-net.ne.jp
FU Ministry of Education, Science, Sports and Culture of Japan
FX Supported by A grant-in-aid from the Ministry of Education, Science,
Sports and Culture of Japan
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NR 34
TC 18
Z9 20
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JAN 14
PY 2009
VL 15
IS 2
BP 231
EP 239
DI 10.3748/wjg.15.231
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 398NS
UT WOS:000262739400016
PM 19132775
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Sy, AM
Ferreira, RD
John, BV
AF Sy, Alexander M.
Ferreira, Raphaella D.
V. John, Binu
TI Hepatocellular Carcinoma in Primary Biliary Cholangitis
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Cirrhosis; Autoimmune liver disease; Epidemiology; Primary liver cancer
ID CLINICAL-PRACTICE GUIDELINES; DIABETES-MELLITUS INCREASES; RISK-FACTORS;
HEPATITIS-C; EXTRAHEPATIC MALIGNANCIES; AUTOIMMUNE HEPATITIS; CIRRHOSIS;
MANAGEMENT; SURVIVAL; PROGRESSION
AB Several studies have shown PBC to confer increased risk to develop HCC. Parameters recognized as risk factors for the development of HCC in PBC include advanced age, male sex, and comorbidities. Advanced liver fibrosis is the most significant risk factor. Moreover, future studies should aim to clarify the role of treatment response as a risk factor for HCC development in PBC patients. To date, the only indication for HCC screening that is agreed on by all scientific societies is in patients with cirrhosis. HCC in PBC carries a poor prognosis compared with other chronic liver diseases with HCC, and liver transplantation offers the best survival rate among available therapies.
C1 [Sy, Alexander M.; Ferreira, Raphaella D.; V. John, Binu] Univ Miami, Miller Sch Med, Dept Med, Miami VA Med Syst,Div Hepatol, 1201 Northwest 16th St, Miami, FL 33125 USA.
[Sy, Alexander M.] Florida Int Univ, Herbert Wertheim Coll Med, Dept Translat Med, Miami, FL 33199 USA.
C3 University of Miami; State University System of Florida; Florida
International University
RP Sy, AM (corresponding author), Univ Miami, Miller Sch Med, Dept Med, Miami VA Med Syst,Div Hepatol, 1201 Northwest 16th St, Miami, FL 33125 USA.; Sy, AM (corresponding author), Florida Int Univ, Herbert Wertheim Coll Med, Dept Translat Med, Miami, FL 33199 USA.
EM alexander.sy3@va.gov
OI Ferreira, Raphaella/0000-0003-4990-4839
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NR 49
TC 14
Z9 15
U1 0
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD NOV
PY 2022
VL 26
IS 4
BP 691
EP 704
DI 10.1016/j.cld.2022.06.011
EA OCT 2022
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 5V4EJ
UT WOS:000877183600010
PM 36270724
DA 2025-01-07
ER
PT J
AU Tadokoro, T
Nomura, T
Fujita, K
Manabe, T
Takuma, K
Nakahara, M
Oura, K
Mimura, S
Tani, J
Morishita, A
Kobara, H
Ono, M
Masaki, T
AF Tadokoro, Tomoko
Nomura, Takako
Fujita, Koji
Manabe, Takushi
Takuma, Kei
Nakahara, Mai
Oura, Kyoko
Mimura, Shima
Tani, Joji
Morishita, Asahiro
Kobara, Hideki
Ono, Masafumi
Masaki, Tsutomu
TI Management of hepatocellular carcinoma, an important cause of death in
Japanese autoimmune hepatitis patients
SO BMC GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune hepatitis; Hepatocellular carcinoma; Molecular-targeted drug;
Immune checkpoint inhibitor; Carcinogenic factor
ID CRITERIA; DIAGNOSIS; SURVIVAL; CANCER
AB Background: Hepatocellular carcinoma (HCC) in autoimmune hepatitis (AIH) was considered rare but is increasing with prolonged prognosis. Its impact on the overall prognosis of AIH is unknown, and treatment has not been established. Aim: To investigate the risk factors and prognosis of HCC in patients with AIH and identify appropriate management strategies. Methods: We studied patients with AIH including background liver disease, sex, age, complications, treatment, response to treatment, liver fibrosis, prognosis, and treatment. Results: In 131 patients, deaths due to liver failure were more common early after the onset of AIH; however, deaths due to HCC increased gradually. HCC was observed in 12 patients (median age, 70 years; male/female, 4/8; cirrhosis at onset, 11; median time to carcinogenesis, 7 years). Cirrhosis at diagnosis was identified as a risk factor for carcinogenesis in the multivariate analysis (odds ratio, 41.36; p < 0.0001) and cumulative cancer rates were high. Multidisciplinary therapy other than immune checkpoint inhibitors was administered as treatment for HCC. Two of the three patients who used molecular-targeted drugs discontinued the treatment because of adverse events. Conclusion: HCC is an important cause of death in patients with AIH. Currently available drug therapies are limited and early detection is desirable.
C1 [Tadokoro, Tomoko; Nomura, Takako; Fujita, Koji; Manabe, Takushi; Takuma, Kei; Nakahara, Mai; Oura, Kyoko; Mimura, Shima; Tani, Joji; Morishita, Asahiro; Kobara, Hideki; Ono, Masafumi; Masaki, Tsutomu] Kagawa Univ, Sch Med, Dept Gastroenterol & Neurol, 1750-1 Ikenobe, Miki, Kagawa 7610793, Japan.
[Nomura, Takako] HITO Med Ctr, Gastroenterol & Hepatol, 788-1 Kamibun Cho, Shikokutyuou, Ehime 7990121, Japan.
[Ono, Masafumi] Kagawa Univ, Fac Med, Div Innovat Med Hepatobiliary & Pancreatol, Sch Med, 1750-1 Ikenobe, Miki, Kagawa 7610793, Japan.
C3 Kagawa University; Kagawa University
RP Tadokoro, T (corresponding author), Kagawa Univ, Sch Med, Dept Gastroenterol & Neurol, 1750-1 Ikenobe, Miki, Kagawa 7610793, Japan.
EM tadokoro.tomoko@kagawa-u.ac.jp
RI Fujita, Koji/X-4478-2019; Ono, Masafumi/IAO-3441-2023; Nomura,
Takako/LFT-3521-2024
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Z9 1
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD APR 1
PY 2024
VL 24
IS 1
AR 123
DI 10.1186/s12876-024-03204-z
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA MS5T8
UT WOS:001195643200002
PM 38561671
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Li, H
Hu, PB
Zou, YJ
Yuan, LJ
Xu, YC
Zhang, XH
Luo, XY
Zhang, ZQ
AF Li, Hu
Hu, Pengbo
Zou, Yajun
Yuan, Lijuan
Xu, Yucheng
Zhang, Xiaohui
Luo, Xiaoyan
Zhang, Zhiqiang
TI Tanshinone IIA and hepatocellular carcinoma: A potential therapeutic
drug
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE Hepatocellular carcinoma; tanshinone IIA; liver fibrosis; nonalcoholic
fatty liver disease (NAFLD); MAPK; rapamycin (mTOR)
ID FATTY LIVER-DISEASE; NF-KAPPA-B; HEPATIC STELLATE CELLS;
SALVIA-MILTIORRHIZA; SIGNALING PATHWAY; IN-VITRO; INSULIN-RESISTANCE;
OXIDATIVE STRESS; MESENCHYMAL TRANSITION; GROWTH
AB Because of its high prevalence and poor long-term clinical treatment effect, liver disease is regarded as a major public health problem around the world. Among them, viral hepatitis, fatty liver, cirrhosis, non-alcoholic fatty liver disease (NAFLD), and autoimmune liver disease are common causes and inducements of liver injury, and play an important role in the occurrence and development of hepatocellular carcinoma (HCC). Tanshinone IIA (TsIIA) is a fat soluble polyphenol of Salvia miltiorrhiza that is extracted from Salvia miltiorrhiza. Because of its strong biological activity (anti-inflammatory, antioxidant), it is widely used in Asia to treat cardiovascular and liver diseases. In addition, TsIIA has shown significant anti-HCC activity in previous studies. It not only has significant anti proliferation and pro apoptotic properties. It can also play an anti-cancer role by mediating a variety of signal pathways, including phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/rapamycin (mTOR), mitogen-activated protein kinase (MAPK), and nuclear factor kappa-B (NF-kappa B). This review not only reviews the existing evidence and molecular mechanism of TsIIA's anti-HCC effect but also reviews the liver-protective effect of TsIIA and its impact on liver fibrosis, NAFLD, and other risk factors for liver cancer. In addition, we also conducted network pharmacological analysis on TsIIA and HCC to further screen and explore the possible targets of TsIIA against hepatocellular carcinoma. It is expected to provide a theoretical basis for the development of anti-HCC-related drugs based on TsIIA.
C1 [Li, Hu; Hu, Pengbo; Yuan, Lijuan; Xu, Yucheng; Zhang, Xiaohui; Luo, Xiaoyan; Zhang, Zhiqiang] Binzhou Med Coll, Affiliated Hosp, Emergency Dept, Binzhou, Peoples R China.
[Hu, Pengbo; Zhang, Zhiqiang] Binzhou Med Univ, Inst Med Sci, Yantai, Peoples R China.
[Zou, Yajun] Anhui Med Univ, Affiliated Hosp 1, Emergency Dept, Hefei, Peoples R China.
C3 Binzhou Medical University; Binzhou Medical University; Anhui Medical
University
RP Zhang, ZQ (corresponding author), Binzhou Med Coll, Affiliated Hosp, Emergency Dept, Binzhou, Peoples R China.; Zhang, ZQ (corresponding author), Binzhou Med Univ, Inst Med Sci, Yantai, Peoples R China.
EM zhangzq678@gmail.com
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OI Zhang, Zhiqiang/0000-0002-7779-2937
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NR 190
TC 10
Z9 10
U1 4
U2 12
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JAN 31
PY 2023
VL 13
AR 1071415
DI 10.3389/fonc.2023.1071415
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8X6WC
UT WOS:000932150900001
PM 36798821
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Tarao, K
Nozaki, A
Ikeda, T
Sato, A
Komatsu, H
Komatsu, T
Taguri, M
Tanaka, K
AF Tarao, Kazuo
Nozaki, Akito
Ikeda, Takaaki
Sato, Akira
Komatsu, Hirokazu
Komatsu, Tatsuji
Taguri, Masataka
Tanaka, Katsuaki
TI Real impact of liver cirrhosis on the development of hepatocellular
carcinoma in various liver diseases-meta-analytic assessment
SO CANCER MEDICINE
LA English
DT Article
DE hepatocellular carcinoma; liver cirrhosis; liver diseases;
meta-analysis; risk of HCC
ID HEPATITIS-C VIRUS; PRIMARY BILIARY-CIRRHOSIS; SERUM ALANINE
AMINOTRANSFERASE; TERM-FOLLOW-UP; POPULATION-BASED COHORT; INCREASED
CANCER-RISK; B-VIRUS; AUTOIMMUNE HEPATITIS; INTERFERON THERAPY;
NATURAL-HISTORY
AB Background It is well known that the incidence of developing hepatocelluler carcinoma (HCC) is increased in liver cirrhosis of different etiologies. However, comparison of HCC incidence in various liver diseases has not yet been estimated. We surveyed this comparison. Methods The PubMed database was examined (1989-2017) for studies published in English language regarding the prospective follow-up results for the development of HCC in various liver diseases. A meta-analysis was performed for each liver disease. Results The annual incidence (%) of HCC in the non-cirrhotic stage and cirrhotic stage, and the ratio of HCC incidence in the cirrhotic stage/non-cirrhotic stage were as follows. (a) hepatitis B virus liver disease: 0.37%-> 3.23% (8.73-fold), (b) hepatitis C virus liver diseases: 0.68%-> 4.81% (7.07-fold), (c) primary biliary cholangitis (0.26%-> 1.79%, 6.88-fold), (d) autoimmune hepatitis (0.19%-> 0.53%, 2.79-fold), and (e) NASH (0.03%-> 1.35%, 45.00-fold). Regarding primary hemochromatosis and alcoholic liver diseases, only follow-up studies in the cirrhotic stage were presented, 1.20% and 2.06%, respectively. Conclusions When the liver diseases advance to cirrhosis, the incidence of HCC is markedly increased. The development of HCC must be closely monitored by ultrasonography, magnetic resonance imaging, and computed tomography, irrespective of the different kinds of liver diseases.
C1 [Tarao, Kazuo] Taraos Gastroenterol Clin, Yokohama, Kanagawa, Japan.
[Nozaki, Akito] Yokohama City Univ, Gastroenterol Ctr, Med Ctr, Yokohama, Kanagawa, Japan.
[Ikeda, Takaaki] Yokosuka Gen Hosp Uwamachi, Gastroenterol Dept, Yokosuka, Kanagawa, Japan.
[Sato, Akira] St Marianna Univ, Yokohama City Scibu Hosp, Dept Internal Med, Div Gastroenterol, Yokohama, Kanagawa, Japan.
[Komatsu, Hirokazu] Yokohama Municipal Citizens Hosp, Dept Gastroenterol, Yokohama, Kanagawa, Japan.
[Komatsu, Tatsuji] Yokohama Med Ctr, Natl Hosp Org, Dept Clin Res, Yokohama, Kanagawa, Japan.
[Taguri, Masataka] Yokohama City Univ, Dept Data Sci, Yokohama, Kanagawa, Japan.
[Tanaka, Katsuaki] Hatano Red Cross Hosp, Hadano, Kanagawa, Japan.
C3 Yokohama City University; Saint Marianna University; Yokohama City
University
RP Tarao, K (corresponding author), Taraos Gastroenterol Clin, Asahi Ku, Yokohama, Kanagawa, Japan.
EM nrg18449@nifty.com
RI Nozaki, Akito/AAT-3562-2021
OI Nozaki, Akito/0000-0002-3310-6632
FU Kanagawa Association of Medical and Dental Practitioners
FX This work was supported by the Kanagawa Association of Medical and
Dental Practitioners.
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NR 133
TC 104
Z9 112
U1 1
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD MAR
PY 2019
VL 8
IS 3
BP 1054
EP 1065
DI 10.1002/cam4.1998
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HQ3YX
UT WOS:000462347500020
PM 30791221
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Ugonabo, O
Pulipati, Y
Elghezewi, A
Miller, V
Logan, L
Pramod, P
AF Ugonabo, Onyinye
Pulipati, Yochita
Elghezewi, Adnan
Miller, Virginia
Logan, Lawrence
Pramod, Pantangi
TI An Unusual Case of Hepatocellular Carcinoma in a Healthy Teenager
SO JOURNAL OF INVESTIGATIVE MEDICINE HIGH IMPACT CASE REPORTS
LA English
DT Article
DE gastroenterology; hematology oncology
ID LIVER
AB Hepatocellular carcinoma (HCC) is a primary liver malignancy known to occur majorly in patients with liver cirrhosis or those with a harbinger of risk factors like viral hepatitis, autoimmune liver disease, alpha-1 antitrypsin deficiency, alcoholic liver disease, and nonalcoholic fatty liver disease. The incidence of HCC has risen in the past 2 decades and currently ranks as the sixth most common cause of cancer-related death worldwide. Most cases are seen in adulthood, and only a very small percentage have been reported in adolescents with risk factors. The 2 pathologic subtypes of pediatric HCC are classic and fibrolamellar. Here, we discussed a very interesting rare case of a healthy male teenager with no apparent liver disease or risk factor who presented with right-upper-quadrant pain, normal alpha-fetoprotein level, and abdominal ultrasound showing a large hepatic mass. A liver biopsy was positive for HCC with fluorescent in situ hybridization showing a PRKACA complex gene pattern, favoring the fibrolamellar type.
C1 [Ugonabo, Onyinye; Elghezewi, Adnan; Miller, Virginia; Logan, Lawrence; Pramod, Pantangi] Marshall Univ, Huntington, WV USA.
[Pulipati, Yochita] Kakatiya Med Coll, Warangal, India.
[Ugonabo, Onyinye] Marshall Univ, Joan C Edwards Sch Med, Internal Med Residency Program, 1249 15th St,Suite 2000, Huntington, WV 25701 USA.
C3 Marshall University; Kakatiya Medical College; Marshall University
RP Ugonabo, O (corresponding author), Marshall Univ, Joan C Edwards Sch Med, Internal Med Residency Program, 1249 15th St,Suite 2000, Huntington, WV 25701 USA.
EM onyinyeugonabo99x@gmail.com
CR Abdelhamed W, 2022, WORLD J GASTRO ONCOL, V14, P1103, DOI 10.4251/wjgo.v14.i6.1103
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NR 12
TC 1
Z9 1
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 2324-7096
J9 J INVEST MED HIGH IM
JI J. Invest. Med. High Impact Case Rep.
PY 2023
VL 11
AR 23247096231165744
DI 10.1177/23247096231165744
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA E8WW6
UT WOS:000978290500001
PM 37119001
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Albishi, AM
Alshahrani, A
Alshahrani, AM
Alahmari, DM
Alqibti, HM
Alsharif, MA
Alshahrani, SM
Alqahtani, MS
Alqahtani, IAS
AF Albishi, Abdullah Mohammed
Alshahrani, Abdulaziz
Alshahrani, Ali Mohammed
Alahmari, Dhafer Mohammed
Alqibti, Hussain Mesfer
Alsharif, Mohammed Ahmed
Alshahrani, Saeed Mohammed
Alqahtani, Mohammed Saeed
Alqahtani, Ibrahim Ayed Saad
TI Public Awareness of Hepatocellular Carcinoma and its Risk Factors Among
General Population in Southern Region, Saudi Arabia, Cross Sectional
Study
SO INTERNATIONAL JOURNAL OF MEDICAL RESEARCH & HEALTH SCIENCES
LA English
DT Article
DE Hepatocellular carcinoma; Liver; cancer; Malignancy; Awareness;
Population; Cirrhosis; Fibrosis
ID LIVER-CANCER
AB Background: Globally, Hepatocellular carcinoma (HCC) is the third leading cause of cancer related mortality. There are many reported causes of HCC including chronic Hepatitis B virus (HBV), Hepatitis C virus (HCV) infection, primary autoimmune hepatitis, hemochromatosis, Budd-Chiari syndrome, and chronic alcohol consumption, which mostly result in liver cirrhosis. Fibrosis and cirrhosis are typically antecedents of HCC. Lack of population awareness may be by itself risk factors for disease and its sequalae. Aim: To assess the general population awareness regarding hepatocellular carcinoma and its risk factors in Southern region, southern of Saudi Arabia. Methodology: A descriptive cross-sectional survey was used targeting all population in Southern region, Saudi Arabia. The study was conducted during the period from February 2020 to May 2020. Data were collected using structured questionnaire included person's socio-demographic data, Participants' awareness regarding HCC. The questionnaire was uploaded online using social media platforms. Results: The study included a total of 956 participants whose ages ranged from 18 to 65 years old with mean age of 31.5 +/- 8.6 years old. Exact of 149 (15.6%) participants had positive family history of liver cancer and 157 (16.4%) had family history of liver cirrhosis. Exact of 78.7% of the respondents reported that they know about liver cancer and 75.2% know about liver cirrhosis. In total, good awareness level regarding liver cirrhosis and cancer was low. Conclusions and recommendations: The study revealed that public awareness regarding HCC and its risk factors were low especially for signs and symptoms which are the early alarming noise for having liver disorder. Health care staff was not the main source of knowledge regarding HCC and liver cirrhosis.
C1 [Albishi, Abdullah Mohammed] Armed Forces Hosp, Khamis Mushayt, Saudi Arabia.
[Alshahrani, Abdulaziz] Najran Univ, Dept Med, Najran, Saudi Arabia.
[Alshahrani, Ali Mohammed] Armed Forces Med Serv Gen Directorate, Riyadh, Saudi Arabia.
[Alahmari, Dhafer Mohammed; Alqibti, Hussain Mesfer; Alsharif, Mohammed Ahmed; Alshahrani, Saeed Mohammed; Alqahtani, Mohammed Saeed; Alqahtani, Ibrahim Ayed Saad] King Khalid Univ, Abha, Saudi Arabia.
C3 Prince Sultan Military Medical City; Najran University; King Khalid
University
RP Albishi, AM (corresponding author), Armed Forces Hosp, Khamis Mushayt, Saudi Arabia.
EM dr.abdullah6975@gmail.com
RI Alqahtani, Ibrahim/ISB-0365-2023; Al-Qahtani, Mohammed/AAZ-1729-2020
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NR 20
TC 0
Z9 0
U1 0
U2 1
PU SUAMTHI PUBLICATIONS
PI AHMEDNAGAR
PA SUAMTHI PUBLICATIONS, AHMEDNAGAR, 00000, INDIA
SN 2319-5886
J9 INT J MED RES HEALTH
JI Int. J. Med. Res. Health Sci.
PY 2020
VL 9
IS 11
BP 46
EP 53
PG 8
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA PH5DE
UT WOS:000600432300007
DA 2025-01-07
ER
PT J
AU Floreani, A
Gabbia, D
De Martin, S
AF Floreani, Annarosa
Gabbia, Daniela
De Martin, Sara
TI Current Perspectives on the Molecular and Clinical Relationships between
Primary Biliary Cholangitis and Hepatocellular Carcinoma
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE PBC; liver cancer; HCC; risk factors; HBV; HCV; UDCA; sex difference
ID URSODEOXYCHOLIC ACID; RISK-FACTORS; CANCER-RISK; BILE-ACIDS;
EXTRAHEPATIC MALIGNANCIES; AUTOIMMUNE HEPATITIS; GENDER DISPARITY;
LIVER-CANCER; FOLLOW-UP; CIRRHOSIS
AB Primary biliary cholangitis (PBC) is an autoimmune liver disease characterised by the immune-mediated destruction of small and medium intrahepatic bile ducts, with variable outcomes and progression. This review summarises the state of the art regarding the risk of neoplastic progression in PBC patients, with a particular focus on the molecular alterations present in PBC and in hepatocellular carcinoma (HCC), which is the most frequent liver cancer in these patients. Major risk factors are male gender, viral infections, e.g., HBV and HCV, non-response to UDCA, and high alcohol intake, as well as some metabolic-associated factors. Overall, HCC development is significantly more frequent in patients with advanced histological stages, being related to liver cirrhosis. It seems to be of fundamental importance to unravel eventual dysfunctional molecular pathways in PBC patients that may be used as biomarkers for HCC development. In the near future, this will possibly take advantage of artificial intelligence-designed algorithms.
C1 [Floreani, Annarosa] Univ Padua, I-35122 Padua, Italy.
[Floreani, Annarosa] Sci Consultant IRCCS Negrar, I-37024 Verona, Italy.
[Gabbia, Daniela; De Martin, Sara] Univ Padua, Dept Pharmaceut & Pharmacol Sci, I-35131 Padua, Italy.
C3 University of Padua; University of Padua
RP De Martin, S (corresponding author), Univ Padua, Dept Pharmaceut & Pharmacol Sci, I-35131 Padua, Italy.
EM annarosa.floreani@unipd.it; daniela.gabbia@unipd.it;
sara.demartin@unipd.it
RI De Martin, Sara/AAC-7396-2022; Gabbia, Daniela/J-9984-2019
OI DE MARTIN, SARA/0000-0001-6398-8237; GABBIA, DANIELA/0000-0003-2247-8227
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NR 128
TC 5
Z9 5
U1 3
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2024
VL 25
IS 4
AR 2194
DI 10.3390/ijms25042194
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA IS2T5
UT WOS:001168262600001
PM 38396870
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Hemminki, K
Sundquist, K
Sundquist, J
Försti, A
Liska, V
Hemminki, A
Li, XJ
AF Hemminki, Kari
Sundquist, Kristina
Sundquist, Jan
Forsti, Asta
Liska, Vaclav
Hemminki, Akseli
Li, Xinjun
TI Autoimmune diseases as comorbidities for liver, gallbladder, and biliary
duct cancers in Sweden
SO CANCER
LA English
DT Article
DE comorbidity; discharge data; hepatocellular cancer; immune disturbance;
risk factor
ID HEPATOCELLULAR-CARCINOMA; INFLAMMATION; IMMUNITY; SMOKING; RISK
AB BackgroundAutoimmune diseases are associated with many cancers but there is a lack of population-based studies with different autoimmune diseases that have a long follow-up. This is also true of hepatobiliary cancers, which include hepatocellular cancer (HCC) and rarer entities of gallbladder cancer (GBC), intra- and extrahepatic cholangiocarcinoma (iCCA and eCCA), and ampullary cancer. MethodsDiagnostic data on 43 autoimmune diseases were collected from the Swedish Inpatient Register from 1987 to 2018, and cancer data were derived from the national cancer registry from 1997 onward. Relative risks were expressed as standardized incidence ratios (SIRs). ResultsIn a population of 13.6 million, 1.1 million autoimmune diseases were diagnosed and subsequent hepatobiliary cancer was diagnosed in 3191 patients (17.2% of cancers). SIRs for HCC were 2.73 (men) and 2.86 (women), 3.74/1.96 for iCCA, 2.65/1.37 for GBC, 2.38/1.64 for eCCA, and 1.80/1.85 for ampullary cancer. Significant associations between autoimmune disease and HCC were observed for 13 autoimmune diseases, with the highest risks being for autoimmune hepatitis (48.92/73.53, men/women) and primary biliary cirrhosis (38.03/54.48). GBC was increased after six autoimmune diseases, with high SIRs for ulcerative colitis (12.22/3.24) and men with Crohn disease (9.16). These autoimmune diseases were also associated with a high risk of iCCA, which had seven other associations, and eCCA, which had five other associations. Ampullary cancer occurrence was increased after four autoimmune diseases. ConclusionAn autoimmune disease is a common precursor condition for hepatobiliary cancers. This calls for careful control of autoimmune disease symptoms in each patient and encouragement to practice a healthy lifestyle.
C1 [Hemminki, Kari; Liska, Vaclav] Charles Univ Prague, Fac Med, Biomed Ctr, Plzen, Czech Republic.
[Hemminki, Kari; Liska, Vaclav] Charles Univ Prague, Biomed Ctr Pilsen, Plzen, Czech Republic.
[Hemminki, Kari] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Hemminki, Kari; Sundquist, Kristina; Sundquist, Jan; Forsti, Asta; Li, Xinjun] Lund Univ, Ctr Primary Hlth Care Res, Malmo, Sweden.
[Sundquist, Kristina; Sundquist, Jan] Icahn Sch Med Mt Sinai, Dept Family Med & Community Hlth, Dept Populat Hlth Sci & Policy, New York, NY USA.
[Sundquist, Kristina; Sundquist, Jan] Shimane Univ, Ctr Community Based Healthcare Res & Educ CoHRE, Sch Med, Dept Funct Pathol, Matsue, Shimane, Japan.
[Forsti, Asta] Hopp Childrens Canc Ctr KiTZ, Heidelberg, Germany.
[Forsti, Asta] German Canc Consortium DKTK, German Canc Res Ctr DKFZ, Div Pediat Neurooncol, Heidelberg, Germany.
[Liska, Vaclav] Charles Univ Prague, Univ Hosp, Sch Med Pilsen, Dept Surg, Plzen, Czech Republic.
[Hemminki, Akseli] Univ Helsinki, Translat Immunol Res Program, Canc Gene Therapy Grp, Helsinki, Finland.
[Hemminki, Akseli] Helsinki Univ Hosp, Comprehens Canc Ctr, Helsinki, Finland.
C3 Charles University Prague; Charles University Prague; Helmholtz
Association; German Cancer Research Center (DKFZ); Lund University;
Icahn School of Medicine at Mount Sinai; Shimane University; Helmholtz
Association; German Cancer Research Center (DKFZ); University Hospital
Plzen; Charles University Prague; University of Helsinki; University of
Helsinki; Helsinki University Central Hospital
RP Hemminki, K (corresponding author), Charles Univ Prague, Fac Med Pilsen, Biomed Ctr, Plzen 30605, Czech Republic.
EM k.hemminki@dkfz.de
RI ; Liska, Vaclav/Q-4402-2017
OI Hemminki, Kari/0000-0002-2769-3316; Hemminki,
Akseli/0000-0001-7103-8530; Liska, Vaclav/0000-0002-5226-0280; Li,
Xinjun/0000-0002-5559-4657
FU European Union's Horizon 2020 research and innovation programme
[856620]; Swedish Research Council; Fourth Framework Programme [856620];
Swedish Research Council; Jane and Aatos Erkko Foundation; Finnish
Cancer Organizations; University of Helsinki; Helsinki University
Central Hospital; Novo Nordisk Foundation; Paivikki and Sakari Sohlberg
Foundation; Sigrid Juselius Foundation; Cooperation Program; Research
Area SURG; National Institute for Cancer Research; European
Union-NextGenerationEU [LX22NPO5102]
FX Fourth Framework Programme, Grant/Award Number: 856620; Swedish Research
Council; Jane and Aatos Erkko Foundation; Finnish Cancer
Organizations;University of Helsinki; Helsinki University Central
Hospital; Novo Nordisk Foundation; Paivikki and Sakari Sohlberg
Foundation; Sigrid Juselius Foundation; Cooperation Program; Research
Area SURG; National Institute for Cancer Research; LX22NPO5102; European
Union-NextGenerationEU
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NR 34
TC 0
Z9 0
U1 1
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD APR 15
PY 2023
VL 129
IS 8
BP 1227
EP 1236
DI 10.1002/cncr.34663
EA JAN 2023
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA A8AN1
UT WOS:000921655200001
PM 36715017
OA hybrid
DA 2025-01-07
ER
PT J
AU Gruden, G
Carucci, P
Barutta, F
Burt, D
Ferro, A
Rolle, E
Pinach, S
Abate, ML
Campra, D
Durazzo, M
AF Gruden, Gabriella
Carucci, Patrizia
Barutta, Federica
Burt, Davina
Ferro, Arianna
Rolle, Emanuela
Pinach, Silvia
Abate, Maria Lorena
Campra, Donata
Durazzo, Marilena
TI Serum levels of anti-heat shock protein 27 antibodies in patients with
chronic liver disease
SO CELL STRESS & CHAPERONES
LA English
DT Article
DE Anti-heat shock protein 27 antibodies; Hepatocellular carcinoma; Liver
cirrhosis; Chronic liver disease
ID HEPATOCELLULAR-CARCINOMA; HSP27; AUTOANTIBODIES; MACROPHAGES; ALCOHOL
AB Heat shock protein 27 (HSP27), an intracellular molecular chaperone, is involved in the pathogenesis of cancer by promoting both tumor cell proliferation and resistance to therapy. HSP27 is also present in the circulation and circulating HSP27 (sHSP27) can elicit an autoimmune response with production of antibodies. Levels of sHSP27 are enhanced in patients with hepatocellular carcinoma (HCC); it is, however, unknown whether changes in HSP27 antibody levels occur in patients with HCC and can be exploited as a circulating biomarker of HCC. Our aim was to assess the potential association between newly diagnosed HCC and serum anti-HSP27 antibody levels. In this cross-sectional study, anti-HSP27 antibody levels were measured in serum samples from 71 HCC patients, 80 subjects with chronic liver disease, and 38 control subjects by immunoenzymatic assay. Anti-HSP27 antibody levels did not differ significantly among groups. However, in patients with chronic active hepatitis/cirrhosis, anti-HSP27 levels were significantly higher in subjects with a positive history of alcoholism (p = 0.03). Our data do not support the hypothesis that anti-HSP27 antibody levels may help identify patients with HCC among subjects with chronic liver disease. However, our finding that alcohol-related liver disease is associated with higher anti-HSP27 levels is novel and deserves further investigations.
C1 [Gruden, Gabriella; Barutta, Federica; Burt, Davina; Ferro, Arianna; Pinach, Silvia; Durazzo, Marilena] Univ Turin, Dept Med Sci, Turin, Italy.
[Carucci, Patrizia; Rolle, Emanuela; Abate, Maria Lorena] Citta Salute & Sci, Dept Gastrohepatol, Turin, Italy.
[Campra, Donata] Citta Salute & Sci, Dept Surg, Turin, Italy.
C3 University of Turin; A.O.U. Citta della Salute e della Scienza di
Torino; A.O.U. Citta della Salute e della Scienza di Torino
RP Gruden, G (corresponding author), Univ Turin, Dept Med Sci, Turin, Italy.
EM gabriella.gruden@unito.it
RI Pinach, Silvia/AAC-7490-2022
OI GRUDEN, GABRIELLA/0000-0001-8906-9589; DURAZZO,
Marilena/0000-0003-2450-5911
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NR 33
TC 2
Z9 2
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1355-8145
EI 1466-1268
J9 CELL STRESS CHAPERON
JI Cell Stress Chaperones
PD JAN
PY 2021
VL 26
IS 1
BP 151
EP 157
DI 10.1007/s12192-020-01164-3
EA SEP 2020
PG 7
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA PF1MB
UT WOS:000566862400001
PM 32895883
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Hemminki, K
Sundquist, K
Sundquist, J
Foersti, A
Liska, V
Hemminki, A
Li, XJ
AF Hemminki, Kari
Sundquist, Kristina
Sundquist, Jan
Foersti, Asta
Liska, Vaclav
Hemminki, Akseli
Li, Xinjun
TI Population-Attributable Fractions of Personal Comorbidities for Liver,
Gallbladder, and Bile Duct Cancers
SO CANCERS
LA English
DT Article
DE hepatocellular carcinoma; comorbidity; risk factor; bile duct infection;
alcohol; viral infection
ID HEPATOCELLULAR-CARCINOMA; INFLAMMATION; TRENDS; RISK
AB Simple Summary Liver cancer is often used as a general term for cancers of the liver (hepatocellular carcinoma, HCC), the gallbladder, and the bile ducts. The well-known risk factors are alcohol and viral hepatitis, but these are risk factors of mainly HCC. For gallbladder cancer, gallstones are important risk factors, and for bile ducts, infections in the ducts are important. For all these cancers, autoimmune diseases and diabetes increase risk. This study shows that these risk factors, in combination, explain 50% or more of the causes of these cancers. The novelty of the present study was the use of national Swedish hospital records for potential risk factors (comorbidities) of hepatobiliary cancers and the estimation of subsequent risks of hepatobiliary cancers in these patients. The underlying mechanism for these cancers is a chronic infection which should be considered a marker of disease progression and a possible target for intervention. Background: We aim to estimate population-attributable fractions (PAF) for 13 comorbidities potentially predisposing to hepatobiliary cancer of hepatocellular carcinoma (HCC), gallbladder cancer (GBC), cancers of the intrahepatic and extrahepatic bile ducts (ICC and ECC), and ampullary cancer. Methods: Patients were identified from the Swedish Inpatient Register from 1987 to 2018 and cancers from the Swedish Cancer Registry from 1997 through 2018. PAFs were calculated for each comorbidity-associated cancer using a cohort study design. Results: For male HCC, the major individual comorbidities (PAF > 10) were diabetes, alcohol-related liver disease, and hepatitis C virus infection. For female HCC, diabetes and autoimmune diseases were important contributors. For female GBC, gallstone disease was an overwhelming contributor, with a PAF of 30.57%, which was also important for men. The overall PAF for male ICC was almost two times higher than the female one. For ECC and ampullary cancer, infection of bile ducts was associated with the highest PAF. Conclusions: The 13 comorbidities accounted for 50% or more of the potential etiological pathways of each hepatobiliary cancer except female ICC. The underlying convergent mechanism for these cancers may be chronic inflammation lasting for decades and thus offering possibilities for intervention and disease monitoring.
C1 [Hemminki, Kari; Liska, Vaclav] Charles Univ Prague, Fac Med, Biomed Ctr, Plzen 32300, Czech Republic.
[Hemminki, Kari; Liska, Vaclav] Charles Univ Prague, Biomed Ctr Pilsen, Plzen 32300, Czech Republic.
[Hemminki, Kari] German Canc Res Ctr, Div Canc Epidemiol, Neuenheimer Feld 580, D-69120 Heidelberg, Germany.
[Hemminki, Kari; Sundquist, Kristina; Sundquist, Jan; Foersti, Asta; Li, Xinjun] Lund Univ, Ctr Primary Hlth Care Res, S-20502 Malmo, Sweden.
[Sundquist, Kristina; Sundquist, Jan] Icahn Sch Med Mt Sinai, Dept Family Med & Community Hlth, New York, NY 10029 USA.
[Sundquist, Kristina; Sundquist, Jan] Shimane Univ, Ctr Community Based Healthcare Res & Educ CoHRE, Sch Med, Dept Funct Pathol, Izumo 6938501, Japan.
[Foersti, Asta] Hopp Childrens Canc Ctr KiTZ, D-69120 Heidelberg, Germany.
[Foersti, Asta] German Canc Res Ctr, German Canc Consortium DKTK, Div Pediat Neurooncol, D-69120 Heidelberg, Germany.
[Liska, Vaclav] Univ Hosp, Sch Med Pilsen, Dept Surg, Plzen 32300, Czech Republic.
[Hemminki, Akseli] Univ Helsinki, Translat Immunol Res Program, Canc Gene Therapy Grp, Helsinki 00290, Finland.
[Hemminki, Akseli] Helsinki Univ Hosp, Comprehens Canc Ctr, Helsinki 00290, Finland.
C3 Charles University Prague; Charles University Prague; Helmholtz
Association; German Cancer Research Center (DKFZ); Lund University;
Icahn School of Medicine at Mount Sinai; Shimane University; Helmholtz
Association; German Cancer Research Center (DKFZ); University Hospital
Plzen; University of Helsinki; University of Helsinki; Helsinki
University Central Hospital
RP Hemminki, K (corresponding author), Charles Univ Prague, Fac Med, Biomed Ctr, Plzen 32300, Czech Republic.; Hemminki, K (corresponding author), Charles Univ Prague, Biomed Ctr Pilsen, Plzen 32300, Czech Republic.; Hemminki, K (corresponding author), German Canc Res Ctr, Div Canc Epidemiol, Neuenheimer Feld 580, D-69120 Heidelberg, Germany.; Hemminki, K (corresponding author), Lund Univ, Ctr Primary Hlth Care Res, S-20502 Malmo, Sweden.
EM k.hemminki@dkfz.de; kristina.sundquist@med.lu.se;
jan.sundquist@med.lu.se; a.foersti@dkfz.de; xinjun.li@med.lu.se
RI ; Liska, Vaclav/Q-4402-2017
OI Hemminki, Kari/0000-0002-2769-3316; Hemminki,
Akseli/0000-0001-7103-8530; Li, Xinjun/0000-0002-5559-4657; Forsti,
Asta/0000-0002-9857-4728; Liska, Vaclav/0000-0002-5226-0280
FU European Union [856620]; Swedish Research Council; Jane and Aatos Erkko
Foundation; Sigrid Juselius Foundation; Novo Nordisk Foundation;
Pauml;ivikki and Sakari Sohlberg Foundation; European Union-Next
Generation EU; Finnish Cancer Organizations; University of Helsinki;
Helsinki University Central Hospital; Finnish Red Cross Blood Service;
National Institute for Cancer Research-NICR; [LX22NPO5102]
FX Supported by the European Union's Horizon 2020 research and innovation
program, grant No 856620 (Chaperon), the Swedish Research Council, Jane
and Aatos Erkko Foundation, Sigrid Juselius Foundation, Finnish Cancer
Organizations, University of Helsinki, Helsinki University Central
Hospital, Novo Nordisk Foundation, Paeivikki and Sakari Sohlberg
Foundation, Finnish Red Cross Blood Service, the Cooperation Program,
research area SURG and the National Institute for Cancer Research-NICR
(Programme EXCELES, ID Project No. LX22NPO5102), funded by the European
Union-Next Generation EU.
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Yi MS, 2022, EUR J CLIN PHARMACOL, V78, P647, DOI 10.1007/s00228-021-03247-1
NR 42
TC 3
Z9 3
U1 2
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2023
VL 15
IS 12
AR 3092
DI 10.3390/cancers15123092
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA K5UN0
UT WOS:001017091000001
PM 37370702
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Peeters, F
Dekervel, J
AF Peeters, Frederik
Dekervel, Jeroen
TI Considerations for individualized first-line systemic treatment in
advanced hepatocellular carcinoma
SO CURRENT OPINION IN PHARMACOLOGY
LA English
DT Article
ID ATEZOLIZUMAB PLUS BEVACIZUMAB; IMMUNE CHECKPOINT INHIBITORS; PREEXISTING
AUTOIMMUNE; MONOCLONAL-ANTIBODY; OPEN-LABEL; SORAFENIB; CANCER;
EFFICACY; SAFETY; DEATH
AB Primary liver cancer is the third most common cause of cancer -related death worldwide and hepatocellular carcinoma (HCC) accounts for approximately 80%-90% of all primary liver ma-lignancies. Until 2007, there was no effective treatment option available for patients diagnosed with advanced HCC, whereas today, both multireceptor tyrosine kinase inhibitors as well as immunotherapy combinations have entered clinical practice. The choice between the different options is a tailor-made de-cision to match the efficacy and safety data of the clinical trials with the specific patient and disease profile. This review pro-vides clinical stepstones to make an individualized decision for every patient with its specific tumor and liver characteristics in mind.
C1 [Peeters, Frederik; Dekervel, Jeroen] Univ Hosp Leuven, Digest Oncol, B-3000 Leuven, Belgium.
C3 KU Leuven; University Hospital Leuven
RP Dekervel, J (corresponding author), Univ Hosp Leuven, Digest Oncol, B-3000 Leuven, Belgium.
EM jeroen.dekervel@uzleuven.be
RI Peeters, Frederik/KHY-5010-2024; Dekervel, Jeroen/A-3582-2019
OI Peeters, Frederik/0000-0002-0081-4800; Dekervel,
Jeroen/0000-0001-7208-3480
CR A-Ag K, 2022, NEJM EVID
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NR 64
TC 6
Z9 6
U1 0
U2 2
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1471-4892
EI 1471-4973
J9 CURR OPIN PHARMACOL
JI Curr. Opin. Pharmacol.
PD JUN
PY 2023
VL 70
AR 102365
DI 10.1016/j.coph.2023.102365
EA MAR 2023
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA D0UI6
UT WOS:000965959200001
PM 36972646
DA 2025-01-07
ER
PT J
AU Athanassiadou, P
Psyhoyiou, H
Grapsa, D
Gonidi, M
Ketikoglou, I
Patsouris, E
AF Athanassiadou, Pauline
Psyhoyiou, Helen
Grapsa, Dimitra
Gonidi, Maria
Ketikoglou, Ioannis
Patsouris, Efstratios
TI Cytokeratin 8 and 18 expression in imprint smears of chronic viral
hepatitis, autoimmune hepatitis and hepatocellular carcinoma - A
preliminary study
SO ACTA CYTOLOGICA
LA English
DT Article
DE cytokeratin 8; cytokeratin 18; liver diseases; liver cancer; imprint
smears
ID KERATIN INTERMEDIATE-FILAMENTS; PRIMARY LIVER CARCINOMAS; HEPATOCYTES;
DISEASE; CYTOSKELETON; HEPATOTOXICITY; SUSCEPTIBILITY; IDENTIFICATION;
ANTIBODIES; MUTATIONS
AB Objective: To investigate whether the expression of cytokeratin (CK) 8 and 18 is altered in chronic active viral hepatitis, autoimmune hepatitis and hepatocellular carcinoma.
Study Design: Cytologic imprint smears were obtained from 53 liver core biopsy specimens and were studied immunocytochemically for the expression of CK8 and 18.
Results: CK8-positive expression was observed in 45.5% of chronic active hepatitis B (CH-B), 20% of chronic active hepatitis C (CH-C), 90% of autoimmune hepatitis (AIH) and 83.3% of hepatocellular carcinoma (HCC) cases. CK18-positive expression was observed in 36.4% of CH-B, 26.7% of CH-C, 70% of AIH and 83.3% of HCC cases. A statistically significant association was found between CK8- and CK18-positive expression and the diagnosis of AIH and HCC. In contrast, CH-C and CH-B were associated with negative CK8 and CK18 expression. In addition, a negative [CK8(-)/CK18(-)] or unbalanced [CK8(-)/CK18(+), CK8(+)/CK18(-)] expression pattern was found in 100.0% and 81.18% of CH-C and CH-B cases, respectively, while the relative percentages of AIH and HCC cases were significantly lower (30.0% and 16.7%, respectively) (p < 0.0001).
Conclusion: Our results indicate that CK8 and 18 expression is maintained in AIH and HCC and altered in CH-B and CH-C. The pathogenetic mechanism of this alteration remains to be clarified.
C1 Univ Athens, Sch Med, Pathol Lab, Cytol Unit, Athens 11527, Greece.
Hippokrateio Hosp, Clin Internal Med, Athens, Greece.
C3 Athens Medical School; National & Kapodistrian University of Athens
RP Grapsa, D (corresponding author), Univ Athens, Sch Med, Pathol Lab, Cytol Unit, 75 Mikras Asias Str, Athens 11527, Greece.
EM dimgrap@yahoo.gr
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NR 33
TC 10
Z9 13
U1 0
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0001-5547
EI 1938-2650
J9 ACTA CYTOL
JI Acta Cytol.
PD JAN-FEB
PY 2007
VL 51
IS 1
BP 61
EP 65
DI 10.1159/000325684
PG 5
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 129YP
UT WOS:000243766300012
PM 17328497
DA 2025-01-07
ER
PT J
AU Chagas, AL
Kikuchi, LOO
Oliveira, CPMS
Vezozzo, DCP
Mello, ES
Oliveira, AC
Cella, LC
Herman, P
Bachella, T
Caldwell, SH
Alves, VAF
Carrilho, FJ
AF Chagas, A. L.
Kikuchi, L. O. O.
Oliveira, C. P. M. S.
Vezozzo, D. C. P.
Mello, E. S.
Oliveira, A. C.
Cella, L. C.
Herman, P.
Bachella, T.
Caldwell, S. H.
Alves, V. A. F.
Carrilho, F. J.
TI Does hepatocellular carcinoma in non-alcoholic steatohepatitis exist in
cirrhotic and non-cirrhotic patients?
SO BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH
LA English
DT Article
DE Hepatocellular carcinoma; Liver cancer; Fatty liver; Steatohepatitis;
Cirrhosis
ID FATTY LIVER-DISEASE; CRYPTOGENIC CIRRHOSIS; ADULTS; RISK
AB Non-alcoholic steatohepatitis (NASH) has been associated with hepatocellular carcinoma (HCC) often arising in histologically advanced disease when steatohepatitis is not active (cryptogenic cirrhosis). Our objective was to characterize patients with HCC and active, histologically defined steatohepatitis. Among 394 patients with HCC detected by ultrasound imaging over 8 years and staged by the Barcelona Clinic Liver Cancer (BCLC) criteria, we identified 7 cases (1.7%) with HCC occurring in the setting of active biopsy-proven NASH. All were negative for other liver diseases such as hepatitis C, hepatitis B, autoimmune hepatitis, Wilson disease, and hemochromatosis. The patients (4 males and 3 females, age 63 +/- 13 years) were either overweight (4) or obese (3); 57% were diabetic and 28.5% had dyslipidemia. Cirrhosis was present in 6 of 7 patients, but 1 patient had well-differentiated HCC in the setting of NASH without cirrhosis (fibrosis stage 1) based on repeated liver biopsies, the absence of portal hypertension by clinical and radiographic evaluations and by direct surgical inspection. Among the cirrhotic patients, 71.4% were clinically staged as Child A and 14.2% as Child B. Tumor size ranged from 1.0 to 5.2 cm and 5 of 7 patients were classified as early stage; 46% of all nodules were hyper-echoic and 57% were <3 cm. HCC was well differentiated in 1/6 and moderately differentiated in 5/6. Alpha-fetoprotein was <100 ng/mL in all patients. HCC in patients with active steatohepatitis is often multifocal, may precede clinically advanced disease and occurs without diagnostic levels of alpha-fetoprotein. Importantly, HCC may occur in NASH in the absence of cirrhosis. More aggressive screening of NASH patients may be warranted.
C1 [Chagas, A. L.; Kikuchi, L. O. O.; Oliveira, C. P. M. S.; Vezozzo, D. C. P.; Oliveira, A. C.; Cella, L. C.; Herman, P.; Bachella, T.; Carrilho, F. J.] Univ Sao Paulo, Fac Med, Dept Gastroenterol LIM 07 37, BR-01246903 Sao Paulo, Brazil.
[Mello, E. S.; Alves, V. A. F.] Univ Sao Paulo, Fac Med, Dept Patol LIM 14, BR-01246903 Sao Paulo, Brazil.
[Caldwell, S. H.] Univ Virginia, Dept Gastroenterol & Hepatol, Charlottesville, VA USA.
C3 Universidade de Sao Paulo; Universidade de Sao Paulo; University of
Virginia
RP Oliveira, CPMS (corresponding author), Univ Sao Paulo, Fac Med, Dept Gastroenterol, Av Dr Arnaldo 455,3 Andar,Sala 3117, BR-01246903 Sao Paulo, Brazil.
EM cpml@usp.br
RI alves, vera/IAO-0451-2023; Oliveira, Claudia/D-1216-2014; Mello,
Evandro/AHD-4795-2022; Carrilho, Flair/I-3046-2012; Chagas,
Aline/X-2059-2019; Paranagua-Vezozzo, Denise/N-7270-2014; Herman,
Paulo/J-5457-2013
OI Alves, Venancio/0000-0001-5285-4460; Carrilho, Flair
Jose/0000-0002-7682-3105; Paranagua-Vezozzo, Denise/0000-0002-9606-4935;
P Oliveira, Claudia/0000-0002-2848-417X; Herman,
Paulo/0000-0003-2859-5846
FU NIDDK NIH HHS [P30 DK067629] Funding Source: Medline
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NR 16
TC 49
Z9 57
U1 0
U2 7
PU ASSOC BRAS DIVULG CIENTIFICA
PI RIBEIRAO PRETO
PA FACULDADE MEDICINA, CASA 10, 14049 RIBEIRAO PRETO, RIBEIRAO PRETO, SP
14049, BRAZIL
SN 0100-879X
EI 1414-431X
J9 BRAZ J MED BIOL RES
JI Brazilian J. Med. Biol. Res.
PD OCT
PY 2009
VL 42
IS 10
BP 958
EP 962
DI 10.1590/S0100-879X2009005000019
PG 5
WC Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Research & Experimental
Medicine
GA 499OO
UT WOS:000270233400014
PM 19787150
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Deng, QM
Zhang, XH
Wan, XF
Zheng, X
Wang, HZ
Zhao, JY
Wang, HQ
Yang, WL
AF Deng, Qingmei
Zhang, Xinhui
Wan, Xiaofeng
Zheng, Xin
Wang, Hongzhi
Zhao, Jingyu
Wang, Hong-Qiang
Yang, Wulin
TI The chemokine CCL20 can assist AFP in serological diagnosis of
hepatocellular carcinoma
SO HELIYON
LA English
DT Article
DE Hepatocellular carcinoma; Serum biomarker; Diagnosis; CCL20; AFP
ID CANCER
AB The chemokine 20 (CCL20) is a member of the CC chemokine family and plays a role in tumor immunity and autoimmune disease. This work investigated the value of CCL20 as a serum diagnostic marker for primary hepatocellular carcinoma (HCC). Based on the data of hepatocellular carcinoma patients in the TCGA database, the up-regulated genes encoding secretory proteins were analyzed in each pathological stage, and the candidate marker CCL20 gene was selected. Serum concentrations of CCL20 in patients with primary HCC, benign liver disease, and healthy subjects were analyzed by enzyme-linked immunosorbent assay (ELISA). The ROC curve evaluated the efficacy of CCL20 alone or in combination with AFP in the diagnosis of HCC. It was found the expression of CCL20 in HCC patients was significantly higher than that in the benign liver disease group and healthy controls (P < 0.05); The AUC of ROC curve to distinguish HCC patients from healthy controls was 0.859, the sensitivity was 73.42%, and the specificity was 86.84%. After combination with AFP, the AUC increased to 0.968, the sensitivity was 88.16%, and the specificity was 97.37%. Although CCL20 was increased in the serum of patients with benign liver diseases, combined with AFP, the AUC to distinguish HCC patients from non-HCC cohorts (benign liver disease group and healthy control group) was 0.902, with a sensitivity of 91.67% and a specificity of 75.26%. Collectively, serum CCL20 is closely related to the occurrence of HCC, and detection of serum CCL20 can assist AFP in improving the diagnostic sensitivity of HCC.
C1 [Deng, Qingmei; Zhang, Xinhui; Wan, Xiaofeng; Wang, Hongzhi; Zhao, Jingyu; Yang, Wulin] Chinese Acad Sci, Inst Hlth & Med Technol, Hefei Inst Phys Sci, Anhui Prov Key Lab Med Phys & Technol, Hefei 230031, Peoples R China.
[Deng, Qingmei; Zhang, Xinhui; Wan, Xiaofeng; Wang, Hongzhi; Zhao, Jingyu; Yang, Wulin] Chinese Acad Sci, Hefei Canc Hosp, Med Pathol Ctr, Hefei 230031, Peoples R China.
[Zhang, Xinhui; Wang, Hongzhi; Yang, Wulin] Anhui Med Univ, Sch Basic Med Sci, Hefei 230032, Peoples R China.
[Zhao, Jingyu] Anhui Univ, Inst Phys Sci & Informat Technol, Hefei 230601, Peoples R China.
[Zheng, Xin] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, Canc Ctr, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.
[Wang, Hong-Qiang] Chinese Acad Sci, Inst Intelligent Machines, Hefei Inst Phys Sci, Biol Mol Informat Syst Lab, Hefei 230031, Peoples R China.
[Wang, Hongzhi; Yang, Wulin] Chinese Acad Sci, Hefei Inst Phys Sci, Inst Hlth & Med Technol, 350 Shushanhu Rd, Hefei 230031, Anhui, Peoples R China.
C3 Chinese Academy of Sciences; Hefei Institutes of Physical Science, CAS;
Chinese Academy of Sciences; Hefei Institutes of Physical Science, CAS;
Anhui Medical University; Anhui University; Sun Yat Sen University;
State Key Lab Oncology South China; Chinese Academy of Sciences; Hefei
Institutes of Physical Science, CAS; Chinese Academy of Sciences; Hefei
Institutes of Physical Science, CAS
RP Wang, HZ; Yang, WL (corresponding author), Chinese Acad Sci, Hefei Inst Phys Sci, Inst Hlth & Med Technol, 350 Shushanhu Rd, Hefei 230031, Anhui, Peoples R China.
EM wanghz@hfcas.ac.cn; yangw@cmpt.ac.cn
RI Wang, Hongzhi/IAP-6964-2023; zhu, y/IVU-7833-2023; Wan,
Xiaofeng/AAG-9967-2020; Wang, Hongqiang/AAY-8288-2021
FU National Natural Science Foundation of China [81872276, 61973295];
Scientific Research Project of Anhui Provincial Health Commission
[AHWJ2021b142]; Hefei municipal Natural Science Foundation [2022050];
Anhui Province's Key Research and Development Project [201904a07020092];
CASHIPS Director's Fund [YZJJ2022QN48]
FX This study was in part supported by the National Natural Science
Foundation of China (81872276, 61973295) , the Scientific Research
Project of Anhui Provincial Health Commission (AHWJ2021b142) , the Hefei
municipal Natural Science Foundation (2022050) , the Anhui Province's
Key Research and Development Project (201904a07020092) , and the CASHIPS
Director's Fund (YZJJ2022QN48) .
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NR 41
TC 1
Z9 1
U1 1
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD MAR 15
PY 2024
VL 10
IS 5
AR e26774
DI 10.1016/j.heliyon.2024.e26774
EA FEB 2024
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA MS9W7
UT WOS:001195752700001
PM 38439882
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Pan, XR
Gao, YZ
Liu, JW
Liu, CY
Xia, Y
AF Pan, Xiaorong
Gao, Yuzhen
Liu, Jianwei
Liu, Chunying
Xia, Yong
TI Progress in studies on autoantibodies against tumor-associated antigens
in hepatocellular carcinoma
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Review
DE Autoantibodies; hepatocellular carcinoma (HCC); screening techniques
ID TISSUE-SPECIFIC EXPRESSION; SERUM ANTI-P53 ANTIBODIES; CHRONIC
LIVER-DISEASE; ALPHA-FETOPROTEIN; AUTOIMMUNE-RESPONSE; P53 ANTIBODIES;
C-MYC; PROGNOSTIC-SIGNIFICANCE; DIAGNOSTIC BIOMARKERS; MINI-ARRAY
AB The diagnosis of hepatocellular carcinoma (HCC) patients using alpha-fetoprotein (AFP) is not accurate enough because of its low specificity. Autoantibodies as a complementary tool to AFP have attracted more and more attention. Although many kinds of autoantibodies are still unknown in patients with various cancers, autoantibodies against tumor-associated antigens (TAAs) have shown high specificities in cancer diagnosis due to the abnormal production of TAAs in cancer patients. At the present, serum proteomics analyses (SERPA), serological analyses of recombinantly expressed cDNA clone (SEREX), phage display technologies and high throughput protein microarray all have been applied in the screening of autoantibodies of HCC patients. Sometimes, the diagnosis value of a single or multiple autoantibodies can be a good complement to AFP. In this review, we describe and summarize the common technologies of screening autoantibodies and the application of autoantibodies in HCC.
C1 [Pan, Xiaorong; Gao, Yuzhen; Liu, Jianwei] Fujian Med Univ, Clin Med Coll 1, Fuzhou 350000, Peoples R China.
[Pan, Xiaorong] Second Mil Med Univ, Tumor Immunol & Gene Therapy Ctr, Shanghai 200438, Peoples R China.
[Gao, Yuzhen] Second Mil Med Univ, Dept Lab Med, Shanghai 200438, Peoples R China.
[Liu, Jianwei; Xia, Yong] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Dept Hepat Surg, Shanghai 200438, Peoples R China.
[Liu, Chunying] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Dept Mol Oncol, Shanghai 200438, Peoples R China.
[Liu, Chunying] Second Mil Med Univ, Natl Ctr Liver Canc, Shanghai 200438, Peoples R China.
C3 Fujian Medical University; Naval Medical University; Naval Medical
University; Naval Medical University; Naval Medical University; Naval
Medical University
RP Xia, Y (corresponding author), Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Dept Hepat Surg, Shanghai 200438, Peoples R China.; Liu, CY (corresponding author), Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Dept Mol Oncol, Shanghai 200438, Peoples R China.; Liu, CY (corresponding author), Second Mil Med Univ, Natl Ctr Liver Canc, Shanghai 200438, Peoples R China.
EM cyliu@sibcb.ac.cn; xia.yong@126.com
OI Gao, Yuzhen/0000-0001-7485-5237
FU Natural Science and Medical Guidance Foundation of Shanghai
[16ZR1400100, 16411966200]; National Natural Science Foundation of
China, Youth Science Fund Project [31301187]
FX This work was supported by the Natural Science and Medical Guidance
Foundation of Shanghai (grant number 16ZR1400100 and 16411966200) and
the National Natural Science Foundation of China, Youth Science Fund
Project (grant number 31301187).
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NR 82
TC 3
Z9 3
U1 1
U2 22
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD DEC
PY 2016
VL 5
IS 6
BP 845
EP 859
DI 10.21037/tcr.2016.11.70
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EJ5YE
UT WOS:000393294300026
DA 2025-01-07
ER
PT J
AU Dragani, TA
AF Dragani, Tommaso A.
TI Risk of HCC: Genetic heterogeneity and complex genetics
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Cirrhosis; Glycogen storage disease; Hemochromatosis; Hepatitis;
Non-alcoholic steatohepatitis; Porphyrias; Tyrosinemia type 1
ID PORPHYRIA-CUTANEA-TARDA; PRIMARY LIVER-CANCER; PRIMARY
HEPATOCELLULAR-CARCINOMA; DISEASE TYPE-I; HEREDITARY HEMOCHROMATOSIS;
HEPATITIS-B; FOLLOW-UP; VIRAL-HEPATITIS; HEPATOCARCINOGENESIS;
SUSCEPTIBILITY
AB Hepatocellular carcinoma (HCC) is a common form of cancer that arises from hepatocytes and whose risk may be affected by several known environmental factors, including hepatitis viruses, alcohol, cigarette smoking, and others. Rare monogenic syndromes, such as alphal-antitrypsin deficiency, glycogen storage disease type 1, hemochromatosis, acute intermittent and cutanea tarda porphyria, as well as hereditary tyrosinemia type I are associated with a high risk of HCC. Several common conditions or diseases inherited as polygenic traits e.g. autoimmune hepatitis, type 2 diabetes, a family history of HCC, hypothyroidism, and non-alcoholic steatohepatitis also show an increased risk of HCC compared to the general Population. Overall, the genetic susceptibility to HCC is characterized by a genetic heterogeneity; a high individual risk of HCC may thus be caused by several unlinked single gene defects, whose carriers are rare in the general Population, or by more common conditions inherited by complex genetics. (C) 2009 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 Fdn IRCCS Ist Nazl Tumori, Dept Expt Oncol & Mol Med, I-20133 Milan, Italy.
C3 Fondazione IRCCS Istituto Nazionale Tumori Milan
RP Dragani, TA (corresponding author), Fdn IRCCS Ist Nazl Tumori, Dept Expt Oncol & Mol Med, Via G Venezian 1, I-20133 Milan, Italy.
EM tommaso.dragani@istitutotumori.mi.it
RI Dragani, Tommaso A./K-4493-2016
OI Dragani, Tommaso A./0000-0001-5915-4598
FU Associazione and Fondazione Italiana per la Ricerca Sul Cancro (AIRC and
FIRC)
FX The author declared that he does not have anything to declare regarding
funding from industry or conflict of interest with respect to this
manuscript. This work was funded in part by grants from Associazione and
Fondazione Italiana per la Ricerca Sul Cancro (AIRC and FIRC).
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NR 73
TC 172
Z9 182
U1 0
U2 13
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD FEB
PY 2010
VL 52
IS 2
BP 252
EP 257
DI 10.1016/j.jhep.2009.11.015
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 566RK
UT WOS:000275390500017
PM 20022654
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Schütte, K
Bornschein, J
Malfertheiner, P
AF Schuette, Kerstin
Bornschein, Jan
Malfertheiner, Peter
TI Hepatocellular Carcinoma - Epidemiological Trends and Risk Factors
SO DIGESTIVE DISEASES
LA English
DT Review
DE HCC, epidemiological trends; HCC, risk factors; Hepatocarcinogenesis;
Viral hepatitis; Hepatitis B-associated HCC; Hepatitis C-associated HCC;
Autoimmune hepatitis (AIH)-related HCC
ID HEPATITIS-C VIRUS; CHRONIC LIVER-DISEASE; HFE GENE-MUTATIONS; RETINOIC
ACID CONCENTRATION; AFLATOXIN B-1 EXPOSURE; TERM-FOLLOW-UP; B E-ANTIGEN;
NATURAL-HISTORY; INTERFERON THERAPY; NONALCOHOLIC STEATOHEPATITIS
AB Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related deaths worldwide with about 600,000 patients dying from the disease annually. In 70-90%, HCC develops on the background of chronic liver cirrhosis or inflammation. Risk factors and etiologies vary among geographical regions. In regions with a high incidence the majority of cases are related to HBV and HCV hepatitis. In developed countries, in addition to virus-related HCC, high consumption of alcohol as well as non-alcoholic fatty liver disease often in the context of metabolic syndromes are the prevalent causes. Improvement in clinical management of patients with liver cirrhosis and the control of related complications are the key for the rising incidence of HCC. This review gives an overview on epidemiological trends and risk factors and their mechanisms involved in the hepatocarcinogenesis. Knowledge of these factors will help to improve current concepts for prevention, screening and treatment of this disease. Copyright (C) 2009 S. Karger AG, Basel
C1 [Schuette, Kerstin; Bornschein, Jan; Malfertheiner, Peter] Otto VonGuericke Univ Magdegurg, Dept Gastroenterol Hepatol & Infect Dis, DE-39120 Magdeburg, Germany.
C3 Otto von Guericke University
RP Malfertheiner, P (corresponding author), Otto VonGuericke Univ Magdegurg, Dept Gastroenterol Hepatol & Infect Dis, Leipziger Str 44, DE-39120 Magdeburg, Germany.
EM peter.malfertheiner@med.ovgu.de
RI Malfertheiner, Peter/AEZ-6553-2022; Bornschein, Jan/U-9402-2018
OI Schutte, Kerstin/0000-0002-1724-3733; Bornschein,
Jan/0000-0001-8673-3122
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NR 138
TC 383
Z9 423
U1 0
U2 61
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PY 2009
VL 27
IS 2
BP 80
EP 92
DI 10.1159/000218339
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 465JB
UT WOS:000267578200002
PM 19546545
DA 2025-01-07
ER
PT J
AU Voiculescu, M
Winkler, RE
Moscovici, M
Neuman, MG
AF Voiculescu, Mihai
Winkler, Robert E.
Moscovici, Marius
Neuman, Manuela G.
TI Chemotherapies and targeted therapies in advanced hepatocellular
carcinoma: from laboratory to clinic
SO JOURNAL OF GASTROINTESTINAL AND LIVER DISEASES
LA English
DT Review
DE alcoholic liver disease; viral hepatitis; cytokines; Fas; hepatocellular
carcinoma; m-Tor inhibitor; primary biliary cirrhosis; protein kinase C;
apoptosis; tumor necrosis factors; vascular endothelial growth factor
ID HEPATITIS-B-VIRUS; LONG-ACTING OCTREOTIDE; MULTICENTER PHASE-II;
E-ANTIGEN; C VIRUS; LIVER-TRANSPLANTATION; ITALIAN PATIENTS;
SURFACE-ANTIGEN; CANCER; EXPRESSION
AB Chronic liver diseases alone or in conjunction with other risk factors result in increased liver damage leading to inflammation and fibrosis of the liver and rising rates of liver cirrhosis, hepatic decompensation and hepatocellular carcinoma (HCC). This review will address the determinants of liver injury at the initiation of the tumor and the risk factors for rapid disease progression. Regardless of the etiology, the unifying feature of these tumors are their propensity to arise upon a background of inflammation and fibrosis. Liver disease is often associated with enhanced hepatocyte apoptosis, which is the case in viral and autoimmune hepatitis, cholestatic diseases, and metabolic disorders. Disruption of apoptosis is responsible for HCC. The mechanisms by which apoptosis occurs in the liver might provide insights into HCC and suggest possible treatments. We aim to better understand the factors that distinguish a relatively long course of HCC from one with rapid progression. We will accomplish this task with three integrated ideas: 1 - the role of epidemiology in establishing the risk factors of co-morbidity with alcohol and hepatitis viruses; 2 - the role of apoptosis and anti-apoptotic signals in the progression of HCC; and 3 - the role of new advancements that have emerged in the field of molecular-directed chemotherapeutics in HCC in recent years. This review will also aim to describe the molecular targeted therapies of non-resectable HCC and the ways of effective combination in this otherwise chemo-resistant tumor.
C1 [Neuman, Manuela G.] Univ Toronto, Ctr Int Hlth,Fac Med, Inst Drug Res, Dept Pharmacol, Toronto, ON M5S 1A1, Canada.
[Voiculescu, Mihai] Fundeni Clin Inst, Ctr Internal Med, Bucharest, Romania.
[Moscovici, Marius] Pharma Clin AG, Zug, Switzerland.
C3 University of Toronto; Institutul Clinic Fundeni
RP Neuman, MG (corresponding author), Univ Toronto, Ctr Int Hlth,Fac Med, Inst Drug Res, Dept Pharmacol, Toronto, ON M5S 1A1, Canada.
EM Manuela.neuman@utoronto.ca
FU Novartis Pharmaceuticals, USA; Bayer- Schering-Pharma, Italy
FX Mihai Voiculescu and Manuela Neuman declare that they do not have
anything to disclose regarding funding frorn industries or conflicts of
interest with respect to this manuscript. Robert Winkler is an employee
of Novartis Pharmaceuticals, USA. Marius Moscovici is a consultant for
"Sorafenib" for Bayer- Schering-Pharma, Italy,
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NR 88
TC 17
Z9 20
U1 0
U2 2
PU MEDICAL UNIV PRESS
PI CLUJ-NAPOCA
PA 3RD MEDICAL CLINIC, STR CROITORILOR NO 19-21, CLUJ-NAPOCA, 400162,
ROMANIA
SN 1841-8724
EI 1842-1121
J9 J GASTROINTEST LIVER
JI J. Gastrointest. Liver Dis.
PD SEP
PY 2008
VL 17
IS 3
BP 315
EP 322
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 354RH
UT WOS:000259656200012
PM 18836626
DA 2025-01-07
ER
PT J
AU Granito, A
Muratori, L
Lalanne, C
Quarneti, C
Ferri, S
Guidi, M
Lenzi, M
Muratori, P
AF Granito, Alessandro
Muratori, Luigi
Lalanne, Claudine
Quarneti, Chiara
Ferri, Silvia
Guidi, Marcello
Lenzi, Marco
Muratori, Paolo
TI Hepatocellular carcinoma in viral and autoimmune liver diseases: Role of
CD4+CD25+Foxp3+regulatory T cells in the immune microenvironment
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Autoimmune liver disease; Hepatitis B virus-related chronic hepatitis;
Hepatitis C virus-related chronic hepatitis; Hepatocellular carcinoma;
Tumor microenvironment
ID HEPATITIS-C VIRUS; SERUM ALANINE AMINOTRANSFERASE; PRIMARY
BILIARY-CIRRHOSIS; IN-VITRO PROLIFERATION; DENDRITIC CELLS; ADVERSE
EVENTS; PREEXISTING AUTOIMMUNE; TUMOR MICROENVIRONMENT; PREDICTIVE
FACTORS; TGF-BETA
AB More than 90% of cases of hepatocellular carcinoma (HCC) occurs in patients with cirrhosis, of which hepatitis B virus and hepatitis C virus are the leading causes, while the tumor less frequently arises in autoimmune liver diseases. Advances in understanding tumor immunity have led to a major shift in the treatment of HCC, with the emergence of immunotherapy where therapeutic agents are used to target immune cells rather than cancer cells. Regulatory T cells (Tregs) are the most abundant suppressive cells in the tumor microenvironment and their presence has been correlated with tumor progression, invasiveness, as well as metastasis. Tregs are characterized by the expression of the transcription factor Foxp3 and various mechanisms ranging from cell-to-cell contact to secretion of inhibitory molecules have been implicated in their function. Notably, Tregs amply express checkpoint molecules such as cytotoxic T lymphocyte-associated antigen 4 and programmed cell-death 1 receptor and therefore represent a direct target of immune checkpoint inhibitor (ICI) immunotherapy. Taking into consideration the critical role of Tregs in maintenance of immune homeostasis as well as avoidance of autoimmunity, it is plausible that targeting of Tregs by ICI immunotherapy results in the development of immune-related adverse events (irAEs). Since the use of ICI becomes common in oncology, with an increasing number of new ICI currently under clinical trials for cancer treatment, the occurrence of irAEs is expected to dramatically rise. Herein, we review the current literature focusing on the role of Tregs in HCC evolution taking into account their opposite etiological function in viral and autoimmune chronic liver disease, and we discuss their involvement in irAEs due to the new immunotherapies.
C1 [Granito, Alessandro] Univ Bologna, IRCCS Azienda Osped Univ Bologna, Div Internal Med Hepatobiliary & Immunoallerg Dis, Via Albertoni 15, I-40138 Bologna, Italy.
[Granito, Alessandro] Univ Bologna, Dept Med & Surg Sci, Ctr Study & Treatment Autoimmune Dis Liver & Bili, I-40138 Bologna, Italy.
[Muratori, Luigi; Lenzi, Marco] Univ Bologna, IRCCS Azienda Osped Univ Bologna, Div Internal Med & Immunorheumatol, Ctr Study & Treatment Autoimmune Dis Liver & Bili, I-40138 Bologna, Italy.
[Muratori, Luigi; Lenzi, Marco] Univ Bologna, Dept Med & Surg Sci, I-40138 Bologna, Italy.
[Lalanne, Claudine; Quarneti, Chiara; Ferri, Silvia; Guidi, Marcello] IRCCS Azienda Osped Univ Bologna, Ctr Study & Treatment Autoimmune Dis Liver & Bili, Div Internal Med, I-40138 Bologna, Italy.
[Muratori, Paolo] Morgagni Pierantoni Hosp, Div Internal Med, I-47100 Forli, Italy.
[Muratori, Paolo] Univ Bologna, Dept Sci Qual Life, I-40138 Bologna, Italy.
C3 IRCCS Azienda Ospedaliero-Universitaria di Bologna; University of
Bologna; University of Bologna; University of Bologna; IRCCS Azienda
Ospedaliero-Universitaria di Bologna; University of Bologna; IRCCS
Azienda Ospedaliero-Universitaria di Bologna; University of Bologna
RP Granito, A (corresponding author), Univ Bologna, IRCCS Azienda Osped Univ Bologna, Div Internal Med Hepatobiliary & Immunoallerg Dis, Via Albertoni 15, I-40138 Bologna, Italy.
EM alessandro.granito@unibo.it
RI Muratori, Luigi/I-3181-2012; Granito, Alessandro/G-9563-2013
OI Granito, Alessandro/0000-0002-0637-739X; Ferri,
Silvia/0000-0002-6033-8594
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PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUN 14
PY 2021
VL 27
IS 22
DI 10.3748/wjg.v27.i22.2994
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA SU4CB
UT WOS:000663086700005
PM 34168403
OA Green Published, hybrid
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Dakhoul, L
Jones, KR
Gawrieh, S
Ghabril, M
McShane, C
Vuppalanchi, R
Vilar-Gomez, E
Nephew, L
Chalasani, N
Lammert, C
AF Dakhoul, Lara
Jones, Keaton R.
Gawrieh, Samer
Ghabril, Marwan
McShane, Chelsey
Vuppalanchi, Raj
Vilar-Gomez, Eduardo
Nephew, Lauren
Chalasani, Naga
Lammert, Craig
TI Older Age and Disease Duration Are Highly Associated with Hepatocellular
Carcinoma in Patients with Autoimmune Hepatitis
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Liver cancer; Autoimmune liver disease; Older age; Disease duration
ID FATTY LIVER-DISEASE; CLINICAL CHARACTERISTICS; PROGNOSIS; CIRRHOSIS
AB BackgroundHepatocellular carcinoma (HCC) is rare in patients with autoimmune hepatitis (AIH). However, the overall burden of AIH cirrhosis in causing HCC and patients' risk factors are not well understood.AimsTo characterize the proportion of HCC linked to AIH at a large academic health center, and to identify variables associated with HCC in patients with AIH in a case-control study design.MethodsOver a 14.5-year period, medical records of all patients with HCC were reviewed. Cases are AIH patients identified from the cohort, and controls are patients with AIH without HCC. Three controls were randomly chosen from the Genetic Repository of Autoimmune Liver Disease and Coexisting Exposures database for each eligible case.ResultsOut of 1250 eligible patients, 20 were linked to AIH (1.6%). Their median age was 64years, 40% men and 100% Caucasian. Ten percent of AIH patients did not have evidence of cirrhosis at HCC diagnosis. The proportion of HCCs due to AIH decreased during the time intervals of the study. Compared to controls, cases were more likely men (40.0% vs. 18%, p=0.049), with longer AIH duration (median 16years vs. 5years, p=0.004). Prolonged AIH duration (OR 1.68, p=0.006) and older age (OR 1.15, p=0.049) were risk factors for HCC.ConclusionsAIH is a rare cause (1.6%) for HCC in Midwestern USA with a decreasing trend over 14.5years. Ten percent of AIH-HCC patients did not have cirrhosis at time of HCC diagnosis. Patients with prolonged duration of the disease and older age are at high risk to develop HCC.
C1 [Dakhoul, Lara; Jones, Keaton R.; Gawrieh, Samer; Ghabril, Marwan; Vuppalanchi, Raj; Vilar-Gomez, Eduardo; Nephew, Lauren; Chalasani, Naga; Lammert, Craig] Indiana Univ, Sch Med, Div Gastroenterol & Hepatol, 702 Rotary Circle,Suite 225, Indianapolis, IN 46202 USA.
[McShane, Chelsey] Indiana Univ Sch Med, Dept Internal Med, Indianapolis, IN 46202 USA.
C3 Indiana University System; Indiana University Indianapolis; Indiana
University System; Indiana University Bloomington
RP Chalasani, N; Lammert, C (corresponding author), Indiana Univ, Sch Med, Div Gastroenterol & Hepatol, 702 Rotary Circle,Suite 225, Indianapolis, IN 46202 USA.
EM ldakhoul@iu.edu; keatjone@gmail.com; sgawrieh@iu.edu; mghabril@iu.edu;
Chelsey.mcshane@gmail.com; rvuppala@iu.edu; evilar@iu.edu;
lnephew@iu.edu; nchalasa@iu.edu; clammert@iu.edu
RI Vilar, Eduardo/H-8556-2019; Gawrieh, Samer/AAS-8904-2020; Nephew,
Lauren/AAY-9123-2021; Vuppalanchi, Raj/AAI-2481-2021; Ghabril,
Marwan/AAF-8661-2020; Lammert, Craig/AAI-3420-2020
OI Ghabril, Marwan/0000-0002-4784-3246; Nephew, Lauren/0000-0003-0837-0746
FU NIDDK NIH HHS [L30 DK106872, K23 DK114561] Funding Source: Medline
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NR 25
TC 12
Z9 12
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD JUN
PY 2019
VL 64
IS 6
BP 1705
EP 1710
DI 10.1007/s10620-018-5441-5
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HY5FM
UT WOS:000468153200040
PM 30617453
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Sharma, R
Verna, EC
Simon, TG
Söderling, J
Hagström, H
Green, PHR
Ludvigsson, JF
AF Sharma, Rajani
Verna, Elizabeth C.
Simon, Tracey G.
Soderling, Jonas
Hagstrom, Hannes
Green, Peter H. R.
Ludvigsson, Jonas F.
TI Cancer Risk in Patients With Autoimmune Hepatitis: A Nationwide
Population-Based Cohort Study With Histopathology
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE cirrhosis; hepatitis; hepatocellular carcinoma; histopathology;
malignancy; population-based
ID TERM-FOLLOW-UP; HEPATOCELLULAR-CARCINOMA; LIVER; INFLAMMATION;
MALIGNANCY; CIRRHOSIS; REGISTER; DISEASES; PROFILE; UPDATE
AB We aimed to determine the risk of incident cancer in autoimmune hepatitis (AIH) compared with the general population and siblings. AIH was defined by the presence of a medical diagnosis of AIH and results of examination of a liver biopsy specimen in a nationwide Swedish population-based cohort study. We identified 5,268 adults with AIH diagnosed during 1969-2016 and 22,996 matched, general population, reference individuals and 4,170 sibling comparators. Using Cox regression, hazard ratios were determined for any incident cancer, and subtypes were determined from the Swedish Cancer Register. During follow-up, a cancer diagnosis was made in 1,119 individuals with AIH (17.2 per 1,000 person-years) and 4,450 reference individuals (12.0 per 1,000 person-years). This corresponded to a hazard ratio of 1.53 (95% confidence interval: 1.42, 1.66). Cancer risk was highest in those with cirrhosis. There was a 29.18-fold increased risk of hepatocellular carcinoma (HCC) (95% confidence interval: 17.52, 48.61). The annual incidence risk of HCC in individuals with AIH who had cirrhosis was 1.1% per year. AIH was also linked to nonmelanoma skin cancer (hazard ratio (HR) = 2.69) and lymphoma (HR = 1.89). Sibling analyses yielded similar risk estimates for any cancer (HR = 1.84) and HCC (HR = 23.10). AIH is associated with an increased risk of any cancer, in particular, HCC and extrahepatic malignancies. The highest risk for cancer, especially HCC, is in patients with cirrhosis.
C1 [Soderling, Jonas; Ludvigsson, Jonas F.] Karolinska Inst, Dept Med Epidemiol & Biostat, C8 MEB Ludvigsson, S-17177 Stockholm, Sweden.
[Sharma, Rajani; Verna, Elizabeth C.] Columbia Univ, Irving Med Ctr, Ctr Liver Dis & Transplantat, Div Digest & Liver Dis, New York, NY USA.
[Sharma, Rajani; Verna, Elizabeth C.; Green, Peter H. R.; Ludvigsson, Jonas F.] Columbia Univ, Coll Phys & Surg, Div Digest & Liver Dis, Dept Med, New York, NY USA.
[Simon, Tracey G.] Massachusetts Gen Hosp, Div Gastroenterol, Transplant Hepatol, Boston, MA USA.
[Hagstrom, Hannes] Karolinska Univ Hosp, Unit Hepatol, Ctr Digest Dis, Stockholm, Sweden.
[Hagstrom, Hannes] Karolinska Inst, Unit Clin Epidemiol, Dept Med, Stockholm, Sweden.
[Green, Peter H. R.] Columbia Univ, Celiac Dis Ctr, Dept Med, Irving Med Ctr, New York, NY USA.
[Ludvigsson, Jonas F.] Orebro Univ Hosp, Dept Pediat, Orebro, Sweden.
[Ludvigsson, Jonas F.] Sch Med, Div Epidemiol & Publ Hlth, Nottingham, England.
[Ludvigsson, Jonas F.] Univ Nottingham, Nottingham, England.
C3 Karolinska Institutet; NewYork-Presbyterian Hospital; Columbia
University; Columbia University; Harvard University; Massachusetts
General Hospital; Karolinska Institutet; Karolinska University Hospital;
Karolinska Institutet; NewYork-Presbyterian Hospital; Columbia
University; Orebro University; University of Nottingham
RP Ludvigsson, JF (corresponding author), Karolinska Inst, Dept Med Epidemiol & Biostat, C8 MEB Ludvigsson, S-17177 Stockholm, Sweden.
EM jonasludvigsson@yahoo.com
RI Hagström, Hannes/I-2036-2019; Ludvigsson, Jonas/A-8560-2012
OI Hagstrom, Hannes/0000-0002-8474-1759
FU Celiac Disease Center at Columbia University Medical Center; Karolinska
Institutet; Stockholm County Council; National Institutes of Health [K23
DK122104]
FX This work was funded by the Celiac Disease Center at Columbia University
Medical Center (to P.H.R.G.) and The Karolinska Institutet (J.F.L.).
H.H. was supported by grants from Stockholm County Council (a clinical
postdoctoral appointment). T.S. is supported by the National Institutes
of Health (grant K23 DK122104).
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NR 32
TC 15
Z9 15
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD JAN 24
PY 2022
VL 191
IS 2
BP 298
EP 319
DI 10.1093/aje/kwab119
PG 22
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Public, Environmental & Occupational Health
GA ZI2IS
UT WOS:000761451100010
PM 33913487
OA Green Published
DA 2025-01-07
ER
PT J
AU Werner, M
Almer, S
Prytz, H
Lindgren, S
Wallerstedt, S
Björsson, E
Bergquist, A
Sandberg-Gertzén, H
Hultcrantz, R
Sangfelt, P
Weiland, O
Danielsson, Å
AF Werner, Marten
Almer, Sven
Prytz, Hanne
Lindgren, Stefan
Wallerstedt, Sven
Bjoersson, Einar
Bergquist, Annika
Sandberg-Gertzen, Hanna
Hultcrantz, Rolf
Sangfelt, Per
Weiland, Ola
Danielsson, Ake
TI Hepatic and extrahepatic malignancies in autoimmune hepatitis. A
long-term follow-up in 473 Swedish patients
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Autoimmune hepatitis; Hepatocellular carcinoma; Lymphoma; Malignancies
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
HEPATOCELLULAR-CARCINOMA; RISK-FACTORS; CANCER; EPIDEMIOLOGY;
POPULATION; STRATEGIES; MANAGEMENT; SWEDEN
AB Background/Aims: Autoimmune Hepatitis (AIH) is a liver disease which may lead to liver cirrhosis. Cirrhosis is a well-known risk factor for hepatocellular cancer. Lymphoma is a disease, where immune modulating drugs as well as the autoimmune disease itself may contribute to the elevated risk. The aim was to investigate the risks of malignancies in a large cohort of AIH patients.
Methods: Four hundred and seventy-three patients with AIH were matched to the Swedish national cancer register as well as to the death cause register.
Results: We found an overall higher risk of malignancies in the cohort of A I H patients from the date of diagnosis with a SIR of 1.51 (95% CI 1.10-2.03). SIR in the subpopulation of well defined catchment areas and complete case finding was 23.28 (95% CI 7.5-54.34) for HCC. Lymphomas were found a SIR of 13.09 (95% CI 4.22-30.56).
Conclusions: There was an overall increased risk of malignancies in a cohort of AIH patients, which manly was caused by hepatobiliary cancers. However, the true risk of HCC in an AIH cirrhotic cohort has yet to be investigated. A significantly higher risk of lymphomas was also found, but no clear cut association to the use of immune modulators. (C) 2008 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Werner, Marten; Danielsson, Ake] Umea Univ Hosp, Dept Med, Sect Hepatol, SE-90185 Umea, Sweden.
[Werner, Marten; Danielsson, Ake] Umea Univ Hosp, Dept Med, Gastroenterol Sect, SE-90185 Umea, Sweden.
[Almer, Sven] Linkoping Univ Hosp, Dept Med, Gastroenterol Sect, Linkoping, Sweden.
[Almer, Sven] Linkoping Univ Hosp, Dept Med, Sect Hepatol, Linkoping, Sweden.
[Prytz, Hanne] Univ Lund Hosp, Dept Med, Sect Hepatol, Lund, Sweden.
[Prytz, Hanne] Univ Lund Hosp, Dept Med, Gastroenterol Sect, Lund, Sweden.
[Lindgren, Stefan] Malmo Univ Hosp, Dept Med, Gastroenterol Sect, Malmo, Sweden.
[Lindgren, Stefan] Malmo Univ Hosp, Dept Med, Sect Hepatol, Malmo, Sweden.
[Bergquist, Annika] Karolinska Univ Hosp Huddinge, Dept Med, Sect Hepatol, Huddinge, Sweden.
[Bergquist, Annika] Karolinska Univ Hosp Huddinge, Dept Med, Gastroenterol Sect, Huddinge, Sweden.
[Sandberg-Gertzen, Hanna] Orebro Univ Hosp, Dept Med, Gastroenterol Sect, Orebro, Sweden.
[Sandberg-Gertzen, Hanna] Orebro Univ Hosp, Dept Med, Sect Hepatol, Orebro, Sweden.
[Hultcrantz, Rolf] Karolinska Univ Hosp Solna, Dept Med, Sect Hepatol, Solna, Sweden.
[Hultcrantz, Rolf] Karolinska Univ Hosp Solna, Dept Med, Gastroenterol Sect, Solna, Sweden.
[Sangfelt, Per] Univ Uppsala Hosp, Dept Med, Gastroenterol Sect, Uppsala, Sweden.
[Sangfelt, Per] Univ Uppsala Hosp, Dept Med, Sect Hepatol, Uppsala, Sweden.
[Weiland, Ola] Karolinska Univ Hosp Huddinge, Dept Infect Dis, Huddinge, Sweden.
C3 Umea University; Umea University; Linkoping University; Linkoping
University; Lund University; Skane University Hospital; Lund University;
Skane University Hospital; Lund University; Skane University Hospital;
Lund University; Skane University Hospital; Karolinska Institutet;
Karolinska University Hospital; Karolinska Institutet; Karolinska
University Hospital; Orebro University; Orebro University; Karolinska
Institutet; Karolinska University Hospital; Karolinska Institutet;
Karolinska University Hospital; Uppsala University; Uppsala University
Hospital; Uppsala University; Uppsala University Hospital; Karolinska
Institutet; Karolinska University Hospital
RP Werner, M (corresponding author), Umea Univ Hosp, Dept Med, Sect Hepatol, SE-90185 Umea, Sweden.
EM marten.werner@vll.se
RI Bergquist, Annika/HOH-4007-2023; Almer, Sven/AFR-5312-2022
OI Bergquist, Annika/0000-0002-3858-6241; Almer, Sven/0000-0001-9334-1821;
Weiland, Ola/0000-0002-6934-9724
FU NSCRI (North Sweden Clinical Research Institute); Bjorn Tavelin.; Bengt
Ihres fund; Umea University; Department of Medicine at Umea University
Hospital; Swedish Internal Medicine Liver Club
FX We received great help from NSCRI (North Sweden Clinical Research
Institute) and especially from Bjorn Tavelin. The Study was Supported by
grants from Bengt Ihres fund, Umea University, and the Department of
Medicine at Umea University Hospital. Meda Sweden AB has throughout the
Study Supported the meetings of the Swedish Internal Medicine Liver
Club.
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NR 20
TC 66
Z9 71
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD FEB
PY 2009
VL 50
IS 2
BP 388
EP 393
DI 10.1016/j.jhep.2008.08.022
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 406QC
UT WOS:000263309000021
PM 19070390
DA 2025-01-07
ER
PT J
AU Hernández-Alvarez, MI
Zorzano, A
AF Hernandez-Alvarez, Maria Isabel
Zorzano, Antonio
TI Mitochondrial Dynamics and Liver Cancer
SO CANCERS
LA English
DT Review
DE hepatocellular carcinoma; chronic liver disease; NASH; liver fibrosis;
insulin resistance; Mitofusin 1; Mitofusin 2; OPA1; DRP1
ID ADVANCED HEPATOCELLULAR-CARCINOMA; ENDOPLASMIC-RETICULUM; MITOFUSIN 2;
FISSION; OPA1; SORAFENIB; MFN2; DRP1; PROTEIN; PROGRESSION
AB Simple Summary
Hepatocellular carcinoma is a leading cause of cancer-related death worldwide. Major risk factors in liver cancer development include chronic hepatitis B or C virus, autoimmune hepatitis, diabetes mellitus, alcohol abuse, and several metabolic diseases, among others. Standard therapy shows low efficacy, and there is an urgent need for novel therapies. Recent data permit to propose that proteins that control mitochondrial morphology through changes in mitochondrial fusion or mitochondrial fission, confer susceptibility or resistance to the development of liver cancer in mouse models. Here, we review the data that suggest mitochondrial dynamics to be involved in the development of liver tumors.
Hepatocellular carcinoma (HCC) is the most prevalent primary liver cancer. Due to its rising incidence and limited therapeutic options, HCC has become a leading cause of cancer-related death worldwide, accounting for 85% of all deaths due to primary liver cancers. Standard therapy for advanced-stage HCC is based on anti-angiogenic drugs such as sorafenib and, more recently, lenvatinib and regorafenib as a second line of treatment. The identification of novel therapeutic strategies is urgently required. Mitochondrial dynamics describes a group of processes that includes the movement of mitochondria along the cytoskeleton, the regulation of mitochondrial morphology and distribution, and connectivity mediated by tethering and fusion/fission events. In recent years, mitochondrial dynamic processes have emerged as key processes in the maintenance of liver mitochondrial homeostasis. In addition, some data are accumulating on the role played by mitochondrial dynamics during cancer development, and specifically on how such dynamics act directly on tumor cells or indirectly on cells responsible for tumor aggression and defense. Here, we review the data that suggest mitochondrial dynamics to be involved in the development of liver tumors.
C1 [Hernandez-Alvarez, Maria Isabel; Zorzano, Antonio] Univ Barcelona, Fac Biol, Dept Bioquim & Biomed Mol, Barcelona 08028, Spain.
[Hernandez-Alvarez, Maria Isabel; Zorzano, Antonio] CIBER Diabet & Enfermedades Metab Asociadas, Barcelona 08028, Spain.
[Hernandez-Alvarez, Maria Isabel] Univ Barcelona, IBUB, Inst Biomed, Barcelona 08028, Spain.
[Zorzano, Antonio] Barcelona Inst Sci & Technol BIST, Inst Res Biomed IRB Barcelona, Barcelona 08028, Spain.
C3 University of Barcelona; CIBER - Centro de Investigacion Biomedica en
Red; CIBERDEM; University of Barcelona; Barcelona Institute of Science &
Technology; Institute for Research in Biomedicine - IRB Barcelona
RP Hernández-Alvarez, MI; Zorzano, A (corresponding author), Univ Barcelona, Fac Biol, Dept Bioquim & Biomed Mol, Barcelona 08028, Spain.; Hernández-Alvarez, MI; Zorzano, A (corresponding author), CIBER Diabet & Enfermedades Metab Asociadas, Barcelona 08028, Spain.; Hernández-Alvarez, MI (corresponding author), Univ Barcelona, IBUB, Inst Biomed, Barcelona 08028, Spain.; Zorzano, A (corresponding author), Barcelona Inst Sci & Technol BIST, Inst Res Biomed IRB Barcelona, Barcelona 08028, Spain.
EM mihernandez@ub.edu; antonio.zorzano@irbbarcelona.org
RI Hernández-Alvarez, María Isabel/Z-4830-2019
OI Hernandez-Alvarez, Maria Isabel/0000-0003-2483-7000
FU MICINN [PID2019-106209RB-I00/AEI/10.13039/501100011033,
PID2019-105466RA-I00 AEI/10.13039/501100011033, RYC2018-024345-I];
Generalitat de Catalunya [2017SGR1015]; CIBERDEM ("Instituto de Salud
Carlos III"); Fundacion Ramon Areces [CIVP18A3942]; Fundacion BBVA;
Fundacio Marato de TV3 [20132330]; EFSD
FX This research was funded by
MICINN(PID2019-106209RB-I00/AEI/10.13039/501100011033,
PID2019-105466RA-I00 AEI/10.13039/501100011033 and RYC2018-024345-I),
the Generalitat de Catalunya (Grant 2017SGR1015), CIBERDEM ("Instituto
de Salud Carlos III"), the Fundacion Ramon Areces (CIVP18A3942), the
Fundacion BBVA, the Fundacio Marato de TV3 (20132330), and EFSD.
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NR 86
TC 26
Z9 30
U1 5
U2 27
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2021
VL 13
IS 11
AR 2571
DI 10.3390/cancers13112571
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SP3WU
UT WOS:000659603200001
PM 34073868
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Koziol, JA
Imai, H
Dai, LP
Zhang, JY
Tan, EM
AF Koziol, James A.
Imai, Haruhiko
Dai, Liping
Zhang, Jian-Ying
Tan, Eng M.
TI Early detection of hepatocellular carcinoma using autoantibody profiles
from a panel of tumor-associated antigens
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Autoantibody profiles; Tumor-associated antigens; Classification;
Hepatocellular carcinoma
ID CANCER; PROTEIN; IMMUNODIAGNOSIS; REPORTERS; DIAGNOSIS; ANTIBODY;
MARKERS; MOTIFS
AB Background Multiple antigen miniarrays used for detecting autoantibodies to tumor-associated antigens (TAAs) can be a useful approach for cancer detection and diagnosis. We here address a very specific question: might there be autoimmune responses to TAAs which precede clinical detection of hepatocellular carcinoma (HCC) in HBV and HCV chronic liver disease patients under continuous medical surveillance, and if so, could these anti-TAAs be added to the armamentarium of diagnostic tests?
Methods We here examine the utility of a panel of 12 TAAs for the diagnosis of hepatocellular carcinoma (HCC). We derived a predictive rule for the presence of HCC based on the panel, from a cohort comprising 160 HCC patients and 90 normals. We then applied this rule to sequential anti-TAA data from a cohort of 17 HCC patients, from whom this information was available prior to diagnosis.
Results The predictors (autoantibodies to HCC1, P16, P53, P90, and survivin) indicated the presence of HCC prior to diagnosis in 16 of the 17 patients, at a median lead time of 0.75 year.
Conclusions We believe these findings warrant further study of anti-TAA profiles as biomarkers for primary or early diagnosis of HCC.
C1 [Koziol, James A.; Tan, Eng M.] Scripps Res Inst, Dept Mol & Expt Med, MEM290,10550 North Torrey Pines Rd, La Jolla, CA 92037 USA.
[Imai, Haruhiko] Okudaira Clin, Matsumoto, Nagano, Japan.
[Dai, Liping; Zhang, Jian-Ying] Zhengzhou Univ, Inst Med & Pharmaceut Sci, Zhengzhou, Henan, Peoples R China.
[Zhang, Jian-Ying] Univ Texas El Paso, El Paso, TX 79968 USA.
C3 Scripps Research Institute; Zhengzhou University; University of Texas
System; University of Texas El Paso
RP Koziol, JA (corresponding author), Scripps Res Inst, Dept Mol & Expt Med, MEM290,10550 North Torrey Pines Rd, La Jolla, CA 92037 USA.
EM koziol@scripps.edu
RI Zhang, Jianying/F-3798-2010
FU National Institutes of Health [1 PO1 HL119165]
FX The authors would like to acknowledge funding received from the National
Institutes of Health: 1 PO1 HL119165 (Koziol).
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NR 22
TC 20
Z9 23
U1 0
U2 13
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
EI 1432-0851
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD MAY
PY 2018
VL 67
IS 5
BP 835
EP 841
DI 10.1007/s00262-018-2135-y
PG 7
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA GE4MQ
UT WOS:000431190400013
PM 29497780
OA Green Published
DA 2025-01-07
ER
PT J
AU Marshall, A
Lukk, M
Kutter, C
Davies, S
Alexander, G
Odom, DT
AF Marshall, Aileen
Lukk, Margus
Kutter, Claudia
Davies, Susan
Alexander, Graeme
Odom, Duncan T.
TI Global Gene Expression Profiling Reveals SPINK1 as a Potential
Hepatocellular Carcinoma Marker
SO PLOS ONE
LA English
DT Article
ID TRYPSIN-INHIBITOR TATI; PRIMARY BILIARY-CIRRHOSIS; RISK-FACTORS; PLASMA
OSTEOPONTIN; PROGNOSTIC-FACTOR; CANCER-RISK; HEREDITARY HEMOCHROMATOSIS;
AUTOIMMUNE HEPATITIS; EARLY RECURRENCE; LIVER-CANCER
AB Background: Liver cirrhosis is the most important risk factor for hepatocellular carcinoma (HCC) but the role of liver disease aetiology in cancer development remains under-explored. We investigated global gene expression profiles from HCC arising in different liver diseases to test whether HCC development is driven by expression of common or different genes, which could provide new diagnostic markers or therapeutic targets.
Methodology and Principal Findings: Global gene expression profiling was performed for 4 normal (control) livers as well as 8 background liver and 7 HCC from 3 patients with hereditary haemochromatosis (HH) undergoing surgery. In order to investigate different disease phenotypes causing HCC, the data were compared with public microarray repositories for gene expression in normal liver, hepatitis C virus (HCV) cirrhosis, HCV-related HCC (HCV-HCC), hepatitis B virus (HBV) cirrhosis and HBV-related HCC (HBV-HCC). Principal component analysis and differential gene expression analysis were carried out using R Bioconductor. Liver disease-specific and shared gene lists were created and genes identified as highly expressed in hereditary haemochromatosis HCC (HH-HCC) were validated using quantitative RT-PCR. Selected genes were investigated further using immunohistochemistry in 86 HCC arising in liver disorders with varied aetiology. Using a 2-fold cut-off, 9 genes were highly expressed in all HCC, 11 in HH-HCC, 270 in HBV-HCC and 9 in HCV-HCC. Six genes identified by microarray as highly expressed in HH-HCC were confirmed by RT qPCR. Serine peptidase inhibitor, Kazal type 1 (SPINK1) mRNA was very highly expressed in HH-HCC (median fold change 2291, p = 0.0072) and was detected by immunohistochemistry in 91% of HH-HCC, 0% of HH-related cirrhotic or dysplastic nodules and 79% of mixed-aetiology HCC.
Conclusion: HCC, arising from diverse backgrounds, uniformly over-express a small set of genes. SPINK1, a secretory trypsin inhibitor, demonstrated potential as a diagnostic HCC marker and should be evaluated in future studies.
C1 [Marshall, Aileen; Lukk, Margus; Kutter, Claudia; Odom, Duncan T.] Li Ka Shing Ctr, Canc Res UK Cambridge Res Inst, Cambridge, England.
[Marshall, Aileen; Davies, Susan] Addenbrookes Hosp, Dept Histopathol, Cambridge CB2 2QQ, England.
[Alexander, Graeme] Addenbrookes Hosp, Cambridge Hepatobiliary Unit, Cambridge, England.
[Odom, Duncan T.] Hutchison MRC Res Ctr, Dept Oncol, Cambridge, England.
C3 CRUK Cambridge Institute; Cancer Research UK; University of Cambridge;
Cambridge University Hospitals NHS Foundation Trust; Addenbrooke's
Hospital; University of Cambridge; Cambridge University Hospitals NHS
Foundation Trust; Addenbrooke's Hospital
RP Marshall, A (corresponding author), Li Ka Shing Ctr, Canc Res UK Cambridge Res Inst, Cambridge, England.
EM aileen.marshall@cruk.cam.ac.uk; duncan.odom@cruk.cam.ac.uk
RI Kutter, Claudia/HHD-1391-2022
OI Lukk, Margus/0000-0002-0701-5358; Odom, Duncan T/0000-0001-6201-5599;
Kutter, Claudia/0000-0002-8047-0058
FU European Research Council; EMBO Young Investigator Program; Cancer
Research UK; University of Cambridge; Swiss National Science Foundation;
Cambridge Biomedical Campus
FX The authors receive support from the European Research Council, EMBO
Young Investigator Program, (D.T.O.), Cancer Research UK (M. L., C. K.),
University of Cambridge (C. K., D.T.O.), Swiss National Science
Foundation (C. K.), and the Cambridge Biomedical Campus (A. M.). These
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 67
TC 58
Z9 65
U1 0
U2 16
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAR 18
PY 2013
VL 8
IS 3
AR e59459
DI 10.1371/journal.pone.0059459
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 109ZS
UT WOS:000316411600058
PM 23527199
OA Green Published, Green Submitted, Green Accepted, gold
DA 2025-01-07
ER
PT J
AU Curran, CS
Sharon, E
AF Curran, Colleen S.
Sharon, Elad
TI PD-1 immunobiology in autoimmune hepatitis and hepatocellular carcinoma
SO SEMINARS IN ONCOLOGY
LA English
DT Review
DE autoimmune hepatitis; hepatocellular carcinoma; programmed cell-death 1
(PD-1); matrix metalloproteinases; IL-18
ID PROGRAMMED DEATH-1; NK CELLS; T-CELLS; MATRIX METALLOPROTEINASES;
DENDRITIC CELLS; STELLATE CELLS; KUPFFER CELLS; LIVER-DISEASE;
PLASMA-CELLS; IFN-GAMMA
AB Disruption of liver immune tolerance allows for the development of autoimmune hepatitis (AIH) and hepatocellular carcinoma (HCC). AIH rarely progresses to HCC but the diseases similarly induce the production of IL-18 and matrix metalloproteinases. These molecules have distinct effects on the immune response, including the programmed cell-death 1 (PD-1) axis. In this review, differences in PD-1 function and possible cell signals in AIH and HCC are highlighted. Published by Elsevier Inc.
C1 [Curran, Colleen S.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Sharon, Elad] NCI, Canc Therapy Evaluat Program, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH Clinical Center (CC);
National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI)
RP Sharon, E (corresponding author), NCI, NIH, 9609 Med Ctr Dr,Room 5W448, Bethesda, MD 20892 USA.
EM sharone@mail.nih.gov
OI Curran, Colleen/0000-0002-4517-6494
FU Intramural NIH HHS [Z99 CA999999, Z99 CL999999] Funding Source: Medline
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NR 73
TC 15
Z9 17
U1 0
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
EI 1532-8708
J9 SEMIN ONCOL
JI Semin. Oncol.
PD DEC
PY 2017
VL 44
IS 6
BP 428
EP 432
DI 10.1053/j.seminoncol.2017.12.001
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GL0GZ
UT WOS:000436649300007
PM 29935904
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Zeng, LL
Zhu, LT
Fu, SS
Li, YA
Hu, KH
AF Zeng, Lianlin
Zhu, Lutao
Fu, Shasha
Li, Yangan
Hu, Kehui
TI Mitochondrial Dysfunction-Molecular Mechanisms and Potential Treatment
approaches of Hepatocellular Carcinoma
SO MOLECULAR AND CELLULAR BIOCHEMISTRY
LA English
DT Review; Early Access
DE Hepatocellular Carcinoma; Mitochondrial dysfunction; Oxidative stress;
Autophagy; Cellular senescence
ID AUTOPHAGY; APOPTOSIS; CELL; MITOPHAGY; DYNAMICS; INSIGHTS; BNIP3
AB Primary liver cancer (PLC), also known as hepatocellular carcinoma (HCC), is a common type of malignant tumor of the digestive system. Its pathological form has a significant negative impact on the patients' quality of life and ability to work, as well as a significant financial burden on society. Current researches had identified chronic hepatitis B virus infection, aflatoxin B1 exposure, and metabolic dysfunction-associated steatotic liver disease (MASLD) as the main causative factors of HCC. Numerous variables, including inflammatory ones, oxidative stress, apoptosis, autophagy, and others, have been linked to the pathophysiology of HCC. On the other hand, autoimmune regulation, inflammatory response, senescence of the hepatocytes, and mitochondrial dysfunction are all closely related to the pathogenesis of HCC. In fact, a growing number of studies have suggested that mitochondrial dysfunction in hepatocytes may be a key factor in the pathogenesis of HCC. In disorders linked to cancer, mitochondrial dysfunction has gained attention in recent 10 years. As the primary producer of adenosine triphosphate (ATP) in liver cells, mitochondria are essential for preserving cell viability and physiological processes. By influencing multiple pathological processes, including mitochondrial fission/fusion, mitophagy, cellular senescence, and cell death, mitochondrial dysfunction contributes to the development of HCC. We review the molecular mechanisms of HCC-associated mitochondrial dysfunction and discuss new directions for quality control of mitochondrial disorders as a treatment for HCC.
C1 [Zeng, Lianlin; Zhu, Lutao; Fu, Shasha; Li, Yangan; Hu, Kehui] Suining Cent Hosp, Dept Rehabil Med, Suining, Sichuan, Peoples R China.
RP Hu, KH (corresponding author), Suining Cent Hosp, Dept Rehabil Med, Suining, Sichuan, Peoples R China.
EM 1452673713@qq.com
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NR 73
TC 0
Z9 0
U1 7
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0300-8177
EI 1573-4919
J9 MOL CELL BIOCHEM
JI Mol. Cell. Biochem.
PD 2024 OCT 27
PY 2024
DI 10.1007/s11010-024-05144-4
EA OCT 2024
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA K5Z5C
UT WOS:001344654900001
PM 39463200
DA 2025-01-07
ER
PT J
AU Ogunwobi, OO
Harricharran, T
Huaman, J
Galuza, A
Odumuwagun, O
Tan, Y
Ma, GX
Nguyen, MT
AF Ogunwobi, Olorunseun O.
Harricharran, Trisheena
Huaman, Jeannette
Galuza, Anna
Odumuwagun, Oluwatoyin
Tan, Yin
Ma, Grace X.
Nguyen, Minhhuyen T.
TI Mechanisms of hepatocellular carcinoma progression
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Hepatocellular carcinoma; Viral/non-viral hepatitis; Alcohol
consumption; Epithelial-mesenchymal transition; Tumor-stromal
interactions; Tumor microenvironment; Cancer stem cells; Circulating
tumor cells; Immunomodulation; Neural regulation
ID CIRCULATING TUMOR-CELLS; CANCER STEM-CELLS; HEPATIC STELLATE CELLS;
ACUTE MYELOID-LEUKEMIA; LIVER-CANCER; MOLECULAR-MECHANISMS; DIURNAL
CORTISOL; PROSTATE-CANCER; NONCODING RNAS; RISK-FACTOR
AB Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver. It is the second leading cause of cancer-related deaths worldwide, with a very poor prognosis. In the United States, there has been only minimal improvement in the prognosis for HCC patients over the past 15 years. Details of the molecular mechanisms and other mechanisms of HCC progression remain undear. Consequently, there is an urgent need for better understanding of these mechanisms. HCC is often diagnosed at advanced stages, and most patients will therefore need systemic therapy, with sorafenib being the most common at the present time. However, sorafenib therapy only minimally enhances patient survival. This review provides a summary of some of the known mechanisms that either cause HCC or contribute to its progression. Included in this review are the roles of viral hepatitis, non-viral hepatitis, chronic alcohol intake, genetic predisposition and congenital abnormalities, toxic exposures, and autoimmune diseases of the liver. Well-established molecular mechanisms of HCC progression such as epithelial-mesenchymal transition, tumor-stromal interactions and the tumor microenvironment, cancer stem cells, and senescence bypass are also discussed. Additionally, we discuss the roles of circulating tumor cells, immunomodulation, and neural regulation as potential new mechanisms of HCC progression. A better understanding of these mechanisms could have implications for the development of novel and more effective therapeutic and prognostic strategies, which are critically needed.
C1 [Ogunwobi, Olorunseun O.; Harricharran, Trisheena; Huaman, Jeannette; Galuza, Anna; Odumuwagun, Oluwatoyin] CUNY Hunter Coll, Dept Biol Sci, 695 Pk Ave, New York, NY 10065 USA.
[Ogunwobi, Olorunseun O.; Harricharran, Trisheena; Huaman, Jeannette] CUNY, Grad Ctr, Dept Biol, New York, NY USA.
[Ogunwobi, Olorunseun O.; Harricharran, Trisheena; Huaman, Jeannette] CUNY, Grad Ctr, Dept Biochem, New York, NY USA.
[Ogunwobi, Olorunseun O.; Harricharran, Trisheena] Cornell Univ, Weill Cornell Med, Joan & Sanford I Weill Dept Med, New York, NY 10065 USA.
[Ogunwobi, Olorunseun O.; Harricharran, Trisheena; Huaman, Jeannette; Galuza, Anna; Odumuwagun, Oluwatoyin] Hunter Coll, CCHDR, New York, NY 10065 USA.
[Tan, Yin; Ma, Grace X.] Temple Univ, Sch Med, Ctr Asian Hlth, Philadelphia, PA 19140 USA.
[Nguyen, Minhhuyen T.] Fox Chase Canc Ctr, Dept Med, Philadelphia, PA 19111 USA.
C3 City University of New York (CUNY) System; Hunter College (CUNY); City
University of New York (CUNY) System; City University of New York (CUNY)
System; Cornell University; Weill Cornell Medicine; City University of
New York (CUNY) System; Hunter College (CUNY); Pennsylvania Commonwealth
System of Higher Education (PCSHE); Temple University; Fox Chase Cancer
Center
RP Ogunwobi, OO (corresponding author), CUNY Hunter Coll, Dept Biol Sci, 695 Pk Ave, New York, NY 10065 USA.
EM ogunwobi@genectr.hunter.cuny.edu
RI TAN, YING/AAT-4671-2020; Ogunwobi, Olorunseun/F-3172-2010
OI Ogunwobi, Olorunseun/0000-0003-3388-2137
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NR 141
TC 171
Z9 187
U1 4
U2 34
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAY 21
PY 2019
VL 25
IS 19
BP 2279
EP 2293
DI 10.3748/wjg.v25.i19.2279
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HY7QC
UT WOS:000468329900002
PM 31148900
OA hybrid, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Manivannan, A
Mazumder, S
Al-Kourainy, N
AF Manivannan, Ahila
Mazumder, Samia
Al-Kourainy, Nabil
TI The Role of Hepatocellular Carcinoma Surveillance in Autoimmune
Hepatitis
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE hepatocellular carcinoma (hcc); autoimmune hepatitis; screening
guidelines
ID EPIDEMIOLOGY
AB Type 1 autoimmune hepatitis (AIH) is a rare inflammatory disorder of the liver that may arise at any age, from infancy to adulthood. Long-standing autoimmune hepatitis may progress to cirrhosis and subsequent hepatocellular carcinoma (HCC). However, the true incidence of HCC in AIH patients is unknown as there is a paucity of published data. Currently, there are no established guidelines on screening patients with AIH for HCC. Without screening protocols, patients with AIH may present with late-stage HCC that may have been detected and treated earlier in the disease course. We describe a case of a patient with type 1 AIH who developed stage IIIB HCC in the absence of appropriate screening protocols with complex social determinants leading to barriers to access regular follow-up care.
C1 [Manivannan, Ahila; Mazumder, Samia; Al-Kourainy, Nabil] Wayne State Univ, Sch Med, Internal Med, Detroit, MI 48202 USA.
C3 Wayne State University
RP Manivannan, A (corresponding author), Wayne State Univ, Sch Med, Internal Med, Detroit, MI 48202 USA.
EM fj0752@wayne.edu
OI Manivannan, Ahila/0000-0001-6757-7048
CR [Anonymous], 2020, CANC FACTS FIGURES 2
Christen U, 2019, CLIN EXP IMMUNOL, V195, P35, DOI 10.1111/cei.13203
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Palle SK, 2019, LIVER INT, V39, P976, DOI 10.1111/liv.14081
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Singal AG, 2015, CLIN GASTROENTEROL H, V13, P2140, DOI 10.1016/j.cgh.2015.08.014
Tansel A, 2017, CLIN GASTROENTEROL H, V15, P1207, DOI 10.1016/j.cgh.2017.02.006
Werner M, 2008, SCAND J GASTROENTERO, V43, P1232, DOI 10.1080/00365520802130183
Yeoman AD, 2008, HEPATOLOGY, V48, P863, DOI 10.1002/hep.22432
Zhang JX, 2020, PLOS ONE, V15, DOI 10.1371/journal.pone.0228857
NR 14
TC 2
Z9 3
U1 0
U2 2
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD OCT 30
PY 2020
VL 12
IS 10
AR e11269
DI 10.7759/cureus.11269
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA OI3LS
UT WOS:000583185100018
PM 33274145
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Kimura, T
Kobayashi, A
Tanaka, N
Sano, K
Komatsu, M
Fujimori, N
Yamazaki, T
Shibata, S
Ichikawa, Y
Joshita, S
Umemura, T
Matsumoto, A
Horiuchi, A
Mori, H
Wada, S
Kiyosawa, K
Miyagawa, S
Tanaka, E
AF Kimura, Takefumi
Kobayashi, Akira
Tanaka, Naoki
Sano, Kenji
Komatsu, Michiharu
Fujimori, Naoyuki
Yamazaki, Tomoo
Shibata, Soichiro
Ichikawa, Yuki
Joshita, Satoru
Umemura, Takeji
Matsumoto, Akihiro
Horiuchi, Akira
Mori, Hiromitsu
Wada, Shuichi
Kiyosawa, Kendo
Miyagawa, Shin-ichi
Tanaka, Eiji
TI Clinicopathological characteristics of non-B non-C hepatocellular
carcinoma without past hepatitis B virus infection
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE diabetes; liver fibrosis; non-B non-B hepatocellular carcinoma; normal
liver; obesity; past HBV infection
ID FATTY LIVER-DISEASE; CLINICAL CHARACTERISTICS; DOWN-REGULATION; PNPLA3;
CANCER; ANTIBODY; ONSET; HBV; EXPRESSION; FEATURES
AB AimPast hepatitis B virus (HBV) infection is considered a risk factor for hepatocarcinogenesis, but the clinicopathological characteristics of non-B non-C hepatocellular carcinoma (NBNC-HCC) excluding past HBV infection have not been investigated. This study aimed to clarify the clinicopathological features of strictly defined NBNC-HCC.
MethodsAmong HCC patients who underwent surgical resection at our affiliated hospitals in Nagano prefecture, Japan, between 1996 and 2012, 77 were negative for serum anti-HBV core/surface antibodies in addition to HBV surface antigen and anti-hepatitis C virus antibody without signs of autoimmune liver disease, Wilson disease, or hemochromatosis. These patients were divided into the alcohol intake-positive group (ethanol intake >20g/day, n=31), non-alcoholic fatty liver group (steatosis >5% and ethanol intake <20g/day, n=30), and cryptogenic group (no ethanol intake or steatosis, n=16). Preoperative clinical parameters, tumor and background liver pathology, and prognosis were analyzed.
ResultsAdvanced fibrosis and steatosis were detected in 64% and 60% of all patients, respectively. Approximately 85% of the alcohol intake-positive patients had advanced fibrosis. Non-alcoholic fatty liver HCC subjects had the highest body mass index and prevalence of diabetes, but 30-40% had none to mild fibrosis. The cryptogenic group of HCC patients had the lowest incidence of accompanying hepatic inflammation/fibrosis but the largest tumor size. Recurrence/survival rates were comparable among the groups.
ConclusionsLiver fibrosis and steatosis are risk factors of HCC regardless of past HBV infection and ethanol consumption. The present results also indicate the possibility of hepatocarcinogenesis independent of hepatic steatosis, inflammation and fibrosis, ethanol intake, and past HBV infection.
C1 [Kimura, Takefumi; Komatsu, Michiharu; Fujimori, Naoyuki; Yamazaki, Tomoo; Shibata, Soichiro; Ichikawa, Yuki; Joshita, Satoru; Umemura, Takeji; Matsumoto, Akihiro; Tanaka, Eiji] Shinshu Univ, Sch Med, Dept Internal Med, Div Gastroenterol, Matsumoto, Nagano, Japan.
[Kobayashi, Akira; Miyagawa, Shin-ichi] Shinshu Univ, Sch Med, Dept Surg, Matsumoto, Nagano, Japan.
[Tanaka, Naoki] Shinshu Univ, Grad Sch Med, Dept Metab Regulat, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan.
[Sano, Kenji] Shinshu Univ Hosp, Dept Lab Med, Matsumoto, Nagano, Japan.
[Kiyosawa, Kendo] Aizawa Hosp, Dept Internal Med, Matsumoto, Nagano, Japan.
[Kimura, Takefumi; Mori, Hiromitsu; Wada, Shuichi] Nagano Red Cross Hosp, Dept Gastroenterol, Nagano, Japan.
[Horiuchi, Akira] Showa Inan Gen Hosp, Digest Dis Ctr, Komagane, Japan.
C3 Shinshu University; Shinshu University; Shinshu University; Shinshu
University; Nagano Red Cross Hospital
RP Tanaka, N (corresponding author), Shinshu Univ, Grad Sch Med, Dept Metab Regulat, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan.
EM naopi@shinshu-u.ac.jp
RI Joshita, Satoru/K-5679-2019; Kimura, Takefumi/D-3412-2011
OI Kimura, Takefumi/0000-0002-1481-1029; Tanaka, Naoki/0000-0002-3212-3836
FU Shinshu Public Utility Foundation for Promotion of Medical Sciences;
Grants-in-Aid for Scientific Research [15H01803] Funding Source: KAKEN
FX THIS STUDY WAS supported by the Shinshu Public Utility Foundation for
Promotion of Medical Sciences (to N.T.). The authors thank Trevor Ralph
for his English editorial assistance.
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Zhang H, 2013, SCAND J GASTROENTERO, V48, P78, DOI 10.3109/00365521.2012.719926
NR 50
TC 26
Z9 27
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD APR
PY 2017
VL 47
IS 5
BP 405
EP 418
DI 10.1111/hepr.12762
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ES7PG
UT WOS:000399741900004
PM 27288988
DA 2025-01-07
ER
PT J
AU West, J
Card, TR
Aithal, GP
Fleming, KM
AF West, J.
Card, T. R.
Aithal, G. P.
Fleming, K. M.
TI Risk of hepatocellular carcinoma among individuals with different
aetiologies of cirrhosis: a population-based cohort study
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID COST-EFFECTIVENESS; VIRUS-INFECTIONS; LIVER-CIRRHOSIS; HEPATITIS;
CANCER; TRENDS; CARE; SURVEILLANCE; DIAGNOSIS; VALIDITY
AB BackgroundAmong patients with cirrhosis, only those determined to be at risk for hepatocellular carcinoma (HCC) should undergo surveillance. However, little is known about how different aetiologies of cirrhosis affect risk for HCC.
AimTo quantify the cumulative incidence of HCC among a representative population of people with cirrhosis of the liver of varying aetiology.
MethodsWe identified subjects with hepatic cirrhosis from the UK's General Practice Research Database (1987-2006). Diagnoses of HCC were obtained from linked national cancer registries (1971-2006). Cox proportional hazards regression was used to estimate hazard ratios. The predicted 10-year cumulative incidence of HCC for each aetiology of cirrhosis was estimated while accounting for competing risks of death from any cause and liver transplant.
ResultsAmong 3107 people with cirrhosis, the adjusted relative risk of HCC was increased twofold to threefold among people with viral and autoimmune/metabolic aetiologies, compared to those with alcohol-associated cirrhosis. The 10-year predicted cumulative incidence estimates of HCC for each aetiology were alcohol, 1.2%; chronic viral hepatitis, 4.0%; autoimmune or metabolic disease, 3.2%; and cryptogenic, 1.1%.
ConclusionsIn a population-based study in the UK, people with cirrhosis have an estimated cumulative 10-year incidence of HCC of 4% or lower. Cumulative incidence varies with aetiology such that individuals with alcohol or cryptogenic cirrhosis have the lowest risk for HCC. These findings provide important information for cost-effectiveness analyses of HCC surveillance.
C1 [West, J.; Card, T. R.; Fleming, K. M.] Univ Nottingham, Div Epidemiol & Publ Hlth, Room B113,Clin Sci Bldg 2,City Hosp Campus, Nottingham NG5 1PB, England.
[Card, T. R.; Aithal, G. P.] Univ Nottingham, Nottingham Univ Hosp NHS Trust, NIHR Nottingham Digest Dis Biomed Res Unit, Nottingham, England.
[Fleming, K. M.] Liverpool John Moores Univ, Inst Publ Hlth, Liverpool, Merseyside, England.
C3 University of Nottingham; Nottingham University Hospital NHS Trust;
Nottingham City Hospital; Nottingham University Hospital NHS Trust;
University of Nottingham; Liverpool John Moores University
RP West, J (corresponding author), Univ Nottingham, Div Epidemiol & Publ Hlth, Room B113,Clin Sci Bldg 2,City Hosp Campus, Nottingham NG5 1PB, England.
EM joe.west@nottingham.ac.uk
RI Card, Timothy/J-8651-2013; West, Joe/I-6637-2012; Fleming,
Kate/A-6475-2010
OI Card, Timothy/0000-0003-2555-2250; West, Joe/0000-0002-1135-9356;
Aithal, Guruprasad/0000-0003-3924-4830; Fleming,
Kate/0000-0002-6572-5016
FU University of Nottingham/Nottingham Hospitals Nottingham NHS Senior
Clinical Research Fellowship; MRC [MR/N005953/1] Funding Source: UKRI
FX JW was funded by a University of Nottingham/Nottingham Hospitals
Nottingham NHS Senior Clinical Research Fellowship during the majority
of the time this paper was worked on. Funding from this fellowship
helped pay for acquisition of the data. The funders had no influence on
the content or interpretation of the work.
CR [Anonymous], 2022, International Statistical Classification of Diseases and Related Health Problems
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World Health Organization, 1977, INT CLASS DIS MAN IN
NR 32
TC 63
Z9 66
U1 1
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD APR
PY 2017
VL 45
IS 7
BP 983
EP 990
DI 10.1111/apt.13961
PG 8
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA EM5SJ
UT WOS:000395372700011
PM 28144999
OA Green Accepted, hybrid
DA 2025-01-07
ER
PT J
AU Chang, ML
Le, PH
Chen, WT
Chen, TD
Chien, RN
AF Chang, Ming-Ling
Le, Puo-Hsien
Chen, Wei-Ting
Chen, Tai-Di
Chien, Rong-Nan
TI Hepatic and Extrahepatic Characteristics of Autoimmune Hepatitis: A
23-year Hospital-Based Cohort Study
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE AIH; HCC; Cirrhosis; Alkaline Phosphatase; ANA
ID CLINICAL-FEATURES; HEPATOCELLULAR-CARCINOMA; LIVER-DISEASES; DIAGNOSIS;
WITHDRAWAL; MANAGEMENT; MORTALITY; CIRRHOSIS; CRITERIA; TAIWAN
AB BackgroundThe characteristics of autoimmune hepatitis (AIH) in Asia mostly remain elusive.MethodsA cohort study of liver biopsy-proven AIH patients was conducted in a tertiary care cancer of Taiwan.ResultsFrom 1999 to 2022, of 13,766 patients who underwent liver biopsy, 150 patients with AIH were enrolled. The female-to-male ratio was 2.26. At baseline, the mean age was 51.09 years, mean alanine aminotransferase level was 494.11 U/L, and 17 (11.3%) had cirrhosis. All except one patient had AIH type 1. The females were older and had higher baseline cirrhosis rates than did the males. The 23-year cumulative incidences of cirrhosis, hepatocellular carcinoma (HCC), mortality/liver transplantation, autoimmune diseases and extrahepatic cancer were 64.2%, 13.3%, 23.4%, 30.7% and 21.2%, respectively. The 1-year, 2-year, 3-year, 5-year, 10-year and 20-year postimmunosuppressive therapy relapse rates were 60%, 78.2%, 81.8%, 89.1%, 94.5% and 100%, respectively. Baseline associations were as follows: alkaline phosphatase (Alk-p) levels with postimmunosuppressive therapy flare [hazard ratio (HR): 1.003; 95% CI HR: 1.000-1.005]; age with HCC (1.072; 1.010-1.138) and all-cause cancer (1.041;1.005-1.079); cirrhosis with mortality/liver transplantation (11.933;1.984-71.787); and antinuclear antibody (ANA) titers with mortality/liver transplantation (1.001;1.000-1.003), cirrhosis (1.001;1.000-1.002), and autoimmune diseases (1.001; 1.000-1.002).ConclusionIn an Asian country endemic for viral hepatitis, the female-to-male and baseline cirrhosis rates of AIH patients were lower than expected, while over 60% of the patients eventually developed cirrhosis. The high posttherapy relapse rate warrants cautious monitoring, particularly for patients with high baseline Alk-p levels. Baseline age, cirrhosis status and ANA titers are crucial for outcomes.
C1 [Chang, Ming-Ling; Le, Puo-Hsien; Chen, Wei-Ting; Chien, Rong-Nan] Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, 5 Fu Hsing St, Taoyuan, Taiwan.
[Chang, Ming-Ling; Le, Puo-Hsien; Chen, Wei-Ting; Chien, Rong-Nan] Chang Gung Univ, Coll Med, Dept Med, Taoyuan, Taiwan.
[Chen, Tai-Di] Chang Gung Mem Hosp, Dept Anat Pathol, Taoyuan, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; Chang Gung Memorial
Hospital
RP Chang, ML (corresponding author), Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, 5 Fu Hsing St, Taoyuan, Taiwan.; Chang, ML (corresponding author), Chang Gung Univ, Coll Med, Dept Med, Taoyuan, Taiwan.
EM mlchang8210@gmail.com
RI CHEN, WEI-TING/AFL-9663-2022; Chen, Tai-Di/JJD-8288-2023
OI Le, Puo-hsien/0000-0002-1100-5371
FU Department of Hepatology and Gastroeneterology, Chang Gung Memorial
Hospital, Taiwan
FX The authors thank Mr. Shuen-Shian Shiau from the Department of
Hepatology and Gastroeneterology, Chang Gung Memorial Hospital, Taiwan,
for his excellent assistance with the data mining.
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US
NR 56
TC 1
Z9 1
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD JUN
PY 2024
VL 69
IS 6
BP 2193
EP 2203
DI 10.1007/s10620-024-08439-0
EA APR 2024
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA TW1N9
UT WOS:001207125600004
PM 38653947
DA 2025-01-07
ER
PT J
AU Fouad, Y
Gaber, Y
Alem, SA
Abdallah, M
Abd-Elsalam, SM
Nafady, S
Attia, D
Eslam, M
AF Fouad, Yasser
Gaber, Yasmine
Alem, Shereen Abdel
Abdallah, Mohamed
Abd-Elsalam, Sherief M.
Nafady, Shaymaa
Attia, Dina
Eslam, Mohamed
TI Changes in the Etiologies of Liver Cancer in Upper Egypt over a Decade
from 2010 to 2020: A Single Tertiary Care Center Study
SO SOUTH ASIAN JOURNAL OF CANCER
LA English
DT Article
DE HCC; Egypt; MAFLD; viral hepatitis; trends
ID HEPATOCELLULAR-CARCINOMA; HEPATITIS-C; ELIMINATION; DISEASE
AB The profile of liver diseases in Egypt is changing dramatically and viral hepatitis is declining, while the fatty liver disease is increasing dramatically. However, the impact of these changes on the profile of hepatocellular carcinoma (HCC) remains uncertain. Therefore, we determined the temporal trends in the etiologies of HCC in Egypt over a decade. We retrospectively analyzed data from consecutive patients who were diagnosed with HCC over 10 years (2010-2020) in a large center in Upper Egypt. Standard tests were utilized to diagnose hepatitis C virus (HCV) and hepatitis B virus. In the absence of other liver disorders, the presence of obesity, or diabetes in the absence of other risk factors, metabolic dysfunction-associated fatty liver disease (MAFLD) was diagnosed. A total of 1,368 HCC patients were included, in which 985 (72%) had HCV, 58 (4%) had hepatitis B virus, and 143 (10.5%) had MAFLD, 1 patient had hemochromatosis, 1 had autoimmune liver disease, and 180 (13%) patients were with unknown cause. The annual proportions of MAFLD-related HCC were increased significantly between 8.3% in 2010 and 20.6% in 2020 (p = 0.001), while HCV-related HCC declined from 84.8 to 66.7% (p = 0.001). Throughout the study period, there were significant increases in the age at diagnosis of HCC, the proportion of female patients, obesity, diabetes, and less severe liver dysfunction at diagnosis (p < 0.05 for all). With the decline of HCV, MAFLD is becoming a major cause of HCC in Egypt, which has increased substantially over the past 10 years. This study urges the creation of comprehensive action strategies to address this growing burden.
C1 [Fouad, Yasser] Minia Univ, Fac Med, Dept Gastroenterol Hepatol & Endem Med, Cairo, Egypt.
[Gaber, Yasmine; Alem, Shereen Abdel] Cairo Univ, Fac Med, Dept Endem Med & Hepatol, Cairo, Egypt.
[Abdallah, Mohamed] Natl Res Ctr, Dept Med Res, Div Med, Giza, Egypt.
[Abd-Elsalam, Sherief M.] Tanta Univ, Fac Med, Trop Med & Infect Dis Dept, Tanta, Egypt.
[Nafady, Shaymaa; Attia, Dina] Beni Suef Univ, Fac Med, Dept Gastroenterol Hepatol & Infect Dis, Bani Suwayf, Egypt.
[Eslam, Mohamed] Univ Sydney, Westmead Hosp, Westmead Inst Med Res, Storr Liver Ctr, Sydney, NSW, Australia.
[Abd-Elsalam, Sherief M.] Tanta Univ, Trop Med & Infect Dis Dept, Tanta 35127, Egypt.
C3 Egyptian Knowledge Bank (EKB); Minia University; Egyptian Knowledge Bank
(EKB); Cairo University; Egyptian Knowledge Bank (EKB); National
Research Centre (NRC); Egyptian Knowledge Bank (EKB); Tanta University;
Egyptian Knowledge Bank (EKB); Beni Suef University; NSW Health;
Westmead Hospital; University of Sydney; Westmead Institute for Medical
Research; Egyptian Knowledge Bank (EKB); Tanta University
RP Abd-Elsalam, SM (corresponding author), Tanta Univ, Trop Med & Infect Dis Dept, Tanta 35127, Egypt.
EM sherif.abdelbaky@med.tanta.edu.eg
RI Alem, Shereen/AAB-9687-2019; Abd-Elsalam, sherief/L-3274-2018; Fouad,
Yasser/Y-7180-2018; Abdallah, Mohamed/ABB-6297-2021; Attia,
Dina/AAP-2462-2020
OI Attia, Dina/0000-0001-8374-2533
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NR 21
TC 0
Z9 0
U1 0
U2 0
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 2278-330X
EI 2278-4306
J9 SOUTH ASIAN J CANCER
JI South Asian J. Cancer
PD JAN
PY 2024
VL 13
IS 01
BP 10
EP 16
DI 10.1055/s-0043-1771440
EA AUG 2023
PG 7
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA PO9L6
UT WOS:001042273600001
PM 38721105
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Ding, WZ
Han, GY
Jin, HH
Zhan, CF
Ji, Y
Huang, XL
AF Ding, Wen-Zhou
Han, Guo-Yong
Jin, Hui-Han
Zhan, Chuan-Fei
Ji, Yuan
Huang, Xin-Li
TI Anti-IL-20 monoclonal antibody suppresses hepatocellular carcinoma
progression
SO ONCOLOGY LETTERS
LA English
DT Article
DE interleukin-20; anti-interleukin-20 monoclonal antibody; hepatocellular
carcinoma; proliferation; metastasis
ID CANCER; ACTIVATION; LIVER; IL-20; EXPRESSION; INTERLEUKIN-20;
IDENTIFICATION; KINASE
AB Interleukin (IL)-20 is a member of the IL-10 family of cytokines, which has been reported to participate in autoimmune inflammatory diseases. However, the potential role of IL-20 in hepatocellular carcinoma (HCC) progression has not yet been investigated. In the present study, it was observed that IL-20 mRNA and protein levels were markedly increased in the HCC tissues examined via reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining. In addition, IL-20 expression was significantly associated with tumor size, metastasis, TNM stage and poor prognosis in patients with HCC. Mouse recombinant IL-20 (mIL-20) enhanced liver cancer cell proliferation, migration and invasion in vitro, while the anti-IL-20 monoclonal antibody (mAb) attenuated the effect of mIL-20, inhibiting cancer cell migration and invasion in vitro and suppressing cell growth in vitro and in vivo. This was detected by Cell Counting Kit-8, colony formation, Transwell assays and a xenograft tumor nude mouse model. Western blotting revealed that IL-20 promoted HCC progression through inducing transforming growth factor-beta and matrix metalloproteinase 9 expression and enhancing the phosphorylation of Jun N-terminal kinase and signal transducer and activator of transcription 3. The results of the present study indicated that IL-20 promotes HCC development. In addition, anti-IL-20 mAb may attenuate the effect of IL-20 and suppress liver tumorigenesis in vitro and in vivo, indicating that anti-IL-20 mAbs may potentially serve as effective therapeutic agents for HCC.
C1 [Ding, Wen-Zhou; Jin, Hui-Han; Ji, Yuan] Nanjing Med Univ, Affiliated Wuxi Hosp 2, Dept Hepatobiliary Surg, Wuxi 214002, Jiangsu, Peoples R China.
[Han, Guo-Yong; Zhan, Chuan-Fei] Nanjing Med Univ, Natl Hlth & Family Planning Commiss, Key Lab Living Donor Liver Transplantat, Dept Liver Surg,Affiliated Hosp 1, Nanjing 210029, Jiangsu, Peoples R China.
[Huang, Xin-Li] Nanjing Univ, Affiliated Hosp, Nanjing Drum Tower Hosp, Dept Hepatobiliary Surg,Med Sch, 321 Zhongshan Rd, Nanjing 210008, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing
University
RP Huang, XL (corresponding author), Nanjing Univ, Affiliated Hosp, Nanjing Drum Tower Hosp, Dept Hepatobiliary Surg,Med Sch, 321 Zhongshan Rd, Nanjing 210008, Jiangsu, Peoples R China.
EM huangxinli@njmu.edu.cn
RI Zhang, Guo-Qiang/AAG-6817-2019
FU Six Talent Peaks Project in Jiangsu Province [2014-WSW-005]
FX The present study was supported by a grant from the Six Talent Peaks
Project in Jiangsu Province (grant no. 2014-WSW-005).
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NR 22
TC 7
Z9 7
U1 0
U2 0
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD NOV
PY 2018
VL 16
IS 5
BP 6156
EP 6162
DI 10.3892/ol.2018.9402
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GY3FG
UT WOS:000448433500084
PM 30333881
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Meza-Junco, J
Montaño-Loza, AJ
Martínez-Benitez, B
Kimura-Hayama, E
AF Meza-Junco, Judith
Montano-Loza, Aldo J.
Martinez-Benitez, Braulio
Kimura-Hayama, Eric
TI Hepatocellular carcinoma in patients with autoimmune liver diseases::
Two case reports and literature review
SO ANNALS OF HEPATOLOGY
LA English
DT Review
DE hepatocellular carcinoma; autoimmune; hepatitis and primary biliary
cirrhosis
ID PRIMARY BILIARY-CIRRHOSIS; MEDICAL PROGRESS; HEPATITIS; SURVIVAL; CANCER
AB Background and aims: Hepatocellular carcinoma has been reported as a rare complication of autoimmune liver diseases. We describe herein two patients with this neoplasia associated with autoimmune hepatitis and primary biliary cirrhosis, and we also review the literature. Cases report: The first case corresponds to a 49-year-old woman presented for evaluation of right upper abdominal pain. She had been diagnosed with antoimmune hepatitis 4 years before. Alpha-fetoprotein was markedly elevated and an abdominal MRI showed a 10 cm x 9.0 cm mass. She received transarterial chemoembolization, and currently the disease has progressed to the lungs and bones, and she is on supportive care. The second case corresponds to a 68-year-old woman presented for evaluation of a liver mass found in a screening ultrasound. She had been diagnosed with primary biliary cirrhosis 5 years previously. At admission alpha-fetoprotein was 1000 ng/mL and an abdominal MRI revealed a 4 cm x 3 cm liver tumor. She was treated with percutaneous radiofrequency ablation getting complete response, and currently she has no evidence of neoplastic disease. These two patients constitute the only cases of hepatocellular carcinoma associated to autoimmune liver diseases that have been attended in our Institute. Conclusion: These cases highlight that hepatocellular carcinoma secondary to autoimmune hepatitis and primary biliary cirrhosis, although rare, can occur in the absence of coexistent viral hepatitis, or excessive alcohol consumption. The utility of screening for hepatocellular carcinoma in antoimmune liver diseases is still not defined.
C1 [Meza-Junco, Judith] INCMNSZ, Dept Oncol, Mexico City 16000, DF, Mexico.
RP Meza-Junco, J (corresponding author), INCMNSZ, Dept Oncol, Vasco Quiroga 15, Mexico City 16000, DF, Mexico.
EM judithmj@quetzal.innsz.mx
RI Montano-Loza, Aldo/B-3092-2013
OI Montano-Loza, Aldo J./0000-0002-2511-7980
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NR 28
TC 10
Z9 10
U1 0
U2 1
PU ELSEVIER ESPANA
PI MADRID
PA CALLE DE ZURBANO, 76-4TH FLR LEFT, MADRID, 28010, SPAIN
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD APR-JUN
PY 2007
VL 6
IS 2
BP 122
EP 126
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 278AX
UT WOS:000254256900011
PM 17519838
DA 2025-01-07
ER
PT J
AU Borssén, ÅD
Almer, S
Prytz, H
Wallerstedt, S
Friis-Liby, IL
Bergquist, A
Nyhlin, N
Hultcrantz, R
Sangfelt, P
Weiland, O
Lindgren, S
Verbaan, H
Werner, M
AF Borssen, Asa Danielsson
Almer, Sven
Prytz, Hanne
Wallerstedt, Sven
Friis-Liby, Inga-Lill
Bergquist, Annika
Nyhlin, Nils
Hultcrantz, Rolf
Sangfelt, Per
Weiland, Ola
Lindgren, Stefan
Verbaan, Hans
Werner, Marten
TI Hepatocellular and extrahepatic cancer in patients with autoimmune
hepatitis - a long-term follow-up study in 634 Swedish patients
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE autoimmune hepatitis; autoimmune liver disease; cancer; extrahepatic
cancer; hepatocellular carcinoma
ID CARCINOMA; RISK; EPIDEMIOLOGY; MALIGNANCIES; CIRRHOSIS
AB Objectives. Cirrhosis is a well-known risk factor for hepatocellular cancer, but the true risk in autoimmune hepatitis (AIH) is scarcely studied. Other cancers may arise after prolonged use of immune-modulating drugs. The aim of this study was to investigate the cancer risk in a large cohort of AIH patients. Material and methods. Six hundred and thirty-four Swedish patients in a well-defined cohort were matched to the Cause of Death Registry and the Cancer Registry. Standard incidence ratios were calculated by relating the incidences in the cohort to an age-matched material from the Swedish background population. Results. A higher overall incidence of malignancies than the background population was found, counting from the date of diagnosis (standard incidence ratio (SIR) 2.08, 95% CI 1.68-2.55). The highest risk was found for hepatocellular carcinoma (HCC). We found 10 cases (4.0%) in 248 patients with cirrhosis, which gives an incidence rate of 0.3%. Standard incidence ratio for developing hepatobiliary cancer was 54.55 (95% CI 19.92-99.99). HCC only occurred in cirrhotic patients. There was also an increased risk for non-melanoma skin cancer (SIR 9.87, 95% CI 6.26-14.81). Conclusion. A slightly enhanced risk for malignancies in general compared to the background population was found. The risk of hepatobiliary cancer was increased, but the annual risk over the observational period was well under the postulated 1.5% when surveillance in cirrhotic patients is considered to be cost-effective.
C1 [Borssen, Asa Danielsson; Werner, Marten] Umea Univ Hosp, Dept Med, Sect Hepatol, SE-90185 Umea, Sweden.
[Borssen, Asa Danielsson; Werner, Marten] Umea Univ Hosp, Dept Med, Gastroenterol Sect, SE-90185 Umea, Sweden.
[Almer, Sven; Bergquist, Annika; Hultcrantz, Rolf; Weiland, Ola] Karolinska Univ Hosp, Dept Med, Sect Hepatol, Stockholm, Sweden.
[Almer, Sven; Bergquist, Annika; Hultcrantz, Rolf; Weiland, Ola] Karolinska Univ Hosp, Dept Med, Gastroenterol Sect, Stockholm, Sweden.
[Prytz, Hanne] Univ Hosp Skane, Dept Med, Sect Hepatol, Lund, Sweden.
[Prytz, Hanne] Univ Hosp Skane, Dept Med, Gastroenterol Sect, Lund, Sweden.
[Wallerstedt, Sven] Ostra Hosp, Sahlgrenska Univ Hosp, Dept Med, Sect Hepatol, Gothenburg, Sweden.
[Wallerstedt, Sven] Ostra Hosp, Sahlgrenska Univ Hosp, Dept Med, Gastroenterol Sect, Gothenburg, Sweden.
[Friis-Liby, Inga-Lill] Sahlgrenska Univ Hosp Sahlgrenska, Dept Med, Sect Hepatol, Gothenburg, Sweden.
[Friis-Liby, Inga-Lill] Sahlgrenska Univ Hosp Sahlgrenska, Dept Med, Gastroenterol Sect, Gothenburg, Sweden.
[Nyhlin, Nils] Orebro Univ Hosp, Dept Med, Sect Hepatol, Orebro, Sweden.
[Nyhlin, Nils] Orebro Univ Hosp, Dept Med, Gastroenterol Sect, Orebro, Sweden.
[Sangfelt, Per] Univ Uppsala Hosp, Dept Med, Sect Hepatol, Uppsala, Sweden.
[Sangfelt, Per] Univ Uppsala Hosp, Dept Med, Gastroenterol Sect, Uppsala, Sweden.
[Lindgren, Stefan; Verbaan, Hans] Univ Hosp Skane, Dept Med, Sect Hepatol, Malmo, Sweden.
[Lindgren, Stefan; Verbaan, Hans] Univ Hosp Skane, Dept Med, Gastroenterol Sect, Malmo, Sweden.
C3 Umea University; Umea University; Karolinska Institutet; Karolinska
University Hospital; Karolinska Institutet; Karolinska University
Hospital; Sahlgrenska University Hospital; Sahlgrenska University
Hospital; Sahlgrenska University Hospital; Sahlgrenska University
Hospital; Orebro University; Orebro University; Uppsala University;
Uppsala University Hospital; Uppsala University; Uppsala University
Hospital
RP Borssén, ÅD (corresponding author), Umea Univ Hosp, Dept Med, SE-90185 Umea, Sweden.
EM asa.danielsson@vll.se
RI Bergquist, Annika/HOH-4007-2023; Almer, Sven/AFR-5312-2022
OI Almer, Sven/0000-0001-9334-1821; Nyhlin, Nils/0000-0002-0942-0816;
Bergquist, Annika/0000-0002-3858-6241; Weiland, Ola/0000-0002-6934-9724
FU Bengt Ihres fund, Umea University; Lions in Umea at Umea University
hospital; Department of Medicine at Umea University hospital
FX The study was supported by grants from Bengt Ihres fund, Umea
University, Lions in Umea and Department of Medicine at Umea University
hospital. Meda AB supported the SILK meetings throughout the study.
Bjorn Tavelin for his help with statistics. Also, a special thanks to
SILK and professor emeritus Ake Danielsson for support and advice.
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NR 34
TC 25
Z9 28
U1 0
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD FEB
PY 2015
VL 50
IS 2
BP 217
EP 223
DI 10.3109/00365521.2014.983154
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AY6RG
UT WOS:000347692700013
PM 25483724
DA 2025-01-07
ER
PT J
AU Mohamed, AA
Omar, AAA
El-Awady, RR
Hassan, SMA
Mohamed, W
Eitah, S
Ahmed, R
Khater, A
Tantawi, OMS
Mohamed, AA
AF Mohamed, Amal Ahmed
Omar, Abdellah Abosrie Ali
El-Awady, Rehab R.
Hassan, Sally Mohamed Aboelsayed
Mohamed, Waleed
Eitah, Soliman
Ahmed, Rehab
Khater, Amir
Tantawi, Omnia Mohamed Saad
Mohamed, Ahmed Abdelhafeez
TI MiR-155 and MiR-665 role as potential non-invasive biomarkers for
hepatocellular carcinoma in Egyptian patients with chronic hepatitis C
virus infection
SO JOURNAL OF TRANSLATIONAL INTERNAL MEDICINE
LA English
DT Article
DE hepatocellular carcinoma (HCC); chronic hepatitis with cirrhosis C and
without HCC (LC); alpha-fetoprotein (AFP); micro RNAs (miRNA)
ID MICRORNA-155; EXPRESSION; CELLS; HEPATOCARCINOGENESIS; PROGRESSION;
METASTASIS; DIAGNOSIS; INVASION; MIRNAS; TARGET
AB Background and Objectives: Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer associated death globally. Serum micro RNAs are full of potential as non-invasive biomarkers. Here, we aim to assess the performance of serum MicroRNA-155 and MicroRNA-665 as diagnostic biomarker for HCC comparing to AFP. Methods: Serum samples were collected from 200 subjects (40 healthy control, 80 chronic hepatitis C patients with cirrhosis and without HCC (LC) and 80 HCC patients currently infected by hepatitis C infection and didn't start the treatment). The HCC patients didn't include alcoholic liver disease, nonalcoholic fatty liver disease nor autoimmune liver disease. MicroRNA-155 and MicroRNA-665 expression were measured by real-time quantitative PCR (RT-qPCR), while AFP level was assessed by ELISA method. Results: Both miR-155 and miR-665 were significantly elevated in HCC group as compared to both control and LC groups. The comparison between LC and HCC patients revealed that the serum level of miR-155 was a significant increase in HCC patients compared to LC patients; however, the serum level of miR-665 didn't show any significant difference between the same two groups. MiR-665 expression level showed a direct correlation with tumor size in HCC patients. Conclusions: Using measurement against AFP level in serum, miR-665 is considered a promising serum biomarker for the diagnosis of HCC patients among the LC patients without HCC. MiR-155 didn't provide a better performance than serum AFP as a diagnostic biomarker among the same group. MiR-665 may serve as a good indicator for HCC prognosis.
C1 [Mohamed, Amal Ahmed] Natl Hepatol & Trop Med Res Inst, Biochem & Mol Biol Dept, Cairo, Egypt.
[Omar, Abdellah Abosrie Ali] Al Azhar Univ Cairo, Fac Med Boys, Med Biochem Dept, Cairo, Egypt.
[El-Awady, Rehab R.; Hassan, Sally Mohamed Aboelsayed] Al Azhar Univ Cairo, Fac Pharm Girls, Biochem Dept, Cairo, Egypt.
[Mohamed, Waleed; Eitah, Soliman] Theodor Bilharz Res Inst, Gastroenterol & Hepatol Dept, Cairo, Egypt.
[Ahmed, Rehab; Khater, Amir] Natl Hepatol & Trop Med Res Inst, Trop Dept, Cairo, Egypt.
[Tantawi, Omnia Mohamed Saad] Cairo Univ, Endem Dis Dept, Cairo, Egypt.
[Mohamed, Ahmed Abdelhafeez] Cairo Univ, Clin Oncol Dept, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); National Hepatology & Tropical Medicine
Research Institute (NHTMRI); Egyptian Knowledge Bank (EKB); Al Azhar
University; Egyptian Knowledge Bank (EKB); Al Azhar University; Egyptian
Knowledge Bank (EKB); Theodor Bilharz Research Institute (TBRI);
Egyptian Knowledge Bank (EKB); National Hepatology & Tropical Medicine
Research Institute (NHTMRI); Egyptian Knowledge Bank (EKB); Cairo
University; Egyptian Knowledge Bank (EKB); Cairo University
RP Mohamed, AA (corresponding author), Cairo Univ, Clin Oncol Dept, Cairo, Egypt.
EM hbaboda@kasralainy.edu.eg
RI Abdelhafeez, Ahmed/AAH-2199-2020; Mohamed, Waleed/Y-2762-2019; El-Awady,
Rehab/HCH-8735-2022; Mohamed, Amal/AAC-9106-2021
OI El-Awady, Rehab/0000-0002-2778-113X; Tantawy, Omnia/0000-0002-7041-7827
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NR 40
TC 44
Z9 45
U1 1
U2 7
PU SCIENDO
PI WARSAW
PA BOGUMILA ZUGA 32A, WARSAW, MAZOVIA, POLAND
SN 2450-131X
EI 2224-4018
J9 J TRANSL INTERN MED
JI J. TRANSL. INTERN. MED.
PY 2020
VL 8
IS 1
BP 32
EP 40
DI 10.2478/jtim-2020-0006
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA LS9FW
UT WOS:000536685400006
PM 32435610
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Arahata, M
Tajiri, K
Nomoto, K
Tsuneyama, K
Minami, S
Shimizu, Y
AF Arahata, Masahisa
Tajiri, Kazuto
Nomoto, Kazuhiro
Tsuneyama, Koichi
Minami, Shinji
Shimizu, Yukihiro
TI A Novel Type of Selective Immunoglobulin M Deficiency in a Patient with
Autoimmune Liver Cirrhosis with Recurrent Hepatocellular Carcinoma: A
Case Report and Review of the Literature
SO INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY
LA English
DT Review
DE Selective immunoglobulin M deficiency; Liver cancer; Autoimmune
hepatitis; Activation-induced cytidine deaminase
ID INDUCED CYTIDINE DEAMINASE; PERIPHERAL-BLOOD LYMPHOCYTES;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; IGM DEFICIENCY; FUNCTIONAL ASSESSMENT;
HUMAN HEPATOCYTES; DISEASE; EXPRESSION; INVITRO
AB A 64-year-old female with advanced liver cirrhosis who had never experienced severe infections presented in 2004 with general malaise. At the time, her serum showed low levels of immunoglobulin (Ig) M (11 mg/dl) with high levels of both IgG (2,942 mg/dl) and IgA (808 mg/dl). Because serum levels of IgG and IgA in previous cases of selective IgM deficiency were normal, this case could have a novel immunological mechanism. By 2006, serum IgM was undetectable (<5 mg/dl). Liver biopsy showed liver cirrhosis from autoimmune hepatitis. She had no other autoimmune diseases or hematological malignancies. She developed hepatocellular carcinoma (HCC) several times and died of liver failure. Immunological analyses performed before the first diagnosis of HCC showed polyclonal gamma-globulin elevation, normal chromosome and normal gene rearrangement of immunoglobulin heavy chain C mu. Peripheral blood showed low count B cells with few surface IgM-positive B lymphocytes, but the percentages of T cell subsets were normal. Expression of activation-induced cytidine deaminase (AID), which plays a critical role in immunoglobin class switching, was found to be over-expressed in the HCC tissue and B cells in bone marrow. This phenomenon could account for the clinical and immunological features of this case. In conclusion, we propose a novel type of selective IgM deficiency in association with the overexpression of AID. Copyright (c) 2012 S. Karger AG, Basel
C1 [Shimizu, Yukihiro] Takaoka City Hosp, Dept Gastroenterol, Takaoka, Toyama 9338550, Japan.
[Arahata, Masahisa; Minami, Shinji] Nanto Municipal Hosp, Dept Internal Med, Nanto, Toyama, Japan.
[Tajiri, Kazuto] Toyama Univ, Fac Med, Dept Internal Med 3, Toyama 930, Japan.
[Nomoto, Kazuhiro; Tsuneyama, Koichi] Toyama Univ, Dept Diagnost Pathol, Grad Sch Med & Pharmaceut Sci, Toyama 930, Japan.
C3 University of Toyama; University of Toyama
RP Shimizu, Y (corresponding author), Takaoka City Hosp, Dept Gastroenterol, 4-1 Takara Machi, Takaoka, Toyama 9338550, Japan.
EM rsf14240@nifty.com
RI Arahata, Masahisa/AGZ-3688-2022
OI Arahata, Masahisa/0000-0002-3759-0724; Tsuneyama,
Koichi/0000-0002-0670-9868
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NR 24
TC 9
Z9 9
U1 1
U2 8
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1018-2438
EI 1423-0097
J9 INT ARCH ALLERGY IMM
JI Int. Arch. Allergy Immunol.
PY 2013
VL 161
IS 1
BP 91
EP 96
DI 10.1159/000343583
PG 6
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA 057UA
UT WOS:000312588300011
PM 23257944
DA 2025-01-07
ER
PT J
AU Yu, X
Lei, XZ
AF Yu, Xian
Lei, Xuezhong
TI Application of the Multi-Omics Liquid Biopsy Method M2P-HCC in Early
Liver Cancer Screening for High-Risk Individuals with Hepatitis
B-Related Liver Cancer
SO DIAGNOSTICS
LA English
DT Article
DE hepatocellular carcinoma; liquid biopsy; HBV; ctDNA; early diagnosis
ID CIRCULATING TUMOR DNA; HEPATOCELLULAR-CARCINOMA; DIAGNOSIS; BIOMARKER;
PROGNOSIS; CHINA
AB Background: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide, with low rates of early diagnosis and surgical resection. In recent years, with the rapid development of liquid biopsy technology, circulating tumor DNA (ctDNA) has emerged as a research hotspot in the field of precision medicine for liver cancer. Existing studies have demonstrated the suitability of ctDNA for combined detection with other liver cancer diagnostic markers, enabling a multi-index analysis. In recent years, a novel prediction model has been developed for early liver cancer screening based on ctDNA liquid biopsy, M2P-HCC (methylation, mutation, and protein-HCC), mainly incorporating methylation changes, gene mutations, and protein markers associated with liver cancer. Preliminary validation in the HCCscreenTM Investigational (HIT, ChiCTR1800020233) study, which focused on screening early liver cancer in communities with Hepatitis B surface antigen (HBsAg) positivity, yielded promising results with 100% sensitivity and 94% specificity. However, it remains uncertain whether M2P-HCC can be effectively applied in high-risk populations for Hepatitis B-associated liver cancer, warranting further research. Methods: Patients who were under long-term follow-up at the outpatient clinic of the Infectious Diseases Center of West China Hospital of Sichuan University from December 2020 to January 2023 were recruited in this prospective observational study and underwent the M2P-HCC test. The study population consisted of high-risk patients with Hepatitis B-related liver cancer who met the inclusion criteria. Patients with a history of previous malignancy, recent blood transfusion, autoimmune diseases, and human immunodeficiency virus (HIV) infection were excluded. Clinical data were collected at a baseline, and all patients underwent the M2P-HCC blood test. Based on the test results, they were categorized into positive, early-warning, and negative groups. Prospective cohort observation and regular follow-ups were performed for 6-8 months. Results: 313 patients met the inclusion criteria and were included in the study. After 6-8 months of follow-up, HCC occurred in 41(13.1%) participants. The M2P-HCC test demonstrated good predictive performance with an area under the curve (AUC) of 0.88 (95% CI: 0.81-0.95, p < 0.001) and a cutoff value of 83 points (sensitivity 82.9% and specificity 85.7%). In contrast, the combination of alpha-fetoprotein (AFP) and ultrasound (US) yielded an inferior predictive performance (AUC 0.76 (95% CI: 0.69-0.84, p < 0.001), sensitivity 58.5%, and specificity 94.1%). Multivariate analyses revealed that M2P-HCC was an independent predictor of increased risk of HCC (OR = 1.16 [1.09-1.22], p < 0.001). Conclusions: M2P-HCC liquid biopsy demonstrated good performance for early liver cancer screening in high-risk populations of Hepatitis B-related liver cancer, exhibiting better sensitivity than the combination of AFP and US.
C1 [Yu, Xian; Lei, Xuezhong] Sichuan Univ, Ctr Infect Dis, West China Hosp, Chengdu 610041, Peoples R China.
C3 Sichuan University
RP Lei, XZ (corresponding author), Sichuan Univ, Ctr Infect Dis, West China Hosp, Chengdu 610041, Peoples R China.
EM yuxian2712@163.com; 18980601317@163.com
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NR 22
TC 3
Z9 3
U1 2
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD AUG
PY 2023
VL 13
IS 15
AR 2484
DI 10.3390/diagnostics13152484
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA O7CJ8
UT WOS:001045342100001
PM 37568847
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Kee, SJ
Kim, TJ
Lee, SJ
Cho, YN
Park, SC
Kim, JS
Kim, JC
Kang, HS
Lee, SS
Park, YW
AF Kee, Seung-Jung
Kim, Tae-Jong
Lee, Sung-Ji
Cho, Young-Nan
Park, Seong-Chang
Kim, Jong-Sun
Kim, Jeong-Chul
Kang, Hyung-Sik
Lee, Shin-Seok
Park, Yong-Wook
TI Dermatomyositis associated with hepatitis B virus-related hepatocellular
carcinoma
SO RHEUMATOLOGY INTERNATIONAL
LA English
DT Article
DE Inflammatory myopathy; Dermatomyositis; Hepatitis B virus;
Hepatocellular carcinoma
ID POLYMYOSITIS; CANCER; HEPATOCARCINOMA; DISEASE; PATIENT
AB Dermatomyositis (DM) is an idiopathic inflammatory myopathy (IIM) with typical cutaneous manifestations. It has been proposed that DM may be caused by autoimmune responses to viral infections, and previous studies have also shown that an association between DM and malignancy. However, chronic hepatitis B virus (HBV) infection associated with DM and hepatocellular carcinoma (HCC) is rarely encountered. The authors report a case of DM and HCC in a patient with a HBV infection. A 58-year-old man presented erythematous skin rashes on a sun-exposed area of 2 year's duration, and recent proximal muscle weakness. His medical history revealed that he had a chronic HBV infection. A diagnosis of DM relies on proximal muscle weakness, elevated muscle enzymes, myopathic changes (demonstrated by electromyography), muscle biopsy evidence of myositis, and its characteristic cutaneous findings. A Liver mass in the left lobe visualized by abdominal computed tomography was confirmed histologically as HCC. This case suggests that DM associated with HCC might be caused by a HBV infection.
C1 [Kim, Tae-Jong; Lee, Sung-Ji; Cho, Young-Nan; Park, Seong-Chang; Kim, Jong-Sun; Lee, Shin-Seok; Park, Yong-Wook] Chonnam Natl Univ, Dept Rheumatol, Sch Med, Kwangju 501757, South Korea.
[Kee, Seung-Jung] Chonnam Natl Univ, Sch Med, Dept Lab Med, Kwangju 501757, South Korea.
[Kim, Jeong-Chul] Chonnam Natl Univ, Dept Gen Surg, Sch Med, Kwangju 501757, South Korea.
[Kang, Hyung-Sik] Chonnam Natl Univ, Sch Biol Sci & Technol, Hormone Res Inst, Kwangju 501757, South Korea.
[Kim, Tae-Jong; Lee, Sung-Ji; Cho, Young-Nan; Park, Seong-Chang; Kim, Jong-Sun; Lee, Shin-Seok; Park, Yong-Wook] Chonnam Natl Univ, Dept Rheumatol, Hosp Med, Kwangju 501757, South Korea.
[Lee, Sung-Ji] Chonnam Natl Univ, Dept Lab Med, Hosp Med, Kwangju 501757, South Korea.
[Kim, Jong-Sun] Chonnam Natl Univ, Dept Gen Surg, Hosp Med, Kwangju 501757, South Korea.
C3 Chonnam National University; Chonnam National University; Chonnam
National University; Chonnam National University; Chonnam National
University; Chonnam National University; Chonnam National University
RP Park, YW (corresponding author), Chonnam Natl Univ, Dept Rheumatol, Sch Med, 8 Hak Dong, Kwangju 501757, South Korea.
EM parkyw@jnu.ac.kr
RI Kim, Dokyun/IYJ-2278-2023; Lee, Shin-Seok/AAC-6779-2021
OI gi, seungjeong/0000-0001-9708-5837; Kim, Tae-Jong/0000-0002-2871-1635
FU Chonnam National University Hospital Research Institute of Clinical
Medicine [CRI08036-1]; Rural Development Administration, Republic of
Korea [20070401-034-026-007-06]
FX This work was supported by a grant (#CRI08036-1) from the Chonnam
National University Hospital Research Institute of Clinical Medicine and
by a grant (20070401-034-026-007-06) from Biogreen 21 project, Rural
Development Administration, Republic of Korea.
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NR 16
TC 18
Z9 18
U1 0
U2 1
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0172-8172
EI 1437-160X
J9 RHEUMATOL INT
JI Rheumatol. Int.
PD MAR
PY 2009
VL 29
IS 5
BP 595
EP 599
DI 10.1007/s00296-008-0718-1
PG 5
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 413GS
UT WOS:000263781500021
PM 18802699
DA 2025-01-07
ER
PT J
AU Wang, S
Dong, V
Montano-Loza, AJ
Mason, AL
AF Wang, Sarah
Dong, Victor
Montano-Loza, Aldo J.
Mason, Andrew L.
TI Autoimmune liver diseases, hepatocellular carcinoma, and recurrence of
autoimmunity postliver transplantation
SO HEPATOMA RESEARCH
LA English
DT Review
DE Recurrence; autoimmune hepatitis; primary biliary cholangitis; primary
sclerosing cholangitis; hepatocellular carcinoma
AB Liver transplantation for the autoimmune liver diseases (AILD), which includes autoimmune hepatitis ( AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC), is indicated in the setting of decompensated cirrhosis, liver failure, and hepatocellular carcinoma (HCC). The risk of HCC is thought to be low in AILD, though data on the risk factors and predictors of HCC are limited in this population. Recurrence of AILD can occur in over half of the patients, complicating the post-transplant course. The pathogenesis of recurrent AILD involves a complex interaction of genetic and environmental influences, as well as a variety of clinical risk factors. Graft and patient survival are negatively impacted by recurrent AILD and the optimal approach to the treatment of AILD recurrence is the subject of ongoing research. This review will address the current literature on the risk of HCC in AILD, as well as the development and management of recurrent AILD post-liver transplantation.
C1 [Wang, Sarah; Dong, Victor; Montano-Loza, Aldo J.; Mason, Andrew L.] Univ Alberta, Div Gastroenterol, Edmonton, AB T6G 2X8, Canada.
[Wang, Sarah; Dong, Victor; Montano-Loza, Aldo J.; Mason, Andrew L.] Univ Alberta, Liver Unit, Edmonton, AB T6G 2X8, Canada.
C3 University of Alberta; University of Alberta
RP Mason, AL (corresponding author), Univ Alberta, Div Gastroenterol, 7 142 KGR,116 St & 85 Ave, Edmonton, AB T6G 2E1, Canada.
EM andrew.mason@ualberta.ca
FU Canadian Institutes for Health Research [PS156013]
FX Mason AL is supported by grants from the Canadian Institutes for Health
Research (PS156013).
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NR 135
TC 2
Z9 3
U1 0
U2 0
PU OAE PUBLISHING INC
PI ALHAMBRA
PA 245 E MAIN ST, ST122, ALHAMBRA, CA 91801 USA
SN 2394-5079
EI 2454-2520
J9 HEPATOMA RES
JI Hepatoma Res.
PY 2021
VL 7
AR 42
DI 10.20517/2394-5079.2020.163
PG 16
WC Oncology; Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Gastroenterology & Hepatology
GA VM9MX
UT WOS:001065282500042
OA gold
DA 2025-01-07
ER
PT J
AU Kim, JW
Ye, QH
Forgues, M
Chen, YD
Budhu, A
Sime, J
Hofseth, LJ
Kaul, R
Wang, XW
AF Kim, JW
Ye, QH
Forgues, M
Chen, YD
Budhu, A
Sime, J
Hofseth, LJ
Kaul, R
Wang, XW
TI Cancer-associated molecular signature in the tissue samples of patients
with cirrhosis
SO HEPATOLOGY
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; GENE-EXPRESSION; RISK-FACTORS; HUMAN LIVER;
EP-CAM; CARCINOGENESIS; IDENTIFICATION; PATHOGENESIS; MICROARRAY;
DISEASE
AB Several types of aggressive cancers, including hepatocellular carcinoma (HCC), often arise as a multifocal primary tumor. This suggests a high rate of premalignant changes in noncancerous tissue before the formation of a solitary tumor. Examination of the messenger RNA expression profiles of tissue samples derived from patients with cirrhosis of various etiologies by complementary DNA (cDNA) microarray indicated that they can be grossly separated into two main groups. One group included hepatitis B and C virus infections, hemochromatosis, and Wilson's disease. The other group contained mainly alcoholic liver disease, autoimmune hepatitis, and primary biliary cirrhosis. Analysis of these two groups by the cross-validated leave-one-out machine-learning algorithms revealed a molecular signature containing 556 discriminative genes (P < .001). It is noteworthy that 273 genes in this signature (49%) were also significantly altered in HCC (P < .001). Many genes were previously known to be related to HCC. The 273-gene signature was validated as cancer-associated genes by matching this set to additional independent tumor tissue samples from 163 patients with HCC, 56 patients with lung carcinoma, and 38 patients with breast carcinoma. From this signature, 30 genes were altered most significantly in tissue samples from high-risk individuals with cirrhosis and from patients with HCC. Among them, 12 genes encoded secretory proteins found in sera. In conclusion, we identified a unique gene signature in the tissue samples of patients with cirrhosis, which may be used as candidate markers for diagnosing the early onset of HCC in high-risk populations and may guide new strategies for chemoprevention.
C1 NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
Fudan Univ, Liver Canc Inst, Shanghai 200433, Peoples R China.
Fudan Univ, Zhongshan Hosp, Shanghai 200433, Peoples R China.
NHGRI, Canc Genet Branch, Bethesda, MD 20892 USA.
Univ Minnesota, Div Pediat Gastroenterol & Nutr, Minneapolis, MN USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI); Fudan University; Fudan University; National Institutes of Health
(NIH) - USA; NIH National Human Genome Research Institute (NHGRI);
University of Minnesota System; University of Minnesota Twin Cities
RP NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, 37 Convent Dr,Bldg 37,Room 3044A, Bethesda, MD 20892 USA.
EM xw3u@nih.gov.fax
RI Wang, Xin Wei/B-6162-2009
OI Wang, Xin Wei/0000-0001-9735-606X
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PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD FEB
PY 2004
VL 39
IS 2
BP 518
EP 527
DI 10.1002/hep.20053
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 805OM
UT WOS:000220375600032
PM 14768006
OA Bronze
DA 2025-01-07
ER
PT J
AU Vitale, G
Gitto, S
Campani, C
Turco, L
Baldan, A
Marra, F
Morelli, MC
AF Vitale, Giovanni
Gitto, Stefano
Campani, Claudia
Turco, Laura
Baldan, Anna
Marra, Fabio
Morelli, Maria Cristina
TI Biological therapies in patients with liver disease: are they really
lifesavers?
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Review
DE Biological therapies; autoimmune liver diseases; autoimmune hepatitis;
primary biliary cholangitis; primary sclerosing cholangitis; liver
cancer; liver transplant
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY CHOLANGITIS; ADVANCED
HEPATOCELLULAR-CARCINOMA; CLINICAL-PRACTICE GUIDELINES; LOW-DOSE
INTERLEUKIN-2; REGULATORY T-CELLS; AUTOIMMUNE HEPATITIS; RENAL-FUNCTION;
DOUBLE-BLIND; TRANSPLANT RECIPIENTS
AB Introduction The liver plays a key role in the setting of immune tolerance. Targeting antigens for presentation by antigen-presenting cells in the liver can induce immune tolerance to either autoantigens from the liver itself or organs outside of the liver. Despite its non-conventional capacity for tolerance induction, the liver remains a target organ for autoimmune diseases. Whereas chronic inflammation and intra-hepatic immuno-suppressive microenvironment occurring during liver fibrosis lead to hepatocellular carcinoma. Monoclonal antibodies have revolutionized the therapeutic strategies of many autoimmune diseases and some cancers. Areas covered We review data from literature regarding the safety and efficacy of biologics in treating hepatobiliary autoimmune diseases and primary liver cancers. Furthermore, we describe their potential use in the setting of liver transplants and their main immune-related liver adverse events. Expert opinion Biological therapies have changed the natural history of main autoimmune diseases and solid cancers. Compared to other organs and disease settings, the liver lags behind in biologics and their applications. The development of novel diagnostic and therapeutic strategies based on the immunological and antigenic characteristics of the hepatobiliary system could reduce mortality and transplant rates linked to chronic liver diseases.
C1 [Vitale, Giovanni; Turco, Laura; Baldan, Anna; Morelli, Maria Cristina] IRCCS Azienda Osped Univ Bologna, Div Internal Med Treatment Severe Organ Failure, Via Albertoni 15, Bologna, Italy.
[Gitto, Stefano; Campani, Claudia; Marra, Fabio] Univ Florence, Dept Expt & Clin Med, Florence, Italy.
C3 IRCCS Azienda Ospedaliero-Universitaria di Bologna; University of
Florence
RP Vitale, G (corresponding author), IRCCS Azienda Osped Univ Bologna, Div Internal Med Treatment Severe Organ Failure, Via Albertoni 15, Bologna, Italy.
EM giovanni.vitale@aosp.bo.it
RI Campani, Claudia/AAC-4021-2022; Gitto, Stefano/J-9922-2018; Marra,
Fabio/K-7263-2016; Vitale, Giovanni/K-6322-2016
OI Gitto, Stefano/0000-0002-8042-6508; Turco, Laura/0000-0001-8148-3769;
Campani, Claudia/0000-0003-3842-782X; morelli, maria
cristina/0000-0002-9742-1981; Marra, Fabio/0000-0001-8629-0878; Vitale,
Giovanni/0000-0003-2603-8245
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NR 176
TC 0
Z9 0
U1 0
U2 12
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1471-2598
EI 1744-7682
J9 EXPERT OPIN BIOL TH
JI Expert Opin. Biol. Ther.
PD APR 3
PY 2022
VL 22
IS 4
BP 473
EP 490
DI 10.1080/14712598.2022.2013799
EA JAN 2022
PG 18
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA ZV3NO
UT WOS:000736365100001
PM 34860629
DA 2025-01-07
ER
PT J
AU Yau, T
Tai, DV
Chan, SL
Huang, YH
Choo, SP
Hsu, C
Cheung, TT
Lin, SM
Yong, WP
Lee, JYY
Leung, T
Shum, T
Yeung, CSY
Tai, AYP
Law, ALY
Cheng, AL
Chen, LT
AF Yau, Thomas
Tai, David
Chan, Stephen Lam
Huang, Yi-Hsiang
Choo, Su Pin
Hsu, Chiun
Cheung, Tan To
Lin, Shi-Ming
Yong, Wei Peng
Lee, Joycelyn
Leung, Thomas
Shum, Tracy
Yeung, Cynthia S. Y.
Tai, Anna Yin-Ping
Law, Ada Lai Yau
Cheng, Ann-Lii
Chen, Li-Tzong
TI Systemic Treatment of Advanced Unresectable Hepatocellular Carcinoma
after First-Line Therapy: Expert Recommendations from Hong Kong,
Singapore, and Taiwan
SO LIVER CANCER
LA English
DT Review
DE Hepatocellular carcinoma; Liver cancer; Systemic treatment
ID CLINICAL-PRACTICE; CANCER-PATIENTS; DOUBLE-BLIND; SORAFENIB; LENVATINIB;
BEVACIZUMAB; PLUS
AB Background: Asia has a high burden of hepatocellular carcinoma (HCC) due to the high rates of chronic hepatitis B infection and accounts for 70% of HCC cases globally. In the past 20 years, the systemic treatment landscape of advanced HCC has evolved substantially - from tyrosine kinase inhibitors to immune-oncology agents plus anti-vascular endothelial growth factor agents. The appropriate sequence of therapies has become critical in optimizing patient outcomes given the increase in systemic therapeutic options. This article evaluates the evidence and provides expert recommendations for the use of systemic therapies after first-line treatment in patients with advanced HCC. Summary: Based on three virtual meetings held in early 2021, a team of 17 experts comprising oncologists, a hepatologist, and a hepatobiliary surgeon from Hong Kong, Singapore, and Taiwan reviewed available data about systemic treatments for HCC after first line and formulated 28 statements. These statements aimed to provide expert guidance on selecting first and subsequent lines of therapies as well as recommending therapies in special circumstances, such as poor liver function, posttransplantation, recent gastrointestinal bleeding, or autoimmune diseases. Data supporting the statements were drawn from clinical trials and real-world studies. The 28 statements were then evaluated anonymously using a 5-point Likert scale, and 24 reached consensus, predefined as achieving 75% agreement. Statements generated covered the selection of first-line systemic therapy, considerations and goals of second-line systemic therapies, treatment selection following first-line therapy, and treatment recommendations following first-line tyrosine kinase inhibitors, immune-oncology monotherapy, or immune-oncology combination therapy. The authors also shared expert opinion on the use of second-line systemic therapy in patients with liver dysfunction, liver transplantation, and recent gastrointestinal or autoimmune disease. Key Messages: These expert statements summarize the latest data and expert opinion on selecting systemic treatment following first-line therapy in patients with unresectable advanced or metastatic HCC.
C1 [Yau, Thomas] Univ Hong Kong, Dept Med, Hong Kong, Peoples R China.
[Tai, David; Lee, Joycelyn] Natl Canc Ctr Singapore, Div Med Oncol, Singapore, Singapore.
[Chan, Stephen Lam] Chinese Univ Hong Kong, Dept Clin Oncol, Hong Kong, Peoples R China.
[Huang, Yi-Hsiang] Taipei Vet Gen Hosp, Div Gastroenterol & Hepatol, Taipei, Taiwan.
[Huang, Yi-Hsiang] Natl Yang Ming Chiao Tung Univ, Sch Med, Einst Clin Med, Taipei, Taiwan.
[Choo, Su Pin] Curie Oncol, Singapore, Singapore.
[Hsu, Chiun] Natl Taiwan Univ Canc Ctr, Dept Med Oncol, Taipei, Taiwan.
[Cheung, Tan To] Univ Hong Kong, Dept Surg, Hong Kong, Peoples R China.
[Lin, Shi-Ming] Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, Linkuo, Taiwan.
[Yong, Wei Peng] Natl Univ Singapore, Dept Haematol Oncol, Singapore, Singapore.
[Leung, Thomas] Hong Kong Sanat & Hosp, Dept Med Oncol, Hong Kong, Peoples R China.
[Shum, Tracy] Princess Margaret Hosp, Dept Oncol, Hong Kong, Peoples R China.
[Yeung, Cynthia S. Y.] Union Hosp, Hong Kong, Peoples R China.
[Tai, Anna Yin-Ping] Queen Elizabeth Hosp, Dept Clin Oncol, Hong Kong, Peoples R China.
[Law, Ada Lai Yau] Chiron Med, Hong Kong, Peoples R China.
[Cheng, Ann-Lii] Natl Taiwan Univ Hosp, Dept Internal Med & Oncol, Taipei, Taiwan.
[Cheng, Ann-Lii] Natl Taiwan Univ, Grad Inst Oncol, Coll Med, Taipei, Taiwan.
[Chen, Li-Tzong] Natl Hlth Res Inst, Natl Inst Canc Res, Tainan, Taiwan.
[Chen, Li-Tzong] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Internal Med, Kaohsiung, Taiwan.
C3 University of Hong Kong; National Cancer Centre Singapore (NCCS);
Chinese University of Hong Kong; Taipei Veterans General Hospital;
National Yang Ming Chiao Tung University; National Taiwan University;
University of Hong Kong; Chang Gung Memorial Hospital; National
University of Singapore; National Taiwan University; National Taiwan
University Hospital; National Taiwan University; National Health
Research Institutes - Taiwan; Kaohsiung Medical University; Kaohsiung
Medical University Hospital
RP Yau, T (corresponding author), Univ Hong Kong, Dept Med, Hong Kong, Peoples R China.
EM the@netvigator.com
RI Cheng, Ann-Lii/ACM-0936-2022; Huang, Yi-Hsiang/ADX-9119-2022; Yau,
Thomas/B-3429-2011; Lee, joycelyn/KIG-1047-2024; CHOO, Su/ABB-3892-2020;
Chan, Stephen/F-9149-2011; Yong, Wei Peng/Y-7260-2018
OI Chan, Stephen/0000-0001-8998-5480; Huang, Yi-Hsiang/0000-0001-5241-5425;
Yong, Wei Peng/0000-0003-4404-3777; Lee, Joycelyn/0000-0002-1070-6125
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NR 69
TC 13
Z9 13
U1 1
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 2235-1795
EI 1664-5553
J9 LIVER CANCER
JI Liver Cancer
PD SEP
PY 2022
VL 11
IS 5
BP 426
EP 439
DI 10.1159/000525582
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 6S9DQ
UT WOS:000893283400003
PM 36158587
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wassef, J
Xu, S
AF Wassef, Jessica
Xu, Shelley
TI Hepatocellular Carcinoma With Tumor Thrombus to the Hepatic Veins and
the Right Atrium: A Case Report and Review Exploring Various
Presentations and Treatment Options
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Review
DE hepatocellular carcinoma; tumor thrombus; inferior vena cava; right
atrium; hepatitis c; hepatitis b; alcohol; cirrhosis; heart; screening
ID PATIENT
AB Hepatocellular carcinoma (HCC) is a leading cause of cancer and cancer-related deaths in the world. Some of the risk factors for the development of HCC include Hepatitis B virus (HBV), Hepatitis C virus (HCV), chronic alcoholism, autoimmune hepatitis, among others. One manifestation of HCC includes tumor thrombus (TT) to the right atrium (RA), which occurs in 0.67-4.1% of patients with HCC. Our case focuses on a unique presentation of HCC with RA 71. with initial symptoms of nausea and vomiting without signs of cardiac &compensation or hemodynamic instability. Although there is no definitive treatment for TT to the RA, there are a variety of proven avenues of management of HCC TT to the RA, especially pertaining to patients with adequate liver function.
A 63-year old female with a past medical history of untreated HCV and alcohol abuse with no previously known liver disease or history of liver decompensation, presented with nausea, vomiting, and diarrhea. Initial labs revealed hypovolemic hyponatremia and transaminitis with negative ethanol levels. The model for end-stage liver disease (MELD-Na) score was calculated at 27, and she had a Child-Pugh class C score. Follow up labs were significant for elevated alpha-fetoprotein (AFP). Triple-phase CT of the liver revealed a large liver mass with extension into the RA with TT and necrosis of the liver. An echocardiogram revealed a RA mass versus thrombus. Throughout her hospitalization, she never admitted to cardiac symptoms, including shortness of breath, palpitations, or chest pain. No tachycardia was noted, and her blood pressure remained stable. She was not a candidate for surgery or chemotherapy. The patient declined any heroic measures, and palliative care was consulted for further management. She was transferred to hospice, where she died one week later.
There are numerous etiologies and clinical presentations of HCC with TT to the RA. Its disease course is insidious and may not present as symptomatic until there is a sizable tumor burden. Therefore, treatment options for HCC with Tr to the RA are reliant on HCC screening for at-risk populations, early diagnosis, and each individual patient's baseline liver function.
C1 [Wassef, Jessica] Broward Hlth Med Ctr, Surg, Ft Lauderdale, FL 33316 USA.
[Wassef, Jessica] Hackensack Meridian Palisades Med Ctr, Gen Surg, North Bergen, NJ 07047 USA.
[Xu, Shelley] Legacy Hlth, Internal Med, Portland, OR USA.
C3 Legacy Health
RP Wassef, J (corresponding author), Broward Hlth Med Ctr, Surg, Ft Lauderdale, FL 33316 USA.; Wassef, J (corresponding author), Hackensack Meridian Palisades Med Ctr, Gen Surg, North Bergen, NJ 07047 USA.
EM jwassef27@gmail.com
OI Wassef, Jessica/0000-0001-9819-6918
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OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhang, CY
Liu, S
Yang, M
AF Zhang, Chun-Ye
Liu, Shuai
Yang, Ming
TI Antioxidant and anti-inflammatory agents in chronic liver diseases:
Molecular mechanisms and therapy
SO WORLD JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Chronic liver disease; Alcoholic liver disease; Non-alcoholic fatty
liver disease; Hepatocellular carcinoma; Natural products; Inflammation;
Oxidative stress; Treatment; Clinical trials
ID ETHANOL-INDUCED HEPATOTOXICITY; INDUCED HEPATIC STEATOSIS; FARNESOID X
RECEPTOR; FATTY LIVER; NONALCOHOLIC STEATOHEPATITIS; OXIDATIVE STRESS;
DOUBLE-BLIND; URSODEOXYCHOLIC ACID; SIGNALING PATHWAY; VITAMIN-E
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C1 [Zhang, Chun-Ye] Univ Missouri, Christopher S Bond Life Sci Ctr, Columbia, MO 65211 USA.
[Liu, Shuai] Zhejiang Univ, Affiliated Hosp 1, Hangzhou 310006, Zhejiang, Peoples R China.
[Yang, Ming] Univ Missouri, Dept Surg, Columbia, MO 65211 USA.
[Yang, Ming] Univ Missouri, Dept Surg, Room 2203,NexGen Precis Bldg,1030 Hitt St, Columbia, MO 65211 USA.
C3 University of Missouri System; University of Missouri Columbia; Zhejiang
University; University of Missouri System; University of Missouri
Columbia; University of Missouri System; University of Missouri Columbia
RP Yang, M (corresponding author), Univ Missouri, Dept Surg, Room 2203,NexGen Precis Bldg,1030 Hitt St, Columbia, MO 65211 USA.
EM yangmin@health.missouri.edu
RI Zhang, Chunye/ABF-8130-2021; Yang, Ming/AAS-8838-2021
OI Yang, Ming/0000-0002-4895-5864
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NR 195
TC 30
Z9 31
U1 2
U2 19
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5182
J9 WORLD J HEPATOL
JI World J. Hepatol.
PD FEB 27
PY 2023
VL 15
IS 2
BP 180
EP 200
DI 10.4254/wjh.v15.i2.180
PG 21
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA A1HV6
UT WOS:000952717700004
PM 36926234
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Colapietro, F
Maisonneuve, P
Lytvyak, E
Beuers, U
Verdonk, RC
van der Meer, AJ
van Hoek, B
Kuiken, SD
Brouwer, JT
Muratori, P
Aghemo, A
Carella, F
van den Berg, AP
Zachou, K
Dalekos, GN
Di Zeo-Sanchez, DE
Robles, M
Andrade, RJ
Montano-Loza, AJ
van den Brand, FF
Slooter, CD
Macedo, G
Liberal, R
de Boer, YS
Lleo, A
AF Colapietro, Francesca
Maisonneuve, Patrick
Lytvyak, Ellina
Beuers, Ulrich
Verdonk, Robert C.
van der Meer, Adriaan J.
van Hoek, Bart
Kuiken, Sjoerd D.
Brouwer, Johannes T.
Muratori, Paolo
Aghemo, Alessio
Carella, Francesco
van den Berg, Ad P.
Zachou, Kalliopi
Dalekos, George N.
Di Zeo-Sanchez, Daniel E.
Robles, Mercedes
Andrade, Raul J.
Montano-Loza, Aldo J.
van den Brand, Floris F.
Slooter, Charlotte D.
Macedo, Guilherme
Liberal, Rodrigo
de Boer, Ynto S.
Lleo, Ana
CA Dutch AIH Study Grp
Int Autoimmune Hepatitis Grp
TI Incidence and predictors of hepatocellular carcinoma in patients with
autoimmune hepatitis
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Autoimmune Hepatitis;
Hepatocellular
carcinoma; Liver cancer; Immunosuppressive therapy
ID COST-EFFECTIVENESS; RISK; PREVALENCE
AB Background and Aims: Autoimmune hepatitis (AIH) is a rare chronic liver disease of unknown aetiology; the risk of hepatocellular carcinoma (HCC) remains unclear and risk factors are not well-defined. We aimed to investigate the risk of HCC across a multicentre AIH cohort and to identify predictive factors. Methods: We performed a retrospective, observational, multicentric study of patients included in the International Autoimmune Hepatitis Group Retrospective Registry. The assessed clinical outcomes were HCC development, liver transplantation, and death. Fine and Gray regression analysis stratified by centre was applied to determine the effects of individual covariates; the cumulative incidence of HCC was estimated using the competing risk method with death as a competing risk. Results: A total of 1,428 patients diagnosed with AIH from 1980 to 2020 from 22 eligible centres across Europe and Canada were included, with a median follow-up of 11.1 years (interquartile range 5.2-15.9). Two hundred and ninety-three (20.5%) patients had cirrhosis at diagnosis. During follow-up, 24 patients developed HCC (1.7%), an incidence rate of 1.44 cases/1,000 patient-years; the cumulative incidence of HCC increased over time (0.6% at 5 years, 0.9% at 10 years, 2.7% at 20 years, and 6.6% at 30 years of follow-up). Patients who developed cirrhosis during follow-up had a significantly higher incidence of HCC. The cumulative incidence of HCC was 2.6%, 4.6%, 5.6% and 6.6% at 5, 10, 15, and 20 years after the development of cirrhosis, respectively. Obesity (hazard ratio [HR] 2.94, p = 0.04), cirrhosis (HR 3.17, p = 0.01), and AIH/PSC variant syndrome (HR 5.18, p = 0.007) at baseline were independent risk factors for HCC development. Conclusions: HCC incidence in AIH is low even after cirrhosis development and is associated with risk factors including obesity, cirrhosis, and AIH/PSC variant syndrome.
C1 [Colapietro, Francesca; Lleo, Ana] Human Univ, Dept Biomed Sci, Milan, Italy.
[Colapietro, Francesca; Aghemo, Alessio; Lleo, Ana] IRCCS Human Res Hosp, Dept Gastroenterol, Div Internal Med & Hepatol, Milan, Italy.
[Maisonneuve, Patrick] IEO European Inst Oncol IRCCS, Div Epidemiol & Biostat, Milan, Italy.
[Lytvyak, Ellina] Univ Alberta, Dept Med, Div Prevent Med, Edmonton, AB, Canada.
[Beuers, Ulrich] Dept Gastroenterol & Hepatol, Amsterdam UMC, AMC, Amsterdam, Netherlands.
[Verdonk, Robert C.] St Antonius Hosp, Dept Gastroenterol & Hepatol, Nieuwegein, Netherlands.
[van der Meer, Adriaan J.] Dept Gastroenterol & Hepatol, Erasmus MC, Rotterdam, Netherlands.
[van Hoek, Bart] Leiden Univ, Med Ctr, Dept Gastroenterol Hepatol, Leiden, Netherlands.
[Kuiken, Sjoerd D.] Dept Gastroenterol & Hepatol, OLVG, Amsterdam, Netherlands.
[Brouwer, Johannes T.] Reinier Graaf Med Ctr, Delft, Netherlands.
[Muratori, Paolo] Morgagni Pierantoni Hosp, Div Internal Med, I-47100 Forli, Italy.
[Muratori, Paolo] Univ Bologna, Dept Sci Qual Life, Bologna, Italy.
[van den Berg, Ad P.] Univ Med Ctr Groningen, Univ Groningen, Groningen, Netherlands.
[Zachou, Kalliopi; Dalekos, George N.] Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Dept Med & Res, Lab Internal Med, Larisa 41110, Greece.
[Di Zeo-Sanchez, Daniel E.; Robles, Mercedes; Andrade, Raul J.] Virgen Victoria Univ Hosp, Univ Malaga, Liver Unit, IBIMA,CIBERehd, Malaga, Spain.
[Montano-Loza, Aldo J.] Univ Alberta, Dept Med, Div Gastroenterol, Liver Unit, Edmonton, AB, Canada.
[van den Brand, Floris F.; Slooter, Charlotte D.; de Boer, Ynto S.] Vrije Univ Amsterdam, Dept Gastroenterol & Hepatol, Amsterdam UMC, Amsterdam, Netherlands.
[Macedo, Guilherme; Liberal, Rodrigo] Ctr Hosp Sao Joao, Dept Gastroenterol & Hepatol, Porto, Portugal.
[Lleo, Ana] Humanitas Univ, IRCCS Human Res Hosp, Dept Biomed Sci, Dept, Via A Manzoni 56, I-20089 Rozzano, Italy.
C3 University of Alberta; University of Amsterdam; Academic Medical Center
Amsterdam; St. Antonius Hospital Utrecht; Erasmus University Rotterdam;
Erasmus MC; Leiden University; Leiden University Medical Center (LUMC);
Leiden University - Excl LUMC; Onze Lieve Vrouwe Gasthuis Hospital;
Reinier de Graaf Hospital; University of Bologna; University of
Groningen; General University Hospital of Larissa; Universidad de
Malaga; CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD;
Instituto de Investigacion Biomedica de Malaga y Plataforma en
Nanomedicina (IBIMA); University of Alberta; Vrije Universiteit
Amsterdam; University of Amsterdam; Sao Joao Hospital; IRCCS Humanitas
Research Hospital; Humanitas University
RP Lleo, A (corresponding author), Humanitas Univ, IRCCS Human Res Hosp, Dept Biomed Sci, Dept, Via A Manzoni 56, I-20089 Rozzano, Italy.
EM ana.lleo@humanitas.it
RI Macedo, Manuel/L-8038-2013; Lleo, Ana/AAA-5759-2019; Aghemo,
Alessio/ABE-5976-2021; van Hoek, Bart/AAU-8953-2020; van den Brand,
Floris/K-9866-2019; Colapietro, Francesca/LFT-8668-2024; Verdonk,
Robert/AIF-4117-2022; Pop, Tudor Lucian/I-4155-2015; de Boer,
Ynto/D-9242-2013
OI Pop, Tudor Lucian/0000-0002-4931-1219; Lytvyak,
Ellina/0000-0001-5651-9010; Trauner, Michael/0000-0002-1275-6425; Di Zeo
Sanchez, Daniel Enrique/0000-0002-9068-0518; Drenth, Joost
PH/0000-0001-8027-3073; Colapietro, Francesca/0000-0002-7520-744X;
Verdonk, Robert/0000-0001-5591-0499; van Hoek, Bart/0000-0001-6527-764X;
de Boer, Ynto/0000-0002-4066-7593; Engel, Bastian/0000-0002-0972-3454
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Sharma R, 2022, AM J EPIDEMIOL, V191, P298, DOI 10.1093/aje/kwab119
Sung H, 2021, CA-CANCER J CLIN, V71, P209, DOI 10.3322/caac.21660
Tansel A, 2017, CLIN GASTROENTEROL H, V15, P1207, DOI 10.1016/j.cgh.2017.02.006
Trivedi PJ, 2021, GUT, V70, P1989, DOI 10.1136/gutjnl-2020-322362
van den Brand FF, 2019, CLIN GASTROENTEROL H, V17, P940, DOI 10.1016/j.cgh.2018.09.046
Viganò L, 2020, UPDATES SURG, V72, P413, DOI 10.1007/s13304-020-00750-5
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Yeoman AD, 2008, HEPATOLOGY, V48, P863, DOI 10.1002/hep.22432
Younossi ZM, 2015, HEPATOLOGY, V62, p739A, DOI 10.1002/hep.28431
Zenouzi R, 2014, CLIN GASTROENTEROL H, V12, P1733, DOI 10.1016/j.cgh.2014.02.008
NR 37
TC 17
Z9 18
U1 9
U2 20
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD JAN
PY 2024
VL 80
IS 1
DI 10.1016/j.jhep.2023.09.010
EA JAN 2024
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HI8X7
UT WOS:001158974300001
PM 37802188
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Hetta, HF
Mekky, MA
Zahran, AM
Abdel-Malek, MO
Ramadan, HK
Shafik, EA
Abbas, WA
El-Masry, MA
Mohamed, NA
Kamel, AA
Marraiki, N
Beshbishy, AM
Batiha, GE
Osman, HA
Koneru, G
El-Mokhtar, MA
AF Hetta, Helal F.
Mekky, Mohamed A.
Zahran, Asmaa M.
Abdel-Malek, Mohamed O.
Ramadan, Haidi K.
Shafik, Engy A.
Abbas, Wael A.
Abbas El-Masry, Muhammad
Mohamed, Nahed A.
Kamel, Amira A.
Marraiki, Najat
Beshbishy, Amany Magdy
Batiha, Gaber El-Saber
Osman, Heba A.
Koneru, Gopala
El-Mokhtar, Mohamed A.
TI Regulatory B Cells and Their Cytokine Profile in HCV-Related
Hepatocellular Carcinoma: Association with Regulatory T Cells and
Disease Progression
SO VACCINES
LA English
DT Article
DE Breg; Treg; HCV; HCC
ID ACTIVATING FACTOR; CANCER; BAFF; AUTOIMMUNITY; SUPPRESSION; EXPRESSION;
IMMUNITY; HEALTH
AB Although regulatory B cells (Bregs) have been proven to play a suppressive role in autoimmune diseases, infections and different tumors, little is known regarding hepatocellular carcinoma (HCC), especially in hepatitis C-related settings. Herein, we analyzed the frequency of circulating Bregs, serum levels of IL-10, IL-35 and B-cell activating factor (BAFF) and investigated their association with regulatory T cells (Tregs) and disease progression in HCV-related HCC. For comparative purposes, four groups were enrolled; chronic HCV (CHC group, n = 35), HCV-related liver cirrhosis (HCV-LC group, n = 35), HCV-related HCC (HCV-HCC group, n = 60) and an apparently healthy control (Control-group, n = 20). HCC diagnosis and staging were in concordance with the Barcelona Clinic Liver Cancer (BCLC) staging system. Analysis of the percentage of Breg cells and peripheral lymphocyte subsets (Treg) was performed by flow cytometry. Serum cytokine levels of IL-10, IL-35 and B-cell activating factor (BAFF) were measured by ELISA. The frequency of Bregs was significantly higher in the HCV-HCC group compared to the other groups and controls. A significant increase was noted in late-HCC versus those in the early stages. The frequency of Bregs was positively correlated with Tregs, serum IL-10, IL-35 and BAFF. In conclusion, Peripheral Bregs were positively correlated with the frequency of Tregs, IL-10, IL-35 and BAFF, and may be associated with HCV-related HCC progression.
C1 [Hetta, Helal F.; Koneru, Gopala] Univ Cincinnati, Coll Med, Dept Internal Med, Cincinnati, OH 45267 USA.
[Hetta, Helal F.; El-Mokhtar, Mohamed A.] Assiut Univ, Dept Med Microbiol & Immunol, Fac Med, Assiut 71515, Egypt.
[Mekky, Mohamed A.; Abdel-Malek, Mohamed O.; Ramadan, Haidi K.] Assiut Univ, Dept Trop Med & Gastroenterol, Fac Med, Assiut 71515, Egypt.
[Zahran, Asmaa M.; Shafik, Engy A.] Assiut Univ, South Egypt Canc Inst, Dept Clin Pathol, Assiut 71515, Egypt.
[Abbas, Wael A.; Abbas El-Masry, Muhammad] Assiut Univ, Div Gastroenterol, Dept Internal Med, Fac Med, Assiut 71515, Egypt.
[Mohamed, Nahed A.; Kamel, Amira A.] Assiut Univ, Dept Med Biochem, Fac Med, Assiut 71515, Egypt.
[Marraiki, Najat] King Saud Univ, Dept Bot & Microbiol, Coll Sci, Riyadh 11451, Saudi Arabia.
[Beshbishy, Amany Magdy] Obihiro Univ Agr & Vet Med, Natl Res Ctr Protozoan Dis, Nishi 2-13,Inada Cho, Obihiro, Hokkaido 0808555, Japan.
[Batiha, Gaber El-Saber] Damanhour Univ, Fac Vet Med, Dept Pharmacol & Therapeut, Damanhur 22511, Egypt.
[Osman, Heba A.] South Valley Univ, Fac Med, Trop Med & Gastroenterol Dept, Hepatol Div, Qena 83523, Egypt.
C3 University System of Ohio; University of Cincinnati; Egyptian Knowledge
Bank (EKB); Assiut University; Egyptian Knowledge Bank (EKB); Assiut
University; Egyptian Knowledge Bank (EKB); Assiut University; Egyptian
Knowledge Bank (EKB); Assiut University; Egyptian Knowledge Bank (EKB);
Assiut University; King Saud University; Obihiro University of
Agriculture & Veterinary Medicine; Egyptian Knowledge Bank (EKB);
Damanhour University; Egyptian Knowledge Bank (EKB); South Valley
University Egypt
RP Hetta, HF (corresponding author), Univ Cincinnati, Coll Med, Dept Internal Med, Cincinnati, OH 45267 USA.; Hetta, HF; El-Mokhtar, MA (corresponding author), Assiut Univ, Dept Med Microbiol & Immunol, Fac Med, Assiut 71515, Egypt.
EM helal.hetta@uc.edu; Mmekky75@yahoo.com; asmaam.zahran@yahoo.com;
momar7619@gmail.com; haidikaram@aun.edu.eg; engyadelshafik@yahoo.com;
drwaelabbas@yahoo.com; Masaeed2@yahoo.com; nahed_eltamawy@yahoo.com;
amira_kamel222@yahoo.com; Najat@ksu.edu.sa; amanimagdi2008@gmail.com;
gaberbatiha@gmail.com; hebaahmed198098@yahoo.com; gkoneru1@gmail.com;
ma_mokhtar@yahoo.com
RI Hetta, Helal/U-6794-2019; Osman, Heba/ABC-3044-2021; Mekky,
Mohamed/A-9892-2018; El-Mokhtar, Mohamed/AAP-4906-2020; Zahran,
Asmaa/N-1920-2019; Ramadan, Haidi/ABA-9666-2020; Kamel,
Amira/AAN-3716-2021; Abourehab, Mohammed/ABH-2907-2021; El-Mokhtar,
Mohamed A./HLQ-5588-2023
OI Zahran, Asmaa/0000-0001-8471-6388; Hetta, Helal F./0000-0001-8541-7304;
Kamel, Amira/0000-0001-7567-7022; El-Mokhtar, Mohamed
A./0000-0003-1943-8419; Batiha, Gaber/0000-0002-7817-425X; Ramadan,
Haidi Karam-Allah/0000-0003-0627-3985; abbas, wael/0000-0001-5554-8207;
Osman Saleh, Heba Ahmed/0000-0001-6302-3443
FU Grant Office, Faculty of Medicine, Assiut University [044-12-2015]
FX The authors are grateful to the Grant Office, Faculty of Medicine,
Assiut University [Grant No 044-12-2015].
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NR 66
TC 16
Z9 19
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-393X
J9 VACCINES-BASEL
JI Vaccines
PD SEP
PY 2020
VL 8
IS 3
AR 380
DI 10.3390/vaccines8030380
PG 12
WC Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Research & Experimental Medicine
GA OD9RW
UT WOS:000580182400001
PM 32664587
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Stern, L
Schmidt, C
Kocheise, L
Joerg, V
Casar, C
Walter, A
Drenth, JPH
Papp, M
Gatselis, NK
Zachou, K
Pinter, M
Scheiner, B
Vogel, A
Kirstein, MM
Finkelmeier, F
Waidmann, O
Weinmann, A
Milkiewicz, P
Thorburn, D
Halliday, N
Lleo, A
Huber, S
Dalekos, GN
Lohse, AW
Wege, H
von Felden, J
Schulze, K
AF Stern, Louisa
Schmidt, Constantin
Kocheise, Lorenz
Joerg, Vincent
Casar, Christian
Walter, Aurelie
Drenth, Joost P. H.
Papp, Maria
Gatselis, Nikolaos K.
Zachou, Kalliopi
Pinter, Matthias
Scheiner, Bernhard
Vogel, Arndt
Kirstein, Martha M.
Finkelmeier, Fabian
Waidmann, Oliver
Weinmann, Arndt
Milkiewicz, Piotr
Thorburn, Douglas
Halliday, Neil
Lleo, Ana
Huber, Samuel
Dalekos, George N.
Lohse, Ansgar W.
Wege, Henning
von Felden, Johann
Schulze, Kornelius
TI Efficacy and safety of palliative treatment in patients with autoimmune
liver disease-associated hepatocellular carcinoma
SO ANNALS OF HEPATOLOGY
LA English
DT Article
ID SORAFENIB; HEPATITIS; CANCER; TRIAL
AB Introduction and Objectives: Autoimmune liver diseases (AILD) are rare causes hepatocellular carcinoma (HCC), and data on the efficacy and tolerability of anti-tumor therapies are scarce. This pan-European study aimed to assess outcomes in AILD-HCC patients treated with tyrosine kinase inhibitors (TKIs) or transarterial chemoembolization (TACE) compared with patients with more common HCC etiologies, including viral, alcoholic or non-alcoholic fatty liver disease. Materials and Methods: 107 patients with HCC-AILD (AIH:55; PBC:52) treated at 13 European centres between 1996 and 2020 were included. 65 received TACE and 28 received TKI therapy. 43 (66%) were female (median age 73 years) with HCC tumor stage BCLC A (34 %), B (46 %), C (9%) or D (11 %). For each treatment type, propensity score matching was used to match AILD to non-AILD-HCC on a 1:1 basis, yielding in a final cohort of 130 TACE and 56 TKI patients for comparative analyses of median overall survival (mOS) and treatment tolerability. Results: HCC-AILD patients showed comparable mOS to controls for both TACE (19.5 vs. 22.1 months, p = 0.9) and TKI (15.4 vs. 15.1 months, p = 0.5). Adverse events were less frequent in AILD-HCC patients than controls (33%% vs. 62%, p = 0.003). For TKIs, there were no significant differences in adverse events (73% vs. 86%, p = 0.2) or interruption rates (44% vs. 36%, p = 0.7). Conclusions: In summary, this study demonstrates comparable mOS for AILD-HCC patients undergoing local and systemic treatments, with better tolerability than HCC of other causes. TKIs remain important therapeu- tic options for AILD-HCC patients, particularly given their exclusion from recent immunotherapy trials. (c) 2024 Fundacion Clinica Medica Sur, A.C. Published by Elsevier Espana, S.L.U. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)
C1 [Stern, Louisa] Univ Med Ctr Hamburg Eppendorf, Dept Gen Visceral & Thorac Surg, Martinistr 52, D-20246 Hamburg, Germany.
[Schmidt, Constantin; Kocheise, Lorenz; Joerg, Vincent; Huber, Samuel; Lohse, Ansgar W.; Wege, Henning; von Felden, Johann; Schulze, Kornelius] Univ Med Ctr Hamburg Eppendorf, Dept Internal Med & Gastroenterol, Martinistr 52, D-20246 Hamburg, Germany.
[Casar, Christian] Univ Med Ctr Hamburg Eppendorf, Bioinformat Core, Martinistr 52, D-20246 Hamburg, Germany.
[Walter, Aurelie] Hop Univ Paris Seine St Denis, Hop Avicenne, AP HP, Serv Hepatol, 125 Rue Stalingrad, F-93000 Bobigny, France.
[Drenth, Joost P. H.] Radboud Univ Nijmegen Med Ctr, Dept Gastroenterol & Hepatol, Geert Grootepl Zuid 8, NL-6525 GA Nijmegen, Netherlands.
[Papp, Maria] Univ Debrecen, Fac Med, Dept Internal Med, Div Gastroenterol, Nagyerde Blvd 98, HU-4026 Debrecen, Hungary.
[Gatselis, Nikolaos K.; Zachou, Kalliopi; Dalekos, George N.] Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Dept Med & Res Lab Internal Med, Larisa 41110, Greece.
[Pinter, Matthias; Scheiner, Bernhard] Med Univ Vienna, Dept Med 3, Div Gastroenterol & Hepatol, A-1090 Vienna, Austria.
[Vogel, Arndt] Med Sch Hannover, Dept Gastroenterol Hepatol & Endocrinol, Carl Neuberg Str 1, D-30625 Hannover, Germany.
[Kirstein, Martha M.] Univ Hosp Schleswig Holstein, Dept Med 1, Ratzeburger Allee 160, D-23538 Lubeck, Germany.
[Finkelmeier, Fabian; Waidmann, Oliver] Univ Hosp Frankfurt, Dept Gastroenterol Hepatol & Endocrinol, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
[Weinmann, Arndt] Univ Hosp Mainz, Dept Gastroenterol & Hepatol, Langenbeckstr 1, D-55131 Mainz, Germany.
[Milkiewicz, Piotr] Dept Gen Transplant & Liver Surg, Liver & Internal Med Unit, Block B,2nd Floor,Banacha 1A, PL-02097 Warsaw, Poland.
[Thorburn, Douglas; Halliday, Neil] Royal Free Hosp, Sheila Sherlock Liver Ctr, London, England.
[Thorburn, Douglas; Halliday, Neil] Royal Free Hosp, UCL Inst Liver & Digest Hlth, London, England.
[Lleo, Ana] Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini 4, I-20090 Milan, Italy.
[Lleo, Ana] Humanitas Res Hosp IRCCS, Dept Gastroenterol, Div Internal Med & Hepatol, Via A Manzoni 56, I-20089 Rozzano, Italy.
[Lleo, Ana] IRCCS Humanitas Res Hosp, Via Manzoni 56, I-20089 Milan, Italy.
[Kocheise, Lorenz; Joerg, Vincent; Drenth, Joost P. H.; Pinter, Matthias; Scheiner, Bernhard; Vogel, Arndt; Lleo, Ana; Dalekos, George N.; Lohse, Ansgar W.; von Felden, Johann; Schulze, Kornelius] European Reference Network Hepatol Dis ERN RARE L, Antwerp, Belgium.
[Milkiewicz, Piotr] Pomeranian Med Univ, Translat Med Grp, Szczecin, Poland.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Hamburg; University Medical Center Hamburg-Eppendorf;
Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
Avicenne - APHP; Universite Paris 13; Radboud University Nijmegen;
University of Debrecen; General University Hospital of Larissa; Medical
University of Vienna; Hannover Medical School; University of Kiel;
Schleswig Holstein University Hospital; Goethe University Frankfurt;
Goethe University Frankfurt Hospital; University Hospital Mainz;
University of London; University College London; UCL Medical School;
Royal Free London NHS Foundation Trust; University of London; University
College London; Royal Free London NHS Foundation Trust; UCL Medical
School; Humanitas University; IRCCS Humanitas Research Hospital;
Pomeranian Medical University
RP Stern, L (corresponding author), Univ Med Ctr Hamburg Eppendorf, Dept Gen Visceral & Thorac Surg, Martinistr 52, D-20246 Hamburg, Germany.
EM sternlouisa@gmail.com
RI Finkelmeier, Fabian/J-8185-2019; Stern, Louisa/JFK-9528-2023; Vogel,
Arndt/A-8437-2012; Lleo, Ana/AAA-5759-2019; Papp, Maria/LMN-8987-2024
OI Papp, Maria/0000-0003-3662-4010; Huber, Samuel/0000-0001-9325-8227;
Schmidt, Constantin/0000-0002-3892-4255; von Felden,
Johann/0000-0003-2839-5174
FU German Research Foundation (DFG); German Federal Ministry of Education
and Research (BMBF) [01EO2106]; German Cancer Aid (Deutsche Krebshilfe);
Wilhelm Sander Foundation
FX JvF is supported by the German Research Foundation (DFG), German Federal
Ministry of Education and Research (BMBF, grant 01EO2106 ), German
Cancer Aid (Deutsche Krebshilfe), and the Wilhelm Sander Foundation.
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NR 16
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER ESPANA
PI MADRID
PA CALLE DE ZURBANO, 76-4TH FLR LEFT, MADRID, 28010, SPAIN
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD NOV-DEC
PY 2024
VL 29
IS 6
AR 101534
DI 10.1016/j.aohep.2024.101534
EA AUG 2024
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA G8F0X
UT WOS:001318920100001
PM 39147132
DA 2025-01-07
ER
PT S
AU Chidambaranathan-Reghupaty, S
Fisher, PB
Sarkar, D
AF Chidambaranathan-Reghupaty, Saranya
Fisher, Paul B.
Sarkar, Devanand
BE Sarkar, D
Fisher, PB
TI Hepatocellular carcinoma (HCC): Epidemiology, etiology and molecular
classification
SO MECHANISMS AND THERAPY OF LIVER CANCER
SE Advances in Cancer Research
LA English
DT Review; Book Chapter
ID HEPATITIS-B-VIRUS; ALCOHOLIC LIVER-DISEASE; TUMOR-SUPPRESSOR GENE;
X-PROTEIN; HEREDITARY HEMOCHROMATOSIS; CELL-PROLIFERATION;
ALPHA(1)-ANTITRYPSIN DEFICIENCY; ALPHA-1-ANTITRYPSIN DEFICIENCY;
AUTOIMMUNE HEPATITIS; CENTROSOME DYNAMICS
AB Hepatocellular carcinoma (HCC), the primary malignancy of hepatocytes, is a diagnosis with bleak outcome. According to National Cancer Institute's SEER database, the average five-year survival rate of HCC patients in the US is 19.6% but can be as low as 2.5% for advanced, metastatic disease. When diagnosed at early stages, it is treatable with locoregional treatments including surgical resection, Radio-Frequency Ablation, Trans-Arterial Chemoembolization or liver transplantation. However, HCC is usually diagnosed at advanced stages when the tumor is unresectable, making these treatments ineffective. In such instances, systemic therapy with tyrosine kinase inhibitors (TKIs) becomes the only viable option, even though it benefits only 30% of patients, provides only a modest (similar to 3 months) increase in overall survival and causes drug resistance within 6 months. HCC, like many other cancers, is highly heterogeneous making a one-size fits all option problematic. The selection of liver transplantation, locoregional treatment, TKIs or immune checkpoint inhibitors as a treatment strategy depends on the disease stage and underlying condition(s). Additionally, patients with similar disease phenotype can have different molecular etiology making treatment responses different. Stratification of patients at the molecular level would facilitate development of the most effective treatment option. With the increase in efficiency and affordability of "omics"level analysis, considerable effort has been expended in classifying HCC at the molecular, metabolic and immunologic levels. This review examines the results of these efforts and the ways they can be leveraged to develop targeted treatment options for HCC.
C1 [Chidambaranathan-Reghupaty, Saranya] Virginia Commonwealth Univ, C Kenneth & Dianne Wright Ctr Clin & Translat Res, Richmond, VA USA.
[Fisher, Paul B.; Sarkar, Devanand] Virginia Commonwealth Univ, Sch Med, Dept Human & Mol Genet, Richmond, VA 23298 USA.
[Fisher, Paul B.; Sarkar, Devanand] Virginia Commonwealth Univ, Sch Med, VCU Inst Mol Med, Richmond, VA 23298 USA.
[Fisher, Paul B.; Sarkar, Devanand] Virginia Commonwealth Univ, VCU Massey Canc Ctr, Richmond, VA 23298 USA.
C3 Virginia Commonwealth University; Virginia Commonwealth University;
Virginia Commonwealth University; Virginia Commonwealth University
RP Sarkar, D (corresponding author), Virginia Commonwealth Univ, Sch Med, Dept Human & Mol Genet, Richmond, VA 23298 USA.; Sarkar, D (corresponding author), Virginia Commonwealth Univ, Sch Med, VCU Inst Mol Med, Richmond, VA 23298 USA.; Sarkar, D (corresponding author), Virginia Commonwealth Univ, VCU Massey Canc Ctr, Richmond, VA 23298 USA.
EM devanand.sarkar@vcuhealth.org
OI Chidambaranathan Reghupaty, Saranya/0000-0001-6660-1296
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[1R01DK107451-01A1]; National Cancer Institute (NCI) [1R01CA230561-01A1,
1R01CA240004-01, 1R01CA244993-01]; Department of Defense (DOD) Grant
[CA170048]; CDMRP [CA170048, 1100630] Funding Source: Federal RePORTER
FX The present study was supported in part by The National Institute of
Diabetes and Digestive and Kidney Diseases (NIDDK) Grant
1R01DK107451-01A1 (D.S.), National Cancer Institute (NCI) Grants
1R01CA230561-01A1 (D.S.), 1R01CA240004-01 (D.S.) and 1R01CA244993-01
(D.S. and P.B.F.), and Department of Defense (DOD) Grant CA170048
(D.S.).
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NR 227
TC 482
Z9 506
U1 21
U2 113
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0065-230X
EI 2162-5557
BN 978-0-12-824030-4
J9 ADV CANCER RES
JI Adv.Cancer Res.
PY 2021
VL 149
BP 1
EP 61
DI 10.1016/bs.acr.2020.10.001
PG 61
WC Oncology; Gastroenterology & Hepatology; Medicine, Research &
Experimental
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology; Research & Experimental
Medicine
GA BS3AJ
UT WOS:000708924200002
PM 33579421
OA Green Accepted
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Ajith, A
Merimi, M
Arki, MK
Hossein-khannazer, N
Najar, M
Vosough, M
Sokal, EM
Najimi, M
AF Ajith, Ananya
Merimi, Makram
Arki, Mandana Kazem
Hossein-khannazer, Nikoo
Najar, Mehdi
Vosough, Massoud
Sokal, Etienne Marc
Najimi, Mustapha
TI Immune regulation and therapeutic application of T regulatory cells in
liver diseases
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE T regulatory cells; foxp3; hepatic microenvironment; liver fibrosis;
liver cirrhosis; HCC; Treg immunotherapy
ID HEPATOCELLULAR-CARCINOMA; TUMOR MICROENVIRONMENT; DENDRITIC CELLS;
EPIGENETIC CONTROL; PERIPHERAL-BLOOD; FOXP3 EXPRESSION; KUPFFER CELLS;
CUTTING EDGE; IMMUNOTHERAPY; MECHANISMS
AB CD4+ CD25+ FOXP3+ T regulatory cells (Tregs) are a subset of the immunomodulatory cell population that can inhibit both innate and adaptive immunity by various regulatory mechanisms. In hepatic microenvironment, proliferation, plasticity, migration, and function of Tregs are interrelated to the remaining immune cells and their secreted cytokines and chemokines. In normal conditions, Tregs protect the liver from inflammatory and auto-immune responses, while disruption of this crosstalk between Tregs and other immune cells may result in the progression of chronic liver diseases and the development of hepatic malignancy. In this review, we analyze the deviance of this protective nature of Tregs in response to chronic inflammation and its involvement in inducing liver fibrosis, cirrhosis, and hepatocellular carcinoma. We will also provide a detailed emphasis on the relevance of Tregs as an effective immunotherapeutic option for autoimmune diseases, liver transplantation, and chronic liver diseases including liver cancer.
C1 [Ajith, Ananya; Sokal, Etienne Marc; Najimi, Mustapha] UCLouvain, Lab Pediat Hepatol & Cell Therapy, Brussels, Belgium.
[Merimi, Makram] Univ Mohammed Premier, Fac Sci, Genet & Immune Cell Therapy Unit, LBBES Lab, Oujda, Morocco.
[Arki, Mandana Kazem] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Gastroenterol & Liver Dis Res Ctr, Tehran, Iran.
[Hossein-khannazer, Nikoo] Shahid Beheshti Univ Med Sci, Sch Adv Technol Med, Dept Tissue Engn & Appl Cell Sci, Tehran, Iran.
[Najar, Mehdi] Univ Montreal Hosp Res Ctr CRCHUM, Dept Med, Osteoarthritis Res Unit, Montreal, PQ, Canada.
[Najar, Mehdi] Univ Libre Bruxelles, Fac Med, Brussels, Belgium.
[Vosough, Massoud] ACECR, Dept Regenerat Med, Royan Inst Stem Cell Biol & Technol, Cell Sci Res Ctr, Tehran, Iran.
[Vosough, Massoud] Inst Lab Med, Karolinska Inst, Expt Canc Med, Huddinge, Sweden.
C3 Universite Catholique Louvain; Mohammed First University of Oujda;
Shahid Beheshti University Medical Sciences; Shahid Beheshti University
Medical Sciences; Universite de Montreal; Universite Libre de Bruxelles;
Academic Center for Education, Culture & Research (ACECR); Karolinska
Institutet
RP Najimi, M (corresponding author), UCLouvain, Lab Pediat Hepatol & Cell Therapy, Brussels, Belgium.
EM mustapha.najimi@uclouvain.be
RI Vosough, Massoud/AAR-8970-2021
OI Vosough, Massoud/0000-0001-5924-4366
FU Fonds National de la Recherche Scientifique (FNRS); Televie; Research
Project (PDR) [PDR-TLV 7.8513.19]
FX The author(s) declare financial support was received for the research,
authorship, and/or publication of this article. This study has received
support from "Fonds National de la Recherche Scientifique (FNRS)",
Televie, and the Research Project (PDR) (Ref: PDR-TLV 7.8513.19).
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NR 150
TC 2
Z9 3
U1 1
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAR 20
PY 2024
VL 15
AR 1371089
DI 10.3389/fimmu.2024.1371089
PG 16
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA MS0N4
UT WOS:001195505700001
PM 38571964
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wei, XX
Yang, CL
Lin, QL
Qiu, MQ
Wen, QP
Zhou, ZH
Jiang, YJ
Chen, PQ
Liang, XM
Cao, J
Tang, J
Wei, YY
Yu, HP
Liu, YC
AF Wei, Xiaoxia
Yang, Chenglei
Lin, Qiuling
Qiu, Moqin
Wen, Qiuping
Zhou, Zihan
Jiang, Yanji
Chen, Peiqin
Liang, Xiumei
Cao, Ji
Tang, Juan
Wei, Yuying
Yu, Hongping
Liu, Yingchun
TI Associations between modifiable risk factors and hepatocellular
carcinoma: a trans-ancestry Mendelian randomization study
SO BMC CANCER
LA English
DT Article
DE Hepatocellular carcinoma; Mendelian randomization; Modifiable risk
factors; Trans-ancestry
ID CAUSAL INFERENCE; CANCER; HEPATITIS; POWER; EPIDEMIOLOGY; METAANALYSIS;
POPULATION; ALCOHOL; MODEL
AB Background Potentially modifiable risk factors for hepatocellular carcinoma (HCC) have been investigated in observational epidemiology studies in East Asian and European populations, whereas the causal associations of most of these risk factors remain unclear. Methods We collected genome-wide association summary statistics of 22 modifiable risk factors in East Asians and 33 risk factors in Europeans. Genetic summary statistics of HCC were sourced from the Biobank Japan study (1,866 cases and 195,745 controls) for East Asians, and the deCODE genetics study (406 cases and 49,302 controls) and the UK Biobank (168 cases and 372 016 controls) for Europeans. Two-sample Mendelian randomization (MR) analyses were performed independently for East Asian and European populations. Results In East Asians, genetically predicted alcohol frequency, ever drinkers, aspartate aminotransferase (AST), hypothyroidism, chronic hepatitis B, and chronic hepatitis C, metabolic dysfunction-associated steatotic liver disease (MASLD), and autoimmune hepatitis were significantly associated with an increased HCC risk (P < 0.05/22). Among European population, alanine transaminase, AST, MASLD, percent liver fat, and liver iron content were significantly associated with a higher risk of HCC (P < 0.05/33). The replication dataset and meta-analysis further confirmed these results. Conclusions Although East Asian and European populations have different factors for HCC, their common modifiable risk factors AST and MASLD for HCC, offer valuable insights for targeted intervention strategies to mitigate society burden of HCC.
C1 [Wei, Xiaoxia; Lin, Qiuling] Guangxi Med Univ, Canc Hosp, Dept Clin Trial Base, Nanning, Guangxi, Peoples R China.
[Yang, Chenglei; Tang, Juan] Guangxi Med Univ, Canc Hosp, Dept Hepatobiliary Surg, Nanning, Guangxi, Peoples R China.
[Qiu, Moqin] Guangxi Med Univ, Canc Hosp, Dept Resp Oncol, Nanning, Guangxi, Peoples R China.
[Wen, Qiuping; Wei, Yuying; Yu, Hongping; Liu, Yingchun] Guangxi Med Univ, Canc Hosp, Dept Expt Res, Nanning, Guangxi, Peoples R China.
[Zhou, Zihan; Cao, Ji] Guangxi Med Univ, Canc Hosp, Dept Canc Prevent & Control, Nanning, Guangxi, Peoples R China.
[Jiang, Yanji] Guangxi Med Univ, Canc Hosp, Dept Sci Res, Nanning, Guangxi, Peoples R China.
[Chen, Peiqin] Guangxi Med Univ, Canc Hosp, Dept Dis Proc Management, Nanning, Guangxi, Peoples R China.
[Liang, Xiumei; Yu, Hongping] Guangxi Med Univ, Key Lab Early Prevent & Treatment Reg High Frequen, Minist Educ, Nanning, Guangxi, Peoples R China.
[Wei, Yuying; Yu, Hongping; Liu, Yingchun] Guangxi Med Univ, Canc Hosp, Key Cultivated Lab Canc Mol Med, Guangxi Hlth Commiss, Nanning, Guangxi, Peoples R China.
C3 Guangxi Medical University; Guangxi Medical University; Guangxi Medical
University; Guangxi Medical University; Guangxi Medical University;
Guangxi Medical University; Guangxi Medical University; Guangxi Medical
University; Guangxi Medical University
RP Yu, HP; Liu, YC (corresponding author), Guangxi Med Univ, Canc Hosp, Dept Expt Res, Nanning, Guangxi, Peoples R China.; Yu, HP (corresponding author), Guangxi Med Univ, Key Lab Early Prevent & Treatment Reg High Frequen, Minist Educ, Nanning, Guangxi, Peoples R China.; Yu, HP; Liu, YC (corresponding author), Guangxi Med Univ, Canc Hosp, Key Cultivated Lab Canc Mol Med, Guangxi Hlth Commiss, Nanning, Guangxi, Peoples R China.
EM yuhongping@stu.gxmu.edu.cn; liuyingchun@stu.gxmu.edu.cn
RI Chen, Peiqin/AHC-2666-2022
FU Natural Science Foundation of Guangxi Province [2023GXNSFBA026091]; Key
Laboratory of Early Prevention and Treatment for Regional High Frequency
Tumor, Ministry of Education [GKE-ZZ202316, GKE-ZZ202118]; Key Project
of Guangxi Natural Science Foundation [2018GXNSFDA050012]; The 111
Projects [D17011]; Youth Science Foundation of Guangxi Medical
University [GXMUYSF202304]; Youth Program of Scientific Research
Foundation of Guangxi Medical University Cancer Hospital [YQJ2022-5]
FX This work was supported by Natural Science Foundation of Guangxi
Province (2023GXNSFBA026091); Key Laboratory of Early Prevention and
Treatment for Regional High Frequency Tumor, Ministry of Education
(GKE-ZZ202316, GKE-ZZ202118); The Key Project of Guangxi Natural Science
Foundation (2018GXNSFDA050012); The 111 Projects (D17011); Youth Science
Foundation of Guangxi Medical University (GXMUYSF202304); Youth Program
of Scientific Research Foundation of Guangxi Medical University Cancer
Hospital (YQJ2022-5).
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NR 45
TC 0
Z9 0
U1 3
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUL 10
PY 2024
VL 24
IS 1
AR 820
DI 10.1186/s12885-024-12525-x
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YN2Y9
UT WOS:001269114300007
PM 38987736
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Okino, H
Satoh, T
Watanabe, J
Masumoto, A
Takeda, S
AF Okino, Hidenobu
Satoh, Takeaki
Watanabe, Jiro
Masumoto, Akihide
Takeda, Shigeaki
TI Hepatocellular carcinoma arising from autoimmune hepatitis: Report of a
case
SO SURGERY TODAY
LA English
DT Article
DE hepatocellular carcinoma; autoimmune hepatitis; hepatitis virus
ID CHRONIC LIVER-DISEASE; PROGNOSIS
AB We describe an operative case of a 64-year-old woman with hepatocellular carcinoma (HCC) associated with autoimmune hepatitis (AIH) during a 4.8-year follow-up. Sixty-seven cases of HCC with AIH have been previously reported as a sporadic complication of AIH. The survival rate after diagnosis with HCC showed the 5-year survival rate to be 10.4%, thus indicating the majority of patients to have either extensive HCC or severe liver dysfunction. Immunosuppressant therapy helped to postpone the hepatocarcinogenesis but it did not improve the prognosis of the patients demonstrating HCC with AIH. A univariate analysis of factors associated with prognosis disclosed that the histology of nontumorous lesion at diagnosis with HCC, tumor size, tumor number, and treatment for HCC were independent prognostic predictors. Patients with AIH were not recognized to be a high-risk group for developing HCC because HCC occasionally occurred even in patients with long-standing cirrhosis in the absence of hepatitis B virus and hepatitis C virus infection.
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Kokura Hosp, Natl Hosp Org, Dept Liver Dis, Kokuraminami Ku, Kitakyushu, Fukuoka 8028533, Japan.
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RP Okino, H (corresponding author), Kokura Hosp, Natl Hosp Org, Dept Surg & Clin Res, Kokuraminami Ku, Kitakyushu, Fukuoka 8028533, Japan.
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TC 6
Z9 6
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013 USA
SN 0941-1291
J9 SURG TODAY
JI Surg. Today
PD AUG
PY 2007
VL 37
IS 8
BP 716
EP 718
DI 10.1007/s00595-007-3483-y
PG 3
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA 192US
UT WOS:000248229500021
PM 17643223
DA 2025-01-07
ER
PT J
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Sun, Chenyu
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Du, Yingying
TI cGAS-STING Signaling Pathway and Liver Disease: From Basic Research to
Clinical Practice
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE CGAS; STING; liver; inflammation; cancer
ID NF-KAPPA-B; VIRUS REPLICATION; INNATE IMMUNITY; DNA SENSOR;
INFLAMMATION; CANCER; CELLS; ACTIVATION; CONTRIBUTES; NARINGENIN
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C1 [Chen, Bangjie; Rao, Xianyue; Luo, Zhipan; Liu, Yuchen; Du, Yingying] Anhui Med Univ, Affiliated Hosp 1, Hefei, Peoples R China.
[Wang, Xinyi; Wang, Jianpeng; Sheng, Shuyan; Zhang, Ning; Jin, Shiyu; Chen, Haosong] Anhui Med Univ, Clin Med Coll 1, Hefei, Peoples R China.
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[Xu, Tao] Inflammat & Immune Mediated Dis Lab Anhui Prov, Hefei, Peoples R China.
[Xu, Tao] Anhui Med Univ, Sch Pharm, Hefei, Peoples R China.
C3 Anhui Medical University; Anhui Medical University; Anhui Medical
University
RP Du, YY (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Hefei, Peoples R China.; Xu, T (corresponding author), Inflammat & Immune Mediated Dis Lab Anhui Prov, Hefei, Peoples R China.; Xu, T (corresponding author), Anhui Med Univ, Sch Pharm, Hefei, Peoples R China.
EM xutao@ahmu.edu.cn; duyingying@126.com
RI Chen, Bangjie/GLU-7441-2022; Wang, Xinyi/HJH-9845-2023; Sheng,
Shuyan/HPC-1871-2023; Sun, Chenyu/M-2322-2019; Xu, Tao/P-9130-2015; liu,
yuchen/GYQ-6286-2022; LIU, zhu/IYS-9390-2023; Chen,
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OI Liu, Yu-Chen/0000-0002-9189-3021; Sheng, Shuyan/0000-0003-2320-7648;
Zhang, Ning/0000-0002-5892-2193; Sun, Chenyu/0000-0003-3812-3164; Wang,
Jianpeng/0009-0003-2664-8956
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PI LAUSANNE
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PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA UM8AX
UT WOS:000693549900001
PM 34483930
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Tai, JNF
Harrison, AP
Chen, HM
Hsu, CY
Hsu, TH
Chen, CJ
Jeng, WJ
Chang, ML
Lu, L
Tai, DI
AF Tai, Jennifer
Harrison, Adam P.
Chen, Hui-Ming
Hsu, Chiu-Yi
Hsu, Tse-Hwa
Chen, Cheng-Jen
Jeng, Wen-Juei
Chang, Ming-Ling
Lu, Le
Tai, Dar-In
TI Acoustic radiation force impulse predicts long-term outcomes in a
large-scale cohort: High liver cancer, low comorbidity in hepatitis B
virus
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Non-alcoholic fatty liver disease; Hepatitis B; Hepatocellular
carcinoma; Acoustic radiation force impulse; Mortality; Comorbidity
ID HEPATOCELLULAR-CARCINOMA; TRANSIENT ELASTOGRAPHY; NATURAL-HISTORY; B/C
INFECTION; RISK; FIBROSIS; STIFFNESS; VALIDATION; ULTRASOUND
AB BACKGROUND Acoustic radiation force impulse (ARFI) is used to measure liver fibrosis and predict outcomes. The performance of elastography in assessment of fibrosis is poorer in hepatitis B virus (HBV) than in other etiologies of chronic liver disease.AIM To evaluate the performance of ARFI in long-term outcome prediction among different etiologies of chronic liver disease.METHODS Consecutive patients who received an ARFI study between 2011 and 2018 were enrolled. After excluding dual infection, alcoholism, autoimmune hepatitis, and others with incomplete data, this retrospective cohort were divided into hepatitis B (HBV, n = 1064), hepatitis C (HCV, n = 507), and non-HBV, non-HCV (NBNC, n = 391) groups. The indexed cases were linked to cancer registration (1987-2020) and national mortality databases. The differences in morbidity and mortality among the groups were analyzed.RESULTS At the enrollment, the HBV group showed more males (77.5%), a higher prevalence of pre-diagnosed hepatocellular carcinoma (HCC), and a lower prevalence of comorbidities than the other groups (P < 0.001). The HCV group was older and had a lower platelet count and higher ARFI score than the other groups (P < 0.001). The NBNC group showed a higher body mass index and platelet count, a higher prevalence of pre-diagnosed non-HCC cancers (P < 0.001), especially breast cancer, and a lower prevalence of cirrhosis. Male gender, ARFI score, and HBV were independent predictors of HCC. The 5-year risk of HCC was 5.9% and 9.8% for those ARFI-graded with severe fibrosis and cirrhosis. ARFI alone had an area under the receiver operating characteristic curve (AUROC) of 0.742 for prediction of HCC in 5 years. AUROC increased to 0.828 after adding etiology, gender, age, and platelet score. No difference was found in mortality rate among the groups.CONCLUSION The HBV group showed a higher prevalence of HCC but lower comorbidity that made mortality similar among the groups. Those patients with ARFI-graded severe fibrosis or cirrhosis should receive regular surveillance.
C1 [Tai, Jennifer; Hsu, Tse-Hwa; Chen, Cheng-Jen; Jeng, Wen-Juei; Chang, Ming-Ling; Tai, Dar-In] Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, 5 Fuxing St, Taoyuan 33305, Taiwan.
[Harrison, Adam P.] Q Bio, Radi Grp, San Carlos, CA 94063 USA.
[Chen, Hui-Ming; Hsu, Chiu-Yi] Chang Gung Mem Hosp, Ctr Big Data Analyt & Stat, Taoyuan 33305, Taiwan.
[Lu, Le] Alibaba Grp, DAMO Acad, New York, NY 10014 USA.
C3 Chang Gung Memorial Hospital; Chang Gung Memorial Hospital; Alibaba
Group
RP Tai, DI (corresponding author), Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, 5 Fuxing St, Taoyuan 33305, Taiwan.
EM tai48978@cgmh.org.tw
RI Lu, Le/AAD-7619-2020
OI Jeng, Wen-Juei/0000-0002-3706-1259
FU Chang Gung Memorial Hospital; PAII Inc [SMRPG3I0011]
FX Supported by the Chang Gung Memorial Hospital and PAII Inc. (a United
States subsidiary company of Ping An Insurance Group), No. SMRPG3I0011.
CR Aoki T, 2017, J GASTROENTEROL, V52, P104, DOI 10.1007/s00535-016-1228-7
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Hsieh AR, 2021, WORLD J GASTROENTERO, V27, P6262, DOI 10.3748/wjg.v27.i37.6262
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Zhang YC, 2021, INT J HYPERTHER, V38, P1052, DOI 10.1080/02656736.2021.1947529
NR 38
TC 0
Z9 0
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD APR 14
PY 2023
VL 29
IS 14
BP 2188
EP 2201
DI 10.3748/wjg.v29.i14.2188
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA F7WA2
UT WOS:000984400300009
PM 37122600
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Jepsen, P
Kraglund, F
West, J
Villadsen, GE
Sorensen, HT
Vilstrup, H
AF Jepsen, Peter
Kraglund, Frederik
West, Joe
Villadsen, Gerda E.
Sorensen, Henrik Toft
Vilstrup, Hendrik
TI Risk of hepatocellular carcinoma in Danish outpatients with
alcohol-related cirrhosis
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Liver cirrhosis; Primary liver cancer; Prognosis; Screening;
Epidemiology
ID MULTISTATE MODELS; LIVER-CIRRHOSIS; CLINICAL-COURSE; DATA QUALITY;
SYSTEM; SURVEILLANCE; REGISTER; DENMARK; PACKAGE
AB Background and Aims: Accurate estimates of hepatocellular carcinoma (HCC) risk in patients with cirrhosis are important to guide surveillance strategies. We described HCC risk among outpatients with alcohol-related cirrhosis and contrasted the risk of death from HCC with the risk of death from variceal bleeding or trauma.
Methods: This was a nationwide, registry-based historical cohort study between 2006 and 2018. We included all Danish outpatients with a hospital diagnosis of alcohol-related cirrhosis, except those with cancer, those with chronic viral hepatitis or autoimmune liver disease, and those older than 80 years. We followed them through 2018 and described the cumulative risk of HCC and the cumulative risk of death from HCC, variceal bleeding, or trauma.
Results: Of the 4,553 patients included, 181 developed HCC and 2,274 died. The cumulative risk of HCC was 0.9% (95% CI 0.7-1.3) after 1 year, 3.6% (95% CI 3.0-4.2) after 5 years, and 6.0% (95% CI 5.1-7.0) after 10 years, or approximately 0.7% per year. Male sex, older age, and decompensated cirrhosis predicted a higher HCC risk. After 10 years, 6.9% of deaths in the cohort could be attributed to HCC, whereas 6.5% could be attributed to variceal bleeding, and 5.0% to trauma.
Conclusions: In 2006-2018, Danish outpatients with alcoholrelated cirrhosis had an HCC risk of 0.7% per year, and they were nearly as likely to die from variceal bleeding or from trauma as from HCC. The implications are that many potentially harmful examinations are required for every HCC found through surveillance, so interventions targeting the prevention of other causes of death might be more cost-effective.
Lay summary: We described the risk of hepatocellular carcinoma (HCC, the most common form of liver cancer originating in the liver) in Danish outpatients with cirrhosis due to harmful alcohol consumption. Accurate data on that risk are important for patient counselling and decisions about screening for HCC. The risk was about 0.7% per year, which is lower than might be expected and suggests that many potentially harmful screening examinations are required for every HCC found through surveillance. (C) 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Jepsen, Peter; Kraglund, Frederik; Villadsen, Gerda E.; Vilstrup, Hendrik] Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Palle Juul Jensens Blvd 99, DK-8200 Aarhus N, Denmark.
[Jepsen, Peter; Sorensen, Henrik Toft] Aarhus Univ Hosp, Dept Clin Epidemiol, Aarhus, Denmark.
[West, Joe] Univ Nottingham, Sch Med, Div Epidemiol & Publ Hlth, Nottingham, England.
[West, Joe] Nottingham Univ Hosp NHS Trust, NIHR Nottingham Biomed Res Ctr BRC, Nottingham, England.
[West, Joe] Univ Nottingham, Nottingham, England.
C3 Aarhus University; Aarhus University; University of Nottingham;
Nottingham University Hospital NHS Trust; University of Nottingham
RP Jepsen, P (corresponding author), Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Palle Juul Jensens Blvd 99, DK-8200 Aarhus N, Denmark.
EM pj@clin.au.dk
RI Sørensen, Henrik/Z-6181-2019; West, Joe/I-6637-2012
OI West, Joe/0000-0002-1135-9356; Jepsen, Peter/0000-0002-6641-1430;
Kraglund, Frederik/0000-0002-7641-6980; Toft Sorensen,
Henrik/0000-0003-4299-7040
FU Novo Nordisk Foundation [NNF18OC0054612]; Danish Cancer Society
[R208-A12410]
FX Peter Jepsen was supported by grants from the Novo Nordisk Foundation
(NNF18OC0054612) and the Danish Cancer Society (R208-A12410). The
funding organizations were not involved in the design and conduct of the
study, or in the decision to submit the manuscript for publication.
CR [Anonymous], 2018, J HEPATOL
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NR 39
TC 23
Z9 28
U1 0
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD NOV
PY 2020
VL 73
IS 5
BP 1030
EP 1036
DI 10.1016/j.jhep.2020.05.043
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA OD4GA
UT WOS:000579809700007
PM 32512015
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Lin, BZ
Lin, TJ
Lin, CL
Liao, LY
Chang, TA
Lu, BJ
Chen, KY
AF Lin, Bou-Zenn
Lin, Tsung-Jung
Lin, Chih-Lin
Liao, Li-Ying
Chang, Ting-An
Lu, Buo-Jia
Chen, Kuan-Yang
TI Differentiation of clinical patterns and survival outcomes of
hepatocellular carcinoma on hepatitis B and nonalcoholic fatty liver
disease
SO JOURNAL OF THE CHINESE MEDICAL ASSOCIATION
LA English
DT Article
DE Fatty liver; Hepatitis B virus (HBV); Hepatocellular carcinoma (HCC);
Nonalcoholic fatty liver disease (NAFLD)
ID METABOLIC SYNDROME; UNITED-STATES; STEATOHEPATITIS; CIRRHOSIS; FIBROSIS;
NAFLD; EPIDEMIOLOGY; CANCER; RISK; PATHOGENESIS
AB Background:
The main etiologies of hepatocellular carcinoma (HCC) were often hepatitis B virus (HBV) or C and alcohol, rarely autoimmune and biliary diseases. Nonalcoholic fatty liver disease (NAFLD) has been an emerging role that could lead to chronic liver disease, nonalcoholic steatohepatitis, cirrhosis, and eventually HCC in recent years. The aim of our study is to investigate and compare the clinical features of HCC in patients with NAFLD and HBV, including age, gender, cirrhosis, liver function tests, largest tumor size, and cancer stage at the time of diagnosis. The survival outcome was compared between the two groups and the significant predictors of mortality were also analyzed in all patients with HCC.
Methods:
Most patients with HCC were recruited from the database of Cancer Registries in Taipei City Hospital, Ren-Ai Branch, from 2011 to 2017; and the other patients consecutively from the HCC multidisciplinary conference between January 2018 and December 2019. NAFLD was defined as nonviral hepatitis B (negative HBsAg and either positive anti-HBs or negative anti-HBc), nonviral hepatitis C (negative antihepatitis C virus [HCV]), nonalcoholic (alcohol consumption of <30 g/d for men and <20 g/d for women) liver disease, or present or past histological or ultrasonographic evidence of fatty liver. Totally, 23 NAFLD-related and 156 HBV-related HCC patients were enrolled in our study for further analysis.
Results:
NAFLD-related HCC patients were significantly older (median age: 70.0 [61.0-79.0] years vs. 63.0 [56.0-72.0] years, p = 0.012) and heavier (median body mass index [BMI]: 26.6 [24.2-30] kg/m(2) vs. 24.8 [22.0-27.1] kg/m(2), p = 0.044) than those with HBV-related HCC. They were also more susceptible to diabetes mellitus (DM), and 60.9% (14 of 23) of them had this comorbidity compared with 29.5% (46 of 156) of those with HBV-related HCC (p = 0.003). Only 34.8% (8 of 23) and 71.2% (111 of 156) of patients with NAFLD- and HBV-related HCC were cirrhotic, respectively (p = 0.001). However, gender, tobacco use, international normalized ratio, albumin, creatinine, and cholesterol levels were not significantly different between the two groups. Tumor characteristics such as the Barcelona clinic liver cancer stage, largest tumor size, tumor number, extrahepatic metastasis, and treatment modalities had no significant difference between such groups.
According to the Kaplan-Meier method analysis, the overall survival was not significantly different between these two patient groups (log-rank test, p = 0.101). To evaluate which patient group would lead to poor prognosis, we analyzed the survival of all patients through multivariate Cox proportional hazard regression after controlling other factors that may influence the hazard ratio. The analysis revealed that NAFLD and HBV infection as the cause of HCC are not risk factors of poor prognosis.
Conclusion:
In conclusion, our study showed NAFLD-related HCC patients were older, heavier, and more had DM than HBV-related. In addition, more NAFLD-related HCC patients were noncirrhotic than HBV-related. The survival rate was similar between NAFLD and HBV-related HCC patients.
C1 [Lin, Bou-Zenn; Lin, Tsung-Jung; Lin, Chih-Lin; Liao, Li-Ying; Chen, Kuan-Yang] Taipei City Hosp, Dept Gastroenterol, Ren Ai Branch, 11F,10,Sect 4,Renai Rd, Taipei 106, Taiwan.
[Chang, Ting-An] Taipei City Hosp, Dept Pathol, Ren Ai Branch, Taipei, Taiwan.
[Lu, Buo-Jia] Taipei Med Univ Hosp, Dept Obstet & Gynecol, Taipei, Taiwan.
[Lin, Tsung-Jung] Univ Taipei, Taipei, Taiwan.
C3 Taipei City Hospital; Taipei City Hospital; Taipei Medical University;
Taipei Medical University Hospital; University of Taipei
RP Lin, TJ (corresponding author), Taipei City Hosp, Dept Gastroenterol, Ren Ai Branch, 11F,10,Sect 4,Renai Rd, Taipei 106, Taiwan.
EM DAB70@tpech.gov.tw
RI chen, ye/HSF-9650-2023
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NR 57
TC 13
Z9 15
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1726-4901
EI 1728-7731
J9 J CHIN MED ASSOC
JI J. Chin. Med. Assoc.
PD JUN
PY 2021
VL 84
IS 6
BP 606
EP 613
DI 10.1097/JCMA.0000000000000530
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA SN7MH
UT WOS:000658471000009
PM 33871391
OA hybrid
DA 2025-01-07
ER
PT J
AU Rallis, KS
Makrakis, D
Ziogas, IA
Tsoulfas, G
AF Rallis, Kathrine S.
Makrakis, Dimitrios
Ziogas, Ioannis A.
Tsoulfas, Georgios
TI Immunotherapy for advanced hepatocellular carcinoma: From clinical
trials to real-world data and future advances
SO WORLD JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
DE Hepatocellular carcinoma; Liver cancer; Immunotherapy; Immune checkpoint
inhibitors; Clinical trials; Real-world data
ID IMMUNE-CHECKPOINT INHIBITORS; PREEXISTING AUTOIMMUNE-DISEASE; INDUCED
KILLER-CELLS; ADJUVANT IMMUNOTHERAPY; COMBINATION THERAPY; ADVANCED
MELANOMA; DOUBLE-BLIND; CANCER; IPILIMUMAB; SORAFENIB
AB Hepatocellular carcinoma (HCC) is a leading cause of cancer-associated mortality worldwide. HCC is an inflammation-associated immunogenic cancer that frequently arises in chronically inflamed livers. Advanced HCC is managed with systemic therapies; the tyrosine kinase inhibitor (TKI) sorafenib has been used in 1st-line setting since 2007. Immunotherapies have emerged as promising treatments across solid tumors including HCC for which immune checkpoint inhibitors (ICIs) are licensed in 1st- and 2nd-line treatment setting. The treatment field of advanced HCC is continuously evolving. Several clinical trials are investigating novel ICI candidates as well as new ICI regimens in combination with other therapeutic modalities including systemic agents, such as other ICIs, TKIs, and anti-angiogenics. Novel immunotherapies including adoptive cell transfer, vaccine-based approaches, and virotherapy are also being brought to the fore. Yet, despite advances, several challenges persist. Lack of real-world data on the use of immunotherapy for advanced HCC in patients outside of clinical trials constitutes a main limitation hindering the breadth of application and generalizability of data to this larger and more diverse patient cohort. Consequently, issues encountered in real-world practice include patient ineligibly for immunotherapy because of contraindications, comorbidities, or poor performance status; lack of response, efficacy, and safety data; and cost-effectiveness. Further real-world data from high-quality large prospective cohort studies of immunotherapy in patients with advanced HCC is mandated to aid evidence-based clinical decision-making. This review provides a critical and comprehensive overview of clinical trials and real-world data of immunotherapy for HCC, with a focus on ICIs, as well as novel immunotherapy strategies underway.
C1 [Rallis, Kathrine S.] Queen Mary Univ London, Barts & London Sch Med & Dent, London E1 2AD, England.
[Rallis, Kathrine S.; Makrakis, Dimitrios; Ziogas, Ioannis A.] Soc Jr Doctors, Surg Working Grp, Athens 15123, Greece.
[Makrakis, Dimitrios] Univ Washington, Div Oncol, Sch Med, Seattle, WA 98195 USA.
[Ziogas, Ioannis A.] Vanderbilt Univ, Med Ctr, Dept Surg, Div Hepatobiliary Surg & Liver Transplantat, Nashville, TN 37232 USA.
[Tsoulfas, Georgios] Aristotle Univ Thessaloniki, Dept Transplantat Surg, Sch Med, 66 Tsimiski St, Thessaloniki 54622, Greece.
C3 University of London; Queen Mary University London; University of
Washington; University of Washington Seattle; Vanderbilt University;
Aristotle University of Thessaloniki
RP Tsoulfas, G (corresponding author), Aristotle Univ Thessaloniki, Dept Transplantat Surg, Sch Med, 66 Tsimiski St, Thessaloniki 54622, Greece.
EM tsoulfasg@gmail.com
RI Tsivgoulis, Georgios/AAD-5360-2020
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NR 161
TC 7
Z9 7
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2218-4333
J9 WORLD J CLIN ONCOL
JI World J. Clin. Oncol.
PD JUN 24
PY 2022
VL 13
IS 6
BP 448
EP 472
DI 10.5306/wjco.v13.i6.448
PG 25
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA 3U1XZ
UT WOS:000840767800003
PM 35949435
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Li, CX
Ling, CC
Shao, Y
Xu, AM
Li, XC
Ng, KTP
Liu, XB
Ma, YY
Qi, X
Liu, H
Liu, J
Yeung, OWH
Yang, XX
Liu, QS
Lam, YF
Zhai, Y
Lo, CM
Man, K
AF Li, Chang Xian
Ling, Chang Chun
Shao, Yan
Xu, Aimin
Li, Xiang Cheng
Ng, Kevin Tak-Pan
Liu, Xiao Bing
Ma, Yuen Yuen
Qi, Xiang
Liu, Hui
Liu, Jiang
Yeung, Oscar Wai Ho
Yang, Xin Xiang
Liu, Qing Sheng
Lam, Yin Fan
Zhai, Yuan
Lo, Chung Mau
Man, Kwan
TI CXCL10/CXCR3 signaling mobilized-regulatory T cells promote liver tumor
recurrence after transplantation
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Liver transplantation; Liver graft injury; Hepatocellular carcinoma;
Tumor recurrence; Regulatory T cells
ID HEPATOCELLULAR-CARCINOMA RECURRENCE; REPERFUSION INJURY; INFLAMMATORY
RESPONSE; ISCHEMIA-REPERFUSION; AUTOIMMUNE-DISEASE; PERIPHERAL-BLOOD;
CANCER-PATIENTS; CUTTING EDGE; GRAFT INJURY; LUNG-CANCER
AB Background & Aims: Liver graft injury and tumor recurrence are the major challenges of liver transplantation for the patients with hepatocellular carcinoma (HCC). Here, we aimed to explore the role and mechanism of liver graft injury mobilizing regulatory T cells (Tregs), which lead to late phase tumor recurrence after liver transplantation.
Methods: The correlation among tumor recurrence, liver graft injury and Tregs mobilization were studied in 257 liver transplant recipients with HCC and orthotopic rat liver transplantation models. The direct roles of CXCL10/CXCR3 signaling on Tregs mobilization and tumor recurrence were investigated in CXCL10(-/-) and CXCR3(-/-) mice models with hepatic IR injury.
Results: Clinically, patients received the graft with graft weight ratio (GWR) <60% had higher HCC recurrence after liver transplantation than the recipients with GWR >= 60% graft. More circulating Tregs and higher intragraft TLR4/CXCL10/CXCR3 levels were detected in recipients with GWR <60% graft. These results were further validated in rat transplantation model. Foxp(3+) cells and expressions of TLR4, CXCL10, TGF beta, CTLA-4 and CD274 were increased in rat liver tumor tissues from small-for-size graft group. In mouse model, the mobilization and recruitment of Tregs were decreased in TLR4(-/-), CXCL10(-/-) and CXCR3(-/-) mice compared to wild-type mice. Moreover, less CXCR3(+) Tregs were recruited into liver in CXCL10(-/-) mice after hepatic IR injury. The knockout of CXCL10 and depletion of Tregs inhibited tumor recurrence after hepatic IR injury.
Conclusion: CXCL10/CXCR3 signaling upregulated at liver graft injury directly induced the mobilization and intragraft recruitment of Tregs, which further promoted HCC recurrence after transplantation.
Lay summary: There were positive correlation among tumor recurrence, circulating Tregs and liver graft injury after human transplantation for HCC patients. The knockout of CXCL10 decreased hepatic recruitment of CXCR3(+) Tregs and late phase tumor recurrence after hepatic IR injury. (C) 2016 European Association for the Study of the Liver. Published by Elsevier B.V.
C1 [Li, Chang Xian; Ling, Chang Chun; Shao, Yan; Ng, Kevin Tak-Pan; Liu, Xiao Bing; Ma, Yuen Yuen; Qi, Xiang; Liu, Hui; Liu, Jiang; Yeung, Oscar Wai Ho; Yang, Xin Xiang; Liu, Qing Sheng; Lam, Yin Fan; Lo, Chung Mau; Man, Kwan] Univ Hong Kong, Dept Surg, L9-55,Fac Med Bldg,21 Sassoon Rd, Hong Kong, Hong Kong, Peoples R China.
[Lo, Chung Mau; Man, Kwan] Univ Hong Kong, Collaborat Innovat Ctr Diag & Treatment Infect Di, Hong Kong, Hong Kong, Peoples R China.
[Ng, Kevin Tak-Pan; Lo, Chung Mau; Man, Kwan] Univ Hong Kong, Shenzhen Inst Res & Innovat, Hong Kong, Hong Kong, Peoples R China.
[Ling, Chang Chun] Nantong Univ, Affiliated Hosp, Dept Gen Surg, Nantong City 226001, Peoples R China.
[Xu, Aimin] Univ Hong Kong, Dept Med, Hong Kong, Hong Kong, Peoples R China.
[Li, Xiang Cheng; Yang, Xin Xiang] Nanjing Med Univ, Affiliated Hosp 1, Liver Transplantat Ctr, Nanjing, Jiangsu, Peoples R China.
[Zhai, Yuan] Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Los Angeles, CA 90095 USA.
C3 University of Hong Kong; Collaborative Innovation Center for Diagnosis &
Treatment of Infectious Diseases; University of Hong Kong; The
University of Hong Kong Shenzhen Institute of Research & Innovation;
University of Hong Kong; Nantong University; University of Hong Kong;
Nanjing Medical University; University of California System; University
of California Los Angeles; University of California Los Angeles Medical
Center; David Geffen School of Medicine at UCLA
RP Man, K (corresponding author), Univ Hong Kong, Dept Surg, L9-55,Fac Med Bldg,21 Sassoon Rd, Hong Kong, Hong Kong, Peoples R China.
EM kwanman@hku.hk
RI Lo, Chung/C-4352-2009; Yang, Xinxiang/ISA-6013-2023; Liu,
Jiang/HCH-0324-2022; NG, Kevin Tak-Pan/J-1510-2018
OI NG, Kevin Tak-Pan/0000-0001-9822-1335
FU Collaborative Research Funding of Research Grant Council, Hong Kong
[HKU3/CRF/11RC7027-14G]; General Research Funding of the Research Grant
Council, Hong Kong [775011M, 17115515, 17115614]; National Science
Foundation of China (NSFC) grants [81470903, 81572945]
FX This study was supported by the Collaborative Research Funding
(HKU3/CRF/11R&C7027-14G) and General Research Funding (775011M,
17115515, & 17115614) of the Research Grant Council, Hong Kong; National
Science Foundation of China (NSFC) grants (81470903 & 81572945).
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NR 46
TC 99
Z9 107
U1 2
U2 19
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD NOV
PY 2016
VL 65
IS 5
BP 944
EP 952
DI 10.1016/j.jhep.2016.05.032
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DZ9IB
UT WOS:000386187400011
PM 27245433
OA Green Accepted, hybrid
DA 2025-01-07
ER
PT J
AU Luo, JR
Chen, SY
Wang, J
Ou, S
Zhang, W
Liu, YQ
Qin, ZL
Xu, J
Lu, QH
Mo, CJ
Li, S
Qin, X
AF Luo, Jingrong
Chen, Siyuan
Wang, Jin
Ou, Shan
Zhang, Wei
Liu, Yanqiong
Qin, Zailong
Xu, Jing
Lu, Qinghua
Mo, Cuiju
Li, Shan
Qin, Xue
TI Genetic polymorphisms in complement receptor 1 gene and its association
with HBV-related liver disease: A case-control study
SO GENE
LA English
DT Article
DE Complement receptor 1; HBV-related liver disease; Genetic variant;
Single nucleotide polymorphism
ID HEPATOCELLULAR-CARCINOMA; CANCER; INFLAMMATION; RISK; SUSCEPTIBILITY;
EXPRESSION; INFECTION; HEPATITIS; VARIANTS; CELLS
AB Background: Several investigators have reported that complement receptor 1 (CR1) likely play a role in the pathogenesis of tumors, autoimmune and inflammatory diseases. However, the association of genetic polymorphisms of CR1 with risk of hepatitis B virus (HBV)-related liver disease remains unexplored.
Methods: In a case control study of 399 HBV-related liver disease patients and 227 healthy controls, we genotyped two SNPs in CR1 (rs3811381 and rs2274567) and assessed their associations with risk of HBV-related liver disease.
Results: No significant differences were observed in the frequency distribution of genotypes or alleles between CR1 rs3811381 and rs2274567 polymorphisms in patients and controls. However, stratification analysis indicated that these two CR1 polymorphisms may contribute to the risk of HBV- hepatocellular carcinoma (HCC) and chronic hepatitis B (CHB) in subgroups of males, alcohol drinkers and nonsmokers. Further, our results showed that the rs3811381 polymorphism may contribute to HBV-HCC risk in subgroups of older and younger subjects, while the G allele, AG and the combined AG + GG genotypes of rs2274567 may be risk factors for HBV-HCC in younger subjects. In addition, our results indicated that subjects who carried the rs3811381 G allele and the rs2274567 AG genotype were at decreased risk of HBV-liver cirrhosis (LC) in subgroups of females.
Conclusions: Our results support the hypothesis that the CR1 gene rs3811381 and rs2274567 polymorphisms may contribute to HBV-HCC and HBV-CHB risk, particularly in subgroups of males, alcohol drinkers, nonsmokers, while these two CR1 polymorphisms were found to associate with decreased risk of HBV-LC, particularly in females. Further validation of these results is warranted.
C1 [Luo, Jingrong; Wang, Jin; Ou, Shan; Qin, Zailong] Guangxi Maternal & Child Hlth Hosp, Dept Genet, 59 Xiangzhu Rd, Nanning, Peoples R China.
[Luo, Jingrong; Wang, Jin; Ou, Shan; Qin, Zailong] Guangxi Maternal & Child Hlth Hosp, Metab Cent Lab, 59 Xiangzhu Rd, Nanning, Peoples R China.
[Chen, Siyuan; Liu, Yanqiong; Lu, Qinghua; Mo, Cuiju; Li, Shan; Qin, Xue] Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, Nanning, Guangxi, Peoples R China.
[Zhang, Wei] Guangxi Med Univ, Affiliated Tumor Hosp, Dept Radiol, Nanning, Peoples R China.
[Xu, Jing] Guangxi Maternal & Child Hlth Hosp, Dept Neonatol, 59 Xiangzhu Rd, Nanning, Peoples R China.
C3 Guangxi Medical University; Guangxi Medical University
RP Li, S; Qin, X (corresponding author), Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, Nanning, Guangxi, Peoples R China.
EM Lis8858@126.com; Qinxue919@126.com
RI qin, xue/KQV-3701-2024; Lu, Qinghua/AAG-3378-2021
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NR 35
TC 9
Z9 9
U1 0
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-1119
EI 1879-0038
J9 GENE
JI Gene
PD MAR 10
PY 2019
VL 688
BP 107
EP 118
DI 10.1016/j.gene.2018.11.082
PG 12
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA HK1JW
UT WOS:000457662200014
PM 30529247
DA 2025-01-07
ER
PT J
AU Wong, DKH
Cheng, SCY
Mak, LLY
To, EWP
Lo, RCL
Cheung, TT
Seto, WK
Fung, J
Man, K
Lai, CL
Yuen, MF
AF Wong, Danny Ka-Ho
Cheng, Serene Ching Yan
Mak, Loey Lung-Yi
To, Elvis Wai-Pan
Lo, Regina Cheuk-Lam
Cheung, Tan-To
Seto, Wai-Kay
Fung, James
Man, Kwan
Lai, Ching-Lung
Yuen, Man-Fung
TI Among Patients with Undetectable Hepatitis B Surface Antigen and
Hepatocellular Carcinoma, a High Proportion Has Integration of HBV DNA
into Hepatocyte DNA and No Cirrhosis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Non-viral Liver Disease; Tumorigenesis; NAFLD; NASH
ID LIVER-DISEASE; VIRUS; INFECTION; RISK
AB BACKGROUND & AIMS: In some individuals with undetectable serum levels of hepatitis B surface antigen (HBsAg), hepatitis B virus (HBV) DNA can still be detected in serum or hepatocytes and HBV replicates at low levels-this is called occult HBV infection (OBI). OBI has been associated with increased risk of hepatocellular carcinoma (HCC). We investigated the incidence of OBI in patients with HCC and other liver diseases. We also investigated whether, in patients with OBI and HCC, HBV DNA has integrated into the DNA of hepatocytes.
METHODS: We collected clinical information and liver tissues from 110 HBsAg-negative patients (90 with HCC and 20 without HCC; median ages at surgical resection and biopsy collection, 64.1 and 48.6 years, respectively) who underwent liver resection or liver biopsy from November 2002 through July 2017 in Hong Kong. HBV DNA and covalently closed circular DNA (cccDNA) were analyzed and quantified by PCR in liver tissues. Integration of HBV DNA into the DNA of liver cells was detected by Alu-PCR.
RESULTS: Of the 90 HBsAg-negative patients with HCC, 18 had alcoholic liver disease (20%), 14 had non-alcoholic fatty liver disease or steatohepatitis (16%), 2 had primary biliary cholangitis, 2 had recurrent pyogenic cholangitis, 1 had autoimmune hepatitis, and 53 had none of these (59%). Among the 20 patients without HCC, 7 had non-alcoholic fatty liver disease or steatohepatitis, 7 had primary biliary cholangitis, and 6 had autoimmune hepatitis. OBI was detected in 62/90 patients with HCC (69%) and 3/20 patients without HCC (15%) (P < .0001). cccDNA was detectable in liver cells of 29 patients with HCC and OBI (47%) and HBV DNA had integrated into DNA of liver cells of 43 patients with HCC and OBI (69%); cccDNA and integrated HBV DNA were not detected in the 3 patients who had OBI without HCC. There were 29 patients with integration of HBV DNA among 33 patients with undetectable cccDNA in liver tissues (88%) and 14 patients with integration of HBV DNA among the 29 patients with cccDNA in liver tissues (48%) (P=.001). HBV DNA was found to integrate near genes associated with hepatocarcinogenesis, such as those encoding telomerase reverse transcriptase, lysine methyltransferase 2B, and cyclin A2. Among the 43 patients with integration of HBV DNA, 39 (91%) did not have cirrhosis.
CONCLUSIONS: In an analysis of clinical data and liver tissues from 90 HBsAg-negative patients with HCC, we found that almost 70% had OBI, of whom 70% had integration of HBV DNA into liver cell DNA; 90% of these patients did not have cirrhosis. HBV DNA integrated near hepatic oncogenes; these integrations might promote development of liver cancer.
C1 [Wong, Danny Ka-Ho; Cheng, Serene Ching Yan; Mak, Loey Lung-Yi; To, Elvis Wai-Pan; Seto, Wai-Kay; Fung, James; Lai, Ching-Lung; Yuen, Man-Fung] Univ Hong Kong, Queen Mary Hosp, Dept Med, Pokfulam Rd, Hong Kong, Peoples R China.
[Wong, Danny Ka-Ho; Lo, Regina Cheuk-Lam; Cheung, Tan-To; Seto, Wai-Kay; Fung, James; Man, Kwan; Lai, Ching-Lung; Yuen, Man-Fung] Univ Hong Kong, Queen Mary Hosp, State Key Lab Liver Res, Hong Kong, Peoples R China.
[Lo, Regina Cheuk-Lam] Univ Hong Kong, Queen Mary Hosp, Dept Pathol, Hong Kong, Peoples R China.
[Cheung, Tan-To; Man, Kwan] Univ Hong Kong, Queen Mary Hosp, Dept Surg, Hong Kong, Peoples R China.
C3 University of Hong Kong; University of Hong Kong; University of Hong
Kong; University of Hong Kong
RP Yuen, MF (corresponding author), Univ Hong Kong, Queen Mary Hosp, Dept Med, Pokfulam Rd, Hong Kong, Peoples R China.
EM mfyuen@hku.hk
RI Mak, Lung Yi (Loey)/ABB-1599-2020; Fung, James/AAG-4832-2020; Seto,
Wai-Kay/H-4452-2012; Yuen, Richard Man Fung/C-4466-2009; Lai,
Ching/C-4298-2009
OI /0000-0001-9078-5005; Mak, Lung Yi/0000-0002-2266-3935;
/0000-0002-9012-313X
CR Cancer Fact Sheets, 2018, CANC FACT SHEETS
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NR 28
TC 44
Z9 48
U1 1
U2 23
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD FEB
PY 2020
VL 18
IS 2
BP 449
EP 456
DI 10.1016/j.cgh.2019.06.029
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA KC0SR
UT WOS:000506898700033
PM 31252193
OA hybrid
DA 2025-01-07
ER
PT J
AU Ru, JN
Lu, JH
Ge, JZ
Ding, B
Su, R
Jiang, YF
Sun, YJ
Ma, J
Li, Y
Sun, JQ
Xu, GM
Tong, RL
Zheng, SS
Yang, B
Wu, J
AF Ru, Junnan
Lu, Jiahua
Ge, Jiangzhen
Ding, Bo
Su, Rong
Jiang, Yifan
Sun, Yujing
Ma, Jun
Li, Yu
Sun, Jingqi
Xu, Guangming
Tong, Rongliang
Zheng, Shusen
Yang, Beng
Wu, Jian
TI IRGM is a novel regulator of PD-L1 via promoting S6K1-mediated
phosphorylation of YBX1 in hepatocellular carcinoma
SO CANCER LETTERS
LA English
DT Article
DE IRGM; Liver cancer; Tumor microenvironment; Immune therapy; Programmed
death-ligand 1
AB Immunity-related GTPase M (IRGM), an Interferon-inducible protein, functions as a pivotal immunoregulator in multiple autoimmune diseases and infection. However, the role of IRGM in hepatocellular carcinoma (HCC) development remains unveiled. Here, we found interferon-gamma (IFN-gamma) treatment in HCC drastically triggered the expression of IRGM, and the high level of IRGM indicated poor prognosis in HCC patients. Functionally, IRGM promoted the malignant progression of HCC. Single-cell sequencing revealed that IRGM inhibition promoted the infiltration of CD8+ cytotoxic T lymphocytes (CTLs) with significant downregulation of PD-L1 expression in HCC. Furthermore, Immunoprecipitation-Mass Spectrometry assay revealed that IRGM interacted with transcription factor YBX1, which facilitated PD-L1 transcription. Mechanistically, IRGM promoted the interaction of YBX1 and phosphokinase S6K1, increasing phosphorylation and nuclear localization of YBX1, transcription of PD-L1. Additionally, the combination of IRGM inhibition with alpha-PD1 demonstrated a stronger anti-tumor effect compared to the single application of alpha-PD1. In summary, IRGM is a novel regulator of PD-L1, which suppresses CD8+ CTLs infiltration and function in HCC, resulting in cancer progression. This study may raise a novel therapeutic strategy combined with immune checkpoint inhibitors (ICIs) against HCC.
C1 [Ru, Junnan; Lu, Jiahua; Ge, Jiangzhen; Ding, Bo; Su, Rong; Jiang, Yifan; Ma, Jun; Li, Yu; Sun, Jingqi; Xu, Guangming; Tong, Rongliang; Zheng, Shusen; Yang, Beng; Wu, Jian] Zhejiang Univ, Div Hepatobiliary & Pancreat Surg, Dept Surg, Affiliated Hosp 1,Sch Med, Hangzhou 310003, Peoples R China.
[Ru, Junnan; Lu, Jiahua; Ge, Jiangzhen; Ding, Bo; Su, Rong; Li, Yu; Xu, Guangming; Tong, Rongliang; Zheng, Shusen; Yang, Beng; Wu, Jian] NHC Key Lab Combined Multiorgan Transplantat, Hangzhou 310003, Peoples R China.
[Ru, Junnan; Ge, Jiangzhen; Su, Rong; Jiang, Yifan; Ma, Jun; Sun, Jingqi; Tong, Rongliang; Zheng, Shusen; Yang, Beng; Wu, Jian] Chinese Acad Med Sci, Res Unit Collaborat Diag & Treatment Hepatobiliar, Key Lab Diag & Treatment Organ Transplantat, Hangzhou, Peoples R China.
[Ru, Junnan; Ge, Jiangzhen; Su, Rong; Jiang, Yifan; Ma, Jun; Sun, Jingqi; Tong, Rongliang; Zheng, Shusen; Yang, Beng; Wu, Jian] Key Lab Organ Transplantat, Hangzhou, Zhejiang, Peoples R China.
[Sun, Yujing] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Gen Practice Dept, Hangzhou, Zhejiang, Peoples R China.
C3 Zhejiang University; Chinese Academy of Medical Sciences - Peking Union
Medical College; Zhejiang University
RP Zheng, SS; Yang, B; Wu, J (corresponding author), Zhejiang Univ, Div Hepatobiliary & Pancreat Surg, Dept Surg, Affiliated Hosp 1,Sch Med, Hangzhou 310003, Peoples R China.
EM shusenzheng@zju.edu.cn; 21518093@zju.edu.cn; drwujian@zju.edu.cn
RI Yang, Beng/GRX-9557-2022; Jiang, Yifan/ABB-4400-2021
OI Lu, Jiahua/0000-0002-6874-0123; Li, Yu/0000-0001-9748-9364
FU Natural Science Foundation of China [82073144]; Department of Science
and Technology of Zhejiang Province [2023C03063]; Huadong Medicine Joint
Funds of the Zhejiang Provincial Natural Science Foundation of China
[LHDMD22H310005]; Health Commission of Zhejiang Province [JBZX-202004]
FX This work was supported by the Natural Science Foundation of China
(82073144) , the Department of Science and Technology of Zhejiang
Province (2023C03063) , Huadong Medicine Joint Funds of the Zhejiang
Provincial Natural Science Foundation of China (LHDMD22H310005) , and
the Health Commission of Zhejiang Province (JBZX-202004) .
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NR 48
TC 9
Z9 9
U1 3
U2 26
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD JAN 28
PY 2024
VL 581
AR 216495
DI 10.1016/j.canlet.2023.216495
EA NOV 2023
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CT0N9
UT WOS:001127375000001
PM 37993085
DA 2025-01-07
ER
PT J
AU Hiraoka, A
Ochi, M
Matsuda, R
Aibiki, T
Okudaira, T
Kawamura, T
Yamago, H
Nakahara, H
Suga, Y
Azemoto, N
Miyata, H
Miyamoto, Y
Ninomiya, T
Hirooka, M
Abe, M
Matsuura, B
Hiasa, Y
Michitaka, K
AF Hiraoka, Atsushi
Ochi, Marie
Matsuda, Rie
Aibiki, Toshihiko
Okudaira, Tomonari
Kawamura, Tomoe
Yamago, Hiroka
Nakahara, Hiromasa
Suga, Yoshifumi
Azemoto, Nobuaki
Miyata, Hideki
Miyamoto, Yasunao
Ninomiya, Tomoyuki
Hirooka, Masashi
Abe, Masanori
Matsuura, Bunzo
Hiasa, Yoichi
Michitaka, Kojiro
TI Ultrasonography screening for hepatocellular carcinoma in Japanese
patients with diabetes mellitus
SO JOURNAL OF DIABETES
LA English
DT Article
DE diabetes mellitus; fatty liver; hepatocellular carcinoma; survey
ID FATTY LIVER-DISEASE; EPIDEMIOLOGIC EVIDENCE; INCREASED RISK; CANCER;
METAANALYSIS; CIRRHOSIS
AB BackgroundEffective surveillance for hepatocellular carcinoma (HCC) in diabetes mellitus (DM) has not been established. We elucidated the risk factors for HCC in DM patients.
MethodsFrom 2000 to 2014, 80 patients diagnosed with HCC for the first time who had concomittant DM but no other etiology of liver disease were enrolled as the DM-HCC group. From 2005 October to 2014, after introduction of the abdominal ultrasonography (US) report database, 2083 DM patients with no viral hepatitis, no known autoimmune hepatic diseases, and/or no evidence of alcohol abuse (>60 g/day) were enrolled as the DM-US group. Findings from the first US screening were evaluated. Elderly patients were defined as those aged >65 years. Clinical features of DM-HCC patients were evaluated and compared with those of DM-US patients.
ResultsIn the DM-HCC group (54 men, 26 women), the mean ( SD age was 74.1 8.5 years, and mean HbA1c and fibrosis-4 (FIB-4) index were 7.3 1.3% and 4.50 3.42, respectively. Mean tumor diameter was 5.7 3.5 cm, there were 63/13/2/2 patients classified as Child-Pugh A/B/C/unknown, and 56/24 were single/multiple lesions. In the DM-US group, HCC was detected in three patients (0.14%; 0.3% of those classified as elderly). The mean age and FIB-4 index of these three patients (one man, two women) were 75.6 years (range 67-92 years) and 4.84 (range 2.87-6.98), respectively. Mean tumor diamter was 7.6 cm and there were one and two single and multiple lesions, respectively. In elderly DM-US patients with a high FIB-4 index (4), the rate of HCC detection was 5.0%.
ConclusionsBeing elderly and having a high FIB-4 index are characteristic features of DM-HCC. Similar characteristics were noted for patients with HCC in the DM-US group. HCC surveillance with US is recommended for DM patients, especially those who are elderly (65 years) and have a high FIB-4 index.
C1 [Hiraoka, Atsushi; Ochi, Marie; Aibiki, Toshihiko; Okudaira, Tomonari; Kawamura, Tomoe; Yamago, Hiroka; Nakahara, Hiromasa; Suga, Yoshifumi; Azemoto, Nobuaki; Miyata, Hideki; Miyamoto, Yasunao; Ninomiya, Tomoyuki; Michitaka, Kojiro] Ehime Prefectural Cent Hosp, Gastroenterol Ctr, Matsuyama, Ehime, Japan.
[Matsuda, Rie] Ehime Prefectural Cent Hosp, Dept Lab, Matsuyama, Ehime, Japan.
[Hirooka, Masashi; Abe, Masanori; Matsuura, Bunzo; Hiasa, Yoichi] Ehime Univ, Grad Sch Med, Dept Gastroenterol & Metabol, Matsuyama, Ehime 790, Japan.
C3 Ehime University
RP Hiraoka, A (corresponding author), Ehime Prefectural Cent Hosp, Kasuga Cho 83, Matsuyama, Ehime 7900024, Japan.
EM hirage@m.ehime-u.ac.jp
RI Hiasa, Yoichi/ABD-2759-2021; Hirooka, Masashi/JUF-2562-2023; Hiraoka,
Atsushi/AFR-0440-2022
OI Hiraoka, Atsushi/0000-0003-1989-0480
CR [Anonymous], 2011, TNM Classification of malignant tumours
[Anonymous], GEN RUL CLIN PATH ST
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NR 16
TC 14
Z9 14
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1753-0393
EI 1753-0407
J9 J DIABETES
JI J. Diabetes
PD SEP
PY 2016
VL 8
IS 5
BP 640
EP 646
DI 10.1111/1753-0407.12340
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA DW1GH
UT WOS:000383390500007
PM 26347476
DA 2025-01-07
ER
PT J
AU Berenguer, M
de Martin, E
Hessheimer, AJ
Levitsky, J
Maluf, DG
Mas, VR
Selzner, N
Hernàndez-Evole, H
Lutu, A
Wahid, N
Zubair, H
AF Berenguer, Marina
de Martin, Eleonora
Hessheimer, Amelia J.
Levitsky, Josh
Maluf, Daniel G.
Mas, Valeria R.
Selzner, Nazia
Hernandez-Evole, Helena
Lutu, Alina
Wahid, Nabeel
Zubair, Haseeb
TI European Society for Organ Transplantation Consensus Statement on
Biomarkers in Liver Transplantation
SO TRANSPLANT INTERNATIONAL
LA English
DT Article
DE liver transplantation; biomarkers; chronic kidney disease;
hepatocellular carcinoma; rejection; recurrent primary diseases
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY-CIRRHOSIS; CHRONIC
KIDNEY-DISEASE; HEPATOCELLULAR-CARCINOMA RECURRENCE; CIRCULATING
TUMOR-CELLS; AUTOIMMUNE HEPATITIS; MESSENGER-RNA; RISK-FACTORS;
OPERATIONAL TOLERANCE; PERIPHERAL-BLOOD
AB Currently, one-year survival following liver transplantation (LT) exceeds 90% in large international registries, and LT is considered definitive treatment for patients with end-stage liver disease and liver cancer. Recurrence of disease, including hepatocellular carcinoma (HCC), significantly hampers post-LT outcomes. An optimal approach to immunosuppression (IS), including safe weaning, may benefit patients by mitigating the effect on recurrent diseases, as well as reducing adverse events associated with over-/under-IS, including chronic kidney disease (CKD). Prediction of these outcome measures-disease recurrence, CKD, and immune status-has long been based on relatively inaccurate clinical models. To address the utility of new biomarkers in predicting these outcomes in the post-LT setting, the European Society of Organ Transplantation (ESOT) and International Liver Transplant Society (ILTS) convened a working group of experts to review literature pertaining to primary disease recurrence, development of CKD, and safe weaning of IS. Summaries of evidence were presented to the group of panelists and juries to develop guidelines, which were discussed and voted in-person at the Consensus Conference in Prague November 2022. The consensus findings and recommendations of the Liver Working Group on new biomarkers in LT, clinical applicability, and future needs are presented in this article.
C1 [Berenguer, Marina] CiberEHD, Hosp Univ Fe IIS La Fe Valencia, Hepatol & Liver Transplantat Unit, Valencia, Spain.
[Berenguer, Marina] Univ Valencia, Valencia, Spain.
[de Martin, Eleonora; Lutu, Alina] Univ Paris Saclay, Hop Paul Brousse, AP HP, Ctr Hepatobiliaire,Inserm,UMR S 1193, Villejuif, France.
[Hessheimer, Amelia J.] Hosp Univ La Paz, Inst Invest Hosp Univ La Paz IdiPAZ, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Gen & Digest Surg, Madrid, Spain.
[Levitsky, Josh; Wahid, Nabeel] Northwestern Univ, Feinberg Sch Med, Comprehens Transplant Ctr, Div Gastroenterol & Hepatol,Dept Med, Chicago, IL USA.
[Maluf, Daniel G.] Univ Maryland, Med Ctr, Dept Surg, Program Transplantat,Sch Med, Baltimore, MD USA.
[Mas, Valeria R.] Univ Maryland, Dept Surg, Chief Surg Sci Div, Surg Sci Res Transplantat,Sch Med, Baltimore, MD USA.
[Selzner, Nazia] Univ Toronto, Toronto Gen Hosp, Ajmera Transplant Ctr, Toronto, ON, Canada.
[Hernandez-Evole, Helena] Hosp Clin Barcelona, Liver Unit, Barcelona, Spain.
[Zubair, Haseeb] Univ Maryland, Sch Med, Surg Sci Div, Baltimore, MD USA.
C3 CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD; University
of Valencia; Institut National de la Sante et de la Recherche Medicale
(Inserm); Assistance Publique Hopitaux Paris (APHP); Hopital
Universitaire Paul-Brousse - APHP; Universite Paris Saclay; Hospital
Universitario La Paz; CIBER - Centro de Investigacion Biomedica en Red;
CIBEREHD; Northwestern University; Feinberg School of Medicine;
University System of Maryland; University of Maryland Baltimore;
University System of Maryland; University of Maryland Baltimore;
University of Toronto; University Health Network Toronto; Toronto
General Hospital; University of Barcelona; Hospital Clinic de Barcelona;
University System of Maryland; University of Maryland Baltimore
RP Berenguer, M (corresponding author), CiberEHD, Hosp Univ Fe IIS La Fe Valencia, Hepatol & Liver Transplantat Unit, Valencia, Spain.; Berenguer, M (corresponding author), Univ Valencia, Valencia, Spain.
EM marina.berenguer@uv.es
RI Levitsky, Josh/AAF-8662-2019; Selzner, Nazia/AAI-1469-2020; Hessheimer,
Amelia/N-1855-2019; Maluf, Daniel/KAM-2337-2024; Berenguer,
Marina/ABG-8602-2020
OI Berenguer, Marina/0000-0001-9246-4264
FU Instituto de Salud Carlos III - European Regional Development Fund "A
way to make Europe" [PI19/01360, INT20/00061]
FX All costs related to taskforce and workgroup meetings were covered by
ESOT, without external funding. MB was granted by the Instituto de Salud
Carlos III and co-funded by European Regional Development Fund "A way to
make Europe" (grants number PI19/01360 and INT20/00061).
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NR 94
TC 2
Z9 2
U1 2
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 0934-0874
EI 1432-2277
J9 TRANSPL INT
JI Transpl. Int.
PD AUG 30
PY 2023
VL 36
AR 11358
DI 10.3389/ti.2023.11358
PG 18
WC Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery; Transplantation
GA R5LR8
UT WOS:001064770700001
PM 37711401
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Pembroke, TPI
John, G
Puyk, B
Howkins, K
Clarke, R
Yousuf, F
Czajkowski, M
Godkin, A
Salmon, J
Yeoman, A
AF Pembroke, Thomas Peter Ignatius
John, Gareth
Puyk, Berry
Howkins, Keith
Clarke, Ruth
Yousuf, Fidan
Czajkowski, Marek
Godkin, Andrew
Salmon, Jane
Yeoman, Andrew
TI Rising incidence, progression and changing patterns of liver disease in
Wales 1999-2019
SO WORLD JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Epidemiology; Cirrhosis; Liver failure; Non-alcoholic fatty liver
disease hepatitis; Hepatocellular carcinoma
ID HEPATITIS-C VIRUS; UNITED-STATES; MORTALITY; CIRRHOSIS; PREVALENCE;
INFECTION; SURVIVAL; PEOPLE; COHORT; LIFE
AB BACKGROUND Liver disease incidence and hence demand on hepatology services is increasing.AIM To describe trends in incidence and natural history of liver diseases in Wales to inform effective provision of hepatology services.METHODS The registry is populated by International Classification of Diseases-10 (ICD-10) code diagnoses for residents derived from mortality data and inpatient/day case activity between 1999-2019. Pseudo-anonymised linkage of: (1) Causative diagnoses; (2) Cirrhosis; (3) Portal hypertension; (4) Decompensation; and (5) Liver cancer diagnoses enabled tracking liver disease progression.RESULTS The population of Wales in 2019 was 3.1 million. Between 1999 and 2019 73054 individuals were diagnosed with a hepatic disorder, including 18633 diagnosed with cirrhosis, 10965 with liver decompensation and 2316 with hepatocellular carcinoma (HCC). Over 21 years the incidence of liver diseases increased 3.6 fold, predominantly driven by a 10 fold increase in non-alcoholic fatty liver disease (NAFLD); the leading cause of liver disease from 2014. The incidence of cirrhosis, decompensation, HCC, and all-cause mortality tripled. Liver-related mortality doubled. Alcohol-related liver disease (ArLD), autoimmune liver disease and congestive hepatopathy were associated with the highest rates of decompensation and all-cause mortality.CONCLUSION A 10 fold increase in NAFLD incidence is driving a 3.6 fold increase in liver disease in Wales over 21 years. Liver-related morbidity and mortality rose more slowly reflecting the lower progression rate in NAFLD. Incidence of ArLD remained stable but was associated with the highest rates of liver-related and all-cause mortality.
C1 [Pembroke, Thomas Peter Ignatius; Godkin, Andrew] Univ Hosp Wales, Dept Gastroenterol & Hepatol, Cardiff CF14 4XN, Wales.
[Pembroke, Thomas Peter Ignatius; Godkin, Andrew] Cardiff Uni, Div Infect & Immun, Cardiff CF14 4XW, Wales.
[John, Gareth; Puyk, Berry; Howkins, Keith; Clarke, Ruth] NHS Wales, Digital Hlth & Care Wales, Cardiff CF11 9AD, Wales.
[Yousuf, Fidan; Czajkowski, Marek; Yeoman, Andrew] Royal Gwent Hosp, Gwent Liver Unit, Newport NP20 2UB, Wales.
[Salmon, Jane] NHS Wales, Publ Hlth Wales, Cardiff CF10 4BZ, Wales.
[Pembroke, Thomas Peter Ignatius] Univ Hosp Wales, Dept Gastroenterol & Hepatol, Heath Pk, Cardiff CF14 4XN, Wales.
C3 Cardiff University; Royal Gwent Hospital
RP Pembroke, TPI (corresponding author), Univ Hosp Wales, Dept Gastroenterol & Hepatol, Heath Pk, Cardiff CF14 4XN, Wales.
EM thomas.pembroke@wales.nhs.uk
OI Pembroke, Thomas/0000-0002-2600-2034
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NR 36
TC 3
Z9 3
U1 0
U2 1
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5182
J9 WORLD J HEPATOL
JI World J. Hepatol.
PD JAN 27
PY 2023
VL 15
IS 1
BP 89
EP 106
DI 10.4254/wjh.v15.i1.89
PG 18
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA 8Y1CY
UT WOS:000932441400007
PM 36744166
OA Green Accepted, gold, Green Published
DA 2025-01-07
ER
PT J
AU Nishiyama, R
Kanai, T
Abe, J
Hara, R
Watahiki, Y
Sakaguchi, T
Nakamura, S
AF Nishiyama, R
Kanai, T
Abe, J
Hara, R
Watahiki, Y
Sakaguchi, T
Nakamura, S
TI Hepatocellular carcinoma associated with autoimmune hepatitis
SO JOURNAL OF HEPATO-BILIARY-PANCREATIC SURGERY
LA English
DT Article
DE hepatocellular carcinoma; autoimmune hepatitis
ID CHRONIC ACTIVE HEPATITIS; LUPOID HEPATITIS; C VIRUS; THERAPY; INFECTION
AB Autoimmune hepatitis (AIH) is a disorder of unknown etiology, which often progresses to cirrhosis and carries a high mortality, even though its treatment with corticosteroids has become common. Hepatocellular carcinoma (HCC) has been reported as a rare complication of AIH. We describe herein a patient with HCC associated with AIH, in whom microwave coagulation therapy provided a means of definitive management, and we also review the literature. Male sex and longstanding cirrhosis seem to be the risk factors for hepatocarcinogenesis in AIR The prognosis of this disease is extremely poor because of the low resectability caused by poor hepatic reserve. It is important to pay attention to hepatic disorders and the possible development of HCC at the time of diagnosis of AIR Surgeons should select suitable treatment, without undue surgical stress, whenever the diagnosis of HCC has been established. Microwave coagulation therapy is a preferred option for the treatment of high-risk patients with poor hepatic reserve or unresectable multiple HCCs.
C1 Inasa Redcross Hosp, Shizuoka 4312213, Japan.
Hamamatsu Univ Sch Med, Dept Surg 2, Hamamatsu, Shizuoka, Japan.
C3 Hamamatsu University School of Medicine
RP Nishiyama, R (corresponding author), Inasa Redcross Hosp, 1020 Kanasashi, Shizuoka 4312213, Japan.
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NR 38
TC 16
Z9 17
U1 0
U2 1
PU SPRINGER TOKYO
PI TOKYO
PA 1-11-11 KUDAN-KITA, CHIYODA-KU, TOKYO, 102-0073, JAPAN
SN 0944-1166
J9 J HEPATO-BILIARY-PAN
JI J. Hepato-Biliary-Pancreatic Surg.
PY 2004
VL 11
IS 3
BP 215
EP 219
DI 10.1007/s00534-003-0878-z
PG 5
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 864DA
UT WOS:000224612200013
PM 15235898
DA 2025-01-07
ER
PT J
AU Pacholczak, R
Bazan-Socha, S
Zdziarska, J
Iwaniec, T
Walocha, JA
Musia, J
Dropiriski, J
AF Pacholczak, Renata
Bazan-Socha, Stanislawa
Zdziarska, Joanna
Iwaniec, Teresa
Walocha, Jerzy A.
Musia, Jacek
Dropiriski, Jerzy
TI Acquired Haemophilia A Associated With Subsequent Hepatocellular
Carcinoma
SO HAMOSTASEOLOGIE
LA English
DT Article
DE acquired haemophilia; hepatocellular carcinoma; haemorrhagic diathesis
ID FACTOR-VIII; SOLID TUMORS; CANCER; PATIENT; COMPLICATIONS; MANAGEMENT
AB Acquired haemophilia A (AHA) is a rare autoimmune disease caused by antibodies directed against clotting factor VIII. About half of cases are idiopathic, but AHA may also be secondary to autoimmune, dermatologic, or oncologic diseases. In approximately 10% of non-idiopathic cases, the disease occurs after or with the diagnosis of cancer as an extremely rare paraneoplastic syndrome. We describe the case of a 73-year-old male patient diagnosed with AHA and successfully treated with recombinant human activated factor Vila and immunosuppression. Two and a half years later, however, the disease relapsed and a routine ultrasound revealed a liver tumour that was then diagnosed as hepatocellular carcinoma. We present this case to increase awareness that this life-threatening condition may develop years prior to the diagnosis of cancer.
C1 [Pacholczak, Renata; Walocha, Jerzy A.] Jagiellonian Univ, Med Coll, Dept Anat, Ul Kopernika 12, PL-33332 Krakow, Poland.
[Pacholczak, Renata] Maria Sklodowska Curie Mem Inst Oncol, Ctr Oncol, Cracow Branch, Krakow, Poland.
[Bazan-Socha, Stanislawa; Iwaniec, Teresa; Musia, Jacek; Dropiriski, Jerzy] Jagiellonian Univ, Med Coll, Dept Internal Med, Krakow, Poland.
[Zdziarska, Joanna] Jagiellonian Univ, Med Coll, Dept Hematol, Krakow, Poland.
C3 Jagiellonian University; Collegium Medicum Jagiellonian University;
Maria Sklodowska-Curie National Research Institute of Oncology;
Jagiellonian University; Collegium Medicum Jagiellonian University;
Jagiellonian University; Collegium Medicum Jagiellonian University
RP Pacholczak, R (corresponding author), Jagiellonian Univ, Med Coll, Dept Anat, Ul Kopernika 12, PL-33332 Krakow, Poland.
EM renata.pacholczak@uj.edu.pl
RI Zdziarska, Joanna/M-2206-2019; Bazan-Socha, Stanislawa/AFK-7047-2022;
Walocha, Jerzy/AAS-9174-2020; Pacholczak-Madej, Renata/ADO-4315-2022
OI Pacholczak-Madej, Renata/0000-0002-6535-4841
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NR 31
TC 2
Z9 2
U1 0
U2 0
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0720-9355
EI 2567-5761
J9 HAMOSTASEOLOGIE
JI Hamostaseologie
PD FEB
PY 2019
VL 39
IS 1
BP 95
EP 99
DI 10.1055/s-0038-1668570
PG 5
WC Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology
GA HN1DM
UT WOS:000459927300013
PM 30112740
DA 2025-01-07
ER
PT J
AU Ahmed, A
Maklad, S
Hussein, G
Badawy, I
Abou Zeid, A
El-Feky, S
AF Ahmed, Amal
Maklad, Sahar
Hussein, Ghada
Badawy, Ingy
Abou Zeid, Alaa
El-Feky, Said
TI Assessment of the Role of Interleukin-18 in diagnosis of Hepatocellular
Carcinoma related to Hepatitis C Virus infection
SO LIFE SCIENCE JOURNAL-ACTA ZHENGZHOU UNIVERSITY OVERSEAS EDITION
LA English
DT Article
DE HCC; HCV; AFP; IL-18
ID LIVER-BIOPSY; THERAPY; MARKERS
AB Background: Hepatocellular carcinoma (HCC) accounts for 90% of primary liver neoplasms. Representing one of the most common cancers and is responsible for up to 1 million deaths annually worldwide. Egypt has the highest prevalence of Hepatitis C Virus (HCV) worldwide and has rising rates of Hepatocellular carcinoma (HCC). The prognosis of most patients is unsatisfactory due to rapid clinical deterioration after the initial diagnosis. Therefore, it is very important to detect HCC and the recurrence at its earlier period. Alpha Feto protein (AFP) has been the most widely used plasma marker for diagnosis, surveillance and as a prognostic indicator of HCC patients' survival. Several studies indicated that high plasma levels of AFP are related to poor prognosis, as well as histological grades of malignancy. However, it has been recognized that AFP has a low sensitivity in detection of HCC, and that AFP level often increases in the absence of HCC. Thus the identification of novel biochemical markers for HCC remains an important goal for many laboratories around the world. Interleukin 18 (IL-18) plays a critical role in the host defense against intracellular microbe's infection and also it induces autoimmune diseases and propagating inflammatory process also it was found that, IL-18 could play a key role in the pathogenesis of HCC. Methods: This study was conducted on a total number of 120 patients admitted to Hepatology and Gastroenterology Department in Faculty of medicines, Ain Shams University. The patients of this study were subdivided as follows. Group I: included 20 normal healthy subjects (as controls). Group II: included 100 patients with Hepatocellular carcinoma confirmed by pathology, cytology, imaging (computer tomography and ultrasound) and serum alpha -fetoprotein. Results: The mean level of IL-18 was significantly higher in HCC patients (238.69 +/- 145.5 pg/ml) compared to the controls (52.8 +/- 13.32 pg/ml), P <0.001). There was significant positive correlation between IL18 and Tumor size. Conclusion: IL-18 could be used as an additional non invasive marker for monitoring the degree of disease severity in Hepatocellular carcinoma. [Amal Ahmed, Sahar Maklad, Ghada Hussein, Ingy Badawy, Alaa Abou Zeid and Said El-Feky Assessment of the Role of Interleukin-18 in diagnosis of Hepatocellular Carcinoma related to Hepatitis C Virus infection] Life Science Journal 2011; 8(4):1154-1158]. (ISSN: 1545-1003). http://www.lifesciencesite.com. 141
C1 [Ahmed, Amal] Natl Hepatol & Trop Med Res Inst, Dept Biochem, Cairo, Egypt.
[Maklad, Sahar] Natl Hepatol & Trop Med Res Inst, Dept Trop, Cairo, Egypt.
[Abou Zeid, Alaa] Cairo Univ, Fac Med, Dept Publ Hlth, Cairo, Egypt.
[El-Feky, Said] Damanhur Natl Med Inst, Dept Biochem, Damanhur, Egypt.
C3 Egyptian Knowledge Bank (EKB); National Hepatology & Tropical Medicine
Research Institute (NHTMRI); Egyptian Knowledge Bank (EKB); National
Hepatology & Tropical Medicine Research Institute (NHTMRI); Egyptian
Knowledge Bank (EKB); Cairo University; Egyptian Knowledge Bank (EKB);
Damanhour University
RP Ahmed, A (corresponding author), Natl Hepatol & Trop Med Inst, Dept Biochem, Cairo, Egypt.
EM amalahmedhcp@yahoo.com
RI Mohamed, Amal/AAC-9106-2021
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NR 21
TC 0
Z9 0
U1 0
U2 1
PU MARSLAND PRESS
PI LANSING
PA PO BOX 21126, LANSING, MI 48909 USA
SN 1097-8135
J9 LIFE SCI J
JI Life Sci. J.
PY 2011
VL 8
IS 4
BP 1154
EP 1158
PG 5
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA 935NN
UT WOS:000303526000141
DA 2025-01-07
ER
PT J
AU Sunwoo, YY
Lee, JH
Jung, HY
Jung, YJ
Park, MS
Chung, YA
Maeng, LS
Han, YM
Shin, HS
Lee, J
Park, SI
AF Sunwoo, Yun-Young
Lee, Jin-Hee
Jung, Ho Yong
Jung, Yu Jin
Park, Moon-Seo
Chung, Yong-An
Maeng, Lee-So
Han, Young-Min
Shin, Hak Soo
Lee, Jisoo
Park, Sang In
TI Oldenlandia diffusa Promotes Antiproliferative and Apoptotic
Effects in a Rat Hepatocellular Carcinoma with Liver Cirrhosis
SO EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
ID ACID INDUCE APOPTOSIS; OLEANOLIC ACID; URSOLIC ACID; MOLECULAR
PATHOGENESIS; HEPATITIS-B; CELLS; INHIBITOR
AB Oldenlandia diffusa (OD) is commonly used with various diseases such as cancer, arthritis, and autoimmune disease. Liver cirrhosis is a predominant risk factor for hepatocellular carcinoma (HCC). Here, we show that the therapeutic effect of OD, which was investigated both in vitro and chemically, induced HCC model. OD significantly enhanced apoptosis and antiproliferative activity and reduced migration ability of HCC cells. In vivo, OD was treated twice a day for 28 days after confirmed HCC model through 2-[F-18]-fluoro-2-deoxy-D-glucose (F-18-FDG) imaging. The survival in OD treated groups was shown to have a greater therapeutic effect than the control group. 28 days after OD treatment, OD treated groups resulted in a significant reduction in tumor number, size, F-18-FDG uptake, and serum levels such as alanine transaminase, aspartate transaminase, and alkaline phosphate compared to the control group. Also, proliferated cells in tumor sites by OD were reduced compared to the control group. Furthermore, several rats in OD treated group survived over 60 days and liver morphology of these rats showed the difference between tumor mass and normal tissue. These results suggest that OD may have antiproliferative activity, inhibition of metastasis, and apoptotic effects in chemically induced HCC model and can have the potential use for clinical application as anticancer drug of the herbal extract.
C1 [Sunwoo, Yun-Young] Catholic Kwandong Univ Korea, Coll Med, Int St Marys Hosp, Comprehens Hosp Adv Canc, Inchon 404834, South Korea.
[Lee, Jin-Hee] Seoul Natl Univ, Coll Pharm, Dept Pharm, Seoul 151742, South Korea.
[Jung, Ho Yong; Park, Moon-Seo; Chung, Yong-An; Maeng, Lee-So; Han, Young-Min; Shin, Hak Soo; Park, Sang In] Catholic Univ Korea, Incheon St Marys Hosp, ICIM, Inchon 403720, South Korea.
[Jung, Yu Jin] Catholic Kwandong Univ Korea, Coll Med, Int St Marys Hosp, EIT LOFUS Res Ctr, Inchon 404834, South Korea.
[Chung, Yong-An] Catholic Univ Korea, Incheon St Marys Hosp, Dept Radiol, Inchon 403720, South Korea.
[Lee, Jisoo] Univ Massachusetts, Sch Med, Dept Internal Med, Worcester, MA 01655 USA.
C3 Catholic Kwandong University; Seoul National University (SNU); Catholic
University of Korea; Catholic Kwandong University; Catholic University
of Korea; University of Massachusetts System; University of
Massachusetts Worcester
RP Maeng, LS (corresponding author), Catholic Univ Korea, Incheon St Marys Hosp, ICIM, Inchon 403720, South Korea.
EM mis1004@olmh.cuk.ac.kr; parksi07@catholic.ac.kr
RI Kim, Jong/M-5732-2019; Chung, Yong An/LNP-9931-2024
FU Incheon St. Mary's Hospital of Catholic University of Korea, through
Institute of Catholic Integrative Medicine Foundation program
FX The research was supported by the Incheon St. Mary's Hospital of
Catholic University of Korea, through Institute of Catholic Integrative
Medicine Foundation program.
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NR 35
TC 21
Z9 22
U1 0
U2 6
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1741-427X
EI 1741-4288
J9 EVID-BASED COMPL ALT
JI Evid.-based Complement Altern. Med.
PY 2015
VL 2015
AR 501508
DI 10.1155/2015/501508
PG 11
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA CH1UW
UT WOS:000353808000001
PM 25852766
OA Green Published, gold
DA 2025-01-07
ER
PT S
AU Baker, SS
Baker, RD
AF Baker, Susan S.
Baker, Robert D.
BE Chen, P
TI Gut Microbiota and Liver Injury (II): Chronic Liver Injury
SO GUT MICROBIOTA AND PATHOGENESIS OF ORGAN INJURY
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
DE Gut microbiota; Viral hepatitis; Nonalcoholic fatty liver disease;
Alcoholic liver disease; Autoimmune hepatitis; Cirrhosis; Hepatocellular
carcinoma
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY CHOLANGITIS; CHAIN
FATTY-ACIDS; HEPATIC-ENCEPHALOPATHY; AUTOIMMUNE HEPATITIS; PATHOGENESIS;
METABOLISM; MANAGEMENT; DYSBIOSIS; DIET
AB Chronic liver injury mainly comprises viral hepatitis, fatty liver disease, autoimmune hepatitis, cirrhosis and liver cancer. It is well established that gut microbiota serves as the key upstream modulator for chronic liver injury progression. Indeed, the term "gut-liver axis" was mostly applied for chronic liver injury. In the current chapter, we will summarize the relationship between gut microbiota and chronic liver injury, including the interaction between them based on latest clinic and basic research.
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[Baker, Susan S.] 39 Irving Pl, Buffalo, NY 14201 USA.
C3 State University of New York (SUNY) System; University at Buffalo, SUNY
RP Baker, SS (corresponding author), SUNY Buffalo, Jacobs Sch Med & Biomed Sci, Dept Pediat, Buffalo, NY 14260 USA.
EM ssbaker@buffalo.edu
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NR 70
TC 9
Z9 9
U1 2
U2 30
PU SPRINGER-VERLAG SINGAPORE PTE LTD
PI SINGAPORE
PA 152 BEACH ROAD, #21-01/04 GATEWAY EAST, SINGAPORE, 189721, SINGAPORE
SN 0065-2598
EI 2214-8019
BN 978-981-15-2385-4; 978-981-15-2384-7
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2020
VL 1238
BP 39
EP 54
DI 10.1007/978-981-15-2385-4_4
D2 10.1007/978-981-15-2385-4
PG 16
WC Gastroenterology & Hepatology; Medicine, Research & Experimental;
Microbiology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Research & Experimental Medicine;
Microbiology
GA BP1EQ
UT WOS:000539027400004
PM 32323179
DA 2025-01-07
ER
PT J
AU Yan, MX
Yang, J
Sun, Q
Liu, CH
Wang, YG
Wang, WQ
AF Yan, Ming-Xian
Yang, Jing
Sun, Qing
Liu, Chang-Hong
Wang, Yi-Guo
Wang, Wen-Qi
TI Hepatocellular carcinoma that arose from primary Sjogren's syndrome
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Autoimmune disease; Hepatic tumor; Surveillance
ID HEPATITIS-C; LIVER-DISEASE; RISK; MANAGEMENT; DIAGNOSIS; CIRRHOSIS
AB Hepatocellular carcinoma (HCC) typically originates from HBV or HCV associated liver cirrhosis. Primary Sjogren's syndrome (pSS) is a kind of autoimmune disease. A sixty-two year old female patient with mild liver damage was diagnosed with pSS after excluding viral, alcoholic and drug-induced hepatitis according to serum immunological detection and liver biopsy. But when she was hospitalized for a second time two years later, a CT scan revealed liver neoplasm. Surgery confirmed HCC and liver cirrhosis by pathology. The elevated level of AFP recovered to normal after tumorectomy. In conclusion, HCC might be a candidate outcome in patients with pSS; it is the doctors' responsibility to keep this kind of patient under surveillance.
C1 [Yan, Ming-Xian; Yang, Jing; Liu, Chang-Hong; Wang, Yi-Guo; Wang, Wen-Qi] Shandong Univ, Sch Med, Shandong Qianfoshan Hosp, Dept Gastroenterol, Jinan 250014, Shandong, Peoples R China.
[Sun, Qing] Shandong Univ, Sch Med, Shandong Qianfoshan Hosp, Dept Pathol, Jinan 250014, Shandong, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
Sciences; Shandong University; Shandong University; Shandong First
Medical University & Shandong Academy of Medical Sciences
RP Yan, MX (corresponding author), Shandong Univ, Sch Med, Shandong Qianfoshan Hosp, Dept Gastroenterol, 16766 Jingshi Rd, Jinan 250014, Shandong, Peoples R China.
EM mingxian.yan@gmail.com
RI Liu, Chang/HOC-0971-2023
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NR 22
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER ESPANA
PI MADRID
PA CALLE DE ZURBANO, 76-4TH FLR LEFT, MADRID, 28010, SPAIN
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD SEP-OCT
PY 2013
VL 12
IS 5
BP 824
EP 829
DI 10.1016/S1665-2681(19)31327-4
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AA0WP
UT WOS:000330818400016
PM 24018503
OA hybrid
DA 2025-01-07
ER
PT J
AU Rimassa, L
Personeni, N
Czauderna, C
Foerster, F
Galle, P
AF Rimassa, Lorenza
Personeni, Nicola
Czauderna, Carolin
Foerster, Friedrich
Galle, Peter
TI Systemic treatment of HCC in special populations
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Hepatocellular carcinoma; Transplant; HIV; Autoimmune diseases;
Diabetes; Metabolic syndrome; Fibrolamellar; Mixed HCC/CCC; Child-Pugh
B; Elderly; Haemodialysis; Vascular invasion
ID ADVANCED HEPATOCELLULAR-CARCINOMA; IMMUNE CHECKPOINT INHIBITORS;
HIV-INFECTED PATIENTS; PHASE-II TRIAL; LIVER-TRANSPLANTATION; PATIENTS
PTS; PORTAL-VEIN; ADVERSE EVENTS; DOUBLE-BLIND; CLINICOPATHOLOGICAL
FEATURES
AB A Summary
Recent years have seen significant progress in the systemic treatment of hepatocellular carcinoma (HCC), including the advent of immunotherapy. While several large phase III trials have provided the evidence for a multi-line treatment paradigm, they have focused on a highly selected group of patients by excluding potentially confounding comorbidities. As a result, high quality evidence for the systemic treatment of HCC in patients with various comorbidities is missing. This review summarises current knowledge on the use of approved medicines in patients with HIV, autoimmune disease, cardiovascular disease, diabetes, fibrola-mellar HCC, mixed HCC-cholangiocarcinoma, decompensated cirrhosis (Child-Pugh B and C), a significant bleeding history, vascular invasion or portal vein thrombosis, as well as the elderly, those on haemodialysis, and those after solid organ transplantation. The article highlights relevant knowledge gaps and current clinical challenges. To improve the safety and efficacy of HCC treatment in these subgroups, future trials should be designed to specifically include patients with comorbidities. (C) 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Rimassa, Lorenza; Personeni, Nicola] Humanitas Clin & Res Ctr, IRCCS, Med Oncol & Hematol Unit, Humanitas Canc Ctr, Via Manzoni 56, I-20089 Milan, Italy.
[Rimassa, Lorenza; Personeni, Nicola] Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini 4, I-20090 Milan, Italy.
[Czauderna, Carolin; Foerster, Friedrich; Galle, Peter] Johannes Gutenberg Univ Mainz, Dept Med I, Univ Med Ctr, Mainz, Germany.
[Czauderna, Carolin] Univ Med Ctr, Dept Med 1, Schleswig Holstein Campus, Lubeck, Germany.
C3 Humanitas University; Johannes Gutenberg University of Mainz
RP Rimassa, L (corresponding author), Humanitas Clin & Res Ctr, IRCCS, Med Oncol & Hematol Unit, Humanitas Canc Ctr, Via Manzoni 56, I-20089 Milan, Italy.; Rimassa, L (corresponding author), Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini 4, I-20090 Milan, Italy.
EM lorenza.rimassa@hunimed.eu
RI foerstfr, foerstfr/KHW-6972-2024; Galle, Peter/ABE-2872-2021; Personeni,
Nicola/ABG-7925-2020; Rimassa, Lorenza/N-4884-2016
OI Rimassa, Lorenza/0000-0001-9957-3615; Personeni,
Nicola/0000-0002-7995-272X; Galle, Peter Robert/0000-0001-8294-0992;
Galle, Peter/0000-0003-1967-0621
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NR 135
TC 81
Z9 83
U1 1
U2 21
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2021
VL 74
IS 4
BP 931
EP 943
DI 10.1016/j.jhep.2020.11.026
EA MAR 2021
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA RB3UF
UT WOS:000632039100017
PM 33248171
OA Bronze
DA 2025-01-07
ER
PT J
AU Aghamiri, S
Jafarpour, A
Gomari, MM
Ghorbani, J
Rajabibazl, M
Payandeh, Z
AF Aghamiri, Shahin
Jafarpour, Ali
Gomari, Mohammad Mahmoudi
Ghorbani, Jaber
Rajabibazl, Masoumeh
Payandeh, Zahra
TI siRNA nanotherapeutics: a promising strategy for anti-HBV therapy
SO IET NANOBIOTECHNOLOGY
LA English
DT Review
DE tumours; drugs; genetics; cellular biophysics; RNA; nanomedicine;
diseases; molecular biophysics; microorganisms; cancer; liver;
nanoparticles; patient treatment; siRNA nanotherapeutics; anti-HBV
therapy; chronic hepatitis B; CHB; HCC; hazardous diseases; cancer;
genetic disease; autoimmune illnesses; viral disorders; hepatitis B
virus infections; naked siRNA delivery; cell membrane; enzymatic
digestion; renal filtration; nanoparticle-mediated delivery systems;
cccDNA formation; HBV infections complete cure; nanosiRNA drugs; siRNA
nanocarrier-mediated delivery systems; HBV infections therapy; liver
cirrhosis; RNA interference; immune response; hepatocellular carcinoma
ID HEPATITIS-B-VIRUS; RNA INTERFERENCE; GENE-THERAPY; CATIONIC LIPIDS;
PROGRESS REPORT; DELIVERY; DNA; NANOPARTICLES; CHALLENGES; PROTEINS
AB Chronic hepatitis B (CHB) is the most common cause of hepatocellular carcinoma (HCC) and liver cirrhosis worldwide. In spite of the numerous advances in the treatment of CHB, drugs and vaccines have failed because of many factors like complexity, resistance, toxicity, and heavy cost. New RNA interference (RNAi)-based technologies have developed innovative strategies to target Achilles' heel of the several hazardous diseases involving cancer, some genetic disease, autoimmune illnesses, and viral disorders particularly hepatitis B virus (HBV) infections. Naked siRNA delivery has serious challenges including failure to cross the cell membrane, susceptibility to the enzymatic digestion, and excretion by renal filtration, which ideally can be addressed by nanoparticle-mediated delivery systems. cccDNA formation is a significant problem in obtaining HBV infections complete cure because of strength, durability, and lack of proper immune response. Nano-siRNA drugs have a great potential to address this problem by silencing specific genes which are involved in cccDNA formation. In this article, the authors describe siRNA nanocarrier-mediated delivery systems as a promising new strategy for HBV infections therapy. Simultaneously, the authors completely represent the clinical trials which use these strategies for treatment of the HBV infections.
C1 [Aghamiri, Shahin] Shahid Beheshti Univ Med Sci, Sch Adv Technol Med, Dept Med Biotechnol, Student Res Comm, Tehran, Iran.
[Jafarpour, Ali] Univ Tehran Med Sci, Sch Publ Hlth, Dept Pathobiol, Virol Div,Students Sci Res Ctr, Tehran, Iran.
[Gomari, Mohammad Mahmoudi] Univ Tehran Med Sci, Sch Med, Dept Microbiol, Tehran, Iran.
[Ghorbani, Jaber] Univ Tehran Med Sci, Sch Adv Technol Med, Dept Med Biotechnol, Tehran, Iran.
[Rajabibazl, Masoumeh] Shahid Beheshti Univ Med Sci, Dept Clin Biochem, Fac Med, Tehran, Iran.
[Rajabibazl, Masoumeh] Shahid Beheshti Univ Med Sci, Sch Adv Technol Med, Dept Tissue Engn & Appl Cell Sci, Tehran, Iran.
[Payandeh, Zahra] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
C3 Shahid Beheshti University Medical Sciences; Tehran University of
Medical Sciences; Tehran University of Medical Sciences; Tehran
University of Medical Sciences; Shahid Beheshti University Medical
Sciences; Shahid Beheshti University Medical Sciences; Tabriz University
of Medical Science
RP Rajabibazl, M (corresponding author), Shahid Beheshti Univ Med Sci, Dept Clin Biochem, Fac Med, Tehran, Iran.; Rajabibazl, M (corresponding author), Shahid Beheshti Univ Med Sci, Sch Adv Technol Med, Dept Tissue Engn & Appl Cell Sci, Tehran, Iran.
EM rajabibazl_m@yahoo.com
RI Mahmoudi Gomari, Mohammad/Y-6938-2018; Aghamiri, Shahin/ABG-4656-2020;
Ghorbani, Jaber/HMU-9065-2023; payandeh, zahra/CAF-0179-2022
OI Aghamiri, Shahin/0000-0003-1083-1409; mahmoudi gomari,
mohammad/0000-0003-4143-2208
FU Student Research Committee, Shahid Beheshti University of Medical
Sciences, Tehran, Iran [16168]; "Student Research Committee" in Shahid
Beheshti University of Medical Sciences
FX This study is related to the project NO. 16168 From Student Research
Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
We also appreciate the "Student Research Committee" and "Research &
Technology Chancellor" in Shahid Beheshti University of Medical Sciences
for their financial support of this study.
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NR 100
TC 11
Z9 11
U1 0
U2 29
PU INST ENGINEERING TECHNOLOGY-IET
PI HERTFORD
PA MICHAEL FARADAY HOUSE SIX HILLS WAY STEVENAGE, HERTFORD SG1 2AY, ENGLAND
SN 1751-8741
EI 1751-875X
J9 IET NANOBIOTECHNOL
JI IET Nanobiotechnol.
PD JUL
PY 2019
VL 13
IS 5
BP 457
EP 463
DI 10.1049/iet-nbt.2018.5286
PG 7
WC Biochemical Research Methods; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Science & Technology - Other Topics
GA ID5NP
UT WOS:000471723400001
OA Green Published
DA 2025-01-07
ER
PT J
AU Castro, FA
Liu, XD
Försti, A
Ji, JG
Sundquist, J
Sundquist, K
Koshiol, J
Hemminki, K
AF Castro, Felipe A.
Liu, Xiangdong
Forsti, Asta
Ji, Jianguang
Sundquist, Jan
Sundquist, Kristina
Koshiol, Jill
Hemminki, Kari
TI Increased Risk of Hepatobiliary Cancers After Hospitalization for
Autoimmune Disease
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Risk Factor; Cohort; Survival; Hepatocellular Carcinoma
ID PRIMARY BILIARY-CIRRHOSIS; POPULATION-BASED COHORT; PRIMARY SCLEROSING
CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE; ULCERATIVE-COLITIS; TRACT
CANCER; HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER; PERNICIOUS-ANEMIA;
CELIAC-DISEASE
AB BACKGROUND & AIMS: Some autoimmune diseases are associated with increased risk of liver cancer. However, there has been no comprehensive evaluation of autoimmune diseases among patients who develop different subtypes of hepatobiliary cancer. We examined the association between autoimmune diseases and cancers of the liver and biliary tract in the Swedish population.
METHODS: We analyzed data from national datasets at the Center for Primary Health Care Research (Lund University, Sweden). Data on patients with autoimmune disorders were retrieved from the Swedish Hospital Discharge Register, from 1964 through 2008; 33 diseases were evaluated. Hepatobiliary cancer cases were retrieved from the Swedish Cancer Registry. We calculated standardized incidence ratios (SIRs) and hazard ratios for incident cancers and deaths from hepatobiliary cancers.
RESULTS: Among 402,462 patients with autoimmune disorders, 582 were diagnosed with primary liver cancer, 330 with gallbladder cancer, 115 with extrahepatic bile duct cancer, and 43 with ampulla of Vater cancers. We identified 14 autoimmune conditions that were significantly associated with increased risk of primary liver cancer (overall SIR [any autoimmune disease], 2.1; 95% confidence interval [CI], 2.0-2.3), 5 conditions associated with gallbladder cancer (overall SIR, 1.3; 95% CI, 1.1-1.4), and 3 associated with extrahepatic bile duct cancer (overall SIR, 1.6; 95% CI, 1.3-1.9). The autoimmune disorders with the strongest association with primary liver cancer were primary biliary cirrhosis (SIR, 39.5; 95% CI, 28.2-53.8) and autoimmune hepatitis (SIR, 29.0; 95% CI, 9.1-68.2); ulcerative colitis was strongly associated with extrahepatic bile duct cancer (SIR, 5.6; 95% CI, 3.6-8.4). Celiac disease, Crohn's disease, systemic sclerosis, and ulcerative colitis were associated with at least 2 types of cancer. Increased hazard ratios were observed only for patients with biliary tract cancer who had been hospitalized for autoimmune conditions.
CONCLUSIONS: In a study of the Swedish population, we identified an increased risk of hepatobiliary cancers among individuals diagnosed with autoimmune disease. Associations among different cancer types indicate that shared immunomodulatory mechanisms determine susceptibility to hepatobiliary cancer.
C1 [Castro, Felipe A.; Koshiol, Jill] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Liu, Xiangdong; Forsti, Asta; Ji, Jianguang; Sundquist, Jan; Sundquist, Kristina; Hemminki, Kari] Lund Univ, Ctr Primary Hlth Care Res, Malmo, Sweden.
[Forsti, Asta; Hemminki, Kari] German Canc Res Ctr, Div Mol Genet Epidemiol, Heidelberg, Germany.
[Sundquist, Jan; Sundquist, Kristina] Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, CA 94305 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI); Lund University; Helmholtz Association; German Cancer Research
Center (DKFZ); Stanford University
RP Castro, FA (corresponding author), NCI Shady Grove, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr 6-E230, Rockville, MD 20850 USA.
EM felipe.castro@nih.gov
RI de Castro, Fabiola/D-4693-2012; koshiol, Jill/L-8686-2014; Ji,
Jianguang/E-9579-2011
OI Ji, Jianguang/0000-0003-0324-9496
FU Deutsche Krebshilfe, ALF project grant, Lund, Sweden; Swedish Council
for Working Life and Social Research; National Institute of Health;
National Cancer Institute, Division of Cancer Epidemiology and Genetics,
USA
FX This work was supported by Deutsche Krebshilfe, ALF project grant, Lund,
Sweden and the Swedish Council for Working Life and Social Research. The
study was also supported by the Intramural Research Program of the
National Institute of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics, USA.
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NR 45
TC 43
Z9 44
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD JUN
PY 2014
VL 12
IS 6
BP 1038
EP +
DI 10.1016/j.cgh.2013.11.007
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AH9ZI
UT WOS:000336504700026
PM 24246767
DA 2025-01-07
ER
PT J
AU Cammarota, A
Zanuso, V
D'Alessio, A
Pressiani, T
Bozzarelli, S
Personeni, N
Rimassa, L
AF Cammarota, Antonella
Zanuso, Valentina
D'Alessio, Antonio
Pressiani, Tiziana
Bozzarelli, Silvia
Personeni, Nicola
Rimassa, Lorenza
TI The dual checkpoint blockade in unresectable hepatocellular carcinoma:
opportunities emerging in clinical trials
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Review
DE CTLA-4; durvalumab; HCC; immune checkpoint inhibitors; immunotherapy;
ipilimumab; nivolumab; PD-1; PD-L1; tremelimumab
ID PREEXISTING AUTOIMMUNE-DISEASE; PHASE-III; SYSTEMIC TREATMENT; PD-L1
EXPRESSION; CANCER-PATIENTS; DOUBLE-BLIND; SORAFENIB; NIVOLUMAB; HCC;
EFFICACY
AB Introduction To prevent damage from an immune response against autoantigens and toxins originating from the gut, the liver promotes an immune-tolerant milieu providing fertile ground for immune escape of cancer cells. Therefore, the use and evaluation of immune checkpoint inhibitors (ICIs) in hepatocellular carcinoma (HCC) is a treatment rationale. Area covered In this article, we discuss the role of the dual ICIs blockade in advanced HCC, covering the biological basis for their combination, their mechanism of action, and the results of the early-phase studies testing nivolumab plus ipilimumab and durvalumab plus tremelimumab. Furthermore, we provide the results of the phase III HIMALAYA trial and an overview of the ongoing trials investigating the dual ICIs in different disease stages. Expert Opinion The potential approval of the dual ICIs blockade strategies for advanced HCC will set the entry of antiangiogenic-free options, expanding the proportion of patients eligible for a first-line treatment. However, it will pose a series of clinical challenges with a sizable proportion of patients, namely Child-Pugh B, elderly, and immunocompromised patients, still marginalized. Also, given the rate of disease progression, identifying reliable predictive biomarkers is crucial to inform treatment choice and sequences. Finally, the compelling response rate of such combinations is paving the way for their evaluation in earlier stages.
C1 [Cammarota, Antonella; Zanuso, Valentina; D'Alessio, Antonio; Personeni, Nicola; Rimassa, Lorenza] Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini 4, I-20072 Milan, Italy.
[Cammarota, Antonella; Zanuso, Valentina; Pressiani, Tiziana; Bozzarelli, Silvia; Personeni, Nicola; Rimassa, Lorenza] IRCCS Humanitas Res Hosp, Med Oncol & Hematol Unit, Humanitas Canc Ctr, Milan, Italy.
[D'Alessio, Antonio] Imperial Coll London, Hammersmith Hosp, Dept Surg & Canc, London, England.
C3 Humanitas University; Imperial College London
RP Rimassa, L (corresponding author), Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini 4, I-20072 Milan, Italy.
EM lorenza.rimassa@hunimed.eu
RI Personeni, Nicola/ABG-7925-2020; D'Alessio, Antonio/ABC-5524-2022;
Cammarota, Antonella/LHA-4361-2024; Rimassa, Lorenza/N-4884-2016;
bozzarelli, silvia/ADF-0978-2022; Pressiani, Tiziana/HDN-8476-2022
OI Rimassa, Lorenza/0000-0001-9957-3615; Cammarota,
Antonella/0000-0001-9967-4694; bozzarelli, silvia/0000-0002-8118-7342;
Pressiani, Tiziana/0000-0001-6919-1536; D'Alessio,
Antonio/0000-0002-9164-3671; Personeni, Nicola/0000-0002-7995-272X
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NR 82
TC 3
Z9 4
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3784
EI 1744-7658
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD APR 3
PY 2022
VL 31
IS 4
SI SI
BP 425
EP 435
DI 10.1080/13543784.2022.2042253
EA FEB 2022
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 0H5NZ
UT WOS:000759261100001
PM 35152830
DA 2025-01-07
ER
PT J
AU Tateishi, R
Okanoue, T
Fujiwara, N
Okita, K
Kiyosawa, K
Omata, M
Kumada, H
Hayashi, N
Koike, K
AF Tateishi, Ryosuke
Okanoue, Takeshi
Fujiwara, Naoto
Okita, Kiwamu
Kiyosawa, Kendo
Omata, Masao
Kumada, Hiromitsu
Hayashi, Norio
Koike, Kazuhiko
TI Clinical characteristics, treatment, and prognosis of non-B, non-C
hepatocellular carcinoma: a large retrospective multicenter cohort study
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Hepatocellular carcinoma; Non-alcoholic fatty liver disease;
Non-alcoholic steatohepatitis; Alcoholic liver disease; Retrospective
study
ID CHRONIC HEPATITIS-B; LIVER-CANCER; RISK; JAPAN; INFECTION; CIRRHOSIS
AB The number of hepatocellular carcinoma (HCC) patients with non-viral etiologies is increasing in Japan. We conducted a nation-wide survey to examine the characteristics of those patients.
After we assessed the trend of patients who were first diagnosed with HCC at 53 tertiary care centers in Japan from 1991 to 2010, we collected detailed data of 5326 patients with non-viral etiology. The etiologies were categorized as autoimmune hepatitis, primary biliary cirrhosis, alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), unclassified, and other. Baseline characteristics at initial diagnosis, the modality of the initial treatment, and survival status were collected via a website. Survival of the patients was assessed by the Kaplan-Meier method and Cox proportional hazard regression.
The proportion of patients with non-viral etiologies increased from 10.0 % in 1991 to 24.1 % in 2010. Of the patients, 92 % were categorized as ALD, NAFLD, or unclassified. Body mass index (BMI) was a parts per thousand yen 25 kg/m(2) in 39 %. Diabetes was most prevalent in NAFLD (63 %), followed by unclassified etiology (46 %) and ALD (45 %). Approximately 80 % of patients underwent radical therapy, including resection, ablation, or transarterial chemoembolization. Survival rates at 3, 5, 10, 15, and 20 years were 58.2, 42.6, 21.5, 15.2, and 15.2 %, respectively. Multivariate analysis revealed that patients with BMI > 22 and a parts per thousand currency sign 25 kg/m(2) showed the best prognosis versus other BMI categories, after adjusting by age, gender, tumor-related factors, and Child-Pugh score.
Most cases of non-B, non-C HCC are related to lifestyle factors, including obesity and diabetes. Slightly overweight patients showed the best prognosis.
C1 [Tateishi, Ryosuke; Fujiwara, Naoto; Koike, Kazuhiko] Univ Tokyo, Dept Gastroenterol, Grad Sch Med, Bunkyo Ku, Tokyo 1138655, Japan.
[Okanoue, Takeshi] Saiseikai Suita Hosp, Suita, Osaka, Japan.
[Okita, Kiwamu] Ajisu Kyoritsu Hosp, Yamaguchi, Japan.
[Kiyosawa, Kendo] Shironishi Hosp, Matsumoto, Nagano, Japan.
[Omata, Masao] Yamanashi Prefectural Hosp Org, Kofu, Yamanashi, Japan.
[Kumada, Hiromitsu] Toranomon Gen Hosp, Tokyo, Japan.
[Hayashi, Norio] Kansai Rosai Hosp, Amagasaki, Hyogo, Japan.
C3 University of Tokyo; Toranomon Hospital; Kansai Rosai Hospital
RP Tateishi, R (corresponding author), Univ Tokyo, Dept Gastroenterol, Grad Sch Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
EM tateishi-tky@umin.ac.jp
RI Fujiwara, Naoto/Y-5938-2019; Tateishi, Ryosuke/G-7758-2014
OI Fujiwara, Naoto/0000-0002-4109-3421; Tateishi,
Ryosuke/0000-0003-3021-2517
FU Ministry of Health, Labour and Welfare of Japan; Eisai Co.
FX This work was supported partly by Health Sciences Research Grants of The
Ministry of Health, Labour and Welfare of Japan (Research on Hepatitis).
Eisai Co. supported the maintenance fee of the website for the data
registration. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
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NR 31
TC 124
Z9 130
U1 0
U2 6
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD MAR
PY 2015
VL 50
IS 3
BP 350
EP 360
DI 10.1007/s00535-014-0973-8
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CD5XN
UT WOS:000351162200013
PM 24929638
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU McDaniel, K
Hall, C
Sato, K
Lairmore, T
Marzioni, M
Glaser, S
Meng, FY
Alpini, G
AF McDaniel, Kelly
Hall, Chad
Sato, Keisaku
Lairmore, Terry
Marzioni, Marco
Glaser, Shannon
Meng, Fanyin
Alpini, Gianfranco
TI Lin28 and let-7: roles and regulation in liver diseases
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Review
DE lethal-7; liver disease; hepatic disorders; hepatocellular carcinoma;
primary biliary cholangitis; primary sclerosing cholangitis; liver
repair
ID MICRORNA BIOGENESIS; UP-REGULATION; STEM-CELLS; EXPRESSION; LIN-28; RNA;
CANCER; PROLIFERATION; PATHOGENESIS; MATURATION
AB McDaniel K, Hall C, Sato K, Lairmore T, Marzioni M, Glaser S, Meng F, Alpini G. Lin28 and let-7: roles and regulation in liver diseases. Am J Physiol Gastrointest Liver Physiol 310: G757-G765, 2016. First published March 24, 2016; doi:10.1152/ajpgi.00080.2016.-The diagnosis and treatment of liver disease remain a major health concern worldwide because of the diverse etiologies of this disease. For this reason, new therapeutic targets are greatly needed to halt the progression of this damaging disease. Upon initiation of liver injury by viral infection, autoimmune disease or toxin, and/or hepatitis, chronic disease may develop, which can progress to cirrhosis, hepatocellular carcinoma (HCC), cholangiocarcinoma, liver failure, or death. The Lin28/lethal-7 (let-7) molecular switch has emerged as a central regulator of multiorgan injuries and cancer development. Lin28 is a stem cell marker vital to initiation or maintenance of a stem cell phenotype. Lin28 has not been extensively studied in the liver, despite its ability to induce tissue regeneration via reprogramming of oxidative enzymes in other tissues and its involvement with numerous upstream regulators and downstream targets in liver disease. Theoretically, overexpression of Lin28 in certain forms of liver disease could be a potential treatment that aids in liver regeneration. Alternatively, Lin28 has been implicated numerous times in the progression of diverse cancer types and is associated with increased severity of disease. In this case, Lin28 could be a potential inhibitory target to prevent malignant transformation in the liver. This review seeks to characterize the role of Lin28 in liver disease.
C1 [McDaniel, Kelly; Glaser, Shannon; Meng, Fanyin; Alpini, Gianfranco] Cent Texas Vet Hlth Care Syst, Res, Temple, TX USA.
[McDaniel, Kelly; Glaser, Shannon; Meng, Fanyin; Alpini, Gianfranco] Scott & White Mem Hosp & Clin, Baylor Scott & White Digest Dis Res Ctr, Temple, TX 76508 USA.
[McDaniel, Kelly; Hall, Chad; Lairmore, Terry; Glaser, Shannon; Meng, Fanyin] Baylor Scott & White, Operat Funds, Temple, TX USA.
[McDaniel, Kelly; Sato, Keisaku; Alpini, Gianfranco] Baylor Scott & White, Dept Med, Temple, TX USA.
[McDaniel, Kelly; Hall, Chad; Sato, Keisaku; Lairmore, Terry; Alpini, Gianfranco] Texas A&M Hlth Sci Ctr, Temple, TX 76504 USA.
[Hall, Chad; Lairmore, Terry] Baylor Scott & White, Dept Surg, Temple, TX USA.
[Marzioni, Marco] Univ Politecn Marche, Dept Med, Ancona, Italy.
C3 Texas A&M University System; Texas A&M University College Station; Texas
A&M Health Science Center; Baylor Health Care System; Scott & White
Medical Center; Baylor Health Care System; Baylor Health Care System;
Texas A&M University System; Texas A&M University College Station; Texas
A&M Health Science Center; Baylor Health Care System; Marche Polytechnic
University
RP Alpini, G (corresponding author), Texas A&M Hlth Sci Ctr, Cent Texas Vet Hlth Care Syst, Coll Med, Olin E Teague Med Ctr, 1901 South 1st St,Bldg 205,1R60, Temple, TX 76504 USA.
EM galpini@tamu.edu
RI Marzioni, Marco/A-8153-2011
OI Mcdaniel, Kelly/0000-0003-4328-8844; Marzioni, Marco/0000-0001-6014-6165
FU Dr. Nicholas C. Hightower Centennial Chair of Gastroenterology from
Scott White; Department of Veterans Affairs Research; Department of
Veterans Affairs Merit Award [5I01BX000574]; Department of Veterans
Affairs Biomedical Laboratory Research Grants [1I01BX001724,
5I01BX002192]; National Institute of Diabetes and Digestive and Kidney
Diseases [R01 DK-058411, DK-076898, DK-107310, DK-062975]; Central Texas
Veterans Health Care System
FX This work was supported in part by the Dr. Nicholas C. Hightower
Centennial Chair of Gastroenterology from Scott & White, a Department of
Veterans Affairs Research Career Scientist Award, Department of Veterans
Affairs Merit Award 5I01BX000574 (to G. Alpini), Department of Veterans
Affairs Biomedical Laboratory Research Grants 1I01BX001724 (to F. Meng)
and 5I01BX002192 (to S. Glaser), and National Institute of Diabetes and
Digestive and Kidney Diseases Grants R01 DK-058411, DK-076898,
DK-107310, and DK-062975 (to G. Alpini, F. Meng, and S. Glaser). This
material is the result of work supported by resources at the Central
Texas Veterans Health Care System.
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NR 88
TC 31
Z9 37
U1 1
U2 11
PU AMER PHYSIOLOGICAL SOC
PI Rockville
PA 6120 Executive Blvd, Suite 600, Rockville, MD, UNITED STATES
SN 0193-1857
EI 1522-1547
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD MAY 15
PY 2016
VL 310
IS 10
BP G757
EP G765
DI 10.1152/ajpgi.00080.2016
PG 9
WC Gastroenterology & Hepatology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Physiology
GA DL7SW
UT WOS:000375841400001
PM 27012771
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Sohal, DPS
Sun, WJ
AF Sohal, Davendra P. S.
Sun, Weijing
TI Hepatocellular Carcinoma: Prevention and Therapy
SO CURRENT ONCOLOGY REPORTS
LA English
DT Article
DE Hepatocellular carcinoma (HCC); Hepatitis B virus (HBV); Hepatitis C
virus (HCV); Nonalcoholic steatohepatitis (NASH); Cirrhosis; Prevention;
Vaccine; Resection; Transplantation; Ablation; Transarterial
chemoembolization (TACE); Chemotherapy; Sorafenib
ID PLUS OXALIPLATIN GEMOX; PHASE-II TRIAL; LIVER-TRANSPLANTATION; ADJUVANT
CHEMOTHERAPY; CHEMOEMBOLIZATION; BEVACIZUMAB; GEMCITABINE; COMBINATION;
RESECTION; HEMOCHROMATOSIS
AB Hepatocellular carcinoma (HCC) is an aggressive malignancy of the liver and occurs most often in the setting of chronic liver disease. The most common acquired causes for this are chronic viral hepatitis infections (mostly HBV and HCV), and alcohol. Other causes include nonalcoholic fatty liver disease-related nonalcoholic steatohepatitis, autoimmune liver disease, and biliary diseases. In addition, certain heritable diseases like hemochromatosis and alpha-1-antitrypsin deficiency can also lead to HCC. Therefore, prevention of HCC can be achieved by preventing and controlling these problems. For treatment, curative modalities are surgical resection and liver transplantation. However, most patients are not candidates for these surgical maneuvers, and outcomes are poor. New therapeutic developments have brought some improvement with both local and systemic disease control.
C1 [Sohal, Davendra P. S.; Sun, Weijing] Univ Penn, Dept Med Hematol & Oncol, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
C3 University of Pennsylvania
RP Sun, WJ (corresponding author), Univ Penn, Dept Med Hematol & Oncol, Abramson Canc Ctr, 16 Penn Tower,3400 Spruce St, Philadelphia, PA 19104 USA.
EM davendra.sohal@uphs.upenn.edu; weijing.sun@uphs.upenn.edu
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[Anonymous], CARDIOVASC INTERVENT
[Anonymous], ONCOLOGY S1
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NR 50
TC 9
Z9 9
U1 0
U2 8
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1523-3790
EI 1534-6269
J9 CURR ONCOL REP
JI Curr. Oncol. Rep.
PD JUN
PY 2011
VL 13
IS 3
BP 186
EP 194
DI 10.1007/s11912-011-0165-0
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 758MX
UT WOS:000290170000005
PM 21409527
OA Bronze
DA 2025-01-07
ER
PT J
AU Lee, M
Kowdley, KV
AF Lee, Maximilian
Kowdley, Kris V.
TI Alcohol's Effect on Other Chronic Liver Diseases
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Alcohol; Autoimmune hepatitis; Fatty liver disease; Hepatitis B;
Hepatitis C; Hemochromatosis; Fibrosis; Cirrhosis
ID HEPATITIS-C VIRUS; HIGH-FAT DIET; HEPATOCELLULAR-CARCINOMA; HEREDITARY
HEMOCHROMATOSIS; FIBROSIS PROGRESSION; METABOLIC SYNDROME; CORE PROTEIN;
B-VIRUS; CIGARETTE-SMOKING; OXIDATIVE STRESS
AB In addition to directly causing liver disease, alcohol consumption is a common comorbid condition with other chronic liver diseases and may exacerbate liver injury, particularly in nonalcoholic fatty liver disease, chronic viral hepatitis, hereditary hemochromatosis, and autoimmune liver diseases. This synergism can result in increased hepatic inflammation and accelerated rates of fibrosis, with more rapid and earlier development of cirrhosis, and also increase the risk for liver cancer and death from liver disease.
C1 [Lee, Maximilian; Kowdley, Kris V.] Virginia Mason Med Ctr, Liver Ctr Excellence, Seattle, WA 98101 USA.
C3 Virginia Mason Medical Center
RP Kowdley, KV (corresponding author), Virginia Mason Med Ctr, Liver Ctr Excellence, 1100 9th Ave,Mailstop C3-GAS, Seattle, WA 98101 USA.
EM kris.kowdley@vmmc.org
RI Kowdley, Kris/AAF-5202-2019
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NR 67
TC 17
Z9 19
U1 0
U2 9
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD NOV
PY 2012
VL 16
IS 4
BP 827
EP +
DI 10.1016/j.cld.2012.08.010
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 058FL
UT WOS:000312619400011
PM 23101984
DA 2025-01-07
ER
PT J
AU Panneerselvam, S
Wilson, C
Kumar, P
Abirami, D
Pamarthi, J
Reddy, MS
Varghese, J
AF Panneerselvam, Sugan
Wilson, Cornelia
Kumar, Prem
Abirami, Dinu
Pamarthi, Jayakrishna
Reddy, Mettu Srinivas
Varghese, Joy
TI Overview of hepatocellular carcinoma: from molecular aspects to future
therapeutic options
SO CELL ADHESION & MIGRATION
LA English
DT Review
DE Circulating tumour cell; HCC biomarkers; immunotherapy; cell signaling
pathways; multi-omics technology
ID TUMOR-INFILTRATING LYMPHOCYTES; CHRONIC HEPATITIS-B; T-REGULATORY CELLS;
VIRUS-INFECTION; DIAGNOSTIC-VALUE; SIGNALING PATHWAYS; RISK-FACTOR;
EXPRESSION; CIRRHOSIS; NAFLD
AB Hepatocellular carcinoma (HCC) is the seventh most highly prevalent malignant tumor globally and the second most common cause of mortality. HCC develops with complex pathways that occur through multistage biological processes. Non-alcoholic fatty liver disease, metabolic-associated fatty liver disease, alcoholic liver disease, autoimmune hepatitis, hepatitis B, and hepatitis C are the causative etiologies of HCC. HCC develops as a result of epigenetic changes, protein-coding gene mutations, and altered signaling pathways. Biomarkers and potential therapeutic targets for HCC open up new possibilities for treating the disease. Immune checkpoint inhibitors are included in the treatment options in combination with molecular targeted therapy.
C1 [Panneerselvam, Sugan; Kumar, Prem] Gleneagles Global Hlth City, Dept Hepatol & Transplant Hepatol, Chennai, Tamil Nadu, India.
[Wilson, Cornelia] Canterbury Christ Church Univ, Sch Psychol & Life Sci, Nat & Appl Sci, Discovery Pk, Sandwich, England.
[Abirami, Dinu; Varghese, Joy] Gleneagles Global Hlth City, Dept Gastroenterol, Chennai, Tamil Nadu, India.
[Pamarthi, Jayakrishna] Madras Med Coll & Govt Gen Hosp, Multidisciplinary Res Unit, Chennai, Tamil Nadu, India.
[Reddy, Mettu Srinivas] Gleneagles Global Hlth City, Chennai, Tamil Nadu, India.
C3 Canterbury Christ Church University; Madras Medical College & General
Hospital
RP Panneerselvam, S (corresponding author), Gleneagles Global Hlth City, Dept Hepatol & Transplant Hepatol, Chennai, Tamil Nadu, India.
EM suganfr@hotmail.com
OI Wilson, Cornelia/0000-0001-6584-6179
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NR 165
TC 8
Z9 9
U1 3
U2 20
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6918
EI 1933-6926
J9 CELL ADHES MIGR
JI Celll Adhes. Migr.
PD DEC 31
PY 2023
VL 17
IS 1
BP 1
EP 21
DI 10.1080/19336918.2023.2258539
PG 21
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA S0OL2
UT WOS:001068248000001
PM 37726886
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Neuberger, J
Jothimani, D
AF Neuberger, J
Jothimani, D
TI Long-term immunosuppression for prevention of nonviral disease
recurrence
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article; Proceedings Paper
CT 3rd International Congress on Immunosuppression
CY DEC 08-11, 2004
CL San Diego, CA
SP Int Soc Heart & Lung Transplantat, Thomson Profess Postgrad Serv, Thomson Amer Hlth Consultants
ID ORTHOTOPIC LIVER-TRANSPLANTATION; PRIMARY SCLEROSING CHOLANGITIS;
INFLAMMATORY-BOWEL-DISEASE; PRIMARY BILIARY-CIRRHOSIS; AUTOIMMUNE
HEPATITIS; HEPATOCELLULAR-CARCINOMA; CANCER PROGRESSION; TUMOR
PROGRESSION; CYCLOSPORINE; GROWTH
AB The choice of immunosuppressive regime used after liver transplantation depends on many factors, which should include the effect of disease recurrence; recurrence of disease after liver transplantation may be affected by the degree and type of immunosuppression used and recurrent disease may affect patient and graft survival. For autoimmune diseases, recurrence of primary biliary cirrhosis develops sooner and more rapidly in those on tacrolimus compared with cyclosporine, but graft loss from recurrent disease is uncommon; recurrence rates of primary sclerosing cholangitis is unaffected by immunosuppressive regimes and recurrence of autoimmune hepatitis may be reduced by prescription of corticosteroids. Whether the immunosuppressive regime affects the pattern of hepatocellular carcinoma recurrence is uncertain. It is probable that the use of calcineurin inhibitor does not have a significant effect and inhibitors of TOR may have an anti-cancer effect, but this still has to be shown clinically. Most metabolic diseases are not affected by the choice of immunosuppression, although recurrence of sarcoidosis may be prevented by corticosteroids.
C1 Queen Elizabeth Hosp, Liver Unit, Birmingham B15 2TH, W Midlands, England.
C3 University of Birmingham
RP Neuberger, J (corresponding author), Queen Elizabeth Hosp, Liver Unit, 3rd Floor, Birmingham B15 2TH, W Midlands, England.
EM J.M.Neuberger@bham.ac.uk
RI Neuberger, James/ABG-3010-2020
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NR 22
TC 5
Z9 6
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0041-1345
J9 TRANSPLANT P
JI Transplant. Proc.
PD MAY
PY 2005
VL 37
IS 4
BP 1671
EP 1674
DI 10.1016/j.transproceed.2005.03.133
PG 4
WC Immunology; Surgery; Transplantation
WE Conference Proceedings Citation Index - Science (CPCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA 931EB
UT WOS:000229467500006
PM 15919426
DA 2025-01-07
ER
PT J
AU Tak, KH
Yu, GI
Lee, MY
Shin, DH
AF Tak, Ki Hong
Yu, Gyeong Im
Lee, Mi Young
Shin, Dong Hoon
TI Association Between Polymorphisms of Interleukin 1 Family Genes and
Hepatocellular Carcinoma
SO MEDICAL SCIENCE MONITOR
LA English
DT Article
DE Carcinoma, Hepatocellular; Interleukin-1; Polymorphism, Single
Nucleotide
ID HEPATITIS; RISK; IL-1; CANCER; SUSCEPTIBILITY; INFECTION; CYTOKINE
AB Background: Hepatocellular carcinoma (HCC) is one of the most common malignancies occurring worldwide and is most frequent type of liver cancer. The risk for developing HCC increases with the severity of inflammation and fibrosis. The members of the interleukin-1 (IL-1) family are primarily proinflammatory cytokines due to their ability to stimulate the expression of genes associated with inflammation and autoimmune diseases. Several studies have suggested that some proinflammatory cytokines, such as the IL-1 family (IL-1 alpha, IL-1 beta, and IL-1 receptor antagonist) are involved in the pathogenesis of HCC.
Material/Methods: This study aimed to determine whether polymorphisms in the IL-1 family of genes are associated with HCC. We analyzed 178 HCC patients and 397 controls to investigate the association between polymorphisms in IL-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1RA) genes and HCC in the Korean population. All subjects were genotyped for the selected SNPs in IL-1 alpha, IL-1 beta, and IL-1RA genes by Golden-Gate SNP Genotyping Assay.
Results: Statistical analysis revealed a significant association at IL-1 beta between HCC and controls. Three individual polymorphisms (rs1143633, rs3917356, and rs1143627) were found to be associated with HCC. The SNPs of IL-1 beta gene (rs1143633A>G and rs1143627T>C) protected against HCC in the dominant model (p=0.027, OR=0.59, 95% CI=0.37-0.94; p=0.019, OR=0.56, 95% CI=0.34-0.91). The SNP of IL-1 beta gene (rs3917356G>A) increased the risk of HCC in the recessive model (p<0.001, OR=2.58, 95% CI=1.53-4.33), whereas other SNPs in IL-1 alpha and IL-1RA showed no significant association between HCC patients and controls.
Conclusions: These results suggest that IL-1 beta in the IL-1 family contributes to HCC susceptibility.
C1 [Tak, Ki Hong] Sungseo Hosp, Dept Occupat & Environm Med, Daegu, South Korea.
[Yu, Gyeong Im; Lee, Mi Young; Shin, Dong Hoon] Keimyung Univ, Sch Med, Dept Prevent Med, Daegu, South Korea.
[Yu, Gyeong Im; Lee, Mi Young; Shin, Dong Hoon] Keimyung Univ, Inst Canc Res, Daegu, South Korea.
C3 Keimyung University; Keimyung University
RP Lee, MY; Shin, DH (corresponding author), Keimyung Univ, Sch Med, Dept Prevent Med, Daegu, South Korea.; Lee, MY; Shin, DH (corresponding author), Keimyung Univ, Inst Canc Res, Daegu, South Korea.
EM mylee@dsmc.or.kr; dhshin@dsmc.or.kr
FU Keimyung University Dongsan Medical Center
FX This work was supported by a Research-Promoting grant from Keimyung
University Dongsan Medical Center in 2008 and 2012
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NR 31
TC 26
Z9 27
U1 0
U2 3
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
SN 1643-3750
J9 MED SCI MONITOR
JI Med. Sci. Monitor
PD MAY 26
PY 2018
VL 24
BP 3488
EP 3495
DI 10.12659/MSM.907524
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA GH1NB
UT WOS:000433168500001
PM 29802240
OA Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU An, Y
Xu, SX
Liu, YT
Xu, XB
Philips, CA
Chen, J
Méndez-Sánchez, N
Guo, XZ
Qi, XS
AF An, Yang
Xu, Shixue
Liu, Yiting
Xu, Xiangbo
Philips, Cyriac Abby
Chen, Jiang
Mendez-Sanchez, Nahum
Guo, Xiaozhong
Qi, Xingshun
TI Role of Galectins in the Liver Diseases: A Systematic Review and
Meta-Analysis
SO FRONTIERS IN MEDICINE
LA English
DT Review
DE galectins; hepatocellular carcinoma; cirrhosis; hepatitis; fibrosis
ID HEPATOCELLULAR-CARCINOMA; SERUM GALECTIN-3; POOR-PROGNOSIS; EXPRESSION;
FIBROSIS; CIRRHOSIS; CANCER; CELLS
AB Background: Galectins, a family of beta-galactoside-binding proteins, are related to the development and progression of various human diseases such as cancer, heart failure, and chronic kidney disease. However, its role in liver diseases is unclear.
Methods: The PubMed, Embase, and Cochrane Library databases were searched. Hazard ratios (HRs), odds ratios (ORs), and mean differences (MDs) with 95% CIs were pooled to evaluate the association of the galectins with the outcomes and risk of liver diseases by a random effects model.
Results: Thirty three studies involving 43 cohorts and 4,168 patients with liver diseases were included. In the patients with hepatocellular carcinoma (HCC), high expression of galectin-1 and -3 in the tissues was significantly associated with worse overall survival (galectin-1: HR = 1.94, 95% CI = 1.61-2.34, p < 0.001; galectin-3: HR = 3.29, 95% CI = 1.62-6.68, p < 0.001) and positive vascular invasion (galectin-1: OR = 1.74, 95% CI = 1.18-2.58, p = 0.005; galectin-3: OR = 2.98, 95% CI = 1.58-5.60, p = 0.001); but, high expression of galectin-4 and -9 in the tissues was significantly associated with better overall survival (galectin-4: HR = 0.53, 95% CI = 0.36-0.79, p = 0.002; galectin-9: HR = 0.56, 95% CI = 0.44-0.71, p < 0.001) and negative vascular invasion (galectin-4: OR = 0.36, 95% CI = 0.19-0.72, p = 0.003; galectin-9: OR = 0.60, 95% CI = 0.37-0.97, p = 0.037). Serum galectin-3 level was significantly higher in HCC (MD = 3.06, 95% CI = 1.79-4.32, p < 0.001), liver failure (MD = 0.44, 95% CI = 0.23-0.66, p < 0.001), liver cirrhosis (MD = 1.83, 95% CI = 1.15-2.51, p < 0.001), and chronic active hepatitis B (MD = 18.95, 95% CI = 10.91-27.00, p < 0.001); serum galectin-9 level was significantly higher in HCC (MD = 3.74, 95% CI = 2.57-4.91, p < 0.001) and autoimmune hepatitis (MD = 8.80, 95% CI = 7.61-9.99, p < 0.001).
Conclusion: High galectin-1 and -3 and low galectin-4 and -9 expression indicate worse outcomes of patients with HCC. Serum galectin-3 and -9 levels are positively associated with the risk of chronic liver diseases.
C1 [An, Yang; Xu, Shixue; Liu, Yiting; Xu, Xiangbo; Chen, Jiang; Guo, Xiaozhong; Qi, Xingshun] Gen Hosp Northern Theater Command, Dept Gastroenterol, Meta Anal Study Grp, Shenyang, Peoples R China.
[An, Yang; Xu, Xiangbo] Shenyang Pharmaceut Univ, Postgrad Coll, Shenyang, Peoples R China.
[Liu, Yiting] China Med Univ, Affiliated Hosp 1, Dept Phys Examinat Ctr, Shenyang, Peoples R China.
[Philips, Cyriac Abby] Cochin Gastroenterol Grp, Liver Unit & Monarch Liver Lab, Ernakulam Med Ctr, Kochi, India.
[Mendez-Sanchez, Nahum] Univ Nacl Autonoma Mexico, Liver Res Unit Med Clin & Fdn, Mexico City, DF, Mexico.
[Mendez-Sanchez, Nahum] Univ Nacl Autonoma Mexico, Fac Med, Mexico City, DF, Mexico.
C3 Shenyang Pharmaceutical University; China Medical University;
Universidad Nacional Autonoma de Mexico; Universidad Nacional Autonoma
de Mexico
RP Qi, XS (corresponding author), Gen Hosp Northern Theater Command, Dept Gastroenterol, Meta Anal Study Grp, Shenyang, Peoples R China.
EM xingshunqi@126.com
RI Qi, Xingshun/M-7063-2013; Guo, Xiaozhong/AAX-5269-2020
OI Guo, Xiaozhong/0000-0002-6397-0501; Philips, Cyriac
Abby/0000-0002-9587-336X
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NR 63
TC 25
Z9 25
U1 0
U2 12
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD OCT 27
PY 2021
VL 8
AR 744518
DI 10.3389/fmed.2021.744518
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA WW0UZ
UT WOS:000717643800001
PM 34778306
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Mukherjee, S
Kar, A
Khatun, N
Datta, P
Biswas, A
Barik, S
AF Mukherjee, Soumyadeep
Kar, Arpita
Khatun, Najma
Datta, Puja
Biswas, Avik
Barik, Subhasis
TI Familiarity Breeds Strategy: In Silico Untangling of the Molecular
Complexity on Course of Autoimmune Liver Disease-to-Hepatocellular
Carcinoma Transition Predicts Novel Transcriptional Signatures
SO CELLS
LA English
DT Article
DE autoimmune liver disease; hepatocellular carcinoma; HCC transcriptomics;
hepatic fibrosis; liver cirrhosis; gene regulatory network
ID HEPATITIS; INFLAMMATION; ENRICHMENT; CIRRHOSIS
AB Autoimmune liver diseases (AILD) often lead to transformation of the liver tissues into hepatocellular carcinoma (HCC). Considering the drawbacks of surgical procedures in such cases, need of successful non-invasive therapeutic strategies and treatment modalities for AILD-associated-HCC still exists. Due to the lack of clear, sufficient knowledge about factors mediating AILD-to-HCC transition, an in silico approach was adopted to delineate the underlying molecular deterministic factors. Parallel enrichment analyses on two different public microarray datasets (GSE159676 and GSE62232) pinpointed the core transcriptional regulators as key players. Correlation between the expression kinetics of these transcriptional modules in AILD and HCC was found to be positive primarily with the advancement of hepatic fibrosis. Most of the regulatory interactions were operative during early (F0-F1) and intermediate fibrotic stages (F2-F3), while the extent of activity in the regulatory network considerably diminished at late stage of fibrosis/cirrhosis (F4). Additionally, most of the transcriptional targets with higher degrees of connectivity in the regulatory network (namely DCAF11, PKM2, DGAT2 and BCAT1) may be considered as potential candidates for biomarkers or clinical targets compared to their low-connectivity counterparts. In summary, this study uncovers new possibilities in the designing of novel prognostic and therapeutic regimen for autoimmunity-associated malignancy of liver in a disease progression-dependent fashion.
C1 [Mukherjee, Soumyadeep; Datta, Puja; Barik, Subhasis] Chittaranjan Natl Canc Inst, Dept In Vitro Carcinogenesis & Cellular Chemother, Kolkata 700026, India.
[Kar, Arpita; Khatun, Najma; Biswas, Avik] Chittaranjan Natl Canc Inst, Dept Signal Transduct & Biogen Amines, Kolkata 700026, India.
RP Barik, S (corresponding author), Chittaranjan Natl Canc Inst, Dept In Vitro Carcinogenesis & Cellular Chemother, Kolkata 700026, India.; Biswas, A (corresponding author), Chittaranjan Natl Canc Inst, Dept Signal Transduct & Biogen Amines, Kolkata 700026, India.
EM mukherjees960@gmail.com; arpitakar2@gmail.com; najma.zhns119@gmail.com;
pujadatta.cell@gmail.com; avikbiswas@cnci.ac.in;
subhasisbarik@cnci.ac.in
RI Kar, Arpita/HOH-7515-2023; Mukherjee, Soumyadeep/HKP-0832-2023
OI Mukherjee, Soumyadeep/0000-0002-7495-0856; Kar,
Arpita/0000-0001-6554-2984
FU DBT-Ramalingaswami Grant [BT/HRD/35/02/2006]; Chittaranjan National
Cancer Institute; Council of Scientific & Industrial Research (CSIR),
India; University Grants Commission (UGC), India; Science and
Engineering Research Board (SERB), India
FX This work was supported by the DBT-Ramalingaswami Grant (D.O.
No.BT/HRD/35/02/2006 Dated: 19 November 2018.) to S.B. and Intramural
funding of Chittaranjan National Cancer Institute. S.M. was supported by
Junior Research Fellowship from Council of Scientific & Industrial
Research (CSIR), India. A.K. and N.K. were supported by Junior Research
Fellowships from University Grants Commission (UGC), India. P.D. was
supported by Junior Research Fellowship from Science and Engineering
Research Board (SERB), India.
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NR 51
TC 13
Z9 13
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD AUG
PY 2021
VL 10
IS 8
AR 1917
DI 10.3390/cells10081917
PG 23
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA UF9CA
UT WOS:000688863000001
PM 34440687
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Loosen, SH
Schöler, D
Luedde, M
Eschrich, J
Luedde, T
Kostev, K
Roderburg, C
AF Loosen, Sven H.
Schoeler, David
Luedde, Mark
Eschrich, Johannes
Luedde, Tom
Kostev, Karel
Roderburg, Christoph
TI Differential role of chronic liver diseases on the incidence of cancer:
a longitudinal analysis among 248,224 outpatients in Germany
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE HCC; Hepatocellular carcinoma; Fib-4; Biomarker; Score
ID HEPATITIS-C VIRUS; HEPATOCELLULAR-CARCINOMA; RISK
AB Background Chronic liver diseases, especially chronic hepatitis, are a known risk factor for the development of liver cancer. However, the risk of total cancer development and malignant potential from these diseases is largely unknown. Systematic data on the risk of cancer development from these diseases are missing. Therefore, the goal of this study is to analyze the risk of total cancer development in chronic liver diseases. Methods A cohort of 15,706 patients with chronic hepatitis and 15,706 patients without hepatitis were matched by propensity scoring from outpatient practices in Germany over a period of 15 years. Cox regression models were conducted to study the association between alcoholic hepatitis, autoimmune hepatitis, hepatitis B, hepatitis C and cancer incidence, including liver, other digestive organs, skin, prostate, breast and lymphoid and hematopoietic tissue cancer. Results Within 10 years of the index date, 19.3% of patients with alcoholic hepatitis and 13.4% of non-hepatitis individuals were diagnosed with cancer (log-rank p = 0.035). These proportions were 15.0 vs. 9.9% (p = 0.078) for autoimmune hepatitis, 8.7 vs. 7.1% (p = 0.015) for hepatitis B, and 12.7 vs. 7.6% (p < 0.001) for hepatitis C. In regression analyses, only alcoholic hepatitis (HR: 1.84, 95% CI 1.32-2.54) and hepatitis C (HR: 2.10, 95% CI 1.77-2.50) were significantly associated with increased risk of cancer. There was a very strong positive association between hepatitis C and liver cancer (HR: 78.2 (95% CI 10.9-560.7). Furthermore, hepatitis C was associated with an increased risk of respiratory organ cancer (HR: 2.59, 95% CI 1.42-4.73). Conclusion This study confirms the strong association between chronic hepatitis and liver cancer, but also with an overall elevated cancer risk, and especially of cancer in the respiratory tract in patients with chronic hepatitis C.
C1 [Loosen, Sven H.; Schoeler, David; Luedde, Tom; Roderburg, Christoph] Heinrich Heine Univ Dusseldorf, Med Fac, Univ Hosp Dusseldorf, Clin Gastroenterol Hepatol & Infect Dis, Moorenstr 5, D-40225 Dusseldorf, Germany.
[Luedde, Mark] KGP Bremerhaven, Bremerhaven, Germany.
[Eschrich, Johannes] Charite Univ Med Ctr, Clin Hepatol & Gastroenterol, Augustenbuger Pl 1, D-13353 Berlin, Germany.
[Kostev, Karel] IQVIA, Epidemiol, Frankfurt, Germany.
C3 Heinrich Heine University Dusseldorf; Heinrich Heine University
Dusseldorf Hospital; Berlin Institute of Health; Free University of
Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
Berlin; IQVIA
RP Loosen, SH; Roderburg, C (corresponding author), Heinrich Heine Univ Dusseldorf, Med Fac, Univ Hosp Dusseldorf, Clin Gastroenterol Hepatol & Infect Dis, Moorenstr 5, D-40225 Dusseldorf, Germany.
EM Sven.Loosen@med.uni-duesseldorf.de;
christoph.roderburg@med.uni-duesseldorf.de
RI Loosen, Sven/AHC-5236-2022; Luedde, Tom/AAE-9135-2022; Kostev,
Karel/S-4755-2019
OI Eschrich, Johannes/0000-0002-7390-6431; Luedde, Tom/0000-0002-6288-8821;
Kostev, Karel/0000-0002-2124-7227
FU European Research Council (ERC) under the European Union's Horizon 2020
research and innovation program through the ERC Consolidator Grant Phase
Control [771083]; German Cancer Aid (Deutsche Krebshilfe) [110043];
German-Research-Foundation [SFB-TRR57/P06, LU 1360/3-1, CRC1380/A01, CA
830/3-1]; German Cancer Aid (Mildred-Scheel-Professorship); Projekt DEAL
FX Open Access funding enabled and organized by Projekt DEAL. There was no
specific funding related to this study. In general, work in the group of
T.L. was funded from the European Research Council (ERC) under the
European Union's Horizon 2020 research and innovation program through
the ERC Consolidator Grant Phase Control (Grant Agreement n degrees
771083). The lab of T.L. was further supported by the German Cancer Aid
(Deutsche Krebshilfe 110043 and a Mildred-Scheel-Professorship) and the
German-Research-Foundation (SFB-TRR57/P06, LU 1360/3-1, CRC1380/A01, and
CA 830/3-1).
CR Allison RD, 2015, J HEPATOL, V63, P822, DOI 10.1016/j.jhep.2015.04.021
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NR 21
TC 2
Z9 2
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD JUL
PY 2023
VL 149
IS 7
BP 3081
EP 3087
DI 10.1007/s00432-022-04198-5
EA JUL 2022
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA L4OB8
UT WOS:000828960600002
PM 35867204
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Luedde, T
Kaplowitz, N
Schwabe, RF
AF Luedde, Tom
Kaplowitz, Neil
Schwabe, Robert F.
TI Cell Death and Cell Death Responses in Liver Disease: Mechanisms and
Clinical Relevance
SO GASTROENTEROLOGY
LA English
DT Article
DE Apoptosis; Necrosis; Necroptosis; Necrosome; DAMP; Viral Hepatitis;
NASH; Clinical Trial; Hepatocellular Carcinoma; Alcoholic Liver Disease;
DILI; Caspases; RIP3; RIP Kinases
ID MITOCHONDRIAL PERMEABILITY TRANSITION; HEPATITIS-C VIRUS; NF-KAPPA-B;
SERUM AMINOTRANSFERASE CONCENTRATION; ENDOPLASMIC-RETICULUM STRESS;
ACUTE ALCOHOLIC HEPATITIS; DOMAIN-LIKE PROTEIN; GROUP BOX-1 PROTEIN;
NONALCOHOLIC STEATOHEPATITIS; HEPATOCELLULAR-CARCINOMA
AB Hepatocellular death is present in almost all types of human liver disease and is used as a sensitive parameter for the detection of acute and chronic liver disease of viral, toxic, metabolic, or autoimmune origin. Clinical data and animal models suggest that hepatocyte death is the key trigger of liver disease progression, manifested by the subsequent development of inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. Modes of hepatocellular death differ substantially between liver diseases. Different modes of cell death such as apoptosis, necrosis, and necroptosis trigger specific cell death responses and promote progression of liver disease through distinct mechanisms. In this review, we first discuss molecular mechanisms by which different modes of cell death, damage-associated molecular patterns, and specific cell death responses contribute to the development of liver disease. We then review the clinical relevance of cell death, focusing on biomarkers; the contribution of cell death to drug-induced, viral, and fatty liver disease and liver cancer; and evidence for cell death pathways as therapeutic targets.
C1 [Luedde, Tom] Univ Hosp RWTH Aachen, Dept Med 3, D-52074 Aachen, Germany.
[Kaplowitz, Neil] Univ So Calif, Keck Sch Med, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90033 USA.
[Schwabe, Robert F.] Columbia Univ, Dept Med, New York, NY 10032 USA.
[Schwabe, Robert F.] Columbia Univ, Inst Human Nutr, New York, NY 10032 USA.
C3 RWTH Aachen University; RWTH Aachen University Hospital; University of
Southern California; Columbia University; Columbia University
RP Luedde, T (corresponding author), Univ Hosp RWTH Aachen, Div GI & Hepatobiliary Oncol, Dept Med 3, Pauwelsstr 30, D-52074 Aachen, Germany.
EM tluedde@ukaachen.de; rfs2102@cumc.columbia.edu
RI Schwabe, Robert/AAY-6506-2021; Luedde, Tom/AAE-9135-2022
OI Luedde, Tom/0000-0002-6288-8821
FU German Cancer Aid (Deutsche Krebshilfe) [110043]; German Research
Foundation [SFB-TRR57/P06]; ERC
[ERC-2007-Stg/208237-Luedde-Med3-Aachen]; EMBO Young Investigator
Program; Ernst Jung Foundation Hamburg; medical faculty of RWTH Aachen;
[5R01DK067215]; [5R01AA014428]; [5P30DK0485]; [1U01AA021912];
[5R01AA020211]; [5U54CA163111]
FX T.L. was supported by the German Cancer Aid (Deutsche Krebshilfe
110043), the German Research Foundation (SFB-TRR57/P06), an ERC Starting
Grant (ERC-2007-Stg/208237-Luedde-Med3-Aachen), the EMBO Young
Investigator Program, the Ernst Jung Foundation Hamburg, and a grant
from the medical faculty of RWTH Aachen. N.K. was supported by grants
5R01DK067215, 5R01AA014428, and 5P30DK0485. R.F.S. was supported by
grants 1U01AA021912, 5R01AA020211, and 5U54CA163111.
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NR 256
TC 553
Z9 607
U1 5
U2 175
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2014
VL 147
IS 4
BP 765
EP U110
DI 10.1053/j.gastro.2014.07.018
PG 23
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AQ0SO
UT WOS:000342493200021
PM 25046161
OA Green Accepted, Bronze
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Amarapurkar, AD
Amarapurkar, DN
Vibhav, S
Patel, ND
AF Amarapurkar, Anjali D.
Amarapurkar, Deepak N.
Vibhav, S.
Patel, Nikhil D.
TI Angiogenesis in chronic liver disease
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE endothelial cells; VEGF; CD 34; hepatocellular carcinoma; viral
hepatitis; neovascularization
ID ENDOTHELIAL GROWTH-FACTOR; HEPATOCELLULAR-CARCINOMA; HEPATITIS-C;
MICROVESSEL DENSITY; CIRRHOTIC LIVER; EXPRESSION; CAPILLARIZATION;
PREREQUISITE; FIBROSIS; CANCER
AB Background: Chronic liver disease is characterized by inflammation and fibrosis. As a consequence angiogenesis leading to new vasculature may have prognostic value in disease progression. Interfering with angiogenesis may be a potential target to avoid progression of liver disease. Hence we planned to evaluate the CD34 and vascular endothelial growth factor (VEGF), the markers for angiogenesis in chronic liver disease. Method: Liver biopsies from 79 patients of chronic liver disease and 21 cases of HCC (M: F = 4:1, age range 22 to 80) were stained for routine HE, CD 34 and VEGF immunostaining (Dako Corp & Santa Cruz respectively). Etiologies of chronic liver disease were alcoholic liver disease, HBV, HCV infection, NAFLD, autoimmune liver disease, and cryptogenic liver disease. Thirty biopsies from normal liver obtained at autopsy were taken as controls. Expressions of CD 34 and VEGF were compared with the stage of fibrosis. Results: Out of 79 patients, angiogenesis was seen in 45.5% cases of chronic liver disease. None of the case with normal liver histology was CD 34 or VEGF positive. No significant correlation of angiogenesis was found between any etiologies of chronic liver disease. CD 34 was positive in 18/21 (85.7%) cases of hepatocellular carcinoma. CD 34 and VEGF positivity was 20.9% and 46.5% in stage 1 and 2 fibrosis while it was 75% and 80% in stage 3 and 4 fibrosis respectively. VEGF appeared more common as compared to CD 34 in early fibrosis. Conclusion: Angiogenesis was present in 45.5% cases of chronic liver disease. It was proportional to the increase in stage of fibrosis. Expression of VEGF was commonly found in early stages of fibrosis. Hence, therapeutic strategies of inhibiting VEGF expression may be of importance in preventing the progression of chronic liver disease in its early stage.
C1 [Patel, Nikhil D.] Bombay Hosp & Med Res Ctr, Dept Gastroenterol & Hepatol, Bombay, Maharashtra, India.
C3 Bombay Hospital & Medical Research Centre
RP Amarapurkar, AD (corresponding author), D 401,Ameya Soc New Prabhadevi Rd, Bombay 400025, Maharashtra, India.
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NR 28
TC 38
Z9 41
U1 0
U2 1
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD JUL-SEP
PY 2007
VL 6
IS 3
BP 170
EP 173
DI 10.1016/S1665-2681(19)31924-6
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 278AY
UT WOS:000254257000007
PM 17786144
OA hybrid
DA 2025-01-07
ER
PT J
AU Migita, K
Watanabe, Y
Jiuchi, Y
Nakamura, Y
Saito, A
Yagura, M
Ohta, H
Shimada, M
Mita, E
Hijioka, T
Yamashita, H
Takezaki, E
Muro, T
Sakai, H
Nakamuta, M
Abiru, S
Komori, A
Ito, M
Yatsuhashi, H
Nakamura, M
Ishibashi, H
AF Migita, Kiyoshi
Watanabe, Yukio
Jiuchi, Yuka
Nakamura, Yoko
Saito, Akira
Yagura, Michiyasu
Ohta, Hajime
Shimada, Masaaki
Mita, Eiji
Hijioka, Taizo
Yamashita, Haruhiro
Takezaki, Eiichi
Muro, Toyokichi
Sakai, Hironori
Nakamuta, Makoto
Abiru, Seigo
Komori, Atsumasa
Ito, Masahiro
Yatsuhashi, Hiroshi
Nakamura, Minoru
Ishibashi, Hiromi
CA Japanese NHO-Liver-Network Study G
TI Hepatocellular carcinoma and survival in patients with autoimmune
hepatitis (Japanese National Hospital Organization-autoimmune hepatitis
prospective study)
SO LIVER INTERNATIONAL
LA English
DT Article
DE autoimmune hepatitis; cirrhosis; hepatocellular carcinoma; multicentre
cohort study; outcome
ID RISK-FACTORS; NATURAL-HISTORY; LIVER-DISEASE; FOLLOW-UP; CIRRHOSIS;
DIAGNOSIS
AB Background/ Aims: Although the outcome of autoimmune hepatitis (AIH) is generally good, the natural course and likelihood of progression to cirrhosis or hepatocellular carcinoma (HCC) remain undefined, and may vary by region and population structure. Our aims were to evaluate risk factors that contribute to poor outcome and particularly development of HCC in a prospective multicentric cohort study of AIH. Methods: The study group comprised 193 Japanese patients with AIH who were prospectively followed up at annual intervals between 1995 and 2008. The mean follow-up period was 8.0 +/- 4.5 years. Results: Twenty-one (10.9%) patients had cirrhosis at presentation and a further 15 (7.8%) developed cirrhosis during the follow-up period. Survival rates were 94.2% at 10 years and 89.3% at 15 years. HCC was diagnosed in seven of the 193 patients. The presence of cirrhosis at presentation was a risk factor for HCC according to a Cox proportional hazard model, and the HCC-free survival rate was significantly lower in those with cirrhosis compared to those without cirrhosis according to Kaplan-Meier analysis. Conclusions: Although the outcome of AIH is as good if not better among Japanese than for other populations, there was an increased risk of HCC in these patients. Cirrhosis at presentation was predictive of development of HCC in AIH in Japan.
C1 [Migita, Kiyoshi; Japanese NHO-Liver-Network Study G] NHO Nagasaki Med Ctr, Clin Res Ctr, Omura 8568652, Japan.
RP Migita, K (corresponding author), NHO Nagasaki Med Ctr, Clin Res Ctr, Kubara 2-1001-1, Omura 8568652, Japan.
EM migita@nmc.hosp.go.jp
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NR 22
TC 43
Z9 43
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD MAY
PY 2012
VL 32
IS 5
BP 837
EP 844
DI 10.1111/j.1478-3231.2011.02734.x
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 921HM
UT WOS:000302468700018
PM 22221966
DA 2025-01-07
ER
PT J
AU Papadatos, D
Fowler, KJ
Kielar, AZ
Cui, J
Sirlin, CB
AF Papadatos, Demetrios
Fowler, Kathryn J.
Kielar, Ania Z.
Cui, Jennifer
Sirlin, Claude B.
TI Cirrhosis and LI-RADS
SO ABDOMINAL RADIOLOGY
LA English
DT Article
DE LI-RADS; Cirrhosis; Fibrosis; Hepatocellular carcinoma; Hepatocellular
nodules; Magnetic resonance imaging
ID NODULAR REGENERATIVE HYPERPLASIA; PRIMARY SCLEROSING CHOLANGITIS;
ATROPHY-HYPERTROPHY COMPLEX; PRIMARY BILIARY-CIRRHOSIS;
BUDD-CHIARI-SYNDROME; HEPATOCELLULAR-CARCINOMA; IMAGING FINDINGS;
AUTOIMMUNE HEPATITIS; PORTAL-HYPERTENSION; ENHANCING LESIONS
AB Chronic liver disease, irrespective of cause, can eventually lead to cirrhosis, which is the primary risk factor for developing hepatocellular carcinoma (HCC). In patients with cirrhosis or appropriate risk factors, HCC can be diagnosed by imaging with high specificity using liver imaging reporting and data system v2017, obviating the need for histologic confirmation. Confident recognition of cirrhosis by conventional imaging alone can be challenging, as radiologists are not always provided with the requisite information to determine if the patient has cirrhosis or other risk factors for HCC. Moreover, cirrhosis-associated abnormalities may impair the diagnostic accuracy of imaging for HCC. This article addresses the diagnosis of cirrhosis by non-invasive imaging and the implications of cirrhosis for imaging interpretation and accuracy.
C1 [Papadatos, Demetrios; Kielar, Ania Z.] Univ Ottawa, Ottawa, ON, Canada.
[Fowler, Kathryn J.] Washington Univ, Sch Med, Dept Radiol, 510 S Kingshighway, St Louis, MO 63110 USA.
[Cui, Jennifer; Sirlin, Claude B.] Univ Calif San Diego, San Diego, CA 92103 USA.
C3 University of Ottawa; Washington University (WUSTL); University of
California System; University of California San Diego
RP Fowler, KJ (corresponding author), Washington Univ, Sch Med, Dept Radiol, 510 S Kingshighway, St Louis, MO 63110 USA.
EM fowlerk@wustl.edu
RI Sirlin, Claude/AAU-1376-2020
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NR 61
TC 10
Z9 10
U1 1
U2 7
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2366-004X
EI 2366-0058
J9 ABDOM RADIOL
JI Abdom. Radiol.
PD JAN
PY 2018
VL 43
IS 1
BP 26
EP 40
DI 10.1007/s00261-017-1425-8
PG 15
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA FT0GK
UT WOS:000422800800004
PM 29218367
DA 2025-01-07
ER
PT J
AU Bergquist, A
Ekstedt, M
Hagström, H
Järnerot, G
Lindgren, S
Nilsson, E
Nyhlin, N
Rorsman, F
Stål, P
Werner, M
Swehep
Kechagias, S
AF Bergquist, Annika
Ekstedt, Mattias
Hagstrom, Hannes
Jarnerot, Gunnar
Lindgren, Stefan
Nilsson, Emma
Nyhlin, Nils
Rorsman, Fredrik
Stal, Per
Werner, Marten
Swehep, Stergios
Kechagias, Stergios
TI Forty years of successful national research collaboration in liver
disease - the Swedish experience
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Primary sclerosing cholangitis; primary biliary cholangitis; autoimmune
hepatitis; cirrhosis; liver steatosis
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
TERM-FOLLOW-UP; AUTOIMMUNE HEPATITIS; HEREDITARY HEMOCHROMATOSIS;
EXTRAHEPATIC MALIGNANCIES; HEPATOCELLULAR-CARCINOMA; URSODEOXYCHOLIC
ACID; NATURAL-HISTORY; CANCER-RISK
AB AimSweden has historically provided a fruitful arena for research in clinical medicine. We here share 40 years of experience of collaboration in the Swedish hepatology research group (SWEHEP) (https://www.swehep.se).MethodsWe describe the way the Swedish hepatology pioneers started the group and how the network continuously developed over the years. Successful projects such as thorough studies of natural history and various clinical aspects of autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis, and steatosis are described.ResultsOver the years, more than 80 publications have been published by the group. A summary of new and ongoing research programs includes the randomized placebo-controlled trial of simvastatin in PSC (PiSCATIN), the prospective BIGMAP (Biochemical and genetic markers for the assessment and prognostication of liver cirrhosis) initiative in patients with liver cirrhosis, and the DETECT-HCC, a prospective multicenter cohort study comparing abbreviated MRI and ultrasound for surveillance of hepatocellular carcinoma every six months over two years. The group philosophy, success factors for the longstanding collaboration as well as experience of failures are shared.ConclusionThe success of hepatology research in Sweden is based on longstanding collaboration over generations of hepatologists, where everyone contributes, regular research meetings, mutual trust, and perseverance.
C1 [Bergquist, Annika; Hagstrom, Hannes; Stal, Per] Karolinska Inst, Karolinska Univ Hosp, Dept Med Huddinge, Div Hepatol,Dept Upper Gastrointestinal Dis, Stockholm, Sweden.
[Ekstedt, Mattias; Swehep, Stergios; Kechagias, Stergios] Linkoping Univ, Dept Hlth Med & Caring Sci, Linkoping, Sweden.
[Ekstedt, Mattias; Kechagias, Stergios] Univ Hosp, Dept Gastroenterol & Hepatol, Linkoping, Sweden.
[Jarnerot, Gunnar; Nyhlin, Nils] Orebro Univ Hosp, Dept Med, Div Gastroenterol, Orebro, Sweden.
[Lindgren, Stefan; Nilsson, Emma] Lund Univ, Skane Univ Hosp, Dept Gastroenterol, Lund, Sweden.
[Rorsman, Fredrik] Uppsala Univ Hosp, Dept Gastroenterol & Hepatol, Uppsala, Sweden.
[Werner, Marten] Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden.
C3 Karolinska Institutet; Karolinska University Hospital; Linkoping
University; Orebro University; Lund University; Skane University
Hospital; Uppsala University; Uppsala University Hospital; Umea
University
RP Bergquist, A (corresponding author), Karolinska Inst, Karolinska Univ Hosp, Dept Med Huddinge, Div Hepatol,Dept Upper Gastrointestinal Dis, Stockholm, Sweden.
EM Annika.Bergquist@ki.se
RI Stål, Per/J-2154-2019; Ekstedt, Mattias/AAP-9770-2020; Hagström,
Hannes/I-2036-2019
OI Stal, Per/0000-0003-2915-1964; Hagstrom, Hannes/0000-0002-8474-1759;
Rorsman, Fredrik/0000-0003-4023-9617; Ekstedt,
Mattias/0000-0002-5590-8601
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NR 44
TC 0
Z9 0
U1 1
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD DEC 1
PY 2024
VL 59
IS 12
BP 1314
EP 1321
DI 10.1080/00365521.2024.2421824
EA NOV 2024
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA N4Z4Y
UT WOS:001347003600001
PM 39485016
OA hybrid
DA 2025-01-07
ER
PT J
AU Pinter, M
Scheiner, B
Peck-Radosavljevic, M
AF Pinter, Matthias
Scheiner, Bernhard
Peck-Radosavljevic, Markus
TI Immunotherapy for advanced hepatocellular carcinoma: a focus on special
subgroups
SO GUT
LA English
DT Article
ID FATTY LIVER-DISEASE; PREEXISTING AUTOIMMUNE-DISEASE; CHECKPOINT
INHIBITOR THERAPY; INFLAMMATORY-BOWEL-DISEASE; DOUBLE-BLIND; PHASE-III;
ADVANCED MELANOMA; RISK-FACTORS; CANCER; BEVACIZUMAB
AB Following the success of immune checkpoint blockers (ICBs) in different cancer types, a large number of studies are currently investigating ICBs in patients with hepatocellular carcinoma (HCC), alone or in combination with other treatments. Both nivolumab and pembrolizumab, as well as the combination of nivolumab plus ipilimumab have been granted accelerated approval by the United States Food and Drug Administration for sorafenib-pretreated patients. While nivolumab and pembrolizumab both failed to meet their primary endpoints in phase III trials, the combination of atezolizumab plus bevacizumab eventually improved overall and progression-free survival compared with sorafenib in a front-line phase III trial, and thus, will become the new standard of care in this setting. Despite this breakthrough, there are patient populations with certain underlying conditions that may not be ideal candidates for this new treatment either due to safety concerns or potential lack of efficacy. In this review, we discuss the safety of ICBs in patients with pre-existing autoimmune disease, IBD or a history of solid organ transplantation. Moreover, we summarise emerging preclinical and clinical data suggesting that ICBs may be less efficacious in patients with underlying non-alcoholic steatohepatitis or HCCs with activated Wnt/beta-catenin signalling.
C1 [Pinter, Matthias; Scheiner, Bernhard] Med Univ Vienna, Dept Internal Med 3, Div Gastroenterol & Hepatol, A-1090 Vienna, Austria.
[Pinter, Matthias; Scheiner, Bernhard] Med Univ Vienna, Liver Canc HCC Study Grp Vienna, Vienna, Austria.
[Peck-Radosavljevic, Markus] Klinikum Klagenfurt Worthersee, Dept Internal Med & Gastroenterol IMuG, Hepatol Endocrinol Rheumatol & Nephrol Including, Klagenfurt, Karnten, Austria.
C3 Medical University of Vienna; Medical University of Vienna
RP Pinter, M (corresponding author), Med Univ Vienna, Dept Internal Med 3, Div Gastroenterol & Hepatol, A-1090 Vienna, Austria.
EM matthias.pinter@meduniwien.ac.at
OI Scheiner, Bernhard/0000-0002-4904-5133; Pinter,
Matthias/0000-0002-7260-532X
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NR 91
TC 168
Z9 178
U1 6
U2 52
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD JAN
PY 2021
VL 70
IS 1
BP 204
EP 214
DI 10.1136/gutjnl-2020-321702
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA PR5UI
UT WOS:000607301000023
PM 32747413
OA Green Published, hybrid
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Zhao, MM
Ying, LX
Wang, RS
Yao, JP
Zhu, LM
Zheng, M
Chen, Z
Yang, ZG
AF Zhao, Miaomiao
Ying, Lixiong
Wang, Rusha
Yao, Jiping
Zhu, Liming
Zheng, Min
Chen, Zhi
Yang, Zhenggang
TI DHX15 Inhibits Autophagy and the Proliferation of Hepatoma Cells
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE DEAH-box helicase 15; RNA helicase; autophagy; mTORC1; HCC cells
AB Autophagy is a highly conserved process by which superfluous or harmful components in eukaryotic cells are degraded by autophagosomes. This cytoprotective mechanism is strongly related to various human diseases, such as cancer, autoimmune diseases, and diabetes. DEAH-box helicase 15 (DHX15), a member of the DEAH box family, is mainly involved in RNA splicing and ribosome maturation. Recently, DHX15 was identified as a tumor-related factor. Although both autophagy and DHX15 are involved in cellular metabolism and cancer progression, their exact relationship and mechanism remain elusive. In this study, we discovered a non-classic function of DHX15 and identified DHX15 as a suppressive protein in autophagy for the first time. We further found that mTORC1 is involved in DHX15-mediated regulation of autophagy and that DHX15 inhibits proliferation of hepatocellular carcinoma (HCC) cells by suppressing autophagy. In conclusion, our study demonstrates a non-classical function of DHX15 as a negative regulator of autophagy related to the mTORC1 pathway and reveals that DHX15-related autophagy dysfunction promotes HCC cell proliferation, indicating that DHX15 may be a target for liver cancer treatment.
C1 [Zhao, Miaomiao; Wang, Rusha; Yao, Jiping; Zheng, Min; Chen, Zhi; Yang, Zhenggang] Zhejiang Univ, State Key Lab Diag & Treatment Infect Dis, Coll Med, Affiliated Hosp 1, Hangzhou, Peoples R China.
[Zhao, Miaomiao; Wang, Rusha; Yao, Jiping; Zheng, Min; Chen, Zhi; Yang, Zhenggang] Collaborat Innovat Ctr Diag & Treatment Infect Di, Hangzhou, Peoples R China.
[Ying, Lixiong] Zhejiang Univ, Affiliated Hosp 1, Dept Pathol, Coll Med, Hangzhou, Peoples R China.
[Zhu, Liming] Zhejiang Canc Hosp, Dept Chemotherapy, Hangzhou, Peoples R China.
C3 Zhejiang University; Collaborative Innovation Center for Diagnosis &
Treatment of Infectious Diseases; Zhejiang University; Zhejiang Cancer
Hospital
RP Yang, ZG (corresponding author), Zhejiang Univ, State Key Lab Diag & Treatment Infect Dis, Coll Med, Affiliated Hosp 1, Hangzhou, Peoples R China.; Yang, ZG (corresponding author), Collaborat Innovat Ctr Diag & Treatment Infect Di, Hangzhou, Peoples R China.
EM yangzg@zju.edu.cn
RI Zheng, Mingyue/HHZ-4062-2022
FU States S&T Projects of the 13th Five Year Plan [2018ZX10302206];
National Key Research and Development Program [2017YFA0503402]; Zhejiang
Provincial Medicine and Health Science Fund [2015KYA031]; Independent
Project Fund of the State Key Laboratory for Diagnosis and Treatment of
Infectious Disease
FX This work was supported by the States S&T Projects of the 13th Five Year
Plan (2018ZX10302206), the National Key Research and Development Program
(2017YFA0503402), and Zhejiang Provincial Medicine and Health Science
Fund (2015KYA031). Independent Project Fund of the State Key Laboratory
for Diagnosis and Treatment of Infectious Disease.
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TC 6
Z9 6
U1 3
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD FEB 11
PY 2021
VL 7
AR 591736
DI 10.3389/fmed.2020.591736
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA QL8ZB
UT WOS:000621368100001
PM 33644083
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Prasad, D
Nguyen, MH
AF Prasad, Debi
Nguyen, Mindie H.
TI Epidemiology, pathogenesis, diagnosis, surveillance, and management of
hepatocellular carcinoma associated with vascular liver disease
SO KAOHSIUNG JOURNAL OF MEDICAL SCIENCES
LA English
DT Review
DE Budd– Chiari syndrome; congenital Porto‐ systemic shunts;
focal nodular hyperplasia; Fontan‐ associated liver disease;
hereditary Haemorrhagic telangiectasia
AB Vascular liver disease (VLD) presents special challenges in the diagnosis, surveillance, and treatment of hepatocellular carcinoma (HCC). HCC arising in the setting of vascular liver disease is often thought to be due to elevated hepatic arterial blood flow, rather than progressive fibrosis from chronic inflammation as with other chronic liver conditions such as viral hepatitis, autoimmune, and metabolic liver diseases. Vascular alteration inherent in VLD often impedes HCC non-invasive diagnosis and loco-regional treatment that depend on vascular properties found in typical liver environment. Benign and pre-malignant liver nodules such as focal nodular hyperplasia and hepatocellular adenoma are also more common in certain VLDs, further adding to surveillance and diagnostic challenges. In this synopsis, we aimed to review available literature on the epidemiology, surveillance, diagnosis, and management of HCC in patients with VLD and specifically Budd-Chiari syndrome, congenital porto-systemic shunts, Fontan-associated liver disease, hereditary hemorrhagic telangiectasia.
C1 [Prasad, Debi] Univ Auckland, Fac Med & Hlth Sci, Auckland, New Zealand.
[Nguyen, Mindie H.] Stanford Univ, Med Ctr, Div Gastroenterol & Hepatol, Palo Alto, CA 94304 USA.
[Nguyen, Mindie H.] Stanford Univ, Med Ctr, Dept Epidemiol & Populat Hlth, Palo Alto, CA 94304 USA.
C3 University of Auckland; Stanford University; Stanford University
RP Nguyen, MH (corresponding author), Stanford Univ, Med Ctr, Med, Epidemiol & Populat Hlth,Gastroenterol Hepatol &, 780 Welch Rd, Palo Alto, CA 94304 USA.
EM mindiehn@stanford.edu
OI Prasad, Debi/0000-0002-1618-2828
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NR 52
TC 5
Z9 5
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1607-551X
EI 2410-8650
J9 KAOHSIUNG J MED SCI
JI Kaohsiung J. Med. Sci.
PD MAY
PY 2021
VL 37
IS 5
BP 355
EP 360
DI 10.1002/kjm2.12368
EA MAR 2021
PG 6
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA SD0LG
UT WOS:000624492600001
PM 33655707
OA gold
DA 2025-01-07
ER
PT J
AU Chandrasekaran, KR
Aftab, S
Al Jajeh, I
Kumar, R
AF Chandrasekaran, Kalki Rajamanickam
Aftab, Syed
Al Jajeh, Issam
Kumar, Rajneesh
TI A Case of Inflammatory Pseudotumour Masquerading as Hepatocellular
Carcinoma
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE igg4 related disease; tumour markers; autoimmune hepatitis;
hepatocellular carcinoma; inflammatory pseudotumour
ID LIVER
AB Inflammatory pseudotumors (IPTs) of the liver can mimic malignant lesions. As the name implies, they are usually associated with an inflammatory process and usually regress with the treatment of the underlying pathology. We report a case of a 67-year-old female who presented with right upper quadrant pain, deranged liver enzymes, elevated tumor markers [alpha-fetoprotein (AFP) and CA 19-9], and a large liver mass on imaging, suspected to be hepatocellular carcinoma (HCC). She was eventually diagnosed with IPT complicating the liver inflammation due to autoimmune hepatitis (AIH). She responded well to treatment with steroids and immunosuppressive therapy.
C1 [Chandrasekaran, Kalki Rajamanickam] Sengkang Gen Hosp, Gastroenterol & Hepatol, Singapore, Singapore.
[Aftab, Syed] Sengkang Gen Hosp, Diag Radiol, Singapore, Singapore.
[Al Jajeh, Issam] Sengkang Gen Hosp, Pathol, Singapore, Singapore.
[Kumar, Rajneesh] Singapore Gen Hosp, Gastroenterol & Hepatol, Singapore, Singapore.
C3 Singapore General Hospital
RP Chandrasekaran, KR (corresponding author), Sengkang Gen Hosp, Gastroenterol & Hepatol, Singapore, Singapore.
EM kalki.rajamanickam.c@singhealth.com.sg
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NR 17
TC 0
Z9 0
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD SEP 25
PY 2023
VL 15
IS 9
AR e45897
DI 10.7759/cureus.45897
PG 7
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA W0WH9
UT WOS:001088914900014
PM 37753063
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Kubo, S
Oba, K
Hirohashi, K
Tanaka, H
Shuto, T
Takemura, S
Yamamoto, T
Tamori, A
Enomoto, M
Nishiguchi, S
AF Kubo, S
Oba, K
Hirohashi, K
Tanaka, H
Shuto, T
Takemura, S
Yamamoto, T
Tamori, A
Enomoto, M
Nishiguchi, S
TI Alcohol abuse as an etiologic factor for hepatocellular carcinoma in
Japan
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE hepatocellular carcinoma; alcoholic liver disease; hepatic fibrosis;
hepatitis virus; hepatitis B x gene
ID HEPATITIS-B-VIRUS; CIGARETTE-SMOKING; SURFACE-ANTIGEN; RISK-FACTORS;
HIGH PREVALENCE; LIVER-DISEASE; INFECTION; CANCER; DNA; CONSUMPTION
AB The etiologic role of alcoholic liver disease for hepatocellular carcinoma is uncertain. To assess the role of alcoholic liver disease on the development of carcinoma, we examined history of alcohol abuse and viral markers in the sera and/or resected specimens in 454 patients who underwent liver resection for hepatocellular carcinoma. Sera from 20 of the 454 patients were negative for hepatitis B, C, and D viruses. Of the 20 patients, one patient had autoimmune hepatitis, one had primary biliary cirrhosis, two had non-alcoholic steatohepatitis. Of the remaining 16 patients, 8 patients were alcohol abusers and 5 of the 8 patients were heavy alcohol abusers. Hepatitis G virus was not detected in sera form the 16 patients. Although hepatitis B x gene was detected in the cancerous and/or non-cancerous tissues in all three alcohol abusers but not heavy abusers and in 5 of 6 non-alcohol abusers whose surgical specimens were available, the gene was detected in only one of the five heavy alcohol abusers. The five heavy alcohol abusers had advanced hepatic fibrosis and active hepatitis. Alcoholic liver disease with advanced hepatic fibrosis and active hepatitis is a possible cause for the development of hepatocellular carcinoma. (c) 2004 Elsevier B.V. All rights reserved.
C1 Osaka City Univ, Grad Sch Med, Dept Gastroenterol, Abeno Ku, Osaka 5458585, Japan.
Osaka City Univ, Grad Sch Med, Dept Hepatobiliary Pancreat Surg, Abeno Ku, Osaka 5458585, Japan.
Osaka City Univ, Grad Sch Med, Dept Hepatol, Abeno Ku, Osaka 5458585, Japan.
C3 Osaka Metropolitan University; Osaka Metropolitan University; Osaka
Metropolitan University
RP Osaka City Univ, Grad Sch Med, Dept Gastroenterol, Abeno Ku, 1-4-3 Asahimachi, Osaka 5458585, Japan.
EM m7696493@msic.med.osaka-cu.ac.jp
RI ENOMOTO, Masaru/I-3864-2019
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NR 50
TC 5
Z9 5
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD FEB
PY 2005
VL 31
IS 2
BP 73
EP 78
DI 10.1016/j.hepres.2004.09.008
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 916ZQ
UT WOS:000228425900003
PM 15716019
DA 2025-01-07
ER
PT J
AU Zhang, XX
Wang, LF
Jin, L
Li, YY
Hao, SL
Shi, YC
Zeng, QL
Li, ZW
Zhang, Z
Lau, GKK
Wang, FS
AF Zhang, Xue-Xiu
Wang, Li-Feng
Jin, Lei
Li, Yuan-Yuan
Hao, Shu-Li
Shi, Yan-Chao
Zeng, Qing-Lei
Li, Zhi-Wei
Zhang, Zheng
Lau, George K. K.
Wang, Fu-Sheng
TI Primary biliary cirrhosis-associated hepatocellular carcinoma in Chinese
patients: Incidence and risk factors
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Primary biliary cirrhosis; Hepatocellular carcinoma; Body mass index;
History of alcohol intake; Case-control study
ID CHRONIC HEPATITIS-B; Y-CHROMOSOME; CANCER-RISK; EXTRAHEPATIC
MALIGNANCIES; URSODEOXYCHOLIC ACID; AUTOIMMUNE HEPATITIS; PROSPECTIVE
COHORT; GENDER DISPARITY; LIVER-DISEASE; POOR SURVIVAL
AB AIM: To investigate the incidence, characteristics, and risk factors for hepatocellular carcinoma (HCC) in Chinese patients with primary biliary cirrhosis (PBC).
METHODS: We reviewed the data of 52 PBC-associated HCC patients treated at Beijing 302 Hospital from January 2002 to December 2013 and analyzed its incidence and characteristics between the two genders. The risk factors for PBC-associated HCC were analyzed via a case-control study comprising 20 PBC patients with HCC and 77 matched controls without HCC. The matched factors included gender, age, follow-up period and Child-Pugh scores. Conditional logistic regression was used to evaluate the odds ratios of potential risk factors for HCC development. A P < 0.05 was considered statistically significant.
RESULTS: The incidence of HCC in Chinese PBC patients was 4.13% (52/1255) and was significantly higher in the males (9.52%) than in the females (3.31%). Among the 52 PBC patients with HCC, 55.76% (29/52) were diagnosed with HCC and PBC simultaneously, and 5.76% (3/52) were diagnosed with HCC before PBC. The males with PBC-associated HCC were more likely than the females to have undergone blood transfusion (18.75% vs 8.33%, P = 0.043), consumed alcohol (31.25% vs 8.33%, P = 0.010), smoked (31.25% vs 8.33%, P = 0.010), had a family history of malignancy (25% vs 5.56%, P = 0.012), and had serious liver inflammation, as indicated by the elevated levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma-glutamyl transpeptidase ( P < 0.05). Conditional logistic regression analysis revealed that body mass index (BMI) = 25 [ adjusted odds ratio (AOR) = 1.116, 95%CI: 1.002-1.244, P = 0.045] and history of alcohol intake (AOR = 10.294, 95%CI: 1.108-95.680, P = 0.040) were significantly associated with increased odds of HCC development in PBC patients.
CONCLUSION: HCC is not rare in Chinese PBC patients. Risk factors for PBC-associated HCC include BMI = 25 and a history of alcohol intake. In addition to regular monitoring, PBC patients may benefit from abstinence from alcohol and body weight control.
C1 [Zhang, Xue-Xiu; Zeng, Qing-Lei; Wang, Fu-Sheng] Peking Univ, Teaching Hosp, Mil Hosp China 302, Inst Translat Hepatol, Beijing 100039, Peoples R China.
[Wang, Li-Feng; Jin, Lei; Li, Yuan-Yuan; Zhang, Zheng; Lau, George K. K.; Wang, Fu-Sheng] Beijing 302 Hosp, Res Ctr Biol Therapy, Beijing 100039, Peoples R China.
[Hao, Shu-Li] Peking Univ, Teaching Hosp, Mil Hosp China 302, Noninfect Liver Dis Diag & Treatment Ctr, Beijing 100039, Peoples R China.
[Shi, Yan-Chao] Peking Univ, Teaching Hosp, Mil Hosp China 302, Res Ctr Liver Transplantat, Beijing 100039, Peoples R China.
[Li, Zhi-Wei] Beijing 302 Hosp, Dept Hepatobiliary Surg, Beijing 100039, Peoples R China.
C3 Peking University; Fifth Medical Center of Chinese PLA General Hospital;
Fifth Medical Center of Chinese PLA General Hospital; Peking University;
Fifth Medical Center of Chinese PLA General Hospital; Fifth Medical
Center of Chinese PLA General Hospital; Peking University; Fifth Medical
Center of Chinese PLA General Hospital
RP Wang, FS (corresponding author), Peking Univ, Teaching Hosp, Mil Hosp China 302, Inst Translat Hepatol, 100 Western 4th Middle Ring Rd, Beijing 100039, Peoples R China.
EM fswang302@163.com
RI Lau, George/AAQ-2085-2021; zhang, zheng/V-9479-2018; li,
yuanyuan/GZA-4435-2022; Zeng, Qing-Lei/ABD-6706-2020
OI Lau, George/0000-0002-8928-3769
FU National Natural Science Foundation of China [81470837, 81101589,
81302593]
FX Supported by National Natural Science Foundation of China, No. 81470837,
No. 81101589 and No. 81302593.
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NR 46
TC 30
Z9 32
U1 0
U2 13
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 28
PY 2015
VL 21
IS 12
BP 3554
EP 3563
DI 10.3748/wjg.v21.i12.3554
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CE5GG
UT WOS:000351858600012
PM 25834320
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU van der Veek, PPJ
Cappel, WHDTN
Langers, AJ
van Hoek, B
AF van der Veek, Patrick P. J.
Cappel, Wouter H. de Vos Tot Nederveen
Langers, AlexandraM. J.
van Hoek, Bart
TI Two Patients with Extremely Elevated Tumor Markers: Where Is the
Malignancy?
SO GASTROENTEROLOGY RESEARCH AND PRACTICE
LA English
DT Article
ID SERUM ALPHA-FETOPROTEIN; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
CA19-9; LEVEL
AB Serum tumor markers are useful to evaluate a cancer's response to treatment, for early detection of cancer relapse, and, in some cases, to diagnose malignancy. In this paper, we present two patients with significantly elevated serum tumor markers without evidence of malignant disease. An 18-year-old patient suffering from autoimmune hepatitis had markedly increased alpha-fetoprotein (aFP) levels (2,002 mu g/L; normal < 10 ug/L). Extensive imaging showed no signs of hepatocellular carcinoma or other cancer, and treatment with Prednisone led to rapid normalization of both liver enzymes and aFP. The second patient, a 60-year-old female with painless jaundice due to biliary stone disease, had very high serum levels of CA19-9 (18,000 kU/L, normal < 27 kU/L). Liver biochemistry and serum CA19-9 concentration decreased to almost normal values (45 kU/L) after biliary stenting. These cases demonstrate that serum tumor markers can be elevated in benign disease and are therefore not appropriate to diagnose cancer.
C1 [van der Veek, Patrick P. J.] Med Ctr Haaglanden, Dept Internal Med, NL-2501 CK The Hague, Netherlands.
[van der Veek, Patrick P. J.] Med Ctr Haaglanden, Dept Gastroenterol, NL-2501 CK The Hague, Netherlands.
[van der Veek, Patrick P. J.] Med Ctr Haaglanden, Dept Hepatol, NL-2501 CK The Hague, Netherlands.
[Cappel, Wouter H. de Vos Tot Nederveen] Isala Clin, Dept Gastroenterol & Hepatol, NL-8000 GM Zwolle, Netherlands.
[Langers, AlexandraM. J.; van Hoek, Bart] Leiden Univ, Dept Gastroenterol & Hepatol, Med Ctr, NL-2300 RC Leiden, Netherlands.
C3 Haaglanden Medical Center; Haaglanden Medical Center; Haaglanden Medical
Center; Isala Clinics; Leiden University - Excl LUMC; Leiden University;
Leiden University Medical Center (LUMC)
RP van der Veek, PPJ (corresponding author), Med Ctr Haaglanden, Dept Internal Med, POB 432, NL-2501 CK The Hague, Netherlands.
EM p.vanderveek@mchaaglanden.nl
RI van Hoek, Bart/AAU-8953-2020; Langers, Alexandra/AAV-9371-2020
OI van Hoek, Bart/0000-0001-6527-764X; Langers,
Alexandra/0000-0003-1627-4324
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NR 14
TC 9
Z9 9
U1 0
U2 0
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-6121
EI 1687-630X
J9 GASTROENT RES PRACT
JI Gastroenterol. Res. Pract.
PY 2011
VL 2011
AR 123743
DI 10.1155/2011/123743
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 802UJ
UT WOS:000293536200001
PM 21760772
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Nishida, N
Kudo, M
AF Nishida, Naoshi
Kudo, Masatoshi
TI Liver damage related to immune checkpoint inhibitors
SO HEPATOLOGY INTERNATIONAL
LA English
DT Review
DE Liver damage; Immune checkpoint inhibitors; Autoimmune hepatitis;
Hepatocellular carcinoma; Granuloma
ID HEPATOCELLULAR-CARCINOMA; COMBINED NIVOLUMAB; CANCER-PATIENTS;
IPILIMUMAB; MANAGEMENT; HEPATITIS; MICROENVIRONMENT; HEPATOTOXICITY;
COMBINATION; BLOCKADE
AB Recently, immune checkpoint inhibitors are becoming one of the key agents of systemic treatment of cancer. The anti-cancer mechanism of this type of agent is totally different from that of conventional therapies; blockade of regulatory receptors and ligand of immune checkpoint molecules arose anti-tumor immunity with durable response. However, owing to its unique action to host immune system, immune checkpoint inhibitors sometimes induce immune-related adverse events (irAEs) which has not been observed for conventional chemotherapies. It has been reported that irAEs are manageable by discontinuation of immune checkpoint inhibitors and corticosteroid. However, severe irAEs might lead to the unsuccessful management of cancer treatment. It is conceivable that irAEs during the treatment of immune checkpoint blockade might mimic the autoimmune disease of the specific organ, such as autoimmune hepatitis (AIH). However, detail of the pathogenesis of irAEs has not been well estimated. In this review, we specially focused on this important issue and discussed the liver toxicity of this type of agent in the context of comparison of clinical and pathological findings of liver damage related to irAEs and AIH.
C1 [Nishida, Naoshi; Kudo, Masatoshi] Kindai Univ, Fac Med, Dept Gastroenterol & Hepatol, 377-2 Ohno Higashi, Osaka 5898511, Japan.
C3 Kindai University (Kinki University)
RP Nishida, N (corresponding author), Kindai Univ, Fac Med, Dept Gastroenterol & Hepatol, 377-2 Ohno Higashi, Osaka 5898511, Japan.
EM naoshi@med.kindai.ac.jp
RI Kudo, Masatoshi/AAA-9744-2019; Naoshi, Nishida/O-2279-2014
OI Naoshi, Nishida/0000-0002-9111-5668
FU Japanese Society for the Promotion of Science [16K09382]; Smoking
Research Foundation
FX This work was supported in part by a Grant-in-Aid for Scientific
Research (KAKENHI: 16K09382) from the Japanese Society for the Promotion
of Science (N. Nishida) and a Grant from the Smoking Research Foundation
(N. Nishida).
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NR 46
TC 36
Z9 38
U1 2
U2 16
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1936-0533
EI 1936-0541
J9 HEPATOL INT
JI Hepatol. Int.
PD MAY
PY 2019
VL 13
IS 3
BP 248
EP 252
DI 10.1007/s12072-018-9921-7
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HZ3LR
UT WOS:000468750700002
PM 30607787
OA Bronze
DA 2025-01-07
ER
PT J
AU Shi, J
Li, X
Hu, Y
Zhang, F
Lv, X
Zhang, X
Chen, Q
Hu, S
AF Shi, J.
Li, X.
Hu, Y.
Zhang, F.
Lv, X.
Zhang, X.
Chen, Q.
Hu, S.
TI MiR-1203 is involved in hepatocellular carcinoma metastases and
indicates a poor prognosis
SO NEOPLASMA
LA English
DT Article
DE miRNA; metastasis; biomarker; HCC; SOCS3
ID EXPRESSION; CELLS; PROMOTES; PATHWAY; METHYLATION; INHIBITOR; MICRORNAS
AB Non-coding RNAs, especially miRNAs, have been shown to be important regulators in multiple human diseases, including malignant tumors, congenital disease, and autoimmune disease. In this study, we screened the metastasis-associated miRNAs in hepatocellular carcinoma (HCC). Based on the miRNA microarray screening, miR-1203 was confirmed to be the most significant miRNA and was also highly associated with HCC metastases. Bioinformatics prediction indicated direct binding of miR-1203 in SOCS3, which was also confirmed by a dual luciferase reporter assay, resulting in suppression of SOCS3. Increased miR-1203 also promoted invasion of HCC cells through suppressing SOCS3, while no effect on cell proliferation or apoptosis was detected. Circulating expression of miR-1203 and SO(S3 might serve as a predictor of metastases and poor prognosis in HCC patients. In conclusion, miR-1203 might promote HCC metastasis by decreasing SOCS3. MiR-1203 predicts a poor outcome in HCC patients and thus might serve as a potential therapeutic target for the prevention of HCC.
C1 [Shi, J.; Hu, S.] Shandong Univ, Shandong Prov Qianfoshan Hosp, Dept Gen Surg, Jinan 250014, Shandong, Peoples R China.
[Shi, J.; Zhang, F.; Lv, X.; Zhang, X.; Chen, Q.] Binzhou Med Univ Hosp, Dept Hepatobiliary Surg, Binzhou 256603, Peoples R China.
[Li, X.] Binzhou Med Univ Hosp, Dept Pediat, Binzhou, Peoples R China.
[Hu, Y.] Nanjing Med Univ, Changzhou Peoples Hosp 2, Dept Hepatobiliary & Pancreat Surg, Changzhou 213000, Peoples R China.
C3 Shandong University; Shandong First Medical University & Shandong
Academy of Medical Sciences; Binzhou Medical University; Binzhou Medical
University; Nanjing Medical University
RP Hu, S (corresponding author), Shandong Univ, Shandong Prov Qianfoshan Hosp, Dept Gen Surg, Jinan 250014, Shandong, Peoples R China.; Chen, Q (corresponding author), Binzhou Med Univ Hosp, Dept Hepatobiliary Surg, Binzhou 256603, Peoples R China.
EM hu_sanyuan@sina.com
FU University-Level Science and Technology Project of Binzhou Medical
University [BY2018KJ09]
FX This study was financed by University-Level Science and Technology
Project of Binzhou Medical University (BY2018KJ09).
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NR 36
TC 14
Z9 14
U1 0
U2 4
PU AEPRESS SRO
PI BRATISLAVA
PA BAJZOVA 7, BRATISLAVA, 821 08, SLOVAKIA
SN 0028-2685
EI 1338-4317
J9 NEOPLASMA
JI Neoplasma
PY 2020
VL 67
IS 2
BP 267
EP 276
DI 10.4149/neo_2019_190414N328
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MB5SY
UT WOS:000542663800006
PM 31847527
OA Bronze
DA 2025-01-07
ER
PT J
AU Albhaisi, SAM
Bajaj, JS
Sanyal, AJ
AF Albhaisi, Somaya A. M.
Bajaj, Jasmohan S.
Sanyal, Arun J.
TI Role of gut microbiota in liver disease
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Review
DE alcoholic hepatitis; bacteria; cirrhosis; gut microbiota; hepatocellular
cancer; intestinal microbiome; metagenomics; nonalcoholic fatty liver
disease; nonalcoholic steatohepatitis
ID PRIMARY SCLEROSING CHOLANGITIS; INCREASED INTESTINAL PERMEABILITY;
BILE-ACIDS; NONALCOHOLIC STEATOHEPATITIS; HEPATOCELLULAR-CARCINOMA;
BACTERIAL TRANSLOCATION; AUTOIMMUNE HEPATITIS; CIRRHOSIS; ENDOTOXEMIA;
DYSBIOSIS
AB The gut microbiome is the natural intestinal inhabitant that has been recognized recently as a major player in the maintenance of human health and the pathophysiology of many diseases. Those commensals produce metabolites that have various effects on host biological functions. Therefore, alterations in the normal composition or diversity of microbiome have been implicated in various diseases, including liver cirrhosis and nonalcoholic fatty liver disease. Moreover, accumulating evidence suggests that progression of dysbiosis can be associated with worsening of liver disease. Here, we review the possible roles for gut microbiota in the development, progression, and complication of liver disease.
C1 [Albhaisi, Somaya A. M.] Virginia Commonwealth Univ, Dept Internal Med, Richmond, VA USA.
[Bajaj, Jasmohan S.; Sanyal, Arun J.] Virginia Commonwealth Univ, Dept Internal Med, Div Gastroenterol Hepatol & Nutr, Richmond, VA USA.
[Bajaj, Jasmohan S.] McGuire Vet Affairs Med Ctr, Richmond, VA USA.
C3 Virginia Commonwealth University; Virginia Commonwealth University;
Hunter Holmes McGuire Veterinary Affairs Medical Center
RP Sanyal, AJ (corresponding author), MCV Box 980341, Richmond, VA 23298 USA.
EM arun.sanyal@vcuhealth.org
RI Albhaisi, Somaya/S-5392-2017
OI Albhaisi, Somaya/0000-0002-7500-4183
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NR 137
TC 86
Z9 90
U1 2
U2 47
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1857
EI 1522-1547
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD JAN
PY 2020
VL 318
IS 1
BP G84
EP G98
DI 10.1152/ajpgi.00118.2019
PG 15
WC Gastroenterology & Hepatology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Physiology
GA KC7ST
UT WOS:000507373700009
PM 31657225
OA Bronze
DA 2025-01-07
ER
PT J
AU Wang, XF
Tian, ZG
AF Wang, Xuefu
Tian, Zhigang
TI γδ T cells in liver diseases
SO FRONTIERS OF MEDICINE
LA English
DT Review
DE gamma delta T cells; liver infection; non-alcoholic fatty liver disease;
autoimmune hepatitis; liver fibrosis and cirrhosis; liver cancer; liver
regeneration
ID HEPATITIS-B-VIRUS; PRIMARY SCLEROSING CHOLANGITIS;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; PERIPHERAL-BLOOD; IMMUNE
TOLERANCE; ALPHA-BETA; MICE; RECEPTOR; INFECTION
AB gamma delta T cells display unique developmental, distributional, and functional patterns and can rapidly respond to various insults and contribute to diverse diseases. Different subtypes of gamma delta T cells are produced in the thymus prior to their migration to peripheral tissues. gamma delta T cells are enriched in the liver and exhibit liver-specific features. Accumulating evidence reveals that gamma delta T cells play important roles in liver infection, non-alcoholic fatty liver disease, autoimmune hepatitis, liver fibrosis and cirrhosis, and liver cancer and regeneration. In this study, we review the properties of hepatic gamma delta T cells and summarize the roles of gamma delta T cells in liver diseases. We believe that determining the properties and functions of gamma delta T cells in liver diseases enhances our understanding of the pathogenesis of liver diseases and is useful for the design of novel gamma delta T cell-based therapeutic regimens for liver diseases.
C1 [Wang, Xuefu] Anhui Med Univ, Sch Pharm, Hefei 230032, Anhui, Peoples R China.
[Tian, Zhigang] Univ Sci & Technol China, Inst Immunol, Sch Life Sci, Hefei 230027, Anhui, Peoples R China.
[Tian, Zhigang] Univ Sci & Technol China, CAS Key Lab Innate Immun & Chron Dis, Sch Life Sci, Hefei 230027, Anhui, Peoples R China.
[Tian, Zhigang] Univ Sci & Technol China, Med Ctr, Hefei 230027, Anhui, Peoples R China.
[Tian, Zhigang] Zhejiang Univ, Collaborat Innovat Ctr Diag & Treatment Infect Di, State Key Lab Diag & Treatment Infect Dis, Affiliated Hosp 1,Coll Med, Hangzhou 310003, Zhejiang, Peoples R China.
C3 Anhui Medical University; Chinese Academy of Sciences; University of
Science & Technology of China, CAS; Chinese Academy of Sciences;
University of Science & Technology of China, CAS; Chinese Academy of
Sciences; University of Science & Technology of China, CAS;
Collaborative Innovation Center for Diagnosis & Treatment of Infectious
Diseases; Zhejiang University
RP Wang, XF (corresponding author), Anhui Med Univ, Sch Pharm, Hefei 230032, Anhui, Peoples R China.
EM wangxuefu@ustc.edu.cn
RI xuefu, wang/HPE-2143-2023; Tian, Zhigang/J-3512-2013
OI Wang, Xuefu/0000-0001-7212-7156
FU Anhui Natural Science Foundation [1708085QH183]; Natural Science
Foundation of China [81302863, 31390433, 91542000]; Ministry of Science
and Technology of China (973 Program) [2013CB944902]
FX This work was supported by the Anhui Natural Science Foundation (No.
1708085QH183), Natural Science Foundation of China (Nos. 81302863,
31390433, and 91542000), and the Ministry of Science and Technology of
China (973 Program, No. 2013CB944902).
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NR 70
TC 28
Z9 32
U1 2
U2 25
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 2095-0217
EI 2095-0225
J9 FRONT MED-PRC
JI Front. Med.
PD JUN
PY 2018
VL 12
IS 3
BP 262
EP 268
DI 10.1007/s11684-017-0584-x
PG 7
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GF9ZB
UT WOS:000432336500003
PM 29441440
DA 2025-01-07
ER
PT J
AU Hernandez, N
Bessone, F
AF Hernandez, Nelia
Bessone, Fernando
TI Hepatotoxicity Induced by Biological Agents: Clinical Features and
Current Controversies
SO JOURNAL OF CLINICAL AND TRANSLATIONAL HEPATOLOGY
LA English
DT Review
DE Hepatotoxicity; Checkpoint inhibitors; Biologics; Autoimmune hepatitis;
Drug-induced liver injury
ID INDUCED LIVER-INJURY; NIVOLUMAB-RELATED CHOLANGITIS; B-VIRUS
REACTIVATION; AUTOIMMUNE HEPATITIS; CANCER-PATIENTS; IPILIMUMAB;
MANAGEMENT; DIAGNOSIS; THERAPY
AB Novel biological agents including cytokines and recombinant fusion proteins are increasingly prescribed for cancer, rheumatologic, autoimmune, and inflammatory diseases, and are currently being evaluated in hepatocellular carcinoma (HCC). They are classified by their mechanism of action and include tumor necrosis factor-alpha (TNF-alpha) antagonists, T cell mediated antitumor inhibitors, interleukin receptor antagonists, and immune checkpoint inhibitors (ICIs). Some ICIs cause frequent hepatotoxicity with a variable clinical, biochemical, and serological presentation, especially in patients receiving another immunomodulatory agent. Half of the cases of liver damage induced by biological agents spontaneously regress after drug withdrawal, but the others require steroid therapy. Unfortunately, there are no widely accepted recommendation for the use of corticosteroids in these patients, even though international cancer societies have their own guidelines. Differentiating drug-induced autoimmune hepatitis (DIAIH) from classic AIH is challenging for pathologists, but liver biopsy is valuable, particularly in cases with unclear clinical presentation. Interesting, novel histological patterns have been described in liver damage induced by these agents (i.e., endothelitis, ring granuloma and secundary sclerosing cholangitis associated with lymphocytic infiltration of cytotoxic CD8+T cells). Here, we describe the clinical and biochemical characteristics of patients with hepatotoxicity induced by TNF-alpha antagonists and ICIs. Controversial issues involved in the administration of corticosteroid therapy, and hepatitis B virus (HBV) reactivation induced by immunosuppressive therapy are also discussed.
C1 [Hernandez, Nelia] Univ Republica, Hosp Clin, Montevideo, Uruguay.
[Bessone, Fernando] Univ Rosario, Sch Med, Hosp Prov Centenario, Rosario, Argentina.
C3 Universidad de la Republica, Uruguay; National University of Rosario
RP Bessone, F (corresponding author), Univ Rosario, Sch Med, Fac Ciencias Med, Hosp Prov Centenario, Rosario, Argentina.
EM bessonefernando@gmail.com
RI hernandez, nelia/GLQ-6250-2022
OI bessone, fernando/0000-0002-8569-8123
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NR 71
TC 10
Z9 13
U1 0
U2 4
PU XIA & HE PUBLISHING INC
PI SUGAR LAND
PA SECOND AFFILIATED HOSP CHONGQING MEDICAL UNIV, 14090 SOUTHWEST FREEWAY,
STE 300, SUGAR LAND, TX 77478 USA
SN 2225-0719
EI 2310-8819
J9 J CLIN TRANSL HEPATO
JI J. Clin. Transl. Hepatol.
PD MAY-JUN
PY 2022
VL 10
IS 3
BP 486
EP 495
DI 10.14218/JCTH.2021.00243
EA JAN 2022
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA F6KU5
UT WOS:000792955900001
PM 35836762
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhang, QX
Li, SL
Yao, YQ
Li, TJ
AF Zhang, Q. X.
Li, S. L.
Yao, Y. Q.
Li, T. J.
TI Association between interleukin-21 gene polymorphisms (rs12508721) and
HBV-related hepatocellular carcinoma
SO INTERNATIONAL JOURNAL OF IMMUNOGENETICS
LA English
DT Article
ID CHRONIC HEPATITIS-B; CANCER; IL-21; INFECTION; LIVER; EXPRESSION;
IMMUNITY; RISK
AB Interleukin-21 (IL-21), as a multifunctional cytokine, plays an important role in many diseases, such as cancer, inflammatory and autoimmune diseases. We aimed to investigate the relationship between polymorphisms of IL-21 gene and susceptibility of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) in a Chinese population. Studied subjects were divided into three groups: 100 patients with HBV-related HCC, 115 patients with chronic HBV infection and 127 healthy controls. Genomic DNA was isolated from peripheral blood, and the polymerase chain reaction-ligase detection reaction (PCR-LDR) method was used to genotype the SNPs (rs2221903, rs907715 and rs12508721) within IL-21 gene. Our results showed that IL-21 polymorphisms were associated with the risk of HCC and chronic HBV infection when compared with healthy controls. The rs2221903A/G AG genotype was associated with a higher risk of chronic HBV infection when compared with healthy controls [AG versus AA + GG, P = 0.036, OR = 1.898, 95% CI = 1.038-3.471]. The rs12508721C/T TT genotype was related with a lower risk of chronic HBV infection and HBV-related HCC than in healthy controls [TT versus CT + CC, P = 0.026, OR = 0.451, 95% CI = 0.221-0.920; P = 0.049, OR = 0.482, 95% CI = 0.231-1.005]. No significant difference in the genotype and allele distrubutions of rs907715G/A SNP was observed in the HBV-related HCC group, chronic HBV-infected group and the healthy control group when compared to each other. Our findings suggest that the rs12508721T/C and rs2221903A/G polymorphisms of IL-21 gene are associated with the susceptibility of HBV-related HCC and chronic HBV infection. The genetic variant may in fact cause protection against the HBV-related HCC. However, the function in these SNPs of IL-21 gene needs to clarify the mechanisms involved in the pathogenesis of HBV-related HCC further.
C1 [Zhang, Q. X.; Yao, Y. Q.; Li, T. J.] Chongqing Med Univ, Affiliated Hosp 1, Dept Infect Dis, Chongqing, Peoples R China.
[Li, S. L.] Chongqing Med Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, Chongqing, Peoples R China.
C3 Chongqing Medical University; Chongqing Medical University
RP Yao, YQ (corresponding author), Youyi Rd 1, Chongqing 400000, Peoples R China.
EM yaoyunqing00@163.com
FU Chongqing Municipal Natural Science Foundation [20021889]; Medical
Science and Technology Fund of Chongqing Municipal Health Bureau
[07-2-062]
FX This work was supported by grants from the Chongqing Municipal Natural
Science Foundation (Grant No. 20021889) and Medical Science and
Technology Fund of Chongqing Municipal Health Bureau (Grant No.
07-2-062).
CR Chisari FV, 2000, AM J PATHOL, V156, P1117, DOI 10.1016/S0002-9440(10)64980-2
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NR 23
TC 12
Z9 12
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1744-3121
EI 1744-313X
J9 INT J IMMUNOGENET
JI Int. J. Immunogenet.
PD JUN
PY 2016
VL 43
IS 3
BP 151
EP 158
DI 10.1111/iji.12263
PG 8
WC Genetics & Heredity; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Immunology
GA DR5DB
UT WOS:000379922100005
PM 27122304
DA 2025-01-07
ER
PT J
AU Sangro, B
Chan, SL
Meyer, T
Reig, M
El-Khoueiry, A
Galle, PR
AF Sangro, Bruno
Chan, Stephen L.
Meyer, Tim
Reig, Maria
El-Khoueiry, Anthony
Galle, Peter R.
TI Diagnosis and management of toxicities of immune checkpoint inhibitors
in hepatocellular carcinoma
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Immunotherapy; Nivolumab; Pembrolizumab; Tremelimumab; Durvalumab;
Ipilimumab; Hepatotoxicity
ID HEPATITIS-B-VIRUS; INTESTINAL BACTERIAL OVERGROWTH; T-CELL RESPONSES;
ADVERSE EVENTS; EXTRAHEPATIC MANIFESTATIONS; HEPATOPULMONARY SYNDROME;
CLINICAL-FEATURES; NIVOLUMAB NIVO; DOUBLE-BLIND; PHASE-III
AB Immune checkpoint inhibitors (ICIs) have reshaped cancer therapy. ICIs enhance T cell activation through various mechanisms and may help reverse the exhausted phenotype of tumour-infiltrating lymphocytes. However, disrupting the key role that checkpoint molecules play in immune homeostasis may result in autoimmune complications. A broad range of immune-related adverse events (irAEs) involve almost every organ but mostly affect the skin, digestive system, lung, endocrine glands, nervous system, kidney, blood cells, and musculoskeletal system. They are usually manageable but can be life-threatening. The incidence of irAEs is not very different in patients with hepatocellular carcinoma (HCC) compared to other tumour types, although there is a trend towards a higher incidence of hepatic irAEs. HCC usually develops on a background of cirrhosis with associated systemic manifestations. Extrahepatic organ dysfunction in cirrhosis may cause signs and symptoms that overlap with irAEs or increase their severity. Available guidelines for the management of irAEs have not specifically considered the assessment of toxicities in the context of patients with liver cancer and cirrhosis. This review addresses the toxicity profile of ICIs in patients with HCC, focusing on the challenges that the underlying liver disease poses to their diagnosis and management. Challenges include late recognition, inadequate work-up and delayed treatment, overdiagnosis and inappropriate interruption of ICIs, complications caused by immunosuppressive therapy, and increased cost. A specific algorithm for the management of hepatic irAEs is provided. (C) 2019 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Sangro, Bruno] Clin Univ Navarra IDISNA, Liver Unit, Avda Pio XII 36, Pamplona 31008, Spain.
[Sangro, Bruno] CIBEREHD, Avda Pio XII 36, Pamplona 31008, Spain.
[Chan, Stephen L.] Dept Clin Oncol, State Key Lab Translat Oncol, Hong Kong, Peoples R China.
[Chan, Stephen L.] Chinese Univ Hong Kong, Sir YK Pao Ctr Canc, Inst Digest Dis, Hong Kong, Peoples R China.
[Meyer, Tim] Royal Free London NHS Fdn Trust & UCL Canc Inst, London, England.
[Reig, Maria] Univ Barcelona, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Barcelona Clin Liver Canc Grp, Liver Unit,Hosp Clin,IDIBAPS, Barcelona, Spain.
[El-Khoueiry, Anthony] Univ Southern Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA 90007 USA.
[Galle, Peter R.] Univ Med Ctr, Med Dept 1, Mainz, Germany.
C3 University of Navarra; CIBER - Centro de Investigacion Biomedica en Red;
CIBEREHD; Chinese University of Hong Kong; CIBER - Centro de
Investigacion Biomedica en Red; CIBEREHD; University of Barcelona;
Hospital Clinic de Barcelona; IDIBAPS; University of Southern
California; Johannes Gutenberg University of Mainz
RP Sangro, B (corresponding author), Clin Univ Navarra IDISNA, Liver Unit, Avda Pio XII 36, Pamplona 31008, Spain.; Sangro, B (corresponding author), CIBEREHD, Avda Pio XII 36, Pamplona 31008, Spain.
EM bsangro@unav.es
RI Galle, Peter/ABE-2872-2021; Chan, Stephen/F-9149-2011; Sangro,
Bruno/AFW-4106-2022; Reig, Maria/ABB-5414-2021
OI Galle, Peter/0000-0003-1967-0621; Reig, Maria/0000-0002-5711-9534;
Meyer, Tim/0000-0003-0782-8647; Sangro, Bruno/0000-0002-4177-6417;
Galle, Peter Robert/0000-0001-8294-0992
FU NIHR University College London Hospitals Biomedical Research Centre,
London, UK
FX TM is part funded by the NIHR University College London Hospitals
Biomedical Research Centre, London, UK.
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NR 122
TC 180
Z9 191
U1 6
U2 36
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD FEB
PY 2020
VL 72
IS 2
SI SI
BP 320
EP 341
DI 10.1016/j.jhep.2019.10.021
PG 22
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA KC8ZV
UT WOS:000507461400010
PM 31954495
OA Green Submitted, Bronze, Green Accepted
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Gufler, S
Seeboeck, R
Schatz, C
Haybaeck, J
AF Gufler, Sabine
Seeboeck, Rita
Schatz, Christoph
Haybaeck, Johannes
TI The Translational Bridge between Inflammation and Hepatocarcinogenesis
SO CELLS
LA English
DT Article
DE acute hepatitis; chronic hepatitis; hepatitis virus; alcoholic liver
disease (ALD); non-alcoholic fatty liver disease (NAFLD); cirrhosis;
steatosis; autoimmune hepatitis; hepatocellular carcinoma (HCC); mTOR
signaling; eukaryotic translation initiation factors (eIFs)
ID FATTY LIVER-DISEASE; CHRONIC VIRAL-HEPATITIS; NONALCOHOLIC
STEATOHEPATITIS; UNITED-STATES; NATURAL-HISTORY; C VIRUS; EPIDEMIOLOGY;
PREVALENCE; TRANSPLANTATION; PATHOGENESIS
AB Viral infections or persistent alcohol or drug abuse, together with intrinsic factors, lead to hepatitis, which often ends in the development of liver cirrhosis or hepatocellular carcinoma (HCC). With this review, we describe inflammatory liver diseases, such as acute liver failure, virus-induced hepatitis, alcoholic- and non-alcoholic steatohepatitis, and autoimmune hepatitis, and highlight their driving mechanisms. These include external factors such as alcohol misuse, viral infection and supernutrition, as well as intrinsic parameters such as genetic disposition and failure, in immune tolerance. Additionally, we describe what is known about the translational machinery within all these diseases. Distinct eukaryotic translation initiation factors (eIFs) with specific functional roles and aberrant expression in HCC are reported. Many alterations to the translational machinery are already triggered in the precancerous lesions described in this review, highlighting mTOR pathway proteins and eIFs to emphasize their putative clinical relevance. Here, we identified a lack of knowledge regarding the roles of single eIF proteins. A closer investigation will help to understand and treat HCC as well as the antecedent diseases.
C1 [Gufler, Sabine; Schatz, Christoph; Haybaeck, Johannes] Med Univ Innsbruck, Inst Pathol Neuropathol & Mol Pathol, A-6020 Innsbruck, Austria.
[Seeboeck, Rita] Karl Landsteiner Univ Hlth Sci, Clin Inst Pathol, Univ Hosp St Poelten, A-3100 St Polten, Austria.
[Seeboeck, Rita] IMC Univ Appl Sci Krems, Dept Life Sci, A-3500 Krems, Austria.
[Haybaeck, Johannes] Med Univ Graz, Inst Pathol, Diagnost & Res Ctr Mol BioMed, A-8010 Graz, Austria.
C3 Medical University of Innsbruck; Medical University of Graz
RP Haybaeck, J (corresponding author), Med Univ Innsbruck, Inst Pathol Neuropathol & Mol Pathol, A-6020 Innsbruck, Austria.; Haybaeck, J (corresponding author), Med Univ Graz, Inst Pathol, Diagnost & Res Ctr Mol BioMed, A-8010 Graz, Austria.
EM sabine.gufler@i-med.ac.at; rita.seeboeck@stpoelten.lknoe.at;
christoph.schatz@i-med.ac.at; johannes.haybaeck@i-med.ac.at
OI Schatz, Christoph/0000-0001-8017-3400
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NR 124
TC 13
Z9 14
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD FEB
PY 2022
VL 11
IS 3
AR 533
DI 10.3390/cells11030533
PG 26
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA YY4ZZ
UT WOS:000754800600001
PM 35159342
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Younossi, ZM
Stepanova, M
Ong, J
Trimble, G
AlQahtani, S
Younossi, I
Ahmed, A
Racila, A
Henrys, L
AF Younossi, Zobair M.
Stepanova, Maria
Ong, Janus
Trimble, Greg
AlQahtani, Saleh
Younossi, Issah
Ahmed, Aijaz
Racila, Andrei
Henrys, Linda
TI Nonalcoholic Steatohepatitis Is the Most Rapidly Increasing Indication
for Liver Transplantation in the United States
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Liver cancer; Incidence; Time periods; Etiology
AB BACKGROUND & AIMS: The profile of chronic liver disease (CLD) in the United States has changed due to obesity trends and advances in treatment of viral hepatitis. We assessed liver transplant listing trends by CLD etiology.
METHODS: Adult candidates for liver transplantation were selected from the Scientific Registry of Transplant Recipients (2002 through 2019). We calculated proportion trends for common CLD etiologies at time of placement on the wait list, including chronic infection with hepatitis B virus, chronic infection with hepatitis C virus (HCV), nonalcoholic steatohepatitis (NASH, including cryptogenic cirrhosis), alcohol-related liver disease (ALD) without or with chronic HCV infection, autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis, in patients with and without hepatocellular carcinoma (HCC).
RESULTS: From the 168,441 patients with known etiology and non-acute liver failure on the liver transplant waitlist, 27,799 patients (16.5%) had HCC. In 2002, the most common etiologies in patients without HCC were chronic HCV infection (37%) and ALD (16%), whereas only 5% had NASH. Among patients with HCC, 58% had chronic HCV infection and 10% had ALD and only 1% had NASH. In 2019, among patients without HCC, NASH was the second leading indication for liver transplantation (28% of patients), after ALD (38% of patients). Among patients with HCC, chronic HCV infection remained the leading indication (40% of patients) but NASH (24% of patients) surpassed ALD (16% of patients) to become the second leading indication. NASH was the leading indication in women without HCC (34%), in patients older than 54 years (36%), and in patients on Medicare (41%). In trend analysis, NASH was the most rapidly increasing indication for liver transplantation in patients without HCC (Kendall tau =0.97; P < .001) and in patients with HCC (tau = 0.94; P < .0001).
CONCLUSIONS: In an analysis of data from the Scientific Registry of Transplant Recipients (2002 through 2019), we found NASH to be the second most common indication for liver transplant in 2019, and the fastest increasing indication. In 2019, NASH was the leading indication for liver transplantation among women without HCC.
C1 [Younossi, Zobair M.; Racila, Andrei] Nova Hlth Syst, Betty & Guy Beatty Ctr Integrated Res, Falls Church, VA USA.
[Younossi, Zobair M.; Trimble, Greg; Racila, Andrei] Nova Fairfax Hosp, Ctr Liver Dis, Dept Med, Falls Church, VA USA.
[Stepanova, Maria; Younossi, Issah; Henrys, Linda] Ctr Outcomes Res Liver Dis, Washington, DC USA.
[Ong, Janus] Univ Philippines, Coll Med, Manila, Philippines.
[AlQahtani, Saleh] Johns Hopkins Univ, Div Gastroenterol & Hepatol, Baltimore, MD USA.
[Ahmed, Aijaz] Stanford Univ, Div Gastroenterol & Hepatol, Med Ctr, Palo Alto, CA USA.
C3 University of the Philippines System; University of the Philippines
Manila; Johns Hopkins University; Stanford University
RP Younossi, ZM (corresponding author), Betty & Guy Beatty Ctr Integrated Res, Claude Moore Hlth Educ & Res Bldg,3300 Gallows Rd, Falls Church, VA 22042 USA.
EM zobair.younossi@inova.org
RI Ahmed, Ahmed/KQU-2025-2024; Stepanova, Maria/V-5513-2019; Younossi,
Zobair M./JRY-9916-2023; Alqahtani, Saleh/ADB-1075-2022
OI Alqahtani, Saleh/0000-0003-2017-3526
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NR 41
TC 319
Z9 327
U1 2
U2 26
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD MAR
PY 2021
VL 19
IS 3
BP 580
EP +
DI 10.1016/j.cgh.2020.05.064
EA FEB 2021
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA QH9ZE
UT WOS:000618634000019
PM 32531342
OA Bronze
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Ward, SC
Deniz, K
Roayaie, S
Qin, LH
AF Ward, Stephen C.
Deniz, Kemal
Roayaie, Sasan
Qin, Lihui
TI Multifocal hepatocellular carcinoma and precancerous lesions in a
patient with autoimmune hepatitis-related cirrhosis
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE autoimmune hepatitis; hepatocellular carcinoma; dysplastic nodule
ID DISEASES; LIVER
AB A 44-year-old woman with a 29-year history of autoimmune hepatitis (AIH) received a living donor liver transplant for multifocal hepatocellular carcinoma (HCC) and cirrhosis in 2007. Her initial laboratory workup at our institution in 1996 revealed a positive antismooth muscle antibody with a titer of 1:640. Serum electrophoresis showed a monoclonal gamma globulin spike with elevated IgG, IgA, and IgM. The patient was negative for hepatitis B and hepatitis C (HCV) by serology and serum polymerase chain reaction. She was treated with corticosteroids and azathioprine, but her disease progressed. In 1997, a liver needle biopsy revealed cirrhosis, and a focus of small cell change. In 2004, a 2-cm exophytic mass was detected on magnetic resonance imaging. Follow-up imaging in 2005 and 2006 showed growth of the exophytic mass and development of new tumors. The exophytic mass was treated with ethanol ablation and she received a transplant. Examination of the explant revealed multiple high-grade dysplastic nodules and four moderately differentiated HCCs, one of which is arising in a high-grade dysplastic nodule. We believe this to be the first case in the English literature documenting the presence of preneoplastic lesions in an HCV-negative patient with AIH who developed HCC.
C1 [Roayaie, Sasan] Mt Sinai Med Ctr, Dept Surg, New York, NY 10029 USA.
Mt Sinai Med Ctr, Lillian & Henry M Stratton Hans Popper Dept Patho, New York, NY 10029 USA.
C3 Icahn School of Medicine at Mount Sinai; Icahn School of Medicine at
Mount Sinai
RP Ward, SC (corresponding author), Mt Sinai Med Ctr, Dept Pathol, 1 Gustave L Levy Pl, New York, NY 10029 USA.
EM Stephen.Ward@mssm.edu
RI Deniz, Kemal/Q-3486-2019; Ward, Stephen/C-5222-2013
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NR 21
TC 4
Z9 4
U1 0
U2 2
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD FEB
PY 2008
VL 28
IS 1
BP 123
EP 127
DI 10.1055/s-2008-1040326
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 300PT
UT WOS:000255838400010
PM 18293282
DA 2025-01-07
ER
PT J
AU Puustinen, L
Barner-Rasmussen, N
Pukkala, E
Färkkilä, M
AF Puustinen, Lauri
Barner-Rasmussen, Nina
Pukkala, Eero
Farkkila, Martti
TI Incidence, prevalence, and causes of death of patients with autoimmune
hepatitis: A nationwide register-based cohort study in Finland
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article
DE Autoimmune liver disease; Epidemiology; Mortality
ID INFLAMMATORY-BOWEL-DISEASE; HEPATOCELLULAR-CARCINOMA; CIRRHOSIS;
DIAGNOSIS; AZATHIOPRINE; EPIDEMIOLOGY; CRITERIA
AB Background: Epidemiological studies of autoimmune hepatitis are scarce and often based on single centre registries.
Aims: We conducted a nationwide register study of incidence, prevalence, survival, and causes of death of autoimmune hepatitis patients in Finland.
Methods: Autoimmune hepatitis cases 1995-2015 were retrieved from the national database of special reimbursements for drugs costs. Data on causes of death were retrieved from Statistics Finland.
Results: After incomplete registration of AIH during the first years, the incidence of autoimmune hepatitis stabilised to 1.1/100,000 person-years (1.6 in women and 0.52 in men) in 2008-2015. The prevalence of autoimmune hepatitis at the end of 2015 was 14.3/100,000, 23.0/100,000 in women and 6.6/100,000 in men. The all-cause standardized mortality ratio (SMR) of autoimmune hepatitis patients was 1.81 (95% confidence interval (CI) 1.47-2.20). The SMR was increased in all age groups and in both sexes. The SMR for hepatocellular carcinoma was 20.6 (95% CI 10.3-36.8), and for digestive diseases in overall 13.5 (95% CI 8.2-20.8), constituting mainly from autoimmune hepatitis and liver cirrhosis.
Conclusion: Incidence of autoimmune hepatitis has remained stable, with clear female predominance. Autoimmune hepatitis is associated with a markedly increased risk of death with hepatocellular cancer forming the greatest risk. (C) 2019 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Puustinen, Lauri; Barner-Rasmussen, Nina; Farkkila, Martti] Univ Helsinki, Helsinki Univ Hosp, Dept Gastroenterol, Helsinki, Finland.
[Pukkala, Eero] Univ Tampere, Fac Social Sci, Tampere, Finland.
[Pukkala, Eero] Inst Stat & Epidemiol Canc Res, Finnish Canc Registry, Helsinki, Finland.
C3 University of Helsinki; Helsinki University Central Hospital; Tampere
University; Finnish Cancer Registry
RP Puustinen, L (corresponding author), Haartmaninkatu 4,POB 340, FI-00280 Helsinki, Finland.
EM lauri.puustinen@helsinki.fi
RI Färkkilä, Martti/AAG-6970-2021
OI Farkkila, Martti/0000-0002-0250-8559
FU Mary och Georg C. Ehrnrooth's foundation
FX The study has been supported by a grant received from Mary och Georg C.
Ehrnrooth's foundation.
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NR 32
TC 36
Z9 37
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD SEP
PY 2019
VL 51
IS 9
BP 1294
EP 1299
DI 10.1016/j.dld.2019.01.015
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IS3ZL
UT WOS:000482092800013
PM 30850346
DA 2025-01-07
ER
PT J
AU Buettner, N
Thimme, R
AF Buettner, Nico
Thimme, Robert
TI Sexual dimorphism in hepatitis B and C and hepatocellular carcinoma
SO SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Review
DE Sexual dimorphism; Hepatitis B virus; Hepatitis C virus; Hepatocellular
carcinoma; Liver disease
ID ESTROGEN-RECEPTOR-BETA; ANDROGEN RECEPTOR; GENE-EXPRESSION;
PEGINTERFERON ALPHA-2B; SPONTANEOUS CLEARANCE; ALCOHOL-CONSUMPTION;
VIRUS REPLICATION; GENDER DISPARITY; TRANSGENIC MICE; NATURAL-HISTORY
AB The incidence of viral hepatitis B or C (HBV/HCV) infection and hepatocellular carcinoma is higher in male compared to female populations, showing a faster disease progression and results in a worse overall survival. Indeed, women are in general better protected from viral infections and show a lower risk of death from malignant cancer in comparison to men. Females mount stronger innate and adaptive immune responses than males, and therefore, most of the autoimmune diseases occur predominantly in females. Next to occupational and/or behavioral factors, cellular and molecular differences between the two sexes contribute to this observation. In this review, we will discuss underlying mechanisms that are important for the observed sex-related differences in liver diseases. A better appreciation of these differences between the two sexes might be of value for better and gender-specific treatment options.
C1 [Buettner, Nico; Thimme, Robert] Univ Freiburg, Fac Med, Med Ctr, Dept Med Gastroenterol Hepatol Endocrinol & Infec, Hugstetter Str 55, D-79106 Freiburg, Germany.
C3 University of Freiburg
RP Thimme, R (corresponding author), Univ Freiburg, Fac Med, Med Ctr, Dept Med Gastroenterol Hepatol Endocrinol & Infec, Hugstetter Str 55, D-79106 Freiburg, Germany.
EM robert.thimme@uniklinik-freiburg.de
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NR 118
TC 12
Z9 13
U1 0
U2 3
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1863-2297
EI 1863-2300
J9 SEMIN IMMUNOPATHOL
JI Semin. Immunopathol.
PD MAR
PY 2019
VL 41
IS 2
SI SI
BP 203
EP 211
DI 10.1007/s00281-018-0727-4
PG 9
WC Immunology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pathology
GA HL1NM
UT WOS:000458465700008
PM 30498927
DA 2025-01-07
ER
PT J
AU Yan, LJ
Yao, SY
Meng, GX
Liu, KX
Li, HC
Ding, ZN
Dong, ZR
Hong, JG
Chen, ZQ
Li, T
AF Yan, Lun-Jie
Yao, Sheng-Yu
Meng, Guang-Xiao
Liu, Kai-Xuan
Li, Hai-Chao
Ding, Zi-Niu
Dong, Zhao-Ru
Hong, Jian-Guo
Chen, Zhi-Qiang
Li, Tao
TI Sex and regional disparities in incidence of hepatocellular carcinoma in
autoimmune hepatitis: a systematic review and meta-analysis
SO HEPATOLOGY INTERNATIONAL
LA English
DT Review
DE Liver; Autoimmune hepatitis; Hepatocellular carcinoma; Incidence;
Prevalence; Sex differences; Regional disparities; Cirrhosis; Risk;
Autoimmune liver disease; Meta-analysis
ID TERM-FOLLOW-UP; RISK; MALIGNANCIES; EPIDEMIOLOGY
AB Background Recent studies have identified an increased risk of hepatocellular carcinoma (HCC) in autoimmune hepatitis (AIH). Sex and regional disparities in incidence of HCC in AIH continue to be reported worldwide. Nevertheless, the magnitude of this gap remains unknown. Method We searched several databases including PubMed, Embase, Web of Science, Cochrane Library, Wanfang Data, CNKI and SinoMed. Incidence rates of HCC in AIH were combined and analyzed following the EBayes method. Incidence rate ratios were pooled to assess the sex differences. The impact of population difference, sex, age, cirrhotic condition was further analyzed with subgroup analysis and linear regression analysis. Result 39 studies meeting our eligibility criteria were chosen for the analysis. The pooled incidence rate of HCC in AIH was 3.54 per 1000 person years (95% CI 2.76-4.55). Pooled IRR for the risk of HCC in male AIH patients compared to female was 2.16 (95% CI 1.25-3.75), with mild heterogeneity among studies. The pooled HCC incidence rate in AIH by continents was as follows: Europe 2.37 per 1000 person-years (95% CI 1.45-3.88), Asia 6.18 per 1000 person-years (95%CI 5.51-6.93), North America 2.97 per 1000 person-years (95%CI 2.40-3.68), Oceania 2.60 (95%CI 0.54-7.58). The pooled HCC incidence rate in AIH-related cirrhosis by continent was as follows: Europe 6.35 per 1000 person-years (95%CI 3.94-10.22), Asia 17.02 per 1000 person-years (95%CI 11.18-25.91), North America 10.89 per 1000 person-years (95%CI 6.69-17.74). Conclusion A higher HCC incidence in AIH was observed among male and in Asian populations. Cirrhosis status at AIH diagnosis is significantly associated with an increased incidence rate for HCC, and routine HCC surveillance is recommended for patients with AIH cirrhosis, especially for those in Asia.
C1 [Yan, Lun-Jie; Yao, Sheng-Yu; Meng, Guang-Xiao; Liu, Kai-Xuan; Li, Hai-Chao; Ding, Zi-Niu; Dong, Zhao-Ru; Hong, Jian-Guo; Chen, Zhi-Qiang; Li, Tao] Shandong Univ, Qilu Hosp, Dept Gen Surg, 107 West Wen Hua Rd, Jinan 250012, Peoples R China.
[Li, Tao] Shandong Univ, Hosp 2, Dept Hepatobiliary Surg, Jinan 250012, Peoples R China.
C3 Shandong University; Shandong University
RP Li, T (corresponding author), Shandong Univ, Qilu Hosp, Dept Gen Surg, 107 West Wen Hua Rd, Jinan 250012, Peoples R China.; Li, T (corresponding author), Shandong Univ, Hosp 2, Dept Hepatobiliary Surg, Jinan 250012, Peoples R China.
EM litao7706@163.com
RI Yan, Lun-Jie/GSJ-4040-2022; Chen, Zhiqiang/AAO-2064-2021
OI Li, Tao/0000-0002-5108-1774
FU Taishan Scholars Program for Young Expert of Shandong Province
[tsqn20161064]; National Natural Science Foundation of China [82073200,
81874178]; founds for Independent Cultivation of Innovative Team from
Universities in Jinan [2020GXRC023]
FX This work was supported by the grants from the Taishan Scholars Program
for Young Expert of Shandong Province (Grant No. tsqn20161064), National
Natural Science Foundation of China (Grant Nos. 82073200 & 81874178),
and founds for Independent Cultivation of Innovative Team from
Universities in Jinan (Grant No.2020GXRC023).
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NR 17
TC 6
Z9 6
U1 1
U2 9
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1936-0533
EI 1936-0541
J9 HEPATOL INT
JI Hepatol. Int.
PD DEC
PY 2021
VL 15
IS 6
BP 1413
EP 1420
DI 10.1007/s12072-021-10249-9
EA SEP 2021
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA XL7PH
UT WOS:000692453100001
PM 34478116
DA 2025-01-07
ER
PT J
AU Hilscher, MB
Shah, VH
AF Hilscher, Moira B.
Shah, Vijay H.
TI Neutrophil Extracellular Traps and Liver Disease
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE portal hypertension; cirrhosis; neutrophil
ID TO-LYMPHOCYTE RATIO; HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC
STEATOHEPATITIS; CLINICAL CHARACTERISTICS; MOLECULAR-MECHANISMS;
INSULIN-RESISTANCE; MURINE MODEL; DNA TRAPS; RELEASE; CANCER
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C1 [Hilscher, Moira B.; Shah, Vijay H.] Mayo Clin, Div Gastroenterol & Hepatol, 200 First St SW, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Shah, VH (corresponding author), Mayo Clin, Div Gastroenterol & Hepatol, 200 First St SW, Rochester, MN 55905 USA.
EM shah.vijay@mayo.edu
FU NIDDK NIH HHS [R01 DK059615] Funding Source: Medline
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NR 125
TC 35
Z9 40
U1 1
U2 22
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD MAY
PY 2020
VL 40
IS 2
BP 171
EP 179
DI 10.1055/s-0039-3399562
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA LL2UB
UT WOS:000531411200008
PM 31726473
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Cripps, JG
Gorham, JD
AF Cripps, James G.
Gorham, James D.
TI MDSC in autoimmunity
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE MDSC; Autoimmunity; Autoimmune hepatitis; EAE; IBD; Nitric oxide
ID CENTRAL-NERVOUS-SYSTEM; SUPPRESSOR-CELLS; T-CELLS; LIVER-DISEASE;
HEPATOCELLULAR-CARCINOMA; ENCEPHALOMYELITIS EAE; MULTIPLE-SCLEROSIS;
IMMUNE-RESPONSES; BONE-MARROW; IFN-GAMMA
AB Myeloid derived suppressor cells (MDSC) were first described nearly two decades ago. Until recently, however, descriptions of MDSC populations were found almost exclusively in animal models of cancer or in cancer patients. Over the last few years, an increasing number of reports have been published describing populations of myeloid cells with MDSC-like properties in murine models of autoimmune disease. In contrast to the proposed deleterious role of MDSC in cancer - where these cells likely inhibit tumor immunity - in the context of autoimmunity, MDSC have the potential to suppress the autoimmune response, thereby limiting tissue injury. A logical corollary of this hypothesis is that a failure of endogenous MDSC to appropriately control autoimmune T cell responses in vivo may actually contribute to the pathogenesis of autoimmune disease. (c) 2011 Elsevier B.V. All rights reserved.
C1 [Cripps, James G.; Gorham, James D.] Dartmouth Med Sch, Dept Microbiol & Immunol, Lebanon, NH 03756 USA.
[Gorham, James D.] Dartmouth Med Sch, Dept Pathol, Lebanon, NH 03756 USA.
C3 Dartmouth College; Dartmouth College
RP Gorham, JD (corresponding author), Dartmouth Med Sch, Dept Microbiol & Immunol, Lebanon, NH 03756 USA.
EM James.D.Gorham@Dartmouth.edu
FU NCI NIH HHS [P30 CA023108] Funding Source: Medline; NIAID NIH HHS [R01
AI078195, R01 AI078195-03] Funding Source: Medline
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NR 46
TC 110
Z9 125
U1 1
U2 45
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD JUL
PY 2011
VL 11
IS 7
SI SI
BP 789
EP 793
DI 10.1016/j.intimp.2011.01.026
PG 5
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA 791IX
UT WOS:000292660000004
PM 21310255
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Zhang, L
Xu, KH
Liu, CM
Chen, JS
AF Zhang, Li
Xu, Kuihua
Liu, Chuanmiao
Chen, Jiasheng
TI Meta-analysis reveals an association between signal transducer and
activator of transcription-4 polymorphism and hepatocellular carcinoma
risk
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE hepatocellular carcinoma; meta-analysis; rs7574865; STAT4
ID HEPATIC ISCHEMIA/REPERFUSION INJURY; STAT4; EPIDEMIOLOGY; REPLICATION;
CYTOKINES; IL-12; MICE
AB AimHepatocellular carcinoma (HCC) is one of the most common causes of cancer-related mortality worldwide. Signal transducer and activator of transcription (STAT) proteins play a multitude of important functions in liver pathophysiology. Recent studies have indicated associations of rs7574865 single nucleotide polymorphism (SNP) in the STAT4 gene with various autoimmune diseases. The association between STAT4 polymorphism and the risk of HCC has been analyzed in several studies, but results remain inconsistent. This study used a meta-analysis approach to comprehensively investigate the correlation between STAT4 polymorphism and HCC risk based on previously published reports.
MethodsStudies were searched from the databases of PubMed, EMBase, Web of Science, and the Chinese National Knowledge Infrastructure up to 31 December 2015. The meta-analysis was carried out based on the statement of Preferred Reporting Items for Systematic Reviews and Meta-Analyses.
ResultsEight published studies, consisting of 7503 HCC patients (cases) and 13831 individuals without HCC (controls), were included in the present study. Meta-analysis of the included studies revealed that STAT4 rs7574865 polymorphism contributed to the risk of HCC under all four genetic models, consisting of the allelic model (G vs. T: odds ratio [OR], 1.25; 95% confidence interval [CI], 1.19-1.30), the dominant effect model (GG+GT vs. TT: OR, 1.52; 95% CI, 1.26-1.84), the recessive effect model (GG vs. GT+TT: OR, 1.35; 95% CI, 1.21-1.50), and the co-dominant effect model (GG vs.. TT: OR, 1.72; 95% CI, 1.42-2.10) comparisons. No publication bias was indicated from either visualization of the funnel plot or Egger's test.
ConclusionA significantly increased risk of HCC associated with the rs7574865 G was found. The rs7574865 polymorphism might be used as one risk factor for HCC.
C1 [Zhang, Li; Xu, Kuihua; Liu, Chuanmiao; Chen, Jiasheng] First Affiliated Hosp Bengbu, Coll Med, Dept Infect Dis, 287 Changhuai Rd, Bengbu, Anhui, Peoples R China.
RP Zhang, L (corresponding author), First Affiliated Hosp Bengbu, Coll Med, Dept Infect Dis, 287 Changhuai Rd, Bengbu, Anhui, Peoples R China.
EM zl_byfy@sina.com
RI Liu, Mingyue/HLQ-3162-2023
OI Chen, Jiasheng/0000-0003-2945-8034
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NR 31
TC 11
Z9 11
U1 0
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD MAR
PY 2017
VL 47
IS 4
BP 303
EP 311
DI 10.1111/hepr.12733
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ER2AT
UT WOS:000398597000006
PM 27126090
DA 2025-01-07
ER
PT J
AU Pang, L
Chen, ZJ
Xu, D
Cheng, WT
AF Pang, Ling
Chen, Zhongju
Xu, Dong
Cheng, Weiting
TI Case report: Mycobacterium neoaurum infection during ICI therapy
in a hepatocellular carcinoma patient with psoriasis
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE immune checkpoint inhibitor (ICI); mycobacterium neoaurum infection;
psoriasis; hepatocellular carcinoma; case report
ID PREEXISTING AUTOIMMUNE; CANCER
AB We report here a patient with advanced hepatocellular carcinoma (HCC) and psoriasis treated with immune checkpoint inhibitor (ICI) therapy who experienced tumor partial response and psoriatic exacerbation. Meanwhile, the patient contracted mycobacterium neoaurum during the treatment period, while it was an opportunistic infection and mainly happened in immunosuppressed patients. We discussed the possibility that this infection was an ICI-associated infection independent of immunosuppression due to dysregulated immunity, which was the result of the effects of immunotherapy and autoimmune disease (AID), and the characteristics and treatment of M. neoaurum, which was rarely reported in China. This case highlights the fact that some infections can be precipitated by ICIs in the absence of immunosuppressive treatment, especially the patients with AID.
C1 [Pang, Ling; Xu, Dong] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Infect Dis, Wuhan, Peoples R China.
[Chen, Zhongju] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Lab Med, Wuhan, Peoples R China.
[Cheng, Weiting] Wuhan 1 Hosp, Dept Oncol, Wuhan, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
Science & Technology
RP Cheng, WT (corresponding author), Wuhan 1 Hosp, Dept Oncol, Wuhan, Peoples R China.
EM weitingcheng@yeah.net
RI vt, cheng/HKE-0837-2023
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NR 19
TC 5
Z9 5
U1 0
U2 2
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD AUG 22
PY 2022
VL 13
AR 972302
DI 10.3389/fimmu.2022.972302
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 4P0DG
UT WOS:000855062400001
PM 36072586
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Tamaki, S
Homma, S
Enomoto, Y
Komita, H
Zeniya, M
Ohno, T
Toda, G
AF Tamaki, S
Homma, S
Enomoto, Y
Komita, H
Zeniya, M
Ohno, T
Toda, G
TI Autoimmune hepatic inflammation by vaccination of mice with dendritic
cells loaded with well-differentiated hepatocellular carcinoma cells and
administration of interleukin-12
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE dendritic cell; cancer vaccine; autommume disease; hepatocellular
carcinoma; interleukin-12; hepatic inflammation
ID NONOBESE DIABETIC MICE; MOUSE BONE-MARROW; T-CELLS; IFN-GAMMA;
ANTITUMOR-ACTIVITY; DISEASE; ANTIGEN; IL-12; INDUCTION; IMMUNOTHERAPY
AB Vaccination of mice with dendritic cells loaded with Hepa1-6, well-differentiated hepatocellular carcinoma cell line (DC/Hepal -6), induced cytotoxic T lymphocytes against Hepa1-6. Liver-specific inflammation was generated by vaccination of mice with DC/Hepa1-6 and subsequent administration of interleukin (IL)-12. Vaccination with DCs loaded with MC38 or B16 and administration of IL-12 did not generate significant liver-specific inflammation. Splenic T cells from DC/Hepa1-6-vaccinated mice showed proliferative response by stimulation with S-100 protein of the liver and showed cytotoxic activity to hepatocytes. Hepatic mononuclear cells from DC/Hepa1-6 + IL-12-treated mice also showed cytotoxic activity to hepatocytes. Adoptive transfer of splenocytes from DC/Hepa1-6-vaccinated mice produced hepatic inflammation in recipient mice that had been pretreated with IL-12. IL-12 upregulated the expression of adhesion molecules and chemokines in the liver. In conclusion, CTLs responsive to hepatocytes induced by DC/Hepa1-6 and enhanced expression of adhesion molecules and chemokines in the liver by IL-12 would produce autoimmune hepatic inflammation. (c) 2005 Elsevier Inc. All rights reserved.
C1 Jikei Univ, Sch Med, Dept Oncol, Inst DNA Med,Minato Ku, Tokyo 1058461, Japan.
Jikei Univ, Sch Med, Div Gastroenterol & Hepatol, Dept Internal Med, Tokyo, Japan.
C3 Jikei University; Jikei University
RP Jikei Univ, Sch Med, Dept Oncol, Inst DNA Med,Minato Ku, 3-25-8 Nishi Shimbashi, Tokyo 1058461, Japan.
EM sahya@jikei.ac.jp
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NR 48
TC 30
Z9 31
U1 1
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
EI 1521-7035
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD DEC
PY 2005
VL 117
IS 3
BP 280
EP 293
DI 10.1016/j.clim.2005.08.010
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 002TA
UT WOS:000234633200010
PM 16246626
DA 2025-01-07
ER
PT J
AU Mailey, B
Buchberg, B
Prendergast, C
Artinyan, A
Khalili, J
Sanchez-Luege, N
Colquhoun, SD
Kim, J
AF Mailey, Brian
Buchberg, Brian
Prendergast, Christie
Artinyan, Avo
Khalili, Joshua
Sanchez-Luege, Nicelio
Colquhoun, Steven D.
Kim, Joseph
TI A Disease-Based Comparison of Liver Transplantation Outcomes
SO AMERICAN SURGEON
LA English
DT Article; Proceedings Paper
CT 20th Annual Scientific Meeting of the Southern California Chapter of the
American-College-of-Surgeons
CY JAN 16-18, 2009
CL Santa Barbara, CA
SP Amer Coll Surg, So Calif Chapter
ID HEPATOCELLULAR-CARCINOMA; MILAN CRITERIA; SURVIVAL; CIRRHOSIS; EXPAND
AB An increasing demand for transplant donor organs has made optimal allocation of resources a priority. Our objective was to evaluate outcomes for orthotopic liver transplantation (OLT) performed in the United States. A query of the United Network for Organ Sharing registry between 1988 and 2007 was performed for patients who underwent OLT for all etiologies. Patients were stratified by pathology necessitating OLT and clinical and pathologic factors were compared. Multivariate Cox-regression analysis was used to assess the association of pathology with survival. Of 61,823 patients, 33 per cent (n = 20,305) of OLTs were secondary to hepatitis C virus, 21 per cent autoimmune disease, 17 per cent alcohol-induced injury, 11 per cent cryptogenic cirrhosis, 8 per cent hepatocellular carcinoma (HCC), 6 per cent hepatitis B virus, and 4 per cent metabolic disease. Patients with autoimmune disease and HCC demonstrated the best and worst survival, respectively, after OLT (median survival 16.0 vs 6.4 yrs, respectively, P < 0.001). By multivariate analysis, OLT for HCC was significantly associated with poorer overall survival (hazard ratio [HR] 2.19, 95% confidence interval [CI]: 2.02-2.37, P < 0.001). Our results indicate that outcomes for liver transplantation vary by primary hepatic pathology with HCC patients having the poorest overall survival. To optimize organ allocation for all patients with end-stage liver disease, a better understanding of poor survival for HCC is necessary.
C1 [Mailey, Brian; Buchberg, Brian; Prendergast, Christie; Artinyan, Avo; Khalili, Joshua; Sanchez-Luege, Nicelio; Kim, Joseph] City Hope Natl Med Ctr, Dept Surg Oncol, Duarte, CA 91010 USA.
[Kim, Joseph] City Hope Natl Med Ctr, Ctr Comprehens Canc, Duarte, CA 91010 USA.
[Colquhoun, Steven D.] Cedars Sinai Med Ctr, Dept Surg, Div Transplantat, Los Angeles, CA 90048 USA.
C3 City of Hope; City of Hope; Cedars Sinai Medical Center
RP Kim, J (corresponding author), City Hope Natl Med Ctr, Dept Surg Oncol, 1500 E Duarte Rd, Duarte, CA 91010 USA.
EM jokim@coh.org
OI Sanchez-Luege, Nicelio/0000-0002-3667-9639
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NR 15
TC 21
Z9 23
U1 0
U2 3
PU SOUTHEASTERN SURGICAL CONGRESS
PI CUMMING
PA 115 SAMARITAN DR, #200, CUMMING, GA 30040-2354 USA
SN 0003-1348
EI 1555-9823
J9 AM SURGEON
JI Am. Surg.
PD OCT
PY 2009
VL 75
IS 10
BP 901
EP 908
PG 8
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Surgery
GA 506SD
UT WOS:000270795300008
PM 19886131
DA 2025-01-07
ER
PT J
AU Gu, X
Qi, P
Zhou, FG
Ji, Q
Wang, H
Dou, TH
Zhao, YP
Gao, CF
AF Gu, Xing
Qi, Peng
Zhou, Feiguo
Ji, Qiang
Wang, Hao
Dou, Tonghai
Zhao, Yunpeng
Gao, Chunfang
TI +49G > A polymorphism in the cytotoxic T-lymphocyte antigen-4 gene
increases susceptibility to hepatitis B-related hepatocellular carcinoma
in a male Chinese population
SO HUMAN IMMUNOLOGY
LA English
DT Article
DE CTLA-4; HBV-related HCC; SNP; Susceptibility
ID A-G POLYMORPHISM; CTLA-4 GENE; METASTATIC MELANOMA; ASSOCIATION; VIRUS;
AUTOIMMUNE; RISK; BLOCKADE; CANCER; POSITION-49
AB Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is an important regulator and functions negatively in immune response. Its nonsynonymous polymorphism +49G > A (dbSNP: rs231775) has been linked to an elevated risk of T-cell-mediated autoimmune diseases, infectious diseases, and even carcinomas. Here, we examined the genotypes at rs231775 of 1003 subjects in a Han Chinese population to detect the association between this single-nucleotide polymorphism (SNP) and hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) Susceptibility, including 375 HBV-related HCC patients, 209 non-HCC patients with HBV infection, and 419 healthy controls. Our results indicated a weak trend for the relationship between rs231775 and HBV-related HCC Susceptibility, although the statistical level was not significant. However, a significant difference was identified in males between HBV-related HCC patients and healthy controls. The data revealed that the frequency of the A/A genotype was higher in patients compared with healthy controls (odds ratio [OR] = 1.79, 95% confidence interval [95% CI] 1.05-3.08). The G allele appeared to have a protective effect in developing HBV-related HCC. Subjects with the A allele had higher HCC Susceptibility than those with the G allele (OR = 1.31, 95% CI 1.03-1.66). These results suggested that the A/A genotype and A allele of rs231775 increased the risk of developing HBV-related HCC in a male Chinese population. (C) 2010 American Society for Histocompatibility and immunogenetics. Published by Elsevier Inc. All rights reserved.
C1 [Gu, Xing; Qi, Peng; Zhou, Feiguo; Ji, Qiang; Zhao, Yunpeng; Gao, Chunfang] Second Mil Med Univ, Eastern Hepatobiliary Hosp, Dept Lab Med, Shanghai 200438, Peoples R China.
[Wang, Hao] Second Mil Med Univ, Changzheng Hosp, Dept Lab Med, Shanghai 200003, Peoples R China.
[Dou, Tonghai] Fudan Univ, Inst Biomed Sci, Shanghai 200032, Peoples R China.
C3 Naval Medical University; Naval Medical University; Fudan University
RP Gao, CF (corresponding author), Second Mil Med Univ, Eastern Hepatobiliary Hosp, Dept Lab Med, Shanghai 200438, Peoples R China.
EM gaocf1115@yahoo.com
RI Zhao, Yunpeng/AAQ-8398-2020; Chen, Gang/G-2722-2010
FU National Natural Science Foundation of China [30770994]
FX The work was supported by National Natural Science Foundation of China
Grant 30770994.
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NR 43
TC 52
Z9 54
U1 0
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0198-8859
EI 1879-1166
J9 HUM IMMUNOL
JI Hum. Immunol.
PD JAN
PY 2010
VL 71
IS 1
BP 83
EP 87
DI 10.1016/j.humimm.2009.09.353
PG 5
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 544JG
UT WOS:000273651600013
PM 19778566
DA 2025-01-07
ER
PT J
AU Floreani, A
Gabbia, D
De Martin, S
AF Floreani, Annarosa
Gabbia, Daniela
De Martin, Sara
TI Are Gender Differences Important for Autoimmune Liver Diseases?
SO LIFE-BASEL
LA English
DT Review
DE gender differences; primary biliary cholangitis; primary sclerosing
cholangitis; AIH; IgG4-related disease
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY-CIRRHOSIS;
INFLAMMATORY-BOWEL-DISEASE; HEPATOCELLULAR-CARCINOMA; CLINICAL-FEATURES;
OVERLAP SYNDROME; GUT MICROBIOTA; HEPATITIS-A; CANCER-RISK; MOUSE MODEL
AB Gender Medicine has had an enormous expansion over the last ten years. Autoimmune liver diseases include several conditions, i.e., autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and conditions involving the liver or biliary tree overlapping with AIH, as well as IgG4-related disease. However, little is known about the impact of sex in the pathogenesis and natural history of these conditions. The purpose of this review is to provide an update of the gender disparities among the autoimmune liver diseases by reviewing the data published from 1999 to 2023. The epidemiology of these diseases has been changing over the last years, due to the amelioration of knowledge in their diagnosis, pathogenesis, and treatment. The clinical data collected so far support the existence of sex differences in the natural history of autoimmune liver diseases. Notably, their history could be longer than that which is now known, with problems being initiated even at a pediatric age. Moreover, gender disparity has been observed during the onset of complications related to end-stage liver disease, including cancer incidence. However, there is still an important debate among researchers about the impact of sex and the pathogenesis of these conditions. With this review, we would like to emphasize the urgency of basic science and clinical research to increase our understanding of the sex differences in autoimmune liver diseases.
C1 [Floreani, Annarosa] Sci Consultant IRCCS Negrar, I-37024 Verona, Italy.
[Floreani, Annarosa] Univ Padua, I-35122 Padua, Italy.
[Gabbia, Daniela; De Martin, Sara] Univ Padua, Dept Pharmaceut & Pharmacol Sci, I-35122 Padua, Italy.
C3 University of Padua; University of Padua
RP Floreani, A (corresponding author), Sci Consultant IRCCS Negrar, I-37024 Verona, Italy.; Floreani, A (corresponding author), Univ Padua, I-35122 Padua, Italy.
EM annarosa.floreani@unipd.it; daniela.gabbia@unipd.it;
sara.demartin@unipd.it
RI De Martin, Sara/AAC-7396-2022; Gabbia, Daniela/J-9984-2019
OI DE MARTIN, SARA/0000-0001-6398-8237; GABBIA, DANIELA/0000-0003-2247-8227
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NR 122
TC 0
Z9 0
U1 4
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-1729
J9 LIFE-BASEL
JI Life-Basel
PD APR
PY 2024
VL 14
IS 4
AR 500
DI 10.3390/life14040500
PG 15
WC Biology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microbiology
GA OX8B6
UT WOS:001210657000001
PM 38672770
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Susanto, H
Wonorahardjo, S
Putra, WE
Taufiq, A
Sunaryono
Fadhilah, DN
Fa'ida, SBRN
Firdaus, SRA
Sholeh, M
Malek, NANN
AF Susanto, Hendra
Wonorahardjo, Surjani
Putra, Wira Eka
Taufiq, Ahmad
Sunaryono, Sunaryono cd Dianvita Nur
Fadhilah, Dianvita Nur
Fa'ida, Siti Bachrotus Recha Nur
Firdaus, Sa'diyatul Rizqie Amaliyah
Sholeh, Moch.
Malek, Nik Ahmad Nizam Nik
TI Phytochemical Profiling and Pharmaceutical Properties of Moringa
oleifera Leaves Powder and Seed Oil Against Hepatocellular Carcinoma
SO MALAYSIAN JOURNAL OF FUNDAMENTAL AND APPLIED SCIENCES
LA English
DT Article
DE Bioactive characterization; Molecular docking; Moringa oleifera;
Hepatocellular Carcinoma; Transforming Growth Factor beta-1
ID MS; EXTRACTS
AB Hepatocellular carcinoma (HCC) is one of the deadliest types of cancer with a mortality rate of 8.9% of the total cancer deaths in Indonesia. This cancer can be caused by exposure to hepatitis B and C viruses, NAFLD, autoimmune, diabetes to sporadic genetic diseases. The development of chronic HCC is generally preceded by the occurrence of severe liver fibrosis and cirrhosis. One of the genes that play a role in fibrosis in the incidence of HCC is TGF-beta 1. As a profibrotic cytokine, the presence of high levels of TGF-beta 1 may be due to oxidative stress activity early in cancer development. One of the natural ingredients with lots of phytochemical content in the form of antioxidants that can reduce this activity is Moringa plant (Moringa oleifera). In this study we used a computational approach using molecular docking on the results of the GC-MS and LC-HRMS tests on Moringa oleifera Seed Oil (MOSEIL) and Moringa oleifera Leaves Powder (MOLP) which are oil and flour products made from moringa. The results of the identification of phytochemical compounds through the GC-MS test showed that the dominant compound in MOSEIL was oleic acid (37.546%) and in MOLP was ester (8.802%) when using n-hexane as solvent. The percentage yield of the dominant compound from the LC-HRMS test in MOSEIL was nitro compound (72.55%) and at MOLP was alcohol (45.87%). These compounds are known to have effects as hepatoprotective agents through antioxidant, anti-inflammatory, and anti-fibrotic activities that can reduce hepatic oxidative stress as an early trigger of cancer development. Through molecular docking, MOSEIL and MOLP showed a lower level of binding affinity when compared to TGF-beta 1 control drugs such as metformin. This data implies MOSEIL and MOLP have a strong interaction to TGF-beta 1 than the control drug. The therapeutic potential of the hepatoprotective properties of MOSEIL and MOLP makes them one of the most-promising therapeutic agents in the initial step of renewable cancer treatment therapy.
C1 [Susanto, Hendra; Putra, Wira Eka; Sunaryono, Sunaryono cd Dianvita Nur; Fa'ida, Siti Bachrotus Recha Nur; Firdaus, Sa'diyatul Rizqie Amaliyah; Sholeh, Moch.] Univ Negeri Malang, Fac Math & Nat Sci, Dept Biol, Malang, East Java, Indonesia.
[Wonorahardjo, Surjani] Univ Negeri Malang, Fac Math & Nat Sci, Dept Chem, Malang, East Java, Indonesia.
[Taufiq, Ahmad] Univ Negeri Malang, Fac Math & Nat Sci, Dept Phys, Malang, East Java, Indonesia.
[Susanto, Hendra; Wonorahardjo, Surjani; Taufiq, Ahmad] Univ Negeri Malang, Ctr Adv Mat Renewable Energy CAMRY, East Java, Indonesia.
[Malek, Nik Ahmad Nizam Nik] Univ Teknol Malaysia UTM, Dept Biosci, Fac Sci, Johor Baharu, Johor, Malaysia.
[Malek, Nik Ahmad Nizam Nik] Univ Teknol Malaysia UTM, Ctr Sustainable Nanomat CSNano, Ibnu Sina Inst Sci & Ind Res ISI ISIR, Utm Johor Bahru 81310, Johor, Malaysia.
C3 Universitas Negeri Malang; Universitas Negeri Malang; Universitas Negeri
Malang; Universitas Negeri Malang; Universiti Teknologi Malaysia;
Universiti Teknologi Malaysia
RP Susanto, H (corresponding author), Univ Negeri Malang, Fac Math & Nat Sci, Dept Biol, Malang, East Java, Indonesia.; Susanto, H (corresponding author), Univ Negeri Malang, Ctr Adv Mat Renewable Energy CAMRY, East Java, Indonesia.
EM hendrabio@um.ac.id
RI Putra, Wira Eka/GQQ-6352-2022; Nik, Malek/K-5227-2016; Wonorahardjo,
Surjani/ABD-6611-2020; Susanto, Hendra/AAM-2189-2021
OI SHOLEH, MOCH/0009-0006-8061-3078; Eka Putra, Wira/0000-0003-4831-3869;
Amaliyah Firdaus, Sa'diyatul Rizqie/0000-0001-8631-5879
FU Universitas Negeri Malang, Indonesia [19.5.897/UN32.20.1/LT/2022]
FX This work is part of a research project with grant number
19.5.897/UN32.20.1/LT/2022, supported by Universitas Negeri Malang,
Indonesia.
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NR 63
TC 0
Z9 0
U1 0
U2 0
PU PENERBIT UTM PRESS
PI JOHOR
PA PENERBIT UTM PRESS, SKUDAI, JOHOR, 81310, MALAYSIA
SN 2289-5981
EI 2289-599X
J9 MALAYS J FUNDAM APPL
JI Malays. J. Fundam. Appl. Sci.
PD JUL-AUG
PY 2023
VL 19
IS 4
BP 691
EP 706
DI 10.11113/mjfas.v19n4.2818
PG 16
WC Multidisciplinary Sciences
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics
GA Q7OJ7
UT WOS:001059378200020
OA gold
DA 2025-01-07
ER
PT J
AU Schulz, PO
Ferreira, FG
Nascimento, MDA
Vieira, A
Ribeiro, MA
David, AI
Szutan, LA
AF Schulz, Perla Oliveira
Ferreira, Fabio Goncalves
Araujo Nascimento, Maria de Fatima
Vieira, Andrea
Ribeiro, Mauricio Alves
David, Andre Ibrahim
Szutan, Luiz Arnaldo
TI Association of nonalcoholic fatty liver disease and liver cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Hepatocellular carcinoma; Colorectal liver metastases; Intrahepatic
cholangiocarcinoma; Liver fibrosis; Nonalcoholic fatty liver disease;
Nonalcoholic steatohepatitis
ID HEPATOCELLULAR-CARCINOMA; HEPATIC STEATOSIS; COLORECTAL METASTASES;
UNITED-STATES; STEATOHEPATITIS; OBESITY; RISK; EPIDEMIOLOGY; PROMOTES;
CHEMOTHERAPY
AB AIM: To investigate the association between nonalcoholic fatty liver disease (NAFLD) and liver cancer, and NAFLD prevalence in different liver tumors.
METHODS: This is a retrospective study of the clinical, laboratory and histological data of 120 patients diagnosed with primary or secondary hepatic neoplasms and treated at a tertiary center where they underwent hepatic resection and/or liver transplantation, with subsequent evaluation of the explant or liver biopsy. The following criteria were used to exclude patients from the study: a history of alcohol abuse, hepatitis B or C infection, no tumor detected in the liver tissue examined by histological analysis, and the presence of chronic autoimmune hepatitis, hemochromatosis, Wilson's disease, or hepatoblastoma. The occurrence of NAFLD and the association with its known risk factors were studied. The risk factors considered were diabetes mellitus, impaired glucose tolerance, impaired fasting glucose, body mass index, dyslipidemia, and arterial hypertension. Presence of reticulin fibers in the hepatic neoplasms was assessed by histological analysis using slide-mounted specimens stained with either hematoxylin and eosin or Masson's trichrome and silver impregnation. Analysis of tumor-free liver parenchyma was carried out to determine the association between NAFLD and its histological grade.
RESULTS: No difference was found in the association of NAFLD with the general population (34.2% and 30.0% respectively, 95% CI: 25.8-43.4). Evaluation by cancer type showed that NAFLD was more prevalent in patients with liver metastasis of colorectal cancer than in patients with hepatocellular carcinoma and intrahepatic cholangiocarcinoma (OR = 3.99, 95%CI: 1.78-8.94, P < 0.001 vs OR = 0.60, 95% CI: 0.18-2.01, P = 0.406 and OR = 0.70, 95%CI: 0.18-2.80, P = 0.613, respectively). There was a higher prevalence of liver fibrosis in patients with hepatocellular carcinoma (OR = 3.50, 95%CI: 1.06-11.57, P = 0.032). Evaluation of the relationship between the presence of NAFLD, nonalcoholic steatohepatitis, and liver fibrosis, and their risk factors, showed no significant statistical association for any of the tumors studied.
CONCLUSION: NAFLD is more common in patients with liver metastases caused by colorectal cancer.
C1 [Schulz, Perla Oliveira; Vieira, Andrea] Santa Casa Sch Med Sci, Dept Internal Med, Gastroenterol Serv, BR-01277900 Sao Paulo, Brazil.
[Araujo Nascimento, Maria de Fatima] Santa Casa Sch Med Sci, Dept Pathol, BR-01277900 Sao Paulo, Brazil.
[David, Andre Ibrahim] Univ Sao Paulo, GI Transplant Serv, Dept Gastroenterol, BR-01246903 Sao Paulo, Brazil.
[Ferreira, Fabio Goncalves; Ribeiro, Mauricio Alves; Szutan, Luiz Arnaldo] Santa Casa Sch Med Sci, Liver & Portal Hypertens Grp, Dept Surg, 1060 Ap 93, BR-01277900 Sao Paulo, Brazil.
C3 Universidade de Sao Paulo
RP Ferreira, FG (corresponding author), Santa Casa Sch Med Sci, Liver & Portal Hypertens Grp, Dept Surg, 1060 Ap 93, BR-01277900 Sao Paulo, Brazil.
EM drfabioferreira@uol.com.br
RI Ferreira, Fabio/AAX-6834-2020; Ribeiro, Mauricio/I-1465-2012; Ferreira,
Fabio/A-3981-2013
OI Ribeiro, Mauricio/0000-0003-4876-2242; Ferreira,
Fabio/0000-0001-8714-2615
FU CAPES-MEC-Brazil
FX Supported by CAPES-MEC-Brazil - Grant master's thesis.
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NR 43
TC 25
Z9 29
U1 1
U2 21
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JAN 21
PY 2015
VL 21
IS 3
BP 913
EP 918
DI 10.3748/wjg.v21.i3.913
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AZ7TA
UT WOS:000348419400019
PM 25624725
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Pascual, S
Miralles, C
Bernabé, JM
Irurzun, J
Planells, M
AF Pascual, Sonia
Miralles, Cayetano
Bernabe, Juan M.
Irurzun, Javier
Planells, Mariana
TI Surveillance and diagnosis of hepatocellular carcinoma: A systematic
review
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Review
DE Surveillance; Hepatocellular carcinoma; Ultrasonography; Cirrhosis;
Imaging diagnosis
ID FATTY LIVER-DISEASE; CHRONIC HEPATITIS-B; RANDOMIZED CONTROLLED-TRIAL;
COST-EFFECTIVENESS ANALYSIS; MR-IMAGING DIAGNOSIS; NATURAL-HISTORY;
SEMIANNUAL SURVEILLANCE; AUTOIMMUNE HEPATITIS; CIRRHOTIC-PATIENTS;
INCREASED SURVIVAL
AB BACKGROUND
Hepatocellular carcinoma (HCC) appears in most of cases in patients with advanced liver disease and is currently the primary cause of death in this population. Surveillance of HCC has been proposed and recommended in clinical guidelines to obtain earlier diagnosis, but it is still controversial and is not accepted worldwide.
AIM
To review the actual evidence to support the surveillance programs in patients with cirrhosis as well as the diagnosis procedure.
METHODS
Systematic review of recent literature of surveillance (tools, interval, cost-benefit, target population) and the role of imaging diagnosis (radiological non-invasive diagnosis, optimal modality and agents) of HCC.
RESULTS
The benefits of surveillance of HCC, mainly with ultrasonography, have been assessed in several prospective and retrospective analysis, although the percentage of patients diagnosed in surveillance programs is still low. Surveillance of HCC permits diagnosis in early stages allows better access to curative treatment and increases life expectancy in patients with cirrhosis. HCC is a tumor with special radiological characteristics in computed tomography and magnetic resonance imaging, which allows highly accurate diagnosis without routine biopsy confirmation. The actual recommendation is to perform biopsy only in indeterminate nodules.
CONCLUSION
The evidence supports the recommendation of performing surveillance of HCC in patients with cirrhosis susceptible of treatment, using ultrasonography every 6 mo. The diagnosis evaluation of HCC can be established based on noninvasive imaging criteria in patients with cirrhosis.
C1 [Pascual, Sonia; Miralles, Cayetano] Hosp Gen Univ Alicante, Liver Unit, Alicante 03010, Spain.
[Pascual, Sonia] CIBEREHD, Alicante 03010, Spain.
[Bernabe, Juan M.; Irurzun, Javier; Planells, Mariana] Hosp Gen Univ Alicante, Radiol Dept, Alicante 03010, Spain.
C3 General University Hospital of Alicante; CIBER - Centro de Investigacion
Biomedica en Red; CIBEREHD; General University Hospital of Alicante
RP Pascual, S (corresponding author), Hosp Gene Univ Alicante, Liver Unit, HGU Alicante, Pintor Baeza 11, Alicante 03010, Spain.
EM pascual_son@gva.es
OI Pascual, Sonia/0000-0002-4265-5019
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NR 89
TC 15
Z9 17
U1 0
U2 5
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD AUG 26
PY 2019
VL 7
IS 16
BP 2269
EP 2286
DI 10.12998/wjcc.v7.i16.2269
PG 18
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA IU1VG
UT WOS:000483364100013
PM 31531321
OA Green Submitted, gold, Green Published
DA 2025-01-07
ER
PT J
AU Wang, L
Cao, ZM
Zhang, LL
Li, JM
Lv, WL
AF Wang, Li
Cao, Zheng-Min
Zhang, Li-Li
Li, Juan-mei
Lv, Wen-liang
TI The Role of Gut Microbiota in Some Liver Diseases: From an Immunological
Perspective
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE gut microbiota; liver diseases; immunity; metabolism; review
ID PRIMARY SCLEROSING CHOLANGITIS; BILIARY EPITHELIAL-CELLS; RANDOMIZED
CLINICAL-TRIAL; BACTERIAL TRANSLOCATION; HEPATIC-ENCEPHALOPATHY;
INTESTINAL MICROBIOTA; BILE-ACID; HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC
STEATOHEPATITIS; AUTOIMMUNE HEPATITIS
AB Gut microbiota is a microecosystem composed of various microorganisms. It plays an important role in human metabolism, and its metabolites affect different tissues and organs. Intestinal flora maintains the intestinal mucosal barrier and interacts with the immune system. The liver is closely linked to the intestine by the gut-liver axis. As the first organ that comes into contact with blood from the intestine, the liver will be deeply influenced by the gut microbiota and its metabolites, and the intestinal leakage and the imbalance of the flora are the trigger of the pathological reaction of the liver. In this paper, we discuss the role of gut microbiota and its metabolites in the pathogenesis and development of autoimmune liver diseases((including autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis), metabolic liver disease such as non-alcoholic fatty liver disease, cirrhosisits and its complications, and liver cancer from the perspective of immune mechanism. And the recent progress in the treatment of these diseases was reviewed from the perspective of gut microbiota.
C1 [Wang, Li; Cao, Zheng-Min; Zhang, Li-Li; Li, Juan-mei; Lv, Wen-liang] China Acad Chinese Med Sci, Guanganmen Hosp, Dept Infect, Beijing, Peoples R China.
C3 Guang'anmen Hospital, CACMS; China Academy of Chinese Medical Sciences
RP Wang, L; Cao, ZM; Li, JM; Lv, WL (corresponding author), China Acad Chinese Med Sci, Guanganmen Hosp, Dept Infect, Beijing, Peoples R China.
EM bucmwangdali@163.com; graycoffee1996@126.com; juanmeili2012@126.com;
lvwenliang@sohu.com
FU National Key Research and Development Program of China [2018YFC1705700]
FX Funding National Key Research and Development Program of China (No.
2018YFC1705700).
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NR 216
TC 40
Z9 43
U1 11
U2 43
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUL 13
PY 2022
VL 13
AR 923599
DI 10.3389/fimmu.2022.923599
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 6J6NI
UT WOS:000886938800001
PM 35911738
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Nakamura, Y
Ito, K
Takemura, N
Inagaki, F
Mihara, F
Kokudo, N
AF Nakamura, Yuki
Ito, Kyoji
Takemura, Nobuyuki
Inagaki, Fuyuki
Mihara, Fuminori
Kokudo, Norihiro
TI Elevation in creatine kinase isoenzyme-MM associated with hepatocellular
carcinoma: a case report and review of literature
SO CLINICAL JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Creatine kinase; CK-MM; Hepatocellular carcinoma; Paraneoplastic
syndrome
ID PARANEOPLASTIC DERMATOMYOSITIS; POLYMYOSITIS; BB; RHABDOMYOLYSIS;
PATIENT
AB We report the case of a 79-year-old woman with hepatocellular carcinoma (HCC) who presented with creatine kinase (CK)-MM elevation. On admission, her serum CK-MM level exceeded 4000 IU/L (normal, 44-206 IU/L), and computed tomography revealed two HCCs in hepatic segment VIII (23 mm, 86 mm). The patient denied experiencing muscular symptoms such as weakness or pain. Hypothyroidism, ischemic heart disease, muscular dystrophy, autoimmune myopathy, drug-induced rhabdomyolysis, and paraneoplastic inflammatory myositis syndrome (PIMS) were included in the differential diagnosis for high CK-MM, but none were suspected. Although the cause of elevated CK-MM was not elucidated, an HCC-related mechanism was considered and the tumor was resected. The CK-MM levels declined gradually to 300 IU/L postoperatively without any special perioperative management. Nineteen cases of HCC-associated CK-MM elevation have been reported in English thus far, in all of which, inflammatory myositis was concluded as the cause of CK-MM elevation. However, in this case, the elevation of CK-MM was associated with HCC-related mechanisms distinct from PIMS, suggesting HCC-related mechanisms should not be excluded as a cause of high CK-MM, even though PIMS is negative.
C1 [Nakamura, Yuki; Ito, Kyoji; Takemura, Nobuyuki; Inagaki, Fuyuki; Mihara, Fuminori; Kokudo, Norihiro] Natl Ctr Global Hlth & Med NCGM, Hepatobiliary Pancreat Surg Div, Dept Surg, Shinjuku Ku, 1-21-1 Toyama, Tokyo 1628655, Japan.
C3 National Center for Global Health & Medicine - Japan
RP Takemura, N (corresponding author), Natl Ctr Global Hlth & Med NCGM, Hepatobiliary Pancreat Surg Div, Dept Surg, Shinjuku Ku, 1-21-1 Toyama, Tokyo 1628655, Japan.
EM ntakemura@hosp.ncgm.go.jp
RI Nobuyuki, Takemura/GLT-3305-2022; Kokudo, Norihiro/AER-1764-2022
OI Nakamura, Yuki/0000-0002-4098-330X
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Z9 1
U1 0
U2 3
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
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EI 1865-7265
J9 CLIN J GASTROENTEROL
JI Clin. J. Gastroenterol.
PD APR
PY 2022
VL 15
IS 2
BP 460
EP 466
DI 10.1007/s12328-022-01612-w
EA FEB 2022
PG 7
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA ZZ5DY
UT WOS:000760044800001
PM 35199319
DA 2025-01-07
ER
PT J
AU Datfar, T
Doulberis, M
Papaefthymiou, A
Hines, IN
Manzini, G
AF Datfar, Toofan
Doulberis, Michael
Papaefthymiou, Apostolis
Hines, Ian N.
Manzini, Giulia
TI Viral Hepatitis and Hepatocellular Carcinoma: State of the Art
SO PATHOGENS
LA English
DT Review
DE viral hepatitis; hepatocellular carcinoma; HCC; cancer; risk factor;
carcinogenesis
ID GROWTH-FACTOR-BETA; B-VIRUS GENOTYPES; CORE PROMOTER MUTATIONS; C VIRUS;
T-CELLS; A VIRUS; DELTA-VIRUS; AUTOIMMUNE HEPATITIS; RISK-FACTORS;
INFECTION
AB Viral hepatitis is one of the main causes leading to hepatocellular carcinoma (HCC). The continued rise in incidence of HCC suggests additional factors following infection may be involved. This review examines recent studies investigating the molecular mechanisms of chronic hepatitis and its association with hepatocarcinogenesis. Hepatitis B virus patients with genotype C display an aggressive disease course leading to HCC more than other genotypes. Furthermore, hepatitis B excretory antigen (HBeAg) seems to be a more sensitive predictive tumor marker exhibiting a six-fold higher relative risk in patients with positive HBsAg and HBeAg than those with HBsAg only. Single or combined mutations of viral genome can predict HCC development in up to 80% of patients. Several mutations in HBx-gene are related with higher HCC incidence. Overexpression of the core protein in HCV leads to hepatocellular lipid accumulation associated with oncogenesis. Reduced number and decreased functionality of natural killer cells in chronic HCV individuals dysregulate their surveillance function in tumor and viral cells resulting in HCC. Furthermore, high T-cell immunoglobulin and mucin 3 levels supress CD8+ T-cells, which lead to immunological dysregulation. Hepatitis D promotes HCC development indirectly via modifications to innate immunity, epigenetic alterations and production of reactive oxygen species with the LHDAg being the most highly associated with HCC development. Summarizing the results, HBV and HCV infection represent the most associated forms of viral hepatitis causing HCC. Further studies are warranted to further improve the prediction of high-risk patients and development of targeted therapeutics preventing the transition from hepatic inflammation-fibrosis to cancer.
C1 [Datfar, Toofan; Manzini, Giulia] Hosp Aarau, Dept Gen & Visceral Surg, CH-5001 Aarau, Switzerland.
[Doulberis, Michael] Hosp Aarau, Dept Gastroenterol & Hepatol, CH-5001 Aarau, Switzerland.
[Papaefthymiou, Apostolis] Univ Hosp Larissa, Dept Gastroenterol, Larisa 41110, Greece.
[Hines, Ian N.] East Carolina Univ, Dept Nutr Sci, Greenville, NC 27858 USA.
C3 General University Hospital of Larissa; University of North Carolina;
East Carolina University
RP Datfar, T (corresponding author), Hosp Aarau, Dept Gen & Visceral Surg, CH-5001 Aarau, Switzerland.
EM t.datfar@gmail.com; michael.doulberis@ksa.ch; appapaef@hotmail.com;
hinesi@ecu.edu; giulia.manzini@ksa.ch
RI ; Papaefthymiou, Apostolis/HPH-4021-2023; Doulberis, Michael/Y-5118-2018
OI Hines, Ian/0000-0002-0201-6992; Papaefthymiou,
Apostolis/0000-0002-3563-4973; Doulberis, Michael/0000-0002-0396-5081
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NR 151
TC 18
Z9 19
U1 0
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-0817
J9 PATHOGENS
JI Pathogens
PD NOV
PY 2021
VL 10
IS 11
AR 1366
DI 10.3390/pathogens10111366
PG 19
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA XJ8AA
UT WOS:000727002300001
PM 34832522
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Suzuki, Y
Ohtake, T
Nishiguchi, S
Hashimoto, E
Aoyagi, Y
Onji, M
Kohgo, Y
AF Suzuki, Yasuaki
Ohtake, Takaaki
Nishiguchi, Shuhei
Hashimoto, Etsuko
Aoyagi, Yutaka
Onji, Morikazu
Kohgo, Yutaka
CA Japan Non-B Non-C Liver Cirrhosis
TI Survey of non-B, non-C liver cirrhosis in Japan
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE alcoholic liver disease; hepatocellular carcinoma; non-alcoholic
steatohepatitis; non-B; non-C liver cirrhosis
ID NONALCOHOLIC STEATOHEPATITIS; HEPATOCELLULAR-CARCINOMA; VIRUS INFECTION;
HEPATITIS-C; DISEASE; FEATURES; OUTCOMES; TISSUE
AB AimThe aim of this survey was to reveal clinical features for each etiology of non-B, non-C liver cirrhosis (NBNC LC) in Japan.
MethodsIn a nationwide survey of NBNC LC in Japan at the 15th General Meeting of the Japan Society of Hepatology, 6999 NBNC LC patients were registered at 48 medical institutions. Epidemiological and clinical factors were investigated.
ResultsThe percentage of NBNC LC among LC patients was 26%. NBNC LC patients were categorized into 11 types according to etiological agents: non-alcoholic steatohepatitis (NASH), 14.5%; alcoholic liver disease (ALD), 55.1%; fatty liver disease (FLD), except NASH, ALD, and other known etiology, 2.5%; primary biliary cirrhosis, 8.0%; other biliary cirrhosis, 0.8%; autoimmune hepatitis, 6.8%; metabolic disease, 0.6%; congestive disease, 0.8%; parasitic disease, 0.2%; other known etiology, 0.2%; and unknown etiology, 10.5%. Compared with previous surveys, the percentage of ALD remained unchanged, whereas that of NASH increased. The mean age and percentage of females were significantly higher in NASH patients than in ALD and FLD patients. Prevalence of diabetes mellitus was significantly higher in NASH and FLD patients than in ALD ones. Prevalence of hepatocellular carcinoma (HCC) in NBNC LC patients was 35.9%. Among NASH, ALD and FLD patients, 50.9%, 34.3% and 54.5% had HCC, respectively. Positivity of hepatitis B core antibody was significantly higher in HCC patients than in those without HCC (41.1% vs 24.8%).
ConclusionThis survey determined the etiology of NBNC LC in Japan. These results should contribute new ideas toward understanding NBNC LC and NBNC HCC.
C1 [Suzuki, Yasuaki; Ohtake, Takaaki; Kohgo, Yutaka] Asahikawa Med Univ, Dept Med, Div Gastroenterol & Hematol Oncol, Asahikawa, Hokkaido 0788510, Japan.
[Nishiguchi, Shuhei] Hyogo Coll Med, Dept Internal Med, Div Hepatobiliary & Pancreat Dis, Nishinomiya, Hyogo 6638501, Japan.
[Hashimoto, Etsuko] Tokyo Womens Med Univ, Inst Gastroenterol, Tokyo, Japan.
[Aoyagi, Yutaka] Niigata Univ, Grad Sch Med & Dent Sci, Div Gastroenterol & Hepatol, Niigata, Japan.
[Onji, Morikazu] Ehime Univ, Grad Sch Med, Dept Gastroenterol & Metabol, Toon, Japan.
C3 Asahikawa Medical College; Hyogo Medical University; Tokyo Women's
Medical University; Niigata University; Ehime University
RP Kohgo, Y (corresponding author), Asahikawa Med Univ, Dept Med, Div Gastroenterol & Hematol Oncol, 2-1 Midorigaoka Higashi, Asahikawa, Hokkaido 0788510, Japan.
EM yk1950@asahikawa-med.ac.jp
RI Kohgo, Yutaka/AAN-4863-2020
FU Grants-in-Aid for Scientific Research [23659395, 23790778] Funding
Source: KAKEN
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NR 18
TC 16
Z9 16
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
J9 HEPATOL RES
JI Hepatol. Res.
PD OCT
PY 2013
VL 43
IS 10
BP 1020
EP 1031
DI 10.1111/hepr.12056
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 229JV
UT WOS:000325260400003
PM 23347437
DA 2025-01-07
ER
PT J
AU Chen, YY
Tian, ZG
AF Chen, Yongyan
Tian, Zhigang
TI Innate lymphocytes: pathogenesis and therapeutic targets of liver
diseases and cancer
SO CELLULAR & MOLECULAR IMMUNOLOGY
LA English
DT Review
DE Innate lymphocyte; Liver disease; Liver cancer; Innate lymphoid cell;
Innate-like T lymphocyte
ID NATURAL-KILLER-CELLS; INVARIANT T-CELLS; CHRONIC HEPATITIS-B;
LYMPHOID-CELLS; NK CELLS; CUTTING EDGE; NONALCOHOLIC STEATOHEPATITIS;
HEPATOCELLULAR-CARCINOMA; MEDIATED ACTIVATION; TISSUE RESIDENCY
AB The liver is a lymphoid organ with unique immunological properties, particularly, its predominant innate immune system. The balance between immune tolerance and immune activity is critical to liver physiological functions and is responsible for the sensitivity of this organ to numerous diseases, including hepatotropic virus infection, alcoholic liver disease, nonalcoholic fatty liver disease, autoimmune liver disease, and liver cancer, which are major health problems globally. In the past decade, with the discovery of liver-resident natural killer cells, the importance of innate lymphocytes with tissue residency has gradually become the focus of research. In this review, we address the current knowledge regarding hepatic innate lymphocytes with unique characteristics, including NK cells, ILC1/2/3s, NKT cells, gamma delta T cells, and MAIT cells, and their potential roles in liver homeostasis maintenance and the progression of liver diseases and cancer. A better understanding of the immunopathogenesis of hepatic innate lymphocytes will be helpful for proposing effective treatments for liver diseases and cancer.
C1 [Chen, Yongyan; Tian, Zhigang] Univ Sci & Technol China, Hefei Natl Lab Phys Sci Microscale, CAS Key Lab Innate Immun & Chron Dis, Sch Basic Med Sci,Div Life Sci & Med, Hefei, Peoples R China.
[Chen, Yongyan; Tian, Zhigang] Univ Sci & Technol China, Inst Immunol, Hefei, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
China, CAS; Chinese Academy of Sciences; University of Science &
Technology of China, CAS
RP Chen, YY (corresponding author), Univ Sci & Technol China, Hefei Natl Lab Phys Sci Microscale, CAS Key Lab Innate Immun & Chron Dis, Sch Basic Med Sci,Div Life Sci & Med, Hefei, Peoples R China.; Chen, YY (corresponding author), Univ Sci & Technol China, Inst Immunol, Hefei, Peoples R China.
EM yychen08@ustc.edu.cn
RI Tian, Zhigang/J-3512-2013
FU National Natural Science Foundation of China [81788101, 91542000,
81671554]; Ministry of Science & Technology of China
[2017ZX10202203-002-001, 2017ZX10202203-009-002]; National Key R&D
Program of China [2019YFA0508503]
FX This work was supported by the National Natural Science Foundation of
China (Grant Nos. 81788101, 91542000, and 81671554), the Ministry of
Science & Technology of China (2017ZX10202203-002-001,
2017ZX10202203-009-002), and the National Key R&D Program of China
(2019YFA0508503).
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NR 215
TC 52
Z9 56
U1 0
U2 35
PU CHIN SOCIETY IMMUNOLOGY
PI BEING
PA 5 DONGDAN SANTIAO, DONGCHEN DISTRICT, BEING, 100005, PEOPLES R CHINA
SN 1672-7681
EI 2042-0226
J9 CELL MOL IMMUNOL
JI Cell. Mol. Immunol.
PD JAN
PY 2021
VL 18
IS 1
BP 57
EP 72
DI 10.1038/s41423-020-00561-z
EA OCT 2020
PG 16
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA PM9GT
UT WOS:000577063900002
PM 33041339
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Gu, DQ
Zhang, M
Wang, YT
Bai, Y
Wang, X
Deng, GH
AF Gu, Dongqing
Zhang, Min
Wang, Yutong
Bai, Ye
Wang, Xin
Deng, Guohong
TI Causal effect of autoimmune liver diseases on cancer: Meta-analyses of
cohort studies and Mendelian randomization study
SO LIVER INTERNATIONAL
LA English
DT Article
DE autoimmune hepatitis; autoimmune liver diseases; cancer; Mendelian
randomization; primary biliary cholangitis; primary sclerosing
cholangitis
ID PRIMARY SCLEROSING CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE; PRIMARY
BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; RISK LOCI; FOLLOW-UP;
MALIGNANCY; SURVIVAL; EPIDEMIOLOGY; PANCREATITIS
AB Background and Aims Prior studies suggested that patients with autoimmune liver diseases (AiLDs) had an increased risk of cancer, whereas the causal effect remained unclear. Methods Meta-analyses concerning the relationship between AiLD and cancer risk were performed to calculate the pooled relative risk (RR) and corresponding 95% confidence intervals (CIs). Then, the associations with a p value of A total of 37 cohort studies covering more than 34 558 patients were included, and we observed an increased risk of overall cancers (pooled RR = 3.64, 95% CI: 2.64-5.03, p < .001) and cancer-related death (pooled RR = 2.48, 95% CI: 1.73-3.53, p < .001) for patients with AiLD. Besides, overall and several site-specific cancers risk were found in patients with primary biliary cholangitis (PBC), autoimmune hepatitis (AIH), and primary sclerosing cholangitis (PSC) (p < .05). However, associations between genetically predisposed AIH, PBC, and PSC and the risk of specific cancers did not reach a significant level, except for PBC and gastric cancer (OR = 0.96, 95% CI: 0.93-0.99; p = .02). Conclusions In addition to hepatobiliary cancer, results from the meta-analyses suggest that patients with AiLD might have an increased risk of several extrahepatobiliary cancers. However, the causal role of AiLD in cancer development needs to be further investigated.
C1 [Gu, Dongqing; Deng, Guohong] Army Med Univ, Affiliated Hosp 1, Dept Infect Dis, 30 Gaotanyan St, Chongqing 400038, Peoples R China.
[Zhang, Min; Bai, Ye] Chongqing Med Univ, Sch Publ Hlth & Management, Chongqing, Peoples R China.
[Wang, Yutong; Wang, Xin] Sichuan Univ, West China Sch Publ Hlth, Dept Epidemiol & Biostat, South Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
C3 Army Medical University; Chongqing Medical University; Sichuan
University
RP Deng, GH (corresponding author), Army Med Univ, Affiliated Hosp 1, Dept Infect Dis, 30 Gaotanyan St, Chongqing 400038, Peoples R China.; Wang, X (corresponding author), Sichuan Univ, West China Sch Publ Hlth, Dept Epidemiol & Biostat, South Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
EM wangxinmarine@126.com; gh_deng@hotmail.com
RI Wang, Xin/N-8865-2018
OI Wang, Xin/0000-0001-9325-3194; Deng, Guo-Hong/0000-0003-1263-7220
FU Chongqing Natural Science Foundation Program [cstc2020jcyj--msxmX0021,
cstc2019jcyj--msxmX0466]; Chongqing Postdoctoral Science Special
Foundation [XmT2018068]; National Natural Science Foundation of China
[81903393, 81903398]
FX Chongqing Natural Science Foundation Program, Grant/Award Number:
cstc2020jcyj--msxmX0021 and cstc2019jcyj--msxmX0466; Chongqing
Postdoctoral Science Special Foundation, Grant/Award Number: XmT2018068;
National Natural Science Foundation of China, Grant/Award Number:
81903393 and 81903398
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NR 49
TC 4
Z9 4
U1 2
U2 22
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD OCT
PY 2022
VL 42
IS 10
BP 2216
EP 2226
DI 10.1111/liv.15355
EA JUL 2022
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 4D6VK
UT WOS:000825843700001
PM 35775855
DA 2025-01-07
ER
PT J
AU Natarajan, S
Thomson, AW
AF Natarajan, Sudha
Thomson, Angus W.
TI Tolerogenic dendritic cells and myeloid-derived suppressor cells:
Potential for regulation and therapy of liver auto- and alloimmunity
SO IMMUNOBIOLOGY
LA English
DT Article
DE Autoimmunity; Dendritic cells; Liver; Myeloid-derived suppressor cells;
Transplantation
ID NOVO AUTOIMMUNE HEPATITIS; CD4(+) T-CELLS; ANTIGEN-SPECIFIC SUPPRESSION;
VERSUS-HOST-DISEASE; TRANSPLANT TOLERANCE; MOLECULAR MIMICRY; REJECTION;
CANCER; CYTOCHROME-P450; DIFFERENTIATION
AB Organ transplantation is now established as an accepted treatment for end-stage liver disease, acute fulminant hepatic liver failure and hepatocellular carcinoma. While early graft acceptance rates have increased markedly due to improved immunosuppressive drug regimens, rates of late graft failure remain largely unchanged. Recent findings suggest that in addition to alloimmunity, chronic rejection of liver allografts may also reflect de novo autoimmune hepatitis or recurrence of pre-existing hepatic autoimmune disease. Dendritic cell (DC)- based therapy is a promising experimental approach to promotion of transplant tolerance and the treatment of autoimmune diseases. Newly emerging evidence also demonstrates the potential efficacy of myeloid-derived suppressor cells (MDSC) in the antigen (Ag)-specific regulation of T-cell responses. Herein, we discuss current understanding of liver autoimmunity post-transplantation, along with current approaches for the development of tolerogenic DC, and the potential use of MDSC for the development of stable, Ag-specific tolerance. Published by Elsevier GmbH.
C1 [Natarajan, Sudha; Thomson, Angus W.] Univ Pittsburgh, Sch Med, Dept Surg, Starzl Transplantat Inst, Pittsburgh, PA 15213 USA.
[Thomson, Angus W.] Univ Pittsburgh, Sch Med, Dept Immunol, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh
RP Thomson, AW (corresponding author), Univ Pittsburgh, 200 Lothrop St,BST W1540, Pittsburgh, PA 15261 USA.
EM thomsonaw@upmc.edu
FU NIH [R01 AI067541, U01 AI051698, P01 AI081678, T32 AI74490]
FX The authors' work is supported by NIH Grants R01 AI067541, U01 AI051698
and P01 AI081678 and by NIH institutional training grant T32 AI74490. We
are grateful to our colleagues for valuable discussion and suggestions.
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NR 72
TC 36
Z9 42
U1 1
U2 11
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0171-2985
J9 IMMUNOBIOLOGY
JI Immunobiology
PD SEP-OCT
PY 2010
VL 215
IS 9-10
SI SI
BP 698
EP 703
DI 10.1016/j.imbio.2010.05.024
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 646JT
UT WOS:000281536800005
PM 20605054
OA Green Accepted, hybrid
DA 2025-01-07
ER
PT J
AU Gnanasegaran, G
Agrawal, K
Wan, SM
AF Gnanasegaran, Gopinath
Agrawal, Kanhaiyalal
Wan, Simon
TI 18F-Flu o rod eoxyg l u cose-PET-Computerized Tomography and non-Fluor
odeoxyglucose PET-Computerized Tomography in Hepatobiliary and
Pancreatic Malignancies
SO PET CLINICS
LA English
DT Article
DE Hepatocellular cancer; Gall bladder cancer; Pancreatic cancer;
Cholangiocarcinoma
ID POSITRON-EMISSION-TOMOGRAPHY; LYMPH-NODE METASTASIS; ISLET-CELL TUMORS;
F-18 FDG PET/CT; HEPATOCELLULAR-CARCINOMA; GALLBLADDER CARCINOMA; LIVER
METASTASES; TRANSARTERIAL CHEMOEMBOLIZATION; AUTOIMMUNE PANCREATITIS;
NEUROENDOCRINE TUMORS
AB PET-CT plays important and expanding roles in the management of patients with hepatobiliary and pancreatic malignancies. In many instances, FDG PET-CT provides complementary information for lesion characterization, staging (especially nodal and distant staging), response evaluation, and detection of recurrent disease, where there are recognized limitations of conventional anatomic imaging in mainstay use. A multitude of non-FDG and novel tracers are in the pipeline with seemingly promising results as summarized in this article and further validation would be necessary before clinical adoption.
C1 [Gnanasegaran, Gopinath] Royal Free NHS Fdn Trust, London, England.
[Agrawal, Kanhaiyalal] All India Inst Med Sci, Bhuba neswar, India.
[Wan, Simon] Univ Coll London Hosp NHS Fdn Trust, London, England.
C3 University College London Hospitals NHS Foundation Trust; University of
London; University College London
RP Gnanasegaran, G (corresponding author), Royal Free NHS Fdn Trust, London, England.
EM gopinath.gnanasegaran@nhs.net
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NR 111
TC 3
Z9 3
U1 0
U2 2
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1556-8598
EI 1559-7814
J9 PET CLIN
JI PET Clin.
PD JUL
PY 2022
VL 17
IS 3
BP 369
EP 388
DI 10.1016/j.cpet.2022.03.007
PG 20
WC Radiology, Nuclear Medicine & Medical Imaging
WE Emerging Sources Citation Index (ESCI)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 2L5DY
UT WOS:000817038400004
PM 35717098
DA 2025-01-07
ER
PT J
AU Kaps, L
Limeres, MJ
Schneider, P
Svensson, M
Zeyn, Y
Fraude, S
Cacicedo, ML
Galle, PR
Gehring, S
Bros, M
AF Kaps, Leonard
Limeres, Maria Jose
Schneider, Paul
Svensson, Malin
Zeyn, Yanira
Fraude, Silvia
Cacicedo, Maximiliano L.
Galle, Peter R.
Gehring, Stephan
Bros, Matthias
TI Liver Cell Type-Specific Targeting by Nanoformulations for Therapeutic
Applications
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE liver; non-parenchymal cells; Kupffer cell; liver sinusoidal endothelial
cell; nanoformulation; hepatitis; fibrosis; hepatocellular carcinoma;
liver metastasis
ID SINUSOIDAL ENDOTHELIAL-CELLS; HEPATIC STELLATE CELLS; GROWTH-FACTOR
RECEPTOR; REGULATORY T-CELLS; A-STORING CELL; HEPATOCELLULAR-CARCINOMA;
DRUG-DELIVERY; TGF-BETA; TUMOR MICROENVIRONMENT; MANNOSE 6-PHOSPHATE
AB Hepatocytes exert pivotal roles in metabolism, protein synthesis and detoxification. Non-parenchymal liver cells (NPCs), largely comprising macrophages, dendritic cells, hepatic stellate cells and liver sinusoidal cells (LSECs), serve to induce immunological tolerance. Therefore, the liver is an important target for therapeutic approaches, in case of both (inflammatory) metabolic diseases and immunological disorders. This review aims to summarize current preclinical nanodrug-based approaches for the treatment of liver disorders. So far, nano-vaccines that aim to induce hepatitis virus-specific immune responses and nanoformulated adjuvants to overcome the default tolerogenic state of liver NPCs for the treatment of chronic hepatitis have been tested. Moreover, liver cancer may be treated using nanodrugs which specifically target and kill tumor cells. Alternatively, nanodrugs may target and reprogram or deplete immunosuppressive cells of the tumor microenvironment, such as tumor-associated macrophages. Here, combination therapies have been demonstrated to yield synergistic effects. In the case of autoimmune hepatitis and other inflammatory liver diseases, anti-inflammatory agents can be encapsulated into nanoparticles to dampen inflammatory processes specifically in the liver. Finally, the tolerance-promoting activity especially of LSECs has been exploited to induce antigen-specific tolerance for the treatment of allergic and autoimmune diseases.
C1 [Kaps, Leonard; Schneider, Paul; Galle, Peter R.] Univ Med Ctr Mainz, Dept Med, Langenbeckstr 1, D-55131 Mainz, Germany.
[Limeres, Maria Jose; Svensson, Malin; Fraude, Silvia; Cacicedo, Maximiliano L.; Gehring, Stephan] Univ Med Ctr, Childrens Hosp, Langenbeckstr 1, D-55131 Mainz, Germany.
[Zeyn, Yanira; Bros, Matthias] Univ Med Ctr Mainz, Dept Dermatol, Langenbeckstr 1, D-55131 Mainz, Germany.
C3 Johannes Gutenberg University of Mainz; Johannes Gutenberg University of
Mainz; Johannes Gutenberg University of Mainz
RP Bros, M (corresponding author), Univ Med Ctr Mainz, Dept Dermatol, Langenbeckstr 1, D-55131 Mainz, Germany.
EM leonardkaps@googlemail.com; mj.limeres@uni-mainz.de;
paschnei@students.uni-mainz.de; malin.svensson@uni-mainz.de;
yanira.zeyn@uni-mainz.de; silvia.fraude@unimedizin-mainz.de;
mcaciced@uni-mainz.de; galle@uni-mainz.de; stephan.gehring@uni-mainz.de;
mbros@uni-mainz.de
RI Galle, Peter/ABE-2872-2021
OI Fraude-El Ghazi, Silvia/0009-0005-9211-2513; Zeyn,
Yanira/0000-0002-2501-8149; Cacicedo, Maximiliano
Luis/0000-0002-3144-8794; Svensson, Malin/0009-0005-9889-6507; Limeres,
Maria Jose/0000-0003-2848-4679
FU Deutsche Forschungsgemeinschaft [SFB1066]
FX L.K., S.G. and M.B. are funded by Deutsche Forschungsgemeinschaft
(SFB1066), grant numbers B15 (S.G., M.B.) and B17 (L.K.).
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NR 254
TC 5
Z9 5
U1 1
U2 20
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2023
VL 24
IS 14
AR 11869
DI 10.3390/ijms241411869
PG 23
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA N7AH4
UT WOS:001038490800001
PM 37511628
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Wang, K
Chen, XY
Zhang, RWY
Yue, Y
Wen, XL
Yang, YS
Han, CY
Ma, Y
Liu, HJ
Zhu, HL
AF Wang, Kai
Chen, Xu-Yang
Zhang, Ren-Wei-Yang
Yue, Ying
Wen, Xiao-Lin
Yang, Yu-Shun
Han, Chen-Yang
Ma, Yuan
Liu, Hong-Ji
Zhu, Hai-Liang
TI Multifunctional fluorescence/photoacoustic bimodal imaging of
γ-glutamyltranspeptidase in liver disorders under different triggering
conditions
SO BIOMATERIALS
LA English
DT Article
DE Bimodal imaging; gamma-Glutamyltranspeptidase; Premonitory induction
stages; Multiple models
ID HEPATOCELLULAR-CARCINOMA; FLUORESCENT-PROBE; TRANSFERASE; DIAGNOSIS;
PATHOGENESIS; DISEASE; INJURY
AB Hepatocellular carcinoma (HCC) seriously threatens the human health. Previous investigations revealed that gamma-glutamyltranspeptidase (GGT) was tightly associated with the chronic injury, hepatic fibrosis, and the development of HCC, therefore might act as a potential indicator for monitoring the HCC-related processes. Herein, with the contribution of a structurally optimized probe ETYZE-GGT , the bimodal imaging in both far red fluorescence (FL) and photoacoustic (PA) modes has been achieved in multiple HCC-related models. To our knowledge, this work covered the most comprehensive models including the fibrosis and developed HCC processes as well as the premonitory induction stages (autoimmune hepatitis, drug-induced liver injury, nonalcoholic fatty liver disease). ETYZE-GGT exhibited steady and practical monitoring performances on reporting the HCC stages via visualizing the GGT dynamics. The two modes exhibited working consistency and complementarity with high spatial resolution, precise apparatus and desirable biocompatibility. In cooperation with the existing techniques including testing serum indexes and conducting pathological staining, ETYZE-GGT basically realized the universal application for the accurate pre-clinical diagnosis of as many HCC stages as possible. By deeply exploring the mechanically correlation between GGT and the HCC process, especially during the premonitory induction stages, we may further raise the efficacy for the early diagnosis and treatment of HCC.
C1 [Wang, Kai; Chen, Xu-Yang; Zhang, Ren-Wei-Yang; Yue, Ying; Wen, Xiao-Lin] Jiangnan Univ, Affiliated Childrens Hosp, Wuxi 214023, Peoples R China.
[Wang, Kai; Chen, Xu-Yang; Yang, Yu-Shun; Zhu, Hai-Liang] Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Nanjing 210023, Peoples R China.
[Ma, Yuan; Liu, Hong-Ji] Hunan Univ, Coll Chem & Chem Engn, State Key Lab Chemo Biosensing & Chemometr, Changsha 410082, Peoples R China.
[Han, Chen-Yang] Jiaxing Univ, Affiliated Hosp 2, Jiaxing 314001, Peoples R China.
C3 Jiangnan University; Nanjing University; Hunan University; Jiaxing
University
RP Zhu, HL (corresponding author), Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Nanjing 210023, Peoples R China.; Ma, Y; Liu, HJ (corresponding author), Hunan Univ, Coll Chem & Chem Engn, State Key Lab Chemo Biosensing & Chemometr, Changsha 410082, Peoples R China.
EM myhnu@hnu.edu.cn; liuhongji@hnu.edu.cn; zhuhl@nju.edu.cn
RI Liu, Hongji/AAE-6274-2021; Yue, Ying/ABY-8206-2022; Ma,
Yuan/P-6460-2019; Chen, Xuyang/JEO-6530-2023
FU China National Postdoctoral Program for Innovative Talents [BX20230111];
Double Innovation Doctor of Jiangsu Province [JSSCBS20221988]; Jiangsu
Provincial Health Commission Project [Z2022066]; Wuxi Science and
Technology Development Fund Project [K20221032]; Science and Technology
Development Fund Project of Nanjing Medical University, China
[NMUB20210311]
FX This work was financially supported by the fellowship of China National
Postdoctoral Program for Innovative Talents (BX20230111) , the Double
Innovation Doctor of Jiangsu Province (JSSCBS20221988) , the Jiangsu
Provincial Health Commission Project (Z2022066) , the Wuxi Science and
Technology Development Fund Project (K20221032) , the Science and
Technology Development Fund Project of Nanjing Medical University, China
(NMUB20210311) . The authors would like to thank Wen-Dong Li from
Shiyanjia Lab ( www.shiyanjia.com ) for the LC-MS analysis.
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NR 68
TC 1
Z9 1
U1 14
U2 17
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0142-9612
EI 1878-5905
J9 BIOMATERIALS
JI Biomaterials
PD OCT
PY 2024
VL 310
AR 122635
DI 10.1016/j.biomaterials.2024.122635
EA MAY 2024
PG 12
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA UG0P1
UT WOS:001246791000001
PM 38810386
DA 2025-01-07
ER
PT J
AU Jakate, S
Yabes, A
Giusto, D
Naini, B
Lassman, C
Yeh, MM
Ferrell, LD
AF Jakate, Shriram
Yabes, Annoel
Giusto, Deborah
Naini, Bita
Lassman, Charles
Yeh, Matthew M.
Ferrell, Linda D.
TI Diffuse Cirrhosis-like Hepatocellular Carcinoma A Clinically and
Radiographically Undetected Variant Mimicking Cirrhosis
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE hepatocellular carcinoma; cirrhosis-like; undetected; variant; diffuse
ID LIVER-TRANSPLANTATION; INTRAHEPATIC METASTASIS; MULTIPLE; SURVIVAL;
HETEROZYGOSITY; CLASSIFICATION; EXPRESSION; ORIGIN
AB A rare variant of hepatocellular carcinoma (HCC) is encountered that produces small cirrhosis-like nodules diffusely throughout the liver (CL-HCC), instead of a larger evident mass. This pattern remains undetected as carcinoma clinically and radiographically and is unexpectedly discovered after liver transplantation in the explanted native liver. We studied 10 such cases (9 males and 1 female, age 35 to 80 y) from 4 medical centers. The pretransplant clinical, laboratory, and radiographical studies were reviewed to determine the cause and stage of liver disease, alpha-fetoprotein (AFP) levels, and detectability of a mass on imaging. All 10 cases had underlying cirrhosis of varying etiology [3 hepatitis C virus (HCV), 3 alcoholic hepatitis, 1 hepatitis B virus, 1 autoimmune, and 2 mixed HCV/alcoholic hepatitis and hemochromatosis/HCV] and underwent orthotopic liver transplantation with no preoperative clinical suspicion of HCC. Ultrasound and/or dynamic imaging showed cirrhosis and no definite HCC. AFP levels were only mildly elevated in only 3 of 10 cases (144, 150, and 252 ng/mL). Grossly, there were innumerable (from about 20 to > 1000) small CL-HCC nodules (0.2 to 0.6 cm) scattered among cirrhotic nodules. Histologically, these were well or moderately differentiated HCC, often with pseudoglandular pattern, perinodular sclerotic rims, cholestasis, frequent Mallory bodies, and small vessel invasion. In addition to the usual HCC immunophenotype, CL-HCC showed frequent ubiquitin and cytoplasmic and membranous CD10 positivity, relatively low Ki-67 proliferative index and absence of AFP immunohistochemically. CL-HCC warrants recognition as a unique HCC variant that evades pretransplant detection despite massive tumor burden, mimics cirrhotic nodules, and shows some uncommon pathologic and immunophenotypical characteristics.
C1 [Jakate, Shriram] Rush Univ, Med Ctr, Dept Pathol, Chicago, IL 60612 USA.
[Yabes, Annoel; Ferrell, Linda D.] Univ Calif San Francisco, Med Ctr, Dept Pathol, San Francisco, CA 94143 USA.
[Naini, Bita; Lassman, Charles] Univ Calif Los Angeles, Med Ctr, Dept Pathol, Los Angeles, CA 90024 USA.
[Giusto, Deborah] Univ Pittsburgh, Dept Pathol, Pittsburgh, PA USA.
[Yeh, Matthew M.] Univ Washington, Dept Pathol, Seattle, WA 98195 USA.
C3 Rush University; University of California System; University of
California San Francisco; University of California System; University of
California Los Angeles; University of California Los Angeles Medical
Center; Pennsylvania Commonwealth System of Higher Education (PCSHE);
University of Pittsburgh; University of Washington; University of
Washington Seattle
RP Jakate, S (corresponding author), Rush Univ, Med Ctr, Dept Pathol, 1750 W Harrison St, Chicago, IL 60612 USA.
EM sjakate@rush.edu
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Z9 32
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
J9 AM J SURG PATHOL
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PY 2010
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BP 935
EP 941
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WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA 615VY
UT WOS:000279167400003
PM 20463569
DA 2025-01-07
ER
PT J
AU Tripathi, D
Neuberger, J
AF Tripathi, Dhiraj
Neuberger, James
TI Autoimmune Hepatitis and Liver Transplantation: Indications, Results,
and Management of Recurrent Disease
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE Autoimmune hepatitis; liver transplantation; recurrence; de novo
autoimmune hepatitis
ID PRIMARY BILIARY-CIRRHOSIS; LATE GRAFT DYSFUNCTION; SINGLE-CENTER
EXPERIENCE; NOVO IMMUNE HEPATITIS; HEPATOCELLULAR-CARCINOMA;
MYCOPHENOLATE-MOFETIL; RISK-FACTORS; FOLLOW-UP; CLINICAL PRESENTATION;
REJECTION
AB For those with autoimmune hepatitis (AIH), indications for liver transplantation include end-stage liver failure (as suggested by a MELD score > 16), the onset of liver cancer, intractable symptoms that make the patient's life intolerable, and fulminant liver failure; outcomes are excellent, with 10-year survival in excess of 70%. For those with a fulminant presentation, the impact of corticosterolds is controversial and liver transplantation may be required. Autoimmune hepatitis recurs in approximately one third and may be detected tip to 10 years or more post-transplant. There are no agreed-on criteria for the diagnosis, and differentiation from rejection and other causes of graft damage call be difficult. There is no strong correlation between the prevalence of recurrent AIH (rAIH) and graft loss from rAIH. Treatment of recurrent disease with the addition or increase in corticosteroids is often successful, although long-term data are lacking and some may progress to graft failure despite increased treatment. There remains controversy over the role for protocol liver biopsies to detect recurrent disease and the best immunosuppressive strategies to prevent and treat recurrence.
C1 [Tripathi, Dhiraj; Neuberger, James] Univ Hosp Birmingham, NHS Fdn Trust, Liver Unit, Birmingham B15 2TH, W Midlands, England.
C3 University of Birmingham; Oxford University Hospitals NHS Foundation
Trust
RP Neuberger, J (corresponding author), Univ Hosp Birmingham, NHS Fdn Trust, Liver Unit, Birmingham B15 2TH, W Midlands, England.
EM James.Neuberger@uhb.nhs.uk
RI Neuberger, James/ABG-3010-2020
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NR 86
TC 29
Z9 32
U1 0
U2 3
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD AUG
PY 2009
VL 29
IS 3
BP 286
EP 296
DI 10.1055/s-0029-1233531
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 483YE
UT WOS:000269008500006
PM 19676001
DA 2025-01-07
ER
PT J
AU Gomes, NBN
Torres, US
Ferraz, MLCG
D'Ippolito, G
AF Nunes Gomes, Natalia Borges
Torres, Ulysses S.
Cardoso Gomes Ferraz, Maria Lucia
D'Ippolito, Giuseppe
TI Autoimmune hepatitis in practice, from diagnosis to complications: What
is the role of imaging? A clinicoradiological review
SO CLINICAL IMAGING
LA English
DT Review
DE Hepatitis; autoimmune; chronic; Diagnostic imaging
ID MULTIPARAMETRIC MAGNETIC-RESONANCE; HEPATOCELLULAR-CARCINOMA; TRANSIENT
ELASTOGRAPHY; HEPATOLOGY RECOMMENDATIONS; BRAZILIAN SOCIETY; OVERLAP
SYNDROMES; LIVER FIBROSIS; MANAGEMENT; MRI; DISEASES
AB Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease of unknown origin that can lead to liver cirrhosis, hepatocellular carcinoma (HCC), liver transplantation or death. The diagnosis is performed upon a multifactorial score. Treatment is based on the combination of immunosuppressants and aims at clinical, laboratory and histological remission, the latter being the most difficult to be achieved and proven. The absence of liver inflammation, defined by biopsy, is the main determinant in remission or therapeutic modification. Imaging exams have a limited role in this clinical management and the main findings are those related to chronic liver disease. Imaging?s relevance, therefore, lies mainly in helping to exclude overlapping syndromes and in assessing complications related to cirrhosis, such as in screening for HCC. In recent years, however, the radiological literature has been witnessing increasing advances with regard to imaging biomarkers in liver disease, leading some authors to consider a future of virtual liver biopsy performed by magnetic resonance imaging. The present study aims to review the role of imaging in the management of AIH in the light of recent advances in the current literature and to provide an illustrated guide with the main findings described in the disease.
C1 [Nunes Gomes, Natalia Borges; Torres, Ulysses S.; D'Ippolito, Giuseppe] Fleury Grp, Rua Cincinato Braga 282, BR-01333010 Sao Paulo, SP, Brazil.
[Nunes Gomes, Natalia Borges; Torres, Ulysses S.; D'Ippolito, Giuseppe] Univ Fed Sao Paulo UNIFESP, Hosp Sao Paulo, Dept Diagnost Imaging, Sao Paulo, Brazil.
[Cardoso Gomes Ferraz, Maria Lucia] Univ Fed Sao Paulo UNIFESP, Hosp Sao Paulo, Dept Gastroenterol, Sao Paulo, Brazil.
C3 FLEURY GROUP; Universidade Federal de Sao Paulo (UNIFESP); Universidade
Federal de Sao Paulo (UNIFESP)
RP Torres, US (corresponding author), Fleury Grp, Rua Cincinato Braga 282, BR-01333010 Sao Paulo, SP, Brazil.
EM ulysses.torres@grupofleury.com.br
RI D'Ippolito, Giuseppe/LGZ-6822-2024; FERRAZ, MARIA/LKJ-5294-2024; Torres,
Ulysses/E-6034-2011
OI D'Ippolito, Giuseppe/0000-0002-2701-1928; Torres,
Ulysses/0000-0002-1911-9090
FU Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior -Brazil
(CAPES) [001]
FX This study was financed in part by the Coordenacao de Aperfeicoamento de
Pessoal de Nivel Superior -Brazil (CAPES) - Finance Code 001.
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NR 57
TC 4
Z9 6
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0899-7071
EI 1873-4499
J9 CLIN IMAG
JI Clin. Imaging
PD JUN
PY 2021
VL 74
BP 31
EP 40
DI 10.1016/j.clinimag.2020.12.032
EA JAN 2021
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA RS5YX
UT WOS:000643855500008
PM 33429144
DA 2025-01-07
ER
PT J
AU Zarrinpar, A
Kim, UB
Boominathan, V
AF Zarrinpar, Ali
Kim, Un Bi
Boominathan, Vijay
TI Phenotypic Response and Personalized Medicine in Liver Cancer and
Transplantation: Approaches to Complex Systems
SO ADVANCED THERAPEUTICS
LA English
DT Article
DE artificial intelligence; immunosuppression; liver cancer; liver
transplants; precision medicine
ID WITHIN-PATIENT VARIABILITY; GENOME-WIDE ASSOCIATION;
HEPATOCELLULAR-CARCINOMA; ACUTE REJECTION; T-CELLS; NONALCOHOLIC
STEATOHEPATITIS; PRECISION MEDICINE; ORGAN-TRANSPLANTATION; AUTOIMMUNE
HEPATITIS; GENE POLYMORPHISMS
AB Rapid improvements in medical technology, big data analysis, and molecular medicine come with promises of revolutionizing medical care. They span the spectrum from diagnostics to genome-based drug selection to multi-biomarker analysis to deciphering large amounts of data. Below, recent developments in personalized and precision medicine are reviewed, focusing specifically on the liver, ranging from fatty liver disease to liver cancer treatment and liver transplantation. Furthermore, current technologies and their advantages and limitations are discussed, in addition to ways in which these disadvantages can be overcome, using phenotypic personalized medicine.
C1 [Zarrinpar, Ali; Kim, Un Bi; Boominathan, Vijay] Univ Florida, Coll Med, Dept Surg, Gainesville, FL 32610 USA.
[Zarrinpar, Ali] Univ Florida, Coll Med, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA.
[Zarrinpar, Ali] Univ Florida, Dept Bioengn, Herbert Wertheim Coll Engn, Gainesville, FL 32610 USA.
C3 State University System of Florida; University of Florida; State
University System of Florida; University of Florida; State University
System of Florida; University of Florida
RP Zarrinpar, A (corresponding author), Univ Florida, Coll Med, Dept Surg, Gainesville, FL 32610 USA.; Zarrinpar, A (corresponding author), Univ Florida, Coll Med, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA.; Zarrinpar, A (corresponding author), Univ Florida, Dept Bioengn, Herbert Wertheim Coll Engn, Gainesville, FL 32610 USA.
EM Ali.Zarrinpar@surgery.ufl.edu
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NR 147
TC 0
Z9 0
U1 1
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2366-3987
J9 ADV THER-GERMANY
JI Adv. Therap.
PD APR
PY 2020
VL 3
IS 4
SI SI
AR 1900167
DI 10.1002/adtp.201900167
EA FEB 2020
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA LH4MG
UT WOS:000512924600001
DA 2025-01-07
ER
PT J
AU Breuhahn, K
Baeuerle, PA
Peters, M
Prang, N
Töx, U
Köhne-Volland, R
Dries, V
Schirmacher, P
Leo, E
AF Breuhahn, K
Baeuerle, PA
Peters, M
Prang, N
Töx, U
Köhne-Volland, R
Dries, V
Schirmacher, P
Leo, E
TI Expression of epithelial cellular adhesion molecule (Ep-CAM) in chronic
(necro-)inflammatory liver diseases and hepatocellular carcinoma
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE Ep-CAM; liver; inflammation; fibrosis; hepatocellular carcinoma;
immunotherapy
ID EPCAM; ANTIBODY; ANTIGEN; TARGET; CANCER; PROTEIN; CELLS
AB Epithelial cell adhesion molecule (Ep-CAM) is expressed in a several epithelial tissues and carcinomas, but not on mature hepatocytes. Here, we analysed the expression of Ep-CAM in 230 patients suffering from various liver diseases like chronic hepatitis B and C (HBV and HCV infection), chronic autoimmune hepatitis (AIH), chronic alcoholic liver disease (ALD), primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), hereditary hemochromatosis and dysplastic nodules (DNs) as well as hepatocellular carcinomas (HCCs) and cholangiocellular carcinomas (CCCs) by immunohistochemistry. De novo hepatocellular Ep-CAM expression was found in 75.9% of ALD (22/29), 63.6% of HCV (21/33) and 55.6% of each AIH and HBV cases (5/9 and 15/27, respectively). Lower Ep-CAM expression levels were observed for primary sclerosing liver diseases (PBC and PSC) with 25% (3/12) and 7.7% (1/13) of cases. Moreover, only 14.3% of HCCs (9/63) manifested expression, while all CCCs showed strong Ep-CAM expression (5/5). For DNs and hereditary hemochromatosis, Ep-CAM expression was found in 10 and 50% (3/30 and 2/4), respectively. In HBV and HCV, Ep-CAM expression correlated significantly with inflammatory activity as assessed by histological parameters and to the extent of fibrosis. In addition, for HCV also transaminase levels correlated significantly with Ep-CAM expression. Our results indicate that de novo Ep-CAM expression in hepatocytes is frequent in inflammatory liver diseases and is potentially linked to regenerative activity. CCCs and Ep-CAM positive HCCs may represent an attractive target group for Ep-CAM-directed immunotherapies, yet unwanted toxicity may limit the use of such strategies due to Ep-CAM expression in biliary epithelium and several chronic liver diseases such as HBV-and HCV-hepatitis. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
C1 Univ Heidelberg Hosp, Inst Pathol, D-69120 Heidelberg, Germany.
Micromet AG, D-81477 Munich, Germany.
Univ Cologne, Dept Med 4, D-50931 Cologne, Germany.
Clin Res GmbH, Metronomia, D-81245 Munich, Germany.
Inst Pathol, D-68055 Mannheim, Germany.
C3 Ruprecht Karls University Heidelberg; Amgen; Amgen Research Munich GmbH;
Micromet AG; University of Cologne
RP Univ Heidelberg Hosp, Inst Pathol, Neuenheimer Feld 220-221, D-69120 Heidelberg, Germany.
EM kai.breuhahn@med.uni-heidelberg.de
OI Breuhahn, Kai/0000-0002-2462-1229
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NR 19
TC 20
Z9 27
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD JAN
PY 2006
VL 34
IS 1
BP 50
EP 56
DI 10.1016/j.hepres.2005.10.006
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 010KQ
UT WOS:000235194000009
PM 16364680
DA 2025-01-07
ER
PT J
AU Zhang, CY
Sui, YX
Liu, S
Yang, M
AF Zhang, Chunye
Sui, Yuxiang
Liu, Shuai
Yang, Ming
TI The Roles of Myeloid-Derived Suppressor Cells in Liver Disease
SO BIOMEDICINES
LA English
DT Article
DE myeloid-derived suppressor cells; liver inflammation; fibrosis;
hepatocellular carcinoma; cell-cell interaction; clinical trials
ID HEPATOCELLULAR-CARCINOMA PATIENTS; MOLECULAR-MECHANISMS; ANTITUMOR
RESPONSE; IMMUNE SUPPRESSION; HEPATITIS; INFLAMMATION; ACCUMULATION;
RECRUITMENT; MICE; MDSC
AB Liver disease-related mortality is a major cause of death worldwide. Hepatic innate and adaptive immune cells play diverse roles in liver homeostasis and disease. Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells. MDSCs can be broadly divided into monocytic MDSCs and polymorphonuclear or granulocytic MDSCs, and they functionally interact with both liver parenchymal and nonparenchymal cells, such as hepatocytes and regulatory T cells, to impact liver disease progression. The infiltration and activation of MDSCs in liver disease can be regulated by inflammatory chemokines and cytokines, tumor-associated fibroblasts, epigenetic regulation factors, and gut microbiota during liver injury and cancer. Given the pivotal roles of MDSCs in advanced liver diseases, they can be targeted to treat primary and metastatic liver cancer, liver generation, alcoholic and nonalcoholic liver disease, and autoimmune hepatitis. Currently, several treatments such as the antioxidant and anti-inflammatory agent berberine are under preclinical and clinical investigation to evaluate their therapeutic efficacy on liver disease and their effect on MDSC infiltration and function. Phenotypic alteration of MDSCs in different liver diseases that are in a model-dependent manner and lack special markers for distinct MDSCs are challenges for targeting MDSCs to treat liver disease. Multi-omics study is an option to uncover the features of disease-specific MDSCs and potential gene or protein targets for liver disease treatment. In summary, MDSCs play important roles in the pathogenesis and progression of liver disease by regulating both intrahepatic innate and adaptive immune responses.
C1 [Zhang, Chunye] Univ Missouri, Christopher S Bond Life Sci Ctr, Columbia, MO 65212 USA.
[Sui, Yuxiang] Shanxi Normal Univ, Sch Life Sci, Linfen 041004, Peoples R China.
[Liu, Shuai] Zhejiang Univ, Affiliated Hosp 1, Hangzhou 310006, Peoples R China.
[Yang, Ming] Univ Missouri, Dept Surg, Columbia, MO 65212 USA.
[Yang, Ming] Univ Missouri, NextGen Precis Hlth Inst, Columbia, MO 65212 USA.
C3 University of Missouri System; University of Missouri Columbia; Shanxi
Normal University; Zhejiang University; University of Missouri System;
University of Missouri Columbia; University of Missouri System;
University of Missouri Columbia
RP Yang, M (corresponding author), Univ Missouri, Dept Surg, Columbia, MO 65212 USA.; Yang, M (corresponding author), Univ Missouri, NextGen Precis Hlth Inst, Columbia, MO 65212 USA.
EM zhangcherryuniversity@gmail.com; yangmin@health.missouri.edu
RI Zhang, Chunye/ABF-8130-2021; Yang, Ming/AAS-8838-2021
OI Yang, Ming/0000-0002-4895-5864; Zhang, Chunye/0000-0003-2567-029X
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NR 110
TC 2
Z9 2
U1 2
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD FEB
PY 2024
VL 12
IS 2
AR 299
DI 10.3390/biomedicines12020299
PG 15
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA ZQ6I4
UT WOS:001276796200001
PM 38397901
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Wuyts, L
Janssens, A
Vonghia, L
Michielsen, P
Raskin, J
Driessen, A
Van Hees, S
Francque, S
Vanwolleghem, T
AF Wuyts, Laura
Janssens, Annelies
Vonghia, Luisa
Michielsen, Peter
Raskin, Jo
Driessen, Ann
Van Hees, Stijn
Francque, Sven
Vanwolleghem, Thomas
TI Nivolumab and anti-HCV activity, a case report
SO ACTA CLINICA BELGICA
LA English
DT Article
DE Nivolumab; anti-PD1; hepatitis C; HCC; immune checkpoint inhibitor
ID IMMUNE CHECKPOINT BLOCKADE; HEPATOCELLULAR-CARCINOMA; HEPATITIS;
IMMUNOTHERAPY; ANTIBODIES
AB Exhaustion of antigen-specific T-cells in order to escape immune destruction is frequently seen in chronic viral infection and different types of cancer. Blockade of overexpressed negative co-stimulatory pathways, a process known as immune checkpoint modulation, is a promising novel therapy that could improve the treatment of liver diseases with features of T cell exhaustion. We present a case of a 54-year-old hepatitis C virus (HCV) positive patient with an acute flare of hepatitis during nivolumab treatment for a stage IV lung carcinoma, an anti-programmed death-1 (PD-1) immunotherapy. Retrospective testing of HCV RNA documented infection more than 6 months ago. Nivolumab treatment was associated with an alanine aminotransferase (ALT) flare reaching a peak value of 663 U/L, along with bilirubin levels of 0.74 mg/dL and no signs of coagulopathy. The assumption of a nivolumab-associated autoimmune hepatitis led to the interruption of the immune checkpoint inhibitor treatment. However, a subsequent 1-log decrease of HCV RNA load was noticed, which raised the possibility of an immune reconstitution against the HCV-infected hepatocytes with cell lysis. Liver biopsy specimen demonstrated no evidence for autoimmune liver disease or fibrosis. Clinical evolution was favorable and serum transaminases returned to normal levels and HCV RNA load increased to baseline values following nivolumab cessation. The current case suggests an anti-HCV activity of anti-PD-1 treatment in the setting of concomitant HCV viremia and lung carcinoma.
C1 [Wuyts, Laura; Vonghia, Luisa; Michielsen, Peter; Van Hees, Stijn; Francque, Sven; Vanwolleghem, Thomas] Antwerp Univ Hosp UZA, Dept Gastroenterol & Hepatol, Wilrijkstr 10, B-2650 Antwerp, Belgium.
[Janssens, Annelies; Raskin, Jo] Antwerp Univ Hosp UZA, Dept Thorac Oncol, Antwerp, Belgium.
[Vonghia, Luisa; Van Hees, Stijn; Francque, Sven; Vanwolleghem, Thomas] Univ Antwerp, Translat Sci Inflammat & Immunol TWI2N, Fac Med & Hlth Sci, Antwerp, Belgium.
[Driessen, Ann] Antwerp Univ Hosp UZA, Dept Pathol, Antwerp, Belgium.
C3 University of Antwerp; University of Antwerp; University of Antwerp;
University of Antwerp
RP Wuyts, L (corresponding author), Antwerp Univ Hosp UZA, Dept Gastroenterol & Hepatol, Wilrijkstr 10, B-2650 Antwerp, Belgium.
EM wuyts.laura8@gmail.com
RI Francque, Sven/E-4526-2017; Vanwolleghem, Thomas/AAD-4094-2022;
Michielsen, Peter/D-7088-2017; Vonghia, Luisa/ABC-4169-2020; Janssens,
Annelies/AGA-9071-2022; Driessen, Ann/D-3768-2017
OI Vanwolleghem, Thomas/0000-0002-0572-8741
CR [Anonymous], 2017, HEMONC TODAY, V18, P46
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NR 19
TC 3
Z9 4
U1 0
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1784-3286
EI 2295-3337
J9 ACTA CLIN BELG
JI Acta Clin. Belg.
PD SEP 3
PY 2021
VL 76
IS 5
BP 392
EP 396
DI 10.1080/17843286.2020.1741897
EA MAR 2020
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA UL8RR
UT WOS:000520556900001
PM 32182200
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Surdea-Blaga, T
Caragut, R
Caraiani, C
Sparchez, Z
al Hajjar, N
Dumitrascu, DL
AF Surdea-Blaga, Teodora
Caragut, Roxana L.
Caraiani, Cosmin
Sparchez, Zeno
al Hajjar, Nadim
Dumitrascu, Dan L.
TI Overlap syndrome of autoimmune hepatitis and primary biliary cholangitis
complicated with atypical hepatocellular carcinoma: a case report
SO JOURNAL OF MEDICAL CASE REPORTS
LA English
DT Article
DE Hepatocellular carcinoma; Primary biliary cholangitis; Autoimmune
hepatitis; Liver cirrhosis; Atypical liver resection; Case report
ID PRIMARY SCLEROSING CHOLANGITIS
AB BackgroundHepatocellular carcinoma (HCC) is a primary tumor of the liver. The majority of HCCs are associated most frequently with chronic B or C viral hepatitis, alcohol intake or aflatoxin exposure. Cirrhosis is a strong risk factor associated with HCC. The causes of liver cirrhosis are chronic viral hepatitis, alcohol intake, metabolic diseases (NAFLD), hemocromathosis, alfa 1 antitrypsisn deficiency. All aetiologic forms of cirrhosis are at risk to be complicated by HCC development, but the risk is higher for patients diagnosed with chronic viral hepatitis. Comparing to the above-mentioned causes, PBC and AIH are less associated with the risk of HCC development.Case summaryA 71-year old Caucasian female previously diagnosed with overlap syndrome (AIH type 1 and PBC-ANA, SMA and AMA antibodies positive), liver cirrhosis, a nodule in the VI/VIIth hepatic segment, systemic sclerosis sine scleroderma, Hashimoto's thyroiditis, antiphospholipid syndrome, gastric antral vascular ectasia (GAVE) (with 2 previous sessions of argon plasma coagulation), cholecystectomy, arterial hypertension and nephro-angiosclerosis presented to the 2nd Department of Internal Medicine in Cluj-Napoca for a follow-up. The patient was following treatment with UDCA (Ursodeoxycholic acid), azathioprine, Plaquenil, calcium channel blockers, angiotensin-converting-enzyme inhibitor, calcium and vitamin D supplementation. The abdominal ultrasound showed a subcapsular hypoechoic nodule with a diameter of 29 mm (at the moment of the diagnosis the diameter was 9/10 mm) in the VI/VIIth hepatic segment. The contrast-enhanced ultrasound (CEUS) characterised the nodule as specific for hepatocellular carcinoma (LI-RADS 5). On MRI with gadoxetate disodium the nodule was hypovascular, non-specific, being classified as LI-RADS 3. An atypical resection of the VIIth hepatic segment was performed and the histohistological examination and imunohistochemistry (Hep Par-a positive, Glypican3 positive, CD34 positive) revealed a moderately differentiated hepatocellular carcinoma (G2), pT2 N0 M0 L0 V1 R0.ConclusionAutoimmune hepatitis, PBC and the overlap syndrome are less associated with the development of liver cirrhosis and HCC than other chronic liver diseases, especially if other risk factors are not associated. This case highlights the importance of a proper surveillance of cirrhotic patients every 6 months including abdominal ultrasound and AFP levels is crucial for an early diagnosis of a HCC.
C1 [Surdea-Blaga, Teodora; Caraiani, Cosmin; Sparchez, Zeno; al Hajjar, Nadim; Dumitrascu, Dan L.] Iuliu Hatieganu Univ Med & Pharm, Cluj Napoca, Romania.
[Surdea-Blaga, Teodora; Dumitrascu, Dan L.] Cty Emergency Hosp, Dept Internal Med 2, Cluj Napoca, Romania.
[Caragut, Roxana L.; Sparchez, Zeno; al Hajjar, Nadim] Reg Inst Gastroenterol & Hepatol, 19 21 Croitorilor St, Cluj Napoca 400162, Romania.
C3 Iuliu Hatieganu University of Medicine & Pharmacy; Regional Institute of
Gastroenterology & Hepatology
RP Caragut, R (corresponding author), Reg Inst Gastroenterol & Hepatol, 19 21 Croitorilor St, Cluj Napoca 400162, Romania.
EM roxanacaragut@gmail.com
RI Surdea-Blaga, Teodora/IAM-5919-2023
OI Caragut, Roxana-Luiza/0000-0003-4174-0390
CR Beuers U, 2009, J HEPATOL, V51, P237, DOI 10.1016/j.jhep.2009.04.009
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Boonstra K, 2012, J HEPATOL, V56, P1181, DOI 10.1016/j.jhep.2011.10.025
Caraiani C, 2021, BIOLOGY-BASEL, V10, DOI 10.3390/biology10050412
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NR 19
TC 1
Z9 1
U1 0
U2 2
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1752-1947
J9 J MED CASE REP
JI J. Med. Case Rep.
PD JUL 25
PY 2023
VL 17
IS 1
AR 328
DI 10.1186/s13256-023-03932-y
PG 8
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA M8BY8
UT WOS:001032426200001
PM 37488645
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Iftikhar, R
Kladney, RD
Havlioglu, N
Schmitt-Gräff, A
Gusmirovic, I
Solomon, H
Luxon, BA
Bacon, BR
Fimmel, CJ
AF Iftikhar, R
Kladney, RD
Havlioglu, N
Schmitt-Gräff, A
Gusmirovic, I
Solomon, H
Luxon, BA
Bacon, BR
Fimmel, CJ
TI Disease- and cell-specific expression of GP73 in human liver disease
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article; Proceedings Paper
CT 53rd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Disease
CY NOV 04, 2002
CL Boston, MA
ID GOLGI MEMBRANE-PROTEIN; GENE-EXPRESSION; HEPATOCELLULAR-CARCINOMA;
INTERFERON-GAMMA; ACUTE HEPATITIS; INFECTION; ETHANOL; CANCER
AB OBJECTIVES: GP73, a Golgi membrane protein, is expressed at high levels in hepatocytes of patients with decompensated cirrhosis. Its expression in other forms of liver disease has not been investigated. Therefore, we studied GP73 expression in patients with noncirrhotic liver disease.
METHODS: GP73 expression was detected immunohistochemically and by immunofluorescence microscopy in patients with acute hepatitis of various etiologies, autoimmune hepatitis, chronic HCV infection, and alcoholic liver disease. In order to quantitate hepatocyte GP73 expression, an immunohistochemical scoring system was developed, and validated by a direct comparison with GP73 protein levels as determined by Western blotting.
RESULTS: GP73 immunostaining and Western blotting data were highly correlated, demonstrating the suitability of the immunohistochemical scoring system to quantitate hepatocyte GP73 expression. Hepatocyte GP73 expression was increased in patients with acute and autoimmune hepatitis. Treatment of autoimmune hepatitis was associated with a normalization of GP73 expression, indicating that the initial upregulation was reversible. Increased levels of GP73 expression were also noted in chronic HCV infection and alcoholic liver disease. Under these conditions, GP73 levels were correlated with disease stage but not grade. GP73 immunoreactivity was occasionally detected in alpha-SMA-positive, sinusoidal lining cells, suggesting activated stellate cells as a potential source of GP73.
CONCLUSIONS: Hepatocyte GP73 levels are upregulated in acute hepatitis and during the progression of liver disease to cirrhosis. This expression pattern suggests the presence of two regulatory mechanisms, the first triggered during acute hepatocellular injury, the second during the progression of chronic liver disease.
C1 St Louis Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol, St Louis, MO 63103 USA.
John Cochran VA Med Ctr, Gastroenterol Sect, St Louis, MO USA.
St Louis Univ, Sch Med, Dept Pathol, St Louis, MO 63103 USA.
Univ Freiburg, Inst Pathol, D-7800 Freiburg, Germany.
St Louis Univ, Sch Med, Dept Surg, St Louis, MO 63103 USA.
St Louis Univ, Ctr Liver, St Louis, MO 63103 USA.
C3 Saint Louis University; Saint Louis University; University of Freiburg;
Saint Louis University; Saint Louis University
RP Fimmel, CJ (corresponding author), St Louis VA Med Ctr, 915 N Grand Blvd, St Louis, MO 63106 USA.
RI Luxon, Bruce/C-9140-2012
CR [Anonymous], 1984, BIOSTATISTICAL ANAL
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NR 26
TC 107
Z9 158
U1 1
U2 20
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD JUN
PY 2004
VL 99
IS 6
BP 1087
EP 1095
DI 10.1111/j.1572-0241.2004.30572.x
PG 9
WC Gastroenterology & Hepatology
WE Conference Proceedings Citation Index - Science (CPCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 830OK
UT WOS:000222131900022
PM 15180730
DA 2025-01-07
ER
PT J
AU Kanaka, S
Kawano, Y
Yokomuro, S
Ando, F
Itokawa, N
Hatori, T
Matsumoto, K
Zen, Y
Miyashita, M
Yoshida, H
AF Kanaka, Shintaro
Kawano, Youichi
Yokomuro, Shigeki
Ando, Fumihiko
Itokawa, Norio
Hatori, Tsutomu
Matsumoto, Koshi
Zen, Yoh
Miyashita, Masao
Yoshida, Hiroshi
TI Hemochromatosis and Hepatocellular Carcinoma Secondary to Immunoglobulin
G4-Related Disease with Hepatopathy: A Case Report
SO JOURNAL OF NIPPON MEDICAL SCHOOL
LA English
DT Article
DE IgG4-related disease; IgG4-hepatopathy; secondary hemochromatosis;
hepatocellular carcinoma
ID AUTOIMMUNE HEPATITIS; DIAGNOSIS
AB Immunoglobulin G4-related disease (IgG4-RD) is a recently characterized illness in which lymphocytes and plasma cells infiltrate various anatomical sites. IgG4-hepatopathy, a manifestation of IgG4-RD, is a broader term covering various patterns of liver injury. The clinical course, including the malignant potential of IgG4-RD, remains unclear. Here we report the first case of secondary hemochromatosis and hepatocellular carcinoma (HCC) developing from IgG4-hepatopathy. A 67-year-old man was admitted to our hospital for treatment of deteriorating glucose tolerance. Blood test results showed hypergam-maglobulinemia, especially IgG4. He was readmitted 2 months later with dyspnea due to lung disease and pleural effusion, and elevated transaminase levels. He underwent liver and lung biopsies. IgG4-RD was diagnosed and he was treated with steroid therapy, which improved serum IgG4 levels and imaging abnormalities. A follow-up computed tomography (CT) scan conducted 38 months later revealed a tumor (diameter, 50 mm) in liver segments 7 and 8. The resected specimen revealed HCC and abundant siderosis in the background liver, indicating a diagnosis of hemochromatosis. IgG4-positive cells were scarce, probably because of corticosteroid therapy. In the present case, IgG4-RD was well controlled with prednisolone (PSL) and an immunosuppressive agent, and chronic hepatitis was not severe, even though the patient subsequently developed HCC. However, extensive siderosis consistent with hemochromatosis was unexpectedly noted. These findings suggest that secondary hemochromatosis and HCC developed during IgG4-RD with hepatopathy. We believe this case sheds light on IgG4-RD.
C1 [Kanaka, Shintaro; Yoshida, Hiroshi] Nippon Med Sch, Dept Surg, Tokyo, Japan.
[Kawano, Youichi; Yokomuro, Shigeki; Ando, Fumihiko; Miyashita, Masao] Nippon Med Sch, Dept Surg, Chiba Hokusoh Hosp, Chiba, Japan.
[Itokawa, Norio] Nippon Med Sch, Dept Internal Med, Div Gastroenterol, Chiba Hokusoh Hosp, Chiba, Japan.
[Hatori, Tsutomu] Nippon Med Sch, Dept Clin Pathol, Chiba Hokusoh Hosp, Chiba, Japan.
[Matsumoto, Koshi] Ebina Gen Hosp, Dept Pathol, Ebina, Kanagawa, Japan.
[Zen, Yoh] Kobe Univ, Dept Diagnost Pathol, Grad Sch Med, Kobe, Hyogo, Japan.
C3 Nippon Medical School; Nippon Medical School; Nippon Medical School;
Nippon Medical School; Kobe University
RP Kanaka, S (corresponding author), Nippon Med Sch, Dept Surg, Bunkyo Ku, 1-1-5 Sendagi, Tokyo 1138603, Japan.
EM ks32814@nms.ac.jp
RI Yoshida, Hiroshi/J-2900-2019
OI Ando, Fumihiko/0000-0002-8192-3055; Yoshida,
Hiroshi/0000-0002-2463-9023; Kanaka, Shintaro/0000-0002-9466-2229
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NR 23
TC 0
Z9 0
U1 0
U2 1
PU MEDICAL ASSOC NIPPON MEDICAL SCH
PI TOKYO
PA 1-1-5, SENDAGI, TOKYO, 113-8602, JAPAN
SN 1345-4676
EI 1347-3409
J9 J NIPPON MED SCH
JI J. Nippon Med. Sch.
PD APR
PY 2021
VL 88
IS 2
BP 138
EP 144
DI 10.1272/jnms.JNMS.2021_88-306
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA TT7HM
UT WOS:000680515600009
PM 32741904
OA gold
DA 2025-01-07
ER
PT J
AU Cho, H
Chang, Y
Lee, JH
Cho, YY
Nam, JY
Lee, YB
Lee, DH
Cho, EJ
Yu, SJ
Kim, YJ
Lee, JM
Yoon, JH
AF Cho, Hyeki
Chang, Young
Lee, Jeong-Hoon
Cho, Young Youn
Nam, Joon Yeul
Lee, Yun Bin
Lee, Dong Ho
Cho, Eun Ju
Yu, Su Jong
Kim, Yoon Jun
Lee, Jeong Min
Yoon, Jung-Hwan
TI Radiologic Nonalcoholic Fatty Liver Disease Increases the Risk of
Hepatocellular Carcinoma in Patients With Suppressed Chronic Hepatitis B
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE nonalcoholic fatty liver disease; biochemical response; hepatocellular
carcinoma; virological suppression; chronic hepatitis B
ID TENOFOVIR DISOPROXIL FUMARATE; METABOLIC SYNDROME INCREASES; ALANINE
AMINOTRANSFERASE; ENTECAVIR TREATMENT; INSULIN-RESISTANCE; VIRUS
INFECTION; E-ANTIGEN; STEATOSIS; DONORS; ASSOCIATION
AB Background and Goals: Although nonalcoholic fatty liver disease (NAFLD) is a risk factor of hepatocellular carcinoma (HCC), it is unclear whether NAFLD additionally increases the risk of HCC among chronic hepatitis B (CHB) patients. This study evaluated the association between NAFLD and the risk of HCC in patients whose hepatitis B virus (HBV) was well controlled. Study: This study included consecutive CHB patients whose serum HBV DNA levels were continuously suppressed <2000 IU/mL with antiviral treatment. Fatty liver was radiologically diagnosed. Patients with concomitant hepatitis C infection, autoimmune hepatitis, or excessive alcohol use were excluded. Results: Among 826 patients, 86 patients (10.4%) developed HCC during the study period (median, 43.1 mo). The patients with NAFLD (N=260) had a significantly higher risk for HCC compared with patients without NAFLD (N=566) (adjusted hazard ratio, 1.67; 95% confidence interval, 1.05-2.63;P=0.03) after adjustment for age, the presence of cirrhosis, hepatitis B envelop antigen positivity, low-level viremia and hypertension. There was significant association between incomplete biochemical response (IBR) (alanine aminotransferase levels >= 40 IU/L) and the presence of NAFLD (P<0.001 by chi(2)test). IBR at the time of virological response was associated with a significantly higher risk of HCC development (adjusted hazard ratio, 1.63; 95% confidence interval, 1.06-2.54;P=0.03). Conclusions: NAFLD increases the risk of HCC in patients with CHB in whom HBV is effectively suppressed by antivirals. Patients with IBR should be suspected of concurrent NAFLD. Further study is warranted to evaluate whether improvement of NAFLD might decrease the risk of HCC development.
C1 [Cho, Hyeki; Chang, Young; Lee, Jeong-Hoon; Cho, Young Youn; Nam, Joon Yeul; Lee, Yun Bin; Cho, Eun Ju; Yu, Su Jong; Kim, Yoon Jun; Yoon, Jung-Hwan] Liver Res Inst, Dept Internal Med, Seoul, South Korea.
[Lee, Dong Ho; Lee, Jeong Min] Seoul Natl Univ, Coll Med, Dept Radiol, Seoul, South Korea.
[Cho, Young Youn] Chung Ang Univ Hosp, Dept Internal Med, Seoul, South Korea.
[Chang, Young] Soonchunhyang Univ, Coll Med, Inst Digest Res, Digest Dis Ctr,Dept Internal Med, Asan, South Korea.
[Nam, Joon Yeul] Ewha Womans Univ, Coll Med, Dept Internal Med, Seoul, South Korea.
[Cho, Hyeki] Dongguk Univ, Ilsan Hosp, Dept Internal Med, Goyang, South Korea.
C3 Seoul National University (SNU); Chung Ang University; Chung Ang
University Hospital; Soonchunhyang University; Ewha Womans University;
NHIS Ilsan Hospital; Dongguk University
RP Lee, JH (corresponding author), Seoul Natl Univ Hosp, Dept Internal Med, 101 Daehak Ro, Seoul 03080, South Korea.
EM pindra@empal.com
RI LEE, JAE SEUNG/KHT-9575-2024; Kim, Sejoong/J-5356-2015; Yoon,
Jung/J-5563-2012; Kim, Yoon/J-2746-2012; Lee, Yoojin/AAB-9799-2022
OI Cho, Eun Ju/0000-0002-2677-3189; Yu, Su Jong/0000-0001-8888-7977; Cho,
Young Youn/0000-0002-9384-5357
FU National R&D Program for Cancer Control, Ministry for Health and
Welfare, Republic of Korea; Seoul National University Hospital Research
Fund [03-2016-0380]; Liver Research Foundation of Korea as part of Bio
Future Strategies Research Project
FX Supported by grants from the National R&D Program for Cancer Control,
Ministry for Health and Welfare, Republic of Korea, from Seoul National
University Hospital Research Fund (grant number 03-2016-0380), and Liver
Research Foundation of Korea as part of Bio Future Strategies Research
Project.
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NR 53
TC 20
Z9 25
U1 1
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD AUG
PY 2020
VL 54
IS 7
BP 633
EP 641
DI 10.1097/MCG.0000000000001217
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA NE7VK
UT WOS:000562811300009
PM 31033805
DA 2025-01-07
ER
PT J
AU Arababadi, MK
Bidaki, MZ
Kennedy, D
AF Arababadi, Mohammad Kazemi
Bidaki, Mohammad Zare
Kennedy, Derek
TI IL-17A in hepatitis B infection: friend or foe?
SO ARCHIVES OF VIROLOGY
LA English
DT Review
ID CD4(+) T-CELLS; TH17 CELLS; VIRUS INFECTION; HEPATOCELLULAR-CARCINOMA;
DISEASE PROGRESSION; TUMOR PROGRESSION; LIVER-FAILURE; TGF-BETA;
EXPRESSION; INTERLEUKIN-17
AB Hepatitis B virus (HBV) is one of the most prevalent and infectious agents that leads to liver disease in humans. Five clinical forms of HBV infection exist, including fulminant, acute, chronic, asymptomatic and occult. The chronic, asymptomatic and occult forms are long-term infections that can lead to hepatocellular carcinoma (HCC) and liver cirrhosis. The mechanisms responsible for progression of these forms of the infection to HCC and liver cirrhosis are not yet clearly understood or characterised. However, genetic and immunological parameters may play important roles in the disease. IL-17A is an important cytokine involved in early immune responses against fungal and bacterial infections, but its role in the response against viral infections is yet to be fully clarified. The crucial roles of IL-17A in the pathogenesis of autoimmune and destructive immune-related diseases have been documented and may provide insights into its functions during hepatitis infection. Therefore, the aim of this review was to address the recent information regarding the status and association of IL-17A during hepatitis B infection and its related disorders, including HCC and liver cirrhosis.
C1 [Arababadi, Mohammad Kazemi; Bidaki, Mohammad Zare] Rafsanjan Univ Med Sci, Immunol Infect Dis Res Ctr, Rafsanjan, Iran.
[Kennedy, Derek] Griffith Univ Nathan, Eskitis Inst Drug Discovery, Sch Biomol & Phys Sci, Nathan, Qld, Australia.
C3 Griffith University
RP Kennedy, D (corresponding author), Griffith Univ Nathan, Eskitis Inst Drug Discovery, Sch Biomol & Phys Sci, Nathan, Qld, Australia.
EM derek.kennedy@griffith.edu.au
RI Arababadi, Mohammad/H-5282-2017; Kennedy, Hendrick/A-7635-2010;
Zare-Bidaki, Mohammad/N-2967-2015
OI Kennedy, Hendrick/0000-0001-7937-3069; Kazemi Arababadi,
Mohammad/0000-0002-4315-8153; Zare-Bidaki, Mohammad/0000-0001-6821-6412
FU Rafsanjan University of Medical Sciences
FX This project was supported by a grant from the Rafsanjan University of
Medical Sciences. None of the authors have any financial, professional
or personal conflicts that are relevant to the manuscript.
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NR 43
TC 28
Z9 30
U1 0
U2 9
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0304-8608
EI 1432-8798
J9 ARCH VIROL
JI Arch. Virol.
PD AUG
PY 2014
VL 159
IS 8
BP 1883
EP 1888
DI 10.1007/s00705-014-2002-x
PG 6
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA AM5HQ
UT WOS:000339888300001
PM 24532300
DA 2025-01-07
ER
PT J
AU Liu, ZK
Dou, CW
Jia, YL
Li, Q
Zheng, X
Yao, YM
Liu, QG
Song, T
AF Liu, Zhikui
Dou, Changwei
Jia, Yuli
Li, Qing
Zheng, Xin
Yao, Yingmin
Liu, Qingguang
Song, Tao
TI RIG-I suppresses the migration and invasion of hepatocellular carcinoma
cells by regulating MMY9
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE retinoic acid-induced protein I; hepatocellular carcinoma;
interferon-alpha therapeutic response; matrix metalloproteinase-9
ID MATRIX METALLOPROTEINASES; INTERFERON-ALPHA; TUMOR MICROENVIRONMENT;
GENE-EXPRESSION; CANCER; METASTASIS; SURVIVAL;
MATRIX-METALLOPROTEINASE-9; IDENTIFICATION; RECURRENCE
AB The retinoic acid-induced protein I (Rig-I/Ddx58), (RIG-I) initiates a signaling cascade that induces innate immune defences which is associated with the production of type I interferons (IFNs) and inflammatory cytokines to establish an antiviral state. Aberrant RIG-I signaling leads to inflammation, autoimmune diseases and cancer. However, the role of RIG-I in hepatocellular carcinoma (HCC) is still unknown. Here, we observed that RIG-I expression was downregulated in HCC tissues and loss of RIG-I expression was correlated with poor clinicopathological features. Additionally, we demonstrated that patients with positive RIG-I expression had a better 3-year survival and RIG-I was an independent factor for predicting the prognosis of HCC patients. Elevated RIG-I expression inhibited the proliferation, migration, and invasion of HCC. Inhibiting RIG-I with its specific si RNA was able to attenuate the malignant behavior of HCC cells. Moreover, RIG-I inhibited the invasive behavior through downregulating matrix metalloproteinase-9 (MMP9). Mechanistically, RIG-I enhances IFN-alpha response by amplifying IFN-a effecter signaling via strengthening STAT1 activation. Addressing this pathway, we identified that RIG-I may serve as a prognostic marker and that MMP9 may be a potential target of RIG-I in HCC.
C1 [Liu, Zhikui; Dou, Changwei; Jia, Yuli; Li, Qing; Zheng, Xin; Yao, Yingmin; Liu, Qingguang; Song, Tao] Xi An Jiao Tong Univ, Dept Hepatobiliary Surg, Affiliated Hosp 1, Coll Med, Xian 710061, Shaanxi, Peoples R China.
C3 Xi'an Jiaotong University
RP Liu, QG (corresponding author), Xi An Jiao Tong Univ, Dept Hepatobiliary Surg, Affiliated Hosp 1, 277 Yanta West Rd, Xian, Shaanxi, Peoples R China.
EM 13572431619@163.com; liuqingguang@vip.sina.com
RI ZHENG, XIN/H-2342-2016
FU National Natural Scientific Foundation of China [81272645, 81072052];
Key Science and Technology Fund of Shaanxi Province [2010K01-131]; Funds
for Creative Research - First Affiliated Hospital of Xi'an Jiaotong
University [14YB10]
FX This study was supported by grants from National Natural Scientific
Foundation of China (nos. 81272645 and 81072052 to Qingguang Liu), Key
Science and Technology Fund of Shaanxi Province to Tao Song
(2010K01-131), and the Funds for Creative Research sponsored by The
First Affiliated Hospital of Xi'an Jiaotong University to Zhikui Liu
(14YB10).
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NR 32
TC 35
Z9 40
U1 0
U2 8
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD APR
PY 2015
VL 46
IS 4
BP 1710
EP 1720
DI 10.3892/ijo.2015.2853
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CC8KE
UT WOS:000350616400032
PM 25626059
OA Bronze
DA 2025-01-07
ER
PT J
AU Thomas, SM
Moke, D
Lopez, R
Hanna, R
Kabbany, MN
Alkhouri, N
AF Thomas, Stefanie M.
Moke, Diana
Lopez, Rocio
Hanna, Rabi
Kabbany, Mohammad Nasser
Alkhouri, Naim
TI Liver Transplantation for Hepatocellular Carcinoma in Young Adults: A
United Network for Organ Sharing Study
SO JOURNAL OF ADOLESCENT AND YOUNG ADULT ONCOLOGY
LA English
DT Article
DE hepatitis B virus; model for end-stage liver disease; surgical oncology
ID CLINICAL CHARACTERISTICS; SURVIVAL; PROGNOSIS; MORTALITY; FEATURES;
COHORT; IMPACT
AB Purpose: Orthotopic liver transplantation (OLT) is curative for hepatocellular carcinoma (HCC). HCC is typically a disease of older adults (OAs); therefore, characteristics and outcomes of OLT for young adults (YAs) (ages 18-40) are not described. The objective of this study was to assess the characteristics and outcomes of YAs with HCC receiving OLT and compare these to OAs (ages >40 years).
Methods: YAs with HCC who had OLT from the United Network for Organ Sharing (UNOS) database were included in this study. As a comparison group, OAs with HCC were matched 4:1 to the YA group. Descriptive statistics of demographics, comorbidities, and outcomes were generated. Kaplan-Meier product limit estimates were used to assess patient and graft survival. Conditional logistic regression and Cox proportional hazards frailty models were used to compare the groups.
Results: A total of 464 YAs received OLT for HCC. The most common underlying liver diseases were hepatitis C virus (21.3%), hepatitis B virus (HBV, 15.5%), and autoimmune/cholestatic disease (12.3%). An increased number of YAs received OLT for HCC after implementation of model for end-stage liver disease scoring. One thousand two hundred eighty OAs served as the comparison group. Post-transplant 5-year survival was 73.1% in YAs with a retransplantation rate of 7.8%. In OAs, survival and retransplantation rates were lower (68.6% p=0.093; 4.3% p=0.001).
Conclusion: Four hundred sixty-four YAs with HCC received OLT in the UNOS database. Compared to the older population, survival and retransplantation rates were higher. HBV, which is vaccine preventable, is a frequent contributor to HCC in YAs.
C1 [Thomas, Stefanie M.; Moke, Diana] Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood Dis, Los Angeles, CA 90027 USA.
[Thomas, Stefanie M.] Univ Southern Calif, Keck Sch Med, Dept Pediat, Div Hematol Oncol & Blood & Marrow Transplantat, Los Angeles, CA 90033 USA.
[Lopez, Rocio] Cleveland Clin, Dept Quantitat Hlth Sci, Cleveland, OH 44106 USA.
[Hanna, Rabi] Cleveland Clin Childrens, Dept Pediat Hematol Oncol & Blood & Marrow Transp, Cleveland, OH USA.
[Kabbany, Mohammad Nasser; Alkhouri, Naim] Cleveland Clin, Dept Pediat Gastroenterol & Hepatol, Cleveland, OH 44106 USA.
[Alkhouri, Naim] Cleveland Clin, Digest Dis Inst, Cleveland, OH 44106 USA.
C3 Children's Hospital Los Angeles; University of Southern California;
Cleveland Clinic Foundation; Cleveland Clinic Foundation; Cleveland
Clinic Foundation; Cleveland Clinic Foundation
RP Thomas, SM (corresponding author), 4650 Sunset Blvd,MS 54, Los Angeles, CA 90027 USA.
EM stthomas@chla.usc.edu
OI Lopez, Ana Rocio/0000-0002-4319-420X; Thomas,
Stefanie/0000-0003-3225-7129
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NR 24
TC 2
Z9 2
U1 0
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 2156-5333
EI 2156-535X
J9 J ADOLESC YOUNG ADUL
JI J. Adolesc. Young Adult Oncol.
PD JUN
PY 2017
VL 6
IS 2
BP 286
EP 293
DI 10.1089/jayao.2016.0048
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EX2LD
UT WOS:000403056900010
PM 27996360
DA 2025-01-07
ER
PT J
AU Qi, JF
Wang, WH
Tang, YM
Lou, SY
Wang, J
Yuan, T
He, QJ
Yang, B
Zhu, H
Cui, SL
AF Qi, Jifeng
Wang, Weihua
Tang, Yongmei
Lou, Shengying
Wang, Jiaer
Yuan, Tao
He, Qiaojun
Yang, Bo
Zhu, Hong
Cui, Sunliang
TI Discovery of Novel Indazoles as Potent and Selective PI3Kδ Inhibitors
with High Efficacy for Treatment of Hepatocellular Carcinoma
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID IN-VIVO EVALUATION; PHOSPHOINOSITIDE 3-KINASES; IDELALISIB;
OPTIMIZATION; DERIVATIVES; THERAPY; DESIGN; DELTA
AB PI3K delta inhibitors have been developed for treatment of B-cell malignancies and inflammatory and autoimmune diseases. However, their therapeutic role in solid tumors like hepatocellular carcinoma (HCC) is rarely reported. Thus, the development of potent and selective PI3K delta inhibitors with a new chemotype and therapy is highly desirable. Through the scaffold-hopping strategy, indazole was first described as the core structure of propeller-shaped PI3K delta inhibitors. A total of 26 indazole derivatives were designed and prepared to identify a novel compound 9x with good isoform selectivity, PK profile, and potency. Compared to Idelalisib and Sorafenib, the pharmacodynamic (PD) studies showed that 9x exhibits superior efficacy in HCC cell lines and xenograft models, and the mechanistic study showed that 9x robustly suppresses the downstream AKT pathway to induce subsequent apoptotic cell death in HCC models. Therefore, this work provides a new structural design of PI3K delta inhibitors for a novel and efficient therapeutic small molecule toward HCC.
C1 [Qi, Jifeng; Tang, Yongmei; Lou, Shengying; Cui, Sunliang] Zhejiang Univ, Coll Pharmaceut Sci, Inst Drug Discovery & Design, Hangzhou 310058, Peoples R China.
[Wang, Weihua; Wang, Jiaer; Yuan, Tao; He, Qiaojun; Yang, Bo; Zhu, Hong] Zhejiang Univ, Coll Pharmaceut Sci, Inst Pharmacol & Toxicol, Hangzhou 310058, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Cui, SL (corresponding author), Zhejiang Univ, Coll Pharmaceut Sci, Inst Drug Discovery & Design, Hangzhou 310058, Peoples R China.; Zhu, H (corresponding author), Zhejiang Univ, Coll Pharmaceut Sci, Inst Pharmacol & Toxicol, Hangzhou 310058, Peoples R China.
EM hongzhu@zju.edu.cn; slcui@zju.edu.cn
RI Cui, Sunliang/F-8232-2011
FU National Natural Science Foundation of China [21971222]; Fundamental
Research Funds for Zhejiang Provincial Universities [2021XZZX036];
Zhejiang Provincial Key RD Program [2021C03082]
FX We are grateful for the financial support from the National Natural
Science Foundation of China (grant number 21971222), the Fundamental
Research Funds for Zhejiang Provincial Universities (grant number
2021XZZX036), and the Zhejiang Provincial Key R&D Program (grant number
2021C03082).
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TC 10
Z9 10
U1 3
U2 28
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD MAR 10
PY 2022
VL 65
IS 5
BP 3849
EP 3865
DI 10.1021/acs.jmedchem.1c01520
PG 17
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Pharmacology & Pharmacy
GA ZX9IG
UT WOS:000772205900010
PM 35191698
DA 2025-01-07
ER
PT J
AU Bei, R
Mizejewski, GJ
AF Bei, Roberto
Mizejewski, Gerald J.
TI Alpha-fetoprotein is an autoantigen in hepatocellular carcinoma and
juvenile Batten disease
SO FRONTIERS IN BIOSCIENCE-LANDMARK
LA English
DT Article
DE Alpha-fetoprotein; Autoimmunity; Antigens; Epitopes; Disordered Protein;
Autoimmune Disorders; Batten Disease; Review
ID T-CELL RESPONSES; MOUSE MODEL; IMMUNE-RESPONSES; CRYPTIC EPITOPES;
SELF-TOLERANCE; AFP; CANCER; PREGNANCY; PEPTIDES; AUTOANTIBODIES
AB Failure of immune tolerance leads to production of autoantibodies to self-antigens. The repertoire of autoantibodies detected in cancer patients can indicate the presence of autoimmune disease. Alpha-fetoprotein (AFP) autoantibodies have been found in patients with hepatocellular carcinoma (HCC) and in juvenile Batten disease (BD), a neurodegenerative condition involving autoimmunity. Variant conformational forms of AFP together with exposed occult antigenic determinant sites on the AFP polypeptide resemble the features of a disordered protein which can impair central immune tolerance. These aberrant structural protein forms can lead to the persistence of autoantibody production by immune sensitized B-lymphocytes. Thus, it is not surprising that AFP, a self-antigen, can induce autoimmune responses in humans. Herein, we discuss the molecular and antigenic properties of AFP which make it a disordered protein, and its ability to induce autoantibody production to AFP cryptic epitopes in both HHC and BD patients. Such insights might aid in the future design of AFP-based vaccines and to discovery of novel pathogenic mechanisms of autoimmune diseases which demonstrate the presence of denatured intermediate forms of AFP.
C1 [Bei, Roberto] Univ Roma Tor Vergata, Dept Clin Sci & Translat Med, I-00133 Rome, Italy.
[Mizejewski, Gerald J.] New York State Dept Hlth, Wadsworth Ctr, Div Translat Med Mol Diagnost, POB 509,Empire State Plaza, Albany, NY 12201 USA.
C3 University of Rome Tor Vergata; Wadsworth Center; State University of
New York (SUNY) System
RP Bei, R (corresponding author), Univ Roma Tor Vergata, Fac Med, Dept Clin Sci & Translat Med, Via Montpellier 1, I-00133 Rome, Italy.
EM bei@med.uniroma2.it
RI Bei, Roberto/W-8023-2019
FU University of Rome "Tor Vergata" (Mission Sustainability, Codice Unico
di Progetto (CUP)) [E81I18000330005]
FX This work was supported by a grant from the University of Rome "Tor
Vergata" (Mission Sustainability, Codice Unico di Progetto (CUP):
E81I18000330005), Italy.
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NR 95
TC 5
Z9 6
U1 0
U2 13
PU FRONTIERS IN BIOSCIENCE INC
PI IRVINE
PA 16471 SCIENTIFIC WAY, IRVINE, CA 92618 USA
SN 1093-9946
EI 1093-4715
J9 FRONT BIOSCI-LANDMRK
JI Front. Biosci.
PD JAN 1
PY 2020
VL 25
BP 912
EP 929
DI 10.2741/4840
PG 18
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA NG1TK
UT WOS:000563769400006
PM 31585923
OA Bronze
DA 2025-01-07
ER
PT J
AU Blachier, M
Leleu, H
Peck-Radosavljevic, M
Valla, DC
Roudot-Thoraval, F
AF Blachier, Martin
Leleu, Henri
Peck-Radosavljevic, Markus
Valla, Dominique-Charles
Roudot-Thoraval, Francoise
TI The burden of liver disease in Europe: A review of available
epidemiological data
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Epidemiology; Burden; Liver disease; Cirrhosis; Primary liver cancer;
Hepatocellular carcinoma; Alcohol-related liver disease; Hepatitis;
NAFLD
ID NONALCOHOLIC FATTY LIVER; HEPATITIS-E-VIRUS; PRIMARY BILIARY-CIRRHOSIS;
PRIMARY SCLEROSING CHOLANGITIS; RISK-FACTORS; GENERAL-POPULATION; C
VIRUS; HEPATOCELLULAR-CARCINOMA; DRUG-USERS; AUTOIMMUNE HEPATITIS
AB To survey the burden of liver disease in Europe and its causes 260 epidemiological studies published in the last five years were reviewed.
The incidence and prevalence of cirrhosis and primary liver cancer are key to understand the burden of liver disease. They represent the end-stage of liver pathology and thus are indicative of the associated mortality. About 0.1% of Hungarian males will die of cirrhosis every year compared with 0.001% of Greek females. WHO estimate that liver cancer is responsible for around 47,000 deaths per year in the EU.
Harmful alcohol consumption, viral hepatitis B and C and metabolic syndromes related to overweight and obesity are the leading causes of cirrhosis and primary liver cancer in Europe.
Chronic hepatitis B affects 0.5-0.7% of the European population. In the last decade the prevalence of chronic hepatitis C was 0.13-3.26%. It is of great concern that about 90% of people in Europe infected by viral hepatitis are unaware of their status. Available data suggest the prevalence rate of NAFLD is 2-44% in the general European population (including obese children) and 42.6-69.5% in people with type 2 diabetes.
Each of these four major causes of liver disease is amenable to prevention and treatment, reducing the burden of liver disease in Europe and saving lives. Further surveys are urgently needed to implement cost-effective prevention programmes and novel treatments to tackle this problem. (C) 2012 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Blachier, Martin; Leleu, Henri; Roudot-Thoraval, Francoise] Univ Paris Est Creteil, Hop Henri Mondor, Dept Publ Hlth, Paris, France.
[Peck-Radosavljevic, Markus] Med Univ Wien, Dept Gastroenterol & Hepatol, A-1090 Vienna, Austria.
[Valla, Dominique-Charles] Univ Paris Diderot, Hop Beaujon, AP HP, Serv Hepatol, Clichy La Garenne, France.
[Valla, Dominique-Charles] INSERM, U773, Clichy La Garenne, France.
C3 Universite Paris-Est-Creteil-Val-de-Marne (UPEC); Assistance Publique
Hopitaux Paris (APHP); Hopital Universitaire Henri-Mondor - APHP;
Medical University of Vienna; Assistance Publique Hopitaux Paris (APHP);
Universite Paris Cite; Hopital Universitaire Beaujon - APHP; Institut
National de la Sante et de la Recherche Medicale (Inserm)
RP Peck-Radosavljevic, M (corresponding author), Med Univ Wien, Dept Gastroenterol & Hepatol, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.
EM markus.peck@meduniwien.ac.at; fran-coise.roudot-thoraval@hmn.aphp.fr
RI Valla, Dominique/IAM-2915-2023; Sirli, Roxana/L-4202-2013;
Peck-Radosavljevic, Markus/J-6353-2013
OI Sirli, Roxana/0000-0002-0179-1014; Valla, Dominique/0000-0002-4460-7643;
Peck-Radosavljevic, Markus/0000-0002-0597-2728; Leleu,
Henri/0000-0003-4930-6767
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Z9 1019
U1 0
U2 148
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD MAR
PY 2013
VL 58
IS 3
BP 593
EP 608
DI 10.1016/j.jhep.2012.12.005
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Gastroenterology & Hepatology
GA 106TK
UT WOS:000316167400027
PM 23419824
OA Green Submitted, hybrid
DA 2025-01-07
ER
PT J
AU Sánchez-Crisóstomo, I
Fernández-Martínez, E
Cariño-Cortés, R
Betanzos-Cabrera, G
Bobadilla-Lugo, RA
AF Sanchez-Crisostomo, Isabel
Fernandez-Martinez, Eduardo
Carino-Cortes, Raquel
Betanzos-Cabrera, Gabriel
Bobadilla-Lugo, Rosa A.
TI Phytosterols and Triterpenoids for Prevention and Treatment of
Metebolic-related Liver Diseases and Hepatocellular Carcinoma
SO CURRENT PHARMACEUTICAL BIOTECHNOLOGY
LA English
DT Review
DE Hepatocellular carcinoma; liver; metabolic syndrome; nuclear receptors;
phytosterols; triterpenes
ID PLANT STEROLS; BETA-SITOSTEROL; INSULIN-RESISTANCE; ALKALINE
SPHINGOMYELINASE; ENDOTHELIAL FUNCTION; METABOLIC SYNDROME; CHOLESTEROL
ABSORPTION; DIETARY PHYTOSTEROLS; PREPUBERTAL CHILDREN; PROTEIN
PHOSPHATASE
AB Background: Liver ailments are the leading causes of death; they originate from viral infections, chronic alcoholism, and autoimmune illnesses, which may chronically be precursors of cirrhosis; furthermore, metabolic syndrome may worsen those hepatopathies or cause Non-alcoholic Fatty Liver Disease (NAFLD) that may advance to non-alcoholic steatohepatitis (NASH). Cirrhosis is the late-stage liver disease and can proceed to hepatocellular carcinoma (HCC). Pharmacological treatment Options for liver diseases, cirrhosis, and HCC, are limited, expensive, and not wholly effective. The use of medicinal herbs and functional foods is growing around the world as natural resources of bioactive compounds that would set the basis for the development of new drugs.
Review and Conclusion: Plant and food-derived sterols and triterpenoids (TTP) possess antioxidant, metabolic-regulating, immunomodulatory, and anti-inflammatory activities, as well as they are recognized as anticancer agents, suggesting their application strongly as an alternative therapy in some chronic diseases. Thus, it is interesting to review current reports about them as hepatoprotective agents, but also because they structurally resemble cholesterol, sexual hormones, corticosteroids and bile acids due to the presence of the steroid nucleus, so they all can share pharmacological properties through activating nuclear and membrane receptors. Therefore, sterols and TTP appear as a feasible option for the prevention and treatment of chronic metabolic-related liver diseases, cirrhosis, and HCC.
C1 [Sanchez-Crisostomo, Isabel; Carino-Cortes, Raquel] Autonomous Univ Hidalgos State, Ctr Res Reprod Biol, Sch Hlth Sci, Pachuca, Mexico.
[Fernandez-Martinez, Eduardo; Betanzos-Cabrera, Gabriel] Autonomous Univ Hidalgos State, Sch Hlth Sci, Dept Med, Lab Med Chem & Pharmacol, St Dr Eliseo Ramirez Ulloa 400, Pachuca 42090, Hidalgo, Mexico.
[Bobadilla-Lugo, Rosa A.] Natl Polytech Inst, Super Sch Med, Mexico City, DF, Mexico.
C3 Universidad Autonoma del Estado de Hidalgo; Universidad Autonoma del
Estado de Hidalgo; Instituto Politecnico Nacional - Mexico
RP Fernández-Martínez, E (corresponding author), Autonomous Univ Hidalgos State, Sch Hlth Sci, Dept Med, Lab Med Chem & Pharmacol, St Dr Eliseo Ramirez Ulloa 400, Pachuca 42090, Hidalgo, Mexico.
EM efernan@uaeh.edu.mx
RI Betanzos, Gabriel/AHB-7550-2022; Fernández-Martínez,
Eduardo/AAJ-4920-2020; Cariño-Cortes, Raquel/E-5302-2018
OI Bobadilla Lugo, Rosa A/0000-0002-5314-1363; Betanzos-Cabrera,
Gabriel/0000-0003-2027-6904; Fernandez-Martinez,
Eduardo/0000-0003-3280-1323
FU Consejo Nacional de Ciencia y Tecnologia (CONACyT), Mexico [363864]
FX The authors would like to thank M.C.E. Luis Carlos Romero-Quezada for
administrative support and to Consejo Nacional de Ciencia y Tecnologia
(CONACyT), Mexico, for the Doctor's degree fellowship to Isabel
Sanchez-Crisostomo (number 363864).
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NR 172
TC 21
Z9 22
U1 5
U2 25
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-2010
EI 1873-4316
J9 CURR PHARM BIOTECHNO
JI Curr. Pharm. Biotechnol.
PY 2019
VL 20
IS 3
BP 197
EP 214
DI 10.2174/1389201020666190219122357
PG 18
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA IA0EA
UT WOS:000469228400003
PM 30806308
DA 2025-01-07
ER
PT J
AU Li, MX
Luo, FZ
Tian, XY
Yin, SY
Zhou, L
Zheng, SS
AF Li, Mengxia
Luo, Fangzhou
Tian, Xinyao
Yin, Shengyong
Zhou, Lin
Zheng, Shusen
TI Chemokine-Like Factor-Like MARVEL Transmembrane Domain-Containing Family
in Hepatocellular Carcinoma: Latest Advances
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE chemokine-like factor– like MARVEL transmembrane domain-containing
family; chemokine-like factor; hepatocellular carcinoma; MARVEL; tumor
suppressor gene
ID TUMOR-SUPPRESSOR; DNA METHYLATION; CELL GROWTH; MESENCHYMAL TRANSITION;
MOLECULAR-CLONING; PROSTATE-CANCER; UP-REGULATION; CMTM3; EXPRESSION;
PROMOTES
AB Chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTMs) is a new gene family, consisting of CKLF and CMTM1 to CMTM8, which plays an important role in hematopoiesis system, autoimmune diseases, male reproduction etc. Abnormal expression of CMTMs is also associated with tumor genesis, development and metastasis. In this review, we briefly describe the characteristics of CMTM family, outline its functions in multiple kinds of carcinomas, and summarize the latest research on their roles in hepatocellular carcinoma which are mainly related to the expression, prognostic effect, potential functions, and mechanism of action. The CMTM family is expected to provide new ideas and targets for HCC diagnosis and treatment.
C1 [Li, Mengxia; Luo, Fangzhou; Tian, Xinyao; Yin, Shengyong; Zhou, Lin; Zheng, Shusen] Zhejiang Univ, Affiliated Hosp 1, Div Hepatobiliary & Pancreat Surg, Dept Surg,Sch Med, Hangzhou, Peoples R China.
[Li, Mengxia; Luo, Fangzhou; Tian, Xinyao] Zhejiang Univ, Sch Med, Hangzhou, Peoples R China.
[Li, Mengxia; Luo, Fangzhou; Tian, Xinyao; Yin, Shengyong; Zhou, Lin; Zheng, Shusen] NHC Key Lab Combined Multiorgan Transplantat, Hangzhou, Peoples R China.
[Li, Mengxia; Luo, Fangzhou; Tian, Xinyao; Yin, Shengyong; Zhou, Lin; Zheng, Shusen] Chinese Acad Med Sci 2019RU019, Key Lab Diag & Treatment Organ Transplantat, Res Unit Collaborat Diag & Treatment Hepatobiliar, Hangzhou, Peoples R China.
[Li, Mengxia; Luo, Fangzhou; Tian, Xinyao; Yin, Shengyong; Zhou, Lin; Zheng, Shusen] Res Ctr Diag & Treatment Hepatobiliary Dis, Key Lab Organ Transplantat, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Zhou, L; Zheng, SS (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Div Hepatobiliary & Pancreat Surg, Dept Surg,Sch Med, Hangzhou, Peoples R China.; Zhou, L; Zheng, SS (corresponding author), NHC Key Lab Combined Multiorgan Transplantat, Hangzhou, Peoples R China.; Zhou, L; Zheng, SS (corresponding author), Chinese Acad Med Sci 2019RU019, Key Lab Diag & Treatment Organ Transplantat, Res Unit Collaborat Diag & Treatment Hepatobiliar, Hangzhou, Peoples R China.; Zhou, L; Zheng, SS (corresponding author), Res Ctr Diag & Treatment Hepatobiliary Dis, Key Lab Organ Transplantat, Hangzhou, Peoples R China.
EM zhoulin99@zju.edu.cn; shusenzheng@zju.edu.cn
RI Luo, Fangzhou/KTI-4889-2024
FU Innovative Research Groups of National Natural Science Foundation of
China [81721091]; National ST Major Project [2017ZX10203205]; Zhejiang
International Science and Technology Cooperation Project [2016C04003];
Research Unit Project of Chinese Academy of Medical Sciences
[2019-I2M-5-030]; Health Commission of Zhejiang Province [JBZX-202004]
FX Innovative Research Groups of National Natural Science Foundation of
China (No. 81721091), National S&T Major Project (No. 2017ZX10203205),
Zhejiang International Science and Technology Cooperation Project (No.
2016C04003), Research Unit Project of Chinese Academy of Medical
Sciences (2019-I2M-5-030), and Grant from Health Commission of Zhejiang
Province (JBZX-202004).
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NR 101
TC 12
Z9 13
U1 2
U2 19
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 13
PY 2020
VL 10
AR 595973
DI 10.3389/fonc.2020.595973
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OV8AU
UT WOS:000592426300001
PM 33282744
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Petrova, M
Kamburov, V
AF Petrova, Mihaela
Kamburov, Victor
TI Epstein-Barr virus: Silent companion or causative agent of chronic liver
disease?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Epstein-Barr virus; Chronic hepatitis; Liver disease; Chronic active
Epstein-Barr virus; Post-transplant lymphoproliferative disorder;
Infectious mononucleosis
ID CD8(+) T-CELLS; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
INFECTION; TRANSPLANT; EBV; IDENTIFICATION; REACTIVATION; EXPRESSION;
DIAGNOSIS
AB The Epstein-Barr virus (EBV) has an important and multifaceted role in liver pathology. As a member of the herpes virus family, EBV establishes a persistent infection in more than 90% of adults. Besides acute hepatitis during primary infection, many clinical syndromes of interest for the hepatologist are associated with EBV infection. The role of EBV in the evolution of chronic hepatitis from hepatotropic viruses is considered. Chronic EBV-associated hepatitis is suspected in immunocompetent adults with compatible serology, suggestive histology and detection of the viral genome in the liver and/or increase of specific circulating cytotoxic T-lymphocytes. EBV is the main cause of post-transplant lymphoproliferative disorders which occur in up to 30% of cases. EBV-driven lymphoproliferative diseases are also recognized in non-immunocompromised patients and liver is involved in up to a third of the cases. Directly implicated in the pathogenesis of different tumors, EBV has a disputable role in hepatocellular carcinoma carcinogenesis. Further research is required in order to establish or reject the role of EBV in human liver cancer. This paper attempts to discuss the range of EBV-associated chronic liver diseases in immunocompetent patients, from mild, self-limiting mononuclear hepatitis to liver cancer. (C) 2010 Baishideng. All rights reserved.
C1 [Petrova, Mihaela] Minist Interior, Gastroenterol Clin, Sofia 1606, Bulgaria.
[Kamburov, Victor] First Multiprofile Hosp Act Treatment, Div Gastroenterol, Sofia 1142, Bulgaria.
C3 Medical University Sofia; Medical Institute of Ministry of Interior,
Sofia, Bulgaria
RP Petrova, M (corresponding author), Minist Interior, Gastroenterol Clin, 79 Skobelev Blvd, Sofia 1606, Bulgaria.
EM mpetrova@gmail.com
RI Petrova, Mihaela/ABG-5124-2020
OI Kamburov, Victor/0000-0002-3111-4081
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NR 59
TC 20
Z9 24
U1 0
U2 11
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD SEP 7
PY 2010
VL 16
IS 33
BP 4130
EP 4134
DI 10.3748/wjg.v16.i33.4130
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 647PH
UT WOS:000281630300003
PM 20806428
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Bittermann, T
Goldberg, DS
Bauer, CM
Khungar, V
AF Bittermann, Therese
Goldberg, David S.
Bauer, Christina M.
Khungar, Vandana
TI Characterizing the Risk of False-Positive Hepatocellular Carcinoma in
Recipients Transplanted With T2 MELD Exceptions
SO TRANSPLANTATION
LA English
DT Article
ID STAGE LIVER-DISEASE; SURVIVAL BENEFIT; AUTOIMMUNE HEPATITIS; EXPLANT
PATHOLOGY; ALPHA-FETOPROTEIN; DIAGNOSIS; ALLOCATION; ABLATION; IMPACT;
RATES
AB Background Patients with hepatocellular carcinoma (HCC) can receive Model for End-Stage Liver Disease (MELD) exception points to increase waitlist priority for liver transplantation. This process does not require a biopsy and is based on radiologic criteria. However, imaging modalities are imperfect, and some will ultimately have no HCC on explant.
Methods This was a retrospective cohort study using national explant pathology data from 2012 to 2015. False-positive HCC was defined as answering no to the question: was evidence of HCC (viable or nonviable) found in the explant? in patients with T2 MELD exceptions.
Results Four thousand one hundred seventeen patients received T2 MELD exceptions, of which 245 (6%) had false-positive HCC. Maximal tumor diameter of 3 to 5 cm and serum fetoprotein (AFP) greater than 100 ng/mL at transplant yielded a 50% lower risk of false-positive HCC (odds ratio [OR], 0.45; 95% confidence interval [CI], 0.27-0.73 and OR, 0.57; 95% CI, 0.37-0.88, respectively). Recipients with immune-mediated liver disease were twice as likely to have no HCC on explant (OR, 2.12; 95% CI, 1.18-3.83) and had a predicted probability of false positive HCC greater than 10% regardless of largest tumor size or AFP. Significant among-center variability in the rate of false-positive HCC was seen.
Conclusions The risk of false-positive HCC is markedly higher in certain groups, such that biopsy may be warranted before T2 MELD exception point approval. Transplant centers with high false-positive HCC rates may benefit from greater oversight.
C1 [Bittermann, Therese; Goldberg, David S.; Khungar, Vandana] Univ Penn, Div Gastroenterol & Hepatol, Philadelphia, PA 19104 USA.
[Goldberg, David S.] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Bauer, Christina M.] Univ N Carolina, Div Gastroenterol & Hepatol, Sch Med, Chapel Hill, NC USA.
C3 University of Pennsylvania; University of Pennsylvania; University of
North Carolina; University of North Carolina Chapel Hill; University of
North Carolina School of Medicine
RP Bittermann, T (corresponding author), Perelman Ctr Adv Med, 3400 Civ Ctr Blvd,South Pavil,7th Floor, Philadelphia, PA 19104 USA.
EM therese.bittermann@uphs.upenn.edu
RI Bittermann, Therese/AAG-1406-2019; Khungar, Vandana/AAJ-3416-2021
FU National Institutes of Health clinical epidemiology institutional
training grant at the University of Pennsylvania [5T32DK007740-20]
FX Dr. Bittermann receives research and educational funding as part of a
National Institutes of Health clinical epidemiology institutional
training grant at the University of Pennsylvania (5T32DK007740-20).
CR American College of Radiology, 2014, LIV IM REP DAT SYST
Berry K, 2015, GASTROENTEROLOGY, V149, P669, DOI 10.1053/j.gastro.2015.05.025
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Organ Procurement and Transplantation Network, OPTN POL 9 ALL LIV L
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NR 34
TC 3
Z9 3
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD MAY
PY 2017
VL 101
IS 5
BP 1099
EP 1105
DI 10.1097/TP.0000000000001660
PG 7
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA EU1GF
UT WOS:000400762500038
PM 28121908
DA 2025-01-07
ER
PT J
AU Dengler, M
Staufer, K
Huber, H
Stauber, R
Bantel, H
Weiss, KH
Starlinger, P
Pock, H
Klöters-Plachky, P
Gotthardt, DN
Rauch, P
Lackner, C
Stift, J
Brostjan, C
Gruenberger, T
Kumada, T
Toyoda, H
Tada, T
Weiss, TS
Trauner, M
Mikulits, W
AF Dengler, Mirko
Staufer, Katharina
Huber, Heidemarie
Stauber, Rudolf
Bantel, Heike
Weiss, Karl Heinz
Starlinger, Patrick
Pock, Hannelore
Kloeters-Plachky, Petra
Gotthardt, Daniel N.
Rauch, Peter
Lackner, Carolin
Stift, Judith
Brostjan, Christine
Gruenberger, Thomas
Kumada, Takashi
Toyoda, Hidenori
Tada, Toshifumi
Weiss, Thomas S.
Trauner, Michael
Mikulits, Wolfgang
TI Soluble Axl is an accurate biomarker of cirrhosis and hepatocellular
carcinoma development: results from a large scale multicenter analysis
SO ONCOTARGET
LA English
DT Article
DE soluble Axl; biomarker; fibrosis; cirrhosis; hepatocellular carcinoma
ID DES-GAMMA-CARBOXYPROTHROMBIN; CHRONIC LIVER-DISEASE; KINASE RECEPTOR
AXL; ALPHA-FETOPROTEIN; PLASMA-CONCENTRATIONS; TYROSINE KINASE; PROTEIN;
GAS6; SAXL; SURVEILLANCE
AB Patients with chronic liver disease (CLD) and cirrhosis are at high risk for hepatocellular carcinoma (HCC). Current diagnostic tools for HCC detection include imaging techniques and serum biomarkers such as a-fetoprotein (AFP). Yet, these methods are limited in sensitivity and specificity to accurately detect early HCC. Here we focused on the potential of soluble Axl (sAxl) as a biomarker in CLD patients by analyzing serum samples of 1067 patients and healthy controls from centers in Europe and Asia. We show that serum concentrations of sAxl were significantly increased at early (82.57 ng/mL) and later stages of HCC (114.50 ng/mL) as compared to healthy controls (40.15 ng/mL). Notably, no elevated sAxl levels were detected in patients with CLD including chronic viral hepatitis, autoimmune hepatitis, cholestatic liver disease, or non-alcoholic fatty liver disease versus healthy controls. Furthermore, sAxl did not rise in liver adenomas or cholangiocarcinoma (CCA). Yet, patients with advanced fibrosis (F3) or cirrhosis (F4) showed enhanced sAxl concentrations (F3: 54.67 ng/mL; F4: 94.74 ng/mL). Hepatic myofibroblasts exhibited an increased release of sAxl, suggesting that elevated sAxl levels arise from these cells during fibrosis. Receiver operating characteristic curve analysis of sAxl displayed a strongly increased sensitivity and specificity to detect both cirrhosis (80.8%/92.0%) and HCC (83.3%/86.7%) with an area under the curve of 0.935/0.903 as compared to AFP. In conclusion, sAxl shows high diagnostic accuracy at early stage HCC as well as cirrhosis, thereby outperforming AFP. Importantly, sAxl remains normal in most common CLDs, liver adenomas and CCA.
C1 [Dengler, Mirko; Huber, Heidemarie; Mikulits, Wolfgang] Med Univ Vienna, Inst Canc Res, Dept Med 1, Comprehens Canc Ctr Vienna, Vienna, Austria.
[Staufer, Katharina] Med Univ Vienna, Div Transplantat, Dept Surg, Vienna, Austria.
[Stauber, Rudolf; Pock, Hannelore] Med Univ Graz, Div Gastroenterol & Hepatol, Dept Internal Med, Graz, Austria.
[Bantel, Heike] Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Hannover, Germany.
[Weiss, Karl Heinz; Kloeters-Plachky, Petra; Gotthardt, Daniel N.] Univ Hosp Heidelberg, Heidelberg, Germany.
[Starlinger, Patrick; Brostjan, Christine; Gruenberger, Thomas] Med Univ Vienna, Div Gen Surg, Dept Surg, Vienna, Austria.
[Rauch, Peter] Candor Biosci GmbH, Wangen Im Allgau, Germany.
[Lackner, Carolin] Med Univ Graz, Inst Pathol, Graz, Austria.
[Stift, Judith] Med Univ Vienna, Clin Inst Pathol, Vienna, Austria.
[Kumada, Takashi; Toyoda, Hidenori; Tada, Toshifumi] Ogaki Municipal Hosp, Dept Gastroenterol, Ogaki, Japan.
[Weiss, Thomas S.] Univ Regensburg Hosp, Childrens Univ Hosp KUNO, Ctr Liver Cell Res, Regensburg, Germany.
[Staufer, Katharina; Trauner, Michael] Med Univ Vienna, Div Gastroenterol & Hepatol, Dept Internal Med 3, Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna; Medical
University of Graz; Hannover Medical School; Ruprecht Karls University
Heidelberg; Medical University of Vienna; Medical University of Graz;
Medical University of Vienna; Ogaki Municipal Hospital; University of
Regensburg; Medical University of Vienna
RP Mikulits, W (corresponding author), Med Univ Vienna, Inst Canc Res, Dept Med 1, Comprehens Canc Ctr Vienna, Vienna, Austria.
EM wolfgang.mikulits@meduniwien.ac.at
RI Brostjan, Christine/LKJ-3842-2024; Mikulits, Wolfgang/AAH-4043-2021;
Weiss, Karl Heinz/AAA-9117-2022; Trauner, Michael/HCH-4032-2022;
Gruenberger, Thomas/ABA-1661-2020; Weiss, Thomas/G-3989-2012
OI Weiss, Thomas/0000-0003-0336-0581; Staufer,
Katharina/0000-0002-1928-3333; Brostjan, Christine/0000-0003-1462-5397;
Trauner, Michael/0000-0002-1275-6425; Gruenberger,
Thomas/0000-0002-2671-0540; Stift, Judith/0000-0001-5334-9343; Mikulits,
Wolfgang/0000-0003-4612-7106
FU Austrian Science Fund, FWF [P25356]; Oesterreichische Nationalbank
(Oesterreichische Nationalbank, Anniversary Fund) [16673]; Austrian
Science Fund (FWF) [P25356] Funding Source: Austrian Science Fund (FWF)
FX This work was supported by the Austrian Science Fund, FWF, P25356 (to
WM) and supported by funds of the Oesterreichische Nationalbank
(Oesterreichische Nationalbank, Anniversary Fund, project number: 16673)
(to WM).
CR Altekruse SF, 2009, J CLIN ONCOL, V27, P1485, DOI 10.1200/JCO.2008.20.7753
[Anonymous], Therap. Adv.
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NR 40
TC 53
Z9 55
U1 0
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JUL 11
PY 2017
VL 8
IS 28
BP 46234
EP 46248
DI 10.18632/oncotarget.17598
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FA5SS
UT WOS:000405504600105
PM 28526812
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Ouyang, BH
Xie, QQ
Huang, WJ
Wang, LC
Tang, SF
Fu, JJ
AF Ouyang, Bohui
Xie, Qing-Qing
Huang, Wenjie
Wang, Linchun
Tang, Shifu
Fu, Jinjian
TI Diagnostic Value of Serum DNASE1L3 in Hepatitis B Virus-Related
Hepatocellular Carcinoma
SO CLINICAL LABORATORY
LA English
DT Article
DE deoxyribonuclease 1-like 3; hepatocellular carcinoma; alpha-fetoprotein;
diagnosis
ID MACROPHAGES; INFILTRATION; ASSOCIATION; RECURRENCE; CHROMATIN
AB Background: Deoxyribonuclease 1-like 3 (DNASE1L3) is an endonuclease associated with many autoimmune diseases and tumors. However, the serum DNASE1L3 level in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) remains unreported. Thus, this study compared the diagnostic value of DNASE1L3 and alpha-fetoprotein (AFP) individually and in combination in HBV-related HCC.
Methods: The study population consisted of 88 patients with HBV-related HCC, 80 patients with HBV-related liver cirrhosis (LC) and 88 control subjects. The serum DNASE1L3 levels were measured using an enzyme-linked immunosorbent assay. The serum AFP was also assayed.
Results: Our data showed that the serum DNASE1L3 levels were significantly higher in patients with HBV-related HCC than in the healthy controls and patients with LC. When the two biomarkers were analyzed individually, the receiver operating characteristic curve analysis showed that the areas under the curve of DNASE1L3 and AFP were 0.898 and 0.866, respectively. When DNASE1L3 and AFP were combined, the area under the curve was 0.951. The sensitivities of DNASE1L3 and AFP were 72.73% and 74.81%, respectively, and the specificities were 93.18% and 92.05%, respectively, in the diagnosis of HBV-related HCC. The sensitivity of the two combined could be improved to 89.77%. However, no correlation was found between serum DNASE1L3 and AFP in HBV-related HCC patients (r = 0.005, p = 0.734).
Conclusions: Serum DNASE1L3 has high sensitivity and specificity in the diagnosis of HCC. DNASE1L3 combined with AFP has higher sensitivity and can improve the diagnostic efficiency of HBV-related HCC.
C1 [Ouyang, Bohui; Xie, Qing-Qing; Wang, Linchun; Tang, Shifu] Guangxi Univ Chinese Med, Affiliated Hosp 3, Dept Clin Lab, Liuzhou, Guangxi, Peoples R China.
[Huang, Wenjie] Guangxi Med Univ, Affiliated Liutie Cent Hosp, Dept Clin Lab, Liuzhou, Guangxi, Peoples R China.
[Fu, Jinjian] Liuzhou Matern & Child Hlth Care Hosp, Dept Clin Lab, Liuzhou, Guangxi, Peoples R China.
C3 Guangxi University of Chinese Medicine; Guangxi Medical University
RP Fu, JJ (corresponding author), Liuzhou Matern & Child Hlth Care Hosp, Dept Prevent & Hlth Care, Dept Pediat, Yingshan Rd 50, Liuzhou 545001, Guangxi, Peoples R China.
EM fujinjianaa@126.com
RI Huang, Wenjie/AFS-0473-2022
FU Guangxi Zhuang Autonomous Region health and Family Planning Commission
[Z20190 220, Z20200093]
FX This study was supported by the self-funded research project of Guangxi
Zhuang Autonomous Region health and Family Planning Commission (grant
No. Z20190 220, Z20200093)
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NR 28
TC 3
Z9 3
U1 1
U2 5
PU CLIN LAB PUBL
PI HEIDELBERG
PA IM BREITSPIEL 15, HEIDELBERG, D-69126, GERMANY
SN 1433-6510
J9 CLIN LAB
JI Clin. Lab.
PY 2021
VL 67
IS 3
BP 731
EP 737
DI 10.7754/Clin.Lab.2020.200627
PG 7
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA RZ6XJ
UT WOS:000648745300011
PM 33739053
DA 2025-01-07
ER
PT J
AU Lammers, WJ
Kowdley, KV
van Buuren, HR
AF Lammers, Willem J.
Kowdley, Kris V.
van Buuren, Henk R.
TI Predicting outcome in primary binary cirrhosis
SO ANNALS OF HEPATOLOGY
LA English
DT Review
DE Prognostic factors; Prediction models; Liver transplant-free survival;
Esophageal varices; Hepatocellular carcinoma
ID PRIMARY BILIARY-CIRRHOSIS; URSODEOXYCHOLIC-ACID THERAPY;
ANTIMITOCHONDRIAL ANTIBODY PROFILES; RANDOMIZED CONTROLLED-TRIALS; EARLY
BIOCHEMICAL RESPONSE; LONG-TERM PROGNOSIS; HEPATOCELLULAR-CARCINOMA;
NATURAL-HISTORY; HISTOLOGICAL PROGRESSION; CLINICAL-FEATURES
AB Primary biliary cirrhosis (PBC) is a slowly progressive autoimmune liver disease that may ultimately result in liver failure and premature death. Predicting outcome is of key importance in clinical management and an essential requirement for patients counselling and timing of diagnostic and therapeutic interventions. The following factors are associated with progressive disease and worse outcome: young age at diagnosis, male gender, histological presence of cirrhosis, accelerated marked ductopenia in relation to the amount of fibrosis, high serum bilirubin, low serum albumin levels, high serum alkaline phosphatase levels, esophageal varices, hepatocellular carcinoma (HCC) and lack of biochemical response to ursodeoxycholic acid (UDCA). The prognostic significance of symptoms at diagnosis is uncertain. UDCA therapy and liver transplantation have a significant beneficial effect on the outcome of the disease. The Mayo risk score in PBC can be used for estimating individual prognosis. The Newcastle Varices in PBC Score may be a useful clinical tool to predict the risk for development of esophageal varices. Male gender, cirrhosis and non-response to UDCA therapy in particular, are risk factors for development of HCC.
C1 [Lammers, Willem J.; van Buuren, Henk R.] Erasmus Univ, Med Ctr, Dept Gastroenterol & Hepatol, NL-3015 CE Rotterdam, Netherlands.
[Kowdley, Kris V.] Virginia Mason Med Ctr, Inst Digest Dis, Liver Ctr Excellence, Seattle, WA 98101 USA.
C3 Erasmus University Rotterdam; Erasmus MC; Virginia Mason Medical Center
RP Lammers, WJ (corresponding author), Erasmus Univ, Med Ctr, Dept Gastroenterol & Hepatol, S Gravendijkwal 230,Room Ca 413, NL-3015 CE Rotterdam, Netherlands.
EM w.lammers@erasmusmc.nl
RI Kowdley, Kris/AAF-5202-2019; Lammers, Willem/P-5456-2014
OI Lammers, Willem/0000-0002-5455-5242
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NR 97
TC 42
Z9 48
U1 0
U2 11
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
PD JUL-AUG
PY 2014
VL 13
IS 4
BP 316
EP 326
DI 10.1016/S1665-2681(19)30838-5
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AO6MX
UT WOS:000341467300001
PM 24927602
OA hybrid
DA 2025-01-07
ER
PT J
AU Jarido, V
Kennedy, L
Hargrove, L
Demieville, J
Thomson, J
Stephenson, K
Francis, H
AF Jarido, Veronica
Kennedy, Lindsey
Hargrove, Laura
Demieville, Jennifer
Thomson, Joanne
Stephenson, Kristen
Francis, Heather
TI The emerging role of mast cells in liver disease
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Review
DE cholangiopathies; disease; liver; mast cells
ID PRIMARY SCLEROSING CHOLANGITIS; HEPATOCELLULAR-CARCINOMA;
HEPATIC-FIBROSIS; FATTY LIVER; NONALCOHOLIC STEATOHEPATITIS; RAT-LIVER;
HISTAMINE-SECRETION; BILIARY HYPERPLASIA; ENDOTHELIAL-CELLS; OXIDATIVE
STRESS
AB The depth of our knowledge regarding mast cells has widened exponentially in the last 20 years. Once thought to be only important for allergy-mediated events, mast cells are now recognized to be important regulators of a number of pathological processes. The revelation that mast cells can influence organs, tissues, and cells has increased interest in mast cell research during liver disease. The purpose of this review is to refresh the reader's knowledge of the development, type, and location of mast cells and to review recent work that demonstrates the role of hepatic mast cells during diseased states. This review focuses primarily on liver diseases and mast cells during autoimmune disease, hepatitis, fatty liver disease, liver cancer, and aging in the liver. Overall, these studies demonstrate the potential role of mast cells in disease progression.
C1 [Kennedy, Lindsey; Demieville, Jennifer; Thomson, Joanne; Francis, Heather] Res Cent Texas Vet Hlth Care Syst, Temple, TX USA.
[Jarido, Veronica; Stephenson, Kristen; Francis, Heather] Baylor Scott & White Hlth & Med, Temple, TX USA.
[Kennedy, Lindsey; Hargrove, Laura; Francis, Heather] Texas A&M Hlth Sci Ctr, Temple, TX USA.
C3 Baylor Health Care System; Texas A&M University System; Texas A&M
University College Station; Texas A&M Health Science Center
RP Francis, H (corresponding author), Texas A&M Univ, Dept Internal Med, Coll Med, CTVHCS,Baylor Scott & White Healthcare, 1901 South 1st St,Bldg 205,1R58, Temple, TX 76502 USA.
EM hfrancis@medicine.tamhsc.edu
FU Department of Veterans Affairs Biomedical Laboratory Research and
Development Service Merit Award [1I01BX003031]; National Institute of
Diabetes and Digestive and Kidney Diseases [RO1 DK-108959]
FX Portions of this work were supported by Department of Veterans Affairs
Biomedical Laboratory Research and Development Service Merit Award
1I01BX003031 and National Institute of Diabetes and Digestive and Kidney
Diseases Grant RO1 DK-108959 to H. Francis. This material is the result
of work supported with resources and the use of facilities at the
Central Texas Veterans Health Care System, Temple, Texas.
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NR 113
TC 35
Z9 39
U1 11
U2 24
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1857
EI 1522-1547
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD AUG
PY 2017
VL 313
IS 2
BP G89
EP G101
DI 10.1152/ajpgi.00333.2016
PG 13
WC Gastroenterology & Hepatology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Physiology
GA FD4GF
UT WOS:000407488900001
PM 28473331
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Zhao, LZ
Yu, GY
Han, Q
Cui, CX
Zhang, B
AF Zhao, Lizhen
Yu, Guoyi
Han, Qi
Cui, Congxian
Zhang, Bei
TI TIM-3: An emerging target in the liver diseases
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Review
DE autoimmune liver disease; Galectin-9; Th1; TIM-3; viral hepatitis
ID T-CELL IMMUNOGLOBULIN; INTERFERON-GAMMA PRODUCTION;
HEPATOCELLULAR-CARCINOMA; MOUSE MODEL; ELEVATED FREQUENCIES; AUTOIMMUNE
HEPATITIS; IMMUNE-RESPONSES; RECEPTOR TIM-3; INNATE; EXPRESSION
AB T cell immunoglobulin domain and mucin domain-containing molecule 3 (TIM-3) is found expression in the surface of terminally differentiated T cells and belongs to the TIM family of type ROMAN NUMERAL ONE transmembrane proteins. It binds to the ligand Galectin-9 and mediates T cell apoptosis. As the research progresses, TIM-3 is also expressed in Th17, NK, monocyte, which binds to ligand and induce immune peripheral tolerance in both mice and man. Numerous researches have demonstrated that TIM-3 influences liver diseases, including liver-associated chronic viral infection, liver fibrosis, liver cancer et al and suggest new approaches to intervention. Currently, targeted therapy of TIM-3 is a new treatment in the field of immunization. Although many studies have proven that TIM-3 has an inhibitory effect in vivo, the specific mechanism is not clear. Herein, we summarize the important role of TIM-3 in the regulation of liver disease and prospects for future clinical research. TIM-3 will provide new targets for improving clinical liver disease.
C1 [Zhao, Lizhen; Han, Qi; Zhang, Bei] Qingdao Univ, Dept Immunol, Coll Med, 308 Ningxia Rd, Qingdao 266071, Shandong, Peoples R China.
[Yu, Guoyi] Journal Qingdao Univ Med Sci, Editorial Off, Qingdao, Peoples R China.
[Cui, Congxian] Qingdao Univ, Coll Med, Affiliated Hosp, Qingdao, Peoples R China.
C3 Qingdao University; Qingdao University
RP Zhang, B (corresponding author), Qingdao Univ, Dept Immunol, Coll Med, 308 Ningxia Rd, Qingdao 266071, Shandong, Peoples R China.
EM Zhangbei124@aliyun.com
OI Zhao, Lizhen/0000-0002-5875-6463
FU National Natural Science Foundation of China [81072398]
FX National Natural Science Foundation of China, Grant/Award Number:
81072398
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NR 93
TC 25
Z9 27
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD APR
PY 2020
VL 91
IS 4
AR e12825
DI 10.1111/sji.12825
EA FEB 2020
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA KX7DU
UT WOS:000511012800001
PM 31486085
OA Bronze
DA 2025-01-07
ER
PT J
AU Lei, YM
Li, SM
He, MX
Ao, ZC
Wang, JD
Wu, QM
Wang, Q
AF Lei, Yumeng
Li, Simin
He, Mingxin
Ao, Zichun
Wang, Jiadun
Wu, Qingming
Wang, Qiang
TI Oral Pathogenic Bacteria and the Oral-Gut-Liver Axis: A New
Understanding of Chronic Liver Diseases
SO DIAGNOSTICS
LA English
DT Review
DE oral-gut-liver axis; oral pathogenic bacteria; oral microbiota; chronic
liver diseases; hepatocellular carcinoma
ID NONALCOHOLIC FATTY LIVER; PORPHYROMONAS-GINGIVALIS;
FUSOBACTERIUM-NUCLEATUM; INTESTINAL MICROBIOTA; COLONIC INFLAMMATION;
RISK-FACTOR; PERIODONTITIS; CIRRHOSIS; EXPRESSION; INCREASE
AB Liver diseases have long been a prevalent cause of morbidity and mortality, and their development and progression involve multiple vital organs throughout the body. Recent studies on the oral-gut-liver axis have revealed that the oral microbiota is associated with the pathophysiology of chronic liver diseases. Since interventions aimed at regulating oral biological disorders may delay the progress of liver disease, it is crucial to better comprehend this process. Oral bacteria with potential pathogenicity have been extensively studied and are closely related to several types of chronic liver diseases. Therefore, this review will systemically describe the emerging role of oral pathogenic bacteria in common liver diseases, including alcoholic liver disease (ALD), non-alcoholic steatohepatitis (NASH), non-alcoholic fatty liver disease (NAFLD), cirrhosis, autoimmune liver diseases (AILD), and liver cancer, and bring in new perspectives for future research.
C1 [Lei, Yumeng; Li, Simin; He, Mingxin; Ao, Zichun; Wang, Jiadun; Wu, Qingming; Wang, Qiang] Wuhan Univ Sci & Technol, Inst Infect Immunol & Tumor Microenvironm, Sch Med, Hubei Prov Key Lab Occupat Hazard Identificat & Co, Wuhan 430065, Peoples R China.
C3 Wuhan University of Science & Technology
RP Wang, Q (corresponding author), Wuhan Univ Sci & Technol, Inst Infect Immunol & Tumor Microenvironm, Sch Med, Hubei Prov Key Lab Occupat Hazard Identificat & Co, Wuhan 430065, Peoples R China.
EM lym8252022@163.com; lsm3667@163.com; mingxin_he2021@163.com;
18871226539@163.com; wangjiadun@wust.edu.cn; wuhe9224@sina.com;
wangqiang@wust.edu.cn
OI wang, haoyu/0009-0001-2467-5331; Wang, Qiang/0000-0001-7420-8646
FU This thesis would not have been possible without the consistent and
valuable references provided by our supervisor, whose insightful
guidance and enthusiastic encouragement in shaping this thesis have
gained our deepest gratitude.
FX This thesis would not have been possible without the consistent and
valuable references provided by our supervisor, whose insightful
guidance and enthusiastic encouragement in shaping this thesis have
gained our deepest gratitude.
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NR 116
TC 4
Z9 4
U1 2
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD NOV
PY 2023
VL 13
IS 21
AR 3324
DI 10.3390/diagnostics13213324
PG 17
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA X6OK1
UT WOS:001099620600001
PM 37958220
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Yoshida, S
Fujita, M
Ishigame, T
Kobayashi, Y
Sumichika, Y
Saito, K
Matsumoto, H
Temmoku, J
Fujita, Y
Matsuoka, N
Asano, T
Sato, S
Watanabe, H
Yoshida, H
Marubashi, S
Hashimoto, Y
Ohira, H
Migita, K
AF Yoshida, Shuhei
Fujita, Masashi
Ishigame, Teruhide
Kobayashi, Yasuyuki
Sumichika, Yuya
Saito, Kenji
Matsumoto, Haruki
Temmoku, Jumpei
Fujita, Yuya
Matsuoka, Naoki
Asano, Tomoyuki
Sato, Shuzo
Watanabe, Hiroshi
Yoshida, Hiroshi
Marubashi, Shigeru
Hashimoto, Yuko
Ohira, Hiromasa
Migita, Kiyoshi
TI Case report: Unusual development of hepatocellular carcinoma during
immunosuppressive treatments against rheumatoid arthritis overlapping
Sjogren's syndrome; cirrhotic steatohepatitis with liver inflammation
and fibrosis lurks in autoimmune disorders
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE methotrexate (MTX); non-alcoholic fatty liver disease (NAFLD);
non-alcoholic steatohepatitis (NASH); rheumatoid arthritis (RA);
Sjogren's syndrome (SS); tumor necrosis factor inhibitors (TNFi);
hepatocellular carcinoma (HCC)
ID RISK-FACTORS; CLASSIFICATION CRITERIA; AMERICAN-COLLEGE; METHOTREXATE;
DISEASE; DRUGS
AB The sequential progression from chronic liver disease to cirrhosis may be a risk factor for hepatocellular carcinoma (HCC) development. Although HCC originates from hepatitis B virus- or hepatitis C virus-associated liver cirrhosis, it has recently been reported in patients with non-alcoholic steatohepatitis (NASH) with advanced fibrosis. However, little is known about the pathophysiological mechanisms linking HCC to rheumatic disorders, including rheumatoid arthritis (RA). Herein, we describe the case of HCC with NASH complicated by RA and Sjogren's syndrome (SS). A fifty-two-year-old patient with RA and diabetes was referred to our hospital for further examination of a liver tumor. She received methotrexate (4 mg/week) for 3 years and adalimumab (40 mg/biweekly) for 2 years. On admission, laboratory data showed mild thrombocytopenia and hypoalbuminemia, with normal hepatitis virus markers or liver enzymes. Anti-nuclear antibodies were positive with high titers (x640), and anti-SS-A/Ro (187.0 U/ml; normal range [NR]: <= 6.9 U/mL) and anti-SS-B/La (320 U/ml; NR: <= 6.9 U/mL) antibodies were also high. Abdominal ultrasonography and computed tomography revealed liver cirrhosis and a tumor in the left lobe (S4) of the liver. She was diagnosed with HCC based on imaging findings, and elevated levels of protein induced by vitamin K absence- II (PIVKA-II) were detected. She underwent laparoscopic partial hepatectomy, and histopathological examination revealed steatohepatitis HCC with background liver cirrhosis. The patient was discharged on the 8(th) day post-operation without any complications. At the 30 months follow-up, no significant evidence of recurrence was observed. Our case suggests that clinical screening for HCC is needed in patients with RA who are at a high risk of NASH, as they may progress to HCC even without elevated liver enzymes.
C1 [Yoshida, Shuhei; Sumichika, Yuya; Saito, Kenji; Matsumoto, Haruki; Temmoku, Jumpei; Fujita, Yuya; Matsuoka, Naoki; Asano, Tomoyuki; Sato, Shuzo; Watanabe, Hiroshi; Migita, Kiyoshi] Fukushima Med Univ, Dept Rheumatol, Sch Med, Fukushima, Japan.
[Fujita, Masashi; Ohira, Hiromasa] Fukushima Med Univ, Dept Gastroenterol, Sch Med, Fukushima, Japan.
[Ishigame, Teruhide; Marubashi, Shigeru] Fukushima Med Univ, Dept Hepatobiliary Pancreat & Transplant Surg, Sch Med, Fukushima, Japan.
[Kobayashi, Yasuyuki; Hashimoto, Yuko] Fukushima Med Univ, Dept Diagnost Pathol, Sch Med, Fukushima, Japan.
[Yoshida, Hiroshi] Kita Fukushima Med Ctr, Dept Internal Med, Date, Japan.
C3 Fukushima Medical University; Fukushima Medical University; Fukushima
Medical University; Fukushima Medical University
RP Migita, K (corresponding author), Fukushima Med Univ, Dept Rheumatol, Sch Med, Fukushima, Japan.
EM migita@fmu.ac.jp
RI Fujita, Masashi/R-6998-2018; Sato, Shuzo/AAC-7025-2019
OI Asano, Tomoyuki/0009-0005-6538-1881; Yoshida,
Shuhei/0000-0001-5123-3136; , Haruki Matsumoto/0009-0006-4305-2048
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NR 39
TC 1
Z9 1
U1 0
U2 2
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD FEB 15
PY 2023
VL 14
AR 1089492
DI 10.3389/fimmu.2023.1089492
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 9J5NL
UT WOS:000940233000001
PM 36875090
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Taylor, SL
Haque, S
AF Taylor, Shari L.
Haque, Salima
TI Hepatobiliary pathology
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Article
DE autoimmune liver disease; hemophagocytic lymphohistiocytosis;
hepatocellular carcinoma; liver pathology; nonalcoholic fatty liver
disease; plasma cell hepatitis
ID NOVO AUTOIMMUNE HEPATITIS; PLASMA-CELL HEPATITIS; FATTY LIVER-DISEASE;
HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC STEATOHEPATITIS;
DIFFERENTIAL-DIAGNOSIS; TRANSPLANTATION; REJECTION; CHILDREN; FEATURES
AB Purpose of review
Recent studies pertaining to the histopathology of the liver and biliary tract are reviewed.
Recent findings
Several studies are reviewed which describe the histologic features and clinical behavior of 'plasma cell hepatitis' in the posttransplant setting. Cytokeratin 7, EMA, and CD68 were found to be useful immunohistochemical stains in fibrolamellar hepatocellular carcinoma and may aid in the distinction between this variant and classic hepatocellular carcinoma. Arginase-1, another immunohistochemical stain, was found to have improved sensitivity over HepPar-1 in the diagnosis of classic hepatocellular carcinoma. Metabolic syndrome is common in children with nonalcoholic fatty liver disease and may be an indicator of more severe disease activity and fibrosis. Histologic features were described that may aid in the distinction between the steroid-responsive IgG4-associated cholangitis and the steroid-nonresponsive primary sclerosing cholangitis. In addition, immunohistochemical stains for IgM and IgG may be helpful in distinguishing between autoimmune liver diseases, with primary biliary cirrhosis and its antimitochondrial-negative variant, autoimmune cholangitis, being the two autoimmune liver diseases with a predominance of IgM-positive plasma cells.
Summary
Several informative studies pertaining to hepatobiliary pathology were published this year, with topics including posttransplant plasma cell hepatitis, familial hemophagocytic lymphohistiocytosis, pediatric nonalcoholic fatty liver disease, and the use of immunohistochemical stains specific for various immunoglobulin subtypes.
C1 [Taylor, Shari L.; Haque, Salima] Caris Life Sci, Irving, TX 75039 USA.
RP Taylor, SL (corresponding author), Caris Life Sci, 6655 N MacArthur Blvd, Irving, TX 75039 USA.
EM staylor@carisls.com
CR [Anonymous], NONALCOHOLIC STEATOH
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NR 43
TC 5
Z9 6
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0267-1379
EI 1531-7056
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD MAY
PY 2011
VL 27
IS 3
BP 248
EP 255
DI 10.1097/MOG.0b013e3283457d43
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 749XM
UT WOS:000289505200008
PM 21423007
DA 2025-01-07
ER
PT J
AU Hamid, S
da Silva, MRA
Burak, KW
Chen, T
Drenth, JPH
Esmat, G
Gaspar, R
LaBrecque, D
Lee, A
Macedo, G
McMahon, B
Ning, Q
Reau, N
Sonderup, M
van Leeuwen, DJ
Armstrong, D
Yurdaydin, C
AF Hamid, Saeed
Alvares da Silva, Mario R.
Burak, Kelly W.
Chen, Tao
Drenth, Joost P. H.
Esmat, Gamal
Gaspar, Rui
LaBrecque, Douglas
Lee, Alice
Macedo, Guilherme
McMahon, Brian
Ning, Qin
Reau, Nancy
Sonderup, Mark
van Leeuwen, Dirk J.
Armstrong, David
Yurdaydin, Cihan
TI WGO Guidance for the Care of Patients With COVID-19 and Liver Disease
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE COVID-19 disease; liver disease; chronic viral hepatitis; metabolic
dysfunction-associated liver disease; autoimmune liver diseases;
hepatocellular carcinoma; liver transplantation
ID CORONAVIRUS; HEPATITIS; HYDROXYCHLOROQUINE; INJURY; SAFETY
AB Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the least deadly but most infectious coronavirus strain transmitted from wild animals. It may affect many organ systems. Aim of the current guideline is to delineate the effects of SARS-CoV-2 on the liver. Asymptomatic aminotransferase elevations are common in coronavirus disease 2019 (COVID-19) disease. Its pathogenesis may be multifactorial. It may involve primary liver injury and indirect effects such as "bystander hepatitis," myositis, toxic liver injury, hypoxia, and preexisting liver disease. Higher aminotransferase elevations, lower albumin, and platelets have been reported in severe compared with mild COVID-19. Despite the dominance of respiratory disease, acute on chronic liver disease/acute hepatic decompensation have been reported in patients with COVID-19 and preexisting liver disease, in particular cirrhosis. Metabolic dysfunction-associated fatty liver disease (MAFLD) has a higher risk of respiratory disease progression than those without MAFLD. Alcohol-associated liver disease may be severely affected by COVID-19-such patients frequently have comorbidities including metabolic syndrome and smoking-induced chronic lung disease. World Gastroenterology Organization (WGO) recommends that interventional procedures such as endoscopy and endoscopic retrograde cholangiopancreatography should be performed in emergency cases or when they are considered strictly necessary such as high risk varices or cholangitis. Hepatocellular cancer surveillance may be postponed by 2 to 3 months. A short delay in treatment initiation and non-surgical approaches should be considered. Liver transplantation should be restricted to patients with high MELD scores, acute liver failure and hepatocellular cancer within Milan criteria. Donors and recipients should be tested for SARS-CoV-2 and if found positive donors should be excluded and liver transplantation postponed until recovery from infection.
C1 [Hamid, Saeed] Aga Khan Univ, Dept Med, Karachi, Pakistan.
[Alvares da Silva, Mario R.] Univ Sao Paulo, Hosp Clin Porto Alegre, GI Liver Unit, Porto Alegre, RS, Brazil.
[Burak, Kelly W.] Univ Calgary, Cumming Sch Med, Dept Med & Oncol, Calgary, AB, Canada.
[Armstrong, David] McMaster Univ, Div Gastroenterol, Med Ctr, Hamilton, ON, Canada.
[Chen, Tao; Ning, Qin] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept & Inst Infect Dis, Wuhan, Peoples R China.
[Drenth, Joost P. H.] Radboud UMC, Dept Gastroenterol & Hepatol, Nijmegen, Netherlands.
[Esmat, Gamal] Cairo Univ, Endem Med & Hepatogastroenterol Dept, Fac Med, Cairo, Egypt.
[Gaspar, Rui; Macedo, Guilherme] Univ Porto, Ctr Hosp Sao Joao, Gastroenterol & Hepatol Dept, Porto, Portugal.
[LaBrecque, Douglas] Univ Iowa Hosp & Clin, Div Gastroenterol & Hepatol, Iowa City, IA 52242 USA.
[Lee, Alice] Univ Sydney, Concord Repatriat Gen Hosp, Hepatitis Program, Sydney, NSW, Australia.
[McMahon, Brian] Alaska Native Tribal Hlth Consortium, Liver Dis & Hepatitis Program, Anchorage, AK USA.
[Reau, Nancy] Rush Univ, Med Ctr, Sect Hepatol, Chicago, IL 60612 USA.
[Sonderup, Mark] Univ Cape Town, Groote Schuur Hosp, Fac Hlth Sci, Dept Med,Div Hepatol, Cape Town, South Africa.
[van Leeuwen, Dirk J.] Dartmouth Hitchcock Med Ctr, Div Gastroenterol & Hepatol, Lebanon, NH 03766 USA.
[Yurdaydin, Cihan] Koc Univ, Med Sch, Dept Gastroenterol & Hepatol, Davutpasa Cad 4, TR-34010 Istanbul, Turkey.
C3 Aga Khan University; Universidade de Sao Paulo; University of Calgary;
McMaster University; Huazhong University of Science & Technology;
Radboud University Nijmegen; Egyptian Knowledge Bank (EKB); Cairo
University; Sao Joao Hospital; Universidade do Porto; University of
Iowa; Concord Repatriation General Hospital; University of Sydney;
Alaska Native Tribal Health Consortium; Rush University; University of
Cape Town; Dartmouth College; Koc University
RP Yurdaydin, C (corresponding author), Koc Univ, Med Sch, Dept Gastroenterol & Hepatol, Davutpasa Cad 4, TR-34010 Istanbul, Turkey.
EM cihan.yurdaydin@medicine.ankara.edu.tr
RI van leeuwen, dirk/S-1659-2019; Drenth, Joost/V-7436-2019; Macedo,
Manuel/L-8038-2013; Alvares-da-Silva, Mario/L-3910-2014
OI Macedo, Guilherme/0000-0002-9387-9872; Drenth, Joost
PH/0000-0001-8027-3073; Alvares-da-Silva, Mario/0000-0002-5001-246X;
Armstrong, David/0000-0003-2487-1479
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NR 82
TC 35
Z9 37
U1 0
U2 18
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD JAN
PY 2021
VL 55
IS 1
BP 1
EP 11
DI 10.1097/MCG.0000000000001459
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA PG4LV
UT WOS:000599709300002
PM 33230011
OA Green Published
DA 2025-01-07
ER
PT J
AU Neuberger, J
AF Neuberger, James
TI An update on liver transplantation: A critical review
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Review
DE Liver transplantation; Machine perfusion; Recurrent disease; Donation
after circulatory; Death; De novo cancer
ID NOVO AUTOIMMUNE HEPATITIS; PLASMA-CELL HEPATITIS;
HEPATOCELLULAR-CARCINOMA; CONSENSUS CONFERENCE; GRAFT-SURVIVAL;
UNITED-STATES; RECIPIENTS; DONATION; RECURRENCE; DISEASE
AB Liver transplantation, although now a routine procedure, with defined indications and usually excellent outcomes, still has challenges. Donor shortage remains a key issue. Transplanted organs are not free of risk and may transmit cancer, infection, metabolic or autoimmune disease. Approaches to the donor shortage include use of organs from donors after circulatory death, from living donors and from those previously infected with Hepatitis B and C and even HIV for selected recipients. Normothermic regional and/or machine perfusion, whether static or pulsatile, normo- or hypothermic, are being explored and will be likely to have a major place in improving donation rates and outcomes. The main indications for liver replacement are alcoholic liver disease, HCV, non-alcoholic liver disease and liver cancer. Recent studies have shown that selected patients with severe alcoholic hepatitis may also benefit from liver transplant. The advent of new and highly effective treatments for HCV, whether given before or after transplant will have a major impact on outcomes. The role of transplantation for those with liver cell cancer continues to evolve as other interventions become more effective. Immunosuppression is usually required life-long and adherence remains a challenge, especially in adolescents. Immunosuppression with calcineurin inhibitors (primarily tacrolimus), antimetabolites (azathioprine or mycophenolate) and corticosteroids remains standard. Outcomes after transplantation are good but not normal in quality or quantity. Premature death may be due to increased risk of cardiovascular disease, de novo cancer, recurrent disease or late technical problems. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Neuberger, James] Queen Elizabeth Hosp, Liver Unit, Birmingham B15 2TH, W Midlands, England.
[Neuberger, James] NHS Blood & Transplant, Organ Donat & Transplantat, Fox Den Rd, Bristol BS34 8RR, Avon, England.
C3 University of Birmingham
RP Neuberger, J (corresponding author), Queen Elizabeth Hosp, Liver Unit, Birmingham B15 2TH, W Midlands, England.
EM james.neuberger@nhsbt.nhs.uk
RI Neuberger, James/ABG-3010-2020
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NR 63
TC 57
Z9 66
U1 0
U2 23
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD JAN
PY 2016
VL 66
SI SI
BP 51
EP 59
DI 10.1016/j.jaut.2015.08.021
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA DC9RB
UT WOS:000369557600006
PM 26350881
DA 2025-01-07
ER
PT J
AU Nocera, A
Andorno, E
Tagliamacco, A
Morelli, N
Bottino, G
Ravazzoni, F
Casaccia, M
Barocci, S
Alice, S
Santori, G
Ghirelli, R
Valente, U
AF Nocera, A.
Andorno, E.
Tagliamacco, A.
Morelli, N.
Bottino, G.
Ravazzoni, F.
Casaccia, M.
Barocci, S.
Alice, S.
Santori, G.
Ghirelli, R.
Valente, U.
TI Sirolimus therapy in liver transplant patients: An initial experience at
a single center
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article; Proceedings Paper
CT 31st Congress of the Italian-Transplantation-Society
CY NOV 28-30, 2007
CL Modena, ITALY
SP Italian Transplantat Soc
ID PNEUMONITIS
AB Sirolimus (SRL) is an mTOR inhibitor that has been shown, in contrast to calcineurin inhibitors (CNI), to inhibit cancers in experimental models. Since February 2005, we introduced SRL in liver transplant patients in group a, in whom the primary disease was hepatocellular carcinoma (HCC) associated with hepatitis B virus (HBV), hepatitis C virus (HCV), alcoholic or autoimmune liver cirrhosis, and group b, HCC-negative patients who developed posttransplantation cancers de novo. Of 18 patients in group a, 11 received SRL ab initio (subgroup a1), starting for 10 patients at 66.1 +/- 29.2 days after surgical healing and after 10 days in I case; the remaining 7 patients (subgroup a2) received SRL at 31.2 +/- 24.2 months. Three patients in group b, included 1. with Kaposi's sarcoma, I with bladder cancer, and I with thyroid cancer. In this group, SRL was introduced at 80.8 +/- 40.4 months. In all patients but one, who received a single 5 mg loading dose, SRL was started at 2 mg/d and adjusted to 6 to 8 ng/mL blood levels. CNI drugs, present as primary therapy, were gradually tapered to low levels and eventually stopped. The following observations were drawn from this initial experience: (1) 4/21 (19.0%) patients had to discontinue SRL because of early and late side effects: thrombocytopenia (n = 2) and headache with leukopenia and leg edema associated with knee joint arthralgia (n = 2); (2) 14 patients (11 in group a and 3 in group b) are still on SRL monotherapy; (3) 1 HCC recurrence and I de novo pancreatic adenocarcinoma were observed at 14 and 16 months, respectively (at the time of transplantation, both patients were beyond the Milan HCC criteria), and (4) 1 patient, from subgroup at, died after 99 days due to pneumonitis and possible relation to SRL lung toxicity. In conclusion, SRL appeared to be an effective immunosuppressant that could be used as monotherapy in liver transplant patients. Any conclusion on SRL anticancer effects can only come from randomized large studies after long follow-up.
C1 [Nocera, A.; Tagliamacco, A.; Barocci, S.; Alice, S.] San Martino Hosp, Transplant Immunol Unit, Dept Transplantat, I-16132 Genoa, Italy.
[Andorno, E.; Morelli, N.; Bottino, G.; Ravazzoni, F.; Casaccia, M.; Santori, G.; Ghirelli, R.; Valente, U.] San Martino Hosp, Transplant Surg Unit, Dept Transplantat, I-16132 Genoa, Italy.
C3 University of Genoa; IRCCS AOU San Martino IST; University of Genoa;
IRCCS AOU San Martino IST
RP Nocera, A (corresponding author), San Martino Hosp, Transplant Immunol Unit, Dept Transplantat, Monoblocco 1F,Largo R Benzi 10, I-16132 Genoa, Italy.
EM arcangelo.nocera@hsanmartino.it
RI Santori, Gregorio/E-8418-2012
OI CASACCIA, MARCO/0000-0001-5048-5091; Santori,
Gregorio/0000-0003-3764-2624
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NR 7
TC 29
Z9 36
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0041-1345
EI 1873-2623
J9 TRANSPL P
JI Transplant. Proc.
PD JUL-AUG
PY 2008
VL 40
IS 6
BP 1950
EP 1952
DI 10.1016/j.transproceed.2008.05.005
PG 3
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Immunology; Surgery; Transplantation
GA 340FG
UT WOS:000258630900044
PM 18675098
DA 2025-01-07
ER
PT J
AU Honma, Y
Shibata, M
Gohda, T
Matsumiya, H
Kumamoto, K
Miyama, A
Morino, K
Koya, Y
Taira, A
Shinohara, S
Hayashi, T
Kusanaga, M
Oe, S
Miyagawa, K
Abe, S
Tanaka, F
Harada, M
AF Honma, Yuichi
Shibata, Michihiko
Gohda, Tomonori
Matsumiya, Hiroki
Kumamoto, Keiichiro
Miyama, Aya
Morino, Kahori
Koya, Yudai
Taira, Akihiro
Shinohara, Shinji
Hayashi, Tsuguru
Kusanaga, Masashi
Oe, Shinji
Miyagawa, Koichiro
Abe, Shintaro
Tanaka, Fumihiro
Harada, Masaru
TI Rapid Progression of Liver Fibrosis Induced by Acute Liver Injury Due to
Immune-related Adverse Events of Atezolizumab
SO INTERNAL MEDICINE
LA English
DT Article
DE atezolizumab; autoimmune hepatitis; immune checkpoint inhibitor;
immune-related adverse event; sequential liver biopsy; liver fibrosis
ID PLUS BEVACIZUMAB; TOXICITIES; IPILIMUMAB; MANAGEMENT; NIVOLUMAB
AB A 72-year-old woman with advanced lung cancer had received systemic chemotherapy including atezolizumab. About three months after the initial administration of atezolizumab, her liver enzyme levels increased. The histopathological findings of the initial liver biopsy revealed acute inflammatory infiltrate, predominantly CD3(+), CD4(+) and CD8(+) T lymphocytes, in the hepatic lobules. We diagnosed her with atezolizumab-induced immune-related acute hepatitis. Oral corticosteroid therapy successfully improved the elevation of serum aminotransferases. A sequential liver biopsy demonstrated the rapid progression of liver fibrosis. Because hepatocellular carcinoma occurs most often in advanced cases of chronic liver disease, we should pay close attention to immune-related acute hepatic injury when treating patients with advanced liver diseases using atezolizumab.
C1 [Honma, Yuichi; Shibata, Michihiko; Gohda, Tomonori; Kumamoto, Keiichiro; Miyama, Aya; Morino, Kahori; Koya, Yudai; Hayashi, Tsuguru; Kusanaga, Masashi; Oe, Shinji; Miyagawa, Koichiro; Abe, Shintaro; Harada, Masaru] Univ Occupat & Environm Hlth, Sch Med, Dept Internal Med 3, Kitakyushu, Fukuoka, Japan.
[Matsumiya, Hiroki; Taira, Akihiro; Shinohara, Shinji; Tanaka, Fumihiro] Univ Occupat & Environm Hlth, Sch Med, Dept Surg 2, Kitakyushu, Fukuoka, Japan.
[Kumamoto, Keiichiro] Univ Occupat & Environm Hlth, Sch Med, Dept Pathol, Kitakyushu, Fukuoka, Japan.
[Koya, Yudai] Moji Med Ctr, Dept Gastroenterol, Kitakyushu, Fukuoka, Japan.
C3 University of Occupational & Environmental Health - Japan; University of
Occupational & Environmental Health - Japan; University of Occupational
& Environmental Health - Japan
RP Honma, Y (corresponding author), Univ Occupat & Environm Hlth, Sch Med, Dept Internal Med 3, Kitakyushu, Fukuoka, Japan.
EM y-homma@med.uoeh-u.ac.jp
RI Koya, Yudai/ABA-3809-2022
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NR 23
TC 14
Z9 15
U1 0
U2 2
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
EI 1349-7235
J9 INTERNAL MED
JI Intern. Med.
PY 2021
VL 60
IS 12
BP 1847
EP 1853
DI 10.2169/internalmedicine.6535-20
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA SW4JK
UT WOS:000664481700007
PM 33456046
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Toma, L
Zgura, A
Isac, T
Simu, R
Mercan-Stanciu, A
Dodot, M
Iliescu, EL
AF Toma, L.
Zgura, A.
Isac, T.
Simu, R.
Mercan-Stanciu, A.
Dodot, M.
Iliescu, E. L.
TI COVID-19 AND THE THYROID FUNCTION IN PATIENTS WITH HCV- ASSOCIATED
HEPATOCELLULAR CARCINOMA
SO ACTA ENDOCRINOLOGICA-BUCHAREST
LA English
DT Article
DE COVID-19; hepatitis C chronic infection; hepatocellular carcinoma;
autoimmune thyroiditis; hypothyroidism; hyperthyroidism
ID ION CHANNELS; HEPATITIS; HYPOTHYROIDISM; PROGRESSION; DISORDERS
AB Context. COVID-19 is more than a respiratory infection, with deep implications regarding multiple systems and organs. Thyroid damage is frequent in COVID-19 and may overlap previous HCV or HCC associated diseases.
Objective. The objective of this study is to determine the effects of COVID-19 in patients with HCV associated HCC and thyroid comorbidities. Design. We performed a retrospective study of the thyroid function tests and autoantibodies in patients with HCV-associated HCC prior and during COVID-19.
Subjects and Methods. We included 52 consecutive patients with HCV-associated HCC and documented thyroid disease, diagnosed with COVID -19 between April and October 2020. Serum values of thyroidstimulating hormone, free T3, free T4, anti-thyroglobulin antibodies and anti-thyroid peroxydase antibodies were determined and compared to baseline levels.
Results. At baseline, 44 patients had positive antithyroid antibodies, 6 had hypothyroidism in substitution and 2 had hyperthyroidism under treatment. During COVID-19 we found an increase in serum values of antithyroid antibodies, and decreased levels of TSH, freeT3 and freeT4 levels. Specific therapies were discontinued in one patient with hyperthyroidism and 3 patients with hypothyroidism.
Conclusion. There is a significant impact of COVID-19 on the thyroid homeostasis; a long-term prognostic value for patients with HCC infected with COVID-19 required further extensive research.
C1 [Toma, L.; Isac, T.; Simu, R.; Mercan-Stanciu, A.; Dodot, M.; Iliescu, E. L.] Fundeni Clin Inst, Dept Internal Med 2, Bucharest 022328, Romania.
[Toma, L.; Zgura, A.; Isac, T.; Mercan-Stanciu, A.; Dodot, M.; Iliescu, E. L.] Carol Davila Univ Med & Pharm, Bucharest, Romania.
C3 Institutul Clinic Fundeni; Carol Davila University of Medicine &
Pharmacy
RP Mercan-Stanciu, A (corresponding author), Fundeni Clin Inst, Dept Internal Med 2, Bucharest 022328, Romania.
EM adriana.mercan@yahoo.ro
RI ILIESCU, Laura/S-2853-2018
OI ILIESCU, Laura/0000-0002-8800-4940
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WHO, PROJ MORT CAUS DEATH
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NR 34
TC 1
Z9 1
U1 0
U2 1
PU EDITURA ACAD ROMANE
PI BUCURESTI
PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
SN 1841-0987
EI 1843-066X
J9 ACTA ENDOCRINOL-BUCH
JI Acta Endocrinol.
PD JUL-SEP
PY 2022
VL 18
IS 3
BP 392
EP 396
DI 10.4183/aeb.2022.392
PG 5
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 8I8WF
UT WOS:000922008200020
PM 36699175
OA Green Published
DA 2025-01-07
ER
PT J
AU Seo, S
Toutounjian, R
Conrad, A
Blatt, L
Tong, MJ
AF Seo, Suk
Toutounjian, Raphael
Conrad, Andrew
Blatt, Larry
Tong, Myron J.
TI Favorable outcomes of autoimmune hepatitis in a community clinic setting
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE autoantibodies; autoimmune hepatitis; hepatocellular carcinoma;
immunosuppression; predictors; prognosis; treatment
ID CHRONIC ACTIVE HEPATITIS; SOLUBLE LIVER ANTIGEN; CORTICOSTEROID-THERAPY;
SUSTAINED REMISSION; JAPANESE PATIENTS; TYPE-1; PROGNOSIS;
AUTOANTIBODIES; DISEASE; SUSCEPTIBILITY
AB Background and Aim: Autoimmune hepatitis (AIH) is an idiopathic disease with diverse clinical manifestations. The aims of the present study were: (i) to describe the clinical characteristics of AIH patients in a community clinic setting; and (ii) to determine factors which were associated with poor clinical outcomes.
Methods: A retrospective review was performed on 72 AIH patients who: (i) had pretreatment sera: (ii) were treatment-naive at presentation; and (iii) had a minimum of 24 months of follow up.
Results: On initial presentation, 22 (30%) had an acute onset of symptoms simulating acute viral hepatitis, 34 (47%) had chronic symptoms of greater than 6 months duration, and the remaining 16 (22%) were asymptomatic. Twenty-six (36%) had coexisting autoimmune diseases. Anti-nuclear antibody (ANA) was positive in 73% of the patients, and antismooth muscle antibody was positive in 15% of ANA-negative patients. Those few patients who tested positive for soluble liver antigen, anti-liver-kidney, microsomal antibody type-1, and anti-mitochondrial antibody were all also ANA positive. The median (range) duration of follow up was 98 (24-331) months. After immunosuppressive therapy, 26 of 72 (36%) remained in remission without further treatment. However, 46 (64%) required maintenance immunosuppression. Three patients who presented under the age of 20 years progressed to liver failure while on therapy and died while waiting for liver transplantation. Two other patients developed hepatocellular carcinoma (HCC) while on therapy and died.
Conclusions: A majority of AIH patients have an excellent prognosis. However, presentation at a younger age is a predictor of poor disease outcome and, although uncommon, HCC may develop during the late stages of cirrhosis.
C1 [Seo, Suk; Tong, Myron J.] Univ Calif Los Angeles, David Geffen Sch Med, Pfleger Liver Inst, Los Angeles, CA 90095 USA.
[Toutounjian, Raphael; Tong, Myron J.] Huntington Med Res Inst, Ctr Liver, Pasadena, CA USA.
[Conrad, Andrew] Natl Inst Genet, Culver City, CA USA.
[Blatt, Larry] Intermune Inc, Brisbane, CA USA.
C3 University of California System; University of California Los Angeles;
University of California Los Angeles Medical Center; David Geffen School
of Medicine at UCLA; Huntington Medical Research Institutes; InterMune,
Inc.
RP Seo, S (corresponding author), Univ Calif Los Angeles, David Geffen Sch Med, Pfleger Liver Inst, 200 Med Plaza,Suite 214,Box 957302, Los Angeles, CA 90095 USA.
EM sseo@mednet.ucla.edu
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NR 28
TC 37
Z9 39
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD SEP
PY 2008
VL 23
IS 9
BP 1410
EP 1414
DI 10.1111/j.1440-1746.2008.05365.x
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 339RV
UT WOS:000258595900019
PM 18373564
DA 2025-01-07
ER
PT J
AU Doulberis, M
Papaefthymiou, A
Polyzos, SA
Vardaka, E
Tzitiridou-Chatzopoulou, M
Chatzopoulos, D
Koffas, A
Papadopoulos, V
Kyrailidi, F
Kountouras, J
AF Doulberis, M.
Papaefthymiou, A.
Polyzos, S. A.
Vardaka, E.
Tzitiridou-Chatzopoulou, M.
Chatzopoulos, D.
Koffas, A.
Papadopoulos, V.
Kyrailidi, F.
Kountouras, J.
TI Local and systemic autoimmune manifestations linked to hepatitis A
infection
SO ACTA GASTRO-ENTEROLOGICA BELGICA
LA English
DT Review
DE Hepatitis A; immune response; autoimmune hepatitis; autoimmune diseases
ID GUILLAIN-BARRE-SYNDROME; RED-CELL APLASIA; T-CELLS; ANTIPHOSPHOLIPID
ANTIBODIES; HEPATOCELLULAR-CARCINOMA; VIRAL-HEPATITIS; VIRUS;
EXPRESSION; PATIENT; CANCER
AB Hepatitis A virus (HAV) represents a global burdening infectious agent causing in the majority of cases a self-limiting acute icteric syndrome, the outcome is related to the hepatic substrate and the potential pre-existing damage, whereas a plethora of extra-hepatic manifestations has also been reported. Despite the absence of post-HAV chronicity it has been associated with an additional burden on existing chronic liver diseases. Moreover, the induced immune response and the antigenic molecular mimicry are considered as triggering factors of autoimmunity with regional and distal impact. Diseases such as autoimmune hepatitis, Guillain-Barre syndrome, rheumatoid arthritis, Still's syndrome, Henoch-Schonlein purpura, autoimmune hemolytic anemia, antiphospholipid syndrome, systematic lupus erythematosus or cryoglobulinemic vasculitis have been described in patients with HAV infection. Although the exact mechanisms remain unclear, this review aims to accumulate and clarify the pathways related to this linkage.
C1 [Doulberis, M.] Kantonsspital Aarau, Med Univ Dept, Dept Gastroenterol & Hepatol, Aarau, Switzerland.
[Doulberis, M.] Univ Zurich, Dept Gastroenterol & Hepatol, Zurich, Switzerland.
[Doulberis, M.; Vardaka, E.; Tzitiridou-Chatzopoulou, M.; Chatzopoulos, D.; Kyrailidi, F.; Kountouras, J.] Aristotle Univ Thessaloniki, Ippokrat Hosp, Dept Internal Med, Med Clin 2, Thessaloniki, Greece.
[Papaefthymiou, A.] Univ Coll London Hosp UCLH, Pancreaticobiliary Med Unit, London, England.
[Papaefthymiou, A.; Polyzos, S. A.] Aristotle Univ Thessaloniki, Lab Pharmacol 1, Thessaloniki, Greece.
[Vardaka, E.] Int Hellen Univ, Sch Hlth Sci, Dept Nutr Sci & Dietet, Thessaloniki, Macedonia, Greece.
[Tzitiridou-Chatzopoulou, M.] Univ Western Macedonia, Dept Midwifery, Macedonia, Greece.
[Koffas, A.] QMUL, Barts Liver Ctr, Ctr Immunobiol, Barts & London Sch Med & Dent,Blizzard Inst, London, England.
[Papadopoulos, V.] Univ Hosp Larissa, Dept Gastroenterol, Larisa, Greece.
[Kountouras, J.] Aristotle Univ Thessaloniki, Med, 8 Fanariou St, Thessaloniki 55133, Macedonia, Greece.
[Kountouras, J.] Aristotle Univ Thessaloniki, 8 Fanariou St, Thessaloniki 55133, Macedonia, Greece.
C3 Kantonsspital Aarau AG (KSA); University of Zurich; Aristotle University
of Thessaloniki; University College London Hospitals NHS Foundation
Trust; Aristotle University of Thessaloniki; International Hellenic
University; University of Western Macedonia; University of London; Queen
Mary University London; General University Hospital of Larissa;
Aristotle University of Thessaloniki; Aristotle University of
Thessaloniki
RP Kountouras, J (corresponding author), Aristotle Univ Thessaloniki, Med, 8 Fanariou St, Thessaloniki 55133, Macedonia, Greece.; Kountouras, J (corresponding author), Aristotle Univ Thessaloniki, 8 Fanariou St, Thessaloniki 55133, Macedonia, Greece.
EM jannis@auth.gr
RI VARDAKA, Elisabeth/ABD-1341-2020; koffas, Apostolos/AAU-6858-2020;
Polyzos, Stergios/H-2844-2019; Doulberis, Michael/Y-5118-2018;
Tzitiridou, Dr. Maria/KHW-8314-2024
OI Doulberis, Michael/0000-0002-0396-5081; Tzitiridou, Dr.
Maria/0000-0001-6051-0860
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NR 66
TC 1
Z9 1
U1 1
U2 3
PU UNIV CATHOLIQUE LOUVAIN-UCL
PI BRUSSELS
PA CLIN UNIV SAINT LUC, AVE HIPPOCRATE 10, BRUSSELS, B-1200, BELGIUM
SN 1784-3227
J9 ACTA GASTRO-ENT BELG
JI Acta Gastro-Enterol. Belg.
PD JUL-SEP
PY 2023
VL 86
IS 3
BP 429
EP 436
DI 10.51821/86.3.11299
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA T1RY5
UT WOS:001075838700001
PM 37814559
OA Bronze
DA 2025-01-07
ER
PT J
AU Adler, M
Tang, I
Gach, MW
MacFaul, G
AF Adler, Maciej
Tang, Ivan
Gach, Michael William
MacFaul, George
TI Recurrent metastatic breast cancer presenting with portal hypertension
and pseudocirrhosis
SO BMJ CASE REPORTS
LA English
DT Article
DE Cirrhosis; Breast cancer
AB We present a case of a 63-year-old woman with an acute history of abdominal distension and shortness of breath. She had no risk factors for liver disease though her prior medical history was positive for breast carcinoma, in remission for 14 years. Examination and investigations were initially consistent with decompensated cirrhosis, thought to be due to subclinical autoimmune hepatitis. Imaging revealed hepatic contour irregularity, atrophy of the liver parenchyma and numerous lesions highly suggestive for multifocal hepatocellular carcinoma. Surprisingly, tissue histology revealed no evidence of cirrhosis, but recurrence of breast cancer which had mimicked cirrhosis. Pseudocirrhosis may be indistinguishable from true cirrhosis without histopathology. It has previously been linked to chemotherapy-induced hepatic injury and nodular regenerative hyperplasia, although our case illustrates an uncommon pathophysiology. Pseudocirrhosis often represents a poor prognosis even with a good baseline performance status, and early involvement of palliative care specialists may be advisable.
C1 [Adler, Maciej; Tang, Ivan; Gach, Michael William] Milton Keynes Univ Hosp NHS Fdn Trust, Dept Med, Milton Keynes, Bucks, England.
[MacFaul, George] Milton Keynes Univ Hosp NHS Fdn Trust, Dept Gastroenterol, Milton Keynes, Bucks, England.
RP Adler, M (corresponding author), Milton Keynes Univ Hosp NHS Fdn Trust, Dept Med, Milton Keynes, Bucks, England.
EM maciej.adler@nhs.net
OI Adler, Maciej/0000-0002-0656-9180
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NR 13
TC 8
Z9 8
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 1757-790X
J9 BMJ CASE REP
JI BMJ Case Rep.
PD NOV
PY 2019
VL 12
IS 11
AR e231044
DI 10.1136/bcr-2019-231044
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA VK1MA
UT WOS:000661454700065
PM 31767605
OA Green Published
DA 2025-01-07
ER
PT J
AU Catamo, E
Zupin, L
Crovella, S
Celsi, F
Segat, L
AF Catamo, Eulalia
Zupin, Luisa
Crovella, Sergio
Celsi, Fulvio
Segat, Ludovica
TI Non-classical MHC-I human leukocyte antigen (HLA-G) in hepatotropic
viral infections and in hepatocellular carcinoma
SO HUMAN IMMUNOLOGY
LA English
DT Review
DE Hepatocellular carcinoma; HLA-G; HCV; HBV
ID HEPATITIS-C VIRUS; G MESSENGER-RNA; 14-BP INSERTION/DELETION
POLYMORPHISM; HUMAN CYTOMEGALOVIRUS-INFECTION; BREAST-CANCER PATIENTS;
CD4(+) T-CELLS; G EXPRESSION; B-VIRUS; NATURAL-HISTORY; G MOLECULES
AB The human leukocyte antigen (HLA)-G is a "nonclassical" major histocompatibility complex (MHC) class lb gene, located at chromosome 6, in the 6p21.3 region.
The HLA-G presents immunomodulatory functions essential in pregnancy for the tolerance of the semi-allogenic fetus, but an abnormal expression of HLA-G has been observed in numerous pathological conditions, such as tumors, autoimmune diseases and viral infections. In recent years, numerous studies have assessed the clinical relevance of HLA-G expression in different types of cancer: in general, a higher HLA-G expression correlates with a lower survival rate or a shorter disease-free survival.
Altered expression of HLA-G has been found in both HCV and HBV infection, and some genetic polymorphisms have been associated with altered susceptibility/disease development for these infections, however, whether the biologic role of HLA-G in HCV and HBV infection is beneficial or hazardous, it is not completely clear. In the context of hepatocellular carcinoma, HLA-G has shown a potential diagnostic role, moreover a prognostic value in HCC patients has been also attributed to HLA-G molecules.
We revise here the role of HLA-G in hepatotropic HBV/HCV infections and in hepatocellular carcinoma (HCC). (C) 2014 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
C1 [Catamo, Eulalia; Crovella, Sergio] Univ Trieste, Dept Med Sci, I-34127 Trieste, Italy.
[Zupin, Luisa; Crovella, Sergio; Celsi, Fulvio; Segat, Ludovica] IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, I-34137 Trieste, Italy.
C3 University of Trieste; IRCCS Burlo Garofolo
RP Segat, L (corresponding author), IRCCS Burlo Garofolo, Via Istria 65-1, I-34137 Trieste, Italy.
EM ludovica.segat@burlo.trieste.it
RI Crovella, Sergio/K-5050-2016; Celsi, Fulvio/H-5134-2013; Zupin,
Luisa/I-5228-2018; Catamo, Eulalia/HKN-7087-2023
OI Zupin, Luisa/0000-0001-5886-9129; Crovella, Sergio/0000-0001-8493-1168;
Segat, Ludovica/0000-0002-6024-1485; Catamo, Eulalia/0000-0002-4701-9134
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NR 93
TC 25
Z9 27
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0198-8859
EI 1879-1166
J9 HUM IMMUNOL
JI Hum. Immunol.
PD DEC
PY 2014
VL 75
IS 12
BP 1225
EP 1231
DI 10.1016/j.humimm.2014.09.019
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AW1HP
UT WOS:000346041100014
PM 25318079
DA 2025-01-07
ER
PT J
AU Yang, HQ
Luo, Y
Lai, XF
AF Yang, Huiqing
Luo, Yan
Lai, Xiaofei
TI The comprehensive role of apoptosis inhibitor of macrophage (AIM) in
pathological conditions
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Review
DE AIM; immunoregulation; inflammation; disease
ID ANTIGEN-LIKE PROTEIN; HEPATOCELLULAR-CARCINOMA; TISSUE MACROPHAGES;
DISEASE-ACTIVITY; OBESITY; CD5L; ACTIVATION; EXPRESSION; SCLEROSIS;
REQUIRES
AB CD5L/AIM (apoptosis inhibitor of macrophage), as an important component in maintaining tissue homeostasis and inflammation, is mainly produced and secreted by macrophages but partially dissociated and released from blood AIM-IgM. AIM plays a regulatory role in intracellular physiological mechanisms, including lipid metabolism and apoptosis. AIM not only increases in autoimmune diseases, directly targets liver cells in liver cancer and promotes cell clearance in acute kidney injury, but also causes arteriosclerosis and cardiovascular events, and aggravates inflammatory reactions in lung diseases and sepsis. Obviously, AIM plays a pleiotropic role in the body. However, to date, studies have failed to decipher the mechanisms behind its different roles (beneficial or harmful) in inflammatory regulation. The inflammatory response is a "double-edged sword," and maintaining balance is critical for effective host defense while minimizing the adverse side effects of acute inflammation. Enhancing the understanding of AIM function could provide the theoretical basis for new therapies in these pathological settings. In this review, we discuss recent studies on the roles of AIM in lipid metabolism, autoimmune diseases and organic tissues, such as liver cancer, myocardial infarction, and kidney disease.
AIM plays a regulatory role in intracellular physiological mechanisms, including lipid metabolism and apoptosis. AIM not only increases its expression in autoimmune diseases, directly targets liver cells in liver cancer and promotes cell clearance in acute kidney injury, but also causes arteriosclerosis and cardiovascular events, and aggravates inflammatory reactions in lung diseases and sepsis. Obviously, AIM plays a pleiotropic role in the body.
C1 [Yang, Huiqing; Luo, Yan; Lai, Xiaofei] Chongqing Med Univ, Affiliated Hosp 1, Dept Lab Med, Chongqing 400016, Peoples R China.
[Luo, Yan; Lai, Xiaofei] Chongqing Med Univ, Affiliated Hosp 1, Dept Lab Med, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China.
C3 Chongqing Medical University; Chongqing Medical University
RP Luo, Y; Lai, XF (corresponding author), Chongqing Med Univ, Affiliated Hosp 1, Dept Lab Med, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China.
EM 87936966@qq.com; luoyan476534@126.com
OI Yang, Huiqing/0000-0003-4388-7468
FU National Natural Science Foundation of China [81901582]; Natural Science
Foundation of Chongqing [cstc2021jcyj-msxmX0123]
FX This review is supported by National Natural Science Foundation of China
(No. 81901582) and Natural Science Foundation of Chongqing (No.
cstc2021jcyj-msxmX0123).
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NR 97
TC 6
Z9 6
U1 3
U2 15
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0009-9104
EI 1365-2249
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD JUN 5
PY 2023
VL 212
IS 3
BP 184
EP 198
DI 10.1093/cei/uxac095
EA MAR 2023
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA I4UT9
UT WOS:000958941300001
PM 36427004
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Tutusaus, A
Morales, A
de Frutos, PG
Marí, M
AF Tutusaus, Anna
Morales, Albert
de Frutos, Pablo Garcia
Mari, Montserrat
TI GAS6/TAM Axis as Therapeutic Target in Liver Diseases
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE phagocytosis; fibrosis; inflammation; cytokine regulation; biomarkers
ID RECEPTOR TYROSINE KINASE; ALPHA-CONVERTING-ENZYME; TYRO-3 FAMILY
RECEPTORS; TAM RECEPTORS; APOPTOTIC CELLS; PROTEIN-S;
HEPATOCELLULAR-CARCINOMA; PROMOTES INFLAMMATION; GAS6/AXL PATHWAY;
IMMUNE CELLS
AB TAM (TYRO3, AXL, and MERTK) protein tyrosine kinase membrane receptors and their vitamin K -dependent ligands GAS6 and protein S (PROS) are well-known players in tumor biology and autoimmune diseases. In contrast, TAM regulation of fibrogenesis and the inflammation mechanisms underlying metabolic dysfunction-associated steatohepatitis (MASH), cirrhosis, and, ultimately, liver cancer has recently been revealed. GAS6 and PROS binding to phosphatidylserine exposed in outer membranes of apoptotic cells links TAMs, particularly MERTK, with hepatocellular damage. In addition, AXL and MERTK regulate the development of liver fibrosis and inflammation in chronic liver diseases. Acute hepatic injury is also mediated by the TAM system, as recent data regarding acetaminophen toxicity and acute-on-chronic liver failure have uncovered. Soluble TAM-related proteins, mainly released from activated macrophages and hepatic stellate cells after hepatic deterioration, are proposed as early serum markers for disease progression. In conclusion, the TAM system is becoming an interesting pharmacological target in liver pathology and a focus of future biomedical research in this field.
C1 [Tutusaus, Anna; Morales, Albert; de Frutos, Pablo Garcia; Mari, Montserrat] IIBB CSIC, IDIBAPS, Dept Cell Death & Proliferat, Barcelona, Catalunya, Spain.
[de Frutos, Pablo Garcia] Ctr Invest Biomed Red Enfermedades Cardiovasc CIBE, Barcelona, Comunidad De Ma, Spain.
[Tutusaus, Anna; Morales, Albert; Mari, Montserrat] Barcelona Clin Liver Canc BCLC Grp, Barcelona, Spain.
[Tutusaus, Anna] Inst Invest Biomed Barcelona IIBB CSIC, C Rossello 161,6th Floor, Barcelona 08036, Catalunya, Spain.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; Consejo
Superior de Investigaciones Cientificas (CSIC); CSIC - Instituto de
Investigaciones Biomedicas de Barcelona (IIBB); CIBER - Centro de
Investigacion Biomedica en Red; CIBERCV; University of Barcelona;
Hospital Clinic de Barcelona; IDIBAPS; Consejo Superior de
Investigaciones Cientificas (CSIC); CSIC - Instituto de Investigaciones
Biomedicas de Barcelona (IIBB)
RP Tutusaus, A (corresponding author), Inst Invest Biomed Barcelona IIBB CSIC, C Rossello 161,6th Floor, Barcelona 08036, Catalunya, Spain.
EM anna.tutusaus@iibb.csic.es
RI MARI, MONTSERRAT/M-2871-2019; Morales, Albert/E-2988-2013; Tutusaus,
Anna/AAA-2353-2020; MARI, MONTSERRAT/A-7376-2013; Garcia de Frutos,
Pablo/B-8594-2011
OI Tutusaus, Anna/0000-0002-1133-321X; MARI,
MONTSERRAT/0000-0002-6116-3247; Garcia de Frutos,
Pablo/0000-0003-1547-1190
FU Instituto de Salud Carlos III [PI22/00475]; Ministerio de Ciencia e
Innovacion (MCIN/AEI) [PID2021-123564OB-I00]; European Union "ERDF A Way
of Making Europe" (Next Generation EU/PRTR); CIBERCV; AGAUR
[2021_SGR_490]; CERCA Programme/Generalitat de Catalunya; Fundacio la
Marato de TV3 [202133-32]; BerGenBio ASA
FX This research was funded by Instituto de Salud Carlos III (Project#
PI22/00475 to M.M.) and by Ministerio de Ciencia e Innovacion
(PID2021-123564OB-I00, MCIN/AEI/10.13039/501100011033 to A.M. and
P.G.F.), and co-funded by the European Union "ERDF A Way of Making
Europe" (Next Generation EU/PRTR); CIBERCV; AGAUR (2021_SGR_490) and
CERCA Programme/Generalitat de Catalunya; and Fundacio la Marato de TV3
(202133-32) to A.M. and P.G.F. This research also received research
funding and Sponsored Research Agreement, from BerGenBio ASA.
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NR 163
TC 2
Z9 2
U1 1
U2 4
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD FEB
PY 2024
VL 44
IS 01
BP 99
EP 114
DI 10.1055/a-2275-0408
EA MAR 2024
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA NT8T7
UT WOS:001188723400001
PM 38395061
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Evans, S
Hofmann, A
AF Evans, Suzanne
Hofmann, Alana
TI Autoimmune Biliary Diseases A Review of Primary Biliary Cholangitis,
Primary Sclerosing Cholangitis, Immunoglobulin G4-Related Sclerosing
Cholangitis, and Autoimmune Hepatitis
SO SURGICAL CLINICS OF NORTH AMERICA
LA English
DT Article
DE Primary biliary cholangitis; Primary sclerosing cholangitis; Autoimmune
hepatitis; IgG4-related sclerosing cholangitis; Autoimmune
cholangiopathy; Cholestasis; Biliary disease
ID HEPATOCELLULAR-CARCINOMA; RISK-FACTORS; PANCREATITIS; DIAGNOSIS;
CIRRHOSIS; EPIDEMIOLOGY; MALIGNANCIES; PATHOLOGY; G4
C1 [Evans, Suzanne] Cincinnati Childrens Hosp, Med Ctr, Dept Pediat & Thorac Surg, 3333 Burnet Ave,C3 163, Cincinnati, OH 45229 USA.
[Hofmann, Alana] Univ Cincinnati, Coll Med, Dept Surg, 231 Albert Sabin Way,MSB 1464, Cincinnati, OH 45267 USA.
C3 Cincinnati Children's Hospital Medical Center; University System of
Ohio; University of Cincinnati
RP Evans, S (corresponding author), Cincinnati Childrens Hosp, Med Ctr, Dept Pediat & Thorac Surg, 3333 Burnet Ave,C3 163, Cincinnati, OH 45229 USA.
EM suzanne.evans@cchmc.org
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NR 60
TC 0
Z9 0
U1 5
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0039-6109
EI 1558-3171
J9 SURG CLIN N AM
JI Surg. Clin.-North Am.
PD DEC
PY 2024
VL 104
IS 6
BP 1249
EP 1261
DI 10.1016/j.suc.2024.04.010
EA OCT 2024
PG 13
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA K9T1N
UT WOS:001347242100001
PM 39448126
DA 2025-01-07
ER
PT J
AU Giannitrapani, L
Soresi, M
Balasus, D
Licata, A
Montalto, G
AF Giannitrapani, Lydia
Soresi, Maurizio
Balasus, Daniele
Licata, Anna
Montalto, Giuseppe
TI Genetic association of interleukin-6 polymorphism (-174 G/C) with
chronic liver diseases and hepatocellular carcinoma
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Single nucleotide polymorphisms; Interleukin-6; Chronic hepatitis; Liver
cirrhosis; Hepatocellular carcinoma
ID CHRONIC HEPATITIS-C; PRIMARY BILIARY-CIRRHOSIS; TYPE-2
DIABETES-MELLITUS; B-VIRUS INFECTION; FACTOR-KAPPA-B; AUTOIMMUNE
HEPATITIS; GLOBAL EPIDEMIOLOGY; PROMOTER POLYMORPHISM; CYTOKINE
SECRETION; IL-6 GENE
AB Interleukin-6 (IL-6) is a pleiotropic cytokine which is expressed in many inflammatory cells in response to different types of stimuli, regulating a number of biological processes. The IL-6 gene is polymorphic in both the 5' and 3' flanking regions and more than 150 single nucleotide polymorphisms have been identified so far. Genetic polymorphisms of IL-6 may affect the outcomes of several diseases, where the presence of high levels of circulating IL-6 have been correlated to the stage and/or the progression of the disease itself. The -174 G/C polymorphism is a frequent polymorphism, that is located in the upstream regulatory region of the IL-6 gene and affects IL-6 production. However, the data in the literature on the genetic association between the -174 G/C polymorphism and some specific liver diseases characterized by different etiologies are still controversial. In particular, most of the studies are quite unanimous in describing a correlation between the presence of the high-producer genotype and a worse evolution of the chronic liver disease. This is valid for patients with hepatitis C virus (HCV)-related chronic hepatitis and liver cirrhosis and hepatocellular carcinoma (HCC) whatever the etiology. Studies in hepatitis B virus-related chronic liver diseases are not conclusive, while specific populations like non alcoholic fatty liver disease/non-alcoholic steatohepatitis, autoimmune and human immunodeficiency virus/HCV co-infected patients show a higher prevalence of the low-producer genotype, probably due to the complexity of these clinical pictures. In this direction, a systematic revision of these data should shed more light on the role of this polymorphism in chronic liver diseases and HCC. (C) 2013 Baishideng. All rights reserved.
C1 [Giannitrapani, Lydia; Soresi, Maurizio; Balasus, Daniele; Licata, Anna; Montalto, Giuseppe] Univ Palermo, Biomed Dept Internal Med & Specialties DiBi MIS, Unit Internal Med, I-90127 Palermo, Italy.
C3 University of Palermo
RP Giannitrapani, L (corresponding author), Univ Palermo, Biomed Dept Internal Med & Specialties, Unit Internal Med, Via Vespro 141, I-90127 Palermo, Italy.
EM lydia.giannitrapani@unipa.it
RI Licata, Anna/ADF-0000-2022; Giannitrapani, Lydia/I-3706-2019; Soresi,
Maurizio/AAY-2045-2020
OI MONTALTO, Giuseppe/0000-0002-8731-8577; Licata,
Anna/0000-0003-0383-6121; Soresi, Maurizio/0000-0001-7850-555X;
Giannitrapani, Lydia/0000-0003-2845-5296
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NR 67
TC 47
Z9 56
U1 0
U2 12
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD APR 28
PY 2013
VL 19
IS 16
BP 2449
EP 2455
DI 10.3748/wjg.v19.i16.2449
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 139ON
UT WOS:000318592400002
PM 23674845
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Li, Y
Zhang, J
Chen, SR
Ke, YN
Li, YM
Chen, Y
AF Li, Yu
Zhang, Jie
Chen, Shurong
Ke, Yini
Li, Youming
Chen, Yi
TI Growth differentiation factor 15: Emerging role in liver diseases
SO CYTOKINE
LA English
DT Article
DE GDF15; MASLD; MASH; Liver fibrosis; HCC
ID HEPATIC STELLATE CELLS; MACROPHAGE-INHIBITORY CYTOKINE; BETA SUPERFAMILY
MEMBER; PROMOTES WEIGHT-LOSS; HEPATOCELLULAR-CARCINOMA; NAG-1/GDF15
EXPRESSION; ENERGY-EXPENDITURE; INSULIN-RESISTANCE; GAMMA LIGAND; GDF15
AB Growth differentiation factor 15 (GDF15) is a cell stress-response cytokine within the transforming growth factor-beta (TGF beta) superfamily. It is known to exert diverse effects on many metabolic pathways through its receptor GFRAL, which is expressed in the hindbrain, and transduces signals through the downstream receptor tyrosine kinase Ret. Since the liver is the core organ of metabolism, summarizing the functions of GDF15 is highly important. In this review, we assessed the relevant literature regarding the main metabolic, inflammatory, fibrogenic, tumorigenic and other effects of GDF15 on different liver diseases, including Metabolic dysfunctionassociated steatotic liver disease(MASLD), alcohol and drug-induced liver injury, as well as autoimmune and viral hepatitis, with a particular focus on the pathogenesis of MASLD progression from hepatic steatosis to MASH, liver fibrosis and even hepatocellular carcinoma (HCC). Finally, we discuss the prospects of the clinical application potential of GDF15 along with its research and development progress. With better knowledge of GDF15, increasing in-depth research will lead to a new era in the field of liver diseases.
C1 [Li, Yu; Zhang, Jie; Chen, Shurong; Li, Youming; Chen, Yi] Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Gastroenterol, Hangzhou 310003, Peoples R China.
[Ke, Yini] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Dept Rheumatol, Hangzhou 310003, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Chen, Y (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Gastroenterol, Hangzhou 310003, Peoples R China.
EM zyyyychen@zju.edu.cn
RI li, youming/GYJ-2598-2022
FU National Natural Science Foundation of China [82170582, 82204229,
82,270,597, U20A20347]; Key R&D & D Program of Zhejiang [2024C03202]
FX This study is supported by National Natural Science Foundation of China
(No.82170582 to Yi Chen, No.82204229 to Yini Ke, No. 82,270,597 and
U20A20347 to Youming Li) and Key R&D & D Program of Zhejiang (No.
2024C03202 to Yi Chen) .
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NR 141
TC 2
Z9 2
U1 3
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2024
VL 182
AR 156727
DI 10.1016/j.cyto.2024.156727
EA AUG 2024
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA C6I5Z
UT WOS:001290389800001
PM 39111112
DA 2025-01-07
ER
PT J
AU Nagao, Y
Sata, M
AF Nagao, Y
Sata, M
TI Hepatitis C virus and lichen planus
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE extrahepatic manifestation; hepatitis C virus; hepatitis C virus RNA;
interferon; lichen planus; oral cancer; oral lichen planus; ribavirin
ID CHRONIC ACTIVE HEPATITIS; PORPHYRIA-CUTANEA-TARDA; SQUAMOUS-CELL
CARCINOMA; INTERFERON ALPHA-2A THERAPY; VAGINAL-GINGIVAL-SYNDROME;
EXTRAHEPATIC MANIFESTATIONS; HEPATOCELLULAR-CARCINOMA; ITALIAN PATIENTS;
HIGH PREVALENCE; HCV INFECTION
AB Hepatitis C virus (HCV) is an important factor in the development of chronic liver disease and hepatocellular carcinoma. In recent years it has become known that HCV induces various extrahepatic manifestations including mixed cryoglobulinemia, membranoproliferative glomerulonephritis, Sjogren's syndrome, autoimmune thyroiditis, malignant lymphoma, porphyria cutanea tarda and lichen planus. Although the mechanisms of extrahepatic manifestations remain unclear, it is known that interferon (IFN) therapy and coadministration of IFN with ribavirin are effective in promoting the disappearance or alleviation of such extrahepatic lesions, which have tended to be overlooked. The present review focuses on lichen planus, one of the major extrahepatic manifestations. (C) 2004 Blackwell Publishing Asia Pty Ltd.
C1 Kurume Univ, Sch Med, Res Ctr Innovat Canc Therapy, Kurume, Fukuoka 8300011, Japan.
Kurume Univ, Sch Med, Dept Med 2, Kurume, Fukuoka 8300011, Japan.
C3 Kurume University; Kurume University
RP Kurume Univ, Sch Med, Res Ctr Innovat Canc Therapy, 67 Asahimachi, Kurume, Fukuoka 8300011, Japan.
EM nagao@med.kurume-u.ac.jp
RI Sata, Masataka/IST-9041-2023
OI Nagao, Yumiko/0000-0002-3971-660X
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NR 152
TC 32
Z9 39
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD OCT
PY 2004
VL 19
IS 10
BP 1101
EP 1113
DI 10.1046/j.1440-1746.2003.03324.x
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 854BL
UT WOS:000223875000002
PM 15377286
DA 2025-01-07
ER
PT J
AU Sayaf, K
Gabbia, D
Russo, FP
De Martin, S
AF Sayaf, Katia
Gabbia, Daniela
Russo, Francesco Paolo
De Martin, Sara
TI The Role of Sex in Acute and Chronic Liver Damage
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE sex; chronic liver disease; acute liver failure; liver regeneration
ID HEPATITIS-B-VIRUS; PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY
CHOLANGITIS; NON-GENOMIC REGULATION; GENDER-DIFFERENCES;
HEPATOCELLULAR-CARCINOMA; RISK-FACTORS; INFLAMMATORY RESPONSES;
GLUCOSE-HOMEOSTASIS; ALCOHOLIC CIRRHOSIS
AB Acute and chronic hepatic damages are caused by xenobiotics or different diseases affecting the liver, characterized by different etiologies and pathological features. It has been demonstrated extensively that liver damage progresses differently in men and women, and some chronic liver diseases show a more favorable prognosis in women than in men. This review aims to update the most recent advances in the comprehension of the molecular basis of the sex difference observed in both acute and chronic liver damage. With this purpose, we report experimental studies on animal models and clinical observations investigating both acute liver failure, e.g., drug-induced liver injury (DILI), and chronic liver diseases, e.g., viral hepatitis, alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), autoimmune liver diseases, and hepatocellular carcinoma (HCC).
C1 [Sayaf, Katia; Russo, Francesco Paolo] Univ Padua, Dept Surg Oncol & Gastroenterol, I-35131 Padua, Italy.
[Gabbia, Daniela; De Martin, Sara] Univ Padua, Dept Pharmaceut & Pharmacol Sci, I-35131 Padua, Italy.
[Russo, Francesco Paolo] Azienda Osped Univ Padova, Gastroenterol & Multivisceral Transplant Units, I-35131 Padua, Italy.
C3 University of Padua; University of Padua; University of Padua; Azienda
Ospedaliera - Universita di Padova
RP Russo, FP (corresponding author), Univ Padua, Dept Surg Oncol & Gastroenterol, I-35131 Padua, Italy.; Russo, FP (corresponding author), Azienda Osped Univ Padova, Gastroenterol & Multivisceral Transplant Units, I-35131 Padua, Italy.
EM francescopaolo.russo@unipd.it
RI Russo, Francesco/ABN-5412-2022; Gabbia, Daniela/J-9984-2019; De Martin,
Sara/AAC-7396-2022
OI GABBIA, DANIELA/0000-0003-2247-8227; RUSSO, FRANCESCO
PAOLO/0000-0003-4127-8941; DE MARTIN, SARA/0000-0001-6398-8237
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NR 161
TC 21
Z9 22
U1 3
U2 15
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2022
VL 23
IS 18
AR 10654
DI 10.3390/ijms231810654
PG 21
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 4R0KE
UT WOS:000856460800001
PM 36142565
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Sharma, SA
Kowgier, M
Hansen, BE
Brouwer, WP
Maan, R
Wong, D
Shah, H
Khalili, K
Yim, C
Heathcote, EJ
Janssen, HLA
Sherman, M
Hirschfield, GM
Feld, JJ
AF Sharma, Suraj A.
Kowgier, Matthew
Hansen, Bettina E.
Brouwer, Willem Pieter
Maan, Raoel
Wong, David
Shah, Hemant
Khalili, Korosh
Yim, Colina
Heathcote, E. Jenny
Janssen, Harry L. A.
Sherman, Morris
Hirschfield, Gideon M.
Feld, Jordan J.
TI Toronto HCC risk index: A validated scoring system to predict 10-year
risk of HCC in patients with cirrhosis
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Cirrhosis; Hepatocellular carcinoma; HCC; Toronto hepatoma risk index
(THRI); Cumulative incidence
ID PRIMARY BILIARY-CIRRHOSIS; HEPATITIS-C VIRUS; HEPATOCELLULAR-CARCINOMA;
GROWTH-RATE; ASSOCIATION; MORTALITY; TRENDS
AB Background & Aims: Current guidelines recommend biannual surveillance for hepatocellular carcinoma (HCC) in all patients with cirrhosis, regardless of etiology. However, HCC incidence is not well established for many causes of cirrhosis. We aimed to assess the disease-specific incidence of HCC in a large cohort of patients with cirrhosis and to develop a scoring system to predict HCC risk.
Methods: A derivation cohort of patients with cirrhosis diagnosed by biopsy or non-invasive measures was identified through retrospective chart review. The disease-specific incidence of HCC was calculated according to etiology of cirrhosis. Factors associated with HCC were identified through multivariable Cox regression and used to develop a scoring system to predict HCC risk. The scoring system was evaluated in an external cohort for validation.
Results: Of 2,079 patients with cirrhosis and >= 6 months follow-up, 226 (10.8%) developed HCC. The 10-year cumulative incidence of HCC varied by etiologic category from 22% in patients with viral hepatitis, to 16% in those with steatohepatitis and 5% in those with autoimmune liver disease (p < 0.001). By multivariable Cox regression, age, sex, etiology and platelets were associated with HCC. Points were assigned in proportion to each hazard ratio to create the Toronto HCC Risk Index (THRI). The 10-year cumulative HCC incidence was 3%, 10% and 32% in the low-risk (< 120 points), medium-risk (120-240) and high-risk (> 240) groups respectively, values that remained consistent after internal validation. External validation was performed on a cohort of patients with primary biliary cirrhosis, hepatitis B viral and hepatitis C viral cirrhosis (n = 1,144), with similar predictive ability (Harrell's c statistic 0.77) in the validation and derivation cohorts.
Conclusion: HCC incidence varies markedly by etiology of cirrhosis. The THRI, using readily available clinical and laboratory parameters, has good predictive ability for HCC in patients with cirrhosis, and has been validated in an external cohort. This risk score may help to guide recommendations regarding HCC surveillance among patients with cirrhosis.
Lay summary: HCC incidence varies markedly depending on the underlying cause of cirrhosis. Herein, using readily available clinical and laboratory parameters we describe a risk score, THRI, which has a good predictive ability for HCC in patients with cirrhosis, and has been validated in an external cohort. This risk score may help to guide recommendations regarding HCC surveillance among patients with cirrhosis. (C) 2017 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Sharma, Suraj A.; Kowgier, Matthew; Wong, David; Shah, Hemant; Yim, Colina; Heathcote, E. Jenny; Janssen, Harry L. A.; Sherman, Morris; Feld, Jordan J.] Univ Toronto, Univ Hlth Network, Toronto Ctr Liver Dis, Toronto, ON, Canada.
[Hansen, Bettina E.; Brouwer, Willem Pieter; Maan, Raoel; Janssen, Harry L. A.] Erasmus MC Univ, Med Ctr, Dept Gastroenterol & Hepatol, Rotterdam, Netherlands.
[Khalili, Korosh] Univ Toronto, Dept Med Imaging, Univ Hlth Network, Toronto, ON, Canada.
[Hirschfield, Gideon M.] Univ Birmingham, Ctr Liver Res, Birmingham, W Midlands, England.
[Hirschfield, Gideon M.] Univ Birmingham, NIHR Biomed Res Unit, Birmingham, W Midlands, England.
[Kowgier, Matthew] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
C3 University of Toronto; University Health Network Toronto; Erasmus
University Rotterdam; Erasmus MC; University of Toronto; University
Health Network Toronto; University of Birmingham; University of
Birmingham; University of Toronto
RP Feld, JJ (corresponding author), Univ Toronto, Univ Hlth Network, Toronto Ctr Liver Dis, Sandra Rotman Ctr Global Hlth, 6B Fell Pavil Rm 158,399 Bathurst St, Toronto, ON M5T 2S8, Canada.
EM Jordan.feld@uhn.ca
RI Kiemeney, Lambertus/D-3357-2009; Feld, Jordan/AAH-5628-2020; Maan,
Raoel/P-5453-2014; Hirschfield, Gideon/M-2143-2015; Brouwer, Willem
Pieter/P-5444-2014
OI Janssen, Harry/0000-0003-2398-8392; Hirschfield,
Gideon/0000-0002-6736-2255; Brouwer, Willem Pieter/0000-0001-8713-1481;
Khalili, Korosh/0000-0002-3496-8744
FU Phelan Family Database, Francis Family Liver Clinic
FX Phelan Family Database, Francis Family Liver Clinic.
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NR 32
TC 138
Z9 147
U1 4
U2 31
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD JAN
PY 2018
VL 68
IS 1
BP 92
EP 99
DI 10.1016/j.jhep.2017.07.033
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FR5HZ
UT WOS:000419098800014
PM 28844936
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Montano-Loza, AJ
Carpenter, HA
Czaja, AJ
AF Montano-Loza, Aldo J.
Carpenter, Herschel A.
Czaja, Albert J.
TI Predictive factors for hepatocellular carcinoma in type 1 autoimmune
hepatitis
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article; Proceedings Paper
CT 58th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY NOV 02-06, 2007
CL Boston, MA
SP Amer Assoc Study Liver Dis
ID CHRONIC ACTIVE HEPATITIS; CORTICOSTEROID-THERAPY; LIVER-DISEASE;
ANTINUCLEAR ANTIBODIES; RISK; HEPATOCARCINOGENESIS; CIRRHOSIS;
IMMUNOFLUORESCENCE; EPIDEMIOLOGY; PREDNISONE
AB OBJECTIVE: Hepatocellular carcinoma (HCC) is an uncommon but serious occurrence in autoimmune hepatitis. Our objective was to determine predictors for this neoplasm to improve screening strategies.
METHODS: Two hundred twenty-seven patients underwent hepatic ultrasonography and serum alpha fetoprotein determinations at 6-12-month intervals.
RESULTS: Nine patients developed HCC (4%), and each had cirrhosis >= 73 months prior to the malignancy (mean, 110 +/- 7 months). By univariate Cox analysis, features at accession associated with a higher risk of HCC were: male gender (Hazard Ratio [HR] 7.0, 95% Confidence Interval [CI] 1.87-26.1, P = 0.004), history of blood transfusion (HR 5.6, 95% CI 1.51-21.1, P = 0.01), thrombocytopenia (HR 7.3, 95% CI 1.89-28.3, P = 0.004), ascites (HR 23.8, 95% CI 4.65-121.8, P = 0.0001), esophageal varices (HR 7.9, 95% CI 1.96-31.8, P = 0.004), and any sign of portal hypertension (HR 19.1, 95% CI 3.91-93.3, P = 0.0003). Features after accession associated with a higher risk of malignancy were: treatment for >= 3 yr (HR 7.6, 95% CI 1.25-18.2, P = 0.02), worsening laboratory tests during corticosteroid therapy (HR 7.6, 95% CI 1.81-32.1, P = 0.006), and cirrhosis for >= 10 yr (HR 8.4, 95% CI 1.69-41.9, P = 0.009).
CONCLUSIONS: Male gender, features of portal hypertension, history of blood transfusions, immunosuppressive treatment for >= 3 yr, treatment failure, and cirrhosis of >= 10 yr duration identify patients at risk for HCC. These risk factors should focus screening in autoimmune hepatitis.
C1 [Carpenter, Herschel A.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
[Montano-Loza, Aldo J.; Czaja, Albert J.] Mayo Clin, Div Gastroenterol, Rochester, MN 55905 USA.
C3 Mayo Clinic; Mayo Clinic
RP Czaja, AJ (corresponding author), Mayo Clin, Div Gastroenterol, 200 1st St SW, Rochester, MN 55905 USA.
RI Montano-Loza, Aldo/B-3092-2013
OI Montano-Loza, Aldo J./0000-0002-2511-7980
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NR 57
TC 72
Z9 74
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD AUG
PY 2008
VL 103
IS 8
BP 1944
EP 1951
DI 10.1111/j.1572-0241.2008.01922.x
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology
GA 335GG
UT WOS:000258278200011
PM 18564111
DA 2025-01-07
ER
PT J
AU González-Moles, MA
de Porras-Carrique, T
Ramos-García, P
AF Gonzalez-Moles, Miguel Angel
de Porras-Carrique, Teresa
Ramos-Garcia, Pablo
TI Association of oral lichen planus with hepatic disorders and
hepatocellular carcinoma: systematic review and meta-analysis
SO MEDICINA ORAL PATOLOGIA ORAL Y CIRUGIA BUCAL
LA English
DT Review
DE Oral lichen planus; hepatocellular carcinoma; hepatitis; systematic
review; meta-analysis
ID VIRUS; PREVALENCE; CANCER; RISK
AB Background: Oral lichen planus (OLP) is a prevalent autoimmune chronic inflammatory disease of unknown etiology. The importance of the association between hepatic disease and OLP lies in the fact that many of these disorders (HC, HB, cirrhosis, hepatic steatosis) behave as risk factors for hepatocellular carcinoma. Material and Methods: We searched PubMed, Embase, Web of Science, and Scopus for studies published before January 2022. We evaluated the quality of studies (Joanna Briggs Institute tool). We performed meta-analyses, investigated the heterogeneity between studies, and we also carried out subgroups, meta-regression, and small -study effects analyses. 146 studies (21,187 patients) were included in this study. Our study aims to evaluate current evidence on the prevalence and magnitude of association between hepatic diseases (especially those with risk of malignancy), hepatocellular carcinoma and OLP. Results: Our results suggest that patients with OLP present a significant tendency to the development of hepatitis B (OR=1.62, 95%CI=1.01-2.40, p=0.02), hepatitis C (OR=4.09, 95%CI=2.77-6.03, p<0.001), cirrhosis (OR=5.58, 95%CI=1.83-16.96, p=0.002), hepatic steatosis (OR=5.71, 95%CI=0.97-33.60, p=0.05) and hepatocellular carci-noma (OR=3.10,95%CI=1.14-8.43, p= 0.03). Conclusions: Patients with OLP should be investigated to rule out the presence of hepatic disease, which can lead to hepatocellular carcinoma, allowing an early diagnosis that would help to a better approach to liver disease and a notable improvement in prognosis in terms of both progression and severity.
C1 [Gonzalez-Moles, Miguel Angel; de Porras-Carrique, Teresa; Ramos-Garcia, Pablo] Univ Granada, Biohlth Res Inst Ibs Granada, Sch Dent, Granada, Spain.
[Gonzalez-Moles, Miguel Angel] Univ Granada, Sch Dent, Oral Med Dept, Paseo Cartuja S N, Granada 18071, Spain.
C3 University of Granada; University of Granada
RP González-Moles, MA (corresponding author), Univ Granada, Sch Dent, Oral Med Dept, Paseo Cartuja S N, Granada 18071, Spain.
EM magonzal@ugr.es
RI González-Moles, MA/AAB-9485-2020; Ramos-Garcia, Pablo/N-1735-2019
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NR 25
TC 9
Z9 9
U1 0
U2 4
PU MEDICINA ORAL S L
PI VALENCIA
PA CALLE DANIEL BALACIART N 4 PTA 17, VALENCIA, 46020, SPAIN
SN 1698-6946
J9 MED ORAL PATOL ORAL
JI Med. Oral Patol. Oral Cir. Bucal
PD MAY 1
PY 2023
VL 28
IS 3
BP E229
EP E237
DI 10.4317/medoral.25661
PG 9
WC Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dentistry, Oral Surgery & Medicine
GA F8NT5
UT WOS:000984867800004
PM 36806023
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhang, XY
Yang, ZY
Fu, CM
Yao, R
Li, H
Peng, F
Li, N
AF Zhang, Xinying
Yang, Ziyue
Fu, Chunmeng
Yao, Run
Li, Huan
Peng, Fang
Li, Ning
TI Emerging roles of liquid-liquid phase separation in liver innate
immunity
SO CELL COMMUNICATION AND SIGNALING
LA English
DT Review
DE Liquid-liquid phase separation; Biomolecular condensates; Liver innate
immunity; Liver disease
ID HEPATITIS-B-VIRUS; HEPATOCELLULAR-CARCINOMA; C VIRUS; AUTOPHAGY;
PROTEIN; STRESS; INFLAMMATION; CONTRIBUTES; PROMOTES; CELLS
AB Biomolecular condensates formed by liquid-liquid phase separation (LLPS) have become an extensive mechanism of macromolecular metabolism and biochemical reactions in cells. Large molecules like proteins and nucleic acids will spontaneously aggregate and assemble into droplet-like structures driven by LLPS when the physical and chemical properties of cells are altered. LLPS provides a mature molecular platform for innate immune response, which tightly regulates key signaling in liver immune response spatially and physically, including DNA and RNA sensing pathways, inflammasome activation, and autophagy. Take this, LLPS plays a promoting or protecting role in a range of liver diseases, such as viral hepatitis, non-alcoholic fatty liver disease, liver fibrosis, hepatic ischemia-reperfusion injury, autoimmune liver disease, and liver cancer. This review systematically describes the whole landscape of LLPS in liver innate immunity. It will help us to guide a better-personalized approach to LLPS-targeted immunotherapy for liver diseases.
C1 [Zhang, Xinying; Yang, Ziyue; Fu, Chunmeng; Yao, Run; Li, Huan; Peng, Fang; Li, Ning] Cent South Univ, Xiangya Hosp, Dept Blood Transfus, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China.
[Zhang, Xinying; Yang, Ziyue; Fu, Chunmeng; Peng, Fang] Cent South Univ, Xiangya Hosp, NHC Key Lab Canc Prote, 87 Xiangya Rd, Changsha 410008, Hunan Province, Peoples R China.
[Zhang, Xinying; Yao, Run; Li, Huan; Li, Ning] Cent South Univ, Xiangya Hosp, Clin Lab, 87 Xiangya Rd, Changsha 410008, Hunan Province, Peoples R China.
[Zhang, Xinying] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, 87 Xiangya Rd, Changsha, Hunan Province, Peoples R China.
C3 Central South University; Central South University; Central South
University; Central South University
RP Peng, F; Li, N (corresponding author), Cent South Univ, Xiangya Hosp, Dept Blood Transfus, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China.; Peng, F (corresponding author), Cent South Univ, Xiangya Hosp, NHC Key Lab Canc Prote, 87 Xiangya Rd, Changsha 410008, Hunan Province, Peoples R China.; Li, N (corresponding author), Cent South Univ, Xiangya Hosp, Clin Lab, 87 Xiangya Rd, Changsha 410008, Hunan Province, Peoples R China.
EM pengfang@csu.edu.cn; liningxy@csu.edu.cn
RI Zhang, xinying/HTO-1396-2023
FU Natural Science Foundation of Hunan Province
FX Not applicable.
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NR 161
TC 0
Z9 0
U1 11
U2 11
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1478-811X
J9 CELL COMMUN SIGNAL
JI Cell Commun. Signal.
PD SEP 3
PY 2024
VL 22
IS 1
AR 430
DI 10.1186/s12964-024-01787-4
PG 15
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA E6I4O
UT WOS:001304019600001
PM 39227829
OA gold
DA 2025-01-07
ER
PT J
AU Baloji, A
Kalra, N
Chaluvashetty, S
Bhujade, H
Chandel, K
Duseja, A
Taneja, S
Gorsi, U
Kumar, R
Singh, H
Sood, A
Bhattacharya, A
Singh, B
Mittal, BR
Singh, V
Sandhu, MS
AF Baloji, Abhiman
Kalra, Naveen
Chaluvashetty, Sreedhara
Bhujade, Harish
Chandel, Karamvir
Duseja, Ajay
Taneja, Sunil
Gorsi, Ujjwal
Kumar, Rajender
Singh, Harmandeep
Sood, Ashwani
Bhattacharya, Anish
Singh, Baljinder
Mittal, Bhagwant R.
Singh, Virendra
Sandhu, Manavjit S.
TI Efficacy of Yttrium-90 Transarterial Radioembolisation in Advanced
Hepatocellular Carcinoma: An Experience With Hybrid Angio-Computed
Tomography and Glass Microspheres
SO JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
LA English
DT Article
DE HCC; angio-CT,; TARE; Yttrium-90; glass microspheres
ID INTERNAL RADIATION-THERAPY; EXTRAHEPATIC METASTASES; RADIOEMBOLIZATION;
SORAFENIB; SURVIVAL; SAFETY; CHEMOEMBOLIZATION; DOSIMETRY; RADIOTHERAPY;
PROGRESSION
AB Background: Hepatocellular carcinoma is one of the most common malignancies worldwide. Transarterial radioembolisation (TARE) involves selective intra-arterial administration of microspheres loaded with a radioactive compound like Yttrium-90 (Y-90). Conventionally, C-arm-based cone-beam computed tomography has been extensively used during TARE. However, angio-computed tomography (CT) is a relatively new modality which combines the advantages of both fluoroscopy and fCT. There is scarce literature detailing the use of angio-CT in Y90 TARE. Methods: This was a retrospective study of primary liver cancer cases in which the TARE procedure was done from November 2017 to December 2021. Glass-based Y-90 microspheres were used in all these cases. All the cases were performed in the hybrid angio-CT suite. A single photon emission computed tomography-computed comography (SPECT-CT) done postplanning session determined the lung shunt fraction and confirmed the accurate targeting of the lesion. Postdrug delivery, positron emission tomography-computed tomography (PET-CT) was obtained to confirm the distribution of the Y-90 particles. The technical success, median follow-up, objective response rate (ORR), progression-free survival (PFS), and overall survival (OS) were recorded. Results: A total of 56 hepatocellular carcinoma patients underwent TARE during this period, out of which 36 patients (30 males and 6 females) underwent Y90 TARE. The aetiology of cirrhosis included non-alcoholic steatohepatitis (NASH) (11), hepatitis C (HCV) (11), hepatitis B (HBV) (9), metabolic dysfunction and alcohol-associated liver disease (MetALD) (2), alcoholic liver disease (ALD) (1), cryptogenic (1), and autoimmune hepatitis (AIH) (1). The technical success was 100 % and the median follow-up was 7 months (range: 1-32 months). The median OS was 15 months (range 10.73-19.27 months; 95 % CI) and the median local PFS was 4 months (range 3.03-4.97 months; 95 % CI). The ORR (best response, CR + PR) was 58 %. No major complications were seen in this study. Conclusion: TARE is a viable option for liver cancer in all stages, but more so in the advanced stages. The use of angio-CT in TARE aids in the precise delivery of the particles to the tumour and avoids non-target embolisation. ( J CLIN EXP HEPATOL 2024;14:101342)
C1 [Baloji, Abhiman; Kalra, Naveen; Chaluvashetty, Sreedhara; Bhujade, Harish; Chandel, Karamvir; Gorsi, Ujjwal; Sandhu, Manavjit S.] Post Grad Inst Med Educ & Res, Dept Radiodiag & Imaging, Chandigarh, India.
[Duseja, Ajay; Taneja, Sunil; Singh, Virendra] Post Grad Inst Med Educ & Res, Dept Hepatol, Chandigarh, India.
[Kumar, Rajender; Singh, Harmandeep; Sood, Ashwani; Bhattacharya, Anish; Singh, Baljinder; Mittal, Bhagwant R.] Post Grad Inst Med Educ & Res, Dept Nucl Med, Chandigarh, India.
C3 Post Graduate Institute of Medical Education & Research (PGIMER),
Chandigarh; Post Graduate Institute of Medical Education & Research
(PGIMER), Chandigarh; Post Graduate Institute of Medical Education &
Research (PGIMER), Chandigarh
RP Kalra, N (corresponding author), Post Grad Inst Med Educ & Res, Dept Radiodiag & Imaging, Chandigarh, India.
EM navkal2004@yahoo.com
RI Bhujade, Harish/ABC-6422-2021; Bhattacharya, Anish/HTP-6468-2023;
Chandel, Karamvir/KTI-0403-2024
OI Chaluvashetty, Sreedhara bettadahally/0000-0001-7526-2185; Baloji,
Abhiman/0000-0002-3369-6409
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NR 58
TC 2
Z9 2
U1 1
U2 2
PU ELSEVIER - DIVISION REED ELSEVIER INDIA PVT LTD
PI NEW DELHI
PA 17-A/1 MAIN RING ROAD, LAJPAT NAGAR IV, NEW DELHI, 110024, INDIA
SN 0973-6883
EI 2213-3453
J9 J CLIN EXP HEPATOL
JI J. Clin. Exp. Hepatol.
PD MAY-JUN
PY 2024
VL 14
IS 3
AR 101342
DI 10.1016/j.jceh.2023.101342
EA JAN 2024
PG 10
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA GU7K5
UT WOS:001155249200001
PM 38283702
DA 2025-01-07
ER
PT J
AU Tapuria, N
Sinha, CK
Michael, NG
Fisher, PW
AF Tapuria, Niteen
Sinha, Chandrasen K.
Michael, N. G.
Fisher, Paul W.
TI Haematogenous metastasis to ascending colon in a patient with
hepatocellular carcinoma and autoimmune hepatitis
SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Article
DE ascending colon metastasis; autoimmune hepatitis; hepatocellular
carcinoma
ID GASTROINTESTINAL-TRACT INVOLVEMENT
AB The association of hepatocellular carcinoma with chronic active autoimmune hepatitis and haematogenous metastasis to ascending colon has not been reported previously in the literature. The patient was asymptomatic for colonic disease and the finding of colonic involvement was incidental on scans subsequently confirmed by colonoscopy. Usually hepatocellular tumour mass would involve the colon by direct contiguity. Owing to haematogenous metastasis, which is extremely rare, the colonic mass was discontiguous from hepatic tumour lesions. The unique presentation of this case and the differential diagnosis of hepatic tumours coexisting with colonic tumours; are highlighted in this case report.
C1 [Tapuria, Niteen] Royal Free Hosp, Acad Dept Surgy, Hampstead NW3 2QG, London, England.
[Sinha, Chandrasen K.; Michael, N. G.; Fisher, Paul W.] Caithnese Gen Hosp, Dept Gen Surg, Wick, Scotland.
C3 University of London; University College London; UCL Medical School
RP Tapuria, N (corresponding author), Royal Free Hosp, Acad Dept Surgy, 9th Floor,Pond St, Hampstead NW3 2QG, London, England.
EM ntapuria@yahoo.com
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NR 10
TC 12
Z9 12
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0954-691X
J9 EUR J GASTROEN HEPAT
JI Eur. J. Gastroenterol. Hepatol.
PD JUL
PY 2007
VL 19
IS 7
BP 607
EP 609
DI 10.1097/MEG.0b013e3281c55f3e
PG 3
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 279LD
UT WOS:000254355800017
PM 17556911
DA 2025-01-07
ER
PT J
AU Groribæk, L
Vilstrup, H
Jepsen, P
AF Groribaek, Lisbet
Vilstrup, Hendrik
Jepsen, Peter
TI Autoimmune hepatitis in Denmark: Incidence, prevalence, prognosis, and
causes of death. A nationwide registry-based cohort study
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Autoimmune liver disease; Incidence; Prevalence; Prognosis; Causes of
death; Hepatocellular carcinoma; Epidemiology
ID TERM-FOLLOW-UP; HEPATOCELLULAR-CARCINOMA; CIRRHOSIS; POPULATION;
EPIDEMIOLOGY; RISK; MORTALITY; SURVIVAL; CRITERIA; DISEASES
AB Background & Aims: Population-based studies of the clinical course of autoimmune hepatitis are scarce. We conducted a nationwide study of incidence, prevalence, prognosis, and causes of death of autoimmune hepatitis in Denmark.
Methods: From nationwide healthcare registries we identified all Danish citizens diagnosed with autoimmune hepatitis in 1994 2012 and their liver biopsy data. We followed patients through January 2013 and examined age-standardized incidence and prevalence, mortality, prognostic factors, risk of hepatocellular carcinoma, and causes of death. We used Cox regression to compare patients' mortality relative to a gender- and age-matched general population sample.
Results: We included 1721 autoimmune hepatitis patients. The incidence rate was 1.68 (95% confidence interval 1.60 to 1.76) per 100,000 population per year, and it doubled during the study period. Of the 1318 patients who were biopsied at diagnosis, 28.3% had cirrhosis. The 10-year cumulative risk of hepatocellular carcinoma was 0.7% (95% confidence interval 0.3 to 1.5). Male gender and cirrhosis were associated with high mortality and development of hepatocellular carcinoma. In the first year after diagnosis, patients with autoimmune hepatitis had six-fold higher mortality than the general population; later, their mortality remained two-fold higher. Their 10-year cumulative mortality was 26.4% (95% confidence interval 23.7 to 29.1). 38.6% of deaths were liver-related including 3.6% from hepatocellular carcinoma.
Conclusions: This nationwide population-based study of autoimmune hepatitis showed that the incidence increased during 1994-2012, and that the disease remains associated with a high mortality, particularly in the first year after diagnosis. Male gender and cirrhosis were adverse prognostic factors. (C) 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Groribaek, Lisbet; Vilstrup, Hendrik; Jepsen, Peter] Aarhus Univ Hosp, Dept Gastroenterol & Hepatol, DK-8000 Aarhus C, Denmark.
[Jepsen, Peter] Aarhus Univ Hosp, Dept Clin Epidemiol, DK-8000 Aarhus C, Denmark.
C3 Aarhus University; Aarhus University
RP Groribæk, L (corresponding author), Aarhus Univ Hosp, Dept Gastroenterol & Hepatol, Norrebrogade 44, DK-8000 Aarhus C, Denmark.
EM groenbaek.lisbet@gmail.com
OI Jepsen, Peter/0000-0002-6641-1430; Gronbaek, Lisbet/0000-0003-0626-179X
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NR 39
TC 248
Z9 259
U1 0
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD MAR
PY 2014
VL 60
IS 3
BP 612
EP 617
DI 10.1016/j.jhep.2013.10.020
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AB0RB
UT WOS:000331498700022
PM 24326217
DA 2025-01-07
ER
PT J
AU Bengsch, B
Thimme, R
AF Bengsch, Bertram
Thimme, Robert
TI Success of immune checkpoint blockade therapies - mechanisms and
implications for hepatology
SO ZEITSCHRIFT FUR GASTROENTEROLOGIE
LA English
DT Review
DE Immunotherapy; checkpoint blockade; liver cancer; autoimmune hepatitis;
PD-1; CTLA-4; IRAE
ID T-CELL RESPONSES; HEPATOCELLULAR-CARCINOMA; CANCER-IMMUNOTHERAPY;
COMBINED NIVOLUMAB; ALPHA-FETOPROTEIN; PD-1 BLOCKADE; CTLA-4; LIVER;
RECEPTOR; IPILIMUMAB
AB The success of immune modulation by checkpoint blockade approaches is currently transforming oncology, with high and long-lasting tumor responses in patients with advanced disease across many cancer entities. Rooted in the reinvigoration of adaptive antitumor immune responses through disinhibition of negative feedback pathways, these approaches are particularly effective in patients with significant preexisting T cell responses in tumors with high neoantigen load. While promising data is starting to emerge from clinical trials in liver cancer patients, the underlying immunobiology remains poorly understood. In this review, we discuss the immunological mechanisms underlying the success of current checkpoint blockade therapies and the implications for hepatology including management of immune-related hepatitis. Checkpoint blockade therapy provides novel therapeutic options for difficult-to-treat liver cancers but also novel clinical challenges for hepatologists facing immune-related adverse events.
C1 [Bengsch, Bertram; Thimme, Robert] Univ Med Ctr Freiburg, Fac Med, Dept Med Gastroenterol Hepatol Endocrinol & Infec, Freiburg, Germany.
[Bengsch, Bertram] Univ Freiburg, Signalling Res Ctr BIOSS, Freiburg, Germany.
[Bengsch, Bertram] Univ Freiburg, Signalling Res Ctr CIBSS, Freiburg, Germany.
C3 University of Freiburg; University of Freiburg; University of Freiburg
RP Bengsch, B (corresponding author), Uniklin Freiburg, Med Klin Abt 2, Hugstetter Str 55, D-79110 Freiburg, Germany.
EM bertram.bengsch@uniklinik-freiburg.de
RI Bengsch, Bertram/ABF-2142-2020
FU German Research Foundation (DFG) [TRR179]; Heisenberg Scholarship of the
DFG [BE5496/2-1]; EXCEL program at the University Medical Center
Freiburg
FX This work was supported by the TRR179 (project 1)1) of the German
Research Foundation (DFG) to RT and project A01 to BB, the Heisenberg
Scholarship BE5496/2-1 of the DFG to BB and the EXCEL program at the
University Medical Center Freiburg (Be).
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NR 112
TC 1
Z9 1
U1 0
U2 6
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0044-2771
EI 1439-7803
J9 Z GASTROENTEROL
JI Z. Gastroent.
PD JAN
PY 2019
VL 57
IS 1
BP 74
EP 86
DI 10.1055/a-0805-6936
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HH4FB
UT WOS:000455675700021
PM 30641606
DA 2025-01-07
ER
PT J
AU Watanabe, Y
Aikawa, M
Oshima, Y
Kato, T
Takase, K
Watanabe, Y
Okada, K
Okamoto, K
Koyama, I
AF Watanabe, Yukihiro
Aikawa, Masayasu
Oshima, Yuhei
Kato, Tomotaka
Takase, Kenichiro
Watanabe, Yuichiro
Okada, Katsuya
Okamoto, Kojun
Koyama, Isamu
TI Short- and long-term outcomes of laparoscopic liver resection for
non-alcoholic fatty liver disease-associated hepatocellular carcinoma: a
retrospective cohort study
SO HPB
LA English
DT Article
ID UNITED-STATES; CIRRHOSIS; NAFLD; DIAGNOSIS; SCORE; HCC; COMPLICATIONS;
EPIDEMIOLOGY; HEPATECTOMY; VALIDATION
AB Background: We compared the recurrence-free survival (RFS), overall survival (OS), and safety of laparoscopic liver resection (LLR) between non-alcoholic fatty liver disease (NAFLD) and non-NAFLD hepatocellular carcinoma (HCC) patients. Methods: Patients with HCC (n = 349) were divided into four groups based on the HCC etiology (NAFLD [n = 71], hepatitis B [n = 27], hepatitis C [n = 187], alcohol/autoimmune hepatitis [AIH] [n = 64]). RFS and OS were assessed by multivariate analysis after adjustment for clinicopathological variables. A subgroup analysis was performed based on the presence (n = 248) or absence (n = 101) of cirrhosis. Results: Compared with the NAFLD group, the hazard ratios (95% confidence intervals) for RFS in the hepatitis B, hepatitis C, and alcohol/AIH groups were 0.49 (0.22-1.09), 0.90 (0.54-1.48), and 1.08 (0.60-1.94), respectively. For OS, the values were 0.28 (0.09-0.84), 0.52 (0.28-0.95), and 0.59 (0.27-1.30), respectively. With cirrhosis, NAFLD was associated with worse OS than hepatitis C (P = 0.010). Without cirrhosis, NAFLD had significantly more complications (P = 0.034), but comparable survival than others. Discussion: Patients with NAFLD-HCC have some disadvantages after LLR. In patients with cirrhosis, LLR is safe, but survival is poor. In patients without cirrhosis, the complication risk is high.
C1 [Watanabe, Yukihiro; Aikawa, Masayasu; Oshima, Yuhei; Kato, Tomotaka; Takase, Kenichiro; Watanabe, Yuichiro; Okada, Katsuya; Okamoto, Kojun; Koyama, Isamu] Saitama Med Univ, Int Med Ctr, Dept Gastroenterol Surg, 1397-1 Yamane, Hidaka, Saitama 3501298, Japan.
C3 Saitama Medical University
RP Watanabe, Y (corresponding author), Saitama Med Univ, Int Med Ctr, Dept Gastroenterol Surg, 1397-1 Yamane, Hidaka, Saitama 3501298, Japan.
EM watanb@saitama-med.ac.jp
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NR 50
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1365-182X
EI 1477-2574
J9 HPB
JI HPB
PD DEC
PY 2023
VL 25
IS 12
BP 1573
EP 1586
DI 10.1016/j.hpb.2023.09.002
EA NOV 2023
PG 14
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA DC0L4
UT WOS:001129715000001
PM 37758580
DA 2025-01-07
ER
PT J
AU Wang, S
Toy, M
Pham, TTH
So, S
AF Wang, Sonia
Toy, Mehlika
Hang Pham, Thi T.
So, Samuel
TI Causes and trends in liver disease and hepatocellular carcinoma among
men and women who received liver transplants in the US, 2010-2019
SO PLOS ONE
LA English
DT Article
ID NONALCOHOLIC STEATOHEPATITIS; UNITED-STATES; VIRUS-INFECTION;
HEPATITIS-B; ALCOHOL-USE; PREVALENCE; CIRRHOSIS; OUTCOMES; OBESITY
AB Background and aims The national Organ Procurement and Transplant Network (OPTN) reported the major indication for liver transplants in 2018 was for other/unknown causes. This study was undertaken to examine all causes and trends in liver disease and hepatocellular carcinoma (HCC) among adults who received liver transplants in the past 10 years. Methods A national cohort study of all adults who received liver transplants from Jan 1, 2010 to Dec 31, 2019 recorded in the OPTN STAR database analyzed by etiology of liver disease and HCC, and gender. Results Adult liver transplants increased from 5,731 in 2010 to 8,345 in 2019 (45.6% increase). Between 2010 and 2014, liver disease and HCC associated with hepatitis C (HCV) was the major cause for liver transplantation. Proportion of liver transplants for HCV associated liver disease and HCC has since decreased to 18.7% in 2019 compared with 44.5% in 2010 [25.8%, (95% CI 24.3% to 27.3%), p<0.001], while liver transplants for liver disease and HCC associated with alcohol-associated liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) increased from 12.7% to 28.8% [16.1%, (95% CI 14.8% to 17.4%), p<0.001], and from 9.1% to 21.5% [12.4%, (95% CI 11.2% to 13.5%), p<0.001], respectively. When all causes of liver disease were examined, only 1.7% of liver transplants had unspecified causes. The five major causes of liver disease and HCC among men receiving liver transplants in 2019 were ALD (33.1%), HCV (21.9%), NAFLD (18.5%), cholestatic liver disease (5.7%) and hepatitis B (4.9%), while the major causes among women were NAFLD (26.8%), ALD (21.1%), HCV (13.1%), cholestatic liver disease (11.1%), and autoimmune liver disease (5.6%). Conclusions Our study found NAFLD in 2017 in women and ALD in 2019 in men have surpassed HCV as the leading causes of liver disease and HCC among adults receiving liver transplants.
C1 [Wang, Sonia; Toy, Mehlika; Hang Pham, Thi T.; So, Samuel] Stanford Univ, Sch Med, Asian Liver Ctr, Dept Surg, Stanford, CA 94305 USA.
C3 Stanford University
RP So, S (corresponding author), Stanford Univ, Sch Med, Asian Liver Ctr, Dept Surg, Stanford, CA 94305 USA.
EM samso@stanford.edu
OI Pham, Thi T. Hang/0000-0002-2480-4586; Toy, Mehlika/0000-0001-7848-4816
FU Asian Liver Center, Department of Surgery, Stanford University School of
Medicine; Health Resources and Services Administration
[234-2005-370011C]
FX All the funding and support for this study is provided by the Asian
Liver Center, Department of Surgery, Stanford University School of
Medicine. There was no additional external funding received for this
study.This work was based on data collected and provided by the Organ
Procurement and Transplant Network which is supported in part by Health
Resources and Services Administration contract 234-2005-370011C. The
content is the responsibility of the authors alone and does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government.
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NR 27
TC 43
Z9 46
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 18
PY 2020
VL 15
IS 9
AR e0239393
DI 10.1371/journal.pone.0239393
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA NU7WV
UT WOS:000573851100081
PM 32946502
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Al-Matham, K
Alabed, I
Zaidi, SZA
Qushmaq, KA
AF Al-Matham, Khalid
Alabed, Iehab
Zaidi, Syed Z. A.
Qushmaq, Khalid A.
TI Cold agglutinin disease in fibrolamellar hepatocellular carcinoma: a
rare association with a rare cancer variant
SO ANNALS OF SAUDI MEDICINE
LA English
DT Article
ID FEATURES; PATIENT
AB Cold agglutinin disease (CAD) is a rare autoimmune hemolytic anemia. Although it can occur secondary to lymphoproliferative disorders and autoimmune or infectious diseases, CAD is rarely reported as secondary to solid tumors. We report a case of a woman aged 18 years diagnosed with a well-differentiated hepatocellular carcinoma of the fibrolamellar subtype, who was shown to have CAD also. Her general condition, including CAD, improved after targeted therapy with sorafenib for the hepatocellular carcinoma and only conservative measures for the CAD that consisted of avoidance of cold. In summary, although it is an extremely rare association and less common than lymphoproliferative disorders, CAD can be associated with solid tumors.
C1 [Al-Matham, Khalid; Alabed, Iehab; Zaidi, Syed Z. A.; Qushmaq, Khalid A.] Main Hosp, Dept Internal Med, Riyadh 11525, Saudi Arabia.
RP Al-Matham, K (corresponding author), Main Hosp, Dept Internal Med, POB 59046, Riyadh 11525, Saudi Arabia.
EM khalidosis@hotmail.com
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Rosse Wendell F, 2004, Hematology Am Soc Hematol Educ Program, P48
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Young S, 2006, ANAESTHESIA, V61, P593, DOI 10.1111/j.1365-2044.2006.04650.x
NR 13
TC 15
Z9 15
U1 0
U2 0
PU K FAISAL SPEC HOSP RES CENTRE
PI RIYADH
PA PUBLICATIONS OFFICE PO BOX 3354, RIYADH 11211, SAUDI ARABIA
SN 0256-4947
EI 1319-9226
J9 ANN SAUDI MED
JI Ann. Saudi Med.
PD MAR-APR
PY 2011
VL 31
IS 2
BP 197
EP 200
DI 10.4103/0256-4947.76409
PG 4
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 740QO
UT WOS:000288809700016
PM 21293066
OA Green Published
DA 2025-01-07
ER
PT J
AU Liao, JY
Zhang, Q
Liao, Y
Cai, B
Chen, J
Li, LX
Wang, LL
AF Liao, Jingyu
Zhang, Qi
Liao, Yun
Cai, Bei
Chen, Jie
Li, Lixin
Wang, Lanlan
TI Association of T-Cell Immunoglobulin and Mucin Domain-Containing
Molecule 3 (Tim-3) Polymorphisms with Susceptibility and Disease
Progression of HBV Infection
SO PLOS ONE
LA English
DT Article
ID ANTITUMOR IMMUNITY; EXPRESSION; BLOCKADE; DYSFUNCTION; EXHAUSTION;
AUTOIMMUNE; INDUCTION; RESPONSES; PD-1
AB Purpose: T-cell immunoglobulin and mucin domain-containing molecule 3 (Tim-3) plays an important role in regulating T cells in hepatitis B virus (HBV) infection and hepatocellular carcinoma (HCC). However, few researches have reported the association of Tim-3 genetic variants with susceptibility and progression of HBV infection. In this study, we focused on the association of Tim-3 polymorphisms with HBV infection, HBsAg seroclearance and hepatocellular carcinoma.
Methods: A total of 800 subjects were involved in this study. Four groups were studied here, including HBV, HBsAg seroclearance, HBV-associated HCC and healthy controls. Three single-nucleotide polymorphisms (SNPs) of Tim-3, rs246871, rs25855 and rs31223 were genotyped to analyze the association of Tim-3 polymorphisms with susceptibility and disease progression of HBV infection.
Results: Our study found that rs31223 and rs246871 were associated with disease progression of HBV infection, while none of the three SNPs was relevant to HBV susceptibility. The minor allele "C'' of rs31223 was found to be associated with an increased probability of HBsAg seroclearance (P = 0.033) and genotype "CC'' of rs246871 to be associated with an increased probability of HBV-associated HCC (P = 0.007). In accordance, haplotypic analysis of the three polymorphisms also showed that the haplotype block CGC* and TGC* were significantly associated with HBsAg seroclearance (P<0.05) while haplotype block CAT*, CGT*, TAC* and TGT* were significantly associated with HBV-associated HCC (all P<0.05).
Conclusions: Genetic variants of Tim-3 have an important impact on disease progression of HBV infection. With specific Tim-3 polymorphisms, patients infected with HBV could be potential candidates of HCC and HBsAg seroclearance.
C1 [Liao, Jingyu; Zhang, Qi; Liao, Yun; Cai, Bei; Chen, Jie; Li, Lixin; Wang, Lanlan] Sichuan Univ, Dept Lab Med, West China Hosp, Chengdu 610064, Sichuan, Peoples R China.
C3 Sichuan University
RP Wang, LL (corresponding author), Sichuan Univ, Dept Lab Med, West China Hosp, Chengdu 610064, Sichuan, Peoples R China.
EM wanglanlan85@126.com
RI Liao, Yun/LKJ-9824-2024
FU National Natural Science Foundation of China [81072443, 81273256]
FX This research was supported by grants from the National Natural Science
Foundation of China (No. 81072443 and 81273256). The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 31
TC 7
Z9 8
U1 0
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 27
PY 2014
VL 9
IS 5
AR e98280
DI 10.1371/journal.pone.0098280
PG 7
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AI5NG
UT WOS:000336914100046
PM 24867713
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Khor, SS
Ueno, K
Nishida, N
Kawashima, M
Kawai, Y
Aiba, Y
Hitomi, Y
Nagasaki, M
Nakamura, M
Tokunaga, K
AF Khor, Seik-Soon
Ueno, Kazuko
Nishida, Nao
Kawashima, Minae
Kawai, Yosuke
Aiba, Yoshihiro
Hitomi, Yuki
Nagasaki, Masao
Nakamura, Minoru
Tokunaga, Katsushi
TI Novel HLA allele associations with susceptibility, staging,
symptomatic state, autoimmune hepatitis and hepatocellular carcinoma
events for primary biliary cholangitis in the Japanese population
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE primary biliary cholangitis; HLA; autoimmune hepatitis; hepatocellular
carcinoma; Scheuer staging system
ID GENOME-WIDE ASSOCIATION; CLASS-II REGION; RISK-FACTORS; CIRRHOSIS;
TYPE-1; GENES; LOCI; POLYMORPHISMS; MULTICENTER; PROGRESSION
AB Primary biliary cholangitis (PBC) is a rare autoimmune disease with a clear predisposition for human leukocyte antigen (HLA)-DR/DQ-associated loss of immune tolerance for the E2 component of the pyruvate dehydrogenase complex. Three-field-resolution HLA imputation of 1,670 Japanese PBC patients and 2,328 healthy controls was conducted using Japanese population-specific HLA reference panels. Eighteen previously reported Japanese PBC-associated HLA alleles were confirmed and extended to 3-field-resolution, including HLA-DRB1*08:03 to HLA-DRB1*08:03:02, HLA-DQB1*03:01 to HLA-DQB1*03:01:01, HLA-DQB1*04:01 to HLA-DQB1*04:01:01 and HLA-DQB1*06:04 to HLA-DQB1*06:04:01. In addition, additional significant novel HLA alleles were identified, including 3 novel susceptible HLA-DQA1 alleles: HLA-DQA1*03:03:01, HLA-DQA1*04:01:01, HLA-DQA1*01:04:01 and 1 novel protective HLA-DQA1 allele, HLA-DQA1*05:05:01. In addition, PBC patients carrying HLA-DRB1*15:01:01 and HLA-DQA1*03:03:01 would have a higher predisposition toward developing concomitant autoimmune hepatitis (AIH). Further, late-stage and symptomatic PBC shared the same susceptible HLA alleles of HLA-A*26:01:01, HLA-DRB1*09:01:02 and HLA-DQB1*03:03:02. Lastly, HLA-DPB1*05:01:01 was identified as a potential risk HLA allele for development of hepatocellular carcinoma (HCC) in PBC patients. In conclusion, we have extended the current knowledge of HLA allele associations to 3-field resolution and identified novel HLA allele associations with predisposition risk, staging, symptomatic state, and AIH and HCC events for Japanese PBC patients.
C1 [Khor, Seik-Soon; Ueno, Kazuko; Nishida, Nao; Kawai, Yosuke; Tokunaga, Katsushi] Natl Ctr Global Hlth & Med, Genome Med Sci Project, Tokyo, Japan.
[Nishida, Nao] Natl Ctr Global Hlth & Med, Res Inst, Res Ctr Hepatitis & Immunol, Ichikawa, Japan.
[Kawashima, Minae] Res Org Informat & Syst, Database Ctr Life Sci DBCLS, Chiba, Japan.
[Aiba, Yoshihiro; Nakamura, Minoru] Natl Hosp Org NHO Nagasaki Med Ctr, Clin Res Ctr, Omura, Japan.
[Hitomi, Yuki] Natl Ctr Global Hlth & Med, Res Inst, Dept Human Genet, Tokyo, Japan.
[Nagasaki, Masao] Kyushu Univ, Med Inst Bioregulat, Med Res Ctr High Depth Om, Fukuoka, Japan.
[Nagasaki, Masao] Kyoto Univ, Ctr Genom Med, Grad Sch Med, Kyoto, Japan.
[Nakamura, Minoru] Nagasaki Univ, Grad Sch Biomed Sci, Dept Hepatol, Omura, Japan.
[Nakamura, Minoru] NHO Nagasaki Med Ctr, Clin Res Ctr, PBC Res NHO Study Grp Liver Dis Japan NHOSLJ, Headquarters Primary Biliary Cholangitis, Omura, Japan.
C3 National Center for Global Health & Medicine - Japan; National Center
for Global Health & Medicine - Japan; Research Organization of
Information & Systems (ROIS); National Center for Global Health &
Medicine - Japan; Kyushu University; Kyoto University; Nagasaki
University
RP Khor, SS; Tokunaga, K (corresponding author), Natl Ctr Global Hlth & Med, Genome Med Sci Project, Tokyo, Japan.
EM skhor@ri.ncgm.go.jp; katokunaga@ri.ncgm.go.jp
RI Hitomi, Yuki/V-8236-2019; Khor, Seik-Soon/C-4700-2015
OI Hitomi, Yuki/0000-0002-6713-7875; Nagasaki, Masao/0000-0002-4292-8785
FU Japan Agency for Medical Research and Development [JP22fk0210111,
20K08370]; Japan Society for Promotion of Science (JSPS) [20590800,
23591006, 26293181]; National Hospital Organization (NHO)
FX This work was supported by the Japan Agency for Medical Research and
Development under grant number JP22fk0210111 and 20K08370, Grants-in-Aid
for Scientific Research from the Japan Society for Promotion of Science
(JSPS) to MN (#20590800, #23591006, #26293181), a Grant-in-Aid for
Clinical Research from the National Hospital Organization (NHO) to MN.
Part of the figure generations was created with BioRender.com.
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NR 49
TC 4
Z9 4
U1 0
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAY 31
PY 2023
VL 14
AR 1151502
DI 10.3389/fimmu.2023.1151502
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA I9RJ9
UT WOS:001006077900001
PM 37325616
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Cindoruk, M
Cirak, MY
Unal, S
Karakan, T
Erkan, G
Engin, D
Dumlu, S
Turet, S
AF Cindoruk, Mehmet
Cirak, Meltem Yalinay
Unal, Selahattin
Karakan, Tarkan
Erkan, Gulbanu
Engin, Doruk
Dumlu, Sukru
Turet, Sevgi
TI Identification of Helicobacter species by 16S rDNA PCR and
sequence analysis in human liver samples from patients with various
etiologies of benign liver diseases
SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Article
DE benign liver disease; chronic hepatitis; Helicobacter pylori; hepatitis
C; nonalcoholic fatty liver disease
ID HEPATITIS-C VIRUS; HEPATOCELLULAR-CARCINOMA; HEPATOBILIARY DISEASES;
PYLORI INFECTION; CIRRHOSIS; DNA; ASSOCIATION; CANCER; HYBRIDIZATION;
STOMACH
AB Background/Aims Several reports indicated an increased prevalence of the Helicobacter species in hepatocellular cancer tissue and in liver samples infected with hepatitis viruses. The frequency of Helicobacter spp. in benign liver diseases was, however, not thoroughly investigated.
Methods Seventy-five consecutive patients with suspected liver disease were enrolled. The indications were hepatitis B virus (n = 30), C virus (n = 8), B and C dual infection (n = 1), nonalcoholic steatohepatitis (n = 27), autoimmune hepatitis (n = 3), primary biliary cirrhosis (n=l) and idiopathic elevation of liver enzymes (n = 5). PCR detection of 16S recombinant RNA gene of Helicobacter spp. was performed on liver samples. PCR products of positive samples were further identified by DNA sequencing. The patients also had upper gastrointestinal endoscopy and gastric biopsy for the detection of H. pylori using histopathology and PCR.
Results Helicobacter spp. DNA was detected in two out of 75 liver biopsy samples (2.6%), which were typed as H. pylori by DNA sequencing. One of these patients had chronic hepatitis C infection (man, 51 years old) and the other had nonalcoholic steatohepatitis (woman, 44 years old). Fifty-two out of 75 of the patients (69.3%) had H. pylori infection in their stomachs.
Conclusion We have found that H. pylori infection is much less prevalent in benign liver diseases. The presence of H. pylori in nonalcoholic steatohepatitis (NASH) patients is a novel finding and this finding should be confirmed in a larger series.
C1 [Cindoruk, Mehmet; Unal, Selahattin; Karakan, Tarkan; Erkan, Gulbanu; Dumlu, Sukru] Gazi Univ, Fac Med, Ankara, Turkey.
[Cirak, Meltem Yalinay; Engin, Doruk; Turet, Sevgi] Dept Gastroenterol & Med Microbiol, Ankara, Turkey.
C3 Gazi University
RP Karakan, T (corresponding author), Gazi Hastanesi Gastroentrol & Med Microbiol, TR-06500 Ankara, Turkey.
EM tkarakan@gmail.com
RI Cindoruk, Mehmet/C-2104-2009; Karakan, Tarkan/A-9875-2016; Engin,
Doruk/O-3604-2014
OI Karakan, Tarkan/0000-0003-1561-8789; Engin, Doruk/0000-0001-9209-8858
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NR 32
TC 34
Z9 40
U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0954-691X
EI 1473-5687
J9 EUR J GASTROEN HEPAT
JI Eur. J. Gastroenterol. Hepatol.
PD JAN
PY 2008
VL 20
IS 1
BP 33
EP 36
DI 10.1097/MEG.0b013e3282efa4f2
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 325ZN
UT WOS:000257627800008
PM 18090988
DA 2025-01-07
ER
PT J
AU John, BV
Dahman, B
Deng, YY
Khakoo, NS
Taddei, TH
Kaplan, DE
Levy, C
AF John, Binu, V
Dahman, Bassam
Deng, Yangyang
Khakoo, Nidah S.
Taddei, Tamar H.
Kaplan, David E.
Levy, Cynthia
TI Rates of decompensation, hepatocellular carcinoma and mortality in
AMA-negative primary biliary cholangitis cirrhosis
SO LIVER INTERNATIONAL
LA English
DT Article
DE antimitochondrial antibodies; autoimmune liver disease; cholestatic
liver disease; decompensation; hepatocellular carcinoma; primary biliary
cholangitis
ID PROGRESSION; ANTIBODIES; PROGNOSIS; FIBROSIS; OUTCOMES; SMOKING
AB Background The natural history of patients with anti-mitochondrial antibody (AMA)-negative Primary Biliary Cholangitis (PBC) cirrhosis has not been well defined, with prior studies showing discordant results. Furthermore, most studies of AMA-negative PBC have limited numbers of patients with cirrhosis and liver-related outcomes. Methods We investigated the association of AMA-negative PBC and the development of death, liver-related death, decompensation and hepatocellular carcinoma (HCC), in a large cohort of predominantly male patients with PBC cirrhosis assembled from the Veterans Health Administration. Results In a cohort of 521 patients with PBC cirrhosis (65 AMA-negative) with a total follow-up of 2504.3 person-years (PY) from cirrhosis diagnosis, patients with AMA-negative PBC were younger and more likely to be black but had similar rates of UDCA response. AMA-negative PBC cirrhosis was associated with similar unadjusted rates of liver-related death (4.6 vs 5.9 per 100 PY, P = .44), overall death (7.7 vs 9.6 per 100 PY, P = .31), decompensation (7.3 vs 5.1 per 100 PY, P = .12) and HCC (0.6 vs 1.0 per 100 PY, P = .63) to AMA-positive PBC. After adjusting for confounders, AMA-negative PBC cirrhosis was associated with similar rates of liver-related death (sub-Hazard Ratio [sHR] 1.27, 95% CI 0.71-2.28, P = .42, death [sHR] 1.24, 95% CI 0.81-1.90, P = .32), decompensation (sHR 1.05, 95% CI 0.56-1.98, P = .87) and HCC (sHR 0.48, 95% CI 0.11-2.10, P = .33) to AMA-positive patients. Conclusion In a cohort of predominantly male patients, AMA-negative PBC cirrhosis was associated with similar rates of overall or liver-related death, HCC or decompensation compared with AMA-positive disease.
C1 [John, Binu, V] Bruce W Carter VA Med Ctr, Div Hepatol, Miami, FL USA.
[John, Binu, V; Levy, Cynthia] Univ Miami, Miller Sch Med, Div Digest Hlth & Liver Dis, Miami, FL 33136 USA.
[Dahman, Bassam; Deng, Yangyang] Virginia Commonwealth Univ, Dept Hlth Behav & Policy, Richmond, VA USA.
[Khakoo, Nidah S.] Jackson Mem Hosp, Dept Med, Miami, FL 33136 USA.
[Taddei, Tamar H.] Yale Sch Med, Sect Digest Dis, New Haven, CT USA.
[Taddei, Tamar H.] VA Connecticut Healthcare Syst, West Haven, CT USA.
[Kaplan, David E.] Univ Penn, Div Gastroenterol & Hepatol, Philadelphia, PA 19104 USA.
[Kaplan, David E.] Corporal Michael J Crescenz VA Med Ctr, Div Gastroenterol & Hepatol, Philadelphia, PA USA.
C3 University of Miami; Virginia Commonwealth University; Yale University;
US Department of Veterans Affairs; Veterans Health Administration (VHA);
VA Connecticut Healthcare System; University of Pennsylvania
RP John, BV (corresponding author), Univ Miami, Miller Sch Med, Miami, FL 33136 USA.; John, BV (corresponding author), Bruce W Carter VA Med Ctr, Hepatol, Miami, FL 33125 USA.
EM Binu.John@va.gov
OI John, Binu V/0000-0002-2002-9682; Levy, Cynthia/0000-0001-5498-6037
FU NIH-NCI Cancer Center Support Grant [P30 CA016059]
FX Services supporting this research project were generated by the VCU
Massey Cancer Center Biostatistics Shared Resource, supported, in part,
with funding from NIH-NCI Cancer Center Support Grant P30 CA016059.
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NR 32
TC 11
Z9 12
U1 1
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD FEB
PY 2022
VL 42
IS 2
BP 384
EP 393
DI 10.1111/liv.15079
EA OCT 2021
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA YO9TE
UT WOS:000706411300001
PM 34614294
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Wild, SH
Morling, JR
McAllister, DA
Kerssens, J
Fischbacher, C
Parkes, J
Roderick, PJ
Sattar, N
Byrne, CD
AF Wild, Sarah H.
Morling, Joanne R.
McAllister, David A.
Kerssens, Jan
Fischbacher, Colin
Parkes, Julie
Roderick, Paul J.
Sattar, Naveed
Byrne, Christopher D.
CA Scottish & Southampton Diabet & Li
Scottish Diabetes Res Network Epid
TI Type 2 diabetes and risk of hospital admission or death for chronic
liver diseases
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Diabetes; Liver disease; Cohort
ID SOCIOECONOMIC-STATUS; HEALTH DISPARITIES; UNITED-STATES; FATTY LIVER;
MORTALITY; ALCOHOL; CANCER; PREVALENCE; OBESITY; BURDEN
AB Background & Aims: The impact of type 2 diabetes (T2DM) on hospital admissions and deaths due to common chronic liver diseases (CLDs) is uncertain. Our aim was to investigate associations between T2DM and CLDs in a national retrospective cohort study and to investigate the role of sex and socio-economic status (SES).
Methods: We used International Classification of Disease codes to identify incident alcoholic liver disease (ALD), autoimmune liver disease, haemochromatosis, hepatocellular carcinoma, non-alcoholic fatty liver disease (NAFLD) and viral liver disease from linked diabetes, hospital, cancer and death records for people of 40-89 years of age in Scotland 2004-2013. We used quasi Poisson regression to estimate rate ratios (RR).
Results: There were 6667 and 33624 first mentions of CLD in hospital, cancer and death records over similar to 1.8 and 24 million person-years in people with and without T2DM, respectively. The most common liver disease was ALD among people without diabetes and was NAFLD among people with T2DM. Age-adjusted RR for T2DM compared to the non-diabetic population (95% confidence intervals) varied between 1.27 (1.04-1.55) for autoimmune liver disease and 5.36 (4.41-6.51) for NAFLD. RRs were lower for men than women and for more compared to less deprived populations for both ALD and NAFLD.
Conclusions: T2DM is associated with increased risk of hospital admission or death for all common CLDs and the strength of the association varies by type of CLD, sex and SES. Increasing prevalence of T2DM is likely to result in increasing burden of all CLDs. (C) 2016 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Wild, Sarah H.; Morling, Joanne R.; McAllister, David A.] Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Ctr Populat Hlth Sci, Teviot Pl, Edinburgh EH8 9AG, Midlothian, Scotland.
[Kerssens, Jan; Fischbacher, Colin] Natl Hlth Serv Natl Serv Scotland, Informat Serv Div, Edinburgh, Midlothian, Scotland.
[Parkes, Julie] Univ Southampton, Fac Med, Southampton SO9 5NH, Hants, England.
[Roderick, Paul J.] Univ Southampton, Primary Care & Populat Sci, Southampton SO9 5NH, Hants, England.
[Roderick, Paul J.] Univ Glasgow, British Heart Fdn Ctr Cardiovasc Sci, Glasgow G12 8QQ, Lanark, Scotland.
[Byrne, Christopher D.] Univ Southampton, Fac Med, Nutr & Metab, Southampton SO9 5NH, Hants, England.
[Byrne, Christopher D.] Southampton Univ Hosp, NIHR Southampton Biomed Res Ctr, Southampton, Hants, England.
C3 University of Edinburgh; NHS National Services Scotland; University of
Southampton; University of Southampton; University of Glasgow;
University of Southampton; University of Southampton
RP Wild, SH (corresponding author), Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Ctr Populat Hlth Sci, Teviot Pl, Edinburgh EH8 9AG, Midlothian, Scotland.
EM sarah.wild@ed.ac.uk
RI Sattar, Naveed/AFN-0504-2022; McAllister, David/AIE-6553-2022; Morling,
Jo/AAH-7385-2020
OI Fischbacher, Colin/0000-0003-3090-1857; Morling,
Joanne/0000-0003-0772-2893; McAllister, David/0000-0003-3550-1764;
Byrne, Christopher D/0000-0001-6322-7753; Parkes,
Julie/0000-0002-6490-395X
FU Scottish Government through the Scottish Diabetes Group; Southampton
National Institute for Health Research Biomedical Research Centre
FX This work was supported by funding from the Scottish Government through
the Scottish Diabetes Group. CDB is supported in part by the Southampton
National Institute for Health Research Biomedical Research Centre.
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NR 30
TC 61
Z9 64
U1 1
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD JUN
PY 2016
VL 64
IS 6
BP 1358
EP 1364
DI 10.1016/j.jhep.2016.01.014
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DL9AS
UT WOS:000375934200022
PM 26812073
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Jensen, MD
Jepsen, P
Vilstrup, H
Gronbæk, L
AF Jensen, Morten D.
Jepsen, Peter
Vilstrup, Hendrik
Gronbaek, Lisbet
TI Increased Cancer Risk in Autoimmune Hepatitis: A Danish Nationwide
Cohort Study
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID TERM-FOLLOW-UP; HEPATOCELLULAR-CARCINOMA; REGRESSION-ANALYSIS;
COLORECTAL-CANCER; LIVER-DISEASES; GUT MICROBIOTA; CIRRHOSIS;
EPIDEMIOLOGY; MALIGNANCIES; PREVENTION
AB INTRODUCTION: Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease and as such may increase the risk of cancer. We examined cancer risks in a nationwide cohort of patients with AIH. METHODS: This study was based on nationwide Danish healthcare registries. We identified all persons diagnosed with AIH between 1994 and 2018. We included 1805 patients with AIH and 16,617 age- and sex-matched population controls. We estimated cumulative risks of cancers and risk ratios (RRs) between patients and controls. Within the cohort of patients with AIH, we examined the impact of immunosuppressive treatment (IST) and cirrhosis on cancer risks. RESULTS: The 10-year risk of any cancer was 13.6% (95% confidence interval [CI] 11.7-15.6) in patients with AIH with an RR of 1.5 (95% CI 1.3-1.7) compared with controls. Patients with AIH had a 10-year risk of 0.5% (95% CI 0.2-1.1) for hepatocellular carcinoma. The 10-year risk was 1.6% (95% CI 1.0-2.5) for colorectal cancer (RR: 2.1 [95% CI 1.3-3.5]) and 4.0% (95% CI 3.0-5.3) for nonmelanoma skin cancer (RR: 1.8 [95% CI 1.3-2.5]). Among patients with AIH, the risk of cancer was higher for those with cirrhosis (hazard ratio: 1.3 [95% CI 1.0-1.7]), and it also increased 1.05-fold (95% CI 1.0-1.1) for every year the patient was on IST. DISCUSSION: AIH was associated with a 1.5-fold increased 10-year risk of cancer compared with age- and sex-matched controls. Among patients with AIH, the risk of cancer was higher for those with cirrhosis, and it also increased slightly with longer duration of IST.
C1 [Jensen, Morten D.; Jepsen, Peter; Vilstrup, Hendrik; Gronbaek, Lisbet] Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Aarhus, Denmark.
[Jepsen, Peter] Aarhus Univ Hosp, Dept Clin Epidemiol, Aarhus, Denmark.
[Gronbaek, Lisbet] Reg Hosp Horsens, Dept Med, Horsens, Denmark.
C3 Aarhus University; Aarhus University
RP Jensen, MD (corresponding author), Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Aarhus, Denmark.
EM moje@clin.au.dk
RI Jensen, Morten Daniel/HDM-8545-2022
OI Gronbaek, Lisbet/0000-0003-0626-179X; Jepsen, Peter/0000-0002-6641-1430;
Jensen, Morten Daniel/0000-0002-5137-7268
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TC 19
Z9 19
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD JAN
PY 2022
VL 117
IS 1
BP 129
EP 137
DI 10.14309/ajg.0000000000001525
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA YB1ID
UT WOS:000738773800021
PM 34622808
DA 2025-01-07
ER
PT J
AU Friedman, SL
Sanyal, AJ
AF Friedman, Scott L. L.
Sanyal, Arun J. J.
TI The future of hepatology
SO HEPATOLOGY
LA English
DT Review
ID FATTY LIVER-DISEASE; NONALCOHOLIC STEATOHEPATITIS;
HEPATOCELLULAR-CARCINOMA; ALCOHOLIC HEPATITIS; TRANSPLANTATION;
EPIDEMIOLOGY; HEALTH; IMPACT; RISK; ASSOCIATION
AB The field of hepatology has made impressive progress over its similar to 75 years of existence. Advances in understanding liver function and its dysregulation in disease, genetic determinants of disease, antiviral therapy, and transplantation have transformed the lives of patients. However, there are still significant challenges that require ongoing creativity and discipline, particularly with the emergence of fatty liver diseases, as well as managing autoimmune disease, cancer, and liver disease in children. Diagnostic advances are urgently needed to accelerate risk stratification and efficient testing of new agents with greater precision in enriched populations. Integrated, holistic care models should be extended beyond liver cancer to diseases like NAFLD with systemic manifestations or extrahepatic comorbidities such as cardiovascular disease, diabetes, addiction, and depressive disorders. To meet the growing burden of asymptomatic liver disease, the workforce will need to be expanded by incorporating more advanced practice providers and educating other specialists. The training of future hepatologists will benefit from incorporating emerging skills in data management, artificial intelligence, and precision medicine. Continued investment in basic and translational science is crucial for further progress. The challenges ahead are significant, but with collective effort, the field of hepatology will continue to make progress and overcome obstacles.
C1 [Friedman, Scott L. L.] Icahn Sch Med Mt Sinai, Dept Med, Div Liver Dis, POB 1123,1425 Madison Ave,Room 1170C, New York, NY 10029 USA.
[Sanyal, Arun J. J.] Virginia Commonwealth Univ, Dept Internal Med, Div Gastroenterol Hepatol & Nutr, Sch Med, MCV POB 980341, Richmond, VA 23298 USA.
C3 Icahn School of Medicine at Mount Sinai; Virginia Commonwealth
University
RP Friedman, SL (corresponding author), Icahn Sch Med Mt Sinai, Dept Med, Div Liver Dis, POB 1123,1425 Madison Ave,Room 1170C, New York, NY 10029 USA.; Sanyal, AJ (corresponding author), Virginia Commonwealth Univ, Dept Internal Med, Div Gastroenterol Hepatol & Nutr, Sch Med, MCV POB 980341, Richmond, VA 23298 USA.
EM scott.friedman@mssm.edu; arun.sanyal@vcuhealth.org
RI Friedman, Scott/AFV-6304-2022
OI Sanyal, Arun/0000-0001-8682-5748; Friedman, Scott/0000-0003-1178-6195
FU FUNDING INFORMATION [R01 DK128289]; Wreschner Research fund;
Stravitz-Sanyal Institute for Liver disease
FX R01 DK128289 and Wreschner Research fund, to Scott L. Friedman;
Stravitz-Sanyal Institute for Liver disease for Arun J. Sanyal.& nbsp;
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NR 106
TC 3
Z9 3
U1 1
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD AUG
PY 2023
VL 78
IS 2
BP 637
EP 648
DI 10.1097/HEP.0000000000000389
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA M7TW8
UT WOS:001032215200040
PM 37013924
DA 2025-01-07
ER
PT J
AU Liu, XQ
Xu, J
AF Liu, Xueqin
Xu, Jian
TI Calling a stage-based treatment model for chronic liver diseases in
China mainland
SO ANNALS OF HEPATOLOGY
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; CIRRHOSIS; TRENDS; EPIDEMIOLOGY; SURVEILLANCE;
POPULATION; MORTALITY; CANCER
AB China is regarded as the "leader in liver diseases" because that one-fifth of the population was affected by some forms of liver diseases in this developing country. In addition to common infectious liver diseases (such as viral hepatitis and parasitic liver diseases), non-infectious liver diseases such as fatty liver diseases (FLD), drug-induced liver injury (DILI), alcoholic liver diseases (ALD), autoimmune liver diseases (AILD), vessel-related liver diseases, genetic metabolic liver diseases and liver masses are present. In recent years, an increasing number of liver diseases have been reported in special populations, including childhood liver diseases, pregnancy-related liver diseases and liver transplant-associated diseases and so on. Absence of characteristic symptoms and signs coupled with a lack of medical knowledge, patients with chronic liver diseases seek medical treatment without a reliable model, which resulted to the chaotic consult medical status in China mainland. This article aims to describe the current seek medical status of chronic liver diseases and discuss a stage-based consulting medical model for chronic liver diseases in China mainland, which would contribute to make rational use of limited medical resources and help to address National Health China 2030 strategy initiated by the Chinese government. (C) 2019 Fundacion Clinica Medica Sur, A.C. Published by Elsevier Espana, S.L.U.
C1 [Liu, Xueqin; Xu, Jian] Fuling Ctr Hosp Chongqing City, Dept Hepatol & Translat Med, Chongqing, Peoples R China.
RP Xu, J (corresponding author), Fuling Ctr Hosp Chongqing City, Dept Hepatol & Translat Med, Chongqing, Peoples R China.
EM 1106134514@qq.com
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NR 31
TC 1
Z9 3
U1 3
U2 26
PU ELSEVIER ESPANA
PI MADRID
PA CALLE DE ZURBANO, 76-4TH FLR LEFT, MADRID, 28010, SPAIN
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD NOV-DEC
PY 2020
VL 19
IS 6
BP 585
EP 589
DI 10.1016/j.aohep.2019.09.007
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA OL4WM
UT WOS:000585342300002
PM 31711913
OA gold
DA 2025-01-07
ER
PT J
AU Du, Y
Zhang, WC
Qiu, H
Xiao, CJ
Shi, J
Reid, LM
He, ZY
AF Du, Yuan
Zhang, Wencheng
Qiu, Hua
Xiao, Canjun
Shi, Jun
Reid, Lola M.
He, Zhiying
TI Mouse Models of Liver Parenchyma Injuries and Regeneration
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE mouse models; liver diseases; liver regeneration; cell transplantation;
cell therapies; transgenic mice
ID HEPATIC STEM-CELLS; EXPERIMENTAL AUTOIMMUNE HEPATITIS; C
VIRUS-INFECTION; PARTIAL-HEPATECTOMY; NONALCOHOLIC STEATOHEPATITIS;
CARBON-TETRACHLORIDE; XENO-REPOPULATION; HUMAN HEPATOCYTES;
IMMUNE-SYSTEM; MURINE MODEL
AB Mice have genetic and physiological similarities with humans and a well-characterized genetic background that is easy to manipulate. Murine models have become the most favored, robust mammalian systems for experimental analyses of biological processes and disease conditions due to their low cost, rapid reproduction, a wealth of mouse strains with defined genetic conditions (both native ones as well as ones established experimentally), and high reproducibility with respect to that which can be done in experimental studies. In this review, we focus on murine models for liver, an organ with renown regenerative capacity and the organ most central to systemic, complex metabolic and physiological functions for mammalian hosts. Establishment of murine models has been achieved for all aspects of studies of normal liver, liver diseases, liver injuries, and regenerative repair mechanisms. We summarize key information on current mouse systems that partially model facets of clinical scenarios, particularly those associated with drug-induced acute or chronic liver injuries, dietary related, non-alcoholic liver disease (NAFLD), hepatitis virus infectious chronic liver diseases, and autoimmune hepatitis (AIH). In addition, we also include mouse models that are suitable for studying liver cancers (e.g., hepatocellular carcinomas), the aging process (senescence, apoptosis), and various types of liver injuries and regenerative processes associated with them.
C1 [Du, Yuan; Qiu, Hua; Xiao, Canjun; Shi, Jun; He, Zhiying] Tongji Univ, Jian Hosp, Shanghai East Hosp, Sch Med,Dept Gen Surg, Jian, Peoples R China.
[Du, Yuan; Zhang, Wencheng; Qiu, Hua; He, Zhiying] Tongji Univ, Shanghai East Hosp, Inst Regenerat Med, Sch Life Sci & Technol, Shanghai, Peoples R China.
[Du, Yuan; Qiu, Hua; Shi, Jun] Nanchang Univ, Affiliated Hosp 1, Nanchang, Peoples R China.
[He, Zhiying] Shanghai Inst Stem CellResearch & Clin Translat, Shanghai, Peoples R China.
[He, Zhiying] Shanghai Engn Res Ctr Stem Cells Translat Med, Shanghai, Peoples R China.
[Reid, Lola M.] UNC Sch Med, Dept Cell Biol & Physiol, Program Mol Biol & Biotechnol, Chapel Hill, NC USA.
C3 Tongji University; Tongji University; Nanchang University; University of
North Carolina School of Medicine
RP Shi, J; He, ZY (corresponding author), Tongji Univ, Jian Hosp, Shanghai East Hosp, Sch Med,Dept Gen Surg, Jian, Peoples R China.; He, ZY (corresponding author), Tongji Univ, Shanghai East Hosp, Inst Regenerat Med, Sch Life Sci & Technol, Shanghai, Peoples R China.; He, ZY (corresponding author), Shanghai Inst Stem CellResearch & Clin Translat, Shanghai, Peoples R China.; He, ZY (corresponding author), Shanghai Engn Res Ctr Stem Cells Translat Med, Shanghai, Peoples R China.; Reid, LM (corresponding author), UNC Sch Med, Dept Cell Biol & Physiol, Program Mol Biol & Biotechnol, Chapel Hill, NC USA.
EM zyhe@tongji.edu.cn; stemcell@med.unc.edu; Lola.M.Reid@gmail.com
RI Zhang, Wencheng/ABF-9335-2021
OI ZHANG, WENCHENG/0000-0003-2848-1611; he, zhiying/0000-0002-0087-2277
FU Major Program of National Key Research and Development Project
[2020YFA0112600, 2019YFA0801502]; Jiangxi Provincial Natural Science
Foundation [20212ACB206033]; National Natural Science Foundation of
China [82173019]; Shanghai Pujiang Program [21PJD059]; Project of
Shanghai Science and Technology Commission [22ZR1451100, 19140902900];
Program of Shanghai Academic/Technology Research Leader [20XD1434000];
Shanghai Engineering Research Center of Stem Cells Translational
Medicine [20DZ2255100]; UNC School of Medicine, Chapel Hill, NC;
Fibrolamellar Carcinoma Foundation (Greenwich, CT); Peak Disciplines
(Type IV) of Institutions of Higher Learning in Shanghai
FX This work was funded by Major Program of National Key Research and
Development Project (2020YFA0112600, 2019YFA0801502), Jiangxi Provincial
Natural Science Foundation (20212ACB206033), National Natural Science
Foundation of China (82173019), Shanghai Pujiang Program (21PJD059), the
Project of Shanghai Science and Technology Commission (22ZR1451100,
19140902900), Program of Shanghai Academic/Technology Research Leader
(20XD1434000), Peak Disciplines (Type IV) of Institutions of Higher
Learning in Shanghai, and Shanghai Engineering Research Center of Stem
Cells Translational Medicine (20DZ2255100). LR was funded by the UNC
School of Medicine, Chapel Hill, NC and by the Fibrolamellar Carcinoma
Foundation (Greenwich, CT).
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NR 133
TC 11
Z9 13
U1 2
U2 27
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD MAY 5
PY 2022
VL 10
AR 903740
DI 10.3389/fcell.2022.903740
PG 16
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA 1J5CR
UT WOS:000797936700001
PM 35721478
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Machida, T
Takahashi, T
Itoh, T
Hirayama, M
Morita, T
Horita, S
AF Machida, Takuro
Takahashi, Toshiyuki
Itoh, Tomoo
Hirayama, Michiaki
Morita, Takayuki
Horita, Shoichi
TI Reactive lymphoid hyperplasia of the liver: A case report and review of
literature
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE reactive lymphoid hyperplasia; pseudolymphoma; hepatocellular carcinoma;
autoimmune thyroiditis; immunohistochemistry
ID MALIGNANT-LYMPHOMA; PSEUDOLYMPHOMA; DISORDER; THERAPY; DISEASE
AB A case of a 53-year-old female patient with reactive lymphoid hyperplasia (RLH), clinically designated as pseudolymphoma of the liver is described in this article. The patient was admitted to our hospital for further evaluation of hepatic tumors incidentally discovered at another hospital. Various diagnostic methods, including ultrasonography (US), computerized tomography (CT), magnetic resonance imaging (MRI) and hepatic angiography displayed three small lesions in the liver with outstanding findings consistent with hepatocellular carcinoma (HCC). Surgical resection was performed and the three lesions were microscopically diagnosed as RLH of the liver. The lesions comprised a massive infiltration of lymphoid cells with follicles and hyalinized interfollicular spaces. Immunohistochemical examination revealed that infiltrating lymphocytes had no prominent nuclear atypia and polyclonality. RLH of the liver is a very rare condition and only twelve cases have been reported in the English literature. Majority of the reported cases were middle-aged women and about half of them had some immunologic abnormalities such as autoimmune thyroiditis, Sjogren's syndrome, primary immunodeficiency, primary biliary cirrhosis. Since they are often clinically misdiagnosed as HCC, surgery is the choice of treatment for these patients. Although their pathology resembles malignant lymphoma, the clinical course is completely benign. The authors propose that RLH of the liver can be discriminated from HCC by its clinical features. (C) 2007 WJG. All rights reserved.
C1 Hokkaido Gastroenterol Hosp, Dept Pathol, Higashi Ku, Sapporo, Hokkaido 0650041, Japan.
Hokkaido Gastroenterol Hosp, Dept Internal Med, Sapporo, Hokkaido 0650041, Japan.
Hokkaido Univ Hosp, Dept Pathol, Sapporo, Hokkaido 0608648, Japan.
Hokkaido Gastroenterol Hosp, Dept Surg, Sapporo, Hokkaido 0650041, Japan.
C3 Hokkaido University
RP Takahashi, T (corresponding author), Hokkaido Gastroenterol Hosp, Dept Pathol, Higashi Ku, 1-1-2-10, Sapporo, Hokkaido 0650041, Japan.
EM ricoh@hgh.or.jp
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NR 19
TC 41
Z9 46
U1 0
U2 4
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD OCT 28
PY 2007
VL 13
IS 40
BP 5403
EP 5407
DI 10.3748/wjg.v13.i40.5403
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 212OM
UT WOS:000249606700022
PM 17879417
OA Green Published
DA 2025-01-07
ER
PT J
AU Kim, J
Kang, W
Sinn, DH
Gwak, GY
Paik, YH
Choi, MS
Lee, JH
Koh, KC
Paik, SW
AF Kim, Jihye
Kang, Wonseok
Sinn, Dong Hyun
Gwak, Geum-Youn
Paik, Yong-Han
Choi, Moon Seok
Lee, Joon Hyeok
Koh, Kwang Cheol
Paik, Seung Woon
TI Potential etiology, prevalence of cirrhosis, and mode of detection among
patients with non-B non-C hepatocellular carcinoma in Korea
SO KOREAN JOURNAL OF INTERNAL MEDICINE
LA English
DT Article
DE Non-B non-C; Carcinoma, hepatocellular; Etiology; Liver cirrhosis
ID FATTY LIVER-DISEASE; VIRUS INFECTION; HEPATITIS; STRATEGIES; FIBROSIS;
NAFLD
AB Background/Aims: We systematically evaluated the clinical characteristics, prevalence of cirrhosis, and mode of detection in virus-unrelated (non-B non-C, NBNC) hepatocellular carcinoma (HCC) patients in Korea.
Methods: A total of 447 consecutive treatment-naive NBNC-HCC adult patients who were registered at the Samsung Medical Center HCC registry in Korea from 2010 to 2013 were analyzed. NBNC was defined as negative hepatitis B surface antigen and negative anti-hepatitis C virus antibody. Presence of cirrhosis was determined based on histological, radiological, endoscopic, and serologic results. Mode of detection was classified as either under surveillance, incidental, or symptomatic.
Results: Heavy alcohol use was the most common potential etiology in NBNC-HCC (NBNC -A, alcohol) (59.7%). Ten patients had other identifiable causes (NBNC-O, other identifiable cause) such as autoimmune hepatitis. The rest (38.0%) had no-identifiable cause (NBNC-NA-NO, non-alcohol, no-other identifiable cause). In NBNC-NA-NO group, 83.5% (96/115) of patients with available hepatitis B core immunoglobulin G antibody (HBcIgG) showed HBcIgG positivity, and 80.6% (137/170) had metabolic risk factors (diabetes, obesity, hypertension, and/ or dyslipidemia). Cirrhosis was present in 90.0%, 70.4%, and 60.0% of NBNC-O, NBNC-A, and NBNC-NA-NO patients, respectively. The proportion of patients diagnosed under surveillance was 25.5% across all patients, with specific proportions being 80.0%, 27.7%, and 18.8% for NBNC-O, NBNC-A, and NBNC-NA-NO, respectively.
Conclusions: Among NBNC-HCC patients, heavy alcohol use or any other identifiable cause was not found in 38.0%. These NBNC-NA-NO HCC patients showed a high prevalence of HBcIgG positivity and metabolic risk factors, suggesting that prior hepatitis B virus infection and metabolic risk factors may be major contributing factors in the hepatocarcinogenesis in NBNC-NA-NO patients.
C1 [Kim, Jihye; Kang, Wonseok; Sinn, Dong Hyun; Gwak, Geum-Youn; Paik, Yong-Han; Choi, Moon Seok; Lee, Joon Hyeok; Koh, Kwang Cheol; Paik, Seung Woon] Sungkyunkwan Univ, Samsung Med Ctr, Dept Med, Sch Med, 81 Irwon Ro, Seoul 06351, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center
RP Paik, SW (corresponding author), Sungkyunkwan Univ, Samsung Med Ctr, Dept Med, Sch Med, 81 Irwon Ro, Seoul 06351, South Korea.
EM sw.paik@samsung.com
RI Sinn, Dong/JAC-4247-2023; Gwak, Geum/F-4605-2014
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NR 28
TC 9
Z9 9
U1 0
U2 5
PU KOREAN ASSOC INTERNAL MEDICINE
PI SEOUL
PA 101-2501 LOTTE CASTLE PRESIDENT, 109 MAPO-DAERO, MAPO-GU, SEOUL, SOUTH
KOREA
SN 1226-3303
EI 2005-6648
J9 KOREAN J INTERN MED
JI Korean J. Intern. Med.
PD JAN
PY 2020
VL 35
IS 1
BP 65
EP +
DI 10.3904/kjim.2018.040
PG 17
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA JZ6IT
UT WOS:000505206100007
PM 31189301
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Du, Y
Chen, X
Huang, ZM
Ye, XH
Niu, Q
AF Du, Yong
Chen, Xin
Huang, Zhi-Ming
Ye, Xiao-Hua
Niu, Qing
TI Increased Frequency of Foxp3+Regulatory T Cells in Mice with
Hepatocellular Carcinoma
SO ASIAN PACIFIC JOURNAL OF CANCER PREVENTION
LA English
DT Article
DE Hepatocellular carcinoma; regulatory T cell; CD4+CD25+T cell; Foxp3;
Granzyme B
ID PERIPHERAL-BLOOD; FOXP3 EXPRESSION; TUMOR; MECHANISM; CANCER;
SUPPRESSION; INDUCTION; SUBSET; CD25
AB The CD4+CD25+ regulatory T cell (Treg) is a special kind of T cell subset. Studies have showed that Treg cells are involved in a number of physiological processes and pathologic conditions such as autoimmune diseases, transplantation tolerance and cancer. Tregs with unique capacity for immune inhibition can impair anti-tumour immunity and help tumor cells to escape from immune surveillance. The aim of our study was to investigate whether Tregs are involved in hepatocellular carcinoma (HCC). A BABL/C mouse with HCC in situ model was established to evaluate the Treg existence in carcinoma tissues and the changes of Tregs in spleen using flow cytometry and immunohistochemistry methods. Granzyme B expression in carcinoma tissues was analyzed by immunohistochemistry to investigate the tumor local immune status. The proportion of CD4+CD25+/CD4+ spleen lymphocytes of tumor bearing mice (18.8%+/- 1.26%) was found to be significantly higher than that in normal mice (9.99%+/- 1.90%) (P<0.01). Immunohistochemistry of spleen tissue also confirmed that there was an increase in Treg in tumor-bearing mice, while in carcinomas it showed Treg cells to be present in tumor infiltrating lymphocyte areas while Granzyme B was rarely observed. Anti-tumour immunity was suppressed, and this might be associated with the increase of Tregs. Our observations suggest that the CD4+CD25+Treg/CD4+ proportion in spleen lymphocytes can be a sensitive index to evaluate the change of Tregs in hepatocellular carcinoma mice and the Treg may be a promising therapeutic target for cancer.
C1 [Du, Yong; Chen, Xin; Huang, Zhi-Ming; Ye, Xiao-Hua] Wenzhou Med Coll, Affiliated Hosp 1, Dept Gastroenterol & Hepatol, Wenzhou, Peoples R China.
[Niu, Qing] Wenzhou Med Coll, Zhejiang Prov Key Lab Med Genet, Wenzhou, Peoples R China.
C3 Wenzhou Medical University; Wenzhou Medical University
RP Huang, ZM (corresponding author), Wenzhou Med Coll, Affiliated Hosp 1, Dept Gastroenterol & Hepatol, Wenzhou, Peoples R China.
EM huangzhiming63@yahoo.cn
FU Foundation of Zhejiang province natural science
FX This research was supported by the Foundation of Zhejiang province
natural science.
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Z9 20
U1 0
U2 8
PU ASIAN PACIFIC ORGANIZATION CANCER PREVENTION
PI GYEONGGI-DO
PA APJCP HEAD OFFICE, KOREAN NATL CANCER CENTER, 323 ILAN -RO,
ILSANDONG-GU, GOYANG-SI, GYEONGGI-DO, 410-769, SOUTH KOREA
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BP 3815
EP 3819
DI 10.7314/APJCP.2012.13.8.3815
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 042GJ
UT WOS:000311459400047
PM 23098476
OA gold
DA 2025-01-07
ER
PT J
AU Manzoor, R
Ahmed, W
Afify, N
Memon, M
Yasin, M
Memon, H
Rustom, M
Al Akeel, M
Alhajri, N
AF Manzoor, Ridda
Ahmed, Weshah
Afify, Nariman
Memon, Mashal
Yasin, Maryam
Memon, Hamda
Rustom, Mohammad
Al Akeel, Mohannad
Alhajri, Noora
TI Trust Your Gut: The Association of Gut Microbiota and Liver Disease
SO MICROORGANISMS
LA English
DT Review
DE dysbiosis; Firmicutes; Bacteroidetes; liver disease; NALFD; ALD; liver
cirrhosis; hepatocellular carcinoma; autoimmune hepatitis
ID PRIMARY SCLEROSING CHOLANGITIS; FECAL BILE-ACID;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; INTESTINAL MICROBIOTA;
NONALCOHOLIC STEATOHEPATITIS; CIRRHOSIS; PROBIOTICS; DYSBIOSIS;
EPIDEMIOLOGY
AB The gut microbiota composition is important for nutrient metabolism, mucosal barrier function, immunomodulation, and defense against pathogens. Alterations in the gut microbiome can disturb the gut ecosystem. These changes may lead to the loss of beneficial bacteria or an increase in potentially pathogenic bacteria. Furthermore, these have been shown to contribute to the pathophysiology of gastrointestinal and extra-intestinal diseases. Pathologies of the liver, such as non-alcoholic liver disease, alcoholic liver disease, cirrhosis, hepatocellular carcinoma, autoimmune hepatitis, viral hepatitis, and primary sclerosing cholangitis have all been linked to changes in the gut microbiome composition. There is substantial evidence that links gut dysbiosis to the progression and complications of these pathologies. This review article aimed to describe the changes seen in the gut microbiome in liver diseases and the association between gut dysbiosis and liver disease, and finally, explore treatment options that may improve gut dysbiosis in patients with liver disease.
C1 [Manzoor, Ridda; Ahmed, Weshah; Afify, Nariman; Memon, Mashal; Yasin, Maryam; Memon, Hamda; Rustom, Mohammad] Khalifa Univ, Coll Med & Hlth Sci, POB 127788, Abu Dhabi, U Arab Emirates.
[Al Akeel, Mohannad] Dept Hlth, Div Family Med, POB 5674, Abu Dhabi, U Arab Emirates.
[Alhajri, Noora] Sheikh Shakhbout Med City SSMC, Dept Med, POB 11001, Abu Dhabi, U Arab Emirates.
C3 Khalifa University of Science & Technology
RP Alhajri, N (corresponding author), Sheikh Shakhbout Med City SSMC, Dept Med, POB 11001, Abu Dhabi, U Arab Emirates.
EM 100052897@ku.ac.ae; 100043004@ku.ac.ae; 100049875@ku.ac.ae;
100049880@ku.ac.ae; 100052896@kmac.ae; 100058242@ku.ac.ae;
100058284@kmac.ae; mohanadalakeel@gmail.com; nalhajri007@gmail.com
OI Rustom, Mohammad/0000-0002-5374-5132; Alhajri, Noora/0000-0001-7205-7493
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NR 161
TC 22
Z9 24
U1 2
U2 27
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-2607
J9 MICROORGANISMS
JI Microorganisms
PD MAY
PY 2022
VL 10
IS 5
AR 1045
DI 10.3390/microorganisms10051045
PG 30
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA 1S8FQ
UT WOS:000804280900001
PM 35630487
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Czaja, AJ
AF Czaja, Albert J.
TI Autoimmune liver disease
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Article
DE diagnostic features; pathogenic mechanisms; therapeutic options
ID PRIMARY BILIARY-CIRRHOSIS; PLASMA-CELL HEPATITIS; REGULATORY T-CELLS;
ANTIMITOCHONDRIAL-ANTIBODIES; CLINICAL-FEATURES;
HEPATOCELLULAR-CARCINOMA; OVERLAP SYNDROMES; VIRUS-INFECTION;
CELIAC-DISEASE; RISK-FACTORS
AB Purpose of review
To review studies that improve the diagnosis and treatment of autoimmune hepatitis and extend the understanding of its pathogenic mechanisms.
Recent findings
A simplified diagnostic scoring system has high sensitivity and specificity. Biliary changes detected by MRI are of uncertain nature and significance. New candidate autoantigens have been identified by proteomic analyses. T regulatory cells suppress disease activity; their adoptive transfer is beneficial in animal models. Budesonide in combination with azathioprine is effective frontline therapy. Bone marrow-derived mesenchymal stem cell transplantation may emerge as salvage therapy. Screening for hepatocellular cancer is justified. Racial disparities in disease severity, mortality, and treatment remain unexplained.
Summary
Diagnosis has been simplified and management strategies have been upgraded. Biliary changes have been recognized but are of uncertain nature and significance. New antigens and antibodies have been described. T-cell populations that modulate disease activity have been characterized, and adoptive transfer of T regulatory cells is possible. Budesonide in combination with azathioprine is effective frontline therapy, and therapeutic interventions that target critical pathogenic mechanisms are feasible.
C1 Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Czaja, AJ (corresponding author), Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, 200 1st St SW, Rochester, MN 55905 USA.
EM czaja.albert@mayo.edu
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NR 68
TC 18
Z9 20
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0267-1379
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD MAY
PY 2009
VL 25
IS 3
BP 215
EP 222
DI 10.1097/MOG.0b013e328324ed06
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 443EH
UT WOS:000265892500008
PM 19387256
DA 2025-01-07
ER
PT J
AU Gelson, W
Hoare, M
Dawwas, MF
Vowler, S
Gibbs, P
Alexander, G
AF Gelson, William
Hoare, Matthew
Dawwas, M. F.
Vowler, Sarah
Gibbs, Paul
Alexander, Graeme
TI The Pattern of Late Mortality in Liver Transplant Recipients in the
United Kingdom
SO TRANSPLANTATION
LA English
DT Article
DE Liver transplantation; Complications of liver transplantation; Immune
suppression
ID SURVIVAL
AB Background. Late survival is not improving after liver transplantation. In this study, possible reasons for this were investigated.
Methods. Mortality rates and causes of death were ascertained in 4483 adult primary liver allograft recipients surviving 1 year or more from engraftment, identified through the UK Transplant Database and transplanted between 1994 and 2007. Associations with death, cause of death, and retransplantation were assessed.
Results. Mortality in those surviving beyond 1 year in UK liver transplant recipients was more than twice that expected in the general population and had not improved during the study period, independent of cause of liver disease, recipient age, recipient gender, and donor age. The major causes of death were malignancy (30.6%), multisystem failure (10.0%), infection (9.8%), cardiac disease (8.7%), and graft failure (9.8%). Associations with death after 1 year were pretransplant etiologies alcohol-related liver disease (hazard ratio [HR] = 2.10), autoimmune hepatitis or cryptogenic (HR = 1.68), hepatitis C virus (HR = 2.51), and hepatocellular carcinoma (HR = 4.19). Associations with retransplantation were recipient age (HR = 0.95 per year), donor age (HR = 1.02 per year), and hepatitis C virus (HR = 2.04). Hepatocellular carcinoma and recipient age were associated with cancer-related death (odds ratio = 1.87 and 1.02 per year). Recipient age was associated with cardiac death (odds ratio = 1.06 per year).
Conclusions. Strategies to reduce late mortality after liver transplantation are required. These may include prevention of disease recurrence, improved recipient selection, and addressing risk factors for death in late survivors of liver transplantation.
C1 [Gelson, William; Hoare, Matthew; Dawwas, M. F.; Alexander, Graeme] Univ Cambridge, Dept Med, Cambridge CB2 2QQ, England.
[Vowler, Sarah] Univ Cambridge, Ctr Appl Med Stat, Cambridge, England.
[Gibbs, Paul] Univ Cambridge, Dept Surg, Cambridge, England.
C3 University of Cambridge; University of Cambridge; University of
Cambridge
RP Alexander, G (corresponding author), Cambridge Univ Hosp NHS Trust, Dept Med, Box 157, Cambridge CB0 2QQ, England.
EM gja1000@doctors.org.uk
OI Hoare, Matthew/0000-0001-5990-9604
FU British Transplantation Society; Wellcome Trust; Frank Litchfield
Charitable Trust; Cambridge Hepatology Endowment Fund
FX This work was supported by the British Transplantation Society (W.G.),
the Wellcome Trust (M.H.), The Frank Litchfield Charitable Trust, and
Cambridge Hepatology Endowment Fund.
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NR 13
TC 74
Z9 75
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD JUN 15
PY 2011
VL 91
IS 11
BP 1240
EP 1244
DI 10.1097/TP.0b013e31821841ba
PG 5
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA 769JN
UT WOS:000291008800016
PM 21516069
OA Bronze
DA 2025-01-07
ER
PT J
AU Goel, A
Kwong, A
AF Goel, Aparna
Kwong, Allison
TI CAQ Corner: Disease recurrence after liver transplantation
SO LIVER TRANSPLANTATION
LA English
DT Review
ID PRIMARY SCLEROSING CHOLANGITIS; HEPATITIS-B-VIRUS; PRIMARY
BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
MANAGEMENT; IMPACT; RISK; MULTICENTER; RECIPIENTS
C1 [Goel, Aparna; Kwong, Allison] Stanford Univ, Div Gastroenterol Hepatol, Palo Alto, CA 94304 USA.
C3 Stanford University
RP Goel, A (corresponding author), 430 Broadway St Pavill C,3rd Floor, Redwood City, CA 94063 USA.
EM goela21@stanford.edu
OI Kwong, Allison/0000-0002-3874-6612; Goel, Aparna/0000-0001-9588-9364
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NR 50
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1527-6465
EI 1527-6473
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD JUL
PY 2023
VL 29
IS 7
BP 768
EP 776
DI 10.1002/lt.26492
EA MAY 2022
PG 9
WC Gastroenterology & Hepatology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA K4TR6
UT WOS:000800212800001
PM 35466545
DA 2025-01-07
ER
PT J
AU Hu, S
Lian, PP
Hu, Y
Zhu, XY
Jiang, SW
Ma, Q
Li, LY
Yang, JF
Yang, L
Guo, HY
Zhou, H
Yang, CC
Meng, XM
Li, J
Li, HW
Xu, T
Zhou, H
AF Hu, Shuang
Lian, Pan-pan
Hu, Ying
Zhu, Xing-yu
Jiang, Shao-wei
Ma, Qiang
Li, Liang-yun
Yang, Jun-fa
Yang, Li
Guo, Hai-yue
Zhou, Hong
Yang, Chen-chen
Meng, Xiao-ming
Li, Jun
Li, Hai-wen
Xu, Tao
Zhou, Huan
TI The Role of IL-35 in the Pathophysiological Processes of Liver Disease
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE Interleukin-35; liver diseases; lipid accumulation; cellular
proliferation; hepatocellular carcinoma
ID CHRONIC HEPATITIS-C; REGULATORY T-CELLS; HELPER 17 CELLS;
CLINICAL-SIGNIFICANCE; AUTOIMMUNE HEPATITIS; EXPRESSION LEVELS;
SUPPRESSOR-CELLS; B-CELLS; INTERLEUKIN-35; FREQUENCY
AB It is known that liver diseases have several characteristics of massive lipid accumulation and lipid metabolic disorder, and are divided into liver inflammation, liver fibrosis, liver cirrhosis (LC), and hepatocellular carcinoma (HCC) in patients. Interleukin (IL)-35, a new-discovered cytokine, can protect the liver from the environmental attack by increasing the ratio of Tregs (T regulatory cells) which can increase the anti-inflammatory cytokines and inhibit the proliferation of immune cellular. Interestingly, two opposite mechanisms (pro-inflammatory and anti-inflammatory) have connection with the ultimate formation of liver diseases, which suggest that IL-35 may play crucial function in the process of liver diseases through immunosuppressive regulation. Besides, some obvious advantages also imply that IL-35 can be considered as a new therapeutic target to control the progression of liver diseases, while its mechanism of function still needs further research.
C1 [Hu, Shuang; Hu, Ying; Li, Liang-yun; Yang, Jun-fa; Yang, Li; Guo, Hai-yue; Zhou, Hong; Yang, Chen-chen; Meng, Xiao-ming; Li, Jun; Xu, Tao] Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Anhui Inst Innovat Drugs, Sch Pharm, Hefei, Peoples R China.
[Hu, Shuang; Hu, Ying; Li, Liang-yun; Yang, Jun-fa; Yang, Li; Guo, Hai-yue; Zhou, Hong; Yang, Chen-chen; Meng, Xiao-ming; Li, Jun; Xu, Tao] Anhui Med Univ, Inst Liver Dis, Hefei, Peoples R China.
[Lian, Pan-pan] Nanjing Univ, Sch Pharm, Nanjing, Peoples R China.
[Zhu, Xing-yu; Zhou, Huan] Bengbu Med Coll, Affiliated Hosp 1, Natl Drug Clin Trial Inst, Bengbu, Peoples R China.
[Jiang, Shao-wei] Anhui Med Univ, Affiliated Hosp 1, Hefei, Peoples R China.
[Ma, Qiang] Anhui Med Univ, Affiliated Hosp 2, Hefei, Peoples R China.
[Li, Hai-wen] Zhengzhou Univ, Affiliated Hosp 1, Affiliated Hosp 3, Anhui Med Univ, Zhengzhou, Peoples R China.
C3 Anhui Medical University; Anhui Medical University; Nanjing University;
Bengbu Medical University; Anhui Medical University; Anhui Medical
University; Zhengzhou University; Anhui Medical University
RP Xu, T (corresponding author), Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Anhui Inst Innovat Drugs, Sch Pharm, Hefei, Peoples R China.; Xu, T (corresponding author), Anhui Med Univ, Inst Liver Dis, Hefei, Peoples R China.; Zhou, H (corresponding author), Bengbu Med Coll, Affiliated Hosp 1, Natl Drug Clin Trial Inst, Bengbu, Peoples R China.
EM xutao@ahmu.edu.cn; zhouhuanbest@163.com
RI Xu, Tao/P-9130-2015; Zhu, Xingyu/KCY-9917-2024; Jiang,
Shaowei/LXA-3944-2024
FU National Natural Science Foundation of China [81700522, 81602344];
Natural Science Foundation of Anhui Province [2008085QH401,
1808085MH235]; 512 Talent Cultivation Plan of Bengbu Medical College
[by51201315]
FX This project was supported by the National Natural Science Foundation of
China (Nos. 81700522, 81602344), Natural Science Foundation of Anhui
Province (1808085MH235), 512 Talent Cultivation Plan of Bengbu Medical
College (by51201315), Natural Science Foundation of Anhui Province
(2008085QH401).
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NR 100
TC 4
Z9 5
U1 3
U2 23
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD JAN 21
PY 2021
VL 11
AR 569575
DI 10.3389/fphar.2020.569575
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA QB6RS
UT WOS:000614268500001
PM 33584256
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Jiang, YT
Chen, SG
Jia, SS
Zhu, ZS
Gao, XR
Dong, D
Gao, YZ
AF Jiang, Yuting
Chen, Shougong
Jia, Shasha
Zhu, Zhansheng
Gao, Xueren
Dong, Dong
Gao, Yuzhen
TI Association of HLA-G 3′ UTR 14-bp Insertion/Deletion
Polymorphism with Hepatocellular Carcinoma Susceptibility in a Chinese
Population
SO DNA AND CELL BIOLOGY
LA English
DT Article
ID RECURRENT SPONTANEOUS-ABORTIONS; ANTIGEN-G EXPRESSION; G GENE; DELETION
POLYMORPHISM; CLINICAL-RELEVANCE; PROGNOSIS; RISK; THERAPY; CANCER;
REGION
AB The 14-bp insertion/deletion (indel) polymorphism located in the 30 UTR of the human leukocyte antigen-G (HLA-G) gene plays a role in several autoimmune and chronic inflammatory diseases. HLA-G expression is associated with hepatocellular carcinoma (HCC) prognosis, especially in early stage, with high expression independently associated with shortened overall survival and increased tumor recurrence. In the present study, we carried out a case-control study in a Chinese population (318 cases and 599 controls) to estimate the susceptibility to HCC associated with the 14-bp indel polymorphism. Logistic regression analysis showed that the heterozygote and the homozygote 14-bp ins/ins confer a lower risk of HCC (adjusted OR = 0.75, 95% CI: 0.57-1.01, p = 0.061; OR = 0.54, 95% CI: 0.30-0.98, p = 0.031, respectively). Hepatitis B virus (HBV) stratification analysis showed that the associations were stronger in the HBV-positive population. Immunohistochemical analysis further showed that HLA-G expression in HCC tissues with 14-bp del/del genotype was more prominent than for heterozygous and 14-bp ins/ins genotype (p < 0.01). Taken together, our results suggested that the HLA-G 14-bp indel polymorphism may be a marker for genetic susceptibility to HCC in Chinese populations. Further studies from different populations with larger sample size are warranted to validate our findings.
C1 [Jiang, Yuting; Chen, Shougong; Jia, Shasha; Zhu, Zhansheng; Gao, Xueren; Dong, Dong; Gao, Yuzhen] Soochow Univ, Coll Med, Dept Forens Med, Suzhou 215123, Jiangsu, Peoples R China.
C3 Soochow University - China
RP Gao, YZ (corresponding author), Soochow Univ, Coll Med, Dept Forens Med, Suzhou 215123, Jiangsu, Peoples R China.
EM yuzhengao@suda.edu.cn
RI Jiang, Yuting/AAR-5384-2021
FU National Natural Science Foundation of China [30800621]; China
Postdoctoral Science Foundation [20080431121, 200902530]; Shanghai Key
Lab of Forensic Medicine [KF0903]
FX This study was supported by grants from National Natural Science
Foundation of China (No. 30800621), China Postdoctoral Science
Foundation (Nos. 20080431121 and 200902530), and Shanghai Key Lab of
Forensic Medicine (No. KF0903).
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NR 31
TC 47
Z9 55
U1 0
U2 23
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5498
J9 DNA CELL BIOL
JI DNA Cell Biol.
PD DEC
PY 2011
VL 30
IS 12
BP 1027
EP 1032
DI 10.1089/dna.2011.1238
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
GA 863GX
UT WOS:000298151900009
PM 21612396
DA 2025-01-07
ER
PT J
AU Shimizu, Y
Nakano, I
Katano, Y
Shimizu, H
Fukuda, Y
AF Shimizu, Y
Nakano, I
Katano, Y
Shimizu, H
Fukuda, Y
TI Clinical implications of measurement of serum nuclear matrix protein
levels in patients with liver disease
SO HEPATO-GASTROENTEROLOGY
LA English
DT Article
DE nuclear matrix protein; viral hepatitis; hepatocellular carcinoma;
primary biliary cirrhosis; fatty liver
ID CANCER
AB Background/Aims: Serum aminotransferase, a sensitive marker of hepatocellular damage, often poorly correlates with the severity of damage. Serum nuclear matrix protein (NMP), a structural protein released from dead cell nuclei, is investigated as a candidate marker of organ damage in liver disease.
Methodology: Serum NMP and aminotransferase levels of 134 patients with various liver diseases and 26 healthy individuals were examined.
Results: Patients with chronic viral hepatitis showed slightly higher NMP levels (17.8 U/mL; 95% Cl 15.0-20.5 U/mL) than those of healthy individuals (6.05 U/mL; 95% Cl 4.82-7.27 U/mL). Their NMP values had no correlation with aminotransferase levels. NMP levels were similar irrespective of liver disease progression, whereas aminotransferase values decreased in parallel with progression. Patients with autoimmune hepatitis or primary biliary cirrhosis who were under an appropriate treatment as well as individuals with fatty liver showed no elevation of serum NMP levels. Patients with acute viral hepatitis showed very high NMP levels (38.8 U/mL; 95%Cl 27.6-50.0 U/mL) that correlated with serum aminotransferase levels in their sera.
Conclusions: In chronic liver diseases, the serum NMP level elevates to various degrees independent from the degree of aminotransferase elevation. Serum NMP, putatively representing the number of dead cells, is a candidate as an indicator of organ damage severity in liver disease.
C1 Nagoya Univ, Sch Med, Dept Internal Med 2, Showa Ku, Nagoya, Aichi 4668550, Japan.
C3 Nagoya University
RP Nagoya Univ, Sch Med, Dept Internal Med 2, Showa Ku, 65 Tsuruma Cho, Nagoya, Aichi 4668550, Japan.
EM is.nakano@adm.nitech.ac.jp
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NR 13
TC 1
Z9 1
U1 0
U2 2
PU H G E UPDATE MEDICAL PUBLISHING S A
PI ATHENS
PA PO BOX 17257, ATHENS GR-10024, GREECE
SN 0172-6390
J9 HEPATO-GASTROENTEROL
JI Hepato-Gastroenterol.
PD NOV-DEC
PY 2005
VL 52
IS 66
BP 1809
EP 1813
PG 5
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 988RT
UT WOS:000233619100037
PM 16334782
DA 2025-01-07
ER
PT J
AU Lafdil, F
Miller, AM
Ki, SH
Gao, B
AF Lafdil, Fouad
Miller, Andrew M.
Ki, Sung Hwan
Gao, Bin
TI Th17 cells and their associated cytokines in liver diseases
SO CELLULAR & MOLECULAR IMMUNOLOGY
LA English
DT Review
DE IL-17; IL-22; hepatitis; alcoholic liver disease; liver cancer
ID REGULATORY T-CELLS; HEPATITIS-B; MEDIATED HEPATITIS; INNATE IMMUNITY;
INTERLEUKIN-17; HEPATOCYTES; IL-22; MECHANISMS; INFECTION; SURVIVAL
AB T helper 17 (Th17) cells are a newly identified subset of T helper cells that play important roles in host defense against extracellular bacteria as well as in the pathogenesis of autoimmune disease. The functions of Th17 cells are mediated via the production of several cytokines including interleukin (IL)-17 and IL-22. Recent studies show that the frequency of IL-17(+) cells is significantly elevated in a variety of chronic liver diseases including alcoholic liver disease, viral hepatitis and hepatocellular carcinoma. IL-17 receptor is expressed virtually on all types of liver cells, while IL-22 receptor expression is restricted to epithelial cells including hepatocytes in the liver. IL-17 seems to play an important role in inducing liver inflammation via stimulating multiple types of liver nonparenchymal cells to produce proinflammatory cytokines and chemokines, while IL-22 appears to be an important factor in promoting hepatocyte survival and proliferation. Cellular & Molecular Immunology (2010) 7, 250-254; doi:10.1038/cmi.2010.5; published online 22 March 2010
C1 [Lafdil, Fouad; Miller, Andrew M.; Ki, Sung Hwan; Gao, Bin] NIAAA, Sect Liver Biol, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Lafdil, Fouad] Hop Henri Mondor, INSERM, U955, F-94010 Creteil, France.
[Lafdil, Fouad] Univ Paris 12, Fac Med, Creteil, France.
C3 National Institutes of Health (NIH) - USA; NIH National Institute on
Alcohol Abuse & Alcoholism (NIAAA); Universite
Paris-Est-Creteil-Val-de-Marne (UPEC); Institut National de la Sante et
de la Recherche Medicale (Inserm); Assistance Publique Hopitaux Paris
(APHP); Hopital Universitaire Henri-Mondor - APHP; Universite
Paris-Est-Creteil-Val-de-Marne (UPEC)
RP Gao, B (corresponding author), NIAAA, Sect Liver Biol, Lab Physiol Studies, NIH, 5625 Fishers Lane, Bethesda, MD 20892 USA.
EM bgao@mail.nih.gov
RI gao, bin/JYW-5418-2024; lafdil, fouad/T-7939-2018
FU NIAAA, NIH
FX This work was supported by the intramural program of NIAAA, NIH.
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NR 59
TC 115
Z9 135
U1 0
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1672-7681
EI 2042-0226
J9 CELL MOL IMMUNOL
JI Cell. Mol. Immunol.
PD JUL
PY 2010
VL 7
IS 4
BP 250
EP 254
DI 10.1038/cmi.2010.5
PG 5
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 620GQ
UT WOS:000279487500002
PM 20305686
OA Green Published
DA 2025-01-07
ER
PT J
AU Nakakuki, N
Maekawa, S
Takano, S
Osawa, L
Komiyama, Y
Takada, H
Muraoka, M
Suzuki, Y
Sato, M
Enomoto, N
AF Nakakuki, Natsuko
Maekawa, Shinya
Takano, Shinichi
Osawa, Leona
Komiyama, Yasuyuki
Takada, Hitomi
Muraoka, Masaru
Suzuki, Yuichiro
Sato, Mitsuaki
Enomoto, Nobuyuki
TI TCR Repertoire Analysis During Therapeutic Interventions in Liver
Diseases Using Next-Generation Sequencing
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article; Early Access
DE AIH; clonotype; HCC; PBC; TCR repertoire
ID T-CELL
AB Background and Aim: The T cell receptor (TCR) can recognize a vast number of antigens and is closely associated with the pathogenesis of various diseases including autoimmune diseases and malignancies. However, the clinical significance of the TCR repertoire and its post-treatment changes remain unclear in liver diseases. Methods: We performed next-generation sequencing (NGS)-based TCR analysis using DNA obtained from peripheral blood mononuclear cells (PBMCs) of healthy donors (HD, n = 5), primary biliary cholangitis (PBC, n = 5), autoimmune hepatitis (AIH, n = 5), and hepatocellular carcinoma (HCC, n = 5) and evaluated the changes after treatment. Results: Baseline TCR repertoire analysis demonstrated that TCR clonotype usage is restricted and diversity is low in all three disease groups (PBC, AIH, and HCC), particularly in PBC and AIH compared to HD (p < 0.05). Following treatment, clonotype usage and diversity did not change significantly, except in AIH, where diversity decreased further (p < 0.05 for clone Shannon diversity and clone evenness). Disease-specific usage of TCR beta genes and specific changes after therapy were observed in all groups. Analysis of clonotypes shared with other individuals (public clonotypes) revealed that nine public clonotypes in PBC, eight in AIH, and eight in HCC disappeared after treatment. Motif analysis identified one characteristic motif (NQPQH) in PBC. Conclusions: The diversity of the TCR repertoire, TCR beta chain usage, clonotypes, and motifs and their post-treatment changes are disease-specific in each liver disease, indicating that further TCR repertoire studies are needed to accelerate the understanding of liver disease pathogenesis from an immunological perspective.
C1 [Nakakuki, Natsuko; Maekawa, Shinya; Takano, Shinichi; Osawa, Leona; Komiyama, Yasuyuki; Takada, Hitomi; Muraoka, Masaru; Suzuki, Yuichiro; Sato, Mitsuaki; Enomoto, Nobuyuki] Univ Yamanashi, Fac Med, Dept Gastroenterol & Hepatol, Chuo, Yamanashi, Japan.
C3 University of Yamanashi
RP Maekawa, S (corresponding author), Univ Yamanashi, Fac Med, Dept Gastroenterol & Hepatol, Chuo, Yamanashi, Japan.
EM maekawa@yamanashi.ac.jp
FU Japan Society for the Promotion of Science
FX This work was supported by Japan Agency for Medical Research and
Development (JP23fk0210104, JP23fk0210113, JP23fk0210122, JP23fk0210126,
and JP23fk0310501) and Japan Society for the Promotion of Science
(JP22H03057, JP22K15600, and JP23K07458).r No Statement Available
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NR 24
TC 0
Z9 0
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD 2024 DEC 2
PY 2024
DI 10.1111/jgh.16835
EA DEC 2024
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA O0Q1V
UT WOS:001368266900001
PM 39618197
DA 2025-01-07
ER
PT J
AU Nagoshi, S
AF Nagoshi, Sumiko
TI Sex- or gender-specific medicine in hepatology
SO HEPATOLOGY RESEARCH
LA English
DT Review
DE hepatocellular carcinoma; liver disease; sex- or gender-specific
medicine
ID CHRONIC HEPATITIS-C; PRIMARY BILIARY-CIRRHOSIS; FATTY LIVER-DISEASE;
PRIMARY SCLEROSING CHOLANGITIS; TYPE-1 AUTOIMMUNE HEPATITIS;
HEPATOCELLULAR-CARCINOMA; NATURAL-HISTORY; VIRUS-INFECTION;
RISK-FACTORS; FIBROSIS PROGRESSION
AB Sex- or gender-specific medicine is an up-to-date medical science in recent medical care. Medical doctors must offer better medical care and should understand and elucidate the mechanisms underlying the sex or gender differences regarding the incidence or etiology, clinical features, and natural history or response to therapies. Sex or gender differences are frequently seen among liver diseases, such as viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis and hepatocellular carcinoma. The mechanisms of sex or gender differences, however, are still unclear. Clinicians and basic scientists are required to cooperatively contribute to the development of sex- or gender-specific medicine to establish an accurate diagnosis and prophylaxis.
C1 Saitama Med Univ, Dept Internal Med, Div Gastroenterol & Hepatol, Saitama, Japan.
C3 Saitama Medical University
RP Nagoshi, S (corresponding author), Saitama Med Univ, Dept Internal Med, Div Gastroenterol & Hepatol, Saitama, Japan.
EM snagoshi@saitama-med.ac.jp
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NR 59
TC 12
Z9 12
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD MAR
PY 2008
VL 38
IS 3
BP 219
EP 224
DI 10.1111/j.1872-034X.2007.00301.x
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 257OV
UT WOS:000252809300001
PM 18047583
DA 2025-01-07
ER
PT J
AU Unagolla, JM
Das, S
Flanagan, R
Oehler, M
Menon, JU
AF Unagolla, Janitha M.
Das, Subarna
Flanagan, Riley
Oehler, Marin
Menon, Jyothi U.
TI Targeting chronic liver diseases: Molecular markers, drug delivery
strategies and future perspectives
SO INTERNATIONAL JOURNAL OF PHARMACEUTICS
LA English
DT Article
DE MASH; MASLD; ALD; Hepatitis; Biomarkers; Liver; Nanoparticles; Drug
delivery
ID HEPATIC STELLATE CELLS; SINUSOIDAL ENDOTHELIAL-CELLS; RANDOMIZED
CONTROLLED-TRIAL; PH-SENSITIVE NANOPARTICLES; SEVERE ALCOHOLIC
HEPATITIS; NONALCOHOLIC STEATOHEPATITIS; KUPFFER CELLS; FATTY LIVER;
HEPATOCELLULAR-CARCINOMA; FIBROSIS
AB Chronic liver inflammation, a pervasive global health issue, results in millions of annual deaths due to its progression from fibrosis to the more severe forms of cirrhosis and hepatocellular carcinoma (HCC). This insidious condition stems from diverse factors such as obesity, genetic conditions, alcohol abuse, viral infections, autoimmune diseases, and toxic accumulation, manifesting as chronic liver diseases (CLDs) such as metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated steatohepatitis (MASH), alcoholic liver disease (ALD), viral hepatitis, drug-induced liver injury, and autoimmune hepatitis. Late detection of CLDs necessitates effective treatments to inhibit and potentially reverse disease progression. However, current therapies exhibit limitations in consistency and safety. A potential breakthrough lies in nanoparticle-based drug delivery strategies, offering targeted delivery to specific liver cell types, such as hepatocytes, Kupffer cells, and hepatic stellate cells. This review explores molecular targets for CLD treatment, ongoing clinical trials, recent advances in nanoparticle-based drug delivery, and the future outlook of this research field. Early intervention is crucial for chronic liver disease. Having a comprehensive understanding of current treatments, molecular biomarkers and novel nanoparticle-based drug delivery strategies can have enormous impact in guiding future strategies for the prevention and treatment of CLDs.
C1 [Unagolla, Janitha M.; Das, Subarna; Menon, Jyothi U.] Univ Rhode Isl, Coll Pharm, Dept Biomed & Pharmaceut Sci, 7 Green House Rd, Kingston, RI 02881 USA.
[Flanagan, Riley; Menon, Jyothi U.] Univ Rhode Isl, Dept Chem Engn, Kingston, RI 02881 USA.
[Oehler, Marin] Univ Rhode Isl, Coll Engn, Dept Biomed Engn, Kingston, RI 02881 USA.
C3 University of Rhode Island; University of Rhode Island; University of
Rhode Island
RP Menon, JU (corresponding author), Univ Rhode Isl, Coll Pharm, Dept Biomed & Pharmaceut Sci, 7 Green House Rd, Kingston, RI 02881 USA.
EM jmenon@uri.edu
RI Unagolla, Janitha/JOZ-5768-2023; Menon, Jyothi/S-9255-2019
FU National Institutes of Health [R21 AA029750, R37 CA283937]
FX The graphical abstract and figures were created with Biorender.com .
This work was supported by the National Institutes of Health [grant
numbers R21 AA029750 and R37 CA283937] to J.U.M.
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U1 3
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-5173
EI 1873-3476
J9 INT J PHARMACEUT
JI Int. J. Pharm.
PD JUL 20
PY 2024
VL 660
AR 124381
DI 10.1016/j.ijpharm.2024.124381
EA JUN 2024
PG 21
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XK7E1
UT WOS:001261635200001
PM 38917958
DA 2025-01-07
ER
PT J
AU Kur, P
Kolasa-Wolosiuk, A
Misiakiewicz-Has, K
Wiszniewska, B
AF Kur, Paulina
Kolasa-Wolosiuk, Agnieszka
Misiakiewicz-Has, Kamila
Wiszniewska, Barbara
TI Sex Hormone-Dependent Physiology and Diseases of Liver
SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
LA English
DT Review
DE gender-dependent liver failure; hepatic glucose metabolism; insulin
resistance; type 2 diabetes; metabolic syndrome; hepatic lipid
metabolism; non-alcoholic fatty liver disease; cirrhosis; hepatocellular
carcinoma; transgenic animal models; clinical cases
ID ESTROGEN-RECEPTOR-ALPHA; HEPATITIS-B-VIRUS; HEPATOCELLULAR-CARCINOMA
CELLS; POLYCYSTIC-OVARY-SYNDROME; NF-KAPPA-B; INSULIN-RESISTANCE;
ANDROGEN RECEPTOR; GENDER DISPARITY; NONALCOHOLIC STEATOHEPATITIS;
CARDIOVASCULAR RISK
AB Sexual dimorphism is associated not only with somatic and behavioral differences between men and women, but also with physiological differences reflected in organ metabolism. Genes regulated by sex hormones differ in expression in various tissues, which is especially important in the case of liver metabolism, with the liver being a target organ for sex hormones as its cells express estrogen receptors (ERs: ER alpha, also known as ESR1 or NR3A; ER beta; GPER (G protein-coupled ER, also known as GPR 30)) and the androgen receptor (AR) in both men and women. Differences in sex hormone levels and sex hormone-specific gene expression are mentioned as some of the main variations in causes of the incidence of hepatic diseases; for example, hepatocellular carcinoma (HCC) is more common in men, while women have an increased risk of autoimmune liver disease and show more acute liver failure symptoms in alcoholic liver disease. In non-alcoholic fatty liver disease (NAFLD), the distinction is less pronounced, but increased incidences are suggested among men and postmenopausal women, probably due to an increased tendency towards visceral fat accumulation.
C1 [Kur, Paulina; Kolasa-Wolosiuk, Agnieszka; Misiakiewicz-Has, Kamila; Wiszniewska, Barbara] Pomeranian Med Univ, Fac Med & Dent, Dept Histol & Embryol, Powst Wlkp 72, PL-70111 Szczecin, Poland.
C3 Pomeranian Medical University
RP Kolasa-Wolosiuk, A (corresponding author), Pomeranian Med Univ, Fac Med & Dent, Dept Histol & Embryol, Powst Wlkp 72, PL-70111 Szczecin, Poland.
EM paulina.kur@pum.edu.pl; agnieszka.kolasa@pum.edu.pl;
kamila.misiakiewicz@pum.edu.pl; barbara.wiszniewska@pum.edu.pl
RI Wiszniewska, Barbara/O-3644-2014; Kolasa, Agnieszka/M-5963-2014;
Misiakiewicz-Has, Kamila/A-3030-2015
OI Wiszniewska, Barbara/0000-0002-9064-6969; Kolasa,
Agnieszka/0000-0002-6933-7643; Misiakiewicz-Has,
Kamila/0000-0001-7880-7507
FU statutory activity of the Pomeranian Medical University
[WLA-167-02/S/16/2020]
FX The publishing and English editing of the publication was financed from
funds for research and development (statutory activity of the Pomeranian
Medical University, WLA-167-02/S/16/2020).
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NR 166
TC 99
Z9 106
U1 2
U2 20
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1660-4601
J9 INT J ENV RES PUB HE
JI Int. J. Environ. Res. Public Health
PD APR
PY 2020
VL 17
IS 8
AR 2620
DI 10.3390/ijerph17082620
PG 26
WC Environmental Sciences; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health
GA LR5OL
UT WOS:000535744100005
PM 32290381
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Adhikary, S
Esmeeta, A
Dey, A
Banerjee, A
Saha, B
Gopan, P
Duttaroy, AK
Pathak, S
AF Adhikary, Subhamay
Esmeeta, Akanksha
Dey, Amit
Banerjee, Antara
Saha, Biki
Gopan, Pournami
Duttaroy, Asim K.
Pathak, Surajit
TI Impacts of gut microbiota alteration on age-related chronic liver
diseases
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Review
DE Gut microbiota; Ageing; Non-alcoholic fatty liver disease (NAFLD); and
non-alcoholic steatohepatitis (NASH); Alcoholic liver disease (ALD);
Liver cirrhosis; Hepatocellular carcinoma; Viral hepatitis; Autoimmune
hepatitis (AIH); Immunomodulation; Gut barrier integrity
ID INTESTINAL PERMEABILITY; HEPATIC-ENCEPHALOPATHY; ACID; BACTERIA; CANCER;
HEALTH; SUSCEPTIBILITY; IDENTIFICATION; PATHOGENESIS; MODULATION
AB The gut microbiome and its metabolites are involved in developing and progressing liver disease. Various liver illnesses, such as non-alcoholic fatty liver disease, alcoholic liver disease, hepatitis C, and hepatocellular carcinoma, are made worse and have worse prognoses with aging. Dysbiosis, which occurs when the symbiosis between the microbiota and the host is disrupted, can significantly negatively impact health. Liver disease is linked to qualitative changes, such as an increase in hazardous bacteria and a decrease in good bacteria, as well as quantitative changes in the overall amount of bacteria (overgrowth). Intestinal gut microbiota and their metabolites may lead to chronic liver disease development through various mechanisms, such as increasing gut permeability, persistent systemic inflammation, production of SCFA, bile acids, and alteration in metabolism. Age-related gut dysbiosis can disrupt the communication between gut microbiota and the host, impacting the host's health and lifespan. With aging, a gradual loss of the ability to maintain homeostasis because of structural alteration and gut dysbiosis leads to the disease progression in end-stage liver disease. Recently chronic liver disease has been identified as a global problem. A large number of patients are receiving liver transplants yearly. Thereby gut microbiome ecology is changing in the patients of the gut due to the changes in pathophysiology during the preoperative stage. The present review summarises the age-associated dysbiosis of gut microbial composition and its contribution to chronic liver disease. This review also provides information about the impact of liver transplant on the gut microbiome and possible disadvantageous effects of alteration in gut microbiota. (c) 2023 The Author(s). Published by Elsevier Ltd on behalf of Editrice Gastroenterologica Italiana S.r.l. This is an open access article under the CC BY license ( http://creativecommons.org/licenses/by/4.0/ )
C1 [Adhikary, Subhamay; Dey, Amit; Banerjee, Antara; Saha, Biki; Gopan, Pournami; Pathak, Surajit] Chettinad Hosp & Res Inst CHRI, Chettinad Acad Res & Educ CARE, Fac Allied Hlth Sci, Kelambakkam 603103, India.
[Esmeeta, Akanksha] Amity Univ, Amity Inst Biotechnol, Sect 125, Noida 201301, Uttar Pradesh, India.
[Duttaroy, Asim K.] Univ Oslo, Inst Basic Med Sci, Fac Med, Dept Nutr, Oslo, Norway.
[Duttaroy, Asim K.] Univ Oslo, Inst Basic Med Sci, Fac Med, Dept Nutr, POB 0317, N-1046 Oslo, Norway.
[Pathak, Surajit] Chettinad Acad Res & Educ, Fac Allied Hlth Sci, Dept Med Biotechnol, Kelambakkam 603103, India.
C3 Amity University Noida; University of Oslo; University of Oslo
RP Duttaroy, AK (corresponding author), Univ Oslo, Inst Basic Med Sci, Fac Med, Dept Nutr, POB 0317, N-1046 Oslo, Norway.; Pathak, S (corresponding author), Chettinad Acad Res & Educ, Fac Allied Hlth Sci, Dept Med Biotechnol, Kelambakkam 603103, India.
EM a.k.duttaroy@medisin.uio.no; drsurajitpathak@care.edu.in
RI Banerjee, Antara/AAH-4044-2020; Duttaroy, Asim/J-9499-2016; Pathak,
Surajit/AAH-4022-2020; Adhikary, Subhamay/JYP-3498-2024
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NR 129
TC 8
Z9 8
U1 2
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD JAN
PY 2024
VL 56
IS 1
BP 112
EP 122
DI 10.1016/j.dld.2023.06.017
EA DEC 2023
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FO6W4
UT WOS:001146830800001
PM 37407321
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Ansari, D
Keussen, I
Andersson, R
AF Ansari, Daniel
Keussen, Inger
Andersson, Roland
TI Positron emission tomography in malignancies of the liver, pancreas and
biliary tract - indications and potential pitfalls
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE F-18-fluorodeoxyglucose; biliary tract carcinoma; colorectal liver
metastases; computed tomography; magnetic resonance imaging; pancreatic
cancer; positron emission tomography
ID HEPATOCELLULAR-CARCINOMA; FDG-PET; AUTOIMMUNE PANCREATITIS; F-18-FDG
PET/CT; GALLBLADDER CANCER; HILAR CHOLANGIOCARCINOMA;
DIFFERENTIAL-DIAGNOSIS; COMPUTED-TOMOGRAPHY; CLINICAL ROLE; METASTASES
AB Malignancies of the hepato-pancreatico-biliary (HPB) system are relatively common and generally characterized by a dismal prognosis. Positron emission tomography (PET) is a functional imaging technique that has emerged as an important modality in oncological decision-making. The principal radiopharmaceutical in PET imaging is the glucose analog F-18-fluorodeoxyglucose, which is able to detect altered glucose metabolism in malignant tissue. PET is typically used in conjunction with computed tomography (CT), and previous studies have supported several uses of PET/CT in HPB malignancies, including staging, differential diagnostics and monitoring of treatment response and progress of disease. A review of PET/CT in the context of HPB malignancies will be presented, including indications and potential pitfalls.
C1 [Ansari, Daniel; Andersson, Roland] Lund Univ, Dept Surg, SE-22185 Lund, Sweden.
[Ansari, Daniel; Keussen, Inger; Andersson, Roland] Skane Univ Hosp, SE-22185 Lund, Sweden.
[Keussen, Inger] Lund Univ, Dept Radiol, SE-22185 Lund, Sweden.
C3 Lund University; Lund University; Skane University Hospital; Lund
University
RP Andersson, R (corresponding author), Lund Univ, Dept Surg, SE-22185 Lund, Sweden.
EM roland.andersson@med.lu.se
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NR 60
TC 9
Z9 9
U1 1
U2 7
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD MAR
PY 2013
VL 48
IS 3
BP 259
EP 265
DI 10.3109/00365521.2012.704936
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 095CX
UT WOS:000315313400001
PM 23148675
DA 2025-01-07
ER
PT J
AU Hu, NH
Liu, J
Xue, XY
Li, YX
AF Hu, Naihua
Liu, Jie
Xue, Xinyan
Li, Yunxia
TI The effect of emodin on liver disease - comprehensive advances in
molecular mechanisms
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE Emodin; Liver; Lipid metabolism; Intrahepatic cholestasis; Fibrosis;
Hepatoma; Liver transplantation
ID HEPATIC STELLATE CELLS; ENDOPLASMIC-RETICULUM STRESS;
ISCHEMIA-REPERFUSION INJURY; PATHWAYS IN-VITRO; POLYGONUM-MULTIFLORUM;
SIGNALING PATHWAYS; DENDRITIC CELLS; ACUTE REJECTION; CYCLOPHILIN D;
RAT-LIVER
AB Liver injury could be caused by a variety of causes, including alcohol, drug poisoning, autoimmune overreaction, etc. In the period of liver injury, hepatic stellate cells (HSCs) will be activated and produce excessive extra cellular matrix (ECM). If injury cannot be suppressed, liver injury will develop into fibrosis, even cirrhosis and liver cancer. It is reported that some monomer components extracted from traditional Chinese medicine have better effects on protecting liver. Emodin, an anthraquinone compound extracted from the traditional Chinese medicine RHEI RADIX ET RHIZOMA, has anti-inflammatory, antioxidant, liver protection and anti-cancer effects, and can prevent liver injury induced by a variety of factors. By searching literatures related to the liver protection of emodin in PUBMED, SINOMED, EBM and CNKI databases, it was found that emodin could inhibit the production and promote the secretion of bile acids, and have a protective effect on intrahepatic cholestasis. Also, emodin reduce collagen synthesis and anti-hepatic fibrosis by inhibiting oxidative stress, TGF-beta/Smad pathway and HSCs proliferation, and promoting apoptosis of HSCs. Emodin can also regulate lipid metabolism and regulate the synthesis and oxidation of lipids and cholesterol to protect the nonalcoholic fatty liver. Besides, emodin can induce the apoptosis of hepatocellular carcinoma cells by acting on the death receptor pathway and mitochondrial apoptosis pathway, thus inhibiting the development of hepatocellular carcinoma. Moreover, emodin can modulate immunity and improve immune rejection in liver transplantation animals. In conclusion, emodin has a good effect on liver protection, but further experimental data are needed to verify it.
C1 [Hu, Naihua; Xue, Xinyan; Li, Yunxia] Chengdu Univ Tradit Chinese Med, Sch Pharm, Key Lab Standardizat Chinese Herbal Med,Minist Ed, Natl Key Lab Breeding Base Systemat Res Dev & Uti, Chengdu 611137, Peoples R China.
[Liu, Jie] Chengdu Univ Tradit Chinese Med, Sch Basic Med, Chengdu, Peoples R China.
C3 Chengdu University of Traditional Chinese Medicine; Chengdu University
of Traditional Chinese Medicine
RP Li, YX (corresponding author), 1166 Liu Tai Ave, Chengdu 611137, Sichuan, Peoples R China.
EM lyxtgyxcdutcm@163.com
RI naihua, hu/GVU-8621-2022
OI hu, naihua/0000-0002-9164-8827
FU National Natural Science Foundation of China [81373943, 81573583];
Sichuan Provincial Science and Technology Department of Youth Science
and technology innovation research team program [2017TD0001, 2016TD007]
FX The research was supported by National Natural Science Foundation of
China (Grant No. 81373943, 81573583) and Sichuan Provincial Science and
Technology Department of Youth Science and technology innovation
research team program (Grant No. 2017TD0001, 2016TD007).
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NR 175
TC 42
Z9 44
U1 3
U2 59
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD SEP 5
PY 2020
VL 882
AR 173269
DI 10.1016/j.ejphar.2020.173269
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA NB6ZK
UT WOS:000560663000005
PM 32553811
DA 2025-01-07
ER
PT J
AU Xue, XY
Wang, J
Fu, K
Dai, S
Wu, R
Peng, C
Li, YX
AF Xue, Xinyan
Wang, Jing
Fu, Ke
Dai, Shu
Wu, Rui
Peng, Cheng
Li, Yunxia
TI The role of miR-155 on liver diseases by modulating immunity,
inflammation and tumorigenesis
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE miR-155; Immunity; Inflammation; Tumorigenesis; Liver diseases
ID SUPPRESSES HEPATOCELLULAR-CARCINOMA; EPITHELIAL-MESENCHYMAL TRANSITION;
ISCHEMIA-REPERFUSION INJURY; HEPATITIS-B-VIRUS; KUPFFER CELLS;
MICRORNA-155 DEFICIENCY; MOLECULAR-MECHANISMS; PERIPHERAL-BLOOD;
UP-REGULATION; CANCER
AB The liver is a well-known metabolic organ that can be susceptible to external stimuli to affect its normal physiological function. Worldwide, the morbidity and mortality of liver diseases are skyrocketing every year, causing human health crises. Recently, new approaches such as biotechnology have been introduced to achieve optimal treatment and prognostic management of liver diseases. microRNAs (miRNAs), a kind of small noncoding RNA molecule, have the advantages of biodiversity, wide distribution and numerous members. Among these miRNAs, miR-155 is an important regulator of inflammation, immunity and tumorigenesis. In this review, the PubMed and Web of Science databases were searched from 2009 to 2022. After inclusion and exclusion, 64 articles were selected for a systematic review to comprehensively summarize the mechanisms of miR-155 regulating inflammation, immunity and tumorigenesis in liver diseases and liver cancer, covering in vitro, in vivo and clinical studies. Existing preclinical studies and clinical trials have listed that the up-regulation and down-regulation of miR-155 are significant in alcoholic liver injury, viral hepatitis, autoimmune hepatitis, infectious liver injury, liver transplantation and liver cancer. The immune and inflammation effects of miR-155 are manifested by regulating macrophage polarization, NK cell killing, Th17 cell and Th1/Th2 cell differentiation. Additionally, miR-155 is also committed to participating in the cell cycle, invasion and metastasis, immune escape and other processes to promote and intensify the development of liver cancer. In conclusion, miR-155 is not only a biomarker for the diagnosis and prognosis of liver diseases, but also plays a therapeutic role via regulating immunity, inflammation and tumorigenesis.
C1 [Xue, Xinyan; Wang, Jing; Fu, Ke; Dai, Shu; Wu, Rui; Peng, Cheng; Li, Yunxia] Chengdu Univ Tradit Chinese Med, Sch Pharm, State Key Lab Southwestern Chinese Med Resources, Key Lab Standardizat Chinese Herbal Med,Minist Edu, Chengdu 611137, Peoples R China.
[Peng, Cheng; Li, Yunxia] 1166 Liu Tai Ave, Chengdu, Sichuan, Peoples R China.
C3 Chengdu University of Traditional Chinese Medicine
RP Peng, C; Li, YX (corresponding author), 1166 Liu Tai Ave, Chengdu, Sichuan, Peoples R China.
EM cdtcmpengcheng@126.com; lyxtgyxcdutcm@163.com
RI CHENG, PENG/HNP-4206-2023
FU National Natural Science Foundation of China [81891012, 81630101,
U19A2010]; Innovation Team and Talents Cultivation Program of National
Administration of Traditional Chinese Medicine [ZYYCXTD-D-202209]
FX Funding This work was supported by the National Natural Science
Foundation of China (NO. 81891012, 81630101, and U19A2010) and
Innovation Team and Talents Cultivation Program of National
Administration of Traditional Chinese Medicine (NO. ZYYCXTD-D-202209) .
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NR 128
TC 10
Z9 11
U1 3
U2 20
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD MAR
PY 2023
VL 116
AR 109775
DI 10.1016/j.intimp.2023.109775
EA FEB 2023
PG 12
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA 8X2OV
UT WOS:000931857800001
PM 36753984
DA 2025-01-07
ER
PT J
AU Mohammadi, M
Attar, A
Mohammadbeigi, M
Peymani, A
Bolori, S
Fardsanei, F
AF Mohammadi, Mahnaz
Attar, Adeleh
Mohammadbeigi, Maryam
Peymani, Amir
Bolori, Shahin
Fardsanei, Fatemeh
TI The possible role of Helicobacter pylori in liver diseases
SO ARCHIVES OF MICROBIOLOGY
LA English
DT Review
DE Helicobacter pylori; Liver diseases; HPV; And HCV
ID UNIDENTIFIED CURVED BACILLI; HEPATIC STELLATE CELLS;
HEPATOCELLULAR-CARCINOMA; FIBROSIS STAGE; INFECTION; DIAGNOSIS;
ASSOCIATION; CIRRHOSIS; SEROPREVALENCE; EPIDEMIOLOGY
AB According to previous studies, Helicobacter pylori infection is associated with liver disease. In order to better understand the risk of acquiring various liver diseases, we reviewed current knowledge on the impact of H. pylori on the onset, intensification, and progression of various liver diseases caused by the infection of H. pylori. It has been estimated that between 50 and 90% of people worldwide have been infected with H. pylori. The bacterium is mostly responsible for inflamed gastric mucosa, ulcers, and cancers associated with the gastric mucosa. Through the active antioxidant system in H. pylori, the bacteria can neutralize free radicals by synthesizing VacA, a toxin that causes cell damage and apoptosis. Furthermore, there is a possibility that CagA genes may play a role in cancer development. People who have been infected with H. pylori are likely to develop lesions in the skin, the circulation system, and the pancreas. Moreover, transferring blood from the stomach may allow H. pylori to colonize the liver. The bacterium worsened liver function during autoimmune inflammation, toxic injury, chronic HCV infection, chronic HBV infection, and liver cirrhosis. Increasing portal pressure, hyperammonemia, and esophageal varices may be associated with H pylori infection. As a result, it is crucial to diagnose and treat this infection in patients with H. pylori.
C1 [Mohammadi, Mahnaz; Attar, Adeleh; Mohammadbeigi, Maryam; Peymani, Amir; Bolori, Shahin; Fardsanei, Fatemeh] Qazvin Univ Med Sci, Med Microbiol Res Ctr, Qazvin, Iran.
C3 Qazvin University of Medical Sciences (QUMS)
RP Fardsanei, F (corresponding author), Qazvin Univ Med Sci, Med Microbiol Res Ctr, Qazvin, Iran.
EM Atefeh_fardsanei@yahoo.com
RI fardsanei, fatemeh/AAZ-7223-2021; Attar, Adeleh/JVD-7902-2023
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NR 147
TC 3
Z9 3
U1 1
U2 11
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0302-8933
EI 1432-072X
J9 ARCH MICROBIOL
JI Arch. Microbiol.
PD AUG
PY 2023
VL 205
IS 8
AR 281
DI 10.1007/s00203-023-03602-z
PG 14
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA L4PU3
UT WOS:001023109400001
PM 37430019
DA 2025-01-07
ER
PT J
AU Park, SM
Rajapaksha, TW
Zhang, ML
Sattar, HA
Fichera, A
Ashton-Rickardt, PG
Peter, ME
AF Park, Sun-Mi
Rajapaksha, Tharinda W.
Zhang, Manling
Sattar, Husain A.
Fichera, Alessandro
Ashton-Rickardt, Philip G.
Peter, Marcus E.
TI CD95 signaling deficient mice with a wild-type hematopoietic system are
prone to hepatic neoplasia
SO APOPTOSIS
LA English
DT Article
DE apoptosis; bone marrow transplantation; Fas; liver cancer; lpr(cg) mice
ID NF-KAPPA-B; AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME;
HEPATOCELLULAR-CARCINOMA; CHEMICAL HEPATOCARCINOGENESIS;
TUMOR-SUPPRESSOR; LIVER-TUMORS; FAS; CELLS; APOPTOSIS; LIGAND
AB Patients with mutations in the death receptor CD95 (Fas/APO-1) frequently develop B-cell lymphoma. However, solid tumors have not been found in the context of defective CD95. This could be due to the fatal autoimmune proliferative disease that develops in the absence of functional CD95 or to a difference in CD95 signaling in lymphoid versus nonlymphoid tissues. To test this we reconstituted mice that harbor a point mutation in the death domain of CD95 (lpr(cg) mice), either in one or in both alleles, with bone marrow from wild-type (wt) mice. After a year one third of the lpr(cg)/lpr(cg) mice developed spontaneous hepatic neoplasms. In contrast only one of the wt/lpr(cg) mice and none of the wt mice developed liver cancer. The agonistic anti-CD95 antibody Jo2 induced massive apoptosis in the liver of wt mice but not in the livers of either wt/lpr(cg) or lpr(cg)/lpr(cg) mice. The susceptibility of lpr(cg)/lpr(cg) mice to liver cancer cannot solely be due to impaired CD95 mediated apoptosis because there was no clear correlation between apoptosis resistance and tumor formation. A gene chip analysis identified genes selectively upregulated in the liver of wt and wt/lpr(cg) mice which may protect these mice from developing liver cancer. Our data represent the first case of CD95 protecting from developing a solid cancer.
C1 [Park, Sun-Mi; Rajapaksha, Tharinda W.; Peter, Marcus E.] Univ Chicago, Ben May Dept Canc Res, Chicago, IL 60637 USA.
[Zhang, Manling; Sattar, Husain A.; Ashton-Rickardt, Philip G.] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
[Fichera, Alessandro] Univ Chicago, Dept Surg, Chicago, IL 60637 USA.
C3 University of Chicago; University of Chicago; University of Chicago
RP Peter, ME (corresponding author), Univ Chicago, Ben May Dept Canc Res, Chicago, IL 60637 USA.
EM mpeter@uchicago.edu
OI Peter, Marcus Ernst/0000-0003-3216-036X
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NR 41
TC 12
Z9 12
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1360-8185
J9 APOPTOSIS
JI Apoptosis
PD JAN
PY 2008
VL 13
IS 1
BP 41
EP 51
DI 10.1007/s10495-007-0149-6
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 250IM
UT WOS:000252293200004
PM 17955374
DA 2025-01-07
ER
PT J
AU Yang, F
Wang, QX
Bian, ZL
Ren, LL
Jia, JD
Ma, X
AF Yang, Fan
Wang, Qixia
Bian, Zhaolian
Ren, Lin-Lin
Jia, Jidong
Ma, Xiong
TI Autoimmune hepatitis: East meets west
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE autoimmune disease; autoimmune hepatitis; autoimmune liver disease;
liver disease
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
LIVER-TRANSPLANTATION; HEPATOCELLULAR-CARCINOMA; CLINICAL-FEATURES;
DIAGNOSTIC-CRITERIA; CONTROLLED-TRIAL; RISK-FACTORS; FOLLOW-UP;
POPULATION
AB Autoimmune hepatitis (AIH) is an inflammatory liver disease with diverse clinical spectrum, which predominantly affects females. This review provides detailed comparisons of epidemiology, genetic predispositions, clinical features, risk factors of hepatocellular carcinoma, and mortality in AIH patients between eastern and western countries. AIH prevalence and incidence are lower in Asia-Pacific area than in Europe and America. European and American patients seem to have more severe disease, characterized with human leukocyte antigen-DR3 haplotype, younger age, more AIH-induced cirrhosis at diagnosis, higher elevated serum immunoglobulin G levels, and positive rate of antisoluble liver antigen/liver pancreatitis. The overall AIH diagnostic accuracy of revised original criteria and simplified scoring system are similar in European/American populations and Asian. Cirrhosis at presentation and non-response to immunosuppressive therapy within 1 year are the most important predictors for poor prognosis of AIH patients.
C1 [Yang, Fan; Wang, Qixia; Bian, Zhaolian; Ren, Lin-Lin; Ma, Xiong] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes, Renji Hosp,Sch Med,Shanghai Canc Inst, Key Lab Gastroenterol & Hepatol,Minist Hlth,Div G, Shanghai 200001, Peoples R China.
[Jia, Jidong] Capital Med Univ, Beijing Friendship Hosp, Liver Res Ctr, Beijing 100050, Peoples R China.
[Jia, Jidong] Capital Med Univ, Beijing Friendship Hosp, Clin Epidemiol & EBM Unit, Beijing 100050, Peoples R China.
C3 Shanghai Jiao Tong University; Capital Medical University; Capital
Medical University
RP Ma, X (corresponding author), Shanghai Jiao Tong Univ, Shanghai Inst Digest Dis, Sch Med, Renji Hosp, 145 Shandong Middle Rd, Shanghai 200001, Peoples R China.
EM jia_jd@ccmu.edu.cn; maxiongmd@hotmail.com
OI Ma, Xiong/0000-0001-9616-4672
FU National Natural Science Foundation of China [81170380, 81325002,
81100271]; Doctoral Innovation Fund Projects from Shanghai Jiaotong
University School of Medicine [BXJ201322, BXJ201321]
FX This work was supported by grants from the National Natural Science
Foundation of China (Nos. 81170380 and 81325002 to X.M.; No. 81100271 to
Q.W.) and the Doctoral Innovation Fund Projects from Shanghai Jiaotong
University School of Medicine (BXJ201322 to L.-L.R. and BXJ201321 to
Z.B.).
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NR 68
TC 30
Z9 46
U1 0
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD AUG
PY 2015
VL 30
IS 8
BP 1230
EP 1236
DI 10.1111/jgh.12952
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CN4YL
UT WOS:000358436400007
PM 25765710
OA Bronze
DA 2025-01-07
ER
PT J
AU Aghabi, YO
Yasin, A
Kennedy, J
Davies, SP
Butler, AE
Stamataki, Z
AF Aghabi, Yara O.
Yasin, Alia
Kennedy, James, I
Davies, Scott P.
Butler, Amber E.
Stamataki, Zania
TI Targeting Enclysis in Liver Autoimmunity, Transplantation, Viral
Infection and Cancer
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE enclysis; hepatitis; transplantation; liver autoimmunity; regulatory T
cells (Treg); immune regulation; tolerance; liver cancer
ID REGULATORY T-CELLS; HEPATOCELLULAR-CARCINOMA; HEPATITIS; THERAPY;
CLEARANCE; DISEASES
AB Persistent liver inflammation can lead to cirrhosis, which associates with significant morbidity and mortality worldwide. There are no curative treatments beyond transplantation, followed by long-term immunosuppression. The global burden of end stage liver disease has been increasing and there is a shortage of donor organs, therefore new therapies are desperately needed. Harnessing the power of the immune system has shown promise in certain autoimmunity and cancer settings. In the context of the liver, regulatory T cell (Treg) therapies are in development. The hypothesis is that these specialized lymphocytes that dampen inflammation may reduce liver injury in patients with chronic, progressive diseases, and promote transplant tolerance. Various strategies including intrinsic and extracorporeal expansion of Treg cells, aim to increase their abundance to suppress immune responses. We recently discovered that hepatocytes engulf and delete Treg cells by enclysis. Herein, we propose that inhibition of enclysis may potentiate existing regulatory T cell therapeutic approaches in patients with autoimmune liver diseases and in patients receiving a transplant. Moreover, in settings where the abundance of Treg cells could hinder beneficial immunity, such us in chronic viral infection or liver cancer, enhancement of enclysis could result in transient, localized reduction of Treg cell numbers and tip the balance towards antiviral and anti-tumor immunity. We describe enclysis as is a natural process of liver immune regulation that lends itself to therapeutic targeting, particularly in combination with current Treg cell approaches.
C1 [Aghabi, Yara O.; Yasin, Alia; Kennedy, James, I; Davies, Scott P.; Butler, Amber E.; Stamataki, Zania] Univ Birmingham, Coll Med & Dent Sci, Inst Immunol & Immunotherapy, Birmingham, W Midlands, England.
C3 University of Birmingham
RP Stamataki, Z (corresponding author), Univ Birmingham, Coll Med & Dent Sci, Inst Immunol & Immunotherapy, Birmingham, W Midlands, England.
EM z.stamataki@bham.ac.uk
RI Davies, Scott/KBQ-1012-2024; Stamataki, Zania/P-4681-2019
OI Stamataki, Zania/0000-0003-3823-4497; Davies, Scott
Philip/0000-0001-6899-1339; Butler, Amber/0000-0002-0792-7672
FU MIBTP studentship [BB/T00746X/1]; NC3R trainee postdoctoral fellowship;
MRF intermediate career fellowship [NC/R002061/1,
MRF-169-0001-F-STAM-C0826]
FX This work is supported by an MIBTP studentship to YA (BBSRC, UKRI, grant
number BB/T00746X/1), an NC3R trainee postdoctoral fellowship to SD
(UKRI) and an MRF intermediate career fellowship to ZS (UKRI, grant
number NC/R002061/1) and an MRF intermediate career fellowship to ZS
(UKRI, grant number MRF-169-0001-F-STAM-C0826).
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NR 145
TC 7
Z9 7
U1 0
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD APR 19
PY 2021
VL 12
AR 662134
DI 10.3389/fimmu.2021.662134
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA RV7YJ
UT WOS:000646044000001
PM 33953725
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Cao, LN
Zhang, T
Zhu, JP
Li, AX
Zheng, K
Zhang, N
Su, B
Xia, W
Wu, H
Li, N
He, QS
AF Cao, Lina
Zhang, Tong
Zhu, Junping
Li, Aixin
Zheng, Kai
Zhang, Nan
Su, Bin
Xia, Wei
Wu, Hao
Li, Ning
He, Qiushui
TI Polymorphism of TLR5 rs5744174 is associated with disease progression in
Chinese patients with chronic HBV infection
SO APMIS
LA English
DT Article
DE Chinese; hepatitis B virus; PCR; sequencing; single nucleotide
polymorphism; TLR5
ID TOLL-LIKE RECEPTOR; B-VIRUS INFECTION; CHRONIC HEPATITIS-B; ADAPTIVE
IMMUNE-RESPONSES; HEPATOCELLULAR-CARCINOMA; GENETIC POLYMORPHISMS;
VIRAL-INFECTION; E-ANTIGEN; INNATE; MICE
AB Toll-like receptors (TLRs) play a crucial role in innate and adaptive immunity, protecting the host from viral pathogens. Studies have implicated that TLR5 is associated with various diseases such as autoimmune and inflammation related diseases. However, little is known about the relationship between TLR5 and hepatitis B virus (HBV) infection. We studied the effect of TLR5 gene polymorphisms on susceptibility to and disease progression of chronic hepatitis B (CHB) infection in Chinese. Blood samples were taken from 636 patients with CHB, HBV-related liver cirrhosis (LC) or hepatocellular carcinoma (HCC) and 273 controls. Polymorphisms of TLR5 (1775A>G rs2072493 and 1846T>C rs5744174) were analyzed by PCR-based sequencing. No difference in genotypic and allelic frequencies of TLR5 rs2072493 and rs5744174 was observed between patients and controls. Significant difference was found in frequency of TLR5 rs5744174 TT genotype between men with CHB and LC (p=0.035). Frequency of TT genotype of TLR5 rs5744174 in patients positive for HBeAg was increased from 53.2% in patients with CHB to 74.1% in those with HCC (p=0.024). Our results indicate that in Chinese genetic variation of TLR5 may be not a determinant of susceptibility to HBV-related diseases but may play a role in development of HBV-related severe liver diseases.
C1 [Cao, Lina; Zhu, Junping; Zheng, Kai; Zhang, Nan; He, Qiushui] Capital Med Univ, Dept Med Microbiol, 10 Xitoutiao, Beijing 100069, Peoples R China.
[Cao, Lina; Zhu, Junping; Zheng, Kai; Zhang, Nan; He, Qiushui] Capital Med Univ, Res Ctr Microbiome, Beijing, Peoples R China.
[Zhang, Tong; Li, Aixin; Su, Bin; Xia, Wei; Wu, Hao; Li, Ning] Capital Med Univ, Beijing Youan Hosp, Dept Infect Dis, Beijing 100069, Peoples R China.
[He, Qiushui] Univ Turku, Dept Med Microbiol & Immunol, Turku, Finland.
C3 Capital Medical University; Capital Medical University; Capital Medical
University; University of Turku
RP He, QS (corresponding author), Capital Med Univ, Dept Med Microbiol, 10 Xitoutiao, Beijing 100069, Peoples R China.; Li, N (corresponding author), Capital Med Univ, Beijing Youan Hosp, Dept Infect Dis, Beijing 100069, Peoples R China.
EM liningbjyah@vip.sina.com; Qiushui.He@utu.fi
RI Wu, Hao/HPE-4844-2023; Li, Wenjing/JMP-8310-2023
FU Collaborative Innovation Center of Infectious Diseases, Capital Medical
University [PXM 2015_014226_000058]; Beijing Key Laboratory [BZ0089];
National Natural Science Foundation of China [81571973]
FX This study was supported by the Collaborative Innovation Center of
Infectious Diseases, Capital Medical University (PXM
2015_014226_000058), by Beijing Key Laboratory (No: BZ0089) and by
National Natural Science Foundation of China (No: 81571973).
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NR 45
TC 7
Z9 10
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0903-4641
EI 1600-0463
J9 APMIS
JI APMIS
PD AUG
PY 2017
VL 125
IS 8
BP 708
EP 716
DI 10.1111/apm.12707
PG 9
WC Immunology; Microbiology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology; Pathology
GA FA9XY
UT WOS:000405800700004
PM 28543911
DA 2025-01-07
ER
PT J
AU Nielsen, KR
Midjord, J
Johannesen, HL
Gronbaek, H
AF Nielsen, Kari Rubek
Midjord, Jongero
Johannesen, Herborg Liggjasardottir
Gronbaek, Henning
TI A nationwide study of autoimmune liver diseases in the Faroe Islands:
Incidence, prevalence, and causes of death 2004-2021
SO INTERNATIONAL JOURNAL OF CIRCUMPOLAR HEALTH
LA English
DT Article
DE autoimmune hepatitis; primary biliary cholangitis; primary sclerosing
cholangitis; epidemiology; incidence; prevalence; Faroe Islands
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; INFLAMMATORY
BOWEL DISEASES; ISOLATED POPULATION; HEPATITIS; EPIDEMIOLOGY; DIAGNOSIS;
IBD; MANAGEMENT; RISK
AB Background and aims: Autoimmune liver diseases are rare diseases, and population-based studies on the epidemiology of autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC) are sparse. We aimed to assess the incidence of AIH, PBC, and PSC in the Faroe Islands. Methods: All cases of AIH, PBC, and PSC diagnosed in the Faroe Islands between January 1(st), 2004, and December 31(st), 2021, were included in this nationwide registry-based cohort study. In addition, we searched all medical records to assess diagnostic criteria and cause of death. Results: The incidences of AIH, PBC, and PSC in the Faroe Islands were 5.2, 2.5 and 0.7 per 100,000 population per year, respectively. Point prevalence per 100,000 population on December 31st 2021, was 71.8 for AIH, 38.5 for PBC, and 11.0 for PSC. Nine AIH patients died after a median of 3 years, three died of hepatocellular carcinoma (HCC), and two died of liver failure. Five PBC patients died after a median of 7 years, one of HCC and one of liver failure. One PSC patient died of cholangiocarcinoma. Conclusion: The incidence and prevalence of AIH, PBC and PSC in the Faroe Islands are among the highest reported in population-based settings.
C1 [Nielsen, Kari Rubek; Midjord, Jongero; Johannesen, Herborg Liggjasardottir] Natl Hosp Faroe Isl, Med Dept, Torshavn, Faroe Islands.
[Nielsen, Kari Rubek; Midjord, Jongero; Johannesen, Herborg Liggjasardottir] Univ Faroe Isl, Fac Hlth Sci & Nursing, Ctr Hlth Sci, Torshavn, Faroe Islands.
[Nielsen, Kari Rubek] Genet Biobank, Torshavn, Faroe Islands.
[Gronbaek, Henning] Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Aarhus, Denmark.
[Gronbaek, Henning] Aarhus Univ, Clin Inst, Aarhus, Denmark.
C3 Aarhus University; Aarhus University
RP Nielsen, KR (corresponding author), Natl Hosp Faroe Isl, Med Dept, Torshavn, Faroe Islands.
EM karirubeknielsen@gmail.com
RI Johannesen, Herborg/AEZ-7783-2022; Gronbaek, Henning/AAJ-3202-2020
OI Gronbaek, Henning/0000-0001-8998-7910; Johannesen, Herborg
Liggjasardottir/0000-0002-9048-3303; Nielsen, Kari
Rubek/0000-0002-1028-644X
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NR 44
TC 5
Z9 5
U1 0
U2 9
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1239-9736
EI 2242-3982
J9 INT J CIRCUMPOL HEAL
JI Int. J. Circumpolar Health
PD DEC 31
PY 2023
VL 82
IS 1
AR 2221368
DI 10.1080/22423982.2023.2221368
PG 6
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA J0WZ0
UT WOS:001006909400001
PM 37300838
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Cao, JG
Mu, QC
Huang, HY
AF Cao, Junguo
Mu, Qingchun
Huang, Haiyan
TI The Roles of Insulin-Like Growth Factor 2 mRNA-Binding Protein 2 in
Cancer and Cancer Stem Cells
SO STEM CELLS INTERNATIONAL
LA English
DT Review
ID CHRONIC LIVER-DISEASE; LONG NONCODING RNA; FACTOR-II; COLORECTAL-CANCER;
BREAST-CANCER; HEPATOCELLULAR-CARCINOMA; TRANSCRIPTION FACTOR;
AUTOIMMUNE-RESPONSE; GASTRIC-CANCER; KH DOMAINS
AB RNA-binding proteins (RBPs) mediate the localization, stability, and translation of the target transcripts and fine-tune the physiological functions of the proteins encoded. The insulin-like growth factor (IGF) 2 mRNA-binding protein (IGF2BP, IMP) family comprises three RBPs, IGF2BP1, IGF2BP2, and IGF2BP3, capable of associating with IGF2 and other transcripts and mediating their processing. IGF2BP2 represents the least understood member of this family of RBPs; however, it has been reported to participate in a wide range of physiological processes, such as embryonic development, neuronal differentiation, and metabolism. Its dysregulation is associated with insulin resistance, diabetes, and carcinogenesis and may potentially be a powerful biomarker and candidate target for relevant diseases. This review summarizes the structural features, regulation, and functions of IGF2BP2 and their association with cancer and cancer stem cells.
C1 [Cao, Junguo; Huang, Haiyan] Jilin Univ, Hosp 1, Dept Neurosurg, Xinmin St 71, Changchun, Jilin, Peoples R China.
[Mu, Qingchun] Mudanjiang Med Univ, Hongqi Hosp, Mudanjiang, Peoples R China.
C3 Jilin University; Mudanjiang Medical University
RP Huang, HY (corresponding author), Jilin Univ, Hosp 1, Dept Neurosurg, Xinmin St 71, Changchun, Jilin, Peoples R China.; Mu, QC (corresponding author), Mudanjiang Med Univ, Hongqi Hosp, Mudanjiang, Peoples R China.
EM muqc@qq.com; huanghy@jlu.edu.cn
OI Mu, Qingchun/0000-0001-7578-5381
FU S&T Development Planning Program of Jilin Province [20150312005ZG]
FX This study was supported by grants from the S&T Development Planning
Program of Jilin Province (nos. 20150312005ZG).
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NR 148
TC 111
Z9 117
U1 0
U2 26
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-966X
EI 1687-9678
J9 STEM CELLS INT
JI Stem Cells Int.
PY 2018
VL 2018
AR 4217259
DI 10.1155/2018/4217259
PG 15
WC Cell & Tissue Engineering
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA GA5DZ
UT WOS:000428353600001
PM 29736175
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Musaddaq, G
Shahzad, N
Ashraf, MA
Arshad, MI
AF Musaddaq, Ghulam
Shahzad, Naveed
Ashraf, Muhammad Adnan
Arshad, Muhammad Imran
TI Circulating liver-specific microRNAs as noninvasive diagnostic
biomarkers of hepatic diseases in human
SO BIOMARKERS
LA English
DT Review
DE Viral hepatitis; human; microRNAs; biomarkers
ID HEPATOCELLULAR-CARCINOMA; POTENTIAL BIOMARKERS; ALANINE
AMINOTRANSFERASE; SERUM MICRORNA-122; EXPRESSION PROFILE;
GENE-EXPRESSION; MIR-122; INJURY; MIRNAS; PLASMA
AB Context: Hepatitis is an endemic disease worldwide leading to chronic and debilitating cancers. The viral agents and hepatotoxic substances lead to damage of hepatocytes and release of damage associated molecules in circulation. The lack of timely and rapid diagnosis of hepatitis results in chronic disease. Objective: The present review aimed to describe regulation, release and functions of microRNAs (miR) during human liver pathology and insights into their promising use as noninvasive biomarkers of hepatitis. Methods: Comprehensive data were collected from PubMed, ScienceDirect and the Web of Science databases utilizing the keywords "biomarkers", "microRNAs" and "hepatic diseases". Results: The miRs are readily released in the body fluids and blood during HBV/HCV associated hepatitis as well as metabolic, alcoholic, drug induced and autoimmune hepatitis. The liver-specific microRNAs including miR-122, miR-130, miR-183, miR-196, miR-209 and miR-96 are potential indicators of liver injury (mainly via apoptosis, necrosis and necroptosis) or hepatitis with their varied expression during acute/fulminant, chronic, liver fibrosis/cirrhosis and hepato-cellular carcinoma. Conclusions: The liver-specific miRs can be used as rapid and noninvasive biomarkers of hepatitis to discern different stages of hepatitis. Blocking or stimulating pathways associated with miR regulation in liver could unveil novel therapeutic strategies in the management of liver diseases.
C1 [Musaddaq, Ghulam; Ashraf, Muhammad Adnan; Arshad, Muhammad Imran] Univ Agr Faisalabad, Inst Microbiol, Faisalabad 38040, Pakistan.
[Shahzad, Naveed] Univ Punjab, SBS, Lahore, Pakistan.
C3 University of Agriculture Faisalabad; University of Punjab
RP Arshad, MI (corresponding author), Univ Agr Faisalabad, Inst Microbiol, Faisalabad 38040, Pakistan.
EM drimranarshad@yahoo.com
RI Musaddaq, Ghulam/AIE-3436-2022; Ashraf, Muhammad Adnan/O-5886-2017;
Arshad, Muhammad Imran/P-5550-2018
OI Ashraf, Muhammad Adnan/0000-0001-8152-5746; Arshad, Muhammad
Imran/0000-0003-2218-9054
FU Endowment Fund Secretariat (EFS), University of Agriculture Faisalabad,
Pakistan [R&D Project 2016-2018]
FX This work was supported by the Endowment Fund Secretariat (EFS),
University of Agriculture Faisalabad, Pakistan under Grant [R&D Project
2016-2018] to Dr. Muhammad Imran Arshad (PI).
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NR 86
TC 27
Z9 30
U1 0
U2 22
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-750X
EI 1366-5804
J9 BIOMARKERS
JI Biomarkers
PD FEB 17
PY 2019
VL 24
IS 2
BP 103
EP 109
DI 10.1080/1354750X.2018.1528631
PG 7
WC Biotechnology & Applied Microbiology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Toxicology
GA HU3FU
UT WOS:000465158700001
PM 30252499
DA 2025-01-07
ER
PT J
AU Zhou, J
Hu, ZH
Zhang, QJ
Li, ZW
Xiang, J
Yan, S
Wu, J
Zhang, M
Zheng, SS
AF Zhou, Jie
Hu, Zhenhua
Zhang, Qijun
Li, Zhiwei
Xiang, Jie
Yan, Sheng
Wu, Jian
Zhang, Min
Zheng, Shusen
TI Spectrum of De Novo Cancers and Predictors in Liver Transplantation:
Analysis of the Scientific Registry of Transplant Recipients Database
SO PLOS ONE
LA English
DT Article
ID LATE MORTALITY; KIDNEY-TRANSPLANTATION; RENAL-TRANSPLANTATION;
ORGAN-TRANSPLANTATION; UNITED-STATES; RISK-FACTORS; MAJOR CAUSE;
MALIGNANCY; SURVIVAL; THERAPY
AB Background
De novo malignancies occur after liver transplantation because of immunosuppression and improved long-term survival. But the spectrums and associated risk factors remain unclear.
Aims
To describe the overall pattern of de novo cancers in liver transplant recipients.
Methods
Data from Scientific Registry of Transplant Recipients from October 1987 to December 2009 were analyzed. The spectrum of de novo cancer was analyzed and logistic-regression was used to identify predictors of do novo malignancies.
Results
Among 89,036 liver transplant recipients, 6,834 recipients developed 9,717 post-transplant malignancies. We focused on non-skin malignancies. A total of 3,845 recipients suffered from 4,854 de novo non-skin malignancies, including 1,098 de novo hematological malignancies, 38 donor-related cases, and 3,718 de novo solid-organ malignancies. Liver transplant recipients had more than 11 times elevated cancer risk compared with the general population. The long-term overall survival was better for recipients without de novo cancer. Multivariate analysis indicated that HCV, alcoholic liver disease, autoimmune liver disease, nonalcoholic steatohepatitis, re-transplantation, combined transplantation, hepatocellular carcinoma, immunosuppression regime of cellcept, cyclosporine, sirolimus, steroids and tacrolimus were independent predictors for the development of solid malignancies after liver transplantation.
Conclusions
De novo cancer risk was elevated in liver transplant recipients. Multiple factors including age, gender, underlying liver disease and immunosuppression were associated with the development of de novo cancer. This is useful in guiding recipient selection as well as post-transplant surveillance and prevention.
C1 [Zhou, Jie; Hu, Zhenhua; Zhang, Qijun; Li, Zhiwei; Xiang, Jie; Yan, Sheng; Wu, Jian; Zhang, Min; Zheng, Shusen] Zhejiang Univ, Sch Med,Div Hepatobiliary & Pancreat Surg, Affiliated Hosp 1,Key Lab Organ Transplantat,Mini, Key Lab Combined Multiorgan Transplantat,Dept Sur, Hangzhou 310003, Zhejiang, Peoples R China.
[Zhou, Jie; Hu, Zhenhua; Zhang, Qijun; Li, Zhiwei; Xiang, Jie; Yan, Sheng; Wu, Jian; Zhang, Min; Zheng, Shusen] Zhejiang Univ, Sch Med, Affiliated Hosp 1,State Key Lab Diag & Treatment, Collaborat Innovat Ctr Diag & Treatment Infect Di, Hangzhou 310003, Zhejiang, Peoples R China.
C3 Zhejiang University; Zhejiang University; Collaborative Innovation
Center for Diagnosis & Treatment of Infectious Diseases
RP Zheng, SS (corresponding author), Zhejiang Univ, Sch Med,Div Hepatobiliary & Pancreat Surg, Affiliated Hosp 1,Key Lab Organ Transplantat,Mini, Key Lab Combined Multiorgan Transplantat,Dept Sur, Hangzhou 310003, Zhejiang, Peoples R China.; Zheng, SS (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 1,State Key Lab Diag & Treatment, Collaborat Innovat Ctr Diag & Treatment Infect Di, Hangzhou 310003, Zhejiang, Peoples R China.
EM shusenzheng@zju.edu.cn
RI Zhang, Min/ADG-4442-2022; Zhou, Jiefeng/HOC-8648-2023; Hu,
Zhenhua/E-3375-2016
FU National ST Major Project [2012ZX10002017]; Foundation for Innovative
Research Groups of the National Natural Science Foundation of China
[81121002]; Medical and health platform project of Zhejiang Province (A
level backbone talent) [2015RCA010]
FX This study was sponsored by grants from the National S&T Major Project
(No. 2012ZX10002017), the Foundation for Innovative Research Groups of
the National Natural Science Foundation of China (Grant No. 81121002)
and Medical and health platform project of Zhejiang Province (A level
backbone talent) (Grant No. 2015RCA010). The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 37
TC 39
Z9 44
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 12
PY 2016
VL 11
IS 5
AR e0155179
DI 10.1371/journal.pone.0155179
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DM8CQ
UT WOS:000376588600130
PM 27171501
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Muriel, P
López-Sánchez, P
Ramos-Tovar, E
AF Muriel, Pablo
Lopez-Sanchez, Pedro
Ramos-Tovar, Erika
TI Fructose and the Liver
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE liver; fructose; uric acid; NLRP3; oxidative stress; inflammation
ID NF-KAPPA-B; FATTY LIVER; OXIDATIVE STRESS; URIC-ACID; DIETARY FRUCTOSE;
HEPATOCELLULAR-CARCINOMA; LIPID-ACCUMULATION; INSULIN-RESISTANCE;
METABOLIC SYNDROME; NONALCOHOLIC STEATOHEPATITIS
AB Chronic diseases represent a major challenge in world health. Metabolic syndrome is a constellation of disturbances affecting several organs, and it has been proposed to be a liver-centered condition. Fructose overconsumption may result in insulin resistance, oxidative stress, inflammation, elevated uric acid levels, increased blood pressure, and increased triglyceride concentrations in both the blood and liver. Non-alcoholic fatty liver disease (NAFLD) is a term widely used to describe excessive fatty infiltration in the liver in the absence of alcohol, autoimmune disorders, or viral hepatitis; it is attributed to obesity, high sugar and fat consumption, and sedentarism. If untreated, NAFLD can progress to nonalcoholic steatohepatitis (NASH), characterized by inflammation and mild fibrosis in addition to fat infiltration and, eventually, advanced scar tissue deposition, cirrhosis, and finally liver cancer, which constitutes the culmination of the disease. Notably, fructose is recognized as a major mediator of NAFLD, as a significant correlation between fructose intake and the degree of inflammation and fibrosis has been found in preclinical and clinical studies. Moreover, fructose is a risk factor for liver cancer development. Interestingly, fructose induces a number of proinflammatory, fibrogenic, and oncogenic signaling pathways that explain its deleterious effects in the body, especially in the liver.
C1 [Muriel, Pablo] Cinvestav IPN, Dept Pharmacol, Lab Expt Hepatol, Apartado Postal 14-740, Mexico City 07300, DF, Mexico.
[Lopez-Sanchez, Pedro; Ramos-Tovar, Erika] Sch Higher Educ Med IPN, Postgrad Studies & Res Sect, Plan San Luis Diaz Miron S-N Casco Santo Tomas, Mexico City 11340, Mexico.
C3 CINVESTAV - Centro de Investigacion y de Estudios Avanzados del
Instituto Politecnico Nacional
RP Ramos-Tovar, E (corresponding author), Sch Higher Educ Med IPN, Postgrad Studies & Res Sect, Plan San Luis Diaz Miron S-N Casco Santo Tomas, Mexico City 11340, Mexico.
EM pmuriel@cinvestav.mx; pelosa651018@yahoo.com; erikaramost@gmail.com
RI Ramos-Tovar, Erika/HRB-9713-2023; Lopez, Pedro/A-1283-2008; Muriel,
Pablo/H-5156-2017
OI Lopez, Pedro/0000-0002-8089-9794; Muriel, Pablo/0000-0002-2236-6631;
Ramos-Tovar, Erika/0000-0002-6616-9760
FU Consejo Nacional de Ciencia y Tecnologia through the Ciencia de Frontera
funding program [53358]
FX This work was financially supported by Consejo Nacional de Ciencia y
Tecnologia through the Ciencia de Frontera funding program, grant number
53358.
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NR 192
TC 73
Z9 77
U1 3
U2 39
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2021
VL 22
IS 13
AR 6969
DI 10.3390/ijms22136969
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA TF8YA
UT WOS:000671000100001
PM 34203484
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Li, YK
You, ZR
Tang, RQ
Ma, X
AF Li, Yikang
You, Zhengrui
Tang, Ruqi
Ma, Xiong
TI Tissue-resident memory T cells in chronic liver diseases: Phenotype,
development and function
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE tissue-resident memory T cells; liver; chronic hepatitis B virus
infection; malaria; autoimmune hepatitis; nonalcoholic fatty liver
disease; hepatocellular carcinoma
ID TGF-BETA; IMMUNE-RESPONSES; HUMAN CD8(+); HEPATITIS; LYMPHOCYTES;
EXPRESSION; MALARIA; SKIN; HBV; DIFFERENTIATION
AB Tissue-resident memory (T-RM) T cells are a unique subset of memory T cells that are critical for the first line of defense against pathogens or antigens in peripheral non-lymphoid tissues such as liver, gut, and skin. Generally, T-RM cells are well adapted to the local environment in a tissue-specific manner and typically do not circulate but persist in tissues, distinguishing them from other memory T cell lineages. There is strong evidence that liver T-RM cells provide a robust adaptive immune response to potential threats. Indeed, the potent effector function of hepatic T-RM cells makes it essential for chronic liver diseases, including viral and parasite infection, autoimmune liver diseases (AILD), nonalcoholic fatty liver disease (NAFLD), hepatocellular carcinoma (HCC) and liver transplantation. Manipulation of hepatic T-RM cells might provide novel promising strategies for precision immunotherapy of chronic liver diseases. Here, we provide insights into the phenotype of hepatic T-RM cells through surface markers, transcriptional profiles and effector functions, discuss the development of hepatic T-RM cells in terms of cellular origin and factors affecting their development, analyze the role of hepatic T-RM cells in chronic liver diseases, as well as share our perspectives on the current status of hepatic T-RM cell research.
C1 [Li, Yikang; You, Zhengrui; Tang, Ruqi; Ma, Xiong] Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Inst Digest Dis, Sch Med,Div Gastroenterol & Hepatol,Key Lab Gastro, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University
RP Ma, X (corresponding author), Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Inst Digest Dis, Sch Med,Div Gastroenterol & Hepatol,Key Lab Gastro, Shanghai, Peoples R China.
EM maxiongmd@hotmail.com
RI you, zhengrui/JYP-7419-2024
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NR 149
TC 10
Z9 10
U1 0
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 12
PY 2022
VL 13
AR 967055
DI 10.3389/fimmu.2022.967055
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 4X1BS
UT WOS:000860586100001
PM 36172356
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Michitaka, K
Nishiguchi, S
Aoyagi, Y
Hiasa, Y
Tokumoto, Y
Onji, M
AF Michitaka, Kojiro
Nishiguchi, Shuhei
Aoyagi, Yutaka
Hiasa, Yoichi
Tokumoto, Yoshio
Onji, Morikazu
CA Japan Etiology Liver Cirrhosis Stu
TI Etiology of liver cirrhosis in Japan: a nationwide survey
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Carcinogenesis; Hepatitis B virus; Hepatitis C virus; Hepatocellular
carcinoma; Nonalcoholic steatohepatitis
ID NONALCOHOLIC FATTY LIVER; C VIRUS-INFECTIONS; HEPATOCELLULAR-CARCINOMA;
HEPATITIS-B; METABOLIC SYNDROME; NATURAL-HISTORY; BLOOD-DONORS; DISEASE;
POPULATION; PREVALENCE
AB Little is understood about worldwide changes in the epidemiological distribution of the etiology of liver cirrhosis (LC). The present study examines the etiology of liver cirrhosis in Japan using a nationwide survey.
We analyzed data from 33,379 patients with LC at 58 hospitals and presented the findings in a poster symposium regarding the etiology and clinical features of LC in Japan that was included in the program of the 44th Annual Meeting of the Japan Society of Hepatology. We identified the distribution of the etiology of LC and compared the present with previous Japanese findings to estimate the future of etiological changes in LC.
The etiological agents were as follows: hepatitis B virus (HBV) 13.9%, hepatitis C virus (HCV) 60.9%, alcohol 13.6%, primary biliary cirrhosis (PBC) 2.4% and autoimmune hepatitis (AIH) 1.9%. Cirrhosis was considered to be related to nonalcoholic steatohepatitis (NASH) in 2.1% of the patients. The ratio of HCV-related LC was significantly higher among patients with hepatocellular carcinoma (HCC) (P < 0.0001) compared to those without, whereas the ratios of alcohol, PBC, AIH were lower. HCC was evident in 31.5% of NASH-related LC.
The major etiology of liver cirrhosis in Japan remains HCV. Our survey revealed the prevalence of NASH-related LC in Japan and the frequency of HCC. Future changes in etiology must be considered in establishing preventive or educational strategies, as well as in developing new treatment strategies.
C1 [Michitaka, Kojiro; Hiasa, Yoichi; Tokumoto, Yoshio; Onji, Morikazu] Ehime Univ, Dept Gastroenterol & Metabol, Grad Sch Med, Toon, Ehime 7910295, Japan.
[Nishiguchi, Shuhei] Hyogo Coll Med, Div Hepatobiliary & Pancreat Dis, Dept Internal Med, Nishinomiya, Hyogo 6638501, Japan.
[Aoyagi, Yutaka] Niigata Univ, Div Gastroenterol & Hepatol, Grad Sch Med & Dent Sci, Niigata 9518122, Japan.
C3 Ehime University; Hyogo Medical University; Niigata University
RP Onji, M (corresponding author), Ehime Univ, Dept Gastroenterol & Metabol, Grad Sch Med, Toon, Ehime 7910295, Japan.
EM kojiromichitaka@gmail.com; nishiguc@hyo-med-ac.jp;
aoy@med.niigata-u.ac.jp; hiasa@m.ehime-u.ac.jp; yotoku@m.ehime-u.ac.jp;
onjimori@m.ehime-u.ac.jp
RI Hiasa, Yoichi/ABD-2759-2021
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NR 24
TC 116
Z9 122
U1 0
U2 3
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JAN
PY 2010
VL 45
IS 1
BP 86
EP 94
DI 10.1007/s00535-009-0128-5
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 546LA
UT WOS:000273811100012
PM 19789837
DA 2025-01-07
ER
PT J
AU Petit, JM
Hamza, S
Rollot, F
Sigonney, V
Crevisy, E
Duvillard, L
Raab, JJ
Bronowicki, JP
Bernard-Chabert, B
Di Martino, V
Doffoel, M
Barraud, H
Richou, C
Jouve, JL
Hillon, P
AF Petit, Jean Michel
Hamza, Samia
Rollot, Fabien
Sigonney, Vanessa
Crevisy, Elodie
Duvillard, Laurence
Raab, Jean Jacques
Bronowicki, Jean Pierre
Bernard-Chabert, Brigitte
Di Martino, Vincent
Doffoel, Michel
Barraud, Helene
Richou, Carine
Jouve, Jean Louis
Hillon, Patrick
TI Impact of liver disease severity and etiology on the occurrence of
diabetes mellitus in patients with liver cirrhosis
SO ACTA DIABETOLOGICA
LA English
DT Article
DE Diabetes mellitus; Cirrhosis; Non-alcoholic fatty liver disease; Viral
hepatitis; Alcoholic liver disease
ID HEPATOCELLULAR-CARCINOMA; HEPATITIS-C; RISK-FACTORS; PREVALENCE;
POPULATION; MANAGEMENT; GLUCOSE; ALCOHOL
AB The association between liver cirrhosis (LC) and diabetes mellitus (DM) is well known. However, the impact of the severity or etiology of LC on the occurrence of DM is relatively unknown. We aimed to determine the prevalence and clinical correlates of DM in a large cohort of patients with cirrhosis. A total of 1,068 patients with LC were included in this cross sectional study (CIRCE study). The diagnosis of cirrhosis irrespective of its etiology was based on histological confirmation by liver biopsy or, in the absence of biopsy, on typical clinical, morphological and biological data. Data related to the cirrhosis etiology: alcohol, viral markers of hepatitis B, C, iron load parameters and autoimmune markers were collected for each patient. Venous blood samples were taken in the morning after 12-h overnight fasting. There were 383 patients with cirrhosis associated with hepatocellular carcinoma (HCC). DM was found in 412 (39.7 %) patients. Patients with DM were older and more likely to be overweight and male, with a family history of DM and a diagnosis of HCC. DM was not associated with a history of stroke or myocardial infarction. Cirrhosis secondary to hepatitis infection was less strongly associated with DM than with NASH or alcoholic cirrhosis. The severity of LC was not associated with DM. In multivariate analysis, the factors associated with DM were age, BMI, a family history of DM, and statin use. There was a significant interaction between HCC and cirrhosis etiology for the risk of DM. Cirrhosis secondary to hepatitis was associated with a lesser presence of DM only in patients with HCC (interaction p = 0.0015). LC was strongly associated with DM, with around 40 % of diabetic patients. In the group of patients with LC without HCC, diabetes was not associated with the etiology of cirrhosis.
C1 [Petit, Jean Michel; Hamza, Samia; Rollot, Fabien; Duvillard, Laurence; Jouve, Jean Louis; Hillon, Patrick] Univ Hosp Dijon, Dijon, France.
[Petit, Jean Michel; Hamza, Samia; Sigonney, Vanessa; Crevisy, Elodie; Duvillard, Laurence; Hillon, Patrick] INSERM, U866, Dijon, France.
[Petit, Jean Michel; Hamza, Samia; Duvillard, Laurence; Hillon, Patrick] Univ Burgundy, Dijon, France.
[Petit, Jean Michel] CHU Bocage, Serv Diabetol & Endocrinol, F-21079 Dijon, France.
[Raab, Jean Jacques] Gen Hosp, Metz, France.
[Bronowicki, Jean Pierre; Barraud, Helene] Univ Hosp Nancy, INSERM 954, Nancy, France.
[Bernard-Chabert, Brigitte] Univ Hosp Reims, Reims, France.
[Di Martino, Vincent; Richou, Carine] Univ Hosp Besancon, Besancon, France.
[Doffoel, Michel] Univ Hosp Strasbourg, Strasbourg, France.
C3 CHU Dijon Bourgogne; Institut Agro; AgroSup Dijon; Universite de
Bourgogne; Institut National de la Sante et de la Recherche Medicale
(Inserm); Universite de Bourgogne; CHU Dijon Bourgogne; CHR
Metz-Thionville; Universite de Lorraine; CHU de Nancy; Institut National
de la Sante et de la Recherche Medicale (Inserm); CHU de Reims;
Universite de Reims Champagne-Ardenne; Universite de Franche-Comte; CHU
Besancon; CHU Strasbourg
RP Petit, JM (corresponding author), CHU Bocage, Serv Diabetol & Endocrinol, BP 77908, F-21079 Dijon, France.
EM jean-michel.petit@chu-dijon.fr
RI Rollot, Fabien/HCI-7357-2022
OI Di Martino, Vincent/0000-0002-2022-690X
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NR 15
TC 21
Z9 25
U1 1
U2 7
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 0940-5429
EI 1432-5233
J9 ACTA DIABETOL
JI Acta Diabetol.
PD JUN
PY 2014
VL 51
IS 3
BP 455
EP 460
DI 10.1007/s00592-013-0538-y
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA AH8PL
UT WOS:000336400100015
PM 24352343
DA 2025-01-07
ER
PT J
AU Strasser, SI
AF Strasser, Simone I.
TI Longterm outcome of the liver graft: A clinician's perspectiverecurrent
disease, the universal shifting
SO LIVER TRANSPLANTATION
LA English
DT Article
ID SOCIETY CONSENSUS STATEMENT; HEPATITIS-C MANAGEMENT; AUTOIMMUNE
HEPATITIS; HEPATOCELLULAR-CARCINOMA; TRANSPLANT CANDIDATES; ANTIVIRAL
THERAPY; TUMOR RECURRENCE; CIRRHOSIS; INFECTION; VELPATASVIR
C1 [Strasser, Simone I.] Royal Prince Alfred Hosp, AW Morrow Gastroenterol & Liver Ctr, Australian Natl Liver Transplant Unit, Missenden Rd, Camperdown, NSW 2050, Australia.
C3 University of Sydney; NSW Health; Royal Prince Alfred Hospital
RP Strasser, SI (corresponding author), Royal Prince Alfred Hosp, AW Morrow Gastroenterol & Liver Ctr, Australian Natl Liver Transplant Unit, Missenden Rd, Camperdown, NSW 2050, Australia.
EM simone.strasser@health.nsw.gov.au
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Bourlière M, 2017, NEW ENGL J MED, V376, P2134, DOI 10.1056/NEJMoa1613512
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NR 32
TC 0
Z9 0
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6465
EI 1527-6473
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD OCT
PY 2017
VL 23
SU 1
BP S64
EP S69
DI 10.1002/lt.24839
PG 6
WC Gastroenterology & Hepatology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA FK5XQ
UT WOS:000413576700011
PM 28779560
DA 2025-01-07
ER
PT J
AU Cheng, JS
Chen, WT
Ku, HP
Chien, RN
Chang, ML
AF Cheng, Jur-Shan
Chen, Wei-Ting
Ku, Hsin-Ping
Chien, Rong-Nan
Chang, Ming-Ling
TI Characteristic geoepidemiology of primary biliary cholangitis in Taiwan:
A nationwide population-based study
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE Asia; female-to-male ratio; incidence; PBC; prevalence
ID AUTOIMMUNE LIVER-DISEASES; HEPATOCELLULAR-CARCINOMA; CEREBROVASCULAR
EVENTS; RISK-FACTORS; FOLLOW-UP; CIRRHOSIS; EPIDEMIOLOGY; OUTCOMES;
CANTERBURY; REGION
AB Aim: Data on the geoepidemiology and outcomes of primary biliary cholangitis (PBC) in Asia are limited; thus, we aimed to collect and assess this information for Taiwan.Methods: A nationwide population-based cohort study was undertaken using data from the Taiwan National Health Insurance Research Database. Primary biliary cholangitis was defined by the International Classification of Diseases, Ninth Revision, Clinical Modification code 571.6 based on alkaline phosphatase and antimitochondrial antibody measurements and ursodeoxycholic acid treatment.Results: During 2002-2015, 2737 patients (2137 female patients; mean age, 57.78 years) had PBC. The average annual age- and sex-adjusted prevalence and incidence rates of PBC were 8.092/10(5) and 1.148/10(5), respectively. Prevalent cases peaked in patients aged 50-59 years; the female-to-male ratio was 4.21. Annual prevalence rates increased with time (average percentage change, 12.03%; p < 0.0001). The annual incidence rates decreased with time (-7.39%; p = 0.000011) in female patients (-8.94%; p = 0.000003) but remained steady in male patients. Female-to-male and northern-to-southern relative risks of PBC incidence rates ranged from 2.2675 to 4.3318 and from 1.5707 to 3.1725, respectively. The 14-year hepatocellular carcinoma (HCC) cumulative incidence was 9.11%, and the mortality rate was 32.44%; the cumulative incidences of dyslipidemia, thyroid disease, and extrahepatic cancers were 65.13%, 24.40%, and 12.79%, respectively. Higher cumulative incidences of HCC (p = 0.0064) and mortality (p < 0.0001) were noted in male than female PBC patients; southern Taiwan PBC patients had higher cumulative incidences of mortality (p < 0.0001) than their northern counterparts.Conclusion: In Taiwan, decreasing trends in incidence rates and the female-to-male ratio of PBC patients and specific sex and geographic impacts on the incidence rates and outcomes of PBC demand further investigation.
C1 [Cheng, Jur-Shan; Ku, Hsin-Ping] Chang Gung Univ, Coll Med, Clin Informat & Med Stat Res Ctr, Keelung, Taiwan.
[Cheng, Jur-Shan; Chen, Wei-Ting; Chien, Rong-Nan; Chang, Ming-Ling] Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, Div Hepatol, Taoyuan 33305, Taiwan.
[Chen, Wei-Ting; Chien, Rong-Nan; Chang, Ming-Ling] Chang Gung Univ, Coll Med, Dept Med, Taoyuan, Taiwan.
C3 Chang Gung University; Chang Gung Memorial Hospital; Chang Gung
University
RP Chang, ML (corresponding author), Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, Div Hepatol, Taoyuan 33305, Taiwan.
EM mlchang8210@gmail.com
FU Chang Gung Medical Research Program [CMRPG3I0413, CMRPG3L1191,
CMRPG3M0211]; National Science Council [110-2629-B-182-001-,
110-2314-B-182-044-, 111-2629-B-182-001, 111-2314-B-182A-156]
FX Chang Gung Medical Research Program,Grant/Award Numbers: CMRPG3I0413 ,
CMRPG3L1191 , CMRPG3M0211 ,CMRPG1K0111-3 ; National Science
Council,Grant/Award
Numbers:110-2629-B-182-001-,110-2314-B-182-044-,111-2629-B-182-001-,111-
2314-B-182A-156
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worldbank, ABOUT US
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NR 61
TC 3
Z9 3
U1 1
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD SEP
PY 2023
VL 53
IS 9
BP 866
EP 877
DI 10.1111/hepr.13910
EA MAY 2023
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA Q9FY5
UT WOS:000982181100001
PM 37060573
DA 2025-01-07
ER
PT J
AU Yao, MJ
Wang, LJ
Leung, PSC
Li, YM
Liu, SH
Wang, L
Guo, XD
Zhou, GD
Yan, Y
Guan, GW
Chen, XM
Bowlus, CL
Liu, TH
Jia, JD
Gershwin, ME
Ma, X
Zhao, JM
Lu, FM
AF Yao, Mingjie
Wang, Leijie
Leung, Patrick S. C.
Li, Yanmei
Liu, Shuhong
Wang, Lu
Guo, Xiaodong
Zhou, Guangde
Yan, Ying
Guan, Guiwen
Chen, Xiangmei
Bowlus, Christopher L.
Liu, Tianhui
Jia, Jidong
Gershwin, M. Eric
Ma, Xiong
Zhao, Jingmin
Lu, Fengmin
TI The Clinical Significance of GP73 in Immunologically Mediated Chronic
Liver Diseases: Experimental Data and Literature Review
SO CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
LA English
DT Review
DE Fibrosis; Chronic liver disease; Liver stiffness; FIB-4; APRI
ID CHRONIC HEPATITIS-B; CARCINOMA CELL-PROLIFERATION; PRIMARY
BILIARY-CIRRHOSIS; PLATELET RATIO INDEX; GOLGI PROTEIN GP73;
HEPATOCELLULAR-CARCINOMA; NATURAL-HISTORY; ALPHA-FETOPROTEIN;
VIRUS-INFECTION; C VIRUS
AB There is significant void in establishing validated non-invasive surrogate biomarkers of liver fibrosis/cirrhosis in chronic liver diseases (CLD). Golgi protein 73 (GP73) has been suggested as a potential serum marker for the diagnosis of hepatocellular carcinoma (HCC). However, significant background of cirrhosis could have accounted for the elevation of serum GP73 in HCC. In this study, we have taken advantage of a well-defined extensive cohort of 3044 patients with either compensated cirrhosis (n = 1247), decompensated cirrhosis (n = 841) or pre-cirrhotic CLD (n = 956) and our ability to quantify serum GP73 to define the potential of serum GP73 as a biomarker of liver cirrhosis/fibrosis in CLD. The diagnostic value of GP73 was compared with aspartate aminotransferase-to-platelet ratio index (APRI), fibrosis index based on four factors (FIB-4) and liver stiffness measurement (LSM). Immunohistochemical analysis was performed to measure hepatic GP73 expression. Receiver operating characteristic curve analysis demonstrated that serum GP73 had a good diagnostic potential for compensated cirrhosis regardless of etiology. The diagnostic performance of GP73 is better than APRI, FIB-4 and similar with LSM, especially in patients with severe inflammation, steatosis and cholestasis. Notably, in patients of autoimmune liver diseases, non-alcoholic fatty liver disease and viral hepatitis, serum GP73 also exhibited diagnostic value for advanced fibrosis as well as cirrhosis. Furthermore, there is also a gradual increase in GP73 expression with disease progression from mild fibrosis to cirrhosis. In conclusion, GP73 is an effective and reliable serological marker for the diagnosis of advanced fibrosis and prediction of appearance of cirrhosis.
C1 [Yao, Mingjie; Wang, Leijie; Wang, Lu; Yan, Ying; Guan, Guiwen; Chen, Xiangmei; Lu, Fengmin] Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Microbiol, 38 Xueyuan Rd, Beijing 100191, Peoples R China.
[Yao, Mingjie; Wang, Leijie; Wang, Lu; Yan, Ying; Guan, Guiwen; Chen, Xiangmei; Lu, Fengmin] Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Infect Dis Ctr, 38 Xueyuan Rd, Beijing 100191, Peoples R China.
[Leung, Patrick S. C.; Gershwin, M. Eric] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Li, Yanmei; Ma, Xiong] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes, Key Lab Gastroenterol & Hepatol,Shanghai Inst Dig, Sch Med,Renji Hosp,Shanghai Canc Inst,Minist Hlth, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.
[Liu, Shuhong; Guo, Xiaodong; Zhou, Guangde; Zhao, Jingmin] Beijing 302 Hosp, Dept Pathol & Hepatol, Beijing 100039, Peoples R China.
[Bowlus, Christopher L.] Univ Calif Davis, Sch Med, Div Gastroenterol & Hepatol, Davis, CA 95616 USA.
[Liu, Tianhui; Jia, Jidong] Capital Med Univ, Liver Res Ctr, Beijing Friendship Hosp, Beijing Key Lab Translat Med Liver Cirrhosis, Beijing 100050, Peoples R China.
[Liu, Tianhui; Jia, Jidong] Natl Clin Res Ctr Digest Dis, Beijing 100050, Peoples R China.
C3 Peking University; Peking University; University of California System;
University of California Davis; Shanghai Jiao Tong University; Fifth
Medical Center of Chinese PLA General Hospital; University of California
System; University of California Davis; Capital Medical University
RP Lu, FM (corresponding author), Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Microbiol, 38 Xueyuan Rd, Beijing 100191, Peoples R China.; Lu, FM (corresponding author), Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Infect Dis Ctr, 38 Xueyuan Rd, Beijing 100191, Peoples R China.; Leung, PSC (corresponding author), Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.; Ma, X (corresponding author), Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes, Key Lab Gastroenterol & Hepatol,Shanghai Inst Dig, Sch Med,Renji Hosp,Shanghai Canc Inst,Minist Hlth, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.; Zhao, JM (corresponding author), Beijing 302 Hosp, Dept Pathol & Hepatol, Beijing 100039, Peoples R China.
EM psleung@ucdavais.edu; maxiongmd@hotmail.com; jmzhao302@163.com;
lu.fengmin@hsc.pku.edu.cn
RI Yan, Ying/HCH-4386-2022; Bowlus, Christopher/N-9276-2016
OI Yao, Mingjie/0000-0002-5341-1714; Bowlus,
Christopher/0000-0002-3906-6811; Ma, Xiong/0000-0001-9616-4672; Guan,
Guiwen/0009-0006-3688-6829; Yan, Ying/0000-0001-8556-7417; Li,
Yanmei/0009-0001-1232-7954
FU National S&T Major Project for Infectious Diseases [2017ZX10302201,
2017ZX10202203]; Beijing Municipal Science and Technology Commission
[Z161100000116047, D161100002716003]; National Natural Science
Foundation of China [81372603, 81471938, 81325002, 81620108002]; 111
Project [B07001]; Research Fund of the Capital Medical Development
[2014-2-5032]; Beijing Municipal Administration of Hospitals Clinical
Medicine Development of Special Funding Support [XMLX201606]
FX This work was supported by the National S&T Major Project for Infectious
Diseases (No. 2017ZX10302201 and 2017ZX10202203), the project from
Beijing Municipal Science and Technology Commission (Z161100000116047
and D161100002716003), the National Natural Science Foundation of China
Grant (No. 81372603, 81471938, 81325002 and 81620108002), the 111
Project (B07001), Research Fund of the Capital Medical Development
(Grant No. 2014-2-5032) and the project from the Beijing Municipal
Administration of Hospitals Clinical Medicine Development of Special
Funding Support (code XMLX201606).
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NR 77
TC 35
Z9 43
U1 0
U2 31
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1080-0549
EI 1559-0267
J9 CLIN REV ALLERG IMMU
JI Clin. Rev. Allergy Immunol.
PD APR
PY 2018
VL 54
IS 2
BP 282
EP 294
DI 10.1007/s12016-017-8655-y
PG 13
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA GA8FN
UT WOS:000428574100007
PM 29256057
DA 2025-01-07
ER
PT J
AU Yeoman, AD
Longhi, MS
Heneghan, MA
AF Yeoman, A. D.
Longhi, M. S.
Heneghan, M. A.
TI Review article: the modern management of autoimmune hepatitis
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
ID REGULATORY T-CELLS; CHRONIC ACTIVE HEPATITIS; PRIMARY BILIARY-CIRRHOSIS;
LONG-TERM MAINTENANCE; SOLUBLE LIVER ANTIGEN; LOW-DOSE TACROLIMUS;
THIOPURINE METHYLTRANSFERASE; MYCOPHENOLATE-MOFETIL; IMMUNOSUPPRESSIVE
THERAPY; HEPATOCELLULAR-CARCINOMA
AB P>Background
The management of autoimmune hepatitis (AIH) continues to be refined. However, several issues remain unresolved, primarily as a consequence of the low incidence of the disease. This factor has contributed both to a lack of understanding of and a paucity of large scale clinical trials involving therapeutic agents.
Aim
To summarize the latest evidence regarding the pathogenesis, diagnosis, therapy and long-term management of AIH with a focus on clinical aspects of the disease.
Method
We searched PUBMED for articles pertaining to AIH, its pathogenesis, treatment and clinical outcomes, combined with the authors' own knowledge of the literature.
Results
Standard therapy (corticosteroids and azathioprine) is effective in more than 80% of patients which renders study of novel agents difficult. Budesonide appears to show equivalence to prednisolone. Available, but limited, data suggest that mycophenolate mofetil, tacrolimus and ciclosporin are all variably effective second line agents. Patients with AIH and cirrhosis are at risk of hepatocellular carcinoma (HCC) and require screening. Patients with end stage liver disease represent excellent candidates for liver transplantation.
Conclusions
Despite ongoing limitations in the understanding of pathogenesis and difficulties in evaluating novel therapies, the management of AIH continues to evolve slowly. Multi-centre collaboration is necessary to obtain sufficient patient numbers to undertake good quality therapeutic studies.
C1 [Yeoman, A. D.; Longhi, M. S.; Heneghan, M. A.] Kings Coll Hosp London, NHS Fdn Trust, Inst Liver Studies, London SE5 9RS, England.
C3 Oxford University Hospitals NHS Foundation Trust; King's College
Hospital NHS Foundation Trust; King's College Hospital; University of
London; King's College London
RP Heneghan, MA (corresponding author), Kings Coll Hosp London, NHS Fdn Trust, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
EM michael.heneghan@kch.nhs.uk
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NR 127
TC 42
Z9 46
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD APR 15
PY 2010
VL 31
IS 8
BP 771
EP 787
DI 10.1111/j.1365-2036.2010.04241.x
PG 17
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 571CC
UT WOS:000275726100001
PM 20096018
DA 2025-01-07
ER
PT J
AU Pekáriková, A
Sánchez, D
Palova-Jelinková, L
Simsová, M
Benes, Z
Hoffmanová, I
Drastich, P
Janatková, I
Mothes, T
Tlaskalová-Hogenová, H
Tucková, L
AF Pekarikova, A.
Sanchez, D.
Palova-Jelinkova, L.
Simsova, M.
Benes, Z.
Hoffmanova, I.
Drastich, P.
Janatkova, I.
Mothes, T.
Tlaskalova-Hogenova, H.
Tuckova, L.
TI Calreticulin is a B cell molecular target in some gastrointestinal
malignancies
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Article
DE antigenic epitopes; autoantibodies; calreticulin; hepatocellular
carcinoma; pancreatic adenocarcinoma
ID BREAST-CANCER; CELIAC-DISEASE; HEPATOCELLULAR-CARCINOMA;
ENDOPLASMIC-RETICULUM; AUTOIMMUNE-DISEASE; COLORECTAL-CANCER;
PANCREATIC-CANCER; HUMORAL IMMUNITY; AUTOANTIBODIES; ANTIBODIES
AB P>Calreticulin, upon translocation to the cell surface, plays a critical role in the recognition of tumour cells and in experimentally induced cellular anti-tumour immunity. However, less is known about anti-calreticulin antibodies and their role in malignancies. Using enzyme-linked immunosorbent assay (ELISA), we found immunoglobulin (Ig)A and/or IgG anti-calreticulin antibodies in sera of approximately 63% of patients with hepatocellular carcinoma (HCC), 57% of patients with colorectal adenocarcinoma (CRA) and 47% of patients with pancreatic adenocarcinoma (PACA), while healthy controls, patients with viral hepatitis C and with chronic pancreatitis reached only 2%, 20% and 31% seropositivity, respectively. We found significantly elevated mean levels of IgA anti-calreticulin antibodies (P < 0 center dot 001) in patients with HCC (78 center dot 7 +/- 52 center dot 3 AU, mean +/- standard deviation), PACA (66 center dot 5 +/- 30 center dot 9 AU) and CRA (61 center dot 8 +/- 25 center dot 8 AU) when compared to healthy controls (41 center dot 4 +/- 19 center dot 2 AU). Significantly elevated mean levels of IgG anti-calreticulin antibodies (P < 0 center dot 001) were detected in patients with HCC (121 center dot 9 +/- 94 center dot 2 AU), gall bladder adenocarcinoma (118 center dot 4 +/- 80 center dot 0 AU) and PACA (88 center dot 7 +/- 55 center dot 6 AU) when compared to healthy controls (56 center dot 7 +/- 22 center dot 9 AU). Pepscan analysis revealed a large number of antigenic epitopes of calreticulin recognized by both IgA and IgG antibodies of patients with HCC and PACA, indicating robust systemic immune response. Moreover, significantly elevated levels of antibodies against peptide KGEWKPRQIDNP (P < 0 center dot 001) in these patients, tested by ELISA, confirmed the distinct character of antibody reactivity against calreticulin. The high occurrence and specificity of serum anti-calreticulin autoantibodies in the majority of patients with some gastrointestinal malignancies provide the evidence for their possible clinical relevance.
C1 [Pekarikova, A.; Sanchez, D.; Palova-Jelinkova, L.; Simsova, M.; Tlaskalova-Hogenova, H.; Tuckova, L.] Acad Sci Czech Republic, Inst Microbiol, Vvi, Dept Immunol, CR-14220 Prague 4, Czech Republic.
[Hoffmanova, I.] Charles Univ Prague, Fac Med 3, Dept Internal Med 2, Prague, Czech Republic.
[Benes, Z.] Thomayers Fac Hosp, Prague, Czech Republic.
[Drastich, P.] Charles Univ Prague, Inst Clin & Expt Med, Prague, Czech Republic.
[Janatkova, I.] Charles Univ Prague, Lab Clin Immunol & Allergol, Inst Clin Biochem, Prague, Czech Republic.
Charles Univ Prague, Diagnost Lab, Gen Teaching Hosp, Prague, Czech Republic.
Charles Univ Prague, Fac Med 1, Prague, Czech Republic.
[Mothes, T.] Univ Hosp, Inst Lab Med Clin Chem & Mol Diagnost, Leipzig, Germany.
C3 Czech Academy of Sciences; Institute of Microbiology of the Czech
Academy of Sciences; Charles University Prague; Thomayer Hospital;
Charles University Prague; Institute for Clinical & Experimental
Medicine (IKEM); Charles University Prague; General University Hospital
Prague; Charles University Prague; Charles University Prague; Leipzig
University
RP Sánchez, D (corresponding author), Acad Sci Czech Republic, Inst Microbiol, Vvi, Dept Immunol, Videnska 1083, CR-14220 Prague 4, Czech Republic.
EM sanchez.cohn@gmail.com
RI Benes, Zdenek/JQX-0143-2023; Sánchez, Daniel/J-6883-2014; Hoffmanova,
Iva/D-7220-2017
OI Hoffmanova, Iva/0000-0002-1546-6853
FU Academy of Sciences of the Czech Republic [A500200709, 500200801,
A500200910]; Grant Agency of the Czech Republic [310/08/H077,
310/07/0414]; Ministry of Education of the Czech Republic [2B06155];
Czech Ministry of Health [NS9705-4/2008]; Institutional Research Concept
[AVOZ50200510]
FX This work was supported by grants A500200709, 500200801, A500200910 from
the Academy of Sciences of the Czech Republic, by grants 310/08/H077,
310/07/0414 from the Grant Agency of the Czech Republic, 2B06155 from
the Ministry of Education of the Czech Republic, NS9705-4/2008 from the
Czech Ministry of Health, and by the Institutional Research Concept
Grant AVOZ50200510.
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NR 32
TC 26
Z9 28
U1 0
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD MAY
PY 2010
VL 160
IS 2
BP 215
EP 222
DI 10.1111/j.1365-2249.2009.04085.x
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 581CT
UT WOS:000276499400009
PM 20030668
OA Green Published
DA 2025-01-07
ER
PT J
AU Zhao, YY
Gong, C
Xu, J
Chen, D
Yang, B
Chen, ZS
Wei, L
AF Zhao, Yuanyuan
Gong, Chen
Xu, Jing
Chen, Dong
Yang, Bo
Chen, Zhishui
Wei, Lai
TI Research Progress of Fecal Microbiota Transplantation in Liver Diseases
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE fecal microbiota transplantation; chronic liver diseases; gut
microbiota; gut-liver axis; liver transplantation
ID PRIMARY SCLEROSING CHOLANGITIS; CLOSTRIDIUM-DIFFICILE INFECTION; B-VIRUS
INFECTION; GUT MICROBIOTA; INTESTINAL MICROBIOTA; AUTOIMMUNE HEPATITIS;
HEPATOCELLULAR-CARCINOMA; MOUSE MODEL; DYSBIOSIS; GUIDELINES
AB A growing body of evidence suggested that gut microbiota is associated with liver diseases through the gut-liver axis. The imbalance of gut microbiota could be correlated with the occurrence, development, and prognosis of a series of liver diseases, including alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), viral hepatitis, cirrhosis, primary sclerosing cholangitis (PSC), and hepatocellular carcinoma (HCC). Fecal microbiota transplantation (FMT) seems to be a method to normalize the patient's gut microbiota. This method has been traced back to the 4th century. In recent decade, FMT has been highly regarded in several clinical trials. As a novel approach to reconstruct the intestinal microecological balance, FMT has been used to treat the chronic liver diseases. Therefore, in this review, the role of FMT in the treatment of liver diseases was summarized. In addition, the relationship between gut and liver was explored through the gut-liver axis, and the definition, objectives, advantages, and procedures of FMT were described. Finally, the clinical value of FMT therapy in liver transplant (LT) recipients was briefly discussed.
C1 [Zhao, Yuanyuan; Xu, Jing; Chen, Dong; Yang, Bo; Chen, Zhishui; Wei, Lai] Huazhong Univ Sci & Technol, Tongji Hosp, Inst Organ Transplantat, Tongji Med Coll, Wuhan 430030, Peoples R China.
[Zhao, Yuanyuan; Xu, Jing; Chen, Dong; Yang, Bo; Chen, Zhishui; Wei, Lai] Minist Educ, Key Lab Organ Transplantat, Wuhan 430030, Peoples R China.
[Zhao, Yuanyuan; Xu, Jing; Chen, Dong; Yang, Bo; Chen, Zhishui; Wei, Lai] Chinese Acad Med Sci, NHC Key Lab Organ Transplantat, Wuhan 430030, Peoples R China.
[Zhao, Yuanyuan; Xu, Jing; Chen, Dong; Yang, Bo; Chen, Zhishui; Wei, Lai] Chinese Acad Med Sci, Key Lab Organ Transplantat, Wuhan 430030, Peoples R China.
[Zhao, Yuanyuan; Xu, Jing; Chen, Dong; Yang, Bo; Chen, Zhishui; Wei, Lai] Chinese Acad Med Sci, Key Lab Organ Transplantat, Wuhan 430030, Peoples R China.
[Gong, Chen] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Oncol, Wuhan 430030, Peoples R China.
C3 Huazhong University of Science & Technology; Chinese Academy of Medical
Sciences - Peking Union Medical College; Chinese Academy of Medical
Sciences - Peking Union Medical College; Chinese Academy of Medical
Sciences - Peking Union Medical College; Huazhong University of Science
& Technology
RP Wei, L (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Inst Organ Transplantat, Tongji Med Coll, Wuhan 430030, Peoples R China.; Wei, L (corresponding author), Minist Educ, Key Lab Organ Transplantat, Wuhan 430030, Peoples R China.; Wei, L (corresponding author), Chinese Acad Med Sci, NHC Key Lab Organ Transplantat, Wuhan 430030, Peoples R China.; Wei, L (corresponding author), Chinese Acad Med Sci, Key Lab Organ Transplantat, Wuhan 430030, Peoples R China.; Wei, L (corresponding author), Chinese Acad Med Sci, Key Lab Organ Transplantat, Wuhan 430030, Peoples R China.
EM weilai@tjh.tjmu.edu.cn
RI YANG, BO/JGM-2237-2023; Nikolli, Pal/O-2733-2014; GONG,
CHEN/JDW-5727-2023; Zhao, Yuanyuan/AAY-6670-2021
OI Zhao, Yuanyuan/0000-0003-0217-3290; Yang, Bo/0000-0002-3183-5567
FU Health Commission of Hubei Province [WJ2021C001]; Key Research and
Development Plan of Hubei Province [2022BCA015]
FX This study was supported by grants from the Health Commission of Hubei
Province (funder: ZS.C; Grant No. WJ2021C001) and Key Research and
Development Plan of Hubei Province (funder: ZS.C; Grant No. 2022BCA015).
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NR 113
TC 20
Z9 20
U1 7
U2 34
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD FEB
PY 2023
VL 12
IS 4
AR 1683
DI 10.3390/jcm12041683
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 9H1EO
UT WOS:000938583100001
PM 36836218
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Ooi, K
Shiraki, K
Morishita, Y
Nobori, T
AF Ooi, Kinue
Shiraki, Katsuya
Morishita, Yoshitaka
Nobori, Tsutomu
TI High-molecular intestinal alkaline phosphatase in chronic liver diseases
SO JOURNAL OF CLINICAL LABORATORY ANALYSIS
LA English
DT Article
DE chronic liver disease; alkaline phosphatase isoenzyme; intestinal
alkaline phosphatase; high-molecular intestinal alkaline phosphatase;
ABO blood group
ID SERUM; ISOENZYMES; ISOFORMS; SECRETOR; VARIANT
AB The presence of high-molecular intestinal alkaline phosphatase (HIALP) different from bone ALP detected in the alpha(2)beta region was recently clarified. In this study we used a novel method in which HIALP was detected after conversion to ALPS by protease to investigate the clinical significance of the appearance of HIALP in patients with chronic liver disease. The subjects were 241 patients with chronic liver disease. When a decrease in ALPS in the alpha(2)beta region and an increase in ALPS in the (3 region were noted, the patient was judged HIALP-positive. In the patients with chronic liver disease, the total ALP activity (T-ALP) increased with progression of the pathology in the order of chronic hepatitis (CH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC). HIALP appeared in 22.4% and 49.3% of patients with CH and LC, respectively, but the positivity rate decreased to 30.4% in HCC. As autoimmune liver diseases, primary biliary cirrhosis (PBC) and autoimmune hepatitis (AIH) were investigated. T-ALP was lower in PBC +AIH than in LC and HCC, but the HIALP-positive rate was high (44.4%). The HIALP-positive rate was dependent on ABO blood groups, and was high in blood groups B and O. In conclusion, the HIALP-positive rate was particularly high in patients with chronic liver disease, and was related to the pathological progression, which suggests that the method is clinically useful.
C1 Mie Univ, Sch Med, Dept Internal Med 1, Tsu, Mie 5148507, Japan.
Mie Univ, Sch Med, Dept Lab Med, Tsu, Mie 5148507, Japan.
C3 Mie University; Mie University
RP Shiraki, K (corresponding author), Mie Univ, Sch Med, Dept Internal Med 1, 2-174 Edobashi, Tsu, Mie 5148507, Japan.
EM katsuyas@clin.medic.mie-u.ac.jp
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NR 20
TC 179
Z9 184
U1 0
U2 55
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0887-8013
EI 1098-2825
J9 J CLIN LAB ANAL
JI J. Clin. Lab. Anal.
PY 2007
VL 21
IS 3
BP 133
EP 139
DI 10.1002/jcla.20178
PG 7
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA 171CK
UT WOS:000246712300001
PM 17506485
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Floreani, A
Spinazzè, A
Caballeria, L
Reig, A
Cazzagon, N
Franceschet, I
Buja, A
Furlan, P
Harada, K
Leung, PSC
Gershwin, ME
Pares, A
AF Floreani, Annarosa
Spinazze, Alice
Caballeria, Llorenc
Reig, Ana
Cazzagon, Nora
Franceschet, Irene
Buja, Alessandra
Furlan, Patrizia
Harada, Kenichi
Leung, Patrick S. C.
Gershwin, M. Eric
Pares, Albert
TI Extrahepatic Malignancies in Primary Biliary Cirrhosis: A Comparative
Study at Two European Centers
SO CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
LA English
DT Review
DE Extrahepatic malignancies; PBC; Cancer; Survival
ID AUTOIMMUNE LIVER-DISEASES; DOSE URSODEOXYCHOLIC ACID; DOMINANT-NEGATIVE
FORM; CD8(+) T-CELLS; HEPATOCELLULAR-CARCINOMA; RISK-FACTORS;
ULCERATIVE-COLITIS; BREAST-CANCER; FOLLOW-UP; CHOLANGITIS
AB Limited information and divergent results are available on the prevalence/incidence, survival, and risk factors for developing extrahepatic malignancies (EMs) in primary biliary cirrhosis (PBC). The aim of the study was to analyze the epidemiology and survival rates for EM in PBC patients. The study was conducted on two series of patients followed up at two European centers (361 in Padova, Italy, and 397 in Barcelona, Spain) for a mean 7.7 +/- 7 and 12.2 +/- 7 years, respectively. The cancer incidence was compared with the standardized incidence ratios (SIRs) calculated using the Cancer Registry of the Veneto Region (Italy) and the Cancer Registry of Tarragona (Spain). Seventy-two patients developed EM. The prevalence of cases was similar in Padova (9.7 %) and Barcelona (9.4 %). The overall cancer incidence was similar to the expected incidence for the general population in the same geographical area (SIR = 1.2), and so was the crude EM rate (855.01 vs 652.86 per 100,000 patient-years, respectively, RR = 1.3). Logistic regression analysis showed that advanced histological stage and extrahepatic autoimmune diseases were significantly associated with the onset of EM. Survival was similar for PBC patients with and without EM (p = n.s.), and actual survival was similar to the one predicted by the Mayo model. The incidence of EM in PBC patients was found similar in Italy and Spain and no different from that of the general population. Advanced histological stage and extrahepatic autoimmune disease were risk factors significantly associated with EM developing in PBC. The onset of cancer in PBC patients does not influence the natural history of their liver disease.
C1 [Floreani, Annarosa; Spinazze, Alice; Cazzagon, Nora; Franceschet, Irene] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
[Caballeria, Llorenc; Reig, Ana; Pares, Albert] Univ Barcelona, Ctr Invest Biomed Red Enfermedades Hepat & Digest, IDIBAPS, Liver Unit,Hosp Clin, Barcelona, Spain.
[Buja, Alessandra; Furlan, Patrizia] Univ Padua, Publ Hlth Sect, Dept Mol Med, Padua, Italy.
[Harada, Kenichi] Kanazawa Univ, Sch Med, Dept Pathol, Kanazawa, Ishikawa 920, Japan.
[Leung, Patrick S. C.; Gershwin, M. Eric] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
C3 University of Padua; University of Barcelona; Hospital Clinic de
Barcelona; IDIBAPS; CIBER - Centro de Investigacion Biomedica en Red;
CIBEREHD; University of Padua; Kanazawa University; University of
California System; University of California Davis
RP Floreani, A (corresponding author), Univ Padua, Dept Surg Oncol & Gastroenterol, Via Giustiniani 2, Padua, Italy.
EM annarosa.floreani@unipd.it
RI Buja, Alessandra/AAN-8141-2020; Pares, Albert/M-6268-2019; Pares,
Albert/G-1328-2011
OI FURLAN, PATRIZIA/0000-0001-5345-7037; Pares, Albert/0000-0002-5413-9687;
Caballeria, Llorenc/0000-0002-7990-0719; Cazzagon,
Nora/0000-0002-6937-8664
FU Padova University
FX The work was partially supported by a Padova University grant (ex 60 %
fund).
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NR 68
TC 16
Z9 16
U1 0
U2 13
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1080-0549
EI 1559-0267
J9 CLIN REV ALLERG IMMU
JI Clin. Rev. Allergy Immunol.
PD JUN
PY 2015
VL 48
IS 2-3
BP 254
EP 262
DI 10.1007/s12016-014-8446-7
PG 9
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA CF6XY
UT WOS:000352701400015
PM 25205363
DA 2025-01-07
ER
PT J
AU Chen, QH
Lu, XY
Zhang, XY
AF Chen, Qianhui
Lu, Xinyu
Zhang, Xiaoyong
TI Noncanonical NF-κB Signaling Pathway in Liver Diseases
SO JOURNAL OF CLINICAL AND TRANSLATIONAL HEPATOLOGY
LA English
DT Review
DE Noncanonical NF-kappa B pathway; NF-kappa B-inducing kinase; Liver
inflammation; Immune responses; Liver diseases
ID CELL-ACTIVATING FACTOR; LYMPHOTOXIN-BETA-RECEPTOR; HEPATITIS-B; KINASE
NIK; HEPATOCELLULAR-CARCINOMA; GENE-EXPRESSION; IKK-ALPHA; BAFF;
INFLAMMATION; STEATOSIS
AB The noncanonical NF-kappa B signaling pathway is an important branch of NF-kappa B signaling. It is involved in regulating multiple important biological processes, including inflammation and host immune response. A central adaptor protein of the noncanonical NF-kappa B pathway is NF-kappa B-inducing kinase (NIK), which activates the downstream kinase IKKa to process p100 to p52, thereby forming the RelB/p52 heterodimer to initiate the expression of target genes. Currently, many specific inhibitors and monoclonal antibodies targeting or triggering this pathway are being developed and tested for various diseases, including cancers, autoimmune diseases, and virus infection. Given that aberrant activation of the noncanonical NF-kappa B pathway is frequently observed in various liver diseases, targeting this pathway may be a promising therapeutic strategy to alleviate liver inflammation. Moreover, activation of this pathway may contribute to the antiviral immune response and promote the clearance of persistent hepatotropic virus infection. Here, we review the role of the noncanonical NF-kappa B pathway in the occurrence and development of different liver diseases, and discuss the potency and application of modulating the noncanonical NF-kappa B pathway for treatment of these liver diseases.
C1 [Chen, Qianhui; Lu, Xinyu; Zhang, Xiaoyong] Southern Med Univ, Nanfang Hosp, Dept Infect Dis, State Key Lab Organ Failure Res,Guangdong Prov Ke, Guangzhou, Guangdong, Peoples R China.
[Zhang, Xiaoyong] Southern Med Univ, Shenzhen Hosp, Hepatol Unit, Shenzhen, Guangdong, Peoples R China.
C3 Southern Medical University - China; Southern Medical University - China
RP Zhang, XY (corresponding author), Southern Med Univ, Nanfang Hosp, Hepatol Unit, 1838 North Guangzhou Ave, Guangzhou 510515, Peoples R China.; Zhang, XY (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Infect Dis, 1838 North Guangzhou Ave, Guangzhou 510515, Peoples R China.
EM xiaoyzhang@smu.edu.cn
RI Lu, Xinyu/KIB-5798-2024
FU National Natural Science Foundation of China [81871664]; National
Science and Technology Major Project [2018ZX10301202-003]
FX This review was partly supported by grants from the National Natural
Science Foundation of China (No. 81871664) and the National Science and
Technology Major Project (No. 2018ZX10301202-003).
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NR 67
TC 23
Z9 27
U1 1
U2 27
PU XIA & HE PUBLISHING INC
PI SUGAR LAND
PA SECOND AFFILIATED HOSP CHONGQING MEDICAL UNIV, 14090 SOUTHWEST FREEWAY,
STE 300, SUGAR LAND, TX 77478 USA
SN 2225-0719
EI 2310-8819
J9 J CLIN TRANSL HEPATO
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PD JAN-FEB
PY 2021
VL 9
IS 1
BP 81
EP 89
DI 10.14218/JCTH.2020.00063
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA QF9FR
UT WOS:000617194500010
PM 33604258
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wang, X
Lin, SX
Tao, J
Wei, XQ
Liu, YT
Chen, YM
Wu, B
AF Wang, Xing
Lin, Shang-Xiong
Tao, Jin
Wei, Xiu-Qing
Liu, Yuan-Ting
Chen, Yu-Ming
Wu, Bin
TI Study of liver cirrhosis over ten consecutive years in Southern China
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Liver cirrhosis; Epidemiology; Etiology; Complication; Hepatocellular
carcinoma; Southern China
ID HEPATITIS-B-VIRUS; PRIMARY SCLEROSING CHOLANGITIS; PRIMARY
BILIARY-CIRRHOSIS; ASIA-PACIFIC REGION; HEPATOCELLULAR-CARCINOMA;
NATURAL-HISTORY; CRYPTOGENIC CIRRHOSIS; AUTOIMMUNE HEPATITIS; DISEASE;
MANAGEMENT
AB AIM: To investigate the etiology and complications of liver cirrhosis (LC) in Southern China.
METHODS: In this retrospective, cross-sectional study, we identified cases of liver cirrhosis admitted between January 2001 to December 2010 and reviewed the medical records. Patient demographics, etiologies and complications were collected, and etiological changes were illustrated by consecutive years and within two time periods (2001-2005 and 2006-2010). All results were expressed as the mean +/- SD or as a percentage. The chi(2) test or Student's t-test was used to analyze the differences in age, gender, and etiological distribution, and one-way analysis of variance was applied to estimate the trends in etiological changes. We analyzed the relationship between the etiologies and complications using unconditioned logistic regression, and the risk of upper gastrointestinal bleeding (UGIB) and hepatocellular carcinoma (HCC) in the major etiological groups was evaluated as ORs. A P value less than 0.05 was considered significant. Statistical computation was performed using SPSS 17.0 software.
RESULTS: In this study, we identified 6719 (83.16%) male patients and 1361 (16.84%) female patients. The average age of all of the patients was 50.5 years at the time of diagnosis. The distribution of etiological agents was as follows: viral hepatitis, 80.62% [hepatitis B virus (HBV) 77.22%, hepatitis C virus (HCV) 2.80%, (HBV + HCV) 0.58%]; alcohol, 5.68%; mixed etiology, 4.95%; cryptogenic, 2.93%; and autoimmune hepatitis, 2.03%; whereas the other included etiologies accounted for less than 4% of the total. Infantile hepatitis syndrome LC patients were the youngest (2.5 years of age), followed by the metabolic LC group (27.2 years of age). Viral hepatitis, alcohol, and mixed etiology were more prevalent in the male group, whereas autoimmune diseases, cryptogenic cirrhosis, and metabolic diseases were more prevalent in the female group. When comparing the etiological distribution in 2001-2005 with that in 2006-2010, the proportion of viral hepatitis decreased from 84.7% to 78.3% (P < 0.001), and the proportion of HBV-induced LC also decreased from 81.9% to 74.6% (P < 0.001). The incidence of mixed etiology, cryptogenic cirrhosis, and autoimmune diseases increased by 3.1% (P < 0.001), 0.5% (P = 0.158), and 1.3% (P < 0.001), respectively. Alcohol-induced LC remained relatively steady over the 10-year period. The ORs of the development of UGIB between HBV and other major etiologies were as fol lows: HCV, 1.07; alcohol, 1.89; autoimmune, 0.90; mixed etiology, 0.83; and cryptogenic, 1.76. The ORs of the occurrence of HCC between HBV and other major etiologies were as follows: HCV, 0.54; alcohol, 0.16; autoimmune, 0.05; mixed etiology, 0.58; and cryptogenic, 0.60.
CONCLUSION: The major etiology of liver cirrhosis in Southern China is viral hepatitis. However, the proportions of viral hepatitis and HBV are gradually decreasing. Alcoholic LC patients exhibit a greater risk of experiencing UGIB, and HBV LC patients may have a greater risk of HCC. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
C1 [Wang, Xing; Lin, Shang-Xiong; Tao, Jin; Wei, Xiu-Qing; Wu, Bin] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Gastroenterol, Guangzhou 510630, Guangdong, Peoples R China.
[Liu, Yuan-Ting] Cent Hosp Panyu Dist, Informat Sect, Guangzhou 511400, Guangdong, Peoples R China.
[Chen, Yu-Ming] Sun Yat Sen Univ, Zhongshan Med Sch, Sch Publ Hlth, Guangzhou 510080, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University
RP Wu, B (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 3, Dept Gastroenterol, 600 Tianhe Rd, Guangzhou 510630, Guangdong, Peoples R China.
EM binwu001@hotmail.com
RI Wang, Xuemei/GXF-3702-2022
OI Wang, Xing/0000-0002-5950-4591
FU Major Projects Incubator Program of National Key Basic Research Program
of China [2012CB526700]; National Natural Science Foundation of China
[81370511]; Natural Science Foundation of Guangdong Province
[S2011020002348]; Fundamental Research Funds for the Central
Universities [13ykjc01, 82000-3281901]
FX Supported by grants (in part) from the Major Projects Incubator Program
of National Key Basic Research Program of China, No. 2012CB526700;
National Natural Science Foundation of China, No. 81370511; Natural
Science Foundation of Guangdong Province, No. S2011020002348; and
Fundamental Research Funds for the Central Universities, No. 13ykjc01
and No. 82000-3281901
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NR 43
TC 58
Z9 79
U1 1
U2 25
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD OCT 7
PY 2014
VL 20
IS 37
BP 13546
EP 13555
DI 10.3748/wjg.v20.i37.13546
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AR9GN
UT WOS:000343881200029
PM 25309085
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Ali, NA
Hamdy, NM
Gibriel, AA
EL Mesallamy, HO
AF Ali, Nermin A.
Hamdy, Nadia M.
Gibriel, Abdullah A.
EL Mesallamy, Hala O.
TI Investigation of the relationship between CTLA4 and the tumor suppressor
RASSF1A and the possible mediating role of STAT4 in a cohort of Egyptian
patients infected with hepatitis C virus with and without hepatocellular
carcinoma
SO ARCHIVES OF VIROLOGY
LA English
DT Article
AB The Ras association domain family 1 isoform A (RASSF1A), cytotoxic T lymphocyte antigen 4 (CTLA-4), and signal transducer and activator of transcription 4 (STAT4) genes play a role in regulating the cell cycle, apoptosis, and the autoimmune response against cancer. We investigated the genotype frequency and the possible association of the rs2073498 (RASSF1A), rs5742909 (CTLA-4) and rs7574865 (STAT4) genetic variants with hepatitis C virus (HCV)-G4-mediated hepatocellular carcinoma (HCC) progression in Egyptian patients. Fifty patients with HCV infection, 50 patients with HCV-mediated HCC, and 50 age- and sex-matched healthy controls were recruited. The investigated variants were genotyped based on polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). The Ser133 mutant G4 variant of the rs2073498 SNP in RASSF1A exhibited a positive correlation with HCC incidence risk (OR = 0.571, 95% CI = 0.175-1.865, P < 0.001). The rs7574865 variant in STAT4 (G/T) occurred frequently in both HCV groups, with a significant incidence risk (OR = 1.583, 95% CI = 1.123-2.232, P = 0.005). The rs5742909 change in CTLA4 (C/T) did not show a significant difference between HCV-mediated HCC cases and the control group (OR = 4.5, 95% CI = 1.326-15.277, P > 0.001). Activation of the immune checkpoint gene CTLA4 or polymorphism in the encoded CTLA4 protein causes phosphorylation of kinases needed for RAS gene activation. This in turn downregulates the tumor suppressor RASSF1, inhibiting apoptosis and leading to HCC development, indicating a negative impact of CTLA4 gene polymorphism on HCV-mediated HCC cases. A major determinant of disease progression could be immune system genetic variants, together with the presence of costimulatory factors. The rs2073498 and rs7574865 variations in the RASSF1A and STAT4 genes, respectively, could be genetic susceptibility factors for Egyptian patients with HCV-mediated HCC.
[GRAPHICS]
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C1 [Ali, Nermin A.; Gibriel, Abdullah A.] British Univ Egypt BUE, Biochem & Mol Biol Dept, Fac Pharm, Cairo, Egypt.
[Hamdy, Nadia M.; EL Mesallamy, Hala O.] Ain Shams Univ, Dept Biochem, Fac Pharm, Cairo 11566, Egypt.
[Gibriel, Abdullah A.] BUE, Ctr Drug Res & Dev CDRD, Fac Pharm, Cairo, Egypt.
[EL Mesallamy, Hala O.] Sinai Univ, Dept Biochem, Fac Pharm, Kantara, Egypt.
C3 Egyptian Knowledge Bank (EKB); British University in Egypt; Egyptian
Knowledge Bank (EKB); Ain Shams University; Egyptian Knowledge Bank
(EKB); British University in Egypt; Egyptian Knowledge Bank (EKB); Sinai
University
RP Hamdy, NM; EL Mesallamy, HO (corresponding author), Ain Shams Univ, Dept Biochem, Fac Pharm, Cairo 11566, Egypt.; EL Mesallamy, HO (corresponding author), Sinai Univ, Dept Biochem, Fac Pharm, Kantara, Egypt.
EM n.abdeldayem@hotmail.com; nadia_hamdy@pharma.asu.edu.eg;
abdullah.gibriel@bue.edu.eg; Hala.elmosalamy@su.edu.eg
RI ; M. Hamdy, Prof. Nadia/AAB-6087-2021
OI Gibriel, Abdullah/0000-0002-1318-4510; M. Hamdy, Prof.
Nadia/0000-0003-2105-107X; El Mesallamy, Hala/0000-0001-8190-536X
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NR 34
TC 26
Z9 26
U1 0
U2 1
PU SPRINGER WIEN
PI Vienna
PA Prinz-Eugen-Strasse 8-10, A-1040 Vienna, AUSTRIA
SN 0304-8608
EI 1432-8798
J9 ARCH VIROL
JI Arch. Virol.
PD JUN
PY 2021
VL 166
IS 6
BP 1643
EP 1651
DI 10.1007/s00705-021-04981-8
EA APR 2021
PG 9
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA SJ9XF
UT WOS:000635940900002
PM 33796885
DA 2025-01-07
ER
PT J
AU Himoto, T
Yoneyama, H
Kurokohchi, K
Inukai, M
Masugata, H
Goda, F
Haba, R
Watanabe, S
Senda, S
Masaki, T
AF Himoto, Takashi
Yoneyama, Hirohito
Kurokohchi, Kazutaka
Inukai, Michio
Masugata, Hisashi
Goda, Fuminori
Haba, Reiji
Watanabe, Seishiro
Senda, Shoichi
Masaki, Tsutomu
TI Clinical significance of autoantibodies to p53 protein in patients with
autoimmune liver diseases
SO CANADIAN JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Antibodies to ds-DNA; Antibodies to p53; Autoimmune hepatitis; Primary
biliary cirrhosis
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; PRIMARY BILIARY-CIRRHOSIS; CHRONIC ACTIVE
HEPATITIS; HEPATOCELLULAR-CARCINOMA; ANTICENTROMERE ANTIBODY; SERA;
DEFINE; DNA; EPITOPES; CANCERS
AB BACKGROUND: Autoantibodies to p53 (anti-p53) are rarely present in the sera of patients with autoimmune diseases or the sera of patients with malignancies.
OBJECTIVE: To examine the prevalence of anti-p53 in patients with autoimmune liver disease including autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), AIH/PBC overlap syndrome (AIH/PBC OS) and primary sclerosing cholangitis (PSC), and to determine the clinical significance of anti-p53 in autoimmune liver diseases.
METHODS: Forty patients with AIH, 41 patients with PBC, eight patients with AIH/PBC OS and five patients with PSC were enrolled. Anti-p53 and antibodies to double-stranded DNA (anti-ds-DNA) were analyzed using commercially available ELISA kits. Demographic, laboratory and histological data were compared between the AIH groups seropositive and seronegative for anti-p53.
RESULTS: Six of 40 (15.0%) patients with AIH and four of eight (50.0%) patients with AIH/PBC OS were positive for anti-p53. One of 41 (2.4%) patients with PBC was also positive for anti-p53, but all five patients with PSC were negative, indicating a significantly higher prevalence of anti-p53 in patients with AIH or AIH/PBC OS compared with patients with PBC. None of the AIH patients positive for anti-p53 progressed to hepatic failure or relapsed after immunosuppressive treatment. Titres of anti-ds-DNA in patients with AIH and AIH/PBC OS significantly correlated with titres of anti-p53 (r=0.511; P=0.0213).
CONCLUSION: The emergence of anti-p53 is likely to be useful for discriminating AIH or AIH/PBC OS from PBC and helpful for predicting favourable prognoses in patients with AIH. DNA damage may trigger the production of anti-p53 in patients with AIH or AIH/PBC OS.
C1 [Himoto, Takashi; Inukai, Michio; Masugata, Hisashi; Goda, Fuminori; Senda, Shoichi] Kagawa Univ, Sch Med, Dept Integrated Med, Miki, Kagawa 7610793, Japan.
[Yoneyama, Hirohito; Kurokohchi, Kazutaka; Masaki, Tsutomu] Kagawa Univ, Sch Med, Dept Gastroenterol & Neurol, Miki, Kagawa 7610793, Japan.
[Haba, Reiji] Kagawa Univ, Sch Med, Dept Diag Pathol, Miki, Kagawa 7610793, Japan.
[Watanabe, Seishiro] Kagawa Prefectural Cent Hosp, Dept Internal Med, Kagawa, Japan.
C3 Kagawa University; Kagawa University; Kagawa University
RP Himoto, T (corresponding author), Kagawa Univ, Sch Med, Dept Integrated Med, 1750-1 Ikenobe, Miki, Kagawa 7610793, Japan.
EM thimoto@med.kagawa-u.ac.jp
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NR 30
TC 14
Z9 14
U1 0
U2 1
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2291-2797
J9 CAN J GASTROENTEROL
JI Can. J. Gastroenterol. Hepatol.
PD MAR
PY 2012
VL 26
IS 3
BP 125
EP 129
DI 10.1155/2012/890698
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 905RI
UT WOS:000301289900002
PM 22408762
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Gatselis, NK
Tornai, T
Shums, Z
Zachou, K
Saitis, A
Gabeta, S
Albesa, R
Norman, GL
Papp, M
Dalekos, GN
AF Gatselis, Nikolaos K.
Tornai, Tamas
Shums, Zakera
Zachou, Kalliopi
Saitis, Asterios
Gabeta, Stella
Albesa, Roger
Norman, Gary L.
Papp, Maria
Dalekos, George N.
TI Golgi protein-73: A biomarker for assessing cirrhosis and prognosis of
liver disease patients
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Biomarker; Golgi protein-73; Hepatic fibrosis; Cirrhosis; Hepatocellular
carcinoma; Hepatitis B; Hepatitis C; Aspartate aminotransferase;
Platelets ratio index score
ID CHRONIC HEPATITIS-B; OLIGOMERIC MATRIX PROTEIN;
HEPATOCELLULAR-CARCINOMA; SIGNIFICANT FIBROSIS; PHOSPHOPROTEIN 2; GP73;
EXPRESSION; RISK; PROLIFERATION; DIAGNOSIS
AB BACKGROUND Reliable biomarkers of cirrhosis, hepatocellular carcinoma (HCC), or progression of chronic liver diseases are missing. In this context, Golgi protein-73 (GP73) also called Golgi phosphoprotein-2, was originally defined as a resident Golgi type II transmembrane protein expressed in epithelial cells. As a result, GP73 expression was found primarily in biliary epithelial cells, with only slight detection in hepatocytes. However, in patients with acute or chronic liver diseases and especially in HCC, the expression of GP73 is significantly up-regulated in hepatocytes. So far, few studies have assessed GP73 as a diagnostic or prognostic marker of liver fibrosis and disease progression. AIM To assess serum GP73 efficacy as a diagnostic marker of cirrhosis and/or HCC or as predictor of liver disease progression. METHODS GP73 serum levels were retrospectively determined by a novel GP73 ELISA (QUANTA Lite(R)GP73, Inova Diagnostics, Inc., Research Use Only) in a large cohort of 632 consecutive patients with chronic viral and non-viral liver diseases collected from two tertiary Academic centers in Larissa, Greece (n= 366) and Debrecen, Hungary (n= 266). Aspartate aminotransferase (AST)/Platelets (PLT) ratio index (APRI) was also calculated at the relevant time points in all patients. Two hundred and three patients had chronic hepatitis B, 183 chronic hepatitis C, 198 alcoholic liver disease, 28 autoimmune cholestatic liver diseases, 15 autoimmune hepatitis, and 5 with other liver-related disorders. The duration of follow-up was 50 (57) mo [median (interquartile range)]. The development of cirrhosis, liver decompensation and/or HCC during follow-up were assessed according to internationally accepted guidelines. In particular, the surveillance for the development of HCC was performed regularly with ultrasound imaging and alpha-fetoprotein (AFP) determination every 6 mo in cirrhotic and every 12 mo in non-cirrhotic patients. RESULTS Increased serum levels of GP73 (> 20 units) were detected at initial evaluation in 277 out of 632 patients (43.8%). GP73-seropositivity correlated at baseline with the presence of cirrhosis (96.4%vs51.5%,P< 0.001), decompensation of cirrhosis (60.3%vs35.5%,P< 0.001), presence of HCC (18.4%vs7.9%,P< 0.001) and advanced HCC stage (52.9%vs14.8%,P= 0.002). GP73 had higher diagnostic accuracy for the presence of cirrhosis compared to APRI score [Area under the curve (AUC) (95%CI): 0.909 (0.885-0.934)vs0.849 (0.813-0.886),P= 0.003]. Combination of GP73 with APRI improved further the accuracy (AUC: 0.925) compared to GP73 (AUC: 0.909,P= 0.005) or APRI alone (AUC: 0.849,P< 0.001). GP73 levels were significantly higher in HCC patients compared to non-HCC [22.5 (29.2)vs16 (20.3) units,P< 0.001) and positively associated with BCLC stage [stage 0: 13.9 (10.8); stage A: 17.1 (16.8); stage B: 19.6 (22.3); stage C: 32.2 (30.8); stage D: 45.3 (86.6) units,P< 0.001] and tumor dimensions [very early: 13.9 (10.8); intermediate: 19.6 (18.4); advanced: 29.1 (33.6) units,P= 0.004]. However, the discriminative ability for HCC diagnosis was relatively low [AUC (95%CI): 0.623 (0.570-0.675)]. Kaplan-Meier analysis showed that the detection of GP73 in patients with compensated cirrhosis at baseline, was prognostic of higher rates of decompensation (P= 0.036), HCC development (P= 0.08), and liver-related deaths (P< 0.001) during follow-up. CONCLUSION GP73 alone appears efficient for detecting cirrhosis and superior to APRI determination. In combination with APRI, its diagnostic performance can be further improved.
Most importantly, the simple GP73 measurement proved promising for predicting a worse outcome of patients with both viral and non-viral chronic liver diseases.
C1 [Gatselis, Nikolaos K.; Zachou, Kalliopi; Saitis, Asterios; Gabeta, Stella; Dalekos, George N.] Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Dept Med, Larisa 41110, Greece.
[Gatselis, Nikolaos K.; Zachou, Kalliopi; Saitis, Asterios; Gabeta, Stella; Dalekos, George N.] Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Res Lab Internal Med, Larisa 41110, Greece.
[Gatselis, Nikolaos K.; Zachou, Kalliopi; Dalekos, George N.] Inst Internal Med & Hepatol, Larisa 41447, Greece.
[Tornai, Tamas; Papp, Maria] Univ Debrecen, Fac Med, Dept Internal Med, Div Gastroenterol, H-4032 Debrecen, Hungary.
[Shums, Zakera; Albesa, Roger; Norman, Gary L.] Inova Diagnost Inc, Dept Res & Dev, San Diego, CA 92131 USA.
C3 General University Hospital of Larissa; General University Hospital of
Larissa; University of Debrecen; Inova Diagnostics, Inc.
RP Dalekos, GN (corresponding author), Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Dept Med, Larisa 41110, Greece.; Dalekos, GN (corresponding author), Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Res Lab Internal Med, Larisa 41110, Greece.
EM georgedalekos@gmail.com
RI Gabeta, Stella/IXW-9909-2023; Papp, Maria/LMN-8987-2024
OI Papp, Maria/0000-0003-3662-4010
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NR 49
TC 28
Z9 34
U1 2
U2 15
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD SEP 14
PY 2020
VL 26
IS 34
BP 5130
EP 5145
DI 10.3748/wjg.v26.i34.5130
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA NW2OK
UT WOS:000574849000006
PM 32982114
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Uchihara, D
Suzuki, T
Koya, Y
Tai, M
Ichii, O
Matsuhashi, N
Ejiri, Y
Kato, T
Honma, Y
Shibata, M
Harada, M
AF Uchihara, Daiki
Suzuki, Tomohiro
Koya, Yudai
Tai, Mayumi
Ichii, Osamu
Matsuhashi, Nobuo
Ejiri, Yutaka
Kato, Tomoya
Honma, Yuichi
Shibata, Michihiko
Harada, Masaru
TI Autoimmune hepatitis complicated by adult-onset Still's disease during
treatment with tocilizumab: A case report from acute onset to recurrence
SO CLINICAL CASE REPORTS
LA English
DT Article
DE adult-onset Still's disease; autoimmune hepatitis; liver biopsy
AB Key Clinical MessageThe characteristics of liver dysfunction due to adult-onset Still's disease are not specific. Differentiating from autoimmune hepatitis is important in deciding whether to continue corticosteroid therapy, and also in terms of management of cirrhosis and surveillance of hepatocellular carcinoma. Liver biopsy is thought to be the most important determinant for differential diagnosis.
C1 [Uchihara, Daiki; Suzuki, Tomohiro; Tai, Mayumi; Ichii, Osamu; Matsuhashi, Nobuo; Ejiri, Yutaka] Fukushima Rosai Hosp, Dept Gastroenterol, Iwaki, Japan.
[Uchihara, Daiki; Koya, Yudai; Tai, Mayumi; Honma, Yuichi; Shibata, Michihiko; Harada, Masaru] Univ Occupat & Environm Hlth, Sch Med, Dept Internal Med 3, Kitakyushu, Japan.
[Kato, Tomoya] Fukushima Rosai Hosp, Dept Pathol, Iwaki, Japan.
C3 University of Occupational & Environmental Health - Japan
RP Uchihara, D (corresponding author), Fukushima Rosai Hosp, Dept Gastroenterol, Iwaki, Japan.
EM uchihara.daiki@gmail.com
RI Ichii, Osamu/JFB-2112-2023; Koya, Yudai/ABA-3809-2022
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NR 20
TC 0
Z9 0
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2050-0904
J9 CLIN CASE REP
JI Clin. Case Rep.
PD JUL
PY 2023
VL 11
IS 7
AR e7530
DI 10.1002/ccr3.7530
PG 6
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA K4QZ7
UT WOS:001016313600001
PM 37397575
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Guo, M
Wang, T
Ge, WJ
Ren, CR
Ko, BCB
Zeng, X
Cao, DL
AF Guo, Min
Wang, Tao
Ge, Wenjun
Ren, Chenran
Ko, Ben Chi-Bun
Zeng, Xi
Cao, Deliang
TI Role of AKR1B10 in inflammatory diseases
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Review
DE IBD; inflammation; NAFLD; T2DM
ID FATTY-ACID SYNTHESIS; KETO REDUCTASE 1B10; NF-KAPPA-B; UP-REGULATION;
LUNG-CANCER; HEPATOCELLULAR-CARCINOMA; OXIDATIVE STRESS; OVEREXPRESSION;
IDENTIFICATION; EXPRESSION
AB Inflammation is an important pathophysiological process in many diseases; it has beneficial and harmful effects. When exposed to various stimuli, the body triggers an inflammatory response to eliminate invaded pathogens and damaged tissues to maintain homeostasis. However, uncontrollable persistent or excessive inflammatory responses may damage tissues and induce various diseases, such as metabolic diseases (e.g. diabetes), autoimmune diseases, nervous system-related diseases, digestive system-related diseases, and even tumours. Aldo-keto reductase 1B10 (AKR1B10) is an important player in the development and progression of multiple diseases, such as tumours and inflammatory diseases. AKR1B10 is upregulated in solid tumours, such as hepatocellular carcinoma (HCC), non-small cell lung carcinoma, and breast cancer, and is a reliable serum marker. However, information on the role of AKR1B10 in inflammation is limited. In this study, we summarized the role of AKR1B10 in inflammatory diseases, including its expression, functional contribution to inflammatory responses, and regulation of signalling pathways related to inflammation. We also discussed the role of AKR1B10 in glucose and lipid metabolism and oxidative stress. This study provides novel information and increases the understanding of clinical inflammatory diseases.
The present article offers a comprehensive overview of the expression levels of AKR1B10 in various inflammation-related diseases and examines its role and potential mechanisms in these conditions, with the aim of providing novel insights for the diagnosis and treatment of related disorders.image
C1 [Guo, Min; Wang, Tao; Ge, Wenjun; Ren, Chenran; Zeng, Xi; Cao, Deliang] Univ South China, Canc Res Inst, Hengyang Med Sch, Hunan Prov Key Lab Tumor Cellular & Mol Pathol, Hengyang 421001, Hunan, Peoples R China.
[Ko, Ben Chi-Bun] Hong Kong Polytech Univ, Dept Appl Biol & Chem Technol, Hong Kong, Peoples R China.
C3 University of South China; Hong Kong Polytechnic University
RP Cao, DL (corresponding author), Univ South China, Canc Res Inst, Hengyang Med Sch, Hunan Prov Key Lab Tumor Cellular & Mol Pathol, Hengyang 421001, Hunan, Peoples R China.
EM dcao@usc.edu.cn
RI Ko, Chi-bun/ACH-7514-2022
OI Zeng, Xi/0000-0001-6835-9691; Ko, Ben Chi Bun/0000-0003-2027-5899
FU Aid Program for Science and Technology Innovative Research Team in
Higher Educational Institutions of Hunan Province; Changsha Science and
Technology Project [kq2303001]; University of South China [211RGC009]
FX This work is supported in part by the Changsha Science and Technology
Project (kq2303001), the Start-up Fund of University of South China
(211RGC009), and the Aid Program for Science and Technology Innovative
Research Team in Higher Educational Institutions of Hunan Province.
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NR 92
TC 3
Z9 3
U1 10
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD AUG
PY 2024
VL 100
IS 2
DI 10.1111/sji.13390
EA MAY 2024
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA YG4Q7
UT WOS:001227478800001
PM 38769661
OA Bronze
DA 2025-01-07
ER
PT J
AU Vierling, JM
AF Vierling, John M.
TI Autoimmune Hepatitis and Overlap Syndromes: Diagnosis and Management
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Autoimmune Hepatitis; Acute Liver Failure; Hepatocellular Carcinoma
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
LIVER-TRANSPLANTATION; MYCOPHENOLATE-MOFETIL; HEPATOCELLULAR-CARCINOMA;
CONTROLLED-TRIAL; FOLLOW-UP; CLINICAL-FEATURES; WILSONS-DISEASE;
AZATHIOPRINE METABOLITES
AB Autoimmune hepatitis (AIH) occurs globally and afflicts children and adults of all ethnicities and races.(1,2) The current hypothesis is that AIH results from hepatocyte injury (caused by environmental exposure to viruses or xenobiotics) that triggers a dysregulated, adaptive immune attack against hepatocyte autoantigens in immunogenetically susceptible persons.(3-5) AIH is characterized by female predilection, elevated aminotransferases, nonspecies or organ-specific autoantibodies, increased levels of g-globulin or immunoglobulin (Ig) G, and interface hepatitis on liver biopsy.(1,3,6) AIH presents rarely as acute liver failure (ALF) and infrequently as acute hepatitis. At diagnosis, 70%-80% of patients have chronic hepatitis, and approximately 33% have cirrhosis,(1,7) indicating that AIH commonly progresses undiagnosed and untreated for prolonged periods. Cirrhotic patients are at risk for complications of portal hypertension, liver failure, and, in a minority, hepatocellular carcinoma (HCC).
AIH is divided into types 1 and 2 (Table 1), which are based on signature expressions of autoantibodies (Table 2). Autoantigenic B-and T-cell epitopes have been identified only for the less frequent type 2. Type 1 AIH can present at any age but is increasingly diagnosed in older women.(8) In contrast, the peak incidence of type 2 AIH occurs in children and adolescents. 9 In European adults, the prevalence of type 2 AIH is higher in the South than in the North.(10) Neither the incidence nor prevalence of type 2 AIH in the United States is known, largely because of failure to test for anti-liver-kidney microsomal antibody 1 (LKM1).(3) A minority of AIH patients develop putative overlap syndromes (OS) with the cholestatic diseases primary biliary cirrhosis (PBC) or primary sclerosing cholangitis (PSC),(3,6,11) but both diagnostic criteria and therapy remain controversial.(12)
C1 [Vierling, John M.] Baylor Coll Med, Dept Med, Baylor St Lukes Med Ctr, Houston, TX 77030 USA.
[Vierling, John M.] Baylor Coll Med, Dept Surg, Baylor St Lukes Med Ctr, Houston, TX 77030 USA.
C3 Baylor College of Medicine; Baylor College of Medicine
RP Vierling, JM (corresponding author), 6620 Main St,Suite 1425, Houston, TX 77030 USA.
EM vierling@bcm.edu
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NR 223
TC 46
Z9 48
U1 0
U2 16
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD NOV
PY 2015
VL 13
IS 12
BP 2088
EP 2108
DI 10.1016/j.cgh.2015.08.012
PG 21
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CT9WB
UT WOS:000363166200007
PM 26284592
OA Bronze
DA 2025-01-07
ER
PT J
AU Oo, YH
Sakaguchi, S
AF Oo, Ye Htun
Sakaguchi, Shimon
TI Regulatory T-cell directed therapies in liver diseases
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Regulatory T cell; Autoimmune hepatitis; Transplantation; Liver cancer;
Cell therapy
ID AUTOIMMUNE HEPATITIS; TOLERANCE; EXPRESSION; EFFECTOR; INTERLEUKIN-2;
RECRUITMENT; HOMEOSTASIS; ACTIVATION; IMPAIRMENT; INDUCTION
C1 [Oo, Ye Htun] Univ Birmingham, Liver Res Ctr, Birmingham B15 2TH, W Midlands, England.
[Oo, Ye Htun] Univ Birmingham, NIHR BRU, Inst Biomed Res, Birmingham B15 2TH, W Midlands, England.
[Oo, Ye Htun] UHB NHS Fdn Trust, Birmingham B15 2TH, W Midlands, England.
[Sakaguchi, Shimon] Osaka Univ, WPI Immunol Frontier Res Ctr, Dept Expt Immunol, Suita, Osaka, Japan.
[Sakaguchi, Shimon] Kyoto Univ, Dept Expt Pathol, Inst Frontier Med Sci, Kyoto, Japan.
C3 University of Birmingham; University of Birmingham; Osaka University;
Kyoto University
RP Oo, YH (corresponding author), Univ Birmingham, Liver Res Ctr, Room 536,5th Floor, Birmingham B15 2TH, W Midlands, England.
EM y.h.oo@bham.ac.uk
RI Sakaguchi, Shimon/C-9535-2009; Oo, Ye Htun/AFC-8888-2022
OI Oo, Ye Htun/0000-0002-0495-6734
FU Medical Research Council Intermediate Clinical Fellowship (Clinician
Scientist) Programme; JST CREST; MRC [G1002552] Funding Source: UKRI
FX Dr Y.H. Oo was funded by Medical Research Council Intermediate Clinical
Fellowship (Clinician Scientist) Programme.Prof Sakaguchi was funded by
Grant-in-Aid for Specially Promoted Research and JST CREST.
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NR 60
TC 40
Z9 41
U1 0
U2 16
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD NOV
PY 2013
VL 59
IS 5
BP 1127
EP 1134
DI 10.1016/j.jhep.2013.05.034
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 235WZ
UT WOS:000325754200032
PM 23727305
OA hybrid
DA 2025-01-07
ER
PT J
AU Keeling, SS
McDonald, MF
Anand, A
Goff, CR
Christmann, CR
Barrett, SC
Kueht, M
Goss, JA
Cholankeril, G
Rana, A
AF Keeling, Stephanie S.
McDonald, Malcolm F.
Anand, Adrish
Goff, Cameron R.
Christmann, Caroline R.
Barrett, Spencer C.
Kueht, Michael
Goss, John A.
Cholankeril, George
Rana, Abbas
TI Do Patients with Autoimmune Conditions Have Less Access to Liver
Transplantation despite Superior Outcomes?
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Article
DE autoimmune liver disease; organ allocation; liver transplantation;
survival
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; LONG-TERM
SURVIVAL; HEPATITIS-C; FOLLOW-UP; NONALCOHOLIC STEATOHEPATITIS;
URSODEOXYCHOLIC-ACID; RECURRENCE; DISEASE; INFECTION
AB Orthotopic liver transplantation (OLT) is a lifesaving therapy for patients with irreversible liver damage caused by autoimmune liver diseases (AutoD) including autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC). Currently, it is unclear how access to transplantation differs among patients with various etiologies of liver disease. Our aim is to evaluate the likelihood of transplant and the long-term patient and graft survival after OLT for each etiology for transplantation from 2000 to 2021. We conducted a large retrospective study of United Network for Organ Sharing (UNOS) liver transplant patients in five 4-year eras with five cohorts: AutoD (PBC, PSC, AIH cirrhosis), alcohol-related liver disease (ALD), hepatocellular carcinoma (HCC), viral hepatitis, and nonalcoholic steatohepatitis (NASH). We conducted a multivariate analysis for probability of transplant. Intent-to-treat (ITT) analysis was performed to assess the 10-year survival differences for each listing diagnosis while accounting for both waitlist and post-transplant survival. Across all eras, autoimmune conditions had a lower adjusted probability of transplant of 0.92 (0.92, 0.93) compared to ALD 0.97 (0.97, 0.97), HCC 1.08 (1.07, 1.08), viral hepatitis 0.99 (0.99, 0.99), and NASH 0.99 (0.99, 1.00). Patients with AutoD had significantly better post-transplant patient and graft survival than ALD, HCC, viral hepatitis, and NASH in each and across all eras (p-values all < 0.001). Patients with AutoD had superior ITT survival (p-value < 0.001, log rank test). In addition, the waitlist survival for patients with AutoD compared to other listing diagnoses was improved with the exception of ALD, which showed no significant difference (p-value = 0.1056, log rank test). Despite a superior 10-year graft and patient survival in patients transplanted for AutoD, patients with AutoD have a significantly lower probability of receiving a liver transplant compared to those transplanted for HCC, ALD, viral hepatitis, and NASH. Patients with AutoD may benefit from improved liver allocation while maintaining superior waitlist and post-transplant survival. Decreased access in spite of appropriate outcomes for patients poses a significant risk for increased morbidity for patients with AutoD.
C1 [Keeling, Stephanie S.; Anand, Adrish; Goff, Cameron R.; Christmann, Caroline R.; Barrett, Spencer C.] Baylor Coll Med, Dept Student Affairs, Houston, TX 77030 USA.
[McDonald, Malcolm F.] Baylor Coll Med, Med Scientist Training Program, Houston, TX 77030 USA.
[Kueht, Michael] Univ Texas Med Branch, Dept Surg, Transplant Surg, Galveston, TX 77555 USA.
[Goss, John A.; Cholankeril, George; Rana, Abbas] Baylor Coll Med, Dept Surg, Div Abdominal Transplant, Houston, TX 77030 USA.
C3 Baylor College of Medicine; Baylor College of Medicine; University of
Texas System; University of Texas Medical Branch Galveston; Baylor
College of Medicine
RP Keeling, SS (corresponding author), Baylor Coll Med, Dept Student Affairs, Houston, TX 77030 USA.
EM keeling@bcm.edu; malcolm.mcdonald@bcm.edu; adrish.anand@bcm.edu;
crgoff@bcm.edu; crchrist@bcm.edu; spencer.barrett2022@gmail.com;
mlkueht@utmb.edu; jgoss@bcm.edu; george.cholankeril@bcm.edu;
abbas.rana@bcm.edu
RI Barrett, Spencer/S-5782-2019
OI Goff, Cameron/0000-0002-4123-8336; Anand, Adrish/0000-0002-6673-6251;
McDonald, Malcolm F./0000-0002-2627-9754; Kueht,
Michael/0000-0003-2509-0877; Keeling, Stephanie/0000-0002-4235-8276
FU McNair Medical Institute; BRASS (Baylor Research Advocates for Student
Scientists)
FX M.F.M. would like to thank the McNair Medical Institute and BRASS
(Baylor Research Advocates for Student Scientists) for their support.
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NR 46
TC 1
Z9 1
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4426
J9 J PERS MED
JI J. Pers. Med.
PD JUL
PY 2022
VL 12
IS 7
AR 1159
DI 10.3390/jpm12071159
PG 12
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA 3I0PX
UT WOS:000832429700001
PM 35887656
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU van Gerven, NMF
Verwer, BJ
Witte, BI
van Erpecum, KJ
van Buuren, HR
Maijers, I
Visscher, AP
Verschuren, EC
van Hoek, B
Coenraad, MJ
Beuers, UHW
de Man, RA
Drenth, JPH
den Ouden, JW
Verdonk, RC
Koek, GH
Brouwer, JT
Guichelaar, MMJ
Vrolijk, JM
Mulder, CJJ
van Nieuwkerk, CMJ
Bouma, G
AF van Gerven, Nicole M. F.
Verwer, Bart J.
Witte, Birgit I.
van Erpecum, Karel J.
van Buuren, Henk R.
Maijers, Ingrid
Visscher, Arjan P.
Verschuren, Edwin C.
van Hoek, Bart
Coenraad, Minneke J.
Beuers, Ulrich H. W.
de Man, Robert A.
Drenth, Joost P. H.
den Ouden, Jannie W.
Verdonk, Robert C.
Koek, Ger H.
Brouwer, Johannes T.
Guichelaar, Maureen M. J.
Vrolijk, Jan Maarten
Mulder, Chris J. J.
van Nieuwkerk, Carin M. J.
Bouma, Gerd
CA Dutch Autoimmune Hepatitis STUDY
TI Epidemiology and clinical characteristics of autoimmune hepatitis in the
Netherlands
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE autoimmune hepatitis; cirrhosis; diagnosis; diagnostic scoring systems;
epidemiology; hepatocellular carcinoma; prevalence; transplantation
ID LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA; FOLLOW-UP; TRANSPLANTATION;
CRITERIA; ASSOCIATION; POPULATION; PREVALENCE; MANAGEMENT; DIAGNOSIS
AB Background and aims. Epidemiological data on autoimmune hepatitis (AIH) are scarce. In this study, we determined the clinical and epidemiological characteristics of AIH patients in the Netherlands (16.7 million inhabitants). Methods. Clinical characteristics were collected from 1313 AIH patients (78% females) from 31 centers, including all eight academic centers in the Netherlands. Additional data on ethnicity, family history and symptoms were obtained by the use of a questionnaire. Results. The prevalence of AIH was 18.3 (95% confidential interval [CI]: 17.3-19.4) per 100,000 with an annual incidence of 1.1 (95% CI: 0.5-2) in adults. An incidence peak was found in middle-aged women. At diagnosis, 56% of patients had fibrosis and 12% cirrhosis in liver biopsy. Overall, 1% of patients developed HCC and 3% of patients underwent liver transplantation. Overlap with primary biliary cirrhosis and primary sclerosing cholangitis was found in 9% and 6%, respectively. The clinical course did not differ between Caucasian and non-Caucasian patients. Other autoimmune diseases were found in 26% of patients. Half of the patients reported persistent AIH-related symptoms despite treatment with a median treatment period of 8 years (range 1-44 years). Familial occurrence was reported in three cases. Conclusion. This is the largest epidemiological study of AIH in a geographically defined region and demonstrates that the prevalence of AIH in the Netherlands is uncommon. Although familial occurrence of AIH is extremely rare, our twin data may point towards a genetic predisposition. The high percentage of patients with cirrhosis or fibrosis at diagnosis urges the need of more awareness for AIH.
C1 [van Gerven, Nicole M. F.; Verwer, Bart J.; Maijers, Ingrid; Visscher, Arjan P.; Verschuren, Edwin C.; Mulder, Chris J. J.; van Nieuwkerk, Carin M. J.; Bouma, Gerd] Vrije Univ Amsterdam, Med Ctr, Dept Gastroenterol & Hepatol, NL-1081 HV Amsterdam, Netherlands.
[Witte, Birgit I.] Vrije Univ Amsterdam, Med Ctr, Dept Epidemiol & Biostat, NL-1081 HV Amsterdam, Netherlands.
[van Erpecum, Karel J.] Univ Med Ctr Utrecht, Dept Gastroenterol & Hepatol, Utrecht, Netherlands.
[van Buuren, Henk R.; de Man, Robert A.] Erasmus Univ, Dept Gastroenterol & Hepatol, Med Ctr, Rotterdam, Netherlands.
[van Hoek, Bart; Coenraad, Minneke J.] Leiden Univ, Dept Gastroenterol & Hepatol, Med Ctr, Leiden, Netherlands.
[Beuers, Ulrich H. W.] Univ Amsterdam, Acad Med Ctr, Dept Gastroenterol & Hepatol, NL-1105 AZ Amsterdam, Netherlands.
[Drenth, Joost P. H.] Radboud Univ Nijmegen, Dept Gastroenterol & Hepatol, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[den Ouden, Jannie W.] Haga Hosp, Dept Gastroenterol & Hepatol, The Hague, Netherlands.
[Verdonk, Robert C.] St Antonius Hosp, Dept Gastroenterol & Hepatol, Nieuwegein, Netherlands.
[Koek, Ger H.] Univ Med Ctr Maastricht, Dept Gastroenterol & Hepatol, Maastricht, Netherlands.
[Brouwer, Johannes T.] Reinier de Graaf Med Ctr, Dept Gastroenterol & Hepatol, Delft, Netherlands.
[Guichelaar, Maureen M. J.] Med Spectrum Twente, Dept Gastroenterol & Hepatol, Enschede, Netherlands.
[Vrolijk, Jan Maarten] Rijnstate Hosp, Dept Gastroenterol & Hepatol, Arnhem, Netherlands.
C3 Vrije Universiteit Amsterdam; Vrije Universiteit Amsterdam; Utrecht
University; Utrecht University Medical Center; Erasmus University
Rotterdam; Erasmus MC; Leiden University; Leiden University Medical
Center (LUMC); Leiden University - Excl LUMC; University of Amsterdam;
Academic Medical Center Amsterdam; Radboud University Nijmegen; Haga
Hospital; St. Antonius Hospital Utrecht; Maastricht University;
Maastricht University Medical Centre (MUMC); Reinier de Graaf Hospital;
Medical Spectrum Twente; Rijnstate Hospital
RP van Gerven, NMF (corresponding author), Vrije Univ Amsterdam, Med Ctr, Dept Gastroenterol & Hepatol, De Boelelaan 1118, NL-1081 HV Amsterdam, Netherlands.
EM n.vangerven@vumc.nl
RI van Hoek, Bart/AAU-8953-2020; Verdonk, Robert/AIF-4117-2022; Coenraad,
Minneke/AAU-1684-2020; bouma, gerd/E-2520-2013; Kluin-Nelemans,
Johanna/F-8658-2018; Drenth, Joost/V-7436-2019; Coenraad,
Minneke/IZD-8288-2023
OI Drenth, Joost PH/0000-0001-8027-3073; Coenraad,
Minneke/0000-0002-3434-4421; Lissenberg-Witte,
Birgit/0000-0001-9448-1826; van Hoek, Bart/0000-0001-6527-764X; Maijers,
Ingrid/0000-0002-4688-4927
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NR 37
TC 130
Z9 135
U1 0
U2 16
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD OCT
PY 2014
VL 49
IS 10
BP 1245
EP 1254
DI 10.3109/00365521.2014.946083
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AP7AB
UT WOS:000342228700011
PM 25123213
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Zhu, SS
Zhang, HM
Bai, L
AF Zhu, Shasha
Zhang, Huimin
Bai, Li
TI NKT cells in liver diseases
SO FRONTIERS OF MEDICINE
LA English
DT Review
DE natural killer T cells; hepatitis B virus and hepatitis C virus
infection; autoimmune liver diseases; alcoholic liver disease;
nonalcoholic fatty liver disease; hepatocellular carcinoma
ID KILLER T-CELLS; ALPHA-GALACTOSYLCERAMIDE KRN7000; CHRONIC
ALCOHOL-CONSUMPTION; ADAPTIVE IMMUNE-RESPONSES; HIGH-FAT DIET;
HEPATITIS-B; PHASE-I; CD1D EXPRESSION; DENDRITIC CELLS; MOUSE MODEL
AB Natural killer T cells are innate-like and tissue-resident lymphocytes, which recognize lipid antigens and are enriched in the liver. Natural killer T cells play important roles in infections, tumors, autoimmune diseases, and metabolic diseases. In this study, we summarize recent findings on biology of natural killer T cells and their roles in hepatitis B virus and hepatitis C virus infection, autoimmune liver diseases, alcoholic liver disease, nonalcoholic fatty liver disease, and hepatocellular carcinoma. Controversial results from previous studies are discussed, and indicate the dynamic alteration in the role of natural killer T cells during the progression of liver diseases, which might be caused by changes in natural killer T subsets, factors skewing cytokine responses, and intercellular crosstalk between natural killer T cells and CD1d-expressing cells or bystander cells.
C1 [Zhu, Shasha; Zhang, Huimin; Bai, Li] Univ Sci & Technol China, CAS Key Lab Innate Immun & Chron Dis, CAS Ctr Excellence Mol Cell Sci, Sch Life Sci, Hefei 230027, Anhui, Peoples R China.
[Zhu, Shasha; Zhang, Huimin; Bai, Li] Univ Sci & Technol China, Med Ctr, Hefei 230027, Anhui, Peoples R China.
[Zhu, Shasha; Zhang, Huimin; Bai, Li] Hefei Natl Lab Phys Sci Microscale, Innovat Ctr Cell Signaling Network, Hefei 230027, Anhui, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
China, CAS; Chinese Academy of Sciences; University of Science &
Technology of China, CAS
RP Bai, L (corresponding author), Univ Sci & Technol China, CAS Key Lab Innate Immun & Chron Dis, CAS Ctr Excellence Mol Cell Sci, Sch Life Sci, Hefei 230027, Anhui, Peoples R China.; Bai, L (corresponding author), Univ Sci & Technol China, Med Ctr, Hefei 230027, Anhui, Peoples R China.; Bai, L (corresponding author), Hefei Natl Lab Phys Sci Microscale, Innovat Ctr Cell Signaling Network, Hefei 230027, Anhui, Peoples R China.
EM baili@ustc.edu.cn
FU National Natural Science Foundation of China [91542203, 31470859,
81771671]; National Key R&D Program of China [2017YFA0505300]; Strategic
Priority Research Program of the Chinese Academy of Sciences
[XDA12030208]; Fundamental Research Funds for the Central Universities
FX Work in the authors' laboratory was supported by National Natural
Science Foundation of China (Nos. 91542203, 31470859, and 81771671),
National Key R&D Program of China (No. 2017YFA0505300), the Strategic
Priority Research Program of the Chinese Academy of Sciences (No.
XDA12030208), the Fundamental Research Funds for the Central
Universities.
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NR 160
TC 31
Z9 37
U1 2
U2 43
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2095-0217
EI 2095-0225
J9 FRONT MED-PRC
JI Front. Med.
PD JUN
PY 2018
VL 12
IS 3
BP 249
EP 261
DI 10.1007/s11684-018-0622-3
PG 13
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GF9ZB
UT WOS:000432336500002
PM 29623561
DA 2025-01-07
ER
PT J
AU Ramos-Tovar, E
Muriel, P
AF Ramos-Tovar, Erika
Muriel, Pablo
TI NLRP3 inflammasome in hepatic diseases: A pharmacological target
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Review
DE Inflammation; Alcoholic liver disease; Non-alcoholic steatohepatitis;
Fibrosis; Cirrhosis; Hepatocellular carcinoma
ID FATTY LIVER-DISEASE; PRIMARY SCLEROSING CHOLANGITIS; CLINICAL-PRACTICE
GUIDELINES; NONALCOHOLIC STEATOHEPATITIS; STELLATE CELLS; ALCOHOLIC
STEATOHEPATITIS; URIC-ACID; HEPATOCYTE PYROPTOSIS; SIGNALING PATHWAY;
OXIDATIVE STRESS
AB The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome pathway is mainly responsible for the activation and release of a cascade of proinflammatory mediators that contribute to the development of hepatic diseases. During alcoholic liver disease development, the NLRP3 inflammasome pathway contributes to the maturation of caspase-1, interleukin (IL)-18, and IL-18, which induce a robust inflammatory response, leading to fibrosis by inducing profibrogenic hepatic stellate cell (HSC) activation. Substantial evidence demonstrates that nonalcoholic fatty liver disease (NAFLD) progresses to nonalcoholic steatohepatitis (NASH) via NLRP3 inflammasome activation, ultimately leading to fibrosis and hepatocellular carcinoma (HCC). Activation of the NLRP3 inflammasome in NASH can be attributed to several factors, such as reactive oxygen species (ROS), gut dysbiosis, leaky gut, which allow triggers such as cardiolipin, cholesterol crystals, endoplasmic reticulum stress, and uric acid to reach the liver. Because inflammation triggers HSC activation, the NLRP3 inflammasome pathway performs a central function in fibrogenesis regardless of the etiology. Chronic hepatic activation of the NLRP3 inflammasome can ultimately lead to HCC; however, inflammation also plays a role in decreasing tumor growth. Some data indicate that NLRP3 inflammasome activation plays an important role in autoimmune hepatitis, but the evidence is scarce. Most researchers have reported that NLRP3 inflammasome activation is essential in liver injury induced by a variety of drugs and hepatotropic virus infection; however, few reports indicate that this pathway can play a beneficial role by inducing liver regeneration. Modulation of the NLRP3 inflammasome appears to be a suitable strategy to treat liver diseases.
C1 [Ramos-Tovar, Erika] Escuela Super Med IPN, Secc Estudios Posgrad Invest, Plan San Luis & Diaz Miron s-n, Mexico City 11340, Mexico.
[Muriel, Pablo] Cinvestav IPN, Dept Farmacol, Lab Hepatol Expt, Mexico City 14740, Mexico.
C3 CINVESTAV - Centro de Investigacion y de Estudios Avanzados del
Instituto Politecnico Nacional
RP Muriel, P (corresponding author), Cinvestav IPN, Dept Farmacol, Lab Hepatol Expt, Mexico City 14740, Mexico.
EM pmuriel@cinvestav.mx
RI Ramos-Tovar, Erika/HRB-9713-2023; Muriel, Pablo/H-5156-2017
OI Muriel, Pablo/0000-0002-2236-6631; Ramos-Tovar,
Erika/0000-0002-6616-9760
FU CONAHCYT [CF2019-53358]
FX This work was funded by CONAHCYT grant No. CF2019-53358 to PM.
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NR 227
TC 15
Z9 16
U1 5
U2 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD NOV
PY 2023
VL 217
AR 115861
DI 10.1016/j.bcp.2023.115861
EA OCT 2023
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FX2X9
UT WOS:001149097500001
PM 37863329
DA 2025-01-07
ER
PT J
AU Miyake, Y
Iwasaki, Y
Terada, R
Okamaoto, R
Ikeda, H
Makino, Y
Kobashi, H
Takaguchi, K
Sakaguchi, K
Shiratori, Y
AF Miyake, Y.
Iwasaki, Y.
Terada, R.
Okamaoto, R.
Ikeda, H.
Makino, Y.
Kobashi, H.
Takaguchi, K.
Sakaguchi, K.
Shiratori, Y.
TI Persistent elevation of serum alanine aminotransferase levels leads to
poor survival and hepatocellular carcinoma development in type 1
autoimmune hepatitis
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID CORTICOSTEROID-THERAPY; URSODEOXYCHOLIC ACID; CIRRHOSIS; FIBROSIS;
PATIENT; TRANSPLANTATION; DIAGNOSIS; REMISSION; PROGNOSIS; DISEASE
AB Background
Although the prognosis of type 1 autoimmune hepatitis is generally good with immunosuppressive treatment, the disease progresses in some patients despite the treatment. The prognosis may be determined by the clinical course.
Aim
To evaluate the long-term prognosis and assess the predictive factors for a serious event, including the development of hepatocellular carcinoma or death.
Methods
Sixty-nine patients with type 1 autoimmune hepatitis were prospectively followed up regularly, with a median follow-up period of 96 months (49-201 months).
Results
During the follow-up period, three patients (4%) developed hepatocellular carcinoma, and two of these three patients died. Another patient died of liver failure. The 10-year survival rate was 98%, and the 10-year hepatocellular carcinoma-free rate was 93%. The four patients experiencing a serious event received higher maintenance doses of corticosteroid during their follow-up periods than those did not. However, serum alanine aminotransferase levels during the follow-up period were higher in these four patients than in the others.
Conclusions
Persistent elevation of serum alanine amniotransferase levels during the follow-up period, rather than factors existing prior to medical treatment is considered to be an important prognostic factor, and it is indicated that poor outcomes may result from the resistance to immunosuppressive treatment.
C1 Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci, Okayama 7008558, Japan.
Hiroshima City Hosp, Dept Internal Med, Hiroshima, Japan.
Kurashiki Cent Hosp, Dept Gastroenterol, Kurashiki, Okayama, Japan.
Natl Hosp Org, Iwakuni Clin Ctr, Dept Gastroenterol, Iwakuni, Japan.
Tsuyama Cent Hosp, Dept Internal Med, Tsuyama, Japan.
Kagawa Prefectural Cent Hosp, Dept Internal Med, Takamatsu, Kagawa, Japan.
C3 Okayama University; Hiroshima City Hospital; Kurashiki Central Hospital
RP Miyake, Y (corresponding author), Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci, 2-5-1 Shikata Cho, Okayama 7008558, Japan.
EM miyakeyasuhiro@hotmail.com
RI Iwasaki, Yoshiaki/B-2538-2011
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NR 28
TC 49
Z9 50
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD OCT 15
PY 2006
VL 24
IS 8
BP 1197
EP 1205
DI 10.1111/j.1365-2036.2006.03113.x
PG 9
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 086FZ
UT WOS:000240660500006
PM 17014578
OA Bronze
DA 2025-01-07
ER
PT J
AU Invernizzi, F
Cilla, M
Trapani, S
Guarino, M
Cossiga, V
Gambato, M
Morelli, MC
Morisco, F
Burra, P
Floreani, A
AF Invernizzi, Federica
Cilla, Marta
Trapani, Silvia
Guarino, Maria
Cossiga, Valentina
Gambato, Martina
Morelli, Maria Cristina
Morisco, Filomena
Burra, Patrizia
Floreani, Annarosa
CA Special Interest Grp Gender Hepato
Italian Assoc Study Liver AISF
TI Gender and Autoimmune Liver Diseases: Relevant Aspects in Clinical
Practice
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Review
DE gender; autoimmune liver diseases; autoimmune hepatitis primary biliary
cirrhosis; primary sclerosing cholangitis; overlap syndromes; liver
transplant
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
INFLAMMATORY-BOWEL-DISEASE; POPULATION-BASED EPIDEMIOLOGY; LONG-TERM
PROGNOSIS; HEPATOCELLULAR-CARCINOMA; URSODEOXYCHOLIC ACID; OVERLAP
SYNDROME; RISK-FACTORS; FOLLOW-UP
AB Autoimmune liver diseases (AILDs) include autoimmune hepatitis, primary biliary cholangitis and primary sclerosing cholangitis. The etiologies of AILD are not well understood but appear to involve a combination of genetic and environmental factors. AILDs commonly affect young individuals and are characterized by a highly variable clinical course. These diseases significantly influence quality of life and can progress toward liver decompensation or the onset of hepatocellular or cholangiocarcinoma; a significant number of patients eventually progress to end-stage liver disease, requiring liver transplantation. In this review, we focus on the sex characteristics and peculiarities of AILD patients and highlight the relevance of a sex-specific analysis in future studies. Understanding the sex differences underlying AILD immune dysregulation may be critical for developing more effective treatments.
C1 [Invernizzi, Federica; Cilla, Marta] IRCCS Osped San Raffaele, Div Internal Med & Hepatol, Ctr Liver Dis, I-20132 Milan, Italy.
[Trapani, Silvia] Italian Natl Transplant Ctr, Natl Inst Hlth, I-00162 Rome, Italy.
[Guarino, Maria; Cossiga, Valentina; Morisco, Filomena] Univ Naples Federico II, Dept Clin Med & Surg, Gastroenterol & Hepatol Unit, I-80138 Naples, Italy.
[Gambato, Martina; Burra, Patrizia] Univ Hosp Padova, Dept Surg Oncol & Gastroenterol Sci, Multivisceral Transplant Unit Gastroenterol, I-35128 Padua, Italy.
[Morelli, Maria Cristina] IRCCS Azienda Osped Univ Bologna, Internal Med Unit Treatment Severe Organ Failure, I-40138 Bologna, Italy.
[Floreani, Annarosa] IRCCS Negrar, I-37024 Verona, Italy.
[Floreani, Annarosa] Univ Padua, I-35131 Padua, Italy.
C3 Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
Istituto Superiore di Sanita (ISS); University of Naples Federico II;
University of Padua; Azienda Ospedaliera - Universita di Padova; IRCCS
Azienda Ospedaliero-Universitaria di Bologna; University of Padua
RP Invernizzi, F (corresponding author), IRCCS Osped San Raffaele, Div Internal Med & Hepatol, Ctr Liver Dis, I-20132 Milan, Italy.
EM invernizzi.federica@hsr.it; cilla.marta@hsr.it; silvia.trapani@iss.it;
maria.guarino86@gmail.com; valentina.cossiga@gmail.com;
martina.gambato@gmail.com; mariacristina.morelli@aosp.bo.it;
filomena.morisco@unina.it; burra@unipd.it; annarosa.floreani@unipd.it
RI Morisco, Filomena/AHI-0851-2022; guarino, maria/AAM-6001-2020; Cossiga,
Valentina/ABB-3331-2021; Burra, Patrizia/AAB-2448-2019; Cilla,
Marta/IQV-0419-2023; Invernizzi, Federica/AAC-3820-2022
OI morisco, filomena/0000-0002-9059-8311; gambato,
martina/0000-0002-0101-1938; Burra, Patrizia/0000-0002-8791-191X;
Morisco, Filomena/0009-0006-1537-5034; morelli, maria
cristina/0000-0002-9742-1981; guarino, Maria/0000-0002-0460-4122;
Trapani, Silvia/0000-0002-8854-7144
FU Department of Surgery, Oncology and Gastroenterology (DiSCOG)-University
of Padua, Italy
FX The APC was funded by Department of Surgery, Oncology and
Gastroenterology (DiSCOG)-University of Padua, Italy.
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NR 122
TC 14
Z9 15
U1 0
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4426
J9 J PERS MED
JI J. Pers. Med.
PD JUN
PY 2022
VL 12
IS 6
AR 925
DI 10.3390/jpm12060925
PG 16
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA 2K3YH
UT WOS:000816275200001
PM 35743710
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Patel, D
Khillan, V
Patel, N
Kale, P
AF Patel, Dhruvi
Khillan, Vikas
Patel, Niharika
Kale, Pratibha
TI Cryptococcosis among HIV negative liver disease patients: Epidemiology,
underlying conditions, antifungal susceptibility profile from tertiary
care hepatobiliary center
SO INDIAN JOURNAL OF MEDICAL MICROBIOLOGY
LA English
DT Article
DE Cirrhosis; Non-HIV; Cryptococcal infection; Antifungal susceptibility;
Liver disease
ID END-POINT DISTRIBUTIONS; GATTII SPECIES COMPLEX; AMPHOTERICIN-B; CUTOFF
VALUES; NEOFORMANS; FLUCONAZOLE; RESISTANCE; CIRRHOSIS; ITRACONAZOLE;
MENINGITIS
AB Purpose: Cryptococcus neoformans is an encapsulated yeast. It is a significant pathogen among immunocompromised people with HIV & Non-HIV vulnerable populations. These conditions include cancer, corticosteroid usage, immunosuppression following sarcoidosis, organ transplantation, immunosuppressive medication, and liver cirrhosis. In cirrhotic, it accounts for 6-21% of systemic infections. Methods: The retrospective study was conducted in tertiary care hepatobiliary center in New Delhi, India. Samples of blood, cerebrospinal fluid (CSF), urine, body fluids, and serum were processed for gram stain, India ink, fungal culture and identification, and cryptococcal antigen. Antifungal susceptibility was assessed using the micro-broth dilution technique. Results: 30 patients with cryptococcal infection were analysed, and 40 isolates from various samples were recovered. Out of 40 samples, C. neoformans was isolated from blood (62.5%), urine (15%), ascitic fluid (10%), MiniBAL (5%), bone marrow, CSF, and pleural fluid in one sample each. India ink positivity was 56% and all samples were positive for Cryptococcal antigen. Alcoholic liver disease & Hepatitis B & C associated chronic liver disease were seen in 43% & 20% of patients. Other underlying conditions were diabetes mellitus (20%), TB (10%), autoimmune hepatitis (6.6%), autoimmune disease (autoimmune hemolytic anemia, Sjogren syndrome) (6.6%), sarcoidosis (3.3%), hepatocellular carcinoma (3.3%). 7.5%, 5%, 2.5%, 7.5%, and 2.5% of C. neoformans strains were the non-wild type to fluconazole, 5-fluorocytosine, amphotericin B, posaconazole, and itraconazole respectively, but all strains were wildtype to voriconazole. Conclusion: According to the study liver conditions are a significant risk factor for cryptococcal infection. Therefore, cryptococcal isolation and antifungal susceptibility testing, as well as appropriate antifungal drug use, should be studied and paid attention too.
C1 [Patel, Dhruvi; Khillan, Vikas; Patel, Niharika; Kale, Pratibha] Inst Liver & Biliary Sci, Dept Microbiol, New Delhi 110070, India.
C3 Institute of Liver & Biliary Sciences (ILBS)
RP Kale, P (corresponding author), Inst Liver & Biliary Sci, Dept Microbiol, New Delhi 110070, India.
EM dr.dhruvi.patel002@gmail.com; khillanv@yahoo.com;
niharikapatelmicro@gmail.com; drpratibhapgi@gmail.com
RI Patel, Dhruvi/KRQ-8646-2024
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NR 27
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0255-0857
EI 1998-3646
J9 INDIAN J MED MICROBI
JI Indian J. Med. Microbiol.
PD NOV-DEC
PY 2023
VL 46
AR 100465
DI 10.1016/j.ijmmb.2023.100465
EA SEP 2023
PG 4
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA T4TM9
UT WOS:001077929400001
PM 37690316
OA gold
DA 2025-01-07
ER
PT J
AU Ramírez, DFB
Gutiérrez, GC
Ramírez, AP
Torres, AV
AF Ramirez, Diana Fernanda Bejarano
Gutierrez, Gabriel Carrasquilla
Ramirez, Alexandra Porras
Torres, Alonso Vera
TI Prevalence of liver disease in Colombia between 2009 and 2016
SO JGH OPEN
LA English
DT Article
DE alcohol consumption; Colombia; immunization; liver disease; obesity;
prevalence; unsatisfied basic needs
ID GLOBAL BURDEN; ALCOHOL; MORTALITY; CIRRHOSIS; CANCER; IMPACT
AB Background and Aim Liver disease refers to a set of pathologies resulting from the interruption of liver function or the poor functioning of the liver. The estimation of morbidity and mortality due to liver disease and the context in which the disease develops are determining factors for public policies related to liver disease and its causes. The primary etiologies are cirrhosis and hepatocellular carcinoma, which are directly related to hepatitis B and C virus and alcohol consumption. Followed by hepatotoxic drug use, autoimmune hepatitis, cholestatic diseases, genetic abnormalities, and nonalcoholic steatohepatitis.
Methods A descriptive cross-sectional study was conducted to estimate the prevalence of liver disease in Colombia between 2009 and 2016. Using the Data Warehouse-Cube of SISPRO as the primary source of the data, prevalence proportions were calculated and adjusted according to the Bennett Horiuchi method. The relationship with alcohol consumption and the index of unsatisfied basic needs based on estimates from 2005 were considered as sociodemographic variables.
Results The prevalence of liver disease differs with regard to the type of illness, sex and age of the patient, access to medical attention, and geographical location.
Conclusions As liver disease is a public health problem, it requires early intervention such as raising awareness and prevention strategies, along with postdiagnosis care channels for treatment, rehabilitation, and palliation. By implementing these strategies, public health will be positively impacted, health care resources will be optimized, and more productive years of life are available for the citizens of the country.
C1 [Ramirez, Diana Fernanda Bejarano; Torres, Alonso Vera] Univ Hosp Fdn Santa Fe Bogota, Transplant Serv, Bogota, Colombia.
[Gutierrez, Gabriel Carrasquilla] Univ Hosp Fdn Santa Fe Bogota, Dept Publ Hlth, Bogota, Colombia.
[Ramirez, Diana Fernanda Bejarano; Gutierrez, Gabriel Carrasquilla; Ramirez, Alexandra Porras] Univ El Bosque, Community Med & Publ Hlth, Bogota, Colombia.
C3 Universidad El Bosque
RP Ramírez, DFB (corresponding author), Univ el Bosque, Fdn Santa Fe Bogota, Carrera 9 131A-02 Founders Bldg,Floor 5, Bogota, Colombia.
EM dfbejaranora@gmail.com
OI Bejarano Ramirez, Diana Fernanda/0000-0002-2753-3961
CR Adler NE, 2002, HEALTH AFFAIR, V21, P60, DOI 10.1377/hlthaff.21.2.60
ALEGRÍA Q. SYLVIA, 2002, Rev. chil. pediatr., V73, P176
Alves de Mattos A, 2016, HEPATOLOGIA CONCEPTO
Andrade Valentina, 2015, Rev. colomb. Gastroenterol., V30, P407
[Anonymous], 2016, EP PROGR AN EP DAT V
[Anonymous], 2016, Stata Statistical Software: Release 12
Arroyave I, 2014, PREV MED, V64, P41, DOI 10.1016/j.ypmed.2014.03.018
Askgaard G, 2015, J HEPATOL, V62, P1061, DOI 10.1016/j.jhep.2014.12.005
Beltrán Galvis Oscar A, 2015, Rev. colomb. Gastroenterol., V30, P89
BENNETT NG, 1984, DEMOGRAPHY, V21, P217, DOI 10.2307/2061041
Bosetti C, 2007, J HEPATOL, V46, P827, DOI 10.1016/j.jhep.2007.01.025
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Collins SE, 2016, ALCOHOL RES-CURR REV, V38, P83
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Guy J, 2009, HEPATOLOGY, V50, P309, DOI 10.1002/hep.22942
IBM Corp, REL 2016 IBM SPSS ST
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Neff Guy W, 2011, Gastroenterol Hepatol (N Y), V7, P661
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NR 37
TC 1
Z9 1
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2397-9070
J9 JGH OPEN
JI JGH Open
PD AUG
PY 2020
VL 4
IS 4
BP 603
EP 610
DI 10.1002/jgh3.12300
EA FEB 2020
PG 8
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA ND2PL
UT WOS:000515279400001
PM 32782945
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Li, S
Deng, Y
Chen, ZP
Huang, S
Liao, XC
Lin, LW
Huang, L
Peng, T
Qin, X
Zhao, JM
AF Li, Shan
Deng, Yan
Chen, Zhi-Ping
Huang, Shan
Liao, Xiang-Cheng
Lin, Li-Wen
Huang, Li
Peng, Tao
Qin, Xue
Zhao, Jin-min
TI Genetic polymorphism of interleukin-16 influences susceptibility to
HBV-related hepatocellular carcinoma in a Chinese population
SO INFECTION GENETICS AND EVOLUTION
LA English
DT Article
DE Hepatocellular carcinoma; IL16; SNP
ID GENOME-WIDE ASSOCIATION; CHRONIC HEPATITIS-B; CHRONIC INFLAMMATION;
T-CELLS; CANCER; RISK; PATHOGENESIS; INFECTION; TUMORIGENESIS;
EXPRESSION
AB Aim: Interleukin-16 (IL16) as a multifunctional cytokine, plays a key role in inflammatory and autoimmune diseases as well as tumour growth and progression. Recently, genetic polymorphisms of IL16 have been reported to be associated with susceptibility to a range of cancers. This study was undertaken to investigate the IL16 gene polymorphisms and determine whether these genetic factors are related to the occurrence of hepatocellular carcinoma (HCC) in a Chinese population.
Methods: We analyzed three polymorphisms of the IL16 gene (rs11556218T/G, rs4072111C/T and rs4778889T/C) in 206 patients with HBV-related HCC, 270 chronic hepatitis B patients and 264 healthy controls, using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and DNA sequencing technology.
Results: IL16 polymorphisms were not associated with risk of HCC when compared with healthy controls. However. IL16 polymorphisms were significantly associated with susceptibility to HBV-related HCC when using chronic hepatitis B patients as controls. The rs11556218T/G TG and GG genotypes were associated with significantly increased risk of HBV-related HCC compared with the IT genotype (OR = 1.96 and OR = 3.33). The data also revealed that subjects with the G allele appeared to have higher susceptibility to HBV-related HCC than those with the T allele (OR = 2.10). Under the dominant model genotype TG + GG appeared to be associated with an increased risk of HBV-related HCC (OR = 2.18). The rs4072111C/T TT genotype was associated with a significantly increased risk of HBV-related HCC compared with the CC genotype (OR = 6.67). Polymorphisms of the IL16 gene were significantly associated with susceptibility to chronic hepatitis B when using healthy subjects as controls. The rs11556218T/G TG and GG genotypes were associated with significantly decreased risk of chronic hepatitis B compared with the TT genotype (OR = 0.49 and OR = 0.29). The data also revealed that subjects with the G allele appeared to have lower susceptibility to chronic hepatitis B than those with the T allele (OR = 0.46). Under the dominant model genotype TG + GC appeared to have lower susceptibility to chronic hepatitis B (OR = 0.44).
Conclusions: This study showed that the genotypes and allele of IL16 SNPs were associated with chronic HBV infection and HCC. However, further investigation with a larger sample size and haplotype analysis with other SNPs may be required to validate the genetic effects of the IL16 polymorphisms on chronic HBV infection and HCC. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Li, Shan; Deng, Yan; Huang, Shan; Liao, Xiang-Cheng; Lin, Li-Wen; Huang, Li; Qin, Xue] Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, Nanning 530021, Guangxi, Peoples R China.
[Chen, Zhi-Ping] Guangxi Med Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Nanning 530021, Guangxi, Peoples R China.
[Peng, Tao] Guangxi Med Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, Nanning 530021, Guangxi, Peoples R China.
[Zhao, Jin-min] Guangxi Med Univ, Affiliated Hosp 1, Dept Orthopaed Trauma Surg, Nanning 530021, Guangxi, Peoples R China.
C3 Guangxi Medical University; Guangxi Medical University; Guangxi Medical
University; Guangxi Medical University
RP Qin, X (corresponding author), Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, Nanning 530021, Guangxi, Peoples R China.
EM qinxue919@yahoo.cn; zhaojinmin@126.com
RI deng, yan/JDW-8815-2023; Peng, Tao/LXB-5171-2024; zhao,
jin/LBH-0351-2024; chen, zhiping/IST-6333-2023; qin, xue/KQV-3701-2024
OI Zhao, Jinmin/0000-0002-1047-8820
FU National Natural Science Foundation [81060199]; Nature Science Fund,
Guangxi Province, China [2010GXNSFA013151]
FX This study was supported by the National Natural Science Foundation (No.
81060199); by Grant from the Nature Science Fund, Guangxi Province,
China (2010GXNSFA013151).
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NR 35
TC 43
Z9 51
U1 0
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-1348
J9 INFECT GENET EVOL
JI Infect. Genet. Evol.
PD DEC
PY 2011
VL 11
IS 8
BP 2083
EP 2088
DI 10.1016/j.meegid.2011.09.025
PG 6
WC Infectious Diseases
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases
GA 871YV
UT WOS:000298774500030
PM 22019522
DA 2025-01-07
ER
PT J
AU Molina, MF
Abdelnabi, MN
Fabre, T
Shoukry, NH
AF Molina, Manuel Flores
Abdelnabi, Mohamed N.
Fabre, Thomas
Shoukry, Naglaa H.
TI Type 3 cytokines in liver fibrosis and liver cancer
SO CYTOKINE
LA English
DT Article; Proceedings Paper
CT 2nd Aegean Conference on Cytokine Signaling in Cancer (ACCSC)
CY MAY 30-JUN 04, 2017
CL Heraklion, GREECE
ID HEPATIC STELLATE CELLS; DELTA-T-CELLS; NF-KAPPA-B; TH17 CELLS; INDUCIBLE
FACTOR; TISSUE-REPAIR; HEPATOCELLULAR-CARCINOMA; PROMOTES ANGIOGENESIS;
PROTECTIVE FUNCTION; BINDING-PROTEIN
AB The type 3 cytokines IL-17 and IL-22 play a crucial, well synchronized physiological role in wound healing and repairing tissue damage due to infections or injury at barrier surfaces. These cytokines act on epithelial cells to induce secretion of early immune mediators, recruitment of inflammatory cells to the site of injury, and to trigger tissue repair mechanisms. However, if the damage persists or if these cytokines are dysregulated, then they contribute to a number of inflammatory pathologies, autoimmune conditions and cancer. The liver is a multifunctional organ that plays an essential role in metabolism, detoxification, and immune surveillance. It is also exposed to a variety of pathogens, toxins and injuries. Over the past decade, IL-17 and IL-22 have been implicated in various aspects of liver inflammation. IL-17 is upregulated in chronic liver injury and associated with liver disease progression. In contrast, IL-22 was shown to be hepatoprotective during acute liver injury but exhibited inflammatory effects in other models. Furthermore, IL-22 and IL-17 are both associated with poor prognosis in liver cancer. Finally, the regulatory mechanisms governing the physiological versus the pathological role of these two cytokines during acute and chronic liver injury remain poorly understood. In this review, we will summarize the current state of knowledge about IL-17 and IL-22 in wound healing during acute and chronic liver injury, their contribution to pathogenesis, their regulation, and their role in the transition from advanced liver disease to liver cancer.
C1 [Molina, Manuel Flores; Abdelnabi, Mohamed N.; Fabre, Thomas; Shoukry, Naglaa H.] CRCHUM, Local R09-414,900 Rue St Denis, Montreal, PQ H2X 0A9, Canada.
[Molina, Manuel Flores; Abdelnabi, Mohamed N.; Fabre, Thomas] Univ Montreal, Fac Med, Dept Microbiol Infectiol & Immunol, Montreal, PQ, Canada.
[Shoukry, Naglaa H.] Univ Montreal, Fac Med, Dept Med, Montreal, PQ, Canada.
C3 Universite de Montreal; Universite de Montreal; Universite de Montreal
RP Shoukry, NH (corresponding author), CRCHUM, Local R09-414,900 Rue St Denis, Montreal, PQ H2X 0A9, Canada.
EM naglaa.shoukry@umontreal.ca
OI Abdelnabi, Mohamed/0009-0000-4012-0494; Flores Molina,
Manuel/0000-0002-2052-9935
FU Canadian Liver Foundation; Canadian Network on Hepatitis C (CanHepC);
Canadian Institutes of Health Research (CIHR) [NHC-142832]; Public
Health Agency of Canada (PHAC); FRQS; Universite de Montreal; CanHepC;
CIHR; Fonds de recherche du Quebec Sante (FRQS) AIDS and Infectious
Disease Network (Reseau SIDA-MI)
FX Our research is supported by grants from the Canadian Liver Foundation,
Fonds de recherche du Quebec Sante (FRQS) AIDS and Infectious Disease
Network (Reseau SIDA-MI) and the Canadian Network on Hepatitis C
(CanHepC). CanHepC is funded by a joint initiative from the Canadian
Institutes of Health Research (CIHR) (NHC-142832) and the Public Health
Agency of Canada (PHAC). MFM is the recipient of a doctoral fellowship
from the FRQS. MNA is supported by fellowships from the Universite de
Montreal and CanHepC. TF received doctoral fellowships from CIHR and
CanHepC.
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NR 155
TC 23
Z9 24
U1 0
U2 8
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD DEC
PY 2019
VL 124
SI SI
AR 154497
DI 10.1016/j.cyto.2018.07.028
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA JN9YM
UT WOS:000497244900002
PM 30097286
DA 2025-01-07
ER
PT J
AU Mishra, B
Tang, Y
Katuri, V
Fleury, T
Said, AH
Rashid, A
Jogunoori, W
Mishra, L
AF Mishra, B
Tang, Y
Katuri, V
Fleury, T
Said, AH
Rashid, A
Jogunoori, W
Mishra, L
TI Loss of cooperative function of transforming growth factor-β signaling
proteins, smad3 with embryonic liver fodrin, a β-spectrin, in primary
biliary cirrhosis
SO LIVER INTERNATIONAL
LA English
DT Article
DE hepatocellular cancer; primary biliary cirrhosis; Smad3; TGF-beta
ID MEMBRANE SKELETON; TGF-BETA; MECHANISMS; CHOLESTASIS; DISRUPTION;
BAND-3; RATS; MICE
AB Modulation of fibrogenesis, epithelial, and mesenchymal cell fates are prominent effects of transforming growth factor-beta (TGF-beta) signaling by Smad proteins. We have previously shown that Smad2 and Smad3 insufficiency leads to a loss of bile ducts. In addition, Smad3/4 activity is mediated by embryonic liver fodrin (ELF), a beta-Spectrin. In mouse elf(-/-) mutants and in liver explant cultures, loss of ELF function results in T lymphocytic proliferation and absent intrahepatic bile ducts. A similar phenotype is seen in a number of cholestatic diseases with progressive loss of intrahepatic bile ducts and fibrosis. However, the expression patterns of Smads or role of ELF in cholestatic and fibrotic liver diseases are not yet known. Methods/results: We investigated the role of ELF in primary biliary cirrhosis (PBC), autoimmune hepatitis C, chronic viral hepatitis and in livers from mice deficient in Smad2/Smad3. We generated elf(+/-) mutant mice and analyzed for chronic liver disease and hepatocellular cancer (HCC) from 6 to 12 months. Perturbations in ELF expression were consistently seen only in PBC tissues. ELF expression was similarly aberrant in tissues from Smad2(+/-)/Smad3(+/-) mutant mice. Further studies indicated that ELF mislocalization is correlated with aberrant localization of Smad3 in some PBC tissues. Thirteen of 17 elf(+/-) mutant mice developed steatosis, fibrosis, hepatic dysplasia, with HCC in two mice. Conclusions: These results suggest that a compromised cytoarchitecture and polarized trafficking of TGF-beta signaling molecules, ELF and Smad3 are involved in the pathogenesis of PBC as well as HCC.
C1 Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, Washington, DC 20057 USA.
DVAMC, Washington, DC USA.
Sibley Mem Hosp, Washington, DC USA.
Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA.
C3 Georgetown University; University of Texas System; UTMD Anderson Cancer
Center
RP Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, 3900 Reservoir Rd NW,Med-Dent NW212, Washington, DC 20057 USA.
EM lm229@georgetown.edu
OI Mishra, Lopa/0000-0002-6850-0808
FU NIDDK NIH HHS [1R01 DK58637, 1R01 DK56111] Funding Source: Medline
CR Alpini Gianfranco, 1994, P623
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NR 27
TC 24
Z9 30
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD DEC
PY 2004
VL 24
IS 6
BP 637
EP 645
DI 10.1111/j.1478-3231.2004.0958.x
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 874NU
UT WOS:000225357900018
PM 15566516
DA 2025-01-07
ER
PT J
AU Waldum, H
Fossmark, R
AF Waldum, Helge
Fossmark, Reidar
TI Inflammation and Digestive Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE carcinogenesis; inflammation; chronic gastritis; gastric cancer; chronic
hepatitis; hepatocellular carcinoma; inflammatory bowel disease; colon
cancer; mechanism; hormonal carcinogenesis
ID HELICOBACTER-PYLORI INFECTION; MULTIPLE ENDOCRINE NEOPLASIA;
ZOLLINGER-ELLISON-SYNDROME; GASTRIC CARCINOID-TUMORS; ECL-CELL
CARCINOIDS; COLORECTAL-CANCER; PERNICIOUS-ANEMIA; BOWEL-DISEASE;
ULCERATIVE-COLITIS; NEUROENDOCRINE DIFFERENTIATION
AB Chronic inflammation is linked to carcinogenesis, particularly in the digestive organs, i.e., the stomach, colon, and liver. The mechanism of this effect has, however, only partly been focused on. In this review, we focus on different forms of chronic hepatitis, chronic inflammatory bowel disease, and chronic gastritis, conditions predisposing individuals to the development of malignancy. Chronic inflammation may cause malignancy because (1) the cause of the chronic inflammation is itself genotoxic, (2) substances released from the inflammatory cells may be genotoxic, (3) the cell death induced by the inflammation induces a compensatory increase in proliferation with an inherent risk of mutation, (4) changes in cell composition due to inflammation may modify function, resulting in hormonal disturbances affecting cellular proliferation. The present review focuses on chronic gastritis (Helicobacter pylori or autoimmune type) since all four mechanisms may be relevant to this condition. Genotoxicity due to the hepatitis B virus is an important factor in hepatocellular cancer and viral infection can similarly be central in the etiology and malignancy of inflammatory bowel diseases. Helicobacter pylori (H. pylori) is the dominating cause of chronic gastritis and has not been shown to be genotoxic, so its carcinogenic effect is most probably due to the induction of atrophic oxyntic gastritis leading to hypergastrinemia.
C1 [Waldum, Helge; Fossmark, Reidar] Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, N-7030 Trondheim, Norway.
C3 Norwegian University of Science & Technology (NTNU)
RP Waldum, H (corresponding author), Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, N-7030 Trondheim, Norway.
EM helge.waldum@ntnu.com; reidar.fossmark@ntnu.no
OI Waldum, Helge/0000-0002-3137-0843
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NR 133
TC 9
Z9 9
U1 6
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2023
VL 24
IS 17
AR 13503
DI 10.3390/ijms241713503
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA R0EW5
UT WOS:001061166700001
PM 37686307
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Elghannam, MT
Hassanien, MH
Ameen, YA
ELattar, GM
ELRay, AA
Turky, EA
ELTalkawy, MD
AF Elghannam, Maged T.
Hassanien, Moataz H.
Ameen, Yosry A.
ELattar, Gamal M.
ELRay, Ahmed A.
Turky, Emad A.
ELTalkawy, Mohammed D.
TI COVID-19 and liver diseases
SO EGYPTIAN LIVER JOURNAL
LA English
DT Review
DE Coronaviruses; SARS-CoV-2; Liver diseases; Hepatocellular carcinoma;
Autoimmune liver disease; Liver transplantation; COVID-19 vaccination
ID PORTAL-VEIN THROMBOSIS; SARS-COV-2 INFECTION; RHEUMATOID-ARTHRITIS;
REPERFUSION INJURY; CYTOKINE; OUTCOMES; TOCILIZUMAB; EXPRESSION;
CIRRHOSIS; ISCHEMIA
AB Coronavirus causes an outbreak of viral pneumonia that spread throughout the world. Liver injury is becoming more widely recognized as a component of the clinical picture of COVID-19 infection. Hepatitis with serum ALT elevation has been reported in up to half of patients. Patients with CLD were at a higher risk of decompensation with liver failure, hospitalization, and mortality. The percentage of acute liver injury (ALI) varied from 5 to 28%. COVID-19 hinders HCV elimination by 2030. It is recommended to continue treatment of chronic HCV and chronic HBV if already receiving treatment. Consider using antiviral therapy to prevent viral flare-ups in patients with occult or resolved HBV and COVID-19 who are receiving immunosuppressive agents. Patients with AIH do not have an increased risk of adverse outcomes even in high-risk areas. There is an association between MAFLD and disease progression. Patients with any type of cancer are at a higher risk of infection and are more likely to develop more severe clinical outcomes. Most societies advise against immunosuppressant modifications in patients with mild COVID-19, whereas in rare cases such as severe lymphopenia, worsening pneumonia, or bacterial or fungal superinfection, reduction or discontinuation of antiproliferative agents and lymphocyte-depleting therapies has been suggested.
C1 [Elghannam, Maged T.; Hassanien, Moataz H.; Ameen, Yosry A.; ELattar, Gamal M.; ELRay, Ahmed A.; Turky, Emad A.; ELTalkawy, Mohammed D.] Theodor Bilharz Res Inst, Giza, Egypt.
C3 Egyptian Knowledge Bank (EKB); Theodor Bilharz Research Institute (TBRI)
RP Elghannam, MT (corresponding author), Theodor Bilharz Res Inst, Giza, Egypt.
EM maged_elghannam@yahoo.com
OI elghannam, maged/0000-0002-3638-5286
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NR 99
TC 5
Z9 5
U1 1
U2 4
PU SPRINGEROPEN
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, GWENT N1 9XW, ENGLAND
SN 2090-6218
EI 2090-6226
J9 EGYPT LIVER J
JI Egypt. Liver J.
PD JUL 21
PY 2022
VL 12
IS 1
AR 43
DI 10.1186/s43066-022-00202-2
PG 9
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA 3C3LW
UT WOS:000828529100001
PM 35880136
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Alqahtani, SA
Stepanova, M
Shah, DP
Al Shabeeb, R
Eberly, KE
Nguyen, V
Ong, J
Younossi, ZM
AF Alqahtani, Saleh A.
Stepanova, Maria
Shah, Dipam
Al Shabeeb, Reem
Eberly, Katherine Elizabeth
Nguyen, Veronica
Ong, Janus
Younossi, Zobair M.
TI Liver Transplantation Profile Among Teenagers in the United States
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Article
DE Acute liver disease; PSC; Autoimmune hepatitis; HCC; Medicaid
ID AMERICAN ASSOCIATION; PRACTICE GUIDELINE; DISEASE; ADOLESCENT; HEALTH;
TRANSITION; RECIPIENTS; OUTCOMES; SOCIETY; BURDEN
AB Purpose: Indications for liver transplantation (LT) vary across age groups. We identified predictors of outcomes for teenage LT waitlisted candidates and recipients in the United States from 2008 to 2022. Methods: The Scientific Registry of Transplant Recipients 2008-2022 provided data (clinical, sociodemographic, indications for LT, outcomes) for all teenagers (13-19 years) waitlisted for LT in the United States. Sociodemographic and clinical characteristics, including primary listing diagnoses, were evaluated and compared by age group (13-16 vs. 17-19 years) among waitlisted teenage candidates. Results: There were 2,813 teenage LT candidates listed between 2008 and 2022. The most common LT indication was acute liver disease (23.5%), followed by biliary atresia or hypoplasia (11.9%), autoimmune hepatitis (11.1%), and primary sclerosing cholangitis (9.7%). In contrast, chronic viral hepatitis, metabolic dysfunction-associated steatotic liver disease, and alcohol-related liver disease (the most common indications in adults) did not exceed 1% each; 2.8% had hepatocellular carcinoma. Excluding the two most recent years, 67.2% of candidates received a transplant; mean time to transplant was 217.0 days (standard deviation 371.6). Independent predictors of receiving a transplant were a more recent calendar year, younger age, higher model for end-stage liver disease score, and an acute liver disease diagnosis (all p < .05). Among the LT group, 3-year survival was 90%, with an improving survival trend. Higher post-transplant mortality was associated with earlier years of transplantation, older age, having Medicaid, being retransplanted, and having hepatocellular carcinoma (adjusted hazard ratios >1, all p < .05). Discussion: Indications for LT among US teenagers are different from adults or younger children. There is a trend toward improved post-transplant outcomes.
C1 [Alqahtani, Saleh A.; Stepanova, Maria; Ong, Janus; Younossi, Zobair M.] Global NASH Council, 2411 1 St, Washington, DC 20037 USA.
[Alqahtani, Saleh A.] King Faisal Specialist Hosp & Res Ctr, Organ Transplant Ctr Excellence, Riyadh, Saudi Arabia.
[Alqahtani, Saleh A.] Johns Hopkins Univ, Div Gastroenterol & Hepatol, Baltimore, MD USA.
[Stepanova, Maria; Shah, Dipam; Eberly, Katherine Elizabeth; Nguyen, Veronica; Younossi, Zobair M.] Inova Hlth Syst, Beatty Liver & Obes Res Program, Falls Church, VA USA.
[Ong, Janus] Univ Philippines, Coll Med, Manila, Philippines.
[Younossi, Zobair M.] Ctr Outcomes Res Liver Dis, Washington, DC USA.
[Younossi, Zobair M.] Global NASH Council, 2411 1 St, Washington, DC 20037 USA.
C3 King Faisal Specialist Hospital & Research Center; Johns Hopkins
University; Inova Health System; University of the Philippines System;
University of the Philippines Manila
RP Younossi, ZM (corresponding author), Global NASH Council, 2411 1 St, Washington, DC 20037 USA.; Younossi, ZM (corresponding author), Global NASH Council, 2411 1 St, Washington, DC 20037 USA.
EM zobair.younossi@cldq.org
RI Younossi, Zobair M./JRY-9916-2023
FU King Faisal Specialist Hospital & Research Centre; Center for Outcomes
Research in Liver Diseases; Beatty Liver and Obesity Research Fund,
Inova Health System, VA, USA
FX This study was partially supported by research funds from King Faisal
Specialist Hospital & Research Centre to the Global NASH Council, by the
Center for Outcomes Research in Liver Diseases, and by the Beatty Liver
and Obesity Research Fund, Inova Health System, VA, USA.
CR [Anonymous], 2022, Data on Excessive Drinking
[Anonymous], Underage drinking
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NR 38
TC 1
Z9 1
U1 3
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1054-139X
EI 1879-1972
J9 J ADOLESCENT HEALTH
JI J. Adolesc. Health
PD OCT
PY 2024
VL 75
IS 4
BP 578
EP 583
DI 10.1016/j.jadohealth.2024.05.009
EA SEP 2024
PG 6
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA G6I0Q
UT WOS:001317640100001
PM 39007787
DA 2025-01-07
ER
PT J
AU Floreani, A
AF Floreani, Annarosa
TI Liver disorders in the elderly
SO BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE Liver diseases; Elderly; Chronic hepatitis; Ageing
ID HEPATITIS-C VIRUS; PRIMARY BILIARY-CIRRHOSIS; I AUTOIMMUNE HEPATITIS;
HEPATOCELLULAR-CARCINOMA; NATURAL-HISTORY; GENERAL-POPULATION;
RISK-FACTORS; FATTY LIVER; NONALCOHOLIC STEATOHEPATITIS; COMBINATION
THERAPY
AB Although there are no specific age-related liver diseases, it is increasingly recognized that the percentage and the actual number of elderly will increase substantially over the next twenty years. Moreover, the developments of new emerging conditions (e.g. non-alcoholic steatohepatitis) and novel therapeutic approaches have provoked increasing enthusiasm among hepatologists. Some liver diseases are particularly frequent in the elderly, e.g. chronic hepatitis C and hepatocellular carcinoma. The clinical course and management of liver disease in the elderly may differ in several aspects from those of younger adults. The problem of whether to offer antiviral treatment to a wide range of patients with chronic hepatitis C has arisen over the last eight to ten years, since the reduction in the risk of hepatocellular carcinoma was analyzed. Selected patients aged 65 and older have a chance of treatment with pegylated interferon plus ribavirin, despite a higher likelihood of side effects. The diagnosis of autoimmune hepatitis should be suspected in a patient over 65 years of age in case of 'acute' presentation with 10-fold increase in transaminases, jaundice and hyper-gammaglobulinemia, to avoid any delay in starting immunosuppressive therapy. The age of an end stage liver disease will increase over the next years, thus we will expects an increasing number of decompensated liver disease and hepatocellular carcinomas. (C) 2009 Elsevier Ltd. All rights reserved.
C1 Univ Padua, Dept Surg & Gastroenterol Sci, I-35128 Padua, Italy.
C3 University of Padua
RP Floreani, A (corresponding author), Univ Padua, Dept Surg & Gastroenterol Sci, Via Giustiniani 2, I-35128 Padua, Italy.
EM annarosa.floreani@unipd.it
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TC 15
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U1 0
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PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1521-6918
EI 1532-1916
J9 BEST PRACT RES CL GA
JI Best Pract. Res. Clin. Gastroenterol.
PD DEC
PY 2009
VL 23
IS 6
BP 909
EP 917
DI 10.1016/j.bpg.2009.10.005
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 537NZ
UT WOS:000273121000011
PM 19942167
DA 2025-01-07
ER
PT J
AU Malik, N
Venkatesh, SK
AF Malik, Neera
Venkatesh, Sudhakar K.
TI Imaging of autoimmune hepatitis and overlap syndromes
SO ABDOMINAL RADIOLOGY
LA English
DT Article
DE Autoimmune hepatitis; Cirrhosis; Primary sclerosing cholangitis; Primary
biliary cirrhosis; MR elastography
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
MAGNETIC-RESONANCE ELASTOGRAPHY; LIVER-DISEASES;
HEPATOCELLULAR-CARCINOMA; MANAGEMENT; DIAGNOSIS; FEATURES; FREQUENCY;
PROGNOSIS
AB Autoimmune hepatitis (AIH) is an uncommon, chronic inflammatory, and relapsing liver disease of unknown origin that may lead to liver cirrhosis, hepatocellular carcinoma, liver transplantation, or death. AIH occurs in all age groups and races but can frequently manifest as acute fulminant hepatitis. Clinical presentation of AIH can have features similar to primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC), and these diseases may coexist leading to overlap syndromes. Although histological diagnosis is necessary, imaging features often can demonstrate characteristics that may be helpful to distinguish these diseases. Imaging features of AIH are those of chronic liver disease, and imaging plays important role in detection of complications and ruling out other possible causes of chronic liver disease. Emerging techniques such as elastography provide non-invasive options for diagnosis of significant fibrosis and cirrhosis during clinical follow-up as well as assessment of response to treatment. In this study, we will describe imaging findings in AIH and overlap syndromes.
C1 [Malik, Neera; Venkatesh, Sudhakar K.] Mayo Clin, Div Abdominal Imaging, Dept Radiol, 200 First St SW, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Venkatesh, SK (corresponding author), Mayo Clin, Div Abdominal Imaging, Dept Radiol, 200 First St SW, Rochester, MN 55905 USA.
EM venkatesh.sudhakar@mayo.edu
RI Venkatesh, Sudhakar/T-9385-2019
OI Venkatesh, Sudhakar/0000-0002-7514-1030
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NR 58
TC 16
Z9 18
U1 0
U2 14
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 2366-004X
EI 2366-0058
J9 ABDOM RADIOL
JI Abdom. Radiol.
PD JAN
PY 2017
VL 42
IS 1
BP 19
EP 27
DI 10.1007/s00261-016-1019-x
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA EI2BQ
UT WOS:000392291700003
PM 27999888
DA 2025-01-07
ER
PT J
AU Schöler, D
Schnabl, B
AF Scholer, David
Schnabl, Bernd
TI The role of the microbiome in liver disease
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Article
DE gut-liver axis; liver disease; microbiome
ID FECAL MICROBIOTA; CLOSTRIDIUM-BUTYRICUM; INTESTINAL VIROME; RESISTANT
STARCH; GUT MICROBIOTA; ALCOHOL-USE; TRANSPLANTATION; ACID; NAFLD;
THERAPY
AB Purpose of reviewThe intestinal microbiome and the gut-liver axis play a major role in health and disease. The human gut harbors trillions of microbes and a disruption of the gut homeostasis can contribute to liver disease. In this review, the progress in the field within the last 3 years is summarized, focusing on metabolic dysfunction-associated steatotic liver disease (MASLD), alcohol-associated liver disease (ALD), autoimmune liver disease (AILD), and hepatocellular carcinoma (HCC).Recent findingsChanges in the fecal virome and fungal mycobiome have been described in patients with various liver diseases. Several microbial derived metabolites including endogenous ethanol produced by bacteria, have been mechanistically linked to liver disease such as MASLD. Virulence factors encoded by gut bacteria contribute to ALD, AILD and HCC. Novel therapeutic approaches focused on the microbiome including phages, pre- and postbiotics have been successfully used in preclinical models. Fecal microbiota transplantation has been effective in attenuating liver disease. Probiotics are safe in patients with alcohol-associated hepatitis and improve liver disease and alcohol addiction.SummaryThe gut-liver axis plays a key role in the pathophysiology of liver diseases. Understanding the microbiota in liver disease can help to develop precise microbiota centered therapies.
C1 [Scholer, David; Schnabl, Bernd] Univ Calif San Diego, Sch Med, MC0063,9500 Gilman Dr, La Jolla, CA 92093 USA.
[Schnabl, Bernd] VA San Diego Healthcare Syst, Dept Med, San Diego, CA USA.
C3 University of California System; University of California San Diego; US
Department of Veterans Affairs; Veterans Health Administration (VHA); VA
San Diego Healthcare System
RP Schnabl, B (corresponding author), Univ Calif San Diego, Sch Med, MC0063,9500 Gilman Dr, La Jolla, CA 92093 USA.
EM beschnabl@health.ucsd.edu
RI Schnabl, Bernd/HCH-3471-2022
FU DFG fellowship [SCHO1910/4-1]; NIH [R01 AA024726, R01 AA020703, U01
AA026939, P30 DK120515, P50 AA011999]; Biomedical Laboratory Research &
Development Service of the VA Office of Research and Development
[BX004594]
FX This work was supported by a DFG fellowship (SCHO1910/4-1) (to D.S.),
NIH grants R01 AA024726, R01 AA020703, U01 AA026939, by Award Number
BX004594 from the Biomedical Laboratory Research & Development Service
of the VA Office of Research and Development (to B.S.) and services
provided by NIH centers P30 DK120515 and P50 AA011999.
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NR 82
TC 3
Z9 4
U1 10
U2 16
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0267-1379
EI 1531-7056
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD MAY
PY 2024
VL 40
IS 3
BP 134
EP 142
DI 10.1097/MOG.0000000000001013
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA SO2V7
UT WOS:001235336600008
PM 38362864
DA 2025-01-07
ER
PT J
AU Okumura, T
Joshita, S
Yamazaki, T
Iwadare, T
Wakabayashi, SI
Kobayashi, H
Yamashita, Y
Sugiura, A
Kimura, T
Ota, M
Umemura, T
AF Okumura, Taiki
Joshita, Satoru
Yamazaki, Tomoo
Iwadare, Takanobu
Wakabayashi, Shun-ichi
Kobayashi, Hiroyuki
Yamashita, Yuki
Sugiura, Ayumi
Kimura, Takefumi
Ota, Masao
Umemura, Takeji
TI HLA-G susceptibility to hepatitis B infection and related hepatocellular
carcinoma in the Japanese population
SO HUMAN IMMUNOLOGY
LA English
DT Article
DE Hepatitis B; Human leukocyte antigen-G; Polymorphisms
ID 14-BP INSERTION/DELETION POLYMORPHISM; G GENE; VIRUS-INFECTION;
NATURAL-HISTORY; CELL; ASSOCIATION; EXPRESSION; REGION; LYSIS
AB Aims: Human leukocyte antigen (HLA)-G plays a role in various physiological immunomodulatory functions. Aberrant HLA-G expression is observed in various disease states, including tumors, autoimmune disorders, and viral infections. The present study investigated the association between HLA-G functional gene polymorphisms (rs1736933 [-486 C > A], rs1049033 [+2018 C > T], 14 bp Insertion [Ins]/Deletion [Del] [+2961 Del > Ins], and rs1063320 [+3142 C > G]) and disease susceptibility, hepatocellular carcinoma (HCC) development, and hepatitis B surface antigen (HBsAg) clearance.Methods: Allele discrimination of the 3 SNPs (-486 C > A, +2018 C > T, +3142 C > G) was determined by a TaqMan 50 exonuclease assay, while the 14 bp Ins/Del polymorphism was typed by fragment analysis using Genetic Analyzer and GeneMapper software. The above polymorphisms were analyzed for 325 Japanese hepatitis B virus (HBV) patients, 355 Japanese healthy subjects (Controls) as healthy controls, and 799 Japanese hepatitis C virus (HCV) patients as disease controls, respectively.Results: The 14 bp Insertion allele was significantly more frequent in HBV patients than Controls (27.1 % vs 20.6 %, odds ratio [OR] 1.43, P = 0.005) but did not differ between HCV patients and Controls. Similar results were found for the rs1063320 G allele (38.9 % vs 26.3 %, OR 1.78, P < 0.001) and the rs1736933 T allele (32.2 % vs 26.9 %, OR 1.29, P = 0.034) between HBV and Controls. The rs1049033 T allele showed a weak but significant association with HCC development in the dominant model (OR 1.95, P = 0.04). Regarding HBsAg clearance, the A allele at rs1736933 was significantly correlated in the recessive model (OR 3.23, P = 0.003).Conclusions: This study revealed significant associations of HLA-G gene polymorphisms with disease susceptibility, HCC development, and HBsAg clearance in HBV patients.
C1 [Okumura, Taiki; Joshita, Satoru; Yamazaki, Tomoo; Iwadare, Takanobu; Wakabayashi, Shun-ichi; Kobayashi, Hiroyuki; Yamashita, Yuki; Sugiura, Ayumi; Kimura, Takefumi; Ota, Masao; Umemura, Takeji] Shinshu Univ, Dept Med, Div Gastroenterol & Hepatol, Sch Med, Matsumoto, Japan.
[Joshita, Satoru; Kobayashi, Hiroyuki; Ota, Masao; Umemura, Takeji] Shinshu Univ, Dept Hlth Promot Med, Sch Med, Matsumoto, Japan.
[Umemura, Takeji] Shinshu Univ, Dept Adv Endoscop Therapy, Sch Med, Matsumoto, Japan.
[Umemura, Takeji] Shinshu Univ Hosp, Consultat Ctr Liver Dis, Matsumoto, Japan.
[Joshita, Satoru; Ota, Masao] Shinshu Univ, Dept Med, Div Gastroenterol & Hepatol, Sch Med, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan.
C3 Shinshu University; Shinshu University; Shinshu University; Shinshu
University; Shinshu University
RP Joshita, S; Ota, M (corresponding author), Shinshu Univ, Dept Med, Div Gastroenterol & Hepatol, Sch Med, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan.
EM joshita@shinshu-u.ac.jp; otamasao@shinshu-u.ac.jp
RI Kimura, Takefumi/D-3412-2011; Joshita, Satoru/K-5679-2019
OI Yamashita, Yuki/0000-0002-0162-4208; Okumura, Taiki/0000-0001-5715-1748;
Ota, Masao/0000-0002-6400-5658; Iwadare, Takanobu/0000-0003-0430-6819;
Joshita, Satoru/0000-0002-6364-9654
FU Japan Society for the Promotion of Science (JSPS) KAKENHI [20K08282,
20K17019]; Japan Agency for Medical Research and Development (AMED)
[JP21fk0210084, JP22fk0210112]
FX Funding statement The authors sincerely appreciate the research support
provided in part by the Japan Society for the Promotion of Science
(JSPS) KAKENHI Grant-in-Aid for Scientific Research (C) (20K08282) ,
Grant-in-Aid for Early-Career Scientists (20K17019) , and the Japan
Agency for Medical Research and Development (AMED) (JP21fk0210084,
JP22fk0210112) .
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NR 30
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0198-8859
EI 1879-1166
J9 HUM IMMUNOL
JI Hum. Immunol.
PD AUG
PY 2023
VL 84
IS 8
BP 401
EP 407
DI 10.1016/j.humimm.2023.05.002
EA JUL 2023
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA P1LK3
UT WOS:001048323000001
PM 37271588
OA Bronze
DA 2025-01-07
ER
PT J
AU López-López, A
López-Gonzálvez, A
Barker-Tejeda, TC
Barbas, C
AF Lopez-Lopez, Angeles
Lopez-Gonzalvez, Angeles
Clive Barker-Tejeda, Tomas
Barbas, Coral
TI A review of validated biomarkers obtained through metabolomics
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE Metabolomics; validation; biomarkers; global profiling
ID SQUAMOUS-CELL CARCINOMA; MAJOR DEPRESSIVE DISORDER; SERUM METABOLOMICS;
LUNG-CANCER; HEPATOCELLULAR-CARCINOMA; POTENTIAL BIOMARKERS;
EARLY-DIAGNOSIS; BLADDER-CANCER; TARGETED METABOLOMICS; METABOLITE
BIOMARKER
AB Introduction: Studying changes in the whole set of small molecules, final products of biochemical reactions in living systems or metabolites, is extremely appealing because they represent the best approach to identifying what occurs in an organism when samples are collected. However, their usefulness as potential biomarkers is limited by discoveries obtained in small groups without proper validation or even confirmation of the chemical structure.Areas covered: During the past 5years, more than 900 papers have been published on metabolomics for biomarker discovery, but the numbers are much lower when some criteria of validation are applied. In total, 102 papers have been included in this review. The most frequent disease areas in which these markers have been discovered include the following: cancer, diabetes, and related diseases and neurodegenerative, cardiovascular, autoimmune, liver, and kidney diseases.Expert commentary: Metabolomics has been demonstrated as rapidly growing due to the improvements in instrumentation, mainly mass spectrometry, and data mining software. For application in the clinic, the results should be validated in different stages, from analytical validation to validation in independent sets of samples, using thousands of samples from different sources.
C1 [Lopez-Lopez, Angeles; Lopez-Gonzalvez, Angeles; Clive Barker-Tejeda, Tomas; Barbas, Coral] Univ CEU San Pablo, Fac Farm, Ctr Metabol & Bioanal CEMBIO, Madrid, Spain.
C3 San Pablo CEU University
RP Barbas, C (corresponding author), Univ CEU San Pablo, Fac Farm, Ctr Metabol & Bioanal CEMBIO, Madrid, Spain.
EM cbarbas@ceu.es
RI López-López, Ángeles/GXH-8429-2022; Barker Tejeda, Tomas
Clive/GVU-5970-2022; Lopez-Gonzalvez, Angeles/K-4361-2014; Barbas,
Coral/K-3871-2014
OI Barker Tejeda, Tomas Clive/0000-0002-2942-5876; Lopez-Gonzalvez,
Angeles/0000-0002-6363-7135; Lopez-Lopez, Angeles/0000-0003-1006-4369;
Barbas, Coral/0000-0003-4722-491X
FU Spanish Ministerio de Economia y Competitividad
FX This article was funded by Spanish Ministerio de Economia y
Competitividad.
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NR 111
TC 64
Z9 68
U1 0
U2 76
PU TAYLOR & FRANCIS AS
PI OSLO
PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY
SN 1473-7159
EI 1744-8352
J9 EXPERT REV MOL DIAGN
JI Expert Rev. Mol. Diagn.
PY 2018
VL 18
IS 6
BP 557
EP 575
DI 10.1080/14737159.2018.1481391
PG 19
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA GJ1IN
UT WOS:000435008800008
PM 29808702
DA 2025-01-07
ER
PT J
AU Qiu, Y
Xu, MB
Yun, MM
Wang, YZ
Zhang, RM
Meng, XK
Ou-Yang, XH
Yun, S
AF Qiu, Ying
Xu, Ming-Bao
Yun, Mark M.
Wang, Yi-Zhong
Zhang, Rui-Ming
Meng, Xing-Kai
Ou-Yang, Xiao-Hui
Yun, Sheng
TI Hepatocellular carcinoma-specific immunotherapy with synthesized
α1,3-galactosyl epitope-pulsed dendritic cells and cytokine-induced
killer cells
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Hepatocellular carcinoma; alpha-Gal epitope; Dendritic cell;
Tumor-associated antigen; Dendritic cell-activated cytokine-induced
killer cell
ID AUTOLOGOUS TUMOR VACCINE; ANTIBODY; THERAPY; CANCER; IMMUNOGENICITY;
COSTIMULATION; RESPONSES
AB AIM: To evaluate the safety and clinical efficacy of a new immunotherapy using both alpha-Gal epitope-pulsed dendritic cells (DCs) and cytokine-induced killer cells.
METHODS: Freshly collected hepatocellular carcinoma (HCC) tumor tissues were incubated with a mixture of neuraminidase and recombinant alpha 1,3-galactosyl-transferase (alpha 1,3GT) to synthesize alpha-Gal epitopes on carbohydrate chains of the glycoproteins of tumor membranes. The subsequent incubation of the processed membranes in the presence of human natural anti-Gal IgG resulted in the effective phagocytosis to the tumor membrane by DCs. Eighteen patients aged 38-78 years with stage. primary HCC were randomLy chosen for the study; 9 patients served as controls, and 9 patients were enrolled in the study group.
RESULTS: The evaluation demonstrated that the procedure was safe; no serious side effects or autoimmune diseases were observed. The therapy significantly prolonged the survival of treated patients as compared with the controls (17.1 +/- 2.01 mo vs 10.1 +/- 4.5 mo, P = 0.00121). After treatment, all patients in the study group had positive delayed hypersensitivity and robust systemic cytotoxicity in response to tumor lysate as measured by interferon-gamma-expression in peripheral blood mononuclear cells using enzyme-linked immunosorbent spot assay. They also displayed increased numbers of CD8-, CD45RO- and CD56-positive cells in the peripheral blood and decreased alpha-fetoprotein level in the serum.
CONCLUSION: This new tumor-specific immunotherapy is safe, effective and has a great potential for the treatment of tumors. (C) 2011 Baishideng. All rights reserved.
C1 [Yun, Sheng] First Teaching Hosp, Inner Mongolia Med Coll, Dept Oncol, Hohhot 010050, Inner Mongolia, Peoples R China.
[Xu, Ming-Bao] Armed Police Gen Hosp, Beijing 100036, Peoples R China.
[Yun, Mark M.] Med Sch UCL, London WC1E 6BT, England.
[Wang, Yi-Zhong; Yun, Sheng] Peking Univ, Aerosp Med Coll, Beijing 100049, Peoples R China.
[Qiu, Ying] Kings Coll Hosp London, Dept Clin Sci, London SE5 9NU, England.
[Yun, Sheng] MRC, Ctr Clin Sci, London W12 0NN, England.
C3 Inner Mongolia Medical University; University of London; University
College London; Peking University; King's College Hospital NHS
Foundation Trust; King's College Hospital
RP Yun, S (corresponding author), First Teaching Hosp, Inner Mongolia Med Coll, Dept Oncol, 1 Tongdao BeiJie, Hohhot 010050, Inner Mongolia, Peoples R China.
EM sheng.yun@hotmail.co.uk
FU Hong Kong Wang Kuan Cheng; Inner Mongolia Stem Cell [kjk10jhg]
FX Supported by Hong Kong Wang Kuan Cheng Grant; and Inner Mongolia Stem
Cell Grant, No. kjk10jhg
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PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD DEC 28
PY 2011
VL 17
IS 48
BP 5260
EP 5266
DI 10.3748/wjg.v17.i48.5260
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 871MI
UT WOS:000298741800004
PM 22219594
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Bezinover, D
Iskandarani, K
Chinchilli, V
McQuillan, P
Saner, F
Kadry, Z
Riley, TR
Janicki, PK
AF Bezinover, Dmitri
Iskandarani, Khaled
Chinchilli, Vernon
McQuillan, Patrick
Saner, Fuat
Kadry, Zakiyah
Riley, Thomas R.
Janicki, Piotr K.
TI Autoimmune conditions are associated with perioperative thrombotic
complications in liver transplant recipients: A UNOS database analysis
SO BMC ANESTHESIOLOGY
LA English
DT Article
DE Liver transplantation; Portal vein thrombosis; Hepatic artery
thrombosis; Autoimmune and oncologic conditions; Antithrombotic
prophylaxis
ID PORTAL-VEIN THROMBOSIS; HEPATIC-ARTERY THROMBOSIS; PRIMARY
BILIARY-CIRRHOSIS; RECURRENT VENOUS THROMBOEMBOLISM;
HEPATOCELLULAR-CARCINOMA; RISK-FACTORS; SURVIVAL BENEFIT; DISEASE;
HYPERCOAGULABILITY; COAGULATION
AB Background: End stage liver disease (ESLD) is associated with significant thrombotic complications. In this study, we attempted to determine if patients with ESLD, due to oncologic or autoimmune diseases, are susceptible to thrombosis to a greater extent than patients with ESLD due to other causes.
Methods: In this retrospective study, we analyzed the UNOS database to determine the incidence of thrombotic complications in orthotopic liver transplant (OLT) recipients with autoimmune and oncologic conditions. Between 2000 and 2012, 65,646 OLTs were performed. We found 4,247 cases of preoperative portal vein thrombosis (PVT) and 1,233 cases of postoperative vascular thrombosis (VT) leading to graft failure.
Results: Statistical evaluation demonstrated that patients with either hepatocellular carcinoma (HCC) or autoimmune hepatitis (AIC) had a higher incidence of PVT (p = 0.05 and 0.03 respectively). Patients with primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and AIC had a higher incidence of postoperative VT associated with graft failure (p < 0.0001, p < 0.0001, p = 0.05 respectively). Patients with preoperative PVT had a higher incidence of postoperative VT (p < 0.0001). Multivariable logistic regression demonstrated that patients with AIC, and BMI >= 40, having had a transjugular intrahepatic portosystemic shunt, and those with diabetes mellitus were more likely to have preoperative PVT: odds ratio (OR)(1.36, 1.19, 1.78, 1.22 respectively). Patients with PSC, PBC, AIC, BMI <= 18, or with a preoperative PVT were more likely to have a postoperative VT: OR (1.93, 2.09, 1.64, 1.60, and 2.01, respectively).
Conclusion: Despite the limited number of variables available in the UNOS database potentially related to thrombotic complications, this analysis demonstrates a clear association between autoimmune causes of ESLD and perioperative thrombotic complications. Perioperative management of patients at risk should include strategies to reduce the potential for these complications.
C1 [Bezinover, Dmitri; McQuillan, Patrick; Janicki, Piotr K.] Penn State Hershey Med Ctr, Dept Anesthesiol, Penn State Coll Med, 500 Univ Dr, Hershey, PA 17033 USA.
[Iskandarani, Khaled; Chinchilli, Vernon] Penn State Hershey Med Ctr, Penn State Coll Med, Dept Publ Hlth Sci, 90 Hope Dr, Hershey, PA 17033 USA.
[Saner, Fuat] Essen Univ, Med Ctr, Dept Gen Visceral & Transplant Surg, Hufelandstr 55, D-45147 Essen, Germany.
[Kadry, Zakiyah] Penn State Hershey Med Ctr, Penn State Coll Med, Dept Surg, 500 Univ Dr, Hershey, PA 17033 USA.
[Riley, Thomas R.] Penn State Hershey Med Ctr, Penn State Coll Med, Dept Gastroenterol, 500 Univ Dr, Hershey, PA 17033 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE);
Pennsylvania State University; Penn State Health; Pennsylvania
Commonwealth System of Higher Education (PCSHE); Pennsylvania State
University; Penn State Health; University of Duisburg Essen;
Pennsylvania Commonwealth System of Higher Education (PCSHE);
Pennsylvania State University; Penn State Health; Pennsylvania
Commonwealth System of Higher Education (PCSHE); Pennsylvania State
University; Penn State Health
RP Bezinover, D (corresponding author), Penn State Hershey Med Ctr, Dept Anesthesiol, Penn State Coll Med, 500 Univ Dr, Hershey, PA 17033 USA.
EM dbezinover@hmc.psu.edu
RI Saner, Fuat/W-8024-2019
OI Riley, Thomas/0000-0002-8678-9836
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NR 57
TC 24
Z9 25
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2253
J9 BMC ANESTHESIOL
JI BMC Anesthesiol.
PD MAY 21
PY 2016
VL 16
AR 26
DI 10.1186/s12871-016-0192-3
PG 7
WC Anesthesiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anesthesiology
GA DM5FU
UT WOS:000376373900001
PM 27207434
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Garg, D
Nagar, A
Philips, S
Takahashi, N
Prasad, SR
Shanbhogue, AK
Sahani, DV
AF Garg, Deepak
Nagar, Arpit
Philips, Shaile
Takahashi, Naoki
Prasad, Srinivasa R.
Shanbhogue, Alampady K.
Sahani, Dushyant V.
TI Immunological diseases of the pancreatico-hepatobiliary system: update
on etiopathogenesis and cross-sectional imaging findings
SO ABDOMINAL IMAGING
LA English
DT Article
DE Autoimmune hepatitis; Primary biliary cirrhosis; Primary sclerosing
cholangitis; IgG-4-related disease; Computed tomography; Magnetic
resonance imaging
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; AUTOIMMUNE
PANCREATITIS; LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA; HEPATITIS; CT;
FEATURES; MANAGEMENT; OVERLAP
AB Immunological diseases of the hepatobiliary system and the pancreas include a broad spectrum of disorders that manifest characteristic histopathology/serology and variable clinical features and imaging findings. Recent studies have thrown fresh light on the complex role of genetics and autoimmunity in the pathogenesis and natural history of these diverse disorders that include autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, IgG4-related cholangitis, overlap/outlier syndromes, and autoimmune pancreatitis.
C1 [Prasad, Srinivasa R.] Univ Texas MD Anderson Canc Ctr, Dept Radiol, Houston, TX 77030 USA.
[Garg, Deepak; Philips, Shaile; Shanbhogue, Alampady K.] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, San Antonio, TX 78229 USA.
[Nagar, Arpit] Ohio State Univ, Dept Radiol, Med Ctr, Columbus, OH 43210 USA.
[Takahashi, Naoki] Mayo Clin, Dept Radiol, Rochester, MN 55905 USA.
[Sahani, Dushyant V.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
Texas System; University of Texas Health Science Center at San Antonio;
University System of Ohio; Ohio State University; Mayo Clinic; Harvard
University; Massachusetts General Hospital
RP Prasad, SR (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Radiol, 1400 Pressler St, Houston, TX 77030 USA.
EM sprasad2@mdander-son.org
RI Prasad, Srinivasa/AAJ-8654-2020
OI Takahashi, Naoki/0000-0002-7946-6078; Shanbhogue, Krishna
Prasad/0000-0002-7071-6077
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NR 54
TC 4
Z9 5
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-8925
EI 1432-0509
J9 ABDOM IMAGING
JI Abdom. Imaging
PD APR
PY 2012
VL 37
IS 2
BP 261
EP 274
DI 10.1007/s00261-011-9759-0
PG 14
WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
GA 918MO
UT WOS:000302254100012
PM 21597892
DA 2025-01-07
ER
PT J
AU Malik, S
Das, R
Thongtan, T
Thompson, K
Dbouk, N
AF Malik, Sheza
Das, Rishi
Thongtan, Thanita
Thompson, Kathryn
Dbouk, Nader
TI AI in Hepatology: Revolutionizing the Diagnosis and Management of Liver
Disease
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE artificial intelligence; machine learning; deep learning; cirrhosis;
hepatocellular carcinoma
ID ARTIFICIAL-INTELLIGENCE; HEPATOCELLULAR-CARCINOMA; MODEL; PREDICTION;
PERFORMANCE; VALIDATION; ALGORITHMS; CHALLENGES; RADIOMICS; MEDICINE
AB The integration of artificial intelligence (AI) into hepatology is revolutionizing the diagnosis and management of liver diseases amidst a rising global burden of conditions like metabolic-associated steatotic liver disease (MASLD). AI harnesses vast datasets and complex algorithms to enhance clinical decision making and patient outcomes. AI's applications in hepatology span a variety of conditions, including autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis, MASLD, hepatitis B, and hepatocellular carcinoma. It enables early detection, predicts disease progression, and supports more precise treatment strategies. Despite its transformative potential, challenges remain, including data integration, algorithm transparency, and computational demands. This review examines the current state of AI in hepatology, exploring its applications, limitations, and the opportunities it presents to enhance liver health and care delivery.
C1 [Malik, Sheza] Rochester Gen Hosp, Dept Internal Med, Rochester, NY 14621 USA.
[Das, Rishi; Thongtan, Thanita; Dbouk, Nader] Emory Univ, Sch Med, Div Digest Dis, Atlanta, GA 30322 USA.
[Das, Rishi; Thongtan, Thanita; Thompson, Kathryn; Dbouk, Nader] Emory Univ, Sch Med, Dept Med, Atlanta, GA 30322 USA.
[Dbouk, Nader] Emory Univ, Sch Med, Emory Transplant Ctr, Atlanta, GA 30322 USA.
RP Dbouk, N (corresponding author), Emory Univ, Sch Med, Div Digest Dis, Atlanta, GA 30322 USA.; Dbouk, N (corresponding author), Emory Univ, Sch Med, Dept Med, Atlanta, GA 30322 USA.; Dbouk, N (corresponding author), Emory Univ, Sch Med, Emory Transplant Ctr, Atlanta, GA 30322 USA.
EM sheza.malik@rochesterregional.org; rishi.das@emory.edu;
thanita.thongtan@emory.edu; kathryn.monti.thompson@emory.edu;
ndbouk@emory.edu
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NR 118
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD DEC
PY 2024
VL 13
IS 24
AR 7833
DI 10.3390/jcm13247833
PG 26
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA Q8A6M
UT WOS:001386840400001
OA gold
DA 2025-01-07
ER
PT J
AU Bowlus, CL
Seeley, EH
Roder, J
Grigorieva, J
Roder, H
Caprioli, RM
Gershwin, ME
AF Bowlus, Christopher L.
Seeley, Erin H.
Roder, Joanna
Grigorieva, Julia
Roder, Heinrich
Caprioli, Richard M.
Gershwin, M. Eric
TI In situ mass spectrometry of autoimmune liver diseases
SO CELLULAR & MOLECULAR IMMUNOLOGY
LA English
DT Article
DE autoimmune hepatitis; mass spectrometry; primary biliary cirrhosis;
primary sclerosing cholangitis
ID PRIMARY BILIARY-CIRRHOSIS; GENE-EXPRESSION PROFILES; TISSUE-SECTIONS;
BREAST-CANCER; LUNG-CANCER; MALDI-MS; HEPATITIS; PROTEINS; CELLS
C1 [Bowlus, Christopher L.] Univ Calif Davis, Div Gastroenterol & Hepatol, Davis, CA 95616 USA.
[Seeley, Erin H.; Caprioli, Richard M.] Vanderbilt Univ, Sch Med, Mass Spectrometry Res Ctr, Nashville, TN 37212 USA.
[Roder, Joanna; Grigorieva, Julia; Roder, Heinrich] Biodesix, Steamboat Springs, CO USA.
[Gershwin, M. Eric] Univ Calif Davis, Div Clin Immunol Allergy & Rheumatol, Davis, CA 95616 USA.
C3 University of California System; University of California Davis;
Vanderbilt University; University of California System; University of
California Davis
RP Bowlus, CL (corresponding author), 4150 V St,PSSB 3500, Sacramento, CA 95817 USA.
EM clbowlus@ucdavis.edu
RI ; Bowlus, Christopher/N-9276-2016
OI Seeley, Erin/0000-0002-8000-5754; Bowlus,
Christopher/0000-0002-3906-6811; Grigorieva, Julia/0000-0001-8136-6167
FU NIH/NIGMS [5R01 GM58008]; Vanderbilt Ingram Cancer Center [P30
CA068485]; NIH [DK39588]; National Foundation for Cancer Research:
Vanderbilt Center for Proteomics and Drug Action
FX This work was supported by NIH/NIGMS 5R01 GM58008, Vanderbilt Ingram
Cancer Center Core Support Grant P30 CA068485, NIH DK39588 and National
Foundation for Cancer Research: Vanderbilt Center for Proteomics and
Drug Action.
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Z9 16
U1 0
U2 7
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PA 5 DONGDAN SANTIAO, DONGCHEN DISTRICT, BEING, 100005, PEOPLES R CHINA
SN 1672-7681
J9 CELL MOL IMMUNOL
JI Cell. Mol. Immunol.
PD MAY
PY 2011
VL 8
IS 3
BP 237
EP 242
DI 10.1038/cmi.2010.72
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WC Immunology
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SC Immunology
GA 758FL
UT WOS:000290147000007
PM 21258365
OA Green Accepted, Green Published
DA 2025-01-07
ER
PT J
AU Brandi, N
Spinelli, D
Granito, A
Tovoli, F
Piscaglia, F
Golfieri, R
Renzulli, M
AF Brandi, Nicolo
Spinelli, Daniele
Granito, Alessandro
Tovoli, Francesco
Piscaglia, Fabio
Golfieri, Rita
Renzulli, Matteo
TI COVID-19: Has the Liver Been Spared?
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE COVID-19; liver; hepatocellular carcinoma; chronic liver disease;
management
ID DISEASE 2019 COVID-19; HEPATOCELLULAR-CARCINOMA; FUNCTIONAL RECEPTOR;
ORGAN-TRANSPLANTATION; AUTOIMMUNE HEPATITIS; CORONAVIRUS; INJURY;
IMPACT; MANAGEMENT; CHEMOEMBOLIZATION
AB The liver is a secondary and often collateral target of COVID-19 disease but can lead to important consequences. COVID-19 might directly cause a high number of complications in patients with pre-existing chronic liver disease, increasing their risk of hepatic decompensation. Moreover, it also determines indirect consequences in the management of patients with liver disease, especially in those suffering from decompensated cirrhosis and HCC, as well as in the execution of their follow-up and the availability of all therapeutic possibilities. Liver imaging in COVID-19 patients proved to be highly nonspecific, but it can still be useful for identifying the complications that derive from the infection. Moreover, the recent implementation of telemedicine constitutes a possible solution to both the physical distancing and the re-organizational difficulties arising from the pandemic. The present review aims to encompass the currently hypothesized pathophysiological mechanisms of liver injury in patients with COVID-19 mediated by both the direct invasion of the virus and its indirect effects and analyze the consequence of the pandemic in patients with chronic liver disease and liver tumors, with particular regard to the management strategies that have been implemented to face this worldwide emergency and that can be further improved.
C1 [Brandi, Nicolo; Spinelli, Daniele; Golfieri, Rita; Renzulli, Matteo] IRCCS Azienda Osped Univ Bologna, Dept Radiol, Via Albertoni 15, I-40138 Bologna, Italy.
[Granito, Alessandro; Tovoli, Francesco; Piscaglia, Fabio] IRCCS Azienda Osped Univ Bologna, Div Internal Med Hepatobiliary & Immunoallerg Dis, I-40138 Bologna, Italy.
C3 IRCCS Azienda Ospedaliero-Universitaria di Bologna; IRCCS Azienda
Ospedaliero-Universitaria di Bologna
RP Brandi, N (corresponding author), IRCCS Azienda Osped Univ Bologna, Dept Radiol, Via Albertoni 15, I-40138 Bologna, Italy.
EM nicolo.brandi@studio.unibo.it
RI Renzulli, Matteo/AAE-1166-2021; Golfieri, Rita/AAB-6252-2022; Piscaglia,
Fabio/AAC-6899-2022; Granito, Alessandro/G-9563-2013; TOVOLI,
FRANCESCO/K-9027-2016
OI Piscaglia, Fabio/0000-0001-8264-1845; Rita,
Golfieri/0000-0001-8809-9989; Renzulli, Matteo/0000-0002-1311-5670;
Brandi, Nicolo/0000-0003-0574-3455; Granito,
Alessandro/0000-0002-0637-739X; TOVOLI, FRANCESCO/0000-0002-8350-1155
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NR 223
TC 8
Z9 9
U1 2
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JAN
PY 2023
VL 24
IS 2
AR 1091
DI 10.3390/ijms24021091
PG 25
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 7Z2WY
UT WOS:000915426200001
PM 36674607
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Qua, CS
Goh, KL
AF Qua, Choon-Seng
Goh, Khean-Lee
TI Liver cirrhosis in Malaysia: Peculiar epidemiology in a multiracial
Asian country
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE ethnic groups; etiology; hepatocellular carcinoma; liver cirrhosis
ID B-VIRUS-INFECTION; FATTY LIVER; NONALCOHOLIC STEATOHEPATITIS;
NATURAL-HISTORY; ALCOHOL-USE; HEPATITIS; DISEASE; CHINA; DEPENDENCE
AB Background and Aim: To determine the etiology of liver cirrhosis and risk factors for hepatocellular carcinoma (HCC) in a multiracial Asian population.
Methods: Consecutive patients with liver cirrhosis presenting to outpatient clinics and inpatient service at the University of Malaya Medical Centre from 1 April 2006 to 31 May 2009 were included.
Results: A total of 460 patients were included in the study: 317 male patients (68.9%) and 143 female patients (31.1%), with a mean age of 58.8 years (range: 15-87 years). The major causes of cirrhosis were: chronic hepatitis B, n = 212, 46.1%; chronic hepatitis C, n = 85, 18.5%; cryptogenic, n = 71, 15.4%; alcohol, n = 58, 12.6% and autoimmune, n = 9, 2.0%. Alcohol was the main etiology in Indians (51.1%) compared to Malay (0%) and Chinese (4.4%) (both P < 0.001). Hepatitis B was the predominant etiology in Malay (47.9%) and Chinese (58.8%) compared to Indians (5.6%) (both P < 0.001). Hepatitis C cirrhosis was highest in Malays (25.0%). 136 patients (29.6%) had concurrent HCC. Male sex (P < 0.001), age > 60 years (P = 0.014), hepatitis B (P < 0.001), hepatitis C (P = 0.006) and cryptogenic cause (P = 0.002) were found to be independent risk factors for HCC.
Conclusions: The etiology of cirrhosis has a peculiar pattern based on racial differences in alcohol intake and in the prevalence of hepatitis B.
C1 [Goh, Khean-Lee] Univ Malaya, Fac Med, Dept Med, Div Gastroenterol & Hepatol, Kuala Lumpur 50603, Malaysia.
C3 Universiti Malaya
RP Goh, KL (corresponding author), Univ Malaya, Fac Med, Dept Med, Div Gastroenterol & Hepatol, Kuala Lumpur 50603, Malaysia.
EM klgoh56@tm.net.my
RI Goh, Khean-Lee/B-6404-2009
OI Qua, Choon Seng/0000-0001-5800-474X
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NR 32
TC 40
Z9 43
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0815-9319
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD AUG
PY 2011
VL 26
IS 8
BP 1333
EP 1337
DI 10.1111/j.1440-1746.2011.06732.x
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 794NZ
UT WOS:000292908400017
PM 21443669
DA 2025-01-07
ER
PT J
AU Arinaga-Hino, T
Ide, T
Miyajima, I
Ogata, K
Kuwahara, R
Amano, K
Kawaguchi, T
Nakamura, T
Kawaguchi, T
Koga, H
Yonemoto, K
Torimura, T
AF Arinaga-Hino, Teruko
Ide, Tatsuya
Miyajima, Ichiro
Ogata, Kei
Kuwahara, Reiichiro
Amano, Keisuke
Kawaguchi, Toshihiro
Nakamura, Toru
Kawaguchi, Takumi
Koga, Hironori
Yonemoto, Koji
Torimura, Takuji
CA Kurume Autoimmune Hepatitis
TI Risk of malignancies in autoimmune hepatitis type 1 patients with a
long-term follow-up in Japan
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE autoimmune hepatitis; extrahepatic malignancy; hepatobiliary cancer;
Japanese; malignancy; risk factors
ID SQUAMOUS-CELL CARCINOMA; DE-NOVO MALIGNANCIES; LIVER-TRANSPLANTATION;
HEPATOCELLULAR-CARCINOMA; RHEUMATOID-ARTHRITIS; CANCER INCIDENCE;
INCIDENCE RATES; HUMAN-PAPILLOMAVIRUS; PREDICTIVE FACTORS; DRUG EXPOSURE
AB Aim: The risk of malignancies in autoimmune diseases is high and is regarded to be due to immunological abnormalities, the use of immunosuppressive agents, and/or chronic inflammation. The aim of this study was to investigate the incidence and risk of malignancies in patients with autoimmune hepatitis (AIH) type 1 in Japan.
Methods: Two hundred and fifty-six patients diagnosed with AIH were enrolled. A person-year calculation was carried out for AIH patients, and the numbers of expected events were clarified using data from "The Monitoring of Cancer Incidence in Japan Project" in order to examine the standard incident rate (SIR) of each type of malignancy. Biochemical data regarding carcinogenesis and its background factors were also examined.
Results: Twenty-seven patients (10.5%) developed malignancies; 11 (4.3%) with hepatobiliary cancer and 16 (6.3%) with extrahepatic malignancies. The overall SIR for malignancies in AIH was significantly high at 2.04 (95% confidence interval [CI], 1.34-2.96), and was high among female patients at 2.49 (95% CI, 1.60-3.71). The SIR for hepatobiliary cancer was 14.14 (95% CI, 7.05-25.30), and was markedly high for female patients at 21.83 (95% CI, 10.45-40.16). The SIR for oral/pharyngeal cancer was significantly high for female patients at 14.61 (95% CI, 1.64-52.77). The risk factors for hepatobiliary cancer at the diagnosis of AIH were low levels of alanine aminotransferase (P = 0.0226), low platelet counts (P < 0.0001), and cirrhosis (P = 0.0004). The risk factor for extrahepatic malignancy was relapse of AIH (P = 0.0485).
Conclusion: The risk of malignancies was generally high among AIH patients. Those with the risk factors of malignancies should be carefully followed up.
C1 [Arinaga-Hino, Teruko; Ide, Tatsuya; Miyajima, Ichiro; Ogata, Kei; Kuwahara, Reiichiro; Amano, Keisuke; Kawaguchi, Toshihiro; Nakamura, Toru; Kawaguchi, Takumi; Koga, Hironori; Torimura, Takuji] Kurume Univ, Div Gastroenterol, Dept Med, Sch Med, 67 Asahi Machi, Kurume, Fukuoka, Japan.
[Yonemoto, Koji] Kurume Univ, Dept Med, Biostat Ctr, Sch Med, Kurume, Fukuoka, Japan.
C3 Kurume University; Kurume University
RP Arinaga-Hino, T (corresponding author), Kurume Univ, Div Gastroenterol, Dept Med, Sch Med, 67 Asahi Machi, Kurume, Fukuoka, Japan.
EM terukoh@med.kurume-u.ac.jp
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NR 42
TC 11
Z9 11
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD FEB
PY 2018
VL 48
IS 3
BP E222
EP E231
DI 10.1111/hepr.12973
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FV8KY
UT WOS:000424837000024
PM 28841782
OA Bronze
DA 2025-01-07
ER
PT J
AU Hadzic, N
Baumann, U
McKiernan, P
McLin, V
Nobili, V
AF Hadzic, Nedim
Baumann, Ulrich
McKiernan, Pat
McLin, Valerie
Nobili, Valerio
TI Paediatric and adolescent liver disease 1 Long-term challenges and
perspectives of pre-adolescent liver disease
SO LANCET GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
ID FAMILIAL INTRAHEPATIC CHOLESTASIS; QUALITY-OF-LIFE; SWEAT CHLORIDE
CONCENTRATION; RANDOMIZED CONTROLLED-TRIAL; HEPATITIS-C VIRUS;
CYSTIC-FIBROSIS; BILIARY ATRESIA; ALPHA-1-ANTITRYPSIN DEFICIENCY;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS
AB Chronic liver disease is a growing problem that has substantial effects on public health. Many paediatric liver conditions are precursors of adult chronic liver disease, cirrhosis, and hepatocellular carcinoma. Clinical management of Wilson's disease, autoimmune liver disease, and chronic biliary disorders, such as biliary atresia, which remains the most common paediatric chronic liver disease and indication for liver transplantation, is similar in children and adults. In the past 10 or so years, paediatric hepatology has expanded into neighbouring clinical areas, such as metabolic liver diseases and systemic conditions with liver involvement. We aim to describe some of these disorders, and outline their natural history and possible differences between management in adults and children to stimulate further debate on the optimal transition of care between paediatric and adult specialists.
C1 [Hadzic, Nedim] Kings Coll Hosp London, Paediat Ctr Hepatol Gastroenterol & Nutr, London, England.
[Baumann, Ulrich] Hannover Med Sch, Paediat Gastroenterol & Hepatol, Hannover, Germany.
[McKiernan, Pat] Univ Pitttsburgh, Div Gastroenterol Hepatol & Nutr, Pittsburgh, PA USA.
[McLin, Valerie] Univ Hosp Geneva, Dept Pediat, Pediat Gastroenterol Unit, Geneva, Switzerland.
[Nobili, Valerio] Bambino Gesu Pediat Hosp, Hepatometab Unit, Rome, Italy.
C3 King's College Hospital NHS Foundation Trust; King's College Hospital;
Hannover Medical School; University of Geneva; IRCCS Bambino Gesu
RP Nobili, V (corresponding author), Bambino Gesu Pediat Hosp, Hepatometab Unit, Rome, Italy.
EM valerio.nobili@opbg.net
RI Hadzic, Nedim/H-7574-2019; Nobili, Valerio/K-8670-2018
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NR 89
TC 22
Z9 22
U1 0
U2 7
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 2468-1253
J9 LANCET GASTROENTEROL
JI Lancet Gastroenterol. Hepatol.
PD JUN
PY 2017
VL 2
IS 6
BP 435
EP 445
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FY6QV
UT WOS:000426981300022
PM 28497759
DA 2025-01-07
ER
PT J
AU Müller, P
Messmer, M
Bayer, M
Pfeilschifter, JM
Hintermann, E
Christen, U
AF Mueller, Peter
Messmer, Marie
Bayer, Monika
Pfeilschifter, Josef M.
Hintermann, Edith
Christen, Urs
TI Non-alcoholic fatty liver disease (NAFLD) potentiates autoimmune
hepatitis in the CYP2D6 mouse model
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Autoimmune hepatitis; NAFLD; CYP2D6; Mouse model; Hepatic fibrosis
ID AUTOANTIBODIES; INFLAMMATION; DIAGNOSIS; FIBROSIS; CRITERIA
AB Non-alcoholic fatty liver disease (NAFLD) and its more severe development non-alcoholic steatohepatitis (NASH) are increasing worldwide. In particular NASH, which is characterized by an active hepatic inflammation, has often severe consequences including progressive fibrosis, cirrhosis, and eventually hepatocellular carcinoma (HCC). Here we investigated how metabolic liver injury is influencing the pathogenesis of autoimmune hepatitis (AIH). We used the CYP2D6 mouse model in which wild type C57BL/6 mice are infected with an Adenovirus expressing the major liver autoantigen cytochrome P450 2D6 (CYP2D6). Such mice display several features of human AIH, including interface hepatitis, formation of LKM-1 antibodies and CYP2D6-specific T cells, as well as hepatic fibrosis. NAFLD was induced with a high-fat diet (HFD). We found that pre-existing NAFLD potentiates the severity of AIH. Mice fed for 12 weeks with a HFD displayed increased cellular infiltration of the liver, enhanced hepatic fibrosis and elevated numbers of liver autoantigen-specific T cells. Our data suggest that a pre-existing metabolic liver injury constitutes an additional risk for the severity of an autoimmune condition of the liver, such as AIH. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Mueller, Peter; Messmer, Marie; Bayer, Monika; Pfeilschifter, Josef M.; Hintermann, Edith; Christen, Urs] Goethe Univ Hosp Frankfurt, Pharmazentrum Frankfurt ZAFES, Frankfurt, Germany.
C3 Goethe University Frankfurt; Goethe University Frankfurt Hospital
RP Christen, U (corresponding author), Univ Hosp Frankfurt, Pharmazentrum Frankfurt Goethe, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
EM christen@med.uni-frankfurt.de
RI Christen, Urs/A-7338-2009
OI Christen, Urs/0000-0003-4165-7976
FU Else Kroner-Fresenius Foundation, Germany; Research Training Group
Translational Research Innovation - Pharma (TRIP); German Research
Foundation [CH 806/1-1, HI 1837/1-1]; Goethe University Hospital
Frankfurt
FX This study was supported by the Else Kroner-Fresenius Foundation,
Germany, Research Training Group Translational Research Innovation -
Pharma (TRIP), the German Research Foundation (CH 806/1-1; HI 1837/1-1),
and the Goethe University Hospital Frankfurt.
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ZANGER UM, 1988, P NATL ACAD SCI USA, V85, P8256, DOI 10.1073/pnas.85.21.8256
NR 36
TC 31
Z9 34
U1 0
U2 11
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD MAY
PY 2016
VL 69
BP 51
EP 58
DI 10.1016/j.jaut.2016.02.007
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA DK4WB
UT WOS:000374919900005
PM 26924542
DA 2025-01-07
ER
PT J
AU Henson, JB
King, LY
AF Henson, Jacqueline B.
King, Lindsay Y.
TI Post-Transplant Management and Complications of Autoimmune Hepatitis,
Primary Biliary Cholangitis, and Primary Sclerosing Cholangitis
including Disease Recurrence
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Liver transplantation; Primary sclerosing cholangitis; Primary biliary
cholangitis; Autoimmune hepatitis; Rejection; Recurrent disease;
Immunosuppression
ID INFLAMMATORY-BOWEL-DISEASE; DONOR LIVER-TRANSPLANTATION; ADULT LIVING
DONOR; TERM-FOLLOW-UP; RISK-FACTORS; ULCERATIVE-COLITIS; URSODEOXYCHOLIC
ACID; AMERICAN ASSOCIATION; ALLOGRAFT-REJECTION; COLORECTAL-CANCER
C1 [Henson, Jacqueline B.] Duke Univ, Sch Med, Dept Med, Div Gastroenterol, DUMC Box 3913, Durham, NC 27710 USA.
[King, Lindsay Y.] Duke Univ, Sch Med, Dept Med, Div Gastroenterol, DUMC Box 3923, Durham, NC 27710 USA.
C3 Duke University; Duke University
RP King, LY (corresponding author), Duke Univ, Sch Med, Dept Med, Div Gastroenterol, DUMC Box 3923, Durham, NC 27710 USA.
EM lindsay.king@duke.edu
RI Henson, Jacqueline/GSD-6547-2022
FU NIH [T32DK007568]
FX J.B. Henson is supported by NIH grant T32DK007568.
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NR 116
TC 3
Z9 3
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD FEB
PY 2024
VL 28
IS 1
BP 193
EP 207
DI 10.1016/j.cld.2023.07.009
EA NOV 2023
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA Z2HR3
UT WOS:001110344900001
PM 37945160
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Sahebjam, F
Vierling, JM
AF Sahebjam, Farhad
Vierling, John M.
TI Autoimmune hepatitis
SO FRONTIERS OF MEDICINE
LA English
DT Review
DE autoimmune hepatitis; autoantibodies; diagnosis; immunological diseases;
drug-induced liver injury; therapy; immunosuppression; outcomes;
hepatocellular carcinoma; liver transplantation
ID PRIMARY BILIARY-CIRRHOSIS; REGULATORY T-CELLS; PRIMARY SCLEROSING
CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE; LIVER-TRANSPLANTATION;
MYCOPHENOLATE-MOFETIL; OVERLAP SYNDROME; HEPATOCELLULAR-CARCINOMA;
CLINICAL-FEATURES; FOLLOW-UP
AB Autoimmune hepatitis is a chronic liver disease putatively caused by loss of tolerance to hepatocyte-specific autoantigens. It is characterized by female predilection, elevated aminotransferase levels, autoantibodies, increased gamma-globulin or IgG levels and biopsy evidence of interface hepatitis. It is currently divided into types 1 and 2, based on expression of autoantibodies. Autoantigenic epitopes have been identified only for the less frequent type 2. Although autoimmune hepatitis occurs in childhood, this review focuses on disease in adults. In the absence of pathognomonic biomarkers, diagnosis requires consideration of clinical, biochemical, serological and histological features, which have been codified into validated diagnostic scoring systems. Since many features also occur in other chronic liver diseases, these scoring systems aid evaluation of the differential diagnosis. New practice guidelines have redefined criteria for remission to include complete biochemical and histological normalization on immunosuppressive therapy. Immunosuppression is most often successful using prednisone or prednisolone and azathioprine; however, the combination of budesonide and azathioprine for non-cirrhotic patients offers distinct advantages. Patients failing standard immunosuppression are candidates for alternative immunosuppressive regimens, yet none of the options has been studied in a randomized, controlled trial. Overlap syndromes with either primary sclerosing cholangitis or primary biliary cirrhosis occur in a minority. Liver transplantation represents a life-saving option for patients presenting with acute liver failure, severely decompensated cirrhosis or hepatocellular carcinoma. Transplant recipients are at risk for recurrent autoimmune hepatitis in the allograft, and de novo disease may occur in patients transplanted for other indications. Patients transplanted for AIH are also at risk for recurrent or de novo inflammatory bowel disease. Progress in our understanding of the immunopathogenesis should lead to identification of specific diagnostic and prognostic biomarkers and new therapeutic strategies.
C1 [Vierling, John M.] Baylor Coll Med, Baylor St Lukes Med Ctr, Dept Med, Houston, TX 77030 USA.
Baylor Coll Med, Baylor St Lukes Med Ctr, Dept Surg, Houston, TX 77030 USA.
C3 Baylor College of Medicine; Baylor College of Medicine
RP Vierling, JM (corresponding author), Baylor Coll Med, Baylor St Lukes Med Ctr, Dept Med, Houston, TX 77030 USA.
EM vierling@bcm.edu
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NR 234
TC 58
Z9 66
U1 0
U2 15
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2095-0217
EI 2095-0225
J9 FRONT MED-PRC
JI Front. Med.
PD JUN
PY 2015
VL 9
IS 2
BP 187
EP 219
DI 10.1007/s11684-015-0386-y
PG 33
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA DB3WQ
UT WOS:000368444400007
PM 25749982
DA 2025-01-07
ER
PT J
AU Zhang, YJ
Kong, DR
Wang, H
AF Zhang, Yujue
Kong, Derun
Wang, Hua
TI Mucosal-Associated Invariant T cell in liver diseases
SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Review
DE alcoholic liver disease; autoimmune liver disease; liver cancer; MAIT
cells; non-alcoholic liver disease
ID CHRONIC HEPATITIS-B; MAIT CELLS; ANTIGEN PRESENTATION; TISSUE-REPAIR;
ACTIVATION; MR1; TCR; BLOOD; HETEROGENEITY; EXPRESSION
AB Mucosal-associated invariant T cells (MAIT cells) are a new population of innate immune cells, which are abundant in the liver and play complex roles in various liver diseases. In this review, we summarize MAIT cells in the liver diseases in recent studies, figure out the role of MAIT cells in various liver disease, including Alcoholic liver disease, Non-alcoholic liver disease, Autoimmune liver diseases, Viral hepatitis and Liver Cancer. Briefly, MAIT cells are involved in anti-bacteria responses in the alcoholic liver diseases. Besides, the activated MAIT cells promote the liver inflammation by secreting inflammatory cytokines and produce regulatory cytokines, which induces anti-inflammatory macrophage polarization. MAIT cells participate in the liver fibrosis via enhancing hepatic stellate cell activation. In viral hepatitis, MAIT cells exhibit a flawed and exhausted phenotype, which results in little effect on controlling the virus and bacteria. In liver cancer, MAIT cells indicate the disease progression and the outcome of therapy. In summary, MAIT cells are attractive biomarkers and therapeutic targets for liver disease.
C1 [Zhang, Yujue; Kong, Derun] Anhui Med Univ, Affiliated Hosp 1, Dept Gastroenterol, Hefei 230032, Anhui, Peoples R China.
[Kong, Derun] Anhui Med Univ, Dept Gastroenterol, Fuyang Hosp, Fuyang 236000, Anhui, Peoples R China.
[Wang, Hua] Anhui Med Univ, Affiliated Hosp 1, Dept Oncol, Hefei 230032, Anhui, Peoples R China.
C3 Anhui Medical University; Anhui Medical University; Anhui Medical
University
RP Kong, DR (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Gastroenterol, Hefei 230032, Anhui, Peoples R China.; Kong, DR (corresponding author), Anhui Med Univ, Dept Gastroenterol, Fuyang Hosp, Fuyang 236000, Anhui, Peoples R China.; Wang, H (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Oncol, Hefei 230032, Anhui, Peoples R China.; Wang, H (corresponding author), Anhui Med Univ, Inst Liver Dis, 218 Jixi Rd, Hefei 230032, Anhui, Peoples R China.
EM kongderun168@163.com; wanghua@ahmu.edu.cn
FU Research fund project of the Anhui provincial institute of translational
medicine [2017zhyx18]; Anhui Science and Technology Department: 2018 Key
research and development plan projects [1804h08020260]
FX The present study was supported by the Research fund project of the
Anhui provincial institute of translational medicine, No. 2017zhyx18 and
the Anhui Science and Technology Department: 2018 Key research and
development plan projects, No. 1804h08020260.
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NR 92
TC 17
Z9 17
U1 0
U2 25
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-2288
J9 INT J BIOL SCI
JI Int. J. Biol. Sci.
PY 2020
VL 16
IS 3
BP 460
EP 470
DI 10.7150/ijbs.39016
PG 11
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA KA6PP
UT WOS:000505919000009
PM 32015682
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Honda, M
Kawai, H
Shirota, Y
Yamashita, T
Kaneko, S
AF Honda, M
Kawai, H
Shirota, Y
Yamashita, T
Kaneko, S
TI Differential gene expression profiles in stage I primary biliary
cirrhosis
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID CHRONIC HEPATITIS; HEPATOCELLULAR-CARCINOMA; BREAST-CANCER;
IDENTIFICATION; HYBRIDIZATION; PROTEIN
AB OBJECTIVES: Primary biliary cirrhosis (PBC) is a progressive disease. However, little is understood about the molecular mechanisms underlying its features.
METHODS: We analyzed gene expression profiles of liver biopsy samples from 16 patients with PBC, seven with autoimmune hepatitis, eight with chronic hepatitis C, and eight normal control livers. In addition to whole liver samples, we selectively analyzed chronic nonsuppurative destructive cholangitis (CNSDC) lesions by laser capture microdissection.
RESULTS: Hierarchical clustering analysis using only early-stage liver disease demonstrated 85 genes were upregulated in stage I PBC specifically. Surprisingly, the expression of these genes was not maintained in advanced-stage PBC, while other gene clusters were upregulated. Expression analysis of CNSDC lesions in stage I PBC showed the presence of active inflammatory changes, characterized by the significant elevation of interferon-gamma and the development and maturation of lymphocytes. Expression of these genes was diminished in lymphoid cells aggregation in stage III PBC, and genes reflecting hepatocyte damage were upregulated with disease progression.
CONCLUSION: Gene expression patterns in stage I PBC are different from others. There are distinct changes in molecular pathology from early- to late-stage PBC, which might be a clue to reveal the etiology and progression of PBC.
C1 Kanazawa Univ, Grad Sch Med, Dept Gastroenterol, Kanazawa, Ishikawa 9208641, Japan.
C3 Kanazawa University
RP Kanazawa Univ, Grad Sch Med, Dept Gastroenterol, Takara Machi 13-1, Kanazawa, Ishikawa 9208641, Japan.
OI Shirota, Yukihiro/0000-0001-6561-4626
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NR 23
TC 21
Z9 23
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD SEP
PY 2005
VL 100
IS 9
BP 2019
EP 2030
DI 10.1111/j.1572-0241.2005.41662.x
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 964BL
UT WOS:000231853600020
PM 16128947
DA 2025-01-07
ER
PT J
AU Yoshioka, Y
Hashimoto, E
Yatsuji, S
Kaneda, H
Taniai, M
Tokushige, K
Shiratori, K
AF Yoshioka, Y
Hashimoto, E
Yatsuji, S
Kaneda, H
Taniai, M
Tokushige, K
Shiratori, K
TI Nonalcoholic steatohepatitis: cirrhosis, hepatocellular carcinoma, and
burnt-out NASH
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE NASH; hepatocellular carcinoma; cryptogenic cirrhosis; burnt-out NASH;
cirrhosis
ID FATTY LIVER-DISEASE; CRYPTOGENIC CIRRHOSIS; NATURAL-HISTORY; FOLLOW-UP;
HEPATITIS; SPECTRUM; OBESITY; NAFLD
AB Nonalcoholic steatohepatitis (NASH) is a liver disease characterized by the histological features of steatohepatitis in the absence of significant alcohol consumption. The natural history of NASH is poorly defined. Here we report our experience with a patient to illustrate the clinical course of cirrhotic NASH. A 67-year-old woman was admitted with hematemesis due to the rupture of esophageal varices. Her varices were treated by endoscopic ligation and endoscopic sclerotherapy. Her medical history was unremarkable. Both the patient and her family members were asked about alcohol intake several times during her illness, but all of them denied a history of alcohol intake. She had insulin resistance, as determined by homeostasis model assessment. Serological tests for viral hepatitis were all negative. Viral hepatitis, autoimmune liver disease, iron overload, and metabolic liver disorders were all excluded. Imaging tests failed to reveal any steatosis, because of the presence of severe fibrosis. Liver biopsy showed moderate steatosis, moderate inflammation, ballooning degeneration, and Mallory bodies. We diagnosed NASH associated with cirrhosis based on the clinicopathological features. Almost 2 years later, she developed hepatocellular carcinoma (HCC) and she died of multiple HCCs. At autopsy, tumor invasion was seen throughout liver segment 8. The noncancerous liver showed burnt-out NASH; the steatosis, necroinflammation, ballooning degeneration, and Mallory bodies had all disappeared. In Japan, the prevalence of nonalcoholic fatty liver disease will increase as obesity has been increasing, so it is important to understand how to diagnose NASH. When a patient has NASH, careful follow-up should be performed.
C1 Tokyo Womens Med Univ, Dept Internal Med & Gastroenterol, Shinjuku Ku, Tokyo 1628666, Japan.
C3 Tokyo Women's Medical University
RP Tokyo Womens Med Univ, Dept Internal Med & Gastroenterol, Shinjuku Ku, 8-1 Kawado Cho, Tokyo 1628666, Japan.
RI taniai, makiko/HZH-7431-2023
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NR 26
TC 89
Z9 95
U1 0
U2 5
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD DEC
PY 2004
VL 39
IS 12
BP 1215
EP 1218
DI 10.1007/s00535-004-1475-x
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 882TS
UT WOS:000225961900015
PM 15622489
DA 2025-01-07
ER
PT J
AU Kumagi, T
Onji, M
AF Kumagi, Teru
Onji, Morikazu
TI Presentation and Diagnosis of Primary Billary Cirrhosis in the 21st
Century
SO CLINICS IN LIVER DISEASE
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; AUTOIMMUNE LIVER-DISEASES; CLINICAL-FEATURES;
HEPATOCELLULAR-CARCINOMA; NATURAL-HISTORY; ANTIMITOCHONDRIAL ANTIBODIES;
PROGNOSTIC IMPORTANCE; SYMPTOM PROGRESSION; FRACTURE RISK; HEPATITIS
AB Primary biliary cirrhosis is a slowly progressive, cholestatic, and chronic liver disease in Which the epithelium of the intrahepatic biliary tree is destroyed by a chronic inflammatory process. The origin of this disease, which mainly affects middle-aged women, is Unknown but has characteristics favoring an autoimmune etiology. This article reviews the presentation and diagnosis of PBC in the 21st century.
C1 [Kumagi, Teru] Univ Toronto, Toronto Western Hosp, Univ Hlth Network, Toronto, ON M5T 2S8, Canada.
[Onji, Morikazu] Ehime Univ, Grad Sch Med, To On, Ehime 7910295, Japan.
C3 University of Toronto; University Health Network Toronto; Ehime
University
RP Kumagi, T (corresponding author), Univ Toronto, Toronto Western Hosp, Univ Hlth Network, 6B Fell 168,399 Bathurst St, Toronto, ON M5T 2S8, Canada.
EM tkumagi@uhnres.utoronto.ca
RI Kumagi, Teru/AAS-7427-2021
OI Kumagi, Teru/0000-0002-2292-7750
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NR 76
TC 14
Z9 18
U1 1
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD MAY
PY 2008
VL 12
IS 2
BP 243
EP +
DI 10.1016/j.cld.2008.02.014
PG 18
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 437LB
UT WOS:000265487900002
PM 18456178
DA 2025-01-07
ER
PT J
AU Carrion, AF
Ghanta, R
Carrasquillo, O
Martin, P
AF Carrion, Andres F.
Ghanta, Ravi
Carrasquillo, Olveen
Martin, Paul
TI Chronic Liver Disease in the Hispanic Population of the United States
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE Ethnicity; Fibrosis; Race; Latino; Risk; Epidemiology
ID NONALCOHOLIC FATTY LIVER; HEPATITIS-C-VIRUS; PRIMARY BILIARY-CIRRHOSIS;
INJECTION-DRUG USERS; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
ETHNIC-DIFFERENCES; RACIAL-DIFFERENCES; PHYSICAL-ACTIVITY;
GENETIC-VARIATION
AB Chronic liver disease is a major cause of morbidity and mortality among Hispanic people living in the United States. Environmental, genetic, and behavioral factors, as well as socioeconomic and health care disparities among this ethnic group have emerged as important public health concerns. We review the epidemiology, natural history, and response to therapy of chronic liver disease in Hispanic patients. The review covers nonalcoholic fatty liver disease, viral hepatitis B and C, coinfection of viral hepatitis with human immunodeficiency virus, alcoholic cirrhosis, hepatocellular carcinoma, autoimmune hepatitis, and primary biliary cirrhosis. For most of these disorders, the Hispanic population has a higher incidence and more aggressive pattern of disease and overall worse treatment outcomes than in the non-Hispanic white population. Clinicians should be aware of these differences in caring for Hispanic patients with chronic liver disease.
C1 [Carrion, Andres F.; Carrasquillo, Olveen] Univ Miami, Miller Sch Med, Div Gen Internal Med, Miami, FL 33136 USA.
[Ghanta, Ravi] Univ Miami, Miller Sch Med, Div Gastroenterol, Miami, FL 33136 USA.
[Martin, Paul] Univ Miami, Miller Sch Med, Div Hepatol, Miami, FL 33136 USA.
C3 University of Miami; University of Miami; University of Miami
RP Carrion, AF (corresponding author), 1611 NW 12th Ave,Cent 600, Miami, FL 33136 USA.
EM acarrionmonsalve@med.miami.edu
FU NCI NIH HHS [U54 CA153705] Funding Source: Medline
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NR 90
TC 70
Z9 75
U1 0
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD OCT
PY 2011
VL 9
IS 10
BP 834
EP 841
DI 10.1016/j.cgh.2011.04.027
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Gastroenterology & Hepatology
GA 831MS
UT WOS:000295735900014
PM 21628000
OA Green Accepted, Bronze
DA 2025-01-07
ER
PT J
AU Miteva, D
Peshevska-Sekulovska, M
Snegarova, V
Peruhova, M
Vasilev, GH
Vasilev, GV
Sekulovski, M
Lazova, S
Gulinac, M
Tomov, L
Mihova, A
Velikova, T
AF Miteva, Dimitrina
Peshevska-Sekulovska, Monika
Snegarova, Violeta
Peruhova, Milena
Vasilev, Georgi H.
Vasilev, Georgi V.
Sekulovski, Metodija
Lazova, Snezhina
Gulinac, Milena
Tomov, Latchezar
Mihova, Antoaneta
Velikova, Tsvetelina
TI Microbiome and Genetic Factors in the Pathogenesis of Liver Diseases
SO GASTROENTEROLOGY INSIGHTS
LA English
DT Review
DE genomics; liver disease; microbiome; gut microbiota; NAFLD; liver
cirrhosis; autoimmune liver disease
ID GENOME-WIDE ASSOCIATION; PRIMARY SCLEROSING CHOLANGITIS;
MUCOSA-ASSOCIATED MICROBIOTA; HEPATOCELLULAR-CARCINOMA; GUT MICROBIOTA;
ALCOHOL-DEPENDENCE; PNPLA3 RS738409; CONFERS SUSCEPTIBILITY; INTESTINAL
MICROBIOTA; DOUBLE-BLIND
AB Our genetic background has not changed over the past century, but chronic diseases are on the rise globally. In addition to the genetic component, among the critical factors for many diseases are inhabitants of our intestines (gut microbiota) as a crucial environmental factor. Dysbiosis has been described in liver diseases with different etiologies like non-alcoholic fatty liver disease (NAFLD), alcohol-related liver disease (ALD), viral hepatitis, autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), primary biliary cholangitis (PBC), cirrhosis, hepatocellular carcinoma (HCC). On the other hand, new technologies have increased our understanding of liver disease genetics and treatment options. Genome-wide association studies (GWAS) identify unknown genetic risk factors, positional cloning of unknown genes associated with different diseases, gene tests for single nucleotide variations (SNVs), and next-generation sequencing (NGS) of selected genes or the complete genome. NGS also allowed studying the microbiome and its role in various liver diseases has begun. These genes have proven their effect on microbiome composition in host genome-microbiome association studies. We focus on altering the intestinal microbiota, and supplementing some bacterial metabolites could be considered a potential therapeutic strategy. The literature data promote probiotics/synbiotics role in reducing proinflammatory cytokines such as TNF-alpha and the interleukins (IL-1, IL-6, IL-8), therefore improving transaminase levels, hepatic steatosis, and NAFLD activity score. However, even though microbial therapy appears to be risk-free, evaluating side effects related to probiotics or synbiotics is imperative. In addition, safety profiles for long-term usage should be researched. Thus, this review focuses on the human microbiome and liver diseases, recent GWASs on liver disease, the gut-liver axis, and the associations with the microbiome and microbiome during/after liver disease therapy.
C1 [Miteva, Dimitrina] Sofia Univ St Kliment Ohridski, Fac Biol, Dept Genet, 8 Dragan Tzankov Str, Sofia 1164, Bulgaria.
[Miteva, Dimitrina; Peshevska-Sekulovska, Monika; Vasilev, Georgi H.; Vasilev, Georgi V.; Sekulovski, Metodija; Lazova, Snezhina; Gulinac, Milena; Tomov, Latchezar; Velikova, Tsvetelina] Sofia Univ St Kliment Ohridski, Med Fac, 1 Kozyak Str, Sofia 1407, Bulgaria.
[Peshevska-Sekulovska, Monika] Univ Hosp Lozenetz, Dept Gastroenterol, 1 Kozyak Str, Sofia 1407, Bulgaria.
[Snegarova, Violeta] Med Univ, Naval Hosp Varna, Mil Med Acad, Med Fac,Clin Internal Dis, Blvd Hristo Smirnenski 3, Varna 9000, Bulgaria.
[Peruhova, Milena] Heart & Brain Hosp, Dept Gastroenterol, Zdrave 1 St, Burgas 8000, Bulgaria.
[Vasilev, Georgi H.] Natl Specialized Hosp Act Treatment Hematol Dis, Lab Cytogenet & Mol Biol, Plovdivsko Pole Str 6, Sofia 1756, Bulgaria.
[Vasilev, Georgi V.] Univ Hosp Sv Georgi, Dept Emergency Med & Clin Neurol, Blvd Peshtersko Shose 66, Plovdiv 4000, Bulgaria.
[Sekulovski, Metodija] Univ Hosp Lozenetz, Dept Anesthesiol & Intens Care, 1 Kozyak Str, Sofia 1407, Bulgaria.
[Lazova, Snezhina] Univ Hosp NI Pirogov, Pediat Dept, 21 Gen Eduard I Totleben Blvd, Sofia 1606, Bulgaria.
[Lazova, Snezhina] Med Univ Sofia, Fac Publ Hlth Tsekomir Vodenicharov, Dept Healthcare, Bialo More 8 Str, Sofia 1527, Bulgaria.
[Gulinac, Milena] Med Univ Plovdiv, Dept Gen & Clin Pathol, Bul Vasil Aprilov 15A, Plovdiv 4000, Bulgaria.
[Tomov, Latchezar] New Bulgarian Univ, Dept Informat, Montevideo 21 Str, Sofia 1618, Bulgaria.
[Mihova, Antoaneta] Dept Immunol, SMDL Ramus, Blvd Kap Spisarevski 26, Sofia 1527, Bulgaria.
C3 University of Sofia; University of Sofia; University of Sofia; Medical
University Varna; Military Medical Academy Sofia; Medical University
Plovdiv; University of Sofia; Medical University Sofia; Medical
University Sofia; Medical University Plovdiv; New Bulgarian University
RP Velikova, T (corresponding author), Sofia Univ St Kliment Ohridski, Med Fac, 1 Kozyak Str, Sofia 1407, Bulgaria.
EM d.georgieva@biofac.uni-sofia.bg; mpesevska93@gmail.com;
violetasnegarova@gmail.com; mperuhova@gmail.com;
drgeorgivasilev@gmail.com; vvasilev.georgi@gmail.com;
metodija.sekulovski@gmail.com; snejina@lazova.com; mgulinac@hotmail.com;
lptomov@nbu.bg; toni02m@yahoo.com; tsvelikova@medfac.mu-sofia.bg
RI Tomov, Latchezar/AAR-2987-2020; GULINAC, MILENA/ABZ-5349-2022; Lazova,
Snezhina/S-5834-2017; Peshevska-Sekulovska, Monika/GMW-7559-2022;
Velikova, Tsvetelina/H-6932-2019; Miteva, Dimitrina/AAL-2547-2021
OI Lazova, Snezhina/0000-0002-5884-7760; Sekulovski,
Metodija/0000-0001-8374-7756; Peshevska-Sekulovska,
Monika/0000-0002-8468-0132; Velikova, Tsvetelina/0000-0002-0593-1272;
Tomov, Latchezar/0000-0003-1902-6473; Miteva,
Dimitrina/0000-0002-5931-2426; Vasilev, Georgi/0000-0002-3280-5060
FU European Union-NextGenerationEU [numero; BG-RRP-2.004-0008-C01];
European Union-NextGenerationEU through the National Recovery and
Resilience Plan of the Republic of Bulgaria
FX This study is financed by the European Union-NextGenerationEU through
the National Recovery and Resilience Plan of the Republic of Bulgaria,
project & numero; BG-RRP-2.004-0008-C01.
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NR 161
TC 1
Z9 1
U1 9
U2 18
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2036-7414
EI 2036-7422
J9 GASTROENTEROL INSIGH
JI Gastroenterol. Insights
PD DEC
PY 2023
VL 14
IS 4
BP 575
EP 597
DI 10.3390/gastroent14040041
PG 23
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA DH5T2
UT WOS:001131158400001
OA gold
DA 2025-01-07
ER
PT J
AU Philips, CA
Madhu, D
Augustine, P
AF Philips, Cyriac Abby
Madhu, Deepak
Augustine, Philip
TI Investigating the correlation between COVID-19 and the progression of
chronic liver disease
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE Cirrhosis; portal hypertension; DILI; coronavirus; covid vaccine;
hepatocellular carcinoma; HBV; HCV
ID SARS-COV-2 INFECTION; AUTOIMMUNE HEPATITIS; CLINICAL-FEATURES;
CHOLANGIOPATHY; PROGNOSIS; OUTCOMES; INJURY; AIH
AB IntroductionThe novel coronavirus disease 2019 has thrown light on various heterogeneous afflictions of newly emerging viruses on the human body. Early reports demonstrated direct effect of novel coronavirus on the liver, but subsequently, this did not stand up to validation. The SARS-CoV-2 virus affects the liver differentially; in healthy compared to those with preexisting liver disease.Areas coveredThis exhaustive paper reviews the current, literature on mechanisms by which COVID-19 affects the healthy liver and those with preexisting liver disease such as alcohol-related and nonalcoholic fatty liver, autoimmune liver disease, chronic liver disease and cirrhosis, hepatocellular carcinoma, viral hepatitis, and liver transplant recipients, with special mention on drug-and herb-induced liver injury with COVID-19 therapies. Search methodology: the review (Dec. 2022 - Jan. 2023) is based on PubMed (NLM) search using the keyword 'COVID' with supplementary searches using 'fibrosis;' 'liver;' 'cirrhosis;' 'CLD;' 'NAFLD;' 'NASH;' 'hepatocellular carcinoma;' 'hepatitis;' 'fatty liver;' 'alcohol;' 'viral;' 'transplant;' and 'liver failure.'Expert opinionDirect liver tropism of SARS-CoV-2 does not cause liver damage. Adverse events following infection depend on the severity of liver disease, the severity of COVID-19, and other risk factors such as metabolic syndrome and older age. Alcohol-related liver disease independently predicts adverse outcomes.
C1 [Philips, Cyriac Abby] Rajagiri Hosp, Liver Inst, Ctr Excellence GI Sci, Clin & Translat Hepatol & Monarch Liver Lab, Aluva, Kerala, India.
[Madhu, Deepak] Lisie Hosp, Dept Gastroenterol, Ernakulam, Kerala, India.
[Augustine, Philip] Rajagiri Hosp, Ctr Excellence GI Sci, Dept Gastroenterol & Adv GI Endoscopy, Aluva, Kerala, India.
[Philips, Cyriac Abby] Rajagiri Hosp, Liver Inst, Ctr Excellence GI Sci, Ground Floor,Phase II, Ernakulam 683112, Kerala, India.
RP Philips, CA (corresponding author), Rajagiri Hosp, Liver Inst, Ctr Excellence GI Sci, Ground Floor,Phase II, Ernakulam 683112, Kerala, India.
EM abbyphilips@theliverinst.in
RI Madhu, Deepak/ABE-3321-2020
OI Philips, Cyriac Abby/0000-0002-9587-336X; Madhu,
Deepak/0000-0002-8613-8670
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NR 83
TC 1
Z9 1
U1 1
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD JUN 3
PY 2023
VL 17
IS 6
BP 603
EP 613
DI 10.1080/17474124.2023.2206564
EA APR 2023
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA K7WR5
UT WOS:000974627100001
PM 37086388
DA 2025-01-07
ER
PT J
AU Chi, G
Pei, JH
Li, XQ
AF Chi, Gang
Pei, Jin-Hong
Li, Xue-Qing
TI EZH2-mediated H3K27me3 promotes autoimmune hepatitis progression by
regulating macrophage polarization
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE EZH2; Macrophage polarization; Autoimmune hepatitis
ID EZH2; CELLS
AB Autoimmune hepatitis (AIH) is a chronic progressive liver disease related to abnormal immune stimulation, leading to liver cirrhosis, liver cancer and liver failure. There is an urgent need to find novel biomarkers and potential drug targets for effective treatment of the disease. Although previous studies have shown that EZH2, as a histone methyltransferase, plays critical roles in tumor and autoimmune diseases, its role in autoimmune hepatitis remains largely unknown. In this study, we reported that the EZH2 and H3K27me3 expression level was significantly upregulated in liver tissues during the progression of AIH. High expression of EZH2 enhanced autoimmune hepatitis, immune response and liver fibrosis through H3K27me3. EZH2 inhibition induced the phenotype of hepatic macrophages to switch from M1 to M2 in the development of AIH. These findings indicated that EZH2-mediated H3K27me3 promoted autoimmune hepatitis by regulating the polarization of hepatic macrophages. EZH2 may be a promising therapeutic target for the prevention or treatment of autoimmune hepatitis.
C1 [Chi, Gang; Pei, Jin-Hong; Li, Xue-Qing] Changzhi Med Coll, Dept Biochem, Changazhi 046000, Shanxi, Peoples R China.
C3 Changzhi Medical College
RP Chi, G (corresponding author), Changzhi Med Coll, Dept Biochem, Changazhi 046000, Shanxi, Peoples R China.
EM cg@czmc.edu.cn
FU Applied Basic Research General Programs of Science and Technology
Foundation of Shanxi Province [201901D111324]; Scientific and
Technologial Innovation Programs of Higher Education Institutions in
Shanxi (STIP) [2021L341]; Scientific Research Starting Foundation for
Doctor of Changzhi Medical College [BS201902]
FX This work was supported by Applied Basic Research General Programs of
Science and Technology Foundation of Shanxi Province [grant numbers
201901D111324], Scientific and Technologial Innovation Programs of
Higher Education Institutions in Shanxi (STIP) [grant numbers 2021L341]
and Scientific Research Starting Foundation for Doctor of Changzhi
Medical College [grant numbers BS201902].
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NR 28
TC 12
Z9 14
U1 3
U2 16
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD MAY
PY 2022
VL 106
AR 108612
DI 10.1016/j.intimp.2022.108612
EA FEB 2022
PG 7
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA 1C6FO
UT WOS:000793212700003
PM 35193055
DA 2025-01-07
ER
PT J
AU Zheng, YC
Xie, FC
Kang, K
Shi, Y
Mao, YL
Sang, XT
Du, SD
AF Zheng, Yong-Chang
Xie, Fu-Cun
Kang, Kai
Shi, Yue
Mao, Yi-Lei
Sang, Xin-Ting
Du, Shun-Da
TI Hepatobiliary case report and literature review of hepatic reactive
lymphoid hyperplasia with positive anti-smooth muscle antibody and
anti-nuclear antibody tests
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Review
DE Reactive lymphoid hyperplasia (RLH); liver; autoimmune hepatitis;
anti-nuclear antibody (ANA); anti-smooth muscle antibody (anti-SMA)
ID NODE RATIO; LIVER; PSEUDOLYMPHOMA; ASSOCIATION; BURDEN
AB Hepatic reactive lymphoid hyperplasia (RLH) is a rare benign tumor of the liver that exhibits similar imaging characteristics to those of other hepatic malignant tumors; therefore, it requires novel biomarkers to be differentiated from the other tumors. A 69-year-old female was found to have a mass in the liver and was admitted to Peking Union Medical College Hospital for further evaluation. Most laboratory tests, including liver function tests, tumor biomarkers, and autoimmune markers were within normal range, except for positive antinuclear antibody and anti-smooth muscle antibody (SMA) tests. Diagnostic imaging, including ultrasonography, computerized tomography and magnetic resonance imaging displayed a small hepatic mass suggestive of hepatocellular carcinoma (HCC). Partial hepatectomy was performed, and histological diagnosis suggested RLH. Postoperative treatments included anti-infection, nutritional enhancement and liver protection. The suspicion of autoimmune hepatitis could not be confirmed. No recurrence or autoimmune disease was observed over 6-month follow-up. Positive anti-nuclear antibody (ANA) and anti-SMA may be potential biomarkers for hepatic RLH.
C1 [Du, Shun-Da] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Liver Surg, 1 Shuaifuyuan Wangfujing, Beijing 100730, Peoples R China.
[Du, Shun-Da] Peking Union Med Coll, 1 Shuaifuyuan Wangfujing, Beijing 100730, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Peking Union Medical College Hospital; Chinese Academy of Medical
Sciences - Peking Union Medical College; Peking Union Medical College
RP Du, SD (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Liver Surg, 1 Shuaifuyuan Wangfujing, Beijing 100730, Peoples R China.; Du, SD (corresponding author), Peking Union Med Coll, 1 Shuaifuyuan Wangfujing, Beijing 100730, Peoples R China.
EM shun-da_du@outlook.com
RI Zheng, Yongchang/KDO-5062-2024
FU Beijing Natural Science Foundation [L172055]; Beijing Municipal Science
& Technology Commission research fund [Z171100000417004]
FX This work was supported by the Beijing Natural Science Foundation
(L172055) and the Beijing Municipal Science & Technology Commission
research fund (Z171100000417004). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 20
TC 3
Z9 3
U1 1
U2 17
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD JUN
PY 2019
VL 8
IS 3
BP 1001
EP 1005
DI 10.21037/tcr.2019.05.32
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IF7VA
UT WOS:000473292100036
PM 35116841
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Arslan, Ç
Kiliçkap, S
Yalçin, S
AF Arslan, Cagatay
Kilickap, Saadettin
Yalcin, Suayib
TI Gastric cancer after cadaveric liver transplantation in a patient with
autoimmune hepatitis: A case report and review of the literature
SO TURKISH JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Gastric cancer; autoimmune hepatitis; liver transplantation;
immunosuppressive therapy
ID DE-NOVO NEOPLASIA; RISK-FACTORS; MALIGNANCIES; EXPERIENCE; KIDNEY
AB The risk of malignancy in transplant patients is higher than in the general population. The risk is increased mostly due to immune alteration and viral infections. While the most common cancers following liver transplantation include skin cancers, lymphoma and Kaposi's sarcoma, gastric cancer is uncommon. Herein, we report a case of gastric adenocarcinoma developing three years after cadaveric liver transplantation in a patient with autoimmune hepatitis. The patient was successfully operated. The patient did not receive any adjuvant therapy, and is free of disease at 9 months' follow-up.
C1 [Arslan, Cagatay; Kilickap, Saadettin; Yalcin, Suayib] Hacettepe Univ, Inst Oncol, Dept Med Oncol, TR-06100 Ankara, Turkey.
C3 Hacettepe University
RP Arslan, Ç (corresponding author), Hacettepe Univ, Inst Oncol, Dept Med Oncol, TR-06100 Ankara, Turkey.
EM arslancagatay@yahoo.com
RI Yalcin, Suayib/KWT-7106-2024; Kilickap, Saadettin/AAP-3732-2021; Aksoy,
Sercan/S-2480-2019
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NR 19
TC 4
Z9 6
U1 0
U2 0
PU TURKISH SOC GASTROENTEROLOGY
PI ABIDINPASA
PA GAZILER SOKAK 22-1, ABIDINPASA, ANKARA 06620, TURKEY
SN 1300-4948
J9 TURK J GASTROENTEROL
JI Turk. J. Gastroenterol.
PD FEB
PY 2011
VL 22
IS 1
BP 73
EP 76
DI 10.4318/tjg.2011.0160
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 752RJ
UT WOS:000289710100013
PM 21480115
DA 2025-01-07
ER
PT J
AU Della Corte, C
Mosca, A
Vania, A
Alterio, A
Alisi, A
Nobili, V
AF Della Corte, Claudia
Mosca, Antonella
Vania, Andrea
Alterio, Arianna
Alisi, Anna
Nobili, Valerio
TI Pediatric liver diseases: current challenges and future perspectives
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE Children; liver disease; nonalcoholic fatty liver disease; treatment;
chronic viral hepatitis; Wilson disease; autoimmune hepatitis
ID CHRONIC HEPATITIS-B; TENOFOVIR DISOPROXIL FUMARATE; NUCLEOTIDE
POLYMERASE INHIBITOR; FATTY LIVER; AUTOIMMUNE HEPATITIS;
CONTROLLED-TRIAL; VITAMIN-E; HEPATOCELLULAR-CARCINOMA; UNIVERSAL
VACCINATION; BARIATRIC SURGERY
AB Chronic liver diseases in children represent a rising problem with significant effects on public health. In fact, several pediatric liver diseases are precursors of adult chronic hepatopathies, cirrhosis and hepatocellular carcinoma. The prevalence of liver diseases in children is unknown. In the USA, every year, 15,000 children are hospitalized for liver diseases, but these disorders continue to be under-recognized or diagnosed late. The main reason is due to the frequent absence of symptoms in the vast majority of liver diseases, especially in the early stages. In the last few decades several advances have been made in understanding the pathogenesis of liver diseases, permitting the discovery of new therapeutic targets to treat liver diseases, thus improving the natural history of these disorders. In this article we discuss the most recent advances in the understanding of the pathogenesis, diagnosis and treatment of the most frequent pediatric liver diseases.
C1 [Della Corte, Claudia; Alterio, Arianna; Nobili, Valerio] Bambino Gesu Pediat Hosp, Hepatometab Dept, IRCCS, Ple S Onofrio 4, I-00165 Rome, Italy.
[Mosca, Antonella; Vania, Andrea] Univ Roma La Sapienza, Pediat Clin, Ctr Dietet & Nutr, Rome, Italy.
[Alisi, Anna] Bambino Gesu Pediat Hosp, IRCCS, Liver Res Unit, I-00165 Rome, Italy.
C3 IRCCS Bambino Gesu; Sapienza University Rome; IRCCS Bambino Gesu
RP Della Corte, C (corresponding author), Bambino Gesu Pediat Hosp, Hepatometab Dept, IRCCS, Ple S Onofrio 4, I-00165 Rome, Italy.
EM claudia.dellacorte@opbg.net
RI Alisi, Anna/A-6469-2010; mosca, antonella/JTS-6893-2023; Nobili,
Valerio/K-8670-2018; VANIA, Andrea/P-8461-2019; Corte,
Claudia/AAA-7478-2020
OI Alisi, Anna/0000-0001-7241-6329; VANIA, Andrea/0000-0001-6158-2495;
Mosca, Antonella/0000-0001-9646-7462; Alterio,
Arianna/0000-0002-8561-1868; nobili, valerio/0000-0002-4570-3979
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NR 83
TC 22
Z9 24
U1 0
U2 13
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD FEB 1
PY 2016
VL 10
IS 2
BP 255
EP 265
DI 10.1586/17474124.2016.1129274
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DC6JT
UT WOS:000369326800001
PM 26641319
DA 2025-01-07
ER
PT J
AU Aslam, H
Oza, F
Ahmed, K
Kopel, J
Aloysius, MM
Ali, A
Dahiya, DS
Aziz, M
Perisetti, A
Goyal, H
AF Aslam, Hunain
Oza, Fouzia
Ahmed, Khalid
Kopel, Jonathan
Aloysius, Mark M. M.
Ali, Aman
Dahiya, Dushyant Singh
Aziz, Muhammad
Perisetti, Abhilash
Goyal, Hemant
TI The Role of Red Cell Distribution Width as a Prognostic Marker in
Chronic Liver Disease: A Literature Review
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE red cell distribution width; viral hepatitis; non-alcoholic fatty liver
disease; autoimmune hepatitis; primary biliary cholangitis;
hepatocellular carcinoma
ID HEPATITIS-C VIRUS; HEPATOCELLULAR-CARCINOMA; INFLAMMATION; FIBROSIS;
SEVERITY; RATIO; RDW
AB Liver disease is one of the leading public health problems faced by healthcare practitioners regularly. As such, there has been a search for an inexpensive, readily available, non-invasive marker to aid in monitoring and prognosticating hepatic disorders. Recently, red blood cell distribution width (RDW) has been found to be associated with various inflammatory conditions with implications for its use as a potential marker for assessing disease progression and prognosis in multiple conditions. Multiple factors effect red blood cell production whereby a dysfunction in any process can lead to anisocytosis. Furthermore, a chronic inflammatory state leads to increased oxidative stress and produces inflammatory cytokines causing dysregulation and increased intracellular uptake and use of both iron and vitamin B12, which leads to a reduction in erythropoiesis causing an increase in RDW. This literature review reviews in-depth pathophysiology that may lead to an increase in RDW and its potential correlation with chronic liver diseases, including hepatitis B, hepatitis C, hepatitis E, non-alcoholic fatty liver disease, autoimmune hepatitis, primary biliary cirrhosis, and hepatocellular carcinoma. In our review, we examine the use of RDW as a prognostic and predictive marker for hepatic injury and chronic liver disease.
C1 [Aslam, Hunain; Oza, Fouzia] Wright Ctr Grad Med Educ, 501 S Washington Ave, Scranton, PA 18505 USA.
[Ahmed, Khalid; Aloysius, Mark M. M.; Ali, Aman] Wright Ctr Grad Med Educ, Dept Med, 501 S Washington Ave, Scranton, PA 18505 USA.
[Kopel, Jonathan] Texas Tech Univ, Hlth Sci Ctr, Dept Internal Med, Lubbock, TX 79430 USA.
[Dahiya, Dushyant Singh] Cent Michigan Univ, Coll Med, Dept Internal Med, Saginaw, MI 48603 USA.
[Aziz, Muhammad] Univ Toledo, Med Ctr, Dept Gastroenterol & Hepatol, Toledo, OH 43614 USA.
[Perisetti, Abhilash] Kansas City VA Med Ctr, Dept Gastroenterol & Hepatol, Kansas City, KS USA.
[Goyal, Hemant] Univ Texas Hlth Sci Ctr Houston, Ctr Intervent Gastroenterol UT iGUT, Div Gastroenterol Hepatol & Nutr, 6431 Fannin,MSB 4-234, Houston, TX 77030 USA.
C3 Texas Tech University System; Texas Tech University Health Science
Center; Central Michigan University; University System of Ohio;
University of Toledo; University of Texas System; University of Texas
Health Science Center Houston
RP Goyal, H (corresponding author), Univ Texas Hlth Sci Ctr Houston, Ctr Intervent Gastroenterol UT iGUT, Div Gastroenterol Hepatol & Nutr, 6431 Fannin,MSB 4-234, Houston, TX 77030 USA.
EM doc.hemant@yahoo.com
RI Goyal, Hemant/E-3153-2012; Aloysius, Mark/GPP-1925-2022; Perisetti,
Abhilash/L-2619-2019; Dahiya, Dushyant/AAV-8203-2020; Kopel,
Jonathan/AAH-9701-2019
OI Perisetti, Abhilash/0000-0003-4074-6395; Aziz,
Muhammad/0000-0001-5620-8597; Aslam, Hunain/0000-0002-1234-1318; Dahiya,
Dushyant/0000-0002-8544-9039; Madhok, Aloysius/0000-0001-6191-0524;
GOYAL, HEMANT/0000-0002-9433-9042; Kopel, Jonathan/0000-0001-5934-2695
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NR 64
TC 13
Z9 14
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2023
VL 24
IS 4
AR 3487
DI 10.3390/ijms24043487
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 9H0PZ
UT WOS:000938545100001
PM 36834895
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Shirabe, K
Bekki, Y
Gantumur, D
Araki, K
Ishii, N
Kuno, A
Narimatsu, H
Mizokami, M
AF Shirabe, Ken
Bekki, Yuki
Gantumur, Dolgormaa
Araki, Kenichiro
Ishii, Norihiro
Kuno, Atsushi
Narimatsu, Hisashi
Mizokami, Masashi
TI Mac-2 binding protein glycan isomer (M2BPGi) is a new serum biomarker
for assessing liver fibrosis: more than a biomarker of liver fibrosis
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Liver fibrosis; M2BPGi; Hepatocarcinogenesis
ID POSITIVE MAC-2-BINDING PROTEIN; CHRONIC HEPATITIS-C;
HEPATOCELLULAR-CARCINOMA DEVELOPMENT; TRANSIENT ELASTOGRAPHY;
CLINICAL-SIGNIFICANCE; GLYCOSYLATION ISOMER; CIRRHOSIS; BIOPSY; MARKER;
WFA(+)-M2BP
AB Assessing liver fibrosis is important for predicting the efficacy of antiviral therapy and patient prognosis. Liver biopsy is the gold standard for diagnosing liver fibrosis, despite its invasiveness and problematic diagnostic accuracy. Although noninvasive techniques to assess liver fibrosis are becoming important, reliable serum surrogate markers are not available. A glycoproteomics study aimed at identifying such markers discovered Mac 2-Binding Protein Gylcan Isomer (M2BPGi), which is a reliable marker for assessing liver fibrosis in patients with viral hepatitis and other fibrotic liver diseases such as primary biliary cholangitis, biliary atresia, autoimmune hepatitis, and nonalcoholic fatty liver disease. M2BPGi predicts the development of hepatocellular carcinoma (HCC) in patients infected with hepatitis B and C as well as the prognosis of liver cirrhosis in those with HCC after therapy. The unique features of M2BPGi are as follows: (1) cut-off values differ for the same stages of fibrosis according to the cause of fibrosis; and (2) M2BPGi levels rapidly decrease after patients achieve a sustained antiviral response to hepatitis C virus. These observations cannot be explained if M2BPGi levels reflect the amount of fibrotic tissue. Hepatic stellate cells (HSCs) secrete M2BPGi, which may serve as a messenger between HSCs and Kupffer cells via Mac-2 (galectin 3) that is expressed in Kupffer cells during fibrosis progression. Here we show that M2BPGi is a surrogate marker for assessing HSC activation. These findings may reveal the roles of HSCs in extrahepatic fibrotic disease progression.
C1 [Shirabe, Ken; Gantumur, Dolgormaa; Araki, Kenichiro; Ishii, Norihiro] Gunma Univ, Grad Sch Med, Div Hepatobiliary & Pancreat Surg, Dept Gen Surg Sci, 3-39-22 Showa Machi, Maebashi, Gunma 3718511, Japan.
[Bekki, Yuki] Kyushu Univ, Grad Sch Med, Dept Surg & Sci, Fukuoka, Fukuoka, Japan.
[Kuno, Atsushi; Narimatsu, Hisashi] Natl Inst Adv Ind Sci & Technol, Res Ctr Med Glycosci, Tsukuba, Ibaraki, Japan.
[Mizokami, Masashi] Natl Ctr Global Hlth & Med, Res Ctr Hepatitis & Immunol, Ichikawa, Chiba, Japan.
C3 Gunma University; Kyushu University; National Institute of Advanced
Industrial Science & Technology (AIST); National Center for Global
Health & Medicine - Japan
RP Shirabe, K (corresponding author), Gunma Univ, Grad Sch Med, Div Hepatobiliary & Pancreat Surg, Dept Gen Surg Sci, 3-39-22 Showa Machi, Maebashi, Gunma 3718511, Japan.
EM kshirabe@gunma-u.ac.jp
RI gantumur, dolgormaa/LPQ-0265-2024; Narimatsu, Hisashi/M-4757-2018;
Shirabe, Ken/AFS-4583-2022; Kuno, Atsushi/M-2151-2018
OI Kuno, Atsushi/0000-0002-6147-6171
FU JSPS KAKENHI [JP1504932, 16K15606]; Grants-in-Aid for Scientific
Research [16K15606] Funding Source: KAKEN
FX This work was supported by JSPS KAKENHI Grants JP1504932 and 16K15606.
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NR 76
TC 132
Z9 133
U1 0
U2 31
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JUL
PY 2018
VL 53
IS 7
BP 819
EP 826
DI 10.1007/s00535-017-1425-z
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GJ7XF
UT WOS:000435602800002
PM 29318378
DA 2025-01-07
ER
PT J
AU Díaz, LA
Villalón, A
Ochoa, G
García, S
Severino, N
Ayares, G
Idalsoaga, F
Dib, M
Briceño, E
Viñuela, E
Martinez, J
Jarufe, N
Rabagliati, R
Meneses, L
Muñoz-Schuffenegger, P
Vargas, JI
Espino, A
Vera, MM
Benítez, C
Wolff, R
Norero, B
Barrera, F
Soza, A
Arrese, M
Arab, JP
AF Diaz, Luis Antonio
Villalon, Alejandro
Ochoa, Gabriela
Garcia, Sergio
Severino, Nicolas
Ayares, Gustavo
Idalsoaga, Francisco
Dib, Martin
Briceno, Eduardo
Vinuela, Eduardo
Martinez, Jorge
Jarufe, Nicolas
Rabagliati, Ricardo
Meneses, Luis
Munoz-Schuffenegger, Pablo
Vargas, Jose Ignacio
Espino, Alberto
Vera, Maria Magdalena
Benitez, Carlos
Wolff, Rodrigo
Norero, Blanca
Barrera, Francisco
Soza, Alejandro
Arrese, Marco
Arab, Juan Pablo
TI Actualizaciones en el manejo general de sus complicaciones más
frecuentes
SO REVISTA MEDICA DE CHILE
LA English
DT Review
DE End Stage Liver Disease; Immunosuppression Therapy; Infections; Liver
Transplantation; Living Donors
ID LIVER-TRANSPLANT RECIPIENTS; HEPATOCELLULAR-CARCINOMA RECURRENCE;
CHRONIC REJECTION; RISK-FACTORS; MYCOPHENOLATE-MOFETIL; BILIARY
STRICTURES; FOLLOW-UP; CYCLOSPORINE; IMMUNOSUPPRESSION; TACROLIMUS
AB Liver transplantation (LT) is a cost-effective therapy for advanced liver disease. Although LT significantly improves long-term survival, it requires strict control of immunosuppressants and their potential complications. Several available immunosuppressive drugs include glucocorticoids, calcineurin inhibitors, mycophenolate, mTOR inhi-bitors, and anti-CD25 antibodies. These drugs act particularly in T lymphocytes, depleting them, deviating their traffic, or blocking their response pathways. The main complications after LT include renal failure and infectious, immunological, biliary, vascular adverse events, metabolic, cardiovascular, and neoplastic diseases, especially during the first months. Bacteria, viruses, and fungi can cause infections in these patients. Prophylaxis against Herpes simplex virus, Varicella zoster virus, Cytomegalovirus, Pneumocystis jirovecii, Candida spp., and Aspergillus spp. should be considered according to the presence of risk factors. Among immunological complications, acute cellular rejection is common (30% of LT) but usually responds to immuno-suppressive escalation. Also, chronic rejection appears in 3-17% of LT, but only half of the recipients respond to increased immunosuppres-sants. Appropriate treatment of the underlying etiology is essential, especially in autoimmune diseases, hepatitis B and C virus infection. Lifestyle changes must be encouraged in all patients, and alcohol consumption avoided (especially in alcohol use disorder). Due to the increased risk of cancer, neoplasms must be actively monitored, as well as osteoporosis and other metabolic disorders such as diabetes and cardiovascular disease
C1 [Diaz, Luis Antonio; Villalon, Alejandro; Ayares, Gustavo; Idalsoaga, Francisco; Vargas, Jose Ignacio; Espino, Alberto; Benitez, Carlos; Wolff, Rodrigo; Norero, Blanca; Barrera, Francisco; Soza, Alejandro; Arrese, Marco; Arab, Juan Pablo] Pontificia Univ Catolica Chile, Escuela Med, Dept Gastroenterol, Marcoleta 367, Santiago, Chile.
[Villalon, Alejandro] Univ Antofagasta, Fac Med & Odontol, Dept Ciencias Med, Antofagasta, Chile.
[Ochoa, Gabriela] Univ Austral Chile, Inst Cirugia, Valdivia, Chile.
[Garcia, Sergio] Pontificia Univ Catolica Chile, Escuela Med, Santiago, Chile.
[Severino, Nicolas; Vera, Maria Magdalena] Pontificia Univ Catolica Chile, Escuela Med, Dept psiquiatria, Santiago, Chile.
[Severino, Nicolas] Pontificia Univ Catolica Chile, Fac Med, Dept Gastroenterol, Santiago, Chile.
[Dib, Martin; Briceno, Eduardo; Vinuela, Eduardo; Martinez, Jorge; Jarufe, Nicolas] Pontificia Univ Catolica Chile, Escuela Med, Dept Cirugia Digest, Santiago, Chile.
[Rabagliati, Ricardo] Pontificia Univ Catolica Chile, Escuela Med, Dept Enfermedades Infecciosas & Inmunol Pediat, Santiago, Chile.
[Meneses, Luis] Pontificia Univ Catolica Chile, Escuela Med, Dept psiquiatria, Santiago, Chile.
[Munoz-Schuffenegger, Pablo] Pontificia Univ Catolica Chile, Escuela Med, Dept Hematol Aoncol, Santiago, Chile.
[Norero, Blanca] Hosp Dr Sotero Del Rio, Serv Radiol, Santiago, Chile.
[Arab, Juan Pablo] Virginia Commonwealth Univ, Div Gastroenterol Hepatol & Nutr, Sch Med, Div Gastroenterol Hepatol & Nutr, Richmond, VA USA.
C3 Pontificia Universidad Catolica de Chile; Universidad de Antofagasta;
Universidad Austral de Chile; Pontificia Universidad Catolica de Chile;
Pontificia Universidad Catolica de Chile; Pontificia Universidad
Catolica de Chile; Pontificia Universidad Catolica de Chile; Pontificia
Universidad Catolica de Chile; Pontificia Universidad Catolica de Chile;
Pontificia Universidad Catolica de Chile; Universidad de Chile; Virginia
Commonwealth University
RP Díaz, LA; Arab, JP (corresponding author), Pontificia Univ Catolica Chile, Dept Gastroenterol, Escuela Med, Marcoleta 367, Santiago, Chile.
EM Indiaz@uc.cl; jparab@uc.cl
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NR 74
TC 0
Z9 0
U1 0
U2 0
PU SOC MEDICA SANTIAGO
PI SANTIAGO 9
PA BERNARDA MORIN 488 PROVIDENCIA, CASILLA 168 CORREO 55, SANTIAGO 9,
00000, CHILE
SN 0034-9887
EI 0717-6163
J9 REV MED CHILE
JI Rev. Medica Chile
PD JUN
PY 2024
VL 152
IS 6
BP 704
EP 717
DI 10.4067/s0034-98872024000600704
PG 14
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA M5S5Q
UT WOS:001358134300007
DA 2025-01-07
ER
PT J
AU Mohammed, A
Paranji, N
Chen, PH
Niu, BL
AF Mohammed, Abdul
Paranji, Neethi
Chen, Po-Hung
Niu, Bolin
TI COVID-19 in Chronic Liver Disease and Liver Transplantation A Clinical
Review
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Review
DE cirrhosis; liver transplantation; hepatitis B; nonalcoholic liver
disease; hepatocellular carcinoma; autoimmune hepatitis; review;
COVID-19; SARS-CoV-2
ID OBESITY; INJURY
AB The coronavirus disease 2019 (COVID-19) pandemic has brought challenges to clinicians caring for patients with chronic liver disease. In the past 6 months, COVID-19 has led to over 150,000 deaths in the United States and over 660,000 deaths around the world. Mounting evidence suggests that chronic liver diseases can have an adverse effect on the clinical outcomes of patients with COVID-19. We present a comprehensive review of the latest literature on preexisting liver diseases and its interrelationship with COVID-19 infection in cirrhosis, hepatocellular carcinoma, nonalcoholic fatty liver disease, autoimmune hepatitis, and viral hepatitis B. As social distancing and telemedicine gain new footing, we synthesize recommendations from 3 major hepatology societies [American Association for the Study of Liver Disease (AASLD), the European Association for the Study of Liver (EASL), and the Asian Pacific Association for the Study of Liver (APASL)] to present the best approaches for caring for patients with liver diseases as well as those requiring liver transplantation.
C1 [Mohammed, Abdul] Cleveland Clin Fdn, Dept Hosp Med, 9500 Euclid Ave, Cleveland, OH 44195 USA.
[Paranji, Neethi; Niu, Bolin] Case Western Reserve Univ, Sch Med, MetroHlth Syst, Div Gastroenterol & Hepatol, Cleveland, OH USA.
[Chen, Po-Hung] Johns Hopkins Med Inst, Johns Hopkins Sch Med, Div Gastroenterol & Hepatol, Baltimore, MD 21205 USA.
C3 Cleveland Clinic Foundation; MetroHealth System; University System of
Ohio; Case Western Reserve University; Johns Hopkins University; Johns
Hopkins Medicine
RP Niu, BL (corresponding author), 2500 Metrohlth Dr, Cleveland, OH 44109 USA.
EM mohamma2@ccf.org; nparanji@metrohealth.org; pchen37@jhmi.edu;
bniu@metrohealth.org
RI Li, Caichen/F-1224-2019
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NR 76
TC 35
Z9 36
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD MAR
PY 2021
VL 55
IS 3
BP 187
EP 194
DI 10.1097/MCG.0000000000001481
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA QN3ED
UT WOS:000622346400003
PM 33394628
OA Green Published
DA 2025-01-07
ER
PT J
AU Mehta, AS
Long, RE
Comunale, MA
Wang, MJ
Rodemich, L
Krakover, J
Philip, R
Marrero, JA
Dwek, RA
Block, TM
AF Mehta, Anand S.
Long, Ronald E.
Comunale, Mary Ann
Wang, Mengjun
Rodemich, Lucy
Krakover, Jonathan
Philip, Ramila
Marrero, Jorge A.
Dwek, Raymond A.
Block, Timothy M.
TI Increased levels of galactose-deficient anti-gal immunoglobulin G in the
sera of hepatitis C virus-infected individuals with fibrosis and
cirrhosis
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RHEUMATOID-ARTHRITIS; HEPATOCELLULAR-CARCINOMA; DISEASE; IGG;
OLIGOSACCHARIDES; IDENTIFICATION; GLYCOPROTEINS; ASSOCIATION;
ANTIBODIES; DIAGNOSIS
AB Hepatitis B and C viruses are major causative agents of liver fibrosis, cirrhosis, and liver cancer. Using comparative glycoproteomics, we identified a glycoprotein that is altered both in amount and in glycosylation as a function of liver fibrosis and cirrhosis. Specifically, this altered glycoprotein is an immunoglobulin G (IgG) molecule reactive to the heterophilic alpha-Gal epitope [Gal alpha-1-3Gal beta 1-(3)4GlcNAc-R]. While similar changes in glycosylation have been observed in several autoimmune diseases, the specific immunoglobulins and their antigen recognition profiles were not determined. Thus, we provide the first report identifying the specific antigenic recognition profile of an immunoglobulin molecule containing altered glycosylation as a function of liver disease. This change in glycosylation allowed increased reactivity with several fucose binding lectins and permitted the development of a plate-based assay to measure this change. Increased lectin reactivity was observed in 100% of the more than 200 individuals with stage III or greater fibrosis and appeared to be correlated with the degree of fibrosis. The reason for the alteration in the glycosylation of anti-Gal IgG is currently unclear but may be related to the natural history of the disease and may be useful in the noninvasive detection of fibrosis and cirrhosis.
C1 [Mehta, Anand S.; Long, Ronald E.; Comunale, Mary Ann; Wang, Mengjun; Rodemich, Lucy; Block, Timothy M.] Drexel Univ, Coll Med, Doylestown, PA 18901 USA.
[Mehta, Anand S.; Long, Ronald E.; Comunale, Mary Ann; Wang, Mengjun; Rodemich, Lucy; Block, Timothy M.] Dept Microbiol & Immunol, Doylestown, PA 18901 USA.
[Mehta, Anand S.; Long, Ronald E.; Comunale, Mary Ann; Wang, Mengjun; Rodemich, Lucy; Block, Timothy M.] Drexel Inst Biotechnol & Virol, Doylestown, PA 18901 USA.
[Krakover, Jonathan; Philip, Ramila] Hepatitis B Fdn, Inst Hepatitis & Virus Res, Doylestown, PA 18901 USA.
[Marrero, Jorge A.] Univ Michigan, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Dwek, Raymond A.] Univ Oxford, Dept Biochem, Oxford Glycobiol Inst, Oxford OX1 3QU, England.
C3 Drexel University; Drexel University; University of Michigan System;
University of Michigan; University of Oxford
RP Mehta, AS (corresponding author), Drexel Univ, Coll Med, 700 E Butler Ave, Doylestown, PA 18901 USA.
EM anand.mehta@drexel.edu
FU NCI NIH HHS [R01 CA120206, U01 CA084951, UO1 CA084951-06, R01
CA120206-01] Funding Source: Medline
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NR 37
TC 98
Z9 121
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD FEB
PY 2008
VL 82
IS 3
BP 1259
EP 1270
DI 10.1128/JVI.01600-07
PG 12
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA 253JH
UT WOS:000252514000020
PM 18045939
OA Green Accepted, Green Published
DA 2025-01-07
ER
PT J
AU Basaranoglu, M
Turhan, N
Sonsuz, A
Basaranoglu, G
AF Basaranoglu, Metin
Turhan, Nesrin
Sonsuz, Abdullah
Basaranoglu, Gokcen
TI Mallory-Denk Bodies in chronic hepatitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Non-alcoholic fatty liver disease; Mallory-Denk Bodies; Hepatitis B and
C; Hepatocellular carcinoma; Primary biliary cirrhosis; Wilson disease
ID FATTY LIVER-DISEASE; NONALCOHOLIC STEATOHEPATITIS; ALCOHOLIC HEPATITIS;
FIBROSIS; INJURY
AB Mallory-Denk Bodies (MDB) are important as investigators, suggesting MDB as an indicator of the histologic severity of chronic hepatitis, causes of which include hepatitis C, primary biliary cirrhosis (PBC), and nonalcoholic fatty liver disease (NAFLD). Matteoni et al scored MDB in patients with NAFLD as none, rare and many, and reported that MDB plays a prominent role in this classification scheme in an earlier classification system. In this study, we evaluated 258 patients with chronic hepatitis due to metabolic, autoimmune and viral etiologies. Liver biopsy samples were evaluated with hematoxylin and eosin, periodic acid-Schiff-diastase, Gordon and Sweet's reticulin, Masson's trichrome, and iron stains. Both staging and grading were performed. Additionally, MDB were evaluated and discussed for each disease. We examined patients with nonalcoholic steatohepatitis (NASH; 50 patients), alcoholic hepatitis (10 patients), PBC (50 patients), Wilson disease (WD; 20 patients), hepatitis B (50 patients), hepatitis C (50 patients) and hepatocellular carcinoma (HCC; 30 patients). Frequency of MDB was as follows; NASH: 10 patients with mild in 60% and moderate in 40% and observed in every stage of the disease and frequently seen in zone 3. PBC: 11 patients with mild in 10%, moderate in 70%, and cirrhosis in 20%, and frequently seen in zone 1. WD: 16 patients with moderate and severe in 60% and cirrhosis in 40% and frequently seen in zone 1. Hep B: 3 patients with mild in 66% and severe in 34%. Hep C: 7 patients with mild in 40% and moderate in 60% and observed in every stage. HCC: 3 patients with hep B in 2 patients. We found that there is no relationship between MDB and any form of chronic hepatitis regarding histologic severity such as alcoholic steatohepatitis and NAFLD and variable zone distribution by etiology. (C) 2011 Baishideng. All rights reserved.
C1 [Basaranoglu, Metin; Turhan, Nesrin] Ankara Yuksek Ihtisas Hosp, Dept Pathol, TR-06420 Ankara, Turkey.
[Sonsuz, Abdullah] Istanbul Univ, Cerrahpasa Med Fac, TR-34500 Istanbul, Turkey.
[Basaranoglu, Gokcen] Vakif Gureba Univ Hosp, Dept Anaesthesiol, TR-34500 Istanbul, Turkey.
C3 Turkey Specialized Higher Education & Research Hospital; Istanbul
University; Istanbul University - Cerrahpasa; Bezmialem Vakif University
RP Basaranoglu, M (corresponding author), Ankara Yuksek Ihtisas Hosp, Dept Pathol, TR-06420 Ankara, Turkey.
EM metin_basaranoglu@yahoo.com
RI Basaranoglu, Metin/X-2412-2018; Başaranoğlu, Gökçen/ACW-4590-2022;
Sonsuz, Abdullah/U-2295-2018
OI Basaranoglu, Gokcen/0000-0002-3093-9049; Sonsuz,
Abdullah/0000-0002-8336-5472
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NR 23
TC 30
Z9 33
U1 0
U2 7
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAY 7
PY 2011
VL 17
IS 17
BP 2172
EP 2177
DI 10.3748/wjg.v17.i17.2172
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 765FP
UT WOS:000290689300002
PM 21633525
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Ishibashi, H
Komori, A
Shimoda, S
Gershwin, ME
AF Ishibashi, Hiromi
Komori, Atsumasa
Shimoda, Shinji
Gershwin, M. Eric
TI Guidelines for therapy of autoimmune liver disease
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE treatment; guideline; autoimmune hepatitis; primary biliary cirrhosis;
primary sclerosing cholangitis; overlapping syndrome
ID PRIMARY BILIARY-CIRRHOSIS; CHRONIC ACTIVE HEPATITIS; PRIMARY SCLEROSING
CHOLANGITIS; URSODEOXYCHOLIC ACID; CORTICOSTEROID-THERAPY;
HEPATOCELLULAR-CARCINOMA; MEDICAL PROGRESS; OVERLAP SYNDROME; CONTROLLED
TRIAL; RISK-FACTORS
AB The principle of therapy for chronic inflammatory liver diseases is the removal of causal agents. For autoimmune liver diseases, however, total removal of causal agents and immune cells is impossible. Therefore, autoimmune liver diseases are presently treated by suppression of the immune response. Autoimmune hepatitis is characteristically responsive to corticosteroids, often used in combination with azathioprine to obtain a steroid-sparing effect. For primary biliary cirrhosis, ursodeoxycholic acid is safe and is the first choice for treatment. Treatment of this autoimmune liver disease should also address various symptoms and complications arising from any associated autoimmune diseases, particularly cholestasis and cirrhosis-related complications. For primary sclerosing cholangitis there are no established immunomodulatory therapies, but medical, endoscopic, and surgical treatments are applicable to this disease. Liver transplantation becomes indicated during the eventual end stages of each of these immune-mediated liver diseases.
C1 Nagasaki Med Ctr, NHO, Clin Res Ctr, Nagasaki 8568562, Japan.
Nagasaki Univ, Grad Sch Biomed Sci, Dept Hepatol, Nagasaki 852, Japan.
Kyushu Univ, Grad Sch Med Sci, Fukuoka 812, Japan.
Univ Calif Davis, Sch Med, Genome & Biomed Sci Facil, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
C3 Nagasaki University; Kyushu University; University of California System;
University of California Davis
RP Ishibashi, H (corresponding author), Nagasaki Med Ctr, NHO, Clin Res Ctr, Kubara 2-1001-1, Nagasaki 8568562, Japan.
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NR 82
TC 26
Z9 33
U1 0
U2 5
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD MAY
PY 2007
VL 27
IS 2
BP 214
EP 226
DI 10.1055/s-2007-979472
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 174TU
UT WOS:000246966500008
PM 17520519
DA 2025-01-07
ER
PT J
AU Chaparro, M
Sanz-Cameno, P
Trapero-Marugán, M
García-Buey, L
Moreno-Otero, R
AF Chaparro, Maria
Sanz-Cameno, Paloma
Trapero-Marugan, Maria
Garcia-Buey, Luisa
Moreno-Otero, Ricardo
TI Mechanisms of angiogenesis in chronic inflammatory liver disease
SO ANNALS OF HEPATOLOGY
LA English
DT Review
DE chronic liver disease; adhesion molecules; angiogenesis; vascular
endothelial growth factor; angiopoietins
ID PRIMARY BILIARY-CIRRHOSIS; ENDOTHELIAL GROWTH-FACTOR; CHRONIC
HEPATITIS-C; OXIDE SYNTHASE EXPRESSION; VIRAL CHRONIC HEPATITIS;
HEPATOCELLULAR-CARCINOMA; X-PROTEIN; MATRIX METALLOPROTEINASES;
VASCULAR-PERMEABILITY; AUTOIMMUNE HEPATITIS
AB Intrahepatic hypoxia may occur during the inflammatory and fibrotic processes that characterize several chronic liver diseases of viral and autoimmune origin. As a consequence, new vascular structures are formed to provide oxygen and nutrients. Angiogenesis involves a tightly regulated network of cellular and molecular mechanisms that result in the formation of functional vessels. Of particular importance are growth factors and molecules involved in matrix remodeling and cell migration, as weel as vessel maturation-related factors. In recent years a number of studies have investigated the expression and function of many pro- and antiangiogenic molecules in chronic liver diseases and liver regeneration. This review examines the potential pathogenic role of angiogenesis in the context of viral hepatitis, autoinmmune hepatitis, primary biliary cirrhosis and hepatocellular carcinoma.
C1 [Chaparro, Maria; Sanz-Cameno, Paloma; Trapero-Marugan, Maria; Garcia-Buey, Luisa; Moreno-Otero, Ricardo] Univ Autonoma Madrid, Univ Hosp La Princesa, Hepatol Dept & Ciberehd, E-28049 Madrid, Spain.
C3 CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD; Autonomous
University of Madrid
RP Chaparro, M (corresponding author), Hosp Univ La Princesa, Unidad Hepatol, C-Diego Leon 62, Madrid 28006, Spain.
EM mariachs2005@gmail.com
RI Sanz, Paloma/C-7799-2014; Chaparro, Maria/I-2500-2016
OI Chaparro, Maria/0000-0002-9275-4242
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NR 43
TC 38
Z9 43
U1 0
U2 5
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD OCT-DEC
PY 2007
VL 6
IS 4
BP 208
EP 213
DI 10.1016/S1665-2681(19)31900-3
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 278AZ
UT WOS:000254257100002
PM 18007549
OA hybrid
DA 2025-01-07
ER
PT J
AU Ekpanyapong, S
Bunchorntavakul, C
Reddy, KR
AF Ekpanyapong, Sirina
Bunchorntavakul, Chalermrat
Reddy, K. Rajender
TI COVID-19 and the Liver: Lessons Learnt from the EAST and the WEST, A
Year Later
SO JOURNAL OF VIRAL HEPATITIS
LA English
DT Review
DE cirrhosis; COVID-19; hepatitis; liver transplant; vaccination
ID CORONAVIRUS DISEASE 2019; TRANSPLANT RECIPIENTS; CLINICAL
CHARACTERISTICS; SARS-COV-2 INFECTION; FEATURES; OUTCOMES; IMPACT;
COMORBIDITIES; CIRRHOSIS; HEPATITIS
AB Globally, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 virus) has been a major cause for significant morbidity and mortality. Since the start of the pandemic, several hepato-biliary manifestations in coronavirus disease 2019 (COVID-19) have been described and unique considerations raised. The review aims to summarize the pathogenesis and hepato-biliary manifestations in COVID-19 and discuss the similarities, contrasting features and disease-specific management across a range of hepato-biliary diseases from the EAST and the WEST. Published studies and regional society guidelines from the EAST and the WEST were comprehensively reviewed and summarized. A wide range of hepato-biliary manifestations, including the infrequent and chronic manifestation of cholangiopathy, has been observed in COVID-19. The pathogenesis of liver injury is multifactorial and with scant evidence for a direct SARS-CoV-2 infection of the liver. Patients with non-alcoholic fatty liver disease, cirrhosis, and liver cancer are potentially at increased risk for severe COVID-19, and there are unique considerations in chronic hepatitis B or C, hepatocellular carcinoma, and in those immunosuppressed such as autoimmune hepatitis or liver transplant recipients. With the surges in SARS-CoV-2 infection, liver transplant activity has variably been impacted. Preliminarily, SARS-CoV-2 vaccines appear to be safe in those with chronic liver disease and in transplant recipients, while emerging data suggest the need for a third dose in immunosuppressed patients. In conclusion, patients with chronic liver disease, particularly cirrhosis, and liver transplant recipients, are vulnerable to severe COVID-19. Over the past year, several unique considerations have been highlighted across a spectrum of hepato-biliary diseases. Vaccination is strongly recommended for those with chronic liver disease and liver transplant recipients.
C1 [Ekpanyapong, Sirina; Bunchorntavakul, Chalermrat] Rajavithi Hosp, Div Gastroenterol & Hepatol, Dept Med, Bangkok, Thailand.
[Reddy, K. Rajender] Univ Penn, Dept Med, Div Gastroenterol & Hepatol, Philadelphia, PA 19104 USA.
C3 Rajavithi Hospital; University of Pennsylvania
RP Reddy, KR (corresponding author), Univ Penn, Med, Div Gastroenterol & Hepatol, HUP, 2 Dulles,3400 Spruce St, Philadelphia, PA 19104 USA.; Reddy, KR (corresponding author), Univ Penn, Hepatol, Div Gastroenterol & Hepatol, HUP, 2 Dulles,3400 Spruce St, Philadelphia, PA 19104 USA.; Reddy, KR (corresponding author), Univ Penn, HUP, Liver Transplantat, Div Gastroenterol & Hepatol, 2 Dulles,3400 Spruce St, Philadelphia, PA 19104 USA.
EM ReddyR@pennmedicine.upenn.edu
OI Ekpanyapong, Sirina/0000-0001-9390-7522
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NR 116
TC 33
Z9 33
U1 1
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1352-0504
EI 1365-2893
J9 J VIRAL HEPATITIS
JI J. Viral Hepatitis
PD JAN
PY 2022
VL 29
IS 1
BP 4
EP 20
DI 10.1111/jvh.13590
EA AUG 2021
PG 17
WC Gastroenterology & Hepatology; Infectious Diseases; Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Infectious Diseases; Virology
GA XQ8DQ
UT WOS:000684350600001
PM 34352133
OA Green Published
DA 2025-01-07
ER
PT J
AU Heller, MT
Borhani, AA
Furlan, A
Tublin, ME
AF Heller, Matthew T.
Borhani, Amir A.
Furlan, Alessandro
Tublin, Mitchell E.
TI Biliary strictures and masses: an expanded differential diagnosis
SO ABDOMINAL IMAGING
LA English
DT Article
DE Biliary; Stricture; Cholangiocarcinoma; Mass
ID PRIMARY SCLEROSING CHOLANGITIS; CHOLEDOCHAL CYSTS; IMAGING FEATURES; MR
CHOLANGIOPANCREATOGRAPHY; AUTOIMMUNE PANCREATITIS;
HEPATOCELLULAR-CARCINOMA; LOW-RISK; DISEASE; CT; CIRRHOSIS
AB Biliary strictures and masses are commonly a result of cholangiocarcinoma. However, there are several congenital, infectious, inflammatory, autoimmune, iatrogenic, and neoplastic etiologies that should also be considered in the differential diagnosis. Knowledge of the key imaging and clinical findings will aid in facilitating the diagnosis and treatment.
C1 [Heller, Matthew T.; Borhani, Amir A.; Furlan, Alessandro; Tublin, Mitchell E.] Univ Pittsburgh, Med Ctr, Dept Radiol, Div Abdominal Imaging, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh
RP Heller, MT (corresponding author), Univ Pittsburgh, Med Ctr, Dept Radiol, Div Abdominal Imaging, 200 Lothrop St,Ste 3950 PST, Pittsburgh, PA 15213 USA.
EM hellermt@upmc.edu
RI Furlan, Alessandro/IZD-6109-2023
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NR 51
TC 6
Z9 6
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0942-8925
EI 1432-0509
J9 ABDOM IMAGING
JI Abdom. Imaging
PD AUG
PY 2015
VL 40
IS 6
BP 1944
EP 1960
DI 10.1007/s00261-014-0336-1
PG 17
WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
GA CO8QM
UT WOS:000359435300062
PM 25542219
DA 2025-01-07
ER
PT J
AU Straub, BK
Esposito, I
Gotthardt, D
Radeleff, B
Antolovic, D
Flechtenmacher, C
Schirmacher, P
AF Straub, Beate K.
Esposito, Irene
Gotthardt, Daniel
Radeleff, Boris
Antolovic, Dalibor
Flechtenmacher, Christa
Schirmacher, Peter
TI IgG4-associated cholangitis with cholangiocarcinoma
SO VIRCHOWS ARCHIV
LA English
DT Article
ID PRIMARY SCLEROSING CHOLANGITIS; IMMUNOGLOBULIN G4-ASSOCIATED
CHOLANGITIS; AUTOIMMUNE PANCREATITIS; DISEASE; CARCINOMA; CANCER; LIVER
C1 [Straub, Beate K.; Flechtenmacher, Christa; Schirmacher, Peter] Univ Hosp, Inst Pathol, D-69120 Heidelberg, Germany.
[Esposito, Irene] Tech Univ Munich, Inst Pathol, D-81675 Munich, Germany.
[Esposito, Irene] Helmholtz Zentrum Munchen, Inst Pathol, D-85764 Neuherberg, Germany.
[Gotthardt, Daniel] Univ Hosp, Dept Internal Med 4, D-69120 Heidelberg, Germany.
[Radeleff, Boris] Univ Hosp, Dept Diagnost & Intervent Radiol, D-69120 Heidelberg, Germany.
[Antolovic, Dalibor] Univ Hosp, Dept Surg, D-69120 Heidelberg, Germany.
C3 Ruprecht Karls University Heidelberg; Technical University of Munich;
Helmholtz Association; Helmholtz-Center Munich - German Research Center
for Environmental Health; Ruprecht Karls University Heidelberg; Ruprecht
Karls University Heidelberg; Ruprecht Karls University Heidelberg
RP Straub, BK (corresponding author), Univ Hosp, Inst Pathol, Neuenheimer Feld 220-221, D-69120 Heidelberg, Germany.
EM beate.straub@med.uni-heidelberg.de
RI Esposito, Irene/AAQ-2891-2021
OI Esposito, Irene/0000-0002-0554-2402; Straub, Beate/0000-0002-4857-1561
FU Medical Faculty of Heidelberg University
FX BKS was supported by a stipend of the Olympia-Morata program of the
Medical Faculty of Heidelberg University.
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NR 15
TC 24
Z9 26
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0945-6317
EI 1432-2307
J9 VIRCHOWS ARCH
JI Virchows Arch.
PD JUN
PY 2011
VL 458
IS 6
BP 761
EP 765
DI 10.1007/s00428-011-1073-2
PG 5
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 771LG
UT WOS:000291158300015
PM 21484428
DA 2025-01-07
ER
PT J
AU Krawitt, EL
AF Krawitt, Edward L.
TI Clinical features and management of autoimmune hepatitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE autoimmunity; autoimmune hepatitis; chronic hepatitis; cirrhosis; liver
disease
ID LIVER-TRANSPLANTATION; HEPATOCELLULAR-CARCINOMA; CORTICOSTEROID-THERAPY;
MYCOPHENOLATE-MOFETIL; F-ACTIN; DISEASE; AUTOANTIBODIES; BUDESONIDE;
RECURRENCE; TACROLIMUS
AB Autoimmune hepatitis (AIH) is a chronic hepatitis of unknown etiology which can progress to cirrhosis. Its clinical manifestations are highly variable and sometimes follow a fluctuating course. Diagnosis is based on characteristic histologic, clinical, biochemical and serological findings. Anti-inflammatory/immunosuppressive treatment frequently induces remission but long-term maintenance therapy is often required. Liver transplantation is generally successful in patients with decompensated cirrhosis unresponsive to or intolerant of medical therapy. (c) 2008 The WJG Press. All rights reserved.
C1 [Krawitt, Edward L.] Univ Vermont, Dept Med, Burlington, VT 05405 USA.
[Krawitt, Edward L.] Dartmouth Coll, Hanover, NH 05405 USA.
C3 University of Vermont; Dartmouth College
RP Krawitt, EL (corresponding author), Univ Vermont, Dept Med, Given C-246, Burlington, VT 05405 USA.
EM edward.krawitt@uvm.edu
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HENNES EM, 2008, HEPATOLOGY, V9999
Ichai P, 2007, LIVER TRANSPLANT, V13, P996, DOI 10.1002/lt.21036
Inductivo-Yu I, 2007, CLIN GASTROENTEROL H, V5, P799, DOI 10.1016/j.cgh.2007.02.030
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Meza-Junco J, 2007, ANN HEPATOL, V6, P122
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Riva S, 2006, LIVER TRANSPLANT, V12, P573, DOI 10.1002/lt.20673
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NR 38
TC 39
Z9 43
U1 0
U2 2
PU W J G PRESS
PI BEIJING
PA APT 1066, YISHOU GARDEN, NO 58, NORTH LANGXINZHUANG RD, PO BOX 2345,
BEIJING 100023, PEOPLES R CHINA
SN 1007-9327
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUN 7
PY 2008
VL 14
IS 21
BP 3301
EP 3305
DI 10.3748/wjg.14.3301
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 312WV
UT WOS:000256704000004
PM 18528927
OA Green Published, Green Submitted, hybrid
DA 2025-01-07
ER
PT J
AU McGee, EE
Castro, FA
Engels, EA
Freedman, ND
Pfeiffer, RM
Nogueira, L
Stolzenberg-Solomon, R
McGlynn, KA
Hemminki, K
Koshiol, J
AF McGee, Emma E.
Castro, Felipe A.
Engels, Eric A.
Freedman, Neal D.
Pfeiffer, Ruth M.
Nogueira, Leticia
Stolzenberg-Solomon, Rachael
McGlynn, Katherine A.
Hemminki, Kari
Koshiol, Jill
TI Associations between autoimmune conditions and hepatobiliary cancer risk
among elderly US adults
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE hepatocellular carcinoma; intrahepatic cholangiocarcinoma; extrahepatic
cholangiocarcinoma; gallbladder cancer; ampulla of Vater cancer
ID PRIMARY SCLEROSING CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE;
BILIARY-TRACT CANCER; UNITED-STATES; HEPATOCELLULAR-CARCINOMA; SYSTEMIC
LUPUS; MEDICARE DATA; CHOLANGIOCARCINOMA; LYMPHOMA; IMMUNE
AB Growing evidence suggests that people with autoimmune conditions may be at increased risk of hepatobiliary tumors. In the present study, we evaluated associations between autoimmune conditions and hepatobiliary cancers among adults aged >= 66 in the United States. We used Surveillance, Epidemiology, and End Results (SEER)-Medicare data (1992-2013) to conduct a population-based, case-control study. Cases (n = 32,443) had primary hepatobiliary cancer. Controls (n = 200,000) were randomly selected, cancer-free adults frequency-matched to cases by sex, age and year of selection. Using multivariable logistic regression, we calculated odds ratios (ORs) and 95% confidence intervals (CIs) for associations with 39 autoimmune conditions identified via Medicare claims. We also conducted separate analyses for diagnoses obtained via inpatient versus outpatient claims. Sixteen conditions were associated with at least one hepatobiliary cancer. The strongest risk estimates were for primary biliary cholangitis with hepatocellular carcinoma (OR: 31.33 [95% CI: 23.63-41.56]) and primary sclerosing cholangitis with intrahepatic cholangiocarcinoma (7.53 [5.73-10.57]), extrahepatic cholangiocarcinoma (5.59 [4.03-7.75]), gallbladder cancer (2.06 [1.27-3.33]) and ampulla of Vater cancer (6.29 [4.29-9.22]). Associations with hepatobiliary-related conditions as a group were observed across nearly all cancer sites (ORs ranging from 4.53 [95% CI: 3.30-6.21] for extrahepatic cholangiocarcinoma to 7.18 [5.94-8.67] for hepatocellular carcinoma). Restricting to autoimmune conditions diagnosed via inpatient claims, 6 conditions remained associated with at least one hepatobiliary cancer, and several risk estimates increased. In the outpatient restricted analysis, 12 conditions remained associated. Multiple autoimmune conditions are associated with hepatobiliary cancer risk in the US Medicare population, supporting a shared immuno-inflammatory etiology to these cancers.
C1 [McGee, Emma E.; Castro, Felipe A.; Engels, Eric A.; Nogueira, Leticia; Koshiol, Jill] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr, Rockville, MD 20852 USA.
[Castro, Felipe A.] Roche, Real World Data Sci RWD S Oncol, Basel, Switzerland.
[Freedman, Neal D.; Stolzenberg-Solomon, Rachael; McGlynn, Katherine A.] NCI, Metab Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Pfeiffer, Ruth M.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Nogueira, Leticia] Amer Canc Soc, Atlanta, GA 30329 USA.
[Hemminki, Kari] German Canc Res Ctr, Div Mol Genet Epidemiol, Heidelberg, Germany.
[Hemminki, Kari] Lund Univ, Ctr Primary Hlth Care Res, Malmo, Sweden.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI); Roche Holding; National Institutes of Health (NIH) - USA; NIH
National Cancer Institute (NCI); National Institutes of Health (NIH) -
USA; NIH National Cancer Institute (NCI); American Cancer Society;
Helmholtz Association; German Cancer Research Center (DKFZ); Lund
University
RP McGee, EE (corresponding author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr, Rockville, MD 20852 USA.
EM emma.mcgee@nih.gov
RI Stolzenberg-Solomon, Rachael/Y-9280-2018; Pfeiffer, Ruth/F-4748-2011; de
Castro, Fabiola/D-4693-2012; Koshiol, Jill/L-8686-2014; Freedman,
Neal/B-9741-2015
OI Koshiol, Jill/0000-0002-3832-6204; McGlynn,
Katherine/0000-0003-2329-9933; Freedman, Neal/0000-0003-0074-1098
FU Intramural Research Program of the National Cancer Institute
FX Grant sponsor: Intramural Research Program of the National Cancer
Institute
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NR 50
TC 22
Z9 25
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD FEB 15
PY 2019
VL 144
IS 4
BP 707
EP 717
DI 10.1002/ijc.31835
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HF2XD
UT WOS:000454099100004
PM 30155920
OA Green Accepted, Bronze
DA 2025-01-07
ER
PT J
AU Floreani, A
Mangini, C
Reig, A
Franceschet, I
Cazzagon, N
Perini, L
Caballería, L
Cocchio, S
Baldo, V
Parés, A
AF Floreani, Annarosa
Mangini, Chiara
Reig, Anna
Franceschet, Irene
Cazzagon, Nora
Perini, Lisa
Caballeria, Llorenc
Cocchio, Silvia
Baldo, Vincenzo
Pares, Albert
TI Thyroid Dysfunction in Primary Biliary Cholangitis: A Comparative Study
at Two European Centers
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID PRIMARY SCLEROSING CHOLANGITIS; AUTOIMMUNE LIVER-DISEASE; BIOCHEMICAL
RESPONSE; URSODEOXYCHOLIC ACID; HASHIMOTOS-THYROIDITIS; L-THYROXINE;
CIRRHOSIS; HYPOTHYROIDISM; PROGNOSIS; HEALTH
AB OBJECTIVES: Primary biliary cholangitis (PBC) is often associated with other autoimmune diseases, but little is known about the influence of thyroid disease (TD) on the natural history of PBC. Our aim is to analyze the association between PBC and TD, and the latter's impact on the natural history of PBC at two European centers.
METHODS: The study involved 921 PBC patients enrolled between 1975 and 2015 in Padova (376 patients) and Barcelona (545 patients), with a mean follow-up of 126.9 +/- 91.7 months. Data were recorded on patients' histological stage at diagnosis, biochemical data, associated extrahepatic autoimmune conditions, and clinical events, including hepatic decompensation.
RESULTS: A total of 150 patients (16.3%) had TD, including 94 patients (10.2%) with Hashimoto's thyroiditis; 15 (1.6%) with Graves' disease; 22 (2.4%) with multinodular goiter; 7 (0.8%) with thyroid cancer; and 12 (1.3%) with other thyroid conditions. The prevalence of different types of TD was similar in Padova and Barcelona, except for Graves' disease and thyroid cancer, which were more frequent in the Padova cohort (15.7 vs. 5.0%, and 8.6 vs. 1.3%, respectively, P <0.05). Overall, there were no differences between PBC patients with and without TD in terms of their histological stage at diagnosis, hepatic decompensation events, occurrence of HCC, or liver transplantation rate. The presence of associated TD was not associated with lower survival for PBC patients in either cohort.
CONCLUSIONS: TDs, and autoimmune TD like Hashimoto's thyroiditis in particular, are often associated with PBC, but the presence of TD does not infl uence the rate of hepatic complications or the natural history of PBC.
C1 [Floreani, Annarosa; Mangini, Chiara; Franceschet, Irene; Cazzagon, Nora; Perini, Lisa] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
[Reig, Anna; Caballeria, Llorenc; Pares, Albert] Univ Barcelona, CIBERehd, Hosp Clin IDIBAPS, Liver Unit, Barcelona, Spain.
[Cocchio, Silvia; Baldo, Vincenzo] Univ Padua, Dept Mol Med, Lab Publ Hlth & Populat Studies, Padua, Italy.
C3 University of Padua; CIBER - Centro de Investigacion Biomedica en Red;
CIBEREHD; University of Barcelona; Hospital Clinic de Barcelona;
IDIBAPS; University of Padua
RP Floreani, A (corresponding author), Univ Padua, Dept Surg Oncol & Gastroenterol DiSCOG, Via Giustiniani 2, I-35128 Padua, Italy.
EM annarosa.floreani@unipd.it
RI Baldo, Vincenzo/V-4005-2019; Cocchio, Silvia/Z-2327-2019; Pares,
Albert/M-6268-2019; Baldo, Vincenzo/D-7822-2018; Pares,
Albert/G-1328-2011
OI Baldo, Vincenzo/0000-0001-6012-9453; Cazzagon, Nora/0000-0002-6937-8664;
Cocchio, Silvia/0000-0003-3801-0901; MANGINI,
CHIARA/0000-0002-9312-0372; Caballeria, Llorenc/0000-0002-7990-0719;
Pares, Albert/0000-0002-5413-9687
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NR 33
TC 28
Z9 31
U1 0
U2 10
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD JAN
PY 2017
VL 112
IS 1
BP 114
EP 119
DI 10.1038/ajg.2016.479
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EK7UX
UT WOS:000394131800021
PM 27779196
OA Green Published
DA 2025-01-07
ER
PT J
AU Rodríguez-Molinero, A
López-Diéguez, M
Banegas, JR
AF Rodriguez-Molinero, Alejandro
Lopez-Dieguez, Maria
Banegas, Jose R.
TI Tissue homeostasis and cancer
SO MEDICAL HYPOTHESES
LA English
DT Review
ID REGULATORY T-CELLS; TUMOR-INFILTRATING LYMPHOCYTES; IMMATURE DENDRITIC
CELLS; TGF-BETA; HEPATOCELLULAR-CARCINOMA; GROWTH-FACTORS; HUMAN COLON;
CHRONIC INFLAMMATION; LIVER-REGENERATION; PERIPHERAL-BLOOD
AB Epithelial, cells are known to release an important amount of cytokines capable to modulate immune system functions. On the other hand, immune system cells can release cytokines, which play an important role in the control of the growth of epithelial cells. In this paper, we stand the hypothesis that a mutual (reciprocal) growth regulation exists between epithelial. cells and immune system. We propose a model describing plausible cytokine circuits that may regulate (inhibit) both epithelial growth and epithelial. inflammation. In addition, we describe how dysfunction of these circuits could lead to tumoral growth, excessive inflammation or both. A failure in the regulation of epithelial growth by the immune system could give rise to a neoplasm, and a failure in the regulation of the immune system by the epithelium could give rise to inflammatory or autoimmune diseases. This model may satisfactorily explain the link between inflammation and cancer. (C) 2006 Elsevier Ltd. All rights reserved.
C1 Univ Autonoma Madrid, Dept Prevent Med & Publ Hlth, Madrid 28029, Spain.
Fdn Hosp Comarcal San Antonio Abad, Clin Res Unit, Barcelona, Spain.
C3 Autonomous University of Madrid
RP Rodríguez-Molinero, A (corresponding author), Univ Autonoma Madrid, Dept Prevent Med & Publ Hlth, Arzobispo Morcillo 2, Madrid 28029, Spain.
EM rodriguez.molinero@gmail.com
OI Rodriguez-Molinero, Alejandro/0000-0002-9678-2654
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NR 101
TC 7
Z9 7
U1 0
U2 3
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0306-9877
EI 1532-2777
J9 MED HYPOTHESES
JI Med. Hypotheses
PY 2007
VL 68
IS 6
BP 1333
EP 1341
DI 10.1016/j.mehy.2006.10.033
PG 9
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 168QV
UT WOS:000246540000025
PM 17157444
DA 2025-01-07
ER
PT J
AU Long, J
Yang, SY
Bian, ZH
Zhu, HX
Ma, M
Wang, XQ
Li, L
Zhang, WC
Han, Y
Gershwin, ME
Lian, ZX
Zhao, ZB
AF Long, Jie
Yang, Si-Yu
Bian, Zhen-Hua
Zhu, Hao-Xian
Ma, Min
Wang, Xiao-Qing
Li, Liang
Zhang, Weici
Han, Ying
Gershwin, M. Eric
Lian, Zhe-Xiong
Zhao, Zhi-Bin
TI PD-1+CD8+ T Cell-Mediated Hepatocyte Pyroptosis
Promotes Progression of Murine Autoimmune Liver Disease
SO ADVANCED SCIENCE
LA English
DT Article; Early Access
DE aire; autoimmune liver disease; dnTGF beta RII; PD-1(+)CD8(+) T cells;
pyroptosis
ID RECEPTORS; MECHANISMS; EXHAUSTION; APOPTOSIS; CLEAVAGE; THERAPY;
RELEASE; CANCER; DEATH; PD-1
AB The specific mechanisms underlying effector pathways in autoimmune liver disease remain enigmatic and therefore constructing appropriate murine models to investigate disease pathogenesis becomes critical. A spontaneous severe murine model of autoimmune liver disease has been previously established in dnTGF beta RII Aire-/- mice, exhibiting disease phenotypes that resemble both human primary biliary cholangitis (PBC) and autoimmune hepatitis (AIH). The data suggests that auto-reactive liver-specific CD8+ T cells are the primary pathogenic cells in liver injury. In this study, these data are advanced through the use of both single-cell sequencing and extensive in vitro analysis. The results identify a specific expanded pathogenic subset of PD-1(+)CD8(+) T cells in the liver, exhibiting strong functional activity and cytotoxicity against target cells. Depletion of PD-1(+)CD8(+ )T cells using CAR-T cells effectively alleviates the disease. GSDMD-mediated pyroptosis is found to be aberrantly activated in the livers of model mice, and treatment with a GSDMD-specific inhibitor significantly inhibits disease progression. In vitro experiments reveal that PD-1(+)CD8(+) T cells can induce the pyroptosis of hepatocytes through elevated production of granzyme B and perforin-1. These results provide a novel explanation for the cytotoxic activity of pathogenic liver PD-1(+)CD8(+) T cells in autoimmune liver diseases and offer potential therapeutic targets.
C1 [Long, Jie; Li, Liang; Zhao, Zhi-Bin] Southern Med Univ, Guangdong Prov Peoples Hosp, Med Res Inst, Guangdong Acad Med Sci, Guangzhou 510080, Peoples R China.
[Yang, Si-Yu] Southern Med Univ, Guangdong Prov Peoples Hosp, Guangdong Cardiovasc Inst, Guangdong Acad Med Sci, Guangzhou 510080, Peoples R China.
[Bian, Zhen-Hua] South China Univ Technol, Sch Biomed Sci & Engn, Guangzhou Int Campus, Guangzhou 511442, Peoples R China.
[Zhu, Hao-Xian; Ma, Min; Wang, Xiao-Qing] South China Univ Technol, Sch Med, Guangzhou 510006, Peoples R China.
[Zhu, Hao-Xian; Ma, Min; Lian, Zhe-Xiong] Southern Med Univ, Guangdong Prov Peoples Hosp, Guangdong Acad Med Sci, Guangzhou 510080, Peoples R China.
[Zhang, Weici; Gershwin, M. Eric] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Han, Ying] Air Force Mil Med Univ, Natl Clin Res Ctr Digest Dis, State Key Lab Canc Biol, Xian 710000, Peoples R China.
[Han, Ying] Air Force Mil Med Univ, Xijing Hosp Digest Dis, Xian 710000, Peoples R China.
C3 Guangdong Academy of Medical Sciences & Guangdong General Hospital;
Southern Medical University - China; Southern Medical University -
China; Guangdong Academy of Medical Sciences & Guangdong General
Hospital; South China University of Technology; South China University
of Technology; Guangdong Academy of Medical Sciences & Guangdong General
Hospital; Southern Medical University - China; University of California
System; University of California Davis; Air Force Military Medical
University
RP Zhao, ZB (corresponding author), Southern Med Univ, Guangdong Prov Peoples Hosp, Med Res Inst, Guangdong Acad Med Sci, Guangzhou 510080, Peoples R China.; Lian, ZX (corresponding author), Southern Med Univ, Guangdong Prov Peoples Hosp, Guangdong Acad Med Sci, Guangzhou 510080, Peoples R China.; Gershwin, ME (corresponding author), Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.; Han, Y (corresponding author), Air Force Mil Med Univ, Natl Clin Res Ctr Digest Dis, State Key Lab Canc Biol, Xian 710000, Peoples R China.; Han, Y (corresponding author), Air Force Mil Med Univ, Xijing Hosp Digest Dis, Xian 710000, Peoples R China.
EM hanying1@fmmu.edu.cn; megershwin@ucdavis.edu; zxlian@gdph.org.cn;
zzbin@mail.ustc.edu.cn
RI Wang, Xiaoqing/ABD-8602-2021; Zhao, Zhibin/V-3278-2017
OI Zhu, Haoxian/0000-0003-3363-7983
FU National Natural Science Foundation of China; [82120108013];
[82370528]; [81820108005]; [32100720]
FX The authors thank Drs. Feng Shao and Zhengfan Jiang for their valuable
advice. This work was supported by the National Natural Science
Foundation of China (82120108013, 82370528, 81820108005 and 32100720).
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NR 58
TC 0
Z9 0
U1 6
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD 2024 NOV 4
PY 2024
DI 10.1002/advs.202407284
EA NOV 2024
PG 17
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA M6D7L
UT WOS:001358427300001
PM 39494472
OA gold
DA 2025-01-07
ER
PT J
AU Cassim, S
Bilodeau, M
Vincent, C
Lapierre, P
AF Cassim, Shamir
Bilodeau, Marc
Vincent, Catherine
Lapierre, Pascal
TI Novel immunotherapies for Autoimmune Hepatitis
SO FRONTIERS IN PEDIATRICS
LA English
DT Review
DE treatment; monoclonal antibodies; autoimmune disease; liver; regulatory
T cells
ID REGULATORY T-CELLS; CHRONIC ACTIVE HEPATITIS; KIDNEY MICROSOME ANTIBODY;
INFLAMMATORY-BOWEL-DISEASE; LOW-DOSE INTERLEUKIN-2;
HEPATOCELLULAR-CARCINOMA; MURINE MODEL; LIVER-DISEASE; TRANSPLANT
RECIPIENTS; TREATMENT WITHDRAWAL
AB Autoimmune hepatitis (AIH) is a multifactorial autoimmune disease of unknown pathogenesis, characterized by a loss of immunological tolerance against liver autoantigens resulting in the progressive destruction of the hepatic parenchyma. Current treatments are based on non-specific immunosuppressive drugs. Although tremendous progress has been made using specific biological agents in other inflammatory diseases, progress has been slow to come for AIH patients. While current treatments are successful in the majority of patients, treatment discontinuation is difficult to achieve, and relapses are frequent. Lifelong immunosuppression is not without risks, especially in the pediatric population; 4% of patient with type 1 AIH will eventually develop hepatocellular carcinoma with a 2.9% probability after 10 years of treatment. Therefore, future treatments should aim to restore tolerance to hepatic autoantigens and induce long-term remission. Promising new immunotherapies have been tested in experimental models of AIH including T and B cell depletion and regulatory CD4(+) T cells infusion. Clinical studies on limited numbers of patients have also shown encouraging results using B-cell-depleting (rituximab) and anti-TNF-alpha (infliximab) antibodies. A better understanding of key molecular targets in AIH combined with effective site-specific immunotherapies could lead to long-term remission without blanket immunosuppression and with minimal deleterious side effects.
C1 [Cassim, Shamir; Bilodeau, Marc; Lapierre, Pascal] CRCHUM, Lab Hepatol Cellulaire, Montreal, PQ, Canada.
[Bilodeau, Marc; Vincent, Catherine; Lapierre, Pascal] Univ Montreal, Dept Med, Montreal, PQ, Canada.
C3 Universite de Montreal; Universite de Montreal
RP Lapierre, P (corresponding author), CRCHUM, Lab Hepatol Cellulaire, Montreal, PQ, Canada.; Lapierre, P (corresponding author), Univ Montreal, Dept Med, Montreal, PQ, Canada.
EM pascal.lapierre.chum@ssss.gouv.qc.ca
RI Lapierre, Pascal/ABD-2247-2021; Bilodeau, Marc/L-2822-2017
OI Lapierre, Pascal/0000-0002-2753-3566; Cassim, Shamir/0000-0003-1072-5868
FU Chaire de recherche en hepatologie Novartis-Fondation canadienne du foie
de l'Universite de Montreal
FX This review was funded by the Chaire de recherche en hepatologie
Novartis-Fondation canadienne du foie de l'Universite de Montreal.
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NR 87
TC 15
Z9 19
U1 0
U2 15
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015,
SWITZERLAND
SN 2296-2360
J9 FRONT PEDIATR
JI Front. Pediatr.
PD JAN 26
PY 2017
VL 5
AR 8
DI 10.3389/fped.2017.00008
PG 8
WC Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics
GA EI7CS
UT WOS:000392655600001
PM 28184367
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Negro, F
AF Negro, Francesco
TI Residual risk of liver disease after hepatitis C virus eradication
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Liver-related mortality; Cirrhosis; Hepatocellular carcinoma; Steatosis;
Antivirals
ID SUSTAINED VIROLOGICAL RESPONSE; ACTING ANTIVIRAL THERAPY;
HEPATOCELLULAR-CARCINOMA DEVELOPMENT; AUTOIMMUNE HEPATITIS;
CLINICAL-OUTCOMES; INTERFERON-ALPHA; CIRRHOSIS; PROGRESSION; FIBROSIS;
MANAGEMENT
AB A Summary Treatment of hepatitis C with direct-acting antivirals is safe and highly efficacious, resulting in viral clearance (sustained virological response [SVR]) in the vast majority of patients. Although SVR is mostly permanent and associated with a significant reduction of liver morbidity and mortality, some patients may still suffer from a major risk of progressive liver damage, potentially leading to severe complications - including liver decompensation, hepatocellular carcinoma and death. This concise review discusses some of the most important features of residual liver disease in patients with chronic hepatitis C who have achieved SVR after antiviral therapy. (C) 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Negro, Francesco] Geneva Univ Hosp, Div Gastroenterol, 4 Rue Gabrielle Perret Gentil, CH-1211 Geneva 14, Switzerland.
[Negro, Francesco] Geneva Univ Hosp, Div Hepatol, 4 Rue Gabrielle Perret Gentil, CH-1211 Geneva 14, Switzerland.
[Negro, Francesco] Geneva Univ Hosp, Div Clin Pathol, 4 Rue Gabrielle Perret Gentil, CH-1211 Geneva 14, Switzerland.
RP Negro, F (corresponding author), Geneva Univ Hosp, Div Gastroenterol, 4 Rue Gabrielle Perret Gentil, CH-1211 Geneva 14, Switzerland.; Negro, F (corresponding author), Geneva Univ Hosp, Div Hepatol, 4 Rue Gabrielle Perret Gentil, CH-1211 Geneva 14, Switzerland.; Negro, F (corresponding author), Geneva Univ Hosp, Div Clin Pathol, 4 Rue Gabrielle Perret Gentil, CH-1211 Geneva 14, Switzerland.
EM Francesco.Negro@hcuge.ch
RI Negro, Francesco/K-1345-2013
OI Negro, Francesco/0000-0003-4046-4806
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NR 87
TC 27
Z9 28
U1 0
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2021
VL 74
IS 4
BP 952
EP 963
DI 10.1016/j.jhep.2020.11.040
EA MAR 2021
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA RB3UF
UT WOS:000632039100019
PM 33276027
OA Bronze
DA 2025-01-07
ER
PT J
AU Manzia, TM
Antonelli, B
Carraro, A
Conte, G
Guglielmo, N
Lauterio, A
Mameli, L
Cillo, U
De Carlis, L
Del Gaudio, M
De Simone, P
Fagiuoli, S
Lupo, F
Tisone, G
Volpes, R
AF Manzia, Tommaso Maria
Antonelli, Barbara
Carraro, Amedeo
Conte, Grazia
Guglielmo, Nicola
Lauterio, Andrea
Mameli, Laura
Cillo, Umberto
De Carlis, Luciano
Del Gaudio, Massimo
De Simone, Paolo
Fagiuoli, Stefano
Lupo, Francesco
Tisone, Giuseppe
Volpes, Riccardo
CA Italian Liver Transplant Working Grp
TI Immunosuppression in adult liver transplant recipients: a 2024 update
from the Italian Liver Transplant Working Group
SO HEPATOLOGY INTERNATIONAL
LA English
DT Review
DE Calcineurin; Hepatocellular cancer; Immunosuppression; Liver
transplantation; Liver metastasis; mTOR inhibitor; Nephrotoxicity;
Rejection; Recurrence
ID PERIHILAR CHOLANGIOCARCINOMA; HEPATOCELLULAR-CARCINOMA; CONSENSUS;
RECOMMENDATIONS; EVEROLIMUS; METASTASES; SARCOPENIA; EFFICACY; TUMOR;
RISK
AB PurposeAdvances in surgical procedures and immunosuppressive therapies have considerably improved the outcomes of patients who have undergone liver transplantation in the past few decades. In 2020, the Italian Liver Transplant Working Group published practice-oriented algorithms for immunosuppressive therapy (IT) in adult liver transplant (LT) recipients. Due to the rapidly evolving LT field, regular updates to the recommendations are required. This review presents a consensus- and evidence-based update of the 2020 recommendations.MethodsThe Italian Liver Transplant Working Group set out to address new IT issues, which were discussed based on supporting literature and the specialists' personal experiences. The panel deliberated on and graded each statement before consensus was reached.ResultsA series of consensus statements were formulated and finalized on: (i) oncologic indications for LT; (ii) management of chronic LT rejection; (iii) combined liver-kidney transplantation; (iv) immunosuppression for transplantation with an organ donated after circulatory death; (v) transplantation in the presence of frailty and sarcopenia; and (vi) ABO blood group incompatibility between donor and recipient. Algorithms were updated in the following LT groups: standard patients, critical patients, oncology patients, patients with specific etiology, and patients at high immunologic risk. A steroid-free approach was generally recommended, except for patients with autoimmune liver disease and those at high immunologic risk.ConclusionThe updated consensus- and evidence-based 2024 recommendations for immunosuppression regimens in adult patients with ABO-compatible LT address a range of clinical variables that should be considered to optimize the choice of the immunosuppression treatment in clinical practice in Italy.
C1 [Manzia, Tommaso Maria] Univ Roma Tor Vergata, Dept Surg Sci, Rome, Italy.
[Antonelli, Barbara] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Milan, Italy.
[Carraro, Amedeo] Univ Hosp Trust Verona, Liver Transplant Unit, Verona, Italy.
[Conte, Grazia] Azienda Osped Univ Marche, Clin Chirurg Epatobiliare Pancreat & Trapianti, Ancona, Italy.
[Guglielmo, Nicola] Azienda Osped San Camillo Forlanini, Gen Surg & Liver Transplantat Unit, Rome, Italy.
[Lauterio, Andrea] Univ Milano Bicocca, ASST Grande Osped Metropolitano Niguarda, Milan, Italy.
[Mameli, Laura; Tisone, Giuseppe] Azienda Osped G Brotzu, Cagliari, Italy.
[Cillo, Umberto] Univ Hosp Padua, Hepatobiliary & Liver Transplant Unit, Padua, Italy.
[De Carlis, Luciano] Osped Niguarda Ca Granda, Dept Gen Surg & Transplantat, Milan, Italy.
[De Carlis, Luciano] Univ Milano Bicocca, Sch Med, Milan, Italy.
[Del Gaudio, Massimo] St Orsola Marcello Malpighi Hosp, Dept Gen Surg & Transplantat, Bologna, Italy.
[De Simone, Paolo] Univ Pisa, Med Sch Hosp, Hepatobiliary Surg & Liver Transplantat Unit, Pisa, Italy.
[Fagiuoli, Stefano] Univ Milano Bicocca, Dept Med, Gastroenterol, Piazza OMS 1, I-24127 Bergamo, Italy.
[Fagiuoli, Stefano] Papa Giovanni XXIII Hosp, Gastroenterol Hepatol & Transplantat, Piazza OMS 1, I-24127 Bergamo, Italy.
[Lupo, Francesco] Azienda Osped Citta Salute & Sci, Dept Gen Surg, Turin, Italy.
[Volpes, Riccardo] Mediterranean Inst Transplantat & Adv Specialized, Palermo, Italy.
[Volpes, Riccardo] Fdn Ist G Giglio Cefalu, Palermo, Italy.
C3 University of Rome Tor Vergata; IRCCS Ca Granda Ospedale Maggiore
Policlinico; University of Verona; Azienda Ospedaliera Universitaria
Integrata Verona; Azienda Ospedaliera San Camillo-Forlanini; University
of Milano-Bicocca; University of Padua; Azienda Ospedaliera - Universita
di Padova; Ospedale Niguarda Ca' Granda; IRCCS Ca Granda Ospedale
Maggiore Policlinico; University of Milano-Bicocca; IRCCS Azienda
Ospedaliero-Universitaria di Bologna; University of Pisa; University of
Milano-Bicocca; ASST Papa Giovanni XXIII; A.O.U. Citta della Salute e
della Scienza di Torino; IRCCS Istituto Mediterraneo per i Trapianti e
Terapie ad Alta Specializzazione (ISMETT)
RP Fagiuoli, S (corresponding author), Univ Milano Bicocca, Dept Med, Gastroenterol, Piazza OMS 1, I-24127 Bergamo, Italy.; Fagiuoli, S (corresponding author), Papa Giovanni XXIII Hosp, Gastroenterol Hepatol & Transplantat, Piazza OMS 1, I-24127 Bergamo, Italy.
EM sfagiuoli@asst-pg23.it
RI Cillo, Umberto/AAC-2591-2019; De Simone, Paolo/AAC-7412-2022; LAUTERIO,
ANDREA/ABE-7865-2020; Manzia, Tommaso/K-4467-2018
FU Novartis Pharma; Novartis Pharma K.K.
FX The authors thank the 20 experts that formed the working group (those in
bold are also authors of this manuscript) Barbara Antonelli, Alfonso
Avolio, Patrizia Boccagni, Marco Bongini, Amedeo Carraro, Antonino
Castellaneta, Matteo Cescon, Alfonso Lanza Galeota, Nicola Guglielmo,
Michela Guizzetti, Andrea Lauterio, Dario Lorenzin, Paolo Magistri,
Laura Mameli, Simona Marenco, Stefano Mirabella, Daniele Nicolini,
Pierluigi Toniutto, Giovanni Vennarecci and Paola Violi. The authors
also thank Nireshnee Ramchundar, PhD, of Springer Healthcare who
prepared the manuscript for submission. This medical writing assistance
was funded by Novartis Pharma K.K.
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NR 67
TC 1
Z9 1
U1 6
U2 6
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1936-0533
EI 1936-0541
J9 HEPATOL INT
JI Hepatol. Int.
PD OCT
PY 2024
VL 18
IS 5
BP 1416
EP 1430
DI 10.1007/s12072-024-10703-4
EA JUL 2024
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA I6K3M
UT WOS:001271167800002
PM 39009897
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Migita, K
Komori, A
Kozuru, H
Jiuchi, Y
Nakamura, M
Yasunami, M
Furukawa, H
Abiru, S
Yamasaki, K
Nagaoka, S
Hashimoto, S
Bekki, S
Kamitsukasa, H
Nakamura, Y
Ohta, H
Shimada, M
Takahashi, H
Mita, E
Hijioka, T
Yamashita, H
Kouno, H
Nakamuta, M
Ario, K
Muro, T
Sakai, H
Sugi, K
Nishimura, H
Yoshizawa, K
Sato, T
Naganuma, A
Komatsu, T
Oohara, Y
Makita, F
Tomizawa, M
Yatsuhashi, H
AF Migita, Kiyoshi
Komori, Atsumasa
Kozuru, Hideko
Jiuchi, Yuka
Nakamura, Minoru
Yasunami, Michio
Furukawa, Hiroshi
Abiru, Seigo
Yamasaki, Kazumi
Nagaoka, Shinya
Hashimoto, Satoru
Bekki, Shigemune
Kamitsukasa, Hiroshi
Nakamura, Yoko
Ohta, Hajime
Shimada, Masaaki
Takahashi, Hironao
Mita, Eiji
Hijioka, Taizo
Yamashita, Haruhiro
Kouno, Hiroshi
Nakamuta, Makoto
Ario, Keisuke
Muro, Toyokichi
Sakai, Hironori
Sugi, Kazuhiro
Nishimura, Hideo
Yoshizawa, Kaname
Sato, Takeaki
Naganuma, Atsushi
Komatsu, Tatsuji
Oohara, Yukio
Makita, Fujio
Tomizawa, Minoru
Yatsuhashi, Hiroshi
TI Circulating microRNA Profiles in Patients with Type-1 Autoimmune
Hepatitis
SO PLOS ONE
LA English
DT Article
ID C VIRUS-INFECTION; HEPATOCELLULAR-CARCINOMA; LIVER-DISEASE;
SERUM-LEVELS; MIR-122; EXPRESSION; MIR-21; CANCER; TARGET; PROGRESSION
AB Recent studies have demonstrated that micro (mi) RNA molecules can be detected in the circulation and can serve as potential biomarkers of various diseases. This study used microarray analysis to identify aberrantly expressed circulating miRNAs in patients with type 1 autoimmune hepatitis (AIH) compared with healthy controls. Patients with well-documented and untreated AIH were selected from the National Hospital Organization (NHO)-AIH-liver-network database. They underwent blood sampling and liver biopsy with inflammation grading and fibrosis staging before receiving treatment. To further confirm the microarray data, circulating expression levels of miR-21 and miR-122 were quantified by real-time quantitative polymerase chain reaction in 46 AIH patients, 40 patients with chronic hepatitis C (CHC), and 13 healthy controls. Consistent with the microarray data, serum levels of miR-21 were significantly elevated in AIH patients compared with CHC patients and healthy controls. miR-21 and miR-122 serum levels correlated with alanine aminotransferase levels. Circulating levels of miR-21 and miR-122 were significantly reduced in AIH patients with liver cirrhosis, and were inversely correlated with increased stages of fibrosis. By contrast, levels of circulating miR-21 showed a significant correlation with the histological grades of inflammation in AIH. We postulate that aberrantly expressed serum miRNAs are potential biomarkers of AIH and could be implicated in AIH pathogenesis. Alternations of miR-21 and miR-122 serum levels could reflect their putative roles in the mediation of inflammatory processes in AIH.
C1 [Migita, Kiyoshi; Komori, Atsumasa; Kozuru, Hideko; Jiuchi, Yuka; Abiru, Seigo; Yamasaki, Kazumi; Nagaoka, Shinya; Hashimoto, Satoru; Bekki, Shigemune; Kamitsukasa, Hiroshi; Nakamura, Yoko; Ohta, Hajime; Shimada, Masaaki; Takahashi, Hironao; Mita, Eiji; Hijioka, Taizo; Yamashita, Haruhiro; Kouno, Hiroshi; Nakamuta, Makoto; Ario, Keisuke; Muro, Toyokichi; Sakai, Hironori; Sugi, Kazuhiro; Nishimura, Hideo; Yoshizawa, Kaname; Sato, Takeaki; Naganuma, Atsushi; Komatsu, Tatsuji; Oohara, Yukio; Makita, Fujio; Tomizawa, Minoru; Yatsuhashi, Hiroshi] Nagasaki Med Ctr, NHO AIH study Grp, Nagasaki 8568562, Japan.
[Nakamura, Minoru] Nagasaki Univ, Grad Sch Biomed Sci, Dept Hepatol, Nagasaki 852, Japan.
[Yasunami, Michio] Nagasaki Univ, Inst Trop Med, Dept Clin Med, Nagasaki 8528501, Japan.
[Furukawa, Hiroshi] Univ Tsukuba, Fac Med, Mol & Genet Epidemiol Lab, Tsukuba, Ibaraki 3058575, Japan.
C3 Nagasaki University; Nagasaki University; University of Tsukuba
RP Migita, K (corresponding author), Nagasaki Med Ctr, NHO AIH study Grp, Kubara 2-1001-1 Omura, Nagasaki 8568562, Japan.
EM migita@nagasaki-mc.com
RI Furukawa, Hiroshi/G-2039-2012
OI Naganuma, Atsushi/0000-0003-0663-0102
FU National Hospital Organization
FX This work was supported by a grant from the National Hospital
Organization.
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Z9 51
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 17
PY 2015
VL 10
IS 11
AR e0136908
DI 10.1371/journal.pone.0136908
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CW7BR
UT WOS:000365153400002
PM 26575387
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Zhou, QH
Wu, FT
Pang, LT
Zhang, TB
Chen, Z
AF Zhou, Qi-Hui
Wu, Feng-Tian
Pang, Lan-Tian
Zhang, Tian-Bao
Chen, Zhi
TI Role of γδT cells in liver diseases and its relationship with intestinal
microbiota
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE gamma delta T cells; Liver diseases; Viral hepatitis; Autoimmune liver
disease; Non-alcoholic fatty liver disease; Liver cirrhosis; Liver
cancer; Intestinal microbiota
ID SCHISTOSOMA-JAPONICUM INFECTION; PERIPHERAL-BLOOD; IMMUNE-RESPONSES;
IL-17 PRODUCTION; PROTECTIVE ROLE; TUMOR-CELLS; HEPATITIS; LYMPHOCYTES;
RECEPTOR; INFLAMMATION
AB gamma delta T cells are unconventional T lymphocytes that bridge innate and adaptive immunity. Based on the composition of T cell receptor and the cytokines produced, gamma delta T cells can be divided into diverse subsets that may be present at different locations, including the liver, epithelial layer of the gut, the dermis and so on. Many of these cells perform specific functions in liver diseases, such as viral hepatitis, autoimmune liver diseases, non-alcoholic fatty liver disease, liver cirrhosis and liver cancers. In this review, we discuss the distribution, subsets, functions of gamma delta T cells and the relationship between the microbiota and gamma delta T cells in common hepatic diseases. As gamma delta T cells have been used to cure hematological and solid tumors, we are interested in gamma delta T cell-based immunotherapies to treat liver diseases.
C1 [Zhou, Qi-Hui; Wu, Feng-Tian; Pang, Lan-Tian; Zhang, Tian-Bao; Chen, Zhi] Zhejiang Univ, Dept Infect Dis,Affiliated Hosp 1, Collaborat Innovat Ctr Diag & Treatment Infect Di, State Key Lab Diag & Treatment Infect Dis,Natl Cl, 79 Qingchun Rd, Hangzhou 310000, Zhejiang, Peoples R China.
C3 Zhejiang University; Collaborative Innovation Center for Diagnosis &
Treatment of Infectious Diseases
RP Chen, Z (corresponding author), Zhejiang Univ, Dept Infect Dis,Affiliated Hosp 1, Collaborat Innovat Ctr Diag & Treatment Infect Di, State Key Lab Diag & Treatment Infect Dis,Natl Cl, 79 Qingchun Rd, Hangzhou 310000, Zhejiang, Peoples R China.
EM zjuchenzhi@zju.edu.cn
RI Zhang, Tianbao/KCY-6752-2024
OI Wu, Fengtian/0000-0001-5047-3701
FU National Science and Technology Major Project of China [2018ZX10302206,
2017ZX10202203-007-010]
FX Supported by the National Science and Technology Major Project of China,
No. 2018ZX10302206 and No. 2017ZX10202203-007-010.
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NR 90
TC 19
Z9 22
U1 0
U2 14
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAY 28
PY 2020
VL 26
IS 20
DI 10.3748/wjg.v26.i20.2559
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA LW6OS
UT WOS:000539264100008
PM 32523311
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Lang, JY
Ma, K
Guo, JX
Zhang, JH
Wang, QF
Sun, H
AF Lang, Junyuan
Ma, Kai
Guo, Jinxiu
Zhang, Jinhui
Wang, Qifeng
Sun, Hui
TI Clinical significance of elevated antinuclear antibodies in patients
with diffuse large B-cell lymphoma: A single center study
SO JOURNAL OF CANCER RESEARCH AND THERAPEUTICS
LA English
DT Article
DE Antinuclear antibodies; diffuse large B-cell lymphoma; indirect
immunofluorescence; prognostic values
ID NON-HODGKINS-LYMPHOMA; SYSTEMIC-LUPUS-ERYTHEMATOSUS; CHRONIC
LIVER-DISEASE; LYMPHOPROLIFERATIVE DISORDERS; HEPATOCELLULAR-CARCINOMA;
SJOGRENS-SYNDROME; AUTOANTIBODIES; AUTOIMMUNITY; CANCER; ASSOCIATION
AB Objective: To investigate the potential diagnostic and prognostic values of antinuclear autoantibodies (ANAs) in diffuse large B-cell lymphoma (DLBCL).
Materials and Methods: Eighty-two DLBCL patients and 120 healthy controls were selected from the Department of Hematology, Jincheng Dayi Hospital between 2005 and 2014. We examined the expression of ANA in the sera of the 82 DLBCL patients at different Ann-Arbor stages (15 at Stage I, 22 at Stage II, 27 at Stage III, and 18 at Stage IV). ANA detection was performed by immunofluorescence, and the results were confirmed by Western blotting analysis.
Result: ANAs were more frequently detected in DLBCL patients than in controls (P < 0.001), with 25 (30.5%) DLBCL patients and 9 (7.5%) controls displaying elevated ANA levels. However, the majority of DLBCL patients in which ANA were detected did not develop autoimmune diseases, suggesting that ANA in DLBCL might not be correlated autoimmune diseases. Furthermore, no correlation was observed between the expression of ANA and the clinical stages of DLBCL. However, ANA-positive DLBCL patients had a better survival rate (P < 0.05).
Conclusions: ANA in DLBCL may be a stage-independent prognostic factor rather than an indication for autoimmune diseases and may represent an effective immune response to the tumor.
C1 [Lang, Junyuan; Sun, Hui] Zhengzhou Univ, Affiliated Hosp 1, Dept Hematol, Zhengzhou 450052, Henan, Peoples R China.
[Lang, Junyuan; Guo, Jinxiu; Zhang, Jinhui] Jincheng Dayi Hosp, Dept Hematol, Jincheng, Peoples R China.
[Ma, Kai] Jincheng Peoples Hosp, Dept Hematol, Jincheng, Peoples R China.
[Wang, Qifeng] Sichuan Canc Hosp, Dept Radiat Oncol, Chengdu, Sichuan, Peoples R China.
C3 Zhengzhou University
RP Sun, H (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Hematol, Zhengzhou 450052, Henan, Peoples R China.
EM sunhui_371@163.com
RI chen, haoran/HJG-8589-2022; Ma, kai/KSL-8338-2024; zhang,
jinhui/GXF-6528-2022
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NR 44
TC 15
Z9 16
U1 0
U2 1
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
INDIA
SN 0973-1482
EI 1998-4138
J9 J CANCER RES THER
JI J. Canc. Res. Ther.
PD JAN
PY 2018
VL 14
IS 1
BP 213
EP 219
DI 10.4103/0973-1482.183559
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FZ1WL
UT WOS:000427368100039
PM 29516988
OA gold
DA 2025-01-07
ER
PT J
AU Janik, MK
Smyk, W
Kruk, B
Szczepankiewicz, B
Górnicka, B
Lebiedzinska-Arciszewska, M
Potes, Y
Simoes, ICM
Weber, SN
Lammert, F
Wieckowski, MR
Milkiewicz, P
Krawczyk, M
AF Janik, Maciej K.
Smyk, Wiktor
Kruk, Beata
Szczepankiewicz, Benedykt
Gornicka, Barbara
Lebiedzinska-Arciszewska, Magdalena
Potes, Yaiza
Simoes, Ines C. M.
Weber, Susanne N.
Lammert, Frank
Wieckowski, Mariusz R.
Milkiewicz, Piotr
Krawczyk, Marcin
TI MARC1 p.A165T variant is associated with decreased markers of
liver injury and enhanced antioxidant capacity in autoimmune hepatitis
SO SCIENTIFIC REPORTS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; PRIMARY BILIARY-CIRRHOSIS; SIMPLE NONINVASIVE
INDEX; HEPATOCELLULAR-CARCINOMA; SIGNIFICANT FIBROSIS;
CLINICAL-FEATURES; RISK LOCI; DISEASE; POLYMORPHISMS; PROTEIN
AB The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to evaluate genetic variants previously associated with fatty liver as potential modulators of the AIH phenotype. The study cohort comprised 313 non-transplanted adults with AIH. In all patients, the MARC1 (rs2642438), HSD17B13 (rs72613567), PNPLA3 (rs738409), TM6SF2 (rs58542926), and MBOAT7 (rs641738) variants were genotyped using TaqMan assays. Mitochondrial damage markers in serum were analyzed in relation to the MARC1 variant. Carriers of the protective MARC1 allele had lower ALT and AST (both P < 0.05). In patients treated for AIH for >= 6 months, MARC1 correlated with reduced AST, ALP, GGT (all P <= 0.01), and lower APRI (P = 0.02). Patients carrying the protective MARC1 genotype had higher total antioxidant activity (P < 0.01) and catalase levels (P = 0.02) in serum. The PNPLA3 risk variant was associated with higher MELD (P = 0.02) in treated patients, whereas MBOAT7 increased the odds for liver cancer (OR = 3.71). None of the variants modulated the risk of death or transplantation. In conclusion, the MARC1 polymorphism has protective effects in AIH. Genotyping of MARC1, PNPLA3, and MBOAT7 polymorphisms might help to stratify patients with AIH.
C1 [Janik, Maciej K.; Smyk, Wiktor; Milkiewicz, Piotr] Med Univ Warsaw, Dept Gen Transplant & Liver Surg, Liver & Internal Med Unit, Warsaw, Poland.
[Janik, Maciej K.; Smyk, Wiktor; Milkiewicz, Piotr] European Reference Network Hepatol Dis ERN RARE L, Hamburg, Germany.
[Kruk, Beata; Krawczyk, Marcin] Med Univ Warsaw, Ctr Preclin Res, Dept Gen Transplant & Liver Surg, Lab Metab Liver Dis, Warsaw, Poland.
[Szczepankiewicz, Benedykt; Gornicka, Barbara] Med Univ Warsaw, Dept Pathol, Warsaw, Poland.
[Lebiedzinska-Arciszewska, Magdalena; Potes, Yaiza; Simoes, Ines C. M.; Wieckowski, Mariusz R.] Polish Acad Sci, Nencki Inst Expt Biol, Lab Mitochondrial Biol & Metab, Warsaw, Poland.
[Weber, Susanne N.; Lammert, Frank; Krawczyk, Marcin] Saarland Univ, Saarland Univ Med Ctr, Dept Med 2, Homburg, Germany.
[Lammert, Frank] Hannover Med Sch, Hannover, Germany.
[Milkiewicz, Piotr] Pomeranian Med Univ, Translat Med Grp, Szczecin, Poland.
C3 Medical University of Warsaw; Medical University of Warsaw; Medical
University of Warsaw; Polish Academy of Sciences; Nencki Institute of
Experimental Biology of the Polish Academy of Sciences;
Universitatsklinikum des Saarlandes; Hannover Medical School; Pomeranian
Medical University
RP Krawczyk, M (corresponding author), Med Univ Warsaw, Ctr Preclin Res, Dept Gen Transplant & Liver Surg, Lab Metab Liver Dis, Warsaw, Poland.; Krawczyk, M (corresponding author), Saarland Univ, Saarland Univ Med Ctr, Dept Med 2, Homburg, Germany.
EM marcin.krawczyk@uks.eu
RI Wieckowski, Mariusz/ABF-1565-2022; Lebiedzińska-Arciszewska,
Magdalena/AAC-5956-2021; Potes, Yaiza/AAU-2188-2021; Krawczyk,
Marcin/AAG-4356-2020
OI Wieckowski, Mariusz/0000-0003-0789-4521; Simoes,
Ines/0000-0002-9701-9431; Janik, Maciej/0000-0003-1941-0336; Krawczyk,
Marcin/0000-0002-0113-0777; Potes, Yaiza/0000-0002-4687-6230; Kruk,
Beata/0000-0001-5558-7636; Lebiedzinska-Arciszewska,
Magdalena/0000-0002-2725-5551
FU Projekt DEAL; National Science Centre, Poland [UMO-2018/29/B/NZ1/00589,
UMO-2020/36/T/NZ1/00004]; FOIE GRASproject; mtFOIE GRAS project;
European Union [722619, 734719]; German Liver Foundation
FX Open Access funding enabled and organized by Projekt DEAL. M.L-A., Y.P.,
I.C.M.S. and M.R.W. were supported by the National Science Centre,
Poland (UMO-2018/29/B/NZ1/00589). I.C.M.S. was supported by the National
Science Centre, Poland (UMO-2020/36/T/NZ1/00004). Moreover, I.C.M.S. and
M.R.W. gratefully acknowledge the financial support for this research
from the FOIE GRAS and mtFOIE GRAS projects. These projects received
funding from the European Union's Horizon 2020 Research and Innovation
program under the Marie Sklodowska-Curie Grant Agreement No. 722619
(FOIE GRAS) and Grant Agreement No. 734719 (mtFOIE GRAS). MK was
supported by the German Liver Foundation.
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NR 38
TC 11
Z9 11
U1 0
U2 2
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD DEC 23
PY 2021
VL 11
IS 1
AR 24407
DI 10.1038/s41598-021-03521-3
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA XU3IP
UT WOS:000734163400001
PM 34949757
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Giard, JM
Terrault, NA
AF Giard, Jeanne-Marie
Terrault, Norah A.
TI Women with Cirrhosis Prevalence, Natural History, and Management
SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Women's health; Cirrhosis; Pregnancy; Hepatitis B; Hepatitis C;
Alcoholic Liver Disease; Nonalcoholic Fatty Liver Disease; Portal
Hypertension
ID STAGE LIVER-DISEASE; CHRONIC HEPATITIS-B; C VIRUS-INFECTION; NATIONAL
EPIDEMIOLOGIC SURVEY; NUTRITION EXAMINATION SURVEY; UNITED-STATES;
PROGNOSTIC INDICATORS; ESOPHAGEAL-VARICES; PORTOPULMONARY HYPERTENSION;
HEPATOCELLULAR-CARCINOMA
AB Cirrhosis is less frequent in women than in men, in large part due to the lower prevalence of hepatitis B, hepatitis C, and alcohol use in women. The most common causes of cirrhosis among women are hepatitis C, autoimmune etiologies, nonalcoholic steatohepatitis, and alcoholic liver disease. For most chronic liver diseases, the risk of progression to cirrhosis and rates of liver failure and hepatocellular carcinoma are lower in women than in men. Pregnancy is very infrequent in women with cirrhosis due to reduced fertility, but when it occurs, requires specialized management.
C1 [Giard, Jeanne-Marie; Terrault, Norah A.] Univ Calif San Francisco, Dept Med, Div Gastroenterol, 400 Parnassus Ave, San Francisco, CA 94143 USA.
C3 University of California System; University of California San Francisco
RP Terrault, NA (corresponding author), 400 Parnassus Ave, San Francisco, CA 94143 USA.
EM norah.terrault@ucsf.edu
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NR 96
TC 14
Z9 17
U1 0
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8553
EI 1558-1942
J9 GASTROENTEROL CLIN N
JI Gastroenterol. Clin. North Am.
PD JUN
PY 2016
VL 45
IS 2
BP 345
EP +
DI 10.1016/j.gtc.2016.02.010
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DP6BJ
UT WOS:000378581600012
PM 27261903
DA 2025-01-07
ER
PT J
AU Chang, ML
Le, PH
Chen, WT
Chen, TD
Su, CW
Chen, CJ
Lin, CY
Wu, CH
Kuo, CJ
Sung, KF
Chien, RN
AF Chang, Ming-Ling
Le, Puo-Hsien
Chen, Wei-Ting
Chen, Tai-Di
Su, Chung-Wei
Chen, Cheng-Jen
Lin, Cheng-Yu
Wu, Chi-Huan
Kuo, Chia-Jung
Sung, Kei-Feng
Chien, Rong-Nan
TI Distinct characteristics of various autoimmune liver diseases: A 22-year
hospital-based study in Taiwan
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE AIH; PBC; PBC-AIH OS
ID PRIMARY BILIARY-CIRRHOSIS; OVERLAP SYNDROME; URSODEOXYCHOLIC ACID;
OBETICHOLIC ACID; HEPATITIS; DIAGNOSIS; CRITERIA; THERAPY; CHOLANGITIS;
GUIDELINES
AB Background and Aim The characteristics of autoimmune liver diseases (AILDs), including primary biliary cholangitis (PBC), autoimmune hepatitis (AIH), and PBC-AIH overlap syndrome (OS), have rarely been investigated and compared in Asia. Methods At the Taiwan tertiary referral center, 330 PBC patients (87% treated with ursodeoxycholic acid [UDCA]), 143 AIH patients (94.4% treated with immunosuppressive therapy [IST]) and 21 PBC-AIH OS patients (85.7% treated with UDCA and IST) were enrolled. Results Compared with AIH patients, PBC patients were older at baseline and had greater female-to-male sex ratios, alkaline phosphatase (ALP) and gamma-glutamyl transferase (gamma-GT) levels, and liver cirrhosis (LC), dyslipidemia, and hepatic and cardiometabolic complication rates. PBC patients had the lowest transaminase levels, whereas AIH patients had the highest transaminase levels. PBC patients had greater 22-year all-cause mortality and liver transplantation (ACMaLT) (43.5 vs 25.4%, P = 0.004), LC (75 vs 58.5%, P < 0.01), dyslipidemia (54.4 vs 45.9%, P = 0.001), and cerebrovascular accident (11.3 vs 0.8%, P = 0.019) cumulative incidences (CIs) than did AIH patients; PBC-AIH OS patients had greater systemic lupus erythematosus (28.9 vs 8.9%, P = 0.009) CI than did PBC patients. Baseline ALP (hazard ratio: 1.001), albumin (0.514), platelet count (0.997), and LC (3.438) were associated with ACMaLT; age (1.110), albumin (0.350), cirrhosis (46.219), and hepatitis C virus antibody positivity (5.068) were associated with hepatocellular carcinoma (HCC); and female sex (2.183) and body mass index (1.054) were associated with autoimmune diseases. Conclusions Compared with AIH patients, PBC patients had greater cardiometabolic CI, and ACMaLT CI, which was associated with cholestasis, liver functional reserve and LC. Older AILD patients with LC and females with obesity demand special caution for the development of HCC and extrahepatic autoimmune diseases, respectively.
C1 [Chang, Ming-Ling; Le, Puo-Hsien; Chen, Wei-Ting; Su, Chung-Wei; Chen, Cheng-Jen; Lin, Cheng-Yu; Wu, Chi-Huan; Kuo, Chia-Jung; Sung, Kei-Feng; Chien, Rong-Nan] Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, New Taipei City, Taiwan.
[Chang, Ming-Ling; Le, Puo-Hsien; Chen, Wei-Ting; Su, Chung-Wei; Chen, Cheng-Jen; Lin, Cheng-Yu; Wu, Chi-Huan; Kuo, Chia-Jung; Sung, Kei-Feng; Chien, Rong-Nan] Chang Gung Univ, Coll Med, Dept Med, Taoyuan, Taiwan.
[Chen, Tai-Di] Chang Gung Mem Hosp, Dept Anat Pathol, Linkou Main Branch, Taoyuan, Taiwan.
[Chen, Tai-Di] Natl Tsing Hua Univ, Sch Med, Hsinchu, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; Chang Gung Memorial
Hospital; National Tsing Hua University
RP Chang, ML (corresponding author), Chang Gung Mem Hosp, Dept Gastroenterol & Hepatol, 5 Fu Hsing St, Taoyuan, Taiwan.
EM mlchang8210@gmail.com
RI CHEN, WEI-TING/HNB-9994-2023; Chen, Tai-Di/JJD-8288-2023
OI Le, Puo-hsien/0000-0002-1100-5371; Chen, Cheng-Jen/0000-0002-0903-0682
FU Chang Gung Medical Research Program; Liver Research Center, Chang Gung
Memorial Hospital, Taiwan
FX The authors thank Mr. Shuen-Shian Shiau from the Liver Research Center,
Chang Gung Memorial Hospital, Taiwan, for his assistance with the data
mining.
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NR 55
TC 0
Z9 0
U1 1
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD DEC
PY 2024
VL 39
IS 12
BP 2835
EP 2844
DI 10.1111/jgh.16736
EA SEP 2024
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA P9Z4W
UT WOS:001318449900001
PM 39307997
DA 2025-01-07
ER
PT J
AU Almomani, A
Kumar, P
Onwuzo, S
Boustany, A
Krishtopaytis, E
Hitawala, A
Alshaikh, D
Albakri, A
Hussein, L
Hussein, E
Asaad, I
AF Almomani, Ashraf
Kumar, Prabhat
Onwuzo, Somtochukwu
Boustany, Antoine
Krishtopaytis, Eduard
Hitawala, Asif
Alshaikh, Dana
Albakri, Almaza
Hussein, Leen
Hussein, Ebrahim
Asaad, Imad
TI Epidemiology and prevalence of lean nonalcoholic fatty liver disease and
associated cirrhosis, hepatocellular carcinoma, and cardiovascular
outcomes in the United States: a population-based study and review of
literature
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE cardiovascular; HCC; lean NAFLD; NAFLD
ID METABOLIC SIGNIFICANCE; NONOBESE; NAFLD; RISK
AB Backgrounds Nonalcoholic fatty liver disease (NAFLD) is linked to obesity and metabolic syndrome conditions. However, a subset of NAFLD patients express a normal or low body mass index (lean NAFLD [L-NAFLD]). Our aim is to compare the prevalence of L-NAFLD to the obesity-associated NAFLD in the United States by assessing prevalence, potential risk factors, liver-related complications, and coronary artery disease outcomes. Methodology A multicenter database (Explorys Inc.) of >70 million patients across the United States was screened. A cohort of patients with "nonalcoholic fatty liver" between 1999 and 2021 was identified. Two sub-cohorts of NAFLD patients were identified: those with a body mass index (BMI) < 25 kg/m(2) (L-NAFLD) and those with a BMI > 30 kg/m(2) (obesity-associated NAFLD). We excluded patients with age <18 and those who have viral hepatitis, hemochromatosis, Wilson's disease, biliary cirrhosis, alcoholic liver disease, cystic fibrosis, alpha-1-antitrypsin deficiency, and autoimmune hepatitis. Multivariate analysis was performed to adjust for confounders. Results 68 892 260 individuals were screened. NAFLD prevalence was four per 100 000, and L-NAFLD prevalence was 0.6 per 100 000. Compared with those without, patients with L-NAFLD tended to be older (OR 2.16), females (OR 1.28), and smokers (OR 4.67) and of Asian race (OR 2.12). L-NAFLD patients were more likely to have acute coronary syndromes (OR 30.00) and metabolic syndrome (OR 2.31) despite the normal/low BMI. Esophageal varices and hepatocellular carcinoma risks were high in both cirrhosis patients. Conclusion This is the largest study to assess L-NAFLD prevalence in the United States. L-NAFLD are at a significantly higher risk for acute coronary syndromes, esophageal varices, and hepatocellular carcinoma.
C1 [Almomani, Ashraf; Kumar, Prabhat; Onwuzo, Somtochukwu; Boustany, Antoine; Krishtopaytis, Eduard; Asaad, Imad] Cleveland Clin Fdn, 9500 Euclid Ave, Cleveland, OH 44195 USA.
[Hitawala, Asif] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Alshaikh, Dana] Mutah Univ, Al Karak, Jordan.
[Albakri, Almaza] Jordanian Royal Med Serv, Amman, Jordan.
[Hussein, Leen; Hussein, Ebrahim] Al Andalus Univ Med Sci, Tartus, Syria.
C3 Cleveland Clinic Foundation; National Institutes of Health (NIH) - USA;
Mutah University
RP Almomani, A (corresponding author), Cleveland Clin Fdn, 9500 Euclid Ave, Cleveland, OH 44195 USA.
EM almomaa@ccf.org
RI Kumar, Prabhat/KKB-7973-2024; Boustany, Antoine/ACC-9168-2022
OI Boustany, Antoine/0000-0002-4661-1443; Hussein,
Leen/0000-0002-3428-9282; Kumar, Prabhat/0000-0001-9768-4223
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NR 32
TC 18
Z9 19
U1 2
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD FEB
PY 2023
VL 38
IS 2
BP 269
EP 273
DI 10.1111/jgh.16049
EA NOV 2022
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 9A7KA
UT WOS:000884496400001
PM 36328950
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Krok, KL
Munoz, SJ
AF Krok, Karen L.
Munoz, Santiago J.
TI Management of Autoimmune and Cholestatic Liver Disorders
SO CLINICS IN LIVER DISEASE
LA English
DT Review
DE Autoimmune hepatitis; Biliary cirrhosis; Sclerosing cholangitis; Overlap
syndrome; Cholestasis; Liver transplantation
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; DOSE
URSODEOXYCHOLIC ACID; PLACEBO-CONTROLLED TRIAL; RANDOMIZED
CONTROLLED-TRIALS; BONE-MINERAL DENSITY; HEPATOCELLULAR-CARCINOMA;
DOUBLE-BLIND; RETROSPECTIVE ANALYSIS; MYCOPHENOLATE-MOFETIL
AB The management of autoimmune and cholestatic liver disorders is a challenging area of hepatology. Autoimmune and cholestatic liver diseases represent a comparatively small proportion of hepatobiliary disorders, yet their appropriate management is of critical importance for patient survival. In this article, management strategies are discussed, including the indications and expectations of pharmacologic therapy, encloscopic approaches, and the role of liver transplantation.
C1 [Munoz, Santiago J.] Temple Univ Hosp & Med Sch, Liver Transplant Program, Philadelphia, PA 19140 USA.
[Krok, Karen L.] Univ Penn, Sch Med, Div Gastroenterol & Hepatol, Philadelphia, PA 19104 USA.
[Munoz, Santiago J.] Temple Sch Med, Philadelphia, PA 19140 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); Temple
University; University of Pennsylvania; Pennsylvania Commonwealth System
of Higher Education (PCSHE); Temple University
RP Munoz, SJ (corresponding author), Temple Univ Hosp & Med Sch, Liver Transplant Program, 3322 N Broad St,Suite 148, Philadelphia, PA 19140 USA.
EM Santiago.Munoz@tuhs.temple.edu
OI Krok, Karen/0000-0001-5849-5251
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NR 132
TC 2
Z9 6
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD MAY
PY 2009
VL 13
IS 2
BP 295
EP +
DI 10.1016/j.cld.2009.02.011
PG 23
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 460SK
UT WOS:000267207200010
PM 19442920
DA 2025-01-07
ER
PT J
AU Li, M
Wei, ZH
Su, JT
Wu, XN
Xie, XQ
You, H
Jia, JD
Kong, YY
AF Li, Min
Wei, Zaihua
Su, Jianting
Wu, Xiaoning
Xie, Xueqin
You, Hong
Jia, Jidong
Kong, Yuanyuan
TI Changing spectrum and mortality disparities of etiology of liver
cirrhosis in Beijing, China
SO JOURNAL OF MEDICAL VIROLOGY
LA English
DT Article
DE cirrhosis; cirrhosis complication; etiology; hepatocellular carcinoma;
liver-related death
ID CLINICAL-PRACTICE GUIDELINES; GLOBAL BURDEN; HEPATITIS-B; DISEASE
AB Liver cirrhosis remains a major health concern globally, but its epidemiology and etiology evolve with time. However, the changing pattern in etiology and cause of liver-related mortality for patients with cirrhosis are not fully elucidated. Herein, our aim was to characterize the temporal trend of the etiological spectrum and evaluate the impact of etiology on liver-related death among patients with compensated cirrhosis (CC) in Beijing, China. Clinical profiles of patients with CC discharged between January 2008 and December 2015 were retrieved from the Beijing hospital discharge database. The mortalities of different etiologies of cirrhosis were calculated. The risks of readmission and liver-related death associated with etiologies were evaluated by the Cox regression model. A total of 23 978 cirrhotic patients were included. The predominant cause was hepatitis B virus (HBV) (58.93%), followed by alcohol (21.35%), autoimmune (14.85%), miscellaneous etiologies (3.55%), and hepatitis C virus (HCV) (1.32%). From 2008 to 2015, the proportion of HBV-related cirrhosis decreased to 28.11%. Meanwhile, the proportions of autoimmune- and miscellaneous-related cirrhosis increased to 28.54% and 13.11%. The risk of liver-related death ranked the highest in patients with miscellaneous cirrhosis, followed by HBV-related cirrhosis, alcohol-related cirrhosis, autoimmune-related cirrhosis, and HCV-related cirrhosis. The 5-year rates of liver-related death were 22.56%, 18.99%, 18.77%, 16.01%, and 10.76%, respectively. HBV-related cirrhosis caused the highest risk of hepatocellular carcinoma (HCC)-related death, whereas alcohol- and miscellaneous-related cirrhosis caused higher risks of decompensation (DC)-related death than HBV-related cirrhosis, with hazard ratios of 1.35 (95% confidence interval [CI]: 1.24-1.48) and 1.20 (95% CI: 1.03-1.40), respectively. HBV remained a common cause of liver cirrhosis but gradually decreased. Mortality disparities existed in etiologies, with higher risks of HCC-related death in HBV-related cirrhosis, and DC-related death in alcohol- and miscellaneous-related cirrhosis.
C1 [Li, Min; Kong, Yuanyuan] Capital Med Univ, Beijing Friendship Hosp, Clin Epidemiol & EBM Unit, Beijing, Peoples R China.
[Li, Min; Kong, Yuanyuan] Beijing Clin Res Inst, Beijing, Peoples R China.
[Li, Min; Kong, Yuanyuan] Natl Clin Res Ctr Digest Dis, Methodol Platform, Beijing, Peoples R China.
[Wei, Zaihua; Su, Jianting] Beijing Ctr Dis Prevent & Control, Stat Ctr, Beijing, Peoples R China.
[Wu, Xiaoning; You, Hong; Jia, Jidong] Capital Med Univ, Beijing Friendship Hosp, Liver Res Ctr, Beijing, Peoples R China.
[Wu, Xiaoning; You, Hong; Jia, Jidong] Natl Clin Res Ctr Digest Dis, Beijing, Peoples R China.
[Xie, Xueqin] Natl Hlth & Family Planning Commiss Peoples Republ, Stat Ctr, Beijing, Peoples R China.
C3 Capital Medical University; Capital Medical University
RP Kong, YY (corresponding author), Capital Med Univ, Beijing Friendship Hosp, Clin Epidemiol & EBM Unit, Beijing, Peoples R China.; Kong, YY (corresponding author), Beijing Clin Res Inst, Beijing, Peoples R China.; Kong, YY (corresponding author), Natl Clin Res Ctr Digest Dis, Methodol Platform, Beijing, Peoples R China.
EM kongyy@ccmu.edu.cn
OI Kong, Yuanyuan/0000-0002-2586-1443; Li, Min/0000-0002-1163-8961
FU Beijing Municipal Science and Technology Commission; National Natural
Science Foundation of China-Youth Science Fund [82103902]; High-level
Public Health Technical Talents of the Beijing Municipal Health
Commission [XUEKEGUGAN-010-018]; [D161100002716003]
FX This study was supported by Beijing Municipal Science and Technology
Commission (No. D161100002716003), the National Natural Science
Foundation of China-Youth Science Fund (No. 82103902), and the
High-level Public Health Technical Talents of the Beijing Municipal
Health Commission (XUEKEGUGAN-010-018).
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NR 26
TC 0
Z9 0
U1 3
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0146-6615
EI 1096-9071
J9 J MED VIROL
JI J. Med. Virol.
PD JAN
PY 2024
VL 96
IS 1
AR e29405
DI 10.1002/jmv.29405
PG 9
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA HI1W5
UT WOS:001158783800035
PM 38235623
DA 2025-01-07
ER
PT J
AU Tamasi, V
Németh, K
Csala, M
AF Tamasi, Viola
Nemeth, Krisztina
Csala, Miklos
TI Role of Extracellular Vesicles in Liver Diseases
SO LIFE-BASEL
LA English
DT Review
DE extracellular vesicles; NAFLD; AFLD; hepatocarcinoma; viral hepatitis;
autoimmune hepatitis; drug-induced hepatitis; liver; hepatocytes
ID HEPATIC STELLATE CELLS; HEPATOCELLULAR-CARCINOMA; C VIRUS;
ENDOTHELIAL-CELLS; T-CELLS; EXOSOMES; RELEASE; EXPRESSION; HEPATOCYTES;
ACTIVATION
AB Extracellular vesicles (EVs) are cell-derived membrane structures that are formed by budding from the plasma membrane or originate from the endosomal system. These microparticles (100 nm-100 mu m) or nanoparticles (>100 nm) can transport complex cargos to other cells and, thus, provide communication and intercellular regulation. Various cells, such as hepatocytes, liver sinusoidal endothelial cells (LSECs) or hepatic stellate cells (HSCs), secrete and take up EVs in the healthy liver, and the amount, size and content of these vesicles are markedly altered under pathophysiological conditions. A comprehensive knowledge of the modified EV-related processes is very important, as they are of great value as biomarkers or therapeutic targets. In this review, we summarize the latest knowledge on hepatic EVs and the role they play in the homeostatic processes in the healthy liver. In addition, we discuss the characteristic changes of EVs and their potential exacerbating or ameliorating effects in certain liver diseases, such as non-alcoholic fatty liver disease (NAFLD), alcoholic fatty liver disease (AFLD), drug induced liver injury (DILI), autoimmune hepatitis (AIH), hepatocarcinoma (HCC) and viral hepatitis.
C1 [Tamasi, Viola; Csala, Miklos] Semmelweis Univ, Dept Mol Biol, H-1094 Budapest, Hungary.
[Nemeth, Krisztina] Semmelweis Univ, Dept Genet Cell and Immunobiol, H-1089 Budapest, Hungary.
[Nemeth, Krisztina] ELKH SE Translat Extracellular Vesicle Res Grp, H-1085 Budapest, Hungary.
C3 Semmelweis University; Semmelweis University
RP Tamasi, V (corresponding author), Semmelweis Univ, Dept Mol Biol, H-1094 Budapest, Hungary.
EM tamasi.viola@semmelweis.hu; nemeth.krisztina1@med.semmelweis-univ.hu;
csala.miklos@semmelweis.hu
RI Csala, Miklos/H-5369-2011
OI Csala, Miklos/0000-0002-3829-4361; Nemeth, Krisztina/0000-0002-3825-2137
FU Ministry of Innovation and Technology of Hungary from the National
Research, Development and Innovation Fund [TKP2021-EGA-24,
TKP2021-EGA-23, TKP2021-EGA]; EU's Horizon 2020 Research and Innovation
Programme [VEKOP-2.3.2-16-2016-000002, VEKOP-2.3.3-15-2017-00016];
National Cardiovascular Laboratory [739593]; ELKH SE Translational
Extracellular Vesicle Research Group [RRF-2.3.1-21-2022-00003]; ministry
for culture and innovation from the source of the national research,
development and innovation fund
FX TKP2021-EGA-24 and TKP2021-EGA-23 were implemented with the support
provided by the Ministry of Innovation and Technology of Hungary from
the National Research, Development and Innovation Fund, and financed
under the TKP2021-EGA funding scheme. Furthermore, this work was
supported by VEKOP-2.3.2-16-2016-000002, VEKOP-2.3.3-15-2017-00016. The
project has received funding from the EU's Horizon 2020 Research and
Innovation Programme under grant agreement No. 739593, the program
RRF-2.3.1-21-2022-00003 National Cardiovascular Laboratory and the ELKH
SE Translational Extracellular Vesicle Research Group. Krisztina Nemeth
was supported by the UNKP-22-4-I-SE-13 new national excellence program
of the ministry for culture and innovation from the source of the
national research, development and innovation fund.
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NR 161
TC 9
Z9 9
U1 4
U2 21
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-1729
J9 LIFE-BASEL
JI Life-Basel
PD APR 30
PY 2023
VL 13
IS 5
AR 1117
DI 10.3390/life13051117
PG 20
WC Biology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microbiology
GA H7WK9
UT WOS:000998019400001
PM 37240762
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Paillet, J
Plantureux, C
Lévesque, S
Le Naour, J
Stoll, G
Sauvat, A
Caudana, P
Boari, JT
Bloy, N
Lachkar, S
Martins, I
Opolon, P
Checcoli, A
Delaune, A
Robil, N
de la Grange, P
Hamroune, J
Letourneur, F
Autret, G
Leung, PSC
Gershwin, ME
Zhu, JS
Kurth, MJ
Lekbaby, B
Augustin, J
Kim, Y
Gujar, S
Coulouarn, C
Fouassier, L
Zitvogel, L
Piaggio, E
Housset, C
Soussan, P
Maiuri, MC
Kroemer, G
Pol, JG
AF Paillet, Juliette
Plantureux, Celeste
Levesque, Sarah
Le Naour, Julie
Stoll, Gautier
Sauvat, Allan
Caudana, Pamela
Boari, Jimena Tosello
Bloy, Norma
Lachkar, Sylvie
Martins, Isabelle
Opolon, Paule
Checcoli, Andrea
Delaune, Agathe
Robil, Noemie
de la Grange, Pierre
Hamroune, Juliette
Letourneur, Franck
Autret, Gwennhael
Leung, Patrick S. C.
Gershwin, M. Eric
Zhu, Jie S.
Kurth, Mark J.
Lekbaby, Bouchra
Augustin, Jeremy
Kim, Youra
Gujar, Shashi
Coulouarn, Cedric
Fouassier, Laura
Zitvogel, Laurence
Piaggio, Eliane
Housset, Chantal
Soussan, Patrick
Maiuri, Maria Chiara
Kroemer, Guido
Pol, Jonathan G.
TI Autoimmunity affecting the biliary tract fuels the immunosurveillance of
cholangiocarcinoma
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID PRIMARY SCLEROSING CHOLANGITIS; T-CELL RESPONSES; NONMELANOMA
SKIN-CANCER; ANIMAL-MODELS; PYRUVATE-DEHYDROGENASE; FUNCTIONAL-ANALYSIS;
INNATE IMMUNITY; B-LYMPHOCYTES; MARABA VIRUS; E2 SUBUNIT
AB Cholangiocarcinoma (CCA) results from the malignant transformation of cholangiocytes. Primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) are chronic diseases in which cholangiocytes are primarily damaged. Although PSC is an inflammatory condition predisposing to CCA, CCA is almost never found in the autoimmune context of PBC. Here, we hypothesized that PBC might favor CCA immunosurveillance. In preclinical murine models of cholangitis challenged with syngeneic CCA, PBC (but not PSC) reduced the frequency of CCA development and delayed tumor growth kinetics. This PBCrelated effect appeared specific to CCA as it was not observed against other cancers, including hepatocellular carcinoma. The protective effect of PBC was relying on type 1 and type 2 T cell responses and, to a lesser extent, on B cells. Single-cell TCR/ RNA sequencing revealed the existence of TCR clonotypes shared between the liver and CCA tumor of a PBC host. Altogether, these results evidence a mechanistic overlapping between autoimmunity and cancer immunosurveillance in the biliary tract.
C1 [Paillet, Juliette; Plantureux, Celeste; Levesque, Sarah; Le Naour, Julie; Stoll, Gautier; Sauvat, Allan; Bloy, Norma; Lachkar, Sylvie; Martins, Isabelle; Maiuri, Maria Chiara; Kroemer, Guido; Pol, Jonathan G.] Univ Paris, Sorbonne Univ, Inst Natl Sante & Rech Med,U1138, Ctr Rech Cordeliers,Equipe Labellisee Ligue Natl, Paris, France.
[Paillet, Juliette; Plantureux, Celeste; Levesque, Sarah; Le Naour, Julie; Stoll, Gautier; Sauvat, Allan; Bloy, Norma; Lachkar, Sylvie; Martins, Isabelle; Maiuri, Maria Chiara; Kroemer, Guido; Pol, Jonathan G.] Gustave Roussy Canc Campus, Metabol & Cell Biol Platforms, Villejuif, France.
[Paillet, Juliette; Plantureux, Celeste; Levesque, Sarah; Le Naour, Julie; Bloy, Norma] Univ Paris Saclay, Fac Med, Le Kremlin Bicetre, France.
[Caudana, Pamela; Boari, Jimena Tosello] Paris Sci & Lettres Res Univ, Inst Curie, Inst Natl Sante & Rech Med U932, Paris, France.
[Opolon, Paule] Gustave Roussy Canc Campus, Villejuif, France.
[Checcoli, Andrea] Paris Sci & Lettres Res Univ, Inst Curie, Paris, France.
[Checcoli, Andrea] Inst Natl Sante & Rech Med, U900, Paris, France.
[Delaune, Agathe; Robil, Noemie; de la Grange, Pierre] GenoSplice Technol, Paris, France.
[Hamroune, Juliette; Letourneur, Franck] Inst Natl Sante & Rech Med U1016, Institut Cochin, Paris, France.
[Autret, Gwennhael] Univ Paris, Paris Cardiovasc Res Ctr, Inst Natl Sante & Rech Med U970, Paris, France.
[Leung, Patrick S. C.; Gershwin, M. Eric] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Zhu, Jie S.; Kurth, Mark J.] Univ Calif Davis, Dept Chem, Davis, CA 95616 USA.
[Lekbaby, Bouchra; Fouassier, Laura; Housset, Chantal; Soussan, Patrick] Sorbonne Univ, Ctr Rech St Antoine, Inst Natl Sante & Rech Med U938, Paris, France.
[Augustin, Jeremy] Sorbonne Univ, Hop Henri Mondor, Assistance Publ Hop Paris,Dept Pathol, Inst Natl Sante & Rech Med U938,Ctr Rech St Antoi, Paris, France.
[Kim, Youra; Gujar, Shashi] Dalhousie Univ, Dept Pathol, Halifax, NS, Canada.
[Gujar, Shashi] Dalhousie Univ, Dept MicroBiol & Immunol, Halifax, NS, Canada.
[Gujar, Shashi] Beatrice Hunter Canc Res Inst, Halifax, NS, Canada.
[Gujar, Shashi] Dalhousie Univ, Dept Biol, Halifax, NS, Canada.
[Coulouarn, Cedric] Univ Rennes 1, Inst Natl Sante & Rech Med, Ctr Lutte Canc Eugene Marquis, Chem Oncogenesis Stress Signaling,UMR S 1242, Rennes, France.
[Zitvogel, Laurence] Univ Paris Saclay, Inst Natl Sante & Rech Med U1015, Gustave Roussy Canc Campus, Villejuif, France.
[Piaggio, Eliane] Inst Curie, Ctr Invest Clin Biotherapie 1428, Paris, France.
[Housset, Chantal] St Antoine Hosp, Assistance Publ Hop Paris, Reference Ctr Inflammatory Biliary Dis & Autoimmu, Dept Hepatol, Paris, France.
[Kroemer, Guido] Inst Univ France, Paris, France.
[Kroemer, Guido] Hop Europeen Georges Pompidou, Assistance Publ Hop Paris, Pole Biol, Paris, France.
[Kroemer, Guido] Chinese Acad Med Sci, Suzhou Inst Syst Med, Suzhou, Peoples R China.
[Kroemer, Guido] Karolinska Univ Hosp, Dept Womens & Childrens Hlth, Karolinska Inst, Stockholm, Sweden.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
Sorbonne Universite; Universite Paris Cite; UNICANCER; Gustave Roussy;
Universite Paris Saclay; Institut National de la Sante et de la
Recherche Medicale (Inserm); UNICANCER; Universite PSL; Institut Curie;
UNICANCER; Gustave Roussy; UNICANCER; Universite PSL; Institut Curie;
Universite PSL; UNICANCER; Institut Curie; Institut National de la Sante
et de la Recherche Medicale (Inserm); Institut National de la Sante et
de la Recherche Medicale (Inserm); Universite Paris Cite; Universite
Paris Cite; Institut National de la Sante et de la Recherche Medicale
(Inserm); University of California System; University of California
Davis; University of California System; University of California Davis;
Institut National de la Sante et de la Recherche Medicale (Inserm);
Sorbonne Universite; Assistance Publique Hopitaux Paris (APHP);
Universite Paris Cite; Hopital Universitaire Saint-Louis - APHP;
Sorbonne Universite; Universite Paris-Est-Creteil-Val-de-Marne (UPEC);
Hopital Universitaire Henri-Mondor - APHP; Institut National de la Sante
et de la Recherche Medicale (Inserm); Dalhousie University; Dalhousie
University; Dalhousie University; UNICANCER; Centre Eugene Marquis;
Universite de Rennes; Institut National de la Sante et de la Recherche
Medicale (Inserm); UNICANCER; Gustave Roussy; Institut National de la
Sante et de la Recherche Medicale (Inserm); Universite Paris Saclay;
UNICANCER; Universite PSL; Institut Curie; Assistance Publique Hopitaux
Paris (APHP); Universite Paris Cite; Hopital Universitaire Saint-Louis -
APHP; Sorbonne Universite; Hopital Universitaire Saint-Antoine - APHP;
Institut Universitaire de France; Assistance Publique Hopitaux Paris
(APHP); Universite Paris Cite; Hopital Universitaire Europeen
Georges-Pompidou - APHP; Hopital Universitaire Saint-Louis - APHP;
Chinese Academy of Medical Sciences - Peking Union Medical College;
Karolinska Institutet; Karolinska University Hospital
RP Kroemer, G; Pol, JG (corresponding author), Univ Paris, Sorbonne Univ, Inst Natl Sante & Rech Med,U1138, Ctr Rech Cordeliers,Equipe Labellisee Ligue Natl, Paris, France.; Kroemer, G; Pol, JG (corresponding author), Gustave Roussy Canc Campus, Metabol & Cell Biol Platforms, Villejuif, France.; Kroemer, G (corresponding author), Inst Univ France, Paris, France.; Kroemer, G (corresponding author), Hop Europeen Georges Pompidou, Assistance Publ Hop Paris, Pole Biol, Paris, France.; Kroemer, G (corresponding author), Chinese Acad Med Sci, Suzhou Inst Syst Med, Suzhou, Peoples R China.; Kroemer, G (corresponding author), Karolinska Univ Hosp, Dept Womens & Childrens Hlth, Karolinska Inst, Stockholm, Sweden.
EM kroemer@orange.fr; pol_jonathan@yahoo.fr
RI Coulouarn, Cedric/E-5472-2011; KROEMER, Guido/B-4263-2013; Pol,
Jonathan/R-6507-2016; Piaggio, Eliane/E-5260-2016; soussan,
patrick/O-9801-2017; Fouassier, Laura/M-7556-2017
OI ZITVOGEL, laurence/0000-0003-1596-0998; Plantureux,
Celeste/0000-0003-4437-0479; Stoll, Gautier/0000-0002-0862-4139;
LACHKAR, SYLVIE/0000-0002-8169-140X; Pol, Jonathan/0000-0002-8355-7562;
Tosello Boari, Jimena/0000-0003-1563-4420; ,
Gwennhael/0000-0001-7335-350X; Paillet, Juliette/0000-0001-7118-7165;
soussan, patrick/0000-0003-2706-7371; Fouassier,
Laura/0000-0001-6377-5610; Checcoli, Andrea/0000-0002-8290-6310;
Hamroune, Juliette/0000-0002-1812-2853; Le Naour,
Julie/0000-0002-3749-2171; Allan, Sauvat/0000-0001-7076-8638
FU Association pour la lutte contre les maladies inflammatoires du foie et
des voies biliaires; Dalhousie Medical Research Foundation; Canadian
Cancer Society; Canadian Institutes of Health Research; Association
Francaise d'Hepatologie; Site de Recherche integree sur le Cancer Cancer
Research and Personalized Medicine; Seerave Foundation; Multi-Organism
Institute (ITMO) Aviesan Cancer (National Alliance for Life Sciences and
Health); Institut National du Cancer; Ligue contre le Cancer (equipe
labellisee); Agence National de la Recherche (ANR) Projets blancs;
Agence National de la Recherche; Association pour la recherche sur le
cancer; Canceropole Ile-de-France; Fondation pour la Recherche
M'edicale; European Union Horizon 2020 Project Oncobiome; Fondation
Carrefour; High-end Foreign Expert Program in China [GDW20171100085,
GDW20181100051]; Inserm Program Heterogeneity of Tumors Ecosystem;
Institut Universitaire de France; LeDucq Foundation; LabEx
Immuno-Oncology; Recherche Hospitalo-Universitaire Torino Lumiere; Site
de Recherche integree sur le Cancer Stratified Oncology Cell DNA Repair
and Tumor Immune Elimination; Cancer Research and Personalized Medicine
FX J. Paillet is supported by the Association pour la lutte contre les
maladies inflammatoires du foie et des voies biliaires. S. Gujar is
supported by Dalhousie Medical Research Foundation, Canadian Cancer
Society, and Canadian Institutes of Health Research. J.G. Pol is
supported by the Association Francaise d'Hepatologie; Site de Recherche
integree sur le Cancer Cancer Research and Personalized Medicine;
Seerave Foundation; Multi-Organism Institute (ITMO) Aviesan Cancer
(National Alliance for Life Sciences and Health); and Institut National
du Cancer. G. Kroemer is supported by the Ligue contre le Cancer (equipe
labellisee); Agence National de la Recherche (ANR) Projets blancs;
Agence National de la Recherche under the frame of E-Rare-2, the ERA-Net
for Research on Rare Diseases; Association pour la recherche sur le
cancer; Canceropole Ile-de-France; Chancellerie des universites de Paris
(Legs Poix), Fondation pour la Recherche M ' edicale; a donation by
Elior; European Research Area Network on Cardiovascular Diseases
(MINOTAUR); Gustave Roussy Odyssea, the European Union Horizon 2020
Project Oncobiome; Fondation Carrefour; High-end Foreign Expert Program
in China (GDW20171100085 and GDW20181100051), Institut National du
Cancer; Inserm Program Heterogeneity of Tumors & Ecosystem; Institut
Universitaire de France; LeDucq Foundation; the LabEx Immuno-Oncology;
the Recherche Hospitalo-Universitaire Torino Lumiere; the Seerave
Foundation; the Site de Recherche integree sur le Cancer Stratified
Oncology Cell DNA Repair and Tumor Immune Elimination; and Cancer
Research and Personalized Medicine.
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NR 117
TC 20
Z9 20
U1 0
U2 10
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA
SN 0022-1007
EI 1540-9538
J9 J EXP MED
JI J. Exp. Med.
PD OCT 4
PY 2021
VL 218
IS 10
AR e20200853
DI 10.1084/jem.20200853
PG 29
WC Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Research & Experimental Medicine
GA UY7HH
UT WOS:000701689800003
PM 34495298
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Seidemann, L
Dietrich, A
AF Seidemann, Lena
Dietrich, Arne
TI Newly diagnosed Crohn's disease, and hepatocellular and renal cell
carcinoma in a bariatric surgery patient-dealing with the complexity of
obesity-associated diseases: a case report and review of the literature
SO JOURNAL OF MEDICAL CASE REPORTS
LA English
DT Review
DE Obesity-associated malignancies; Inflammatory bowel disease;
Hepatocellular carcinoma; Renal cell carcinoma; Bariatric surgery; Case
report
AB BackgroundBariatric surgery candidates commonly suffer from conditions that constitute the metabolic syndrome. But they also have a higher risk for autoimmune and malignant diseases. Obesity-associated comorbidities aside from the metabolic syndrome are often given insufficient attention in the clinical routine, including preoperative work-ups for bariatric surgery.Case presentationWe retrospectively report the case of a 65 years old Caucasian patient who was diagnosed with Crohn's disease prior to, a hepatocellular carcinoma during, and a renal cell carcinoma post bariatric surgery. The relevance of these diseases for decision making in bariatric procedures and current recommendations for preoperative bariatric work-ups are discussed. In our case, the diagnosis of Crohn's disease led to the performance of a sleeve gastrectomy instead of a Roux-en-Y gastric bypass and a previously unknown hepatocellular carcinoma was simultaneously removed by hepatic wedge resection.ConclusionsPreoperative endoscopy and imaging techniques can be valuable since surprising pre- and intraoperative findings can force the bariatric surgeon to change the initially planned operative strategy. But the diagnostic accuracy of abdominal ultrasound may be limited in bariatric surgery patients. With the expansion of bariatric surgery, the complexity of bariatric surgery patients is also likely to increase. However, with the appropriate awareness and strategies, bariatric surgery can be safely executed and even contribute to the treatment of severe comorbidities that exceed the metabolic spectrum.
C1 [Seidemann, Lena; Dietrich, Arne] Univ Leipzig Med Ctr, Dept Bariatr Metab & Endocrine Surg, Clin Visceral Transplant Thorac & Vasc Surg, Liebigstr 20, D-04103 Leipzig, Germany.
C3 Leipzig University
RP Seidemann, L (corresponding author), Univ Leipzig Med Ctr, Dept Bariatr Metab & Endocrine Surg, Clin Visceral Transplant Thorac & Vasc Surg, Liebigstr 20, D-04103 Leipzig, Germany.
EM lena.seidemann@medizin.uni-leipzig.de
OI Seidemann, Lena/0000-0002-1531-7735
FU The authors cordially thank the entire interdisciplinary team that is
involved in the treatment of obesity at University of Leipzig Medical
Center.
FX The authors cordially thank the entire interdisciplinary team that is
involved in the treatment of obesity at University of Leipzig Medical
Center.
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NR 23
TC 0
Z9 0
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1752-1947
J9 J MED CASE REP
JI J. Med. Case Rep.
PD SEP 5
PY 2023
VL 17
IS 1
AR 379
DI 10.1186/s13256-023-04111-9
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA Q5YM7
UT WOS:001058277500001
PM 37667406
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Vuerich, M
Robson, SC
Longhi, MS
AF Vuerich, Marta
Robson, Simon C.
Longhi, Maria Serena
TI Ectonucleotidases in Intestinal and Hepatic Inflammation
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE ectonucleotidase; ATP; adenosine; T-cell; intestine; liver
ID REGULATORY T-CELLS; BOWEL-DISEASE; HEPATOCELLULAR-CARCINOMA; CYTOKINE
PRODUCTION; INDUCED GASTRITIS; CD39 EXPRESSION; HELPER-CELLS; TH17
CELLS; ADENOSINE; CD73
AB Purinergic signaling modulates systemic and local inflammatory responses. Extracellular nucleotides, including eATP, promote inflammation, at least in part via the inflammasome upon engagement of P2 purinergic receptors. In contrast, adenosine generated during eATP phosphohydrolysis by ectonucleotidases, triggers immunosuppressive/anti-inflammatory pathways. Mounting evidence supports the role of ectonucleotidases, especially ENTPD1/CD39 and CD73, in the control of several inflammatory conditions, ranging from infectious disease, organ fibrosis to oncogenesis. Our experimental data generated over the years have indicated both CD39 and CD73 serve as pivotal regulators of intestinal and hepatic inflammation. In this context, immune cell responses are regulated by the balance between eATP and adenosine, potentially impacting disease outcomes as in gastrointestinal infection, inflammatory bowel disease, ischemia reperfusion injury of the bowel and liver, autoimmune or viral hepatitis and other inflammatory conditions, such as cancer. In this review, we report the most recent discoveries on the role of ENTPD1/CD39, CD73, and other ectonucleotidases in the regulation of intestinal and hepatic inflammation. We discuss the present knowledge, highlight the most intriguing and promising experimental data and comment on important aspects that still need to be addressed to develop purinergic-based therapies for these important illnesses.
C1 [Vuerich, Marta; Robson, Simon C.; Longhi, Maria Serena] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Anesthesia, Boston, MA 02115 USA.
[Robson, Simon C.; Longhi, Maria Serena] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med, Div Gastroenterol, Boston, MA 02115 USA.
C3 Harvard University; Harvard Medical School; Beth Israel Deaconess
Medical Center; Harvard University; Harvard Medical School; Beth Israel
Deaconess Medical Center
RP Robson, SC; Longhi, MS (corresponding author), Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Anesthesia, Boston, MA 02115 USA.; Robson, SC; Longhi, MS (corresponding author), Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med, Div Gastroenterol, Boston, MA 02115 USA.
EM srobson@bidmc.harvard.edu; mlonghi@bidmc.harvard.edu
RI Robson, Simon/AAA-8537-2021
FU National Institute of Health [R01 DK108894, P01 HL107152, R21 CA164970];
AASLD Pilot Research Award; Pfizer; Helmsley Charitable Trust
[281574.5069091.0010]; Department of Defense [W81XWH-16-0464]
FX This work has been supported by the National Institute of Health (R01
DK108894 to MSL; P01 HL107152 and R21 CA164970 to SCR); AASLD Pilot
Research Award (to MSL); Pfizer research support to SCR; the Helmsley
Charitable Trust (grant 281574.5069091.0010 to SCR); and by the
Department of Defense Award W81XWH-16-0464 (to SCR).
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NR 101
TC 36
Z9 36
U1 2
U2 10
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAR 19
PY 2019
VL 10
AR 507
DI 10.3389/fimmu.2019.00507
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA HP3RS
UT WOS:000461595600001
PM 30941139
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zheng, MH
Gu, DN
Braddock, M
Leishman, AJ
Jin, C
Wen, JS
Gong, YW
Chen, YP
AF Zheng, Ming-Hua
Gu, Dian-Na
Braddock, Martin
Leishman, Andrew J.
Jin, Chang
Wen, Jin-Sheng
Gong, Yue-Wen
Chen, Yong-Ping
TI CD4+CD25+ regulatory T cells:: a therapeutic
target for liver diseases
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
DE autoimmune liver disease; chronic hepatitis B; chronic hepatitis C;
hepatocellular carcinoma; immune therapy; regulatory T cells; T-regs
ID HEPATITIS-C VIRUS; TUMOR-INFILTRATING LYMPHOCYTES; GROWTH-FACTOR-BETA;
ANTIVIRAL IMMUNE-RESPONSE; CHRONIC ACTIVE HEPATITIS; CTL-ASSOCIATED
ANTIGEN-4; INDUCED TNF RECEPTOR; HEPATOCELLULAR-CARCINOMA; IN-VITRO;
DENDRITIC CELLS
AB Background: Regulatory T cells (T-regs) have been shown to play an important role in maintaining peripheral immune homeostasis by suppressing autoreactive and allergen-specific T cells and turning off the immune response after the pathogen has been cleared. However, in certain situations T-regs can impair effective immunity to some pathogens and tumour cells. Objective: To review the role of T-regs in liver pathology and to assess the potential to enhance or inhibit their function as applied to the treatment of liver disease. Methods: The literature was reviewed using standard indexing terms and incorporating publications up to and including those published in 2007. Results/conclusions: T-regs are therapeutic targets for modulation in autoimmune disease and may provide new opportunities for application to human liver conditions.
C1 [Zheng, Ming-Hua; Gu, Dian-Na; Chen, Yong-Ping] First Affiliated Hosp, Wenzhou Med Coll, Dept Infect & Liver Dis, Wenzhou 325000, Zhejiang, Peoples R China.
[Braddock, Martin; Leishman, Andrew J.] AstraZeneca R&D Charnwood, Discovery Biosci, Loughborough LE11 5RH, Leics, England.
[Jin, Chang] Wenzhou Med Coll, Sch Optometry & Ophthalmol, Wenzhou 325000, Zhejiang, Peoples R China.
[Wen, Jin-Sheng] Wenzhou Med Coll, Dept Microbiol & Immunol, Wenzhou 325000, Zhejiang, Peoples R China.
[Gong, Yue-Wen] Univ Manitoba, Fac Pharm, Winnipeg, MB R3T 2N2, Canada.
C3 Wenzhou Medical University; AstraZeneca; Wenzhou Medical University;
Wenzhou Medical University; University of Manitoba
RP Chen, YP (corresponding author), First Affiliated Hosp, Wenzhou Med Coll, Dept Infect & Liver Dis, Wenzhou 325000, Zhejiang, Peoples R China.
EM ypchen77@hotmail.com
RI Gong, Yuewen/ABA-5742-2020
OI Zheng, Ming-Hua/0000-0003-4984-2631; Gong, Yuewen/0000-0001-7929-1979;
Leishman, Andrew/0000-0003-4273-8188
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NR 183
TC 6
Z9 8
U1 0
U2 4
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1472-8222
EI 1744-7631
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD MAR
PY 2008
VL 12
IS 3
BP 313
EP 326
DI 10.1517/14728222.12.3.313
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 274VP
UT WOS:000254031200006
PM 18269341
DA 2025-01-07
ER
PT J
AU Sapmaz, F
Kalkan, IH
Kisa, Ü
Guliter, S
AF Sapmaz, Ferdane
Kalkan, Ismail H.
Kisa, Ucler
Guliter, Sefa
TI A very rare cause of markedly elevated CA 19.9: Autoimmune hepatitis
SO ACTA CLINICA BELGICA
LA English
DT Article
DE Autoimmune hepatitis; CA19; 9; Elevated; Benign disease
ID DIFFERENTIAL-DIAGNOSIS; ANTIGEN; CANCER; CA19-9; BENIGN
AB Carbohydrate antigen 19.9 (CA 19.9) is a specific tumour marker of the biliary, pancreatic and gastrointestinal tracts. Autoimmune hepatitis is a chronic immune-mediated liver disorder characterised by female predominance. We report a case of approximately 30-fold increased serum CA 19.9 in a 57-year-old woman who was diagnosed with autoimmune hepatitis. She had no evidence of any malignant disease in pancreatobiliary or gastrointestinal tracts. CA 19.9 levels decreased to normal levels with immunosuppressive treatment. Markedly elevated serum CA 19.9 levels might be encountered with benign liver diseases such as autoimmune hepatitis.
C1 [Sapmaz, Ferdane; Kalkan, Ismail H.; Kisa, Ucler; Guliter, Sefa] Kirikkale Univ, Dept Gastroenterol, Fac Med, Kirikkale, Turkey.
[Kisa, Ucler] Kirikkale Univ, Dept Biochem, Fac Med, Kirikkale, Turkey.
C3 Kirikkale University; Kirikkale University
RP Sapmaz, F (corresponding author), Kirikkale Univ, Fac Med, Dept Gastroenterol, Kirikkale Univ Kampusu Ankara Yolu 7 Km, TR-71450 Kirikkale, Turkey.
EM ferda-sapmaz@hotmail.com
RI KISA, UCLER/V-5443-2017
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NR 13
TC 0
Z9 0
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1784-3286
EI 2295-3337
J9 ACTA CLIN BELG
JI Acta Clin. Belg.
PD OCT
PY 2016
VL 71
IS 5
BP 331
EP 333
DI 10.1080/17843286.2015.1115601
PG 3
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DX8XF
UT WOS:000384674200012
PM 27098926
DA 2025-01-07
ER
PT J
AU Graziadei, I
Zoller, H
Fickert, P
Schneeberger, S
Finkenstedt, A
Peck-Radosavljevic, M
Müller, H
Kohl, C
Sperner-Unterweger, B
Eschertzhuber, S
Hofer, H
Öfner, D
Tilg, H
Vogel, W
Trauner, M
Berlakovich, G
AF Graziadei, Ivo
Zoller, Heinz
Fickert, Peter
Schneeberger, Stefan
Finkenstedt, Armin
Peck-Radosavljevic, Markus
Mueller, Helmut
Kohl, Claudia
Sperner-Unterweger, Barbara
Eschertzhuber, Stephan
Hofer, Harald
Oefner, Dietmar
Tilg, Herbert
Vogel, Wolfgang
Trauner, Michael
Berlakovich, Gabriela
TI Indications for liver transplantation in adults
SO WIENER KLINISCHE WOCHENSCHRIFT
LA English
DT Article
DE Liver cirrhosis; Acute liver failure; Hepatocellular carcinoma;
Cholangiocellular carcinoma; Chronic hepatitis
ID PRIMARY SCLEROSING CHOLANGITIS; RECURRENT HEPATITIS-C;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; INTRAHEPATIC
CHOLANGIOCARCINOMA; HEREDITARY HEMOCHROMATOSIS; SLEEVE GASTRECTOMY;
NATURAL-HISTORY; WILSON-DISEASE; SURVIVAL
AB Liver transplantation has emerged as an established and well-accepted therapeutic option for patients with acute and chronic liver failure and hepatocellular carcinoma. The disproportion between recipients and donors is still an ongoing problem that has only been solved partially over the last centuries. For several patients no life-saving organs can be distributed. Therefore, objective and internationally established recommendations regarding indication and organ allocation are imperative. The aim of this article is to establish evidence-based recommendations regarding the evaluation and assessment of adult candidates for liver transplantation. This publication is the first Austrian consensus paper issued and approved by the Austrian Society of Gastroenterology and Hepatology in cooperation with the Austrian Society of Transplantation, Infusion and Genetics.
C1 [Graziadei, Ivo] Acad Teaching Hosp Hall IT, Dept Internal Med, Milserstr 10, A-6060 Hall In Tirol, Austria.
[Graziadei, Ivo; Zoller, Heinz; Finkenstedt, Armin; Vogel, Wolfgang] Med Univ Innsbruck, Dept Internal Med 2, Innsbruck, Austria.
[Fickert, Peter] Med Univ Graz, Dept Gastroenterol & Hepatol, Graz, Austria.
[Schneeberger, Stefan; Oefner, Dietmar] Med Univ Innsbruck, Dept Visceral Transplant & Thorax Surg, Innsbruck, Austria.
[Peck-Radosavljevic, Markus; Hofer, Harald; Trauner, Michael] Med Univ Vienna, Dept Internal Med 3, Div Gastroenterol & Hepatol, Vienna, Austria.
[Mueller, Helmut] Med Univ Graz, Dept Transplant Surg, Graz, Austria.
[Kohl, Claudia; Sperner-Unterweger, Barbara] Med Univ Innsbruck, Dept Psychiat, Innsbruck, Austria.
[Eschertzhuber, Stephan] Med Univ Innsbruck, Dept Anesthesiol & Intens Care Med, Innsbruck, Austria.
[Tilg, Herbert] Med Univ Innsbruck, Dept Internal Med 1, Innsbruck, Austria.
[Berlakovich, Gabriela] Med Univ Vienna, Dept Transplantat, Vienna, Austria.
C3 Medical University of Innsbruck; Medical University of Graz; Medical
University of Innsbruck; Medical University of Vienna; Medical
University of Graz; Medical University of Innsbruck; Medical University
of Innsbruck; Medical University of Innsbruck; Medical University of
Vienna
RP Graziadei, I (corresponding author), Acad Teaching Hosp Hall IT, Dept Internal Med, Milserstr 10, A-6060 Hall In Tirol, Austria.
EM ivo.graziadei@tirol-kliniken.at
RI Öfner, Dietmar/JJF-9514-2023; Schneeberger, Stefan/S-9329-2019;
Trauner, Michael/HCH-4032-2022; Tilg, Herbert/AEO-9569-2022; Zoller,
Heinz/AAD-7225-2019
OI Trauner, Michael/0000-0002-1275-6425; Sperner-Unterweger,
Barbara/0000-0001-8936-676X; Berlakovich, Gabriela/0000-0001-8850-7874
FU University of Innsbruck; Medical University of Innsbruck
FX Open access funding provided by University of Innsbruck and Medical
University of Innsbruck.
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NR 68
TC 37
Z9 40
U1 0
U2 4
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0043-5325
EI 1613-7671
J9 WIEN KLIN WOCHENSCHR
JI Wien. Klin. Wochen.
PD OCT
PY 2016
VL 128
IS 19-20
BP 679
EP 690
DI 10.1007/s00508-016-1046-1
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DY8GM
UT WOS:000385367100001
PM 27590261
OA Green Published
DA 2025-01-07
ER
PT J
AU Gieseler, RK
Schreiter, T
Canbay, A
AF Gieseler, Robert K. K.
Schreiter, Thomas
Canbay, Ali
TI The Aging Human Liver: The Weal and Woe of Evolutionary Legacy
SO ZEITSCHRIFT FUR GASTROENTEROLOGIE
LA English
DT Review
DE liver regeneration; inflammaging; biotransformation; nonalcoholic fatty
liver disease; hepatocellular carcinoma; Horvath clock
ID EPIDERMAL-GROWTH-FACTOR; PARTIAL-HEPATECTOMY; BRUNNERS GLANDS; CELL;
AGE; REGENERATION; ACTIVATION; MICROBIOME; FIBROSIS; DISEASE
AB Aging is characterized by the progressive decline of biological integrity and its compensatory mechanisms as well as immunological dysregulation. This goes along with an increasing risk of frailty and disease. Against this background, we here specifically focus on the aging of the human liver. For the first time, we shed light on the intertwining evolutionary underpinnings of the liver's declining regenerative capacity, the phenomenon of inflammaging, and the biotransformation capacity in the process of aging. In addition, we discuss how aging influences the risk for developing nonalcoholic fatty liver disease, hepatocellular carcinoma, and/or autoimmune hepatitis, and we describe chronic diseases as accelerators of biological aging.
C1 [Gieseler, Robert K. K.; Schreiter, Thomas; Canbay, Ali] Univ klinikum Knappschaftskrankenhaus Bochum GmbH, Med Klin, Bochum, Germany.
[Gieseler, Robert K. K.] Univ klinikum Knappschaftskrankenhaus Bochum GmbH, Med Klin, Schornau 23-25, D-44892 Bochum, Germany.
C3 Ruhr University Bochum; Ruhr University Bochum
RP Gieseler, RK (corresponding author), Univ klinikum Knappschaftskrankenhaus Bochum GmbH, Med Klin, Schornau 23-25, D-44892 Bochum, Germany.
EM rk.gieseler@gmx.de
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NR 121
TC 4
Z9 4
U1 0
U2 2
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0044-2771
EI 1439-7803
J9 Z GASTROENTEROL
JI Z. Gastroent.
PD JAN
PY 2023
VL 61
IS 01
BP 83
EP 94
DI 10.1055/a-1955-5297
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 9J3WH
UT WOS:000940120800023
PM 36623546
OA Bronze
DA 2025-01-07
ER
PT J
AU Miyake, Y
Yamamoto, K
AF Miyake, Yasuhiro
Yamamoto, Kazuhide
TI Current status of autoimmune hepatitis in Japan
SO ACTA MEDICA OKAYAMA
LA English
DT Review
DE autoimmune hepatitis; epidemiology; pathogenesis; diagnosis; prognosis
ID CHRONIC ACTIVE HEPATITIS; SOLUBLE LIVER ANTIGEN; REGULATORY T-CELLS;
BILE-DUCT INJURY; CLINICAL-FEATURES; SCORING SYSTEM;
HEPATOCELLULAR-CARCINOMA; CORTICOSTEROID-THERAPY; SUSCEPTIBLE
INDIVIDUALS; SCLEROSING CHOLANGITIS
AB Autoimmune hepatitis (AIH) is a chronic and progressive disease characterized by histological interface hepatitis, hypergammaglobulinemia, and circulating autoantibodies. Multiple factors, including molecular mimicry, a genetic background including major histocompatibility complex class 11, and defective function of regulatory T-cells, are involved in the pathogenesis. The diagnosis is made based on the scoring system of the International Autoimmune Hepatitis Group, the sensitivity and specificity of which are > 90%, respectively. AIH is classified into 3 sub-types based on the profiles of circulating autoantibodies: anti-nuclear antibody and/or smooth muscle anti body-positive (type 1), anti-liver-kidney microsomal antibody-positive (type 2), and anti-soluble liver antigen/liver-pancreas antigen antibody-positive (type 3). Recently, however, the number of atypical cases lacking the usual features has increased-for example, patients with acute-onset or fulminant-type AIH, autoantibody-negative patients, male patients, and patients with bile duct injury-and thus the clinical features of AIH have been diversified. AIH is responsive to immunosuppressive treatment in most cases; however, relapse occurs in more than 80% of patients within I year after immunosuppressive treatment withdrawal. The 10-year survival rate and the 10-year hepatocellular carcinoma-free rate are > 90%, respectively, indicating that some patients reach liver failure or develop hepatocellular carcinoma. To improve the prognosis of these patients, persistent normalization of transaminase is required.
C1 [Miyake, Yasuhiro; Yamamoto, Kazuhide] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Gastroenterol & Hepatol, Okayama 7008558, Japan.
C3 Okayama University
RP Miyake, Y (corresponding author), Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Gastroenterol & Hepatol, Okayama 7008558, Japan.
EM miyake43@md.okayama-u.ac.jp
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NR 81
TC 11
Z9 12
U1 0
U2 0
PU OKAYAMA UNIV MED SCHOOL
PI OKAYAMA
PA EDITORIAL OFFICE, ACTA MEDICA OKAYAMA OKAYAMA UNIVERSITY MEDICAL SCHOOL
2-5-1 SHIKATA-CHO, KITA-KU, OKAYAMA, 700-8558, JAPAN
SN 0386-300X
J9 ACTA MED OKAYAMA
JI Acta Med. Okayama
PD AUG
PY 2008
VL 62
IS 4
BP 217
EP 226
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 340YM
UT WOS:000258680900001
PM 18766204
DA 2025-01-07
ER
PT J
AU Kemmer, N
Neff, GW
AF Kemmer, Nyingi
Neff, Guy W.
TI Ethnic variations in chronic liver diseases
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE ethnicity; liver disease; race
ID HEPATITIS-C VIRUS; NONALCOHOLIC FATTY LIVER; 3RD NATIONAL-HEALTH;
UNITED-STATES; RACIAL-DIFFERENCES; B-VIRUS; HEPATOCELLULAR-CARCINOMA;
AUTOIMMUNE HEPATITIS; METABOLIC SYNDROME; AFRICAN-AMERICANS
AB Chronic liver disease is a major source of morbidity and mortality in the United States today. There is little information on the interethnic variation in the clinical presentation, therapeutic responses and prognosis of individuals with liver disease. This review will discuss the ethnic variations and implications of the most common liver diseases.
C1 [Kemmer, Nyingi; Neff, Guy W.] Univ Cincinnati, Med Ctr, Cincinnati, OH 45267 USA.
C3 University System of Ohio; University of Cincinnati
RP Kemmer, N (corresponding author), Univ Cincinnati, Med Ctr, 231 Albert Sabin Way,MSB Room 6363, Cincinnati, OH 45267 USA.
EM Nyingi.Kemmer@uc.edu
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NR 85
TC 9
Z9 10
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD MAY
PY 2008
VL 53
IS 5
BP 1339
EP 1344
DI 10.1007/s10620-007-9992-0
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 286LU
UT WOS:000254848200026
PM 17934812
DA 2025-01-07
ER
PT J
AU Padgett, KA
Lan, RY
Leung, PC
Lleo, A
Dawson, K
Pfeiff, J
Mao, TK
Coppel, RL
Ansari, AA
Gershwin, ME
AF Padgett, Kerstien A.
Lan, Ruth Y.
Leung, Patrick C.
Lleo, Ana
Dawson, Kevin
Pfeiff, Janice
Mao, Tin K.
Coppel, Ross L.
Ansari, Aftab A.
Gershwin, M. Eric
TI Primary biliary cirrhosis is associated with altered hepatic microRNA
expression
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Autoimmune liver diseases; MicroRNA; Primary biliary cirrhosis
ID HUMAN HEPATOCELLULAR-CARCINOMA; GENE-EXPRESSION; BIOLOGICAL NETWORKS;
CYTOSCAPE PLUGIN; AUTOIMMUNITY; CELLS; DISEASE; TIME; ANTIGEN;
IDENTIFICATION
AB MicroRNAs (miRNAs) are small RNA molecules that negatively regulate protein coding gene expression and are thought to play a critical role in many biological processes. Aberrant levels of miRNAs have been associated with numerous diseases and cancers, and as such, miRNAs have gain much interests as diagnostic biomarkers, and as therapeutic targets. However, their role in autoimmunity is largely unknown. The aims of this study are to: (1) identify differentially expressed miRNAs in human primary biliary cirrhosis (PBC); (2) validate these independently; and (3) identify potential targets of differentially expressed miRNAs. We compared the expression of 377 miRNAs in explanted livers form subjects with PBC versus controls with normal liver histology. A total of 35 independent miRNAs were found to be differentially expressed in PBC (p < 0.001). Quantitative PCR was employed to validate down-regulation of microRNA-122a (miR-122a) and miR-26a and the increased expression of miR-328 and miR-299-5p. The predicted targets of these miRNAs are known to affect cell proliferation, apoptosis, inflammation, oxidative stress, and metabolism. Our data are the first to demonstrate that PBC is characterized by altered expression of hepatic miRNA; however additional studies are required to demonstrate a causal link between those miRNA and the development of PBC. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Gershwin, M. Eric] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Sch Med, Genome & Biomed Sci Facil,Dept Internal Med, Davis, CA 95616 USA.
[Padgett, Kerstien A.] Univ Calif Davis, Dept Med Microbiol & Immunol, Davis, CA 95616 USA.
[Dawson, Kevin] Univ Calif Davis, Ctr Excellence Nutr Genom, Davis, CA 95616 USA.
[Pfeiff, Janice] Univ Calif Davis, Sch Vet Med, Arraycore Facil, Davis, CA 95616 USA.
[Mao, Tin K.] Tacere Therapeut, San Jose, CA USA.
[Coppel, Ross L.] Monash Univ, Dept Med Microbiol, Melbourne, Vic 3004, Australia.
[Ansari, Aftab A.] Emory Univ, Sch Med, Dept Pathol, Atlanta, GA 30322 USA.
C3 University of California System; University of California Davis;
University of California System; University of California Davis;
University of California System; University of California Davis;
University of California System; University of California Davis; Monash
University; Emory University
RP Gershwin, ME (corresponding author), Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Sch Med, Genome & Biomed Sci Facil,Dept Internal Med, 451 Hlth Sci Dr,Suite 6510, Davis, CA 95616 USA.
EM megershwin@ucdavis.edu
RI Coppel, Ross/A-6626-2008; LLEO, Ana/AAA-5759-2019
OI Coppel, Ross/0000-0002-4476-9124; LLEO, Ana/0000-0002-0561-7902
FU National Institutes of Health [DK 39588]; NCMHD/NIH [P60/MD00222]
FX This work was supported by National Institutes of Health Grant DK 39588
and NCMHD/NIH P60/MD00222.
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NR 52
TC 173
Z9 195
U1 0
U2 8
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD MAY-JUN
PY 2009
VL 32
IS 3-4
SI SI
BP 246
EP 253
DI 10.1016/j.jaut.2009.02.022
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 451ZV
UT WOS:000266510300015
PM 19345069
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Mansueto, P
Patti, AM
Seidita, A
D'Alcamo, A
Adragna, F
Di Stefano, L
Drago, G
Passiglia, F
Zappalà, F
Affronti, M
Rini, G
AF Mansueto, Pasquale
Patti, Angelo Maria
Seidita, Aurelio
D'Alcamo, Alberto
Adragna, Floriana
Di Stefano, Laura
Drago, Giuseppe
Passiglia, Francesco
Zappala, Francesco
Affronti, Marco
Rini, Giovambattista
TI AUTOIMMUNE LIVER DISEASE IN A SICILIAN WOMAN
SO ACTA MEDICA MEDITERRANEA
LA English
DT Article
DE autoimmune hepatitis; autoantibodies; corticosteroids
ID CLINICAL CHALLENGES; HEPATITIS; MANAGEMENT; DIAGNOSIS
AB Autoimmune hepatitis (AIH) is a chronic liver disease characterized by clinical features analogue to viral and non-autoimmune liver disorders, but with distinct sero-autoimmunologic properties. The disease results from a network of complex interactions involving genetic predisposition, triggering factors, autoantigens and immunoregulatory system. Diagnosis of AIH relies on positive autoantibodies determination and on liver core biopsy histological appearance. Corticosteroid and immunosuppressive drugs are generally useful in the treatment of disease. However, when inflammation cannot be controlled, progression from chronic hepatitis to cirrhosis is often observed and hepatocellular carcinoma may appear at the end stage. Here we reported a case of a woman, affected with AIH. The patient presented features of chronic liver disease of neither viral nor alcoholic aetiology. Serum evidence of hypertraminasemia, hypergammaglobulinemia and specific autoantibodies were the leading points to final diagnosis, which was validated by liver biopsy. The patient was, finally, successfully treated with steroids.
C1 [Mansueto, Pasquale; Patti, Angelo Maria; Seidita, Aurelio; D'Alcamo, Alberto; Adragna, Floriana; Di Stefano, Laura; Drago, Giuseppe; Passiglia, Francesco; Zappala, Francesco; Affronti, Marco; Rini, Giovambattista] Univ Hosp Palermo, Dept Internal & Specialist Med, Palermo, Italy.
C3 University of Palermo; Policlinico Paolo Giaccone
RP Mansueto, P (corresponding author), Azienda Osped Univ Policlin P Giaccone, Dipartimento Med Clin & Patol Emergenti, Via Vespro 141, I-90127 Palermo, Italy.
RI Passiglia, Francesco/AAC-7794-2022; Mansueto, Pasquale/K-3458-2016;
Seidita, Aurelio/IQT-5629-2023; Affronti, Marco/IQT-5717-2023
OI Seidita, Aurelio/0000-0003-4080-2641; Affronti,
Marco/0009-0008-0136-5518
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NR 25
TC 0
Z9 0
U1 0
U2 0
PU CARBONE EDITORE
PI PALERMO
PA VIA QUINTINO SELLA, 68, PALERMO, 90139, ITALY
SN 0393-6384
EI 2283-9720
J9 ACTA MEDICA MEDITERR
JI Acta Medica Mediterr.
PY 2012
VL 28
IS 1
BP 13
EP 18
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 970UK
UT WOS:000306157600002
DA 2025-01-07
ER
PT J
AU Hrad, V
Abebe, Y
Ali, SH
Velgersdyk, J
Al Hallak, M
Imam, M
AF Hrad, Valery
Abebe, Yoftahe
Ali, Syed Haris
Velgersdyk, Jared
Al Hallak, Mohammed
Imam, Mohamad
TI Risk and Surveillance of Cancers in Primary Biliary Tract Disease
SO GASTROENTEROLOGY RESEARCH AND PRACTICE
LA English
DT Review
ID PRIMARY SCLEROSING CHOLANGITIS; CONFOCAL LASER ENDOMICROSCOPY;
TERM-FOLLOW-UP; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
EXTRAHEPATIC MALIGNANCIES; ULCERATIVE-COLITIS; INTRAHEPATIC
CHOLANGIOCARCINOMA; PERORAL CHOLANGIOSCOPY; COLORECTAL NEOPLASIA
AB Primary biliary diseases have been associated in several studies with various malignancies. Understanding the risk and optimizing surveillance strategy of these malignancies in this specific subset of patients are an important facet of clinical care. For instance, primary sclerosing cholangitis is associated with an increased risk for cholangiocarcinoma (which is very challenging to diagnose) and when IBD is present for colorectal cancer. On the other hand, primary biliary cirrhosis patients with cirrhosis or not responding to 12 months of ursodeoxycholic acid therapy are at increased risk of hepatocellular carcinoma. In this review we will discuss in detail the risks and optimal surveillance strategies for patients with primary biliary diseases.
C1 [Hrad, Valery; Abebe, Yoftahe; Ali, Syed Haris; Velgersdyk, Jared; Imam, Mohamad] Univ N Dakota, Dept Internal Med, Fargo, ND 58102 USA.
[Al Hallak, Mohammed] MD Anderson Canc Ctr, Dept Gen Internal Med, Houston, TX 77030 USA.
C3 University of North Dakota Grand Forks; University of Texas System; UTMD
Anderson Cancer Center
RP Imam, M (corresponding author), Univ N Dakota, Dept Internal Med, Fargo, ND 58102 USA.
EM mohamad.imam@sanfordhealth.org
OI Al Hallak, Mohammed/0000-0002-4598-8177
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NR 104
TC 10
Z9 10
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1687-6121
EI 1687-630X
J9 GASTROENT RES PRACT
JI Gastroenterol. Res. Pract.
PY 2016
VL 2016
AR 3432640
DI 10.1155/2016/3432640
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DQ2YG
UT WOS:000379069000001
PM 27413366
OA Green Submitted, gold, Green Published
DA 2025-01-07
ER
PT J
AU Czaja, AJ
AF Czaja, A. J.
TI Review article: the management of autoimmune hepatitis beyond consensus
guidelines
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
ID ACTIVE LIVER-DISEASE; THIOPURINE METHYLTRANSFERASE ACTIVITY;
INFLAMMATORY-BOWEL-DISEASE; KIDNEY MICROSOME ANTIBODY; PRIMARY
BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; MYCOPHENOLATE-MOFETIL;
CORTICOSTEROID-THERAPY; CLINICAL-FEATURES; ALPHA-FETOPROTEIN
AB BackgroundConsensus guidelines aid in the diagnosis and management of autoimmune hepatitis, but they are frequently based on low-quality clinical evidence, conflicting experiences and divergent opinions. Recommendations may be weak, discrepant or non-existent at critical decision points.
AimsTo identify the decision points where guidelines are weak or non-existent and review the evidence essential in the decision process.
MethodsFull-text articles published in English using the keyword autoimmune hepatitis' were identified by PubMed from 1972 to 2013. Personal experience and investigations in autoimmune hepatitis also identified important contributions.
ResultsSeventy per cent of the guidelines developed by the American Association for the Study of Liver Diseases and 48% of those proposed by the British Society of Gastroenterology are based on low-quality evidence, conflicting experiences or divergent opinions. The key uncertainties in diagnosis relate to the timing of liver biopsy, recognising acute severe (fulminant) disease, interpreting coincidental nonclassical histological changes, accommodating atypical or deficient features in non-White patients, differentiating drug-induced from classical disease and identifying overlap syndromes. The key uncertainties in management relate to pre-treatment testing for thiopurine methyltransferase activity, treating asymptomatic mild disease, determining treatment end points, managing suboptimal responses, incorporating nonstandard medications as front-line and salvage agents, using azathioprine in pregnancy and instituting surveillance for hepatocellular carcinoma.
ConclusionsConsensus guidelines are fraught with uncertainties in the diagnosis and management of autoimmune hepatitis. Each decision point must counterbalance the current available evidence and tailor the application of this evidence to the individual patient.
C1 [Czaja, A. J.] Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Czaja, AJ (corresponding author), Mayo Clin, Coll Med, 200 1st St SW, Rochester, MN 55905 USA.
EM czaja.albert@mayo.edu
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NR 208
TC 43
Z9 44
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD AUG
PY 2013
VL 38
IS 4
BP 343
EP 364
DI 10.1111/apt.12381
PG 22
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 182VU
UT WOS:000321773700002
PM 23808490
DA 2025-01-07
ER
PT J
AU Bocedi, A
Noce, A
Marrone, G
Noce, G
Cattani, G
Gambardella, G
Di Lauro, M
Di Daniele, N
Ricci, G
AF Bocedi, Alessio
Noce, Annalisa
Marrone, Giulia
Noce, Gianluca
Cattani, Giada
Gambardella, Giorgia
Di Lauro, Manuela
Di Daniele, Nicola
Ricci, Giorgio
TI Glutathione Transferase P1-1 an Enzyme Useful in Biomedicine and as
Biomarker in Clinical Practice and in Environmental Pollution
SO NUTRIENTS
LA English
DT Review
DE glutathione; glutathione transferase; biomarker; cancer;
neurodegenerative disease; liver disease; hemodialysis; chronic kidney
disease; kidney transplantation; environmental pollution
ID AMYOTROPHIC-LATERAL-SCLEROSIS; GSTP1 GENE POLYMORPHISMS; S-TRANSFERASE;
ERYTHROCYTE GLUTATHIONE; OXIDATIVE STRESS; HEPATOCELLULAR-CARCINOMA; PI
EXPRESSION; POSITIVE COOPERATIVITY; PRENEOPLASTIC LESIONS; CATALYTIC
MECHANISM
AB Glutathione transferase P1-1 (GSTP1-1) is expressed in some human tissues and is abundant in mammalian erythrocytes (here termed e-GST). This enzyme is able to detoxify the cell from endogenous and exogenous toxic compounds by using glutathione (GSH) or by acting as a ligandin. This review collects studies that propose GSTP1-1 as a useful biomarker in different fields of application. The most relevant studies are focused on GSTP1-1 as a biosensor to detect blood toxicity in patients affected by kidney diseases. In fact, this detoxifying enzyme is over-expressed in erythrocytes when unusual amounts of toxins are present in the body. Here we review articles concerning the level of GST in chronic kidney disease patients, in maintenance hemodialysis patients and to assess dialysis adequacy. GST is also over-expressed in autoimmune disease like scleroderma, and in kidney transplant patients and it may be used to check the efficiency of transplanted kidneys. The involvement of GSTP in the oxidative stress and in other human pathologies like cancer, liver and neurodegenerative diseases, and psychiatric disorders is also reported. Promising applications of e-GST discussed in the present review are its use for monitoring human subjects living in polluted areas and mammals for veterinary purpose.
C1 [Bocedi, Alessio; Cattani, Giada; Gambardella, Giorgia; Ricci, Giorgio] Univ Roma Tor Vergata, Dept Chem Sci & Technol, Via Ric Sci 1, I-00133 Rome, Italy.
[Noce, Annalisa; Marrone, Giulia; Di Lauro, Manuela; Di Daniele, Nicola] Univ Roma Tor Vergata, UOC Internal Med Ctr Hypertens & Nephrol, Dept Syst Med, Via Montpellier 1, I-00133 Rome, Italy.
[Marrone, Giulia] Univ Roma Tor Vergata, PhD Sch Appl Med Surg Sci, Via Montpellier 1, I-00133 Rome, Italy.
[Noce, Gianluca] Univ Roma Tor Vergata, Dept Biomed & Prevent, Sect Legal Med Social Secur & Forens Toxicol, Via Montpellier 1, I-00133 Rome, Italy.
C3 University of Rome Tor Vergata; University of Rome Tor Vergata;
University of Rome Tor Vergata; University of Rome Tor Vergata
RP Ricci, G (corresponding author), Univ Roma Tor Vergata, Dept Chem Sci & Technol, Via Ric Sci 1, I-00133 Rome, Italy.
EM riccig@uniroma2.it
RI Marrone, Giulia/IQR-7760-2023; Noce, Annalisa/B-5558-2019; Di Lauro,
Manuela/AAB-9784-2022
OI Cattani, Giada/0000-0002-6217-2209; Di Lauro,
Manuela/0000-0001-8118-1330; Marrone, Giulia/0000-0002-5854-2086; NOCE,
ANNALISA/0000-0003-1310-3730
FU University of Rome Tor Vergata [2817/2016]; Federazione Medico Sportiva
Italiana
FX This research was funded by University of Rome Tor Vergata Grant
Mission: Sustainability (Decreto Rettorale 2817/2016) to A.B.;
Federazione Medico Sportiva Italiana by a financial support to N.D.D.
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NR 196
TC 50
Z9 52
U1 2
U2 14
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD AUG
PY 2019
VL 11
IS 8
AR 1741
DI 10.3390/nu11081741
PG 34
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA IV8HH
UT WOS:000484506000051
PM 31357662
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Chalasani, N
AF Chalasani, N
TI Statins and hepatotoxicity: Focus on patients with fatty liver
SO HEPATOLOGY
LA English
DT Article
ID LIPID-LOWERING DRUGS; NONALCOHOLIC STEATOHEPATITIS; AUTOIMMUNE
HEPATITIS; DIABETES-MELLITUS; CLINICAL-TRIALS; UNITED-STATES; DISEASE;
PRAVASTATIN; CANCER; SAFETY
C1 Indiana Univ, Sch Med, Indianapolis, IN 46202 USA.
C3 Indiana University System; Indiana University Indianapolis
RP Indiana Univ, Sch Med, 1001 W 10th St,WD OPW 2005, Indianapolis, IN 46202 USA.
EM nchalasa@iupui.edu
FU NIDDK NIH HHS [U01 DK065211] Funding Source: Medline
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*WWW DRUGTOPICS CO, PHARM FACTS FIG
NR 49
TC 211
Z9 233
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD APR
PY 2005
VL 41
IS 4
BP 690
EP 695
DI 10.1002/hep.20671
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 911MD
UT WOS:000228006000001
PM 15789367
OA Bronze
DA 2025-01-07
ER
PT J
AU Shen, XH
Li, N
Li, H
Zhang, T
Wang, F
Li, QA
AF Shen, Xiaohong
Li, Na
Li, Hui
Zhang, Ti
Wang, Feng
Li, Qiang
TI Increased prevalence of regulatory T cells in the tumor microenvironment
and its correlation with TNM stage of hepatocellular carcinoma
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Hepatocellular carcinoma; Regulatory T cell; Tumor microenvironment
ID TRANSCRIPTION FACTOR FOXP3; PERIPHERAL-BLOOD; AUTOIMMUNE-DISEASE;
SUBPOPULATION; EXPRESSION; TOLERANCE; RATES
AB Few detailed studies about the correlations among the expanded prevalence, elevated function of Treg cells in tumor microenvironment of hepatocellular carcinoma (HCC), and different clinical tumor stage were reported. The purpose of the present study was to examine the presence and functions of CD4(+)CD25(high) regulatory T cell (Treg cell) in tumor microenvironment from early and late stages and reveal the potential underlying mechanisms that may be responsible.
The prevalence of Treg in peripheral blood and fresh tissue samples from 31 patients with HCC after radical hepatectomy and 9 controls was detected. CD127 was selected as a Treg cell maker to test the cell populations and compared its expressions with ICOS. The expressions of FOXP3 mRNA were analyzed. The migration, proliferation, and suppression functions of Treg cell were observed. IFN-gamma., IL-10, TGF-, CCL-17, CCL-22, and SDF-1 in cell supernatant were detected. Among all of the tests, the relations among the different TNM tumor stages, populations, and functions of Treg cells were evaluated.
The prevalence of Treg cell was significantly higher in the peripheral blood and in tumor tissue compared with those in normal donors. Increased numbers of Treg cell were showed in peripheral blood as well as in tumor tissue. High levels of IL-10 and TGF-, but little IFN-gamma, were detected in the tumor microenvironment. Treg cells potently suppressed the functions and proliferation of CD4(+)CD25(-) T cells. High levels of SDF-1 were detected in malignant biopsies compared with those in benign regions, significantly increased in stage III. Plasma from the same patient was able to chemoattract Treg cell but that was lesser extent than those in tumor supernatant. Also, supernatant in advanced stage tumors exhibited powerful chemoattractic activity. SDF-1 played an important role in the recruited functions of Treg cell into tumor microenvironment of early and advanced stages. The expressions of Foxp3 mRNA increased in different TNM stages. The increased prevalence and expanded function of Treg cells in the tumor microenvironment of HCC were correlated with the cancer stage.
The increase in frequency of Treg cells might play a role in modulation of the immune response against HCC in different TNM stages. The substance secreted in tumor microenvironment recruited CD4(+)CD25(+) Treg cells to tumor sites to contribute to the prosperity and growth of the tumors. The performance of Treg cells in different TNM stages of tumor microenvironment might be acted as the route to evaluate the immunotherapy-based methods, promote therapy effect, and consequently to increase the survival rate in HCC.
C1 [Li, Qiang] Tianjin Med Univ, Canc Hosp, Dept Hepatobiliary, Tianjin 300060, Peoples R China.
[Shen, Xiaohong; Li, Na] Nankai Univ, Sch Med, Tianjin 300071, Peoples R China.
[Li, Hui] Tianjin Med Univ, Canc Hosp, Dept Immunol, Tianjin 300060, Peoples R China.
[Zhang, Ti; Wang, Feng] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
C3 Tianjin Medical University; Nankai University; Tianjin Medical
University; University of Texas System; UTMD Anderson Cancer Center
RP Li, QA (corresponding author), Tianjin Med Univ, Canc Hosp, Dept Hepatobiliary, Tianjin 300060, Peoples R China.
EM liqiang4016@yahoo.cn
RI LI, NA/G-4083-2015; Cai, Lin/C-3286-2016; Li, Qiang/HGT-8278-2022
FU Department of Hepatobiliary Surgery, Cancer Hospital of Tianjin Medical
University
FX This study was funded by: supported by the department of Hepatobiliary
Surgery, Cancer Hospital of Tianjin Medical University with the patients
collection and providing samples. The authors thank department of
Clinical Immunology, Cancer Research Institute of Tianjin Medical
University and Department of Pathology, University of Texas M. D.
Anderson Cancer Center for their technical support.
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NR 24
TC 79
Z9 91
U1 0
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0171-5216
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD NOV
PY 2010
VL 136
IS 11
BP 1745
EP 1754
DI 10.1007/s00432-010-0833-8
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 654QS
UT WOS:000282183700014
PM 20221638
DA 2025-01-07
ER
PT J
AU Liu, LJ
Liao, JM
Zhu, F
AF Liu, Li-Juan
Liao, Jian-Ming
Zhu, Fan
TI Proliferating cell nuclear antigen clamp associated factor, a potential
proto-oncogene with increased expression in malignant gastrointestinal
tumors
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Proliferating cell nuclear antigen; Proliferating cell nuclear antigen
clamp associated factor; Transcript variant; Gastrointestinal cancers;
Signal pathway; Biological therapeutic
ID PCNA-ASSOCIATED FACTOR; HEPATOCELLULAR-CARCINOMA; MESSENGER-RNA;
KIAA0101 EXPRESSION; ESOPHAGEAL CANCER; PARK7 INTERACTOME;
PERIPHERAL-BLOOD; POOR-PROGNOSIS; GENE; PROTEIN
AB Gastrointestinal (GI) cancers, including malignancies in the gastrointestinal tract and accessory organs of digestion, represent the leading cause of death worldwide due to the poor prognosis of most GI cancers. An investigation into the potential molecular targets of prediction, diagnosis, prognosis, and therapy in GI cancers is urgently required. Proliferating cell nuclear antigen (PCNA) clamp associated factor (PCLAF), which plays an essential role in cell proliferation, apoptosis, and cell cycle regulation by binding to PCNA, is a potential molecular target of GI cancers as it contributes to a series of malignant properties, including tumorigenesis, epithelial-mesenchymal transition, migration, and invasion. Furthermore, PCLAF is an underlying plasma prediction target in colorectal cancer and liver cancer. In addition to GI cancers, PCLAF is also involved in other types of cancers and autoimmune diseases. Several pivotal pathways, including the Rb/E2F pathway, NF-kappa B pathway, and p53-p21 cascade, are implicated in PCLAF-mediated diseases. PCLAF also contributes to some diseases through dysregulation of the p53 pathway, WNT signal pathway, MEK/ERK pathway, and PI3K/AKT/mTOR signal cascade. This review mainly describes in detail the role of PCLAF in physiological status and GI cancers. The signaling pathways involved in PCLAF are also summarized. Suppression of the interaction of PCLAF/PCNA or the expression of PCLAF might be potential biological therapeutic strategies for GI cancers.
C1 [Liu, Li-Juan; Liao, Jian-Ming; Zhu, Fan] Wuhan Univ, Sch Med, Dept Med Microbiol, State Key Lab Virol, 185 Donghu Rd, Wuhan 430071, Hubei, Peoples R China.
[Liu, Li-Juan; Liao, Jian-Ming; Zhu, Fan] Wuhan Univ, Sch Med, Dept Med Microbiol, Hubei Prov Key Lab Allergy & Immunol, 185 Donghu Rd, Wuhan 430071, Hubei, Peoples R China.
[Liao, Jian-Ming] Wuhan Univ, Renmin Hosp, Dept Neurosurg, Wuhan 430060, Hubei, Peoples R China.
C3 Wuhan University; Wuhan University; Wuhan University
RP Zhu, F (corresponding author), Wuhan Univ, Sch Med, Dept Med Microbiol, State Key Lab Virol, 185 Donghu Rd, Wuhan 430071, Hubei, Peoples R China.; Zhu, F (corresponding author), Wuhan Univ, Sch Med, Dept Med Microbiol, Hubei Prov Key Lab Allergy & Immunol, 185 Donghu Rd, Wuhan 430071, Hubei, Peoples R China.
EM fanzhu@whu.edu.cn
RI Liao, Jian/GRX-4579-2022; zhu, fan/HMK-5557-2023
OI zhu, fan/0000-0001-7031-2956
FU National Natural Science Foundation of China [81971943, 81772196]; Hubei
Provincial Natural Science Foundation of China [2020CFB656]
FX Supported by the National Natural Science Foundation of China, No.
81971943 and No. 81772196; and the Hubei Provincial Natural Science
Foundation of China, No. 2020CFB656.
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NR 89
TC 7
Z9 7
U1 0
U2 6
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD OCT 15
PY 2021
VL 13
IS 10
BP 1425
EP 1439
DI 10.4251/wjgo.v13.i10.1425
PG 15
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA XB8VS
UT WOS:000721601200013
PM 34721775
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kavgaci, G
Sahin, TK
Sokmensuer, C
Balaban, HY
Aksoy, S
AF Kavgaci, Gozde
Sahin, Taha Koray
Sokmensuer, Cenk
Balaban, Hatice Yasemin
Aksoy, Sercan
TI Ribociclib-induced autoimmune-like hepatitis: a case report
SO JOURNAL OF CHEMOTHERAPY
LA English
DT Article; Early Access
DE Breast cancer; ribociclib; drug-induced liver injury; autoimmune-like
hepatitis
ID BREAST-CANCER; THERAPY; FULVESTRANT; PALBOCICLIB
AB Hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative breast cancer represents the most prevalent subtype of breast cancer. Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors, in combination with endocrine therapy (ET), have shown substantial benefits in improving progression-free survival and, for ribociclib, an overall survival advantage. Despite clinical benefits, ribociclib is associated with elevated liver enzymes and severe liver dysfunction. We present a 44-year-old Caucasian woman with HR-positive, HER2-negative metastatic breast cancer who developed drug-induced autoimmune-like hepatitis (DI-ALH) after ribociclib therapy. Initially treated for early-stage disease with surgery, chemotherapy, radiotherapy, and ET, she progressed to metastatic disease and received ribociclib, letrozole, and goserelin, achieving a partial response. Treatment was complicated by grade 3 hepatotoxicity, confirmed as DI-ALH by liver biopsy. Managed with prednisolone and azathioprine, ribociclib was reintroduced at a reduced dose and later escalated to full dose. This case report highlights the importance of a multidisciplinary approach to balance oncologic efficacy with hepatologic safety.
C1 [Kavgaci, Gozde; Sahin, Taha Koray; Aksoy, Sercan] Hacettepe Univ, Canc Inst, Dept Med Oncol, Mehmet Akif Ersoy Sk 19 A, TR-06230 Ankara, Turkiye.
[Sokmensuer, Cenk] Hacettepe Univ, Fac Med, Dept Pathol, Ankara, Turkiye.
[Balaban, Hatice Yasemin] Hacettepe Univ, Fac Med, Dept Gastroenterol, Ankara, Turkiye.
C3 Hacettepe University; Hacettepe University; Hacettepe University
RP Kavgaci, G (corresponding author), Hacettepe Univ, Canc Inst, Dept Med Oncol, Mehmet Akif Ersoy Sk 19 A, TR-06230 Ankara, Turkiye.
EM drgozdekavgaci@gmail.com
RI Sahin, Taha Koray/ABH-1748-2020
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NR 31
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1120-009X
EI 1973-9478
J9 J CHEMOTHERAPY
JI J. Chemother.
PD 2024 NOV 22
PY 2024
DI 10.1080/1120009X.2024.2433368
EA NOV 2024
PG 6
WC Oncology; Infectious Diseases; Pathology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Infectious Diseases; Pathology; Pharmacology & Pharmacy
GA N9I1T
UT WOS:001367378500001
PM 39610055
DA 2025-01-07
ER
PT J
AU Shalapy, NM
Liu, M
Kang, WY
AF Shalapy, Nashwa M.
Liu, Ming
Kang, Wenyi
TI Protective effects of hepatic diseases by bioactive phytochemicals in
Fusarium oxysporum - A review
SO HELIYON
LA English
DT Review
DE Fusarium oxysporum; Hepatic disorders; Alcoholic liver disease;
Non-alcoholic fatty liver disease; Liver inflammatory disease;
Cirrhosis; Oxidative stress; Fungal bioactive compounds; Therapeutic
effects; Efficacy
ID 2 ENDOPHYTIC STRAINS; CHEMICAL-CONSTITUENTS; ISOSORBIDE DINITRATE;
LIVER; ACID; NAPHTHOQUINONES; NANOPARTICLES; PURIFICATION; ANTIOXIDANT;
FUSARUSIDE
AB Lately, liver diseases were categorized as one of the most prevalent health problems globally as it causes a severe threat to mankind all over the world due to the wide range of occurrence. There are multiple factors causing hepatic disorders, such as alcohol, virus, poisons, adverse effects of drugs, poor diet, inherited conditions and obesity. Liver diseases have various types including alcoholic liver disease, non-alcoholic fatty liver disease, autoimmune hepatitis, liver cancer, hepatocellular carcinoma, liver fibrosis and hepatic inflammation. Therefore, it is imperative to find effective and efficacious agents in managing liver diseases. Fusarium oxysporum, an endophytic fungus and containing many bioactive compounds, could be served as a forked medication for enormous number and types of maladies. It was characterized by producing biochemical compounds which had rare pharmacological properties as it may be found in a limit number of other medicinal plants. The majority of the past researches related to Fusarium oxysporum recited the fungal negative field either on the pathogenic effects of the fungus on economical crops or on the fungal chemical components to know how to resist it. The present review will highlight on the bright side of Fusarium oxysporum and introduce the functional activities of its chemical compounds for treating its target diseases. The key point of illustrated studies in this article is displaying wide range of detected bioactive compounds isolated from Fusarium oxysporum and in other illustrated studies it was elucidated the therapeutical and pharmacological potency of these biologically active compounds (isolated from medicinal plants sources) against different types of liver diseases including non-alcoholic fatty liver disease, alcoholic liver disease, cirrhosis and others. It was demonstrated that F. oxysporum contains unique types of isoflavones, flavonoids, phenols and another active chemical compounds, and these compounds showed recently a fabulous clinical contribution in the therapy of liver injury diseases, which opens new and unprecedented way for evaluating the maintaining efficacy of Fusarium oxysporum bioactive compounds in dealing with hepatic complications and its remedy impacting on liver diseases and injured hepatocytes through recommending implement a practical study.
C1 [Shalapy, Nashwa M.; Liu, Ming; Kang, Wenyi] Henan Univ, Natl R&D Ctr Edible Fungus Proc Technol, Kaifeng 475004, Peoples R China.
[Shalapy, Nashwa M.] Natl Res Ctr, Biotechnol Res Inst, Microbial Chem Dept, Cairo, Egypt.
[Kang, Wenyi] Joint Int Res Lab Food & Med Resource Funct, Kaifeng 475004, Henan, Peoples R China.
C3 Henan University; Egyptian Knowledge Bank (EKB); National Research
Centre (NRC)
RP Shalapy, NM; Kang, WY (corresponding author), Henan Univ, Natl R&D Ctr Edible Fungus Proc Technol, Kaifeng 475004, Peoples R China.; Kang, WY (corresponding author), Joint Int Res Lab Food & Med Resource Funct, Kaifeng 475004, Henan, Peoples R China.
EM nashwa.mustafa410@yahoo.com; kangweny@hotmail.com
OI kang, wenyi/0000-0002-1822-6249; Shalapy, Nashwa/0000-0002-9605-8471
FU Research on Precision Nutrition and Health Food, Department of Science
and Technology of Henan Province [CXJD2021006]
FX The authors declare the following financial interests/personal
relationships which may be considered as potential competing in-terests:
Wenyi Kang reports financial support was provided by Research on
Precision Nutrition and Health Food, Department of Science and
Technology of Henan Province (CXJD2021006) . Wenyi Kang reports a
relationship with Research on Precision Nutrition and Health Food,
Department of Science and Technology of Henan Province (CXJD2021006) .
that includes: funding grants. There is no room for wrong interpretation
by the reader as conflict of interest.
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NR 99
TC 1
Z9 1
U1 10
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD MAR 15
PY 2024
VL 10
IS 5
AR e26562
DI 10.1016/j.heliyon.2024.e26562
EA MAR 2024
PG 18
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA NJ5W5
UT WOS:001200108400001
PM 38455549
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Chen, LJ
Zhang, N
Huang, YQ
Zhang, Q
Fang, YX
Fu, JM
Yuan, Y
Chen, L
Chen, X
Xu, ZY
Li, YF
Izawa, H
Xiang, C
AF Chen, Lijun
Zhang, Ning
Huang, Yuqi
Zhang, Qi
Fang, Yangxin
Fu, Jiamin
Yuan, Yin
Chen, Lu
Chen, Xin
Xu, Zhenyu
Li, Yifei
Izawa, Hiromi
Xiang, Charlie
TI Multiple Dimensions of using Mesenchymal Stem Cells for Treating Liver
Diseases: From Bench to Beside
SO STEM CELL REVIEWS AND REPORTS
LA English
DT Article
DE Cellular therapy; Clinical research; Liver diseases; Mesenchymal stem
cells; Regenerative medicine
ID HEPATIC STELLATE CELLS; EXPERIMENTAL AUTOIMMUNE HEPATITIS; HUMAN
ADIPOSE-TISSUE; STROMAL CELLS; HEPATOCELLULAR-CARCINOMA; IN-VITRO;
B-VIRUS; EXTRACELLULAR VESICLES; HEPATOCYTE DIFFERENTIATION;
THERAPEUTIC-EFFICACY
AB Liver diseases impose a huge burden worldwide. Although hepatocyte transplantation has long been considered as a potential strategy for treating liver diseases, its clinical implementation has created some obvious limitations. As an alternative strategy, cell therapy, particularly mesenchymal stem cell (MSC) transplantation, is widely used in treating different liver diseases, including acute liver disease, acute-on-chronic liver failure, hepatitis B/C virus, autoimmune hepatitis, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, alcoholic liver disease, liver fibrosis, liver cirrhosis, and hepatocellular carcinoma. Here, we summarize the status of MSC transplantation in treating liver diseases, focusing on the therapeutic mechanisms, including differentiation into hepatocyte-like cells, immunomodulating function with a variety of immune cells, paracrine effects via the secretion of various cytokines and extracellular vesicles, and facilitation of homing and engraftment. Some improved perspectives and current challenges are also addressed. In summary, MSCs have great potential in the treatment of liver diseases based on their multi-faceted characteristics, and more accurate mechanisms and novel therapeutic strategies stemming from MSCs will facilitate clinical practice.
C1 [Chen, Lijun; Zhang, Ning; Huang, Yuqi; Zhang, Qi; Fang, Yangxin; Fu, Jiamin; Yuan, Yin; Li, Yifei; Xiang, Charlie] Zhejiang Univ, Affiliated Hosp 1, Natl Clin Res Ctr Infect Dis, Natl Med Ctr Infect Dis,Sch Med,State Key Lab Diag, Hangzhou 310003, Zhejiang, Peoples R China.
[Chen, Lijun; Zhang, Ning; Huang, Yuqi; Zhang, Qi; Fang, Yangxin; Fu, Jiamin; Yuan, Yin; Li, Yifei; Xiang, Charlie] Chinese Acad Med Sci, Res Unit Infect Dis, Hangzhou 310003, Zhejiang, Peoples R China.
[Chen, Lijun; Zhang, Ning; Huang, Yuqi; Zhang, Qi; Fang, Yangxin; Fu, Jiamin; Yuan, Yin; Xiang, Charlie] Chinese Acad Med Sci, Res Unit Microecol, Hangzhou 310003, Zhejiang, Peoples R China.
[Chen, Lu; Xu, Zhenyu] Innovat Precis Med IPM Grp, Hangzhou 311215, Zhejiang, Peoples R China.
[Chen, Xin] Zhejiang Univ, Affiliated Hangzhou Peoples Hosp 1, Dept Hematol, Sch Med, Hangzhou 310027, Zhejiang, Peoples R China.
[Izawa, Hiromi] Jingugaien Woman Life Clin, Jingu Gaien 3-39-5 2F,Shibuya Ku, Tokyo, Japan.
C3 Zhejiang University; Chinese Academy of Medical Sciences - Peking Union
Medical College; Chinese Academy of Medical Sciences - Peking Union
Medical College; Zhejiang University
RP Xiang, C (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Natl Clin Res Ctr Infect Dis, Natl Med Ctr Infect Dis,Sch Med,State Key Lab Diag, Hangzhou 310003, Zhejiang, Peoples R China.; Xiang, C (corresponding author), Chinese Acad Med Sci, Res Unit Infect Dis, Hangzhou 310003, Zhejiang, Peoples R China.; Xiang, C (corresponding author), Chinese Acad Med Sci, Res Unit Microecol, Hangzhou 310003, Zhejiang, Peoples R China.
EM cxiang@zju.edu.cn
RI li, yifei/HJO-9520-2023; Zhenyu, Xu/AAW-7042-2020; Chen,
Lijun/AAV-2714-2021; huang, yuqi/HJI-9038-2023
OI Li, YiFei/0000-0001-9055-6034; Chen, Lijun/0000-0001-9374-6466
FU National Key Ramp;D Program of China [2022YFA1105603, 2022YFC2304405];
National Natural Science Foundation of China [81900563]; Hangzhou
Science and Technology Project [20200224]; Independent Task of State Key
Laboratory for Diagnosis and Treatment of Infectious Diseases;
Fundamental Research Funds for the Central Universities [2022ZFJH003];
CAMS Innovation Fund for Medical Sciences [2019-I2M-5045]
FX This work was supported by the National Key R&D Program of China
(2022YFA1105603 and 2022YFC2304405), the National Natural Science
Foundation of China (81900563), the Hangzhou Science and Technology
Project (20200224), the Independent Task of State Key Laboratory for
Diagnosis and Treatment of Infectious Diseases, the Fundamental Research
Funds for the Central Universities (2022ZFJH003), and CAMS Innovation
Fund for Medical Sciences (2019-I2M-5-045).
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NR 261
TC 7
Z9 7
U1 7
U2 21
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2629-3269
EI 2629-3277
J9 STEM CELL REV REP
JI Stem Cell Rev. Rep.
PD OCT
PY 2023
VL 19
IS 7
BP 2192
EP 2224
DI 10.1007/s12015-023-10583-5
EA JUL 2023
PG 33
WC Cell & Tissue Engineering; Cell Biology; Medicine, Research &
Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA U5AZ2
UT WOS:001038562500001
PM 37498509
DA 2025-01-07
ER
PT J
AU Bat-Erdene, O
Miura, K
Maeda, H
Watanabe, S
Tsukui, M
Takaoka, Y
Nomoto, H
Goka, R
Morimoto, N
Yamamoto, H
AF Bat-Erdene, Oyunjargal
Miura, Kouichi
Maeda, Hiroshi
Watanabe, Shunji
Tsukui, Mamiko
Takaoka, Yoshinari
Nomoto, Hiroaki
Goka, Rie
Morimoto, Naoki
Yamamoto, Hironori
TI The Frequency and Characteristics of Severe Liver-Related Adverse Events
in Patients with Chronic Liver Diseases after Vaccination against Severe
Acute Respiratory Syndrome Coronavirus 2: A Retrospective Study
SO GASTROINTESTINAL DISORDERS
LA English
DT Article
DE SARS-CoV-2; COVID-19; vaccine; liver dysfunction; liver disease;
autoimmune disease
ID MESSENGER-RNA; COVID-19; INFECTION; VACCINES; CANCER
AB Background: Vaccination against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is recommended for patients with chronic liver diseases as the vaccine can prevent and/or reduce the severity of SARS-CoV-2 infection. However, we have little information on the often-reported liver-related adverse events (LrAEs) caused by the mRNA vaccine. Methods: We retrospectively investigated the frequency and details of severe LrAEs and changes in liver function tests in patients with chronic liver diseases. Results: Among 431 patients with chronic liver diseases, 416 (96.5%) had received the SARS-CoV-2 vaccine >= 2 times. Among the 345 patients included in the analysis, 6 (1.7%) had severe LrAEs; 3 ascites, 2 increases in transaminases, and 1 an increase in total bilirubin. Multivariate analysis demonstrated that cirrhosis and autoimmune disease were risk factors for severe LrAEs. In contrast, the liver function reserve assessed by the Child-Pugh and ALBI scores did not markedly change after vaccination in patients with cirrhosis and/or autoimmune diseases despite a small increase in transaminase levels. Conclusion: SARS-CoV-2 mRNA vaccines, which were used in most of our patients, are safe in patients with chronic liver diseases, but the frequency of severe LrAEs is slightly increased in patients with cirrhosis and/or autoimmune diseases.
C1 [Bat-Erdene, Oyunjargal; Miura, Kouichi; Maeda, Hiroshi; Watanabe, Shunji; Tsukui, Mamiko; Takaoka, Yoshinari; Nomoto, Hiroaki; Goka, Rie; Morimoto, Naoki; Yamamoto, Hironori] Jichi Med Univ, Dept Med, Div Gastroenterol, Sch Med, 3311-1 Yakushiji, Shimotsuke, Tochigi 3290498, Japan.
C3 Jichi Medical University
RP Miura, K (corresponding author), Jichi Med Univ, Dept Med, Div Gastroenterol, Sch Med, 3311-1 Yakushiji, Shimotsuke, Tochigi 3290498, Japan.
EM miura385@jichi.ac.jp
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NR 18
TC 0
Z9 0
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2624-5647
J9 GASTROINTEST DISORD
JI Gastrointest. Disord.
PD MAR
PY 2023
VL 5
IS 1
BP 15
EP 27
DI 10.3390/gidisord5010002
PG 13
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA A9GE2
UT WOS:000958121400001
OA gold
DA 2025-01-07
ER
PT J
AU Takahashi, A
Ohira, H
AF Takahashi, Atsushi
Ohira, Hiromasa
TI Autoimmune hepatitis, fatty liver, and Fukushima
SO FUKUSHIMA JOURNAL OF MEDICAL SCIENCE
LA English
DT Review
DE autoimmune hepatitis; non-alcoholic fatty liver disease; the Great East
Japan Earth-quake; the Fukushima Heath Management Survey
ID EAST JAPAN EARTHQUAKE; POWER-PLANT ACCIDENT; CORTICOSTEROID-THERAPY;
RESISTANCE EXERCISE; MANAGEMENT; EVACUATION; DISEASE; RELAPSE; RISK;
REMISSION
AB The use of direct antiviral agents (DAAs) for hepatitis C virus has led to a paradigm shift from viral hepatitis to non-viral disease. Autoimmune hepatitis (AIH) remains to be an issue in liver disease after the DAAs era. Moreover, fatty liver had been increasing in incidence and has attracted attention because of its risk for hepatocellular carcinoma. In 2011, the Great East Japan Earthquake, with the associated tsunami and accident at Fukushima Daiichi Nuclear Power Plant, has changed the lifestyle of residents in Fukushima prefecture. In this manuscript, we outlined the recent topics about AIH, fatty liver, and Fukushima.
C1 [Takahashi, Atsushi; Ohira, Hiromasa] Fukushima Med Univ, Dept Gastroenterol, Sch Med, Fukushima, Japan.
C3 Fukushima Medical University
RP Takahashi, A (corresponding author), Fukushima Med Univ, Dept Gastroenterol, Sch Med, Fukushima, Japan.
EM junior@fmu.ac.jp
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NR 44
TC 0
Z9 1
U1 0
U2 1
PU FUKUSHIMA SOC MEDICAL SCIENCE
PI FUKUSHIMA
PA FUKUSHIMA MEDICAL UNIV LIBRARY, 1 HIKARIGAOKA,, FUKUSHIMA, 960-1297,
JAPAN
SN 0016-2590
EI 2185-4610
J9 FUKUSHIMA J MED SCI
JI Fukushima J. Med. Sci.
PY 2019
VL 65
IS 2
BP 25
EP 29
DI 10.5387/fms.2019-13
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA JW3PE
UT WOS:000502966400001
PM 31270280
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Sandrasegaran, K
Menias, CO
AF Sandrasegaran, Kumaresan
Menias, Christine O.
TI Imaging in Autoimmune Pancreatitis and Immunoglobulin G4-Related Disease
of the Abdomen
SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Autoimmune pancreatitis; Systemic IgG4 disease; IgG4 sclerosing
cholangitis; Pancreas cancer; Cholangiocarcinoma; Primary sclerosing
cholangitis
ID IGG4-RELATED SCLEROSING DISEASE; NATIONWIDE SURVEY; SERUM IGG4;
DIAGNOSIS; DIFFERENTIATION; MANAGEMENT; CANCER; CT; CHOLANGIOPATHY;
INVOLVEMENT
AB Autoimmune pancreatitis (AIP) is a steroid-responsive fibroinflammatory disorder of the pancreas. There are 2 distinct subtypes of AIP, types 1 and 2. Type 1 is associated with systemic immunoglobulin (Ig)G4 disease and may affect multiple organs in the body. Type 2 is confined to the pancreas and shows an association with ulcerative colitis. This article describes the imaging findings of AIP and IgG4 disease in the liver, bile ducts, kidneys, and retroperitoneal regions. The imaging differentiation of AIP from pancreas cancer is discussed.
C1 [Sandrasegaran, Kumaresan] Indiana Univ Sch Med, Dept Radiol, 550 North Univ Blvd,UH0279, Indianapolis, IN 46202 USA.
[Menias, Christine O.] Mayo Clin Hosp, Mayo Clin Sch Med, Dept Radiol, 5777 East Mayo Blvd, Phoenix, AZ 85054 USA.
C3 Indiana University System; Indiana University Bloomington; Mayo Clinic;
Mayo Clinic Phoenix
RP Sandrasegaran, K (corresponding author), Indiana Univ Sch Med, Dept Radiol, 550 North Univ Blvd,UH0279, Indianapolis, IN 46202 USA.
EM ksandras@iupui.edu
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NR 40
TC 12
Z9 14
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8553
EI 1558-1942
J9 GASTROENTEROL CLIN N
JI Gastroenterol. Clin. North Am.
PD SEP
PY 2018
VL 47
IS 3
BP 603
EP +
DI 10.1016/j.gtc.2018.04.007
PG 18
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GU5IX
UT WOS:000445320300011
PM 30115440
DA 2025-01-07
ER
PT J
AU Kobashi-Margáin, RA
Gutiérrez-Grobe, Y
Ponciano-Rodríguez, G
Uribe, M
Méndez-Sánchez, N
AF Arturo Kobashi-Margain, Ramon
Gutierrez-Grobe, Ylse
Ponciano-Rodriguez, Guadalupe
Uribe, Misael
Mendez-Sanchez, Nahum
TI Prevalence of type 2 diabetes mellitus and chronic liver disease: A
retrospective study of the association of two increasingly common
diseases in Mexico
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Chronic liver disease; Insulin resistance; Nonalcoholic fatty liver
disease; Cirrhosis; Hepatocellular carcinoma
ID HEPATITIS-C VIRUS; HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC
STEATOHEPATITIS; CLINICAL-IMPLICATIONS; AUTOIMMUNE HEPATITIS;
RISK-FACTORS; HEMOCHROMATOSIS; MANAGEMENT; CIRRHOSIS; FIBROSIS
AB Background. Recent studies have demonstrated a relationship between insulin resistance (IR) and type 2 diabetes mellitus (T2DM). The aim of this study was to determine the prevalence of 12DM among patients with liver disease. Methods. A retrospective study was performed by examining the charts of patients who presented with a diagnosis of liver disease at a university hospital between January 2006 and April 2010. Results. Liver disease was found in 129 patients. The most prevalent liver disease was cirrhosis, with 61 patients (47.2%), 44 patients had hepatitis C virus (34.1%) and 28 patients had hepatocellular carcinoma (21.7%). 12DM was diagnosed in 30 patients, 18 of whom were male (18/60; 30%) and 12 of whom were female (12/69; 17.4%). Only liver cirrhosis was significantly related to 12DM (21 of 61 patients; 34.4%, p < 0.004). Conclusions. The prevalence of T2DM among patients with liver disease (23.2%) is well established and similar to that reported in Western and some Eastern countries.
C1 [Arturo Kobashi-Margain, Ramon; Gutierrez-Grobe, Ylse; Uribe, Misael; Mendez-Sanchez, Nahum] Med Sur Clin & Fdn, Liver Unit, Mexico City, DF, Mexico.
[Ponciano-Rodriguez, Guadalupe] Univ Nacl Autonoma Mexico, Fac Med, Mexico City 04510, DF, Mexico.
C3 Universidad Nacional Autonoma de Mexico
RP Méndez-Sánchez, N (corresponding author), Med Sur Clin & Fdn, Liver Res Unit, Puente Piedra 150,Col Toriello Guerra, Mexico City, DF, Mexico.
EM nmendez@medicasur.org.mx
OI Uribe, Misael/0000-0002-6514-7869
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NR 44
TC 15
Z9 17
U1 0
U2 1
PU ELSEVIER ESPANA
PI MADRID
PA CALLE DE ZURBANO, 76-4TH FLR LEFT, MADRID, 28010, SPAIN
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD JUL-SEP
PY 2010
VL 9
IS 3
BP 282
EP 288
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 638HW
UT WOS:000280885300007
PM 20720269
DA 2025-01-07
ER
PT J
AU Covini, G
Bredi, E
Badalamenti, S
Roncalli, M
Aghemo, A
Colombo, M
AF Covini, Giovanni
Bredi, Elena
Badalamenti, Salvatore
Roncalli, Massimo
Aghemo, Alessio
Colombo, Massimo
TI Autoimmune Hepatitis During Ledipasvir/Sofosbuvir Treatment of Hepatitis
C: A Case Report
SO HEPATOLOGY COMMUNICATIONS
LA English
DT Article
ID EXTRAHEPATIC MANIFESTATIONS; HEPATOCELLULAR-CARCINOMA; LIVER-INJURY;
DIAGNOSIS; MANAGEMENT; RECURRENCE; INFECTION; GUIDELINE
AB We report the case of a woman with chronic hepatitis C and idiopathic thrombocytopenic purpura (ITP) who developed autoimmune hepatitis (AIH) during antiviral therapy with ledipasvir (LDV)/sofosbuvir (SOF). The onset of acute hepatitis rose two weeks after starting treatment with LDV/SOF when HCV-RNA tested negative, suggesting a link between rapid HCV clearance and de novo autoimmune diseases. Conclusion: This case report proposes new immunologic scenarios in patients with hepatitis C virus (HCV) with laboratory or clinical signs of autoimmunity during direct-acting antiviral (DAA) therapy.
C1 [Covini, Giovanni] Humanitas Clin & Res Ctr, Liver Unit, Rozzano, Italy.
[Covini, Giovanni] Humanitas Clin & Res Ctr, Ctr Autoimmune Liver Dis, Rozzano, Italy.
[Bredi, Elena] Humanitas Clin & Res Ctr, Clin Invest Lab, Rozzano, Italy.
[Badalamenti, Salvatore] Humanitas Clin & Res Ctr, Nephrol & Dialysis Unit, Rozzano, Italy.
[Roncalli, Massimo] Humanitas Clin & Res Ctr, Dept Pathol, Rozzano, Italy.
[Aghemo, Alessio; Colombo, Massimo] Humanitas Univ, Liver Unit, Rozzano, Italy.
[Aghemo, Alessio; Colombo, Massimo] Humanitas Univ, Dept Biomed Sci, Rozzano, Italy.
C3 IRCCS Humanitas Research Hospital; IRCCS Humanitas Research Hospital;
IRCCS Humanitas Research Hospital; IRCCS Humanitas Research Hospital;
IRCCS Humanitas Research Hospital; Humanitas University; IRCCS Humanitas
Research Hospital; IRCCS Humanitas Research Hospital; Humanitas
University
RP Covini, G (corresponding author), Liver Unit, Via Manzoni 56, I-20089 Rozzano, Italy.; Covini, G (corresponding author), Ctr Autoimmune Liver Dis, Via Manzoni 56, I-20089 Rozzano, Italy.
EM giovanni.covini@humanitas.it
RI Aghemo, Alessio/ABE-5976-2021; Roncalli, Massimo/HJZ-1838-2023
OI BADALAMENTI, SALVATORE/0000-0002-0394-0730; Covini,
Giovanni/0000-0003-1632-3907; Roncalli, Massimo/0000-0002-7901-8910
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NR 25
TC 9
Z9 10
U1 0
U2 1
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
EI 2471-254X
J9 HEPATOL COMMUN
JI Hepatol. Commun.
PD OCT
PY 2018
VL 2
IS 10
BP 1179
EP 1183
DI 10.1002/hep4.1248
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HD3ZN
UT WOS:000452465000005
PM 30288473
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Lefkowitch, JH
AF Lefkowitch, Jay H.
TI Recent developments in liver pathology
SO HUMAN PATHOLOGY
LA English
DT Review
DE Liver; Liver biopsy; Fatty liver; Liver tumors; Glypican-3; Iron;
Mallory-Denk body
ID HEPATITIS-E VIRUS; PLASMA-CELL HEPATITIS; HEPATOCELLULAR-CARCINOMA;
GENE-EXPRESSION; GLYPICAN-3 EXPRESSION; AUTOIMMUNE HEPATITIS; CENTRAL
PERIVENULITIS; CENTRAL VENULITIS; PROGENITOR CELLS; NATURAL-HISTORY
AB Progress in liver histopathology continues to be made, as evidenced by recent publications in all areas of hepatobiliary disease. Multinucleated giant hepatocytes, known to be associated with autoimmune and drug hepatitis, now have been seen in chronic hepatitis C with or without HIV infection and in patients with infection by human herpesvirus-6A. The new term Mallory-Denk body (formerly the Mallory body) recognizes the substantial contributions to this field by Prfessor Helmut Denk of Austria. The problems of fatly liver and hepatic iron overload have been addressed ill Studies highlighting their complex pathogenesis. Genomic and immunohistochemical analysis of liver tumors provides important diagnostic information, particularly regarding the use of glypican-3 in the diagnosis Of hepatocellular carcinoma. (C) 2009 Elsevier Inc. All rights reserved.
C1 Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA.
C3 Columbia University
RP Lefkowitch, JH (corresponding author), Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA.
EM jhl3@columbia.edu
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NR 108
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Z9 5
U1 0
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD APR
PY 2009
VL 40
IS 4
BP 445
EP 455
DI 10.1016/j.humpath.2008.12.014
PG 11
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 430LI
UT WOS:000264990200001
PM 19289183
DA 2025-01-07
ER
PT J
AU Chi, G
Feng, XX
Ru, YX
Xiong, T
Gao, Y
Wang, H
Luo, ZL
Mo, R
Guo, F
He, YP
Zhang, GM
Tian, DA
Feng, ZH
AF Chi, Gang
Feng, Xin-Xia
Ru, Ying-Xia
Xiong, Ting
Gao, Yuan
Wang, Han
Luo, Zhen-Long
Mo, Ran
Guo, Fang
He, Yong-Pei
Zhang, Gui-Mei
Tian, De-An
Feng, Zuo-Hua
TI TLR2/4 ligand-amplified liver inflammation promotes initiation of
autoimmune hepatitis due to sustained IL-6/IL-12/IL-4/IL-25 expression
SO MOLECULAR IMMUNOLOGY
LA English
DT Article
DE Autoimmune hepatitis; TLR ligands; Inflammation; Treg cells; Th1/Th2
responses
ID REGULATORY T-CELLS; DISEASE; HEPATOCARCINOMA; METASTASIS; SUPPRESSES;
INHIBITION; APOPTOSIS; CYTOKINES; FIBROSIS; UPDATE
AB Autoimmune hepatitis (AII-1), a serious autoimmune liver disease, can be a lifelong illness, leading to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). So far the mechanisms for disease initiation are largely unknown. Here we report that the amplified non-AIH liver inflammation could promote the initiation of AIH due to the sustained increase of IL-6, IL-12, IL-4, and IL-25 in the liver. The liver injury resulting from virus (adenovirus) or chemicals (CCl4) could induce an amplified (stronger/long-lasting) hepatic inflammation by releasing the ligands for TLR2/TLR4. The amplified inflammation resulted in the increase of multiple cytokines and chemokines in the liver. Among them, the sustained increase of IL-6/IL-12 resulted in the activation of STAT3 and STAT4 in hepatic CD4(+)CD25(+) Treg cells, thus suppressing Foxp3 gene expression to reduce the suppressive function of Treg cells in the liver, but not those in the spleen. The increase of IL-12 and the impairment of Treg function promoted Th1 response in presence of self-mimicking antigen (human CYP2D6). Intriguingly, the amplified inflammation resulted in the increase of IL-4 and IL-25 in the liver. The moderate increase of IL-4 was sufficient for cooperating with IL-25 to initiate Th2 response, but inefficient in suppressing Th1 response, favoring the initiation of autoimmune response. Consequently, either adenovirus/CYP2D6 or CCl4/CYP2D6 could induce the autoimmune response and AIH in the mice, leading to hepatic fibrosis. The findings in this study suggest that the amplified non-AIH inflammation in the liver could be a driving force for the initiation of autoimmune response and AIH.
C1 [Chi, Gang; Ru, Ying-Xia; Mo, Ran; Guo, Fang; He, Yong-Pei; Zhang, Gui-Mei; Feng, Zuo-Hua] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Basic Med, Dept Biochem & Mol Biol, Wuhan 430030, Hubei, Peoples R China.
[Feng, Xin-Xia; Xiong, Ting; Gao, Yuan; Wang, Han; Luo, Zhen-Long; Tian, De-An] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Gastroenterol, Wuhan 430030, Hubei, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
Science & Technology
RP Feng, XX; Feng, ZH (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Wuhan 430030, Hubei, Peoples R China.
EM fengxinxia@163.com; fengzhg_tj@163.com
RI Zhang, Guimei/JAO-1883-2023; Guo, Fang/L-2273-2017
OI Wang, Han/0000-0002-1253-5972
FU National Natural Science Foundation of China [81600448, 81472704]
FX This work was supported by National Natural Science Foundation of China
[grant numbers 81600448, 81472704]. We thank Zhi-Hui Liang, Hui-Fen Zhu
and Wen-Hong Lu for technical assistance.
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NR 51
TC 32
Z9 37
U1 0
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD JUL
PY 2018
VL 99
BP 171
EP 181
DI 10.1016/j.molimm.2018.05.005
PG 11
WC Biochemistry & Molecular Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Immunology
GA GL3ND
UT WOS:000437042200019
PM 29793131
DA 2025-01-07
ER
PT J
AU Voss, J
Schneider, CV
Kleinjans, M
Bruns, T
Trautwein, C
Strnad, P
AF Voss, Jessica
Schneider, Carolin V.
Kleinjans, Moritz
Bruns, Tony
Trautwein, Christian
Strnad, Pavel
TI Hepatobiliary phenotype of individuals with chronic intestinal disorders
SO SCIENTIFIC REPORTS
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; GLUTEN-FREE DIET; CELIAC-DISEASE; SCLEROSING
CHOLANGITIS; SEVERE STEATOHEPATITIS; LIVER; PREVALENCE; RISK;
MANIFESTATIONS; COMPLICATIONS
AB Despite the known functional relationship between the gut and the liver, the clinical consequences of this circuit remain unclear. We assessed the hepatobiliary phenotype of cohorts with celiac disease (CeD), Crohn ' s disease (CD) and ulcerative colitis (UC). Baseline liver function tests and the frequency of hepatobiliary diseases were analyzed in 2377 CeD, 1738 CD, 3684 UC subjects and 488,941 controls from the population-based UK Biobank cohort. In this cohort study associations were adjusted for age, sex, BMI, diabetes, and alcohol consumption. Compared to controls, cohorts with CeD, but not CD/UC displayed higher AST/ALT values. Subjects with CD/UC but not CeD had increased GGT levels. Elevated ALP and cholelithiasis were significantly more common in all intestinal disorders. Non-alcoholic steatohepatitis and hepatocellular carcinoma (HCC) were enriched in CeD and CD (NASH: (t)aOR = 4.9 [2.2-11.0] in CeD, aOR = 4.2 [1.7-10.3] in CD, HCC: aOR = 4.8 [1.8-13.0] in CeD, aOR = 5.9 [2.2-16.1] in CD), while cholangitis was more common in the CD/UC cohorts (aOR = 11.7 [9.1-15.0] in UC, aOR = 3.5 [1.8-6.8] in CD). Chronic hepatitis, autoimmune hepatitis (AIH) and cirrhosis were more prevalent in all intestinal disorders. In UC/CD, a history of intestinal surgery was associated with elevated liver enzymes and increased occurrence of gallstones (UC: aOR = 2.9 [2.1-4.1], CD: 1.7 [1.2-2.3]). Our data demonstrate that different intestinal disorders predispose to distinct hepatobiliary phenotypes. An increased occurrence of liver cirrhosis, NASH, AIH and HCC and the impact of surgery warrant further exploration.
C1 [Voss, Jessica; Schneider, Carolin V.; Kleinjans, Moritz; Bruns, Tony; Trautwein, Christian; Strnad, Pavel] Univ Hosp RWTH Aachen, Med Clin Gastroenterol Metab Dis & Intens Care 3, Pauwelsstr 30, D-52074 Aachen, Germany.
C3 RWTH Aachen University; RWTH Aachen University Hospital
RP Strnad, P (corresponding author), Univ Hosp RWTH Aachen, Med Clin Gastroenterol Metab Dis & Intens Care 3, Pauwelsstr 30, D-52074 Aachen, Germany.
EM pstrnad@ukaachen.de
RI Schneider, Carolin/AAZ-4832-2021; Strnad, Pavel/HPG-1883-2023; Bruns,
Tony/C-5720-2011
OI Schneider, Carolin V/0000-0002-6728-9246; Bruns,
Tony/0000-0002-5576-6914
FU Projekt DEAL; German Research Foundation (DFG) [CRC/SFB 1382, 403224013,
STR 1095/6-1]
FX Open Access funding enabled and organized by Projekt DEAL. P.S., T.B.
and C.T. are supported by the German Research Foundation (DFG)
consortium CRC/SFB 1382 "Gut-liver axis" (ID 403224013), P.S. is also
supported by DFG grant STR 1095/6-1 (Heisenberg professorship). This
research has been conducted using the UK Biobank Resource under
Application Number 47527.
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NR 47
TC 9
Z9 9
U1 1
U2 3
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD OCT 7
PY 2021
VL 11
IS 1
AR 19954
DI 10.1038/s41598-021-98843-7
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA WF5XG
UT WOS:000706376200032
PM 34620902
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Wang, HW
Zhang, J
Liu, JQ
Jiang, YF
Fu, L
Peng, SF
AF Wang, Huiwen
Zhang, Jian
Liu, Jinqing
Jiang, Yongfang
Fu, Lei
Peng, Shifang
TI Identification of AKR1B10 as a key gene in primary biliary cholangitis
by integrated bioinformatics analysis and experimental validation
SO FRONTIERS IN MOLECULAR BIOSCIENCES
LA English
DT Article
DE primary biliary cholangitis; integrated bioinformatics; differentially
expressed genes; hub genes
ID HEPATOCELLULAR-CARCINOMA; REDUCTASE; EXPRESSION; CIRRHOSIS; CELLS;
RESISTANCE; OVEREXPRESSION; PATHOGENESIS; GENDER; CXCR3
AB Background: Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease that eventually progresses to cirrhosis and hepatocellular carcinoma (HCC) in the absence of proper treatment. However, Gene expression and molecular mechanisms involved in the pathogenesis of PBC have not been completely elucidated. Methods: Microarray expression profiling dataset GSE61260 was downloaded from the Gene Expression Omnibus (GEO) database. Data were normalized to screen differentially expressed genes (DEGs) using the limma package in R. Moreover, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analyses were performed. A protein-protein interaction (PPI) network was constructed to identify hub genes and an integrative regulatory network of transcriptional factor-DEG-microRNA was established. Gene Set Enrichment Analysis (GSEA) was used to analyze differences in biological states for groups with different expressions of aldo-keto reductase family 1 member B10 (AKR1B10). Immunohistochemistry (IHC) analysis was performed to validate the expression of hepatic AKR1B10 in patients with PBC. The association of hepatic AKR1B10 levels with clinical parameters was evaluated using one-way analysis of variance (ANOVA) and Pearson's correlation analysis. Results: This study identified 22 upregulated and 12 downregulated DEGs between patients with PBC and healthy controls. GO and KEGG analysis revealed that DEGs were mainly enriched in immune reactions. AKR1B10 was identified as a key gene and was further analyzed by screening out hub genes from the PPI network. GSEA analysis indicated that high expression of AKR1B10 might promote PBC to develop into HCC. Immunohistochemistry results verified the increased expression of hepatic AKR1B10 in patients with PBC and demonstrated its positive correlation with the severity of PBC. Conclusion: AKR1B10 was identified as a hub gene in PBC by integrated bioinformatics analysis and clinical validation. The increase of AKR1B10 expression in patients with PBC was associated with disease severity and might promote the progression of PBC to HCC.
C1 [Wang, Huiwen; Zhang, Jian; Liu, Jinqing; Fu, Lei; Peng, Shifang] Cent South Univ, Xiangya Hosp, Dept Infect Dis, Changsha, Peoples R China.
[Jiang, Yongfang] Cent South Univ, Xiangya Hosp 2, Dept Infect Dis, Changsha, Peoples R China.
C3 Central South University; Central South University
RP Fu, L; Peng, SF (corresponding author), Cent South Univ, Xiangya Hosp, Dept Infect Dis, Changsha, Peoples R China.
EM fulei92@126.com; sfp1988@csu.edu.cn
RI Wang, Huiwen/JED-3206-2023
OI Zhang, Jian/0000-0001-9231-0724
FU National Natural Science Foundation of China [81974080, 82170640,
2021039]; Natural Science Foundation of Hunan Province [2022JJ30954]
FX Funding This work was supported by the National Natural Science
Foundation of China (No. 81974080 and 82170640), WANG Bao-En Liver
Fibrosis Research Fund (No. 2021039), Natural Science Foundation of
Hunan Province (No. 2022JJ30954).
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NR 55
TC 0
Z9 0
U1 2
U2 15
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-889X
J9 FRONT MOL BIOSCI
JI Front. Mol. Biosci.
PD FEB 9
PY 2023
VL 10
AR 1124956
DI 10.3389/fmolb.2023.1124956
PG 12
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 9E8JJ
UT WOS:000937025400001
PM 36845547
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Shouval, D
Shibolet, O
AF Shouval, Daniel
Shibolet, Oren
TI Immunosuppression and HBV Reactivation
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE hepatitis; immunosuppression; hepatitis B virus (HBV); chemotherapy;
reactivation; antiviral; preemptive
ID HEPATITIS-B-VIRUS; RECEIVING CYTOTOXIC CHEMOTHERAPY; ACTIVE
ANTIRETROVIRAL THERAPY; HUMAN-IMMUNODEFICIENCY-VIRUS;
BONE-MARROW-TRANSPLANTATION; BREAST-CANCER PATIENTS; SURFACE-ANTIGEN;
HEPATOCELLULAR-CARCINOMA; PREEMPTIVE LAMIVUDINE; LYMPHOMA PATIENTS
AB Hepatitis B virus (HBV) reactivation following immunosuppression is defined by an abrupt rise in HBV replication followed by laboratory signs of hepatocellular injury in a "silent" hepatitis B surface antigen (HBsAg) carrier. Reactivation can also occur, albeit at a lower rate, in patients with occult HBV infection. The clinical presentation of reactivation is variable ranging from an asymptomatic course to severe hepatitis, liver failure, and death. It is most frequently observed in patients with lymphoma treated with rituximab and corticosteroids as well as in patients undergoing stem cell and bone marrow transplantation. Other risk groups include patients with solid tumors, subjects infected with human immunodeficiency virus, organ transplant recipients, and those with autoimmune diseases (i.e., inflammatory bowel disease, rheumatoid arthritis). In cancer patients, HBV reactivation can lead to interruption of chemotherapy with serious impact on prognosis. In HBsAg-positive patients who are candidates for chemotherapy or treatment with biologic agents, preemptive treatment with an antiviral agent such as lamivudine, and lately with the more potent tenofovir or entecavir, has become a standard of care, effectively preventing HBV reactivation. Patients with occult HBV should be monitored for alanine aminotransferase and HBV DNA during the course of immunosuppression. Prompt administration of a potent antiviral agent upon diagnosis of reactivation may be lifesaving in such patients.
C1 [Shouval, Daniel] Hadassah Hebrew Univ Hosp, Liver Unit, IL-91120 Jerusalem, Israel.
[Shibolet, Oren] Tel Aviv Univ, Dept Gastroenterol, Liver Unit, Tel Aviv Med Ctr, IL-69978 Tel Aviv, Israel.
[Shibolet, Oren] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel.
C3 Hebrew University of Jerusalem; Hadassah University Medical Center; Tel
Aviv University; Tel Aviv University
RP Shouval, D (corresponding author), Hadassah Hebrew Univ Hosp, Liver Unit, POB 12000, IL-91120 Jerusalem, Israel.
EM shouval@hadassah.org.il
RI Shouval, Daniel/U-2779-2017
OI Shouval, Daniel/0000-0002-0512-6513
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NR 102
TC 125
Z9 136
U1 0
U2 21
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD MAY
PY 2013
VL 33
IS 2
BP 167
EP 177
DI 10.1055/s-0033-1345722
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 159FG
UT WOS:000320029900010
PM 23749673
DA 2025-01-07
ER
PT J
AU Gaspar, R
Branco, CC
Macedo, G
AF Gaspar, Rui
Branco, Catarina Castelo
Macedo, Guilherme
TI Liver and COVID-19: From care of patients with liver diseases to liver
injury
SO WORLD JOURNAL OF HEPATOLOGY
LA English
DT Review
DE COVID-19; Liver diseases; Vaccination; SARS-CoV-2
ID HEPATOCELLULAR-CARCINOMA; TRANSPLANT RECIPIENTS; SARS-COV-2 INFECTION;
POSITION PAPER; IMPACT; SURVEILLANCE; INVOLVEMENT; MANAGEMENT; OUTCOMES
AB The global pandemic of coronavirus disease 2019 (COVID-19) changed dramatically all priorities on medical society and created several challenges for clinicians caring for patients with liver diseases. We performed a comprehensive review about how COVID-19 can affect the liver, the influence of liver diseases on the risk of developing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and COVID-19 severity and also some strategies to overcome all the challenges clinicians have to face in the management of patients with liver diseases in a period of time when all the focus turned on COVID-19. We analyze the relationship between COVID-19 and non-alcoholic fatty liver disease, alcoholic liver disease, viral hepatitis, autoimmune liver disease, cirrhosis, hepatocellular carcinoma and liver transplantation, as well as the approach to SARS-CoV-2 vaccination.
C1 [Gaspar, Rui; Macedo, Guilherme] Ctr Hosp Sao Joao, Dept Gastroenterol & Hepatol, Alameda Prof Hernani Monteiro, P-4200 Porto, Portugal.
[Branco, Catarina Castelo] Ctr Hosp & Univ Porto, Dept Internal Med, P-4100 Porto, Portugal.
C3 Sao Joao Hospital; Universidade do Porto
RP Gaspar, R (corresponding author), Ctr Hosp Sao Joao, Dept Gastroenterol & Hepatol, Alameda Prof Hernani Monteiro, P-4200 Porto, Portugal.
EM ruilopesgaspar@gmail.com
RI Macedo, Manuel/L-8038-2013
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NR 75
TC 7
Z9 7
U1 1
U2 5
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5182
J9 WORLD J HEPATOL
JI World J. Hepatol.
PD OCT 27
PY 2021
VL 13
IS 10
BP 1367
EP 1377
DI 10.4254/wjh.v13.i10.1367
PG 11
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA XB7KF
UT WOS:000721503600012
PM 34786172
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Gu, JN
Yan, W
Gao, QL
Chen, L
AF Gu, Ji-Na
Yan, Wang
Gao, Qiao-Ling
Chen, Lin
TI Anti-OJ antibody-positive anti-synthetase syndrome with repeated
arthritis, fever, and recurrent liver cancer: a case report
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Case report; anti-synthetase syndrome (ASS); anti-OJ
(anti-isoleucyl-transfer RNA synthetase) antibody; arthritis;
polymyositis
ID CLINICAL CHARACTERISTICS
AB Background: Anti-isoleucyl-transfer RNA synthetase (anti-OJ) autoantibody-positive anti-synthetase syndrome (ASS) is a rare systemic autoimmune disease that manifests as an inflammatory myopathy and interstitial lung disease. We present a case of an anti-OJ antibody-positive ASS, with recurrent joint pain and fever, significantly elevated inflammatory markers, occult myositis but no interstitial pneumonia. This clinical presentation of an anti-OJ antibody-positive ASS has not been reported before.Case Description: A 75-year-old male, was admitted to our hospital complaining of recurrent joint pain for more than 1 year, recurrent fever for 6 months, and recurrence of joint pain and fever for 1 week. The patient had a history of chronic viral hepatitis B, hepatocellular carcinoma (HCC) surgery 11 years ago, hypertension and type 2 diabetes. In the past year, the patient visited Departments of orthopedics, Infectious Medicine and rheumatology for many times, and has undergone positron emission tomography-computed tomography (PET-CT), bone marrow puncture and other examinations, but the cause was still unknown. On admission, physical examination showed that the temperature was 39.6 celcius, and there was tenderness in multiple joints and muscles, such as the left ankle, the right shoulder, the left wrist, biceps brachii and quadriceps femoris, and so on. The laboratory results showed white blood cell (WBC) count of 30,500/mu L (neutrophils: 90.1%), C-reactive protein (CRP): 140.79 mg/dL,Creatine Kinase and creatine kinase-MB were normal. Because of the muscle tenderness, myositis antibody tests were performed and the anti-OJ autoantibody was positive. Asking the medical history in detail, the patient had myasthenia, which was covered up due to prominent joint pain and fever. The patient had no interstitial pneumonia and mechanic's hand. Recurrent hepatocellular carcinoma was confirmed 1 year after the diagnosis of ASS, and the clinical symptoms were relieved after surgical resection. Conclusions: We report this rare case of anti-OJ antibody-positive ASS with atypical manifestations to raise awareness of the disease for clinicians. For patients with recurrent unexplained arthritis with fever, we should consider ASS, and myositis antibody tests should be performed if necessary. Patients with a history of tumours should be monitored for tumour recurrence.
C1 [Gu, Ji-Na; Chen, Lin] Univ Chinese Acad Sci, Hwa Mei Hosp, Dept Infect Med, Ningbo, Peoples R China.
[Yan, Wang] Univ Chinese Acad Sci, Hwa Mei Hosp, Dept Neurol, Ningbo, Peoples R China.
[Gao, Qiao-Ling] Univ Chinese Acad Sci, Hwa Mei Hosp, Dept Radiol, Ningbo, Peoples R China.
[Chen, Lin] Univ Chinese Acad Sci, Hwa Mei Hosp, Dept Infect Med, Ningbo 315800, Peoples R China.
C3 Chinese Academy of Sciences; University of Chinese Academy of Sciences,
CAS; Chinese Academy of Sciences; University of Chinese Academy of
Sciences, CAS; Chinese Academy of Sciences; University of Chinese
Academy of Sciences, CAS; Chinese Academy of Sciences; University of
Chinese Academy of Sciences, CAS
RP Chen, L (corresponding author), Univ Chinese Acad Sci, Hwa Mei Hosp, Dept Infect Med, Ningbo 315800, Peoples R China.
EM chenlin2111@163.com
RI wang, yingying/M-6676-2015
FU Key Medical Subjects of Joint Construction Between Provinces and Cites
(Infectious Diseases) , China [2016-S04]; Key Discipline Foundation of
Hwa Mei Hospital, University of Chinese Academy of Sciences
[2020ZDXK03]; Medical Scientific Research Foundation of Zhejiang
Province, China [2019KY598]
FX This work was supported by Key Medical Subjects of Joint Construction
Between Provinces and Cites (Infectious Diseases) , China (Grant No.
2016-S04) ; the Key Discipline Foundation of Hwa Mei Hospital,
University of Chinese Academy of Sciences (Grant No.2020ZDXK03) ;
Medical Scientific Research Foundation of Zhejiang Province, China
(Grant No. 2019KY598) . The funding bodies supported the publication
fees but had no influence on the diagnosis and treatment of the patient,
or the writing of manuscript.
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NR 21
TC 2
Z9 2
U1 0
U2 1
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD OCT
PY 2022
VL 13
IS 5
BP 2672
EP 2678
DI 10.21037/jgo-22-720
EA AUG 2022
PG 7
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 6M4BF
UT WOS:000858883100001
PM 36388687
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Wei, QJ
Jiang, YT
Xie, JW
Yang, MC
Zhang, YL
Wu, ZM
Chen, SH
Liao, ZT
Lin, ZM
Gu, JR
AF Wei, Qiujing
Jiang, Yutong
Xie, Jiewen
Yang, Mingcan
Zhang, Yanli
Wu, Zhongming
Chen, Shuhong
Liao, Zetao
Lin, Zhiming
Gu, Jieruo
TI Investigation and analysis of HEp 2 indirect immunofluorescence titers
and patterns in various liver diseases
SO CLINICAL RHEUMATOLOGY
LA English
DT Article
DE Antinuclear antibodies; Autoimmune diseases; Autoimmune hepatitis; Liver
diseases; Primary biliary cirrhosis
ID CLASSIFICATION CRITERIA; ANTINUCLEAR ANTIBODIES; AMERICAN-COLLEGE;
AUTOANTIBODIES; ANA; CONSENSUS; HEPATITIS
AB Introduction Antinuclear antibody (ANA) testing using indirect immunofluorescence assay (IIFA) is a common and economical method which contributes to detect systemic autoimmune diseases (SARD) and autoimmune liver diseases (AILD). The primary aim of our study was to investigate ANA positivity and their patterns in multiple liver diseases, including primary biliary cirrhosis (PBC), autoimmune hepatitis (AIH), hepatitis B virus infection (HBV), hepatitis C virus infection (HCV), and hepatic carcinoma (HCC). Besides, we also compared the ANA titers and patterns in patients with liver disease, SARD, and healthy controls (HC). Methods A total of 2537 patients with SARD, 137 PBC cases, 57 AIH cases, 3420 HBV cases, 769 HCV cases, 268 HCC cases, and 1073 HC were retrospectively assessed. The titers and patterns of ANA were detected with the IIFA method. Results ANA positivity rate was considerably discernible between these diseases, which is 90.1% in SARD, 93.4% in PBC, 49.1% in AIH, 19.1% in HBV, 13.9% in HCV, and 23.5% in HCC. Moreover, only 4.9% of HCC cases, 2.5% of HBV patients, and 1.6% of HCV patients had an ANA titer >= 1:320. The mixed pattern which composed of at least two patterns majorly lied in PBC. AC-15 and AC-21 was frequently related to liver diseases; the former pattern was more frequently found in AIH (84.2%) and PBC (8.8%), and the latter pattern was easily seen in PBC (62.2%) and HCC (22.6%). The positive rate of ANA in HC was 12.2%, and its major pattern was AC-2. Conclusions There are differences in ANA positivity among patients with SARD and various liver diseases. Some mixed patterns may provide important evidence for the diagnosis of PBC. Clinicians should pay attention to ANA patterns and titer during the interpretation of this test.
C1 [Wei, Qiujing; Jiang, Yutong; Xie, Jiewen; Yang, Mingcan; Zhang, Yanli; Wu, Zhongming; Chen, Shuhong; Liao, Zetao; Lin, Zhiming; Gu, Jieruo] Sun Yat Sen Univ, Dept Rheumatol, Affiliated Hosp 3, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University
RP Gu, JR (corresponding author), Sun Yat Sen Univ, Dept Rheumatol, Affiliated Hosp 3, Guangzhou, Guangdong, Peoples R China.
EM gujieruo@163.com
RI Jiang, Yutong/KUF-1282-2024
OI gu, jieruo/0000-0002-8785-0600
FU Sun Yat-sen University [82000-31143401]; National key research and
development project [2016YFC0903501]; Guangzhou Health and Medical
Collaborative InnovationMajor Projects [201604020013]; health management
platform for ankylosing spondylitis and hyperuricemia [A2968]
FX The study was funded by three major construction project of Sun Yat-sen
University [grant number 82000-31143401], the establishment of a health
management platform for ankylosing spondylitis and hyperuricemia [grant
number A2968], National key research and development project [grant
number 2016YFC0903501], and Guangzhou Health and Medical Collaborative
InnovationMajor Projects [grant number 201604020013].
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NR 28
TC 10
Z9 11
U1 0
U2 1
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0770-3198
EI 1434-9949
J9 CLIN RHEUMATOL
JI Clin. Rheumatol.
PD AUG
PY 2020
VL 39
IS 8
BP 2425
EP 2432
DI 10.1007/s10067-020-04950-7
EA FEB 2020
PG 8
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA MF9QW
UT WOS:000516789700002
PM 32103375
DA 2025-01-07
ER
PT J
AU Heneghan, MA
Yeoman, AD
Verma, S
Smith, AD
Longhi, MS
AF Heneghan, Michael A.
Yeoman, Andrew D.
Verma, Sumita
Smith, Alastair D.
Longhi, Maria Serena
TI Autoimmune hepatitis
SO LANCET
LA English
DT Article
ID CHRONIC ACTIVE HEPATITIS; PRIMARY BILIARY-CIRRHOSIS; SOLUBLE LIVER
ANTIGEN; REGULATORY T-CELLS; PRIMARY SCLEROSING CHOLANGITIS;
MYCOPHENOLATE-MOFETIL; CORTICOSTEROID-THERAPY; OVERLAP SYNDROME;
JAPANESE PATIENTS; CONTROLLED-TRIAL
AB Autoimmune hepatitis is a disease of the hepatic parenchyma that can present in acute or chronic forms. In common with many autoimmune diseases, autoimmune hepatitis is associated with non-organ-specific antibodies in the context of hepatic autoimmunity. This dichotomy has made definition of a unifying hypothesis in the pathophysiology of the disease difficult, although data from the past 8 years have drawn attention to the role of regulatory T cells. Several triggers have been identified, and the disease arises in genetically susceptible individuals. Clinical and biochemical remission is achievable in up to 85% of cases. For the remaining patients, alternative immunosuppression strategies are an option. Liver transplantation provides an excellent outcome for patients with acute liver failure or complications of end-stage liver disease, including hepatocellular carcinoma. Variant or overlapping syndromes are worthy of consideration when unexpected disease features arise.
C1 [Heneghan, Michael A.; Yeoman, Andrew D.; Longhi, Maria Serena] Kings Coll Hosp NHS Fdn Trust, Inst Liver Studies, London SE5 9RS, England.
[Verma, Sumita] Brighton & Sussex Med Sch, Dept Med, Brighton, E Sussex, England.
[Smith, Alastair D.] Duke Univ, Med Ctr, Div Gastroenterol & Hepatol, Durham, NC USA.
C3 University of London; King's College London; King's College Hospital NHS
Foundation Trust; University of Sussex; University of Brighton; Duke
University
RP Heneghan, MA (corresponding author), Kings Coll Hosp NHS Fdn Trust, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
EM michael.heneghan@nhs.net
OI Verma, Sumita/0000-0001-7021-8409
FU Wellcome Trust; Kelly Group; Medical Research Council; MRC [G0902288]
Funding Source: UKRI
FX MAH is the recipient of research funding from the Wellcome Trust and The
Kelly Group. MSL is the recipient of a Medical Research Council
Clinician Scientist Fellowship. We thank Alberto Quaglia (King's College
Hospital London, UK) for histological images.
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NR 174
TC 207
Z9 224
U1 1
U2 22
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD OCT 26
PY 2013
VL 382
IS 9902
BP 1433
EP 1444
DI 10.1016/S0140-6736(12)62163-1
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 242JW
UT WOS:000326237500028
PM 23768844
DA 2025-01-07
ER
PT J
AU Yao, JP
Liang, X
Liu, YN
Zheng, M
AF Yao, Jiping
Liang, Xue
Liu, Yanning
Zheng, Min
TI Neddylation: A Versatile Pathway Takes on Chronic Liver Diseases
SO FRONTIERS IN MEDICINE
LA English
DT Review
DE neddylation; HBV; NAFLD; liver fibrosis; HCC; therapy; MLN4924
ID NEDD8-ACTIVATING ENZYME-INHIBITOR; E3 UBIQUITIN LIGASE; FACTOR-KAPPA-B;
BETA-TRCP; PROTEIN NEDDYLATION; DNA-DAMAGE; MTOR INHIBITOR;
UP-REGULATION; HIF-ALPHA; NEDD8
AB Neddylation is a ubiquitin-like posttranslational modification that conjugates neural precursor cell expressed developmentally downregulated-8 (Nedd8) to specific substrates for regulation of protein activity. In light of current researches, the neddylation pathway is aberrant in the pathogenesis of many diseases. In our review, we summarize the versatile roles of neddylation in chronic liver diseases (CLDs). CLDs are one of the leading causes of chronic disease-associated deaths worldwide. There are diverse etiologic agents causing CLDs, mainly including hepatitis B virus (HBV) infection, nonalcoholic fatty liver disease (NAFLD), chronic exposure to alcohol or drugs, and autoimmune causes. So far, however, there remains a paucity of effective therapeutic approach to CLDs. In this review, we summarized the role of the neddylation pathway which runs through the chronic hepatitis B/NAFLD-liver fibrosis-cirrhosis-hepatocellular carcinoma (HCC) axis, a canonical pattern in the process of CLD development and progression. The dysregulation of neddylation may provide a better understanding of CLD pathology and even a novel therapeutic strategy. Correspondingly, inhibiting neddylation via MLN4924, a small molecule compound targeting NEDD8-activating enzyme (NAE), can potently alleviate CLD progression and improve the outcome. On this basis, profiling and characterization of the neddylation pathway can provide new insights into the CLD pathology as well as novel therapeutic strategies, independently of the etiology of CLD.
C1 [Yao, Jiping; Liang, Xue; Liu, Yanning; Zheng, Min] Zhejiang Univ, Collaborat Innovat Ctr Diag & Treatment Infect Di, State Key Lab Diag & Treatment Infect Dis,Coll Me, Natl Clin Res Ctr Infect Dis,Affiliated Hosp 1, Hangzhou, Peoples R China.
C3 Collaborative Innovation Center for Diagnosis & Treatment of Infectious
Diseases; Zhejiang University
RP Zheng, M (corresponding author), Zhejiang Univ, Collaborat Innovat Ctr Diag & Treatment Infect Di, State Key Lab Diag & Treatment Infect Dis,Coll Me, Natl Clin Res Ctr Infect Dis,Affiliated Hosp 1, Hangzhou, Peoples R China.
EM minzheng@zju.edu.cn
RI Zheng, Mingyue/HHZ-4062-2022
FU National Nature Science Foundation of China [81871646]; State S & T
Project of 13th Five Year [2018ZX10302206]
FX This study was supported by Grants from the National Nature Science
Foundation of China, No. 81871646; the State S & T Project of 13th Five
Year, No. 2018ZX10302206.
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NR 128
TC 23
Z9 26
U1 0
U2 15
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD OCT 19
PY 2020
VL 7
AR 586881
DI 10.3389/fmed.2020.586881
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OI4RY
UT WOS:000583269000001
PM 33195347
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Larrey, D
Bozonnat, MC
Kain, I
Pageaux, GP
Assenat, E
AF Larrey, Dominique
Bozonnat, Marie-Cecile
Kain, Ihab
Pageaux, Georges-Philippe
Assenat, Eric
TI Is chronic hepatitis C virus infection a risk factor for breast cancer?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Breast tumors; Breast cancer; Hepatitis C virus infection; Risk factor
ID HEPATOCELLULAR-CARCINOMA; LIVER FIBROSIS; EPIDEMIOLOGY; PREVALENCE;
MARKERS; FRANCE; WOMEN; TIME
AB AIM: To evaluate the prevalence of breast tumors in adult females with chronic hepatitis C virus (HCV) infection.
METHODS: Prospective, single-center study, based on female outpatients consulting in a liver unit, for 1 year. The study group included females with present and/or past history of chronic infection by HCV. Patients with spontaneous recovery were excluded. Chronic hepatitis had been proved by liver biopsy in the majority of cases and/or biological markers of inflammation and fibrosis. The control group included female patients with other well documented chronic liver diseases: chronic hepatitis B, alcoholic liver disease, autoimmune hepatitis, hemochromatosis, non alcoholic liver disease, chronic cholangitis. Participating patients were prospectively questioned during consultation about past breast history and follow-up by mammography.
RESULTS: Breast carcinoma was recorded in 17/294 patients with HCV infection (5.8%, 95% CI: 3.1-8.4) vs 5/107 control patients (4.7%, 95% CI: 0.67-8.67). Benign tumors of the breast (mastosis, nodules, cysts) were recorded in 75/294 patients with HCV infection (25.5%, 95% CI: 20.5-30.5) vs 21/107 (19.6%, 95% CI: 12.1-27.1) in the control group. No lesion was noted in 202 patients with HCV (68.7%, 95% CI: 63.4-74) vs 81 control patients (75.7%, 95% CI: 67.6-83.8). Despite a trend to an increased prevalence in the group with HCV infection, the difference was not significant compared to the control group (P = NS). In patients over 40 years, the results were, respectively, as follows: breast cancer associated with HCV: 17/266 patients (6.3%, 95% CI: 3.4-9.3) vs 5/95 patients (5.2%, 95% CI: 0.7-9.7) in the control group; benign breast tumors: 72/266 patients with HCV infection (27%, 95% CI: 21.7-32.4) vs 18/95 patients (18.9%, 95% CI: 11-26.8) in the control group; no breast lesion 177/266 (66.5%, 95% CI: 60.9-72.2) in patients with HCV infection vs 72/95 (75.7%, 95% CI: 67.1-84.4) in the control group. The differences were not significant (P = NS).
CONCLUSION: These results suggest that chronic HCV infection is not a strong promoter of breast carcinoma in adult females of any age. (C) 2010 Baishideng. All rights reserved.
C1 [Larrey, Dominique; Pageaux, Georges-Philippe] Univ Montpellier, Liver Unit, F-34295 Montpellier 5, France.
[Larrey, Dominique; Pageaux, Georges-Philippe] Univ Montpellier, INSERM, Unit 632, St Eloi Hosp, F-34295 Montpellier 5, France.
[Bozonnat, Marie-Cecile] Univ Montpellier, Dept Biostat, Intitut Univ Rech Clin, F-34295 Montpellier 5, France.
[Kain, Ihab] Univ Montpellier, Liver Unit, St Eloi Hosp, F-34295 Montpellier 5, France.
[Assenat, Eric] Univ Montpellier, Med Oncol Unit, St Eloi Hosp, F-34295 Montpellier 5, France.
C3 Universite de Montpellier; Universite de Montpellier; CHU de
Montpellier; Institut National de la Sante et de la Recherche Medicale
(Inserm); Universite de Montpellier; Universite de Montpellier; CHU de
Montpellier; Universite de Montpellier; CHU de Montpellier
RP Larrey, D (corresponding author), Univ Montpellier, Liver Unit, 80 Rue Augustin Fliche, F-34295 Montpellier 5, France.
EM dom-larrey@chu-montpellier.fr
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NR 28
TC 11
Z9 11
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD AUG 7
PY 2010
VL 16
IS 29
BP 3687
EP 3691
DI 10.3748/wjg.v16.i29.3687
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 636ET
UT WOS:000280712500010
PM 20677341
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Nevens, F
AF Nevens, Frederik
TI PBC-transplantation and disease recurrence
SO BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE Primary biliary cholangitis; Pruritus; Mortality liver transplantation;
Transplantation rejection; PBC recurrence
ID PRIMARY BILIARY-CIRRHOSIS; AUTOIMMUNE LIVER-DISEASES; LONG-TERM
OUTCOMES; HEPATOCELLULAR-CARCINOMA; ALLOGRAFT-REJECTION;
CONTROLLED-TRIAL; NATURAL-HISTORY; LIST MORTALITY; RISK-FACTORS;
FOLLOW-UP
AB Despite near universal use of ursodeoxycholic acid (UDCA) several patients with PBC still progress to liver transplant (LT) or death. Pruritus and fatigue are the most common symptoms. Liver transplantation for pruritus is highly effective but fatigue will not disappear in the majority of the patients. In contrast to other liver diseases, portal hypertension may develop in pre-cirrhotic patients with PBC. Patients with PBC have an incidence rate of 3.4 hepatocellular carcinoma cases for every 1000 patient-years and risk factors are advanced stage of the disease and male sex. For the appropriate timing of LT the utility of prognostic models (bilirubin, Mayo risk score and MELD, in particular) and standard exception points in case of HCC are established. However, recent data from different part of the world demonstrated that PBC patients compared to patients with PSC have higher waiting-list mortality. Hyperlipidemia can be present in up to 80% of the patients but there is no evidence for an elevated cardiovascular risk, certainly not in relationship with LT. Patients transplanted for PBC suffer more frequently from acute cellular and also late cellular rejection. However, 5-year patient survival rates after LT of 80-85% is better than for most other indications. Recurrent PBC is reported in a range from 14% up to 42% after LT but in contrast to other autoimmune diseases graft loss due to recurrent disease is not a major issue. The type of immunosuppression after LT was found to be associated with the incidence of recurrence but since mediate term impact on overall and graft survival is negligible, tacrolimus-based regimens remain standard at most centers. Observational studies suggest that long-term administration of UDCA following LT has a beneficial effect on recurrence of PBC. Therefore biomarkers after LT that may identify patients at risk for recurrence should be further explored to allows early medical intervention. (C) 2018 Published by Elsevier Ltd.
C1 [Nevens, Frederik] Univ Hosp KU Leuven, Dept Gastroenterol & Hepatol, Leuven, Belgium.
C3 KU Leuven; University Hospital Leuven
RP Nevens, F (corresponding author), Univ Hosp KU Leuven, Dept Gastroenterol & Hepatol, Leuven, Belgium.
EM Frederik.Nevens@uzleuven.be
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NR 56
TC 15
Z9 17
U1 1
U2 4
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1521-6918
EI 1532-1916
J9 BEST PRACT RES CL GA
JI Best Pract. Res. Clin. Gastroenterol.
PD JUN-AUG
PY 2018
VL 34-35
BP 107
EP 111
DI 10.1016/j.bpg.2018.09.001
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GZ5FZ
UT WOS:000449445900013
PM 30343704
DA 2025-01-07
ER
PT J
AU Wang, QX
Yan, L
Ma, X
AF Wang, Qi-Xia
Yan, Li
Ma, Xiong
TI Autoimmune Hepatitis in the Asia-Pacific Area
SO JOURNAL OF CLINICAL AND TRANSLATIONAL HEPATOLOGY
LA English
DT Review
DE Autoimmune hepatitis; Outcome; Personalized management; Asia-Pacific
area
ID PRIMARY BILIARY-CIRRHOSIS; CHRONIC ACTIVE HEPATITIS; SINGLE-CENTER
EXPERIENCE; CLINICAL-FEATURES; HEPATOCELLULAR-CARCINOMA; OVERLAP
SYNDROME; LIVER-DISEASE; AZATHIOPRINE INTOLERANCE;
MYCOPHENOLATE-MOFETIL; DIAGNOSTIC-CRITERIA
AB Autoimmune hepatitis has been considered as a relatively rare immunological liver disease, especially in the Asia-Pacific area. Although the diagnosis criteria and immunosuppressive treatment regimens have been established, there are still some challenges. According to the different presentations, the personalized management of patients who suffer from this disease, including those with chronic or acute severe onset, the autoantibody-negative phenotype and cirrhosis are necessarily descriptive. Each subgroup of patients should receive an individualized therapy. Here, we review the recent studies of autoimmune hepatitis, mainly focusing on the epidemiology and genetics, personalized diagnostics, individualized treatment strategies, special subgroups and outcomes. Most of the research in the literature is based on Japanese and Chinese populations.
C1 [Wang, Qi-Xia; Yan, Li; Ma, Xiong] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes, Sch Med,Key Lab Gastroenterol & Hepatol,Shanghai, Div Gastroenterol & Hepatol,Renji Hosp,Minist Hlt, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University
RP Ma, X (corresponding author), Shanghai Jiao Tong Univ, Renji Hosp, Sch Med, Shanghai Inst Digest Dis, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.
EM maxiongmd@163.com
OI Ma, Xiong/0000-0001-9616-4672
FU National Natural Science Foundation of China [81325002, 81620108002,
81570511, 81770564]; Foundation for Innovative Research Groups of the
National Natural Science Foundation of China [81421001]; Municipal Human
Resources Development Program for Outstanding Young Talents in Medical
and Health Sciences in Shanghai [2017YQ037]
FX This work was supported by grants from the National Natural Science
Foundation of China (No. 81325002 and No. 81620108002 to X Ma, No.
81570511 and No. 81770564 to QX Wang), the Foundation for Innovative
Research Groups of the National Natural Science Foundation of China (No.
81421001), and the Municipal Human Resources Development Program for
Outstanding Young Talents in Medical and Health Sciences in Shanghai
(No. 2017YQ037 to QX Wang).
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NR 119
TC 19
Z9 23
U1 0
U2 10
PU XIA & HE PUBLISHING INC
PI SUGAR LAND
PA 14090 SOUTHWEST FREEWAY, STE 300, SUGAR LAND, TX 77478 USA
SN 2225-0719
EI 2310-8819
J9 J CLIN TRANSL HEPATO
JI J. Clin. Transl. Hepatol.
PD JAN-MAR
PY 2018
VL 6
IS 1
BP 48
EP 56
DI 10.14218/JCTH.2017.00032
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GH8EL
UT WOS:000433899900007
PM 29577032
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Chang, LY
Lin, YC
Chiang, JM
Mahalingam, J
Su, SH
Huang, CT
Chen, WT
Huang, CH
Jeng, WJ
Chen, YC
Lin, SM
Sheen, IS
Lin, CY
AF Chang, Li-Yuan
Lin, Yung-Chang
Chiang, Jy-Ming
Mahalingam, Jayashri
Su, Shih-Huan
Huang, Ching-Tai
Chen, Wei-Ting
Huang, Chien-Hao
Jeng, Wen-Juei
Chen, Yi-Cheng
Lin, Shi-Ming
Sheen, I-Shyan
Lin, Chun-Yen
TI Blockade of TNF-α signaling benefits cancer therapy by suppressing
effector regulatory T cell expansion
SO ONCOIMMUNOLOGY
LA English
DT Article
DE colorectal cancer; cyclophosphamide; effector regulatory T cells;
hepatocellular carcinoma; TNF-alpha; TNFR2
ID TUMOR-NECROSIS-FACTOR; AUTOIMMUNE-DISEASE; OVARIAN-CANCER;
IMMUNE-SYSTEM; BREAST-CANCER; PHASE-II; TGF-BETA; ETANERCEPT; CARCINOMA;
IMMUNOTHERAPY
AB Effector but not naive regulatory T cells (Treg cells) can accumulate in the peripheral blood as well as the tumor microenvironment, expand during tumor progression and be one of the main suppressors for antitumor immunity. However, the underlying mechanisms for effector Treg cell expansion in tumor are still unknown. We demonstrate that effector Treg cell-mediated suppression of antitumor CD8(+) T cells is tumor-nonspecific. Furthermore, TNFR2 expression is increased in these Treg cells by Affymetrix chip analysis which was confirmed by monoclonal antibody staining in both hepatocellular carcinoma (HCC) and colorectal cancer (CRC) patients and murine models. Correspondingly, increased levels of TNF-alpha in both tissue and serum were also demonstrated. Interestingly, TNF-alpha could not only expand effector Treg cells through TNFR2 signaling, but also enhanced their suppressive activity against antitumor immunity of CD8(+) T cells. Furthermore, targeting TNFR2 signaling with a TNF-alpha inhibitor could selectively reduce rapid resurgence of effector Treg cells after cyclophosphamide-induced lymphodepletion and markedly inhibit the growth of established tumors. Herein, we propose a novel mechanism in which TNF-alpha could promote tumor-associated effector Treg cell expansion and suggest a new cancer immunotherapy strategy using TNF-alpha inhibitors to reduce effector Treg cells expansion after cyclophosphamide-induced lymphodepletion.
C1 [Chang, Li-Yuan; Mahalingam, Jayashri; Chen, Wei-Ting; Huang, Chien-Hao; Jeng, Wen-Juei; Chen, Yi-Cheng; Lin, Shi-Ming; Sheen, I-Shyan; Lin, Chun-Yen] Chang Gung Mem Hosp, Div Hepatol, Dept Gastroenterol & Hepatol, Linkou Med Ctr, Taoyuan, Taiwan.
[Lin, Yung-Chang; Chiang, Jy-Ming; Su, Shih-Huan; Huang, Ching-Tai; Chen, Wei-Ting; Chen, Yi-Cheng; Lin, Shi-Ming; Sheen, I-Shyan; Lin, Chun-Yen] Chang Gung Univ, Coll Med, Taoyuan, Taiwan.
[Lin, Yung-Chang] Chang Gung Mem Hosp, Dept Hematol Oncol, Linkou Med Ctr, Taoyuan, Taiwan.
[Chiang, Jy-Ming] Chang Gung Mem Hosp, Colorectal Surg Sect, Linkou Med Ctr, Dept Surg, Taoyuan, Taiwan.
[Huang, Ching-Tai] Chang Gung Mem Hosp, Dept Infect Dis, Linkou Med Ctr, Taoyuan, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; Chang Gung Memorial
Hospital; Chang Gung Memorial Hospital; Chang Gung Memorial Hospital
RP Lin, CY (corresponding author), Chang Gung Mem Hosp, Div Hepatol, Dept Gastroenterol & Hepatol, Linkou Med Ctr, Taoyuan, Taiwan.
EM chunyenlin@gmail.com
RI Lin, Chiu-Yue/AFE-3858-2022; CHEN, WEI-TING/AFL-9663-2022; Chung,
Chi-Hsiang/AAY-3386-2021; Chen, Yi-Cheng/AFK-2872-2022; Huang,
Chien-Hao/AGG-4501-2022
OI Lin, Chun-Yen/0000-0003-3007-3190; Jeng, Wen-Juei/0000-0002-3706-1259;
Huang, Chien-Hao/0000-0003-1689-3221
FU Chang Gung Memorial Hospital [CMRPG 380363, CMRPG 390363, CMRPG 3D0041,
CMRPG3C0653]; National Health Research Institutes, Taiwan [NHRI EX
102-1010BI]; Ministry of Science and Technology, Taiwan [NMRPG3C6332]
FX This work was supported by CMRPG 380363; CMRPG 390363; CMRPG 3D0041;
CMRPG3C0653 from Chang Gung Memorial Hospital and NHRI EX 102-1010BI
from The National Health Research Institutes, Taiwan and NMRPG3C6332
from Ministry of Science and Technology, Taiwan.
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NR 42
TC 43
Z9 47
U1 0
U2 13
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 2162-402X
J9 ONCOIMMUNOLOGY
JI OncoImmunology
PY 2015
VL 4
IS 10
AR e1040215
DI 10.1080/2162402X.2015.1040215
PG 12
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA CP9UT
UT WOS:000360241200014
PM 26451304
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Tao, L
Ren, XM
Zhai, WH
Chen, Z
AF Tao, Li
Ren, Xiaomeng
Zhai, Wenhui
Chen, Zheng
TI Progress and Prospects of Non-Canonical NF-κB Signaling Pathway in the
Regulation of Liver Diseases
SO MOLECULES
LA English
DT Review
DE non-canonical NF-kappa B signaling pathway; NF-kappa B-inducing kinase;
liver diseases; NF-kappa B2; metabolism
ID CELL-ACTIVATING FACTOR; HEPATIC ISCHEMIA/REPERFUSION INJURY;
ISCHEMIA-REPERFUSION INJURY; LYMPHOTOXIN-BETA-RECEPTOR;
HEPATOCELLULAR-CARCINOMA; CARBON TETRACHLORIDE; HEPATOCYTE APOPTOSIS;
TISSUE INFLAMMATION; INSULIN-RESISTANCE; OXIDATIVE STRESS
AB Non-canonical nuclear factor kappa B (NF-kappa B) signaling pathway regulates many physiological and pathological processes, including liver homeostasis and diseases. Recent studies demonstrate that non-canonical NF-kappa B signaling pathway plays an essential role in hyperglycemia, non-alcoholic fatty liver disease, alcoholic liver disease, liver regeneration, liver injury, autoimmune liver disease, viral hepatitis, and hepatocellular carcinoma. Small-molecule inhibitors targeting to non-canonical NF-kappa B signaling pathway have been developed and shown promising results in the treatment of liver injuries. Here, the recent advances and future prospects in understanding the roles of the non-canonical NF-kappa B signaling pathways in the regulation of liver diseases are discussed.
C1 [Tao, Li; Zhai, Wenhui] 305 Hosp Peoples Liberat Army, Emergency Dept, Beijing 100017, Peoples R China.
[Ren, Xiaomeng] Shenyang Univ Chem Technol, Coll Pharmaceut & Biol Engn, Shenyang 110142, Peoples R China.
[Chen, Zheng] Harbin Inst Technol, Sch Life Sci & Technol, Hit Ctr Life Sci, Harbin 150001, Peoples R China.
C3 Shenyang University of Chemical Technology; Harbin Institute of
Technology
RP Ren, XM (corresponding author), Shenyang Univ Chem Technol, Coll Pharmaceut & Biol Engn, Shenyang 110142, Peoples R China.; Chen, Z (corresponding author), Harbin Inst Technol, Sch Life Sci & Technol, Hit Ctr Life Sci, Harbin 150001, Peoples R China.
EM taolistar@163.com; renxm@syuct.edu.cn; pla305hos@126.com;
chenzheng@hit.edu.cn
RI chen, zheng/J-4600-2014; TAO, Li/HIR-4254-2022
OI , zheng/0000-0001-7129-6644
FU National Natural Science Foundation of China [92057110, 31971083]; Young
Scientists Nurturing Program from the Department of Education of
Liaoning Province [LQ2020022]; 305 Hospital of People's Liberation Army
Research Grant [17YQ01]
FX This research was funded by the National Natural Science Foundation of
China Grant [92057110 and 31971083], the Young Scientists Nurturing
Program from the Department of Education of Liaoning Province
[LQ2020022] and 305 Hospital of People's Liberation Army Research Grant
[17YQ01]. The APC was funded by 305 Hospital of People's Liberation Army
Research Grant [17YQ01].
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NR 97
TC 5
Z9 7
U1 3
U2 26
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD JUL
PY 2022
VL 27
IS 13
AR 4275
DI 10.3390/molecules27134275
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 2W0JA
UT WOS:000824219900001
PM 35807520
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Guo, YX
Wang, N
Wu, WC
Li, CQ
Chen, RH
Zhang, Y
Li, X
AF Guo, Yu-Xin
Wang, Na
Wu, Wen-Cheng
Li, Cui-Qin
Chen, Rui-Heng
Zhang, Yuan
Li, Xing
TI The Role of miR-23b in Cancer and Autoimmune Disease
SO JOURNAL OF ONCOLOGY
LA English
DT Review
ID HEPATOCELLULAR-CARCINOMA; LUNG-CANCER; INCIDENCE TRENDS; POOR-PROGNOSIS;
UP-REGULATION; T-CELLS; MIRNA; MICRORNAS; GENE; EXPRESSION
AB Short-stranded miRNAs are single-stranded RNA molecules involved in the regulation of gene expression. miRNAs are involved in a variety of cellular physiological processes, including cell proliferation, differentiation, and apoptosis. miR-23b have been identified to act both as oncogenes and as tumor suppressors. In addition, miR-23b is related to inflammation resistance to various autoimmune diseases and restrained inflammatory cell migration. The characterization of the specific alterations in the patterns of miR-23b expression in cancer and autoimmune disease has great potential for identifying biomarkers for early disease diagnosis, as well as for potential therapeutic intervention in various diseases. In this review, we summarize the ever-expanding role of miR-23b and its target genes in different models and offer insight into how this multifunctional miRNA modulates tumor cell proliferation and apoptosis or inflammatory cell activation, differentiation, and migration.
C1 [Guo, Yu-Xin; Wu, Wen-Cheng; Li, Cui-Qin; Zhang, Yuan; Li, Xing] Shaanxi Normal Univ, Minist Educ, Coll Life Sci,Key Lab Med Resources & Nat Pharmac, Nat Engn Lab Resource Dev Endangered Crude Drugs, Xian 710119, Shaanxi, Peoples R China.
[Wang, Na] First Peoples Hosp Tianshui, Surg Oncol Dept, Tianshui 741000, Gansu, Peoples R China.
[Chen, Rui-Heng] Shaanxi Normal Univ, High Sch Affiliated, Xian 710119, Shaanxi, Peoples R China.
C3 Shaanxi Normal University; Shaanxi Normal University
RP Zhang, Y; Li, X (corresponding author), Shaanxi Normal Univ, Minist Educ, Coll Life Sci,Key Lab Med Resources & Nat Pharmac, Nat Engn Lab Resource Dev Endangered Crude Drugs, Xian 710119, Shaanxi, Peoples R China.
EM 2326424138@qq.com; wangna_wn2002@hotmail.com; wuwencheng122@163.com;
licuiqin16@snnu.edu.cn; 731053922@qq.com; yuanzhang_bio@126.com;
xingli_xian@126.com
OI , Yuan/0000-0002-2463-4599; Li, Xing/0000-0002-0742-1364
FU Chinese National Natural Science Foundation [31970771, 82071396,
81771345]; Natural Science Foundation of Shaanxi Province, China
[2021ZDLSF03-09, 2020SF-314]; Fundamental Research Funds for the Central
Universities [GK202007022, GK202105002, GK202006003, TD2020039Y,
2020CSZL009]
FX AcknowledgmentsThis study was supported by the Chinese National Natural
Science Foundation (Grant nos. 31970771, 82071396, and 81771345), the
Natural Science Foundation of Shaanxi Province, China (Grant nos.
2021ZDLSF03-09 and 2020SF-314), and the Fundamental Research Funds for
the Central Universities (Grant nos. GK202007022, GK202105002,
GK202006003, TD2020039Y, and 2020CSZL009).
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NR 106
TC 20
Z9 21
U1 0
U2 3
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-8450
EI 1687-8469
J9 J ONCOL
JI J. Oncol.
PD NOV 3
PY 2021
VL 2021
AR 6473038
DI 10.1155/2021/6473038
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WY8EB
UT WOS:000719509500001
PM 34777498
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Tan, JT
Tang, XW
He, YX
Xu, XM
Qiu, DP
Chen, JF
Zhang, QH
Zhang, LQ
AF Tan, Juntao
Tang, Xuewen
He, Yuxin
Xu, Xiaomei
Qiu, Daoping
Chen, Jianfei
Zhang, Qinghua
Zhang, Lingqin
TI In-patient Expenditure Between 2012 and 2020 Concerning Patients With
Liver Cirrhosis in Chongqing: A Hospital-Based Multicenter Retrospective
Study
SO FRONTIERS IN PUBLIC HEALTH
LA English
DT Article
DE liver cirrhosis; medical expenditure; multiple linear regression; time
trends; China
ID HEPATITIS-B; HEPATOCELLULAR-CARCINOMA; ECONOMIC BURDEN; EPIDEMIOLOGY;
READMISSIONS; MANAGEMENT; DISEASE; CANCER
AB BackgroundLiver cirrhosis is a major global health and economic challenge, placing a heavy economic burden on patients, families, and society. This study aimed to investigate medical expenditure trends in patients with liver cirrhosis and assess the drivers for such medical expenditure among patients with liver cirrhosis. MethodsMedical expenditure data concerning patients with liver cirrhosis was collected in six tertiary hospitals in Chongqing, China, from 2012 to 2020. Trends in medical expenses over time and trends according to subgroups were described, and medical expenditure compositions were analyzed. A multiple linear regression model was constructed to evaluate the factors influencing medical expenditure. All expenditure data were reported in Chinese Yuan (CNY), based on the 2020 value, and adjusted using the year-specific health care consumer price index for Chongqing. ResultsMedical expenditure for 7,095 patients was assessed. The average medical expenditure per patient was 16,177 CNY. An upward trend in medical expenditure was observed in almost all patient subgroups. Drug expenses were the largest contributor to medical expenditure in 2020. A multiple linear regression model showed that insurance type, sex, age at diagnosis, marital status, length of stay, smoking status, drinking status, number of complications, autoimmune liver disease, and the age-adjusted Charlson comorbidity index score were significantly related to medical expenditure. ConclusionConservative estimates suggest that the medical expenditure of patients with liver cirrhosis increased significantly from 2012 to 2020. Therefore, it is necessary to formulate targeted measures to reduce the personal burden on patients with liver cirrhosis.
C1 [Tan, Juntao; Qiu, Daoping] Peoples Hosp Chongqing Banan Dist, Med Records & Stat Room, Chongqing, Peoples R China.
[Tang, Xuewen; Chen, Jianfei] Peoples Hosp Chongqing Banan Dist, Dept Cardiol, Chongqing, Peoples R China.
[He, Yuxin] Peoples Hosp Chongqing Banan Dist, Dept Med Adm, Chongqing, Peoples R China.
[Xu, Xiaomei] Fifth Peoples Hosp Chengdu, Dept Gastroenterol, Chengdu, Peoples R China.
[Xu, Xiaomei] Chongqing Med Univ, Dept Infect Dis, Affiliated Hosp 1, Chongqing, Peoples R China.
[Zhang, Qinghua] Peoples Hosp Chongqing Banan Dist, Dept Sci & Educ, Chongqing, Peoples R China.
[Zhang, Lingqin] Peoples Hosp Chongqing Bishan Dist, Dept Biomed Equipment, Chongqing, Peoples R China.
C3 Chongqing Medical University
RP Tang, XW (corresponding author), Peoples Hosp Chongqing Banan Dist, Dept Cardiol, Chongqing, Peoples R China.
EM xuewentang_bnrmyy@163.com
RI Zhang, Qinghua/G-3980-2019; zhang, lidong/GSA-0096-2022
CR Allen AM, 2016, HEPATOLOGY, V64, P2165, DOI 10.1002/hep.28812
Bailey DE, 2021, WESTERN J NURS RES, V43, P509, DOI 10.1177/0193945920952059
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Bajaj JS, 2016, HEPATOLOGY, V64, P200, DOI 10.1002/hep.28414
Berman K, 2011, CLIN GASTROENTEROL H, V9, P254, DOI 10.1016/j.cgh.2010.10.035
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Das UN, 2019, J ADV RES, V17, P17, DOI 10.1016/j.jare.2018.12.006
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Dimitrova M, 2017, FRONT MED-LAUSANNE, V4, DOI 10.3389/fmed.2017.00125
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National Bureau of Statistics of China, 2020, HUBEI STAT YB
Neff Guy W, 2011, Gastroenterol Hepatol (N Y), V7, P661
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Raffetti E, 2016, LIVER INT, V36, P1239, DOI 10.1111/liv.13142
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Xu XY, 2019, WORLD J GASTROENTERO, V25, P5403, DOI 10.3748/wjg.v25.i36.5403
Zeng YB, 2019, INT J EQUITY HEALTH, V18, DOI 10.1186/s12939-019-0933-2
Zhang H, 2015, ASIA-PAC J PUBLIC HE, V27, p41S, DOI 10.1177/1010539514560057
Zheng M, 2021, RISK MANAG HEALTHC P, V14, P2133, DOI 10.2147/RMHP.S298145
Zheng Y, 2020, VIROL J, V17, DOI 10.1186/s12985-020-01393-z
Zhu K, 2017, INT J EQUITY HEALTH, V16, DOI 10.1186/s12939-017-0690-z
NR 40
TC 3
Z9 3
U1 1
U2 16
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-2565
J9 FRONT PUBLIC HEALTH
JI Front. Public Health
PD MAR 8
PY 2022
VL 10
AR 780704
DI 10.3389/fpubh.2022.780704
PG 11
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA 0C3GM
UT WOS:000775205800001
PM 35350474
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Huang, Y
Joseph, J
Bastiaan de Boer, W
Cheng, W
Adams, LA
MacQuillan, G
Garas, G
Raftopoulos, S
Jeffrey, GP
AF Huang, Yi
Joseph, John
Bastiaan de Boer, W.
Cheng, Wendy
Adams, Leon A.
MacQuillan, Gerry
Garas, George
Raftopoulos, Spiro
Jeffrey, Gary P.
TI Long-term Liver-related Outcomes of Patients With Chronic Liver Diseases
in Australia
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Survival; ALD; HCC; Cirrhosis
ID HEPATITIS-C VIRUS; FIBROSIS PROGRESSION; COMPETING RISKS;
NATURAL-HISTORY; CLINICAL-COURSE; MORTALITY; ALCOHOL; EPIDEMIOLOGY;
PREVALENCE; INFECTION
AB BACKGROUND & AIMS: Chronic liver disease is a major health burden that produces significant liver-related morbidity and mortality. We aimed to evaluate liver-related outcomes of patients with different causes of chronic liver disease in Australia.
METHODS: We collected data from 10,933 patients with chronic liver disease assessed by Hepascore (a serum fibrosis model) in Western Australia from 2004 through 2015. We obtained records of liver-related death, transplantation, decompensation, and hepatocellular carcinoma from WA Data Linkage Unit databases. Competing risk analysis was used to calculate the cumulative risk of each clinical endpoint, and risks for clinical endpoints were compared among all causes of chronic liver disease.
RESULTS: In our final cohort for analysis, 5566 patients had hepatitis C virus (HCV) infection, 1989 had HBV infection, 119 were infected with HBV and HCV, 955 had alcohol-associated liver disease, 1597 had non-alcoholic fatty liver disease (NAFLD), 123 had alcohol-associated liver disease and metabolic risk factors, 561 had autoimmune liver disease without overlap syndrome, and 23 autoimmune overlap syndrome. Significant differences among chronic liver diseases were observed in risk of all-cause death (P < .001), liver-related death (P < .001), liver transplantation (P < .001), and decompensation (P < .001) but not hepatocellular carcinoma (P = .095). Patients with alcohol-associated liver disease had the highest 5-year cumulative risk of liver-related death (17.1%) and the second-highest 5-year cumulative risk of decompensation (29.2%). Multivariate analysis found patients with alcohol-associated liver disease had significantly higher risks of liver-related death and decompensation than patients with HCV infection with hazard ratios (HRs) of 2.39 (95% CI, 1.88-3.03) and 3.42 (95% CI, 2.74-4.27), respectively. Patients with NAFLD had a significantly lower risk of liver related death and decompensation than patients with HCV infection, with HRs of 0.67 (95% CI, 0.48-0.95) and 0.70 (95% CI, 0.52-0.94) respectively.
CONCLUSIONS: In an analysis of patients in Western Australia, we found patients with alcohol-associated liver disease to have significantly higher risk of decompensation and liver-related death than patients with HCV infection, whereas patients with NAFLD have significantly lower risks of either outcome.
C1 [Huang, Yi; Adams, Leon A.; MacQuillan, Gerry; Garas, George; Jeffrey, Gary P.] Univ Western Australia, Sch Med & Pharmacol, Perth, WA, Australia.
[Huang, Yi; Adams, Leon A.; MacQuillan, Gerry; Garas, George; Raftopoulos, Spiro; Jeffrey, Gary P.] Sir Charles Gairdner Hosp, Dept Hepatol, Perth, WA, Australia.
[Joseph, John] PathWest Lab Med, Dept Biochem, Perth, WA, Australia.
[Bastiaan de Boer, W.] PathWest Lab Med, Dept Anat Pathol, Perth, WA, Australia.
[Cheng, Wendy] Royal Perth Hosp, Dept Gastroenterol & Hepatol, Perth, WA, Australia.
C3 University of Western Australia; University of Western Australia; Sir
Charles Gairdner Hospital; Pathwest Laboratory Medicine; Pathwest
Laboratory Medicine; University of Western Australia; East Metropolitan
Health Service; Royal Perth Hospital
RP Jeffrey, GP (corresponding author), Univ Western Australia, Sch Med & Pharmacol, Harry Perkins Inst Med Res, 5th Floor,6 Verdun St, Nedlands, WA 6009, Australia.
EM gary.jeffrey@uwa.edu.au
RI Raftopoulos, Spiro/HDL-7127-2022
FU National Health and Medical Research Council, Australia; Cancer Council
Western Australia; Research Advisory Committee Project grant, Sir
Charles Gairdner Hospital
FX Supported by project grant, National Health and Medical Research
Council, Australia; postdoctoral fellowship grant, Cancer Council
Western Australia; and Research Advisory Committee Project grant, Sir
Charles Gairdner Hospital. The University of Western Australia (employer
of LAA and GPJ) hold the patent for Hepascore and have a licencing
agreement with Quest Diagnostics.
CR Adams LA, 2005, GASTROENTEROLOGY, V129, P113, DOI 10.1053/j.gastro.2005.04.014
Adams LA, 2005, CLIN CHEM, V51, P1867, DOI 10.1373/clinchem.2005.048389
Amin J, 2006, J HEPATOL, V45, P197, DOI 10.1016/j.jhep.2006.02.014
Bellentani S, 2000, ANN INTERN MED, V132, P112, DOI 10.7326/0003-4819-132-2-200001180-00004
Boberg KM, 2011, J HEPATOL, V54, P374, DOI 10.1016/j.jhep.2010.09.002
Dominguez M, 2008, AM J GASTROENTEROL, V103, P2747, DOI 10.1111/j.1572-0241.2008.02104.x
European Assoc Study Liver, 2017, J HEPATOL, V67, P370, DOI 10.1016/j.jhep.2017.03.021
GESA, EC COST HLTH BURD LI
Huang Y, 2015, INTERN MED J, V45, P48, DOI 10.1111/imj.12626
Huang Y, 2017, LIVER INT, V37, P121, DOI 10.1111/liv.13116
Jepsen P, 2015, HEPATOLOGY, V62, P292, DOI 10.1002/hep.27598
Jepsen P, 2010, HEPATOLOGY, V51, P1675, DOI 10.1002/hep.23500
Kim D, 2013, HEPATOLOGY, V57, P1357, DOI 10.1002/hep.26156
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Poupon R, 2006, HEPATOLOGY, V44, P85, DOI 10.1002/hep.21229
Poynard T, 2003, J HEPATOL, V38, P257, DOI 10.1016/S0168-8278(02)00413-0
Raynard B, 2002, HEPATOLOGY, V35, P635, DOI 10.1053/jhep.2002.31782
Ruhl CE, 2005, CLIN GASTROENTEROL H, V3, P1260, DOI 10.1016/S1542-3565(05)00743-3
Sagnelli E, 2004, INFECTION, V32, P144, DOI 10.1007/s15010-004-3080-6
Satagopan JM, 2004, BRIT J CANCER, V91, P1229, DOI 10.1038/sj.bjc.6602102
Thein HH, 2008, HEPATOLOGY, V48, P418, DOI 10.1002/hep.22375
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Younossi ZM, 2016, HEPATOLOGY, V64, P73, DOI 10.1002/hep.28431
NR 26
TC 13
Z9 13
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD FEB
PY 2020
VL 18
IS 2
BP 496
EP +
DI 10.1016/j.cgh.2019.07.013
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA KC0SR
UT WOS:000506898700038
PM 31319186
DA 2025-01-07
ER
PT J
AU Boonstra, K
Weersma, RK
van Erpecum, KJ
Rauws, EA
Spanier, BWM
Poen, AC
van Nieuwkerk, KM
Drenth, JP
Witteman, BJ
Tuynman, HA
Naber, AH
Kingma, PJ
van Buuren, HR
van Hoek, B
Vleggaar, FP
van Geloven, N
Beuers, U
Ponsioen, CY
AF Boonstra, Kirsten
Weersma, Rinse K.
van Erpecum, Karel J.
Rauws, Erik A.
Spanier, B. W. Marcel
Poen, Alexander C.
van Nieuwkerk, Karin M.
Drenth, Joost P.
Witteman, Ben J.
Tuynman, Hans A.
Naber, Anton H.
Kingma, Paul J.
van Buuren, Henk R.
van Hoek, Bart
Vleggaar, Frank P.
van Geloven, Nan
Beuers, Ulrich
Ponsioen, Cyriel Y.
CA EpiPSCPBC Study Grp
TI Population-Based Epidemiology, Malignancy Risk, and Outcome of Primary
Sclerosing Cholangitis
SO HEPATOLOGY
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; PRIMARY BILIARY-CIRRHOSIS; DOSE
URSODEOXYCHOLIC ACID; NATURAL-HISTORY; HEPATOCELLULAR-CARCINOMA;
AUTOIMMUNE HEPATITIS; PROGNOSTIC-FACTORS; LIVER-DISEASE; CANCER;
CHOLANGIOCARCINOMA
AB Extensive population-based studies are much needed to accurately establish epidemiology and disease course in patients with primary sclerosing cholangitis (PSC). We aimed to obtain population-based prevalence and incidence figures, insight in disease course with regard to survival, liver transplantation (LT), and occurrence of malignancies, as well as risk factors thereof. Four independent hospital databases were searched in 44 hospitals in a large geographically defined area of the Netherlands, comprising 50% of the population. In addition, all PSC patients in the three Dutch liver transplant centers and all inflammatory bowel disease (IBD) patients in the adherence area of a large district hospital were identified. All medical records were reviewed on-site, verifying diagnosis. Five hundred and ninety PSC patients were identified, resulting in an incidence of 0.5 and a point prevalence of 6.0 per 100,000. Median follow up was 92 months. Estimated median survival from diagnosis until LT or PSC-related death in the entire cohort was 21.3 years, as opposed to 13.2 years in the combined transplant centers cohort (n = 422; P < 0.0001). Colorectal carcinoma (CRC) risk was 10-fold increased, as compared to ulcerative colitis controls, and developed at a much younger age (39 years; range, 26-64), compared to IBD controls (59 years; range, 34-73; P = 0.019). Colonoscopic surveillance was associated with significantly better outcome. Conclusion: This study exemplifies that, for relatively rare diseases, it is paramount to collect observational data from large, population-based cohorts, because incidence and prevalence rates of PSC are markedly lower and survival much longer than previously reported. The selection of a bias-free, population-based cohort showed a significantly longer survival, compared to the tertiary referral cohort. CRC can develop at an early age, warranting surveillance from time of PSC diagnosis. (Hepatology 2013; 58:2045-2055)
C1 [Boonstra, Kirsten; Beuers, Ulrich; Ponsioen, Cyriel Y.] Acad Med Ctr, Dept Gastroenterol & Hepatol, NL-1100 DE Amsterdam, Netherlands.
[Weersma, Rinse K.] Univ Groningen, Univ Med Ctr Groningen, Dept Gastroenterol & Hepatol, Groningen, Netherlands.
[Weersma, Rinse K.] Univ Groningen, Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
[van Erpecum, Karel J.; Vleggaar, Frank P.] Univ Med Ctr Utrecht, Dept Gastroenterol & Hepatol, Utrecht, Netherlands.
[Spanier, B. W. Marcel] Rijnstate Hosp, Dept Gastroenterol & Hepatol, Arnhem, Netherlands.
[Poen, Alexander C.] Isala Clin, Dept Gastroenterol & Hepatol, Zwolle, Netherlands.
[van Nieuwkerk, Karin M.] Vrije Univ Amsterdam Med Ctr, Dept Gastroenterol & Hepatol, Amsterdam, Netherlands.
[Drenth, Joost P.] Radboud Univ Nijmegen, Dept Gastroenterol & Hepatol, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Witteman, Ben J.] Gelderse Vallei Hosp, Dept Gastroenterol & Hepatol, Ede, Netherlands.
[Tuynman, Hans A.] Med Ctr Alkmaar, Dept Gastroenterol & Hepatol, Alkmaar, Netherlands.
[Naber, Anton H.; Kingma, Paul J.] Tergooiziekenhuizen, Dept Gastroenterol & Hepatol, Hilversum Blaricum, Netherlands.
[van Buuren, Henk R.] Erasmus Univ, Med Ctr, Dept Gastroenterol & Hepatol, Rotterdam, Netherlands.
[van Hoek, Bart] Leiden Univ, Med Ctr, Dept Gastroenterol & Hepatol, Leiden, Netherlands.
[van Geloven, Nan] Acad Med Ctr, Clin Res Unit, NL-1100 DE Amsterdam, Netherlands.
C3 University of Amsterdam; Academic Medical Center Amsterdam; University
of Groningen; University of Groningen; Utrecht University; Utrecht
University Medical Center; Rijnstate Hospital; Isala Clinics; Vrije
Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER; Radboud University
Nijmegen; Gelderse Vallei Hospital; Medical Center Of Alkmaar; Erasmus
University Rotterdam; Erasmus MC; Leiden University; Leiden University
Medical Center (LUMC); Leiden University - Excl LUMC; University of
Amsterdam; Academic Medical Center Amsterdam
RP Ponsioen, CY (corresponding author), Acad Med Ctr, Dept Gastroenterol & Hepatol, POB 22700, NL-1100 DE Amsterdam, Netherlands.
EM c.y.ponsioen@amc.uva.nl
RI van Hoek, Bart/AAU-8953-2020; Spanier, Marcel/HKE-2275-2023; Weersma,
Rinse/ABE-3807-2021; Drenth, Joost/V-7436-2019
OI Drenth, Joost PH/0000-0001-8027-3073; Boonstra,
Kirsten/0009-0000-6181-1227; van Hoek, Bart/0000-0001-6527-764X
FU AbbVie Inc. (Hoofddorp, the Netherlands); Tramedico Inc. (Weesp the
Netherlands); Dr. Falk Pharma Benelux Inc. ( Breda, Netherlands);
Netherlands Organization for Scientific Research (NWO) [90.700.281]
FX This research was supported by unrestricted grants from AbbVie Inc.
(Hoofddorp, the Netherlands), Tramedico Inc. (Weesp the Netherlands),
and Dr. Falk Pharma Benelux Inc. (Breda, Netherlands). R. K. W. is
supported by a clinical fellowship grant (90.700.281) from the
Netherlands Organization for Scientific Research (NWO).
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Boberg KM, 1998, SCAND J GASTROENTERO, V33, P99
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WIESNER RH, 1989, HEPATOLOGY, V10, P430, DOI 10.1002/hep.1840100406
NR 41
TC 460
Z9 482
U1 0
U2 44
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD DEC
PY 2013
VL 58
IS 6
BP 2045
EP 2055
DI 10.1002/hep.26565
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 257LH
UT WOS:000327385000052
PM 23775876
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Saito, M
Ogasawara, R
Izumiyama, K
Mori, A
Kondo, T
Tanaka, M
Morioka, M
Ieko, M
AF Saito, Makoto
Ogasawara, Reiki
Izumiyama, Koh
Mori, Akio
Kondo, Takeshi
Tanaka, Masanori
Morioka, Masanobu
Ieko, Masahiro
TI Acquired hemophilia A in solid cancer: Two case reports and review of
the literature
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Review
DE Acquired hemophilia A; Coagulation factor VIII; Solid cancer; Gastric
cancer; Hepatocellular carcinoma; Case report
ID FACTOR-VIII; INHIBITORS; PATIENT
AB Acquired hemophilia A (AHA) is a rare, hemorrhagic autoimmune disease, whose pathogenesis involves reduced coagulation factor VIII (FVIII) activity related to the appearance of inhibitors against FVIII. Common etiological factors include autoimmune diseases, malignancy, and pregnancy. We report two cases of AHA in solid cancer. The first case is a 63-year-old man who developed peritoneal and intestinal bleeding after gastrectomy for gastric cancer. He was diagnosed with AHA, and was treated with prednisone, followed by cyclophosphamide. In the second case, a 68-year-old man developed a subcutaneous hemorrhage. He was diagnosed with AHA in hepatocellular carcinoma on CT imaging, and treated with rituximab alone. Hemostasis was achieved for both patients without bypassing agents as the amount of inhibitors was reduced and eradicated. However, both patients died within 1 year due to cancer progression. Successful treatment for AHA in solid cancer can be difficult because treatment of the underlying malignancy is also required.
C1 [Saito, Makoto; Ogasawara, Reiki; Izumiyama, Koh; Mori, Akio; Kondo, Takeshi; Tanaka, Masanori; Morioka, Masanobu] Aiiku Hosp, Dept Internal Med & Hematol, Sapporo, Hokkaido 0640804, Japan.
[Ieko, Masahiro] Hlth Sci Univ Hokkaido, Dept Internal Med, Toubetsu 0610293, Japan.
C3 Health Sciences University of Hokkaido
RP Saito, M (corresponding author), Aiiku Hosp, Dept Internal Med & Hematol, Chuo Ku, Minami 4 Nishi 25, Sapporo, Hokkaido 0640804, Japan.
EM ikyoku@aiiku-hp.or.jp
RI Kondo, Takeshi/G-2103-2012
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NR 22
TC 7
Z9 7
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD NOV 26
PY 2018
VL 6
IS 14
BP 781
EP 785
DI 10.12998/wjcc.v6.i14.781
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HB7TV
UT WOS:000451284700008
PM 30510943
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Nagashima, K
Sano, I
Kobayashi, T
Eto, K
Nagai, K
Ninomiya, R
Suzuki, A
Oohata, Y
Konishi, K
Nakano, T
Yamamoto, F
AF Nagashima, Kazunori
Sano, Itsuki
Kobayashi, Tomoe
Eto, Kazunori
Nagai, Kosuke
Ninomiya, Ryusuke
Suzuki, Akira
Oohata, Yoshihiro
Konishi, Kouhei
Nakano, Tsuyoshi
Yamamoto, Fumiyasu
TI IgG4-related Lung Pseudotumor and Pleural Inflammation with Autoimmune
Hepatitis
SO INTERNAL MEDICINE
LA English
DT Article; Proceedings Paper
CT 276th Hokkaido Area Meeting of the Japanese-Society-of-Internal-Medicine
CY FEB, 2016
CL Sapporo, JAPAN
SP Japanese Soc Internal Med
DE IgG4; lung pseudotumor; autoimmune hepatitis
ID SYSTEMIC-DISEASE; PLASMA-CELLS; FDG PET/CT; PANCREATITIS; DIAGNOSIS;
FEATURES; CANCER; COHORT
AB A 63-year-old man was admitted to our department following a secondary medical examination. Blood tests showed high levels of liver enzymes, IgG, IgG4, and antinuclear antibody. Computed tomography showed tumors in the bilateral lower lobes of the lungs and pleural thickening. After pleural and liver biopsy procedures, he was conclusively diagnosed with IgG4-related lung pseudotumor and pleural inflammation with autoimmune hepatitis. We started treatment with prednisolone 40 mg/day, and chest radiograph and blood tests showed signs of improvement. This was a rare case that suggested an association between IgG4-related disease and autoimmune hepatitis.
C1 [Nagashima, Kazunori; Kobayashi, Tomoe; Eto, Kazunori; Nagai, Kosuke; Konishi, Kouhei; Yamamoto, Fumiyasu] Tomakomai City Hosp, Gastroenterol Med, Tomakomai, Hokkaido, Japan.
[Sano, Itsuki] Hokkaido Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sapporo, Hokkaido, Japan.
[Ninomiya, Ryusuke; Oohata, Yoshihiro; Nakano, Tsuyoshi] Tomakomai City Hosp, Resp Med, Tomakomai, Hokkaido, Japan.
[Suzuki, Akira] Tomakomai City Hosp, Dept Pathol, Tomakomai, Hokkaido, Japan.
[Suzuki, Akira] KKR Sapporo Med Ctr, Dept Pathol, Sapporo, Hokkaido, Japan.
C3 Hokkaido University
RP Nagashima, K (corresponding author), Tomakomai City Hosp, Gastroenterol Med, Tomakomai, Hokkaido, Japan.
EM 1-tetsu@frontier.hokudai.ac.jp
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NR 26
TC 8
Z9 8
U1 0
U2 3
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
EI 1349-7235
J9 INTERNAL MED
JI Intern. Med.
PY 2018
VL 57
IS 1
BP 43
EP 48
DI 10.2169/internalmedicine.9026-17
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC General & Internal Medicine
GA FT1AW
UT WOS:000422866000007
PM 29033427
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Czaja, AJ
AF Czaja, Albert J.
TI Autoimmune hepatitis in diverse ethnic populations and geographical
regions
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE autoimmune hepatitis; cholestasis; ethnic background; genetic
predispositions; non-white patients; regional differences
ID PRIMARY BILIARY-CIRRHOSIS; CHRONIC LIVER-DISEASE; HUMAN-LEUKOCYTE
ANTIGEN; PRIMARY SCLEROSING CHOLANGITIS; CRYPTOGENIC CHRONIC HEPATITIS;
MICROSOMAL ANTIBODY TYPE-1; DOSE URSODEOXYCHOLIC ACID; CHRONIC ACTIVE
HEPATITIS; D-RECEPTOR POLYMORPHISMS; HEPATOCELLULAR-CARCINOMA
AB Autoimmune hepatitis has diverse clinical phenotypes and outcomes in ethnic groups within a country and between countries, and these differences may reflect genetic predispositions, indigenous etiological agents, pharmacogenomic mechanisms and socioeconomic reasons. In the USA, African-American patients have cirrhosis more commonly, treatment failure more frequently and higher mortality than white American patients. Survival is poorest in Asian-American patients. Autoimmune hepatitis in other countries is frequently associated with genetic predispositions that may favor susceptibility to indigenous etiological agents. Cholestatic features influence treatment response; acute-on-chronic liver disease increases mortality and socioeconomic and cultural factors affect prognosis. Ethnic-based deviations from classical phenotypes and the frequency of late-stage disease can complicate the diagnosis and management of autoimmune hepatitis in non-white populations.
C1 Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Czaja, AJ (corresponding author), Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
EM czaja.albert@mayo.edu
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NR 227
TC 47
Z9 48
U1 0
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD MAY
PY 2013
VL 7
IS 4
BP 365
EP 385
DI 10.1586/EGH.13.21
PG 21
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 138YS
UT WOS:000318548700015
PM 23639095
DA 2025-01-07
ER
PT J
AU Dumortier, J
Besch, C
Moga, L
Coilly, A
Conti, F
Corpechot, C
Del Bello, A
Faitot, F
Francoz, C
Hilleret, MN
Houssel-Debry, P
Jezequel, C
Lavayssière, L
Neau-Cransac, M
Erard-Poinsot, D
de Lédinghen, V
Bourlière, M
Bureau, C
Ganne-Carrié, N
AF Dumortier, Jerome
Besch, Camille
Moga, Lucile
Coilly, Audrey
Conti, Filomena
Corpechot, Christophe
Del Bello, Arnaud
Faitot, Francois
Francoz, Claire
Hilleret, Marie-Noelle
Houssel-Debry, Pauline
Jezequel, Caroline
Lavayssiere, Laurence
Neau-Cransac, Martine
Erard-Poinsot, Domitille
de Ledinghen, Victor
Bourliere, Marc
Bureau, Christophe
Ganne-Carrie, Nathalie
TI Non-invasive diagnosis and follow-up in liver transplantation
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Article
ID HEPATIC-ARTERY THROMBOSIS; PRIMARY SCLEROSING CHOLANGITIS; PRIMARY
BILIARY-CIRRHOSIS; TRANSIENT ELASTOGRAPHY; HEPATOCELLULAR-CARCINOMA;
ACUTE REJECTION; AUTOIMMUNE HEPATITIS; MEDIATED REJECTION; RISK-FACTORS;
C VIRUS
AB The field of liver transplantation directly or indirectly embodies all liver diseases, in addition to specific ones related to organ rejection (cellular and humoral). The recommended non-invasive methods for determining the indication for liver transplantation are the Model for End-stage Liver Disease score, and the alpha-foetoprotein score in case of hepatocellular carcinoma. Radiological methods are the cornerstones for the diagnosis of vascular and biliary complications after liver transplantation. The possible diseases of the liver graft after transplantation are multiple and often intertwined. Non-invasive diagnostic methods have been poorly evaluated in this context, apart from the recurrence of hepatitis C. Liver biopsy remains the gold standard for evaluating graft lesions in the majority of cases, especially graft rejection. (C) 2021 Published Elsevier Masson SAS.
C1 [Dumortier, Jerome; Erard-Poinsot, Domitille] CHU Lyon, Hop Edouard Herriot HCL, Unite Transplantat Hepat, Serv Hepatogastroenterol, Lyon, France.
[Besch, Camille; Faitot, Francois] CHRU Strasbourg, Hop Hautepierre, Serv Chirurg Hepatobiliopancreat & Transplantat H, Strasbourg, France.
[Moga, Lucile; Francoz, Claire] Hop Beaujon, AP HP, Serv Hepatol & Transplantat Hepat, Clichy, France.
[Coilly, Audrey] Hop Paul Brousse, AP HP, Ctr Hepatobiliaire, Villejuif, France.
[Conti, Filomena] Hop La Pitie Salpetriere, AP HP, Serv Hepatol & Transplantat Hepat, Paris, France.
[Corpechot, Christophe] Hop St Antoine, AP HP, Serv Hepatogastroenterol, Paris, France.
[Del Bello, Arnaud; Lavayssiere, Laurence] CHU Toulouse, Hop Rangueil, Dept Nephrol & Transplantat Organes, Toulouse, France.
[Hilleret, Marie-Noelle] CHU Grenoble, Serv Hepatogastroenterol, Grenoble, France.
[Houssel-Debry, Pauline; Jezequel, Caroline] CHU Rennes Pontchaillou, Serv Malad Foie, Rennes, France.
[Neau-Cransac, Martine; de Ledinghen, Victor] CHU Bordeaux, Unite Transplantat Hepat, Hop Haut Leveque, Bordeaux, France.
[Bourliere, Marc] Aix Marseille Univ, Serv Hepatogastroenterol, Hop St Joseph, Marseille, France.
[Bourliere, Marc] Aix Marseille Univ, INSERM UMR 1252 IRD SESSTIM, Marseille, France.
[Bureau, Christophe] CHU Toulouse, Serv Hepatol, Hop Rangueil, Toulouse, France.
[Ganne-Carrie, Nathalie] Univ Sorbonne Paris Nord, Hop Avicenne, AP HP, Serv Hepatol, Bobigny, France.
[Ganne-Carrie, Nathalie] Univ Paris, Ctr Rech Cordeliers, INSERM UMR 1138, Paris, France.
C3 CHU Lyon; CHU Strasbourg; Universites de Strasbourg Etablissements
Associes; Universite de Strasbourg; Universite Paris Cite; Assistance
Publique Hopitaux Paris (APHP); Hopital Universitaire Beaujon - APHP;
Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
Paul-Brousse - APHP; Sorbonne Universite; Assistance Publique Hopitaux
Paris (APHP); Hopital Universitaire Pitie-Salpetriere - APHP; Assistance
Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
Universitaire Saint-Antoine - APHP; CHU de Toulouse; Universite de
Toulouse; Universite Toulouse III - Paul Sabatier; Communaute Universite
Grenoble Alpes; Universite Grenoble Alpes (UGA); CHU Grenoble Alpes;
Universite de Rennes; CHU Rennes; Universite de Bordeaux; CHU Bordeaux;
Aix-Marseille Universite; Institut National de la Sante et de la
Recherche Medicale (Inserm); Aix-Marseille Universite; CHU de Toulouse;
Universite de Toulouse; Universite Toulouse III - Paul Sabatier;
Universite Paris 13; Assistance Publique Hopitaux Paris (APHP); Hopital
Universitaire Avicenne - APHP; Sorbonne Universite; Universite Paris
Cite; Institut National de la Sante et de la Recherche Medicale (Inserm)
RP Dumortier, J (corresponding author), CHU Lyon, Hop Edouard Herriot HCL, Unite Transplantat Hepat, Serv Hepatogastroenterol, Lyon, France.
EM jerome.dumortier@chu-lyon.fr
RI Dumortier, Jerome/J-2029-2014; Erard, Domitille/AAB-4991-2022; Faitot,
François/Y-9465-2019
OI Moga, Lucile/0000-0002-9083-2315; Faitot, Francois/0000-0001-6514-0774
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NR 86
TC 3
Z9 4
U1 0
U2 3
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD JAN
PY 2022
VL 46
IS 1
AR 101774
DI 10.1016/j.clinre.2021.101774
EA OCT 2021
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WS1XB
UT WOS:000714981300006
PM 34332131
DA 2025-01-07
ER
PT J
AU Federico, A
D'Aiuto, E
Borriello, F
Barra, G
Gravina, AG
Romano, M
De Palma, R
AF Federico, Alessandro
D'Aiuto, Elena
Borriello, Francesco
Barra, Giusi
Gravina, Antonietta Gerarda
Romano, Marco
De Palma, Raffaele
TI Fat: A matter of disturbance for the immune system
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Adipocytokine; Adipose tissue; Fat; Immune system; Kupffer cell; Natural
killer; Steatosis
ID KILLER T-CELLS; LIVER-DISEASE; NONALCOHOLIC STEATOHEPATITIS;
INSULIN-RESISTANCE; INNATE IMMUNITY; ADIPOSE-TISSUE; NKT CELLS;
ALTERNATIVE ACTIVATION; METABOLIC SYNDROME; ALPHA PRODUCTION
AB Obesity is increasingly being recognized as a risk factor for a number of benign and malignant gastrointestinal conditions. However, literature on the underlying pathophysiological mechanisms is sparse and ambiguous. There is compelling evidence that both overnutrition and undernutrition negatively interfere with the immune system. Overnutrition has been found to increase susceptibility to the development of inflammatory diseases, autoimmune diseases and cancer. In the regulation of immune and inflammatory processes, white adipose tissue plays a critical role, not only as an energy store but also as an important endocrine organ. The obese state is characterised by a low-grade systemic inflammation, mainly as a result of increased adipocytes as well as fat resident- and recruited-macrophage activity. In the past few years, various products of adipose tissue including adipokines and cytokines have been characterised and a number of pathways linking adipose tissue metabolism with the immune system have been identified. Activation of the innate immune system plays a major role in hepatic steatosis. Non-alcoholic fatty liver disease includes a wide spectrum of diseases, from pure steatosis to non-alcoholic steatohepatitis in the absence of significant alcohol consumption. Although steatosis is considered a non-progressive disease, non-alcoholic steatohepatitis may deteriorate in advanced chronic liver diseases, cirrhosis, and hepatocellular carcinoma. An important parallel between obesity-related pathology of adipose tissue and liver pertains to the emerging role of macrophages, and growing evidence suggests that Kupffer cells critically contribute to progression of non-alcoholic fatty liver disease. Moreover, a close link between specific immune activation and atherosclerosis has been well established, suggesting that fat can directly trigger immune responses. This review discusses the role of fat as "a matter of disturbance for the immune system" with a focus on hepatic steatosis.
C1 [D'Aiuto, Elena; Borriello, Francesco; Barra, Giusi; De Palma, Raffaele] Univ Naples 2, Clin Immunol Sect, Dept Clin & Expt Med, I-80131 Naples, Italy.
[Federico, Alessandro; Gravina, Antonietta Gerarda; Romano, Marco] Univ Naples 2, Gastroenterol Sect, Dept Clin & Expt Med, I-80131 Naples, Italy.
C3 Universita della Campania Vanvitelli; Universita della Campania
Vanvitelli
RP De Palma, R (corresponding author), Univ Naples 2, Clin Immunol Sect, Dept Clin & Expt Med, C-O 2 Policlin Ed 3,Via S Pansini 5, I-80131 Naples, Italy.
EM raffaele.depalma@unina2.it
RI Gravina, Antonietta Gerarda/AAC-1528-2019; Federico,
Alessandro/AAB-3893-2019
OI Barra, Giusi/0000-0003-2395-6710; ROMANO, Marco/0000-0002-3271-349X;
Borriello, Francesco/0000-0001-9074-4828; Gravina, Antonietta
Gerarda/0000-0001-8049-0115; De Palma, Raffaele/0000-0001-9070-8878;
Federico, Alessandro/0000-0002-0885-0793
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NR 104
TC 60
Z9 68
U1 0
U2 13
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD OCT 14
PY 2010
VL 16
IS 38
BP 4762
EP 4772
DI 10.3748/wjg.v16.i38.4762
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 667IF
UT WOS:000283185800002
PM 20939104
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Landgren, AM
Landgren, O
Gridley, G
Dores, GM
Linet, MS
Morton, LM
AF Landgren, Anne M.
Landgren, Ola
Gridley, Gloria
Dores, Grace M.
Linet, Martha S.
Morton, Lindsay M.
TI Autoimmune Disease and Subsequent Risk of Developing Alimentary Tract
Cancers Among 4.5 Million US Male Veterans
SO CANCER
LA English
DT Article
DE alimentary; gastrointestinal; autoimmune disease; inflammation; cancer
ID INFLAMMATORY-BOWEL-DISEASE; COMPLICATING CROHNS-DISEASE; PRIMARY
BILIARY-CIRRHOSIS; POPULATION-BASED COHORT; MULTIPLE-SCLEROSIS;
CELIAC-DISEASE; PERNICIOUS-ANEMIA; RHEUMATOID-ARTHRITIS;
POLYARTERITIS-NODOSA; HELICOBACTER-PYLORI
AB BACKGROUND: Autoimmunity is clearly linked with hematologic malignancies, but less is known about autoimmunity and alimentary tract cancer risk, despite the specific targeting of alimentary organs and tissues by several autoimmune diseases. The authors therefore conducted the first systematic evaluation of a broad range of specific autoimmune diseases and risk for subsequent alimentary tract cancer. METHODS: On the basis of 4,501,578 US male veterans, the authors identified 96,277 men who developed alimentary tract cancer during up to 26.2 years of follow-up. By using Poisson regression methods, the authors calculated relative risks (RRs) and 95% confidence intervals. RESULTS: A history of autoimmune disease with localized alimentary tract effects generally increased cancer risks in the organ(s) affected by the autoimmune disease, such as primary biliary cirrhosis and liver cancer (RR, 6.01; 95% confidence interval [Cl], 4.76-7.57); pernicious anemia and stomach cancer (RR, 3.17; 95% Cl, 2.47-4.07); and ulcerative colitis and small intestine, colon, and rectal cancers (RR, 2.53; 95% Cl, 1.05-6.11; RR, 2.06; 95% Cl, 1.70-2.48; and RR, 2.07; 95% Cl, 1.62-2.64, respectively). In addition, a history of celiac disease, reactive arthritis (Reiter disease), and systemic sclerosis all were associated significantly with increased risk of esophageal cancer (RR, 1.86-2.86). Autoimmune diseases without localized alimentary tract effects generally were not associated with alimentary tract cancer risk, with the exception of decreased risk for multiple alimentary tract cancers associated with a history of multiple sclerosis. CONCLUSIONS: These findings support the importance of localized inflammation in alimentary tract carcinogenesis. Future research is needed to confirm the findings and improve understanding of underlying mechanisms by which autoimmune diseases contribute to alimentary tract carcinogenesis. Cancer 2011;117:1163-71. Published 2010 by the American Cancer Society*
C1 [Landgren, Anne M.; Dores, Grace M.; Linet, Martha S.; Morton, Lindsay M.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Rockville, MD 20852 USA.
[Landgren, Anne M.] Mid Sweden Univ, Dept Hlth Sci, Sundsvall, Sweden.
[Landgren, Ola] NCI, Med Oncol Branch, Ctr Canc Res, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Gridley, Gloria] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Dores, Grace M.] Dept Vet Affairs Med Ctr, Med Serv, Oklahoma City, OK USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI); Mid-Sweden University; National Institutes of Health (NIH) - USA;
NIH National Cancer Institute (NCI); National Institutes of Health (NIH)
- USA; NIH National Cancer Institute (NCI); University of Oklahoma
System; University of Oklahoma Health Sciences Center
RP Morton, LM (corresponding author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, 6120 Execut Blvd,EPS 7040,MSC 7238, Rockville, MD 20852 USA.
EM mortonli@mail.nih.gov
RI ; Morton, Lindsay/B-5234-2015
OI Dores, Graca/0000-0002-3985-2935; Morton, Lindsay/0000-0001-9767-2310
FU National Cancer Institute, National Institutes of Health, Department of
Health and Human Services
FX This research was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health, Department of
Health and Human Services.
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NR 57
TC 111
Z9 120
U1 1
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD MAR 15
PY 2011
VL 117
IS 6
BP 1163
EP 1171
DI 10.1002/cncr.25524
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 734PZ
UT WOS:000288349300008
PM 21381009
OA Green Accepted, Green Submitted
DA 2025-01-07
ER
PT J
AU Jensen, ASH
Ytting, H
Winther-Sorensen, M
Burisch, J
Bergquist, A
Gluud, LL
Albrechtsen, NWJ
AF Jensen, Anne-Sofie H.
Ytting, Henriette
Winther-Sorensen, Marie
Burisch, Johan
Bergquist, Annika
Gluud, Lise Lotte
Wewer Albrechtsen, Nicolai J.
TI Autoimmune liver diseases and diabetes
SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE autoimmune hepatitis; autoimmune liver disease; diabetes; glucose;
primary biliary cholangitis; primary sclerosing cholangitis
ID PRIMARY SCLEROSING CHOLANGITIS; CLINICAL-PRACTICE GUIDELINES; PRIMARY
BILIARY-CIRRHOSIS; GENOME-WIDE ASSOCIATION; INSULIN-RESISTANCE;
RISK-FACTORS; HEPATOCELLULAR-CARCINOMA; GLYCOSYLATED HEMOGLOBIN;
EUROPEAN ASSOCIATION; MANAGEMENT
AB Autoimmune liver diseases include autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis. They are chronic, heterogenous diseases affecting the liver which is a key metabolic organ that ensures glucose homeostasis. It is well known that patients with other chronic liver diseases such as cirrhosis and nonalcoholic fatty liver disease (NAFLD) display glucose disturbances like insulin resistance and have an increased risk of diabetes. Previous evidence on glucose disturbances in patients with autoimmune liver disease is scarce but does point towards a potentially increased risk of type 1 diabetes and type 2 diabetes. The underlying mechanisms are unknown but may reflect genetic predisposition, concurrent NAFLD and or cirrhosis development, and treatment (steroid) related impairment of glucose homeostasis. Therefore, increased awareness and surveillance of diabetes development in patients with autoimmune liver disease may be important. Overall, detection and treatment of diabetes generally follow the usual diabetes guidelines; however, in patients with advanced liver cirrhosis, HbA1c may not be a reliable marker of average glucose levels, and treatment with insulin is generally recommended. In addition, it has recently been suggested that sodium-glucose cotransporter 2 inhibitors may be beneficial in treating refractory ascites. Further research on diabetes risk in autoimmune liver disease is warranted.
C1 [Jensen, Anne-Sofie H.; Winther-Sorensen, Marie; Wewer Albrechtsen, Nicolai J.] Univ Copenhagen, Novo Nord Fdn Ctr Prot Res, Fac Hlth & Med Sci, Copenhagen, Denmark.
[Jensen, Anne-Sofie H.; Ytting, Henriette; Burisch, Johan; Bergquist, Annika; Gluud, Lise Lotte] Copenhagen Univ Hosp, Amager Hvidovre Hosp, Gastro Unit, Hvidovre, Denmark.
[Ytting, Henriette] Rigshosp, European Reference Network Hepatol Dis ERN RARE LI, Copenhagen, Denmark.
[Ytting, Henriette; Gluud, Lise Lotte] Univ Copenhagen, Inst Clin Med, Fac Hlth & Med Sci, Copenhagen, Denmark.
[Bergquist, Annika] Karolinska Univ Hosp, Karolinska Inst, Dept Upper GI Dis, Dept Med, Stockholm, Sweden.
[Wewer Albrechtsen, Nicolai J.] Copenhagen Univ Hosp, Bispebjerg Frederiksberg Hosp, Dept Clin Biochem, Copenhagen, Denmark.
[Jensen, Anne-Sofie H.] Copenhagen Univ Hosp, Amager & Hvidovre Hosp, Gastro Unit, Kettegard Alle 30, DK-2650 Hvidovre, Denmark.
C3 University of Copenhagen; University of Copenhagen; University of
Copenhagen; Rigshospitalet; University of Copenhagen; Karolinska
Institutet; Karolinska University Hospital; University of Copenhagen;
Bispebjerg Hospital; University of Copenhagen
RP Jensen, ASH (corresponding author), Copenhagen Univ Hosp, Amager & Hvidovre Hosp, Gastro Unit, Kettegard Alle 30, DK-2650 Hvidovre, Denmark.
EM anne-sofie.houlberg.jensen@regionh.dk
RI Winther-Sørensen, Marie/GVS-7537-2022; Ytting, Henriette/ABA-9518-2021;
Gluud, Lise/AAY-2120-2020; Burisch, Johan/AGJ-3893-2022; Bergquist,
Annika/HOH-4007-2023
OI Winther-Sorensen, Marie/0000-0003-2144-1385; Jensen, Anne-Sofie
Houlberg/0000-0002-5982-8684; Burisch, Johan/0000-0002-3312-5139
FU Novo Nordisk Foundation Excellence Emerging Investigator Grant -
Endocrinology and Metabolism [NNF19OC0055001]; European Foundation
[NNF21SA0072746]; Independent Research Fund Denmark, Sapere Aude
[1052-00003B]; Novo Nordisk Foundation [NNF14CC0001]
FX A.-S.H.J and N.J.W.A. were supported by Novo Nordisk Foundation
Excellence Emerging Investigator Grant - Endocrinology and Metabolism
(Application No. NNF19OC0055001), European Foundation for the Study of
Diabetes Future Leader Award (NNF21SA0072746) and Independent Research
Fund Denmark, Sapere Aude (1052-00003B). Novo Nordisk Foundation Center
for Protein Research is supported financially by the Novo Nordisk
Foundation (Grant agreement NNF14CC0001). The funding was not involved
in this study.
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NR 122
TC 6
Z9 6
U1 4
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0954-691X
EI 1473-5687
J9 EUR J GASTROEN HEPAT
JI Eur. J. Gastroenterol. Hepatol.
PD SEP
PY 2023
VL 35
IS 9
BP 938
EP 947
DI 10.1097/MEG.0000000000002594
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA N6JA2
UT WOS:001038039100002
PM 37505973
DA 2025-01-07
ER
PT J
AU Wang, PL
Djerboua, M
Flemming, JA
AF Wang, Peter L.
Djerboua, Maya
Flemming, Jennifer A.
TI Cause-specific mortality among patients with cirrhosis in a
population-based cohort study in Ontario (2000-2017)
SO HEPATOLOGY COMMUNICATIONS
LA English
DT Article
ID GENERAL-POPULATION; LIVER-CIRRHOSIS; PEOPLE; TRENDS; DEATH
AB Background: Although patients with cirrhosis are at increased risk of death, the exact causes of death have not been reported in the contemporary era. This study aimed to describe cause-specific mortality in patients with cirrhosis in the general population. Methods: Retrospective cohort study using administrative health care data from Ontario, Canada. Adult patients with cirrhosis from 2000-2017 were identified. Cirrhosis etiologies were defined as HCV, HBV, alcohol associated liver disease (ALD), NAFLD, or autoimmune liver disease/other with validated algorithms. Patients were followed until death, liver transplant, or end of study. Primary outcome was the cause of death as liver-related, cardiovascular disease, non-hepatic malignancy, and external causes (accident/self-harm/suicide/homicide). Nonparametric analyses were used to describe the cumulative incidence of cause-specific death by cirrhosis etiology, sex, and compensation status. Results: Overall, 202,022 patients with cirrhosis were identified (60% male, median age 56 y (IQR 46-67), 52% NAFLD, 26% alcohol-associated liver disease, 11% HCV). After a median follow-up of 5 years (IQR 2-12), 81,428 patients died, and 3024 (2%) received liver transplant . Patients with compensated cirrhosis mostly died from non-hepatic malignancies and cardiovascular disease (30% and 27%, respectively, in NAFLD). The 10-year cumulative incidence of liver-related deaths was the highest among those with viral hepatitis (11%-18%) and alcohol-associated liver disease (25%), those with decompensation (37%) and/or HCC (50%-53%). Liver transplant occurred at low rates (< 5%), and in men more than women. Conclusions: Cardiovascular disease and cancer-related mortality exceed liver-related mortality in patients with compensated cirrhosis.
C1 [Wang, Peter L.; Flemming, Jennifer A.] Dept Med, Kingston, ON, Canada.
[Djerboua, Maya; Flemming, Jennifer A.] Queens Univ, ICES, Kingston, ON, Canada.
[Flemming, Jennifer A.] Queens Univ, Publ Hlth Sci, Kingston, ON, Canada.
C3 Queens University - Canada; Queens University - Canada
RP Flemming, JA (corresponding author), Queens Univ, Hotel Dieu Hosp Site, Kingston Hlth Sci Ctr, Dept Med, 166 Brock St, Kingston, ON K7L 5M2, Canada.; Flemming, JA (corresponding author), Queens Univ, Hotel Dieu Hosp Site, Kingston Hlth Sci Ctr, Dept Publ Hlth Sci, 166 Brock St, Kingston, ON K7L 5M2, Canada.
EM 13plw3@queensu.ca; maya.djerboua@ices.on.ca;
Jennifer.Flemming2@kingstonhsc.ca
RI Flemming, Jennifer/L-4228-2018
OI Flemming, Jennifer/0000-0002-9911-0925
FU ICES - Ontario Ministry of Health (MOH); Ministry of Long-Term Care
(MLTC); American Association for the Study of Liver Disease Foundation
Clinical, Translational, and Outcomes Research Award in Liver Disease;
Southeastern Ontario New Clinician Scientist Award
FX This study was supported by ICES, which is funded by an annual grant
from the Ontario Ministry of Health (MOH) and the Ministry of Long-Term
Care (MLTC). This study also received funding from the American
Association for the Study of Liver Disease Foundation Clinical,
Translational, and Outcomes Research Award in Liver Disease (Jennifer A.
Flemming) and the Southeastern Ontario New Clinician Scientist Award
(Jennifer A. Flemming).
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Yeung DF, 2012, CAN MED ASSOC J, V184, pE765, DOI 10.1503/cmaj.111958
NR 26
TC 3
Z9 3
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2471-254X
J9 HEPATOL COMMUN
JI Hepatol. Commun.
PD JUL
PY 2023
VL 7
IS 7
AR e00194
DI 10.1097/HC9.0000000000000194
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA L2NE9
UT WOS:001021670100001
PM 37378630
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Suda, T
Kobayashi, M
Kurokawa, K
Matsushita, E
AF Suda, Tsuyoshi
Kobayashi, Masako
Kurokawa, Koji
Matsushita, Eiki
TI Simultaneous occurrence of autoimmune pancreatitis and sclerosing
cholangitis as immune-related adverse events of pembrolizumab
SO BMJ CASE REPORTS
LA English
DT Article
DE oncology; pancreas and biliary tract; liver disease
ID CANCER; CHEMOTHERAPY; INHIBITORS
AB A 57-year-old man with lung cancer, previously treated with the programmed death-1 inhibitor pembrolizumab, was evaluated for liver injury and acute pancreatitis. Serum IgG4 levels were not elevated. Contrast-enhanced CT showed pancreatic swelling, contrast unevenness in the liver and thickening of the common bile duct and gall bladder. Magnetic resonance cholangial pancreatography revealed beads in the left intrahepatic bile duct and localised narrowing of the head and body of the central pancreatic duct. Endoscopic ultrasound-guided fine-needle and liver needle biopsy showed CD8+ and CD4+ T lymphocyte aggregates, whereas immunostaining revealed greater infiltration by CD8+ cells than CD4+ cells. IgG4-related disease was ruled out based on serum and pathological findings. The patient simultaneously presented with immune-related adverse events, autoimmune pancreatitis-like features and sclerosing cholangitis, which were ameliorated by steroid therapy. CD8+ lymphocytes were the dominant infiltrating cells in autoimmune pancreatitis and sclerosing cholangitis.
C1 [Suda, Tsuyoshi; Matsushita, Eiki] Kanazawa Municipal Hosp, Dept Gastroenterol, Kanazawa, Ishikawa, Japan.
[Kobayashi, Masako] Kanazawa Municipal Hosp, Dept Pathol, Kanazawa, Ishikawa, Japan.
[Kurokawa, Koji] Kanazawa Municipal Hosp, Dept Resp Med, Kanazawa, Ishikawa, Japan.
RP Suda, T (corresponding author), Kanazawa Municipal Hosp, Dept Gastroenterol, Kanazawa, Ishikawa, Japan.
EM t.suda1112@gmail.com
RI suda, tsuyoshi/KIJ-2082-2024
OI Suda, Tsuyoshi/0000-0001-9608-0444
CR Friedman CF, 2016, JAMA ONCOL, V2, P1346, DOI 10.1001/jamaoncol.2016.1051
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NR 15
TC 10
Z9 10
U1 0
U2 3
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 1757-790X
J9 BMJ CASE REP
JI BMJ Case Rep.
PD JUN
PY 2021
VL 14
IS 6
AR e243360
DI 10.1136/bcr-2021-243360
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA SR2ML
UT WOS:000660877400002
PM 34088696
OA Green Published
DA 2025-01-07
ER
PT J
AU Dimitroulis, D
Valsami, S
Stamopoulos, P
Kouraklis, G
AF Dimitroulis, Dimitrios
Valsami, Serena
Stamopoulos, Paraskevas
Kouraklis, Gregory
TI Immunological HCV-Associated Thrombocytopenia: Short Review
SO CLINICAL & DEVELOPMENTAL IMMUNOLOGY
LA English
DT Review
ID C VIRUS-INFECTION; HEPATITIS-C; EXTRAHEPATIC MANIFESTATIONS;
HEPATOCELLULAR-CARCINOMA; INTERFERON-ALPHA; IMMUNE THROMBOCYTOPENIA;
UNITED-STATES; PURPURA; PREVALENCE; THERAPY
AB Infection with Hepatitis C virus (HCV) is affecting about 3% of the world's population, leading to liver damage, end-stage liver disease, and development of hepatocellular carcinoma, being thus the first indication for liver transplantation in the USA. Apart from the cirrhotic-liver-derived clinical signs and symptoms several conditions with immunological origin can also arise, such as, glomerulonephritis, pulmonary fibrosis, and thrombocytopenia. HCV-related autoimmune thrombocytopenia shows specific pathogenetic characteristics as well as symptoms and signs that differ in severity and frequency from symptoms in patients that are not HCV infected. Aim of this short paper is to estimate the epidemiological characteristics of the disease, to investigate the pathogenesis and clinical manifestation, and to propose treatment strategies according to the pertinent literature.
C1 [Dimitroulis, Dimitrios; Stamopoulos, Paraskevas; Kouraklis, Gregory] Univ Athens, Laiko Hosp, Sch Med, Dept Propaedeut Surg 2, Athens 17455, Greece.
[Valsami, Serena] Univ Athens, Arete Hosp, Sch Med, Blood Transfus Dept, Athens 11528, Greece.
C3 Laiko General Hospital; Athens Medical School; National & Kapodistrian
University of Athens; National & Kapodistrian University of Athens;
Athens Medical School
RP Dimitroulis, D (corresponding author), Univ Athens, Laiko Hosp, Sch Med, Dept Propaedeut Surg 2, Sakellariou 4 St, Athens 17455, Greece.
EM dimitroulisdimitrios@yahoo.com
RI VALSAMI, SERENA/AAB-4895-2020; Kouraklis, Gregory/AAA-3561-2020
OI Valsami, Serena/0000-0002-1034-6510
CR Agence Nationale d'Accreditation et d'Evaluation en Sante (ANAES), 2002, Gastroenterol Clin Biol, V26 Spec No 2, pB303
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NR 43
TC 8
Z9 11
U1 0
U2 1
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1740-2522
EI 1740-2530
J9 CLIN DEV IMMUNOL
JI Clin. Dev. Immunol.
PY 2012
AR 378653
DI 10.1155/2012/378653
PG 5
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 989WL
UT WOS:000307591600001
PM 22829850
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Migita, K
Nakamura, M
Aiba, Y
Kozuru, H
Abiru, S
Komori, A
Fujita, Y
Temmoku, J
Asano, T
Sato, S
Furuya, M
Naganuma, A
Yoshizawa, K
Shimada, M
Ario, K
Mannami, T
Kohno, H
Kaneyoshi, T
Komura, T
Ohira, H
Yatsuhashi, H
AF Migita, Kiyoshi
Nakamura, Minoru
Aiba, Yoshihiro
Kozuru, Hideko
Abiru, Seigo
Komori, Atsumasa
Fujita, Yuya
Temmoku, Junpei
Asano, Tomoyuki
Sato, Shuzo
Furuya, Makiko
Naganuma, Atsushi
Yoshizawa, Kaname
Shimada, Masaaki
Ario, Keisuke
Mannami, Tomohiko
Kohno, Hiroshi
Kaneyoshi, Toshihiko
Komura, Takuya
Ohira, Hiromasa
Yatsuhashi, Hiroshi
TI Association of soluble T cell immunoglobulin domain and mucin-3 (sTIM-3)
and mac-2 binding protein glycosylation isomer (M2BPGi) in patients with
autoimmune hepatitis
SO PLOS ONE
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; TIM-3; DIAGNOSIS
AB Background
Autoimmune hepatitis (AIH) is a disorder of unknown etiology in which immune-mediated liver injury progress to cirrhosis or hepatocellular carcinoma (HCC). The aim of the present study was to determine whether circulating soluble TIM3 (sTIM3) is elevated in patients with AIH patients and whether sTIM-3 levels are associated with clinical parameters of AIH.
Methods
We enrolled 123 Japanese patients with AIH who were identified from the National Hospital Organization-AIH-liver-network database, as well as 32 patients with chronic hepatitis C (CHC), 30 patients with primary biliary cholangitis (PBC) and healthy control subjects. Serum sTIM-3 concentrations were quantified by ELISA.
Results
Serum levels of sTIM-3 were significantly higher in AIH patients (median 4865 pg/ml; [interquartile range (IQR); 3122-7471]) compared to those in CHC (1026 pg/ml [IQR: 806-1283] p<0.001), PBC (2395 pg/ml [IQR: 2012-3422] p<0.001) or healthy controls (1285 pg/ml [IQR: 1098-1812] p<0.001). In AIH group, serum sTIM-3 were correlated with alanine aminotransferase (ALT), or total bilirubin (TB) and negatively correlated with serum levels of albumin (Alb). Serum levels of sTIM-3 were also strongly correlated with Mac-2 binding protein glycosylation isomer (M2BPGi) levels, but did not correlate with the histological grade of liver fibrosis. Steroid treatment of AIH patients significantly reduced serum sTIM-3 levels (2147 +/- 623pg/ml versus 1321 +/- 378pg/ml, p<0.001).
Conclusions
Circulating sTIM-3 levels were elevated in AIH patients and are associated with AIH disease activity and AIH-related liver damage. These findings indicate that serum sTIM-3 correlated with disease status of AIH and could be useful biomarkers to detect autoimmune-mediated liver injury. Our data suggest a possible link between the TIM-3/GAL-9 pathway and AIH severity or phenotype, and further investigations of the TIM-3 pathway and AIH pathophysiology is warranted.
C1 [Migita, Kiyoshi; Nakamura, Minoru; Aiba, Yoshihiro; Kozuru, Hideko; Abiru, Seigo; Komori, Atsumasa; Yatsuhashi, Hiroshi] Nagasaki Med Ctr, Clin Res Ctr, Nagasaki, Japan.
[Migita, Kiyoshi; Fujita, Yuya; Temmoku, Junpei; Asano, Tomoyuki; Sato, Shuzo; Furuya, Makiko] Fukushima Med Univ, Dept Rheumatol, Fukushima, Japan.
[Naganuma, Atsushi] Natl Hosp Org, Takasaki Med Ctr, Takasaki, Gumma, Japan.
[Yoshizawa, Kaname] Natl Hosp Org, Shinsyu Ueda Med Ctr, Ueda, Nagano, Japan.
[Shimada, Masaaki] Natl Hosp Org, Nagoya Med Ctr, Nagoya, Aichi, Japan.
[Ario, Keisuke] Natl Hosp Org, Ureshino Med Ctr, Ureshino, Saga, Japan.
[Mannami, Tomohiko] Natl Hosp Org, Okayama Med Ctr, Okayama, Okayama, Japan.
[Kohno, Hiroshi] Natl Hosp Org, Kure Med Ctr, Kure, Hiroshima, Japan.
[Kaneyoshi, Toshihiko] Natl Hosp Org, Fukuyama Med Ctr, Kanazawa, Ishikawa, Japan.
[Komura, Takuya] Natl Hosp Org, Kanazawa Med Ctr, Kanazawa, Ishikawa, Japan.
[Ohira, Hiromasa] Fukushima Med Univ, Dept Gastroenterol, Fukushima, Japan.
C3 Fukushima Medical University; Nagoya Medical Center; Fukushima Medical
University
RP Migita, K (corresponding author), Nagasaki Med Ctr, Clin Res Ctr, Nagasaki, Japan.; Migita, K (corresponding author), Fukushima Med Univ, Dept Rheumatol, Fukushima, Japan.
EM migita@fmu.ac.jp
RI Sato, Shuzo/AAC-7025-2019; Mannami, Tomohiko/GRY-5310-2022
OI Sato, Shuzo/0000-0002-8110-8261; Asano, Tomoyuki/0009-0005-6538-1881
FU National Hospital Organization [H29-NHOL-01]
FX The study was supported by a grant from the National Hospital
Organization (grant number H29-NHOL-01). The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 33
TC 6
Z9 6
U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 21
PY 2020
VL 15
IS 12
AR e0238540
DI 10.1371/journal.pone.0238540
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA PL4CD
UT WOS:000603071100066
PM 33347507
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Dirchwolf, M
Marciano, S
Giunta, DH
Posadas-Martínez, ML
Biggins, SW
Ruf, AE
AF Dirchwolf, Melisa
Marciano, Sebastian
Giunta, Diego H.
Posadas-Martinez, Maria L.
Biggins, Scott W.
Ruf, Andres E.
TI Trends in liver transplantation for hepatitis C in a country with
reduced access to direct-acting antiviral agents
SO CLINICAL TRANSPLANTATION
LA English
DT Article
DE direct-acting antivirals; hepatitis C; joinpoint regression analysis;
liver transplantation; trends; waiting list analysis
ID SUSTAINED VIROLOGICAL RESPONSE; HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC
STEATOHEPATITIS; VIRUS-INFECTION; CIRRHOSIS; FUTURE; ERA; INTERFERON;
CANDIDATES; THERAPY
AB Background: Hepatitis C virus (HCV)-related cirrhosis is a leading indication for liver transplantation (LT) worldwide. Access to effective HCV treatment is inequitable globally. We aimed to analyze whether the introduction of effective HCV treatment caused an impact in LT trends in a middle-income country.
Methods: Cross-sectional analysis of all adult patients who were listed/received a LT in Argentina for HCV, alcohol-related liver disease (ALD), or autoimmune hepatitis/primary biliary cirrhosis (AIH/PBC) from 2007 to 2017. Joinpoint regression analysis was used to identify changes in the cumulative incidence rates in waiting list (WL) registration, WL mortality, and LT.
Results: Liver transplantation WL for HCV increased significantly between 2007 and 2014, with an annual percentage change (APC) +7.8%, P=.01, followed by a downward slope from 2014 to 2017 with an APC-9.8%, P=.1. There were no significant changes in WL mortality. LT trends remained stable. LT for HCV without MELD exception points for HCC decreased (APC-6.6%, P=.01), whereas LT for HCV with HCC exception points increased (APC + 11.1, P=.01) during the study period.
Conclusion: Waiting list and LT for HCV without HCC decreased, whereas LT for HCV and HCC increased; this may be related to selective antiviral treatment access for patients with advanced fibrosis.
C1 [Dirchwolf, Melisa; Ruf, Andres E.] Hosp Privado Rosario, Liver Unit, Rosario, Santa Fe, Argentina.
[Marciano, Sebastian] Hosp Italiano Buenos Aires, Liver Unit, Buenos Aires, DF, Argentina.
[Marciano, Sebastian; Giunta, Diego H.; Posadas-Martinez, Maria L.] Hosp Italiano Buenos Aires, Dept Res, Buenos Aires, DF, Argentina.
[Biggins, Scott W.] Univ Washington, Seattle, WA 98195 USA.
[Ruf, Andres E.] Fdn Docencia & Invest Enfermedades Higado FUNDIEH, Buenos Aires, DF, Argentina.
C3 Hospital Italiano de Buenos Aires; University of Buenos Aires;
University of Buenos Aires; Hospital Italiano de Buenos Aires;
University of Washington; University of Washington Seattle
RP Dirchwolf, M (corresponding author), Hosp Privado Rosario, Liver Unit, Rosario, Santa Fe, Argentina.
EM mdirchwolf@outlook.com
RI biggins, scott/AAQ-6532-2020; Giunta, Diego Hernan/AAJ-6928-2021
OI Giunta, Diego Hernan/0000-0002-8427-6033; Posadas-Martinez, Ma.
Lourdes/0000-0003-1403-7069
CR [Anonymous], 2001, GPE Discussion Paper Series: No.31
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NR 24
TC 3
Z9 3
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0902-0063
EI 1399-0012
J9 CLIN TRANSPLANT
JI Clin. Transplant.
PD APR
PY 2018
VL 32
IS 4
AR e13230
DI 10.1111/ctr.13230
PG 8
WC Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery; Transplantation
GA GJ6NE
UT WOS:000435500100022
PM 29485711
DA 2025-01-07
ER
PT J
AU Singh, RP
Hasan, S
Sharma, S
Nagra, S
Yamaguchi, DT
Wong, DTW
Hahn, BH
Hossain, A
AF Singh, Ram Pyare
Hasan, Sascha
Sharma, Sherven
Nagra, Saranpreet
Yamaguchi, Dean T.
Wong, David T. W.
Hahn, Bevra H.
Hossain, Awlad
TI Th17 cells in inflammation and autoimmunity
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE Th17; Sex hormones; Autoimmunity; Systemic lupus erythematosus; Cancer;
Mesenchymal stem cells
ID MESENCHYMAL STEM-CELLS; REGULATORY T-CELLS; TUMOR-INFILTRATING
LYMPHOCYTES; SJOGRENS-SYNDROME; HEPATOCELLULAR-CARCINOMA; HELPER-CELLS;
HOST-DEFENSE; INTERLEUKIN-17 PRODUCTION; RHEUMATOID-ARTHRITIS;
PERIPHERAL-BLOOD
AB T helper 17 (Th17), a distinct subset of CD4(+) T cells with IL-17 as their major cytokine, orchestrate the pathogenesis of inflammatory and autoimmune diseases. Dysregulated Th17 cells contribute to inflammatory and autoimmune diseases. Candidate biologics are in development for targeting IL-17, IL-17 receptors or IL-17 pathways. Several drugs that impact the IL-17 pathway are already in clinical trials for the treatment of autoimmune diseases. In this review we provide evidence for the role of Th17 cells in immune-mediated diseases. An understanding of the role of Th17 in these conditions will provide important insights and unravel novel targets for therapeutic intervention. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Singh, Ram Pyare; Nagra, Saranpreet; Hahn, Bevra H.; Hossain, Awlad] Univ Calif Los Angeles, David Geffen Sch Med, Div Rheumatol, Los Angeles, CA 90095 USA.
[Hasan, Sascha] Univ Calif Los Angeles, David Geffen Sch Med, Sanguine Biosci Inc, Los Angeles, CA 90095 USA.
[Sharma, Sherven; Yamaguchi, Dean T.] Univ Calif Los Angeles, David Geffen Sch Med, Vet Affairs Greater Los Angeles Hlth Care Syst, Res Serv, Los Angeles, CA 90095 USA.
[Wong, David T. W.] Univ Calif Los Angeles, David Geffen Sch Med, Sch Dent, Los Angeles, CA 90095 USA.
C3 University of California System; University of California Los Angeles;
University of California Los Angeles Medical Center; David Geffen School
of Medicine at UCLA; University of California System; University of
California Los Angeles; University of California Los Angeles Medical
Center; David Geffen School of Medicine at UCLA; US Department of
Veterans Affairs; Veterans Health Administration (VHA); VA Greater Los
Angeles Healthcare System; University of California System; University
of California Los Angeles; University of California Los Angeles Medical
Center; David Geffen School of Medicine at UCLA; University of
California System; University of California Los Angeles; University of
California Los Angeles Medical Center; David Geffen School of Medicine
at UCLA
RP Singh, RP (corresponding author), Univ Calif Los Angeles, David Geffen Sch Med, Div Rheumatol, Los Angeles, CA 90095 USA.
EM rsingh@ucla.edu
RI Singh, Ram/JMC-0997-2023
OI Singh, Ram/0000-0002-3203-4454
FU NIH [AR54034, AI 083894, AI65645]; UCLA Senate Core Grant; UCLA
Oppenheimer Clinical Seed Grant; American Autoimmune Related Disease
Association; Lupus Foundation of America; VA Merit Review Award [2101
BX000170-05]
FX Supported by NIH grants AR54034, AI 083894, AI65645 to RPS, UCLA Senate
Core Grant to BHH and RPS, UCLA Oppenheimer Clinical Seed Grant and
American Autoimmune Related Disease Association and the Lupus Foundation
of America Awards to RPS, and VA Merit Review Award 2101 BX000170-05 to
DTY.
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NR 117
TC 165
Z9 196
U1 0
U2 56
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD DEC
PY 2014
VL 13
IS 12
BP 1174
EP 1181
DI 10.1016/j.autrev.2014.08.019
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AT8TC
UT WOS:000345203800002
PM 25151974
DA 2025-01-07
ER
PT J
AU Sheng, LL
Jena, PK
Hu, Y
Liu, HX
Nagar, N
Kalanetra, KM
French, SW
French, SW
Mills, DA
Wan, YJY
AF Sheng, Lili
Jena, Prasant Kumar
Hu, Ying
Liu, Hui-Xin
Nagar, Nidhi
Kalanetra, Karen M.
French, Samuel William
French, Samuel Wheeler
Mills, David A.
Wan, Yu-Jui Yvonne
TI Hepatic inflammation caused by dysregulated bile acid synthesis is
reversible by butyrate supplementation
SO JOURNAL OF PATHOLOGY
LA English
DT Article
DE short-chain fatty acids; hepatitis; liver cancer; gut microbiota;
probiotics; FXR
ID CHAIN FATTY-ACIDS; HEPATOCELLULAR-CARCINOMA; DIETARY FIBER;
LIVER-CANCER; RECEPTOR; GUT; MICROBIOTA; EXPRESSION; FXR; ACTIVATION
AB Dysregulated bile acid (BA) synthesis or reduced farnesoid X receptor (FXR) levels are found in patients having metabolic diseases, autoimmune hepatitis, and liver cirrhosis or cancer. The objective of this study was to establish the relationship between butyrate and dysregulated BA synthesis-induced hepatitis as well as the effect of butyrate in reversing the liver pathology. Wild-type (WT) and FXR knockout (KO) male mice were placed on a control (CD) or western diet (WD) for 15 months. In the presence or absence of butyrate supplementation, feces obtained from 15-month-old WD-fed FXR KO mice, which had severe hepatitis and liver tumors, were transplanted to 7-month-old WD-fed FXR KO for 3 months. Hepatic phenotypes, microbiota profile, and BA composition were analyzed. Butyrate-generating bacteria and colonic butyrate concentration were reduced due to FXR inactivation and further reduced by WD intake. In addition, WD-fed FXR KO male mice had the highest concentration of hepatic beta-muricholic acid (beta-MCA) and bacteria-generated deoxycholic acid (DCA) accompanied by serious hepatitis. Moreover, dysregulated BA and reduced SCFA signaling co-existed in both human liver cancers and WD-fed FXR KO mice. Microbiota transplantation using butyrate-deficient feces derived from 15-month-old WD-fed FXR KO mice increased hepatic lymphocyte numbers as well as hepatic beta-MCA and DCA concentrations. Furthermore, butyrate supplementation reduced hepatic beta-MCA as well as DCA and eliminated hepatic lymphocyte infiltration. In conclusion, reduced butyrate contributes to the development of hepatitis in the FXR KO mouse model. In addition, butyrate reverses dysregulated BA synthesis and its associated hepatitis. Copyright (C) 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
C1 [Sheng, Lili; Jena, Prasant Kumar; Hu, Ying; Liu, Hui-Xin; Nagar, Nidhi; Wan, Yu-Jui Yvonne] Univ Calif Davis, Dept Med Pathol & Lab Med, Sacramento, CA 95817 USA.
[Nagar, Nidhi] Calif State Univ East Bay, Dept Biol Sci, Hayward, CA USA.
[Kalanetra, Karen M.; Mills, David A.] Univ Calif Davis, Dept Food Sci & Technol, Dept Viticulture & Enol, Davis, CA 95616 USA.
[French, Samuel William] Harbor UCLA Med Ctr, Dept Pathol, Torrance, CA 90509 USA.
[French, Samuel Wheeler] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
C3 University of California System; University of California Davis;
California State University System; California State University East
Bay; University of California System; University of California Davis;
University of California System; University of California Los Angeles;
University of California Los Angeles Medical Center; University of
California System; University of California Los Angeles; University of
California Los Angeles Medical Center; David Geffen School of Medicine
at UCLA
RP Wan, YJY (corresponding author), Univ Calif Davis, Davis Hlth Syst, Dept Med Pathol & Lab Med, Room 3400B,Res Bldg 3,4645 2nd Ave, Sacramento, CA 95817 USA.
EM yjywan@ucdavis.edu
RI Kalanetra, Karen/AAP-3669-2021; Jena, Prasant/L-4339-2017; Mills, David
Andrew/G-2282-2011
OI Mills, David Andrew/0000-0003-1913-9865; Liu,
Hui-Xin/0000-0002-8981-9981
FU National Institutes of Health [U01CA179582]
FX We thank Dr Frank J. Gonzalez at NCI for providing FXR KO mice and Niki
Taylor DeGeorge for editing the manuscript. This work was supported by
National Institutes of Health, Grant U01CA179582.
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NR 62
TC 97
Z9 97
U1 2
U2 60
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3417
EI 1096-9896
J9 J PATHOL
JI J. Pathol.
PD DEC
PY 2017
VL 243
IS 4
BP 431
EP 441
DI 10.1002/path.4983
PG 11
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA FN0RF
UT WOS:000415685900004
PM 28892150
OA Green Submitted, Green Accepted
DA 2025-01-07
ER
PT J
AU Zhu, H
Zhao, M
Chang, C
Chan, V
Lu, QJ
Wu, HJ
AF Zhu, Huan
Zhao, Ming
Chang, Christopher
Chan, Vera
Lu, Qianjin
Wu, Haijing
TI The complex role of AIM2 in autoimmune diseases and cancers
SO IMMUNITY INFLAMMATION AND DISEASE
LA English
DT Review
DE AIM2; autoimmune diseases; cancers; cGAS-STING
ID SQUAMOUS-CELL CARCINOMA; MELANOMA 2; LUNG-CANCER; DNA SENSOR;
INFLAMMASOME ACTIVATION; CASPASE-3 CLEAVAGE; CO-IMMUNIZATION;
GENE-EXPRESSION; UP-REGULATION; TUMOR-CELLS
AB Absent in melanoma 2 (AIM2) is a novel member of interferon (IFN)-inducible PYHIN proteins. In innate immune cells, AIM2 servers as a cytoplasmic double-stranded DNA sensor, playing a crucial role in the initiation of the innate immune response as a component of the inflammasome. AIM2 expression is increased in patients with systemic lupus erythematosus (SLE), psoriasis, and primary Sjogren's syndrome, indicating that AIM2 might be involved in the pathogenesis of autoimmune diseases. Meanwhile, AIM2 also plays an antitumorigenesis role in an inflammasome independent-manner. In melanoma, AIM2 is initially identified as a tumor suppressor factor. However, A1M2 is also found to contribute to lung tumorigenesis via the inflammasome-dependent release of interleukin 1 beta and regulation of mitochondrial dynamics. Additionally, AIM2 reciprocally dampening the cGAS-STING pathway causes immunosuppression of macrophages and evasion of antitumor immunity during antibody treatment. To summarize the complicated effect and role of AIM2 in autoimmune diseases and cancers, herein, we provide an overview of the emerging research progress on the function and regulatory pathway of AIM2 in innate and adaptive immune cells, as well as tumor cells, and discuss its pathogenic role in autoimmune diseases, such as SLE, psoriasis, primary Sjogren's syndrome, and cancers, such as melanomas, non-small-cell lung cancer, colon cancer, hepatocellular carcinoma, renal carcinoma, and so on, hopefully providing potential therapeutic and diagnostic strategies for clinical use.
C1 [Zhu, Huan; Zhao, Ming; Lu, Qianjin; Wu, Haijing] Cent South Univ, Hunan Key Lab Med Epigen, Dept Dermatol, Xiangya Hosp 2, 139 Middle Renmin Rd, Changsha 410011, Hunan, Peoples R China.
[Chang, Christopher] Univ Calif Davis, Davis Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Chan, Vera] Univ Hong Kong, Dept Med, Div Rheumatol & Clin Immunol, Hong Kong, Peoples R China.
[Lu, Qianjin] Chinese Acad Med Sci & Peking Union Med Coll, Inst Dermatol, Nanjing, Peoples R China.
C3 Central South University; University of California System; University of
California Davis; University of Hong Kong; Chinese Academy of Medical
Sciences - Peking Union Medical College; Peking Union Medical College;
Institute of Dermatology - CAMS
RP Lu, QJ; Wu, HJ (corresponding author), Cent South Univ, Hunan Key Lab Med Epigen, Dept Dermatol, Xiangya Hosp 2, 139 Middle Renmin Rd, Changsha 410011, Hunan, Peoples R China.
EM qianlu5860@csu.edu.cn; chriswu1010@csu.edu.cn
FU Hunan Outstanding Young Investigator [2020JJ2055]; Hunan Talent Young
Investigator [2019RS2012]; National Natural Science Foundation of China
[81972943, 81830097]
FX Hunan Outstanding Young Investigator, Grant/Award Number: 2020JJ2055;
Hunan Talent Young Investigator, Grant/Award Number: 2019RS2012;
National Natural Science Foundation of China, Grant/Award Numbers:
81972943, 81830097
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NR 162
TC 29
Z9 36
U1 6
U2 27
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2050-4527
J9 IMMUN INFLAMM DIS
JI IMMUN. INFLAMM. DIS.
PD SEP
PY 2021
VL 9
IS 3
BP 649
EP 665
DI 10.1002/iid3.443
EA MAY 2021
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA TV0TS
UT WOS:000652197000001
PM 34014039
OA Green Published
DA 2025-01-07
ER
PT J
AU Songtanin, B
Nugent, K
AF Songtanin, Busara
Nugent, Kenneth
TI Burden, Outcome, and Comorbidities of Extrahepatic Manifestations in
Hepatitis C Virus Infection
SO BIOLOGY-BASEL
LA English
DT Review
DE extrahepatic manifestation; hepatitis C virus; hepatitis C infection;
antiviral therapy; burden; morbidity; mortality
ID ORAL LICHEN-PLANUS; SUSTAINED VIROLOGICAL RESPONSE;
PORPHYRIA-CUTANEA-TARDA; INTERFERON ALPHA-2A THERAPY; CHRONIC
KIDNEY-DISEASE; NON-HODGKIN LYMPHOMAS; INSULIN-RESISTANCE; MIXED
CRYOGLOBULINEMIA; SJOGRENS-SYNDROME; DIABETES-MELLITUS
AB Simple Summary Hepatitis C is a liver infection caused by the hepatitis C virus and is a major health problem that contributes to the global burden of chronic disease. Chronic infection can lead to liver cancer and death from end-organ damage. Despite the introduction of novel anti-viral therapy, the disease burden is still high. This review focuses on the various extrahepatic manifestations of the hepatitis C virus, including frequency, mechanism, and outcomes. Despite the introduction of direct-acting antiviral drugs which have more than a 90% rate of sustained virologic responses, about one-third of patients with chronic HCV infections still develop at least one extrahepatic manifestation. Hepatitis C virus (HCV) is a significant cause of chronic liver diseases worldwide and is associated with negative consequences, including cirrhosis, hepatic decompensation, hepatocellular carcinoma, and increased risk of mortality. In addition to liver-related morbidities, HCV is also associated with several extrahepatic manifestations, including mixed cryoglobulinemia, diabetes mellitus, cardiocerebrovascular disease, lymphoma, and autoimmune diseases. These non-liver-related complications of HCV increase the complexity of this disease and can contribute to the economic burden, morbidity, quality of life, and mortality throughout the world. Therefore, understanding how this virus can contribute to each extrahepatic manifestation is worth investigating. Currently, the advancement of HCV treatment with the advent of direct-acting anti-viral agents (DAAs) has led to a high cure rate as a result of sustained virologic response and tremendously reduced the burden of extrahepatic complications. However, HCV-associated extrahepatic manifestations remain a relevant concern, and this review aims to give an updated highlight of the prevalence, risk factors, associated burdens, and treatment options for these conditions.
C1 [Songtanin, Busara; Nugent, Kenneth] Texas Tech Univ, Dept Internal Med, Hlth Sci Ctr, Lubbock, TX 79430 USA.
C3 Texas Tech University System; Texas Tech University Health Science
Center
RP Songtanin, B (corresponding author), Texas Tech Univ, Dept Internal Med, Hlth Sci Ctr, Lubbock, TX 79430 USA.
EM busara.songtanin@ttuhsc.edu
OI Songtanin, Busara/0000-0002-4117-4272
CR AASLD/IDSA HCV, GUID PAN REC TEST MA
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NR 184
TC 11
Z9 11
U1 0
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2079-7737
J9 BIOLOGY-BASEL
JI Biology-Basel
PD JAN
PY 2023
VL 12
IS 1
AR 23
DI 10.3390/biology12010023
PG 23
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA 7X7OD
UT WOS:000914386100001
PM 36671716
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Chlamydas, S
Markouli, M
Strepkos, D
Piperi, C
AF Chlamydas, Sarantis
Markouli, Mariam
Strepkos, Dimitrios
Piperi, Christina
TI Epigenetic mechanisms regulate sex-specific bias in disease
manifestations
SO JOURNAL OF MOLECULAR MEDICINE-JMM
LA English
DT Review
DE X-inactivation; Epigenetics; Sex bias; Hormones; COVID-19; X-linked
genes; Autoimmune disorders; Liver fibrosis; Neuropsychiatric diseases;
Cancer
ID X-CHROMOSOME INACTIVATION; GENE-EXPRESSION; ASTHMA DEVELOPMENT;
GENDER-DIFFERENCES; CHROMATIN; HISTONE; SUSCEPTIBILITY; POLYCOMB;
CANCER; TRITHORAX
AB Sex presents a vital determinant of a person's physiology, anatomy, and development. Recent clinical studies indicate that sex is also involved in the differential manifestation of various diseases, affecting both clinical outcome as well as response to therapy. Genetic and epigenetic changes are implicated in sex bias and regulate disease onset, including the inactivation of the X chromosome as well as sex chromosome aneuploidy. The differential expression of X-linked genes, along with the presence of sex-specific hormones, exhibits a significant impact on immune system function. Several studies have revealed differences between the two sexes in response to infections, including respiratory diseases and COVID-19 infection, autoimmune disorders, liver fibrosis, neuropsychiatric diseases, and cancer susceptibility, which can be explained by sex-biased immune responses. In the present review, we explore the input of genetic and epigenetic interplay in the sex bias underlying disease manifestation and discuss their effects along with sex hormones on disease development and progression, aiming to reveal potential new therapeutic targets. Key messages Sex is involved in the differential manifestation of various diseases. Epigenetic modifications influence X-linked gene expression, affecting immune response to infections, including COVID-19. Epigenetic mechanisms are responsible for the sex bias observed in several respiratory and autoimmune disorders, liver fibrosis, neuropsychiatric diseases, and cancer.
C1 [Chlamydas, Sarantis; Markouli, Mariam; Strepkos, Dimitrios; Piperi, Christina] Natl & Kapodistrian Univ Athens, Med Sch, Dept Biol Chem, 75 M Asias St Bldg 16, Athens 11527, Greece.
[Chlamydas, Sarantis] Olink Prote, Uppsala, Sweden.
C3 National & Kapodistrian University of Athens
RP Piperi, C (corresponding author), Natl & Kapodistrian Univ Athens, Med Sch, Dept Biol Chem, 75 M Asias St Bldg 16, Athens 11527, Greece.
EM cpiperi@med.uoa.gr
RI Markouli, Mariam/HNB-4965-2023; Piperi, Christina/AAF-2009-2020
OI Piperi, Christina/0000-0002-2701-0618; Strepkos,
Dimitrios/0000-0001-6623-1715
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NR 115
TC 16
Z9 17
U1 2
U2 8
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0946-2716
EI 1432-1440
J9 J MOL MED
JI J. Mol. Med.
PD AUG
PY 2022
VL 100
IS 8
BP 1111
EP 1123
DI 10.1007/s00109-022-02227-x
EA JUN 2022
PG 13
WC Genetics & Heredity; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Research & Experimental Medicine
GA 3G3SM
UT WOS:000817816300001
PM 35764820
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Samonakis, DN
Gatselis, N
Bellou, A
Sifaki-Pistolla, D
Mela, M
Demetriou, G
Thalassinos, E
Rigopoulou, EI
Kevrekidou, P
Tziortziotis, I
Azariadi, K
Kavousanaki, M
Digenakis, E
Vassiliadis, T
Kouroumalis, EA
Dalekos, GN
AF Samonakis, Dimitrios N.
Gatselis, Nikolaos
Bellou, Aristea
Sifaki-Pistolla, Dimitra
Mela, Maria
Demetriou, George
Thalassinos, Evangelos
Rigopoulou, Eirini I.
Kevrekidou, Polyxeni
Tziortziotis, Ioannis
Azariadi, Kalliopi
Kavousanaki, Melina
Digenakis, Emmanuel
Vassiliadis, Themistoklis
Kouroumalis, Elias A.
Dalekos, George N.
TI Spontaneous bacterial peritonitis: a prospective Greek multicenter study
of its epidemiology, microbiology, and outcomes
SO ANNALS OF GASTROENTEROLOGY
LA English
DT Article
DE Cirrhosis; spontaneous bacterial peritonitis; mortality; lactate; MELD
score
ID PROTON PUMP INHIBITORS; CIRRHOTIC-PATIENTS; RESISTANT BACTERIA; SEPTIC
SHOCK; RISK-FACTORS; MORTALITY; INFECTIONS; INCREASE; THERAPY; FAILURE
AB Background Spontaneous bacterial peritonitis (SBP) is an ominous complication of decompensated cirrhosis. This study aimed to assess several epidemiological, clinical, microbiological and outcome characteristics in Greek patients with SBP, as no solid representative nationwide data of this type was available.
Methods During a 3-year period, 77 consecutive patients with SBP (61 male; median age: 67 years; model for end-stage liver disease [MELD] score: 20), diagnosed and followed in 5 tertiary liver units, were prospectively recruited and studied. Various prognostic factors for disease outcome were studied.
Results Thirty-eight patients had alcohol-related cirrhosis, 17 viral hepatitis, 6 non-alcoholic steatohepatitis, 6 autoimmune liver diseases, and 10 cryptogenic cirrhosis. Hepatocellular carcinoma (HCC) was present in 23 (29.9%), whereas 10 (13%) had portal vein thrombosis. The first SBP episode at baseline was community-acquired in 53 (68.8%), while in 24 (31.1%) was hospital-acquired, with predominant symptoms abdominal pain and encephalopathy. A positive ascitic culture was documented in 36% of patients in the initial episode, with almost equal gram (+) and gram (-) pathogens, including 3 multidrug-resistant pathogens. Significant factors for 6-month survival were: higher MELD score, previous beta-blocker use, lower serum albumin, higher lactate on admission and need for vasopressors, while factors for 12-month survival were MELD score and lactate. For overall survival, higher MELD score and lactate along with HCC presence were negative predictive factors.
Conclusions MELD score, lactate, albumin, HCC and treatment with vasopressors were predictive of survival in SBP patients. In hospital-acquired SBP the prevalence of difficult-to-treat pathogens was higher.
C1 [Samonakis, Dimitrios N.; Demetriou, George; Digenakis, Emmanuel; Kouroumalis, Elias A.] Univ Hosp Heraklion, Dept Gastroenterol & Hepatol, Iraklion 71110, Crete, Greece.
[Gatselis, Nikolaos; Bellou, Aristea; Rigopoulou, Eirini I.; Azariadi, Kalliopi; Dalekos, George N.] Gen Univ Hosp Larissa, Dept Med, Natl Expertise Ctr Greece Autoimmune Liver Dis, Larisa, Greece.
[Gatselis, Nikolaos; Bellou, Aristea; Rigopoulou, Eirini I.; Azariadi, Kalliopi; Dalekos, George N.] Gen Univ Hosp Larissa, Res Lab Internal Med, Natl Expertise Ctr Greece Autoimmune Liver Dis, Larisa, Greece.
[Bellou, Aristea; Kevrekidou, Polyxeni; Vassiliadis, Themistoklis] Aristotle Univ Thessaloniki, Dept Internal Med 3, Papageorgiou Gen Hosp, Thessaloniki, Greece.
[Sifaki-Pistolla, Dimitra; Tziortziotis, Ioannis] Univ Crete, Sch Med, Clin Social & Family Med, Iraklion, Crete, Greece.
[Mela, Maria] Evangelismos Med Ctr, Dept Gastroenterol, Athens, Greece.
[Thalassinos, Evangelos; Kavousanaki, Melina] Venizele Hosp, Dept Internal Med, Iraklion, Crete, Greece.
C3 University Hospital of Heraklion; General University Hospital of
Larissa; General University Hospital of Larissa; Papageorgiou Hospital;
Aristotle University of Thessaloniki; University of Crete; Evangelismos
Hospital
RP Samonakis, DN (corresponding author), Univ Hosp Heraklion, Dept Gastroenterol & Hepatol, Iraklion 71110, Crete, Greece.
EM dsamonakis@gmail.com
OI Sifaki-Pistolla, Dimitra/0000-0001-9345-6266
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NR 45
TC 2
Z9 3
U1 0
U2 4
PU HELLENIC SOC GASTROENTEROLOGY
PI ATHENS
PA DEMOKRATIAS AVE 67, ATHENS, 15451, GREECE
SN 1108-7471
EI 1792-7463
J9 ANN GASTROENTEROL
JI Ann. Gastroenterol.
PY 2022
VL 35
IS 1
BP 80
EP 87
DI 10.20524/aog.2021.0674
EA NOV 2021
PG 8
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA YI3JC
UT WOS:000719988900001
PM 34987293
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Piñero, F
da Fonseca, LG
AF Pinero, Federico
da Fonseca, Leonardo Gomes
TI Trial eligibility in advanced hepatocellular carcinoma: Does it support
clinical practice in underrepresented subgroups?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Eligibility; Systemic therapies; End-stage; Hepatocellular carcinoma
ID ATEZOLIZUMAB PLUS BEVACIZUMAB; LIVER-DISEASE; LATIN-AMERICA; SORAFENIB;
MULTICENTER; LENVATINIB; ETIOLOGY
AB Although hepatocellular carcinoma is considered a highly lethal malignancy, recent therapeutic advances have been achieved during the last 10 years. This scenario resulted in an unprecedented improvement in survival for patients with advanced hepatocellular carcinoma, almost reaching 20-26 mo of overall survival after first-second line sequential treatment. The advent of the combination of atezolizumab with bevacizumab showed, for the first time, superiority over sorafenib with improvement in overall survival. However, first and second-line trials were correctly based on the premise that a strict selection of patients enhances the power to capture the positive effect of treatment by excluding competing risks for mortality such as liver failure, decompensated cirrhosis or other underlying medical conditions. As a result, the inclusion criteria used in clinical trials do not support the use of novel therapies in several real-world scenarios involving underrepresented subgroups, such as patients with unpreserved liver function, other comorbid conditions, a history of solid-organ transplantation, autoimmune disorders and those with a high risk of bleeding. The present text aims at discussing treatment strategies in these subgroups.
C1 [Pinero, Federico] Austral Univ, Hosp Univ Austral, Sch Med, Hepatol & Liver Unit, Av Presidente Peron 1500,Pilar, Buenos Aires, DF, Argentina.
[da Fonseca, Leonardo Gomes] Univ Sao Paulo, Inst Canc Estado Sao Paulo, Clin Oncol, BR-05403000 Sao Paulo, Brazil.
C3 Austral University; Hospital Universitario Austral; Universidade de Sao
Paulo
RP Piñero, F (corresponding author), Austral Univ, Hosp Univ Austral, Sch Med, Hepatol & Liver Unit, Av Presidente Peron 1500,Pilar, Buenos Aires, DF, Argentina.
EM fpinerof@cas.austral.edu.ar
RI Fonseca, Leonardo/JCD-5745-2023
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NR 50
TC 4
Z9 4
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUN 28
PY 2021
VL 27
IS 24
BP 3429
EP 3439
DI 10.3748/wjg.v27.i24.3429
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA TE4RL
UT WOS:000669998400001
PM 34239261
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Xu, XL
Jiang, LS
Wu, CS
Pan, LY
Lou, ZQ
Peng, CT
Dong, Y
Ruan, B
AF Xu, Xiao-lan
Jiang, Lu-shun
Wu, Chen-si
Pan, Li-ya
Lou, Zhuo-qi
Peng, Chun-ting
Dong, Yin
Ruan, Bing
TI The role of fibrosis index FIB-4 in predicting liver fibrosis stage and
clinical prognosis: A diagnostic or screening tool?
SO JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION
LA English
DT Review
DE Acute liver injury; Chronic liver disease; Liver fibrosis; Non-invasive;
Prognosis
ID CHRONIC HEPATITIS-B; MAGNETIC-RESONANCE ELASTOGRAPHY; PLATELET RATIO
INDEX; TRANSIENT ELASTOGRAPHY; HEPATOCELLULAR-CARCINOMA; NONINVASIVE
ASSESSMENT; AUTOIMMUNE HEPATITIS; NATURAL-HISTORY; SCORING SYSTEMS;
SERUM MARKERS
AB This review evaluates the ability of the fibrosis index based on four factors (FIB-4) identifying fibrosis stages, long-time prognosis in chronic liver disease, and short-time outcomes in acute liver injury. FIB-4 was accurate in predicting the absence or presence of advanced fibrosis with cut-offs of 1.0 and 2.65 for viral hepatitis B, 1.45 and 3.25 for viral hepatitis C, 1.30 (<65 years), 2.0 (>65 years), and 2.67 for non-alcoholic fatty liver disease (NAFLD), respectively, but had a low-to-moderate accuracy in alcoholic liver disease (ALD) and autoimmune hepatitis. It performed better in excluding fibrosis, so we built an algorithm for identifying advanced fibrosis by combined methods and giving work-up and follow-up suggestions. High FIB-4 in viral hepatitis, NAFLD, and ALD was associated with significantly high hepatocellular carcinoma incidence and mortality. Additionally, FIB-4 showed the ability to predict high-risk varices with cut-offs of 2.87 and 3.91 in cirrhosis patients and predict long-term survival in hepatocellular carcinoma patients after hepatectomy. In acute liver injury caused by COVID-19, FIB-4 had a predictive value for mechanical ventilation and 30-day mortality. Finally, FIB-4 may act as a screening tool in the secondary prevention of NAFLD in the high-risk population. Copyright 2021, Formosan Medical Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by- nc-nd/4.0/).
C1 [Xu, Xiao-lan; Jiang, Lu-shun; Wu, Chen-si; Pan, Li-ya; Lou, Zhuo-qi; Peng, Chun-ting; Ruan, Bing] Zhejiang Univ, Affiliated Hosp 1, Coll Med,Collaborat Innovat Ctr Diag & Treatment, State Key Lab Diag & Treatment Infect Dis,Natl Cl, Hangzhou, Peoples R China.
[Dong, Yin] Peoples Hosp Med Community Yuhuan Cty, Taizhou, Zhejiang, Peoples R China.
C3 Zhejiang University; Collaborative Innovation Center for Diagnosis &
Treatment of Infectious Diseases
RP Ruan, B (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Coll Med, 79 Qingchun Rd, Hangzhou, Peoples R China.
EM xxl66@zju.edu.cn; 21818032@zju.edu.cn; 11918233@zju.edu.cn;
11818050@zju.edu.cn; louzhuoqigl@163.com; pengct420@zju.edu.cn;
9597082@qq.com; ruanbing@zju.edu.cn
FU National Science and Tech-nology Major Project of China
[2017ZX10105001]; Na-tional Human Genetic Resources Sharing Service
Platform [2005DKA21300]
FX The work was funded by the National Science and Tech-nology Major
Project of China (2017ZX10105001) and Na-tional Human Genetic Resources
Sharing Service Platform (Grant No. 2005DKA21300) .
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NR 97
TC 32
Z9 33
U1 2
U2 18
PU ELSEVIER TAIWAN
PI TAIPEI
PA RM N-412, 4F, CHIA HSIN BUILDING 11, NO 96, ZHONG SHAN N ROAD SEC 2,
TAIPEI, 10449, TAIWAN
SN 0929-6646
EI 1876-0821
J9 J FORMOS MED ASSOC
JI J. Formos. Med. Assoc.
PD FEB
PY 2022
VL 121
IS 2
BP 454
EP 466
DI 10.1016/j.jfma.2021.07.013
EA JAN 2022
PG 13
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA YR4UO
UT WOS:000749987400003
PM 34325952
OA gold
DA 2025-01-07
ER
PT J
AU Kardashian, A
Serper, M
Terrault, N
Nephew, LD
AF Kardashian, Ani
Serper, Marina
Terrault, Norah
Nephew, Lauren D.
TI Health disparities in chronic liver disease
SO HEPATOLOGY
LA English
DT Review
ID HEPATITIS-C VIRUS; PRIMARY SCLEROSING CHOLANGITIS; UNITED-STATES;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; AFRICAN-AMERICANS;
URSODEOXYCHOLIC ACID; ETHNIC DISPARITIES; RACIAL DISPARITIES; NATIONAL
TRENDS
AB The syndemic of hazardous alcohol consumption, opioid use, and obesity has led to important changes in liver disease epidemiology that have exacerbated health disparities. Health disparities occur when plausibly avoidable health differences are experienced by socially disadvantaged populations. Highlighting health disparities, their sources, and consequences in chronic liver disease is fundamental to improving liver health outcomes. There have been large increases in alcohol use disorder in women, racial and ethnic minorities, and those experiencing poverty in the context of poor access to alcohol treatment, leading to increasing rates of alcohol-associated liver diseases. Rising rates of NAFLD and associated fibrosis have been observed in Hispanic persons, women aged > 50, and individuals experiencing food insecurity. Access to viral hepatitis screening and linkage to treatment are suboptimal for racial and ethnic minorities and individuals who are uninsured or underinsured, resulting in greater liver-related mortality and later-stage diagnoses of HCC. Data from more diverse cohorts on autoimmune and cholestatic liver diseases are lacking, supporting the need to study the contemporary epidemiology of these disorders in greater detail. Herein, we review the existing literature on racial and ethnic, gender, and socioeconomic disparities in chronic liver diseases using a social determinants of health framework to better understand how social and structural factors cause health disparities and affect chronic liver disease outcomes. We also propose potential solutions to eliminate disparities, outlining health-policy, health-system, community, and individual solutions to promote equity and improve health outcomes.
C1 [Kardashian, Ani; Terrault, Norah] Univ Southern Calif, Div Gastrointestinal & Liver Dis, Los Angeles, CA USA.
[Serper, Marina] Univ Penn, Div Gastroenterol & Hepatol, Perelman Sch Med, Philadelphia, PA USA.
[Serper, Marina] Corporal Michael J Crescenz VA Med Ctr, Philadelphia, PA USA.
[Serper, Marina] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA USA.
[Nephew, Lauren D.] Indiana Univ Sch Med, Div Gastroenterol & Hepatol, Dept Med, Indianapolis, IN USA.
[Nephew, Lauren D.] Indiana Univ, Simon Comprehens Canc Ctr, Indianapolis, IN USA.
C3 University of Southern California; University of Pennsylvania;
University of Pennsylvania; Indiana University System; Indiana
University Bloomington; Indiana University System; Indiana University
Indianapolis
RP Nephew, LD (corresponding author), Indiana Univ Sch Med, Div Gastroenterol & Hepatol, Dept Med, 702 Rotary Circle, Indianapolis, IN 46202 USA.
EM lnephew@iu.edu
RI Nephew, Lauren/AAY-9123-2021
OI Terrault, Norah/0000-0003-4143-1950; Nephew, Lauren/0000-0003-0837-0746;
Serper, Marina/0000-0003-4899-2160
FU American Association for the Study of Liver Diseases; National Institute
of Diabetes and Digestive and Kidney Diseases [DK115897]
FX American Association for the Study of Liver Diseases, Grant/Award
Number: Advanced/Transplant Hepatology Award; National Institute of
Diabetes and Digestive and Kidney Diseases, Grant/Award Number: DK115897
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NR 179
TC 85
Z9 85
U1 9
U2 26
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD APR
PY 2023
VL 77
IS 4
BP 1382
EP 1403
DI 10.1002/hep.32743
EA SEP 2022
PG 22
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA Q6PJ1
UT WOS:000849516800001
PM 35993341
OA Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Kanno, A
Satoh, K
Kimura, K
Masamune, A
Asakura, T
Unno, M
Matsuno, S
Moriya, T
Shimosegawa, T
AF Kanno, A
Satoh, K
Kimura, K
Masamune, A
Asakura, T
Unno, M
Matsuno, S
Moriya, T
Shimosegawa, T
TI Autoimmune pancreatitis with hepatic inflammatory pseudotumor
SO PANCREAS
LA English
DT Article
DE pancreatitis; autoimmune; inflammatory pseudotumor
ID SCLEROSING PANCREATITIS; RETROPERITONEAL FIBROSIS; F-18
FLUORODEOXYGLUCOSE; PET; DISEASE; CANCER
AB We report a case of autoimmune pancreatitis (AIP) with hepatic inflammatory pseudotumor (IP). The patient was clinically diagnosed as having multiple metastatic tumors originated from cholangiocellular carcinoma as well as autoimmune pancreatitis and underwent left lobectomy of the liver. Histological examination showed a diffuse or dense lymphoplasmacytic infiltration with obliterating phlebitis but an absence of neoplastic proliferation both in the liver tumor and in the biopsy specimen of the pancreas. Abundant IgG4-positive plasma cells were seen in the lesions. This is the first case report that shows a simultaneous occurrence of hepatic IP and AIP, suggesting that these lesions appeared on the background of the recently proposed entity of IgG4-related systemic disease.
C1 Tohoku Univ, Grad Sch Med, Div Gastroenterol, Aoba Ku, Sendai, Miyagi 9808574, Japan.
Tohoku Univ, Grad Sch Med, Dept Surg Gastroenterol, Sendai, Miyagi 9808574, Japan.
Tohoku Univ, Grad Sch Med, Dept Pathol, Sendai, Miyagi 9808574, Japan.
C3 Tohoku University; Tohoku University; Tohoku University
RP Tohoku Univ, Grad Sch Med, Div Gastroenterol, Aoba Ku, 1-1 Seiryo Machi, Sendai, Miyagi 9808574, Japan.
EM atsushih@cocoa.ocn.ne.jp
RI Unno, Michiaki/AAX-5246-2020; Kanno, Atsushi/J-2685-2019; Moriya,
Takuya/AAM-6974-2020
OI Masamune, Atsushi/0000-0001-7184-7282
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NR 14
TC 41
Z9 45
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2005
VL 31
IS 4
BP 420
EP 423
DI 10.1097/01.mpa.0000179732.46210.da
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 980KM
UT WOS:000233017400019
PM 16258381
DA 2025-01-07
ER
PT J
AU Piantanida, E
Ippolito, S
Gallo, D
Masiello, E
Premoli, P
Cusini, C
Rosetti, S
Sabatino, J
Segato, S
Trimarchi, F
Bartalena, L
Tanda, ML
AF Piantanida, E.
Ippolito, S.
Gallo, D.
Masiello, E.
Premoli, P.
Cusini, C.
Rosetti, S.
Sabatino, J.
Segato, S.
Trimarchi, F.
Bartalena, L.
Tanda, M. L.
TI The interplay between thyroid and liver: implications for clinical
practice
SO JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
LA English
DT Review
DE Hypothyroidism; Hyperthyroidism; Antithyroid drugs; Chronic hepatitis C;
Thyroid autoimmunity
ID CHRONIC HEPATITIS-C; INTERFERON-ALPHA THERAPY; VIRUS-INFECTION;
GRAVES-DISEASE; HEPATOCELLULAR-CARCINOMA; PRIMARY HYPOTHYROIDISM;
AUTOIMMUNE DISORDERS; PLUS RIBAVIRIN; FUNCTION TESTS; SERUM TSH
AB A complex relationship exists between thyroid and liver in health and disease. Liver plays an essential physiological role in thyroid hormone activation and inactivation, transport, and metabolism. Conversely, thyroid hormones affect activities of hepatocytes and hepatic metabolism. Serum liver enzyme abnormalities observed in hypothyroidism may be related to impaired lipid metabolism, hepatic steatosis or hypothyroidism-induced myopathy. Severe hypothyroidism may have biochemical and clinical features, such as hyperammonemia and ascites, mimicking those of liver failure. Liver function tests are frequently abnormal also in hyperthyroidism, due to oxidative stress, cholestasis, or enhanced osteoblastic activity. Antithyroid drug-associated hepatotoxicity is a rare event, likely related mainly to an idiosyncratic mechanism, ranging from a mild hepatocellular damage to liver failure. Propylthiouracil-induced liver damage is usually more severe than that caused by methimazole. On the other hand, thyroid abnormalities can be found in liver diseases, such as chronic hepatitis C, liver cirrhosis, hepatocellular carcinoma, and cholangiocarcinoma. In particular, autoimmune thyroid diseases are frequently found in patients with hepatitis C virus infection. These patients, especially if thyroid autoimmunity preexists, are at risk of hypothyroidism or, less frequently, thyrotoxicosis, during and after treatment with interpheron-alpha alone or in combination with ribavirin, commonly used before the introduction of new antiviral drugs. The present review summarizes both liver abnormalities related to thyroid disorders and their treatment, and thyroid abnormalities related to liver diseases and their treatment.
C1 [Piantanida, E.; Ippolito, S.; Gallo, D.; Masiello, E.; Premoli, P.; Cusini, C.; Rosetti, S.; Sabatino, J.; Bartalena, L.; Tanda, M. L.] Univ Insubria, Dept Med & Surg, Endocrine Unit, ASST Sette Laghi,Osped Circolo, Viale Borri 57, Varese, Italy.
[Segato, S.] ASST Sette Laghi, Dept Specialist Med, Gastroenterol & Gastrointestinal Endoscop Unit, Varese, Italy.
[Trimarchi, F.] Univ Messina, Accademia Peloritana Pericolanti, Messina, Italy.
C3 Ospedale Circolo & Fondazione Macchi; University of Insubria; University
of Messina
RP Piantanida, E; Bartalena, L (corresponding author), Univ Insubria, Dept Med & Surg, Endocrine Unit, ASST Sette Laghi,Osped Circolo, Viale Borri 57, Varese, Italy.
EM eliana.piantanida@uninsubria.it; luigi.bartalena@uninsubria.it;
maria.tanda@uninsubria.it
RI Ippolito, Silvia/AAI-1361-2021; Tanda, Maria/AAD-4071-2020; Gallo,
Daniela/AAD-7839-2019
OI Gallo, Daniela/0000-0002-1873-3048
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NR 169
TC 80
Z9 93
U1 4
U2 28
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0391-4097
EI 1720-8386
J9 J ENDOCRINOL INVEST
JI J. Endocrinol. Invest.
PD JUL
PY 2020
VL 43
IS 7
BP 885
EP 899
DI 10.1007/s40618-020-01208-6
PG 15
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA LZ2FA
UT WOS:000541042800003
PM 32166702
DA 2025-01-07
ER
PT S
AU Wirtz, TH
Brandt, EF
Berres, ML
AF Wirtz, Theresa Hildegard
Brandt, Elisa Fabiana
Berres, Marie-Luise
BE Lhuillier, C
Galluzzi, L
TI Liver DCs in health and disease
SO IMMUNOBIOLOGY OF DENDRITIC CELLS, PT A
SE International Review of Cell and Molecular Biology
LA English
DT Review; Book Chapter
ID PLASMACYTOID DENDRITIC CELLS; HEPATIC STELLATE CELLS; REGULATORY
T-CELLS; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; IN-VIVO;
TOLERANCE; MACROPHAGES; IMMUNITY; TISSUE
AB Hepatic dendritic cells represent a unique and multifaceted subset of antigen-presenting leukocytes that orchestrate specified immune responses in the liver. They are constantly exposed to antigens and signals derived not only from the hepatic micro-environment and the systemic circulation but also from the portal vein draining the gut and conveying food antigens as well as microbial compounds. Modulated by these various factors they shape intrahepatic immune responses during acute and chronic liver diseases, hepatocellular carcinoma and allograft tolerance as well as systemic responses to gut-derived components. Hence, hepatic DC are central targets to decipher and fine-tune innate and adaptive hepatic immune responses as well as tolerance. This review focuses on the origin of hepatic DC, the different DC subsets present in the liver and their functionality during different acute and chronic liver diseases in mice and men and will discuss potential DC directed therapeutic interventions in liver disease.
C1 [Wirtz, Theresa Hildegard; Brandt, Elisa Fabiana; Berres, Marie-Luise] Univ Hosp RWTH Aachen, Med Dept 3, Aachen, Germany.
C3 RWTH Aachen University; RWTH Aachen University Hospital
RP Berres, ML (corresponding author), Univ Hosp RWTH Aachen, Med Dept 3, Aachen, Germany.
EM mberres@ukaachen.de
RI Wirtz, Theresa/KIJ-5676-2024; Berres, Marie-Luise/AAN-5351-2021
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NR 128
TC 11
Z9 15
U1 0
U2 5
PU ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD
PI LONDON
PA 125 LONDON WALL, LONDON EC2Y 5AS, ENGLAND
SN 1937-6448
BN 978-0-12-818352-6; 978-0-12-818351-9
J9 INT REV CEL MOL BIO
JI Int. Rev. Cell Mol. Biol.
PY 2019
VL 348
BP 263
EP 299
DI 10.1016/bs.ircmb.2019.08.001
PG 37
WC Cell Biology; Immunology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Immunology
GA BO3YH
UT WOS:000513136000007
PM 31810555
DA 2025-01-07
ER
PT J
AU Sureka, B
Bansal, K
Patidar, Y
Kumar, S
Arora, A
AF Sureka, Binit
Bansal, Kalpana
Patidar, Yashwant
Kumar, Sachin
Arora, Ankur
TI Thoracic perspective revisited in chronic liver disease
SO GASTROENTEROLOGY REPORT
LA English
DT Review
DE cirrhosis; infection; portosystemic; portopulmonary; computed tomography
ID HEPATOPULMONARY SYNDROME; HEPATITIS-C; CIRRHOSIS; COMPLICATIONS
AB A variety of chest manifestations are seen in patients with chronic liver diseases, namely hepatopulmonary syndrome, portopulmonary hypertension, intrathoracic portosystemic collaterals, hepatic hydrothorax, infections, drug-induced changes, manifestations of hepatocellular carcinoma, gynecomastia, acute respiratory distress syndrome, autoimmune changes, aspiration pneumonitis and changes due to alpha(1)-antitrypsin deficiency. Gastroenterologists and radiologists should be aware of these entities; knowledge of the imaging findings specific to each condition is of prime importance for managing such patients.
C1 [Sureka, Binit; Bansal, Kalpana; Patidar, Yashwant; Arora, Ankur] Inst Liver & Biliary Sci, Dept Radiol Intervent Radiol, New Delhi 110070, India.
[Kumar, Sachin] Inst Liver & Biliary Sci, Dept Pulm Med, New Delhi 110070, India.
C3 Institute of Liver & Biliary Sciences (ILBS); Institute of Liver &
Biliary Sciences (ILBS)
RP Sureka, B (corresponding author), Inst Liver & Biliary Sci, Dept Radiol Intervent Radiol, D-1 Vasant Kunj, New Delhi 110070, India.
EM binitsurekapgi@gmail.com
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[Anonymous], 2014, NEW INDIAN EXPR 0419
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NR 25
TC 5
Z9 6
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 2052-0034
J9 GASTROENTEROL REP
JI Gastroenterol. Rep.
PD AUG
PY 2015
VL 3
IS 3
BP 194
EP 200
DI 10.1093/gastro/gov017
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CP5DA
UT WOS:000359900300003
PM 25969457
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Liu, Q
Liu, YY
Yang, ZY
AF Liu, Qi
Liu, Yuyang
Yang, Zhanyu
TI Leukocyte immunoglobulin-like receptor B4: A keystone in immune
modulation and therapeutic target in cancer and beyond
SO CANCER INNOVATION
LA English
DT Review
DE cancer therapy; immune checkpoint; immunotherapy; leukocyte
immunoglobulin-like receptor B4; monoclonal antibodies
ID T-CELL RESPONSES; INHIBITORY-RECEPTOR; DENDRITIC CELLS; TRANSCRIPT 3;
NEGATIVE REGULATION; UP-REGULATION; ILT3; EXPRESSION; INDUCTION;
ACTIVATION
AB Leukocyte immunoglobulin-like receptor B4 (LILRB4) significantly impacts immune regulation and the pathogenesis and progression of various cancers. This review discusses LILRB4's structural attributes, expression patterns in immune cells, and molecular mechanisms in modulating immune responses. We describe the influence of LILRB4 on T cells, dendritic cells, NK cells, and macrophages, and its dual role in stimulating and suppressing immune activities. The review discusses the current research on LILRB4's involvement in acute myeloid leukemia, chronic lymphocytic leukemia, and solid tumors, such as colorectal cancer, pancreatic cancer, non-small cell lung cancer, hepatocellular carcinoma, and extramedullary multiple myeloma. The review also describes LILRB4's role in autoimmune disorders, infectious diseases, and other conditions. We evaluate the recent advancements in targeting LILRB4 using monoclonal antibodies and peptide inhibitors and their therapeutic potential in cancer treatment. Together, these studies underscore the need for further research on LILRB4's interactions in the tumor microenvironment and highlight its importance as a therapeutic target in oncology and for future clinical innovations.
Interaction of LILRB4 with Immune Cells: This diagram showcases the interactions between LILRB4 and various immune cells, including T cells, dendritic cells (DCs), natural killer (NK) cells, macrophages, and myeloid-derived suppressor cells (MDSCs). Key pathways and molecules involved in these interactions, such as SHP1/2, HLA-G, and ILT3-Fc, are indicated, demonstrating how LILRB4 modulates immune responses. Role of LILRB4 in Different Diseases: The schematic map presents the diverse diseases associated with LILRB4 expression, categorized by the system. These include blood system diseases (CLL, AML, extramedullary multiple myeloma), digestive system diseases (pancreatic cancer, colorectal cancer, liver cancer, NAFLD, and IBD), respiratory system diseases (NSCLC, COPD, and ALI), immune system disorders (SLE, multiple sclerosis, transplant tolerance, and vitamin D deficiency-related immune disorders), infectious diseases (HIV, bacterial infections, COVID-19, and parasitic infections), neurological diseases (Alzheimer's disease), cardiovascular diseases (aortic dissection, pathological cardiac hypertrophy), and pediatric diseases (Kawasaki disease). image
C1 [Liu, Qi; Yang, Zhanyu] Chinese Peoples Liberat Army Gen Hosp, Fac Hepatopancreato Biliary Surg, Med Ctr 1, 28 Fuxing Rd, Beijing 100853, Peoples R China.
[Liu, Qi] Med Sch Chinese Peoples Liberat Army, Beijing, Peoples R China.
[Liu, Yuyang] 920th Hosp Joint Logist Support Force, Dept Neurosurg, Kunming, Yunnan, Peoples R China.
C3 Chinese People's Liberation Army General Hospital
RP Yang, ZY (corresponding author), Chinese Peoples Liberat Army Gen Hosp, Fac Hepatopancreato Biliary Surg, Med Ctr 1, 28 Fuxing Rd, Beijing 100853, Peoples R China.
EM zhanyuyang@163.com
OI Liu, Qi/0009-0007-0384-6668
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NR 88
TC 0
Z9 0
U1 3
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2770-9191
EI 2770-9183
J9 CANCER INNOV
JI Cancer Innov.
PD DEC
PY 2024
VL 3
IS 6
AR e153
DI 10.1002/cai2.153
PG 13
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA J6A5C
UT WOS:001337872600001
PM 39444949
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Covelli, C
Sacchi, D
Sarcognato, S
Cazzagon, N
Grillo, F
Baciorri, F
Fanni, D
Cacciatore, M
Maffeis, V
Guido, M
AF Covelli, Claudia
Sacchi, Diana
Sarcognato, Samantha
Cazzagon, Nora
Grillo, Federica
Baciorri, Francesca
Fanni, Daniela
Cacciatore, Matilde
Maffeis, Valeria
Guido, Maria
TI Pathology of autoimmune hepatitis
SO PATHOLOGICA
LA English
DT Review
DE autoimmune hepatitis; histology; liver biopsy; interface hepatitis
ID CHRONIC VIRAL-HEPATITIS; CLINICOPATHOLOGICAL FEATURES;
HEPATOCELLULAR-CARCINOMA; SERUM AUTOANTIBODIES; HISTOLOGIC FEATURES;
SIMPLIFIED CRITERIA; DIAGNOSIS; MANAGEMENT; DISEASE; GUIDELINES
AB Autoimmune hepatitis (AIH) is a relatively rare non-resolving chronic liver disease, which mainly affects women. It is characterized by hypergammaglobulinemia, circulating autoantibodies, interface hepatitis on liver histology and a favourable response to immunosuppression. The putative mechanism for the development of autoimmune hepatitis is thought to be the interaction between genetic predisposition, environmental triggers and failure of the native immune system.
AIH still remains a major diagnostic and therapeutic challenge, mainly because it is a very heterogeneous disease. Prompt and timely diagnosis is crucial since, if left untreated, AIH has a high mortality rate. Histological demonstration of hepatitis is required for the diagnosis of AIH and, therefore, liver biopsy is mandatory in the initial diagnostic work-up, before treatment. In this review, we summarize the histological features of AIH with the main aim of highlighting the most important clinical-pathological hallmarks useful in the routine diagnostic practice.
C1 [Covelli, Claudia] Fdn IRCCS Casa Sollievo della Sofferenza, Pathol Unit, San Giovanni Rotondo, Italy.
[Sacchi, Diana; Sarcognato, Samantha; Baciorri, Francesca; Cacciatore, Matilde; Maffeis, Valeria; Guido, Maria] Pathol Dept Azienda ULSS 2 Marca Trevigiana, Treviso, Italy.
[Cazzagon, Nora] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
[Grillo, Federica] Univ Genoa, Dept Surg Sci & Integrated Diagnost Disc, Unit Anat Pathol, Genoa, Italy.
[Grillo, Federica] Osped Policlin San Martino IRCCS, Genoa, Italy.
[Fanni, Daniela] Univ Cagliari, Dept Med Sci, Pathol Unit, Cagliari, Italy.
[Guido, Maria] Univ Padua, Dept Med DIMED, Padua, Italy.
C3 University of Padua; University of Genoa; University of Cagliari;
University of Padua
RP Covelli, C (corresponding author), Fdn IRCCS Casa Sollievo della Sofferenza, I-71013 San Giovanni Rotondo, Italy.
EM cla.covelli85@gmail.com
RI Grillo, Federica/AAA-6422-2020; Fanni, Daniela/ABD-9643-2020
OI guido, maria/0000-0002-8558-0723; Grillo, Federica/0000-0001-6477-3182;
Cazzagon, Nora/0000-0002-6937-8664
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NR 55
TC 35
Z9 37
U1 0
U2 8
PU PACINI EDITORE
PI PISA
PA VIA DELLA GHERARDESCA-ZONA INDUSTRIALE OSPEDALETTO, 56121 PISA, ITALY
SN 0031-2983
EI 1591-951X
J9 PATHOLOGICA
JI Pathologica
PD JUN
PY 2021
VL 113
IS 3
BP 185
EP 193
DI 10.32074/1591-951X-241
PG 9
WC Pathology
WE Emerging Sources Citation Index (ESCI)
SC Pathology
GA XQ6BV
UT WOS:000731631300004
PM 34294936
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Xia, DC
Chen, DZ
Cai, TC
Zhu, LJ
Lin, YH
Yu, SJ
Zhu, KL
Wang, XD
Xu, LM
Chen, YP
AF Xia, Dingchao
Chen, Dazhi
Cai, Tingchen
Zhu, Lujian
Lin, Yanhan
Yu, Sijie
Zhu, Kailu
Wang, Xiaodong
Xu, Lanman
Chen, Yongping
TI Nimbolide attenuated the inflammation in the liver of autoimmune
hepatitis's mice through regulation of HDAC3
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Autoimmune Hepatitis; Nimbolide; HDAC3; NF-?B
ID NF-KAPPA-B; HISTONE DEACETYLASE INHIBITOR; STAT3; TRICHOSTATIN;
EXPRESSION; CANCER; ALPHA
AB A chronic liver disease named autoimmune hepatitis (AIH) will carry elevated levels of inflammatory cytokines, but there is currently no effective treatment to cure it. Histone deacetylase 3 (HDAC3) takes an important position in regulating the expression of inflammatory genes. Nimbolide (NIB) is a limonoid extracted from the neem tree (Azadirachta indica) that has been found to be effective against many diseases, including cancer, scleroderma, and acute respiratory distress syndrome. Here, we investigated the protective effect of nimbolide on AIH liver. Mice and AML12 cells were employed to establish AIH model with liver antigen S100 and cell injury model of LPS, and then treated with different concentrations of nimbolide. After the successful establishment of the animal model and cell model, inflammatory cytokines of IL-1 beta, IL-6 and TNF-alpha as well as cellular signaling related to inflammation such as STAT3, I kappa B-alpha and NF-kappa B were examined. We observed for the first time about nimbolide can effectively inhibit inflammation in AIH mice's liver and AML12 cells by inhibiting HDAC3 expression. HDAC3 knocked down by siRNA in cells can also effectively alleviate the inflammation in AML12 cells, further confirming that HDAC3 plays an important role in the inflammation of liver cells. These results suggest nimbolide could be a potential new treatment for autoimmune hepatitis, and HDAC3 may become a new target for autoimmune hepatitis.
C1 [Xia, Dingchao; Cai, Tingchen; Zhu, Lujian; Lin, Yanhan; Yu, Sijie; Zhu, Kailu; Wang, Xiaodong; Chen, Yongping] Wenzhou Med Univ, Hepatol Inst Wenzhou Med Univ, Dept Infect Dis, Zhejiang Prov Key Lab Accurate Diag & Treatment Ch, Wenzhou 325006, Peoples R China.
[Chen, Dazhi] First Hosp Peking Univ, Dept Gastroenterol, Beijing 100032, Peoples R China.
[Xu, Lanman] Ningbo Univ, Ningbo Med Ctr Lihuili Hosp, Dept Infect Dis & Liver Dis, Affiliated Hosp, Ningbo 315040, Zhejiang, Peoples R China.
C3 Wenzhou Medical University; Ningbo University
RP Chen, YP (corresponding author), Wenzhou Med Univ, Hepatol Inst Wenzhou Med Univ, Dept Infect Dis, Zhejiang Prov Key Lab Accurate Diag & Treatment Ch, Wenzhou 325006, Peoples R China.; Xu, LM (corresponding author), Ningbo Univ, Ningbo Med Ctr Lihuili Hosp, Dept Infect Dis & Liver Dis, Affiliated Hosp, Ningbo 315040, Zhejiang, Peoples R China.
EM 13587646315@163.com; did@wzhospital.cn
FU Wenzhou Science and Technology Bureau Major Scientific and Technological
Innovation to attack health care projects [ZY2019008]; Zhejiang
Provincial Natural Science Foundation of China [LD21H030002]; National
Natural Science Foundation of China [81770585, 82070593]
FX Acknowledgments This research was supported by Wenzhou Science and
Technology Bureau Major Scientific and Technological Innovation to
attack health care projects (No. ZY2019008) , Zhejiang Provincial
Natural Science Foundation of China (No. LD21H030002) and the National
Natural Science Foundation of China (No.81770585 and No.82070593) .
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NR 41
TC 6
Z9 7
U1 2
U2 25
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD JAN 1
PY 2022
VL 434
AR 115795
DI 10.1016/j.taap.2021.115795
PG 11
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA 0X9AM
UT WOS:000789991800007
PM 34780724
OA hybrid
DA 2025-01-07
ER
PT J
AU Karaosmanoglu, AD
Uysal, A
Karcaaltincaba, M
Akata, D
Ozmen, MN
Kraeft, J
Hahn, PF
AF Karaosmanoglu, Ali Devrim
Uysal, Aycan
Karcaaltincaba, Musturay
Akata, Deniz
Ozmen, Mustafa Nasuh
Kraeft, Jessica
Hahn, Peter F.
TI Non-neoplastic hepatopancreatobiliary lesions simulating malignancy: can
we differentiate?
SO INSIGHTS INTO IMAGING
LA English
DT Review
DE Hepatobiliary; Pancreas; Neoplasm; Mimicker; Radiology
ID HEPATIC INFLAMMATORY PSEUDOTUMOR; ISOLATED PANCREATIC TUBERCULOSIS;
AUTOIMMUNE PANCREATITIS; IGG4-RELATED DISEASE; TERTIARY SYPHILIS;
XANTHOGRANULOMATOUS CHOLECYSTITIS; HEPATOBILIARY TUBERCULOSIS;
HEPATOSPLENIC CANDIDIASIS; HEPATOCELLULAR-CARCINOMA; LIVER
AB Despite the success of cross-sectional imaging in evaluating hepatopancreatobiliary system malignancies, several non-malignant disease processes may closely mimic malignancy. Differentiating these benign diseases from malignancy may be difficult, or even impossible, even in the hands of experienced imagers. In this manuscript, we present benign mimics involving the hepatopancreatobiliary system and try to increase awareness of these potential pitfalls.
C1 [Karaosmanoglu, Ali Devrim; Karcaaltincaba, Musturay; Akata, Deniz; Ozmen, Mustafa Nasuh] Hacettepe Univ, Dept Radiol, Sch Med, TR-06100 Ankara, Turkey.
[Uysal, Aycan] Gulhane Training & Res Hosp, Dept Radiol, TR-06010 Ankara, Turkey.
[Kraeft, Jessica] Univ Colorado, Dept Radiol, Sch Med, Aurora, CO 80045 USA.
[Hahn, Peter F.] Harvard Med Sch, Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
C3 Hacettepe University; Gulhane Training & Research Hospital; University
of Colorado System; University of Colorado Anschutz Medical Campus;
Harvard University; Massachusetts General Hospital; Harvard Medical
School
RP Karaosmanoglu, AD (corresponding author), Hacettepe Univ, Dept Radiol, Sch Med, TR-06100 Ankara, Turkey.
EM alidevrim76@yahoo.com
RI uysal, aycan/ITU-7151-2023; Karaosmanoglu, Ali/D-8624-2015;
Karcaaltincaba, Musturay/A-3866-2016; Ozmen, Mustafa Nasuh/I-9398-2013
OI Ozmen, Mustafa Nasuh/0000-0002-9910-4808
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NR 82
TC 2
Z9 2
U1 0
U2 7
PU SPRINGEROPEN
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1869-4101
J9 INSIGHTS IMAGING
JI Insights Imaging
PD FEB 10
PY 2020
VL 11
IS 1
AR 21
DI 10.1186/s13244-019-0813-8
PG 19
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA KV5HX
UT WOS:000520514900002
PM 32040641
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Khoshpouri, P
Habibabadi, RR
Hazhirkarzar, B
Ameli, S
Ghadimi, M
Ghasabeh, MA
Menias, CO
Kim, A
Li, ZP
Kamel, IR
AF Khoshpouri, Pegah
Habibabadi, Roya Rezvani
Hazhirkarzar, Bita
Ameli, Sanaz
Ghadimi, Maryam
Ghasabeh, Mounes Aliyari
Menias, Christine O.
Kim, Amy
Li, Zhiping
Kamel, Ihab R.
TI Imaging Features of Primary Scle-rosing Cholangitis: From Diagnosis to
Liver Transplant Follow-up
SO RADIOGRAPHICS
LA English
DT Article
ID PRIMARY SCLEROSING CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE;
MAGNETIC-RESONANCE CHOLANGIOGRAPHY; GALLBLADDER POLYPS; AUTOIMMUNE
PANCREATITIS; DOMINANT STRICTURES; BILIARY STRICTURES; MR; CT; RISK
AB Primary sclerosing cholangitis (PSC) is a chronic progressive inflammatory disease of the bile ducts that leads to multifocal bile duct fibrosis, strictures, cholestasis, liver parenchymal changes, and ultimately cirrhosis. It more commonly occurs in young adults, with a variety of clinical and imaging manifestations. The cause of the disease is not known, but it has a strong association with inflammatory bowel disease and can overlap with other autoimmune diseases, including autoimmune hepatitis and immunoglobulin G4-related disease. Patients are predisposed to various hepatic and extrahepatic deteriorating complications, such as bile duct and gallbladder calculi, acute bacterial cholangitis, liver abscess, and portal hypertension, as well as malignancies including cholangiocarcinoma (CCA), gallbladder cancer, and colorectal carcinoma. Imaging has an essential role in diagnosis, surveillance, and detection of complications. MR cholangiopancreatography and endoscopic retrograde cholangiopancreatography have high specificity and sensitivity for detection of primary disease and assessment of disease progression. However, many patients with PSC are still diagnosed incidentally at US or CT. Novel imaging techniques such as transient elastography and MR elastography are used to survey the grade of liver fibrosis. Annual cancer surveillance is necessary in all PSC patients to screen for CCA and gallbladder cancer. Familiarity with PSC pathogenesis and imaging features across various classic imaging modalities and novel imaging techniques can aid in correct imaging diagnosis and guide appropriate management. The imaging features of the biliary system and liver parenchyma in PSC across various imaging modalities are reviewed. Imaging characteristics of the differential diagnosis of PSC, clinical associations, and complications are described. Finally, the role of imaging in evaluation of PSC progression, pre-liver transplant assessment, and post-liver transplant disease recurrence are discussed. (C) RSNA, 2019
C1 [Khoshpouri, Pegah; Habibabadi, Roya Rezvani; Hazhirkarzar, Bita; Ameli, Sanaz; Ghadimi, Maryam; Ghasabeh, Mounes Aliyari; Kim, Amy; Li, Zhiping; Kamel, Ihab R.] Johns Hopkins Univ, Russell H Morgan Dept Radiol & Radiol Sci, Sch Med, 600 N Wolfe St,MRI Room 143, Baltimore, MD 21287 USA.
[Menias, Christine O.] Mayo Clin Phoenix, Dept Radiol, Scottsdale, AZ USA.
C3 Johns Hopkins University; Mayo Clinic; Mayo Clinic Phoenix
RP Kamel, IR (corresponding author), Johns Hopkins Univ, Russell H Morgan Dept Radiol & Radiol Sci, Sch Med, 600 N Wolfe St,MRI Room 143, Baltimore, MD 21287 USA.
EM ikamel@jhmi.edu
RI LI, Zhen/AAL-4559-2021; Ghadimi, Maryam/AAC-9149-2019
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NR 105
TC 41
Z9 43
U1 1
U2 11
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0271-5333
J9 RADIOGRAPHICS
JI Radiographics
PD NOV-DEC
PY 2019
VL 39
IS 7
BP 1938
EP 1964
DI 10.1148/rg.2019180213
PG 27
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA JL9YN
UT WOS:000495881600006
PM 31626561
DA 2025-01-07
ER
PT J
AU Goel, A
Kwo, P
AF Goel, Aparna
Kwo, Paul
TI Treatment of Autoimmune Hepatitis
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Autoimmune hepatitis; Treatment failure; Biochemical remission;
Immunosuppression; Liver transplant; Recurrent autoimmune hepatitis
ID TRANSIENT ELASTOGRAPHY; MYCOPHENOLATE-MOFETIL; LIVER-TRANSPLANTATION;
CONTROLLED-TRIAL; REMISSION; EFFICACY; AZATHIOPRINE; PREDNISONE;
RECURRENCE; TACROLIMUS
AB The goal of autoimmune hepatitis treatment is to achieve clinical and biochemical remission, which is associated with significantly improved outcomes. Induction treatment with corticosteroids and the subsequent addition of steroid-sparing therapy with gradual tapering of corticosteroids remains the standard of care. Several alternatives to azathioprine and second-line agents, such as mycophenolate mofetil, tacrolimus, cyclosporine, sirolimus, or rituximab, have been evaluated in those with intolerance or inadequate response to standard-of-care therapy. Treatment withdrawal is achievable in less than 20% of patients after 2 years of sustained remission. Liver transplantation should be considered in those with progressive liver disease or those with complications such as hepatocellular carcinoma.
C1 [Goel, Aparna; Kwo, Paul] Stanford Univ, Div Gastroenterol & Hepatol, Palo Alto, CA 94043 USA.
[Goel, Aparna; Kwo, Paul] 430 Broadway St,Pavil C,3rd Floor, Redwood City, CA 94043 USA.
C3 Stanford University
RP Goel, A (corresponding author), 430 Broadway St,Pavil C,3rd Floor, Redwood City, CA 94043 USA.
EM goela21@stanford.edu
OI Goel, Aparna/0000-0001-9588-9364
CR [Anonymous], Early treatment response predicts the need for liver transplantation in autoimmune hepatitis - Tan - 2005, DOI [10.1111/j.1478-3231.2005.01121.x, DOI 10.1111/J.1478-3231.2005.01121.X]
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NR 39
TC 4
Z9 4
U1 1
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD FEB
PY 2024
VL 28
IS 1
BP 51
EP 61
DI 10.1016/j.cld.2023.07.001
EA NOV 2023
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA Z2KK4
UT WOS:001110416000001
PM 37945162
DA 2025-01-07
ER
PT J
AU Hsu, C
Marshall, JL
He, AR
AF Hsu, Christine
Marshall, John L.
He, Aiwu Rum
TI Workup and Management of Immune-Mediated Hepatobiliary Pancreatic
Toxicities That Develop During Immune Checkpoint Inhibitor Treatment
SO ONCOLOGIST
LA English
DT Article
ID HEPATITIS-B REACTIVATION; CELL LUNG-CANCER; ADVANCED MELANOMA;
OPEN-LABEL; IPILIMUMAB; NIVOLUMAB; CHEMOTHERAPY; HYPERAMYLASEMIA;
PEMBROLIZUMAB; MULTICENTER
AB Immune checkpoint inhibitor treatment has been approved by the U.S. Food and Drug Administration for the treatment of a wide range of cancer types, including hepatocellular carcinoma. Workup and management of immune-mediated hepatitis, pancreatitis, or cholangitis that develops during immune checkpoint inhibitor treatment can be challenging. Immune-mediated hepatitis can be particularly challenging if patients have underlying viral hepatitis or autoimmune hepatitis. Patients with positive hepatitis B virus DNA should be referred to a hepatologist for antiviral therapy prior to immune checkpoint inhibitor treatment. With untreated hepatitis C virus (HCV) and elevated liver enzymes, a liver biopsy should be obtained to differentiate between HCV infection and immune-mediated hepatitis due to anti-programmed cell death protein 1 (PD-1) therapy. If autoimmune serologies are negative, then this supports a case of immune-mediated hepatitis secondary to anti-PD-1 therapy, rather than autoimmune hepatitis. In this case, an empiric steroid therapy is reasonable; however, if the patient does not respond to steroid therapy in 3-5 days, then liver biopsy should be pursued. The incidence of immune checkpoint-induced pancreatitis is low, but when it does occur, diagnosis is not straightforward. Although routine monitoring of pancreatic enzymes is not generally recommended, when pancreatitis is suspected, serum levels of amylase and lipase should be checked. Once confirmed, a steroid or other immunosuppressant (if steroids are contraindicated) should be administered along with close monitoring, and a slow tapering dosage once the pancreatitis is under control. Patients should then be monitored for recurrent pancreatitis. Finally, immune therapy-related cholangitis involves elevated bilirubin and alkaline phosphatase and, once diagnosed, is managed in the same way as immune-mediated hepatitis. Key Points
Immune-mediated hepatitis, pancreatitis, and cholangitis are found in patients receiving or who have previously received immune checkpoint inhibitors. To work up immune-mediated hepatitis, viral, and autoimmune serologies, liver imaging will help to differentiate immune-mediated hepatitis from hepatitis of other etiology. Hepatology consult may be considered in patients with a history of chronic liver disease who developed hepatitis during immune checkpoint inhibitor treatment. Liver biopsy should be considered to clarify the diagnosis for case in which the hepatitis is refractory to steroid or immunosuppressant treatment. Immune-mediated pancreatitis is treated with steroid or other immunosuppressant with a slow tapering and should be monitored for recurrence. Implications for Practice All patient receiving or who have previously received immune checkpoint inhibitors should be monitored closely for immune-mediated hepatitis, pancreatitis, and cholangitis. Workup and management of immune-mediated hepatitis, pancreatitis, and cholangitis should follow the package insert of immune checkpoint inhibitors. Hepatology consultation should be considered in patients with a history of chronic liver disease.
C1 [Hsu, Christine] MedStar Georgetown Transplant Inst, Pasquerilla Healthcare Ctr, Washington, DC USA.
[Marshall, John L.; He, Aiwu Rum] Georgetown Univ, Lombardi Comprehens Canc Ctr, 3800 Reservoir Rd NW, Washington, DC 20007 USA.
C3 Georgetown University
RP He, AR (corresponding author), Georgetown Univ, Lombardi Comprehens Canc Ctr, 3800 Reservoir Rd NW, Washington, DC 20007 USA.
EM arh29@georgetown.edu
OI He, Aiwu/0000-0002-2104-0816; Hsu, Christine/0000-0001-8779-9422
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NR 46
TC 29
Z9 30
U1 1
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD FEB
PY 2020
VL 25
IS 2
BP 105
EP 111
DI 10.1634/theoncologist.2018-0162
EA SEP 2019
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KK0QF
UT WOS:000485636400001
PM 32043797
OA Bronze, Green Published
DA 2025-01-07
ER
PT J
AU Sharma, R
Simon, TG
Hagström, H
Lochhead, P
Roelstraete, B
Söderling, J
Verna, EC
Emond, J
Ludvigsson, JF
AF Sharma, Rajani
Simon, Tracey G.
Hagstrom, Hannes
Lochhead, Paul
Roelstraete, Bjorn
Soderling, Jonas
Verna, Elizabeth C.
Emond, Jean
Ludvigsson, Jonas F.
TI Statins Are Associated With a Decreased Risk of Severe Liver Disease in
Individuals With Noncirrhotic Chronic Liver Disease
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Cirrhosis; Hepatocellular Carcinoma; Fibrosis
ID CIRRHOSIS; DECOMPENSATION; REGISTER; COHORT
AB BACKGROUND & AIMS: Little is known about the potential impact of statins on the progression of noncirrhotic chronic liver diseases (CLDs) to severe liver disease. METHODS: Using liver histopathology data in a nationwide Swedish cohort, we identi fi ed 3862 noncirrhotic individuals with CLD and statin exposure, de fi ned as a statin prescription fi lled for 30 or more cumulative de fi ned daily doses. Statin users were matched to 3862 (statin) nonusers with CLD through direct 1:1 matching followed by propensity score matching. Cox regression was used to estimate hazard ratios (HRs) for the primary outcome of incident severe liver disease (a composite of cirrhosis, hepatocellular carcinoma, and liver transplantation/liverrelated mortality). RESULTS: A total of 45.3% of CLD patients had nonalcoholic fatty liver disease, 21.9% had alcohol -related liver disease, 17.7% had viral hepatitis, and 15.1% had autoimmune hepatitis. During follow-up evaluation, 234 (6.1%) statin users vs 276 (7.1%) nonusers developed severe liver disease. Statin use was associated with a decreased risk of developing severe liver disease (HR, 0.60; 95% CI, 0.48 - 0.74). Statistically signi fi cantly lower rates of severe liver disease were seen in alcohol -related liver disease (HR, 0.30; 95% CI, 0.19 - 0.49) and in nonalcoholic fatty liver disease (HR, 0.68; 95% CI, 0.45 - 1.00), but not in viral hepatitis (HR, 0.76; 95% CI, 0.51 - 1.14) or autoimmune hepatitis (HR, 0.88; 95% CI, 0.48 - 1.58). Statin use had a protective association in both pre fi brosis and fi brosis stages at diagnosis. Statin use was associated with lower rates of progression to cirrhosis (HR, 0.62; 95% CI, 0.49 - 0.78), hepatocellular carcinoma (HR, 0.44; 95% CI, 0.27 - 0.71), and liver -related mortality (HR, 0.55; 95% CI, 0.36 - 0.82). CONCLUSIONS: Among individuals with noncirrhotic CLD, incident statin use was linked to lower rates of severe liver disease, suggesting a potential disease -modifying role.
C1 [Sharma, Rajani; Verna, Elizabeth C.; Emond, Jean] Columbia Univ, Ctr Liver Dis & Transplantat, Div Digest & Liver Dis, Irving Med Ctr, New York, NY USA.
[Sharma, Rajani; Verna, Elizabeth C.; Ludvigsson, Jonas F.] Columbia Univ, Dept Med, Div Digest & Liver Dis, Coll Phys & Surg, New York, NY USA.
[Simon, Tracey G.; Soderling, Jonas] Massachusetts Gen Hosp, Liver Ctr, Div Gastroenterol, Boston, MA USA.
[Hagstrom, Hannes] Karolinska Univ Hosp, Ctr Digest Dis, Unit Hepatol, Stockholm, Sweden.
[Hagstrom, Hannes] Karolinska Inst, Dept Med, Div Clin Epidemiol, Stockholm, Sweden.
[Hagstrom, Hannes] Karolinska Inst, Dept Med Huddinge, Stockholm, Sweden.
[Lochhead, Paul] GlaxoSmithKline PLC, London, England.
[Roelstraete, Bjorn; Ludvigsson, Jonas F.] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Ludvigsson, Jonas F.] Orebro Univ Hosp, Dept Pediat, Orebro, Sweden.
[Ludvigsson, Jonas F.] Univ Nottingham, Sch Med, Div Epidemiol & Publ Hlth, Nottingham, England.
[Sharma, Rajani] Columbia Univ, Ctr Liver Dis & Transplantat, Irving Med Ctr, 622 West 168th St,PH14,Suite 202, New York, NY 10032 USA.
C3 Columbia University; NewYork-Presbyterian Hospital; Columbia University;
Harvard University; Massachusetts General Hospital; Karolinska
Institutet; Karolinska University Hospital; Karolinska Institutet;
Karolinska Institutet; GlaxoSmithKline; Karolinska Institutet; Orebro
University; University of Nottingham; Columbia University;
NewYork-Presbyterian Hospital
RP Sharma, R (corresponding author), Columbia Univ, Ctr Liver Dis & Transplantat, Irving Med Ctr, 622 West 168th St,PH14,Suite 202, New York, NY 10032 USA.
EM rs3333@cumc.columbia.edu
RI Ludvigsson, Jonas/A-8560-2012
OI Hagstrom, Hannes/0000-0002-8474-1759
FU Karolinska Institutet; Columbia University Irving Medical Center;
Swedish Research Council, Center for Innovative Medicine (CIMED);
Swedish Cancer Society; National Institutes of Health [K23 DK122104]
FX This project received funding through Karolinska Institutet (J.F.L.) ,
and the Columbia University Irving Medical Center (J.E.) . Supported by
grants from The Swedish Research Council, Center for Innovative Medicine
(CIMED) , and The Swedish Cancer Society (H.H.) ; and by National
Institutes of Health grant K23 DK122104 (T.G.S.) . None of the funding
organizations had any role in the design and conduct of the study; in
the collection, management, and analysis of the data; or in the
preparation, review, and approval of the manuscript.
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NR 23
TC 10
Z9 9
U1 6
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD APR
PY 2024
VL 22
IS 4
DI 10.1016/j.cgh.2023.04.017
EA MAR 2024
PG 30
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA QA4U0
UT WOS:001218154500001
PM 37121528
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Wehrle, CJ
Panconesi, R
Satish, S
Maspero, M
Jiao, CB
Sun, KY
Karakaya, O
Allkushi, E
Esfeh, JM
Linganna, MW
Ma, WW
Fujiki, M
Hashimoto, K
Miller, C
Kwon, DCH
Aucejo, F
Schlegel, A
AF Wehrle, Chase J.
Panconesi, Rebecca
Satish, Sangeeta
Maspero, Marianna
Jiao, Chunbao
Sun, Keyue
Karakaya, Omer
Allkushi, Erlind
Esfeh, Jamak Modaresi
Linganna, Maureen Whitsett
Ma, Wen Wee
Fujiki, Masato
Hashimoto, Koji
Miller, Charles
Kwon, David C. H.
Aucejo, Federico
Schlegel, Andrea
TI The Impact of Biliary Injury on the Recurrence of Biliary Cancer and
Benign Disease after Liver Transplantation: Risk Factors and Mechanisms
SO CANCERS
LA English
DT Review
DE liver transplantation; biliary complications; cholangiocarcinoma; benign
disease recurrence
ID PRIMARY SCLEROSING CHOLANGITIS; POUCH-ANAL ANASTOMOSIS; ISCHEMIC
CHOLANGIOPATHY; CIRCULATORY DEATH; HEPATITIS-C; AUTOIMMUNE HEPATITIS;
DONATION; CHOLANGIOCARCINOMA; TIME; REPERFUSION
AB Simple Summary Ischemia-reperfusion injury (IRI) is the source of significant graft inflammation in liver transplantation. Such injuries can lead to increased recurrence of both benign and malignant diseases of the biliary tree after transplant. Herein, we review the mechanisms and risk factors for the link between IRI and biliary recurrence, as well as evidence for strategies to mitigate this damage.Abstract Liver transplantation is known to generate significant inflammation in the entire organ based on the metabolic profile and the tissue's ability to recover from the ischemia-reperfusion injury (IRI). This cascade contributes to post-transplant complications, affecting both the synthetic liver function (immediate) and the scar development in the biliary tree. The new occurrence of biliary strictures, and the recurrence of malignant and benign liver diseases, such as cholangiocarcinoma (CCA) and primary sclerosing cholangitis (PSC), are direct consequences linked to this inflammation. The accumulation of toxic metabolites, such as succinate, causes undirected electron flows, triggering the releases of reactive oxygen species (ROS) from a severely dysfunctional mitochondrial complex 1. This initiates the inflammatory IRI cascade, with subsequent ischemic biliary stricturing, and the upregulation of pro-tumorigenic signaling. Such inflammation is both local and systemic, promoting an immunocompromised status that can lead to the recurrence of underlying liver disease, both malignant and benign in nature. The traditional treatment for CCA was resection, when possible, followed by cytotoxic chemotherapy. Liver transplant oncology is increasingly recognized as a potentially curative approach for patients with intrahepatic (iCCA) and perihilar (pCCA) cholangiocarcinoma. The link between IRI and disease recurrence is increasingly recognized in transplant oncology for hepatocellular carcinoma. However, smaller numbers have prevented similar analyses for CCA. The mechanistic link may be even more critical in this disease, as IRI causes the most profound damage to the intrahepatic bile ducts. This article reviews the underlying mechanisms associated with biliary inflammation and biliary pathology after liver transplantation. One main focus is on the link between transplant-related IRI-associated inflammation and the recurrence of cholangiocarcinoma and benign liver diseases of the biliary tree. Risk factors and protective strategies are highlighted.
C1 [Wehrle, Chase J.; Satish, Sangeeta; Allkushi, Erlind; Fujiki, Masato; Hashimoto, Koji; Miller, Charles; Kwon, David C. H.; Aucejo, Federico; Schlegel, Andrea] Cleveland Clin, Transplantat Ctr, Cleveland, OH 44195 USA.
[Panconesi, Rebecca; Satish, Sangeeta; Jiao, Chunbao; Sun, Keyue; Karakaya, Omer; Schlegel, Andrea] Cleveland Clin, Dept Inflammat & Immun, Lerner Res Inst, Cleveland, OH 44195 USA.
[Maspero, Marianna] IRCCS Ist Tumori, Gen Surg & Liver Transplantat Unit, I-20133 Milan, Italy.
[Esfeh, Jamak Modaresi; Linganna, Maureen Whitsett] Cleveland Clin, Dept Gastroenterol & Transplant Hepatol, Cleveland, OH 44195 USA.
[Ma, Wen Wee] Cleveland Clin, Novel Therapeut Ctr, Taussig Canc Inst, Cleveland, OH 44195 USA.
C3 Cleveland Clinic Foundation; Cleveland Clinic Foundation; Fondazione
IRCCS Istituto Nazionale Tumori Milan; Cleveland Clinic Foundation;
Cleveland Clinic Foundation
RP Schlegel, A (corresponding author), Cleveland Clin, Transplantat Ctr, Cleveland, OH 44195 USA.; Schlegel, A (corresponding author), Cleveland Clin, Dept Inflammat & Immun, Lerner Res Inst, Cleveland, OH 44195 USA.
EM wehrlec@ccf.org; panconr@ccf.org; jiaoc@ccf.org; aucejof@ccf.org;
schlega4@ccf.org
RI Murray, Charles/T-7847-2019; Kapadia, Samir/AGU-1915-2022; Schlegel,
Andrea/LFT-9832-2024; Jiao, Chunbao/LKK-5227-2024; Hashmani,
Shahrukh/LSJ-8362-2024; Rezaee, Fariba/AAI-1437-2021; Maspero,
Marianna/KGK-8232-2024; Fujiki, Masato/ABB-8738-2021
OI Panconesi, Rebecca/0000-0003-2708-1261; Wehrle,
Chase/0000-0002-9275-4744; Fujiki, Masato/0000-0002-1118-0081; Jiao,
Chunbao/0000-0002-9566-8243; Maspero, Marianna/0000-0002-7589-4489;
Modaresi Esfeh, Jamak/0000-0002-9429-5465; Ma, Wen
Wee/0000-0001-5899-4034
FX This research received no external funding.
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NR 138
TC 0
Z9 0
U1 1
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD AUG
PY 2024
VL 16
IS 16
AR 2789
DI 10.3390/cancers16162789
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA E7W5E
UT WOS:001305070700001
PM 39199562
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Umeshappa, CS
Mbongue, J
Singha, S
Mohapatra, S
Yamanouchi, J
Lee, JA
Nanjundappa, RH
Shao, K
Christen, U
Yang, Y
Ellestad, KK
Santamaria, P
AF Umeshappa, Channakeshava Sokke
Mbongue, Jacques
Singha, Santiswarup
Mohapatra, Saswat
Yamanouchi, Jun
Lee, Justin A.
Nanjundappa, Roopa Hebbandi
Shao, Kun
Christen, Urs
Yang, Yang
Ellestad, Kristofor K.
Santamaria, Pere
TI Ubiquitous antigen-specific T regulatory type 1 cells variably suppress
hepatic and extrahepatic autoimmunity
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
AB Peptide MHC class II-based (pMHCII-based) nanomedicines trigger the formation of multicellular regulatory networks by reprogramming autoantigen-experienced CD4(+) T cells into autoimmune disease-suppressing T regulatory type 1 (TR1) cells. We have shown that pMHCII-based nanomedicines displaying liver autoimmune disease-relevant yet ubiquitously expressed antigens can blunt various liver autoimmune disorders in a non-disease-specific manner without suppressing local or systemic immunity against infectious agents or cancer. Here, we show that such ubiquitous autoantigen-specific T cells are also awakened by extrahepatic tissue damage and that the corresponding TR1 progeny can suppress experimental autoimmune encephalomyelitis (EAE) and pancreatic beta cell autoreactivity. In mice having EAE, nanomedicines displaying either ubiquitous or CNS-specific epitopes triggered the formation and expansion of cognate TR1 cells and their recruitment to the CNS-draining lymph nodes, sparing their liver-draining counterparts. Surprisingly, in mice having both liver autoimmunity and EAE, liver inflammation sequestered these ubiquitous or even CNS-specific TR1 cells away from the CNS, abrogating their antiencephalitogenic activity. In these mice, only the ubiquitous antigen-specific TR1 cells suppressed liver autoimmunity. Thus, the scope of antigen spreading in autoimmune disorders is larger than previously anticipated, involving specificities expected to be silenced by mechanisms of tolerance; the regulatory activity, but not the retention of autoreactive TR1 cells, requires local autoantigen expression.
C1 [Umeshappa, Channakeshava Sokke; Mbongue, Jacques; Singha, Santiswarup; Mohapatra, Saswat; Yamanouchi, Jun; Lee, Justin A.; Nanjundappa, Roopa Hebbandi; Shao, Kun; Yang, Yang; Ellestad, Kristofor K.; Santamaria, Pere] Univ Calgary, Julia McFarlane Diabet Res Ctr JMDRC, Cumming Sch Med, Snyder Inst Chron Dis, Calgary, AB, Canada.
[Umeshappa, Channakeshava Sokke; Mbongue, Jacques; Singha, Santiswarup; Mohapatra, Saswat; Yamanouchi, Jun; Lee, Justin A.; Nanjundappa, Roopa Hebbandi; Shao, Kun; Yang, Yang; Ellestad, Kristofor K.; Santamaria, Pere] Univ Calgary, Snyder Inst Chron Dis, Cumming Sch Med, Dept Microbiol Immunol & Infect Dis, Calgary, AB, Canada.
[Umeshappa, Channakeshava Sokke; Mbongue, Jacques; Singha, Santiswarup; Mohapatra, Saswat; Yamanouchi, Jun; Lee, Justin A.; Nanjundappa, Roopa Hebbandi; Shao, Kun; Yang, Yang; Ellestad, Kristofor K.; Santamaria, Pere] Univ Calgary, Hotchkiss Brain Inst, Cumming Sch Med, Calgary, AB, Canada.
[Christen, Urs] Klinikum Goethe Univ Frankfurt, Pharmazentrum Frankfurt, Frankfurt, Germany.
[Yang, Yang] Univ Calgary, Cumming Sch Med, Dept Biochem & Mol Biol, Calgary, AB, Canada.
[Santamaria, Pere] Inst Invest Biomed August Pi I Sunyer, Barcelona, Spain.
C3 University of Calgary; University of Calgary; University of Calgary;
Goethe University Frankfurt; Goethe University Frankfurt Hospital;
University of Calgary; University of Barcelona; Hospital Clinic de
Barcelona; IDIBAPS
RP Santamaria, P (corresponding author), Univ Calgary, Cumming Sch Med, Dept Microbiol Immunol & Infect Dis, Calgary, AB T2N 4N1, Canada.
EM psantama@ucalgary.ca
RI Christen, Urs/A-7338-2009; Santamaria, Pere/ABF-6823-2021; mohapatra,
saswat/AFP-1328-2022
OI Christen, Urs/0000-0003-4165-7976; Mohapatra,
Saswat/0000-0002-7430-7289; Mbongue, Jacques
Christian/0000-0002-7123-3480; Shao, Kun/0000-0001-6876-4697
FU Canadian Institutes of Health Research (CIHR); Diabetes Canada; Multiple
Sclerosis Society of Canada; Crohn's and Colitis Foundation of Canada;
MINECO [RTI2018-093964-B-I00]; CIHR; Banting-CIHR fellowships;
Alberta-Innovates-Health-Solutions
FX We thank H. Jamaleddine and A. Khadra for theoretical contributions to
the concept of competitive autoimmunity; S. Thiessen, J. Erickson, G.
Mendizabal and J. Fetsch, Y. Liu, L. Kennedy, and K. Poon for technical
contributions; and the staff of the Nicole Perkins Microbial Communities
Core. This work was funded by the Canadian Institutes of Health Research
(CIHR), Diabetes Canada, the Multiple Sclerosis Society of Canada, the
Crohn's and Colitis Foundation of Canada, and MINECO
(RTI2018-093964-B-I00). CSU was supported by CIHR,
Alberta-Innovates-Health-Solutions, and Banting-CIHR fellowships. The
JMDRC was supported by Diabetes Canada.
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NR 11
TC 31
Z9 31
U1 0
U2 5
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD APR 1
PY 2020
VL 130
IS 4
BP 1823
EP 1829
DI 10.1172/JCI130670
PG 7
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA LJ3XK
UT WOS:000530101000030
PM 32125290
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Minlikeeva, AN
Freudenheim, JL
Eng, KH
Cannioto, RA
Friel, G
Szender, JB
Segal, B
Odunsi, K
Mayor, P
Diergaarde, B
Zsiros, E
Kelemen, LE
Köel, M
Steed, H
deFazio, A
Jordan, SJ
Fasching, PA
Beckmann, MW
Risch, HA
Rossing, MA
Doherty, JA
Chang-Claude, J
Goodman, MT
Dörk, T
Edwards, R
Modugno, F
Ness, RB
Matsuo, K
Mizuno, M
Karlan, BY
Goode, EL
Kjær, SK
Hogdall, E
Schildkraut, JM
Terry, KL
Cramer, DW
Bandera, EV
Paddock, LE
Kiemeney, LA
Massuger, LFAG
Sutphen, R
Anton-Culver, H
Ziogas, A
Menon, U
Gayther, SA
Ramus, SJ
Gentry-Maharaj, A
Pearce, CL
Wu, AH
Kupryjanczyk, J
Jensen, A
Webb, PM
Moysich, KB
AF Minlikeeva, Albina N.
Freudenheim, Jo L.
Eng, Kevin H.
Cannioto, Rikki A.
Friel, Grace
Szender, J. Brian
Segal, Brahm
Odunsi, Kunle
Mayor, Paul
Diergaarde, Brenda
Zsiros, Emese
Kelemen, Linda E.
Kobel, Martin
Steed, Helen
deFazio, Anna
Jordan, Susan J.
Fasching, Peter A.
Beckmann, Matthias W.
Risch, Harvey A.
Rossing, Mary Anne
Doherty, Jennifer A.
Chang-Claude, Jenny
Goodman, Marc T.
Doerk, Thilo
Edwards, Robert
Modugno, Francesmary
Ness, Roberta B.
Matsuo, Keitaro
Mizuno, Mika
Karlan, Beth Y.
Goode, Ellen L.
Kjaer, Susanne K.
Hogdall, Estrid
Schildkraut, Joellen M.
Terry, Kathryn L.
Cramer, Daniel W.
Bandera, Elisa V.
Paddock, Lisa E.
Kiemeney, Lambertus A.
Massuger, Leon F. A. G.
Sutphen, Rebecca
Anton-Culver, Hoda
Ziogas, Argyrios
Menon, Usha
Gayther, Simon A.
Ramus, Susan J.
Gentry-Maharaj, Aleksandra
Pearce, Celeste L.
Wu, Anna H.
Kupryjanczyk, Jolanta
Jensen, Allan
Webb, Penelope M.
Moysich, Kirsten B.
CA Australian Ovarian Canc Study Grp
Ovarian Canc Assoc Consortium
TI History of Comorbidities and Survival of Ovarian Cancer Patients,
Results from the Ovarian Cancer Association Consortium
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID CO-MORBIDITY; AGE
AB Background: Comorbidities can affect survival of ovarian cancer patients by influencing treatment efficacy. However, little evidence exists on the association between individual concurrent comorbidities and prognosis in ovarian cancer patients.
Methods: Among patients diagnosed with invasive ovarian carcinoma who participated in 23 studies included in the Ovarian Cancer Association Consortium, we explored associations between histories of endometriosis; asthma; depression; osteoporosis; and autoimmune, gallbladder, kidney, liver, and neurological diseases and overall and progression-free survival. Using Cox proportional hazards regression models adjusted for age at diagnosis, stage of disease, histology, and study site, we estimated pooled HRs and 95% confidence intervals to assess associations between each comorbidity and ovarian cancer outcomes.
Results: None of the comorbidities were associated with ovarian cancer outcome in the overall sample nor in strata defined by histologic subtype, weight status, age at diagnosis, or stage of disease (local/regional vs. advanced).
Conclusions: Histories of endometriosis; asthma; depression; osteoporosis; and autoimmune, gallbladder, kidney, liver, or neurologic diseases were not associated with ovarian cancer overall or progression-free survival.
Impact: These previously diagnosed chronic diseases do not appear to affect ovarian cancer prognosis. (C) 2017 AACR.
C1 [Minlikeeva, Albina N.; Cannioto, Rikki A.; Moysich, Kirsten B.] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
[Freudenheim, Jo L.; Moysich, Kirsten B.] Univ Buffalo, Dept Epidemiol & Environm Health, Buffalo, NY USA.
[Eng, Kevin H.] Roswell Pk Canc Inst, Dept Biostatist & Bioinformat, Buffalo, NY 14263 USA.
[Friel, Grace] Independent Health, New York, NY USA.
[Szender, J. Brian; Odunsi, Kunle; Mayor, Paul] Roswell Pk Canc Inst, Dept Surg, Div Gynecol Oncol, Buffalo, NY 14263 USA.
[Segal, Brahm] Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA.
[Segal, Brahm; Moysich, Kirsten B.] Roswell Pk Canc Inst, Dept Immunol, New York, NY USA.
[Odunsi, Kunle; Zsiros, Emese] Roswell Pk Canc Inst, Ctr Immunotherapy, Buffalo, NY 14263 USA.
[Diergaarde, Brenda] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
[Diergaarde, Brenda] Univ Pittsburgh, Canc Inst, Pittsburgh, PA USA.
[Kelemen, Linda E.] Med Univ South Carolina, Dept Publ Hlth Sci, Charleston, SC USA.
Univ Calgary, Dept Pathol, Foothills Med Ctr, Calgary, AB, Canada.
[Kobel, Martin] Univ Calgary, Dept Pathol & Lab Med, Foothills Med Ctr, Calgary, AB, Canada.
[Steed, Helen] Royal Alexandra Hosp, Div Gynecol Oncol, Dept Obstet & Gynecol, Edmonton, AB, Canada.
[deFazio, Anna] Univ Sydney, Dept Gynecol Oncol, Westmead Hosp, Sydney, NSW, Australia.
[deFazio, Anna] Univ Sydney, Westmead Millenium Inst Med Res, Sydney, NSW, Australia.
[Jordan, Susan J.; Webb, Penelope M.] QIMR Berghofer Med Res Inst, Populat Hlth Dept, Brisbane, Qld, Australia.
[Fasching, Peter A.] Univ Calif Los Angeles, Dept Med, Div Hematol & Oncol, David Geffen Sch Med, Los Angeles, CA 90024 USA.
[Fasching, Peter A.; Beckmann, Matthias W.] Friedrich Alexander Univ Erlangen Nuremberg, Erlangen Univ Hosp, Comprehens Canc Ctr Erlangen EMN, Dept Gynecol & Obstet, Erlangen, Germany.
[Risch, Harvey A.] Yale Sch Publ Hlth, Dept Chron Dis Epidemiol, New Haven, CT USA.
[Rossing, Mary Anne] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Doherty, Jennifer A.] Geisel Sch Med Dartmouth Med, Dept Epidemiol, Hanover, NH USA.
[Chang-Claude, Jenny] German Canc Res Canc, Div Canc Epidemiol, Heidelberg, Germany.
[Chang-Claude, Jenny] Univ Canc Ctr Hamburg, Univ Med Ctr Hamburg Eppendorf Hamburg, Hamburg, Germany.
[Goodman, Marc T.] Cedars Sinai Med Ctr, Samuel Oschin Com prehens Canc Inst, Canc Prevent & Control, Los Angeles, CA 90048 USA.
[Doerk, Thilo] Hannover Med Sch, Dept Obstet & Gynaecol, Hannover, Lower Saxony, Germany.
[Edwards, Robert; Modugno, Francesmary] Univ Pittsburgh, Sch Med, Dept Obstet Gynecol & Reprod Sci, Div Gynecol Oncol, Pittsburgh, PA USA.
[Edwards, Robert; Modugno, Francesmary] Magee Womens Res Inst, Womens Canc Res Program, Ovarian Canc Ctr Excellence, Pittsburgh, PA USA.
[Edwards, Robert; Modugno, Francesmary] Univ Pittsburgh, Canc Inst, Pittsburgh, PA USA.
[Modugno, Francesmary] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
[Ness, Roberta B.] Univ Texas Houston, Sch Publ Hlth, Houston, TX USA.
[Matsuo, Keitaro] Aichi Canc Ctr, Res Inst, Div Mol Med, Nagoya, Aichi, Japan.
[Mizuno, Mika] Aichi Canc Ctr Hosp, Dept Gynecol Oncol, Nagoya, Aichi, Japan.
[Karlan, Beth Y.] Cedars Sinai Med Ctr, Womens Canc Program, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
[Goode, Ellen L.] Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN USA.
[Kjaer, Susanne K.; Hogdall, Estrid; Jensen, Allan] Danish Canc Soc, Res Ctr, Dept Virus Lifestyle & Genes, Copenhagen, Denmark.
[Kjaer, Susanne K.] Univ Copenhagen, Dept Gynaecol, Rigshosp, Copenhagen, Denmark.
[Hogdall, Estrid] Univ Copenhagen, Dept Pathol, Herlev Hosp, Copenhagen, Denmark.
[Schildkraut, Joellen M.] Univ Virginia, Sch Med, Dept Publ Hlth Sci, Charlottesville, VA 22908 USA.
[Terry, Kathryn L.; Cramer, Daniel W.] Brigham & Womens Hosp, Obstet & Gynecol Epidemiol Ctr, 75 Francis St, Boston, MA 02115 USA.
[Terry, Kathryn L.; Cramer, Daniel W.] Harvard TH Chan Sch Publ Hlth, Boston, MA USA.
[Bandera, Elisa V.] Rutgers Canc Inst New Jersey, Canc Prevent & Control Program, New Brunswick, NJ USA.
[Paddock, Lisa E.] New Jersey Dept, Hlth & Senior Serv, Trenton, NJ USA.
[Paddock, Lisa E.] Univ Med & Dent New Jersey, Sch Publ Hlth, Piscataway, NJ 08854 USA.
[Kiemeney, Lambertus A.] Radboud Univ Nijmegen, Med Ctr, Radboud Inst Hlth Sci, Nijmegen, Netherlands.
[Massuger, Leon F. A. G.] Radboud Univ Nijmegen, Med Ctr, Dept Gynaecol, Radboud Inst Mol Life Sci, Nijmegen, Netherlands.
[Sutphen, Rebecca] Univ S Florida, Coll Med, Epidemiol Ctr, Tampa, FL USA.
[Anton-Culver, Hoda] Univ Calif Irvine, Sch Med, Ctr Canc Genet Res & Prevent, Genet Epidemiol Res Inst, Irvine, CA 92717 USA.
[Anton-Culver, Hoda; Ziogas, Argyrios] Univ Calif Irvine, Dept Epidemiol, Irvine, CA USA.
[Menon, Usha] UCL, Womens Canc Inst Womens Hlth, London, England.
[Gayther, Simon A.] Ctr Canc Prevent & Translat Genom, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA USA.
[Gayther, Simon A.] Cedars Sinai Med Ctr, Dept Biomed Sci, Los Angeles, CA 90048 USA.
[Ramus, Susan J.] Univ New South Wales, Sch Womens & Childrens Hlth, Sydney, NSW, Australia.
[Ramus, Susan J.] Kinghorn Canc Ctr, Garvan Inst Med Res, Darlinghurst, NSW, Australia.
[Gentry-Maharaj, Aleksandra] UCL, Womens Canc, Inst Womens Hlth, London, England.
[Pearce, Celeste L.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Pearce, Celeste L.; Wu, Anna H.] Univ South Calif, Dept Prevent Med, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
[Kupryjanczyk, Jolanta] Maria Sklodowska Curie Mem Canc Ctr, Dept Pathol, Warsaw, Poland.
[Kupryjanczyk, Jolanta] Maria Sklodowska Curie Mem Canc Ctr, Lab Diagnost, Warsaw, Poland.
[Kupryjanczyk, Jolanta] Inst Oncol, Warsaw, Poland.
C3 Roswell Park Comprehensive Cancer Center; State University of New York
(SUNY) System; University at Buffalo, SUNY; Roswell Park Comprehensive
Cancer Center; Roswell Park Comprehensive Cancer Center; Roswell Park
Comprehensive Cancer Center; Roswell Park Comprehensive Cancer Center;
Roswell Park Comprehensive Cancer Center; Pennsylvania Commonwealth
System of Higher Education (PCSHE); University of Pittsburgh;
Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Medical University of South Carolina; University of
Calgary; University of Calgary; Royal Alexandra Hospital; NSW Health;
Westmead Hospital; University of Sydney; University of Sydney; QIMR
Berghofer Medical Research Institute; University of California System;
University of California Los Angeles; University of California Los
Angeles Medical Center; David Geffen School of Medicine at UCLA;
University of Erlangen Nuremberg; Yale University; Fred Hutchinson
Cancer Center; University of Hamburg; University Medical Center
Hamburg-Eppendorf; Cedars Sinai Medical Center; Hannover Medical School;
Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh; Magee-Womens Research Institute;
Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh; University of Texas System;
University of Texas Health Science Center Houston; University of Texas
School Public Health; Aichi Cancer Center; Aichi Cancer Center; Cedars
Sinai Medical Center; Mayo Clinic; Danish Cancer Society;
Rigshospitalet; University of Copenhagen; University of Copenhagen;
Herlev & Gentofte Hospital; University of Virginia; Harvard University;
Brigham & Women's Hospital; Harvard University; Harvard T.H. Chan School
of Public Health; Rutgers University System; Rutgers University New
Brunswick; Rutgers University Biomedical & Health Sciences; Rutgers
Cancer Institute of New Jersey; Rutgers University System; Rutgers
University New Brunswick; Rutgers University Biomedical & Health
Sciences; Radboud University Nijmegen; Radboud University Nijmegen;
State University System of Florida; University of South Florida;
University of California System; University of California Irvine;
University of California System; University of California Irvine;
University of London; University College London; Cedars Sinai Medical
Center; Cedars Sinai Medical Center; University of New South Wales
Sydney; The Kinghorn Cancer Centre; Garvan Institute of Medical
Research; University of London; University College London; University of
Michigan System; University of Michigan; University of Southern
California; Maria Sklodowska-Curie National Research Institute of
Oncology; Maria Sklodowska-Curie National Research Institute of
Oncology; Maria Sklodowska-Curie National Research Institute of Oncology
RP Moysich, KB (corresponding author), Roswell Pk Canc Inst, A-352 Carlton House,Elm & Carlton Streets, Buffalo, NY 14263 USA.
EM kirsten.moysich@roswellpark.org
RI Modugno, Francesmary/AIB-6722-2022; Massuger, Leon/H-8072-2014; Zsiros,
Emese/AAM-4469-2021; Jensen, Allan/LPQ-7837-2024; Ramus,
Susan/AAG-8352-2019; Matsuo, Keitaro/H-6758-2019; Köbel,
Martin/A-7373-2011; Jordan, Susan/AAE-6356-2020; Segal,
Brahm/AAW-2706-2020; Menon, Usha/C-4716-2008; Fasching,
Peter/ABH-9912-2020; Webb, Penelope/D-5736-2013; Jordan,
Susan/G-2519-2010; Bowtell, David/H-1007-2016; Kiemeney,
Lambertus/D-3357-2009; Dork, Thilo/J-8620-2012; DeFazio,
Anna/D-3939-2013
OI Hogdall, Estrid/0000-0003-4689-5658; Menon, Usha/0000-0003-3708-1732;
Webb, Penelope/0000-0003-0733-5930; Jensen, Allan/0000-0001-8124-4880;
Steed, Helen/0000-0002-0539-8906; Matsuo, Keitaro/0000-0003-1761-6314;
Jordan, Susan/0000-0002-4566-1414; Ramus, Susan/0000-0003-0005-7798;
Freudenheim, Jo/0000-0002-9301-0499; Bowtell, David/0000-0001-9089-7525;
Kobel, Martin/0000-0002-6615-2037; Goodman, Marc/0000-0002-4839-3021;
Kiemeney, Lambertus/0000-0002-2368-1326; Kupryjanczyk,
Jolanta/0000-0001-5820-0214; Diergaarde, Brenda/0000-0002-3578-6547;
Eng, Kevin/0000-0001-5636-0812; Dork, Thilo/0000-0002-9458-0282; Zsiros,
Emese/0000-0003-0142-7375; DeFazio, Anna/0000-0003-0057-4744
FU NCI Interdisciplinary Training Grant in Cancer Epidemiology
[R25CA113951]; NIH/NCI [R01CA126841, 2R25CA113951, R01CA095023,
P50CA159981, K07-CA080668, R01-CA95023, P50-CA159981, R01-CA126841,
R01-CA61107, K07 CA095666, K22-CA138563, P30-CA072720]; NIH/NLM
[K01LM012100]; Roswell Park Alliance Foundation; NCI [5T32CA108456]; NIH
[R01CA188900, R01-CA074850, R01-CA080742, R01-CA112523, R01-CA87538,
R01-CA58598, N01-CN-55424, N01-PC-67001, R01-CA122443, P30-CA15083,
P50-CA136393, R01-CA76016, R01-CA54419, P50-CA105009, R01-CA106414-A2,
R01-CA058860]; Canadian Institutes for Health Research [MOP-86727]; Army
Medical Research and Materiel Command [DAMD17-01-1-0729]; National
Health & Medical Research Council of Australia [199600, 400281]; Cancer
Councils of New South Wales, Victoria, Queensland, South Australia and
Tasmania; Cancer Foundation of Western Australia; ELAN Funds of the
University of Erlangen-Nuremberg; German Federal Ministry of Education
and Research, Program of Clinical Biomedical Research [01GB9401]; German
Cancer Research Center; Rudolf-Bartling Foundation; Department of
Defense (DOD) [DAMD17-02-1-0669]; Ministry of Health, Labour and
Welfare; American Cancer Society Early Detection Professorship
[SIOP-06-258-01-COUN]; National Center for Advancing Translational
Sciences (NCATS) [UL1TR000124]; Mayo Foundation; Minnesota Ovarian
Cancer Alliance; Fred C. and Katherine B. Anderson Foundation; Danish
Cancer Society [94 222 52]; Mermaid I project; DOD [DAMD17-02-1-0666,
DAMD17-98-1-8659]; Cancer Institute of New Jersey; Radboud University
Medical Centre; American Cancer Society [CRTG-00-196-01-CCE]; Celma
Mastery Ovarian Cancer Foundation; Lon V Smith Foundation grant
[LVS-39420]; Eve Appeal (Oak Foundation); National Institute for Health
Research University College London Hospitals Biomedical Research Centre;
California Cancer Research Program [00-01389V-20170, 2II0200]; Polish
Ministry of Science and Higher Education [4 PO5C 028 14, 2 PO5A 068 27];
Maria Sklodowska-CurieMemorial Cancer Cente; Institute of Oncology,
Warsaw, Poland; [P01CA17054]; [P30CA14089]; [R01CA61132];
[N01PC67010]; [R03CA113148]; [R03CA115195]; [N01CN025403]
FX A.N. Minlikeeva was supported by NCI Interdisciplinary Training Grant in
Cancer Epidemiology (R25CA113951). J.L. Freudenheim was supported by
NIH/NCI (2R25CA113951). G. Friel was supported by NIH/NCI (R01CA095023
and R01CA126841). K.H. Eng was supported by NIH/NLM (K01LM012100) and
the Roswell Park Alliance Foundation. J.B. Szender was supported by NCI
(5T32CA108456). B.H. Segal was supported by NIH (R01CA188900). K.B.
Moysich was supported by NIH/NCI (2R25CA113951, R01CA095023,
R01CA126841, P50CA159981) and the Roswell Park Alliance Foundation. AOV
was supported by the Canadian Institutes for Health Research
(MOP-86727). AUS was supported by U.S. Army Medical Research and
Materiel Command (DAMD17-01-1-0729), National Health & Medical Research
Council of Australia (199600 and 400281), Cancer Councils of New South
Wales, Victoria, Queensland, South Australia and Tasmania, Cancer
Foundation of Western Australia. BAV was supported by ELAN Funds of the
University of Erlangen-Nuremberg. CON was supported by NIH (R01-CA074850
and R01-CA080742). DOV was supported by NIH (R01-CA112523 and
R01-CA87538). GER was supported by German Federal Ministry of Education
and Research, Program of Clinical Biomedical Research (01GB9401) and
German Cancer Research Center. HAW was supported by NIH (R01-CA58598,
N01-CN-55424, and N01-PC-67001). HJO was supported by Intramural
funding; Rudolf-Bartling Foundation. HOP was supported by Department of
Defense (DOD): DAMD17-02-1-0669 and NIH/NCI (K07-CA080668, R01-CA95023,
P50-CA159981, and R01-CA126841). JPN was supported by Grant-in-Aid for
the Third Term Comprehensive 10-Year Strategy for Cancer Control from
the Ministry of Health, Labour and Welfare. LAX was supported by
American Cancer Society Early Detection Professorship
(SIOP-06-258-01-COUN) and the National Center for Advancing
Translational Sciences (NCATS; UL1TR000124). MAC and MAY were supported
by NIH (R01-CA122443, P30-CA15083, and P50-CA136393), Mayo Foundation,
Minnesota Ovarian Cancer Alliance, and Fred C. and Katherine B. Anderson
Foundation. MAL was supported by NIH/NCI (R01-CA61107), Danish Cancer
Society (research grant 94 222 52), and the Mermaid I project. NCO was
supported by NIH (R01-CA76016) and the DOD (DAMD17-02-1-0666). NEC was
supported by NIH (R01-CA54419 and P50-CA105009) and DOD
(W81XWH-10-1-02802). NJO was supported by NIH/NCI (K07 CA095666,
K22-CA138563, and P30-CA072720) and the Cancer Institute of New Jersey.
NTH was supported by Radboud University Medical Centre. TBO was
supported by NIH (R01-CA106414-A2), American Cancer Society
(CRTG-00-196-01-CCE), DOD (DAMD17-98-1-8659), and Celma Mastery Ovarian
Cancer Foundation. UCI was supported by NIH (R01-CA058860) and the Lon V
Smith Foundation grant (LVS-39420). UKO was funded by The Eve Appeal
(The Oak Foundation) and supported by the National Institute for Health
Research University College London Hospitals Biomedical Research Centre.
USC was supported by (P01CA17054, P30CA14089, R01CA61132, N01PC67010,
R03CA113148, R03CA115195, and N01CN025403) and California Cancer
Research Program (00-01389V-20170, 2II0200). WOC was supported by Polish
Ministry of Science and Higher Education (4 PO5C 028 14, 2 PO5A 068 27),
The Maria Sklodowska-CurieMemorial Cancer Center, and Institute of
Oncology, Warsaw, Poland.
CR Hemminki K, 2012, GYNECOL ONCOL, V127, P180, DOI 10.1016/j.ygyno.2012.07.100
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O'Malley CD, 2003, GYNECOL ONCOL, V91, P608, DOI 10.1016/j.ygyno.2003.08.010
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NR 8
TC 8
Z9 10
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD SEP
PY 2017
VL 26
IS 9
BP 1470
EP 1473
DI 10.1158/1055-9965.EPI-17-0367
PG 4
WC Oncology; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Public, Environmental & Occupational Health
GA FI7DZ
UT WOS:000412157800016
PM 28864456
OA Green Submitted, Bronze, Green Accepted
DA 2025-01-07
ER
PT J
AU Manno, V
Gerussi, A
Carbone, M
Minelli, G
Taruscio, D
Conti, S
Invernizzi, P
AF Manno, Valerio
Gerussi, Alessio
Carbone, Marco
Minelli, Giada
Taruscio, Domenica
Conti, Susanna
Invernizzi, Pietro
TI A National Hospital-Based Study of Hospitalized Patients With Primary
Biliary Cholangitis
SO HEPATOLOGY COMMUNICATIONS
LA English
DT Article
ID NATURAL-HISTORY; RISK-FACTORS; CIRRHOSIS; EPIDEMIOLOGY;
HYPERCHOLESTEROLEMIA; COMORBIDITIES; SURVIVAL; OUTCOMES; LIVER
AB Epidemiological studies on primary biliary cholangitis (PBC) have been based primarily on tertiary referral case series. We aimed to estimate the incidence and prevalence and describe comorbidities in hospitalized patients with PBC in Italy using a national hospital-based data source. Data were extracted from the National Hospital Discharge Database, which includes all Italian individuals discharged from any hospital in the country. All adults diagnosed with biliary cirrhosis (International Classification of Diseases, Ninth Revision, Clinical Modification, 571.6) as the primary or secondary diagnosis from 2011 to 2015 were included. To determine whether a comorbidity was either more or less frequent in PBC patients compared with the general hospitalized Italian population, the standardized hospitalization ratio (SHR) was calculated. A total of 5,533 incident cases were identified from 2011 to 2015, 3,790 of whom were females (68.5%; female to male [F:M] ratio, 2.2:1). Prevalent cases were 9,664, of whom 7,209 were females (74.6%; F:M ratio, 2.9:1). The incident rate was 1.03 x 100,000 in males and 1.92 x 100,000 in females; prevalence was 1.89 x 100,000 in males and 4.75 x 100,000 in females. Extrahepatic autoimmune diseases, malignant neoplasms of liver and intrahepatic biliary ducts, and malignant neoplasms of gallbladder and extrahepatic bile ducts were found more frequently in PBC patients than in the general hospitalized population (SHR > 100), whereas cerebrovascular diseases and ischemic heart diseases were less frequent in PBC individuals (SHR < 100). Conclusion: This national study provides a survey of comorbidities associated with PBC. Hospitalized patients with PBC are more likely to have extrahepatic autoimmune diseases, hepatocellular carcinoma, and biliary tract cancers and a low risk of cardiovascular events.
C1 [Manno, Valerio; Minelli, Giada; Conti, Susanna] Natl Inst Hlth, Serv Stat, Rome, Italy.
[Gerussi, Alessio; Carbone, Marco; Invernizzi, Pietro] Univ Milano Bicocca, Div Gastroenterol, Via Cadore 48, I-20900 Monza, MB, Italy.
[Gerussi, Alessio; Carbone, Marco; Invernizzi, Pietro] Univ Milano Bicocca, Ctr Autoimmune Liver Dis, Dept Med & Surg, Via Cadore 48, I-20900 Monza, MB, Italy.
[Taruscio, Domenica] Natl Ctr Rare Dis, Natl Inst Hlth, Rome, Italy.
C3 Istituto Superiore di Sanita (ISS); University of Milano-Bicocca;
University of Milano-Bicocca; Istituto Superiore di Sanita (ISS)
RP Invernizzi, P (corresponding author), Univ Milano Bicocca, Div Gastroenterol, Via Cadore 48, I-20900 Monza, MB, Italy.; Invernizzi, P (corresponding author), Univ Milano Bicocca, Ctr Autoimmune Liver Dis, Dept Med & Surg, Via Cadore 48, I-20900 Monza, MB, Italy.
EM pietro.invernizzi@unimib.it
RI Invernizzi, Pietro/AAB-8367-2022; Gerussi, Alessio/AAM-5199-2020;
Minelli, Giada/AAC-2787-2021; TARUSCIO, DOMENICA/A-6646-2015; Manno,
Valerio/GSI-4281-2022
OI Gerussi, Alessio/0000-0002-5086-0514; Manno, Valerio/0000-0003-0382-5940
FU Italian Ministry of Health in the role of auto-reactive hepatic natural
killer cells in the pathogenesis of primary biliary cholangitis
[PE-2016-02363915, GR-2018-12367794]
FX Supported by the Italian Ministry of Health in the role of auto-reactive
hepatic natural killer cells in the pathogenesis of primary biliary
cholangitis (PE-2016-02363915) and in the biocompatible nano-assemblies
to increase the safety and the efficacy of steroid treatment against
liver inflammation (GR-2018-12367794).
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NR 33
TC 10
Z9 11
U1 0
U2 2
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
EI 2471-254X
J9 HEPATOL COMMUN
JI Hepatol. Commun.
PD SEP
PY 2019
VL 3
IS 9
BP 1250
EP 1257
DI 10.1002/hep4.1407
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IU5TV
UT WOS:000483651100009
PM 31497745
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Menias, CO
Surabhi, VR
Prasad, SR
Wang, HL
Narra, VR
Chintapalli, KN
AF Menias, Christine O.
Surabhi, Venkateswar R.
Prasad, Srinivasa R.
Wang, Hanlin L.
Narra, Vamsi R.
Chintapalli, Kedar N.
TI Mimics of cholangiocarcinoma: Spectrum of disease
SO RADIOGRAPHICS
LA English
DT Article; Proceedings Paper
CT 92nd Scientific Assembly and Annual Meeting of the
Radiological-Society-of-North-America
CY NOV 26-DEC 01, 2006
CL Chicago, IL
SP Radiol Soc N Amer
ID PRIMARY SCLEROSING CHOLANGITIS; EXTRAHEPATIC BILE-DUCTS; INFLAMMATORY
MYOFIBROBLASTIC TUMOR; RECURRENT PYOGENIC CHOLANGITIS;
NON-HODGKINS-LYMPHOMA; OF-THE-LITERATURE; BILIARY-TRACT;
OBSTRUCTIVE-JAUNDICE; MIRIZZI-SYNDROME; XANTHOGRANULOMATOUS
CHOLECYSTITIS
AB Cholangiocarcinoma is the second most common primary malignant hepatobiliary neoplasm, accounting for approximately 15% of liver cancers. Diagnosis of cholangiocarcinoma is challenging and the prognosis is uniformly poor, with recurrence rates of 60%-90% after surgical resection. A wide spectrum of neoplastic and nonneoplastic conditions of the biliary tract may masquerade as cholangiocarcinoma, adding to the complexity of management in patients suspected to have cholangiocarcinoma. Mimics of cholangiocarcinoma constitute a heterogeneous group of entities that includes primary sclerosing cholangitis, recurrent pyogenic cholangitis, acquired immunodeficiency syndrome cholangiopathy, autoimmune pancreatitis, inflammatory pseudotumor, Mirizzi syndrome, xanthogranulomatous cholangitis, sarcoidosis, chemotherapy-induced sclerosis, hepatocellular carcinoma, metastases, melanoma, lymphoma, leukemia, and carcinoid tumors. These entities demonstrate characteristic histomorphology and variable clinicobiologic behaviors. The imaging findings of these disparate entities are protean and may be indistinguishable from those of cholangiocarcinoma. In most cases, a definitive diagnosis can be established only with histopathologic examination of a biopsy specimen. (C) RSNA, 2008.
C1 [Surabhi, Venkateswar R.; Prasad, Srinivasa R.; Chintapalli, Kedar N.] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, San Antonio, TX 78229 USA.
[Menias, Christine O.; Narra, Vamsi R.] Washington Univ, Med Ctr, Mallinckrodt Inst Radiol, Dept Radiol, St Louis, MO 63110 USA.
[Wang, Hanlin L.] Washington Univ, Dept Pathol, St Louis, MO 63130 USA.
C3 University of Texas System; University of Texas Health Science Center at
San Antonio; Washington University (WUSTL); Washington University
(WUSTL)
RP Prasad, SR (corresponding author), Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, 703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM prasads@uthscsa.edu
RI Prasad, Srinivasa/AAJ-8654-2020
OI Prasad, Srinivasa/0000-0003-4594-2117
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NR 70
TC 87
Z9 95
U1 0
U2 6
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0271-5333
J9 RADIOGRAPHICS
JI Radiographics
PD JUL-AUG
PY 2008
VL 28
IS 4
BP 1115
EP 1129
DI 10.1148/rg.284075148
PG 15
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 323HX
UT WOS:000257438300014
PM 18635632
DA 2025-01-07
ER
PT J
AU Jiao, GH
Wang, BM
AF Jiao, Guohui
Wang, Bangmao
TI NK Cell Subtypes as Regulators of Autoimmune Liver Disease
SO GASTROENTEROLOGY RESEARCH AND PRACTICE
LA English
DT Review
ID NATURAL-KILLER-CELLS; INNATE LYMPHOID-CELLS; ADAPTIVE IMMUNITY;
PERIPHERAL-BLOOD; CHEMOKINES; RECEPTORS; HEPATITIS; LYMPHOCYTES;
CYTOKINE; BIOLOGY
AB As major components of innate immunity, NK cells not only exert cell-mediated cytotoxicity to destroy tumors or infected cells, but also act to regulate the functions of other cells in the immune system by secreting cytokines and chemokines. Thus, NK cells provide surveillance in the early defense against viruses, intracellular bacteria, and cancer cells. However, the effecter function of NK cells must be exquisitely controlled to prevent inadvertent attack against normal "self" cells. In an organ such as the liver, where the distinction between immunotolerance and immune defense against routinely processed pathogens is critical, the plethora of NK cells has a unique role in the maintenance of homeostasis. Once self-tolerance is broken, autoimmune liver disease resulted. NK cells act as a "two-edged weapon" and even play opposite roles with both regulatory and inducer activities in the hepatic environment. That is, NK cells act not only to produce inflammatory cytokines and chemokines, but also to alter the proliferation and activation of associated lymphocytes. However, the precise regulatory mechanisms at work in autoimmune liver diseases remain to be identified. In this review, we focus on recent research with NK cells and their potential role in the development of autoimmune liver disease.
C1 [Jiao, Guohui; Wang, Bangmao] Tianjin Med Univ, Gen Hosp, Dept Gastroenterol, Tianjin 300052, Peoples R China.
C3 Tianjin Medical University
RP Wang, BM (corresponding author), Tianjin Med Univ, Gen Hosp, Dept Gastroenterol, Tianjin 300052, Peoples R China.
EM tjmughgi@hotmail.com
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NR 71
TC 14
Z9 14
U1 0
U2 4
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-6121
EI 1687-630X
J9 GASTROENT RES PRACT
JI Gastroenterol. Res. Pract.
PY 2016
VL 2016
AR 6903496
DI 10.1155/2016/6903496
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DR4LA
UT WOS:000379871800001
PM 27462349
OA gold, Green Submitted, Green Published
DA 2025-01-07
ER
PT J
AU Clendenon, JN
Aranda-Michel, J
Krishna, M
Taner, CB
Willingham, DL
AF Clendenon, Jacob N.
Aranda-Michel, Jaime
Krishna, Murli
Taner, C. Burcin
Willingham, Darrin L.
TI Recurrent liver failure caused by IgG4 associated cholangitis
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Autoimmune cholangitis; Autoimmune diseases; Immunoglobulin G4; Bile
duct diseases
ID SCLEROSING PANCREATO-CHOLANGITIS; OF-THE-LITERATURE; AUTOIMMUNE
PANCREATITIS; DISEASE; ENTITY
AB Immunoglobulin G4 associated cholangitis (IAC) is an autoimmune disease associated with autoimmune pancreatitis (AIP). It presents with clinical and radiographic findings similar to primary sclerosing cholangitis (PSC). IAC commonly has a faster, more progressive onset of symptoms and it is more common to see obstructive jaundice in IAC patients compared to those with PSC. One of the hallmarks of IAC is its responsiveness to steroid therapy. Current recommendations for treatment of AIP demonstrate excellent remission of the disease and associated symptoms with initiation of steroid therapy followed by steroid tapering. If untreated, it can progress to irreversible liver failure. This report describes a 59 year-old female with undiagnosed IAC who previously had undergone a pancreaticoduodenectomy for a suspected pancreatic cancer and later developed liver failure from presumed PSC. The patient underwent an uncomplicated liver transplantation at our institution, but experienced allograft failure within five years due to progressive and irreversible bile duct injury. Radiology and histology suggested recurrence of PSC, but the diagnosis of IAC was suspected based on her past history and confirmed when IgG4 positive cells were found within the intrahepatic bile duct walls on a liver biopsy. A successful liver retransplantation was performed and the patient is currently on triple immunosuppressive therapy. Our experience in this case and review of the current literature regarding IAC management suggest that patients with suspected or recurrent PSC with atypical features including history of pancreatitis should undergo testing for IAC as this entity is highly responsive to steroid therapy.
C1 [Clendenon, Jacob N.; Aranda-Michel, Jaime; Taner, C. Burcin; Willingham, Darrin L.] Mayo Clin Florida, Dept Transplantat, Jacksonville, FL 32224 USA.
[Krishna, Murli] Mayo Clin Florida, Dept Lab Med & Pathol, Jacksonville, FL 32224 USA.
C3 Mayo Clinic; Mayo Clinic
RP Aranda-Michel, J (corresponding author), Mayo Clin Florida, Dept Transplantat, 4500 San Pablo Rd, Jacksonville, FL 32224 USA.
EM arandamichel.jaime@mayo.edu
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NR 12
TC 5
Z9 6
U1 0
U2 2
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD OCT-DEC
PY 2011
VL 10
IS 4
BP 562
EP 564
DI 10.1016/S1665-2681(19)31527-3
PG 3
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 843LF
UT WOS:000296672600021
PM 21911900
OA hybrid
DA 2025-01-07
ER
PT J
AU Uhl, P
Fricker, G
Haberkorn, U
Mier, W
AF Uhl, Philipp
Fricker, Gert
Haberkorn, Uwe
Mier, Walter
TI Current Status in the Therapy of Liver Diseases
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE hepatic diseases; hepatitis; entry inhibitors; molecular mechanisms;
liver cirrhosis; hepatocellular carcinoma
ID HEPATITIS-B-VIRUS; PEGYLATED INTERFERON; CONTROLLED-TRIAL; RIBAVIRIN;
ENTRY; PIOGLITAZONE; ABSORPTION; PREVENTION; DIAGNOSIS; ALPHA-2A
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C1 [Uhl, Philipp; Haberkorn, Uwe; Mier, Walter] Univ Heidelberg Hosp, Dept Nucl Med, D-69120 Heidelberg, Germany.
[Fricker, Gert] Heidelberg Univ, Inst Pharm & Mol Biotechnol, D-69120 Heidelberg, Germany.
C3 Ruprecht Karls University Heidelberg; Ruprecht Karls University
Heidelberg
RP Mier, W (corresponding author), Univ Heidelberg Hosp, Dept Nucl Med, Neuenheimer Feld 400, D-69120 Heidelberg, Germany.
EM philipp.uhl@med.uni-heidelberg.de; gert.fricker@uni-hd.de;
uwe.haberkorn@med.uni-heidelberg.de; walter.mier@med.uni-heidelberg.de
OI Uhl, JunProf. Dr. Philipp/0000-0002-8616-5599
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NR 38
TC 35
Z9 40
U1 0
U2 15
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD MAY
PY 2014
VL 15
IS 5
BP 7500
EP 7512
DI 10.3390/ijms15057500
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA AI4NJ
UT WOS:000336841800026
PM 24786290
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Uchida, K
Satoi, S
Miyoshi, H
Hachimine, D
Ikeura, T
Shimatani, M
Matsushita, M
Takaoka, M
Takai, S
Ashida, K
Okazaki, K
AF Uchida, Kazushige
Satoi, Sohei
Miyoshi, Hideaki
Hachimine, Daisaku
Ikeura, Tsukasa
Shimatani, Masaaki
Matsushita, Mitsunobu
Takaoka, Makoto
Takai, Soichiro
Ashida, Kiyoshi
Okazaki, Kazuichi
TI Inflammatory pseudotumors of the pancreas and liver with infiltration of
IgG4-positive plasma cells
SO INTERNAL MEDICINE
LA English
DT Article
DE autoimmune pancreatitis; inflammatory pseudotumor; pancreatic cancer
ID AUTOIMMUNE-RELATED PANCREATITIS; SCLEROSING PANCREATITIS; CHOLANGITIS;
DISEASE
AB Recently, it has been reported that autoimmune pancreatitis (AIP) can be complicated with various extra-pancreatic lesions. Here, we report a very rare case of pancreatic and hepatic inflammatory pseudotumor (IPT) with the infiltration of IgG4-positive plasmacytes. The patient showed pancreatic and hepatic masses with elevated levels of serum IgG4. Endoscopic retrograde cholangiopancreatography revealed narrowing of the intrapancreatic bile duct. Fluorine-18fluorodeoxyglucose positron emission tomography suggested pancreatic cancer with hepatic metastasis. Histopathologic findings showed fibrosis and infiltration of IgG4-positive plasmacytes, suggesting IPT. The present case suggests a possible common mechanism in the development of AIP and IPT of the liver.
C1 [Uchida, Kazushige; Miyoshi, Hideaki; Hachimine, Daisaku; Ikeura, Tsukasa; Shimatani, Masaaki; Matsushita, Mitsunobu; Takaoka, Makoto; Okazaki, Kazuichi] Kansai Med Univ, Dept Internal Med 3, Moriguchi, Osaka 570, Japan.
[Satoi, Sohei; Takai, Soichiro] Kansai Med Univ, Dept Surg, Hirakata, Osaka, Japan.
[Ashida, Kiyoshi] Osaka Saiseikai Nakatsu Hosp, Dept Gastroenterol, Osaka, Japan.
C3 Kansai Medical University; Kansai Medical University
RP Uchida, K (corresponding author), Kansai Med Univ, Dept Internal Med 3, Moriguchi, Osaka 570, Japan.
EM uchidak@hirakata.kmu.ac.jp
RI Uchida, Kazushige/AAD-4966-2020
OI Uchida, Kazushige/0000-0002-3160-3184
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NR 14
TC 30
Z9 33
U1 0
U2 1
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
J9 INTERNAL MED
JI Intern. Med.
PY 2007
VL 46
IS 17
BP 1409
EP 1412
DI 10.2169/internalmedicine.46.6430
PG 4
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 343HV
UT WOS:000258845000014
PM 17827840
OA hybrid
DA 2025-01-07
ER
PT J
AU Lleo, A
Colapietro, F
AF Lleo, Ana
Colapietro, Francesca
TI Changes in the Epidemiology of Primary Biliary Cholangitis
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Geoepidemiology; Personalized medicine; Female prevalence; Primary
biliary cholangitis
ID PRIMARY SCLEROSING CHOLANGITIS; GENOME-WIDE ASSOCIATION; ACID-TREATED
PATIENTS; RISK-FACTORS; URSODEOXYCHOLIC ACID; X-CHROMOSOME; BIOCHEMICAL
RESPONSE; SUSCEPTIBILITY LOCI; ANTIMITOCHONDRIAL ANTIBODIES;
HEPATOCELLULAR-CARCINOMA
AB Primary biliary cholangitis (PBC) is considered a model autoimmune disease, characterized by circulating antimitochondrial antibodies and a selective autoimmune destruction of intrahepatic cholangiocytes. PBC is heterogeneous in its presentation, symptomatology, disease progression, and response to therapy. The pathogenesis is still largely unknown, and epidemiologic studies have facilitated the identification of risk factors and the understanding of disease prevalence, geographic variations, heterogeneity, and differences in sex ratio. Recent studies from large international cohorts have better identified prognostic factors, suggesting a change in patient management based on risk-stratification tools to identify subgroups at greatest potential benefit from second-line therapies.
C1 [Lleo, Ana; Colapietro, Francesca] Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini 4, I-20090 Milan, Italy.
[Lleo, Ana] Humanitas Clin & Res Ctr, Liver Unit, Ctr Autoimmune Liver Dis, I-20089 Milan, Italy.
C3 Humanitas University
RP Lleo, A (corresponding author), Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini 4, I-20090 Milan, Italy.
EM ana.lleo@humanitas.it
RI Colapietro, Francesca/LFT-8668-2024; LLEO, Ana/AAA-5759-2019
OI Colapietro, Francesca/0000-0002-7520-744X; LLEO, Ana/0000-0002-0561-7902
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NR 82
TC 20
Z9 21
U1 0
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD AUG
PY 2018
VL 22
IS 3
BP 429
EP +
DI 10.1016/j.cld.2018.03.001
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GP0WC
UT WOS:000440531300002
PM 30259845
DA 2025-01-07
ER
PT J
AU Strauss, O
Dunbar, PR
Bartlett, A
Phillips, A
AF Strauss, Otto
Dunbar, P. Rod
Bartlett, Adam
Phillips, Anthony
TI The immunophenotype of antigen presenting cells of the mononuclear
phagocyte system in normal human liver - A systematic review
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Human; Macrophages; Dendritic cells; Monocytes; Antigen presenting
cells; Mononuclear phagocyte system; Kupffer cell; Review
ID MYELOID DENDRITIC CELLS; SINUSOIDAL ENDOTHELIAL-CELLS; ACUTE CELLULAR
REJECTION; HUMAN KUPFFER CELLS; IMMUNOHISTOCHEMICAL ANALYSIS; CHRONIC
HEPATITIS; HEPATOCELLULAR-CARCINOMA; MACROPHAGE POPULATIONS;
MONOCLONAL-ANTIBODIES; TISSUE DISTRIBUTION
AB The mononuclear phagocytic system (MPS), comprised of monocytes, macrophages, and dendritic cells, is essential in tissue homeostasis and in determining the balance of the immune response through its role in antigen presentation. It has been identified as a therapeutic target in infectious disease, cancer, autoimmune disease and transplant rejection. Here, we review the current understanding of the immunophenotype and function of the MPS in normal human liver. Using well-defined selection criteria, a search of MEDLINE and EMBASE databases identified 76 appropriate studies. The majority (n = 67) described Kupffer cells (KCs), although the definition of KC differs between sources, and little data were available regarding their function. Only 10 papers looked at liver dendritic cells (DCs), and largely confirmed the presence of the major dendritic cell subsets identified in human blood. Monocytes were thoroughly characterized in four studies that utilized flow cytometry and fluorescent microscopy and highlighted their prominent role in liver homeostasis and displayed subtle differences from circulating monocytes. There was some limited evidence that liver DCs are tolerogenic but neither liver dendritic cell subsets nor macrophages have been thoroughly characterized, using either multi-colour flow cytometry or multi-parameter fluorescence microscopy. The lobular distribution of different subsets of liver MPS cells was also poorly described, and the ability to distinguish between passenger leukocytes and tissue resident cells remains limited. It was apparent that further research, using modern immunological techniques, is now required to accurately characterize the cells of the MPS in human liver. (C) 2014 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Strauss, Otto; Bartlett, Adam; Phillips, Anthony] Univ Auckland, Fac Med Hlth Sci, Dept Surg, Auckland 1, New Zealand.
[Strauss, Otto; Dunbar, P. Rod; Bartlett, Adam; Phillips, Anthony] Univ Auckland, Maurice Wilkins Ctr Mol Biodiscovery, Auckland 1, New Zealand.
[Strauss, Otto; Dunbar, P. Rod; Phillips, Anthony] Univ Auckland, Fac Sci, Sch Biol Sci, Auckland 1, New Zealand.
C3 University of Auckland; University of Auckland; University of Auckland
RP Bartlett, A (corresponding author), Univ Auckland, Fac Med Hlth Sci, Dept Surg, Auckland Publ Hosp, Level 12 Support Bldg,Pk Rd, Auckland 1, New Zealand.
EM AdamB@adhb.govt.nz
RI Dunbar, Rod/C-2570-2012; Phillips, Anthony/HNB-5734-2023; Bartlett,
Adam/A-9853-2017
OI Dunbar, Rod/0000-0001-9626-2600
FU Department of Surgery Lectureship grant; Auckland Medical Research
Foundation Doctoral Scholarship; MercyAscot Doctoral Scholarship
FX We are grateful for the funding support from the following grants; the
Department of Surgery Lectureship grant, Auckland Medical Research
Foundation Doctoral Scholarship, MercyAscot Doctoral Scholarship.
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NR 134
TC 46
Z9 58
U1 1
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD FEB
PY 2015
VL 62
IS 2
BP 458
EP 468
DI 10.1016/j.jhep.2014.10.006
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AZ2CZ
UT WOS:000348043600029
PM 25315649
OA hybrid
DA 2025-01-07
ER
PT J
AU Pellicano, R
Ferro, A
Cicerchia, F
Mattivi, S
Fagoonee, S
Durazzo, M
AF Pellicano, Rinaldo
Ferro, Arianna
Cicerchia, Francesca
Mattivi, Simone
Fagoonee, Sharmila
Durazzo, Marilena
TI Autoimmune Hepatitis and Fibrosis
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE autoimmune hepatitis; liver fibrosis; liver diseases
ID REGULATORY T-CELLS; TRANSIENT ELASTOGRAPHY; LIVER FIBROSIS;
DIAGNOSTIC-ACCURACY; MYCOPHENOLATE-MOFETIL; CYCLOSPORINE-A;
HEPATOCELLULAR-CARCINOMA; MONONUCLEAR-CELLS; CLINICAL-PRACTICE; DISEASE
AB Autoimmune hepatitis (AIH) is a chronic immune-inflammatory disease of the liver, generally considered a rare condition. The clinical manifestation is extremely varied and can range from paucisymptomatic forms to severe hepatitis. Chronic liver damage causes activation of hepatic and inflammatory cells leading to inflammation and oxidative stress through the production of mediators. This results in increased collagen production and extracellular matrix deposition leading to fibrosis and even cirrhosis. The gold standard for the diagnosis of fibrosis is liver biopsy; however, there are serum biomarkers, scoring systems, and radiological methods useful for diagnosis and staging. The goal of AIH treatment is to suppress fibrotic and inflammatory activities in the liver to prevent disease progression and achieve complete remission. Therapy involves the use of classic steroidal anti-inflammatory drugs and immunosuppressants, but in recent years scientific research has focused on several new alternative drugs for AIH that will be discussed in the review.
C1 [Pellicano, Rinaldo] Citta Salute & Sci Hosp, Unit Gastroenterol, Cso Bramante 88, I-10126 Turin, Italy.
[Ferro, Arianna; Cicerchia, Francesca; Mattivi, Simone; Durazzo, Marilena] Univ Turin, Dept Med Sci, Cso AM Dogliotti 14, I-10126 Turin, Italy.
[Fagoonee, Sharmila] CNR, Inst Biostruct & Bioimaging, Mol Biotechnol Ctr, I-10126 Turin, Italy.
C3 A.O.U. Citta della Salute e della Scienza di Torino; University of
Turin; Consiglio Nazionale delle Ricerche (CNR); Istituto di
Biostrutture e Bioimmagini (IBB-CNR)
RP Durazzo, M (corresponding author), Univ Turin, Dept Med Sci, Cso AM Dogliotti 14, I-10126 Turin, Italy.
EM marilena.durazzo@unito.it
RI Pellicano, Rinaldo/K-2575-2016; Fagoonee, Sharmila/L-1940-2019
OI DURAZZO, Marilena/0000-0003-2450-5911; PELLICANO,
RINALDO/0000-0003-3438-0649; Mattivi, Simone/0000-0002-5261-718X;
FAGOONEE, SHARMILA/0000-0001-6070-6716
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Xue TX, 2021, PHARMACOL RES, V173, DOI 10.1016/j.phrs.2021.105910
Yasui S, 2011, J GASTROENTEROL, V46, P378, DOI 10.1007/s00535-010-0316-3
Yu ZJ, 2019, EUR J GASTROEN HEPAT, V31, P873, DOI 10.1097/MEG.0000000000001367
Yuan XL, 2019, EUR J GASTROEN HEPAT, V31, P1467, DOI 10.1097/MEG.0000000000001437
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NR 122
TC 10
Z9 10
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD MAR
PY 2023
VL 12
IS 5
AR 1979
DI 10.3390/jcm12051979
PG 18
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 9U2NC
UT WOS:000947553300001
PM 36902767
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Ji, D
Shao, Q
Han, P
Li, F
Li, B
Zang, H
Niu, XX
Li, ZB
Xin, SJ
Chen, GF
AF Ji, Dong
Shao, Qing
Han, Ping
Li, Fan
Li, Bing
Zang, Hong
Niu, Xiaoxia
Li, Zhongbin
Xin, Shaojie
Chen, Guofeng
TI The Frequency and Determinants of Liver Stiffness Measurement Failure: A
Retrospective Study of "Real-Life'' 38,464 Examinations
SO PLOS ONE
LA English
DT Article
ID HEPATITIS-C VIRUS; TRANSIENT ELASTOGRAPHY; DIAGNOSTIC PERFORMANCE;
NONINVASIVE MARKERS; XL PROBE; FIBROSIS; CIRRHOSIS; FIBROSCAN(R);
FEASIBILITY; DISEASE
AB Objective: To investigate the frequency and determinants of liver stiffness measurement (LSM) failure by means of FibroScan in "real-life'' Chinese patients.
Methods: A total of 38,464 "real-life'' Chinese patients in 302 military hospital of China through the whole year of 2013, including asymptomatic carrier, chronic hepatitis B, chronic hepatitis C, liver cirrhosis (LC), alcoholic liver disease, autoimmune liver disease, hepatocellular carcinoma (HCC) and other, were enrolled, their clinical and biological parameters were retrospectively investigated. Liver fibrosis was evaluated by FibroScan detection. S probe (for children with height less than 1.20 m) and M probe (for adults) were used. LSM failure defined as zero valid shots (unsuccessful LSM), or the ratio of the interquartile range to the median of 10 measurements (IQR/M) greater than 0.30 plus median LSM greater or equal to 7.1 kPa (unreliable LSM).
Results: LSM failure occurred in 3.34% of all examinations (1286 patients out of 38,464), among them, there were 958 cases (2.49%) with unsuccessful LSM, and 328 patients (0.85%) with unreliable LSM. Statistical analyses showed that LSM failure was independently associated with body mass index (BMI) greater than 30 kg/m(2), female sex, age greater than 50 years, intercostal spaces (IS) less than 9 mm, decompensated liver cirrhosis and HCC patients. There were no significant differences among other diseases. By changing another skilled operator, success was achieved on 301 cases out of 1286, which reduced the failure rate to 2.56%, the decrease was significant (P<0.0001).
Conclusions: The principal reasons of LSM failure are ascites, obesity and narrow of IS. The failure rates of HCC, decompensated LC, elder or female patients are higher. These results emphasize the need for adequate operator training, technological improvements and optimal criteria for specific patient subpopulations.
C1 [Ji, Dong; Shao, Qing; Li, Fan; Li, Bing; Niu, Xiaoxia; Li, Zhongbin; Chen, Guofeng] 302 Mil Hosp China, Liver Fibrosis Diag & Treatment Ctr, Beijing, Peoples R China.
[Han, Ping] 302 Mil Hosp China, Tumor Radiotherapy Ctr, Beijing, Peoples R China.
[Zang, Hong; Xin, Shaojie] 302 Mil Hosp China, Liver Failure Diag & Treatment Ctr, Beijing, Peoples R China.
C3 Fifth Medical Center of Chinese PLA General Hospital; Fifth Medical
Center of Chinese PLA General Hospital; Fifth Medical Center of Chinese
PLA General Hospital
RP Xin, SJ (corresponding author), 302 Mil Hosp China, Liver Failure Diag & Treatment Ctr, Beijing, Peoples R China.
EM XinShaojie302@163.com; bjchen302@aliyun.com
RI Li, Fan/GRX-7461-2022; Li, Zhongbin/J-5387-2014; Ji, Dong/AAF-6364-2019
OI Ji, Dong/0000-0001-8214-462X
FU Beijing Natural Science Foundation [7122177]; National Natural Science
Foundation of China [81371799]
FX This work was supported by Beijing Natural Science Foundation (7122177,
http://www.bjnsf.org/) and National Natural Science Foundation of China
(81371799, http://www.nsfc.gov.cn/). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
CR Afdhal Nezam H, 2012, Gastroenterol Hepatol (N Y), V8, P605
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NR 37
TC 10
Z9 13
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 14
PY 2014
VL 9
IS 8
AR e105183
DI 10.1371/journal.pone.0105183
PG 6
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AO0QT
UT WOS:000341017000103
PM 25122123
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Coukos, A
Vionnet, J
Obeid, M
Bouchaab, H
Peters, S
Latifyan, S
Wicky, A
Michielin, O
Chtioui, H
Moradpour, D
Fasquelle, F
Sempoux, C
Fraga, M
AF Coukos, Alexander
Vionnet, Julien
Obeid, Michel
Bouchaab, Hasna
Peters, Solange
Latifyan, Sofiya
Wicky, Alexandre
Michielin, Olivier
Chtioui, Haithem
Moradpour, Darius
Fasquelle, Francois
Sempoux, Christine
Fraga, Montserrat
TI Systematic comparison with autoimmune liver disease identifies specific
histological features of immune checkpoint inhibitor-related adverse
events
SO JOURNAL FOR IMMUNOTHERAPY OF CANCER
LA English
DT Article
DE immunotherapy; cytotoxicity; immunologic; programmed cell death 1
receptor; CTLA-4 antigen; autoimmunity
ID PREEXISTING AUTOIMMUNE; ADVANCED MELANOMA; CLINICOPATHOLOGICAL FEATURES;
IPILIMUMAB; NIVOLUMAB; THERAPY; CANCER; PEMBROLIZUMAB; MANAGEMENT;
PATHWAYS
AB Background Immune checkpoint inhibitors (ICIs) have become a mainstay of cancer treatment. Their immune-boosting quality has one major drawback, their proclivity to induce a broad array of immune-related adverse events (irAEs) affecting, among others, the liver and sharing some similarities with classic autoimmune liver diseases (AILD).We aimed to compare clinical, laboratory and histological features of patients with liver-related irAEs and AILD. Methods We systematically compared liver irAEs with AILD, namely autoimmune hepatitis (AIH) and primary biliary cholangitis, regarding their clinical, laboratory, and histological features. Results Twenty-seven patients with liver irAEs (ICI group) and 14 patients with AILD were identified. We observed three distinct ICI-induced histological liver injury patterns: hepatitic (52%), cholangitic (19%), and mixed (29%). When comparing the ICI and AILD groups, centrilobular injury as well as granuloma formation were more prevalent in the former (p=0.067 and 0.002, respectively). CD4+/CD8+ T cell ratios were heterogeneous between the two groups, without statistically significant difference but with a trend toward increased CD8+ T cells among hepatitic irAEs as compared with AIH. Pattern of liver function test alteration was predictive for the type of irAEs but did not correlate with histological severity. Conclusions Liver irAEs have broad clinical, laboratory and histological presentations. Histological features of irAEs and AILD are distinct, likely underpinning their different immunological mechanisms.
C1 [Coukos, Alexander; Vionnet, Julien; Moradpour, Darius; Fraga, Montserrat] CHU Vaudois, Gastroenterol & Hepatol, Lausanne, Switzerland.
[Vionnet, Julien] CHU Vaudois, Transplantat Ctr, Lausanne, Switzerland.
[Obeid, Michel] CHU Vaudois, Immunol Div, Lausanne, Switzerland.
[Bouchaab, Hasna; Peters, Solange; Latifyan, Sofiya; Wicky, Alexandre] CHU Vaudois, Dept Med Oncol, Lausanne, Switzerland.
[Michielin, Olivier] Lausanne Univ Hosp, Dept Med Oncol, Lausanne, Switzerland.
[Chtioui, Haithem] CHU Vaudois, Div Clin Pharmacol, Lausanne, Switzerland.
[Fasquelle, Francois; Sempoux, Christine] CHU Vaudois, Dept Pathol, Lausanne, Switzerland.
C3 University of Lausanne; Centre Hospitalier Universitaire Vaudois (CHUV);
University of Lausanne; Centre Hospitalier Universitaire Vaudois (CHUV);
University of Lausanne; Centre Hospitalier Universitaire Vaudois (CHUV);
University of Lausanne; Centre Hospitalier Universitaire Vaudois (CHUV);
University of Lausanne; Centre Hospitalier Universitaire Vaudois (CHUV);
University of Lausanne; Centre Hospitalier Universitaire Vaudois (CHUV);
University of Lausanne; Centre Hospitalier Universitaire Vaudois (CHUV)
RP Fraga, M (corresponding author), CHU Vaudois, Gastroenterol & Hepatol, Lausanne, Switzerland.
EM Montserrat.Fraga@chuv.ch
RI Wicky, Alexandre/JOJ-6559-2023; OBEID, Pr Michel/HCI-9145-2022;
Michielin, Olivier/JAO-0968-2023; Fasquelle, François/AAE-7818-2021
OI Chtioui, Haithem/0000-0003-3821-6942; Coukos,
Alexander/0000-0003-4869-3160; Obeid, Michel/0000-0003-2095-2677;
Peters, Solange/0000-0002-0412-7143; Michielin,
Olivier/0000-0003-4926-6355
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NR 50
TC 19
Z9 20
U1 0
U2 5
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 2051-1426
J9 J IMMUNOTHER CANCER
JI J. Immunother. Cancer
PD OCT
PY 2022
VL 10
IS 10
AR e005635
DI 10.1136/jitc-2022-005635
PG 12
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA 5Y6KM
UT WOS:000879391200003
PM 36283734
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Matsuoka, N
Kozuru, H
Koga, T
Abiru, S
Yamasaki, K
Komori, A
Fujita, Y
Tenmoku, J
Asano, T
Sato, S
Suzuki, E
Furuya, M
Kobayashi, H
Watanabe, H
Naganuma, A
Yoshizawa, K
Shimada, M
Ario, K
Yamashita, H
Kohno, H
Kaneyoshi, T
Nakamura, M
Furukawa, H
Takahashi, A
Kawakami, A
Ohira, H
Yatsuhashi, H
Migita, K
AF Matsuoka, Naoki
Kozuru, Hideko
Koga, Tomohiro
Abiru, Seigo
Yamasaki, Kazumi
Komori, Atsumasa
Fujita, Yuya
Tenmoku, Junpei
Asano, Tomoyuki
Sato, Shuzo
Suzuki, Eiji
Furuya, Makiko
Kobayashi, Hiroko
Watanabe, Hiroshi
Naganuma, Atsushi
Yoshizawa, Kaname
Shimada, Masaaki
Ario, Keisuke
Yamashita, Haruhiro
Kohno, Hiroshi
Kaneyoshi, Toshihiko
Nakamura, Minoru
Furukawa, Hiroshi
Takahashi, Atsushi
Kawakami, Atsushi
Ohira, Hiromasa
Yatsuhashi, Hiroshi
Migita, Kiyoshi
TI Galectin-9 in autoimmune hepatitis Correlation between serum levels of
galectin-9 and M2BPGi in patients with autoimmune hepatitis
SO MEDICINE
LA English
DT Article
DE autoimmune hepatitis; CXCL10; cytokine; galectin-9; M2BPGi; systemic
lupus erythematosus
ID CELLS; DIAGNOSIS; IMMUNITY; TIM-3
AB Autoimmune hepatitis (AIH) is a disorder of unknown etiology in which immune-mediated liver damage progresses to cirrhosis or hepatocellular carcinoma (HCC). The mainstay therapy for AIH is steroids and other immunosuppressive treatments. Currently, there are no validated markers for monitoring immune-mediated hepatic inflammation. Galectin-9 has recently been identified as a potential biomarker in patients with chronic liver disease. The objective of this study was to determine whether Galectin-9 and other serum proteins are associated with active disease in AIH patients.
We enrolled 77 Japanese patients with well-documented AIH who were identified from the National Hospital Organization-AIH-liver-network database, as well as 32 patients with chronic hepatitis C (CHC), 27 patients with SLE, and 17 healthy control subjects.
Serum levels of galectin-9, and markers of liver injury were measured and compared between groups. Serum levels of galectin-9 were significantly higher in AIH patients than in CHC patients (13.8 +/- 4.9ng/mL vs 8.9 +/- 3.0ng/mL, P<.001) or healthy controls (13.8 +/- 4.9ng/mL vs 5.0 +/- 1.3ng/mL, P<.001). In AIH group, serum galectin-9 levels weakly correlated with alanine aminotransferase levels or total bilirubin (TB) and strongly correlated with C-X-C motif chemokine 10 (CXCL10) and Mac-2 binding protein glycosylation isomer (M2BPGi) levels, but did not correlate with the histological grade of liver fibrosis. Steroid treatment of AIH patients significantly reduced serum galectin-9 levels (14.1 +/- 4.9ng/mL vs 8.3 +/- 3.8 ng/mL, P<.001). SLE patients exhibited higher galectin-9 levels, whereas the galectin-9 levels did not correlate with liver function tests such as alanine aminotransferase levels.
Serum galectin-9 correlated with disease status in AIH patients and could thus be useful biomarkers to detect hepatic autoimmunity. Because circulating galectin-9 reflects autoimmune-mediated inflammation, it may have additional utility as a biomarker for other autoimmune disorders.
C1 [Matsuoka, Naoki; Kozuru, Hideko; Abiru, Seigo; Yamasaki, Kazumi; Komori, Atsumasa; Yatsuhashi, Hiroshi; Migita, Kiyoshi] Nagasaki Med Ctr, Clin Res Ctr, Nagasaki, Japan.
[Matsuoka, Naoki; Fujita, Yuya; Tenmoku, Junpei; Asano, Tomoyuki; Sato, Shuzo; Suzuki, Eiji; Furuya, Makiko; Kobayashi, Hiroko; Watanabe, Hiroshi; Migita, Kiyoshi] Fukushima Med Univ, Dept Rheumatol, Fukushima, Japan.
[Koga, Tomohiro; Kawakami, Atsushi] Nagasaki Univ, Grad Sch Biomed Sci, Unit Translat Med, Dept Immunol & Rheumatol, Nagasaki, Japan.
[Naganuma, Atsushi] Natl Hosp Org, Takasaki Med Ctr, Takasaki, Gunma, Japan.
[Yoshizawa, Kaname] Natl Hosp Org, Shinsyu Ueda Med Ctr, Ueda, Nagano, Japan.
[Shimada, Masaaki] Natl Hosp Org, Nagoya Med Ctr, Nagoya, Aichi, Japan.
[Ario, Keisuke] Natl Hosp Org, Ureshino Med Ctr, Saga, Japan.
[Yamashita, Haruhiro] Natl Hosp Org, Okayama Med Ctr, Okayama, Japan.
[Kohno, Hiroshi] Natl Hosp Org, Kure Med Ctr, Kure, Japan.
[Kaneyoshi, Toshihiko] Natl Hosp Org, Fukuyama Med Ctr, Fukuyama, Hiroshima, Japan.
[Nakamura, Minoru] Nagasaki Univ, Grad Sch Biomed Sci, Dept Hepatol, Nagasaki, Japan.
[Furukawa, Hiroshi] Univ Tsukuba, Fac Med, Mol & Genet Epidemiol Lab, Tsukuba, Ibaraki, Japan.
[Takahashi, Atsushi; Ohira, Hiromasa] Fukushima Med Univ, Dept Gastroenterol, Fukushima, Japan.
C3 Fukushima Medical University; Nagasaki University; Nagoya Medical
Center; Nagasaki University; University of Tsukuba; Fukushima Medical
University
RP Migita, K (corresponding author), Fukushima Med Univ, Sch Med, Dept Rheumatol, 1 Hikarigaoka, Fukushima, Fukushima 9601295, Japan.
EM migita@fmu.ac.jp
RI Koga, Tomohiro/AAU-9697-2020; Kawakami, Atsushi/D-3785-2019; Sato,
Shuzo/AAC-7025-2019
OI Asano, Tomoyuki/0009-0005-6538-1881; Koga, Tomohiro/0000-0003-2077-4428;
Sato, Shuzo/0000-0002-8110-8261; Naganuma, Atsushi/0000-0003-0663-0102
FU National Hospital Organization
FX This work was supported by a grant from the National Hospital
Organization.
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NR 29
TC 13
Z9 13
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD AUG
PY 2019
VL 98
IS 35
AR e16924
DI 10.1097/MD.0000000000016924
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA IY2RU
UT WOS:000486239900040
PM 31464928
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Puri, P
Malik, S
AF Puri, Pankaj
Malik, Sarthak
TI Liver Transplantation: Contraindication and Ineligibility
SO JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
LA English
DT Review
DE liver transplantation; contraindications; ineligibility; chronic liver
disease; acute liver failure
ID PRIMARY BILIARY-CIRRHOSIS; CORONARY-ARTERY-DISEASE; PRIMARY SCLEROSING
CHOLANGITIS; SEVERE AUTOIMMUNE HEPATITIS; BUDD-CHIARI-SYNDROME; C
VIRUS-INFECTION; HEPATOCELLULAR-CARCINOMA; BIOCHEMICAL RESPONSE;
NATURAL-HISTORY; CARDIOVASCULAR RISK
AB Liver transplantation (LT) is a life-saving therapeutic modality for patients with various advanced liver diseases. It is crucial to identify that the patient's illness is sufficiently advanced and unlikely to improve with medical management to justify the need for transplantation. At the same time, it is crucial to identify patients with co-morbidities and far advanced disease that would result in an unacceptable outcome after LT. Specific care also is required before deciding on LT in the elderly, acute on chronic liver disease, patients with comorbidities, and hepatocellular carcinoma. Transplantation needs to be timed appropriately to avoid unnecessary LT and ensure that the decision is not left too late to avoid losing the patient without a transplant. Also, important is the decision as to when not to transplant. The current review explores some of these issues of contraindications and ineligibility for LT. ( J CLIN EXP HEPATOL 2023;13:1116-1129)
C1 [Puri, Pankaj] Fortis Escorts Hosp, Fortis Escorts Liver & Digest Dis Inst, New Delhi 110025, India.
[Malik, Sarthak] Manipal Hosp, Dept Gastroenterol, New Delhi 110075, India.
[Puri, Pankaj] Fortis Escorts Hosp, Fortis Escorts Liver & Digest Dis Inst, Okhla Rd, New Delhi 110025, India.
C3 Fortis Escorts Hospital; Fortis Escorts Hospital
RP Puri, P (corresponding author), Fortis Escorts Hosp, Fortis Escorts Liver & Digest Dis Inst, Okhla Rd, New Delhi 110025, India.
EM puripankaj@gmail.com
RI Puri, Pankaj/KYQ-4180-2024
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NR 117
TC 1
Z9 1
U1 0
U2 2
PU ELSEVIER - DIVISION REED ELSEVIER INDIA PVT LTD
PI NEW DELHI
PA 17-A/1 MAIN RING ROAD, LAJPAT NAGAR IV, NEW DELHI, 110024, INDIA
SN 0973-6883
EI 2213-3453
J9 J CLIN EXP HEPATOL
JI J. Clin. Exp. Hepatol.
PD NOV-DEC
PY 2023
VL 13
IS 6
BP 1116
EP 1129
DI 10.1016/j.jceh.2023.04.005
EA NOV 2023
PG 14
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA Y7GX4
UT WOS:001106919700001
PM 37975058
DA 2025-01-07
ER
PT J
AU Shin, SW
Kim, Y
Jeong, WK
Kim, J
Kim, MY
Oh, YH
Pyo, JY
AF Shin, Sang-Wook
Kim, Yongsoo
Jeong, Woo Kyoung
Kim, Jinoo
Kim, Min Yeong
Oh, Young Ha
Pyo, Ju Yeon
TI Isolated IgG4-related cholecystitis mimicking gallbladder cancer: a case
report
SO CLINICAL IMAGING
LA English
DT Article
DE Cholecystitis; IgG4-related sclerosing disease; Pancreas; Computed
tomography; Magnetic resonance
ID AUTOIMMUNE PANCREATITIS; SCLEROSING DISEASE
AB A 58-year-old man with right upper quadrant pain was referred to the radiology department. The patient underwent computed tomography and magnetic resonance imaging, which suggested the diagnosis of gallbladder cancer invading the liver. After surgical removal of the gallbladder, and the adjacent liver parenchyma was performed, the histologic diagnosis of IgG4-related cholecystitis was made. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Shin, Sang-Wook; Kim, Yongsoo; Jeong, Woo Kyoung; Kim, Jinoo; Kim, Min Yeong] Hanyang Univ, Guri Hosp, Dept Radiol, Guri Si 471701, Kyounggi Do, South Korea.
[Oh, Young Ha; Pyo, Ju Yeon] Hanyang Univ, Guri Hosp, Dept Pathol, Guri Si 471701, Kyounggi Do, South Korea.
C3 Hanyang University; Hanyang University
RP Kim, Y (corresponding author), Hanyang Univ, Guri Hosp, Dept Radiol, Guri Si 471701, Kyounggi Do, South Korea.
EM ysookim@hanyang.ac.kr
RI Kim, Seung/T-5133-2017; Kim, Ho Cheol/LIJ-9487-2024; Kim,
Minyeong/JHU-5269-2023; Jeong, Woo/ABE-7025-2021
OI Kim, Jinoo/0000-0001-7238-2528
CR Abraham SC, 2003, AM J SURG PATHOL, V27, P441, DOI 10.1097/00000478-200304000-00003
Detlefsen S, 2009, SCAND J GASTROENTERO, V44, P1391, DOI 10.3109/00365520903358881
Kamisawa T, 2003, J GASTROENTEROL, V38, P982, DOI 10.1007/s00535-003-1175-y
Kamisawa T, 2008, WORLD J GASTROENTERO, V14, P3948, DOI 10.3748/wjg.14.3948
Kamisawa T, 2006, WORLD J GASTROENTERO, V12, P3736, DOI 10.3748/wjg.v12.i23.3736
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Soyer P, 1997, AM J ROENTGENOL, V169, P781, DOI 10.2214/ajr.169.3.9275896
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Wang WL, 2009, HISTOPATHOLOGY, V54, P829, DOI 10.1111/j.1365-2559.2009.03315.x
NR 9
TC 14
Z9 16
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0899-7071
J9 CLIN IMAG
JI Clin. Imaging
PD SEP-OCT
PY 2013
VL 37
IS 5
BP 969
EP 971
DI 10.1016/j.clinimag.2013.01.015
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 220TS
UT WOS:000324610400031
PM 23751265
DA 2025-01-07
ER
PT J
AU Lakkasani, S
Jagirdhar, GSK
Qirem, M
Digiacomo, SW
Pantula, S
AF Lakkasani, Saraswathi
Jagirdhar, Gowthami Sai Kogilathota
Qirem, Murad
Digiacomo, Scott W.
Pantula, Srinivasa
TI A Rare Case of Primary Sclerosing Cholangitis Overlapped With Autoimmune
Hepatitis and Ulcerative Colitis
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE autoimmune hepatitis; cholestasis; ursodeoxycholic acid; ulcerative
colitis; primary sclerosing cholangitis (psc)
ID INFLAMMATORY-BOWEL-DISEASE; HEPATOBILIARY MANIFESTATIONS
AB Primary sclerosing cholangitis (PSC) is a liver disease of idiopathic origin, displaying a diverse and varied nature, which leads to cholestasis. It is characterized by continuous, advancing inflammation and fibrosis in the bile ducts. PSC is closely linked with inflammatory bowel disease and poses a risk for colon, bile duct, and gallbladder cancer. Unfortunately, there is currently no effective medical treatment available for this condition. In some cases, the disease may progress to end-stage liver failure, making liver transplantation a possible necessity for affected individuals. PSC association with autoimmune hepatitis (AIH) is very rare. This is a case of PSC that is overlapped with AIH. Screening colonoscopy showed colitis, and a biopsy was consistent with ulcerative colitis without any colitis symptoms, emphasizing the need for ruling out any other associated conditions, which respond well to the effective treatment to avoid morbidity and mortality in PSC.
C1 [Lakkasani, Saraswathi] St Michaels Hosp, Gastroenterol, Newark, NJ 07102 USA.
[Jagirdhar, Gowthami Sai Kogilathota] Harvard Med Sch, Res, Boston, MA USA.
[Jagirdhar, Gowthami Sai Kogilathota] St Michaels Hosp, Internal Med, Newark, NJ USA.
[Qirem, Murad] St Michaels Hosp, Med Educ, Newark, NJ USA.
[Digiacomo, Scott W.] St Michaels Hosp, Gastroenterol & Hepatol, Newark, NJ USA.
[Pantula, Srinivasa] Prime Healthcare, Gen Med, Ontario, CA USA.
C3 Harvard University; Harvard Medical School
RP Lakkasani, S (corresponding author), St Michaels Hosp, Gastroenterol, Newark, NJ 07102 USA.
EM dr.saraswathi.l@gmail.com
RI Lakkasani, Saraswathi/KIJ-0653-2024
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NR 13
TC 0
Z9 0
U1 0
U2 1
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD AUG 13
PY 2023
VL 15
IS 8
DI 10.7759/cureus.43403
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA P8EF0
UT WOS:001052940500038
PM 37706140
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Drummer, C
Saaoud, F
Jhala, NC
Cueto, R
Sun, Y
Xu, KM
Shao, Y
Lu, YF
Shen, HM
Yang, L
Zhou, Y
Yu, J
Wu, S
Snyder, NW
Hu, WH
Zhuo, JJ
Zhong, YH
Jiang, XH
Wang, H
Yang, XF
AF Drummer, Charles
Saaoud, Fatma
Jhala, Nirag C.
Cueto, Ramon
Sun, Yu
Xu, Keman
Shao, Ying
Lu, Yifan
Shen, Huimin
Yang, Ling
Zhou, Yan
Yu, Jun
Wu, Sheng
Snyder, Nathaniel W.
Hu, Wenhui
Zhuo, Jia Joe
Zhong, Yinghui
Jiang, Xiaohua
Wang, Hong
Yang, Xiaofeng
TI Caspase-11 promotes high-fat diet-induced NAFLD by increasing
glycolysis, OXPHOS, and pyroptosis in macrophages
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis
(NASH); caspase-11; inflammation; pyroptosis
ID LIVER-DISEASE; NONALCOHOLIC STEATOHEPATITIS; ENDOTHELIAL-CELLS;
INFLAMMASOME ACTIVATION; UNITED-STATES; FIBROSIS; EXPRESSION; BURDEN;
DIFFERENTIATION; CENICRIVIROC
AB Introduction: Non-alcoholic fatty liver disease (NAFLD) has a global prevalence of 25% of the population and is a leading cause of cirrhosis and hepatocellular carcinoma. NAFLD ranges from simple steatosis (non-alcoholic fatty liver) to non-alcoholic steatohepatitis (NASH). Hepatic macrophages, specifically Kupffer cells (KCs) and monocyte-derived macrophages, act as key players in the progression of NAFLD. Caspases are a family of endoproteases that provide critical connections to cell regulatory networks that sense disease risk factors, control inflammation, and mediate inflammatory cell death (pyroptosis). Caspase-11 can cleave gasdermin D (GSDMD) to induce pyroptosis and specifically defends against bacterial pathogens that invade the cytosol. However, it's still unknown whether high fat diet (HFD)-facilitated gut microbiota- generated cytoplasmic lipopolysaccharides (LPS) activate caspase-11 and promote NAFLD.
Methods: To examine this hypothesis, we performed liver pathological analysis, RNA- seq, FACS, Western blots, Seahorse mitochondrial stress analyses of macrophages and bone marrow transplantation on HFD-induced NAFLD in WT and Casp11-/- mice.
Results and Discussion: Our results showed that 1) HFD increases body wight, liver wight, plasma cholesterol levels, liver fat deposition, and NAFLD activity score (NAS score) in wild-type (WT) mice; 2) HFD increases the expression of caspase-11, GSDMD, interleukin-1b, and guanylate-binding proteins in WT mice; 3) Caspase-11 deficiency decreases fat liver deposition and NAS score; 4) Caspase-11 deficiency decreases bone marrow monocyte-derived macrophage (MDM) pyroptosis (inflammatory cell death) and inflammatory monocyte ( IM) surface GSDMD expression; 5) Caspase-11 deficiency re- programs liver transcriptomes and reduces HFD-induced NAFLD; 6) Caspase-11 deficiency decreases extracellular acidification rates (glycolysis) and oxidative phosphorylation (OXPHOS) in inflammatory fatty acid palmitic acid-stimulated macrophages, indicating that caspase-11 significantly contributes to maintain dual fuel bioenergetics-glycolysis and OXPHOS for promoting pyroptosis in macrophages. These results provide novel insights on the roles of the caspase- 11-GSDMD pathway in promoting hepatic macrophage inflammation and pyroptosis and novel targets for future therapeutic interventions involving the transition of NAFLD to NASH, hyperlipidemia, type II diabetes, metabolic syndrome, metabolically healthy obesity, atherosclerotic cardiovascular diseases, autoimmune diseases, liver transplantation, and hepatic cancers.
C1 [Drummer, Charles; Saaoud, Fatma; Sun, Yu; Xu, Keman; Shao, Ying; Lu, Yifan; Yang, Xiaofeng] Temple Univ, Ctr Cardiovasc Res, Lewis Katz Sch Med, Philadelphia, PA 19122 USA.
[Jhala, Nirag C.] Temple Univ, Dept Pathol & Lab Med, Lewis Katz Sch Med, Philadelphia, PA USA.
[Cueto, Ramon; Shen, Huimin; Yu, Jun; Wu, Sheng; Snyder, Nathaniel W.; Hu, Wenhui; Jiang, Xiaohua; Wang, Hong; Yang, Xiaofeng] Temple Univ, Metab Dis Res & Thrombosis Res Ctr, Dept Cardiovasc Sci, Lewis Katz Sch Med, Philadelphia, PA 19122 USA.
[Yang, Ling] Temple Univ, Dept Med Genet & Mol Biochem, Lewis Katz Sch Med, Philadelphia, PA USA.
[Zhou, Yan] Temple Hlth, Fox Chase Canc Ctr, Biostat & Bioinformat Facil, Philadelphia, PA USA.
[Zhuo, Jia Joe] Tulane Univ, Tulane Hypertens & Renal Ctr Excellence, Sch Med, New Orleans, LA USA.
[Zhong, Yinghui] Drexel Univ, Sch Biomed Engn Sci & Hlth Syst, Philadelphia, PA USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); Temple
University; Pennsylvania Commonwealth System of Higher Education
(PCSHE); Temple University; Pennsylvania Commonwealth System of Higher
Education (PCSHE); Temple University; Pennsylvania Commonwealth System
of Higher Education (PCSHE); Temple University; Fox Chase Cancer Center;
Tulane University; Drexel University
RP Yang, XF (corresponding author), Temple Univ, Ctr Cardiovasc Res, Lewis Katz Sch Med, Philadelphia, PA 19122 USA.; Yang, XF (corresponding author), Temple Univ, Metab Dis Res & Thrombosis Res Ctr, Dept Cardiovasc Sci, Lewis Katz Sch Med, Philadelphia, PA 19122 USA.
EM xfyang@temple.edu
RI XU, KEMAN/JJC-6529-2023; 仲, 英惠/HZH-3357-2023
OI Hu, Wenhui/0000-0001-8152-6116; Lu, Yifan/0000-0003-4461-0698
FU National Institutes of Health (NIH)/National Heart, Lung, and Blood
Institute [HL131460, HL132399, HL138749, HL147565, DK104116, DK113775]
FX Funding Our research activities are supported by grants from the
National Institutes of Health (NIH)/National Heart, Lung, and Blood
Institute (HL131460, HL132399, HL138749, HL147565, DK104116, and
DK113775). The content in this article is solely the responsibility of
the authors and does not necessarily represent the official views of the
NIH. We are very grateful to Dr. Edward A. Miao in the Department of
Immunology at Duke University School of Medicine for his most insightful
advices and corrections.
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NR 145
TC 33
Z9 34
U1 6
U2 30
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 26
PY 2023
VL 14
AR 1113883
DI 10.3389/fimmu.2023.1113883
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 8S7JS
UT WOS:000928753600001
PM 36776889
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Zwolak, A
Jastrzebska, I
Surdacka, A
Kasztelan-Szczerbinska, B
Lozowski, CT
Rolinski, J
Skrzydio-Radomanska, B
Radwan, P
Daniluk, J
AF Zwolak, A.
Jastrzebska, I.
Surdacka, A.
Kasztelan-Szczerbinska, B.
Lozowski, C. T.
Rolinski, J.
Skrzydio-Radomanska, B.
Radwan, P.
Daniluk, J.
TI Peripheral blood dendritic cells in alcoholic and autoimmune liver
disorders
SO HUMAN & EXPERIMENTAL TOXICOLOGY
LA English
DT Article
DE dendritic cells; alcoholic liver disease; autoimmune hepatitis; primary
biliary cirrhosis; immunotoxicology/immunology; hepatic toxicology
ID PRIMARY BILIARY-CIRRHOSIS; CHRONIC ETHANOL INGESTION; C VIRUS-INFECTION;
IN-VITRO; IL-12 PRODUCTION; HEPATITIS; SUBSETS; CONSUMPTION; ACTIVATION;
EXPRESSION
AB Little is known about effects of alcohol consumption on dendritic cell (DC) function and resultant immune response. However, quantitative and qualitative disturbances of DCs are speculated to be involved in alcohol-related as well as in other liver pathology. The present study aimed to evaluate changes in circulating DC subsets in alcoholic liver disease (N = 43), autoimmune hepatitis (N = 26) and primary biliary cirrhosis (N = 20). DCs isolated from the peripheral blood of recruited participants were stained with monoclonal antibodies against blood dendritic cell antigens (BDCAs) and estimated using the flow cytometry. Myeloid DCs were defined as BDCA-1(+)/CD19(-) cells, and lymphoid DCs as BDCA-2(+)/CD123(+) cells. Total numbers of circulating DCs in subjects with some liver diseases were markedly lower than in the healthy participants (p = 0.03). There was a significantly lower percentage of circulating BDCA-2(+)/CD123(+) (p = 0.02), and a tendency for the percentage of circulating BDCA-1(+)/CD19(-) cells to decrease in patients with liver diseases compared to the controls (p = 0.09). These results may suggest that decreased numbers of DCs may be responsible for reduced adaptive immune responses and increased susceptibility to infections and cancer development observed in patients exposed to alcohol. Moreover, numerical abnormalities of DCs may contribute to the breakdown of self-tolerance, a feature of autoimmune diseases.
C1 [Zwolak, A.; Jastrzebska, I.; Daniluk, J.] Med Univ Lublin, Dept Internal Med & Internal Med Nursing, PL-20954 Lublin, Poland.
[Surdacka, A.; Rolinski, J.] Med Univ Lublin, Dept Clin Immunol, PL-20954 Lublin, Poland.
[Kasztelan-Szczerbinska, B.; Lozowski, C. T.; Skrzydio-Radomanska, B.; Radwan, P.; Daniluk, J.] Med Univ Lublin, Dept & Clin Gastroenterol, PL-20954 Lublin, Poland.
C3 Medical University of Lublin; Medical University of Lublin; Medical
University of Lublin
RP Zwolak, A (corresponding author), Med Univ Lublin, Dept Internal Med & Internal Med Nursing, 8 Jaczewskiego Str, PL-20954 Lublin, Poland.
EM zwolakag@wp.pl
RI Rolinski, Jacek/K-5178-2013; Kasztelan-Szczerbinska, Beata/H-2854-2019;
Jastrzebska, Iwona/U-7175-2018
OI Rolinski, Jacek Mariusz/0000-0001-5596-2651; Zwolak,
Agnieszka/0000-0002-2556-4705; Kasztelan-Szczerbinska,
Beata/0000-0002-7198-4428; Rolinski, Jacek/0000-0003-4841-6120; Daniluk,
Jadwiga/0000-0002-0635-2221; Surdacka, Agata/0000-0002-0307-7535;
Jastrzebska, Iwona/0000-0002-4808-6275
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Zhu XY, 2004, ALCOHOL, V32, P91, DOI 10.1016/j.alcohol.2004.01.004
NR 35
TC 4
Z9 4
U1 0
U2 12
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0960-3271
J9 HUM EXP TOXICOL
JI Hum. Exp. Toxicol.
PD MAY
PY 2012
VL 31
IS 5
BP 438
EP 446
DI 10.1177/0960327111426582
PG 9
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA 935WH
UT WOS:000303552400002
PM 22076495
OA Bronze
DA 2025-01-07
ER
PT J
AU White, FV
Dehner, LR
AF White, FV
Dehner, LR
TI Viral diseases of the liver in children: Diagnostic and differential
diagnostic considerations
SO PEDIATRIC AND DEVELOPMENTAL PATHOLOGY
LA English
DT Review
DE hepatitis; liver disease; hepatotropic viruses; pediatric; childhood
ID CHRONIC HEPATITIS-C; PARVOVIRUS B19 INFECTION; GIANT-CELL HEPATITIS; B
VIRUS-INFECTION; PRIMARY HEPATOCELLULAR-CARCINOMA; HUMAN HERPESVIRUS-6
INFECTION; IMMUNE-DEFICIENCY-SYNDROME; AUTOIMMUNE-HEPATITIS;
FULMINANT-HEPATITIS; SPORADIC HEPATITIS
AB This review summarizes the general histologic features of acute and chronic hepatitides and highlights those morphologic findings that may suggest or be diagnostic of a specific agent or etiology. The main epidemiologic, clinical, and pathologic features of the hepatotropic viruses are discussed, with an emphasis on pediatric studies and the differential diagnosis of hepatitis in childhood.
C1 Washington Univ, Med Ctr, St Louis Childrens Hosp,Dept Pathol & Immunol, Lauren V Ackerman Lab Surg Pathol, St Louis, MO 63110 USA.
C3 Washington University (WUSTL); St. Louis Children's Hospital
RP Washington Univ, Med Ctr, St Louis Childrens Hosp,Dept Pathol & Immunol, Lauren V Ackerman Lab Surg Pathol, 660 S Euclid Ave, St Louis, MO 63110 USA.
EM fwhite@path.wustl.edu
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NR 110
TC 11
Z9 11
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1093-5266
EI 1615-5742
J9 PEDIATR DEVEL PATHOL
JI Pediatr. Dev. Pathol.
PD NOV-DEC
PY 2004
VL 7
IS 6
BP 552
EP 567
DI 10.1007/s10024-004-8101-z
PG 16
WC Pathology; Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Pediatrics
GA 883QU
UT WOS:000226031600001
PM 15630523
DA 2025-01-07
ER
PT J
AU Novotny, I
Díte, P
Lata, J
Nechutová, H
Kianicka, B
AF Novotny, I.
Dite, P.
Lata, J.
Nechutova, H.
Kianicka, B.
TI Autoimmune Pancreatitis - Recent Advances
SO DIGESTIVE DISEASES
LA English
DT Article
DE Autoimmune pancreatitis; IgG4-related sclerosing disease; Corticosteroid
therapy; Granulocyte epithelial lesion
ID DIAGNOSTIC-CRITERIA; DISEASE; PROPOSAL; CANCER; EPIDEMIOLOGY;
PATHOGENESIS
AB Autoimmune pancreatitis (AIP) is recognized as a distinct clinical entity, identified as a chronic inflammatory process of the pancreas in which the autoimmune mechanism is involved. Clinically and histologically, AIP has two subsets: type 1 - lymphoplasmatic sclerosing pancreatitis with abundant infiltration of the pancreas and other affected organs with immunoglobulin G4-positive plasma cells, and type 2 - duct centric fibrosis, characterized by granulocyte epithelial lesions in the pancreas without systemic involvement. In the diagnosis of AIP, two diagnostic criterions are used - the HISORt criteria and Asian Diagnostic Criteria. In the differential diagnosis, the pancreatic cancer must be excluded by endosonographically guided pancreatic biopsy. Typical signs of AIP are concomitant disorders in other organs (kidney, liver, biliary tract, salivary glands, colon, retroperitoneum, prostate). Novel clinicopathological entity was proposed as an 'IgG4-related sclerosing disease' (IgG4-RSC). Extensive IgG4-positive plasma cells and T lymphocyte infiltration is a common characteristics of this disease. Recently, IgG4-RSC syndrome was extended to a new entity, characterized by IgG4 hypergammaglobulinemia and IgG4-positive plasma cell infiltration, this being considered an expression of a lymphoproliferative disease, 'IgG4-positive multiorgan lymphoproliferative syndrome'. This syndrome includes Mikulicz's disease, mediastinal fibrosis, autoimmune hypophysitis, and inflammatory pseudotumor - lung, liver, breast. In the therapy of AIP, steroids constitute first-choice treatment. High response to the corticosteroid therapy is an important diagnostic criterion. In the literature, there are no case-control studies that determine if AIP predisposes to pancreatic cancer. Undoubtedly, AIP is currently a hot topic in pancreatology. Copyright (C) 2010 S. Karger AG, Basel
C1 [Dite, P.] Univ Hosp Brno, Internal Clin3, Jihlavska St 20, CZ-60000 Brno, Czech Republic.
[Lata, J.] Univ Ostrava, Fac Med, Ostrava, Czech Republic.
C3 University Hospital Brno; University of Ostrava
RP Díte, P (corresponding author), Univ Hosp Brno, Internal Clin3, Jihlavska St 20, CZ-60000 Brno, Czech Republic.
EM pdite@med.muni.cz
RI KIanička, Bohuslav/AAC-8558-2022
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NR 33
TC 3
Z9 4
U1 0
U2 7
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PY 2010
VL 28
IS 2
BP 334
EP 338
DI 10.1159/000319410
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 647GT
UT WOS:000281607100006
PM 20814208
DA 2025-01-07
ER
PT J
AU Zen, Y
Yeh, MM
AF Zen, Yoh
Yeh, Matthew M.
TI Hepatotoxicity of immune checkpoint inhibitors: a histology study of
seven cases in comparison with autoimmune hepatitis and idiosyncratic
drug-induced liver injury
SO MODERN PATHOLOGY
LA English
DT Article
ID CELL LUNG-CANCER; NIVOLUMAB; IPILIMUMAB; MELANOMA; ANTIBODIES;
EXPRESSION; ZONATION; CTLA-4
AB The adverse effects of immune checkpoint inhibitors in various organs may be attributed to immune-mediated processes triggered by disrupted self-tolerance; however, it remains unclear whether they are similar or dissimilar to classic organ-specific autoimmune diseases. The present study aimed to compare clinicopathologic features between checkpoint inhibitor-induced liver injury and acutely presenting autoimmune hepatitis or idiosyncratic drug-induced liver injury. Seven patients treated with nivolumab (n = 5) or ipilimumab (n = 2) presented with liver dysfunction a median of 41 days (range 21-120) after the initiation of immunotherapy. All patients had elevated liver enzymes, whereas hyper-bilirubinemia was less common. None of the patients had antinuclear antibodies or IgG elevations. Stopping the immunotherapy and additional immunosuppression with corticosteroids normalized or decreased liver enzymes in all patients treated. Histologically, all biopsies showed predominantly lobular hepatitis with milder portal inflammation. Centrilobular confluent necrosis and plasmacytosis were observed in a single case, and were markedly less common and milder than those in autoimmune hepatitis (p = 0.017 and p < 0.001, respectively). Bile duct injury, micro-abscesses, and extramedullary hematopoiesis were also found in one case each. Immunostaining revealed the presence of large numbers of CD3+ and CD8+ lymphocytes, whereas CD20+ B cells and CD4+ T cells were fewer in checkpoint inhibitor-induced liver injury than in autoimmune hepatitis or drug-induced liver injury. In conclusion, liver injury caused by cancer immunotherapy shares some features with injury of autoimmune hepatitis; however, there are obvious differences between the two conditions. Checkpoint inhibitor-induced liver injury may represent an immune-mediated, less zone-selective hepatocyte necrosis not requiring the strong activation of helper T cells and immunoglobulin production.
C1 [Zen, Yoh] Kobe Univ, Grad Sch Med, Dept Diagnost Pathol, Kobe, Hyogo, Japan.
[Yeh, Matthew M.] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA.
C3 Kobe University; University of Washington; University of Washington
Seattle
RP Zen, Y (corresponding author), Kobe Univ, Grad Sch Med, Dept Diagnost Pathol, Kobe, Hyogo, Japan.
EM yohzen@med.kobe-u.ac.jp
FU Grants-in-Aid for Scientific Research [15K08345] Funding Source: KAKEN
CR Abdel-Wahab N, 2016, PLOS ONE, V11, DOI 10.1371/journal.pone.0160221
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NR 29
TC 194
Z9 200
U1 0
U2 31
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
EI 1530-0285
J9 MODERN PATHOL
JI Mod. Pathol.
PD JUN
PY 2018
VL 31
IS 6
BP 965
EP 973
DI 10.1038/s41379-018-0013-y
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA GJ1CH
UT WOS:000434991000012
PM 29403081
OA Bronze
DA 2025-01-07
ER
PT J
AU Nandi, N
Fraquelli, M
AF Nandi, Nicoletta
Fraquelli, Mirella
TI The role of elastography in viral hepatitis and autoimmune hepatitis
SO MINERVA GASTROENTEROLOGY
LA English
DT Review
DE Elasticity imaging techniques; Hepatitis C; chronic; Hepatitis B;
chronic; Hepatitis; autoimmune
ID LIVER STIFFNESS MEASUREMENT; TRANSIENT ELASTOGRAPHY; DIAGNOSTIC
PERFORMANCE; NONINVASIVE ASSESSMENT; FIBROSIS; BIOPSY; ACCURACY; MARKER;
REPRODUCIBILITY; PREDICTION
AB The prognosis of chronic liver diseases, which represent a major public health problem, is mainly linked to the extent and progression of liver fibrosis and the subsequent risk of developing cirrhosis and related complications, mainly hepatocellular carcinoma. During the past decade many noninvasive methods and in particular electrographic techniques, have been developed to reduce the need for liver biopsy in staging fibrosis and to overcome whenever possible its limitations, mainly: invasiveness, costs, low reproducibility and poor acceptance by patients. The aim of this review was to provide a comprehensive review of the role of elastography techniques in viral chronic liver diseases and autoimmune hepatitis, with the focus on the possible advantages and limitations of these techniques and on their diagnostic accuracy in predicting the stage of liver fibrosis.
C1 [Nandi, Nicoletta; Fraquelli, Mirella] Univ Milan, Fdn IRCCS Ca Granda Osped Maggiore Policlin, Unit Gastroenterol & Endoscopy, Via Francesco Sforza 35, I-20122 Milan, Italy.
C3 University of Milan; IRCCS Ca Granda Ospedale Maggiore Policlinico
RP Fraquelli, M (corresponding author), Univ Milan, Fdn IRCCS Ca Granda Osped Maggiore Policlin, Unit Gastroenterol & Endoscopy, Via Francesco Sforza 35, I-20122 Milan, Italy.
EM mfraquelli@yahoo.it
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NR 58
TC 1
Z9 1
U1 0
U2 6
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 2724-5985
EI 2724-5365
J9 MINERVA GASTROENTERO
JI Minerva Gastroenterol.
PD JUN
PY 2021
VL 67
IS 2
BP 141
EP 150
DI 10.23736/S2724-5985.21.02788-4
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA SJ3LW
UT WOS:000655435100005
PM 34027931
DA 2025-01-07
ER
PT J
AU Yamac, D
Gunel, N
Goker, B
Coskun, U
Erdem, O
Akyol, G
Ozenirler, S
AF Yamac, D
Gunel, N
Goker, B
Coskun, U
Erdem, O
Akyol, G
Ozenirler, S
TI Polymyositis and hepatitis concurrent with breast cancer
SO MEDICAL PRINCIPLES AND PRACTICE
LA English
DT Article
DE breast cancer; polymyositis; hepatitis; paraneoplastic syndrome
ID DERMATOMYOSITIS; MALIGNANCIES; AUTOIMMUNE
AB Objective: To present a rare case of breast cancer associated with both inflammatory muscle disease and liver disease as a paraneoplastic syndrome. Clinical Presentation and Intervention: A woman with breast cancer presented with elevated liver enzymes and progressive proximal muscle weakness. Liver biopsy was consistent with hepatitis and muscle biopsy revealed myositis. The start of corticosteroid therapy was followed by relief of the myopathic symptoms and regression of hepatitis histopathologically. Conclusion: A case of polymyositis and hepatitis associated with breast cancer and their flare-up with recurrence of malignancy is presented. In this case, the temporal relation with malignancy following its concurrent remission and relapse suggests a paraneoplastic mechanism. Copyright (C) 2004 S. Karger AG, Basel.
C1 Gazi Univ, Sch Med, Dept Med Oncol, Ankara, Turkey.
Gazi Univ, Sch Med, Dept Rheumatol, Ankara, Turkey.
Gazi Univ, Sch Med, Dept Pathol, Ankara, Turkey.
Gazi Univ, Sch Med, Dept Gastroenterol, Ankara, Turkey.
C3 Gazi University; Gazi University; Gazi University; Gazi University
RP Yamac, D (corresponding author), Mertler Sokak 31-5, TR-06510 Ankara, Turkey.
EM dyamac@gazi.edu.tr
RI AKYOL, Gulen/AHB-7455-2022
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NR 9
TC 2
Z9 2
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1011-7571
J9 MED PRIN PRACT
JI Med. Princ. Pract.
PY 2004
VL 13
IS 3
BP 171
EP 175
DI 10.1159/000076959
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 809QB
UT WOS:000220650100012
PM 15073432
OA Bronze
DA 2025-01-07
ER
PT J
AU Theocharidou, E
Heneghan, MA
AF Theocharidou, Eleni
Heneghan, Michael A.
TI Current and future perspectives in autoimmune hepatitis
SO BRITISH JOURNAL OF HOSPITAL MEDICINE
LA English
DT Review
ID CHRONIC ACTIVE HEPATITIS; LIVER-DISEASE; CORTICOSTEROID WITHDRAWAL;
OVERLAP SYNDROME; CONTROLLED-TRIAL; NATURAL-HISTORY; RISK-FACTORS;
REMISSION; TYPE-1; AZATHIOPRINE
AB Autoimmune hepatitis occurs in genetically susceptible individuals as a result of loss of immunological tolerance to hepatic autoantigens that can be precipitated by environmental triggers. The clinical manifestation is usually insidious but can be also acute with liver failure. The diagnosis is made on the basis of antibody positivity, elevated immunoglobulin G levels and interface hepatitis on liver histology. Induction of remission is achieved with high-dose steroids in the majority of cases, and maintenance of remission with azathioprine. Treatment withdrawal is achievable only in a small proportion of patients. Patients with acute liver failure unresponsive to steroids or those with end-stage liver failure or hepatocellular carcinoma may require liver transplantation. Variant forms of overlapping autoimmune hepatitis with either primary biliary cholangitis or sclerosing cholangitis are associated with worse outcomes. New insights into the pathophysiology of the disease may provide novel therapeutic targets and a more individualized approach to treatment of autoimmune hepatitis.
C1 [Theocharidou, Eleni; Heneghan, Michael A.] Kings Coll Hosp NHS Fdn Trust, Inst Liver Studies, London SE5 9RS, England.
C3 University of London; King's College London; King's College Hospital NHS
Foundation Trust
RP Heneghan, MA (corresponding author), Kings Coll Hosp NHS Fdn Trust, Inst Liver Studies, London SE5 9RS, England.
EM michael.heneghan@nhs.net
OI Theocharidou, Eleni/0000-0001-8136-3927
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NR 65
TC 5
Z9 5
U1 0
U2 8
PU MA HEALTHCARE LTD
PI LONDON
PA ST JUDES CHURCH, DULWICH ROAD, LONDON SE24 0PB, ENGLAND
SN 1750-8460
EI 1759-7390
J9 BRIT J HOSP MED
JI Br. J. Hosp. Med.
PD MAR
PY 2018
VL 79
IS 3
BP 151
EP 159
DI 10.12968/hmed.2018.79.3.151
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA FZ1DT
UT WOS:000427317000019
PM 29528732
OA Bronze
DA 2025-01-07
ER
PT J
AU Ye, C
Li, WY
Zheng, MH
Chen, YP
AF Ye, Chao
Li, Wen-yuan
Zheng, Ming-hua
Chen, Yong-ping
TI T-helper 17 cell: A distinctive cell in liver diseases
SO HEPATOLOGY RESEARCH
LA English
DT Review
DE autoimmune; inflammatory; liver; regulatory T cell; T-helper 17 cell
ID PRIMARY BILIARY-CIRRHOSIS; GROWTH-FACTOR-BETA; TH17 CELLS; TGF-BETA;
INTERLEUKIN-17 PRODUCTION; RHEUMATOID-ARTHRITIS; CYTOKINE PROFILE;
IMMUNE-RESPONSE; INNATE IMMUNITY; ACUTE REJECTION
AB T-helper (Th)17 cells, a new population of effector CD4+ T cells, are characterized by the secretion of interleukin (IL)-17. It has been demonstrated that Th17 cells are distinct from Th1 and Th2 cells; they play important roles in the pathogenesis of numerous inflammatory and autoimmune diseases; and are closely related to host defense, tumorigenesis and transplant rejection. Moreover, it has been found that these cells have a close and intricate connection with the regulatory T cells, which play an important role in maintaining self-tolerance and down-tuning immune responses. In the present review, we find that they are significantly elevated in various kinds of liver diseases including liver autoimmunity and inflammatory diseases, alcoholic liver disease and hepatocellular carcinoma.
C1 [Ye, Chao; Li, Wen-yuan; Zheng, Ming-hua; Chen, Yong-ping] Affiliated Hosp 1, Wenzhou Med Coll, Dept Infect & Liver Dis, Liver Res Ctr, Wenzhou 325000, Zhejiang, Peoples R China.
C3 Wenzhou Medical University
RP Chen, YP (corresponding author), Affiliated Hosp 1, Wenzhou Med Coll, Dept Infect & Liver Dis, Liver Res Ctr, 2 Fuxue Lane, Wenzhou 325000, Zhejiang, Peoples R China.
EM ypchen77@gmail.com
RI Zheng, Ming-Hua/H-5584-2019
OI Ye, Chao/0000-0003-0740-7850; Zheng, Ming-Hua/0000-0003-4984-2631; Li,
Wenyuan/0000-0001-7404-1575
FU Zhejiang Provincial Natural Science Foundation of China [Y207464];
Scientific Research Foundation of Wenzhou, Zhejiang Province, China
[H20090014, Y20090269]; Research Foundation of Education Bureau of
Zhejiang Province [Y201009942]; Health Bureau of Zhejiang Province
[2010KYB070]
FX THIS WORK WAS supported by grants from Zhejiang Provincial Natural
Science Foundation of China (Y207464), Scientific Research Foundation of
Wenzhou, Zhejiang Province, China (H20090014, Y20090269), Research
Foundation of Education Bureau of Zhejiang Province (Y201009942), and
Health Bureau of Zhejiang Province (2010KYB070).
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NR 97
TC 21
Z9 23
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD JAN
PY 2011
VL 41
IS 1
BP 22
EP 29
DI 10.1111/j.1872-034X.2010.00744.x
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 700ZD
UT WOS:000285783200002
PM 21108703
DA 2025-01-07
ER
PT J
AU Birn-Rydder, R
Jensen, MD
Jepsen, P
Gronbæk, L
AF Birn-Rydder, Rasmine
Jensen, Morten D.
Jepsen, Peter
Gronbaek, Lisbet
TI Extrahepatic autoimmune diseases in autoimmune hepatitis: Effect on
mortality
SO LIVER INTERNATIONAL
LA English
DT Article
DE autoimmune diseases; autoimmune hepatitis; epidemiology; mortality;
prognosis; registries
ID REGISTRY; RISK
AB Background and Aims Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease associated with an increased prevalence of extrahepatic autoimmune diseases and an increased mortality compared with the general population. The contribution of extrahepatic autoimmune diseases to the increased mortality has not been clarified. Our aim was to determine the effect of extrahepatic autoimmune diseases on mortality in AIH patients. Methods This nationwide register-based cohort study included all Danish patients diagnosed with AIH between 1995 and 2019. We examined the presence of extrahepatic autoimmune diseases and compared the mortality between AIH patients with and without extrahepatic autoimmune diseases. We adjusted our analysis for age, sex, calendar year of AIH diagnosis, cirrhosis, cancer, chronic obstructive pulmonary disease and ischaemic heart disease. Results We included 2479 AIH patients of whom 19.8% had one extrahepatic autoimmune disease and 3.3% had multiple. The adjusted 10-year cumulative mortality was 27.2% (95% confidence interval [CI]: 25.2-29.4) for patients with extrahepatic autoimmune diseases and 21.6% (95% CI: 19.9-23.6) for patients without. The adjusted mortality hazard ratio was 1.30 (95% CI: 1.12-1.52) for AIH patients with versus without extrahepatic autoimmune diseases; it was 1.25 (95% CI: 1.06-1.48) for patients with one extrahepatic autoimmune disease and 1.54 (95% CI: 1.15-2.05) for those with more than one. Conclusions Extrahepatic autoimmune diseases increased the mortality in patients with AIH. Patients with multiple extrahepatic autoimmune diseases had a higher mortality than patients with just one extrahepatic autoimmune disease.
C1 [Birn-Rydder, Rasmine; Jensen, Morten D.; Jepsen, Peter; Gronbaek, Lisbet] Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Aarhus, Denmark.
[Gronbaek, Lisbet] Reg Hosp Horsens, Dept Med, Horsens, Denmark.
C3 Aarhus University
RP Birn-Rydder, R (corresponding author), Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Aarhus, Denmark.
EM rasbir@rm.dk
RI Jensen, Morten Daniel/HDM-8545-2022
OI Gronbaek, Lisbet/0000-0003-0626-179X; Jepsen, Peter/0000-0002-6641-1430;
Birn-Rydder, Rasmine/0000-0003-4584-7275; Jensen, Morten
Daniel/0000-0002-5137-7268
FU A.P. Moller Foundation for the Advancement of Medical Science; Novo
Nordisk Foundation
FX The A.P. Moller Foundation for the Advancement of Medical Science; The
Novo Nordisk Foundation
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Statistics Denmark, DEATHS
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JI Liver Int.
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VL 42
IS 11
BP 2466
EP 2472
DI 10.1111/liv.15382
EA AUG 2022
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 4V0WX
UT WOS:000842536000001
PM 35924431
OA Green Published
DA 2025-01-07
ER
PT J
AU Gidwaney, NG
Pawa, S
Das, KM
AF Gidwaney, Neelam G.
Pawa, Swati
Das, Kiron M.
TI Pathogenesis and clinical spectrum of primary sclerosing cholangitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Primary sclerosing cholangitis; cholestasis; inflammatory bowel disease;
autoimmune; gallbladder neoplasia; cholangiocarcinoma; IgG4 related
disease; colon cancer; liver transplant
ID INFLAMMATORY-BOWEL-DISEASE; PRIMARY BILIARY-CIRRHOSIS; GENOME-WIDE
ASSOCIATION; IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; ANTINEUTROPHIL
CYTOPLASMIC ANTIBODIES; DOSE URSODEOXYCHOLIC ACID; BILE-DUCT STENOSES;
ULCERATIVE-COLITIS; LIVER-TRANSPLANTATION; AUTOIMMUNE PANCREATITIS
AB Primary sclerosing cholangitis (PSC) is a disease of the biliary tract, which has been documented in the literature since 1867. This disease has a strong predilection for affecting men and can be seen in individuals as young as 2 years of age. PSC has a strong associated with inflammatory bowel disease, more commonly with ulcerative colitis, and is also part of the clinical spectrum of IgG4-related diseases. Small-duct PSC, a variant of PSC, also has an association with inflammatory bowel disease. The exact pathogenesis of PSC is not well understood at present, however, is likely a combination of a genetic predisposition with alteration of the molecular structure of the gut. Abnormal serum liver chemistry and presence of certain autoimmune markers are usually the first indicators leading to a diagnosis of PCS, however, these may often be normal in early stages of this disease. The diagnosis is made by cholangiography, which is now considered the gold standard. PSC is a known pre-malignant condition. Such patients have an increased risk of developing cholangiocarcinoma, gallbladder neoplasia, and colon cancer. Many new treatment modalities have emerged in the recent past, including anti-tumor necrosis factora and anti-integrins; however, liver transplantation is the only known cure for PSC. Despite past and present research, PSC remains an enigmatic biliary disease with few viable treatment options.
C1 [Gidwaney, Neelam G.; Pawa, Swati; Das, Kiron M.] Rutgers Robert Wood Johnson Med Sch, Div Gastroenterol & Hepatol, One Robert Wood Johnson Pl,Med Educ Bldg 478B, New Brunswick, NJ 08903 USA.
C3 Rutgers University System; Rutgers University New Brunswick; Rutgers
University Biomedical & Health Sciences
RP Das, KM (corresponding author), Rutgers Robert Wood Johnson Med Sch, Div Gastroenterol & Hepatol, One Robert Wood Johnson Pl,Med Educ Bldg 478B, New Brunswick, NJ 08903 USA.
EM daskm@rwjms.rutgers.edu
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NR 137
TC 28
Z9 35
U1 1
U2 3
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD APR 14
PY 2017
VL 23
IS 14
BP 2459
EP 2469
DI 10.3748/wjg.v23.i14.2459
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ES4BW
UT WOS:000399475100002
PM 28465630
OA Green Published, hybrid, Green Submitted
DA 2025-01-07
ER
PT J
AU Eichhorst, ST
AF Eichhorst, ST
TI Modulation of apoptosis as a target for liver disease
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
ID TUMOR-NECROSIS-FACTOR; MITOCHONDRIAL PERMEABILITY TRANSITION; VIRUS CORE
PROTEIN; ISCHEMIA-REPERFUSION INJURY; ENDOTHELIAL-CELL APOPTOSIS;
SURVIVAL SIGNALING CASCADE; ETHANOL-INDUCED APOPTOSIS; ACID-INDUCED
APOPTOSIS; TRANSFORMING GROWTH FACTOR-BETA(1); HUMAN
HEPATOCELLULAR-CARCINOMA
AB Apoptosis mediated via extrinsic or intrinsic pathways is essential for maintaining cellular homeostasis in the liver. The extrinsic pathway is triggered from the cell surface by engagement of death receptors as CD95, TRAIL (TNF-related apoptosis inducing ligand) and TNF (tumour necrosis factor) or TGF-beta (transforming growth factor beta) receptors. The intrinsic pathway is initiated from the mitochondria and can be influenced by Bcl-2 family members. Both pathways are intertwined and play a physiological role in the liver. Dysregulation of apoptosis pathways contributes to diseases as hepatocellular carcinoma, viral hepatitis, autoimmune hepatitis, ischaemia-reperfusion injury, iron or copper deposition disorders, toxic liver damage and acute liver failure. The apoptosis defects are often central pathogenetic events; hence molecular mechanisms of apoptosis give not only insight into disease mechanisms but also provide potential corresponding therapeutic candidates in liver disease. The focus of this review is the identification of apoptotic signalling components in the liver as therapeutic targets.
C1 Univ Munich, Klinikum Grosshadern, Dept Internal Med 2, Res Lab B 5 E01 308, D-81377 Munich, Germany.
C3 University of Munich
RP Univ Munich, Klinikum Grosshadern, Dept Internal Med 2, Res Lab B 5 E01 308, Marchioninistr 15, D-81377 Munich, Germany.
EM S.Eichhorst@mail.com
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NR 209
TC 48
Z9 52
U1 1
U2 8
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1472-8222
EI 1744-7631
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD FEB
PY 2005
VL 9
IS 1
BP 83
EP 99
DI 10.1517/14728222.9.1.83
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 901AT
UT WOS:000227256100006
PM 15757484
DA 2025-01-07
ER
PT J
AU Luo, MJ
Ballester, MP
Soffientini, U
Jalan, R
Mehta, G
AF Luo, Mingjia
Ballester, Maria Pilar
Soffientini, Ugo
Jalan, Rajiv
Mehta, Gautam
TI SARS-CoV-2 infection and liver involvement
SO HEPATOLOGY INTERNATIONAL
LA English
DT Review
DE SARS-CoV-2; COVID-19; Liver injury; Chronic liver disease; Cirrhosis;
Alcohol-related liver disease; Autoimmune liver disease; Non-alcoholic
fatty liver disease; Hepatitis B virus infection; Vaccination
ID MESSENGER-RNA; COVID-19; CIRRHOSIS; DISEASE; INJURY; DEATH
AB The COVID-19 pandemic is the largest public health challenge in living memory. Patients with underlying liver disease have been disproportionately affected, experiencing high morbidity and mortality. In addition, elevated liver enzymes appear to be a risk factor for disease progression, even in the absence of underlying liver disease. Nevertheless, the mechanism of liver injury in SARS-CoV-2 infection remains largely unknown. This review aims to provide an overview of the mechanisms by which SARS-CoV-2 induces liver injury, and the impact of COVID-19 on cirrhosis, alcohol-related liver disease, autoimmune liver disease, non-alcoholic fatty liver disease, hepatitis B and C virus infection, liver-transplant recipients and patients with hepatocellular carcinoma. Finally, emerging data on vaccination in liver diseases is discussed, to help inform public health policy.
C1 [Luo, Mingjia] UCL, Div Med, London, England.
[Ballester, Maria Pilar] Univ Valencia, Hosp Clin, Digest Dis Dept, Valencia, Spain.
[Ballester, Maria Pilar] INCLIVA Biomed Res Inst, Valencia, Spain.
[Soffientini, Ugo; Mehta, Gautam] Fdn Liver Res, Roger Williams Inst Hepatol, London, England.
[Soffientini, Ugo; Jalan, Rajiv; Mehta, Gautam] UCL, Liver Failure Grp, UCL Med Sch, Inst Liver & Dis Hlth, Royal Free Campus,Rowland Hill St, London NW3 2PF, England.
C3 University of London; University College London; University of Valencia;
University of London; University College London; University of London;
University College London
RP Mehta, G (corresponding author), Fdn Liver Res, Roger Williams Inst Hepatol, London, England.; Mehta, G (corresponding author), UCL, Liver Failure Grp, UCL Med Sch, Inst Liver & Dis Hlth, Royal Free Campus,Rowland Hill St, London NW3 2PF, England.
EM gautam.mehta@ucl.ac.uk
RI Mehta, Gautam/AAJ-8510-2020; Ballester, Maria Pilar/I-5516-2017
OI Mehta, Gautam/0000-0002-5696-359X; Ballester, Maria
Pilar/0000-0001-7177-5696
FU COBALT consortium; EF-Clif
FX The authors acknowledge support from the COBALT consortium and EF-Clif.
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NR 59
TC 37
Z9 37
U1 1
U2 24
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1936-0533
EI 1936-0541
J9 HEPATOL INT
JI Hepatol. Int.
PD AUG
PY 2022
VL 16
IS 4
BP 755
EP 774
DI 10.1007/s12072-022-10364-1
EA JUN 2022
PG 20
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 3M8QZ
UT WOS:000818648200003
PM 35767172
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Chuang, HC
Tan, TH
AF Chuang, Huai-Chia
Tan, Tse-Hua
TI MAP4K3/GLK in autoimmune disease, cancer and aging
SO JOURNAL OF BIOMEDICAL SCIENCE
LA English
DT Review
DE HPK1; Autoimmune disease; Cancer metastasis; Aging; IL-17A; PKC theta;
IQGAP1; Autophagy; Verteporfin
ID N-TERMINAL KINASE; HEMATOPOIETIC PROGENITOR KINASE; PHOTODYNAMIC
THERAPY; FAMILY KINASES; PROTEIN-KINASE; LUNG-CANCER; TUMOR-CELLS;
ACTIVATION; PATHWAY; PHOSPHORYLATION
AB MAP4K3 (also named GLK) is a serine/threonine kinase, which belongs to the mammalian Ste20-like kinase family. At 22 years of age, GLK was initially cloned and identified as an upstream activator of the MAPK JNK under an environmental stress and proinflammatory cytokines. The data derived from GLK-overexpressing or shRNA-knockdown cell lines suggest that GLK may be involved in cell proliferation through mTOR signaling. GLK phosphorylates the transcription factor TFEB and retains TFEB in the cytoplasm, leading to inhibition of cell autophagy. After generating and characterizing GLK-deficient mice, the important in vivo roles of GLK in T-cell activation were revealed. In T cells, GLK directly interacts with and activates PKC theta through phosphorylating PKC theta at Ser-538 residue, leading to activation of IKK/NF-kappa B. Thus, GLK-deficient mice display impaired T-cell-mediated immune responses and decreased inflammatory phenotypes in autoimmune disease models. Consistently, the percentage of GLK-overexpressing T cells is increased in the peripheral blood from autoimmune disease patients; the GLK-overexpressing T cell population is correlated with disease severity of patients. The pathogenic mechanism of autoimmune disease by GLK overexpression was unraveled by characterizing T-cell-specific GLK transgenic mice and using biochemical analyses. GLK overexpression selectively promotes IL-17A transcription by inducing the AhR-ROR gamma t complex in T cells. In addition, GLK overexpression in cancer tissues is correlated with cancer recurrence of human lung cancer and liver cancer; the predictive power of GLK overexpression for cancer recurrence is higher than that of pathologic stage. GLK directly phosphorylates and activates IQGAP1, resulting in induction of Cdc42-mediated cell migration and cancer metastasis. Furthermore, treatment of GLK inhibitor reduces disease severity of mouse autoimmune disease models and decreases IL-17A production of human autoimmune T cells. Due to the inhibitory function of HPK1/MAP4K1 in T-cell activation and the promoting effects of GLK on tumorigenesis, HPK1 and GLK dual inhibitors could be useful therapeutic drugs for cancer immunotherapy. In addition, GLK deficiency results in extension of lifespan in Caenorhabditis elegans and mice. Taken together, targeting MAP4K3 (GLK) may be useful for treating/preventing autoimmune disease, cancer metastasis/recurrence, and aging.
C1 [Chuang, Huai-Chia; Tan, Tse-Hua] Natl Hlth Res Inst, Immunol Res Ctr, 35 Keyan Rd, Zhunan 35053, Taiwan.
[Tan, Tse-Hua] Baylor Coll Med, Dept Pathol & Immunol, Houston, TX 77030 USA.
C3 National Health Research Institutes - Taiwan; Baylor College of Medicine
RP Tan, TH (corresponding author), Natl Hlth Res Inst, Immunol Res Ctr, 35 Keyan Rd, Zhunan 35053, Taiwan.; Tan, TH (corresponding author), Baylor Coll Med, Dept Pathol & Immunol, Houston, TX 77030 USA.
EM ttan@nhri.edu.tw
RI Chuang, Huai-Chia/E-9486-2016; Tan, Tse-Hua/ABD-7080-2021; Tan,
Tse-Hua/E-3983-2010
OI Tan, Tse-Hua/0000-0003-4969-3170
FU National Health Research Institutes, Taiwan [IM-107-PP-01, IM-107-SP-01,
IM-107-PP-06]; Ministry of Science and Technology, Taiwan
[MOST-106-2321-B-400-013]
FX This work was supported by grants from the National Health Research
Institutes, Taiwan (IM-107-PP-01 and IM-107-SP-01, to T.-H.T.;
IM-107-PP-06, to H.-C.C.) and Ministry of Science and Technology, Taiwan
(MOST-106-2321-B-400-013 to T.-H.T.).
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NR 56
TC 29
Z9 35
U1 0
U2 38
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1021-7770
EI 1423-0127
J9 J BIOMED SCI
JI J. Biomed. Sci.
PD OCT 22
PY 2019
VL 26
IS 1
AR 82
DI 10.1186/s12929-019-0570-5
PG 8
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA JG3SS
UT WOS:000491994900001
PM 31640697
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kotlyar, DS
Campbell, MS
Reddy, KR
AF Kotlyar, David S.
Campbell, Mical S.
Reddy, K. Rajender
TI Recurrence of diseases following orthotopic liver transplantation
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY-CIRRHOSIS; HEPATITIS-C
INFECTION; SINGLE-CENTER EXPERIENCE; LONG-TERM OUTCOMES;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; FIBROSIS PROGRESSION;
CRYPTOGENIC CIRRHOSIS; COMBINATION THERAPY
AB Long-term graft survival and mortality after liver transplantation continue to improve. However, disease recurrence remains a major stumbling block, especially among patients with hepatitis C. Chronic hepatitis C recurs to varying degrees in nearly all patients who undergo transplantation. Transplantation for hepatitis C is associated with higher rates of graft failure and death compared with transplantation for other indications, and retransplantation for hepatitis C related liver failure remains controversial. Recurrence of hepatitis B has been markedly reduced with improved prophylactic regimens. Further, rates of hepatocellular carcinoma recurrence have also decreased, as improved patient selection criteria have prioritized transplantation for those with a low risk of recurrence. Primary biliary cirrhosis recurs in some patients, but it is often relatively mild. Autoimmune liver disease has also been shown to have a relatively benign post-transplantation course, but some studies have indicated that it slowly progresses in most recipients. It has been recently reported that alcoholic liver disease liver transplant recipients who return to drinking have worsened mortality. In such patients worse outcomes are not due to graft failure, but instead to other comorbidities. Recurrences of other diseases, including nonalcoholic steatohepatitis and primary sclerosing cholangitis, are now being recognized as having potentially detrimental effects on graft survival and mortality. Expert clinical management may help prevent and treat complications associated with disese recurrence.
C1 Univ Penn, G1 Div, Sch Med, Philadelphia, PA 19104 USA.
Univ Penn, Hlth Syst, Div Gastroenterol, Philadelphia, PA 19104 USA.
C3 University of Pennsylvania; University of Pennsylvania
RP Reddy, KR (corresponding author), Univ Penn, G1 Div, Sch Med, 3 Ravdin,3400 Spruce St, Philadelphia, PA 19104 USA.
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NR 85
TC 50
Z9 53
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD JUN
PY 2006
VL 101
IS 6
BP 1370
EP 1378
DI 10.1111/j.1572-0241.2006.00586.x
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 047HS
UT WOS:000237871000034
PM 16771963
DA 2025-01-07
ER
PT J
AU Cui, YZ
Hettinghouse, A
Liu, CJ
AF Cui, Yazhou
Hettinghouse, Aubryanna
Liu, Chuan-ju
TI Progranulin: A conductor of receptors orchestra, a chaperone of
lysosomal enzymes and a therapeutic target for multiple diseases
SO CYTOKINE & GROWTH FACTOR REVIEWS
LA English
DT Review
DE Progranulin; Membrane receptors; Inflammation; Autoimmune diseases;
Neurodegenerative diseases; Cancer; Lysosomal storage diseases
ID GRANULIN-EPITHELIN PRECURSOR; FRONTOTEMPORAL LOBAR DEGENERATION;
GROWTH-FACTOR; SERUM PROGRANULIN; CANCER CELLS; MOUSE MODEL;
HEPATOCELLULAR-CARCINOMA; INFLAMMATORY DISEASE; DOWNSTREAM MOLECULE;
PROMOTES MIGRATION
AB Progranulin (PGRN), a widely expressed glycoprotein with pleiotropic function, has been linked to a host of physiological processes and diverse pathological states. A series of contemporary preclinical disease models and clinical trials have evaluated various therapeutic strategies targeting PGRN, highlighting PGRN as a promising therapeutic target. Herein we summarize available knowledge of PGRN targeting in various kinds of diseases, including common neurological diseases, inflammatory autoimmune diseases, cancer, tissue repair, and rare lysosomal storage diseases, with a focus on the functional domain-oriented drug development strategies. In particular, we emphasize the role of extracellular PGRN as a non-conventional, extracellular matrix bound, growth factor-like conductor orchestrating multiple membrane receptors and intracellular PGRN as a chaperone/co-chaperone that mediates the folding and traffic of its various binding partners.
C1 [Cui, Yazhou; Hettinghouse, Aubryanna; Liu, Chuan-ju] NYU, Med Ctr, Dept Orthopaed Surg, New York, NY 10003 USA.
[Cui, Yazhou] Shandong Acad Med Sci, Shandong Med Biotechnol Ctr, Jinan 250062, Shandong, Peoples R China.
[Liu, Chuan-ju] NYU, Sch Med, Dept Cell Biol, New York, NY 10016 USA.
C3 New York University; University of Jinan; Shandong First Medical
University & Shandong Academy of Medical Sciences; New York University
RP Liu, CJ (corresponding author), NYU, Sch Med, Dept Orthopaed Surg, HJD, Rm 1608,301 East 17th St, New York, NY 10003 USA.; Liu, CJ (corresponding author), NYU, Sch Med, Dept Cell Biol, 301 East 17th St, New York, NY 10003 USA.
EM chuanju.liu@nyumc.org
RI Liu, Chuan-ju/AAT-8165-2021
OI liu, chuanju/0000-0002-7181-8032
FU NIH [R01NS103931, R01AR062207, R01AR061484]; DOD [W81XWH-16-1-0482];
National Natural Science Foundation of China [81772300]
FX CJ Liu is grateful to his gifted collaborators who made the explorations
in his laboratory possible. We apologize to the colleagues whose
publications are not included due to the space limitation. This work was
supported partly by NIH research grants R01NS103931, R01AR062207,
R01AR061484, and a DOD research grant W81XWH-16-1-0482 (CJ Liu). YZ Cui
was funded by National Natural Science Foundation of China (81772300).
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NR 138
TC 65
Z9 66
U1 0
U2 20
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6101
EI 1879-0305
J9 CYTOKINE GROWTH F R
JI Cytokine Growth Factor Rev.
PD FEB
PY 2019
VL 45
SI SI
BP 53
EP 64
DI 10.1016/j.cytogfr.2019.01.002
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA HN4LI
UT WOS:000460155000006
PM 30733059
OA Bronze, Green Accepted
DA 2025-01-07
ER
PT J
AU Nishikawa, H
Fukunishi, S
Asai, A
Yokohama, K
Ohama, H
Nishiguchi, S
Higuchi, K
AF Nishikawa, Hiroki
Fukunishi, Shinya
Asai, Akira
Yokohama, Keisuke
Ohama, Hideko
Nishiguchi, Shuhei
Higuchi, Kazuhide
TI Dysbiosis and liver diseases (Review)
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Review
DE dysbiosis; liver disease; molecular mechanism; disease progression;
carcinogenesis
ID PRIMARY BILIARY CHOLANGITIS; HEPATIC STELLATE CELLS; HUMAN GUT
MICROBIOME; NONALCOHOLIC STEATOHEPATITIS; AUTOIMMUNE HEPATITIS;
HEPATOCELLULAR-CARCINOMA; INTESTINAL MICROBIOTA; PATHOGENESIS;
CIRRHOSIS; ALCOHOL
AB Dysbiosis, a qualitative and quantitative aberrancy of gut microbiota, has attracted marked attention. At present, advances in molecular biological techniques have made it possible to analyze gut microbiota at the DNA and RNA levels without culturing, and methods such as 16S ribosomal RNA targeting analysis and metagenomic analysis using next-generation sequencers have been developed. The relationship between gut microbiota and various diseases has been extensively examined. Gut microbiota are essential for the immune system, energy intake and fat storage, and humans use them to build complex immune regulatory mechanisms and to obtain energy from food. The liver is the first organ to be nourished by the portal blood flow of intestinal origin, and liver diseases can be strongly influenced by various factors of intestinal origin, such as intestinal bacteria, bacterial components, and intestinal bacterial metabolites. Rigorous research has revealed that the composition of the gut microbiota is altered and the diversity of bacteria is reduced in liver diseases. Significance of various factors transported to the liver by portal vein blood flow from the intestine has been extensively investigated. Gut microbiota in liver disease can be associated with disease progression regardless of disease etiology and even with carcinogenesis. The relationship between gut microbiota and liver diseases (hepatitis virus-related diseases, autoimmune liver diseases, alcoholic liver disease, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma) and the treatments of dysbiosis (antibiotics, prebiotics, probiotics and fecal microbiota transplantation) in liver disease are outlined based on the current evidence.
C1 [Nishikawa, Hiroki; Fukunishi, Shinya; Asai, Akira; Yokohama, Keisuke; Ohama, Hideko; Higuchi, Kazuhide] Osaka Med & Pharmaceut Univ, Dept Internal Med 2, 2-7 Daigakumachi St, Takatsuki, Osaka 5698686, Japan.
[Nishikawa, Hiroki; Fukunishi, Shinya] Osaka Med & Pharmaceut Univ, Premier Dept Med Res, Takatsuki, Osaka 5698686, Japan.
[Nishiguchi, Shuhei] Kano Gen Hosp, Dept Internal Med, Osaka 5310041, Japan.
C3 Osaka Medical & Pharmaceutical University; Osaka Medical &
Pharmaceutical University
RP Nishikawa, H (corresponding author), Osaka Med & Pharmaceut Univ, Dept Internal Med 2, 2-7 Daigakumachi St, Takatsuki, Osaka 5698686, Japan.
EM nishikawa_6392_0207@yahoo.co.jp
RI Ohama, Hideko/HJH-2482-2023
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NR 113
TC 6
Z9 7
U1 1
U2 14
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD SEP
PY 2021
VL 48
IS 3
AR 183
DI 10.3892/ijmm.2021.5016
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA TY3DB
UT WOS:000683663200001
PM 34328191
OA hybrid
DA 2025-01-07
ER
PT J
AU Dasgupta, A
Tsay, E
Federman, N
Lechner, MG
Su, MA
AF Dasgupta, Aditi
Tsay, Eric
Federman, Noah
Lechner, Melissa G.
Su, Maureen A.
TI Polyendocrine Autoimmunity and Diabetic Ketoacidosis Following Anti-PD-1
and Interferon α
SO PEDIATRICS
LA English
DT Article
ID IMMUNE CHECKPOINT INHIBITORS; BLOCKADE; THERAPY
AB Immune checkpoint inhibitor (ICI) therapies are now first-line therapy for many advanced malignancies in adults, with emerging use in children. With increasing ICI use, prompt recognition and optimal management of ICI-associated immune-related adverse events (IRAEs) are critical. Nearly 60% of ICI-treated adults develop IRAEs, which commonly manifest as autoimmune skin, gastrointestinal, and endocrine disease and can be life-threatening. The incidence, presentation, and disease course of spontaneous autoimmune diseases differ between adults and children, but the pattern of pediatric IRAEs is currently unclear. We report a case of a pediatric patient presenting with new onset autoimmune diabetes mellitus and diabetic ketoacidosis during ICI treatment of fibrolamellar hepatocellular carcinoma (FLC). Distinct from spontaneous type 1 diabetes mellitus (T1DM), this patient progressed rapidly and was negative for known beta cell autoantibodies. Additionally, the patient was positive for 21-hydroxylase autoantibodies, suggesting development of concomitant adrenal autoimmunity. Current guidelines for the management of IRAEs in adults may not be appropriate for the management of pediatric patients, who may have different autoimmune risks in a developmental context.
C1 [Dasgupta, Aditi] UCLA, Dept Pediat, Geffen Sch Med, Los Angeles, CA USA.
[Tsay, Eric; Su, Maureen A.] UCLA, Div Pediat Endocrinol, Geffen Sch Med, Los Angeles, CA USA.
[Federman, Noah] UCLA, Div Pediat Hematol & Oncol, Geffen Sch Med, Los Angeles, CA USA.
[Lechner, Melissa G.] UCLA, Div Endocrinol Diabet & Metab, Geffen Sch Med, Los Angeles, CA USA.
[Su, Maureen A.] UCLA, Dept Microbiol Immunol & Mol Genet, Geffen Sch Med, 615 S Charles & Young Dr,BSRB 257, Los Angeles, CA 90095 USA.
C3 University of California System; University of California Los Angeles;
University of California Los Angeles Medical Center; David Geffen School
of Medicine at UCLA; University of California System; University of
California Los Angeles; University of California Los Angeles Medical
Center; David Geffen School of Medicine at UCLA; University of
California System; University of California Los Angeles; University of
California Los Angeles Medical Center; David Geffen School of Medicine
at UCLA; University of California System; University of California Los
Angeles; University of California Los Angeles Medical Center; David
Geffen School of Medicine at UCLA; University of California System;
University of California Los Angeles; University of California Los
Angeles Medical Center; David Geffen School of Medicine at UCLA
RP Su, MA (corresponding author), UCLA, Dept Microbiol Immunol & Mol Genet, Geffen Sch Med, 615 S Charles & Young Dr,BSRB 257, Los Angeles, CA 90095 USA.
EM MaSu@mednet.ucla.edu
FU NIH [R01DK119445, K08DK129829]; National Institute of Diabetes and
Digestive and Kidney Diseases [R01DK119445, K08DK129829] Funding Source:
NIH RePORTER
FX Dr Su receives funding from NIH grant R01DK119445 and Dr Lechner
receives funding from NIH grant K08DK129829.
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NR 34
TC 2
Z9 3
U1 0
U2 0
PU AMER ACAD PEDIATRICS
PI Itasca
PA 345 Park Boulevard, Itasca, IL, UNITED STATES
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD APR
PY 2022
VL 149
IS 4
AR e2021053363
DI 10.1542/peds.2021-053363
PG 5
WC Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics
GA 8D3OE
UT WOS:000918205700014
PM 35274131
OA Green Accepted, Green Submitted
DA 2025-01-07
ER
PT J
AU Sadri, M
Shafaghat, Z
Roozbehani, M
Hoseinzadeh, A
Mohammadi, F
Arab, FL
Minaeian, S
Fard, SR
Faraji, F
AF Sadri, Maryam
Shafaghat, Zahra
Roozbehani, Mona
Hoseinzadeh, Akram
Mohammadi, Fatemeh
Arab, Fahimeh Lavi
Minaeian, Sara
Fard, Soheil Rahmani
Faraji, Fatemeh
TI Effects of Probiotics on Liver Diseases: Current In Vitro and
In Vivo Studies
SO PROBIOTICS AND ANTIMICROBIAL PROTEINS
LA English
DT Review; Early Access
DE Probiotics; Liver diseases; Hepatic diseases; In vivo and in vitro
studies
ID GUT MICROBIOTA; HEPATOCELLULAR-CARCINOMA; LACTOBACILLUS-PLANTARUM;
INTESTINAL PERMEABILITY; AUTOIMMUNE HEPATITIS; INSULIN-RESISTANCE;
FERMENTED MILK; RISK-FACTORS; RHAMNOSUS; CIRRHOSIS
AB Various types of liver or hepatic diseases cause the death of about 2 million people worldwide every year, of which 1 million die from the complications of cirrhosis and another million from hepatocellular carcinoma and viral hepatitis. Currently, the second most common solid organ transplant is the liver, and the current rate represents less than 10% of global transplant requests. Hence, finding new approaches to treat and prevent liver diseases is essential. In liver diseases, the interaction between the liver, gut, and immune system is crucial, and probiotics positively affect the human microbiota. Probiotics are a non-toxic and biosafe alternative to synthetic chemical compounds. Health promotion by lowering cholesterol levels, stimulating host immunity, the natural gut microbiota, and other functions are some of the activities of probiotics, and their metabolites, including bacteriocins, can exert antimicrobial effects against a broad range of pathogenic bacteria. The present review discusses the available data on the results of preclinical and clinical studies on the effects of probiotic administration on different types of liver diseases.
C1 [Sadri, Maryam; Shafaghat, Zahra] Iran Univ Med Sci, Dept Immunol, Tehran, Iran.
[Roozbehani, Mona] Iran Univ Med Sci, Vaccine Res Ctr, Tehran, Iran.
[Hoseinzadeh, Akram] Semnan Univ Med Sci, Canc Res Ctr, Fac Med, Semnan, Iran.
[Mohammadi, Fatemeh; Arab, Fahimeh Lavi] Mashhad Univ Med Sci, Sch Med, Dept Immunol, Mashhad, Iran.
[Minaeian, Sara; Fard, Soheil Rahmani; Faraji, Fatemeh] Iran Univ Med Sci, Inst Immunol & Infect Dis, Antimicrobial Resistance Res Ctr, Tehran, Iran.
RP Faraji, F (corresponding author), Iran Univ Med Sci, Inst Immunol & Infect Dis, Antimicrobial Resistance Res Ctr, Tehran, Iran.
EM maryam.sadr91@gmail.com; zahrashafaghat75@gmail.com;
mona.roozbehani@yahoo.com; Hoseinzadehak961@semums.ac.ir;
fs.mohammadi55@gmail.com; fahime.lavi@gmail.com;
sara.minaeian@gmail.com; faraji.fat@iums.ac.ir
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NR 191
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1867-1306
EI 1867-1314
J9 PROBIOTICS ANTIMICRO
JI Probiotics Antimicrob. Proteins
PD 2024 DEC 30
PY 2024
DI 10.1007/s12602-024-10431-z
EA DEC 2024
PG 23
WC Biotechnology & Applied Microbiology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Microbiology
GA Q8Q4W
UT WOS:001387253100001
PM 39739162
DA 2025-01-07
ER
PT J
AU Bei, R
Masuelli, L
Palumbo, C
Modesti, M
Modesti, A
AF Bei, R.
Masuelli, L.
Palumbo, C.
Modesti, M.
Modesti, A.
TI A common repertoire of autoantibodies is shared by cancer and autoimmune
disease patients: Inflammation in their induction and impact on tumor
growth
SO CANCER LETTERS
LA English
DT Review
DE Tumor antigens; Anti-cancer immunity; Immune tolerance; Autoantibodies;
Inflammation
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; ANTI-DNA ANTIBODIES; B-CELL EPITOPE;
RIBOSOMAL-P-PROTEINS; OF-THE-LITERATURE; LUNG-CANCER; P53
AUTOANTIBODIES; IMMUNE-RESPONSE; SELF-ANTIGENS; HEPATOCELLULAR-CARCINOMA
AB The repertoire of autoantibodies found in cancer patients partly overlaps with that typical of patients with autoimmune diseases. Beside the biochemical and immunological properties of the target antigens and their altered expression in tumor tissues, the intratumoral inflammatory context can play a key role in the induction of autoimmune disease-associated autoantibodies in cancer patients. Furthermore, the impact of such antibodies on cancer growth and progression can be deeply influenced by the interplay with inflammation. The characterization of the spontaneous humoral responses occurring in cancer patients, of the mechanisms that trigger and sustain the autoantibody response and of the biological effects of such autoantibodies may help the rational design of anti-cancer immunotherapeutic protocols. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Bei, R.; Palumbo, C.; Modesti, A.] Univ Tor Vergata, Dept Expt Med & Biochem Sci, I-00133 Rome, Italy.
[Masuelli, L.] Univ Sapienza, Dept Expt Med, Rome, Italy.
[Modesti, M.] Univ Sapienza, Dept Surg Sci, Rome, Italy.
C3 University of Rome Tor Vergata; Sapienza University Rome; Sapienza
University Rome
RP Bei, R (corresponding author), Univ Tor Vergata, Dept Expt Med & Biochem Sci, Via Montpellier 1, I-00133 Rome, Italy.
EM bei@med.uniroma2.it
RI Bei, Roberto/W-8023-2019; Masuelli, Laura/AGW-4259-2022; Modesti,
Mauro/D-6258-2017; Palumbo, Carla/E-5802-2012
OI MASUELLI, Laura/0000-0001-8174-8034; Palumbo,
Camilla/0000-0001-5087-7140
FU Italian Ministry of University and Research (PRIN 2007)
FX This work was supported by grants from the Italian Ministry of
University and Research (PRIN 2007, R.B., L.M. and A.M.). We thank
Barbara Bulgarini for assistance in manuscript preparation. We apologize
to the colleagues whose articles have not been cited in this review
because of space limitations.
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EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD AUG 18
PY 2009
VL 281
IS 1
BP 8
EP 23
DI 10.1016/j.canlet.2008.11.009
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 465KD
UT WOS:000267581600002
PM 19091462
DA 2025-01-07
ER
PT J
AU Chen, JH
Deshpande, V
AF Chen, Jonathan H.
Deshpande, Vikram
TI IgG4-related Disease and the Liver
SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE IgG4-related disease; IgG4; IgG4-related sclerosing cholangitis; Primary
sclerosing cholangitis; Autoimmune pancreatitis
ID PRIMARY SCLEROSING CHOLANGITIS; IMMUNOGLOBULIN G4-ASSOCIATED
CHOLANGITIS; MULTICENTRIC CASTLEMANS-DISEASE; NATIONWIDE EPIDEMIOLOGIC
SURVEY; SERUM IGG4 LEVELS; AUTOIMMUNE PANCREATITIS; G4-RELATED DISEASE;
PLASMA-CELLS; EXTRAHEPATIC CHOLANGIOCARCINOMA; IGG4-ASSOCIATED
CHOLANGITIS
AB Pathologists are likely to encounter IgG4-related disease in several organ systems. This article focuses on helping pathologists diagnose IgG4-related disease in the hepatobiliary system. Missing the diagnosis can result in unnecessary organ damage and/or unnecessary surgical and cancer therapy. In the liver, tumefactive lesion(s) involving the bile ducts with storiform fibrosis and an IgG4-enriched lymphoplasmacytic infiltrate are highly concerning for IgG4-related disease. The recent identification of oligoclonal populations of T cells and B cells in IgG4-related disease may lead to molecular tests, new therapeutics, and a greater mechanistic understanding of the disease.
C1 [Chen, Jonathan H.; Deshpande, Vikram] Harvard Med Sch, Massachusetts Gen Hosp, Dept Pathol, 55 Fruit St, Boston, MA 01224 USA.
C3 Harvard University; Massachusetts General Hospital; Harvard Medical
School
RP Deshpande, V (corresponding author), Harvard Med Sch, Massachusetts Gen Hosp, Dept Pathol, 55 Fruit St, Boston, MA 01224 USA.
EM vikramdirdeshpande@gmail.com
RI Deshpande, Vikram/AEN-2602-2022
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NR 81
TC 29
Z9 34
U1 0
U2 13
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8553
EI 1558-1942
J9 GASTROENTEROL CLIN N
JI Gastroenterol. Clin. North Am.
PD JUN
PY 2017
VL 46
IS 2
BP 195
EP +
DI 10.1016/j.gtc.2017.01.001
PG 23
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EX2CU
UT WOS:000403033900003
PM 28506361
DA 2025-01-07
ER
PT J
AU Albright, CM
Fay, EE
AF Albright, Catherine M.
Fay, Emily E.
TI Chronic Liver Disease in the Obstetric Patient
SO CLINICAL OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE chronic liver disease; pregnancy; review
ID BUDD-CHIARI-SYNDROME; PRIMARY BILIARY-CIRRHOSIS; PENICILLAMINE-TREATED
PATIENTS; WILSONS-DISEASE; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE
HEPATITIS; URSODEOXYCHOLIC ACID; TRANSPLANT RECIPIENTS; SPONTANEOUS
RUPTURE; PREGNANT-WOMEN
AB Chronic liver disease in pregnancy is rare. Historically, many chronic liver diseases were considered contraindications to pregnancy; however, with current monitoring and treatment strategies, pregnancy may be considered in many cases. Preconception and initial antepartum consultation should focus on disease activity, medication safety, risks of pregnancy, as well as the need for additional monitoring during pregnancy. In most cases, a multidisciplinary approach is necessary to ensure optimal maternal and fetal outcomes. Despite improving outcomes, pregnancy in women with the chronic liver disease remains high risk.
C1 [Albright, Catherine M.; Fay, Emily E.] Univ Washington, Med Ctr, Dept Obstet & Gynecol, Div Maternal Fetal Med, Box 356460, Seattle, WA 98195 USA.
C3 University of Washington; University of Washington Seattle
RP Albright, CM (corresponding author), Univ Washington, Med Ctr, Dept Obstet & Gynecol, Div Maternal Fetal Med, Box 356460, Seattle, WA 98195 USA.
EM cmalbrig@uw.edu
OI Fay, Emily/0000-0001-5582-2835
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TC 2
Z9 3
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0009-9201
EI 1532-5520
J9 CLIN OBSTET GYNECOL
JI Clin. Obstet. Gynecol.
PD MAR
PY 2020
VL 63
IS 1
BP 193
EP 210
DI 10.1097/GRF.0000000000000502
PG 18
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA KF5OC
UT WOS:000509290300020
PM 31789831
DA 2025-01-07
ER
PT J
AU Geng, QS
Cao, XX
Fan, DP
Wang, Q
Wang, X
Zhang, MX
Zhao, L
Jiao, Y
Deng, TT
Liu, HL
Zhou, J
Lou, YN
Liang, J
Xiao, C
AF Geng, Qishun
Cao, Xiaoxue
Fan, Danping
Wang, Qiong
Wang, Xing
Zhang, Mengxiao
Zhao, Lu
Jiao, Yi
Deng, Tingting
Liu, Honglin
Zhou, Jing
Lou, Yanni
Liang, Jing
Xiao, Cheng
TI Potential medicinal value of N6-methyladenosine in autoimmune diseases
and tumours
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Review; Early Access
DE autoimmune diseases; m6A; medicinal value; targets; tumours
ID HEPATOCELLULAR-CARCINOMA; CONCISE GUIDE; FAT MASS; M(6)A; METHYLATION;
CANCER; IDENTIFICATION; PROLIFERATION; SUPPRESSES; APOPTOSIS
AB Autoimmune diseases (ADs) are closely related to malignant tumours. On the one hand, ADs can increase the incidence of tumours; on the other hand, malignant tumours can cause rheumatic disease-like manifestations. With the increasing depth of analysis into the mechanism of N-6-methyladenosine (m6A) modification, it has been found that changes in m6A-related modification enzymes are closely related to the occurrence and development of ADs and malignant tumours. In this review, we explore the pathogenesis of ADs and tumours based on m6A modification. According to systematic assessment of the similarities between ADs and tumours, m6A may represent a common target of both diseases. At present, most of the drugs targeting m6A are in the research and development stage, not in clinical trials. Therefore, advancing the development of drugs targeting m6A is of great significance for both the combined treatment of ADs and malignant tumours and improving the quality of life and prognosis of patients.
C1 [Geng, Qishun; Cao, Xiaoxue; Zhang, Mengxiao; Deng, Tingting; Liu, Honglin; Xiao, Cheng] China Japan Friendship Hosp, Inst Clin Med, Beijing, Peoples R China.
[Geng, Qishun; Cao, Xiaoxue; Xiao, Cheng] Chinese Acad Med Sci & Peking Union Med Coll, China Japan Friendship Hosp, Inst Clin Med Sci, Beijing, Peoples R China.
[Fan, Danping] China Acad Chinese Med Sci, Expt Res Ctr, Beijing Key Lab Res Chinese Med Prevent & Treatmen, Beijing, Peoples R China.
[Wang, Qiong; Wang, Xing; Jiao, Yi] Beijing Univ Chinese Med, China Japan Friendship Clin Med Coll, Beijing, Peoples R China.
[Zhao, Lu] Capital Med Univ, China Japan Friendship Hosp, Beijing, Peoples R China.
[Zhou, Jing] Guangxi Med Univ, Sch Basic Med Sci, Dept Physiol, Nanning, Peoples R China.
[Lou, Yanni] China Japan Friendship Hosp, Oncol Dept Integrated Tradit Chinese & Western Med, Beijing, Peoples R China.
[Liang, Jing] China Japan Friendship Hosp, Dept Obstet & Gynecol, Beijing, Peoples R China.
[Xiao, Cheng] China Japan Friendship Hosp, Dept Emergency, Beijing, Peoples R China.
C3 China-Japan Friendship Hospital; Chinese Academy of Medical Sciences -
Peking Union Medical College; Peking Union Medical College; China-Japan
Friendship Hospital; Experimental Research Center, CACMS; China Academy
of Chinese Medical Sciences; Beijing University of Chinese Medicine;
Capital Medical University; China-Japan Friendship Hospital; Guangxi
Medical University; China-Japan Friendship Hospital; China-Japan
Friendship Hospital; China-Japan Friendship Hospital
RP Xiao, C (corresponding author), China Japan Friendship Hosp, Inst Clin Med, Beijing, Peoples R China.; Lou, YN (corresponding author), China Japan Friendship Hosp, Oncol Dept Integrated Tradit Chinese & Western Med, Beijing, Peoples R China.; Liang, J (corresponding author), China Japan Friendship Hosp, Dept Obstet & Gynecol, Beijing, Peoples R China.
EM louyanni@hotmail.com; jacyliang@sina.com; xc2002812@126.com
RI Liu, Honglin/AAA-9488-2022; mengxiao, zhang/GYU-3986-2022; Xiao,
Cheng/AAM-7764-2020
OI xiao, Cheng/0000-0002-5601-9670
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NR 94
TC 6
Z9 6
U1 2
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1188
EI 1476-5381
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD 2023 FEB 1
PY 2023
DI 10.1111/bph.16030
EA FEB 2023
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 8G4EN
UT WOS:000920299100001
PM 36624563
OA Bronze
DA 2025-01-07
ER
PT J
AU Willuweit, K
Heinold, A
Rashidi-Alavijeh, J
Heinemann, FM
Horn, PA
Paul, A
Gerken, G
Herzer, K
AF Willuweit, Katharina
Heinold, Andreas
Rashidi-Alavijeh, Jassin
Heinemann, Falko M.
Horn, Peter A.
Paul, Andreas
Gerken, Guido
Herzer, Kerstin
TI Immunosuppression with mTOR inhibitors prevents the development of
donor-specific antibodies after liver transplant
SO CLINICAL TRANSPLANTATION
LA English
DT Article
DE donor-specific antibodies; everolimus; hepatocellular carcinoma; human
leukocyte antigen antibodies; liver transplantation
ID ANTI-HLA ANTIBODIES; MEDIATED REJECTION; CALCINEURIN INHIBITORS;
ALLOGRAFT RECIPIENTS; CYCLOSPORINE; EVEROLIMUS; TOLERANCE; DISEASES; C4D
AB Background: Donor-specific antibodies (DSAs) are an important cause of complications after solid organ transplant. Risk factors and, thus, strategies for preventing DSA development are not well defined.
Methods: The DSA status of 400 patients who underwent liver transplant (LT) at the outpatient clinic of the University Hospital Essen was determined. Human leukocyte antigen (HLA) antibodies were detected by single-antigen bead technology. The strength of DSAs was reported as mean fluorescence intensity.
Results: Detectable DSAs were found in 74 (18.5%) patients and significantly more often in patients who underwent LT for autoimmune liver disease than for all other indications (29.3%; P=.022), but significantly less often found in patients who underwent LT for hepatocellular carcinoma (7.6%, P=.005). The incidence of DSAs increased with time after LT, and the risk was generally higher for female patients. The frequency of DSA detection was significantly lower (10.6%) for patients receiving immunosuppressive treatment with mammalian target of rapamycin (mTOR) inhibitors than for those receiving other regimens (20.5%; P=.025).
Conclusion: Autoimmune liver diseases, female sex, and time of more than 8 years since LT predispose patients to the development of DSAs. Immunosuppression with the mTOR inhibitor everolimus protects against DSA development after liver transplant.
C1 [Willuweit, Katharina; Rashidi-Alavijeh, Jassin; Gerken, Guido; Herzer, Kerstin] Univ Duisburg Essen, Univ Hosp Essen, Dept Gastroenterol & Hepatol, Duisburg, Germany.
[Willuweit, Katharina; Rashidi-Alavijeh, Jassin; Paul, Andreas; Herzer, Kerstin] Univ Duisburg Essen, Univ Hosp Essen, Dept Gen Visceral & Transplantat Surg, Duisburg, Germany.
[Heinold, Andreas; Heinemann, Falko M.; Horn, Peter A.] Univ Duisburg Essen, Univ Hosp Essen, Inst Transfus Med, Duisburg, Germany.
C3 University of Duisburg Essen; University of Duisburg Essen; University
of Duisburg Essen
RP Herzer, K (corresponding author), Univ Duisburg Essen, Univ Hosp Essen, Dept Gastroenterol & Hepatol, Duisburg, Germany.; Herzer, K (corresponding author), Univ Duisburg Essen, Univ Hosp Essen, Dept Gen Visceral & Transplantat Surg, Duisburg, Germany.
EM kerstin.herzer@uk-essen.de
FU Office of the Dean of the Faculty of Medicine, University of
Duisburg-Essen
FX Office of the Dean of the Faculty of Medicine, University of
Duisburg-Essen
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PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0902-0063
EI 1399-0012
J9 CLIN TRANSPLANT
JI Clin. Transplant.
PD JUN
PY 2017
VL 31
IS 6
AR e12974
DI 10.1111/ctr.12974
PG 8
WC Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery; Transplantation
GA EZ8KZ
UT WOS:000404975900012
PM 28345271
DA 2025-01-07
ER
PT J
AU Wu, S
Li, XF
Wu, YY
Yin, SQ
Huang, C
Li, J
AF Wu, Sha
Li, Xiao-Feng
Wu, Yuan-Yuan
Yin, Su-Qin
Huang, Cheng
Li, Jun
TI N6 -Methyladenosine and Rheumatoid Arthritis: A
Comprehensive Review
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE N-6; -methyladenosine; rheumatoid arthritis; immune cells; autoimmune
disease; cancers
ID METHYLTRANSFERASE METTL3 PROMOTES; NATURAL-KILLER-CELLS; MESSENGER-RNA;
HEPATOCELLULAR-CARCINOMA; STRUCTURAL BASIS; DENDRITIC CELLS;
NUCLEAR-RNA; M(6)A RNA; CANCER; TRANSLATION
AB Rheumatoid arthritis (RA), one of the most common autoimmune diseases, is characterized by immune cell infiltration, fibroblast-like synovial cell hyperproliferation, and cartilage and bone destruction. To date, numerous studies have demonstrated that immune cells are one of the key targets for the treatment of RA. N-6-methyladenosine (m(6)A) is the most common internal modification to eukaryotic mRNA, which is involved in the splicing, stability, export, and degradation of RNA metabolism. m(6)A methylated-related genes are divided into writers, erasers, and readers, and they are critical for the regulation of cell life. They play a significant role in various biological processes, such as virus replication and cell differentiation by controlling gene expression. Furthermore, a growing number of studies have indicated that m(6)A is associated with the occurrence of numerous diseases, such as lung cancer, bladder cancer, gastric cancer, acute myeloid leukemia, and hepatocellular carcinoma. In this review, we summarize the history of m6A research and recent progress on RA research concerning m(6)A enzymes. The relationship between m(6)A enzymes, immune cells, and RA suggests that m(6)A modification offers evidence for the pathogenesis of RA, which will help in the development of new therapies for RA.
C1 [Wu, Sha; Li, Xiao-Feng; Wu, Yuan-Yuan; Yin, Su-Qin; Huang, Cheng; Li, Jun] Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Key Lab Antiinflammatory & Immune Med, Anhui Inst Innovat Drugs,Minist Educ,Sch Pharm, Hefei, Peoples R China.
[Li, Xiao-Feng] Anhui Med Univ, Postdoctoral Stn Clin Med, Hefei, Peoples R China.
C3 Anhui Medical University; Anhui Medical University
RP Li, J (corresponding author), Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Key Lab Antiinflammatory & Immune Med, Anhui Inst Innovat Drugs,Minist Educ,Sch Pharm, Hefei, Peoples R China.
EM lj@ahmu.edu.cn
RI li, xiaofeng/GXF-9442-2022; wu, yunayuan/IST-4642-2023
FU National Natural Science Foundation of China [82002269]; China
Postdoctoral Science Foundation [2020M671839]; Postdoctoral Science
Foundation from Anhui Medical University [BSH201902]; Anhui Provincial
Science and Technology Major Project [8212929035]
FX This study was supported by the National Natural Science Foundation of
China (No. 82002269), China Postdoctoral Science Foundation (No.
2020M671839), Postdoctoral Science Foundation from Anhui Medical
University (No. BSH201902), and Anhui Provincial Science and Technology
Major Project (8212929035).
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NR 117
TC 33
Z9 34
U1 0
U2 16
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 24
PY 2021
VL 12
AR 731842
DI 10.3389/fimmu.2021.731842
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA WE8PK
UT WOS:000705881100001
PM 34630412
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Song, Y
Zhao, YY
Wang, F
Tao, LC
Xiao, JJ
Yang, CQ
AF Song, Yang
Zhao, Yingying
Wang, Fei
Tao, Lichan
Xiao, Junjie
Yang, Changqing
TI Autophagy in Hepatic Fibrosis
SO BIOMED RESEARCH INTERNATIONAL
LA English
DT Review
ID PROTEIN-DEGRADATION PATHWAYS; ENDOPLASMIC-RETICULUM STRESS;
STARVATION-INDUCED AUTOPHAGY; STELLATE CELLS; C VIRUS; LIVER FIBROSIS;
ALPHA-1-ANTITRYPSIN DEFICIENCY; INTRACELLULAR INCLUSIONS;
HEPATOCELLULAR-CARCINOMA; MESENCHYMAL TRANSITION
AB Hepatic fibrosis is a leading cause of morbidity and mortality worldwide. Hepatic fibrosis is usually associated with chronic liver diseases caused by infection, drugs, metabolic disorders, or autoimmune imbalances. Effective clinical therapies are still lacking. Autophagy is a cellular process that degrades damaged organelles or protein aggregation, which participates in many pathological processes including liver diseases. Autophagy participates in hepatic fibrosis by activating hepatic stellate cells and may participate as well through influencing other fibrogenic cells. Besides that, autophagy can induce some liver diseases to develop while it may play a protective role in hepatocellular abnormal aggregates related liver diseases and reduces fibrosis. With a better understanding of the potential effects of autophagy on hepatic fibrosis, targeting autophagy might be a novel therapeutic strategy for hepatic fibrosis in the near future.
C1 [Song, Yang; Zhao, Yingying; Wang, Fei; Xiao, Junjie; Yang, Changqing] Tongji Univ, Sch Med, Shanghai Tongji Hosp, Div Gastroenterol & Hepatol,Digest Dis Inst, Shanghai 200065, Peoples R China.
[Tao, Lichan; Xiao, Junjie] Shanghai Univ, Sch Life Sci, Regenerat Lab, Shanghai 200444, Peoples R China.
[Tao, Lichan; Xiao, Junjie] Shanghai Univ, Sch Life Sci, Expt Ctr Life Sci, Shanghai 200444, Peoples R China.
[Tao, Lichan] Nanjing Med Univ, Affiliated Hosp 1, Dept Cardiol, Nanjing 210029, Jiangsu, Peoples R China.
[Xiao, Junjie] Shanghai Univ, Sch Life Sci, Shanghai Key Lab Bioenergy Crops, Shanghai 200444, Peoples R China.
C3 Tongji University; Shanghai University; Shanghai University; Nanjing
Medical University; Shanghai University
RP Xiao, JJ (corresponding author), Tongji Univ, Sch Med, Shanghai Tongji Hosp, Div Gastroenterol & Hepatol,Digest Dis Inst, 389 Xincun Rd, Shanghai 200065, Peoples R China.
EM junjiexiao@shu.edu.cn; changqingyang_tj@hotmail.com
RI TAO, Li/HIR-4254-2022
OI Song, Yang/0009-0006-2123-1600
FU National Natural Science Foundation of China [81200169, 81070343,
81370559]; Shanghai Innovation Program [12431901002]; Innovation Program
of Shanghai Municipal Education Commission [13YZ014]; Foundation for
University Young Teachers by Shanghai Municipal Education Commission;
Innovation Foundation of Shanghai University [sdcx2012038]; Leading
Academic Discipline Project of Shanghai Municipal Education Commission
"Molecular Physiology"; Shanghai Municipal Science and Technology
Committee [13DZ2272100]
FX This work was supported by the Grants from National Natural Science
Foundation of China (81200169 to Junjie Xiao; 81070343 and 81370559 to
Changqing Yang), funds from Shanghai Innovation Program (12431901002 to
Changqing Yang), Innovation Program of Shanghai Municipal Education
Commission (13YZ014 to Junjie Xiao), Foundation for University Young
Teachers by Shanghai Municipal Education Commission (year 2012, to
Junjie Xiao), Innovation Foundation of Shanghai University (sdcx2012038,
to Junjie Xiao), and partially by Leading Academic Discipline Project of
Shanghai Municipal Education Commission "Molecular Physiology" and
Shanghai Municipal Science and Technology Committee (13DZ2272100).
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NR 104
TC 43
Z9 49
U1 5
U2 36
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-6133
EI 2314-6141
J9 BIOMED RES INT
JI Biomed Res. Int.
PY 2014
VL 2014
AR 436242
DI 10.1155/2014/436242
PG 8
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA AE3VH
UT WOS:000333906000001
PM 24779010
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Bave, AL
von Seth, E
Ingre, M
Nordenvall, C
Bergquist, A
AF Lundberg Bave, Aiva
von Seth, Erik
Ingre, Michael
Nordenvall, Caroline
Bergquist, Annika
TI Autoimmune diseases in primary sclerosing cholangitis and their
first-degree relatives
SO HEPATOLOGY
LA English
DT Article
DE Inflammatory bowel disease; first-degree relatives; genetics; heredity
ID IBD IMMUNOLOGICAL DISEASES; GENOME-WIDE ASSOCIATION; RISK; REGISTER;
GENETICS
AB Background:Primary sclerosing cholangitis (PSC) is linked to inflammatory bowel disease (IBD). However, there is limited overlap between IBD and PSC risk genes, but a stronger association between PSC and other autoimmune conditions. We aimed to assess coexistence and familial association of autoimmune disorders in PSC, and the influence of autoimmune co-morbidity on severe outcomes. Method:In a matched cohort study, 1,378 individuals with PSC and 13,549 general population comparators and their first-degree relatives were evaluated. National registries provided data on diagnoses and outcomes (liver transplantation, hepatobiliary cancer, liver related death). Odds ratio (OR) of autoimmune disease was estimated by logistic regression. Fine & Gray competing risk regression estimated hazard ratios (HRs) for severe outcomes. Results:Prevalence of non-IBD, non-autoimmune hepatitis (AIH), autoimmune disease was 18% in PSC and 11% in comparators, OR 1.77(95%CI; 1.53-2.05). Highest odds were seen for celiac disease [OR 4.36(95%CI; 2.44-7.49)], sarcoidosis [OR 2.74(95%CI; 1.29-5.33)], diabetes type 1 [OR 2.91(95%CI; 2.05-4.05)], and autoimmune skin disease [OR 2.15(95%CI; 1.52-2.96)]. First-degree relatives of individuals with PSC had higher odds for developing IBD, AIH and any autoimmune disease than relatives of the comparators [OR 3.25 95% CI (2.68-3.91); OR 5.94 95% CI (2.82-12.02); OR 1.34 (95% CI: 1.19-1.50)]. Autoimmune co-morbidity in PSC was not associated with poorer outcome, HR 0.96 (95%CI; 0.71-1.28). Conclusion:Individuals with PSC and their first-degree relatives had higher odds for autoimmune disease compared to matched comparators. This finding provides validation for prior genetic discoveries at a phenotypic level. Autoimmune comorbidity did not impact severe outcome.
C1 [Lundberg Bave, Aiva; von Seth, Erik; Ingre, Michael; Bergquist, Annika] Karolinska Univ Hosp, Karolinska Inst, Dept Upper GI Dis, Div Hepatol,Dept Med Huddings, Stockholm, Sweden.
[Nordenvall, Caroline] Karolinska Univ Hosp, Karolinska Inst, Dept Mol Med & Surg, Dept Pelv Canc, Stockholm, Sweden.
C3 Karolinska Institutet; Karolinska University Hospital; Karolinska
Institutet; Karolinska University Hospital
RP Bave, AL (corresponding author), Karolinska Univ Hosp, Karolinska Inst, Dept Upper GI Dis, Div Hepatol,Dept Med Huddings, Stockholm, Sweden.
EM aiva.lundberg.bave@ki.se; erik.von.seth@ki.se; michael.ingre@ki.se;
caroline.nordenvall@ki.se; annika.bergquist@ki.se
RI Nordenvall, Caroline/C-4058-2016
OI Nordenvall, Caroline/0000-0002-5112-8894
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NR 36
TC 2
Z9 2
U1 3
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD SEP
PY 2024
VL 80
IS 3
BP 527
EP 535
DI 10.1097/HEP.0000000000000823
EA MAR 2024
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA E1G8V
UT WOS:001199819500002
PM 38441983
DA 2025-01-07
ER
PT J
AU Lefkowitch, JH
AF Lefkowitch, Jay H.
TI Advances in Hepatobiliary Pathology: Update for 2010
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Hepatology; Hepatic pathology; Hepatobiliary pathology; Liver tumors;
Cholangiocarcinoma; Primary sclerosing cholangitis
ID PRIMARY BILIARY-CIRRHOSIS; HEPATITIS-C VIRUS; PRIMARY SCLEROSING
CHOLANGITIS; INTRAHEPATIC CHOLESTASIS TYPE-1; FATTY LIVER-DISEASE;
HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC STEATOHEPATITIS; AUTOIMMUNE
HEPATITIS; RISK-FACTORS; DIAGNOSIS
AB Recent publications on hepatology and hepatic pathology provide a wealth of new information on wideranging topics Morphologic aspects of liver disease associated with hepatitis B and C viruses autoimmune hepatitis and HIV infection were addressed as was the prevalent problem of nonalcoholic fatty liver disease Advances in diagnosis and pathogenesis of primary biliary cirrhosis primary sclerosing cholangitis and the increasingly complex spectrum of IgG4 hepatobiliary diseases were also reported The histologic and immunohistochemical features of the rare calcifying nested stromal-epithelial tumor of the liver were described in a 9-case series For benign and malignant liver tumors immunohistochemistry plays a major diagnostic role and several recent studies demonstrate the value of immunostains in distinguishing between liver-cell adenoma and focal nodular hyperplasia
C1 Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA.
C3 Columbia University
RP Lefkowitch, JH (corresponding author), Columbia Univ, Coll Phys & Surg, Dept Pathol, 630 W 168th St PH 15 W,Room 1574, New York, NY 10032 USA.
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NR 87
TC 1
Z9 3
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD NOV
PY 2010
VL 14
IS 4
BP 747
EP +
DI 10.1016/j.cld.2010.07.007
PG 18
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 688OG
UT WOS:000284859900014
PM 21055694
DA 2025-01-07
ER
PT J
AU Delire, B
De Martin, E
Meunier, L
Larrey, D
Horsmans, Y
AF Delire, Benedicte
De Martin, Eleonora
Meunier, Lucy
Larrey, Dominique
Horsmans, Yves
TI Immunotherapy and Gene Therapy: New Challenges in the Diagnosis and
Management of Drug-Induced Liver Injury
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE immunotherapy; immune checkpoint inhibitors; immune-mediated hepatitis;
gene therapy; drug-induced liver injury (DILI)
ID IMMUNE CHECKPOINT INHIBITORS; ADVANCED HEPATOCELLULAR-CARCINOMA;
PREEXISTING AUTOIMMUNE; ADVERSE EVENTS; CAUSALITY ASSESSMENT; METASTATIC
MELANOMA; COMBINED NIVOLUMAB; DOUBLE-BLIND; HEPATITIS; IPILIMUMAB
AB In the last 5 years, the landscape of oncologic treatment has been deeply modified with the development and use of immune checkpoint inhibitors (ICIs) that exert their antitumoral effect by reverting the exhausted phenotype of tumor-infiltrating lymphocytes. This innovative therapeutic strategy has widely changed the prognosis of some advanced neoplastic diseases such as melanoma and lung cancer, providing durable remission for a significant number of patients. Unfortunately, immune-related adverse events (irAEs), especially ICI-induced hepatitis, may be very severe in some cases, impairing the prognosis of the patient. Guidelines available today on the diagnosis and management of ICI-induced hepatitis are mainly based on expert opinions and case series. This lack of large data is explained not only by the low incidence of hepatic adverse events but also by their clinical heterogeneity and variable severity. In this article, we will review the clinical, biological, and histological characteristics of ICI-induced liver injury. We will discuss the current knowledge on their pathological mechanisms and their therapeutic strategy based on immunosuppressive treatment for more severe cases. Regarding severity assessment, we will discuss the gap between the oncologist and the hepatologist's point of view, highlighting the need for multidisciplinary management. While initially developed for notably less frequent diseases than neoplastic ones, gene therapy is going to be a revolution for the treatment of diseases not responding to pharmacological therapy. Limited but growing data describe liver injury after the administration of such therapy whose exact physiopathology remains unknown. In this article, we will discuss the available data supporting the role of gene therapies in the onset of drug-induced liver injury and related mechanisms. We will describe the clinical context, the biological and histological features, and the management currently proposed.
C1 [Delire, Benedicte; Horsmans, Yves] Catholic Univ Louvain, Clin Univ St Luc, Dept Gastroenterol, Brussels, Belgium.
[Delire, Benedicte; Horsmans, Yves] Catholic Univ Louvain, Inst Rech Clin IREC, Brussels, Belgium.
[De Martin, Eleonora] Univ Paris Saclay, Hop Paul Brousse, AP HP, Ctr Hepatobiliaire,INSERM,Unit 1193, Villejuif, France.
[Meunier, Lucy; Larrey, Dominique] St Eloi Hosp, Montpellier Sch Med, INSERM 1183, Liver Unit, Montpellier, France.
C3 Universite Libre de Bruxelles; Universite Catholique Louvain; Cliniques
Universitaires Saint-Luc; Universite Catholique Louvain; Universite
Paris Saclay; Assistance Publique Hopitaux Paris (APHP); Hopital
Universitaire Paul-Brousse - APHP; Institut National de la Sante et de
la Recherche Medicale (Inserm); Institut National de la Sante et de la
Recherche Medicale (Inserm); Universite de Montpellier; CHU de
Montpellier
RP Horsmans, Y (corresponding author), Catholic Univ Louvain, Clin Univ St Luc, Dept Gastroenterol, Brussels, Belgium.; Horsmans, Y (corresponding author), Catholic Univ Louvain, Inst Rech Clin IREC, Brussels, Belgium.
EM yves.horsmans@saintluc.uclouvain.be
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NR 117
TC 12
Z9 13
U1 0
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD JAN 19
PY 2022
VL 12
AR 786174
DI 10.3389/fphar.2021.786174
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA YR3AA
UT WOS:000749866000001
PM 35126126
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Medina, J
Arroyo, AG
Sánchez-Madrid, F
Moreno-Otero, R
AF Medina, J
Arroyo, AG
Sánchez-Madrid, F
Moreno-Otero, R
TI Angiogenesis in chronic inflammatory liver disease
SO HEPATOLOGY
LA English
DT Review
ID ENDOTHELIAL GROWTH-FACTOR; OXIDE SYNTHASE EXPRESSION; TUMOR-CELL
INVASION; CHRONIC HEPATITIS-C; MATRIX METALLOPROTEINASES;
PARTIAL-HEPATECTOMY; HEPATOCELLULAR-CARCINOMA; EXTRACELLULAR-MATRIX;
TRANSFORMING-GROWTH; FACTOR RECEPTORS
AB Intrahepatic hypoxia may occur during the inflammatory and fibrotic processes that characterize several chronic liver diseases of viral and autoimmune origin. As a consequence, new vascular structures are formed to provide oxygen and nutrients. Angiogenesis involves a tightly regulated network of cellular and molecular mechanisms that result in the formation of functional vessels. Of particular importance are growth factors, molecules involved in matrix remodeling and cell migration, and vessel maturation-related factors. In recent years, a number of studies have examined the expression and function of many pro- and antiangiogenic molecules in the setting of nontumoral chronic liver diseases and liver regeneration. This review examines the potential pathogenetic role of angiogenesis in the context of viral hepatitis, cirrhosis, autoimmune hepatitis, primary biliary cirrhosis, and alcoholic liver disease. The future perspectives for research in this field are outlined.
C1 Univ Autonoma Madrid, Hosp Princesa, Liver Unit, E-28049 Madrid, Spain.
Univ Autonoma Madrid, Hosp Princesa, Serv Immunol, E-28049 Madrid, Spain.
C3 Autonomous University of Madrid; Hospital de La Princesa; Autonomous
University of Madrid; Hospital de La Princesa
RP Hosp Univ Princesa, Unidad Hepatol, Diego de Leon 62,Planta 3, E-28006 Madrid, Spain.
EM rmoreno.hlpr@salud.madrid.org
RI Arroyo, Alicia/M-2507-2018; Medina, Jesus/J-4785-2015; Sanchez-Madrid,
Francisco/M-7889-2016; Garcia Arroyo, Alicia/L-2796-2014
OI Sanchez-Madrid, Francisco/0000-0001-5303-0762; Garcia Arroyo,
Alicia/0000-0002-1536-3846
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NR 118
TC 185
Z9 211
U1 0
U2 15
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD MAY
PY 2004
VL 39
IS 5
BP 1185
EP 1195
DI 10.1002/hep.20193
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 815NX
UT WOS:000221050100001
PM 15122744
OA Bronze
DA 2025-01-07
ER
PT J
AU Brancatelli, G
Federle, MP
Ambrosini, R
Lagalla, R
Carriero, A
Midiri, M
Vilgrain, V
AF Brancatelli, Giuseppe
Federle, Michael P.
Ambrosini, Roberta
Lagalla, Roberto
Carriero, Alessandro
Midiri, Massimo
Vilgrain, Valrie
TI Cirrhosis: CT and MR imaging evaluation
SO EUROPEAN JOURNAL OF RADIOLOGY
LA English
DT Article
DE liver; cirrhosis; computed tomography; magnetic resonance imaging
ID CONGENITAL HEPATIC-FIBROSIS; BUDD-CHIARI-SYNDROME;
HEPATOCELLULAR-CARCINOMA; LIVER-DISEASE; PATHOLOGICAL CORRELATION;
REGENERATIVE NODULES; COMPUTED-TOMOGRAPHY; BILIARY-CIRRHOSIS;
MORPHOLOGY; DIAGNOSIS
AB In this article, we present the CT and MR imaging characteristics of the cirrhotic liver. We describe the altered liver morphology in different forms of viral, alcoholic and autoimmune end-stage liver disease. We present the spectrum of imaging findings in portal hypertension, such as splenomegaly, ascites and varices. We describe the patchy and lacelike patterns of fibrosis, along with the focal confluent form. The process of hepatocarcinogenesis is detailed, from regenerative to dysplastic nodules to overt hepatocellular carcinoma. Different types of non-neoplastic focal liver lesions occurring in the cirrhotic liver are discussed, including arterially enhancing nodules, hemangiomas and peribiliary cysts. We show different conditions causing liver morphology changes that can mimic cirrhosis, such as congenital hepatic fibrosis, "pseudo-cirrhosis" due to breast metastases treated with chemotherapy, Budd-Chiari syndrome, sarcoidosis and cavernous transformation of the portal vein. (C) 2006 Elsevier Ireland Ltd. All rights reserved.
C1 Saverio Bellis IRCCS, Osped Specializzato Gastroenterol, Sez Radiol, I-70013 Bari, Italy.
Univ Palermo, Dipartimento Biotecnol Med & Med Legale, Sez Sci Radiol, I-90127 Palermo, Italy.
Univ Pittsburgh, Med Ctr, Dept Radiol, Pittsburgh, PA 15213 USA.
A Avogadro Eastern Piemonte Univ, Maggiore Carita Univ Hosp, Dept Diagnost & Intervent Radiol, Novara, Italy.
Hop Beaujon, Serv Radiol, F-92118 Clichy, France.
C3 IRCCS Saverio de Bellis; University of Palermo; Pennsylvania
Commonwealth System of Higher Education (PCSHE); University of
Pittsburgh; University of Eastern Piedmont Amedeo Avogadro; Assistance
Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
Universitaire Beaujon - APHP
RP Brancatelli, G (corresponding author), Via Villaermosa 29, I-90139 Palermo, Italy.
EM gbranca@yahoo.com
RI Ambrosini, Roberta/J-6711-2019; brancatelli, giuseppe/ADI-3570-2022;
CARRIERO, Alessandro/AAL-3790-2020
OI BRANCATELLI, Giuseppe/0000-0001-6136-9088; Ambrosini,
Roberta/0000-0002-4082-2303
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NR 40
TC 110
Z9 123
U1 0
U2 11
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0720-048X
EI 1872-7727
J9 EUR J RADIOL
JI Eur. J. Radiol.
PD JAN
PY 2007
VL 61
IS 1
BP 57
EP 69
DI 10.1016/j.ejrad.2006.11.003
PG 13
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 130KZ
UT WOS:000243799800008
PM 17145154
DA 2025-01-07
ER
PT J
AU Kubiatowski, T
Nicos, M
Krawczyk, P
AF Kubiatowski, Tomasz
Nicos, Marcin
Krawczyk, Pawel
TI Lung Cancer Immunotherapy in Transplant Patients and in Patients With
Autoimmune Diseases
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE programmed cell death receptor type 1; PD-1 ligand; cytotoxic T
lymphocyte-associated antigen; preexisting autoimmune disease;
transplant recipients
ID IMMUNE CHECKPOINT INHIBITORS; PREEXISTING AUTOIMMUNE; OPEN-LABEL;
IPILIMUMAB; NIVOLUMAB; DOCETAXEL; ATEZOLIZUMAB; MULTICENTER;
PEMBROLIZUMAB; CHEMOTHERAPY
AB The use of immune checkpoint inhibitors (ICIs) delivered great and new possibilities in modern treatment of many types of cancers. This therapy based on blockade of such molecules as CTLA-4 (cytotoxic T lymphocyte-associated antigen), PD-1 (programmed cell death receptor type 1), or PD-1 ligand (PD-L1) brings a new hope for patients with non-small cell lung cancer (NSCLC), melanoma, or head and neck squamous carcinoma. Efficacy of immunotherapy was proven in many clinical trials. Unfortunately, ICIs treatment was not addressed to the patients with preexisting allogeneic transplants or autoimmune diseases mainly due to high risk of transplant rejection, exacerbation of autoimmune diseases, and risk of serious toxicity. However, it is possible to receive anti-tumor response to ICIs treatment avoiding graft rejection by adjusting the immunosuppression. Obviously, it depends on the type of transplants: the use of immunotherapy is usually possible in kidney or corneal recipients, but it could be difficult in patients with liver and heart transplant. Therefore, the development of biomarkers for tumor response and transplant rejection in ICIs treated patients is essential. Data coming from published literature support the possibilities of using ICIs in patients with preexisting autoimmune diseases who undergoing proper management of side effects of immunotherapy or when the potential benefits of such treatment outweigh the potential risks. This depends on the type of autoimmune disease and may be difficult or not feasible in patients with systemic lupus erythematosus or systemic sclerosis. Therefore, it may be appropriate to include cancer patients with preexisting autoimmune disease or with allogeneic transplants in clinical trials using immunotherapy when no other effective cancer treatment options exist.
C1 [Kubiatowski, Tomasz] Ctr Oncol Lublin Reg, Dept Med Oncol, Lublin, Poland.
[Nicos, Marcin; Krawczyk, Pawel] Med Univ Lublin, Dept Pneumonol Oncol & Allergol, Lublin, Poland.
[Nicos, Marcin] Karolinska Inst, Dept Med Biochem & Biophys, Sci Life Lab, Stockholm, Sweden.
C3 Medical University of Lublin; Karolinska Institutet
RP Kubiatowski, T (corresponding author), Ctr Oncol Lublin Reg, Dept Med Oncol, Lublin, Poland.
EM tkubiatowski@cozl.eu
OI Nicos, Marcin/0000-0002-9566-113X; Krawczyk, Pawel/0000-0001-8400-4452
FU Medical University of Lublin; Foundation for Polish Science (FNP)
FX This work was supported by Funds from Medical University of Lublin to PK
and a START scholarship from the Foundation for Polish Science (FNP) to
MN.
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NR 44
TC 1
Z9 1
U1 0
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 19
PY 2020
VL 10
AR 568081
DI 10.3389/fonc.2020.568081
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OZ7OM
UT WOS:000595110800001
PM 33330040
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Liu, SQ
Wang, JS
Guo, CM
Qi, HB
Sun, MZ
AF Liu, Shuqing
Wang, Jiasheng
Guo, Chunmei
Qi, Houbao
Sun, Ming-Zhong
TI Annexin A11 knockdown inhibits in vitro proliferation and
enhances survival of Hca-F cell via Akt2/FoxO1 pathway and MMP-9
expression
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Anxa11; Hepatocarcinoma; Proliferation; Apoptosis; Akt2/FoxO1 pathway
ID MATRIX-METALLOPROTEINASE (MMP)-2; LYMPH-NODE METASTASIS;
HEPATOCELLULAR-CARCINOMA; SIGNALING PATHWAY; HEPATOCARCINOMA CELLS;
COLORECTAL-CANCER; LIVER-CANCER; APOPTOSIS; AKT; PHOSPHORYLATION
AB Annexin A11 (Anxa11), a Ca2+-regulated phospholipid-binding protein, is involved in cell apoptosis, differentiation, vesicle trafficking, cancer progression and autoimmune diseases. Previous study from our group indicated that Anxa11 was associated with lymphatic metastatic potential of murine hepatocarcinoma cells. Herein, we investigated the effects and action mechanism of Anxa11 knockdown on in vitro cell proliferation and apoptosis of Hca-F, a murine hepatocarcinoma cell with similar to 75% lymph node metastatic potential. Real-time PCR and western blotting assays indicated that Anxa11 was significantly downregulated in monoclonal Anxa11-shRNA-transfected Hca-F cells. Anxa11 knockdown in Hca-F suppressed its in vitro proliferation and cell apoptosis capacities. Following Anxa11 knockdown in Hca-F cells, Bax/Bcl-2 expression level ratio, Akt2 and FoxO1 (pSer319) expression levels as well as MMP-9 mRNA and active MMP-9 protein levels were significantly elevated in Hca-F cells. In conclusion, Annexin A11 knockdown inhibits the in vitro proliferation and cell apoptosis of Hca-F cell via Akt2/FoxO1 and/or MMP-9 expression pathway. Anxa11 might play an important role in hepatocarcinoma cell invasion and metastasis and hepatocarcinoma malignancy. (C) 2015 Elsevier Masson SAS. All rights reserved.
C1 [Liu, Shuqing] Dalian Med Univ, Dept Biochem, Dalian 116044, Peoples R China.
[Wang, Jiasheng; Guo, Chunmei; Qi, Houbao; Sun, Ming-Zhong] Dalian Med Univ, Dept Biotechnol, Dalian 116044, Peoples R China.
C3 Dalian Medical University; Dalian Medical University
RP Sun, MZ (corresponding author), Dalian Med Univ, Dept Biotechnol, 9 West Lvshun Southern Rd, Dalian 116044, Peoples R China.
EM mingzhongsun@dlmedu.edu.cn
RI wang, wei/JYP-7819-2024; Li, xiaolong/GRS-9148-2022
FU National Natural Science Foundation of China [81171957, 81272186,
81050010]; Distinguished Young Scholars of Liaoning College and
University [LJQ2011094]; Liaoning BaiQianWan Talent Project [2012921015]
FX This work was supported by the grants from National Natural Science
Foundation of China (81171957; 81272186; 81050010), the Distinguished
Young Scholars of Liaoning College and University (LJQ2011094), and the
Liaoning BaiQianWan Talent Project (2012921015).
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NR 37
TC 14
Z9 16
U1 1
U2 10
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD MAR
PY 2015
VL 70
BP 58
EP 63
DI 10.1016/j.biopha.2015.01.011
PG 6
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA CD3YI
UT WOS:000351019300011
PM 25776480
DA 2025-01-07
ER
PT J
AU Tiegs, G
Horst, AK
AF Tiegs, Gisa
Horst, Andrea K.
TI TNF in the liver: targeting a central player in inflammation
SO SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Review
DE TNF signalling; Inflammation; Apoptosis; Viral hepatitis; Non-alcoholic
fatty liver disease; Autoimmune hepatitis; Primary sclerosing
cholangitis
ID TUMOR-NECROSIS-FACTOR; HEPATITIS-B-VIRUS; PRIMARY SCLEROSING
CHOLANGITIS; PROTEIN-KINASE 3; CD4(+) T-CELLS; FACTOR-ALPHA;
NONALCOHOLIC STEATOHEPATITIS; MICE LACKING; FACTOR RECEPTOR; IN-VIVO
AB Tumour necrosis factor-alpha (TNF) is a multifunctional cytokine. First recognized as an endogenous soluble factor that induces necrosis of solid tumours, TNF became increasingly important as pro-inflammatory cytokine being involved in the immunopathogenesis of several autoimmune diseases. In the liver, TNF induces numerous biological responses such as hepatocyte apoptosis and necroptosis, liver inflammation and regeneration, and autoimmunity, but also progression to hepatocellular carcinoma. Considering these multiple functions of TNF in the liver, we propose anti-TNF therapies that specifically target TNF signalling at the level of its specific receptors.
C1 [Tiegs, Gisa; Horst, Andrea K.] Univ Med Ctr Hamburg Eppendorf, Inst Expt Immunol & Hepatol, Hamburg, Germany.
[Tiegs, Gisa; Horst, Andrea K.] Univ Med Ctr Hamburg Eppendorf, Hamburg Ctr Translat Immunol, Hamburg, Germany.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Hamburg; University Medical Center Hamburg-Eppendorf
RP Tiegs, G (corresponding author), Univ Med Ctr Hamburg Eppendorf, Inst Expt Immunol & Hepatol, Hamburg, Germany.; Tiegs, G (corresponding author), Univ Med Ctr Hamburg Eppendorf, Hamburg Ctr Translat Immunol, Hamburg, Germany.
EM g.tiegs@uke.de
FU Deutsche Forschungsgemeinschaft (DFG) [SFB 841, KFO306]
FX Open Access funding enabled and organized by Projekt DEAL. This work was
supported by the Deutsche Forschungsgemeinschaft (DFG): SFB 841 project
B1 granted to G.T. and A.K.H., and KFO306 project 4 granted to G.T.
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NR 127
TC 75
Z9 80
U1 7
U2 31
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1863-2297
EI 1863-2300
J9 SEMIN IMMUNOPATHOL
JI Semin. Immunopathol.
PD JUL
PY 2022
VL 44
IS 4
SI SI
BP 445
EP 459
DI 10.1007/s00281-022-00910-2
EA FEB 2022
PG 15
WC Immunology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pathology
GA 2R3EO
UT WOS:000751198800001
PM 35122118
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Huang, QR
Xiao, B
Ma, XT
Qu, MJ
Li, YM
Nagarkatti, P
Nagarkatti, M
Zhou, JH
AF Huang, Qingrong
Xiao, Bo
Ma, Xinting
Qu, Mingjuan
Li, Yanmin
Nagarkatti, Prakash
Nagarkatti, Mitzi
Zhou, Juhua
TI MicroRNAs associated with the pathogenesis of multiple sclerosis
SO JOURNAL OF NEUROIMMUNOLOGY
LA English
DT Review
DE MicroRNAs; Multiple sclerosis; Pathogenesis; Diagnosis; Treatment
ID BLOOD-BRAIN-BARRIER; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CANCER
CELL-PROLIFERATION; INHIBITS PROLIFERATION; COLORECTAL-CANCER;
CARCINOMA-CELLS; MESSENGER-RNA; BREAST-CANCER; B-CELLS;
HEPATOCELLULAR-CARCINOMA
AB Multiple sclerosis (MS) is not only an autoimmune disease in which autoreactive immune cells against myelin damage axons and nerves in the central nervous system, but also a neurodegenerative disease, in which progressive loss of structure and function of neurons occurs. The mechanisms of MS pathogenesis have not been fully understood. It has been reported that miRNAs may play a critical role in MS pathogenesis. In this review, we have extensively discussed the alterations in the expression of miRNAs detected in patients with MS. The dysregulated miRNAs have been shown to be associated with the pathogenesis of MS. We suggest that such dysregulated miRNAs may potentially be used as biomarkers in the diagnosis of MS, to discover new therapeutic targets for MS treatment, and to predict prognostic markers in responses to MS treatment. (C) 2016 Elsevier B.V. All rights reserved.
C1 [Huang, Qingrong; Xiao, Bo; Ma, Xinting; Qu, Mingjuan; Li, Yanmin; Zhou, Juhua] Ludong Univ, Sch Life Sci, Inst Tumor Immunol, 186 Hongqi Middle Rd, Yantai 264025, Shandong, Peoples R China.
[Nagarkatti, Prakash; Nagarkatti, Mitzi] Univ S Carolina, Dept Pathol Microbiol & Immunol, Sch Med, 6439 Garners Ferry Rd, Columbia, SC 29209 USA.
C3 Ludong University; University of South Carolina System; University of
South Carolina Columbia
RP Zhou, JH (corresponding author), Ludong Univ, Sch Life Sci, Inst Tumor Immunol, 186 Hongqi Middle Rd, Yantai 264025, Shandong, Peoples R China.
EM juhua.zhou@gmail.com
RI Li, Yan/JQI-3638-2023
OI Nagarkatti, Mitzi/0000-0002-5977-5615; Nagarkatti,
Prakash/0000-0003-2663-0759
FU National Natural Science Foundation of China [81341037]; "Taishan
Scholar" Special Fund from the Shandong Government, China [109, 2012]
FX This work was supported by a grant (#81341037 to JZ) from the National
Natural Science Foundation of China and "Taishan Scholar" Special Fund
(#109, 2012 to JZ) from the Shandong Government, China. The funding
sources were not involved in study design, the collection, analysis and
interpretation of data, the writing of the report and the decision to
submit the article for publication.
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NR 182
TC 51
Z9 56
U1 0
U2 32
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0165-5728
EI 1872-8421
J9 J NEUROIMMUNOL
JI J. Neuroimmunol.
PD JUN 15
PY 2016
VL 295
BP 148
EP 161
DI 10.1016/j.jneuroim.2016.04.014
PG 14
WC Immunology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Neurosciences & Neurology
GA DO5KM
UT WOS:000377822000020
PM 27235360
DA 2025-01-07
ER
PT J
AU Couvreur, P
Gref, R
Andrieux, K
Maivy, C
AF Couvreur, P.
Gref, R.
Andrieux, K.
Malvy, C.
TI Nanotechnologies for drug delivery: Application to cancer and autoimmune
diseases
SO PROGRESS IN SOLID STATE CHEMISTRY
LA English
DT Article; Proceedings Paper
CT Meeting of the European-Materials-Research-Society
CY MAY 30-JUN 03, 2005
CL Strasbourg, FRANCE
SP European Materials Res Soc
ID NANOPARTICLES; TUMOR; BRAIN; MICE
AB Polymer-based nanotechnologies are now proposed as an alternative to classical formulations for drug administration, delivery and targeting. Therapeutic applications of the first generation of nanotechnologies include the treatment of cancer liver diseases. Avoiding the recognition by the liver is also possible by developing long circulating polymeric colloidal carriers ("stealth" systems) able to avoid the opsonization process and the recognition by the macrophages. The design of such carriers of second generation is based on the physico-chemical concept of the "steric repulsion" by grafting polyethyleneglycol chains at the surface of nanoparticles, the adsorption of steric proteins may be dramatically reduced due to steric hindrance. Such an approach allows maintaining the drug carrier for a longer time into the circulation and the resulting extravasation towards non reticuloendothelial-located cancers may become possible. Now, new applications and exciting perspectives are proposed for the delivery of drugs to previously non accessible diseased sanctuaries, like the brain (treatment of glioma and autoimmune diseases of the brain) or the ocular tissues (treatment of the autoimmune uveitis). Finally, the use of nanotechnologies for the delivery of nucleic acids (oligonucleotides) is also discussed in this review. (C) 2005 Elsevier Ltd. All rights reserved.
C1 Univ Paris Sud, Ctr Etud Pharmaceut, CNRS, UMR 8612, F-92296 Chatenay Malabry, France.
C3 Universite Paris Saclay; Centre National de la Recherche Scientifique
(CNRS); CNRS - Institute of Chemistry (INC)
RP Couvreur, P (corresponding author), Univ Paris Sud, Ctr Etud Pharmaceut, CNRS, UMR 8612, F-92296 Chatenay Malabry, France.
EM patrick.couvreur@cep.u-psud.fr
RI COUVREUR, Patrick/AAY-7568-2020; Patrick, COUVREUR/G-4844-2011;
Andrieux, Karine/P-3010-2017; Gref, Ruxandra/F-1487-2011
OI Patrick, COUVREUR/0000-0001-7961-5443; Andrieux,
Karine/0000-0002-2002-7556; Gref, Ruxandra/0000-0002-7869-0908
CR Brandt H, 2004, JOM-US, V56, P16
Brigger I, 2002, J PHARMACOL EXP THER, V303, P928, DOI 10.1124/jpet.102.039669
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NR 10
TC 74
Z9 80
U1 0
U2 45
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0079-6786
J9 PROG SOLID STATE CH
JI Prog. Solid State Chem.
PY 2006
VL 34
IS 2-4
SI SI
BP 231
EP 235
DI 10.1016/j.progsolidstchem.2005.11.009
PG 5
WC Chemistry, Inorganic & Nuclear
WE Conference Proceedings Citation Index - Science (CPCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA 064FG
UT WOS:000239074000017
DA 2025-01-07
ER
PT J
AU Zhao, N
Liu, X
Guo, H
Zhao, XN
Qiu, YJ
Wang, W
AF Zhao, Na
Liu, Xin
Guo, Hao
Zhao, Xiangnan
Qiu, Yujie
Wang, Wei
TI Interleukin-35: An emerging player in the progression of liver diseases
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Review
DE Interleukin-35; Liver immune; Hepatitis; Hepatocellular carcinoma
AB Interleukin-35(IL-35), a newly identified immunosuppressive cytokine, has recently been shown to play a significant role in the progression of various autoimmune diseases and malignant tumors. The liver is the largest organ in the body and is generally regarded as an important lymphoid organ by an increasing number of immunologists. A number of reports have demonstrated that IL-35 plays essential roles in maintaining the immune homeostasis of the liver microenvironment. This review summarizes the existing studies of IL-35 in liver diseases, including viral hepatitis, immune liver injury, liver cirrhosis and carcinoma. We aimed to provide a comprehensive overview of the vital roles of IL-35 in hepatic damage and explore new alternative therapeutic targets for these diseases. (c) 2020 Elsevier Masson SAS. All rights reserved.
C1 [Zhao, Na; Liu, Xin; Guo, Hao; Zhao, Xiangnan; Qiu, Yujie; Wang, Wei] Tianjin Med Univ, Gen Hosp, Dept Gen Surg, Tianjin 300052, Peoples R China.
C3 Tianjin Medical University
RP Zhao, N (corresponding author), Tianjin Med Univ, Gen Hosp, Dept Gen Surg, Tianjin 300052, Peoples R China.
EM nasy3367@126.com
FU Tianjin Science and Technology Foundation [18JCYBJC26400]
FX This work was supported by the Tianjin Science and Technology Foundation
(grant number 18JCYBJC26400).
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NR 44
TC 2
Z9 3
U1 0
U2 5
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD JAN
PY 2021
VL 45
IS 1
DI 10.1016/j.clinre.2020.07.023
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA RM1ZT
UT WOS:000639459300010
PM 33387857
DA 2025-01-07
ER
PT J
AU Marjot, T
Eberhardt, CS
Boettler, T
Belli, LS
Berenguer, M
Buti, M
Jalan, R
Mondelli, MU
Moreau, R
Shouval, D
Berg, T
Cornberg, M
AF Marjot, Thomas
Eberhardt, Christiane S.
Boettler, Tobias
Belli, Luca S.
Berenguer, Marina
Buti, Maria
Jalan, Rajiv
Mondelli, Mario U.
Moreau, Richard
Shouval, Daniel
Berg, Thomas
Cornberg, Markus
TI Impact of COVID-19 on the liver and on the care of patients with chronic
liver disease, hepatobiliary cancer, and liver transplantation: An
updated EASL position paper
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE SARS-CoV-2; COVID-19; cirrhosis; liver transplantation; chronic liver
disease; hepatobiliary cancer; vaccination
ID PORTAL-VEIN THROMBOSIS; AUTOIMMUNE HEPATITIS; HOSPITALIZED-PATIENTS;
MESSENGER-RNA; SARS-COV-2 INFECTION; CHADOX1 NCOV-19;
RHEUMATOID-ARTHRITIS; HCV ELIMINATION; OPEN-LABEL; VACCINE
AB The COVID-19 pandemic has presented a serious challenge to the hepatology community, particularly healthcare professionals and patients. While the rapid development of safe and effective vaccines and treatments has improved the clinical landscape, the emergence of the omicron variant has presented new challenges. Thus, it is timely that the European Association for the Study of the Liver provides a summary of the latest data on the impact of COVID-19 on the liver and issues guidance on the care of patients with chronic liver disease, hepatobiliary cancer, and previous liver transplantation, as the world continues to deal with the consequences of the COVID-19 pandemic.(c) 2022 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Marjot, Thomas] Oxford Univ Hosp NHS Fdn Trust, John Radcliffe Hosp, Oxford Liver Unit, Oxford, England.
[Marjot, Thomas] Univ Oxford, Nuffield Dept Med, Translat Gastroenterol Unit, Oxford, England.
[Eberhardt, Christiane S.] Univ Geneva, Ctr Vaccinol & Neonatal Immunol, Dept Pathol & Immunol, Geneva, Switzerland.
[Eberhardt, Christiane S.] Univ Geneva, Geneva Univ Hosp, Fac Med, Ctr Vaccinol,Div Gen Pediat,Dept Woman Child & Ad, Geneva, Switzerland.
[Boettler, Tobias] Univ Freiburg, Dept Med 2, Fac Med, Med Ctr, Freiburg, Germany.
[Belli, Luca S.] GOM Niguarda, Dept Hepatol & Gastroenterol, Milan, Italy.
[Berenguer, Marina] IISLaFe, Liver Transplantat & Hepatol Unit & Ciberehd, Valencia, Spain.
[Berenguer, Marina] Hosp Univ & Politecn La Fe, Valencia, Spain.
[Berenguer, Marina] Univ Valencia, Dept Med, Valencia, Spain.
[Buti, Maria] Hosp Univ Valle Hebron, Liver Unit, Barcelona, Spain.
[Buti, Maria] Inst Carlos II, CIBEREHD, Dept Med 2, Div Hepatol, Barcelona, Spain.
[Jalan, Rajiv] UCL, Liver Failure Grp, Inst Liver & Digest Hlth, Royal Free Campus, London, England.
[Jalan, Rajiv] European Fdn Study Chron Liver Failure, Barcelona, Spain.
[Mondelli, Mario U.] Univ Pavia, Fdn IRCCS Policlin San Matteo, Div Clin Immunol & Infect Dis, Hannover, Germany.
[Mondelli, Mario U.] German Ctr Infect Res DZ, Dept Internal Med & Therapeut, Partner Site Hannover Braunschweig, Hannover, Germany.
[Moreau, Richard] Hop Beaujon, AP HP, Serv Hepatol, Clichy, France.
[Moreau, Richard] European Fdn Study Chron Liver Failure, Barcelona, Spain.
[Moreau, Richard] INSERM, Ctr Rech Inflammat, Paris, France.
[Moreau, Richard] Univ Paris Cite, Paris, France.
C3 University of Oxford; Oxford University Hospitals NHS Foundation Trust;
University of Oxford; University of Geneva; University of Geneva;
University of Freiburg; Hospital Universitari i Politecnic La Fe;
University of Valencia; Hospital Universitari Vall d'Hebron; CIBER -
Centro de Investigacion Biomedica en Red; CIBEREHD; University of
London; University College London; Universite Paris Cite; Assistance
Publique Hopitaux Paris (APHP); Hopital Universitaire Beaujon - APHP;
Universite Paris Cite; Institut National de la Sante et de la Recherche
Medicale (Inserm); Universite Paris Cite
RP Cornberg, M (corresponding author), Hannover Med Sch MHH, Dept Gastroenterol Hepatol & Endocrinol, Hannover, Germany.
EM cornberg.markus@mh-hannover.de
RI Cornberg, Markus/HSE-4367-2023; Mondelli, Mario/J-5375-2016; Eberhardt,
Christiane/ABB-8432-2020; Buti, MARIA/A-5327-2019; Boettler,
Tobias/E-3331-2012; Moreau, Richard/N-2197-2017; Berenguer,
Marina/ABG-8602-2020
OI Boettler, Tobias/0000-0002-1195-055X; Moreau,
Richard/0000-0003-0862-403X; Berenguer, Marina/0000-0001-9246-4264;
Belli, Luca Saverio/0000-0001-8714-2439; Eberhardt, Christiane
Sigrid/0000-0001-7495-258X; Jalan, Rajiv/0000-0002-7747-4015
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NR 333
TC 44
Z9 46
U1 1
U2 23
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD OCT
PY 2022
VL 77
IS 4
BP 1161
EP 1197
DI 10.1016/j.jhep.2022.07.008
EA SEP 2022
PG 37
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 4Z5RP
UT WOS:000862265900006
PM 35868584
OA Bronze, Green Published
DA 2025-01-07
ER
PT J
AU Tuohy, VK
Jaini, R
AF Tuohy, Vincent K.
Jaini, Ritika
TI Prophylactic cancer vaccination by targeting functional non-self
SO ANNALS OF MEDICINE
LA English
DT Article
DE Autoimmune; cancer vaccine; tumor immunotherapy
ID MAMMARY-TUMOR VIRUS; MOUSE ALPHA-LACTALBUMIN; T-CELL REPERTOIRE;
HUMAN-PAPILLOMAVIRUS; BREAST CARCINOMAS; HEPATOCELLULAR-CARCINOMA;
IMMUNE-RESPONSE; PROSTATE-CANCER; EXPRESSION; GENE
AB Despite the monumental success of childhood prophylactic vaccination, there is no similar program designed to provide protection as we age against adult onset diseases like breast cancer. Instead, the predominant focus of current cancer vaccine strategy is to vaccinate after the tumors become established. This strategy has at best provided incremental improvement in overall survival. We propose the development of an adult vaccination program modeled on the childhood program that provides protection against diseases we confront as we enter our middle age. Since most cases of adult cancers are not associated with definitive etiopathogenic viruses, we propose extending our selection of vaccine targets to tissue-specific self proteins that are over-expressed in developing tumors but are no longer expressed in normal tissues (''retired or former self''), are expressed in normal tissues under readily avoidable conditions (''conditional self''), or are incapable of targeting any clinically significant autoimmune complications (''irrelevant self''). By extending prophylactic vaccination to such ""functional non-self"" targets, prophylactic vaccination against adult onset diseases like breast cancer may occur safely in the absence of any autoimmune inflammatory complications and may potentially reduce disease incidence in a manner that mimics the impact of childhood vaccination on diseases like measles and polio.
C1 [Tuohy, Vincent K.; Jaini, Ritika] Cleveland Clin, Lerner Res Inst, Dept Immunol, Cleveland, OH 44195 USA.
[Tuohy, Vincent K.] Case Western Reserve Univ, Cleveland Clin, Lerner Coll Med, Dept Mol Med, Cleveland, OH 44106 USA.
C3 Cleveland Clinic Foundation; Cleveland Clinic Foundation; University
System of Ohio; Case Western Reserve University
RP Tuohy, VK (corresponding author), Cleveland Clin, Lerner Res Inst, Dept Immunol, NB30,9500 Euclid Ave, Cleveland, OH 44195 USA.
EM tuohyv@ccf.org
OI Jaini, Ritika/0000-0002-4580-8789
FU U.S. National Institutes of Health [R01CA-14035]
FX This work was supported by U.S. National Institutes of Health grant
R01CA-14035 (V. K. T.). The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institutes of Health.
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NR 75
TC 11
Z9 16
U1 0
U2 7
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0785-3890
EI 1365-2060
J9 ANN MED
JI Ann. Med.
PD AUG
PY 2011
VL 43
IS 5
BP 356
EP 365
DI 10.3109/07853890.2011.565065
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 779OT
UT WOS:000291789800004
PM 21651440
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Mathavan, A
Mathavan, A
Krekora, U
Daily, K
AF Mathavan, Akash
Mathavan, Akshay
Krekora, Urszula
Daily, Karen
TI Immune-mediated herb-induced liver injury: a potential association with
herbal artemisinin use as supported by the updated RUCAM
SO BMJ CASE REPORTS
LA English
DT Article
DE Liver disease; Immunology; Vitamins and supplements; Unwanted effects;
adverse reactions
ID COMBINATION; CANCER; HEPATITIS
AB Immune-mediated herb-induced liver injury (HILI) is an acute or chronic inflammatory liver disease precipitated by a hepatotoxic agent with a presentation similar to acute autoimmune hepatitis. It is distinguished in clinical course from true autoimmune hepatitis by remission on drug discontinuation and immunosuppressive treatment. We report a potential case of immune-mediated HILI associated with artemisinin use, an herb underlying first-line malarial treatments, in a woman undergoing radiotherapy for right-sided pelvic sarcoma. A probable association in this case is supported by causality assessment using the updated Roussel Uclaf Causality Assessment Method (score of 6). She achieved clinical improvement with a course of oral corticosteroids and remained stable without relapse following discontinuation. Increased awareness of this complication is imperative, as literature to date only documents direct hepatocellular and cholestatic liver injury from artemisinin use, and should augment clinician counsel regarding complementary medicine administration, especially in high-risk individuals like those with cancer.
C1 [Mathavan, Akash; Mathavan, Akshay] Univ Florida, Coll Med, Gainesville, FL 32611 USA.
[Krekora, Urszula] Univ Cent Florida, Coll Med, Orlando, FL USA.
[Daily, Karen] Univ Florida, Hematol & Oncol, Gainesville, FL USA.
C3 State University System of Florida; University of Florida; State
University System of Florida; University of Central Florida; State
University System of Florida; University of Florida
RP Mathavan, A (corresponding author), Univ Florida, Coll Med, Gainesville, FL 32611 USA.
OI Mathavan, Akshay/0000-0002-3850-834X; Mathavan,
Akash/0000-0003-3496-2542
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NR 33
TC 0
Z9 0
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 1757-790X
J9 BMJ CASE REP
JI BMJ Case Rep.
PD MAY
PY 2023
VL 16
IS 5
DI 10.1136/bcr-2022-251852
PG 7
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA F8DK5
UT WOS:000984596500016
PM 37142282
DA 2025-01-07
ER
PT J
AU Cripps, JG
Wang, J
Maria, A
Blumenthal, I
Gorham, JD
AF Cripps, James G.
Wang, Jing
Maria, Ann
Blumenthal, Ian
Gorham, James D.
TI Type 1 T Helper Cells Induce the Accumulation of Myeloid-Derived
Suppressor Cells in the Inflamed Tgfb1 Knockout Mouse Liver
SO HEPATOLOGY
LA English
DT Article
ID AUTOIMMUNE HEPATITIS; HEPATOCELLULAR-CARCINOMA; GENETIC-REGULATION;
TUMOR PROGRESSION; IFN-GAMMA; MICE; INFLAMMATION; DISEASE; CANCER;
INJURY
AB Immune-mediated liver injury in hepatitis is due to activated T cells producing interferon-gamma (IFN-gamma). It is important to identify negative feedback immune mechanisms that can regulate T cell activity. In this study, we demonstrate that liver inflammation mediated by type 1 T helper (Thl) cells can induce the accumulation of myeloid-derived suppressor cells (MDSCs), pleiomorphic cells capable of modulating T cell mediated immunity, that heretofore have been studied almost exclusively in the context of tumor-associated inflammation. Mice deficient in the gene encoding transforming growth factor-beta 1 (Tgfb1(-/-) mice) acutely develop liver necroinflammation caused by IFN-gamma-producing clusters of differentiation 4 positive (CD4(+)) T cells. Liver Th1 cell accumulation was accompanied by myeloid cells expressing CD11b and Grl, phenotypic hallmarks of MDSCs. Isolated Tgfb1(-/-) liver CD11b(+)Gr1(+) cells were functional MDSCs, readily suppressing T cell proliferation in vitro. Pharmacologic inhibitors of inducible nitric oxide (NO) synthase completely eliminated suppressor function. Suppressor function and the production of NO were dependent on cell cell contact between MDSCs and T cells, and upon IFN-gamma, and were specifically associated with the "monocytic" CD11b(+)Ly6G Ly6C(hi) subset of liver Tgfb1(-/-) CD11b(+) cells. The rapid accumulation of CD11b(+)Gr1(+) cells in Tgfb1(-/-) liver was abrogated when mice were either depleted of CD4(+) T cells or rendered unable to produce IFN-gamma, showing that Th1 activity induces MDSC accumulation. Conclusion: Th1 liver inflammation mobilizes an MDSC response that, through the production of NO, can inhibit T cell proliferation. We propose that MDSCs serve an important negative feedback function in liver immune homeostasis, and that insufficient or inappropriate activity of this cell population may contribute to inflammatory liver pathology. (HEPATOLoGY 2010;52:1350-1359)
C1 [Wang, Jing; Blumenthal, Ian; Gorham, James D.] Dartmouth Med Sch, Dept Pathol, Lebanon, NH 03756 USA.
[Cripps, James G.; Maria, Ann; Gorham, James D.] Dartmouth Med Sch, Dept Microbiol & Immunol, Lebanon, NH 03756 USA.
C3 Dartmouth College; Dartmouth College
RP Gorham, JD (corresponding author), Dartmouth Med Sch, Dept Pathol, 1 Med Ctr Dr, Lebanon, NH 03756 USA.
EM James.D.Gorham@dartmouth.edu
FU National Institutes of Health; National Center for Research Resources
[P20RR16437]; Hitchcock Foundation; American Liver Foundation; National
Institutes of Health [T32AI07363]; [AI078195]
FX This work was supported by National Institutes of Health grants AI078195
("D.C.) and P20RR16437 from the COBRE Program of the National Center for
Research Resources, as well as by a grant from the Hitchcock Foundation
(J.D.G.). J.W was supported by a Samuel A. Hamacher Autoimmune Hepatitis
Postdoctoral Research Fellowship from the American Liver Foundation.
J.G.C. was supported by National Institutes of Health training grant
T32AI07363.
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NR 36
TC 77
Z9 86
U1 0
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2010
VL 52
IS 4
BP 1350
EP 1359
DI 10.1002/hep.23841
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 660BK
UT WOS:000282613000022
PM 20803559
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Krivosheev, AB
Khvan, LA
Morozov, DV
Krivosheeva, IA
Spitsina, SV
Dobracheva, OA
Eremeeva, SA
Levekina, EE
AF Krivosheev, Alexandr B.
Khvan, Liudmila A.
V. Morozov, Dmitry
Krivosheeva, Inga A.
V. Spitsina, Svetlana
Dobracheva, Olga A.
Eremeeva, Svetlana A.
Levekina, Elena E.
TI Case of multiple systemic (extrahepatic) manifestations of chronic HCV
infection (analysis of the literature and own observations). Case report
SO TERAPEVTICHESKII ARKHIV
LA English
DT Article
DE ?hronic HCV infection; extrahepatic manifestations; porphyria cutanea
tarda; mixed cryoglobulenemia; autoimmune thyroiditis; psoriasis;
paraneoplastic diseases; hepatocellular carcinoma
AB The article presents a description of a patient with chronic HCV infection and multiple extrahepatic manifestations, which manifested in dynamics and were recorded with a different sequence during 15 years of follow-up. In the patient we observed, the most frequently recorded extrahepatic manifestations were verified: porphyria cutanea tarda, mixed cryoglobulenemia, and utoimmune thyroiditis. Chronic HCV infection is often diagnosed in the presence of psoriasis was assessed as a paraneoplastic disease.
C1 [Krivosheev, Alexandr B.] Novosibirsk State Med Univ, Novosibirsk, Russia.
[Khvan, Liudmila A.; V. Morozov, Dmitry; Krivosheeva, Inga A.; Dobracheva, Olga A.; Eremeeva, Svetlana A.; Levekina, Elena E.] City Clin Hosp 1, Novosibirsk, Russia.
[V. Spitsina, Svetlana] Novosibirsk Reg Clin Cardiol Dispensary, Novosibirsk, Russia.
C3 Novosibirsk State Medical University
RP Krivosheev, AB (corresponding author), Novosibirsk State Med Univ, Novosibirsk, Russia.
EM krivosheev-ab@narod.ru
RI Eremeeva, Svetlana/HKN-0033-2023
CR Dedkova EM, 1977, PARANEOPLASTICHESKIE
Ignatova T M, 2005, Klin Med (Mosk), V83, P37
[Ивашкин В.Т. Ivashkin V.T.], 2019, [Российский журнал гастроэнтерологии, гепатологии, колопроктологии, Russian Journal of Gastroenterology, Hepatology, Coloproctology, Rossiiskii zhurnal gastroenterologii, gepatologii, koloproktologii], V29, P53
Korotaeva IA, 2015, J DERMATOLOGY VENERE, V91, P90, DOI [10.25208/0042-4609-2015-91-4-90-94, DOI 10.25208/0042-4609-2015-91-4-90-94]
[Кривошеев А.Б. Krivosheev A.B.], 2020, [Экспериментальная и клиническая гастроэнтерология, Experimental and Clinical Gastroenterology Journal, Eksperimental'naya i klinicheskaya gastroenterologiya], P96, DOI 10.31146/1682-8658-ecg-182-10-96-100
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Maev IV, 2014, TERAPEVT ARKH, V86, P108
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[Павлов А.И. Pavlov A.I.], 2008, [Российский журнал гастроэнтерологии, гепатологии, колопроктологии, Rossiiskii zhurnal gastroenterologii, gepatologii, koloproktologii], V18, P51
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NR 15
TC 0
Z9 0
U1 0
U2 0
PU CJSC CONSILIUM MEDICUM
PI MOSCOW
PA NOVIY ZIKOVSKIY PROEZD, D 3, 40, MOSCOW, 125167, RUSSIA
SN 0040-3660
EI 2309-5342
J9 TERAPEVT ARKH
JI Ter. Arkhiv
PY 2022
VL 94
IS 11
BP 1303
EP 1309
DI 10.26442/00403660.2022.11.201935
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 7M2VC
UT WOS:000906512200012
PM 37167169
OA gold
DA 2025-01-07
ER
PT J
AU Kemp, W
Majeed, A
Mitchell, J
Majumdar, A
Tse, E
Skoien, R
Croagh, D
Dev, A
Gao, H
Weltman, M
Craig, P
Stuart, K
Cheng, W
Edmunds, S
Lee, E
Sood, S
Metz, A
Thompson, A
Sinclair, M
Beswick, L
Nicoll, A
Riordan, S
Braund, A
Muller, K
MacQuillan, G
Sandanayake, N
Shackel, N
Roberts, SK
AF Kemp, William
Majeed, Ammar
Mitchell, Joanne
Majumdar, Avik
Tse, Edmund
Skoien, Richard
Croagh, Daniel
Dev, Anouk
Gao, Hugh
Weltman, Martin
Craig, Philip
Stuart, Katherine
Cheng, Wendy
Edmunds, Simon
Lee, Eric
Sood, Siddharth
Metz, Andrew
Thompson, Alexander
Sinclair, Marie
Beswick, Lauren
Nicoll, Amanda
Riordan, Stephen
Braund, Alicia
Muller, Kate
MacQuillan, Gerry
Sandanayake, Neomal
Shackel, Nicholas
Roberts, Stuart Keith
TI Management, outcomes and survival of an Australian IgG4-SC cohort: The
MOSAIC study
SO LIVER INTERNATIONAL
LA English
DT Article
DE autoimmune; biliary disease; cancer; cholangitis
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; AUTOIMMUNE PANCREATITIS;
SCLEROSING CHOLANGITIS; DIAGNOSIS
AB Background and Aims IgG4 sclerosing cholangitis (IgG4-SC) is the biliary component of the multisystem IgG4-related disease. We aimed to investigate the clinical features, demographics, treatment response and outcomes of IgG4-SC in a large Australian cohort. Methods We conducted nationwide retrospective cohort via the Australian Liver Association Clinical Trials Network (ALA-CRN). 39 sites were invited to participate. IgG4-SC was defined by the clinical diagnostic criteria established by the Japanese Biliary Association in 2012. Data were collected on patient demographic, clinical and laboratory information, presenting features, response to therapy and clinical outcomes. Results 67 patients meet inclusion criteria from 22 sites. 76% were male with mean age of 63.3 +/- 14.5 years and a median IgG4 level of 3.6 g/L [0.09-67.1]. The most frequent presenting symptom was jaundice (62%) and abdominal pain (42%) and Type 1 biliary stricturing (52%) at the distal common bile duct was the most frequent biliary tract finding. Prednisolone was used as a primary treatment in 61 (91%) and partial or complete response occurred in 95% of subjects. Relapse was common (42%) in those who ceased medical therapy. After a median follow up of 3.9 years there was one hepatocellular carcinoma and no cholangiocarcinomas. Conclusions Our study confirms the preponderance of IgG4-SC in males and highlights the steroid response nature of this condition although relapse is common after steroid cessation. Progression to malignancy was uncommon.
C1 [Kemp, William; Majeed, Ammar; Mitchell, Joanne; Roberts, Stuart Keith] Alfred Hosp, Melbourne, Vic, Australia.
[Kemp, William; Majeed, Ammar; Roberts, Stuart Keith] Monash Univ, Melbourne, Vic, Australia.
[Majumdar, Avik] Royal Prince Alfred Hosp, Sydney, NSW, Australia.
[Tse, Edmund] Royal Adelaide Hosp, Adelaide, SA, Australia.
[Skoien, Richard] Royal Brisbane & Womens Hosp, Brisbane, Qld, Australia.
[Croagh, Daniel; Dev, Anouk; Gao, Hugh] Monash Med Ctr, Melbourne, Vic, Australia.
[Weltman, Martin] Nepean Hosp, Sydney, NSW, Australia.
[Craig, Philip] St George Hosp, Sydney, NSW, Australia.
[Stuart, Katherine] Greenslopes Private Hosp, Brisbane, Qld, Australia.
[Cheng, Wendy; Edmunds, Simon] Royal Perth Hosp, Perth, WA, Australia.
[Lee, Eric] Westmead Hosp, Sydney, NSW, Australia.
[Sood, Siddharth; Metz, Andrew] Royal Melbourne Hosp, Melbourne, Vic, Australia.
[Thompson, Alexander] St Vincents Hosp, Melbourne, Vic, Australia.
[Sinclair, Marie] Austin Hlth, Melbourne, Vic, Australia.
[Beswick, Lauren] Geelong Hosp, Geelong, Vic, Australia.
[Nicoll, Amanda] Eastern Hlth, Melbourne, Vic, Australia.
[Riordan, Stephen] Prince Wales Hosp, Sydney, NSW, Australia.
[Braund, Alicia] Gold Coast Univ Hosp, Gold Coast, Qld, Australia.
[Muller, Kate] Flinders Med Ctr, Adelaide, SA, Australia.
[MacQuillan, Gerry] Sir Charles Gairdner Hosp, Perth, WA, Australia.
[Sandanayake, Neomal] Royal North Shore Hosp, St Leonards, NSW, Australia.
[Shackel, Nicholas] Liverpool Hosp, Sydney, NSW, Australia.
C3 Florey Institute of Neuroscience & Mental Health; Monash University;
University of Sydney; NSW Health; Royal Prince Alfred Hospital; Royal
Adelaide Hospital; Royal Brisbane & Women's Hospital; Monash University;
Nepean Hospital; St George Hospital; Greenslopes Private Hospital; East
Metropolitan Health Service; Royal Perth Hospital; University of Western
Australia; University of Sydney; NSW Health; Westmead Hospital;
Melbourne Health; Royal Melbourne Hospital; NSW Health; St Vincents
Hospital Sydney; St Vincent's Health; St Vincent's Hospital Melbourne;
Austin Research Institute; Florey Institute of Neuroscience & Mental
Health; Barwon Health; Geelong Hospital; Eastern Health; University of
New South Wales Sydney; Prince of Wales Hospital (POWH); Gold Coast
University Hospital; Flinders Medical Centre; University of Western
Australia; Sir Charles Gairdner Hospital; Royal North Shore Hospital;
Liverpool Hospital
RP Kemp, W (corresponding author), Alfred Hosp, Gastroenterol Dept, 55 Commercial Rd, Melbourne, Vic 3004, Australia.
EM w.kemp@alfred.org.au
RI Skoien, Richard/G-4704-2012; Kemp, William/IRZ-5250-2023; Craig,
Paul/G-4248-2011; Majumdar, Avik/KIJ-2479-2024; Sinclair,
Marie/AAY-1302-2020; Mitchell, Joanne/KWE-2976-2024
OI sinclair, marie/0000-0003-0657-3048; Roberts,
Stuart/0000-0002-9015-7997; Sood, Siddharth/0000-0002-9341-4792; Kemp,
William/0000-0002-0787-7273; Majumdar, Avik/0000-0003-2975-4327
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NR 23
TC 2
Z9 5
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD DEC
PY 2021
VL 41
IS 12
BP 2934
EP 2943
DI 10.1111/liv.15036
EA SEP 2021
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA XR8QI
UT WOS:000692461700001
PM 34392596
DA 2025-01-07
ER
PT J
AU You, YL
Qian, ZW
Jiang, Y
Chen, LY
Wu, DP
Liu, L
Zhang, F
Ning, X
Zhang, Y
Xiao, JP
AF You, Yilan
Qian, Zhiwen
Jiang, Ying
Chen, Lingyan
Wu, Danping
Liu, Lu
Zhang, Feng
Ning, Xin
Zhang, Yan
Xiao, Jianping
TI Insights into the pathogenesis of gestational and hepatic diseases: the
impact of ferroptosis
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE ferroptosis; pregnancy; placenta; liver diseases; pathogenesis
ID PLACENTAL OXIDATIVE STRESS; FATTY LIVER-DISEASE; INTRAHEPATIC
CHOLESTASIS; CELL-DEATH; LIPID-PEROXIDATION; REPERFUSION INJURY; IRON
OVERLOAD; CYSTINE/GLUTAMATE ANTIPORTER; DICTATES FERROPTOSIS; PROMOTES
FERROPTOSIS
AB Ferroptosis, a distinct form of non-apoptotic cell death characterized by iron dependency and lipid peroxidation, is increasingly linked to various pathological conditions in pregnancy and liver diseases. It plays a critical role throughout pregnancy, influencing processes such as embryogenesis, implantation, and the maintenance of gestation. A growing body of evidence indicates that disruptions in these processes can precipitate pregnancy-related disorders, including pre-eclampsia (PE), gestational diabetes mellitus (GDM), and intrahepatic cholestasis of pregnancy (ICP). Notably, while ICP is primarily associated with elevated maternal serum bile acid levels, its precise etiology remains elusive. Oxidative stress induced by bile acid accumulation is believed to be a significant factor in ICP pathogenesis. Similarly, the liver's susceptibility to oxidative damage underscores the importance of lipid metabolism dysregulation and impaired iron homeostasis in the progression of liver diseases such as alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), cholestatic liver injury, autoimmune hepatitis (AIH), acute liver injury, viral hepatitis, liver fibrosis, and hepatocellular carcinoma (HCC). This review discusses the shared signaling mechanisms of ferroptosis in gestational and hepatic diseases, and explores recent advances in understanding the mechanisms of ferroptosis and its potential role in the pathogenesis of gestational and hepatic disorders, with the aim of identifying viable therapeutic targets.
C1 [You, Yilan; Qian, Zhiwen; Chen, Lingyan; Zhang, Feng; Zhang, Yan; Xiao, Jianping] Nanjing Med Univ, Wuxi Maternal & Child Healthcare Hosp, Wuxi Med Ctr, Dept Obstet & Gynecol, Wuxi, Peoples R China.
[Jiang, Ying; Wu, Danping; Liu, Lu; Ning, Xin; Zhang, Yan; Xiao, Jianping] Jiangnan Univ, Womens Hosp Jiangnan Univ, Wuxi Matern & Child Healthcare Hosp, Dept Obstet & Gynecol, Wuxi, Peoples R China.
C3 Nanjing Medical University; Jiangnan University
RP Zhang, Y; Xiao, JP (corresponding author), Nanjing Med Univ, Wuxi Maternal & Child Healthcare Hosp, Wuxi Med Ctr, Dept Obstet & Gynecol, Wuxi, Peoples R China.; Zhang, Y; Xiao, JP (corresponding author), Jiangnan Univ, Womens Hosp Jiangnan Univ, Wuxi Matern & Child Healthcare Hosp, Dept Obstet & Gynecol, Wuxi, Peoples R China.
EM fuyou2007@126.com; jianpingx999@126.com
RI 陈, 凌燕/HLQ-3324-2023; Xiao, Jianping/B-8028-2012
FU National Natural Science Foundation of China [82472842]; Wuxi
Double-Hundred Talent Fund Project [BJ2023075]
FX The author(s) declare that financial support was received for the
research, authorship, and/or publication of this article. The study was
supported by the National Natural Science Foundation of China (82472842)
and Wuxi Double-Hundred Talent Fund Project (BJ2023075).
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NR 230
TC 0
Z9 0
U1 2
U2 2
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD NOV 12
PY 2024
VL 12
AR 1482838
DI 10.3389/fcell.2024.1482838
PG 21
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA N2K7J
UT WOS:001362692900001
PM 39600338
OA gold
DA 2025-01-07
ER
PT J
AU Fox, AN
Brown, RS
AF Fox, Alyson N.
Brown, Robert S., Jr.
TI Is the Patient a Candidate for Liver Transplantation?
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Liver failure; Transplantation; Hepatic decompensation; Liver disease;
Transplant evaluation
ID TERM-FOLLOW-UP; PRIMARY BILIARY-CIRRHOSIS; AUTOIMMUNE HEPATITIS; MELD
SCORE; INTESTINE TRANSPLANTATION; HEPATOCELLULAR-CARCINOMA;
NATURAL-HISTORY; IRON OVERLOAD; UNITED-STATES; SURVIVAL
AB Identifying whether someone is a good candidate for liver transplantation is a complex process that requires a team approach. There are several medical and psychosocial considerations involved, each of which is thoroughly explored during the evaluation process. Both the indications and contraindications to transplantation can change over time, reflecting advances in understanding of, and ability to treat, certain disease processes. Ultimately, the goal of liver transplantation remains to provide a survival benefit to those with acute or chronic liver diseases.
C1 [Fox, Alyson N.] Weill Cornell Med Ctr, New York, NY 10021 USA.
[Fox, Alyson N.; Brown, Robert S., Jr.] New York Presbyterian Hosp, Ctr Liver Dis & Transplantat, New York, NY USA.
[Brown, Robert S., Jr.] Columbia Univ Coll Phys & Surg, New York, NY 10032 USA.
C3 Cornell University; Weill Cornell Medicine; NewYork-Presbyterian
Hospital; Columbia University
RP Fox, AN (corresponding author), Weill Cornell Med Ctr, 1305 York Ave, New York, NY 10021 USA.
EM alf9011@med.cornell.edu
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NR 51
TC 18
Z9 19
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD MAY
PY 2012
VL 16
IS 2
BP 435
EP +
DI 10.1016/j.cld.2012.03.014
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 949JL
UT WOS:000304572400016
PM 22541708
DA 2025-01-07
ER
PT J
AU Wu, D
Struwe, WB
Harvey, DJ
Ferguson, MAJ
Robinson, CV
AF Wu, Di
Struwe, Weston B.
Harvey, David J.
Ferguson, Michael A. J.
Robinson, Carol V.
TI N-glycan microheterogeneity regulates interactions of plasma proteins
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE glycoprotein; mass spectrometry; protein interactions
ID HUMAN ALPHA(1)-ACID GLYCOPROTEIN; ELECTROSPRAY MASS-SPECTROMETRY;
GROWTH-FACTOR RECEPTOR; HEPATOCELLULAR-CARCINOMA; ALPHA-1-ACID
GLYCOPROTEIN; BINDING-CAPACITIES; BIOLOGICAL ROLES; LIVER-CIRRHOSIS;
SITE OCCUPANCY; HAPTOGLOBIN
AB Altered glycosylation patterns of plasma proteins are associated with autoimmune disorders and pathogenesis of various cancers. Elucidating glycoprotein microheterogeneity and relating subtle changes in the glycan structural repertoire to changes in protein-protein, or protein-small molecule interactions, remains a significant challenge in glycobiology. Here, we apply mass spectrometry-based approaches to elucidate the global and site-specific microheterogeneity of two plasma proteins: alpha 1-acid glycoprotein (AGP) and haptoglobin (Hp). We then determine the dissociation constants of the anticoagulant warfarin to different AGP glycoforms and reveal how subtle N-glycan differences, namely, increased antennae branching and terminal fucosylation, reduce drug-binding affinity. Conversely, similar analysis of the haptoglobin-hemoglobin (Hp-Hb) complex reveals the contrary effects of fucosylation and N-glycan branching on Hp-Hb interactions. Taken together, our results not only elucidate how glycoprotein microheterogeneity regulates protein-drug/protein interactions but also inform the pharmacokinetics of plasma proteins, many of which are drug targets, and whose glycosylation status changes in various disease states.
C1 [Wu, Di; Struwe, Weston B.; Robinson, Carol V.] Univ Oxford, Dept Chem, Oxford OX1 3QZ, England.
[Struwe, Weston B.] Univ Oxford, Oxford Glycobiol Inst, Dept Biochem, Oxford OX1 3QU, England.
[Harvey, David J.] Univ Oxford, Nuffield Dept Med, Target Discovery Inst, Oxford OX3 7FZ, England.
[Ferguson, Michael A. J.] Univ Dundee, Sch Life Sci, Wellcome Ctr Anti Infect Res, Dundee DD1 5EH, Scotland.
C3 University of Oxford; University of Oxford; University of Oxford;
University of Dundee
RP Robinson, CV (corresponding author), Univ Oxford, Dept Chem, Oxford OX1 3QZ, England.
EM carol.robinson@chem.ox.ac.uk
RI Ferguson, Michael/F-7829-2010; Harvey, David/A-5579-2013; Wu,
Di/AAF-2276-2020; Robinson, Christopher/H-7992-2019; Struwe,
Weston/D-6180-2018
OI robinson, carol/0000-0001-7829-5505; Harvey, David/0000-0003-0544-771X;
Ferguson, Michael/0000-0003-1321-8714; Struwe,
Weston/0000-0003-0594-226X
FU Medical Research Council [MR/N020413/1]; European Research Council
Advanced Grant ENABLE [641317]; Wellcome Trust [104633/Z/14/Z]; MRC
[MR/N020413/1] Funding Source: UKRI
FX We thank Joseph Gault, Hsin-Yung Yen, and Manman Guo (Nuffield
Department of Orthopaedics, Rheumatology, and Musculoskeletal Sciences,
University of Oxford) for useful discussions in native MS, glycobiology,
and glycoproteomics analysis. We acknowledge funding from Medical
Research Council Programme Grant MR/N020413/1, European Research Council
Advanced Grant ENABLE (641317), and Wellcome Trust Investigator Award
104633/Z/14/Z.
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NR 58
TC 87
Z9 109
U1 0
U2 34
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD AUG 28
PY 2018
VL 115
IS 35
BP 8763
EP 8768
DI 10.1073/pnas.1807439115
PG 6
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GR7ID
UT WOS:000442861600054
PM 30111543
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Martin-Orozco, N
Dong, C
AF Martin-Orozco, Natalia
Dong, Chen
TI The IL-17/IL-23 axis of inflammation in cancer: Friend or foe?
SO CURRENT OPINION IN INVESTIGATIONAL DRUGS
LA English
DT Review
DE Cancer immunity; IL-17; IL-23; immunotherapy; Th17
ID REGULATORY T-CELLS; NF-KAPPA-B; AUTOIMMUNE INFLAMMATION; TH17 CELLS;
TGF-BETA; HEPATOCELLULAR-CARCINOMA; TUMOR MICROENVIRONMENT; LYMPHOPENIC
HOSTS; ADAPTIVE IMMUNITY; INNATE IMMUNITY
AB IL-17, a proinflammatory cytokine that is regulated by IL-23, is crucial for the development of a novel CD4+ T-cell subset called T-helper 17 (Th17) cells, which promotes tissue inflammation in host defense responses against infection, as well as in chronic autoimmune diseases. IL-17 and IL-23 expression, as well as the presence of Th17 cells, have been documented in several human carcinomas, but their function in tumors remains controversial. This review summarizes the current literature on IL-17, IL-23 and Th17 cells in human tumors and animal models of cancer, discussing their possible roles in cancer development and cancer immunity, and presenting a personal perspective of this research area.
C1 [Martin-Orozco, Natalia; Dong, Chen] Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Dong, C (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Immunol, 7455 Fannin St, Houston, TX 77030 USA.
EM cdong@mdanderson.org
RI Orozco, Natalia/E-4794-2010; dong, chen/B-3181-2009
FU NIH; Center for Targeted Therapy; Research Institute Investigator award;
Leukemia and Lymphoma Society Scholar award; American Lung Association
Career Investigator award; Trust Fellowship
FX The authors would like to thank their colleagues and collaborators for
their help and useful discussions. This work was supported in part by
grants from the NIH (to CD) and grants from the Center for Targeted
Therapy of MD Anderson Cancer Center (to CD and NMO). CD receives a
Cancer Research Institute Investigator award, a Leukemia and Lymphoma
Society Scholar award, an American Lung Association Career Investigator
award and a Trust Fellowship from the MD Anderson Cancer Center.
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NR 72
TC 64
Z9 74
U1 0
U2 8
PU THOMSON REUTERS (SCIENTIFIC) LTD
PI LONDON
PA 77 HATTON GARDEN, LONDON, EC1N 8JS, ENGLAND
SN 1472-4472
EI 2040-3429
J9 CURR OPIN INVEST DR
JI Curr. Opin. Investig. Drugs
PD JUN
PY 2009
VL 10
IS 6
BP 543
EP 549
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 454OV
UT WOS:000266692900004
PM 19513943
DA 2025-01-07
ER
PT J
AU Jeong, JJ
Park, HJ
Cha, MG
Park, E
Won, SM
Ganesan, R
Gupta, H
Gebru, YA
Sharma, SP
Lee, SB
Kwon, GH
Jeong, MK
Min, BH
Hyun, JY
Eom, JA
Yoon, SJ
Choi, MR
Kim, DJ
Suk, KT
AF Jeong, Jin-Ju
Park, Hee Jin
Cha, Min Gi
Park, Eunju
Won, Sung-Min
Ganesan, Raja
Gupta, Haripriya
Gebru, Yoseph Asmelash
Sharma, Satya Priya
Lee, Su Been
Kwon, Goo Hyun
Jeong, Min Kyo
Min, Byeong Hyun
Hyun, Ji Ye
Eom, Jung A.
Yoon, Sang Jun
Choi, Mi Ran
Kim, Dong Joon
Suk, Ki Tae
TI The Lactobacillus as a Probiotic: Focusing on Liver Diseases
SO MICROORGANISMS
LA English
DT Review
DE probiotics; liver disease; Lactobacillus
ID RHAMNOSUS GG; DOUBLE-BLIND; HEPATOCELLULAR-CARCINOMA; INTESTINAL
PERMEABILITY; POTENTIAL PROBIOTICS; LIPID-METABOLISM; GUT MICROBIOTA;
ACIDOPHILUS; BACTERIA; PLACEBO
AB Over the past decade, scientific evidence for the properties, functions, and beneficial effects of probiotics for humans has continued to accumulate. Interest in the use of probiotics for humans has increased tremendously. Among various microorganisms, probiotics using bacteria have been widely studied and commercialized, and, among them, Lactobacillus is representative. This genus contains about 300 species of bacteria (recently differentiated into 23 genera) and countless strains have been reported. They improved a wide range of diseases including liver disease, gastrointestinal diseases, respiratory diseases, and autoimmune diseases. Here, we intend to discuss in depth the genus Lactobacillus as a representative probiotic for chronic liver diseases.
C1 [Jeong, Jin-Ju; Park, Hee Jin; Cha, Min Gi; Park, Eunju; Won, Sung-Min; Ganesan, Raja; Gupta, Haripriya; Gebru, Yoseph Asmelash; Sharma, Satya Priya; Lee, Su Been; Kwon, Goo Hyun; Jeong, Min Kyo; Min, Byeong Hyun; Hyun, Ji Ye; Eom, Jung A.; Yoon, Sang Jun; Choi, Mi Ran; Kim, Dong Joon; Suk, Ki Tae] Hallym Univ, Inst Liver & Digest Dis, Coll Med, Chunchon 24252, South Korea.
C3 Hallym University
RP Suk, KT (corresponding author), Hallym Univ, Inst Liver & Digest Dis, Coll Med, Chunchon 24252, South Korea.
EM jj_jeong@hallym.ac.kr; heejin773@gmail.com; qjarlf987@naver.com;
epark312@hallym.ac.kr; lionbanana@hallym.ac.kr; vraja.ganesan@gmail.com;
phr.haripriya13@gmail.com; yagebru@gmail.com; satyapriya83@gmail.com;
qlstn5549@gmail.com; ninetjd@naver.com; astella525@gmail.com;
wooju7023@gmail.com; jiy25n@naver.com; eomjunga32@naver.com;
ysjtthuman@gmail.com; choimi316@naver.com; djkim@hallym.ac.kr;
ktsuk@hallym.ac.kr
RI Kim, Jeong-Han/JDM-6716-2023; won, sungmin/AAH-8401-2021; Ganesan,
Raja/AAW-3703-2021; Gupta, Haripriya/ADF-9486-2022
OI Suk, Ki Tae/0000-0002-9206-9245; Gebru, Yoseph
Asmelash/0000-0001-5133-3620; Yoon, Sang Jun/0000-0003-4712-6359;
Ganesan, Raja/0000-0003-3060-6217; Gupta, Haripriya/0000-0002-6008-1143;
Jeong, Jin-Ju/0000-0001-5728-9886; Kim, Dong Joon/0000-0002-5792-1500
FU Hallym University Research Fund; Basic Science Research Program through
the National Research Foundation of Korea - Ministry of Education,
Science and Technology [NRF-2018M3A9F3020956, NRF-2019R1I1A3A01060447,
NRF-2020R1I1A3073530, NRF-2020R1A6A1A03043026]
FX This research was supported by Hallym University Research Fund, the
Basic Science Research Program through the National Research Foundation
of Korea funded by the Ministry of Education, Science and Technology
(NRF-2018M3A9F3020956, NRF-2019R1I1A3A01060447, NRF-2020R1I1A3073530,
and NRF-2020R1A6A1A03043026).
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NR 118
TC 34
Z9 37
U1 6
U2 33
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-2607
J9 MICROORGANISMS
JI Microorganisms
PD FEB
PY 2022
VL 10
IS 2
AR 288
DI 10.3390/microorganisms10020288
PG 20
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA 2V8TJ
UT WOS:000824111000004
PM 35208742
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Yamaura, Y
Tatsumi, N
Takagi, S
Tokumitsu, S
Fukami, T
Tajiri, K
Minemura, M
Yokoi, T
Nakajima, M
AF Yamaura, Yu
Tatsumi, Naoyuki
Takagi, Shingo
Tokumitsu, Shinsaku
Fukami, Tatsuki
Tajiri, Kazuto
Minemura, Masami
Yokoi, Tsuyoshi
Nakajima, Miki
TI Serum microRNA profiles in patients with chronic hepatitis B, chronic
hepatitis C, primary biliary cirrhosis, autoimmune hepatitis,
nonalcoholic steatohepatitis, or drug-induced liver injury
SO CLINICAL BIOCHEMISTRY
LA English
DT Article
DE Circulating miRNA; miRNA profile; Biomarker; Liver disease; Array
analysis; PCA
ID CIRCULATING MICRORNAS; CANCER-DETECTION; BIOMARKERS; DISEASE; PLASMA;
INFORMATION; CELLS
AB Purpose: Some blood biomarkers or histological examination by liver biopsy are used for the diagnosis of liver diseases in clinics. However, conventional blood biomarkers show poor specificity and sensitivity, and liver biopsy is highly invasiveness. Therefore, to overcome such disadvantages, specific/sensitive and noninvasive options are desirable. In recent years, circulating microRNAs (miRNAs) have been acknowledged for their potential as disease markers. Actually, several miRNAs have been reported to be biomarker candidates of liver diseases. However, these earlier studies were performed for one disease. Therefore, the specificity as biomarkers was not guaranteed, because they didn't study for the other types of liver injury. In this study, we examined if circulating miRNA could distinguish different types of liver diseases.
Methods: Serum miRNA profiles in 28 patients with chronic hepatitis B, chronic hepatitis C, primary biliary cirrhosis, autoimmune hepatitis, nonalcoholic steatohepatitis or drug-induced liver injury as well as 4 control subjects were determined by TaqMan MicroRNA Array analysis. Principal component analysis (PCA) of selected miRNAs was performed.
Results: We identified 37 miRNAs whose levels were significantly different between any of the groups. Although individual miRNAs could not distinguish different types of liver diseases, probably because of similar liver pathology, their profiling by PCA could classify different liver disease groups.
Conclusions: The profiling of the selected miRNAs can be useful to distinguish different types of liver diseases.
C1 [Yamaura, Yu; Tatsumi, Naoyuki; Takagi, Shingo; Tokumitsu, Shinsaku; Fukami, Tatsuki; Yokoi, Tsuyoshi; Nakajima, Miki] Kanazawa Univ, Drug Metab & Toxicol, Fac Pharmaceut Sci, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
[Tajiri, Kazuto; Minemura, Masami] Univ Toyama, Grad Sch Med & Pharmaceut Sci, Sugitani, Toyama 9300194, Japan.
C3 Kanazawa University; University of Toyama
RP Nakajima, M (corresponding author), Kanazawa Univ, Drug Metab & Toxicol, Fac Pharmaceut Sci, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
EM nmiki@p.kanazawa-u.ac.jp
RI Nakajima, Miki/C-3990-2015; Fukami, Tatsuki/C-8907-2015; yokoi,
tsuyoshi/I-7115-2014
OI Fukami, Tatsuki/0000-0003-2416-5988; Yokoi, Tsuyoshi/0000-0002-3239-2817
FU Health and Labor Science Research Grants from the Ministry of Health,
Labor, and Welfare of Japan [H20-BIO-G001]
FX This work was supported in part by Health and Labor Science Research
Grants from the Ministry of Health, Labor, and Welfare of Japan
(H20-BIO-G001).
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NR 37
TC 16
Z9 16
U1 0
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0009-9120
EI 1873-2933
J9 CLIN BIOCHEM
JI Clin. Biochem.
PD DEC
PY 2017
VL 50
IS 18
BP 1034
EP 1039
DI 10.1016/j.clinbiochem.2017.08.010
PG 6
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA FN4OT
UT WOS:000415987300011
PM 28823616
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Kountouras, J
Zavos, C
Chatzopoulos, D
AF Kountouras, J
Zavos, C
Chatzopoulos, D
TI A concept on the role of Helicobacter pylori infection in
autoimmune pancreatitis
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE autoimmune pancreatitis; Helicobacter pylori; molecular mimicry;
apoptosis; T cells
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
PYRUVATE-DEHYDROGENASE COMPLEX; CELLULAR IMMUNE-RESPONSE;
HEPATOCELLULAR-CARCINOMA; HEPATITIS-C; OPEN-ANGLE; T-CELLS; APOPTOSIS;
LIVER
AB Autoimmune pancreatitis, an inflammatory process of the pancreas due to an autoimmune mechanism establishing etiology of chronic pancreatitis, is characterized by the presence of autoantibodies, hypergammaglobulinemia, pancreatic enlargement, pancreatic duct strictures, and pathologic features of fibrotic changes with intense, mainly lymphocytic infiltrations, which may contribute to tissue destruction probably by apoptosis. In almost 60% of the cases, this type of pancreatitis coexists with other autoimmune diseases such as Sjogren's syndrome, sclerosing extrahepatic cholangitis, primary biliary cirrhosis, autoimmune hepatitis, or other extrapancreatic disorders, and recently with gastric peptic ulceration. The diversity of extrapancreatic lesions with similar histopathologic findings suggests general involvement of the digestive system in this disease, although the presence of such involvement has not been fully elucidated. Similarly, Helicobacter pylori (H. pylori) infection, a well known cause of gastric ulcer, has been associated, via molecular mimicry of host structures by its constituents with the same autoimmune conditions, also characterized by fibrotic changes and/or lymphoplasmacytic inflammations, accompanied by aberrations of T cell apoptosis that contribute to hepatobiliary- or extrahepatic-tissue destruction. Considering that H. pylori is involved in the pathogenesis and pathophysiology of these autoimmune disorders, we propose that this organism might trigger autoimmune pancreatitis through induction of autoimmunity and apoptosis.
C1 Aristotle Univ Thessaloniki, Ippokrat Hosp, Med Clin 2, Dept Med, GR-54006 Thessaloniki, Greece.
C3 Aristotle University of Thessaloniki
RP 8 Fanariou St,Byzantio 551 33, Thessaloniki, Macedonia, Greece.
EM jannis@med.auth.gr
RI Zavos, Christos/N-8618-2015
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NR 66
TC 81
Z9 88
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD JAN-MAR
PY 2005
VL 9
IS 1
BP 196
EP 207
DI 10.1111/j.1582-4934.2005.tb00349.x
PG 12
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA 915KB
UT WOS:000228302000019
PM 15784177
OA Green Published
DA 2025-01-07
ER
PT J
AU Morihisa, Y
Chung, H
Towatari, S
Yamashita, D
Inokuma, T
AF Morihisa, Yoshiki
Chung, Hobyung
Towatari, Shuichiro
Yamashita, Daisuke
Inokuma, Tetsuro
TI Autoimmune hepatitis and primary sclerosing cholangitis after
direct-acting antiviral treatment for hepatitis C virus: A case report
SO WORLD JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Liver; Hepatitis C virus; Autoimmune hepatitis; Primary sclerosing
cholangitis; Immune system; Case report
ID INVARIANT T-CELLS; LIVER
AB BACKGROUND Chronic hepatitis C virus (HCV) infection is a major global health concern that leads to liver fibrosis, cirrhosis, and cancer. Regimens containing direct-acting antivirals (DAAs) have become the mainstay of HCV treatment, achieving a high sustained virological response (SVR) with minimal adverse events.
CASE SUMMARY A 74-year-old woman with chronic HCV infection was treated with the DAAs ledipasvir, and sofosbuvir for 12 wk and achieved SVR. Twenty-four weeks after treatment completion, the liver enzyme and serum IgG levels increased, and antinuclear antibody became positive without HCV viremia, suggesting the development of autoimmune hepatitis (AIH). After liver biopsy indicated AIH, a definite AIH diagnosis was made and prednisolone was initiated. The treatment was effective, and the liver enzyme and serum IgG levels normalized. However, multiple strictures of the intrahepatic and extrahepatic bile ducts with dilatation of the peripheral bile ducts appeared on magnetic resonance cholangiopancreatography after 3 years of achieving SVR, which were consistent with primary sclerosing cholangitis.
CONCLUSION The potential risk of developing autoimmune liver diseases after DAA treatment should be considered.
C1 [Morihisa, Yoshiki; Chung, Hobyung; Towatari, Shuichiro; Inokuma, Tetsuro] Kobe City Med Ctr Gen Hosp, Dept Gastroenterol & Hepatol, 2-1-1 Minatojimaminami Machi,Chuo Ku, Kobe, Hyogo 6500047, Japan.
[Yamashita, Daisuke] Kobe City Med Ctr Gen Hosp, Dept Pathol, Kobe, Hyogo 6500047, Japan.
C3 Kobe City Medical Center General Hospital; Kobe City Medical Center
General Hospital
RP Chung, H (corresponding author), Kobe City Med Ctr Gen Hosp, Dept Gastroenterol & Hepatol, 2-1-1 Minatojimaminami Machi,Chuo Ku, Kobe, Hyogo 6500047, Japan.
EM teihiroshi@gmail.com
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,, 2011, Journal of Hepatology, V55, P245, DOI [10.1016/j.jhep.2013.11.003, 10.1016/j.jhep.2011.02.023]
NR 31
TC 2
Z9 2
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5182
J9 WORLD J HEPATOL
JI World J. Hepatol.
PD FEB 27
PY 2024
VL 16
IS 2
DI 10.4254/wjh.v16.i2.286
PG 9
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA LV9C6
UT WOS:001189683700020
PM 38495284
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Ngu, JH
Gearry, RB
Frampton, CM
Stedman, CAM
AF Ngu, Jing Hieng
Gearry, Richard Blair
Frampton, Chris Miles
Stedman, Catherine Ann Malcolm
TI Mortality and the risk of malignancy in autoimmune liver diseases: A
population-based study in Canterbury, New Zealand
SO HEPATOLOGY
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; EXTRAHEPATIC
MALIGNANCIES; HEPATOCELLULAR-CARCINOMA; FOLLOW-UP; SYMPTOM PROGRESSION;
BREAST-CANCER; SINGLE-CENTER; HEPATITIS; COHORT
AB Population-based quantitative data on the mortality and cancer incidence of autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC) are scarce. Our aim was to systematically investigate the survival and risk of malignancy on population-based cohorts of AIH, PBC, and PSC in Canterbury, New Zealand. Multiple case-finding methods were employed, including searches of all public and private, adult and pediatric outpatient clinics, hospital notes, laboratory, radiology, and pathology reports. Cases that fulfilled standardized diagnostic criteria were included. Kaplan-Meier survival estimates, standardized mortality ratios (SMR), and standard incidence ratios (SIR) for malignancy were calculated. A total of 130 AIH, 70 PBC, and 81 PSC patients were included contributing to 1,156, 625, and 613 person-years at risk, respectively. For AIH, PBC, and PSC cohorts, SMRs for all-cause mortality were 2.1 (95% confidence interval [CI] 1.4-3.1), 2.7 (95% CI 1.7-4.0), and 4.1 (95% CI 2.6-6.3), SMRs for hepatobiliary mortality were 42.3 (95% CI 20.3-77.9), 71.2 (95% CI 30.7-140.3), and 116.9 (95% CI 66.8-189.8), SIRs for all cancers were 3.0 (95% CI 2.0-4.3), 1.6 (95% CI 0.8-2.9), and 5.2 (95% CI 3.3-7.8), and SIRs for extrahepatic malignancy were 2.7 (95% CI 1.8-3.9), 1.6 (95% CI 0.8-2.9), and 3.0 (95% CI 1.6-5.1), respectively. Conclusion: This is the first population-based study to examine and compare the survival and cancer incidence in AIH, PBC, and PSC in the same population. The mortality for all three cohorts was significantly increased due to liver-related death, demonstrating the inadequacy of current management strategies. The risk of hepatic and extrahepatic malignancy was significantly increased in AIH and PSC patients. (HEPATOLOGY 2012)
C1 [Ngu, Jing Hieng; Gearry, Richard Blair; Stedman, Catherine Ann Malcolm] Christchurch Hosp, Dept Gastroenterol, Christchurch, New Zealand.
[Ngu, Jing Hieng; Gearry, Richard Blair; Stedman, Catherine Ann Malcolm] Univ Otago, Canterbury, New Zealand.
C3 Christchurch Hospital New Zealand; University of Otago
RP Stedman, CAM (corresponding author), Christchurch Hosp, Dept Gastroenterol, Private Bag 4710, Christchurch, New Zealand.
EM catherine.stedman@cdhb.health.nz
RI Stedman, Catherine/AFM-4210-2022; Gearry, Richard/H-3959-2019
OI Gearry, Richard/0000-0002-2298-5141
FU Health Research Council of New Zealand; Ferring/New Zealand Society of
Gastroenterology; Canterbury Medical Research Foundation; Royal
Australasia College of Physicians
FX Dr. Ngu's stipend is supported by Clinical Research Training Fellowship
from the Health Research Council of New Zealand (2011-2013), Ferring/New
Zealand Society of Gastroenterology Fellowship and Canterbury Medical
Research Foundation Fellowship (2010). Research related expenses were
supported by grant from the Royal Australasia College of Physicians.
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NR 39
TC 79
Z9 81
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD FEB
PY 2012
VL 55
IS 2
BP 522
EP 529
DI 10.1002/hep.24743
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 883KM
UT WOS:000299632900021
PM 21994151
OA Bronze
DA 2025-01-07
ER
PT J
AU O'Grady, JG
AF O'Grady, J. G.
TI Phenotypic Expression of Recurrent Disease After Liver Transplantation
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Review
DE HLA matching; immunosuppression; liver transplantation; phenotype;
recurrent disease
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; AUTOIMMUNE
HEPATITIS; IMMUNOSUPPRESSIVE REGIMENS; HEPATOCELLULAR-CARCINOMA;
CRYPTOGENIC CIRRHOSIS; VIRUS-INFECTION; HCV; OUTCOMES; THERAPY
AB Recurrence of the primary disease has become a major focus for transplant hepatologists both when investigating graft dysfunction and when tailoring immunosuppression to maximize graft survival. However, disease recurrence varies in penetrance, can be predictable or random, and does not always conform to the expected pattern of disease. The cholestatic hepatitis syndromes associated with hepatitis B and C are the most dramatic examples of phenotypic change. Being on immunosuppressive drugs may intensify the progression of infectious and malignant diseases, but this effect is not predictable. A significant minority of patients with each of the autoimmune diseases, counter-intuitively, get recurrent disease despite immunosuppression of a potency that is adequate to prevent rejection of the liver graft. Disease patterns emerge after liver transplantation for cryptogenic cirrhosis that shed light on the cause of the native liver disease, for example, nonalcohol-related fatty liver disease and autoimmune hepatitis. The phenotypic expression of disease recurrence can be modified by specific drugs used for immunosuppression and by HLA-antigen matching profiles. Understanding and modifying the phenotypic expression of recurrent disease after liver transplantation is a fertile area for research and continued refinement of clinical care.
C1 Kings Coll Hosp London, Inst Liver Studies, London SE5 8RX, England.
C3 University of London; King's College London; King's College Hospital NHS
Foundation Trust; King's College Hospital
RP O'Grady, JG (corresponding author), Kings Coll Hosp London, Inst Liver Studies, Denmark Hill, London SE5 8RX, England.
EM john.ogrady@kcl.ac.uk
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NR 33
TC 17
Z9 17
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-6135
EI 1600-6143
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD MAY
PY 2010
VL 10
IS 5
BP 1149
EP 1154
DI 10.1111/j.1600-6143.2010.03080.x
PG 6
WC Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery; Transplantation
GA 586OZ
UT WOS:000276921600008
PM 20353464
OA hybrid
DA 2025-01-07
ER
PT J
AU Durazzo, M
Ponzo, E
Bonetto, S
Fagoonee, S
Pellicano, R
AF Durazzo, Marilena
Ponzo, Elena
Bonetto, Silvia
Fagoonee, Sharmila
Pellicano, Rinaldo
TI Liver diseases in the elderly
SO MINERVA MEDICA
LA English
DT Review
DE Aged; Liver diseases; Hepatitis; Liver cirrhosis
ID PRIMARY BILIARY-CIRRHOSIS; C VIRUS-INFECTION; POPULATION-BASED
EPIDEMIOLOGY; TYPE-1 AUTOIMMUNE HEPATITIS; ACG CLINICAL GUIDELINE;
HEPATOCELLULAR-CARCINOMA; RISK-FACTORS; RADIOFREQUENCY ABLATION;
OLD-AGE; TRANSPLANTATION
AB Due to the progressive increase in life expectancy, the number of elderly people in the world is growing rapidly. Although there are no liver diseases specific of older age, the ageing liver shows some anatomical and physiological changes that can affect the frequency and the clinical behavior of most hepatopathies. In particular, these changes tend to cause an increased vulnerability to acute liver injury and an increased susceptibility to liver fibrosis, accounting for the predisposition to a generally more severe course of liver diseases compared to younger patients. Furthermore, advanced age is also associated with immune system alterations, influencing the manifestation of those hepatopathies that are mediated by host immune response, like viral hepatitis, autoimmune hepatitis but also hepatocellular carcinoma. Despite these changes, total liver function and laboratory values tend to be well maintained in healthy elderly, so that every enzymatic alteration in a geriatric patient should be investigated with the same attention as in a younger one. A proper and early diagnosis is of great importance both considering the age-related more aggressive course of hepatopathies and that age itself does not seem to be a limit for most treatment options, even if specific data are often lacking. This paper focuses on the peculiarities of main liver diseases in geriatrics, with respect to epidemiology, clinical presentation, diagnosis and management, which can be more challenging in advanced age because of the frequent comorbidities and polytherapies.
C1 [Durazzo, Marilena; Bonetto, Silvia] Univ Turin, Molinette Hosp, Dept Med Sci, Unit Med Citta Salute & Sci 3, Turin, Italy.
[Ponzo, Elena; Pellicano, Rinaldo] Molinette SGAS Hosp, Unit Gastroenterol, Turin, Italy.
[Fagoonee, Sharmila] CNR, Mol Biotechnol Ctr, Inst Biostruct & Bioimaging, Turin, Italy.
C3 University of Turin; A.O.U. Citta della Salute e della Scienza di
Torino; AOU San Giovanni Battista-Molinette; A.O.U. Citta della Salute e
della Scienza di Torino; AOU San Giovanni Battista-Molinette; Consiglio
Nazionale delle Ricerche (CNR); Istituto di Biostrutture e Bioimmagini
(IBB-CNR)
RP Durazzo, M (corresponding author), Univ Turin, Dept Med Sci, Corso AM Dogliotti 14, I-10126 Turin, Italy.
EM marilena.durazzo@unito.it
RI Fagoonee, Sharmila/L-1940-2019
OI DURAZZO, Marilena/0000-0003-2450-5911; FAGOONEE,
SHARMILA/0000-0001-6070-6716; PELLICANO, RINALDO/0000-0003-3438-0649
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NR 99
TC 19
Z9 19
U1 0
U2 10
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 0026-4806
EI 1827-1669
J9 MINERVA MED
JI Minerva Med.
PD FEB
PY 2019
VL 110
IS 1
BP 35
EP 51
DI 10.23736/S0026-4806.18.05858-5
PG 17
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HP5RH
UT WOS:000461735900006
PM 30334441
DA 2025-01-07
ER
PT J
AU Capurso, G
Pedica, F
Palumbo, D
Della-Torre, E
AF Capurso, Gabriele
Pedica, Federica
Palumbo, Diego
Della-Torre, Emanuel
TI IgG4-related autoimmune liver disease
SO MINERVA GASTROENTEROLOGY
LA English
DT Review
DE Immunoglobin G4-related disease; Immunoglobin G; Autoimmune
pancreatitis; Cholangitis; Liver; Hepa-titis
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; FINE-NEEDLE BIOPSY; SCLEROSING
CHOLANGITIS; SYSTEMIC-DISEASE; SERUM IGG4; DIAGNOSTIC-CRITERIA;
PANCREATITIS; ASSOCIATION; FEATURES; TYPE-1
AB The term IgG4-related autoimmune liver disease (AILD) refers to hepato-biliary manifestations of Immunoglobin G4 -related disease (IgG4-RD) including IgG4-related sclerosing cholangitis and IgG4-related pseudotumor. The association of some forms of autoimmune hepatitis to IgG4-RD remains controversial. Although autoimmune phenomena have not been clearly observed in IgG4-AILD, perturbation of the adaptive immune system and activation of the humoral response represent established pathophysiological hallmarks and potential therapeutic targets. Clinical manifestations of IgG4-AILD are virtually indistinguishable from bile duct cancer or primary sclerosing cholangitis and are due to mass forming lesions and thickening of the biliary tract that progressively lead to biliary ducts obstruction. There are no current reliable biomarkers for IgG4-AILD and diagnosis should rely on the integration of clinical, serological, radiological, and histo-logical findings. In analogy to most IgG4-RD manifestations, and in contrast to its major mimickers, IgG4-AILD prompt-ly responds to glucocorticoids but frequently relapses, thus requiring long-term maintenance therapy to avoid progressive fibrosclerotic disease and liver cirrhosis. Accumulating evidence on the efficacy of B-cell depletion therapy in patients with systemic IgG4-RD is gradually changing the treatment paradigm of IgG4-AILD and biologics will be increasingly used also for gastroenterological manifestations of IgG4-RD to spare glucocorticoids and traditional immunosuppressive agents. Looking ahead, identification of reliable biomarkers and of mini-invasive strategies to obtain informative biopsies from the biliary tree represent unavoidable priorities to optimize diagnosis and management of IgG4-AILD.
C1 [Capurso, Gabriele; Pedica, Federica; Palumbo, Diego; Della-Torre, Emanuel] Univ Vita Salute San Raffaele, IRCCS San Raffaele Hosp, Milan, Italy.
[Capurso, Gabriele] IRCCS San Raffaele Hosp, Div Pancreato Biliary Endoscopy & Endosonog, Milan, Italy.
[Capurso, Gabriele; Della-Torre, Emanuel] IRCCS San Raffaele Hosp, Div Pancreat Surg, Pancreas Translat & Clin Res Ctr, Milan, Italy.
[Pedica, Federica] IRCCS San Raffaele Hosp, Unit Pathol, Milan, Italy.
[Palumbo, Diego] IRCCS San Raffaele Hosp, Unit Clin & Expt Radiol, Expt Imaging Ctr, Milan, Italy.
[Della-Torre, Emanuel] IRCCS San Raffaele Hosp, Unit Immunol Rheumatol Allergy & Rare Dis UnIRAR, Milan, Italy.
C3 Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele
RP Della-Torre, E (corresponding author), Univ Vita Salute San Raffaele, IRCCS San Raffaele Hosp, Div Pancreat Surg,Pancreas Translat & Clin Res Ct, Unit Immunol Rheumatol Allergy & Rare Dis UnIRAR, Via Olgettina 60, I-20132 Milan, Italy.
EM dellatorre.emanuel@hsr.it
RI Palumbo, Diego/AAN-6709-2020; Capurso, Gabriele/AAB-1389-2019
OI Capurso, Gabriele/0000-0002-0019-8753
FU Cariplo Foundation
FX The authors acknowledge Cariplo Foundation for supporting Dr. Della
Torre salary thanks to a "Cariplo Giovani Ricercatori 2018" award.
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NR 108
TC 0
Z9 0
U1 0
U2 1
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 2724-5985
EI 2724-5365
J9 MINERVA GASTROENTERO
JI Minerva Gastroenterol.
PD MAR
PY 2023
VL 69
IS 1
BP 23
EP 49
DI 10.23736/S2724-5895.20.02794-4
PG 27
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WS2J2
UT WOS:001256794200005
PM 33267565
DA 2025-01-07
ER
PT J
AU Gu, XP
Lu, Q
Zhang, CC
Tang, ZW
Chu, LX
AF Gu, Xinpei
Lu, Qin
Zhang, Chengcheng
Tang, Zhewei
Chu, Liuxi
TI Clinical Application and Progress of Fecal Microbiota Transplantation in
Liver Diseases: A Review
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE gut microbiota; microbiota imbalance; liver diseases; microbiome
ID CLOSTRIDIUM-DIFFICILE INFECTION; FATTY LIVER; GUT MICROBIOME;
HEPATIC-ENCEPHALOPATHY; SIGNATURE; DYSBIOSIS; SEVERITY; FIBROSIS;
CANCER; INJURY
AB The human gut harbors a dense and highly diverse microbiota of approximately 1,000 bacterial species. The interaction between the host and gut bacteria strongly influences human health. Numerous evidence suggest that intestinal flora imbalance is closely associated with the development and treatment of liver diseases, including acute liver injury and chronic liver diseases (cirrhosis, autoimmune liver disease, and fatty liver). Therefore, regulating the gut microbiota is expected to be a new method for the adjuvant treatment of liver diseases. Fecal microbiota transplantation (FMT) is defined as the transplantation of gut microbiota from healthy donors to sick patients via the upper or lower gastrointestinal route to restore the normal intestinal balance. In this study, we briefly review the current research on the gut microbiota and its link to liver diseases and then summarize the evidence to elucidate the clinical application and development of FMT in liver disease treatment.
C1 [Gu, Xinpei] Shandong First Med Univ & Shandong Acad Med Sci, Dept Human Anat, Tai An, Shandong, Peoples R China.
[Lu, Qin] Hebei Univ Chinese Med, Sch Basic Med Sci, Dept Prescript Sci, Shijiazhuang, Hebei, Peoples R China.
[Zhang, Chengcheng; Tang, Zhewei] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, Shanghai, Peoples R China.
[Chu, Liuxi] Southeast Univ, Sch Biol Sci & Med Engn, Inst Child Dev & Educ, Nanjing 210096, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
Sciences; Hebei University of Chinese Medicine; Shanghai University of
Traditional Chinese Medicine; Southeast University - China
RP Chu, LX (corresponding author), Southeast Univ, Sch Biol Sci & Med Engn, Inst Child Dev & Educ, Nanjing 210096, Peoples R China.
EM clx@seu.edu.cn
OI Gu, Xinpei/0000-0002-3577-4538; Chu, Liuxi/0000-0002-6071-1870
FU National Natural Science Foundation of China [81904129]; College Student
Innovation Funds Project for the Hebei University of Chinese Medicine
[31800952, 202014432203]; Fundamental Research Funds for the Southeast
University [3218006405, 2242019s10024]
FX National Natural Science Foundation of China (81904129), the College
Student Innovation Funds Project for the Hebei University of Chinese
Medicine (31800952, 202014432203), the Fundamental Research Funds for
the Southeast University (3218006405, 2242019s10024) sponsored this
study.
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NR 95
TC 14
Z9 14
U1 4
U2 60
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD NOV
PY 2021
VL 41
IS 04
BP 495
EP 506
DI 10.1055/s-0041-1732319
EA JUL 2021
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WB6VO
UT WOS:000673464000001
PM 34261137
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Piconese, S
Cammarata, I
Barnaba, V
AF Piconese, Silvia
Cammarata, Ilenia
Barnaba, Vincenzo
TI Viral hepatitis, inflammation, and cancer: A lesson for autoimmunity
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE HCV; HBV; Immune checkpoints; Tregs; Wnt
ID REGULATORY T-CELLS; B-VIRUS INFECTION; BETA-CATENIN; TREG CELLS;
IMMUNE-RESPONSES; CUTTING EDGE; EFFECTOR; LIVER; PD-1; TOLERANCE
AB In the present review, we analyzed the various overlapping and non-mutually exclusive mechanisms that intersect and form complex and highly flexible immunological networks allowing the defense against liver infections and tumors. Liver immunity results from the combination of the skills of systemic and local immune system(s) to sense and recognize pathogen or tumor antigens, to sensitize a wide range of innate and adaptive immune cells, and to clear the "invaders", through the establishment of a transient liver immunopathology state undergoing resolution/control of infections or tumors, and memory development. Then, a special emphasis is placed on discussing about the capacity of the immune system(s) to develop a state of chronic low-level immunopathology adapting through the intervention of simultaneous immunoregulatory mechanisms, when the liver is infected by highly mutable viruses (e.g., hepatitis B or C viruses [HBV or HCV]) capable to escape from the immune recognition. The establishment of chronic inflammation represents an advantage for the species survival, because it guarantees the long-term survival of human hosts despite the virus persistence. However, chronic inflammation, in the long run, can evolve towards severe consequences (decompensated cirrhosis and hepatocellular carcinoma) in some individuals, finding requiring the impelling need of discovering new therapeutic anti-viral and immunostimulatory agents addressed, in combination, to fight especially HBV that, in contrast to HCV, lacks antivirals capable to eradicate the virus. Finally, we discussed the concept proposing that the divergent immunoregulatory mechanisms that develop in persisting infections or tumors, on the one hand, and autoimmunity, on the other hand, are the mirror image of each other, whose understanding is also relevant for preparing novel immunotherapeutic approaches in autoimmune diseases.
C1 [Piconese, Silvia; Cammarata, Ilenia; Barnaba, Vincenzo] Sapienza Univ Rome, Dipartimento Med Interne & Specialita Med, Viale Policlin 155, I-00161 Rome, Italy.
[Piconese, Silvia; Barnaba, Vincenzo] Fdn Cenci Bolognetti, Ist Pasteur Italia, Rome, Italy.
[Barnaba, Vincenzo] Ist Italian Tecnol, Ctr Life Nano Sci, Rome, Italy.
C3 Sapienza University Rome; Fondazione Cenci Bolognetti; Istituto Italiano
di Tecnologia - IIT
RP Barnaba, V (corresponding author), Sapienza Univ Rome, Dipartimento Med Interne & Specialita Med, Viale Policlin 155, I-00161 Rome, Italy.
EM vincenzo.barnaba@uniroma1.it
RI Barnaba, Vincenzo/AAB-1945-2019
OI Piconese, Silvia/0000-0002-9685-5227
FU Associazione Italiana per la Ricerca sul Cancro (AIRC) [15199, 19784,
19939]; Ministero della Salute [RF-2010-2310438, RF 2010-2318269];
Fondazione Italiana Sclerosi Multipla (FISM) onlus [2015/R/04];
Ministero dell'Istruzione, dell'Universita e della Ricerca (MIUR)
[2010LC747T_004]; Fondo per gli investimenti di ricerca di base (FIRB)
[RBAP10TPXK]; Istituto Pasteur Italia - Fondazione Cenci Bolognetti;
International Network Institut Pasteur, Paris - "Programmes Transversaux
De Recherche" [20-16]
FX This work was supported by the following grants: Associazione Italiana
per la Ricerca sul Cancro (AIRC) (progetti "Investigator Grant"
[IG]-2014 id. 15199 and IG-2017 id. 19939 to VB, and IG-2017 id. 19784
to SP); Ministero della Salute (Ricerca finalizzata [RF-2010-2310438 and
RF 2010-2318269]); Fondazione Italiana Sclerosi Multipla (FISM) onlus
(cod. 2015/R/04); Ministero dell'Istruzione, dell'Universita e della
Ricerca (MIUR) (PRIN 2010-2011 prot. 2010LC747T_004); Fondo per gli
investimenti di ricerca di base (FIRB)-2011/13 (no. RBAP10TPXK);
Istituto Pasteur Italia - Fondazione Cenci Bolognetti (grant 2014-2016);
International Network Institut Pasteur, Paris - "Programmes Transversaux
De Recherche" (PTR n. 20-16).
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NR 106
TC 30
Z9 32
U1 0
U2 15
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD DEC
PY 2018
VL 95
SI SI
BP 58
EP 68
DI 10.1016/j.jaut.2018.10.021
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA HE6DA
UT WOS:000453492300006
PM 30509387
DA 2025-01-07
ER
PT J
AU Wang, TT
Men, RT
Hu, MX
Fan, XL
Yang, XX
Huang, XJ
Ye, TH
Yang, L
AF Wang, Tingting
Men, Ruoting
Hu, Mingxing
Fan, Xiaoli
Yang, Xiaoxue
Huang, Xiaojun
Ye, Tinghong
Yang, Li
TI Protective effects of Punica granatum (pomegranate) peel extract
on concanavalin A-induced autoimmune hepatitis in mice
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Punica granatum peel extract (PoPx); Concanavalin A; Autoimmune
hepatitis; Immune cells; Mouse model
ID CHINESE HERBAL MEDICINES; OXIDATIVE STRESS; LIVER-INJURY; ANTIOXIDANT
ACTIVITY; SELF-TOLERANCE; BREAST-CANCER; LUNG-CANCER; IN-VITRO; T-CELLS;
DISEASE
AB Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease of an unknown etiology, glucocorticoid therapy is currently recognized as an effective treatment for AIH, but conventional application and patient compliance are both hindered by its side effects. The exploration of the AIH pathogenesis and the searching for the new candidate drugs that exert potential activity and low toxicity are urgently needed. Pomegranate peel extract (PoPx) is a natural extract of Punica granatum and has been reported to have anti-inflammatory and antioxidative properties. The present study aimed to clarify the effect of PoPx on the concanavalin A (ConA)induced autoimmune hepatitis in a mouse model that is well established at 12h after tail vein injection with a dose of 20 mg/kg of ConA. C57BL/6 female mice were pretreated with PoPx (250 mg/kg, once daily for 3 days) followed by a ConA challenge. Pretreatment with PoPx significantly alleviated ConA-induced liver injury by down-regulating the levels of plasma alanine transaminase (ALT), aspartate transaminase (AST) and cytokine, including TNF-alpha, interferon (IFN) -gamma and interleukin (IL)-6. Moreover, liver hematoxylin and eosin (H&E) staining displayed a lighter inflammatory infiltration around the portal area in the PoPx-pretreated mice. In addition, the flow cytometry (FCM) data showed that the immune response in the liver was died down in the PoPx-pretreated condition. Specially, pretreatment with PoPx reduced the infiltration of activated CD4(+) and CD8(+) T cells in the liver. Taken together, these findings contributed to a better understanding of the actions of PoPx against acute AIH and indicated that PoPx might be a potential compound in treating T cell-mediated autoimmune liver injury.
C1 [Wang, Tingting; Men, Ruoting; Fan, Xiaoli; Yang, Xiaoxue; Yang, Li] Sichuan Univ, West China Hosp, Div Gastroenterol & Hepatol, Chengdu 610041, Peoples R China.
[Hu, Mingxing; Ye, Tinghong] Sichuan Univ, West China Hosp, Lab Liver Surg, Chengdu 610041, Peoples R China.
[Huang, Xiaojun] Jinan Univ, Shenzhen Peoples Hosp, Dept Hepatobiliary & Pancreas Surg, Clin Med Coll 2, Shenzhen, Guangdong, Peoples R China.
C3 Sichuan University; Sichuan University; Jinan University
RP Yang, L (corresponding author), Sichuan Univ, West China Hosp, Div Gastroenterol & Hepatol, Chengdu 610041, Peoples R China.
EM yangli_hx@scu.edu.cn
RI YE, Ting-Hong/HLW-3123-2023; wang, tingting/AAK-2640-2020
FU National Natural Science Foundation of China [81500054, 81570554];
Science & Technology Department of Sichuan Province, China [2017JY0071]
FX The authors would like to thank Chen Fan and Ten Ling for their
additional work. This research was supported by the National Natural
Science Foundation of China (81500054 and 81570554) and the Key Project
(Grant No: 2017JY0071) of the Science & Technology Department of Sichuan
Province, China.
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NR 54
TC 28
Z9 33
U1 1
U2 27
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD APR
PY 2018
VL 100
BP 213
EP 220
DI 10.1016/j.biopha.2017.12.110
PG 8
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA FZ5PZ
UT WOS:000427649200027
PM 29428670
DA 2025-01-07
ER
PT J
AU Zhang, L
Zhou, XM
Dai, YP
Lv, CY
Wu, J
Wu, QQ
Li, T
Wang, YG
Xia, PG
Pei, H
Huang, B
AF Zhang, Li
Zhou, Xiumei
Dai, Yaping
Lv, Chunyan
Wu, Jian
Wu, Qingqing
Li, Ting
Wang, Yigang
Xia, Penguo
Pei, Hao
Huang, Biao
TI Establishment of interleukin-18 time-resolved fluorescence immunoassay
and its preliminary application in liver disease
SO JOURNAL OF CLINICAL LABORATORY ANALYSIS
LA English
DT Article
DE ELISA; interferon‐ γ interleukin 18; liver disease;
time‐ resolved fluorescence immunoassay
AB Background To establish a time-resolved fluorescence immunoassay of interleukin (IL)-18 (IL-18-TRFIA) and detect its concentration in different liver disease serum samples.
Methods The IL-18 coating antibody and the Eu3+-labeled detection antibody were used for the IL-18-TRFIA to detect serum IL-18 concentration in patients with liver cancer, hepatitis B, hepatitis C, autoimmune hepatitis, fatty liver disease, and healthy controls. The double-antibody sandwich method was used and methodological evaluation was performed.
Results The average intra- and inter-assay coefficient of variation for IL-18-TRFIA was 4.80% and 5.90%, respectively. The average recovery rate was 106.19 +/- 3.44%. The sensitivity (10.96 pg/mL) was higher than that obtained using the ELISA method (62.5 pg/mL). The detection range was 10.96-1000 pg/mL. IL-6 and galectin-3 did not cross-react with IL-18-TRFIA. The serum concentration of IL-18 was (776.99; 653.48-952.39 pg/mL) in hepatitis C, (911; 775.55-1130.03 pg/mL) in fatty liver, (1048.88; 730.04-1185.10 pg/mL) in liver cancer, and (949.12; 723.70-1160.28 pg/mL) in hepatitis B. Moreover, IL-18 serum levels were significantly higher in patients than the healthy controls (483.09; 402.52-599.70/mL) (p < 0.0001). Autoimmune hepatitis with a serum IL-18 concentration of 571.62; 502.47-730.31 pg/mL was not significantly different from the healthy controls (p > 0.05).
Conclusion We established a highly sensitive IL-18-TRFIA method that successfully detected serum IL-18 concentrations in different liver diseases. Furthermore, IL-18 serum concentration was higher in patients with liver cancer, hepatitis C, hepatitis B, and fatty liver disease compared to healthy controls.
C1 [Zhang, Li; Zhou, Xiumei; Wu, Qingqing; Li, Ting; Wang, Yigang; Xia, Penguo; Huang, Biao] Zhejiang Sci Tech Univ, Coll Life Sci & Med, Hangzhou, Peoples R China.
[Dai, Yaping; Lv, Chunyan; Pei, Hao] Wuxi 5 Peoples Hosp, Wuxi, Jiangsu, Peoples R China.
[Wu, Jian] First Peoples Hosp Yancheng City, Dept Lab Med, Yancheng, Peoples R China.
C3 Zhejiang Sci-Tech University
RP Huang, B (corresponding author), Zhejiang Sci Tech Univ, Coll Life Sci & Med, Hangzhou, Peoples R China.; Pei, H (corresponding author), Wuxi 5 Peoples Hosp, Wuxi, Jiangsu, Peoples R China.
EM peihao1008@126.com; jswxhb@163.com
RI Huang, B/HGA-7110-2022
OI Wu, Jian/0000-0003-0087-3744; WU, QINGQING/0000-0002-0539-0947; Li,
Ting/0000-0001-6213-2496
FU Social Development Fund of Zhejiang Province [LGF20H200008]; Wuxi Key
Laboratory of Infectious Disease Prevention and Control [CXPT(SYS)001];
Key Research and Development Program of Zhejiang Province [2020C03066]
FX The Social Development Fund of Zhejiang Province, Grant/Award Number:
LGF20H200008; Wuxi Key Laboratory of Infectious Disease Prevention and
Control, Grant/Award Number: CXPT(SYS)001; The Key Research and
Development Program of Zhejiang Province, Grant/Award Number: 2020C03066
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NR 32
TC 4
Z9 4
U1 2
U2 36
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0887-8013
EI 1098-2825
J9 J CLIN LAB ANAL
JI J. Clin. Lab. Anal.
PD MAY
PY 2021
VL 35
IS 5
AR e23758
DI 10.1002/jcla.23758
EA MAR 2021
PG 8
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA SD1WH
UT WOS:000628861100001
PM 33720453
OA Green Published
DA 2025-01-07
ER
PT J
AU Male, V
Stegmann, KA
Easom, NJ
Maini, MK
AF Male, Victoria
Stegmann, Kerstin A.
Easom, Nicholas J.
Maini, Mala K.
TI Natural Killer Cells in Liver Disease
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE NK cells; liver residence; fibrosis; viral hepatitis; alcoholic liver
disease; non-alcoholic fatty liver disease; hepatocellular carcinoma;
autoimmune; transplantation
ID CHRONIC HEPATITIS-B; PRIMARY SCLEROSING CHOLANGITIS; C VIRUS-INFECTION;
PRIMARY BILIARY-CIRRHOSIS; INDUCED HEPATOCELLULAR-CARCINOMA; CHRONIC
ALCOHOL-CONSUMPTION; ADAPTIVE IMMUNE-RESPONSES; APOPTOSIS-INDUCING
LIGAND; ACTIVATED STELLATE CELLS; CD56(BRIGHT) NK CELLS
AB Natural killer (NK) cells comprise one of the most abundant immune cell populations in human liver and the nature and functions of these cells have been a focus of recent interest. Here, we consider the possible roles of NK cells in diverse liver diseases, concentrating on data from patient studies. NK cells can be protective, killing virally infected and cancerous cells in the liver and limiting fibrosis by eliminating hepatic stellate cells. However, they can also be deleterious, contributing to pathology in viral hepatitis by killing hepatocytes and downregulating virus-specific T-cell responses. It has recently emerged that a large fraction of hepatic NK cells constitute a distinct liver-resident subset and we highlight the need to distinguish between circulating and liverresident NK cells in future studies. There is also a need for further investigation into how NK cells are influenced by the liver microenvironment and what scope there is to harness their immunotherapeutic potential.
C1 [Male, Victoria] UCL, Inst Immun & Transplantat, UCL Med Sch, Div Infect & Immun, Rowland Hill St, London NW3 2PF, England.
[Stegmann, Kerstin A.; Easom, Nicholas J.; Maini, Mala K.] UCL, Div Infect & Immun, London, England.
C3 University of London; University College London; University of London;
University College London
RP Male, V (corresponding author), UCL, Inst Immun & Transplantat, UCL Med Sch, Div Infect & Immun, Rowland Hill St, London NW3 2PF, England.
EM v.male@ucl.ac.uk
OI Male, Victoria/0000-0001-5654-5083; Maini, Mala/0000-0001-6384-1462
FU Royal Society/Wellcome Trust Sir Henry Dale Fellowship WT [105677];
Wellcome Trust Investigator Award; Wellcome Trust [101849/Z/13/Z]
Funding Source: Wellcome Trust; MRC [MR/M020126/1] Funding Source: UKRI
FX Victoria Male is supported by a Royal Society/Wellcome Trust Sir Henry
Dale Fellowship WT 105677. Mala Maini is supported by a Wellcome Trust
Investigator Award.
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NR 144
TC 20
Z9 21
U1 0
U2 19
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD AUG
PY 2017
VL 37
IS 3
BP 198
EP 209
DI 10.1055/s-0037-1603946
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FE7SI
UT WOS:000408406800002
PM 28847031
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Bach, JP
Rinn, B
Meyer, B
Dodel, R
Bacher, M
AF Bach, Jan-Philipp
Rinn, Birgit
Meyer, Bernhard
Dodel, Richard
Bacher, Michael
TI Role of MIF in Inflammation and Tumorigenesis
SO ONCOLOGY
LA English
DT Review
DE Angiogenesis; Autoimmune diseases; Inflammation; MIF; Tumor
ID MIGRATION-INHIBITORY FACTOR; ACTIVATED PROTEIN-KINASE; TUMOR-CELL
GROWTH; REGULATORY ROLE; FACTOR GENE; HEPATOCELLULAR-CARCINOMA; CYTOKINE
PRODUCTION; CRYSTAL-STRUCTURE; MELANOMA-CELLS; MACROPHAGE
AB MIF has been described as a protein that plays an essential role in both innate and acquired immunity. Previous studies have demonstrated that MIF activates lymphocytes, granulocytes and monocytes/macrophages. Furthermore, MIF can counteract the physiological function of steroids, thus playing a role in immune system regulation. Further evidence for a role of MIF in immunity was obtained in mouse models of autoimmune disorders, where the inhibition of MIF resulted in a more benign disease progression. This observation made MIF an attractive therapeutic target for the treatment of these disorders. Moreover, MIF expression was found to be upregulated in a variety of different tumor cells, a finding that further attracted interest. This review provides an overview of the involvement of MIF in both autoimmune disorders and tumorigenesis and summarizes the molecular action of MIF in this context. Copyright (c) 2008 S. Karger AG, Basel
C1 [Bach, Jan-Philipp; Dodel, Richard; Bacher, Michael] Univ Marburg, Dept Neurol, DE-35039 Marburg, Germany.
[Rinn, Birgit; Bacher, Michael] Univ Marburg, Inst Immunol, DE-35039 Marburg, Germany.
[Meyer, Bernhard] Tech Univ Munich, Dept Neurosurg, Munich, Germany.
C3 Philipps University Marburg; Philipps University Marburg; Technical
University of Munich
RP Dodel, R (corresponding author), Univ Marburg, Dept Neurol, Rudolf Bultmannstr 8, DE-35039 Marburg, Germany.
EM dodel@med.uni-marburg.de
RI Meyer, Bernhard/Q-9413-2016
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NR 69
TC 101
Z9 110
U1 0
U2 13
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0030-2414
J9 ONCOLOGY-BASEL
JI Oncology
PY 2008
VL 75
IS 3-4
BP 127
EP 133
DI 10.1159/000155223
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 362ZL
UT WOS:000260235600001
PM 18791328
DA 2025-01-07
ER
PT J
AU Geng, N
Xin, YN
Xia, HHX
Jiang, M
Wang, J
Liu, Y
Chen, LZ
Xuan, SY
AF Geng, Ning
Xin, Yong-Ning
Xia, Harry Hua-Xiang
Jiang, Man
Wang, Jian
Liu, Yang
Chen, Li-Zhen
Xuan, Shi-Ying
TI Association of PNPLA3 I148M Variant With Chronic Viral Hepatitis,
Autoimmune Liver Diseases and Outcomes of Liver Transplantation
SO HEPATITIS MONTHLY
LA English
DT Review
DE PNPLA3; Polymorphism; Hepatitis B; Chronic; Hepatitis C; Chronic;
Autoimmune Hepatitis; Liver Transplantation
ID HEPATOCELLULAR-CARCINOMA; C-VIRUS; FIBROSIS PROGRESSION;
INSULIN-RESISTANCE; METABOLIC SYNDROME; GENETIC-VARIANTS; RISK-FACTOR;
STEATOSIS; GENOTYPE; HCV
AB Context: The PNPLA3 I148M variant has been recognized as a genetic determinant of liver fat content and a genetic risk factor of liver damage progression associated with steatohepatitis. The I148M variant is associated with many chronic liver diseases. However, its potential association with inflammatory and autoimmune liver diseases has not been established.
Evidence Acquisition: We systemically reviewed the potential associations of I148M variant with chronic viral hepatitis, autoimmune liver diseases and the outcome of liver transplantation, explored the underlying molecular mechanisms and tried to translate them into more individualized decision-making and personalized medicine.
Results: There were associations between I148M variant and chronic viral hepatitis and autoimmune liver diseases and differential associations of I148M variant in donors and recipients with post-liver transplant outcomes. I148M variant may activate the development of steatosis caused by host metabolic disorders in chronic viral hepatitis, but few researches were found to illustrate the mechanisms in autoimmune liver diseases. The peripherally mediated mechanism (via extrahepatic adipose tissue) may play a principal role in triglyceride accumulation regardless of adiponutrin activity in the graft liver.
Conclusions: Evidences have shown the associations between I148M variant and mentioned diseases. I148M variant induced steatosis may be involved in the mechanism of chronic viral hepatitis and genetic considered personalized therapies, especially for PSC male patients. It is also crucial to pay attention to this parameter in donor selection and prognosis estimation in liver transplantation.
C1 [Geng, Ning; Wang, Jian; Liu, Yang; Chen, Li-Zhen] Qingdao Univ, Qingdao Municipal Hosp, Coll Med, Qingdao 266071, Peoples R China.
[Xin, Yong-Ning; Jiang, Man; Xuan, Shi-Ying] Qingdao Municipal Hosp, Dept Gastroenterol, Qingdao, Peoples R China.
[Xia, Harry Hua-Xiang] Qingdao Univ, Qingdao Municipal Hosp, Qingdao 266071, Peoples R China.
C3 Qingdao Municipal Hospital; Qingdao University; Qingdao Municipal
Hospital; Qingdao Municipal Hospital; Qingdao University
RP Xin, YN (corresponding author), Qingdao Municipal Hosp, Dept Gastroenterol, POB 266021, Qingdao, Peoples R China.
EM xinyongning@gmail.com; dxyxyn@gmail.com
RI Chen, Liú/KWU-4813-2024; dong, quanjiang/AAD-3581-2019
FU National Natural Science Foundation of China (NSFC) [81170337]
FX This review was supported by the National Natural Science Foundation of
China (NSFC, No. 81170337 (http://www.nsfc.gov.cn/).
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NR 64
TC 4
Z9 5
U1 1
U2 9
PU KOWSAR PUBL
PI HOENSBROEK
PA PATERSWEG 22,, HOENSBROEK, LIMBURG 6431 GC, NETHERLANDS
SN 1735-143X
EI 1735-3408
J9 HEPAT MON
JI Hepat. Mon.
PD APR
PY 2015
VL 15
IS 4
AR e26459
DI 10.5812/hepatmon.15(4)2015.26459
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CI0FG
UT WOS:000354411400005
PM 26034504
OA Green Published, Green Accepted, hybrid
DA 2025-01-07
ER
PT J
AU Ferro, A
Saccu, G
Mattivi, S
Gaido, A
Sanchez, MBH
Haque, S
Silengo, L
Altruda, F
Durazzo, M
Fagoonee, S
AF Ferro, Arianna
Saccu, Gabriele
Mattivi, Simone
Gaido, Andrea
Sanchez, Maria Beatriz Herrera
Haque, Shafiul
Silengo, Lorenzo
Altruda, Fiorella
Durazzo, Marilena
Fagoonee, Sharmila
TI Extracellular Vesicles as Delivery Vehicles for Non-Coding RNAs:
Potential Biomarkers for Chronic Liver Diseases
SO BIOMOLECULES
LA English
DT Review
DE chronic liver diseases; non-coding RNAs; diagnosis; extracellular
vesicles; biomarkers
ID HEPATIC STELLATE CELLS; TISSUE GROWTH-FACTOR; CIRCULATING MICRORNAS;
AUTOIMMUNE HEPATITIS; LIQUID BIOPSY; EXOSOMES; FIBROSIS; HEPATOCYTES;
INJURY; SERUM
AB In recent years, EVs have emerged as promising vehicles for coding and non-coding RNAs (ncRNAs), which have demonstrated remarkable potential as biomarkers for various diseases, including chronic liver diseases (CLDs). EVs are small, membrane-bound particles released by cells, carrying an arsenal of ncRNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and other ncRNA species, such as piRNAs, circRNAs, and tsRNAs. These ncRNAs act as key regulators of gene expression, splicing, and translation, providing a comprehensive molecular snapshot of the cells of origin. The non-invasive nature of EV sampling, typically via blood or serum collection, makes them highly attractive candidates for clinical biomarker applications. Moreover, EV-encapsulated ncRNAs offer unique advantages over traditional cell-free ncRNAs due to their enhanced stability within the EVs, hence allowing for their detection in circulation for extended periods and enabling more sensitive and reliable biomarker measurements. Numerous studies have investigated the potential of EV-enclosed ncRNAs as biomarkers for CLD. MiRNAs, in particular, have gained significant attention due to their ability to rapidly respond to changes in cellular stress and inflammation, hallmarks of CLD pathogenesis. Elevated levels of specific miRNAs have been consistently associated with various CLD subtypes, including metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated steatohepatitis (MASH), and chronic hepatitis B and C. LncRNAs have also emerged as promising biomarkers for CLD. These transcripts are involved in a wide range of cellular processes, including liver regeneration, fibrosis, and cancer progression. Studies have shown that lncRNA expression profiles can distinguish between different CLD subtypes, providing valuable insights into disease progression and therapeutic response. Promising EV-enclosed ncRNA biomarkers for CLD included miR-122 (elevated levels of miR-122 are associated with MASLD progression and liver fibrosis), miR-21 (increased expression of miR-21 is linked to liver inflammation and fibrosis in CLD patients), miR-192 (elevated levels of miR-192 are associated with more advanced stages of CLD, including cirrhosis and HCC), LncRNA HOTAIR (increased HOTAIR expression is associated with MASLD progression and MASH development), and LncRNA H19 (dysregulation of H19 expression is linked to liver fibrosis and HCC progression). In the present review, we focus on the EV-enclosed ncRNAs as promising tools for the diagnosis and monitoring of CLD of various etiologies.
C1 [Ferro, Arianna; Saccu, Gabriele; Mattivi, Simone; Gaido, Andrea; Durazzo, Marilena] Univ Turin, Dept Med Sci, I-10126 Turin, Italy.
[Sanchez, Maria Beatriz Herrera] Univ Torino, Soc Gest incubatore Imprese & Trasferimento Tecnol, 2i3T, I-10126 Turin, Italy.
[Sanchez, Maria Beatriz Herrera; Silengo, Lorenzo; Altruda, Fiorella] Mol Biotechnol Ctr MBC Guido Tarone, I-10126 Turin, Italy.
[Haque, Shafiul] Jazan Univ, Coll Nursing & Hlth Sci, Res & Sci Studies Unit, Jazan 45142, Saudi Arabia.
[Haque, Shafiul] Ajman Univ, Ctr Med & Bioallied Hlth Sci Res, Ajman 13306, U Arab Emirates.
[Haque, Shafiul] Lebanese Amer Univ, Gilbert & Rose Marie Chagoury Sch Med, Beirut 11022801, Lebanon.
[Fagoonee, Sharmila] Natl Res Council CNR, Mol Biotechnol Ctr Guido Tarone, Inst Biostruct & Bioimaging, I-10126 Turin, Italy.
C3 University of Turin; University of Turin; Jazan University; Ajman
University; Lebanese American University; Consiglio Nazionale delle
Ricerche (CNR); Istituto di Biostrutture e Bioimmagini (IBB-CNR)
RP Fagoonee, S (corresponding author), Natl Res Council CNR, Mol Biotechnol Ctr Guido Tarone, Inst Biostruct & Bioimaging, I-10126 Turin, Italy.
EM arianna.ferro@unito.it; gabriele.saccu@unito.it;
simone.mattivi@unito.it; andrea.gaido@unito.it; maria.herrera@2i3t.it;
shafiul.haque@hotmail.com; lorenzo.silengo@unito.it;
fiorella.altruda@unito.it; marilena.durazzo@unito.it;
sharmila.fagoonee@unito.it
RI herrera sanchez, Maria beatriz/KBQ-4678-2024; Fagoonee,
Sharmila/L-1940-2019; Haque, Shafiul/AAN-2946-2020
OI Herrera Sanchez, Maria Beatriz/0000-0002-5272-6773; Haque,
Shafiul/0000-0002-2989-121X; FAGOONEE, SHARMILA/0000-0001-6070-6716;
Saccu, Gabriele/0000-0002-3637-7227; Altruda,
Fiorella/0000-0002-6238-1860
FU Deputyship for Research & Innovation, Ministry of Education in Saudi
Arabia [2022]
FX We apologize to all the investigators whose important works have not
been cited due to space restrictions. We thank Emanuela Tolosano for
assistance with the Biorender images. A few sentences were improved
using ChatGPT, a language model developed by OpenAI, for text generation
and linguistic analysis in this study. ChatGPT is a state-of-the-art
natural language processing model based on the GPT-3.5 architecture
(OpenAI, 2022).
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NR 168
TC 8
Z9 8
U1 3
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD MAR
PY 2024
VL 14
IS 3
AR 277
DI 10.3390/biom14030277
PG 25
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA MD9N1
UT WOS:001191806300001
PM 38540698
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhou, QH
Shi, Y
Chen, C
Wu, FT
Chen, Z
AF Zhou, Qihui
Shi, Yu
Chen, Chao
Wu, Fengtian
Chen, Zhi
TI A narrative review of the roles of indoleamine 2,3-dioxygenase and
tryptophan-2,3-dioxygenase in liver diseases
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Indoleamine 2; 3-dioxygenase (IDO); viral hepatitis; autoimmune liver
diseases; liver fibrosis and cirrhosis; liver tumors
ID REGULATORY T-CELLS; DENDRITIC CELLS; IDO EXPRESSION; UP-REGULATION;
TOLERANCE; INHIBITION; KYNURENINE; INDUCTION;
INDOLEAMINE-2,3-DIOXYGENASE; ACTIVATION
AB Indoleamine 2,3-dioxygenase (IDO) and tryptophan-2,3-dioxygenase (TDO) are induced by several immune factors, such as interferon-gamma, and act as intracellular enzymes that catabolize essential amino acid tryptophan into kynurenine and other downstream metabolites, including kynurenic acid (KYNA), xanthurenic acid (XA) and so on. IDO and TDO work as a double-edge sword. On one hand, they exert the immunomodulatory effects, especially immunosuppressive effects on the microenvironment including infections, pregnancy, tumor cells escape and transplantation. TDO plays the major role under basal conditions, while IDO comes into play under different circumstances of immune activation, thus IDO has a wider spectrum of immune regulation. On the other hand, these enzymes also inhibit pathogens such as Chlamydia pneumoniae, Staphylococcus aureus, Toxoplasma gondii and so on. Moreover, IDO regulates metabolic health through shaping intestinal microbiota. Recently, these enzymes have attracted more and more attention in liver diseases. Several studies have indicated that IDO and TDO can modulate viral hepatitis, autoimmune liver diseases, non-alcoholic fatty liver disease (NAFLD), liver cirrhosis, liver cancer even liver transplantation. Targeting them or their antagonists may provide novel therapeutic treatments for liver diseases. In this review, we will discuss the exact roles that IDO and TDO play in diverse hepatic diseases.
C1 [Zhou, Qihui; Shi, Yu; Chen, Chao; Wu, Fengtian; Chen, Zhi] Zhejiang Univ, Dept Infect Dis,Coll Med,Affiliated Hosp 1, State Key Lab Diag & Treatment Infect Dis, Natl Clin Res Ctr Infect Dis,Collaborat Innovat C, Hangzhou 310000, Peoples R China.
C3 Zhejiang University
RP Chen, Z (corresponding author), Zhejiang Univ, Dept Infect Dis,Coll Med,Affiliated Hosp 1, State Key Lab Diag & Treatment Infect Dis, Natl Clin Res Ctr Infect Dis,Collaborat Innovat C, Hangzhou 310000, Peoples R China.
EM zjuchenzhi@zju.edu.cn
RI REN, CHAO/KRO-9616-2024
FU National Science and Technology Major Project of China [2018ZX10302206,
2017ZX10202203]
FX This work was supported by the National Science and Technology Major
Project of China [grant number 2018ZX10302206, 2017ZX10202203].
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NR 57
TC 19
Z9 20
U1 3
U2 22
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD JAN
PY 2021
VL 9
IS 2
AR 174
DI 10.21037/atm-20-3594
PG 9
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA QG9ES
UT WOS:000617883200017
PM 33569476
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Jensen, ASH
Ytting, H
Werge, MP
Rashu, EB
Hetland, LE
Thing, M
Nabilou, P
Burisch, J
Bojsen-Moller, KN
Junker, AE
Hobolth, L
Mortensen, C
Tofteng, F
Bendtsen, F
Moller, S
Vyberg, M
Serizawa, RR
Gluud, LL
Albrechtsen, NJW
AF Jensen, Anne-Sofie H.
Ytting, Henriette
Werge, Mikkel P.
Rashu, Elias B.
Hetland, Liv E.
Thing, Mira
Nabilou, Puria
Burisch, Johan
Bojsen-Moller, Kirstine N.
Junker, Anders E.
Hobolth, Lise
Mortensen, Christian
Tofteng, Flemming
Bendtsen, Flemming
Moller, Soren
Vyberg, Mogens
Serizawa, Reza R.
Gluud, Lise L.
Albrechtsen, Nicolai J. Wewer
TI Patients with autoimmune liver disease have glucose disturbances that
mechanistically differ from steatotic liver disease
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Article
DE autoimmune hepatitis; diabetes; incretin; primary biliary cholangitis;
primary sclerosing cholangitis
ID CLINICAL-PRACTICE GUIDELINES; HEPATIC INSULIN-CLEARANCE; GLUCAGON-LIKE
PEPTIDE-1; INTRAHEPATIC CHOLESTASIS; HEPATOCELLULAR-CARCINOMA;
EUROPEAN-ASSOCIATION; RISK-FACTORS; VALIDATION; METABOLISM; RESISTANCE
AB Autoimmune liver diseases are associated with an increased risk of diabetes, yet the underlying mechanisms remain unknown. In this cross-sectional study, we investigated the glucose-regulatory disturbances in patients with autoimmune hepatitis (AIH, n = 19), primary biliary cholangitis (PBC, n = 15), and primary sclerosing cholangitis (PSC, n = 6). Healthy individuals (n = 24) and patients with metabolic dysfunction-associated steatotic liver disease (MASLD, n = 18) were included as controls. Blood samples were collected during a 120-min oral glucose tolerance test. We measured the concentrations of glucose, C-peptide, insulin, glucagon, and the two incretin hormones, glucose insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1). We calculated the homeostasis model assessment of insulin resistance (HOMA-IR), whole body insulin resistance (Matsuda index), insulin clearance, and insulinogenic index. All patient groups had increased fasting plasma glucose and impaired glucose responses compared with healthy controls. Beta-cell secretion was increased in AIH, PBC, and MASLD but not in PSC. Patients with AIH and MASLD had hyperglucagonemia and hepatic, as well as peripheral, insulin resistance and decreased insulin clearance, resulting in hyperinsulinemia. Patients with autoimmune liver disease had an increased GIP response, and those with AIH or PBC had an increased GLP-1 response. Our data demonstrate that the mechanism underlying glucose disturbances in patients with autoimmune liver disease differs from that underlying MASLD, including compensatory incretin responses in patients with autoimmune liver disease. Our results suggest that glucose disturbances are present at an early stage of the disease. NEW & NOTEWORTHY Patients with autoimmune liver disease but without overt diabetes display glucose disturbances early on in their disease course. We identified pathophysiological traits specific to these patients including altered incretin responses.
C1 [Jensen, Anne-Sofie H.; Ytting, Henriette; Werge, Mikkel P.; Rashu, Elias B.; Hetland, Liv E.; Thing, Mira; Nabilou, Puria; Burisch, Johan; Junker, Anders E.; Hobolth, Lise; Mortensen, Christian; Tofteng, Flemming; Bendtsen, Flemming; Gluud, Lise L.] Copenhagen Univ Hosp, Amager & Hvidovre Hosp, Gastro Unit, Hvidovre, Denmark.
[Jensen, Anne-Sofie H.; Albrechtsen, Nicolai J. Wewer] Copenhagen Univ Hosp, Bispebjerg & Frederiksberg Hosp, Dept Clin Biochem, Copenhagen, Denmark.
[Jensen, Anne-Sofie H.; Albrechtsen, Nicolai J. Wewer] Univ Copenhagen, Novo Nord Fdn Ctr Prot Res, Fac Hlth & Med Sci, Copenhagen, Denmark.
[Ytting, Henriette; Burisch, Johan; Bojsen-Moller, Kirstine N.; Bendtsen, Flemming; Moller, Soren; Gluud, Lise L.] Univ Copenhagen, Fac Hlth & Med Sci, Dept Clin Med, Copenhagen, Denmark.
[Bojsen-Moller, Kirstine N.] Copenhagen Univ Hosp, Amager & Hvidovre Hosp, Dept Endocrinol, Hvidovre, Denmark.
[Moller, Soren] Copenhagen Univ Hosp, Amager & Hvidovre Hosp, Ctr Funct & Diagnost Imaging & Res, Dept Clin Physiol & Nucl Med, Hvidovre, Denmark.
[Vyberg, Mogens; Serizawa, Reza R.] Copenhagen Univ Hosp, Amager & Hvidovre Hosp, Dept Pathol, Hvidovre, Denmark.
[Vyberg, Mogens] Aalborg Univ, Ctr RNA Med, Dept Clin Med, Copenhagen, Denmark.
C3 University of Copenhagen; University of Copenhagen; Bispebjerg Hospital;
University of Copenhagen; University of Copenhagen; University of
Copenhagen; University of Copenhagen; University of Copenhagen; Aalborg
University
RP Albrechtsen, NJW (corresponding author), Copenhagen Univ Hosp, Bispebjerg & Frederiksberg Hosp, Dept Clin Biochem, Copenhagen, Denmark.; Albrechtsen, NJW (corresponding author), Univ Copenhagen, Novo Nord Fdn Ctr Prot Res, Fac Hlth & Med Sci, Copenhagen, Denmark.
EM nicolai.albrechtsen@regionh.dk
RI Werge, Mikkel/P-2055-2019; Møller, Søren/JVO-5643-2024; Ytting,
Henriette/ABA-9518-2021; Nabilou, Puria/IVV-1613-2023
OI Burisch, Johan/0000-0002-3312-5139; Rashu, Elias
Badal/0000-0002-9958-9024; Thing, Mira/0009-0009-8924-9534; Hetland,
Liv/0000-0001-8753-4096; Bojsen-Moller, Kirstine
Nyvold/0000-0003-1962-5302; Nabilou, Puria/0000-0002-4764-4423; Jensen,
Anne-Sofie Houlberg/0000-0002-5982-8684; Ytting,
Henriette/0000-0001-5018-5232; Werge, Mikkel/0000-0002-9980-1072
FU Novo Nordisk Foundation [NNF19OC0055001, NNF14CC0001]; European
Foundation for the Study of Diabetes Future Leader [NNF21SA0072746];
Independent Research Fund Denmark; Sapere Aude [1052-00003B]; Project
Grant in Clinical and Translational Medicine [NNF23OC0084970]
FX A.-S.H.J. and N.J.W.A. were supported by Novo Nordisk Foundation
Excellence Emerging Investigator Grant-Endocrinology and Metabolism
under Application No. NNF19OC0055001, European Foundation for the Study
of Diabetes Future Leader Award NNF21SA0072746, Independent Research
Fund Denmark, Sapere Aude 1052-00003B, and Project Grant in Clinical and
Translational Medicine NNF23OC0084970. Novo Nordisk Foundation Center
for Protein Research is supported financially by the Novo Nordisk
Foundation under Grant Agreement NNF14CC0001. The funding did not
pertain to this study.
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PU AMER PHYSIOLOGICAL SOC
PI Rockville
PA 6120 Executive Blvd, Suite 600, Rockville, MD, UNITED STATES
SN 0193-1857
EI 1522-1547
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD JUN 16
PY 2024
VL 326
IS 6
BP G736
EP G746
DI 10.1152/ajpgi.00047.2024
PG 11
WC Gastroenterology & Hepatology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Physiology
GA TK4U4
UT WOS:001241151400002
PM 38625142
DA 2025-01-07
ER
PT J
AU Van Roosbroeck, K
Pollet, J
Calin, GA
AF Van Roosbroeck, Katrien
Pollet, Jeroen
Calin, George A.
TI miRNAs and long noncoding RNAs as biomarkers in human diseases
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE autoimmune diseases; biomarkers; cancer; cardiovascular diseases;
infectious diseases; miRNAs; molecular diagnostics; neurological
diseases; noncoding RNAs
ID BINDING-SITE POLYMORPHISMS; PROFILING MICRORNA EXPRESSION; GENOME-WIDE
ANALYSIS; CELL LUNG-CANCER; PROSTATE-CANCER; CIRCULATING MICRORNAS;
BREAST-CANCER; DRUG-RESISTANCE; UP-REGULATION; HEPATOCELLULAR-CARCINOMA
AB Noncoding RNAs (ncRNAs) are transcripts that have no apparent protein-coding capacity; however, many ncRNAs have been found to play a major biological role in human physiology. Their deregulation is implicated in many human diseases, but their exact roles are only beginning to be elucidated. Nevertheless, ncRNAs are extensively studied as a novel source of biomarkers, and the fact that they can be detected in body fluids makes them extremely suitable for this purpose. The authors mainly focus on ncRNAs as biomarkers in cancer, but also touch on other human diseases such as cardiovascular diseases, autoimmune diseases, neurological disorders and infectious diseases. The authors discuss the established methods and provide a selection of emerging new techniques that can be used to detect and quantify ncRNAs. Finally, the authors discuss ncRNAs as a new strategy for therapeutic interventions.
C1 [Van Roosbroeck, Katrien; Calin, George A.] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Unit 1950, Houston, TX 77054 USA.
[Pollet, Jeroen] Univ Houston, Dept Chem & Biomol Engn, Houston, TX 77204 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
Houston System; University of Houston
RP Calin, GA (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Unit 1950, 1881 East Rd, Houston, TX 77054 USA.
EM gcalin@mdanderson.org
RI Calin, George/E-9390-2011
OI Pollet, Jeroen/0000-0003-1420-4015; Calin, George/0000-0001-6704-5615;
Calin, George/0000-0002-7427-0578
FU Henri Benedictus Fund/Belgian American Education Foundation; Fulbright
Association; Belgian American Education Foundation; University of Texas
MD Anderson Research Trust; University of Texas System Regents Research
Scholar; CLL Global Research Foundation; NIH/NCI [CA135444]; Department
of Defense Breast Cancer Idea Award; Developmental Research Awards in
Breast Cancer, Ovarian Cancer, Brain Cancer, Prostate Cancer, Multiple
Myeloma, Leukemia [P50 CA100632]; Developmental Research Awards in Head
and Neck [P50 CA097007]; SPOREs, a SINF MDACC_DKFZ grant in CLL; Laura
and John Arnold Foundation; RGK Foundation; Estate of CG Johnson Jr.
FX K Van Roosbroeck is supported by a fellowship of the Henri Benedictus
Fund/Belgian American Education Foundation. J Pollet is supported by
fellowships of the Fulbright Association and the Belgian American
Education Foundation. GA Calin is an Alan M Gewirtz Leukemia & Lymphoma
Society Scholar. He is also supported as a Fellow at The University of
Texas MD Anderson Research Trust, as a University of Texas System
Regents Research Scholar, and by the CLL Global Research Foundation.
Work in GA Calin's laboratory is supported in part by the NIH/NCI
(CA135444), a Department of Defense Breast Cancer Idea Award,
Developmental Research Awards in Breast Cancer, Ovarian Cancer, Brain
Cancer, Prostate Cancer, Multiple Myeloma, Leukemia (P50 CA100632) and
Head and Neck (P50 CA097007) SPOREs, a SINF MDACC_DKFZ grant in CLL, the
Laura and John Arnold Foundation, the RGK Foundation and the Estate of
CG Johnson Jr. The authors have no other relevant affiliations or
financial involvement with any organization or entity with a financial
interest in or financial conflict with the subject matter or materials
discussed in the manuscript apart from those disclosed.
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NR 305
TC 113
Z9 121
U1 0
U2 58
PU TAYLOR & FRANCIS AS
PI OSLO
PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY
SN 1473-7159
EI 1744-8352
J9 EXPERT REV MOL DIAGN
JI Expert Rev. Mol. Diagn.
PD MAR
PY 2013
VL 13
IS 2
BP 183
EP 204
DI 10.1586/ERM.12.134
PG 22
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 105EW
UT WOS:000316049700012
PM 23477558
DA 2025-01-07
ER
PT J
AU Kozlowska, D
Mysliwiec, H
Flisiak, I
AF Kozlowska, Dorota
Mysliwiec, Hanna
Flisiak, Iwona
TI Inflammation and lipid metabolism as a strong background connecting
psoriasis and liver diseases
SO PRZEGLAD DERMATOLOGICZNY
LA English
DT Review
DE metabolic syndrome; psoriasis; inflammation; lipids; non-alcoholic;
fatty liver disease
ID FATTY LIVER; BILIARY-CIRRHOSIS; HEPATITIS; RISK; CERAMIDES; ARTHRITIS;
PROFILE; NAFLD; IL-6
AB Psoriasis is not an isolated pathology of the skin and joints, but is also characterized by multiple extracutaneous systemic manifestations. Beside the co-occurrence of obesity, arterial hypertension, dyslipidemia, and type 2 diabetes mellitus, there is a strong correlation with many liver disturbances. The most common liver comorbid disease coexisting with psoriasis is non-alcoholic fatty liver disease, which is a hepatic manifestation of metabolic syndrome. Both diseases share the same molecular mechanisms: chronic systemic inflammation, oxidative stress, disturbances of lipid metabolism, immune pathways and secretions of bioactive molecules. Additionally, patients with psoriasis have an increased risk of developing autoimmune liver disease and also liver cancer in comparison to the heathy population. Moreover, drugs used in treatment of psoriasis and psoriatic arthritis augment the hepatotoxic effect on the liver. The study below presents the most recent data on the liver diseases and their pathogenesis in patients with psoriasis.
C1 [Kozlowska, Dorota; Mysliwiec, Hanna; Flisiak, Iwona] Med Univ Bialystok, Dept Dermatol & Venereol, Bialystok, Poland.
C3 Medical University of Bialystok
RP Kozlowska, D (corresponding author), Uniwersytet Med Bialymstoku, Klin Dermatol & Wenerol, Ul Zurawia 14, PL-15540 Bialystok, Poland.
EM dorota.kozlowska@umb.edu.pl
RI Kozłowska, Dorota/T-4060-2018; Myśliwiec, Hanna/S-6326-2018; Flisiak,
Iwona/R-5874-2018
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NR 77
TC 1
Z9 1
U1 0
U2 4
PU TERMEDIA PUBLISHING HOUSE LTD
PI POZNAN
PA KLEEBERGA ST 2, POZNAN, 61-615, POLAND
SN 0033-2526
EI 2084-9893
J9 PRZ DERMATOL
JI Prz. Dermatol.
PY 2020
VL 107
IS 3
BP 257
EP 272
DI 10.5114/dr.2020.97819
PG 16
WC Dermatology
WE Emerging Sources Citation Index (ESCI)
SC Dermatology
GA NJ2GT
UT WOS:000565864500006
OA gold
DA 2025-01-07
ER
PT J
AU Manoukian, G
Hagemeister, F
AF Manoukian, George
Hagemeister, Fred
TI Denileukin diftitox: a novel immunotoxin
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Article
DE chemotherapy; denileukin diftitox; IL-2; immunotherapy; lymphoma; Ontak
ID T-CELL LYMPHOMA; CHRONIC LYMPHOCYTIC-LEUKEMIA; NON-HODGKINS-LYMPHOMA;
PHASE-II TRIAL; FUSION-PROTEIN; IL-2 RECEPTOR; INTERLEUKIN-2;
DAB(389)IL-2; DEPLETION; MELANOMA
AB Objective: To review FDA approved and other potential uses of Ontak, denileukin diftitox. Methods: information was obtained via the internet and a journal literature review. Results: In 1999, the FDA approved the use of denileukin diftitox for patients with persistent or relapsed CD25-positive cutaneous T-cell lymphoma (CTCL), but Ontak has been reported to be an effective therapy for other neoplastic and non-neoplastic conditions. Oncological uses include therapy for CD25-negative T-cell lymphoma, recurrent and refractory chronic lymphocytic leukemia (CLL), non-Hodgkin's B-cell lymphoma (NHL), and human T-cell lymphotropic virus-1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATL). Potential additional uses of Ontak include: therapy of graft-versus-host disease (GvHD) and autoimmune conditions, including psoriasis, rheumatoid arthritis (RA), systemic lupus, scleroderma and vasculitis. Denileukin diftitox's effect has also been studied for patients with hepatocellular carcinoma (HCC) and HIV, but conclusive data are still pending. Conclusion: There are many potential uses for denileukin diftitox, in both malignant and benign disorders. More human trials are needed to demonstrate further efficacy for a wide range of diseases.
C1 [Hagemeister, Fred] MD Anderson Canc Ctr Lymphoma Myeloma, Houston, TX 77030 USA.
[Manoukian, George; Hagemeister, Fred] Univ Texas Houston Internal Med, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Hagemeister, F (corresponding author), MD Anderson Canc Ctr Lymphoma Myeloma, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM fhagemei@mdanderson.org
CR [Anonymous], 2008, Cancer Facts Figures 2008
[Anonymous], CUTANEOUS T CELL LYM
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WAINSCOAT B, HUMAN T CELL LYMPHOT
Wong BY, 2008, AM J HEMATOL, V83, P596, DOI 10.1002/ajh.21177
NR 37
TC 74
Z9 81
U1 0
U2 7
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1471-2598
EI 1744-7682
J9 EXPERT OPIN BIOL TH
JI Expert Opin. Biol. Ther.
PD NOV
PY 2009
VL 9
IS 11
BP 1445
EP 1451
DI 10.1517/14712590903348135
PG 7
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA 515FX
UT WOS:000271454300009
PM 19817678
DA 2025-01-07
ER
PT J
AU Kocheise, L
Piseddu, I
Vonderlin, J
Tjwa, ET
Buescher, G
Meunier, L
Goeggelmann, P
Fianchi, F
Dumortier, J
Barciela, MR
Gevers, TJG
Beretta-Piccoli, BT
Londoño, MC
Frankova, S
Roesner, T
Joerg, V
Schmidt, C
Glaser, F
Sutter, JP
Fründt, TW
Lohse, AW
Huber, S
von Felden, J
Sebode, M
Schulze, K
AF Kocheise, Lorenz
Piseddu, Ignazio
Vonderlin, Joscha
Tjwa, Eric T.
Buescher, Gustav
Meunier, Lucy
Goeggelmann, Pia
Fianchi, Francesca
Dumortier, Jerome
Riveiro Barciela, Mar
Gevers, Tom J. G.
Terziroli Beretta-Piccoli, Benedetta
Londono, Maria-Carlota
Frankova, Sona
Roesner, Thomas
Joerg, Vincent
Schmidt, Constantin
Glaser, Fabian
Sutter, Jan P.
Fruendt, Thorben W.
Lohse, Ansgar W.
Huber, Samuel
von Felden, Johann
Sebode, Marcial
Schulze, Kornelius
TI PD-1/PD-L1 immune checkpoint therapy demonstrates favorable safety
profile in patients with autoimmune and cholestatic liver disease
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE autoimmune disease (AID); immune checkpoint inhibitors (ICI); autoimmune
liver diseases (AILD); immune related adverse effects (irAEs);
PD-1/PD-L1 immune checkpoint inhibitors; autoimmune hepatitis (AIH);
primary sclerosing cholangites (PSC); primary biliary cholangitis (PBC)
ID CHOLANGITIS; RISK
AB IntroductionImmune checkpoint inhibitors (ICI) have revolutionized the treatment of many malignancies in recent years. However, immune-related adverse events (irAE) are a frequent concern in clinical practice. The safety profile of ICI for the treatment of malignancies in patients diagnosed with autoimmune and cholestatic liver disease (AILD) remains unclear. Due to this uncertainty, these patients were excluded from ICI clinical trials and ICI are withheld from this patient group. In this retrospective multicenter study, we assessed the safety of ICI in patients with AILD.MethodsWe contacted tertiary referral hospitals for the identification of AILD patients under ICI treatment in Europe via the European Reference Network on Hepatological Diseases (ERN RARE-LIVER). Fourteen centers contributed data on AILD patients with malignancies being treated with ICI, another three centers did not treat these patients with ICI due to fear of irAEs.ResultsIn this study, 22 AILD patients under ICI treatment could be identified. Among these patients, 12 had primary biliary cholangitis (PBC), five had primary sclerosing cholangitis (PSC), four had autoimmune hepatitis (AIH), and one patient had an AIH-PSC variant syndrome. Eleven patients had hepatobiliary cancers and the other 11 patients presented with non-hepatic tumors. The applied ICIs were atezolizumab (n=7), durvalumab (n=5), pembrolizumab (n=4), nivolumab (n=4), spartalizumab (n=1), and in one case combined immunotherapy with nivolumab plus ipilimumab. Among eight patients who presented with grade 1 or 2 irAEs, three demonstrated liver irAEs. Cases with grades >= 3 irAEs were not reported. No significant changes in liver tests were observed during the first year after the start of ICI.DiscussionThis European multicenter study demonstrates that PD-1/PD-L1 inhibitors appear to be safe in patients with AILD. Further studies on the safety of more potent dual immune checkpoint therapy are needed. We conclude that immunotherapy should not categorically be withheld from patients with AILD.
C1 [Kocheise, Lorenz; Buescher, Gustav; Joerg, Vincent; Schmidt, Constantin; Glaser, Fabian; Sutter, Jan P.; Fruendt, Thorben W.; Lohse, Ansgar W.; Huber, Samuel; von Felden, Johann; Sebode, Marcial; Schulze, Kornelius] Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Hamburg, Germany.
[Kocheise, Lorenz; Piseddu, Ignazio; Vonderlin, Joscha; Tjwa, Eric T.; Buescher, Gustav; Meunier, Lucy; Fianchi, Francesca; Dumortier, Jerome; Riveiro Barciela, Mar; Gevers, Tom J. G.; Terziroli Beretta-Piccoli, Benedetta; Londono, Maria-Carlota; Frankova, Sona; Joerg, Vincent; Schmidt, Constantin; Glaser, Fabian; Sutter, Jan P.; Fruendt, Thorben W.; Lohse, Ansgar W.; Huber, Samuel; von Felden, Johann; Sebode, Marcial; Schulze, Kornelius] European Reference Network Hepatol Dis ERN RARE LI, Hamburg, Germany.
[Piseddu, Ignazio] Ludwig Maximilians Univ LMU Munchen, Univ Hosp, Dept Med 2, Munich, Germany.
[Vonderlin, Joscha] Charite Univ Med Berlin, Dept Hepatol & Gastroenterol, Berlin, Germany.
[Tjwa, Eric T.] Radboud Univ Nijmegen, Radboud Inst Mol Life Sci, Med Ctr, Dept Gastroenterol & Hepatol, Nijmegen, Netherlands.
[Meunier, Lucy] CHU Montpellier, Hop St Eloi, Serv Hepatogastro Enterol, Montpellier, France.
[Goeggelmann, Pia] Univ Hosp Regensburg, Dept Internal Med 1, Regensburg, Germany.
[Fianchi, Francesca] Univ Cattolica Sacro Cuore, Fdn Policlin Univ Gemelli IRCCS, CEMAD Ctr Malattie Apparat Digerente, Rome, Italy.
[Dumortier, Jerome] Univ Lyon, Hop Edouard Herriot, Hosp Civils Lyon, Serv Hepatogastroenterol, Lyon, France.
[Riveiro Barciela, Mar] Univ Autonoma Barcelona, Hosp Univ Valle dHebron, Dept Internal Med, Liver Unit, Barcelona, Spain.
[Gevers, Tom J. G.] Maastricht Univ, Med Ctr, Dept Gastroenterol & Hepatol, Maastricht, Netherlands.
[Gevers, Tom J. G.] Maastricht Univ, Nutrim Sch Nutr & Translat Res Metab, Maastricht, Netherlands.
[Terziroli Beretta-Piccoli, Benedetta] Epatoctr Ticino, Lugano, Switzerland.
[Terziroli Beretta-Piccoli, Benedetta] Univ Svizzera Italiana, Fac Biomed Sci, Lugano, Switzerland.
[Terziroli Beretta-Piccoli, Benedetta] Kings Coll London, Kings Coll Hosp, Fac Life Sci & Med, MowatLabs, London, England.
[Londono, Maria-Carlota] Univ Barcelona, Hosp Clin Barcelona, Liver Unit, FCRB IDIBAPS, Barcelona, Spain.
[Frankova, Sona] Inst Clin & Expt Med, Dept Hepatogastroenterol, Prague, Czech Republic.
[Roesner, Thomas] Natl Ctr Tumor Dis NCT Heidelberg, Dept Med Oncol, Heidelberg, Germany.
[Roesner, Thomas] Univ Klinikum Heidelberg, Heidelberg, Germany.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Munich; Berlin Institute of Health; Free University of
Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
Berlin; Radboud University Nijmegen; Universite de Montpellier; CHU de
Montpellier; University of Regensburg; Catholic University of the Sacred
Heart; IRCCS Policlinico Gemelli; CHU Lyon; Autonomous University of
Barcelona; Maastricht University; Maastricht University; Maastricht
University Medical Centre (MUMC); Universita della Svizzera Italiana;
University of London; King's College London; King's College Hospital NHS
Foundation Trust; King's College Hospital; University of Barcelona;
Hospital Clinic de Barcelona; IDIBAPS; Institute for Clinical &
Experimental Medicine (IKEM); Helmholtz Association; German Cancer
Research Center (DKFZ); Ruprecht Karls University Heidelberg; Ruprecht
Karls University Heidelberg
RP Kocheise, L (corresponding author), Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Hamburg, Germany.; Kocheise, L (corresponding author), European Reference Network Hepatol Dis ERN RARE LI, Hamburg, Germany.
EM l.kocheise@uke.de
RI Buescher, Gustav/AAN-9362-2021; MEUNIER, Lucy/JMB-9041-2023; Londono,
Maria/KMA-4581-2024; Beretta-Piccoli, Benedetta/U-8460-2019; Dumortier,
Jerome/J-2029-2014
OI Huber, Samuel/0000-0001-9325-8227; Schmidt,
Constantin/0000-0002-3892-4255; von Felden, Johann/0000-0003-2839-5174;
Terziroli Beretta-Piccoli, Benedetta/0000-0001-5004-5029; Londono,
Maria-Carlota/0000-0002-6533-1586
FU Open Access Publication Fund of UKE - Universitatsklinikum
Hamburg-Eppendorf; DFG - German Research Foundation
FX The author(s) declare financial support was received for the research,
authorship, and/or publication of this article. We acknowledge financial
support from the Open Access Publication Fund of UKE -
Universitatsklinikum Hamburg-Eppendorf and DFG - German Research
Foundation.
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Berry P, 2023, LIVER INT, V43, P147, DOI 10.1111/liv.15340
Bhave P, 2018, J HEPATOL, V69, P976, DOI 10.1016/j.jhep.2018.06.012
Boland P, 2020, J IMMUNOTHER CANCER, V8, DOI 10.1136/jitc-2019-000356
Brown LJ, 2021, J IMMUNOTHER CANCER, V9, DOI 10.1136/jitc-2020-002121
Cai Q, 2022, HUM VACC IMMUNOTHER, DOI 10.1080/21645515.2022.2145102
Chanza NM, 2020, J IMMUNOTHER CANCER, V8, DOI 10.1136/jitc-2020-000538
Cohen JV, 2021, MODERN PATHOL, V34, P426, DOI 10.1038/s41379-020-00653-1
Cortellini A, 2019, ONCOLOGIST, V24, pE327, DOI 10.1634/theoncologist.2018-0618
Coukos A, 2022, J IMMUNOTHER CANCER, V10, DOI 10.1136/jitc-2022-005635
De Martin E, 2020, JHEP REP, V2, DOI 10.1016/j.jhepr.2020.100170
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Onoyama T, 2020, WORLD J GASTROENTERO, V26, P353, DOI 10.3748/wjg.v26.i3.353
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NR 33
TC 4
Z9 4
U1 1
U2 12
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 10
PY 2024
VL 14
AR 1326078
DI 10.3389/fimmu.2023.1326078
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA FQ0I5
UT WOS:001147191600001
PM 38268921
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Das, N
Paul, S
Chatterjee, D
Banerjee, N
Majumder, NS
Sarma, N
Sau, TJ
Basu, S
Banerjee, S
Majumder, P
Bandyopadhyay, AK
States, JC
Giri, AK
AF Das, Nandana
Paul, Somnath
Chatterjee, Debmita
Banerjee, Nilanjana
Majumder, Niladri S.
Sarma, Nilendu
Sau, Tanmoy J.
Basu, Santanu
Banerjee, Saptarshi
Majumder, Papiya
Bandyopadhyay, Apurba K.
States, J. Christopher
Giri, Ashok K.
TI Arsenic exposure through drinking water increases the risk of liver and
cardiovascular diseases in the population of West Bengal, India
SO BMC PUBLIC HEALTH
LA English
DT Article
DE Arsenic; Antinuclear antibody; Liver function tests; Cytokines
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; ANTI-DSDNA ANTIBODIES; SKIN-LESIONS;
ALKALINE-PHOSPHATASE; INDIVIDUALS; GROUNDWATER; POLYMORPHISMS;
ABERRATIONS; MECHANISMS; DISTRICTS
AB Background: Arsenic is a natural drinking water contaminant affecting 26 million people in West Bengal, India. Chronic arsenic exposure causes cancer, cardiovascular disease, liver disease, neuropathies and ocular diseases. The aims of the present study were to assess bioindicators of hepatocellular injury as indicated by the levels of liver enzymes, to determine the auto immune status, as indicated by the amounts of anti-nuclear antibodies (ANA) and anti-dsDNA antibodies in their serum, and to predict cardiovascular risk in the arsenic exposed population.
Methods: Effect of chronic arsenic exposure on liver was determined by liver function tests. Autoimmune status was measured by measuring ANA and anti-dsDNA in serum. Inflammatory cytokines associated with increased cardiovascular disease risk, IL6, IL8 and MCP-1 were determined.
Results: Our results indicated that serum levels of bilirubin, alanine transaminase, aspartate transaminase, alkaline phosphatase and ANA were increased in the arsenic exposed population. Serum levels of IL6 and IL8 also increased in the arsenic exposed group.
Conclusions: Chronic arsenic exposure causes liver injury, increases the serum levels of autoimmune markers and imparts increased cardiovascular risk.
C1 [Das, Nandana; Paul, Somnath; Chatterjee, Debmita; Banerjee, Nilanjana; Majumder, Niladri S.; Bandyopadhyay, Apurba K.; Giri, Ashok K.] CSIR Indian Inst Chem Biol, Mol & Human Genet Div, Kolkata 700032, India.
[Sarma, Nilendu] Sir Nil Ratan Sircar Med Coll & Hosp, Kolkata 700014, India.
[Sau, Tanmoy J.] Calcutta Natl Med Coll, Dept Med, Kolkata 700017, W Bengal, India.
[Basu, Santanu] Sri Aurobindo Seva Kendra, Dept Gen Med, Kolkata 700068, W Bengal, India.
[Banerjee, Saptarshi] Calcutta Med Coll, Reg Inst Opthalmol, Kolkata 700073, W Bengal, India.
[Majumder, Papiya] Tata Main Hosp, Jamshedpur 831001, Jharkhand, India.
[States, J. Christopher] Univ Louisville, Dept Pharmacol & Toxicol, Louisville, KY 40209 USA.
C3 Council of Scientific & Industrial Research (CSIR) - India; CSIR -
Indian Institute of Chemical Biology (IICB); University of Louisville
RP Giri, AK (corresponding author), CSIR Indian Inst Chem Biol, Mol & Human Genet Div, 4 Raja SC Mullick Rd, Kolkata 700032, India.
EM akgiri15@yahoo.com
RI States, J./H-4246-2011; PAUL, SOMNATH/C-7372-2013
OI Giri, Ashok/0000-0002-2646-4087; Chatterjee,
Debmita/0000-0003-0218-5654; States, J. Christopher/0000-0003-4717-4422;
PAUL, SOMNATH/0000-0003-4104-9209
FU Council of Scientific and Industrial Research, Government of India
[NWP-0004, NWP-0052]; U.S. Public Health Service [ES011314, ES014443]
FX Authors are grateful to Fogarty International Training Program
(2D43TW000815-11) jointly with University of California, Berkeley, for
providing training to S.P., N.B. N. D., N.S.M. and S.B. for research on
molecular epidemiology and environmental health. This study was funded
by Council of Scientific and Industrial Research, Government of India
(NWP-0004 and NWP-0052); U.S. Public Health Service (ES011314, ES014443)
to J.C.S.
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NR 62
TC 112
Z9 130
U1 1
U2 28
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2458
J9 BMC PUBLIC HEALTH
JI BMC Public Health
PD AUG 10
PY 2012
VL 12
AR 639
DI 10.1186/1471-2458-12-639
PG 9
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Public, Environmental & Occupational Health
GA 004TX
UT WOS:000308705100002
PM 22883023
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Vojdani, A
AF Vojdani, A.
TI ANTIBODIES AS PREDICTORS OF COMPLEX AUTOIMMUNE DISEASES AND CANCER
SO INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY
LA English
DT Article
DE predictive antibodies; neuroimmune disorders; autoimmune diseases;
cancer; environmental triggers; polyreactive antibodies;
ELISAIntroduction
ID BRAIN-BARRIER DISRUPTION; MULTIPLE-SCLEROSIS; B-CELLS; AUTOANTIBODIES;
ACTIVATION; RECEPTORS; EPITOPES; PROTEIN; MYELIN; IDENTIFICATION
AB The pathologic role of autoantibodies in many autoimmune diseases is widely accepted. An enzyme immunoassay was used for measurement of antibodies against disease-specific antigens and etiologic agents for cross-reactive antigens associated with them. This antibody assay was applied to a panel of antigens for the detection of different neuroautoimmune diseases that included multiple sclerosis, motor peripheral neuropathies, multifocal motor neuropathy, amyotrophic lateral sclerosis and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection. We studied women with pregnancies complicated by neural tube defect, neuroborreliosis, autism and patients with possible somatic hypermutation. Antibodies were also measured against antigens and etiologic agents associated with primary biliary cirrhosis and chronic obstructive pulmonary disease. And, finally, antibodies were measured against several tumor antigens or peptides which are expressed in prostatic, breast and colon tissues. This panel of different autoantibodies was applied to 290 patients with neuroautoimmune disorders, cancer, and possible somatic hypermutation. The levels of these antibodies against different tissue-specific antigens and etiologic agents associated with them were significantly elevated in patients versus controls. We hope that this novel 96 antigen-specific ELISA will be used in additional studies that will prove its clinical efficacy, not only for the early diagnosis of many neuroautoimmune, liver and lung autoimmune disorders, but also for prognosis and the implementation of preventive steps for many complex diseases.
C1 [Vojdani, A.] Immunisci Lab Inc, Beverly Hills, CA USA.
RP Vojdani, A (corresponding author), 8693 Wilshire Blvd,Suite 200, Beverly Hills, CA 90211 USA.
EM immunsci@ix.netcom.com
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NR 40
TC 20
Z9 21
U1 0
U2 8
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0394-6320
EI 2058-7384
J9 INT J IMMUNOPATH PH
JI Int. J. Immunopathol. Pharmacol.
PD JUL-SEP
PY 2008
VL 21
IS 3
BP 553
EP 566
DI 10.1177/039463200802100308
PG 14
WC Immunology; Pathology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pathology; Pharmacology & Pharmacy
GA 359KR
UT WOS:000259986100008
PM 18831922
OA Bronze
DA 2025-01-07
ER
PT J
AU Saglam, A
Singh, K
Gollapudi, S
Kumar, J
Brar, N
Butzmann, A
Warnke, R
Ohgami, RS
AF Saglam, Arzu
Singh, Kunwar
Gollapudi, Sumanth
Kumar, Jyoti
Brar, Nivaz
Butzmann, Alexandra
Warnke, Roger
Ohgami, Robert S.
TI Indolent T-lymphoblastic proliferation: A systematic review of the
literature analyzing the epidemiologic, clinical, and pathologic
features of 45 cases
SO INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY
LA English
DT Review; Early Access
DE Castleman disease; indolent T-lymphoblastic proliferation; TdT;
T-lymphoblastic lymphoma
ID TRANSFERASE-POSITIVE CELLS; HEPATOCELLULAR-CARCINOMA; CASTLEMAN DISEASE;
STEM-CELLS; THYMUS; LIVER; INTERLEUKIN-6; ASSOCIATION; PRECURSORS;
CHIMERISM
AB An indolent T-lymphoblastic proliferation (iT-LBP) is a rare benign disorder characterized by an abnormal expansion of immature T-cells, which morphologically can mimic malignancy. Since the first case was described in 1999, dozens more have been reported in the literature. However, the epidemiologic, clinical, pathologic, and biologic features of this disease have not been well described. Here, we retrospectively reviewed all known cases reported in the literature to better understand this entity. A PubMed search up to January 2022 highlighted 25 papers describing cases/case series of iT-LBP, one of which was a case presentation in a slide workshop. Except for 9 of the cases in one of the papers, where it was evident that the number of CD3+/TdT+ cells were too few to conform with a diagnosis of iT-LBP, all papers and all the cases reported were included in the study amounting to a total of 45 cases. Clinicopathologic characteristics were analyzed using descriptive statistics and frequencies. Our analysis highlighted the previously known association with Castleman disease and Castleman-like features and underlined its association with dendritic cell proliferations in general, as well as uncovering high frequency of concurrence with hepatocellular carcinoma and autoimmune diseases, most notably myasthenia gravis, paraneoplastic pemphigus and paraneoplastic autoimmune multiorgan syndrome. Furthermore, the co-expression of CD4 and CD8 and high prevalence of extranodal disease and recurrences were other less well described features that were revealed.
C1 [Saglam, Arzu] Hacettepe Univ, Dept Pathol, Ankara, Turkey.
[Singh, Kunwar; Gollapudi, Sumanth; Butzmann, Alexandra; Ohgami, Robert S.] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA.
[Kumar, Jyoti; Brar, Nivaz; Warnke, Roger] Stanford Univ, Dept Pathol, Stanford, CA 94305 USA.
C3 Hacettepe University; University of California System; University of
California San Francisco; Stanford University
RP Saglam, A (corresponding author), Hacettepe Univ, Sch Med, Dept Pathol, TR-06230 Ankara, Turkey.
EM eminearzusaglam@yahoo.com
RI Ayhan, Arzu/AAB-9393-2020
OI Saglam, Arzu/0000-0002-0076-8293
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NR 54
TC 6
Z9 6
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-5521
EI 1751-553X
J9 INT J LAB HEMATOL
JI Int. J. Lab. Hematol.
PD 2022 MAY 16
PY 2022
DI 10.1111/ijlh.13873
EA MAY 2022
PG 12
WC Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology
GA 1H0WA
UT WOS:000796266300001
PM 35577551
DA 2025-01-07
ER
PT J
AU Smyk, DS
Koutsoumpas, AL
Mytilinaiou, MG
Rigopoulou, EI
Sakkas, LI
Bogdanos, DP
AF Smyk, Daniel S.
Koutsoumpas, Andreas L.
Mytilinaiou, Maria G.
Rigopoulou, Eirini I.
Sakkas, Lazaros I.
Bogdanos, Dimitrios P.
TI Helicobacter pylori and autoimmune disease: Cause or bystander
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmunity; Helicobacter pylori; Infection; Gastritis; Mimicry;
Rheumatology
ID PRIMARY BILIARY-CIRRHOSIS; IDIOPATHIC THROMBOCYTOPENIC PURPURA;
NEUTROPHIL-ACTIVATING PROTEIN; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
LYMPHOID-TISSUE LYMPHOMA; MULTIPLE-SCLEROSIS; MOLECULAR MIMICRY;
RHEUMATOID-ARTHRITIS; CHRONIC URTICARIA; WEGENERS-GRANULOMATOSIS
AB Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjorens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Smyk, Daniel S.; Koutsoumpas, Andreas L.; Mytilinaiou, Maria G.; Sakkas, Lazaros I.; Bogdanos, Dimitrios P.] Kings Coll Hosp London, Kings Coll London, Sch Med, Inst Liver Studies,Div Transplantat Immunol & Muc, London SE5 9RS, England.
[Koutsoumpas, Andreas L.; Rigopoulou, Eirini I.; Bogdanos, Dimitrios P.] Univ Thessaly, Fac Med, Sch Hlth Sci, Dept Med, Larisa 41110, Greece.
[Sakkas, Lazaros I.] Univ Thessaly, Fac Med, Sch Hlth Sci, Dept Rheumatol, Larisa 41110, Greece.
[Bogdanos, Dimitrios P.] Inst REs & Technol THessaly I RE TE TH, Ctr Res & TEchnol Hellas CE R T H, Cellular Immunotherapy & Mol Immunodiagnost Biome, Thessaloniki, Greece.
C3 University of London; King's College London; King's College Hospital NHS
Foundation Trust; King's College Hospital; University of Thessaly;
University of Thessaly; Centre for Research & Technology Hellas
RP Bogdanos, DP (corresponding author), Univ Thessaly, Fac Med, Sch Hlth Sci, Dept Med, Mezourlo Campus, Larisa 41110, Greece.
EM dimitrios.bogdanos@kcl.ac.uk
RI Bogdanos, Dimitrios/AAF-8620-2020; Mytilinaiou, Maria/HPE-8131-2023
OI Bogdanos, Dimitrios/0000-0002-9697-7902
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NR 159
TC 106
Z9 117
U1 0
U2 32
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JAN 21
PY 2014
VL 20
IS 3
BP 613
EP 629
DI 10.3748/wjg.v20.i3.613
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AA1KZ
UT WOS:000330856400001
PM 24574735
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Kim, BH
Choi, HY
Ki, M
Kim, KA
Jang, ES
Jeong, SH
AF Kim, Bo Hyun
Choi, Hwa Young
Ki, Moran
Kim, Kyung-Ah
Jang, Eun Sun
Jeong, Sook-Hyang
TI Population-based prevalence, incidence, and disease burden of autoimmune
hepatitis in South Korea
SO PLOS ONE
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; LIVER-DISEASE; FOLLOW-UP; EPIDEMIOLOGY;
NATIONWIDE; CRITERIA; WOMEN; AREA
AB Background and aim
Little is known about population-based epidemiology and disease burden of autoimmune hepatitis (AIH). The aim of this study was to investigate the prevalence, incidence, comorbidity and direct medical cost of AIH in South Korea.
Methods
The data was from the nationwide, population-based National Health Insurance Service claims database and the Rare Intractable Disease registration program. Age and gender-specific prevalence rates were calculated, and data on comorbidity, diagnostic tests, prescribed drugs, and medical costs were retrieved for patients registered under the disease code K75.4 (AIH) from 2009 to 2013.
Results
A total of 4,085 patients with AIH were identified between 2009 and 2013 with a female-tomale ratio of 6.4. The age-adjusted prevalence rate was 4.82/100,000 persons and gender adjusted prevalence rates were 8.35 in females and 1.30 in males. The age-adjusted calculated incidence rate was 1.07/100,000 persons (gender-adjusted 1.83 in females and 0.31 in males). Ascites, variceal bleeding, and hepatocellular carcinoma were found in 1.4%, 1.3%, and 2.2% of the patients, respectively. Forty-six patients (1.1%) underwent liver transplantation during the study period. Case-fatality was 2.18%. Corticosteroid and azathioprine were prescribed in 44.1% and 38.0% of prevalent patients with AIH in 2013, respectively. The nationwide total direct medical cost was less than 4.0 million USD, and the average cost for each patient was 1,174 USD in 2013.
Conclusion
This is the first report on the nationwide epidemiology of AIH in Korea, and it showed a lower prevalence than that of Western countries with considerable disease burden.
C1 [Kim, Bo Hyun] Natl Canc Ctr, Ctr Liver Canc, Goyang, South Korea.
[Choi, Hwa Young; Ki, Moran] Grad Sch Canc Sci, Dept Canc Control & Policy, Goyang, South Korea.
[Choi, Hwa Young; Ki, Moran] Policy Natl Canc Ctr, Goyang, South Korea.
[Kim, Kyung-Ah] Inje Univ, Dept Internal Med, Ilsan Paik Hosp, Goyang, South Korea.
[Jang, Eun Sun; Jeong, Sook-Hyang] Seoul Natl Univ, Dept Internal Med, Bundang Hosp, Coll Med, Seoul, South Korea.
C3 National Cancer Center - Korea (NCC); Inje University; Seoul National
University (SNU); Seoul National University Hospital
RP Jeong, SH (corresponding author), Seoul Natl Univ, Dept Internal Med, Bundang Hosp, Coll Med, Seoul, South Korea.
EM jsh@snubh.org
RI Choi, Youn/AAS-3301-2021; Jeong, Sook-Hyang/J-5642-2012; Ki,
Moran/R-6600-2019
OI Ki, Moran/0000-0002-8892-7104
FU Korean Association for the Study of the Liver (KASL); National Cancer
Center, Korea [NCC-1410860]
FX This work was supported in part by a research grant from Korean
Association for the Study of the Liver (KASL academic research fund
2013), and from the National Cancer Center, Korea (NCC-1410860). The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 25
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Z9 36
U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 3
PY 2017
VL 12
IS 8
AR e0182391
DI 10.1371/journal.pone.0182391
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA FC5AR
UT WOS:000406853600099
PM 28771543
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Magen, I
Avraham, Y
Berry, E
Mechoulam, R
AF Magen, Iddo
Avraham, Yosefa
Berry, Elliot
Mechoulam, Raphael
TI Endocannabinoids in liver disease and hepatic encephalopathy
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
ID CANNABINOID RECEPTOR ANTAGONISM; ACTIVATED PROTEIN-KINASE; AUTOPSIED
BRAIN-TISSUE; ACID AMIDE HYDROLASE; ISCHEMIA/REPERFUSION INJURY;
CIRRHOTIC RATS; CB1 RECEPTORS; HEPATOCELLULAR-CARCINOMA;
BILIARY-CIRRHOSIS; FATTY LIVER
AB Chronic liver disease results from a variety of causes such as hepatitis virus infections, autoimmune processes and alcohol consumption. Its complications include fat deposition, hemodynamic changes and fibrosis. Clinically there may be progression to portal-hypertension and porto-systemic encephalopathy. Pioneering research from the laboratory of Kunos at NIH has stressed the importance of endocannabinoids (ECs) as mediators of some of the pathological processes in chronic liver disease. The present review summarizes the literature on the association between ECs and liver disease, as well as the therapeutic potential of ECs and exogenous cannabinoids in liver disease with emphasis on hepatic encephalopathy.
C1 [Magen, Iddo; Avraham, Yosefa; Berry, Elliot] Hebrew Univ Jerusalem, Fac Med, Dept Nutr & Metab, IL-91120 Jerusalem, Israel.
[Magen, Iddo; Mechoulam, Raphael] Hebrew Univ Jerusalem, Fac Med, Dept Med Chem & Nat Prod, IL-91120 Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hebrew University of Jerusalem
RP Magen, I (corresponding author), Hebrew Univ Jerusalem, Fac Med, Dept Nutr & Metab, Kerem campus, IL-91120 Jerusalem, Israel.
EM iddo.magen@mail.huji.ac.il; mechou@cc.huji.ac.il
RI Magen, Iddo/KCJ-7148-2024
OI Magen, Iddo/0000-0002-3011-3175
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NR 85
TC 16
Z9 18
U1 0
U2 2
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD AUG
PY 2008
VL 14
IS 23
BP 2362
EP 2369
DI 10.2174/138161208785740063
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 351TF
UT WOS:000259448100012
PM 18781986
DA 2025-01-07
ER
PT J
AU Liu, K
Strasser, SI
Koorey, DJ
Leong, RW
Solomon, M
McCaughan, GW
AF Liu, Ken
Strasser, Simone I.
Koorey, David J.
Leong, Rupert W.
Solomon, Michael
McCaughan, Geoffrey W.
TI Interactions between primary sclerosing cholangitis and inflammatory
bowel disease: implications in the adult liver transplant setting
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE Primary sclerosing cholangitis; inflammatory bowel disease; ulcerative
colitis; Crohn's disease; liver transplantation; colorectal cancer;
cholangiocarcinoma
ID ULCERATIVE-COLITIS PATIENTS; POUCH-ANAL ANASTOMOSIS; DE-NOVO
CHOLANGIOCARCINOMA; NATURAL-HISTORY MODEL; FECAL BILE-ACIDS;
RISK-FACTORS; COLORECTAL-CANCER; URSODEOXYCHOLIC ACID; CLINICAL-COURSE;
BILIARY RECONSTRUCTION
AB Introduction: Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease which is associated with inflammatory bowel disease (IBD) in most cases. As there is currently no medical therapy which alters the natural history of PSC, liver transplantation may be required.
Areas covered: We searched for articles in PubMed and critically reviewed current literature on the interrelationship between PSC and IBD with a specific focus on considerations for patients in the liver transplant setting.
Expert commentary: PSC is an uncommon disease which limits available studies to be either retrospective or contain relatively small numbers of patients. Based on observations from these studies, the behavior and complications of PSC and IBD impact on each other both before and after a liver transplant. Both these autoimmune conditions and their associated cancer risk also influence patient selection for transplantation and may be impacted by immunosuppression use post-transplant. Hence, a complex interplay exists between PSC, IBD and liver transplantation which requires clarification with ongoing research.
C1 [Liu, Ken; Strasser, Simone I.; Koorey, David J.; Leong, Rupert W.; Solomon, Michael; McCaughan, Geoffrey W.] Univ Sydney, Sydney Med Sch, Sydney, NSW, Australia.
[Liu, Ken; Strasser, Simone I.; Koorey, David J.; McCaughan, Geoffrey W.] Royal Prince Alfred Hosp, AW Morrow Gastroenterol & Liver Ctr, Sydney, NSW, Australia.
[Liu, Ken; McCaughan, Geoffrey W.] Univ Sydney, Centenary Inst, Liver Injury & Canc Program, Sydney, NSW, Australia.
[Leong, Rupert W.] Concord Hosp, Gastroenterol & Liver Serv, Sydney, NSW, Australia.
[Solomon, Michael] Royal Prince Alfred Hosp, Dept Colorectal Surg, Sydney, NSW, Australia.
C3 University of Sydney; University of Sydney; NSW Health; Royal Prince
Alfred Hospital; University of Sydney; Centenary Institute; Concord
Repatriation General Hospital; NSW Health; Royal Prince Alfred Hospital;
University of Sydney
RP McCaughan, GW (corresponding author), Univ Sydney, Royal Prince Alfred Hosp, AW Morrow Gastroenterol & Liver Ctr, Liver Immunobiol Program,Centenary Res Inst, Sydney, NSW, Australia.; McCaughan, GW (corresponding author), Univ Sydney, Royal Prince Alfred Hosp, Australian Liver Transplant Unit, Sydney, NSW, Australia.
EM g.mccaughan@centenary.usyd.edu.au
RI Liu, Ken/I-1559-2019; Leong, Rupert/J-7839-2012
OI Leong, Rupert/0000-0001-5944-3488; MCCAUGHAN,
GEOFFREY/0000-0002-1483-1636
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NR 140
TC 3
Z9 5
U1 0
U2 4
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PY 2017
VL 11
IS 10
BP 949
EP 960
DI 10.1080/17474124.2017.1343666
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FN3TW
UT WOS:000415924800008
PM 28627935
DA 2025-01-07
ER
PT J
AU Tsioumpekou, M
Krijgsman, D
Leusen, JHW
Olofsen, PA
AF Tsioumpekou, Maria
Krijgsman, Danielle
Leusen, Jeanette H. W.
Olofsen, Patricia A.
TI The Role of Cytokines in Neutrophil Development, Tissue Homing, Function
and Plasticity in Health and Disease
SO CELLS
LA English
DT Review
DE neutrophils; cytokines; tissue-resident neutrophils; autoimmune
diseases; cancer; tumor microenvironment; TME; NETs; cytokine
therapeutics; immunocytokines; immunotherapy
ID COLONY-STIMULATING FACTOR; TUMOR-ASSOCIATED NEUTROPHILS; MYELOID
SUPPRESSOR-CELLS; DELTA T-CELLS; G-CSF; IN-VIVO; LYMPH-NODES;
INFLAMMASOME ACTIVATION; COLORECTAL-CANCER; PERIPHERAL-BLOOD
AB Neutrophils are crucial innate immune cells and comprise 50-70% of the white blood cell population under homeostatic conditions. Upon infection and in cancer, blood neutrophil numbers significantly increase because of the secretion of various chemo- and cytokines by, e.g., leukocytes, pericytes, fibroblasts and endothelial cells present in the inflamed tissue or in the tumor microenvironment (TME). The function of neutrophils in cancer has recently gained considerable attention, as they can exert both pro- and anti-tumorigenic functions, dependent on the cytokine milieu present in the TME. Here, we review the effect of cytokines on neutrophil development, tissue homing, function and plasticity in cancer and autoimmune diseases as well as under physiological conditions in the bone marrow, bloodstream and various organs like the spleen, kidney, liver, lung and lymph nodes. In addition, we address several promising therapeutic options, such as cytokine therapy, immunocytokines and immunotherapy, which aim to exploit the anti-tumorigenic potential of neutrophils in cancer treatment or block excessive neutrophil-mediated inflammation in autoimmune diseases.
C1 [Tsioumpekou, Maria; Krijgsman, Danielle; Leusen, Jeanette H. W.; Olofsen, Patricia A.] Univ Med Ctr Utrecht, Ctr Translat Immunol, NL-3584 CX Utrecht, Netherlands.
[Krijgsman, Danielle] Univ Med Ctr Utrecht, Ctr Mol Med, NL-3584 CX Utrecht, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
University; Utrecht University Medical Center
RP Olofsen, PA (corresponding author), Univ Med Ctr Utrecht, Ctr Translat Immunol, NL-3584 CX Utrecht, Netherlands.
EM m.tsioumpekou@umcutrecht.nl; d.krijgsman-4@umcutrecht.nl;
jleusen@umcutrecht.nl; p.a.olofsen@umcutrecht.nl
RI Krijgsman, Daniëlle/Y-3829-2018; , Jeanette/AAG-3736-2019
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NR 197
TC 17
Z9 18
U1 3
U2 14
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD AUG
PY 2023
VL 12
IS 15
AR 1981
DI 10.3390/cells12151981
PG 24
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA O7EX5
UT WOS:001045409200001
PM 37566060
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Ko, HBM
Hernandez-Prera, JC
Zhu, HF
Dikman, SH
Sidhu, HK
Ward, SC
Thung, SN
AF Ko, Huaibin M.
Hernandez-Prera, Juan C.
Zhu, Hongfa
Dikman, Steven H.
Sidhu, Harleen K.
Ward, Stephen C.
Thung, Swan N.
TI Morphologic Features of Extrahepatic Manifestations of Hepatitis C Virus
Infection
SO CLINICAL & DEVELOPMENTAL IMMUNOLOGY
LA English
DT Review
ID NON-HODGKIN-LYMPHOMA; NECROLYTIC ACRAL ERYTHEMA; INTERFERON-ALPHA
THERAPY; CRYOGLOBULINEMIA TYPE-II; MIXED CRYOGLOBULINEMIA; MEMBRANOUS
GLOMERULONEPHRITIS; HEPATOCELLULAR-CARCINOMA; INSULIN-RESISTANCE;
DIABETES-MELLITUS; SJOGRENS-SYNDROME
AB Cirrhosis and hepatocellular carcinoma are the prototypic complications of chronic hepatitis C virus infection in the liver. However, hepatitis C virus also affects a variety of other organs that may lead to significant morbidity and mortality. Extrahepatic manifestations of hepatitis C infection include a multitude of disease processes affecting the small vessels, skin, kidneys, salivary gland, eyes, thyroid, and immunologic system. The majority of these conditions are thought to be immune mediated. The most documented of these entities is mixed cryoglobulinemia. Morphologically, immune complex depositions can be identified in small vessels and glomerular capillary walls, leading to leukoclastic vasculitis in the skin and membranoproliferative glomerulonephritis in the kidney. Other HCV-associated entities include porphyria cutanea tarda, lichen planus, necrolytic acral erythema, membranous glomerulonephritis, diabetic nephropathy, B-cell non-Hodgkin lymphomas, insulin resistance, sialadenitis, sicca syndrome, and autoimmune thyroiditis. This paper highlights the histomorphologic features of these processes, which are typically characterized by chronic inflammation, immune complex deposition, and immunoproliferative disease in the affected organ.
C1 [Ko, Huaibin M.; Hernandez-Prera, Juan C.; Zhu, Hongfa; Dikman, Steven H.; Sidhu, Harleen K.; Ward, Stephen C.; Thung, Swan N.] Mt Sinai Sch Med, Lillian & Henry M Stratton Hans Popper Dept Patho, New York, NY 10029 USA.
C3 Icahn School of Medicine at Mount Sinai
RP Ko, HBM (corresponding author), Mt Sinai Sch Med, Lillian & Henry M Stratton Hans Popper Dept Patho, New York, NY 10029 USA.
EM mabel.ko@mssm.edu
RI Ward, Stephen/C-5222-2013; HernandezPrera, Juan/LBH-6479-2024; Ko,
Huaibin Mabel/AAO-2767-2020
OI Ko, Huaibin Mabel/0000-0003-1062-2383
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NR 74
TC 33
Z9 33
U1 0
U2 4
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 1740-2522
J9 CLIN DEV IMMUNOL
JI Clin. Dev. Immunol.
PY 2012
AR 740138
DI 10.1155/2012/740138
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 997XT
UT WOS:000308202000001
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Tanoue, S
Kanmura, S
Hinokuchi, M
Arima, S
Sasaki, F
Hashimoto, S
Ido, A
AF Tanoue, Shiroh
Kanmura, Shuji
Hinokuchi, Makoto
Arima, Shiho
Sasaki, Fumisato
Hashimoto, Shinichi
Ido, Akio
TI Role of apoptosis inhibitor of macrophages in patients with IgG4-related
disease/autoimmune pancreatitis and the clinical characteristics
associated with this condition
SO BIOMEDICAL REPORTS
LA English
DT Article
DE apoptosis inhibitor of macrophages; IgG4-related disease; autoimmune
pancreatitis; pancreatic cancer
ID AUTOIMMUNE PANCREATITIS; DIAGNOSTIC-CRITERIA; SERUM IGG4; ACTIVATION;
FIBROSIS; DISEASE; AIM
AB Type 1 autoimmune pancreatitis (AIP) is a pancreatic manifestation of IgG4-related disease (IgG4-RD) and is a unique chronic inflammatory disease characterized by fibrosis. IgG4-RD is caused by an autoimmune mechanism that mimics malignant tumors and inflammatory disorders. Apoptosis inhibitor of macrophages (AIM) can function as a biomarker of autoimmune or inflammatory diseases with tissue fibrosis, including in inflammatory bowel disease and chronic liver disease. Therefore, the aim of the present study was to clarify the role of serum AIM levels and the clinical characteristics of patients with IgG4-RD and AIP. For this purpose, serum AIM concentrations were assessed using ELISA and the association between AIM and the laboratory and clinical data from patients with IgG4-RD/AIP, patients with pancreatic cancer (PC) and healthy controls (HCs), was determined. The results demonstrated that the serum AIM concentrations were not associated with the laboratory data. However, the serum AIM levels were significantly elevated in patients with AIP compared with the HCs and patients with PC. Furthermore, the serum AIM levels significantly decreased following steroid therapy in patients with AIP who were in remission. Overall, the present study demonstrates that serum AIM levels may be a potentially useful biomarker for the differential diagnosis of AIP and for evaluating the therapeutic reactivity of affected patients.
C1 [Tanoue, Shiroh; Kanmura, Shuji; Hinokuchi, Makoto; Arima, Shiho; Sasaki, Fumisato; Hashimoto, Shinichi; Ido, Akio] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Digest & Lifestyle Dis, Kagoshima 8908544, Japan.
[Tanoue, Shiroh] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Epidemiol & Prevent Med, Kagoshima 8908544, Japan.
[Tanoue, Shiroh] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Digest & Lifestyle Dis, 8-35-1 Sakuragaoka, Kagoshima 8908544, Japan.
C3 Kagoshima University; Kagoshima University; Kagoshima University
RP Tanoue, S (corresponding author), Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Digest & Lifestyle Dis, 8-35-1 Sakuragaoka, Kagoshima 8908544, Japan.
RI Hashimoto, Shinichi/AAA-4028-2022; Sasaki, Fumisato/AAQ-6470-2020
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NR 33
TC 3
Z9 3
U1 2
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 2049-9434
EI 2049-9442
J9 BIOMED REP
JI Biomed. Rep.
PD OCT
PY 2022
VL 17
IS 4
AR 82
DI 10.3892/br.2022.1565
PG 9
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA 4Z8JO
UT WOS:000862447900001
PM 36158321
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Zigmond, E
Shalev, Z
Pappo, O
Alper, R
Zolotarov, L
Ilan, Y
AF Zigmond, Ehud
Shalev, Zvi
Pappo, Orit
Alper, Roslana
Zolotarov, Lidya
Ilan, Yaron
TI NKT lymphocyte polarization determined by microenvironment signaling: A
role for CD8+ lymphocytes and β-glycosphingolipids
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Natural killer T cells; Glycolipids; Immune regulation
ID KILLER T-CELLS; HEPATOCELLULAR-CARCINOMA GROWTH; ACTIVATION IN-VIVO;
AUTOIMMUNE-DISEASES; IMMUNE REGULATION; DENDRITIC CELLS; MURINE MODEL;
LIVER-INJURY; MICE; GALACTOSYLCERAMIDE
AB Natural killer T-cell (NKT) regulatory lymphocytes have been shown to behave differently in various immune settings. The aim of the present study was to determine the effect of microenvironmental signaling on NKT polarization and the process of active CD8 and NKT intrahepatic lymphocyte sequestration. In an in vitro assay, double negative (DN) NKT hybridoma cells were incubated with Hep3B hepatoma cells. This caused a significant increase in the secretion of alpha-fetoprotein (AFP) from Hep3B cells. When NKT cells were exposed to beta-glucoslyceramide (beta-GC) prior to incubation, Hep3B cells exhibited increased Proliferation, increased IFN secretion, and reduced AFP secretion. In vivo, the adoptive transfer of naive DN NKT cells into athymic nude-nu mice transplanted with human Hep3B hepatocellular carcinoma (HCC) caused accelerated tumor growth. This effect was inhibited by prior ex vivo exposure of DN NKT lymphocytes to P-GC. To assess the effect of the immunological enviromment on NKT cells, immune mediated hepatitis and colitis were induced simultaneously in mice. Induction of TNBS colitis prior to administration of concanavalin A (Con A) hepatitis resulted in an aggravation of the liver damage caused by Con A hepatitis alone. This effect was associated with reduced intrahepatic CD8(+) T cell trapping and an increase in intrahepatic NKT cells. The presence of different ligands altered host microenvironment signaling and influenced the fate and polarization of NKT cells and the sequestration of active intrahepatic lymphocytes. These data support the notion that NKT regulatory lymphocytes have an inherent plasticity that may be important for their regulatory function. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Zigmond, Ehud; Shalev, Zvi; Alper, Roslana; Zolotarov, Lidya; Ilan, Yaron] Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Med, Liver Unit, IL-91120 Jerusalem, Israel.
[Pappo, Orit] Hadassah Hebrew Univ, Med Ctr, Dept Pathol, Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hadassah University Medical Center;
Hebrew University of Jerusalem; Hadassah University Medical Center
RP Ilan, Y (corresponding author), Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Med, Liver Unit, POB 12000, IL-91120 Jerusalem, Israel.
EM ilan@hadassah.org.il
FU ENZO Biochem, NYC, NY; Roaman-Epstein Liver Research Foundation
FX This work was supported in part by the following grants: ENZO Biochem,
NYC, NY, and The Roaman-Epstein Liver Research Foundation.
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NR 61
TC 21
Z9 21
U1 0
U2 5
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD SEP
PY 2008
VL 31
IS 2
BP 188
EP 195
DI 10.1016/j.jaut.2008.07.003
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 357XO
UT WOS:000259880700015
PM 18710796
DA 2025-01-07
ER
PT J
AU Xu, MY
Luo, KK
Li, JJ
Li, Y
Zhang, YX
Yuan, ZY
Xu, Q
Wu, XD
AF Xu, Mengyi
Luo, Kangkang
Li, Junjie
Li, Yu
Zhang, Yuxuan
Yuan, Zhiyao
Xu, Qiang
Wu, Xudong
TI Role of Intestinal Microbes in Chronic Liver Diseases
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE intestinal microbes; bacterial metabolites; chronic liver diseases;
probiotics and prebiotics
ID NONALCOHOLIC FATTY LIVER; CHRONIC HEPATITIS-C; GUT MICROBIOTA; PRECISION
MEDICINE; NATURAL-HISTORY; FERMENTED MILK; DYSBIOSIS; DIET; FIBROSIS;
ALCOHOL
AB With the recent availability and upgrading of many emerging intestinal microbes sequencing technologies, our research on intestinal microbes is changing rapidly. A variety of investigations have found that intestinal microbes are essential for immune system regulation and energy metabolism homeostasis, which impacts many critical organs. The liver is the first organ to be traversed by the intestinal portal vein, and there is a strong bidirectional link between the liver and intestine. Many intestinal factors, such as intestinal microbes, bacterial composition, and intestinal bacterial metabolites, are deeply involved in liver homeostasis. Intestinal microbial dysbiosis and increased intestinal permeability are associated with the pathogenesis of many chronic liver diseases, such as alcoholic fatty liver disease (AFLD), non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), chronic hepatitis B (CHB), chronic hepatitis C (CHC), autoimmune liver disease (AIH) and the development of hepatocellular carcinoma (HCC). Intestinal permeability and dysbacteriosis often lead to Lipopolysaccharide (LPS) and metabolites entering in serum. Then, Toll-like receptors activation in the liver induces the exposure of the intestine and liver to many small molecules with pro-inflammatory properties. And all of these eventually result in various liver diseases. In this paper, we have discussed the current evidence on the role of various intestinal microbes in different chronic liver diseases. As well as potential new therapeutic approaches are proposed in this review, such as antibiotics, probiotics, and prebiotics, which may have an improvement in liver diseases.
C1 [Xu, Mengyi; Luo, Kangkang; Li, Junjie; Li, Yu; Zhang, Yuxuan; Xu, Qiang; Wu, Xudong] Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Nanjing 210023, Peoples R China.
[Yuan, Zhiyao] Nanjing Univ, Nanjing Stomatol Hosp, Med Sch, Nanjing 210008, Peoples R China.
C3 Nanjing University; Nanjing University
RP Xu, Q; Wu, XD (corresponding author), Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Nanjing 210023, Peoples R China.
EM qiangxu@nju.edu.cn; xudongwu@nju.edu.cn
RI wu, xudong/KGL-1857-2024
OI Wu, Xudong/0000-0003-2260-035X; Yuan, Zhiyao/0000-0002-2406-0281
FU National Natural Science Foundation of China [82173871, 81872916];
Natural Science Foundation of Jiangsu Province [BK20201256]; Fundamental
Research Funds for the Central Universities [021414380503]; Open Project
of State Key Laboratory of Pharmaceutical Biotechnology of Nanjing
University [KF-GN-202101]
FX This study was supported by the National Natural Science Foundation of
China (82173871, 81872916), Natural Science Foundation of Jiangsu
Province (BK20201256), Fundamental Research Funds for the Central
Universities (021414380503), and Open Project of State Key Laboratory of
Pharmaceutical Biotechnology of Nanjing University (KF-GN-202101).
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NR 146
TC 14
Z9 15
U1 6
U2 42
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2022
VL 23
IS 20
AR 12661
DI 10.3390/ijms232012661
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 5P5PI
UT WOS:000873202300001
PM 36293518
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Lefkowitch, JH
AF Lefkowitch, Jay H.
TI Hepatobiliary pathology
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Article
DE ductular reaction; hemochromatosis; hepatocellular carcinoma; liver
pathology; viral hepatitis; Wilson disease
ID HEPATITIS-C VIRUS; HEPATOCELLULAR-CARCINOMA; LIVER-TRANSPLANTATION;
DUCTULAR REACTIONS; DISEASE; CELLS; CLASSIFICATION; ADENOMA;
CHOLANGIOCARCINOMA; DIFFERENTIATION
AB Purpose of review
Studies are reviewed from the past year concerning the histopathology of liver and biliary diseases and their pathogenesis.
Recent findings
Several cases of acute hepatitis E showed portal and periportal hepatitis, with polarization of neutrophils to the interface region and lymphocytes more centrally in the portal tracts. Transfection of hepatitis C virus into cultured fetal hepatocytes resulted in sustained growth of 50-90 nm diameter viral particles. The ductular reaction in nonalcoholic steatohepatitis appears to evolve with fibrosis in response to hepatocyte replicative senescence. Hepatocellular release of hepcidin is critical for iron homeostasis in a manner analogous to pancreatic insulin for glucose homeostasis; this 'endocrine' focus was elaborated in an overview of hemochromatosis. Specific microscopic features of liver-cell adenomas combined with genetic analysis for hepatocyte nuclear factor 1 alpha and beta-catenin mutations allows differentiation into four variants. Steroid-sensitive biliary strictures resembling primary sclerosing cholangitis but with increased serum immunoglobulin G4 and infiltrating immunoglobulin G4-positive plasma cells ('immunoglobulin associated cholangitis') are part of a spectrum of disorders including autoimmune pancreatitis and inflammatory pseudotumor.
Summary
Pathologic features of viral hepatitis C and E, immunohistochemistry for the ductular reaction and malignant liver tumors and several systemic disorders are among recent important pathology studies.
C1 Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA.
C3 Columbia University
RP Lefkowitch, JH (corresponding author), Columbia Univ, Coll Phys & Surg, Dept Pathol, 630 W 168th St,PH 15 W-1574, New York, NY 10032 USA.
EM jhl3@columbia.edu
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NR 63
TC 3
Z9 4
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0267-1379
EI 1531-7056
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD MAY
PY 2008
VL 24
IS 3
BP 269
EP 277
DI 10.1097/MOG.0b013e3282f8e28f
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 298SM
UT WOS:000255707400002
PM 18408454
DA 2025-01-07
ER
EF
FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Schroeder, SM
Matsukuma, KE
Medici, V
AF Schroeder, Shannon M.
Matsukuma, Karen E.
Medici, Valentina
TI Wilson disease and the differential diagnosis of its hepatic
manifestations: a narrative review of clinical, laboratory, and liver
histological features
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Wilson disease (WD); copper; diagnosis; histology; fatty liver
ID URINARY COPPER EXCRETION; AUTOIMMUNE HEPATITIS; SCORING SYSTEM;
NONALCOHOLIC STEATOHEPATITIS; HEPATOCELLULAR MITOCHONDRIA;
ASPARTATE-AMINOTRANSFERASE; FAILURE; ATP7B; GENE; ZINC
AB Objective: The goal of the present work is to provide an overview of the differential diagnosis of Wilson disease. Background: Wilson disease is a rare condition due to copper accumulation primarily in the liver and brain. Although there is no definitive cure, current anti-copper treatments are associated with better outcomes if initiated early and if the diagnosis is made promptly. However, diagnostic delays are frequent and often Wilson disease represents a diagnostic challenge. The diagnosis ultimately relies on a combination of clinical, laboratory and genetic findings, and it is crucial that clinicians list Wilson disease in their differential diagnosis, especially in patients presenting with a hepatocellular pattern of liver injury. Some biochemical and liver histological features of Wilson disease overlap with those of more common conditions including nonalcoholic fatty liver disease, alcohol-associated liver disease, and autoimmune hepatitis. In particular, hepatic steatosis, hepatocyte glycogenated nuclei, ballooning degeneration, and Mallory-Denk bodies are often identified in Wilson disease as well as more common liver diseases. In addition, the natural history of liver damage in Wilson disease and the risk of developing liver cancer are largely understudied. Methods: We conducted an enlarged review of published papers on Wilson disease focusing on its diagnosis and distinctive clinical and liver pathology features in relation to common non-cholestatic liver diseases with the final goal in aiding clinicians in the diagnostic process of this rare but treatable condition. Conclusions: Aside from markedly altered copper metabolism, Wilson disease has essentially no pathognomonic features that can distinguish it from more common liver diseases. Clinicians should be aware of this challenge and consider Wilson disease in patients presenting with a hepatocellular pattern of liver injury.
C1 [Schroeder, Shannon M.] Univ Calif Davis, Dept Internal Med, Sacramento, CA 95817 USA.
[Matsukuma, Karen E.] Univ Calif Davis, Dept Pathol & Lab Med, Sacramento, CA 95817 USA.
[Medici, Valentina] Univ Calif Davis, Dept Internal Med, Div Gastroenterol & Hepatol, 4150 St,PSSB Suite 3500, Sacramento, CA 95817 USA.
C3 University of California System; University of California Davis;
University of California System; University of California Davis;
University of California System; University of California Davis
RP Medici, V (corresponding author), Univ Calif Davis, Dept Internal Med, Div Gastroenterol & Hepatol, 4150 St,PSSB Suite 3500, Sacramento, CA 95817 USA.
EM vmedici@ucdavis.edu
FU National Institutes of Health [R01DK104770]
FX The research was supported by the National Institutes of Health through
grant number R01DK104770 (to VM).
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NR 117
TC 18
Z9 19
U1 1
U2 16
PU AME PUBL CO
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD SEP
PY 2021
VL 9
IS 17
DI 10.21037/atm-21-2264
EA JUL 2021
PG 16
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA UY0SV
UT WOS:000689708700001
PM 34733946
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wang, NP
Zhu, P
Xiang, Y
Tao, LP
Huang, T
Feng, ZS
AF Wang, Nanping
Zhu, Peng
Xiang, Yue
Tao, Liping
Huang, Tao
Feng, Zhisong
TI IgG4-related autoimmune pancreatitis and sclerosing cholangitis: A case
report and literature review
SO MEDICINE
LA English
DT Article
DE AIP; diabetes; IgG4; IgG4-related sclerosing cholangitis; liver
cirrhosis
ID INTERNATIONAL CONSENSUS; DISEASE; CRITERIA
AB Rationale:Immunoglobulin G4-related disease (IgG4-RD) can involve various organs throughout the body, primarily manifesting as endocrine dysfunction, visual impairment, jaundice, and limited sexual function. IgG4-related autoimmune pancreatitis is triggered by autoimmune reactions and characterized by structural changes in the pancreas and pancreatic ducts. The disease mainly affects middle-aged and elderly males, typically presenting as progressive painless jaundice and misdiagnosed as cholangiocarcinoma or pancreatic cancer.Patient concerns:This study reports a 54-year-old male who consulted with different institutions multiple times due to diabetes, pancreatitis, elevated liver enzymes, and jaundice.Diagnoses:Magnetic resonance imaging revealed swollen head of the pancreas and atrophic tail. Liver and pancreatic tissue pathology showed IgG4 plasma cell infiltration, while liver biopsy indicated interface hepatitis, liver fibrosis, and pseudolobule formation, with no evidence of bile duct damage.Interventions:Following hormone therapy, the patient's serum IgG4 levels and liver enzyme levels returned to normal.Outcomes:The disease relapsed 2 years after maintaining hormone therapy, and the patient underwent additional hormone-induced remission therapy combined with azathioprine.Lessons:The purpose of this research report is to enhance the awareness and understanding of IgG4-RD, emphasizing the necessity for personalized treatment strategies that take into account its recurrence, associations, and imaging features. This report provides valuable insights and guidance for clinicians in managing and diagnosing patients with IgG4-RD.
C1 [Wang, Nanping; Tao, Liping; Huang, Tao; Feng, Zhisong] North Sichuan Med Coll, Affiliated Hosp, Dept Gastroenterol, Maoyuan South Rd, Nanchong, Sichuan, Peoples R China.
[Zhu, Peng] Fifth Peoples Hosp, Dept Hepatobiliary Surg, Nanchong, Sichuan, Peoples R China.
[Xiang, Yue] North Sichuan Med Coll, Affiliated Hosp, Dept Pathol, Nanchong, Sichuan, Peoples R China.
C3 North Sichuan Medical University; North Sichuan Medical University
RP Wang, NP (corresponding author), North Sichuan Med Coll, Affiliated Hosp, Dept Gastroenterol, Maoyuan South Rd, Nanchong, Sichuan, Peoples R China.
EM 416617650@qq.com; 411403665@qq.com; 544532166@qq.com; 36013436@qq.com;
514663870@qq.com; 2694063459@qq.com
FU College-level Youth Research Program at the North Sichuan Medical
College [CBY23-QNA21]
FX College-level Youth Research Program at the North Sichuan Medical
College (CBY23-QNA21).
CR Aithal GP, 2001, NEW ENGL J MED, V345, P147
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[Anonymous], CHRONIC INFLAMMATORY
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TC 1
Z9 1
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD APR 26
PY 2024
VL 103
IS 17
AR e37922
DI 10.1097/MD.0000000000037922
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OP9R6
UT WOS:001208602100057
PM 38669380
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Bhandari, BM
Bayat, H
Rothstein, KD
AF Bhandari, Bhavik M.
Bayat, Hasan
Rothstein, Kenneth D.
TI Primary Biliary Cirrhosis
SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Primary biliary cirrhosis; Ursodeoxycholic acid; Liver failure
ID PRIMARY BILLARY CIRRHOSIS; QUALITY-OF-LIFE; URSODEOXYCHOLIC ACID;
NATURAL-HISTORY; RISK-FACTORS; LIVER-TRANSPLANTATION; BREAST-CANCER;
SERUM-LIPIDS; PATHOGENESIS; FATIGUE
AB Primary biliary cirrhosis is a chronic autoimmune inflammatory disease of the liver with a striking female preponderance. It has an insidious onset and typically affects middle-aged women. The disease manifests gradually with symptoms of fatigue, pruritis, and increased alkaline phosphatase levels on laboratory evaluation. The hallmark of the disease is the circulating antimitochondrial antibody. Histology is characterized by inflammation of the bile ducts, destruction of cholangiocytes, and subsequent cholestasis, progressing to biliary cirrhosis. The standard treatment for primary biliary cirrhosis is ursodeoxycholic acid, which improves survival, but the disease can still lead to cirrhosis and liver failure over decades.
C1 [Bhandari, Bhavik M.; Rothstein, Kenneth D.] Drexel Univ, Div Gastroenterol & Hepatol, Coll Med, Dept Med, Philadelphia, PA 19107 USA.
C3 Drexel University
RP Bhandari, BM (corresponding author), Drexel Univ, Div Gastroenterol & Hepatol, Coll Med, Dept Med, 219 N Broad St,5th Floor, Philadelphia, PA 19107 USA.
EM bhandabh@gmail.com
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NR 83
TC 13
Z9 16
U1 1
U2 16
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8553
EI 1558-1942
J9 GASTROENTEROL CLIN N
JI Gastroenterol. Clin. North Am.
PD JUN
PY 2011
VL 40
IS 2
BP 373
EP +
DI 10.1016/j.gtc.2011.03.008
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 780XJ
UT WOS:000291894100007
PM 21601785
DA 2025-01-07
ER
PT J
AU Stoess, C
Choi, YK
Onyuru, J
Friess, H
Hoffman, HM
Hartmann, D
Feldstein, AE
AF Stoess, Christian
Choi, Yeon-Kyung
Onyuru, Janset
Friess, Helmut
Hoffman, Hal M.
Hartmann, Daniel
Feldstein, Ariel E.
TI Cell Death in Liver Disease and Liver Surgery
SO BIOMEDICINES
LA English
DT Review
DE cell death; pyroptosis; apoptosis; ferroptosis; cancer; liver surgery;
liver disease
ID ISCHEMIA-REPERFUSION INJURY; HEPATIC STELLATE CELLS; NLRP3 INFLAMMASOME;
APOPTOTIC CELLS; DANGER SIGNALS; NONALCOHOLIC STEATOHEPATITIS;
MITOCHONDRIAL DYSFUNCTION; ALCOHOLIC STEATOHEPATITIS; INACTIVATION
PROTECTS; KUPFFER CELLS
AB Cell death is crucial for maintaining tissue balance and responding to diseases. However, under pathological conditions, the surge in dying cells results in an overwhelming presence of cell debris and the release of danger signals. In the liver, this gives rise to hepatic inflammation and hepatocellular cell death, which are key factors in various liver diseases caused by viruses, toxins, metabolic issues, or autoimmune factors. Both clinical and in vivo studies strongly affirm that hepatocyte death serves as a catalyst in the progression of liver disease. This advancement is characterized by successive stages of inflammation, fibrosis, and cirrhosis, culminating in a higher risk of tumor development. In this review, we explore pivotal forms of cell death, including apoptosis, pyroptosis, and necroptosis, examining their roles in both acute and chronic liver conditions, including liver cancer. Furthermore, we discuss the significance of cell death in liver surgery and ischemia-reperfusion injury. Our objective is to illuminate the molecular mechanisms governing cell death in liver diseases, as this understanding is crucial for identifying therapeutic opportunities aimed at modulating cell death pathways.
C1 [Stoess, Christian; Choi, Yeon-Kyung; Feldstein, Ariel E.] Univ Calif San Diego, Dept Pediat Gastroenterol, 9500 Gilman Dr, La Jolla, CA 92093 USA.
[Stoess, Christian; Friess, Helmut; Hartmann, Daniel] Tech Univ Munich, TUM Sch Med, Dept Surg, Klinikum Rechts Der Isar, D-81675 Munich, Germany.
[Choi, Yeon-Kyung] Kyungpook Natl Univ, Chilgok Hosp, Sch Med, Dept Internal Med, Daegu 41404, South Korea.
[Onyuru, Janset; Hoffman, Hal M.] Univ Calif San Diego, Dept Pediat Allergy Immunol & Rheumatol, La Jolla, CA 92093 USA.
[Feldstein, Ariel E.] Novo Nord, Global Drug Discovery, Orestads Blvd 108, DK-2300 Copenhagen, Denmark.
C3 University of California System; University of California San Diego;
Technical University of Munich; Kyungpook National University (KNU);
University of California System; University of California San Diego;
Novo Nordisk
RP Feldstein, AE (corresponding author), Univ Calif San Diego, Dept Pediat Gastroenterol, 9500 Gilman Dr, La Jolla, CA 92093 USA.; Hartmann, D (corresponding author), Tech Univ Munich, TUM Sch Med, Dept Surg, Klinikum Rechts Der Isar, D-81675 Munich, Germany.; Feldstein, AE (corresponding author), Novo Nord, Global Drug Discovery, Orestads Blvd 108, DK-2300 Copenhagen, Denmark.
EM christian.stoess@tum.de; daniel.hartmann@tum.de;
afeldstein@health.ucsd.edu
RI Friess, Helmut/ABO-1348-2022; Stoess, Christian/HJZ-4129-2023
OI Hartmann, Daniel/0000-0003-4366-8986; Stoess,
Christian/0000-0002-0682-8808; Choi, Yeon-Kyung/0000-0003-0996-6437
FU National Institutes of Health
FX No Statement Available
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NR 266
TC 1
Z9 1
U1 3
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD MAR
PY 2024
VL 12
IS 3
AR 559
DI 10.3390/biomedicines12030559
PG 34
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA MC7T8
UT WOS:001191500700001
PM 38540172
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Sun, QQ
Dai, H
Wang, SL
Chen, YY
Shi, HL
AF Sun, Qianqian
Dai, Heng
Wang, Siliang
Chen, Yuanyuan
Shi, Huilian
TI Progress in research on the role played by myeloid-derived suppressor
cells in liver diseases
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Review
DE immunosuppression; immunotherapy; liver diseases; myeloid-derived
suppressor cells
ID HEPATOCELLULAR-CARCINOMA; PERIPHERAL-BLOOD; T-CELLS; NK CELLS;
HEPATITIS; RESPONSES; INHIBITION; BLOCKADE; IMMUNOSUPPRESSION;
DIFFERENTIATION
AB Myeloid-derived suppressor cells (MDSCs) refer to a group of immature myeloid cells with potent immunosuppressive capacity upon activation by pathological conditions. Because of their potent immunosuppressive ability, MDSCs have garnered extensive attention in the past few years in the fields of oncology, infection, chronic inflammation and autoimmune diseases. Research on MDSCs in liver diseases has gradually increased, and their potential therapeutic roles will be further explored. This review presents a summary of the involvement and the role played by MDSCs in liver diseases, thus identifying their potential targets for the treatment of liver diseases and providing new directions for liver disease-related research.
C1 [Sun, Qianqian; Dai, Heng] Nanjing Univ Chinese Med, Affiliated Hosp, Nanjing, Peoples R China.
[Wang, Siliang] Nanjing Univ, Nanjing Drum Tower Hosp, Affiliated Hosp, Med Sch,Dept Pharm, Nanjing, Peoples R China.
[Chen, Yuanyuan] Nanjing Med Univ, Dept Biochem & Mol Biol, Nanjing, Peoples R China.
[Shi, Huilian] Nanjing Univ Chinese Med, Jiangsu Prov Hosp Chinese Med, Affiliated Hosp, Dept Infect Dis, Nanjing, Peoples R China.
[Shi, Huilian] Nanjing Univ Chinese Med, Jiangsu Prov Hosp Chinese Med, Affiliated Hosp, Dept Infect Dis, 155 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
[Wang, Siliang] Nanjing Univ, Nanjing Drum Tower Hosp, Affiliated Hosp, Med Sch,Dept Pharm, 321 Zhongshan Rd, Nanjing 210008, Peoples R China.
[Chen, Yuanyuan] Nanjing Med Univ, Dept Biochem & Mol Biol, 101 Longmian Ave, Nanjing 211166, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University; Nanjing
Medical University; Nanjing University of Chinese Medicine; Nanjing
University of Chinese Medicine; Nanjing University; Nanjing Medical
University
RP Shi, HL (corresponding author), Nanjing Univ Chinese Med, Jiangsu Prov Hosp Chinese Med, Affiliated Hosp, Dept Infect Dis, 155 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.; Wang, SL (corresponding author), Nanjing Univ, Nanjing Drum Tower Hosp, Affiliated Hosp, Med Sch,Dept Pharm, 321 Zhongshan Rd, Nanjing 210008, Peoples R China.; Chen, YY (corresponding author), Nanjing Med Univ, Dept Biochem & Mol Biol, 101 Longmian Ave, Nanjing 211166, Jiangsu, Peoples R China.
EM wsl_dth@126.com; yuanyuanch@njmu.edu.cn; shihuilian820@163.com
RI Wang, Siliang/ABH-1536-2021; Sun, Qianqian/KVY-2334-2024
OI Wang, Siliang/0000-0003-1228-869X; Shi, Huilian/0000-0003-2437-2573
FU National Natural Science Foundation of China (NSFC) [31101011, 82070804,
81903974]; Natural Science Foundation of Jiangsu Province [BK20221421];
Open project of Nanjing Research Center for Infectious Diseases of
Integrated Traditional Chinese and Western Medicine [NCMIC-2022-01]
FX National Natural Science Foundation of China, Grant/Award Number:
31101011, 81903974 and 82070804; the Natural Science Foundation of
Jiangsu Province, Grant/Award Number: BK20221421; The Open Project of
Nanjing Research Center for infectious Diseases of Integrated
Traditional Chinese and Western Medicine, Grant/Award Number:
NCMIC-2022-01
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NR 100
TC 0
Z9 0
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD OCT
PY 2023
VL 98
IS 4
DI 10.1111/sji.13312
EA AUG 2023
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA R9ME4
UT WOS:001044197900001
PM 38441348
OA Bronze
DA 2025-01-07
ER
PT J
AU Patra, MC
Shah, M
Choi, S
AF Patra, Mahesh Chandra
Shah, Masaud
Choi, Sangdun
TI Toll-like receptor-induced cytokines as immunotherapeutic targets in
cancers and autoimmune diseases
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Autoimmune disease; Cancer; Cytokine; Innate immunity; Toll-like
receptor
ID TUMOR-NECROSIS-FACTOR; CHRONIC LYMPHOCYTIC-LEUKEMIA;
NATURAL-KILLER-CELLS; ANTIINTERFERON-MONOCLONAL-ANTIBODY;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; INNATE IMMUNE-RESPONSES; HUMAN
ENDOTHELIAL-CELLS; CD4(+) T-CELLS; RHEUMATOID-ARTHRITIS;
HEPATOCELLULAR-CARCINOMA
AB Immune cells of the myeloid and lymphoid lineages express Toll-like receptors (TLRs) to recognize pathogenic components or cellular debris and activate the immune system through the secretion of cytokines. Cytokines are signaling molecules that are structurally and functionally distinct from one another, although their secretion profiles and signaling cascades often overlap. This situation gives rise to pleiotropic cell-to-cell communication pathways essential for protection from infections as well as cancers. Nonetheless, deregulated signaling can have detrimental effects on the host, in the form of inflammatory or autoimmune diseases. Because cytokines are associated with numerous autoimmune and cancerous conditions, therapeutic strategies to modulate these molecules or their biological responses have been immensely beneficial over the years. There are still challenges in the regulation of cytokine function in patients, even in those who take approved biological therapeutics. In this review, our purpose is to discuss the differential expression patterns of TLR-regulated cytokines and their cell type specificity that is associated with cancers and immune-system-related diseases. In addition, we highlight key structural features and molecular recognition of cytokines by receptors; these data have facilitated the development and approval of several biologics for the treatment of autoimmune diseases and cancers.
C1 [Patra, Mahesh Chandra; Shah, Masaud; Choi, Sangdun] Ajou Univ, Dept Mol Sci & Technol, Suwon 16499, South Korea.
C3 Ajou University
RP Choi, S (corresponding author), Ajou Univ, Dept Mol Sci & Technol, Suwon 16499, South Korea.
EM sangdunchoi@ajou.ac.kr
RI Shah, Masaud/K-8748-2016; Patra, Mahesh/I-9746-2014
OI Shah, Masaud/0000-0002-6923-0010; Patra, Mahesh/0000-0003-0471-6236
FU Commercializations Promotion Agency for R&D Outcomes - Ministry of
Science and ICT [2018K000369]; National Research Foundation of Korea
[NRF-2019R1H1A2039674]
FX This work was supported by the Commercializations Promotion Agency for
R&D Outcomes funded by the Ministry of Science and ICT (2018K000369) and
the National Research Foundation of Korea (NRF-2019R1H1A2039674).
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NR 261
TC 52
Z9 57
U1 1
U2 33
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
EI 1096-3650
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD AUG
PY 2020
VL 64
SI SI
BP 61
EP 82
DI 10.1016/j.semcancer.2019.05.002
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LW8HT
UT WOS:000539384700008
PM 31054927
DA 2025-01-07
ER
PT J
AU Cheng, SX
Jiang, DW
Lan, XL
Liu, K
Fan, C
AF Cheng, Sixuan
Jiang, Dawei
Lan, Xiaoli
Liu, Kun
Fan, Cheng
TI Voltage-gated potassium channel 1.3: A promising molecular target in
multiple disease therapy
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Kv1.3 channel; Channel inhibitors; Autoimmune diseases;
Neuroinflammation; Cancer; Molecular imaging
ID KV1.3 CHANNEL; K+-CHANNEL; ION CHANNELS; K(V)1.3 CHANNELS;
CROHNS-DISEASE; LIVER-INJURY; T-CELLS; BLOCKER; INHIBITION; EXPRESSION
AB Voltage-gated potassium channel 1.3 (Kv1.3) has emerged as a pivotal player in numerous biological processes and pathological conditions, sparking considerable interest as a potential therapeutic target across various diseases. In this review, we present a comprehensive examination of Kv1.3 channels, highlighting their fundamental characteristics and recent advancements in utilizing Kv1.3 inhibitors for treating autoimmune disorders, neuroinflammation, and cancers. Notably, Kv1.3 is prominently expressed in immune cells and implicated in immune responses and inflammation associated with autoimmune diseases and chronic inflammatory conditions. Moreover, its aberrant expression in certain tumors underscores its role in cancer progression. While preclinical studies have demonstrated the efficacy of Kv1.3 inhibitors, their clinical translation remains pending. Molecular imaging techniques offer promising avenues for tracking Kv1.3 inhibitors and assessing their therapeutic efficacy, thereby facilitating their development and clinical application. Challenges and future directions in Kv1.3 inhibitor research are also discussed, emphasizing the significant potential of targeting Kv1.3 as a promising therapeutic strategy across a spectrum of diseases.
C1 [Cheng, Sixuan; Jiang, Dawei; Lan, Xiaoli] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Nucl Med, Wuhan 430022, Peoples R China.
[Cheng, Sixuan; Jiang, Dawei; Lan, Xiaoli] Hubei Key Lab Mol Imaging, Wuhan 430022, Peoples R China.
[Liu, Kun] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Cardiol, 1277 Jiefang Ave, Wuhan 430022, Peoples R China.
[Fan, Cheng] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Geriatr, 1277 Jiefang Ave, Wuhan 430022, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
Science & Technology; Huazhong University of Science & Technology
RP Liu, K (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Cardiol, 1277 Jiefang Ave, Wuhan 430022, Peoples R China.; Fan, C (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Geriatr, 1277 Jiefang Ave, Wuhan 430022, Peoples R China.
EM liukun@hust.edu.cn; kristyfan@hust.edu.cn
RI Li, xiaofei/GXF-7187-2022; Fan, Cheng/GXW-3204-2022; Jiang,
Dawei/J-6148-2019
OI Fan, Cheng/0000-0002-3440-3276
FU National Natural Science Foundation of China [82271621, 82070514,
22277031]; National Key Research and Development Program of China
[2022YFB3808200]; Key Project of Hubei Province Natural Science
Foundation [2021CFA008]
FX This work was supported by the National Natural Science Foundation of
China (Grant Number 82271621, 82070514, 22277031) , National Key
Research and Development Program of China (2022YFB3808200) and Key
Project of Hubei Province Natural Science Foundation (2021CFA008) .
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NR 138
TC 5
Z9 5
U1 3
U2 6
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD JUN
PY 2024
VL 175
AR 116651
DI 10.1016/j.biopha.2024.116651
EA APR 2024
PG 14
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA SW4P0
UT WOS:001237475100001
PM 38692062
OA gold
DA 2025-01-07
ER
PT J
AU Wu, L
Yang, LL
AF Wu, Lei
Yang, Lili
TI The function and mechanism of HMGB1 in lung cancer and its potential
therapeutic implications
SO ONCOLOGY LETTERS
LA English
DT Review
DE high-mobility group protein B1; lung cancer; proliferation; function
ID GLYCATION END-PRODUCTS; GROUP BOX-1 PROTEIN; BRONCHIAL EPITHELIAL-CELLS;
TOLL-LIKE RECEPTORS; BACTERIAL CPG-DNA; HEPATOCELLULAR-CARCINOMA;
INFLAMMATORY RESPONSES; ADENOCARCINOMA CELLS; REGULATES AUTOPHAGY;
SODIUM-SALICYLATE
AB As a non-histone chromatin-associated protein, high-mobility group box-1 (HMGB1) performs a pivotal function in various human diseases, including autoimmune diseases, neurodegenerative diseases and cancer. Overexpression of HMGB1 has been demonstrated in numerous types of cancer, including breast cancer, colorectal cancer, lung cancer and hepatocellular carcinoma. However, the underlying mechanism of HMGB1 function in lung cancer remains to be elucidated. The present study aimed to analyze, and summarize the role and mechanism of HMGB1 in lung cancer by retrieving available literature regarding HMGB1 in association with lung cancer. It provides comprehensive information on the association of HMGB1 with the carcinogenesis and progression of lung cancer, and discusses the molecular mechanism of these processes. HMGB1 may induce tumorigenesis, metastasis and chemotherapy resistance in lung cancer. Overall, it is evident that HMGB1 serves an important role in the development and progression of lung cancer, and this review warrants further investigation into HMGB1 as a novel target for cancer therapy.
C1 [Wu, Lei; Yang, Lili] Tianjin Med Univ, Tianjin Canc Inst & Hosp, Dept Immunol, Huanhuxi Rd, Tianjin 300060, Peoples R China.
[Wu, Lei; Yang, Lili] Tianjin Med Univ, Natl Clin Res Ctr Canc, Tianjin Canc Inst & Hosp, Tianjin 300060, Peoples R China.
[Wu, Lei; Yang, Lili] Tianjin Med Univ, Key Lab Canc Immunol & Biotherapy, Tianjin Canc Inst & Hosp, Tianjin 300060, Peoples R China.
C3 Tianjin Medical University; Tianjin Medical University; Tianjin Medical
University
RP Yang, LL (corresponding author), Tianjin Med Univ, Tianjin Canc Inst & Hosp, Dept Immunol, Huanhuxi Rd, Tianjin 300060, Peoples R China.
EM yanglili@tjmuch.com
FU National Key Technology RD Program [2015BAI12B12]; Key Projects of
Tianjin Health Industry [15KG145]; National Natural Science Foundation
of China [81572265, 31500736]
FX The present study was supported by the National Key Technology R&D
Program (grant no. 2015BAI12B12), Key Projects of Tianjin Health
Industry (grant no. 15KG145) and the National Natural Science Foundation
of China (grant no. 81572265 and 31500736).
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NR 90
TC 57
Z9 62
U1 2
U2 17
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD MAY
PY 2018
VL 15
IS 5
BP 6799
EP 6805
DI 10.3892/ol.2018.8215
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GF3DN
UT WOS:000431825900094
PM 29725415
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wingren, C
AF Wingren, Christer
TI Novel type of protein chip for multiplex detection of autoantibodies
SO EXPERT REVIEW OF PROTEOMICS
LA English
DT Review
DE biomarker discovery; denatured probes; immobilization; oligo-cysteine
tag; protein array; protein chip
ID TUMOR-ASSOCIATED ANTIGENS; HEPATOCELLULAR-CARCINOMA; ANTIBODY
MICROARRAYS; IMMOBILIZATION; BIOMARKERS
AB Evaluation of: Akada J, Kamei S, Ito A et al. A new type of protein chip to detect hepatocellular carcinoma-related autoimmune antibodies in the sera of hepatitis C virus-positive patients. Proteome Sci. 11(1), 33 (2013). Unlocking the proteome and delivering biomarkers to the clinic will be critical for early and improved diagnosis and prognosis. Conventional protein microarrays have evolved as a promising proteomic technology with great potential for protein expression profiling in health and disease. In this study, Akada et al. explore a new type of protein chip, interfaced with a dual-color fluorescence-based read-out, for screening of autoantibodies in serum. Uniquely, the recombinant antigens were microarray adapted by molecular design to contain a five-cysteine tag for immobilization and green fluorescent protein for detection (color 1). The engineered antigens were immobilized on in-house-designed maleimide-incorporated diamond-like carbon substrates and subsequently heat treated in a solution of denaturing and reducing agents before any specifically bound serum autoantibodies were detected (color 2). The authors used a 4-plex array targeting hepatocellular carcinoma-related autoantibodies in the sera of hepatitis C virus-positive patients as model system to demonstrate proof-of-concept.
C1 Lund Univ, Dept Immunotechnol, SE-22381 Lund, Sweden.
C3 Lund University
RP Wingren, C (corresponding author), Lund Univ, Dept Immunotechnol, SE-22381 Lund, Sweden.
EM christer.wingren@immun.lth.se
FU Greta and Johan Kock Foundation; Swedish National Research Council
(VR-NT); Swedish National Research Council (VR-M); SSF - the foundation
of Strategic Research (Strategic Center for Translational Cancer
Research - CREATE Health); Vinnova
FX The author is a co-founder of a small startup biotechnology company that
uses antibody-based microarrays for detecting disease-associated
biomarkers. The author was supported by grants from Greta and Johan Kock
Foundation, the Swedish National Research Council (VR-NT and VR-M), SSF
- the foundation of Strategic Research (Strategic Center for
Translational Cancer Research - CREATE Health) and Vinnova. The author
has no other relevant affiliations or financial involvement with any
organization or entity with a financial interest in or financial
conflict with the subject matter or materials discussed in the
manuscript apart from those disclosed.
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NR 20
TC 0
Z9 0
U1 0
U2 24
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1478-9450
EI 1744-8387
J9 EXPERT REV PROTEOMIC
JI Expert Rev. Proteomics
PD OCT
PY 2013
VL 10
IS 5
BP 417
EP 420
DI 10.1586/14789450.2013.842900
PG 4
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 301LW
UT WOS:000330534800008
PM 24088012
DA 2025-01-07
ER
PT J
AU Zimmermann, T
Hoppe-Lotichius, M
Tripkovic, V
Barreiros, AP
Wehler, TC
Zimmermann, A
Schattenberg, JM
Heise, M
Biesterfeld, S
Galle, PR
Otto, G
Schuchmann, M
AF Zimmermann, Tim
Hoppe-Lotichius, Maria
Tripkovic, Vuk
Barreiros, Ana P.
Wehler, Thomas C.
Zimmermann, Anca
Schattenberg, Jorn M.
Heise, Michael
Biesterfeld, Stefan
Galle, Peter R.
Otto, Gerd
Schuchmann, Marcus
TI Liver transplanted patients with preoperative autoimmune hepatitis and
immunological disorders are at increased risk for Post-Transplant
Lymphoproliferative Disease (PTLD)
SO EUROPEAN JOURNAL OF INTERNAL MEDICINE
LA English
DT Article
DE Liver transplantation; Autoimmune liver disease; Immunological disorder;
Preoperative immunosuppression; PTLD
ID SOLID-ORGAN TRANSPLANTATION; NON-HODGKINS-LYMPHOMA; EPSTEIN-BARR-VIRUS;
CANCER; ASSOCIATION; RECIPIENTS; THERAPY; ADULTS
AB Background: Long term immunosuppression and therapy of acute rejections result in a 20-120-fold increased risk to develop Non Hodgkin lymphoma (NHL). Since immunosuppressive therapy and immunological disorders are major risk factors for the development of NHL in the non-transplant population we aimed to analyze risk factors for PTLD in our cohort of liver transplanted (LT) patients.
Methods: We analyzed retrospectively 431 patients liver transplanted between 1998 and 2008.
Results: PTLD was diagnosed in eleven of 431 patients (2.6%). PTLD, especially late PTLD, was significantly more frequent in patients who received steroids before LT (Kaplan-Meier: p<0.001). Moreover PTLD in immunocompromised patients with preoperative steroid treatment occurred at a significantly younger age (49.5 +/- 4.7 years) compared to patients without steroids (60.6 +/- 5.1 years; p = 0.006). Multivariate analysis revealed pretransplant steroid treatment and liver transplantation for autoimmune hepatitis as main risk factors for the development of PTLD after liver transplantation (p<0.001).
Conclusion: Liver transplanted patients who received steroids before LT due to immunological disorders and patients with autoimmune hepatitis seem to be at particular high risk to develop PTLD. Prospective cohort studies including immunoepidemiologic investigations of abnormalities of cellular, humoral and innate immunity should be carried out to identify predictive factors and patients at risk. (C) 2010 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
C1 [Zimmermann, Tim; Tripkovic, Vuk; Barreiros, Ana P.; Zimmermann, Anca; Schattenberg, Jorn M.; Galle, Peter R.; Schuchmann, Marcus] Johannes Gutenberg Univ Mainz, Dept Med 1, D-55101 Mainz, Germany.
[Hoppe-Lotichius, Maria; Heise, Michael; Otto, Gerd] Johannes Gutenberg Univ Mainz, Dept Transplantat Surg, D-55101 Mainz, Germany.
[Wehler, Thomas C.] Johannes Gutenberg Univ Mainz, Dept Med 3, D-55101 Mainz, Germany.
[Biesterfeld, Stefan] Johannes Gutenberg Univ Mainz, Inst Pathol, D-55101 Mainz, Germany.
C3 Johannes Gutenberg University of Mainz; Johannes Gutenberg University of
Mainz; Johannes Gutenberg University of Mainz; Johannes Gutenberg
University of Mainz
RP Schuchmann, M (corresponding author), Johannes Gutenberg Univ Mainz, Dept Med 1, Langenbeck Str 1, D-55101 Mainz, Germany.
EM schuchmann@1-med.klinik.uni-mainz.de
RI Galle, Peter/ABE-2872-2021; Wehler, Thomas/AAY-6362-2020; Schattenberg,
Jörn/C-1301-2013
OI Galle, Peter Robert/0000-0001-8294-0992; Schattenberg, Jorn
M./0000-0002-4224-4703
CR Aucejo F, 2006, J HEPATOL, V44, P19, DOI 10.1016/j.jhep.2005.10.008
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NR 30
TC 20
Z9 20
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0953-6205
EI 1879-0828
J9 EUR J INTERN MED
JI Eur. J. Intern. Med.
PD JUN
PY 2010
VL 21
IS 3
BP 208
EP 215
DI 10.1016/j.ejim.2010.02.009
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 622MP
UT WOS:000279668200015
PM 20493424
DA 2025-01-07
ER
PT J
AU Zhao, YP
Liu, RR
Li, MM
Liu, PF
AF Zhao, Yaping
Liu, Rongrong
Li, Miaomiao
Liu, Pengfei
TI The spleen tyrosine kinase (SYK): A crucial therapeutic target for
diverse liver diseases
SO HELIYON
LA English
DT Review
DE Spleen tyrosine kinase (SYK); Liver diseases; Small molecule inhibitor;
Therapy target
ID HEPATOCELLULAR-CARCINOMA; AMELIORATES INFLAMMATION; MYELOID CELLS;
INHIBITION; RECEPTOR; ACTIVATION; EXPRESSION; MACROPHAGE; STEATOSIS;
DISCOVERY
AB Spleen tyrosine kinase (SYK) is an enigmatic protein tyrosine kinase, and involved in signal transduction related with lots of cellular processes. It's highly expressed in the cells of hematopoietic origin and acts as an important therapeutic target in the treatment of autoimmune diseases and allergic disorders. In recent years, more and more evidences indicate that SYK is expressed in non-hematopoietic cells and effectively regulates various non-immune biological responses as well. In this review, we mainly summary the role of SYK in different liver diseases. Robust SYK expression has been discovered in hepatocytes, hepatic stellate cells, as well as Kupffer cells, which participates in the regulation of numerous signal transduction in various liver diseases (e.g. hepatitis, liver fibrosis and hepatocellular carcinoma). In addition, the blockage of SYK activity using small molecule modulators is considered as a significant therapeutic strategy against liver diseases, and both hepatic SYK and non-hepatic SYK could become highly promising therapeutic targets. Totally, even though some critical points about the significance of SYK in liver diseases treatment still need further elaboration, more reliable biotechnical or pharmacological therapy modes will be established based on the better understanding of the relationship between SYK and liver diseases.
C1 [Zhao, Yaping; Liu, Rongrong; Li, Miaomiao; Liu, Pengfei] Xi An Jiao Tong Univ, Affiliated Hosp 2, Natl & Local Joint Engn Res Ctr Biodiag & Biothera, Xian, Peoples R China.
[Zhao, Yaping; Liu, Rongrong; Li, Miaomiao; Liu, Pengfei] Xi An Jiao Tong Univ, Affiliated Hosp 2, Int Joint Res Ctr Cell Stress & Dis Diag & Therapy, Xian, Peoples R China.
[Zhao, Yaping; Liu, Rongrong] Xi An Jiao Tong Univ, Affiliated Hosp 2, Shaanxi Prov Clin Res Ctr Hepat & Splen Dis, Xian, Peoples R China.
[Liu, Pengfei] Jilin Univ, Sch Pharmaceut Sci, Dept Regenerat Med, Changchun, Peoples R China.
[Liu, Pengfei] Xi An Jiao Tong Univ, Key Lab Environm & Genes Related Dis, Minist Educ China, Xian, Peoples R China.
C3 Xi'an Jiaotong University; Xi'an Jiaotong University; Xi'an Jiaotong
University; Jilin University; Xi'an Jiaotong University
RP Liu, PF (corresponding author), Xi An Jiao Tong Univ, Affiliated Hosp 2, Natl & Local Joint Engn Res Ctr Biodiag & Biothera, Xian, Peoples R China.; Liu, PF (corresponding author), Xi An Jiao Tong Univ, Affiliated Hosp 2, Int Joint Res Ctr Cell Stress & Dis Diag & Therapy, Xian, Peoples R China.; Liu, PF (corresponding author), Jilin Univ, Sch Pharmaceut Sci, Dept Regenerat Med, Changchun, Peoples R China.; Liu, PF (corresponding author), Xi An Jiao Tong Univ, Key Lab Environm & Genes Related Dis, Minist Educ China, Xian, Peoples R China.
EM liupengfei@xjtu.edu.cn
RI Liu, Pengfei/LTF-3543-2024
OI Liu, Pengfei/0000-0003-0172-189X
FU "The Young Talent Support Plan" of Xi'an Jiaotong University; National
Natural Science Foundation of China [31900547]; Introducing overseas
high-level talent intelligence projects of Xi'an City
[2022JH-GCRC-0063]; Medical "Base-Clinic" Integrated Innovation Project
of Xi'an Jiaotong University
FX This study was supported by "The Young Talent Support Plan" of Xi'an
Jiaotong University (For P. Liu), National Natural Science Foundation of
China (31900547), Introducing overseas high-level talent intelligence
projects of Xi'an City (2022JH-GCRC-0063) and Medical "Base-Clinic"
Integrated Innovation Project of Xi'an Jiaotong University.
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NR 71
TC 4
Z9 4
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD DEC
PY 2022
VL 8
IS 12
AR e12130
DI 10.1016/j.heliyon.2022.e12130
EA DEC 2022
PG 7
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 7L7CX
UT WOS:000906120000017
PM 36568669
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Kumar, S
Diamond, T
AF Kumar, S.
Diamond, T.
TI Paraneoplastic syndrome - a rare but treatable cause of
non-thyroid-related extraocular muscle enlargement
SO ORBIT-THE INTERNATIONAL JOURNAL ON ORBITAL DISORDERS-OCULOPLASTIC AND
LACRIMAL SURGERY
LA English
DT Article
DE Thyroid; orbitopathy; extraocular muscle; cancer; paraneoplastic
syndrome
ID DISTANT METASTASES; CLINICAL-VALUE; BREAST; CARCINOMA; EXOPHTHALMOS;
DIAGNOSIS; SEMINOMA; TUMORS; LUNG; CEA
AB Paraneoplastic syndrome is a rare but reversible cause of non-thyroid-related extraocular muscle enlargement. We present a 71-year-old lady with diplopia, restricted eye movements, suppressed thyroid-stimulating hormone and enlargement of all extraocular muscles while on thyroxine replacement for hypothyroidism. She had distant history of metastatic breast cancer treated with chemotherapy, surgical resection and tamoxifen. She had negative anti-thyroid autoantibodies and thyroid ultrasound was not consistent with autoimmune thyroid disease. Carcinoembryonic antigen and cancer antigens 15-3, 125 and 72-4 were elevated, and whole-body positron emission tomography-computed tomography showed avid liver, left adrenal and skeletal lesions, with liver biopsy confirming breast cancer recurrence. She received prednisone and chemotherapy (letrozole, palbociclib) and achieved normalisation of eye movements and reduction in her EOME at 9-month follow-up. Our case highlights the importance of exploring paraneoplastic syndrome as a treatable cause of EOME in a patient lacking features of thyroid orbitopathy and autoimmune thyroid disease.
C1 [Kumar, S.] UNSW, St George Publ Hosp, Kogarah, NSW, Australia.
[Diamond, T.] St George Publ Hosp, Endocrinol, Kogarah, NSW, Australia.
C3 St George Hospital; University of New South Wales Sydney; St George
Hospital
RP Kumar, S (corresponding author), UNSW, St George Publ Hosp, 106 Boundary Rd, Sydney, NSW 2223, Australia.
EM shejil_kumar@hotmail.com
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NR 25
TC 1
Z9 1
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0167-6830
EI 1744-5108
J9 ORBIT-ABINGDON
JI Orbit
PY 2019
VL 38
IS 6
BP 468
EP 473
DI 10.1080/01676830.2018.1550790
PG 6
WC Ophthalmology
WE Emerging Sources Citation Index (ESCI)
SC Ophthalmology
GA JD1JH
UT WOS:000489730500006
PM 30523726
DA 2025-01-07
ER
PT J
AU Lanfranca, MP
Lin, YW
Fang, JY
Zou, WP
Frankel, T
AF Lanfranca, Mirna Perusina
Lin, Yanwei
Fang, Jingyuan
Zou, Weiping
Frankel, Timothy
TI Biological and pathological activities of interleukin-22
SO JOURNAL OF MOLECULAR MEDICINE-JMM
LA English
DT Review
DE IL-22; Th22; ILC22; Cancer; Tcell; Cancer; Autoimmune; Infection;
IL-22R; IL-22BP
ID INNATE LYMPHOID-CELLS; DELTA T-CELLS; INTESTINAL EPITHELIAL-CELLS;
ARYL-HYDROCARBON RECEPTOR; HEPATITIS-B-VIRUS; ROR-GAMMA-T; CONVENTIONAL
NK CELLS; BINDING-PROTEIN; HEPATOCELLULAR-CARCINOMA; INDUCIBLE FACTOR
AB Interleukin (IL)-22, a member of the IL-10 family, is a cytokine secreted by several types of immune cells including IL-22(+)CD4(+) T cells (Th22) and IL-22 expressing innate leukocytes (ILC22). Recent studies have demonstrated that IL-22 is a key component in mucosal barrier defense, tissue repair, epithelial cell survival, and proliferation. Furthermore, accumulating evidence has defined both protective and pathogenic properties of IL-22 in a number of conditions including autoimmune disease, infection, and malignancy. In this review, we summarize the expression and signaling pathway and functional characteristics of the IL-22 and IL-22 receptor axis in physiological and pathological scenarios and discuss the potential to target IL-22 signaling to treat human diseases.
C1 [Lanfranca, Mirna Perusina; Lin, Yanwei; Zou, Weiping; Frankel, Timothy] Univ Michigan, Sch Med, Dept Surg, 109 Zina Pitcher Pl, Ann Arbor, MI 48109 USA.
[Lin, Yanwei; Fang, Jingyuan] Shanghai Jiao Tong Univ, Sch Med, Div Gastroenterol & Hepatol, Renji Hosp, Shanghai 200001, Peoples R China.
[Zou, Weiping; Frankel, Timothy] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Zou, Weiping] Univ Michigan, Grad Programs Immunol & Tumor Biol, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan; Shanghai Jiao
Tong University; University of Michigan System; University of Michigan;
University of Michigan System; University of Michigan
RP Zou, WP (corresponding author), Univ Michigan, Sch Med, Dept Surg, 109 Zina Pitcher Pl, Ann Arbor, MI 48109 USA.; Zou, WP; Frankel, T (corresponding author), Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.; Zou, WP (corresponding author), Univ Michigan, Grad Programs Immunol & Tumor Biol, Ann Arbor, MI 48109 USA.
EM wzou@med.umich.edu; timofran@med.umich.edu
RI FANG, Jing-Yuan/JOZ-1388-2023
OI Frankel, Timothy/0000-0001-5987-0404; Perusina Lanfranca,
Mirna/0000-0002-3845-2585
FU NCI NIH HHS [R01 CA193136, R01 CA190176, R01 CA171306, R01 CA152470]
Funding Source: Medline
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NR 182
TC 100
Z9 109
U1 1
U2 32
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0946-2716
EI 1432-1440
J9 J MOL MED
JI J. Mol. Med.
PD MAY
PY 2016
VL 94
IS 5
BP 523
EP 534
DI 10.1007/s00109-016-1391-6
PG 12
WC Genetics & Heredity; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Research & Experimental Medicine
GA DL5ZG
UT WOS:000375715200005
PM 26923718
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Agmon-Levin, N
Kopilov, R
Selmi, C
Nussinovitch, U
Sánchez-Castañón, M
López-Hoyos, M
Amital, H
Kivity, S
Gershwin, EM
Shoenfeld, Y
AF Agmon-Levin, Nancy
Kopilov, Ron
Selmi, Carlo
Nussinovitch, Udi
Sanchez-Castanon, Maria
Lopez-Hoyos, Marcos
Amital, Howie
Kivity, Shaye
Gershwin, Eric M.
Shoenfeld, Yehuda
TI Vitamin D in primary biliary cirrhosis, a plausible marker of advanced
disease
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Vitamin D; PBC (primary biliary cirrhosis); Autoimmunity;
Autoantibodies; Liver
ID MUSCULOSKELETAL HEALTH; CARDIOVASCULAR-DISEASE; BIOCHEMICAL RESPONSE;
BONE-DISEASE; RISK-FACTORS; RECOMMENDATIONS; AUTOIMMUNITY; ENVIRONMENT;
PREDICTION; CANCER
AB Vitamin D immune-modulating effects were extensively studied, and low levels have been linked with autoimmune diseases. The associations of vitamin D with autoimmune diseases of the liver, and particularly primary biliary cirrhosis (PBC), are yet to be defined. Hence, in this study, serum levels of vitamin D were determined in 79 patients with PBC and 70 age- and sex-matched controls by the LIAISON chemiluminescent immunoassays (DiaSorin-Italy). Clinical and serological parameters of patients were analyzed with respect to vitamin D status. Mean levels of vitamin D were significantly lower among patients with PBC compared with controls (16.8 +/- A 9 vs. 22.1 +/- A 9 ng/ml; p = 0.029), and vitamin D deficiency (a parts per thousand currency sign10 ng/ml) was documented in 33 % of patients with PBC versus 7 % of controls (p < 0.0001). Vitamin D levels inversely correlated with advanced liver damage and the presence of concomitant autoimmune diseases. In contrast, higher levels of vitamin D were observed among patients with PBC treated with ursodeoxycholic acid (UDCA). In conclusion, low vitamin D levels are common among patients with PBC and correlate with advanced disease, lack of UDCA therapy and autoimmune comorbidity. This alludes to the plausible roles of vitamin D as a prognostic marker of PBC severity, and as a potential player in this disease pathogenesis. While further studies are awaited, monitoring vitamin D in patients with PBC and use of supplements may be advisable.
C1 [Agmon-Levin, Nancy; Kopilov, Ron; Nussinovitch, Udi; Amital, Howie; Kivity, Shaye; Shoenfeld, Yehuda] Chaim Sheba Med Ctr, Zabludowicz Ctr Autoimmune Dis, IL-52621 Tel Hashomer, Israel.
[Agmon-Levin, Nancy; Amital, Howie; Kivity, Shaye] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel.
[Selmi, Carlo] Humanitas Clin & Res Ctr, Div Rheumatol & Clin Immunol, Milan, Italy.
[Selmi, Carlo; Gershwin, Eric M.] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Nussinovitch, Udi] Technion Israel Inst Technol, Bruce Rappaport Fac Med, IL-31096 Haifa, Israel.
[Sanchez-Castanon, Maria; Lopez-Hoyos, Marcos] Hosp Univ Marques de Valdecilla IDIVAL, Serv Inmunol, Santander 39008, Spain.
[Amital, Howie] Chaim Sheba Med Ctr, Dept Internal Med B, IL-52621 Tel Hashomer, Israel.
[Kivity, Shaye] Chaim Sheba Med Ctr, Dr Pinchas Borenstein Talpiot Med Leadership Prog, IL-52621 Tel Hashomer, Israel.
[Shoenfeld, Yehuda] Tel Aviv Univ, Incumbent Laura Schwarz Kipp Chair Res Autoimmune, IL-69978 Tel Aviv, Israel.
C3 Chaim Sheba Medical Center; Tel Aviv University; University of
California System; University of California Davis; Technion Israel
Institute of Technology; Rappaport Faculty of Medicine; Hospital
Universitario Marques de Valdecilla (HUMV); Chaim Sheba Medical Center;
Chaim Sheba Medical Center; Tel Aviv University
RP Shoenfeld, Y (corresponding author), Chaim Sheba Med Ctr, Zabludowicz Ctr Autoimmune Dis, IL-52621 Tel Hashomer, Israel.
EM shoenfel@post.tau.ac.il
RI López-Hoyos, Marcos/ABC-1024-2020; Schoenfeld, Yehuda/I-1525-2016;
Selmi, Carlo/ABG-4899-2021
OI SANCHEZ CASTANON, MARIA/0009-0006-0740-1837; Lopez-Hoyos,
Marcos/0000-0003-0562-427X
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NR 40
TC 45
Z9 50
U1 0
U2 9
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD FEB
PY 2015
VL 61
IS 1-2
SI SI
BP 141
EP 146
DI 10.1007/s12026-014-8594-0
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CA6FK
UT WOS:000349004900021
PM 25424577
DA 2025-01-07
ER
PT J
AU Karatas, A
Küçük, OG
Aytaç, E
Hamzaoglu, I
AF Karatas, Adem
Kucuk, Ozan Gultekin
Aytac, Erman
Hamzaoglu, Ismail
TI Recurrent bleeding of parastomal varices: Case report
SO TURKISH JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune hepatitis; parastomal varices; bleeding; cyanoacrylate;
polidocanol
ID STOMAL VARICES; PORTOSYSTEMIC SHUNT; PERISTOMAL VARICES; SCLEROTHERAPY;
EMBOLIZATION; HEMORRHAGE; INJECTION; GLUE
AB Bleeding of parastomal varices is an unusual complication of portal hypertension. We report a case with recurrent parastomal variceal bleeding who had chronic liver disease secondary to autoimmune hepatitis and who had undergone abdominoperineal resection for rectal cancer. She presented four episodes of parastomal variceal bleeding in one month and was successfully treated with combined polidocanol and cyanoactylate glue.
C1 [Karatas, Adem; Kucuk, Ozan Gultekin; Aytac, Erman; Hamzaoglu, Ismail] Istanbul Univ, Cerrahpasa Med Fac, Dept Gen Surg, Istanbul, Turkey.
C3 Istanbul University - Cerrahpasa; Istanbul University
RP Aytaç, E (corresponding author), Istanbul Univ, Cerrahpasa Med Fac, Dept Gen Surg, Istanbul, Turkey.
EM eaytactr@yahoo.com
RI Kucuk, Gultekin Ozan/ABH-2997-2021; Aytac, Erman/T-7533-2017
OI Aytac, Erman/0000-0002-8803-0874; Kucuk, Gultekin
Ozan/0000-0002-6415-0900
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NR 15
TC 1
Z9 1
U1 0
U2 0
PU AVES
PI SISLI
PA BUYUKDERE CAD 105-9, MECIDIYEKOY, SISLI, ISTANBUL 34394, TURKEY
SN 1300-4948
EI 2148-5607
J9 TURK J GASTROENTEROL
JI Turk. J. Gastroenterol.
PD JUN
PY 2011
VL 22
IS 3
BP 329
EP 332
DI 10.4318/tjg.2011.0221
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 801JH
UT WOS:000293434100015
PM 21805411
DA 2025-01-07
ER
PT J
AU Herreros-Villanueva, M
Hijona, E
Cosme, A
Bujanda, L
AF Herreros-Villanueva, Marta
Hijona, Elizabeth
Cosme, Angel
Bujanda, Luis
TI Spontaneous regression of pancreatic cancer: Real or a misdiagnosis?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune pancreatitis; Insulinoma; Pancreatic cancer; Pancreatic
ductal adenocarcinoma; Spontaneous regression
ID SOLID-PSEUDOPAPILLARY TUMOR; RENAL-CELL CARCINOMA; HUMAN-MELANOMA CELLS;
LONG-TERM SURVIVAL; AUTOIMMUNE PANCREATITIS; HEPATOCELLULAR-CARCINOMA;
SPONTANEOUS REMISSION; FUNCTIONING INSULINOMA; DIAGNOSTIC-CRITERIA;
TELOMERASE ACTIVITY
AB Spontaneous tumor regression has been subject of numerous studies and speculations for many years. This phenomenon is exceptional, but well reported, in some types of tumors, but not in pancreatic cancer. Pancreatic cancer has the worst five-year survival rate of any cancer. Despite numerous molecular studies and clinical approaches, using several mouse models, this cancer responds poorly to the existing chemotherapeutic agents and progress on treatment remains elusive. Although pancreatic cancer tumors seldom undergo spontaneous regression, and some authors take that with skepticism, there are some cases reported in the literature. However, the variability in the description of the reports and technical details could make this process susceptible to misdiagnosis. Distinguishing between different types of pancreatic carcinoma should be taken with caution as they have wide differences in malignant potential. Diseases such as pancreatic benign tumors, insulinomas, or autoimmune pancreatitis could be responsible for this misdiagnosis as a pancreatic cancer. Here we review different cases reported, their clinical characteristics, and possible mechanisms leading to spontaneous regression of pancreatic cancer. We also discuss the possibilities of misdiagnosis. (C) 2012 Baishideng. All rights reserved.
C1 [Hijona, Elizabeth; Cosme, Angel; Bujanda, Luis] Univ Basque Country, Dept Gastroenterol, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Donostia Hosp,Biodonostia Inst, San Sebastian 20014, Spain.
[Herreros-Villanueva, Marta] Mayo Clin, Schulze Ctr Novel Therapeut, Div Oncol Res, Dept Med, Rochester, MN 55905 USA.
C3 University Hospital Donostia; University of Basque Country; CIBER -
Centro de Investigacion Biomedica en Red; CIBEREHD; Instituto de
Investigacion Sanitaria Biogipuzkoa; Mayo Clinic
RP Bujanda, L (corresponding author), Univ Basque Country, Dept Gastroenterol, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Donostia Hosp,Biodonostia Inst, Paseo Dr Beguiristain S-N, San Sebastian 20014, Spain.
EM luis.bujanda@osakidetza.net
RI , Herreros-Villanueva/M-5702-2016; Bujanda, Luis/AAB-2485-2021
OI Bujanda, Luis/0000-0002-4353-9968
FU Instituto Salud Carlos III
FX Supported by Instituto Salud Carlos III
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NR 74
TC 11
Z9 12
U1 0
U2 11
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUN 21
PY 2012
VL 18
IS 23
BP 2902
EP 2908
DI 10.3748/wjg.v18.i23.2902
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 012BR
UT WOS:000309210900003
PM 22736913
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Ramos-Casals, M
Trejo, O
García-Carrasco, M
Cervera, R
De la Red, G
Gil, V
López-Guillermo, A
Ingelmo, M
Font, J
AF Ramos-Casals, M
Trejo, O
García-Carrasco, M
Cervera, R
De la Red, G
Gil, V
López-Guillermo, A
Ingelmo, M
Font, J
TI Triple association between hepatitis C virus infection, systemic
autoimmune diseases, and B cell lymphoma
SO JOURNAL OF RHEUMATOLOGY
LA English
DT Article
DE cryoglobulinemia; B cell lymphoma; systemic lupus erythematosus;
Sjogren's syndrome; hepatitis C virus; polyarteritis nodosa
ID NON-HODGKINS-LYMPHOMAS; SJOGRENS-SYNDROME; LYMPHOPROLIFERATIVE DISEASES;
MIXED CRYOGLOBULINEMIA; CRITERIA; CLASSIFICATION; PREVALENCE; FRANCE;
LIVER
AB Objective. To analyze the clinical characteristics of patients from a Department of Autoimmune Diseases presenting chronic hepatitis C virus (HCV) infection, systemic autoimmune disease, and B cell lymphoma.
Methods. We analyzed the records of 100 consecutive patients with systemic autoimmune diseases and associated HCV infection seen in our department between 1994 and 2000. We retrospectively investigated the development of B cell malignancies after the diagnosis of HCV related autoimmune disease.
Results. Six patients with HCV related systemic autoimmune disease presented B cell non-Hodgkin's lymphoma (NHL). These patients fulfilled the diagnostic criteria for Sjogren's syndrome (n = 4) and polyarteritis nodosa (PAN; n = 2). Four patients were female and 2 male, with a mean age at lymphoma diagnosis of 62 years (range 45-78). The main immunologic markers were hypocomplementemia in all patients and cryoglobulinemia in 5 (83%). Primary extranodal localization of lymphoma was observed in 3 (50%) patients: prostate (n = 1), liver and ovary (n = 1), and ocular annexa (n = 1). Clinically, NHL was classified as indolent lymphoma in 3 patients and aggressive lymphoma in 3. NHL histologic types were diffuse large cell lymphoma (n = 4), extranodal marginal zone B cell lymphoma (n = 1), MALT lymphoma (n = 1), and lymphoplasmacytic lymphoma (n = 1).
Conclusion. We describe 6 patients with a triple association of HCV infection, systemic autoimmune disease, and NHL. Characteristics of these patients included a high prevalence of cryoglobulinemia (that clearly contributes to fulfilment of diagnostic criteria for PAN) and an elevated frequency of primary extranodal involvement. We recommend careful evaluation of patients with B cell NHL to detect silent autoimmune or chronic viral diseases. This triple association reinforces the suspected links between autoimmunity, infection, and cancer.
C1 Univ Barcelona, Hosp Clin, Serv Malalties Autoimmunes, Dept Autoimmuno Dis,IDIBAPS, E-08036 Barcelona, Spain.
Univ Barcelona, Hosp Clin, Serv Malalties Autoimmunes, Dept Hematol,IDIBAPS, E-08036 Barcelona, Spain.
Univ Barcelona, Barcelona, Spain.
Benemerita Univ Autonoma Puebla, Rheumatol Unit, Puebla, Mexico.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS;
University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS;
University of Barcelona; Benemerita Universidad Autonoma de Puebla
RP Univ Barcelona, Hosp Clin, Serv Malalties Autoimmunes, Dept Autoimmuno Dis,IDIBAPS, C Villarroel 170, E-08036 Barcelona, Spain.
EM mramos@clinic.ub.es
RI Ramos-Casals, Manuel/IUQ-6082-2023; Lopez-Guillermo,
Armando/Z-5684-2019; Carrasco, Mario/AAU-5477-2021
OI Trejo Gutierrez, Olga/0000-0002-7482-0584; Ramos-Casals,
Manuel/0000-0001-5709-6734
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NR 35
TC 49
Z9 55
U1 0
U2 4
PU J RHEUMATOL PUBL CO
PI TORONTO
PA 365 BLOOR ST E, STE 901, TORONTO, ONTARIO M4W 3L4, CANADA
SN 0315-162X
EI 1499-2752
J9 J RHEUMATOL
JI J. Rheumatol.
PD MAR
PY 2004
VL 31
IS 3
BP 495
EP 499
PG 5
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 802FF
UT WOS:000220148700016
PM 14994393
DA 2025-01-07
ER
PT J
AU Sahu, R
Goswami, S
Sastry, GN
Rawal, RK
AF Sahu, Rakesh
Goswami, Sourav
Narahari Sastry, G.
Rawal, Ravindra K.
TI The Preventive and Therapeutic Potential of the Flavonoids in Liver
Cirrhosis: Current and Future Perspectives
SO CHEMISTRY & BIODIVERSITY
LA English
DT Review
DE liver cirrhosis; NAFLD; flavonoid; ECM; PDGF; HSCs
ID HEPATIC STELLATE CELL; NF-KAPPA-B; TNF-ALPHA; DOWN-REGULATION; KUPFFER
CELLS; NONALCOHOLIC STEATOHEPATITIS; ANTIFIBROTIC ACTIVITY; HEPATOCYTE
APOPTOSIS; DIETARY FLAVONOIDS; NATURAL-HISTORY
AB Non-alcoholic fatty liver disease (NAFLD) may vary from moderately mild non-alcohol fatty liver (NAFL) towards the malignant variant known as non-alcoholic steatohepatitis (NASH), which is marked by fatty liver inflammation and may progress to liver cirrhosis (LC), liver cancer, fibrosis, or liver failure. Flavonoids can protect the liver from toxins through their anti-inflammatory, antioxidant, anti-cancer, and antifibrogenic pharmacological activities. Furthermore, flavonoids protect against LC by regulation of hepatic stellate cells (HSCs) trans-differentiation, inhibiting growth factors like TGF-beta and platelets-derived growth factor (PDGF), vascular epithelial growth factor (VEGF), viral infections like hepatitis-B, C and D viruses (HBV, HCV & HDV), autoimmune-induced, alcohol-induced, metabolic disorder-induced, causing by apoptosis, and regulating MAPK pathways. These flavonoids may be explored in the future as a therapeutic solution for hepatic diseases.
C1 [Sahu, Rakesh; Goswami, Sourav; Narahari Sastry, G.; Rawal, Ravindra K.] CSIR North East Inst Sci & Technol, Chem Sci & Technol Div, Nat Prod Chem Grp, Jorhat 785006, Assam, India.
[Narahari Sastry, G.; Rawal, Ravindra K.] Acad Sci & Innovat Res AcSIR, Ghaziabad 201002, Uttar Pradesh, India.
C3 Council of Scientific & Industrial Research (CSIR) - India; CSIR - North
East Institute of Science & Technology (NEIST); Academy of Scientific &
Innovative Research (AcSIR)
RP Rawal, RK (corresponding author), CSIR North East Inst Sci & Technol, Chem Sci & Technol Div, Nat Prod Chem Grp, Jorhat 785006, Assam, India.; Rawal, RK (corresponding author), Acad Sci & Innovat Res AcSIR, Ghaziabad 201002, Uttar Pradesh, India.
EM rawal.ravindra@gmail.com
RI Sahu, Rakesh/M-3535-2013; Rawal, Ravindra/F-9486-2010
OI , Rakesh Sahu/0000-0002-3997-7770; Rawal, Ravindra/0000-0001-9035-3579
FU CSIR, Government of India [4/25/Immunity/202-1IMD, HCP-035]
FX RKR thanks CSIR, Government of India, for the financial assistance in
the form of research grant (Ref. No.: 4/25/Immunity/202-1IMD; HCP-035,
2021). RS and SG also thank CSIR, Government of India, for providing
research fellowship.
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NR 140
TC 6
Z9 7
U1 4
U2 25
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1612-1872
EI 1612-1880
J9 CHEM BIODIVERS
JI Chem. Biodivers.
PD FEB
PY 2023
VL 20
IS 2
DI 10.1002/cbdv.202201029
EA JAN 2023
PG 23
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA T5BO9
UT WOS:000921276000001
PM 36703592
DA 2025-01-07
ER
PT J
AU Michielsen, P
Vandewoude, M
AF Michielsen, P.
Vandewoude, M.
TI Liver diseases in the older adult
SO ACTA GASTRO-ENTEROLOGICA BELGICA
LA English
DT Review
DE aging; liver disease; older adults; viral hepatitis; liver surgery;
liver transplantation
ID CHRONIC HEPATITIS-C; HEPATOCELLULAR-CARCINOMA; FIBROSIS PROGRESSION;
PLUS RIBAVIRIN; AUTOIMMUNE HEPATITIS; CLINICAL-FEATURES;
ELDERLY-PATIENTS; RISK-FACTORS; DONOR AGE; TRANSPLANTATION
AB Although there are no liver diseases specific to advanced age, the clinical course and management of liver disease in the older adult may differ from those in younger people. Changes in hepatic morphology with aging may lead to changes in liver function. Disturbances in laboratory liver function tests are similar as in younger people and should lead to the same vigilance in investigating for liver disease. Changes in immune function lead to more symptomatic acute hepatitis A, more progression to chronicity in hepatitis B and more fibrosis progression in chronic hepatitis C, especially after liver transplantation with livers from older donors. Treatment for chronic hepatitis C or autoimmune hepatitis is similar for younger or older adults, but side effects may be more prominent in older people. Comprehensive geriatric assessment should be part of the preliminary evaluation of the older patient with liver disease. (Acta gastroenterol. belg., 2010, 73, 1-4).
C1 [Michielsen, P.] Univ Antwerp Hosp, Div Hepatogastroenterol, B-2650 Edegem, Belgium.
[Vandewoude, M.] Univ Antwerp, Univ Dept Geriatr, B-2000 Antwerp, Belgium.
[Vandewoude, M.] ZNA, B-2000 Antwerp, Belgium.
C3 University of Antwerp; University of Antwerp; ZNA Stuivenberg
RP Michielsen, P (corresponding author), Univ Antwerp Hosp, Div Hepatogastroenterol, Wilrijkstr 10, B-2650 Edegem, Belgium.
EM peter.michielsen@uza.be
RI Michielsen, Peter/D-7088-2017
OI Michielsen, Peter/0000-0001-7232-8927
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SN 1784-3227
J9 ACTA GASTRO-ENT BELG
JI Acta Gastro-Enterol. Belg.
PD JAN-MAR
PY 2010
VL 73
IS 1
BP 1
EP 4
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 590UU
UT WOS:000277254600001
PM 20458843
DA 2025-01-07
ER
PT J
AU Brewer, GJ
Dick, R
Zeng, CH
Hou, GQ
AF Brewer, George J.
Dick, Robert
Zeng, Chunhua
Hou, Guoqing
TI The use of tetrathiomolybdate in treating fibrotic, inflammatory, and
autoimmune diseases, including the non-obese diabetic mouse model
SO JOURNAL OF INORGANIC BIOCHEMISTRY
LA English
DT Article; Proceedings Paper
CT 12th International Conference on Biological Inorganic Chemistry
CY JUL 31-AUG 05, 2005
CL Ann Arbor, MI
DE copper; tetrathiomolybdate; diabetes; fibrotic disease; inflammatory
diseases
ID THERAPY PROTECTS; INITIAL THERAPY; TUMOR-GROWTH; COPPER; SUPPRESSION;
ANTICOPPER; CERULOPLASMIN; ANGIOGENESIS; DOXORUBICIN; METASTASIS
AB Tetrathiomolybdate was originally developed for use in Wilson's disease. However, lowering copper levels to below normal levels with tetrathiomolybdate has been found to have efficacy in cancer, probably by turning down signaling by angiogenic cytokines. More recently, we have shown in animals models that tetrathiomolybdate dramatically inhibits pulmonary and liver fibrosis. In other animal models, we have shown that the drug also inhibits liver damage from concanavalin A and acetaminophen, and heart damage from doxorubicin. These studies are briefly reviewed, and we then present data on tetrathiomolybdate's partially protective effect against diabetes in non-obese diabetic mice, an autoimmune model of type I diabetes. Possible mechanisms of tetrathiomolybdate's protective effect are briefly considered. (c) 2005 Elsevier Inc. All rights reserved.
C1 Univ Michigan, Sch Med, Dept Human Genet, Ann Arbor, MI 48109 USA.
Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan; University of
Michigan System; University of Michigan
RP Brewer, GJ (corresponding author), Univ Michigan, Sch Med, Dept Human Genet, 5022 Kresge Bldg 2, Ann Arbor, MI 48109 USA.
EM brewergj@umich.edu
RI Zeng, Chunhua/ABB-2231-2020
OI Zeng, Chunhua/0000-0001-5954-1803
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NR 30
TC 32
Z9 33
U1 2
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0162-0134
EI 1873-3344
J9 J INORG BIOCHEM
JI J. Inorg. Biochem.
PD MAY
PY 2006
VL 100
IS 5-6
BP 927
EP 930
DI 10.1016/j.jinorgbio.2005.10.007
PG 4
WC Biochemistry & Molecular Biology; Chemistry, Inorganic & Nuclear
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Biochemistry & Molecular Biology; Chemistry
GA 049GR
UT WOS:000238004700006
PM 16321443
DA 2025-01-07
ER
PT J
AU Czaja, AJ
AF Czaja, Albert J.
TI Cryptogenic Chronic Hepatitis and Its Changing Guise in Adults
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Review
DE Cryptogenic hepatitis; Autoantibody-negative; Chronic hepatitis
ID FATTY LIVER-DISEASE; SEN VIRUS-INFECTION; ANTINEUTROPHIL CYTOPLASMIC
ANTIBODIES; MZ ALPHA-1-ANTITRYPSIN DEFICIENCY; INHERITED METABOLIC
DISEASE; CHRONIC ACTIVE HEPATITIS; AUTOIMMUNE HEPATITIS; C VIRUS;
WILSON-DISEASE; NONALCOHOLIC STEATOHEPATITIS
AB Cryptogenic chronic hepatitis is a disease that is unexplained by conventional clinical, laboratory and histological findings, and it can progress to cirrhosis, develop hepatocellular carcinoma, and require liver transplantation. The goals of this review are to describe the changing phenotype of cryptogenic chronic hepatitis in adults, develop a diagnostic algorithm appropriate to current practice, and suggest treatment options. The frequency of cryptogenic hepatitis is estimated at 5.4%. Cryptogenic cirrhosis is diagnosed in 5-30% of patients with cirrhosis, and it is present in 3-14% of adults awaiting liver transplantation. Nonalcoholic fatty liver disease has been implicated in 21-63% of patients, and autoimmune hepatitis is a likely diagnosis in 10-54% of individuals. Viral infections, hereditary liver diseases, celiac disease, and unsuspected alcohol or drug-induced liver injury are recognized infrequently in the current cryptogenic population. Manifestations of the metabolic syndrome heighten the suspicion of nonalcoholic fatty liver disease, and the absence of hepatic steatosis does not discount this possibility. The diagnostic scoring system of the International Autoimmune Hepatitis Group can support the diagnosis of autoimmune hepatitis in some patients. Certain genetic mutations may have disease-specificity, and they suggest that some patients may have an independent and uncharacterized disease. Corticosteroid therapy is effective in patients with autoimmune features, and life-style changes and specific therapies for manifestations of the metabolic syndrome are appropriate for all obese patients. The 1- and 5-year survivals after liver transplantation have ranged from 72-85% to 58-73%, respectively.
C1 Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Czaja, AJ (corresponding author), Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, 200 1st St SW, Rochester, MN 55905 USA.
EM czaja.albert@mayo.edu
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NR 223
TC 34
Z9 43
U1 0
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD DEC
PY 2011
VL 56
IS 12
BP 3421
EP 3438
DI 10.1007/s10620-011-1769-9
PG 18
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 857UM
UT WOS:000297747300004
PM 21647651
DA 2025-01-07
ER
PT J
AU Kahraman, A
Gerken, G
Canbay, A
AF Kahraman, Alisan
Gerken, Guido
Canbay, Ali
TI Apoptosis in Immune-Mediated Liver Diseases
SO DIGESTIVE DISEASES
LA English
DT Article; Proceedings Paper
CT Falk Workshop on Immunology and Liver Disease/Falk Symposium 171 on
Liver and Metabolic Syndrome
CY OCT 15-18, 2009
CL Hannover, GERMANY
DE Apoptosis; Autoimmunity; Cholestasis; Stress-induced ligands
ID PRIMARY BILIARY-CIRRHOSIS; HUMAN HEPATOCELLULAR CARCINOMAS; AUTOIMMUNE
HEPATITIS; URSODEOXYCHOLIC ACID; CHAIN-A; EXPRESSION; CELLS; BILE;
FIBROSIS; CHOLANGITIS
AB Autoimmune diseases of the liver are chronic inflammatory processes leading to injury of hepatocytes and cholangiocytes. Cell death by apoptosis is a prominent feature in a variety of liver diseases. It is likely that apoptosis is the initial cellular response to liver and biliary injury and may thus initiate several cellular and cytokine cascades. Obviously, this cascade of events is of particular clinical importance. This short overview will focus on the role of apoptosis in immune-mediated liver diseases. Recently, also soluble forms of major histocompatibility complex class I-related chains A and closely related B (MIC A and B) were reported to be increased in the sera of patients with autoimmune and cholestatic liver diseases, and also in non-alcoholic steatohepatitis. MIC A and B are cell surface glycoproteins that function as indicators for cellular stress by displaying peptides derived from proteins degraded in the cytosol on the cell surface, and thus facilitate the recognition of intracellular antigens by circulating cytotoxic natural killer cells, leading to enhanced cell death. Nowadays rational-based strategies are being developed to suppress apoptotic cell death as a novel therapeutic option for the treatment of these liver diseases. Copyright (C) 2010 S. Karger AG, Basel
C1 [Kahraman, Alisan; Gerken, Guido; Canbay, Ali] Univ Duisburg Essen, Univ Clin Essen, Div Gastroenterol & Hepatol, DE-45122 Essen, Germany.
C3 University of Duisburg Essen
RP Canbay, A (corresponding author), Univ Duisburg Essen, Univ Clin Essen, Div Gastroenterol & Hepatol, Hufelandstr 55, DE-45122 Essen, Germany.
EM Ali.Canbay@uni-due.de
RI Canbay, Ali/AAL-9620-2020
OI Canbay, Ali/0000-0001-6069-7899; Gerken, Guido/0000-0001-6734-5001
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NR 32
TC 16
Z9 19
U1 0
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PY 2010
VL 28
IS 1
BP 144
EP 149
DI 10.1159/000299799
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology
GA 594YY
UT WOS:000277578800020
PM 20460903
DA 2025-01-07
ER
PT J
AU Scott, JD
Garland, N
AF Scott, John D.
Garland, Naomi
TI Chronic liver disease in Aboriginal North Americans
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE hepatitis C virus; hepatitis B virus; American Indian; Alaska native;
chronic liver disease
ID B-VIRUS-INFECTION; PRIMARY HEPATOCELLULAR-CARCINOMA; PRIMARY
BILIARY-CIRRHOSIS; HEPATITIS-C INFECTION; AUTOIMMUNE-HEPATITIS;
VIRAL-HEPATITIS; ALASKA NATIVES; UNITED-STATES; ALCOHOLIC CIRRHOSIS;
SURFACE-ANTIGEN
AB A structured literature review was performed to detail the frequency and etiology of chronic liver disease (CLD) in Aboriginal North Americans. CLD affects Aboriginal North Americans disproportionately and is now one of the most common causes of death. Alcoholic liver disease is the leading etiology of CLD, but viral hepatitis, particularly hepatitis C, is an important and growing cause of CLD. High rates of autoimmune hepatitis and primary biliary cirrhosis (PBC) are reported in regions of coastal British Columbia and southeastern Alaska. Non-alcoholic liver disease is a common, but understudied, cause of CLD. Future research should monitor the incidence and etiology of CLD and should be geographically inclusive. In addition, more research is needed on the treatment of hepatitis C virus (HCV) infection and non-alcoholic fatty liver disease (NAFLD) in this population. (c) 2008 The WJG Press. All rights reserved.
C1 [Scott, John D.] Univ Washington, Dept Med, Div Allergy & Infect Dis, Harborview Med Ctr, Seattle, WA 98144 USA.
[Garland, Naomi] Univ Washington, Dept Lab Med, Seattle, WA 98144 USA.
C3 Harborview Medical Center; University of Washington; University of
Washington Seattle; University of Washington; University of Washington
Seattle
RP Scott, JD (corresponding author), Univ Washington, Dept Med, Div Allergy & Infect Dis, Harborview Med Ctr, 325 9th Ave,Box 359938, Seattle, WA 98144 USA.
EM jdscott@u.washington.edu
FU NCRR NIH HHS [K23 RR022206, 5K23 RR 02206] Funding Source: Medline
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2003, MMWR MORB MORTAL WKL, V52, P1148
NR 71
TC 25
Z9 30
U1 0
U2 7
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD AUG 7
PY 2008
VL 14
IS 29
BP 4607
EP 4615
DI 10.3748/wjg.14.4607
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 338YE
UT WOS:000258544500003
PM 18698674
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Chan, EY
Larson, AM
Gernsheimer, TB
Kowdley, KV
Carithers, RL
Reyes, JD
Perkins, JD
AF Chan, Edie Y.
Larson, Anne M.
Gernsheimer, Terry B.
Kowdley, Kris V.
Carithers, Robert L., Jr.
Reyes, Jorge D.
Perkins, James D.
TI Recipient and donor factors influence the incidence of graft-vs.-host
disease in liver transplant patients
SO LIVER TRANSPLANTATION
LA English
DT Article
ID V-ALPHA-24J-ALPHA-Q T-CELLS; CHIMERISM; DIAGNOSIS; CONFIRMATION;
MIGRATION; RECEPTOR; HEALTH
AB Acute cellular graft-vs.-host disease (GVHD) following liver transplantation has an incidence of 1 to 2% and a mortality rate of 85%. Our aim was to identify a patient population at high risk for developing GVHD using a large clinical database to study both recipient and donor factors. We compared our liver transplant patients who developed GVHD to those that did not for recipient and donor factors and combinations of factors. For 2003-2004 we had 205 first-time liver transplant patients surviving >30 days, From this group, 4 (1.9%) developed GVHD. Compared to the control group, there were no significant differences in recipient age, recipient gender, donor age, donor gender, total ischemia time, donor-recipient human leukocyte antigen (HLA) mismatch, or donor-recipient age difference. Percentages of liver disease etiologies among the patients who developed GVHD were as follows: 16% (1/6) autoimmune hepatitis (AIH) (P = 0.003), 5.6% (3/54) alcoholic liver disease (ALD) (P = 0.057), and 7.1% (3/42) hepatocellular carcinoma (HCC) (P = 0.026). The incidence of GVHD in patients with glucose intolerance (either Type I or Type II diabetes mellitus [DM]) was significant (P = 0.022). Focusing on patients only with high-risk factors for GVHD during the years 2003-2005, we had 19 such patients. Four of these high-risk patients developed GVHD. Three of these 4 patients had received a donor liver with steatosis of degree >= mild compared to only 2 of the 15 high-risk patients who did not develop GVHD (P = 0.037). In conclusion, we have identified liver transplant patients with AIH or the combination of ALD, HCC, and glucose intolerance who receive a steatotic donor liver as being at high risk for developing GVHD.
C1 Univ Washington, Dept Surg, Div Transplantat, Seattle, WA 98195 USA.
Univ Washington, Dept Med, Div Gastroenterol, Seattle, WA USA.
Univ Washington, Dept Med, Div Hematol, Seattle, WA 98195 USA.
C3 University of Washington; University of Washington Seattle; University
of Washington; University of Washington Seattle; University of
Washington; University of Washington Seattle
RP Perkins, JD (corresponding author), Univ Washington, Dept Surg, Div Transplantat, Box 356410, Seattle, WA 98195 USA.
EM theperk@u.washington.edu
RI Larson, Anne/I-2087-2019; Kowdley, Kris/AAF-5202-2019; Perkins,
James/AAF-1323-2019
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NR 58
TC 51
Z9 55
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6465
EI 1527-6473
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD APR
PY 2007
VL 13
IS 4
BP 516
EP 522
DI 10.1002/lt.21082
PG 7
WC Gastroenterology & Hepatology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA 155RT
UT WOS:000245596400009
PM 17394149
OA Bronze
DA 2025-01-07
ER
PT J
AU Oda, H
Ishihara, M
Miyahara, Y
Nakamura, J
Kozuka, Y
Iwasa, M
Tsunoda, A
Yamashita, Y
Saito, K
Mizuno, T
Shiku, H
Katayama, N
AF Oda, Hiroyasu
Ishihara, Mikiya
Miyahara, Yoshihiro
Nakamura, Junko
Kozuka, Yuji
Iwasa, Motoh
Tsunoda, Akira
Yamashita, Yoshiki
Saito, Kanako
Mizuno, Toshiro
Shiku, Hiroshi
Katayama, Naoyuki
TI First Case of Cytokine Release Syndrome after Nivolumab for Gastric
Cancer
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE Cytokine release syndrome; Gastric cancer; Nivolumab; Liver injury;
TNF-alpha
ID PRIMARY BILIARY-CIRRHOSIS
AB Introduction: Cytokine release syndrome (CRS) is a potentially life-threatening systemic disease that has been observed after treatment with antibodies and adoptive T cell therapies. In this case, we observed nivolumab-induced CRS in a patient with gastric cancer. Case Presentation: A 43-year-old male with advanced gastric cancer was treated with nivolumab as a third-line chemotherapy. He had no history of allergies. Eight days after the first administration of nivolumab, fever, tachycardia, appetite loss and increases in liver and biliary enzymes were observed. Computed tomography revealed neither bile duct obstruction nor progression of liver metastases but showed that there was edema of the Gleason sheath. Histopathological analysis of the liver revealed cholestatic liver injury with CD8+ T lymphocyte and macrophage infiltration. Neither viral infection nor autoimmune disease was revealed. His symptoms were similar to those of CRS observed after T cell therapy. We diagnosed his disease as nivolumab-induced liver injury and cholangitis accompanied by CRS based on his serum cytokine levels. Discussion/Conclusion: To the best of our knowledge, this is the first report of nivolumab-induced CRS in a patient with gastric cancer. (C) 2019 The Author(s) Published by S. Karger AG, Basel
C1 [Oda, Hiroyasu; Ishihara, Mikiya; Tsunoda, Akira; Yamashita, Yoshiki; Saito, Kanako; Mizuno, Toshiro] Mie Univ Hosp, Dept Med Oncol, 174 Edobashi 2 Chome, Tsu, Mie 5148507, Japan.
[Miyahara, Yoshihiro; Nakamura, Junko; Shiku, Hiroshi] Mie Univ, Grad Sch Med, Dept Immunogene Therapy, Tsu, Mie, Japan.
[Kozuka, Yuji] Mie Univ, Grad Sch Med, Dept Pathol, Tsu, Mie, Japan.
[Iwasa, Motoh] Mie Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Tsu, Mie, Japan.
[Katayama, Naoyuki] Mie Univ, Grad Sch Med, Dept Hematol & Oncol, Tsu, Mie, Japan.
C3 Mie University; Mie University; Mie University; Mie University; Mie
University
RP Ishihara, M (corresponding author), Mie Univ Hosp, Dept Med Oncol, 174 Edobashi 2 Chome, Tsu, Mie 5148507, Japan.
EM mishihara@clin.medic.mie-u.ac.jp
RI Shiku, Hiroshi/U-7321-2019
OI Shiku, Hiroshi/0000-0002-0362-755X; ISHIHARA,
Mikiya/0000-0002-7581-2615; Miyahara, Yoshihiro/0000-0002-6458-3167
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NR 15
TC 26
Z9 27
U1 0
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-6575
J9 CASE REP ONCOL
JI Case Rep. Oncol.
PY 2019
VL 12
IS 1
BP 147
EP 156
DI 10.1159/000496933
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA HX8GG
UT WOS:000467643700024
PM 31043953
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Roberts, EA
AF Roberts, Eve A.
TI Autoimmune hepatitis from the paediatric perspective
SO LIVER INTERNATIONAL
LA English
DT Review
DE autoimmune; children; hepatobiliary
ID CHRONIC ACTIVE HEPATITIS; PRIMARY SCLEROSING CHOLANGITIS; KIDNEY
MICROSOME ANTIBODY; A VIRUS-INFECTION; CORTICOSTEROID-THERAPY;
CONTROLLED-TRIAL; HEPATOCELLULAR-CARCINOMA; CELIAC-DISEASE;
LIVER-FAILURE; FOLLOW-UP
AB Autoimmune hepatitis (AIH) is an important entity within the broad spectrum of autoimmune hepatobiliary disease comprised of AIH, primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). Since the 1960s, AIH has been investigated with extensive clinical research aimed at effective therapeutic intervention. It was one of the first liver diseases where treatment was demonstrated to prolong survival. AIH occurs in children, as well as in adults. Its clinical manifestations in children may differ from classic adult AIH. These differences have elucidated certain aspects of AIH and hepatobiliary disease in general. There are two major patterns of AIH: type 1, with anti-smooth muscle antibodies and type 2, with anti-liver/kidney microsomal antibodies. The second type of AIH was first identified in children and is more common in younger patients. AIH often presents as acute disease in children and also in adults: the nomenclature has dropped the allusion to chronicity. Some children who have sclerosing cholangitis present with clinical disease closely resembling AIH; this AIH-like PSC, termed autoimmune sclerosing cholangitis (ASC), is also found in adults. Children with AIH may have identifiable monogenic disorders of immune regulation such as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). Like adults with AIH, children with AIH usually respond very favourably to immunosuppressive treatment with corticosteroids +/- azathioprine. True cures seem to be rare, although many children achieve a stable remission. Nonetheless children with AIH may develop cirrhosis and some require liver transplantation. Early diagnosis and improved treatment strategies may further improve the outlook for children with AIH.
C1 [Roberts, Eve A.] Univ Toronto, Hosp Sick Children, Div Gastroenterol Hepatol & Nutr, Toronto, ON M5G 1X8, Canada.
[Roberts, Eve A.] Univ Toronto, Dept Paediat, Toronto, ON M5G 1X8, Canada.
[Roberts, Eve A.] Univ Toronto, Dept Med, Toronto, ON M5G 1X8, Canada.
[Roberts, Eve A.] Univ Toronto, Dept Pharmacol, Toronto, ON M5G 1X8, Canada.
C3 University of Toronto; Hospital for Sick Children (SickKids); University
of Toronto; University of Toronto; University of Toronto
RP Roberts, EA (corresponding author), Univ Toronto, Hosp Sick Children, Div Gastroenterol Hepatol & Nutr, Room 8263,555 Univ Ave, Toronto, ON M5G 1X8, Canada.
EM eve.roberts@utoronto.ca
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NR 68
TC 18
Z9 20
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD NOV
PY 2011
VL 31
IS 10
BP 1424
EP 1431
DI 10.1111/j.1478-3231.2011.02603.x
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 837YM
UT WOS:000296249800003
PM 22093323
DA 2025-01-07
ER
PT J
AU Azariadis, K
Gatselis, NK
Lyberopoulou, A
Arvaniti, P
Zachou, K
Gabeta, S
Dalekos, GN
AF Azariadis, Kalliopi
Gatselis, Nikolaos K.
Lyberopoulou, Aggeliki
Arvaniti, Pinelopi
Zachou, Kalliopi
Gabeta, Stella
Dalekos, George N.
TI PNPLA3 I148 M genetic variant in autoimmune hepatitis characterises
advanced disease at diagnosis and reduced survival free of cirrhotic
events and liver-related mortality
SO JOURNAL OF TRANSLATIONAL AUTOIMMUNITY
LA English
DT Article
DE Autoimmune hepatitis; PNPLA3 I148 M; Polymorphisms; Biomarker;
Liver-related mortality
ID GENOME-WIDE ASSOCIATION; HEPATOCELLULAR-CARCINOMA; HISTOLOGICAL
SEVERITY; POLYMORPHISM; METAANALYSIS; STEATOSIS; RS738409; RISK;
SUSCEPTIBILITY; MYCOPHENOLATE
AB Background: Autoimmune hepatitis (AIH) is a relatively rare autoimmune disease with a strong genetic background. The patatin-like phospholipase domain-containing protein 3 (PNPLA3) I148 M (rs738409 C/G) variant has been associated with hepatic inflammation and fibrosis in chronic hepatic diseases beyond metabolic dysfunction-associated steatotic liver disease (MASLD). Aim: Our aim was to investigate the significance of PNPLA3 I148 M variant in AIH. Method: Two hundred AIH patients, followed in our centre, were evaluated while 100 healthy subjects served as controls. Genotyping was performed with allelic discrimination end -point polymerase chain reaction (PCR). Results: The I148 M variant was present in 95/200 (47.5 %) AIH patients compared to 47/100 (47 %) healthy controls (p = 1.000). Patients with GG/CG genotypes were more likely to present with decompensated cirrhosis at diagnosis (GG/CG 6.3 % vs. CC 1 %, p = 0.039). Comorbidity with cardiometabolic risk factors and concurrence of MASLD was similar across genotypes. Simple steatosis was present in 37/186 (19.9 %) and steatohepatitis in 14/186 (7.5 %) patients with available liver biopsy without correlation with PNPLA3 genotype. Fibrosis stage and grade of inflammation were not correlated with any genotype. Response to treatment was also independent of the presence of the I148 M variant, even though a longer time was needed to achieve complete biochemical response in those carrying the GG/CG genotypes (p = 0.07). On Kaplan Meier analysis homozygosity for the G allele corelated with reduced survival free of decompensation (p = 0.006), cirrhotic events (decompensation, liver transplantation, hepatocellular carcinoma; p = 0.001) and liver-related death or liver transplantation (p = 0.011) in treated patients. Conclusions: The PNPLA3 I148 M variant in AIH patients is associated with increased risk of advanced disease at diagnosis and reduced survival free of cirrhotic events and liver-related death or liver transplantation, regardless of the presence of MASLD. This signifies a potential role for the PNPLA3 I148 M variant as a new AIH biomarker allowing to identify patients at increased risk of disease progression.
C1 [Azariadis, Kalliopi; Gatselis, Nikolaos K.; Lyberopoulou, Aggeliki; Arvaniti, Pinelopi; Zachou, Kalliopi; Gabeta, Stella; Dalekos, George N.] Gen Univ Hosp Larissa, Dept Med, Larisa, Greece.
[Azariadis, Kalliopi; Gatselis, Nikolaos K.; Lyberopoulou, Aggeliki; Arvaniti, Pinelopi; Zachou, Kalliopi; Gabeta, Stella; Dalekos, George N.] Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Res Lab Internal Med, Larisa, Greece.
[Azariadis, Kalliopi; Gatselis, Nikolaos K.; Lyberopoulou, Aggeliki; Arvaniti, Pinelopi; Zachou, Kalliopi; Gabeta, Stella; Dalekos, George N.] Gen Univ Hosp Larissa, European Reference Network Hepatol Dis ERN Rare Li, Larisa, Greece.
C3 General University Hospital of Larissa; General University Hospital of
Larissa; General University Hospital of Larissa
RP Dalekos, GN (corresponding author), Gen Univ Hosp Larissa, Dept Med, Larisa 41110, Greece.; Dalekos, GN (corresponding author), Gen Univ Hosp Larissa, Expertise Ctr Greece Autoimmune Liver Dis, Res Lab Internal Med, European Reference Network Hepatol Dis ERN RARE LI, Larisa 41110, Greece.
EM kazariadis@hotmail.com; gatselis@me.com; aglyber@gmail.com;
peni.arvaniti@gmail.com; zachoukalliopi@gmail.com; s_gampeta@yahoo.com;
georgedalekos@gmail.com
RI Gabeta, Stella/IXW-9909-2023
OI Dalekos, George/0000-0001-7075-8464; Arvaniti,
Pinelopi/0000-0002-0278-3518; Gabeta, Stella/0000-0003-4779-8155
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NR 62
TC 1
Z9 1
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2589-9090
J9 J TRANSL AUTOIMMUN
JI J. Transl. Autoimmun.
PD DEC
PY 2024
VL 9
AR 100243
DI 10.1016/j.jtauto.2024.100243
EA JUN 2024
PG 8
WC Immunology
WE Emerging Sources Citation Index (ESCI)
SC Immunology
GA WI9Z3
UT WOS:001254372700001
PM 38974691
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Miyake, Y
Iwasaki, Y
Terada, R
Nagano, T
Kobashi, H
Sakaguchi, K
Shiratori, Y
AF Miyake, Yasuhiro
Iwasaki, Yoshiaki
Terada, Ryo
Nagano, Takuya
Kobashi, Haruhiko
Sakaguchi, Kohsaku
Shiratori, Yasushi
TI A model for estimating cirrhosis in patients with type 1 autoimmune
hepatitis
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE AST/ ALT ratio; autoimmune hepatitis; cirrhosis; immunoglobulin A;
platelet
ID HEPATOCELLULAR-CARCINOMA; CORTICOSTEROID-THERAPY;
ASPARTATE-AMINOTRANSFERASE; C VIRUS; FIBROSIS; DIAGNOSIS; PREDICTION;
INFECTION; MARKER; TESTS
AB Aim: Longstanding cirrhosis has been recognized as a risk factor for the development of hepatocellular carcinoma in patients with autoimmune hepatitis (AIH). Thus, the accurate determination of cirrhosis is important for prognostication, decisions regarding treatment and monitoring of disease progression. The aim of this study was to identify independent predictors of cirrhosis and to develop a model for estimating cirrhosis in patients with type 1 AIH.
Methods: Using the training sample, consisting of 121 patients with type 1 AIH, we retrospectively examined independent predictors of cirrhosis and constructed a model for estimating cirrhosis. Validation was prospectively performed in the validation sample, consisting of 35 patients.
Results: Using a stepwise multiple linear regression analysis, three predictors of serum immunoglobulin A level, ratio of aspartate aminotransferase to alanine aminotransferase, and platelet count were elicited, and a model for estimating cirrhosis was determined as follows: risk score = -0.113 + 0.0006056 x immunoglobulin A (mg/dL) + 0.155 x ratio of aspartate aminotransferase to alanine aminotransferase - 0.007079 x platelet (x10(4)/mm(3)). In the training sample, the sensitivity and specificity were 90% and 83%, respectively, when patients presenting a risk score >= 0.20 were estimated to be cirrhotic. When this model was applied to the validation sample, the sensitivity, specificity, positive predictive value, negative predictive value and accuracy were 83%, 97%, 83%, 97% and 94%, respectively.
Conclusion: It is suggested that this model could be useful for the estimation of cirrhosis in patients with type 1 autoimmune hepatitis.
C1 [Miyake, Yasuhiro; Iwasaki, Yoshiaki; Terada, Ryo; Kobashi, Haruhiko; Sakaguchi, Kohsaku; Shiratori, Yasushi] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Gastroenterol & Hepatol, Okayama 7008558, Japan.
[Nagano, Takuya] Kagawa Prefectural Cent Hosp, Dept Internal Med, Takamatsu, Kagawa, Japan.
C3 Okayama University
RP Miyake, Y (corresponding author), Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Gastroenterol & Hepatol, 2-5-1 Shikata Cho, Okayama 7008558, Japan.
EM miyakeyasuhiro@hotmail.com
RI Iwasaki, Yoshiaki/B-2538-2011
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NR 29
TC 5
Z9 5
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD JUL
PY 2008
VL 38
IS 7
BP 658
EP 663
DI 10.1111/j.1872-034X.2008.00329.x
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 307WX
UT WOS:000256351300003
PM 18328063
DA 2025-01-07
ER
PT J
AU Ivanenkov, YA
Maklakova, SY
Beloglazkina, EK
Zyk, NV
Nazarenko, AG
Tonevitsky, AG
Kotelianski, VE
Majouga, AG
AF Ivanenkov, Yan A.
Maklakova, Svetlana Yu.
Beloglazkina, Elena K.
Zyk, Nikolay V.
Nazarenko, Anton G.
Tonevitsky, Alexander G.
Kotelianski, Victor E.
Majouga, Alexander G.
TI Development of liver cell-targeted drug delivery systems: experimental
approaches
SO RUSSIAN CHEMICAL REVIEWS
LA English
DT Review
ID CHRONIC HEPATITIS-C; HUMAN ASIALOGLYCOPROTEIN RECEPTOR; BLOCK-COPOLYMER
MICELLES; HUMAN HEPATOCELLULAR-CARCINOMA; SOLID LIPID NANOPARTICLES;
LOW-DENSITY-LIPOPROTEIN; BOVINE SERUM-ALBUMIN; IN-VITRO; GENE DELIVERY;
STELLATE CELLS
AB The review is devoted to liver cell-targeted drug delivery systems. Primary attention is paid to the therapy of hepatocellular carcinoma, liver fibrosis, liver cirrhosis, viral hepatitis (A G), cholangiocarcinoma, autoimmune liver diseases and some metabolic disorders. A general overview, modern classification and specific features of drug delivery systems are presented. The key characteristics and parameters of these systems and their advantages and restrictions for clinical applications are discussed. A considerable body of information is presented as summary tables convenient for perception and comparison. The data presented are critically analyzed and an expert evaluation of the therapeutic potential of the drug delivery systems in question is given. Discussion of invasive local delivery approaches, transmembrane systems and implants, as well as prodrugs is beyond the scope of the review, except for a few examples.
The bibliography includes 344 references.
C1 [Ivanenkov, Yan A.; Maklakova, Svetlana Yu.; Beloglazkina, Elena K.; Zyk, Nikolay V.; Majouga, Alexander G.] Lomonosov Moscow State Univ, Dept Chem, Leninskie Gory 1,Stroenie 3, Moscow 119991, Russia.
[Ivanenkov, Yan A.] MIPT, Inst Per 9, Dolgoprudnyi 141700, Moscow Reg, Russia.
[Nazarenko, Anton G.; Majouga, Alexander G.] Gen Management Dept President Russian Federat, Clin Hosp, Losinoostrovskaya Ul 45, Moscow 107105, Russia.
[Tonevitsky, Alexander G.] Scie Res Ctr BioClinicum, Ugreshskaya Ul 2,Stroenie 85, Moscow 115088, Russia.
[Tonevitsky, Alexander G.] P Herzen Moscow Oncol Res Inst, 2 Oy Botkinskiy Pr 3, Moscow 125284, Russia.
[Kotelianski, Victor E.] Skolkovo Innovat Ctr, Skolkovo Inst Sci & Technol, Ul Nobel 3, Moscow 143026, Russia.
[Majouga, Alexander G.] Natl Univ Sci & Technol MISiS, Leninsky Prosp 4, Moscow 119049, Russia.
C3 Lomonosov Moscow State University; Moscow Institute of Physics &
Technology; Skolkovo Institute of Science & Technology; National
University of Science & Technology (MISIS)
RP Ivanenkov, YA (corresponding author), Lomonosov Moscow State Univ, Dept Chem, Leninskie Gory 1,Stroenie 3, Moscow 119991, Russia.; Ivanenkov, YA (corresponding author), MIPT, Inst Per 9, Dolgoprudnyi 141700, Moscow Reg, Russia.
EM yai@pharmcluster.ru; maklakova.svetlana91@gmail.com;
bel@org.chem.msu.ru; zyk@org.chem.msu.ru; info@presidentclinic.ru;
tonevitsky@mail.ru; V.Kotelianski@skoltech.ru;
alexander.majouga@gmail.com
RI Ivanenkov, Yan/B-3653-2014; Majouga, Alexander/I-4099-2012; Nazarenko,
Anton/AAW-8202-2021; Tonevitsky, Alexander/R-5596-2019; Maklakova,
Svetlana/E-5512-2019
OI Maklakova, Svetlana/0000-0001-5290-9353; ivanenkov,
yan/0000-0002-8968-0879; Zyk, Nikolai/0000-0002-3771-116X
FU Russian Science Foundation [17-14-01316]; National University of Science
and Technology MISiS; Ministry of Education and Science of Russian
Federation [20.9907.2017/BU]; Russian Science Foundation [17-14-01316]
Funding Source: Russian Science Foundation
FX The review has been written with the financial support from the Russian
Science Foundation (Project No 17-14-01316), National University of
Science and Technology MISiS and the Ministry of Education and Science
of the Russian Federation (State Assignment No. 20.9907.2017/BU).
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NR 317
TC 16
Z9 16
U1 3
U2 36
PU ND Zelinsky Inst Organic Chemistry, RAS - ZIOC RAS
PI Moscow
PA 47 Leninsky Pr, Moscow, RUSSIA
SN 0036-021X
EI 1468-4837
J9 RUSS CHEM REV+
JI Russ. Chem. Rev.
PY 2017
VL 86
IS 8
BP 750
EP 776
DI 10.1070/RCR4707
PG 27
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA FE9HW
UT WOS:000408515800002
DA 2025-01-07
ER
PT J
AU Sasahira, N
Kawabe, T
Nakamura, A
Shimura, K
Shimura, H
Itobayashi, E
Asada, M
Shiratori, Y
Omata, M
AF Sasahira, Naoki
Kawabe, Takao
Nakamura, Akira
Shimura, Kenji
Shimura, Haruhisa
Itobayashi, Ei
Asada, Manabu
Shiratori, Yasushi
Omata, Masao
TI Inflammatory pseudotumor of the liver and peripheral eosinophilia in
autoimmune pancreatitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Inflammatory pseudotumor; Autoimmune pancreatitis
ID HYPEREOSINOPHILIC SYNDROME; SCLEROSING CHOLANGITIS; REGRESSION; THERAPY;
DISEASE; TUMOR; CHILD
AB AIM: Inflammatory pseudotumor (IPT) of the liver is a rare benign lesion, the etiology of which remains obscure. It is not associated with any particular diseases apart from phlebitis and Crohn's disease.
METHODS: A middle-aged male with hepatic IPT and peripheral eosinophilia associated with autoimmune pancreatitis (AIP) was selected for this study and review of literature.
RESULTS: A 59-year-old male was admitted with obstructive jaundice, marked eosinophilia (1 343/mm(3)) and hypergammaglobulinemia (4 145 mg/dL). Imaging techniques revealed dilatation of the intrahepatic bile duct, stenosis of the common bile duct with diffuse wall thickening, gallbladder wall thickening, irregular narrowing of the pancreatic duct, and swelling of the pancreatic parenchyma. Multiple liver masses were also demonstrated and diagnosed as IPT by biopsy specimens. Six months later, the abnormal features of the biliary tree remarkably improved by the oral administration of prednisolone, and the liver masses disappeared. The swelling of the pancreatic head also improved. The peripheral eosinophil count normalized. IPT associated with AIP, as we know, has not been reported in the literature. The clinical features of the present case mimicked those of pancreatic cancer with liver metastasis. This case deserves to be documented to prevent misdiagnosis of similar cases. (C) 2005 The WJG Press and Elsevier Inc. All rights reserved.
C1 [Sasahira, Naoki] Univ Tokyo, Dept Gastroenterol, Bunkyo Ku, Tokyo 1138655, Japan.
[Nakamura, Akira; Shimura, Kenji; Shimura, Haruhisa; Itobayashi, Ei; Asada, Manabu] Asahi Gen Hosp, Dept Gastroenterol, Chiba, Japan.
[Shiratori, Yasushi] Okayama Univ, Dept Gastroenterol, Okayama 7008530, Japan.
C3 University of Tokyo; Okayama University
RP Sasahira, N (corresponding author), Univ Tokyo, Dept Gastroenterol, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
EM sasahira-tky@umin.ac.jp
RI Sasahira, Naoki/JNT-5053-2023
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NR 29
TC 36
Z9 37
U1 0
U2 0
PU BAISHIDENG PUBL GRP CO LTD
PI BEIJING
PA RM 903, BLDG D, OCEAN INTERNATIONAL CTR, NO 62 DONGSIHUAN ZHONGLU,
BEIJING, CHAOYANG DISTRICT 100025, PEOPLES R CHINA
SN 1007-9327
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD FEB 14
PY 2005
VL 11
IS 6
BP 922
EP 925
DI 10.3748/wjg.v11.i6.922
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA V19VQ
UT WOS:000208100300030
PM 15682495
OA Green Published, hybrid
DA 2025-01-07
ER
PT S
AU Duan-Porter, WD
Casciola-Rosen, L
Rosen, A
AF Duan-Porter, WD
Casciola-Rosen, L
Rosen, A
BE Steinman, RM
TI Autoantigens - The critical partner in initiating and propagating
systemic autoimmunity
SO HUMAN IMMUNOLOGY: PATIENT-BASED RESEARCH
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Human Immunology
CY MAY 16-18, 2005
CL New York, NY
SP NY Acad Sci, Dana Fdn
DE autoimmunity; autoantigens; cancer; nucleophosmin; myositis; B23
ID PARANEOPLASTIC NEUROLOGICAL DEGENERATIONS; TUMOR-SUPPRESSOR PROTEIN;
REQUIRE GRANZYME-B; LUPUS-ERYTHEMATOSUS; BREAST-CANCER; NUCLEOLAR
PHOSPHOPROTEIN; HEPATOCELLULAR-CARCINOMA; INFLAMMATORY MYOPATHY; RAPID
INDUCTION; TOPOISOMERASE-I
AB The increasing recognition that cancer is frequently associated with an autoantibody response, and observations that systemic autoimmunity is sometimes associated with the diagnosis of a variety of malignancies (many detected near the onset of autoimmune disease), strongly underscore a potential mechanistic connection between cancer immunity and systemic autoimmunity. Accumulating data suggest that autoantigens are critical partners in driving the autoimmune response. Futhermore, unique changes in antigen expression and conformation in the immunizing tumor and the target tissue may play a role in antigen selection and ongoing damage. This construct has important implications for disgnosis, monitoring, and treatment of autoimmunity and, potentially, cancer immunotherapy.
C1 Johns Hopkins Univ, Div Rheumatol, Baltimore, MD 21224 USA.
C3 Johns Hopkins University
RP Rosen, A (corresponding author), Johns Hopkins Univ, Div Rheumatol, Mason F Lord Bldg,Cent Tower,Suite 4100,Room 411, Baltimore, MD 21224 USA.
EM arosen@jhmi.edu
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NR 63
TC 2
Z9 2
U1 0
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-606-7
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2005
VL 1062
BP 127
EP 136
DI 10.1196/annals.1358.015
PG 10
WC Immunology; Multidisciplinary Sciences
WE Conference Proceedings Citation Index - Science (CPCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Science & Technology - Other Topics
GA BEA65
UT WOS:000236473100013
PM 16461795
DA 2025-01-07
ER
PT J
AU Buechter, M
Dorn, D
Moehlendick, B
Siffert, W
Baba, HA
Gerken, G
Kahraman, A
AF Buechter, Matthias
Dorn, Dominik
Moehlendick, Birte
Siffert, Winfried
Baba, Hideo A. A.
Gerken, Guido
Kahraman, Alisan
TI Characteristics and Long-Term Outcome of 535 Patients with Autoimmune
Hepatitis-The 20-Year Experience of a High-Volume Tertiary Center
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE autoimmune hepatitis; immunosuppression; liver transplantation
ID SIMPLIFIED DIAGNOSTIC-CRITERIA; ACUTE LIVER-FAILURE; EPIDEMIOLOGY;
MANAGEMENT; REMISSION; PROGNOSIS; DISEASE; MAINTENANCE; VALIDATION;
CIRRHOSIS
AB Background and aims: Autoimmune hepatitis (AIH) is a complex and progressive inflammatory liver disease characterized by immune-mediated destruction of the liver parenchyma, hypergammaglobulinemia, the presence of circulating autoantibodies, and good response to immunosuppressive therapy. Since the prevalence of AIH is relatively rare, data on the clinical course and the long-term outcome are scarce. Patients and methods: We retrospectively analyzed the data of 535 well-documented AIH patients treated at the University Hospital Essen between 2000 and 2020. Results: The majority of patients were middle-aged females (75% women, mean age 45 years) with AIH type 1 (97%). Approximately 32% of patients were diagnosed with cirrhosis due to AIH, 29% had concomitant autoimmune (predominantly autoimmune thyroiditis), and 10% had psychiatric diseases, respectively. Skin tumors were the most common malignant diseases (47% of all tumors), while hepatocellular carcinoma rarely occurred (only six cases). Overall long-term mortality and liver-associated mortality were 9.16% and 4.67%, respectively. However, long-term survival was strongly associated with disease remission. Conclusions: Although AIH is a silent disease and cirrhosis is present in many cases, a favorable long-term prognosis can be achieved by consequent immunosuppressive therapy. The incidence of (liver-associated) complications seems to be lower in comparison to other etiologies, such as viral hepatitis or NASH, and mainly depends on the long-term side effects of immunosuppressive therapy.
C1 [Buechter, Matthias; Dorn, Dominik; Gerken, Guido; Kahraman, Alisan] Univ Duisburg Essen, Univ Clin Essen, Dept Gastroenterol & Hepatol, D-45122 Essen, Germany.
[Buechter, Matthias] Elisabeth Hosp, Dept Gastroenterol & Hepatol, D-58638 Iserlohn, Germany.
[Moehlendick, Birte; Siffert, Winfried] Univ Duisburg Essen, Univ Clin Essen, Inst Pharmacogenet, D-45122 Essen, Germany.
[Baba, Hideo A. A.] Univ Duisburg Essen, Univ Clin Essen, Inst Pathol, D-45122 Essen, Germany.
[Gerken, Guido] Helios Clin, Dept Gastroenterol & Hepatol, D-42549 Velbert, Germany.
[Kahraman, Alisan] Max Grundig Clin, Dept Gastroenterol & Hepatol, D-77815 Buhl, Germany.
C3 University of Duisburg Essen; University of Duisburg Essen; University
of Duisburg Essen
RP Gerken, G; Kahraman, A (corresponding author), Univ Duisburg Essen, Univ Clin Essen, Dept Gastroenterol & Hepatol, D-45122 Essen, Germany.; Gerken, G (corresponding author), Helios Clin, Dept Gastroenterol & Hepatol, D-42549 Velbert, Germany.; Kahraman, A (corresponding author), Max Grundig Clin, Dept Gastroenterol & Hepatol, D-77815 Buhl, Germany.
EM guido@clausgerken.de; alisan.kahraman@max-grundig-clinic.de
RI ; Mohlendick, Birte/IXW-5627-2023
OI Gerken, Guido/0000-0001-5734-8006; Mohlendick,
Birte/0000-0001-9093-8585; Buechter, Matthias/0000-0003-3394-5492
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NR 54
TC 2
Z9 2
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD JUL
PY 2023
VL 12
IS 13
AR 4192
DI 10.3390/jcm12134192
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA M1ZQ0
UT WOS:001028237000001
PM 37445225
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Moon, SK
Yoo, JJ
Kim, SG
Kim, YS
AF Moon, Seung Ki
Yoo, Jeong-Ju
Kim, Sang Gyune
Kim, Young Seok
TI Extremely rare case of necrotizing gastritis in a patient with
autoimmune hepatitis: A case report
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Article
DE Autoimmune hepatitis; Azathioprine; Case report
ID EMPHYSEMATOUS-GASTRITIS; AZATHIOPRINE; PREDNISONE; MANAGEMENT; DISEASE
AB BACKGROUND
Autoimmune hepatitis can cause liver fibrosis, liver cirrhosis, and hepatocellular carcinoma. Its treatment option include the use of steroids and/or immune-suppressive agents such as azathioprine. However, these drugs have some side effects. Thus, close follow-up is needed during treatment. Here, we present an extremely rare case of a patient with an autoimmune hepatitis who died from necrotizing gastritis during immunosuppressive treatment.
CASE SUMMARY
A 52-year-old female patient was diagnosed with autoimmune hepatitis. We treated this patient with immunosuppressive agents. High-dose steroid treatment was initially started. Then azathioprine treatment was added while steroid was tapering. Five weeks after the start of treatment, she visited the emergency room due to generalized abdominal pain and vomiting. After computed tomography scan, the patient was diagnosed with necrotizing gastritis and the patient progressed to septic shock. Treatment for sepsis was continued in the intensive care unit. However, the patient died at 6 h after admission to the emergency room.
CONCLUSION
In patients with autoimmune infections undergoing immunosuppressant therapy, rare complications such as necrotizing gastritis may occur, thus requiring clinical attention.
C1 [Moon, Seung Ki] Soonchunhyang Univ, Bucheon Hosp, Dept Internal Med, Bucheon 14584, South Korea.
[Yoo, Jeong-Ju; Kim, Sang Gyune; Kim, Young Seok] Soonchunhyang Univ, Sch Med, Dept Gastroenterol & Hepatol, 170 Jomaru Ro, Bucheon 14584, South Korea.
C3 Soonchunhyang University; Soonchunhyang University
RP Yoo, JJ (corresponding author), Soonchunhyang Univ, Sch Med, Dept Gastroenterol & Hepatol, 170 Jomaru Ro, Bucheon 14584, South Korea.
EM puby17@naver.com
RI Kim, Sang/AAI-5704-2020
OI Yoo, Jeong-Ju/0000-0002-7802-0381
FU Soonchunhyang University Research Fund [20200037]
FX Supported by The Soonchunhyang University Research Fund, No. 20200037.
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NR 29
TC 0
Z9 0
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD MAY 16
PY 2021
VL 9
IS 14
BP 3472
EP 3477
DI 10.12998/wjcc.v9.i14.3472
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA SA7DA
UT WOS:000649459600029
PM 34002160
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Chen, EQ
Shi, Y
Tang, H
AF Chen, En-Qiang
Shi, Ying
Tang, Hong
TI New insight of vitamin D in chronic liver diseases
SO HEPATOBILIARY & PANCREATIC DISEASES INTERNATIONAL
LA English
DT Review
DE vitamin D; deficiency; viral hepatitis; chronic liver diseases
ID PRIMARY BILIARY-CIRRHOSIS; D-RECEPTOR POLYMORPHISMS; HEPATITIS-C VIRUS;
COMMON GENETIC-DETERMINANTS; D SERUM-LEVELS; HEPATOCELLULAR-CARCINOMA; D
SUPPLEMENTATION; VIROLOGICAL RESPONSE; SEVERE FIBROSIS; D DEFICIENCY
AB BACKGROUND: Vitamin D is a fat-soluble sterol derivative that is predominantly synthesized in the liver and has multiple functions. The accumulative data showed that the clinical manifestations and prognosis of chronic liver diseases are associated with serum vitamin D levels.
DATA SOURCES: A Pub Med and Google Scholar search using terms: "vitamin D", "25 (OH) D", "liver disease", "viral hepatitis", "non-alcoholic fatty liver disease", "liver fibrosis", "cirrhosis", "hepatocellular carcinoma" and "autoimmune liver disease" was performed, and relevant articles published in English between January 2000 and March 2014 were reviewed. Full-text publications relevant to the field were selected and relevant articles from reference lists were also included.
RESULTS: The insufficiency or deficiency of vitamin D is common in various kinds of chronic liver diseases including viral hepatitis B and C. Serum 25-hydroxyvitamin D and vitamin D receptors are possibly interrelated with the incidence, treatment and prognosis of diseases. Though the evidence of vitamin D supplementation in viral hepatitis and associated liver diseases is still limited, there is great potential to apply this adjuvant therapy to improve the treatments.
CONCLUSIONS: Although the exact role and mechanisms of vitamin D have not been fully elucidated in chronic liver diseases, it is potentially beneficial in the treatment of chronic liver diseases. Further mechanistic studies are needed to validate its clinical application.
C1 [Chen, En-Qiang; Shi, Ying; Tang, Hong] Sichuan Univ, West China Hosp, Ctr Infect Dis, Chengdu 610041, Peoples R China.
[Chen, En-Qiang; Shi, Ying; Tang, Hong] Sichuan Univ, Div Infect Dis, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University
RP Tang, H (corresponding author), Sichuan Univ, West China Hosp, Ctr Infect Dis, Chengdu 610041, Peoples R China.
EM htang6198@hotmail.com
RI Chen, En-Qiang/S-7967-2019
FU National Twelve-Five Project of China [2012ZX10002007-001-003]; Chinese
Foundation for Hepatitis Prevention and Control-TianQing Liver Disease
Research Fund [cfhpc20132047]
FX This study was supported by grants from the National Twelve-Five Project
of China (2012ZX10002007-001-003), and the Chinese Foundation for
Hepatitis Prevention and Control-TianQing Liver Disease Research Fund
(cfhpc20132047).
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NR 59
TC 26
Z9 27
U1 1
U2 24
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1499-3872
EI 2352-9377
J9 HEPATOB PANCREAT DIS
JI Hepatob. Pancreatic. Dis. Int.
PD DEC 15
PY 2014
VL 13
IS 6
BP 580
EP 585
DI 10.1016/S1499-3872(14)60295-2
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AW4AI
UT WOS:000346223600002
PM 25475859
DA 2025-01-07
ER
PT J
AU Han, HT
Jin, WL
Li, X
AF Han, Heng-Tong
Jin, Wei-Lin
Li, Xun
TI Mesenchymal stem cells-based therapy in liver diseases
SO MOLECULAR BIOMEDICINE
LA English
DT Review
DE Chronic liver diseases; Mesenchymal stem cells; Immune regulation; Liver
regeneration; Liver immune microenvironment
ID HEPATITIS-B-VIRUS; REGULATORY T-CELLS; TOLL-LIKE RECEPTORS; EXPERIMENTAL
AUTOIMMUNE HEPATITIS; HEPATOCELLULAR-CARCINOMA CELLS; SINUSOIDAL
ENDOTHELIAL-CELLS; PLASMACYTOID DENDRITIC CELLS; HIGH-FAT DIET; STROMAL
CELLS; STELLATE CELLS
AB Multiple immune cells and their products in the liver together form a complex and unique immune microenvironment, and preclinical models have demonstrated the importance of imbalances in the hepatic immune microenvironment in liver inflammatory diseases and immunocompromised liver diseases. Various immunotherapies have been attempted to modulate the hepatic immune microenvironment for the purpose of treating liver diseases. Mesenchymal stem cells (MSCs) have a comprehensive and plastic immunomodulatory capacity. On the one hand, they have been tried for the treatment of inflammatory liver diseases because of their excellent immunosuppressive capacity; On the other hand, MSCs have immune-enhancing properties in immunocompromised settings and can be modified into cellular carriers for targeted transport of immune enhancers by genetic modification, physical and chemical loading, and thus they are also used in the treatment of immunocompromised liver diseases such as chronic viral infections and hepatocellular carcinoma. In this review, we discuss the immunological basis and recent strategies of MSCs for the treatment of the aforementioned liver diseases. Specifically, we update the immune microenvironment of the liver and summarize the distinct mechanisms of immune microenvironment imbalance in inflammatory diseases and immunocompromised liver diseases, and how MSCs can fully exploit their immunotherapeutic role in liver diseases with both immune imbalance patterns.
C1 [Han, Heng-Tong; Jin, Wei-Lin; Li, Xun] Lanzhou Univ, Sch Clin Med 1, Lanzhou 730000, Peoples R China.
[Jin, Wei-Lin; Li, Xun] Lanzhou Univ, Hosp 1, Med Frontier Innovat Res Ctr, 1 West Donggang Rd, Lanzhou 730000, Peoples R China.
[Li, Xun] Lanzhou Univ, Hosp 1, Dept Gen Surg, Lanzhou 730000, Peoples R China.
[Li, Xun] Key Lab Biotherapy & Regenerat Med Gansu Prov, Lanzhou 730000, Peoples R China.
C3 Lanzhou University; Lanzhou University; Lanzhou University
RP Li, X (corresponding author), Lanzhou Univ, Sch Clin Med 1, Lanzhou 730000, Peoples R China.; Li, X (corresponding author), Lanzhou Univ, Hosp 1, Med Frontier Innovat Res Ctr, 1 West Donggang Rd, Lanzhou 730000, Peoples R China.; Li, X (corresponding author), Lanzhou Univ, Hosp 1, Dept Gen Surg, Lanzhou 730000, Peoples R China.; Li, X (corresponding author), Key Lab Biotherapy & Regenerat Med Gansu Prov, Lanzhou 730000, Peoples R China.
EM lix@lzu.edu.cn
RI han, hengtong/LWI-0886-2024; Li, Xiaohan/KDN-3542-2024
OI Jin, Wei-Lin/0000-0001-8011-2405; Han, Heng-Tong/0000-0001-7671-944X
FU Regional Project of National Natural Science Foundation of China
[82060119]; Major Science and Technology Projects of Gansu Province
[1602FKDA001]; Scientific Research Project of health industry in Gansu
Province [GSWSKY-2015-49]; Gansu Science and Technology Program
[18JR2TA018]; Key Laboratory of Gansu Province [145RTSA002]; Gansu Fund
Project for Guiding Scientific and Technological Innovation and
Development [32]
FX This work was supported in part by the Regional Project of National
Natural Science Foundation of China (No. 82060119), Major Science and
Technology Projects of Gansu Province (No. 1602FKDA001), Scientific
Research Project of health industry in Gansu Province (No.
GSWSKY-2015-49), and Gansu Science and Technology Program (No.
18JR2TA018), Key Laboratory of Gansu Province (No.145RTSA002), Gansu
Fund Project for Guiding Scientific and Technological Innovation and
Development (No. GCK [2018] No.32).
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NR 608
TC 9
Z9 9
U1 1
U2 16
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2662-8651
J9 MOL BIOMED
JI Mol. Biomed.
PD JUL 27
PY 2022
VL 3
IS 1
AR 23
DI 10.1186/s43556-022-00088-x
PG 51
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
WE Emerging Sources Citation Index (ESCI)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 6W3RP
UT WOS:000895648900001
PM 35895169
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Jeffery, HC
Braitch, MK
Brown, S
Oo, YH
AF Jeffery, Hannah C.
Braitch, Manjit Kaur
Brown, Solomon
Oo, Ye Htun
TI Clinical Potential of Regulatory T Cell Therapy in Liver Diseases: An
Overview and Current Perspectives
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE regulatory T cells; microenvironment; metabolites; microbes
ID PRIMARY BILIARY-CIRRHOSIS; TRANS-RETINOIC ACID; PRIMARY SCLEROSING
CHOLANGITIS; SOLID-ORGAN TRANSPLANTATION; INFLAMMATORY-BOWEL-DISEASE;
LOW-DOSE INTERLEUKIN-2; HUMAN DENDRITIC CELLS; VERSUS-HOST-DISEASE;
GROWTH-FACTOR-BETA; IMMUNE-RESPONSES
AB The increasing demand for liver transplantation and the decline in donor organs has highlighted the need for alternative novel therapies to prevent chronic active hepatitis, which eventually leads to liver cirrhosis and liver cancer. Liver histology of chronic hepatitis is composed of both effector and regulatory lymphocytes. The human liver contains different subsets of effector lymphocytes that are kept in check by a subpopulation of T cells known as Regulatory T cells (Treg). The balance of effector and regulatory lymphocytes generally determines the outcome of hepatic inflammation: resolution, fulminant hepatitis, or chronic active hepatitis. Thus, maintaining and adjusting this balance is crucial in immunological manipulation of liver diseases. One of the options to restore this balance is to enrich Treg in the liver disease patients. Advances in the knowledge of Treg biology and development of clinical grade isolation reagents, cell sorting equipment, and good manufacturing practice facilities have paved the way to apply Treg cells as a potential therapy to restore peripheral self-tolerance in autoimmune liver diseases (AILD), chronic rejection, and posttransplantation. Past and on-going studies have applied Treg in type-1 diabetes mellitus, systemic lupus erythematosus, graft versus host diseases, and solid organ transplantations. There have not been any new therapies for the AILD for more than three decades; thus, the clinical potential for the application of autologous Treg cell therapy to treat autoimmune liver disease is an attractive and novel option. However, it is fundamental to understand the deep immunology, genetic profiles, biology, homing behavior, and microenvironment of Treg before applying the cells to the patients.
C1 [Jeffery, Hannah C.; Braitch, Manjit Kaur; Brown, Solomon; Oo, Ye Htun] Univ Birmingham, NIHR Biomed Res Unit Liver Dis, Liver Res Ctr, Inst Immunol & Immunotherapy, Birmingham, W Midlands, England.
[Oo, Ye Htun] Univ Hosp NHS Fdn Trust, Liver & Hepatobiliary Unit, Birmingham, W Midlands, England.
C3 University of Birmingham
RP Oo, YH (corresponding author), Univ Birmingham, NIHR Biomed Res Unit Liver Dis, Liver Res Ctr, Inst Immunol & Immunotherapy, Birmingham, W Midlands, England.; Oo, YH (corresponding author), Univ Hosp NHS Fdn Trust, Liver & Hepatobiliary Unit, Birmingham, W Midlands, England.
EM Y.H.Oo@bham.ac.uk
RI Oo, Ye Htun/AFC-8888-2022
OI Oo, Ye Htun/0000-0002-0495-6734
FU MRC Clinician Scientist Award [G1002552]; Queen Elizabeth Hospital
Charity, Bowel Disease Research Foundation; National Institute of Health
Research Birmingham Liver Biomedical Research Unit; MRC; National
Institute of Health Research Rare Disease Translational Research
Collaborative Grant (UK-Autoimmune Hepatitis); MRC [G1002552] Funding
Source: UKRI
FX Dr. YO was funded by MRC Clinician Scientist Award (G1002552), Queen
Elizabeth Hospital Charity, Bowel Disease Research Foundation. Dr. HJ
was funded by the National Institute of Health Research Birmingham Liver
Biomedical Research Unit and MRC. Ms. MB was funded by National
Institute of Health Research Rare Disease Translational Research
Collaborative Grant (UK-Autoimmune Hepatitis).
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NR 95
TC 49
Z9 52
U1 1
U2 22
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015,
SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 6
PY 2016
VL 7
AR 334
DI 10.3389/fimmu.2016.00334
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA DU9DO
UT WOS:000382516700001
PM 27656181
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Chen, HY
Wang, JM
Zhang, CY
Ding, PL
Tian, SX
Chen, JM
Ji, G
Wu, T
AF Chen, Hongyu
Wang, Junmin
Zhang, Caiyun
Ding, Peilun
Tian, Shuxia
Chen, Junming
Ji, Guang
Wu, Tao
TI Sphingosine 1-phosphate receptor, a new therapeutic direction in
different diseases
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE S1PR; S1P Immune system; Pulmonary disease; Liver disease; Cancer
ID T-CELLS; CROSS-TALK; SPHINGOSINE-1-PHOSPHATE; MIGRATION; INHIBITION;
SYSTEM; ACID; PROLIFERATION; CONTRIBUTES; DISRUPTION
AB Sphingosine 1-phosphate receptor (S1PR), as a kind of G protein-coupled receptor, has five subtypes, including S1PR1, S1PR2, S1PR3, S1PR4, and S1PR5. Sphingosine 1-phosphate receptor (S1P) and S1PR regulate the trafficking of neutrophils and some cells, which has great effects on immune systems, lung tissue, and liver tissue. Presently, many related reports have proved that S1PR has a strong effect on the migration of lymphocytes, tumor cells, neutrophils, and many other cells via the regulation of signals, pathways, and enzymes. In this way, S1PR can regulate the relative response of the organism. Thus, S1PR has become a possible target for the treatment of autoimmune diseases, pulmonary disease, liver disease, and cancer. In this review, we mainly focus on the research of the S1PR for the new therapeutic directions of different diseases and is expected to assist support in the clinic and drug use.
C1 [Chen, Hongyu; Tian, Shuxia; Chen, Junming] Fudan Univ, Minhang Hosp, Xinsong Rd 170, Shanghai 201199, Peoples R China.
[Chen, Hongyu; Wang, Junmin; Zhang, Caiyun; Ding, Peilun; Wu, Tao] Shanghai Univ Tradit Chinese Med, Inst Interdisciplinary Integrat Med Res, Cailun Rd 1200, Shanghai 201203, Peoples R China.
[Ji, Guang] Shanghai Univ Tradit Chinese Med, Longhua Hosp, Inst Digest Dis, South Wanping Rd 725, Shanghai 200032, Peoples R China.
C3 Fudan University; Shanghai University of Traditional Chinese Medicine;
Shanghai University of Traditional Chinese Medicine
RP Chen, JM (corresponding author), Fudan Univ, Minhang Hosp, Xinsong Rd 170, Shanghai 201199, Peoples R China.; Wu, T (corresponding author), Shanghai Univ Tradit Chinese Med, Inst Interdisciplinary Integrat Med Res, Cailun Rd 1200, Shanghai 201203, Peoples R China.; Ji, G (corresponding author), Shanghai Univ Tradit Chinese Med, Longhua Hosp, Inst Digest Dis, South Wanping Rd 725, Shanghai 200032, Peoples R China.
EM chjm2008@126.com; jg@shutcm.edu.cn; wutao001827@163.com
RI li, fangyu/KCY-0521-2024; 田, 淑侠/ABG-4867-2020; chen,
hongyu/HHS-4314-2022
OI Chen, Hongyu/0000-0001-8244-2889
FU National Natural Science Foundation of China [81873076, 81774061];
Hundred Talents Program from Shanghai University of Traditional Chinese
Medicine and Innovation Project for Undergraduates of Shanghai
University of Traditional Chi- nese Medicine [202210268231]
FX This work was supported by the National Natural Science Foundation of
China (81873076, 81774061) , the Hundred Talents Program from Shanghai
University of Traditional Chinese Medicine and Innovation Project for
Undergraduates of Shanghai University of Traditional Chi- nese Medicine
(202210268231) .
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NR 126
TC 35
Z9 37
U1 6
U2 37
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD SEP
PY 2022
VL 153
AR 113341
DI 10.1016/j.biopha.2022.113341
EA JUL 2022
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 4F6WJ
UT WOS:000848650600005
PM 35785704
DA 2025-01-07
ER
PT J
AU Lemoine, M
Ingiliz, P
AF Lemoine, Maud
Ingiliz, Patrick
TI Liver injury in HIV monoinfected patients: Should we turn a blind eye to
it?
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Review
ID HUMAN-IMMUNODEFICIENCY-VIRUS; NONALCOHOLIC FATTY LIVER; HEPATITIS-E
VIRUS; NODULAR REGENERATIVE HYPERPLASIA; INFECTED PATIENTS;
RISK-FACTORS; INSULIN-RESISTANCE; HEPATOCELLULAR-CARCINOMA;
ALCOHOL-CONSUMPTION; AUTOIMMUNE HEPATITIS
AB With the advent of combined antiretroviral therapies, liver diseases have emerged as a key issue in the management of HIV infection. In addition to hepatitis co-infection, a large spectrum of liver diseases can affect the prognosis of HIV infection. Acute or progressive hepatic injuries require an accurate diagnosis for a better clinical management. Here, we provide an overview of the main liver diseases associated with HIV infection, which are not covered by the widely documented field of viral hepatitis co-infection. (c) 2012 Elsevier Masson SAS. All rights reserved.
C1 [Lemoine, Maud] Imperial Coll London, Med Res Council, Hepatitis Dept, Fajara, Gambia.
[Ingiliz, Patrick] Med Ctr Infect Dis, D-13353 Berlin, Germany.
C3 University of London; London School of Hygiene & Tropical Medicine
RP Lemoine, M (corresponding author), Imperial Coll London, Med Res Council, Hepatitis Dept, Atlantic Rd, Fajara, Gambia.
EM mlemoine@mrc.gm; ingiliz@mvz-mib.de
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NR 62
TC 6
Z9 6
U1 0
U2 3
PU ELSEVIER MASSON, CORPORATION OFFICE
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD OCT
PY 2012
VL 36
IS 5
BP 441
EP 447
DI 10.1016/j.clinre.2012.06.002
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 057UP
UT WOS:000312589800017
PM 23079114
DA 2025-01-07
ER
PT J
AU Harrison, L
Gleeson, D
AF Harrison, Laura
Gleeson, Dermot
TI Stopping immunosuppressive treatment in autoimmune hepatitis (AIH): Is
it justified (and in whom and when)?
SO LIVER INTERNATIONAL
LA English
DT Review
DE autoimmune hepatitis; immunosuppressive treatment; liver; relapse;
withdrawal
ID INFLAMMATORY-BOWEL-DISEASE; ACTIVE LIVER-DISEASE;
CORTICOSTEROID-THERAPY; CONTROLLED-TRIAL; TREATMENT WITHDRAWAL;
AZATHIOPRINE METABOLITES; TRANSIENT ELASTOGRAPHY; BIOCHEMICAL REMISSION;
CLINICAL-SIGNIFICANCE; SUSTAINED REMISSION
AB Background Initial treatment of autoimmune hepatitis (AIH) with prednisolone +/- azathioprine is based on randomised controlled trials. Many patients receive long-term immunosuppressive treatment to prevent disease relapse; this strategy has a weaker evidence base. Aim To consider whether immunosuppressive treatment (IST) withdrawal in AIH is justified and to develop a rationale for patient selection.
Methods We reviewed published papers between 1972 and 2018, which addressed the outcomes of IST withdrawal and/or complications of IST in AIH.
Results (1) AIH relapse rates after withdrawal of IST vary between 25% and 100%. There is heterogeneity in these studies regarding relapse definition, IST duration prior to withdrawal and criteria for biochemical and histological remission prior to withdrawal. (2) Factors associated with relapse following IST withdrawal include: (a) absence of an identifiable initial disease trigger, (b) presence of other autoimmune diseases, (c) longer time to biochemical remission and (d) elevated serum transaminases on treatment withdrawal. Reports of associations between relapse and age, IST duration and failure of histological remission have been inconsistent. (3) Continued IST reduces risk of AIH relapse over at least 5 years. However, there is no evidence that routine (as opposed to selective) long-term IST improves disease outcome. (4) Patients with AIH have an increased risk of extrahepatic cancer, notably non-melanoma skin cancer, to which long-term IST may contribute. Long-term corticosteroid therapy is associated with weight gain, low-trauma fractures, diabetes and possibly vascular disease.
Conclusions While further studies are needed, evidence supports a strategy of IST withdrawal in some patients with AIH who have achieved remission.
C1 [Harrison, Laura; Gleeson, Dermot] Northern Gen Hosp, Sheffield Teaching Hosp NHS Fdn Trust, Liver Unit, Sheffield, S Yorkshire, England.
[Harrison, Laura] Univ Sheffield, Med Sch, Dept Infect Immun & Cardiovasc Dis, Sheffield, S Yorkshire, England.
C3 Northern General Hospital; University of Sheffield; University of
Sheffield
RP Harrison, L (corresponding author), Northern Gen Hosp, Liver Unit, Sheffield, S Yorkshire, England.
EM laura.harrison11@nhs.net
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NR 91
TC 24
Z9 25
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD APR
PY 2019
VL 39
IS 4
BP 610
EP 620
DI 10.1111/liv.14051
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HQ7AW
UT WOS:000462572800002
PM 30667576
OA Bronze
DA 2025-01-07
ER
PT J
AU Zúñigaa, S
Firrincieli, D
Housset, C
Chignard, N
AF Zunigaa, Silvia
Firrincieli, Delphine
Housset, Chantal
Chignard, Nicolas
TI Vitamin D and the vitamin D receptor in liver pathophysiology
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Review
ID PRIMARY BILIARY-CIRRHOSIS; D-BINDING PROTEIN; ISOLATED EPITHELIAL-CELLS;
FARNESOID-X-RECEPTOR; CHRONIC HEPATITIS-C; BILE-ACID SYNTHESIS; D
NUCLEAR RECEPTOR; GENE POLYMORPHISMS; IN-VITRO; 1,25-DIHYDROXYVITAMIN
D-3
AB Vitamin D through the vitamin D nuclear receptor (VDR) plays a key role in mineral ion homeostasis. The liver is central in vitamin D synthesis, however the direct involvement of the vitamin D-VDR axis on the liver remains to be evaluated. In this review, we will describe vitamin D metabolism and the mechanisms of homeostatic control. We will also address the associations between the vitamin D-VDR axis and pathological liver entities, such as non-alcoholic fatty liver disease, autoimmune liver disease, viral hepatitis and liver cancer. The link between liver diseases and the vitamin D-VDR axis will be discussed in light of evidences arising from in vitro and in vivo studies. Finally, we will consider the therapeutic potential of the vitamin D-VDR axis in liver diseases. (C) 2011 Elsevier Masson SAS. All rights reserved.
C1 [Zunigaa, Silvia; Firrincieli, Delphine; Housset, Chantal; Chignard, Nicolas] Univ Paris 06, UMR S 938, CdR St Antoine, F-75005 Paris, France.
[Zunigaa, Silvia; Firrincieli, Delphine; Housset, Chantal; Chignard, Nicolas] INSERM, UMR S 938, CdR St Antoine, F-75012 Paris, France.
[Zunigaa, Silvia] Pontificia Univ Catolica Chile, Santiago, Chile.
[Housset, Chantal] Hop St Antoine, Serv Hepatol, AP HP, F-75020 Paris, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
Sorbonne Universite; Sorbonne Universite; Institut National de la Sante
et de la Recherche Medicale (Inserm); Pontificia Universidad Catolica de
Chile; Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite;
Hopital Universitaire Saint-Antoine - APHP
RP Chignard, N (corresponding author), UPMC, UMR S 938, CdR St Antoine, 27 Rue Chaligny, F-75571 Paris 12, France.
EM nicolas.chignard@upmc.fr
RI Firrincieli, Delphine/K-8663-2018; Chignard, Nicolas/B-2835-2008
OI Housset, Chantal/0000-0001-6469-0651; Chignard,
Nicolas/0000-0002-2680-1864
FU French Association for the Study of the Liver (AFEF) Association pour la
lutte contre les maladies inflammatoires du foie et des voies biliaires
(ALBI); European Community [FP7/2007-2013, HEALT-HF2-2009-241762]
FX This work was supported by the French Association for the Study of the
Liver (AFEF) Association pour la lutte contre les maladies
inflammatoires du foie et des voies biliaires (ALBI) and by the European
Community's Seventh Framework Programme (FP7/2007-2013) under agreement
no HEALT-HF2-2009-241762 for the project FLIP.
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NR 91
TC 60
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U2 29
PU ELSEVIER MASSON, CORPORATION OFFICE
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD APR
PY 2011
VL 35
IS 4
BP 295
EP 302
DI 10.1016/j.clinre.2011.02.003
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 754FI
UT WOS:000289839700008
PM 21440524
DA 2025-01-07
ER
PT J
AU Hirschfield, GM
Kumagi, T
Heathcote, EJ
AF Hirschfield, Gideon M.
Kumagi, Teru
Heathcote, E. Jenny
TI Preventative hepatology: minimising symptoms and optimising care
SO LIVER INTERNATIONAL
LA English
DT Review
DE autoimmune liver disease; cholestasis; chronic liver disease; chronic
viral hepatitis; cirrhosis; hepatocellular carcinoma; osteoporosis;
pregnancy and liver disease; safe prescribing; travel health
ID PRIMARY BILIARY-CIRRHOSIS; CHRONIC LIVER-DISEASE; QUALITY-OF-LIFE;
PRIMARY SCLEROSING CHOLANGITIS; DOSE URSODEOXYCHOLIC ACID; VITAMIN-D
SUPPLEMENTATION; RANDOMIZED CONTROLLED-TRIAL; BONE-MINERAL DENSITY;
CHRONIC HEPATITIS-B; INTRAHEPATIC CHOLESTASIS
AB Most care of liver disease is in the ambulatory setting, and therefore the clinical needs of patients represent those of any other chronic illness. Emphasis must be given to preventative strategies such that liver lifetime (including pre-emptive strategies related to potential allograft survival) is maximised through timely intervention and avoidance of side effects. This review addresses the pertinent practical clinical concerns faced by clinicians as they manage adult patients with chronic liver disease, with an emphasis on preventing and managing symptoms and complications directly and indirectly related to the underlying disease.
C1 [Hirschfield, Gideon M.; Kumagi, Teru; Heathcote, E. Jenny] Univ Toronto, Toronto Western Hosp, Univ Hlth Network, Toronto, ON M5T 2S8, Canada.
C3 University of Toronto; University Health Network Toronto
RP Hirschfield, GM (corresponding author), Univ Toronto, Toronto Western Hosp, Univ Hlth Network, 399 Bathurst St, Toronto, ON M5T 2S8, Canada.
EM gideon.hirschfield@uhn.on.ca
RI Kumagi, Teru/AAS-7427-2021; Hirschfield, Gideon/M-2143-2015
OI Hirschfield, Gideon/0000-0002-6736-2255; Kumagi,
Teru/0000-0002-2292-7750
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NR 134
TC 25
Z9 25
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD AUG
PY 2008
VL 28
IS 7
BP 922
EP 934
DI 10.1111/j.1478-3231.2008.01816.x
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 327CG
UT WOS:000257706600005
PM 18783540
OA Bronze
DA 2025-01-07
ER
PT J
AU Zhu, LR
Li, SS
Zheng, WQ
Ni, WJ
Cai, M
Liu, HP
AF Zhu, Li-Ran
Li, Shan-Shan
Zheng, Wan-Qun
Ni, Wei-Jian
Cai, Ming
Liu, Hai-Peng
TI Targeted modulation of gut microbiota by traditional Chinese medicine
and natural products for liver disease therapy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE liver disease; gut microbiota; traditional Chinese medicine; natural
product; therapeutic strategy
ID INTESTINAL PERMEABILITY; AXIS; METABOLISM; DYSBIOSIS; INJURY; ACIDS;
MICE
AB The gut microbiota not only constitutes intestinal microenvironment homeostasis and human health but also exerts indispensable roles in the occurrence and progression of multiple liver diseases, including alcohol-related liver disease, nonalcoholic fatty liver disease, autoimmune liver disease and liver cancer. Given the therapeutic status of these diseases, their prevention and early therapy are crucial, and the detailed mechanism of gut microbiota in liver disease urgently needs to be explored. Meanwhile, multiple studies have shown that various traditional Chinese medicines, such as Si Miao Formula, Jiangzhi Granules, Liushen Capsules, Chaihu-Shugan Power, Cassiae Semen and Gynostemma, as well as some natural products, including Costunolide, Coprinus comatus polysaccharide, Antarctic krill oil, Oridonin and Berberine, can repair liver injury, improve fatty liver, regulate liver immunity, and even inhibit liver cancer through multiple targets, links, and pathways. Intriguingly, the aforementioned effects demonstrated by these traditional Chinese medicines and natural products have been shown to be closely related to the gut microbiota, directly driving the strategy of traditional Chinese medicines and natural products to regulate the gut microbiota as one of the breakthroughs in the treatment of liver diseases. Based on this, this review comprehensively summarizes and discusses the characteristics, functions and potential mechanisms of these medicines targeting gut microbiota during liver disease treatment. Research on the potential effects on gut microbiota and the regulatory mechanisms of traditional Chinese medicine and natural products provides novel insights and significant references for developing liver disease treatment strategies. In parallel, such explorations will enhance the comprehension of traditional Chinese medicine and natural products modulating gut microbiota during disease treatment, thus facilitating their clinical investigation and application.
C1 [Zhu, Li-Ran; Liu, Hai-Peng] Anhui Prov Childrens Hosp, Anhui Inst Pediat Res, Hefei, Anhui, Peoples R China.
[Zhu, Li-Ran] Chinese Acad Sci, Inst Hlth & Med Technol, Hefei Inst Phys Sci, Anhui Prov Key Lab Med Phys & Technol, Hefei, Anhui, Peoples R China.
[Li, Shan-Shan] Anhui Prov Childrens Hosp, Dept Sci Res & Educ, Hefei, Anhui, Peoples R China.
[Zheng, Wan-Qun] Anhui Med Univ, Dept Chinese Med, Affiliated Hosp 1, Hefei, Anhui, Peoples R China.
[Ni, Wei-Jian] Univ Sci & Technol China, Anhui Prov Hosp, Affiliated Hosp 1, Dept Pharm,USTC,Div Life Sci & Med, Hefei, Anhui, Peoples R China.
[Ni, Wei-Jian] Anhui Med Univ, Anhui Inst Innovat Drugs, Sch Pharm, Inflammat & Immune Mediated Dis Lab Anhui Prov,Key, Hefei, Anhui, Peoples R China.
[Cai, Ming] Anhui Univ Tradit Chinese Med, Dept Pharm, Affiliated Hosp 2, Hefei, Anhui, Peoples R China.
[Cai, Ming] Anhui Univ Tradit Chinese Med, Anhui Acupuncture & Moxibust Clin Med Res Ctr, Affiliated Hosp 2, Hefei, Anhui, Peoples R China.
C3 Chinese Academy of Sciences; Hefei Institutes of Physical Science, CAS;
Anhui Medical University; Chinese Academy of Sciences; University of
Science & Technology of China, CAS; Anhui Medical University; Anhui
University of Chinese Medicine; Anhui University of Chinese Medicine
RP Liu, HP (corresponding author), Anhui Prov Childrens Hosp, Anhui Inst Pediat Res, Hefei, Anhui, Peoples R China.; Ni, WJ (corresponding author), Univ Sci & Technol China, Anhui Prov Hosp, Affiliated Hosp 1, Dept Pharm,USTC,Div Life Sci & Med, Hefei, Anhui, Peoples R China.; Ni, WJ (corresponding author), Anhui Med Univ, Anhui Inst Innovat Drugs, Sch Pharm, Inflammat & Immune Mediated Dis Lab Anhui Prov,Key, Hefei, Anhui, Peoples R China.; Cai, M (corresponding author), Anhui Univ Tradit Chinese Med, Dept Pharm, Affiliated Hosp 2, Hefei, Anhui, Peoples R China.; Cai, M (corresponding author), Anhui Univ Tradit Chinese Med, Anhui Acupuncture & Moxibust Clin Med Res Ctr, Affiliated Hosp 2, Hefei, Anhui, Peoples R China.
EM niweijian@ustc.edu.cn; hefeicaiming@126.com; itishaipeng@yeah.net
RI Liu, Haipeng/A-1879-2012
OI Ni, Wei-Jian/0000-0002-9844-0578
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NR 96
TC 25
Z9 28
U1 14
U2 96
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD FEB 2
PY 2023
VL 14
AR 1086078
DI 10.3389/fimmu.2023.1086078
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 9F1TF
UT WOS:000937256900001
PM 36817459
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Morgan, MA
Khot, R
Sundaram, KM
Ludwig, DR
Nair, RT
Mittal, PK
Ganeshan, DM
Venkatesh, SK
AF Morgan, Matthew A.
Khot, Rachita
Sundaram, Karthik M.
Ludwig, Daniel R.
Nair, Rashmi T.
Mittal, Pardeep K.
Ganeshan, Dhakshina M.
Venkatesh, Sudhakar K.
TI Primary sclerosing cholangitis: review for radiologists
SO ABDOMINAL RADIOLOGY
LA English
DT Review
DE Liver; MRI; Elastography; Biliary; Cholangitis; Primary sclerosing
cholangitis
ID MAGNETIC-RESONANCE ELASTOGRAPHY; LIVER-TRANSPLANTATION; OVERLAP
SYNDROME; RISK-FACTORS; AUTOIMMUNE HEPATITIS; CANCER SURVEILLANCE;
GALLBLADDER POLYPS; DISEASE; CHOLANGIOCARCINOMA; MRI
AB Primary sclerosing cholangitis is a rare chronic inflammatory disease affecting the bile ducts, which can eventually result in bile duct strictures, cholestasis and cirrhosis. Patients are often asymptomatic but may present with clinical features of cholestasis. Imaging plays an important role in the diagnosis and management. This review covers the pathophysiology, clinical features, imaging findings as well as methods of surveillance and post-transplant appearance.
[GRAPHICS]
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C1 [Morgan, Matthew A.; Sundaram, Karthik M.] Univ Penn Hlth Syst, Dept Radiol, 1 Silverstein,3400 Spruce St, Philadelphia, PA USA.
[Khot, Rachita] Univ Virginia Hlth, Radiol & Med Imaging, 1215 Lee St, Charlottesville, VA USA.
[Ludwig, Daniel R.] Washington Univ, Sch Med, Mallinckrodt Inst Radiol, 510 S Kingshighway Blvd,Campus Box 8131, St Louis, MO USA.
[Nair, Rashmi T.] Univ Kentucky, Dept Radiol, 800 Rose St,Room HX 313B, Lexington, KY 40536 USA.
[Mittal, Pardeep K.] Augusta Univ, Med Coll Georgia, 1120 15th St BA-1411, Augusta, GA 30912 USA.
[Ganeshan, Dhakshina M.] Univ Texas MD Anderson Canc Ctr, 1400 Pressler St,Unit 1473, Houston, TX 77030 USA.
[Venkatesh, Sudhakar K.] Mayo Clin, Dept Radiol, Abdominal Imaging, Rochester, MN 55905 USA.
C3 University of Pennsylvania; University of Virginia; Washington
University (WUSTL); University of Kentucky; University System of
Georgia; Augusta University; University of Texas System; UTMD Anderson
Cancer Center; Mayo Clinic
RP Morgan, MA (corresponding author), Univ Penn Hlth Syst, Dept Radiol, 1 Silverstein,3400 Spruce St, Philadelphia, PA USA.
EM Matthew.Morgan@pennmedicine.upenn.edu; rk9j@virginia.edu;
Karthik.Sundaram@Pennmedicine.upenn.edu; ludwigd@wustl.edu;
rtna222@uky.edu; pmittal@augusta.edu; dganeshan@mdanderson.org;
venkatesh.sudhakar@mayo.edu
RI Mittal, Pardeep/H-8537-2019; Morgan, Matthew/KFS-1478-2024; Sundaram,
Karthik/HGT-8743-2022; Venkatesh, Sudhakar/T-9385-2019
OI Sundaram, Karthik/0000-0001-9392-7910; Morgan,
Matthew/0000-0001-8956-4483; Mittal, Pardeep/0000-0002-3302-8590;
Venkatesh, Sudhakar/0000-0002-7514-1030
FU U.S. Department of Defense [W81XWH-19-1-0583-01]; NIH R01Grant
[EB001981]
FX Dr. Venkatesh acknowledges support from NIH R01Grant EB001981 and U.S.
Department of Defense Grant W81XWH-19-1-0583-01.
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NR 72
TC 8
Z9 8
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2366-004X
EI 2366-0058
J9 ABDOM RADIOL
JI Abdom. Radiol.
PD JAN
PY 2023
VL 48
IS 1
SI SI
BP 136
EP 150
DI 10.1007/s00261-022-03655-6
EA SEP 2022
PG 15
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA A1EM0
UT WOS:000850047300002
PM 36063181
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Arora, GS
Javed, H
Kaur, P
Singh, S
AF Arora, Gagandeep Singh
Javed, Hamna
Kaur, Parneet
Singh, Simran
TI Hepatopulmonary Syndrome in a Patient With Autoimmune Hepatitis and
Chronic Hepatitis C: A Case Report Highlighting Typical Echo Findings
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE liver transplantation; symptom management; respiratory failure;
echocardiography; chronic hepatitis c; autoimmune hepatitis; arterial
hypoxemia; intrapulmonary vascular dilatations; hepatopulmonary syndrome
AB Hepatopulmonary syndrome (HPS) is a rare complication of liver disease characterized by intrapulmonary vascular dilatations leading to arterial hypoxemia. We present the case of a 59-year-old female with a past medical history of bilateral breast cancer status post mastectomy who presented with progressive dyspnea on exertion and fatigue. A comprehensive diagnostic workup was conducted to exclude other cardiac, pulmonary, and systemic etiologies. She was diagnosed with autoimmune hepatitis along with chronic hepatitis C. Echocardiography revealed characteristic findings of intrapulmonary shunting characteristic of HPS. The patient showed improvement in pulmonary symptoms and oxygenation status following the initiation of steroid therapy. Although corticosteroids are not the definitive treatment for HPS, they were considered a supportive measure in this case. However, it is important to note that liver transplantation remains the definitive treatment for HPS. This case underscores the importance of echocardiography and the potential role of supportive measures, like corticosteroids, in managing HPS-related symptoms, particularly in patients with autoimmune hepatitis, as a bridging therapy while awaiting liver transplantation.
C1 [Arora, Gagandeep Singh] Univ Calif Riverside, Internal Med, San Bernardino, CA 92521 USA.
[Javed, Hamna] St Agnes Med Ctr, Internal Med, Fresno, CA USA.
[Kaur, Parneet] Suburban Community Hosp, Internal Med, Philadelphia, PA USA.
[Singh, Simran] Jinnah Sindh Med Univ SMC, Internal Med, Karachi, Pakistan.
C3 Jinnah Sindh Medical University - Pakistan
RP Arora, GS (corresponding author), Univ Calif Riverside, Internal Med, San Bernardino, CA 92521 USA.
EM gagan89arora@gmail.com
RI Kaur, Parneet/ISA-2806-2023
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NR 10
TC 1
Z9 1
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD JUL 7
PY 2023
VL 15
IS 7
DI 10.7759/cureus.41491
PG 6
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA CG6U8
UT WOS:001124148600015
PM 37484786
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Chrostek, L
Cylwik, B
Panasiuk, A
Brodowska-Adamusiak, D
Gruszewska, E
AF Chrostek, Lech
Cylwik, Bogdan
Panasiuk, Anatol
Brodowska-Adamusiak, Dorota
Gruszewska, Ewa
TI Lipid-bound sialic acid (LSA) in liver diseases of different etiologies
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Lipid-bound sialic acid; Sialylation; Glycosylation; Liver diseases
ID SERUM; LIPOPROTEINS; GANGLIOSIDES
AB Objective. There are evidences that the changes in glycosylation and sialylation of proteins and lipids play an important role in the pathogenesis and progression of various liver diseases. The aim of this study was to evaluate the changes in the sialylation of serum lipids measured by the level of lipid-bound sialic acid (LSA) in liver diseases of different etiologies. Materials and methods. Tested group consisted of 303 patients suffering from liver diseases: alcoholic and non-alcoholic cirrhosis, chronic non-viral hepatitis, toxic hepatitis, chronic viral C and B hepatitis, autoimmune hepatitis, primary liver cancer, liver cancer and cirrhosis (mixed group), acute hepatitis B, primary biliary cirrhosis and fatty liver. LSA was determined by the method of Katopodis and co-workers. Results. There were significant differences in the serum LSA concentrations between liver diseases of different etiologies. The level of LSA in liver tumors was higher than that in both types of cirrhosis: alcoholic and non-alcoholic. In turn, LSA level in non-alcoholic cirrhosis was lower than in toxic hepatitis and mixed group. There was no difference in LSA concentration between tumor and mixed group. Similarly to LSA, AFP level in tumor group was also higher than that in both cirrhotic groups, but there was no difference in AFP concentration between tumor and mixed group. Conclusions. The sialylation of serum lipids alters in liver diseases of different etiologies. Given the importance of glycans in biological systems we can speculate that the changes in lipids sialylation play an important role in liver pathology, especially in primary cancer, cirrhosis and toxic hepatitis.
C1 [Chrostek, Lech; Cylwik, Bogdan; Brodowska-Adamusiak, Dorota; Gruszewska, Ewa] Med Univ, Dept Biochem Diagnost, PL-15274 Bialystok, Poland.
[Panasiuk, Anatol] Med Univ, Dept Infect Dis, PL-15274 Bialystok, Poland.
C3 Medical University of Bialystok; Medical University of Bialystok
RP Chrostek, L (corresponding author), Med Univ, Dept Biochem Diagnost, Waszyngtona 15A St, PL-15274 Bialystok, Poland.
EM chrostek@umwb.edu.pl
RI Gruszewska, Ewa/T-1062-2018; Cylwik, Bogdan/S-5063-2018; Chrostek,
Lech/T-2219-2018
OI Cylwik, Bogdan/0000-0002-9890-7334; Gruszewska, Ewa/0000-0002-7702-5148;
Chrostek, Lech/0000-0001-6701-1861
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NR 16
TC 11
Z9 16
U1 0
U2 3
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD APR-JUN
PY 2011
VL 10
IS 2
BP 150
EP 154
DI 10.1016/S1665-2681(19)31563-7
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 764NJ
UT WOS:000290636300005
PM 21502676
OA hybrid
DA 2025-01-07
ER
PT J
AU Altieri, B
Muscogiuri, G
Barrea, L
Mathieu, C
Vallone, CV
Mascitelli, L
Bizzaro, G
Altieri, VM
Tirabassi, G
Balercia, G
Savastano, S
Bizzaro, N
Ronchi, CL
Colao, A
Pontecorvi, A
Della Casa, S
AF Altieri, Barbara
Muscogiuri, Giovanna
Barrea, Luigi
Mathieu, Chantal
Vallone, Carla V.
Mascitelli, Luca
Bizzaro, Giorgia
Altieri, Vincenzo M.
Tirabassi, Giacomo
Balercia, Giancarlo
Savastano, Silvia
Bizzaro, Nicola
Ronchi, Cristina L.
Colao, Annamaria
Pontecorvi, Alfredo
Della Casa, Silvia
TI Does vitamin D play a role in autoimmune endocrine disorders? A proof of
concept
SO REVIEWS IN ENDOCRINE & METABOLIC DISORDERS
LA English
DT Review
DE Vitamin D; Autoimmunity; Type 1 diabetes mellitus; Addison's disease;
Hashimoto's thyroiditis; Graves' disease; Autoimmune polyendocrine
syndromes; Environment; Lifestyle
ID D-RECEPTOR GENE; TYPE-1 DIABETES-MELLITUS; BETA-CELL FUNCTION; COD-LIVER
OIL; 1,25-DIHYDROXYVITAMIN D-3; GRAVES-DISEASE; D DEFICIENCY;
ADDISONS-DISEASE; THYROID-DISEASES; IMMUNE-SYSTEM
AB In the last few years, more attention has been given to the "non-calcemic" effect of vitamin D. Several observational studies and meta-analyses demonstrated an association between circulating levels of vitamin D and outcome of many common diseases, including endocrine diseases, chronic diseases, cancer progression, and autoimmune diseases. In particular, cells of the immune system (B cells, T cells, and antigen presenting cells), due to the expression of 1 alpha-hydroxylase (CYP27B1), are able to synthesize the active metabolite of vitamin D, which shows immunomodulatory properties. Moreover, the expression of the vitamin D receptor (VDR) in these cells suggests a local action of vitamin D in the immune response. These findings are supported by the correlation between the polymorphisms of the VDR or the CYP27B1 gene and the pathogenesis of several autoimmune diseases. Currently, the optimal plasma 25-hydroxyvitamin D concentration that is necessary to prevent or treat autoimmune diseases is still under debate. However, experimental studies in humans have suggested beneficial effects of vitamin D supplementation in reducing the severity of disease activity. In this review, we summarize the evidence regarding the role of vitamin D in the pathogenesis of autoimmune endocrine diseases, including type 1 diabetes mellitus, Addison's disease, Hashimoto's thyroiditis, Graves' disease and autoimmune polyendocrine syndromes. Furthermore, we discuss the supplementation with vitamin D to prevent or treat autoimmune diseases.
C1 [Altieri, Barbara; Pontecorvi, Alfredo; Della Casa, Silvia] Univ Cattolica Sacro Cuore, Inst Med Pathol, Div Endocrinol & Metab Dis, Rome, Italy.
[Muscogiuri, Giovanna; Barrea, Luigi] Univ Federico II, Ios & Coleman Med Futura Med Ctr, Naples, Italy.
[Mathieu, Chantal] Katholieke Univ Leuven, Clin & Expt Endocrinol, Leuven, Belgium.
[Vallone, Carla V.] Fdn Poliambulanza, Ist Osped, Emergency Dept, Brescia, Italy.
[Mascitelli, Luca] Comando Brigata Alpina Julia Multinatl Land Force, Med Serv, Udine, Italy.
[Bizzaro, Giorgia] TSEM Med Swiss SA, Lugano, Switzerland.
[Altieri, Vincenzo M.] Bolognini Hosp, Dept Urol, Seriate, Italy.
[Tirabassi, Giacomo; Balercia, Giancarlo] Polytech Univ Marche, Div Endocrinol, Dept Clin & Mol Sci, Umberto Hosp 1, Ancona, Italy.
[Savastano, Silvia; Colao, Annamaria] Univ Naples Federico II, Dept Clin Med & Surg, Naples, Italy.
[Bizzaro, Nicola] San Antonio Hosp, Clin Pathol Lab, Tolmezzo, Italy.
[Ronchi, Cristina L.] Univ Hosp Wuerzburg, Div Endocrinol & Diabet, Dept Internal Med 1, Wurzburg, Germany.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
University of Naples Federico II; KU Leuven; Marche Polytechnic
University; University of Naples Federico II; University of Wurzburg
RP Altieri, B (corresponding author), Univ Cattolica Sacro Cuore, Inst Med Pathol, Div Endocrinol & Metab Dis, Rome, Italy.
EM altieri.barbara@gmail.com
RI Pontecorvi, Alfredo/K-5146-2016; Altieri, Barbara/HMP-1607-2023; Colao,
Annamaria/A-7671-2011; mathieu, chantal/ABD-5505-2021; Muscogiuri,
Giovanna/K-5817-2016; Barrea, Luigi/K-6551-2016; Savastano,
Silvia/K-6546-2016
OI Mathieu, Chantal/0000-0002-4055-5233; Altieri,
Barbara/0000-0003-2616-3249; Barrea, Luigi/0000-0001-9054-456X; Ronchi,
Cristina/0000-0001-5020-2071; Savastano, Silvia/0000-0002-3211-4307
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NR 105
TC 131
Z9 137
U1 2
U2 40
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1389-9155
EI 1573-2606
J9 REV ENDOCR METAB DIS
JI Rev. Endocr. Metab. Disord.
PD SEP
PY 2017
VL 18
IS 3
BP 335
EP 346
DI 10.1007/s11154-016-9405-9
PN 2
PG 12
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA FC4SS
UT WOS:000406831500005
PM 28070798
DA 2025-01-07
ER
PT J
AU Maheshwari, A
Thuluvath, PJ
AF Maheshwari, Anurag
Thuluvath, Paul J.
TI Endocrine Diseases and the Liver
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Endocrine disorders; Fatty liver disease; Abnormal liver function test
result
ID NONALCOHOLIC FATTY LIVER; GROWTH-HORMONE DEFICIENCY; HEPATITIS-C VIRUS;
ADRENAL INSUFFICIENCY; INSULIN-RESISTANCE; ORAL-CONTRACEPTIVES;
METABOLIC SYNDROME; HEPATOCELLULAR-CARCINOMA; PLASMA ADIPONECTIN;
DIABETES-MELLITUS
AB Liver disease and endocrine disorders, both common in the general population, have a bidirectional and complex relationship. Certain liver diseases are more commonly associated with endocrine disorders, including nonalcoholic fatty liver disease, autoimmune hepatitis, and primary biliary cirrhosis. There may be an association between hepatitis C and type 2 diabetes mellitus as well as thyroid disorders, and sex hormonal preparations may cause specific hepatic lesions. The presence of relative adrenal insufficiency in patients with end-stage liver disease may have therapeutic implications in patients admitted with acute-on-chronic liver failure. The objective of this review is to focus on the effect of endocrine disorders on liver.
C1 [Thuluvath, Paul J.] Georgetown Univ, Sch Med, Baltimore, MD 21202 USA.
[Maheshwari, Anurag; Thuluvath, Paul J.] Mercy Med Ctr, Inst Digest Hlth & Liver Dis, Baltimore, MD 21202 USA.
C3 Georgetown University; Mercy Medical Center - Maryland
RP Thuluvath, PJ (corresponding author), Georgetown Univ, Sch Med, 301 St Paul Pl,Phys Off Bldg, Baltimore, MD 21202 USA.
EM thuluvath@gmail.com
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NR 68
TC 26
Z9 29
U1 9
U2 90
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD FEB
PY 2011
VL 15
IS 1
BP 55
EP +
DI 10.1016/j.cld.2010.09.008
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 701VB
UT WOS:000285850600005
PM 21111993
DA 2025-01-07
ER
PT J
AU Yang, WT
Guo, GY
Sun, C
AF Yang, Wanting
Guo, Gaoyue
Sun, Chao
TI Therapeutic potential of rifaximin in liver diseases
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Rifaximin; Liver disease; Gut microbiota; Antibiotic; Liver cirrhosis
ID PREGNANE-X-RECEPTOR; SPONTANEOUS BACTERIAL PERITONITIS; PRIMARY
SCLEROSING CHOLANGITIS; IRRITABLE-BOWEL-SYNDROME; IN-VITRO ACTIVITY;
ANTIBACTERIAL ACTIVITY; GUT MICROBIOTA; MACROPHAGE ACTIVATION;
CLOSTRIDIUM-DIFFICILE; REFRACTORY ASCITES
AB Rifaximin, derived from rifamycin, is a broad-spectrum antibiotic by inhibiting bacterial RNA synthesis. Rifaximin has a very low intestinal absorption and exerts its antimicrobial activity primarily in the intestinal tract. It regulates the gut microbiota with limited side effects systemically. Rifaximin has been recommended for the treatment of hepatic encephalopathy but some studies shed light on its medicinal effects in many other diseases. For instance, rifaximin may suppress the progression of liver fibrosis and its related complications, and ameliorate metabolic dysfunction-associated steatotic liver disease and alcohol-associated liver disease, etc. Rifaximin can also mediate anti-inflammation, antiproliferation, and proapoptotic events by activating pregnane X receptor, which is efficious in cancers such as colon cancer. In addition, some investigations have shown rifaximin may play a therapeutic role in various autoimmune and neurological disorders. However, these findings still need more real-world practices and in-depth investigations to obtain more precise indications and fully elucidate the multifaceted potentials of rifaximin.
C1 [Yang, Wanting; Guo, Gaoyue; Sun, Chao] Tianjin Med Univ, Gen Hosp, Dept Gastroenterol & Hepatol, Anshan Rd 154, Tianjin 300052, Peoples R China.
[Yang, Wanting; Guo, Gaoyue; Sun, Chao] Tianjin Med Univ, Gen Hosp, Airport Hosp, Dept Gastroenterol, East St 6,Tianjin Airport Econ Area, Tianjin 300308, Peoples R China.
C3 Tianjin Medical University; Tianjin Medical University
RP Sun, C (corresponding author), Tianjin Med Univ, Gen Hosp, Dept Gastroenterol & Hepatol, Anshan Rd 154, Tianjin 300052, Peoples R China.
EM chaosun@tmu.edu.cn
RI Yang, Wanting/AAZ-6192-2020
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NR 131
TC 1
Z9 1
U1 5
U2 5
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD SEP
PY 2024
VL 178
AR 117283
DI 10.1016/j.biopha.2024.117283
EA AUG 2024
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA D2W5L
UT WOS:001294842500001
PM 39126775
OA gold
DA 2025-01-07
ER
PT J
AU Xu, LY
Ling, JW
Su, C
Su, YW
Xu, Y
Jiang, ZZ
AF Xu, Lingyan
Ling, Jiawei
Su, Chang
Su, Yu-Wen
Xu, Yan
Jiang, Zhenzhou
TI Emerging Roles on Immunological Effect of Indoleamine 2,3-Dioxygenase in
Liver Injuries
SO FRONTIERS IN MEDICINE
LA English
DT Review
DE IDO; liver injury; kynurenine pathway; immunoregulation; liver diseases
ID CYTOTOXIC T-LYMPHOCYTES; LONG-TERM SURVIVAL; DENDRITIC CELLS;
CARBON-TETRACHLORIDE; IFN-GAMMA; TRYPTOPHAN-METABOLISM; HEPATITIS-B;
KYNURENINE PATHWAY; PERIPHERAL-BLOOD; IMMUNE-RESPONSES
AB Indoleamine 2,3-dioxygenase (IDO) is one of the initial rate-limiting enzymes of the kynurenine pathway (KP), which causes immune suppression and induction of T cell anergy. It is associated with the imbalance of immune homeostasis in numerous diseases including cancer, chronic viral infection, allergy, and autoimmune diseases. Recently, IDO has extended its role to liver field. In this review, we summarize the dysregulation and potentials of IDO in the emerging field of liver injuries, as well as current challenges for IDO targets. In particular, we discuss unexpected conclusions against previous work published. IDO is induced by pro-inflammatory cytokines in liver dysfunction and exerts an immunosuppressive effect, whereas the improvement of liver injury may require consideration of multiple factors besides IDO.
C1 [Xu, Lingyan; Su, Chang; Su, Yu-Wen; Xu, Yan] Nanjing Med Univ, Sir Run Run Hosp, Nanjing, Peoples R China.
[Ling, Jiawei] Chinese Univ Hong Kong, Inst Chinese Med, Hong Kong, Peoples R China.
[Ling, Jiawei] Chinese Univ Hong Kong, State Key Lab Res Bioact & Clin Applicat Med Plan, Hong Kong, Peoples R China.
[Su, Yu-Wen] Nanjing Med Univ, Sch Pharm, Nanjing, Peoples R China.
[Jiang, Zhenzhou] China Pharmaceut Univ, New Drug Screening Ctr, Jiangsu Ctr Pharmacodynam Res & Evaluat, Nanjing, Peoples R China.
C3 Nanjing Medical University; Chinese University of Hong Kong; Chinese
University of Hong Kong; Nanjing Medical University; China
Pharmaceutical University
RP Jiang, ZZ (corresponding author), China Pharmaceut Univ, New Drug Screening Ctr, Jiangsu Ctr Pharmacodynam Res & Evaluat, Nanjing, Peoples R China.
EM beaglejiang@cpu.edu.cn
RI Su, Yu-Wen/V-4948-2018
OI Su, Yu-wen/0000-0001-6730-8219
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NR 142
TC 4
Z9 4
U1 0
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD NOV 18
PY 2021
VL 8
AR 756435
DI 10.3389/fmed.2021.756435
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA XI5NF
UT WOS:000726157400001
PM 34869457
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU MacArthur, KL
Forouhar, F
Wu, GYH
AF MacArthur, Kristin Loening
Forouhar, Faripour
Wu, George Yung-Hsing
TI Intra-abdominal Complications of Sarcoidosis
SO JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION
LA English
DT Review
DE gastrointestinal; hepatic; pancreatic; peritoneal; splenic
ID OF-THE-LITERATURE; GASTROINTESTINAL SARCOIDOSIS; PERITONEAL SARCOIDOSIS;
HEPATIC SARCOIDOSIS; HEPATOCELLULAR-CARCINOMA; ESOPHAGEAL SARCOIDOSIS;
SYSTEMIC SARCOIDOSIS; SPLENIC SARCOIDOSIS; GASTRIC SARCOIDOSIS;
INVOLVEMENT
AB Sarcoidosis is an inflammatory disease characterized by non-caseating granulomas in the absence of other autoimmune processes, infectious diseases, or foreign agents. The etiology of sarcoidosis is not completely understood. Several organ systems can be affected, of which the most frequently involved include the lungs and lymph nodes. Intra-abdominal sarcoidosis is less common, but can be found in the absence of pulmonary or lymphatic disease. Intra-abdominal sarcoidosis is most often asymptomatic. However, long-standing unrecognized disease can result in life-threatening complications. The identification, monitoring and prevention of these complications will be discussed, with emphasis on both clinical and histological presentations of intra-abdominal sarcoidosis.
C1 [Wu, George Yung-Hsing] Univ Connecticut, Ctr Hlth, Dept Med, Div Gastroenterol Hepatol, Farmington, CT 06030 USA.
[Forouhar, Faripour] Univ Connecticut, Ctr Hlth, Dept Anat Pathol, Farmington, CT 06030 USA.
C3 University of Connecticut; University of Connecticut
RP Wu, GYH (corresponding author), Univ Connecticut, Ctr Hlth, Dept Med, Div Gastroenterol Hepatol, Rm AM 044,263 Farmington Ave, Farmington, CT 06030 USA.
EM wu@nso.uchc.edu
RI Wu, George/JCE-1302-2023
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NR 66
TC 22
Z9 23
U1 0
U2 0
PU ELSEVIER TAIWAN
PI TAIPEI
PA RM N-412, 4F, CHIA HSIN BUILDING 11, NO 96, ZHONG SHAN N ROAD SEC 2,
TAIPEI, 10449, TAIWAN
SN 0929-6646
EI 1876-0821
J9 J FORMOS MED ASSOC
JI J. Formos. Med. Assoc.
PD JUL
PY 2010
VL 109
IS 7
BP 484
EP 492
DI 10.1016/S0929-6646(10)60082-4
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 632IS
UT WOS:000280416800002
PM 20654787
DA 2025-01-07
ER
PT J
AU Hübscher, SG
AF Hübscher, SG
TI Recurrent and de-novo disease in the liver allograft
SO CURRENT OPINION IN ORGAN TRANSPLANTATION
LA English
DT Review
DE de-novo disease; liver transplantation; recurrent disease
ID HEPATITIS-C VIRUS; STELLATE CELL ACTIVATION; HEPATOCELLULAR-CARCINOMA;
AUTOIMMUNE HEPATITIS; HISTOLOGIC RECURRENCE; FIBROSIS PROGRESSION;
CIRRHOTIC EVOLUTION; TRANSPLANT PATIENTS; ACUTE REJECTION; RISK-FACTORS
AB Purpose of review
This article reviews recent studies of recurrent and de-novo disease in the liver allograft. Particular attention has been given to areas in which histological assessments have been important, either in clinical management or in understanding pathogenetic mechanisms.
Recent findings
Several studies have focused on posttransplant biopsies from patients with recurrent hepatitis C virus infection. These include problems with distinguishing recurrent hepatitis C virus from acute rejection and identifying early histological predictors of rapidly progressive hepatitis C virus-related disease. De-novo autoimmune hepatitis is emerging as an important complication, particularly in the paediatric population. Novel immunopathogenetic mechanisms have been identified that may help with the diagnosis and management of de-novo autoimmune hepatitis. Some patients develop histological features of chronic hepatitis, not obviously related to recurrent or de-novo disease. Serial biopsies have shown that a substantial proportion of these cases may develop fibrosis or cirrhosis.
Summary
Histological assessments continue to be important in the assessment of long-term survivors following liver transplantation. Many of the changes seen in biopsies obtained more than 12 months following transplant can be attributed to recurrent or de-novo disease. Clinically significant histological abnormalities may be seen in people who are apparently well with good graft function.
C1 Univ Birmingham, Dept Pathol, Birmingham B15 2TT, W Midlands, England.
C3 University of Birmingham
RP Hübscher, SG (corresponding author), Univ Birmingham, Dept Pathol, Edgbaston, Birmingham B15 2TT, W Midlands, England.
EM s.g.hubscher@bham.ac.uk
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NR 48
TC 5
Z9 6
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1087-2418
J9 CURR OPIN ORGAN TRAN
JI Curr. Opin. Organ Transpl.
PD JUN
PY 2006
VL 11
IS 3
BP 283
EP 288
PG 6
WC Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Transplantation
GA 054BR
UT WOS:000238351200014
DA 2025-01-07
ER
PT J
AU Dimitriadis, K
Katelani, S
Pappa, M
Fragkoulis, GE
Androutsakos, T
Squadrito, G
AF Dimitriadis, Konstantinos
Katelani, Stamatia
Pappa, Maria
Fragkoulis, George E.
Androutsakos, Theodoros
Squadrito, Giovanni
TI The Role of Interleukins in HBV Infection: A Narrative Review
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Review
DE Hepatitis B virus; interleukins; chronic liver disease; immune response
ID HEPATITIS-B-VIRUS; REGULATORY T-CELLS; BLOOD MONONUCLEAR-CELLS; CHRONIC
LIVER-FAILURE; PERIPHERAL-BLOOD; TH17 CELLS; INTERFERON-GAMMA; VIRAL
CLEARANCE; IMMUNE-RESPONSE; UP-REGULATION
AB Hepatitis B virus (HBV) infection is a worldwide medical issue with significant morbidity and mortality, as it is the main cause of chronic liver disease and hepatocellular carcinoma (HCC). Both innate and adaptive immune responses play a key role in HBV replication and suppression. Recently, the pathophysiological function of interleukins (IL) in the natural course of HBV has gained much attention as a result of the broad use of anti-interleukin agents for a variety of autoimmune diseases and the accompanying risk of HBV reactivation. We present a narrative review regarding the role of IL in HBV infection. Collectively, the pro-inflammatory ILs, namely IL-1, IL-5, IL-6, IL-12 and IL-21, seem to play a critical role in the suppression of HBV replication. In contrast, the anti-inflammatory cytokines IL-10, IL-23 and IL-35 probably act as HBV replication enhancers, while IL-17 has been correlated with HBV-related liver injury. Interestingly enough, IL-2, IL-4 and IL-12 have been tried as therapeutic options against HBV infection with contradictory results. Lastly, the role of IL-22 remains largely ill defined, although preliminary data suggest that it may play a significant role in HBV replication, proliferation and subsequent liver damage.
C1 [Dimitriadis, Konstantinos; Katelani, Stamatia; Androutsakos, Theodoros] Natl & Kapodistrian Univ Athens, Med Sch, Dept Pathophysiol, Athens 11527, Greece.
[Pappa, Maria; Fragkoulis, George E.] Natl & Kapodistrian Univ Athens, Laiko Hosp, Dept Internal Med 1, Propaedeut Clin, Athens 11527, Greece.
[Fragkoulis, George E.] Univ Glasgow, Inst Infect Immun & Inflammat, Glasgow G12 8QQ, Scotland.
C3 National & Kapodistrian University of Athens; National & Kapodistrian
University of Athens; Laiko General Hospital; University of Glasgow
RP Androutsakos, T (corresponding author), Natl & Kapodistrian Univ Athens, Med Sch, Dept Pathophysiol, Athens 11527, Greece.
EM kdimitriadis@med.uoa.gr; stamkatelani@med.uoa.gr;
mariakpappa@med.uoa.gr; geofragkoul@med.uoa.gr; tandroutsak@med.uoa.gr
RI Androutsakos, Theodoros/AAF-5209-2020
OI Androutsakos, Theodoros/0000-0003-2556-6230
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NR 185
TC 6
Z9 6
U1 2
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4426
J9 J PERS MED
JI J. Pers. Med.
PD DEC
PY 2023
VL 13
IS 12
AR 1675
DI 10.3390/jpm13121675
PG 17
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA DF1J2
UT WOS:001130520500001
PM 38138902
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Pickartz, T
Pickartz, H
Lochs, H
Ockenga, J
AF Pickartz, T
Pickartz, H
Lochs, H
Ockenga, J
TI Overlap syndrome of autoimmune pancreatitis and cholangitis associated
with secondary Sjogren's syndrome
SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Article
DE overlap syndrome; autoimmune pancreatitis; cholangitis; associated;
Sjogren's syndrome; biliary obstruction; pancreatic cancer
ID SCLEROSING PANCREATITIS; CLASSIFICATION; RECURRENT; DISEASE
AB In approximately 25% of patients with acute or chronic pancreatitis the cause remains unclear. Despite progress in understanding so-called idiopathic pancreatitis, more diagnostic criteria are needed. We report on a patient who presented with jaundice, but without pain or fever. Under the assumption of pancreatic cancer the patient underwent hemipancreatoduodenectomy. Histological examination showed chronic sclerosing inflammation of the pancreas and bile ducts without any signs of malignancy. Ten weeks later he developed bilateral parotid swelling and recurrent bouts of fever. Again liver enzymes were elevated and unsuccessfully treated with antibiotics for bacterial cholangitis. Further biopsies from submandibular gland, lymph nodes and liver again showed chronic sclerosing inflammation with lymphoplasmacytic infiltration. For sicca symptoms the diagnosis of a primary Sjogren's syndrome was proposed. However, with corticosteroid treatment the patient improved remarkably but after tapering he relapsed. On the basis of established criteria, we diagnosed autoimmune pancreatitis with (1) diffuse swelling of the pancreas, (2) irregularities of the pancreatic duct, (3) lymphoplasmacytic infiltration, (4) response to corticosteroids, (5) hypergammaglobulinaemia, and (6) disproportionately raised IgG4. In addition, the patient fulfilled the criteria for secondary Sjogren's syndrome. Autoimmune pancreatitis may present as an isolated or syndromic disease. It is an autoimmune disorder of unknown cause and should be included in the differential diagnosis of pancreatic disorders. (C) 2004 Lippincott Williams Wilkins.
C1 Humboldt Univ, Dept Gastroenterol Hepatol Endocrinol Metab & Nut, Med Fac Charite, D-1086 Berlin, Germany.
Evangel Waldkrankenhaus, Inst Pathol, Berlin, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
University of Berlin; Charite Universitatsmedizin Berlin
RP Univ Klinikum Charite, Campus Mitte,Schumannstr 20-21, D-10117 Berlin, Germany.
EM johann.ockenga@charite.de
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NR 15
TC 22
Z9 23
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0954-691X
EI 1473-5687
J9 EUR J GASTROEN HEPAT
JI Eur. J. Gastroenterol. Hepatol.
PD NOV
PY 2004
VL 16
IS 12
BP 1295
EP 1299
DI 10.1097/00042737-200412000-00010
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 877IK
UT WOS:000225561400010
PM 15618835
DA 2025-01-07
ER
PT J
AU Liu, XR
Li, JJ
Bai, L
Yu, ZJ
Kan, QC
AF Liu, Xiaorui
Li, Jingjing
Bai, Lu
Yu, Zujiang
Kan, Quancheng
TI Identification of the risk factors for liver-related mortality in
primary biliary cirrhosis patients: a case-control study in China
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Article
DE Primary biliary cirrhosis; liver-related mortality; hepatocellular
carcinoma; risk factor; case-control study
ID URSODEOXYCHOLIC-ACID THERAPY; HEPATOCELLULAR-CARCINOMA; PROGRESSION;
PREDICTION; METAANALYSIS; PROGNOSIS; SURVIVAL; TRIALS; COHORT
AB Background: Primary biliary cirrhosis (PBC) is an autoimmune liver condition with relatively slow progression, leading to liver failure and death. We retrospectively investigated potential risk factors of liver-related mortality in patients with PBC. Methods: The data of patients with PBC at the First Affiliated Hospital of Zhengzhou University in China from 2007 to 2013 were included, specifically that of 91 deceased and 364 living (control) patients. Univariate and multivariate conditional logistic regression models were applied to determine potential risk factors of liver-related mortality, with calculations of odds ratios (ORs) and 95% confidence intervals (CIs). Results: The following features were statistically similar between the deceased and living patients: age, gender, nationality, the status of anti-human immunodeficiency virus antibody, anti-hepatitis C virus antibody, and hepatitis B surface antigen. A large proportion of deceased PBC patients (92.31%) had died of decompensated cirrhosis; the most common immediate cause was hemorrhagic shock (41.75%), then hepatic encephalopathy (38.45%). Independent risk factors for liver-related mortality were: hepatocellular carcinoma, elevated total bilirubin (TBIL), decreased albumin (ALB) and platelet levels, and non-response to ursodeoxycholic acid (P<0.001, all). Cutoff values of TBIL and ALB for prediction of poor prognosis were determined as 38.65 mu mol/L and 34.8 g/L, respectively; the areas under the ROC curve were 0.771 and 0.758 (P<0.001), respectively. Conclusions: PBC patients with hepatocellular carcinoma, high total bilirubin, low albumin or platelet levels at the initial diagnosis of disease, or who do not response to UDCA, are prone to liver-related death.
C1 [Liu, Xiaorui; Li, Jingjing; Bai, Lu; Yu, Zujiang; Kan, Quancheng] Zhengzhou Univ, Affiliated Hosp 1, Dept Infect Dis, 1 Jianshe East Rd, Zhengzhou 450052, Peoples R China.
[Liu, Xiaorui; Li, Jingjing; Kan, Quancheng] Zhengzhou Univ, Affiliated Hosp 1, Dept Pharm, 1 Jianshe East Rd, Zhengzhou 450052, Peoples R China.
C3 Zhengzhou University; Zhengzhou University
RP Kan, QC (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Infect Dis, 1 Jianshe East Rd, Zhengzhou 450052, Peoples R China.; Kan, QC (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Pharm, 1 Jianshe East Rd, Zhengzhou 450052, Peoples R China.
EM grklxr@163.com
RI Liu, Xiaorui/L-6602-2018
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ter Borg PCJ, 2006, AM J GASTROENTEROL, V101, P2044, DOI 10.1111/j.1572-0241.2006.00699.x
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NR 33
TC 0
Z9 0
U1 0
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1940-5901
J9 INT J CLIN EXP MED
JI Int. J. Clin. Exp. Med.
PY 2016
VL 9
IS 11
BP 21996
EP 22003
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA EG7UD
UT WOS:000391260800172
DA 2025-01-07
ER
PT J
AU Chi, G
Pei, JH
Ma, QY
Ru, YX
Feng, ZH
AF Chi, Gang
Pei, Jin-hong
Ma, Qin-ya
Ru, Ying-Xia
Feng, Zuo-hua
TI Chemical induced inflammation of the liver breaks tolerance and results
in autoimmune hepatitis in Balb/c mice
SO IMMUNOLOGY LETTERS
LA English
DT Article
DE Autoimmune hepatitis; Liver tolerance; Chemical induced inflammation;
Balb/c mice
ID GENETIC PREDISPOSITION; MOLECULAR MIMICRY; MOUSE MODELS; MURINE MODEL;
VIRUS; CYTOCHROME-P450; SUSCEPTIBILITY; INFECTION
AB Autoimmune hepatitis (AIH) is a chronic liver disease mediated by immunity, and could lead to liver fibrosis and hepatocellular carcinoma. However, the mechanisms for breaking hepatic tolerance and driving AIH still remain elusive. We herein reported that the non-specific liver inflammation triggered by carbon tetrachloride (CCl4) recruited high numbers of CD4 + T, CD8 + T and B cells, and elevated the expression of proinflammaitory cytokines in Balb/c mice, further breaking liver tolerance and inducing autoimmune response, AIH inflammation and liver fibrosis in the presence of CYP2D6 antigen mimicry. In contrast, adenovirus infection could not break liver tolerance and induce AIH in Balb/c mice even in the presence of CYP2D6 antigen mimicry. These results suggested that genetic predisposition could determine liver tolerance in Balb/c mice. The chemical induced inflammation in the liver breaks tolerance and might be considered important for the initiation and development of AIH in Balb/c mice.
C1 [Chi, Gang; Pei, Jin-hong] Changzhi Med Coll, Dept Biochem, Changzhi 046000, Shanxi, Peoples R China.
[Ru, Ying-Xia; Feng, Zuo-hua] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Basic Med, Dept Biochem & Mol Biol, Wuhan 430030, Peoples R China.
[Ma, Qin-ya] Changzhi Publ Secur Bur, DNA Lab, Changzhi 046000, Shanxi, Peoples R China.
C3 Changzhi Medical College; Huazhong University of Science & Technology
RP Chi, G (corresponding author), Changzhi Med Coll, Dept Biochem, Changzhi 046000, Shanxi, Peoples R China.; Feng, ZH (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Basic Med, Dept Biochem & Mol Biol, Wuhan 430030, Peoples R China.
EM cg@czmc.edu.cn; tgyouxiang@163.com
FU Scientific Research Starting Foundation for Doctor of Changzhi Medical
College [BS201902]; Scientific and Technologial Innovation Programs of
Higher Education Institutions in Shanxi (STIP) [2019L0667]
FX This work was supported by Scientific Research Starting Foundation for
Doctor of Changzhi Medical College [grant numbers BS201902], Scientific
and Technologial Innovation Programs of Higher Education Institutions in
Shanxi (STIP) [grant numbers 2019L0667].
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NR 37
TC 8
Z9 8
U1 1
U2 11
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29a, 1043 NX AMSTERDAM, NETHERLANDS
SN 0165-2478
EI 1879-0542
J9 IMMUNOL LETT
JI Immunol. Lett.
PD FEB
PY 2020
VL 218
BP 44
EP 50
DI 10.1016/j.imlet.2019.11.010
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA KH9EX
UT WOS:000510953000007
PM 31794800
DA 2025-01-07
ER
PT J
AU Mercado, LA
Gil-Lopez, F
Chirila, RM
Harnois, DM
AF Mercado, Lydia A.
Gil-Lopez, Fernando
Chirila, Razvan M.
Harnois, Denise M.
TI Autoimmune Hepatitis: A Diagnostic and Therapeutic Overview
SO DIAGNOSTICS
LA English
DT Review
DE autoimmune hepatitis; immunosuppression; liver disease; autoantibodies;
remission
ID INDUCED LIVER-INJURY; PRIMARY BILIARY-CIRRHOSIS; THIOPURINE
METHYLTRANSFERASE DEFICIENCY; OVERLAP SYNDROME;
HEPATOCELLULAR-CARCINOMA; CLINICAL CHARACTERISTICS; SCLEROSING
CHOLANGITIS; CORTICOSTEROID-THERAPY; MYCOPHENOLATE-MOFETIL; SIMPLIFIED
CRITERIA
AB Autoimmune hepatitis is an immune-mediated inflammatory condition of the liver of undetermined cause that affects both sexes, all ages, races, and ethnicities. Its clinical presentation can be very broad, from having an asymptomatic and silent course to presenting as acute hepatitis, cirrhosis, and acute liver failure potentially requiring liver transplantation. The diagnosis is based on histological abnormalities (interface hepatitis), characteristic clinical and laboratory findings (increased aspartate aminotransferase, alanine aminotransferase, and serum IgG concentration), and the presence of one or more characteristic autoantibodies. The large heterogeneity of these clinical, biochemical, and histological findings can sometimes make a timely and proper diagnosis a difficult task. Treatment seeks to achieve remission of the disease and prevent further progression of liver disease. First-line therapy includes high-dose corticosteroids, which are later tapered to decrease side effects, and azathioprine. In the presence of azathioprine intolerance or a poor response to the standard of care, second-line therapy needs to be considered, including mycophenolate mofetil. AIH remains a diagnostic and therapeutic challenge, and a further understanding of the pathophysiological pathways of the disease and the implementation of randomized controlled trials are needed.
C1 [Mercado, Lydia A.; Gil-Lopez, Fernando; Harnois, Denise M.] Mayo Clin Florida, Dept Liver Transplant, Jacksonville, FL 32224 USA.
[Chirila, Razvan M.] Mayo Clin Florida, Dept Gen Internal Med, Jacksonville, FL 32224 USA.
[Harnois, Denise M.] Mayo Clin Florida, Dept Gastroenterol & Hepatol, Jacksonville, FL 32224 USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic
RP Harnois, DM (corresponding author), Mayo Clin Florida, Dept Liver Transplant, Jacksonville, FL 32224 USA.; Harnois, DM (corresponding author), Mayo Clin Florida, Dept Gastroenterol & Hepatol, Jacksonville, FL 32224 USA.
EM chirila.razvan@mayo.edu; harnois.denise@mayo.edu
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NR 142
TC 1
Z9 1
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD FEB
PY 2024
VL 14
IS 4
AR 382
DI 10.3390/diagnostics14040382
PG 20
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA IS6Z1
UT WOS:001168372800001
PM 38396421
OA gold
DA 2025-01-07
ER
PT J
AU Montano-Loza, AJ
Allegretti, JR
Cheung, A
Ebadi, M
Jones, D
Kerkar, N
Levy, C
Rizvi, S
Vierling, JM
Alvarez, F
Bai, WN
Gilmour, S
Gulamhusein, A
Guttman, O
Hansen, BE
MacParland, S
Mason, A
Onofrio, F
Santamaria, P
Stueck, A
Swain, M
Vincent, C
Ricciuto, A
Hirschfield, G
AF Montano-Loza, Aldo J.
Allegretti, Jessica R.
Cheung, Angela
Ebadi, Maryam
Jones, David
Kerkar, Nanda
Levy, Cynthia
Rizvi, Sumera
Vierling, John M.
Alvarez, Fernando
Bai, Wayne
Gilmour, Susan
Gulamhusein, Aliya
Guttman, Orlee
Hansen, Bettina E.
MacParland, Sonya
Mason, Andrew
Onofrio, Fernanda
Santamaria, Pere
Stueck, Ashley
Swain, Mark
Vincent, Catherine
Ricciuto, Amanda
Hirschfield, Gideon
TI Single Topic Conference on Autoimmune Liver Disease from the Canadian
Association for the Study of the Liver
SO CANADIAN LIVER JOURNAL
LA English
DT Article
DE autoimmune hepatitis; cirrhosis; overlap syndrome; primary biliary
cirrhosis; primary sclerosing cholangitis
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY-CIRRHOSIS;
INFLAMMATORY-BOWEL-DISEASE; GENOME-WIDE ASSOCIATION; HUMAN-LEUKOCYTE
ANTIGEN; URSODEOXYCHOLIC ACID; INADEQUATE RESPONSE; RISK-FACTORS;
OBETICHOLIC ACID; NATURAL-HISTORY
AB Autoimmune liver disease (AILD) spans a spectrum of chronic disorders affecting the liver parenchyma and biliary system. Three main categories of AILD are autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC). This review condenses the presentation and discussions of the Single Topic Conference (STC) on AILD that was held in Ottawa, Ontario, in November 2019. We cover generalities regarding disease presentation and clinical diagnosis; mechanistic themes; treatment paradigms; clinical trials, including approaches and challenges to new therapies; and looking beyond traditional disease boundaries. Although these diseases are considered autoimmune, the etiology and role of environmental triggers are poorly understood. AILDs are progressive and chronic conditions that affect survival and quality of life. Advances have been made in PBC treatment because second-line treatments are now available (obeticholic acid, bezafibrate); however, a significant proportion still present suboptimal response. AIH treatment has remained unchanged for several decades, and data suggest that fewer than 50% of patients achieve a complete response and as many as 80% develop treatment-related side effects. B-cell depletion therapy to treat AIH is in an early stage of development and has shown promising results. An effective treatment for PSC is urgently needed. Liver transplant remains the best option for patients who develop decompensated cirrhosis or hepatocellular carcinoma within specific criteria, but recurrent AILD might occur. Continued efforts are warranted to develop networks for AILD aimed at assessing geo-epidemiological, clinical, and biochemical differences to capture the new treatment era in Canada.
C1 [Montano-Loza, Aldo J.; Ebadi, Maryam; Bai, Wayne; Mason, Andrew] Univ Alberta, Div Gastroenterol, Edmonton, AB, Canada.
[Montano-Loza, Aldo J.; Ebadi, Maryam; Bai, Wayne; Mason, Andrew] Univ Alberta, Liver Unit, Edmonton, AB, Canada.
[Allegretti, Jessica R.] Harvard Med Sch, Brigham & Womens Hosp, Div Gastroenterol, Boston, MA 02115 USA.
[Cheung, Angela; Rizvi, Sumera] Mayo Clin, Coll Med & Sci, Rochester, MN USA.
[Jones, David] Newcastle Univ, Fac Med Sci, Newcastle Upon Tyne, Tyne & Wear, England.
[Kerkar, Nanda] Univ Rochester, Div Gastroenterol Hepatol & Nutr, Golisano Childrens Hosp Strong, Med Ctr, New York, NY USA.
[Levy, Cynthia] Univ Miami, Schiff Ctr Liver Dis, Miami, FL USA.
[Vierling, John M.] Baylor Coll Med, Houston, TX 77030 USA.
[Alvarez, Fernando] Univ Montreal, Dept Pediat, Hop St Justine, Montreal, PQ, Canada.
[Gilmour, Susan] Univ Alberta, Stollery Childrens Hosp, Edmonton, AB, Canada.
[Gulamhusein, Aliya; Hansen, Bettina E.; MacParland, Sonya; Onofrio, Fernanda] Univ Toronto, Ajmera Family Transplant Ctr, Toronto Gen Res Inst, Dept Lab Med, Toronto, ON, Canada.
[Gulamhusein, Aliya; Hansen, Bettina E.; MacParland, Sonya; Onofrio, Fernanda] Univ Toronto, Ajmera Family Transplant Ctr, Toronto Gen Res Inst, Dept Pathobiol, Toronto, ON, Canada.
[Gulamhusein, Aliya; Hansen, Bettina E.; MacParland, Sonya; Onofrio, Fernanda] Univ Toronto, Ajmera Family Transplant Ctr, Toronto Gen Res Inst, Dept Immunol, Toronto, ON, Canada.
[Guttman, Orlee] British Columbia Childrens Hosp, Div Gastroenterol Hepatol & Nutr, Vancouver, BC, Canada.
[Santamaria, Pere] Univ Calgary, Dept Microbiol Immunol & Infect Dis, Calgary, AB, Canada.
[Stueck, Ashley] Dalhousie Univ, Dept Pathol, Halifax, NS, Canada.
[Swain, Mark] Univ Calgary, Div Gastroenterol & Hepatol, Calgary Liver Unit, Calgary, AB, Canada.
[Vincent, Catherine] Univ Montreal, Dept Med, Montreal, PQ, Canada.
[Ricciuto, Amanda] Hosp Sick Children, Div Gastroenterol Hepatol & Nutr, Toronto, ON, Canada.
[Hirschfield, Gideon] Univ Hlth Network, Toronto Ctr Liver Dis, Toronto, ON, Canada.
[Hirschfield, Gideon] Univ Toronto, Inst Hlth Policy Management & Evaluat, Toronto, ON, Canada.
C3 University of Alberta; University of Alberta; Harvard University;
Brigham & Women's Hospital; Harvard Medical School; Mayo Clinic;
Newcastle University - UK; University of Rochester; University of Miami;
Baylor College of Medicine; Universite de Montreal; University of
Alberta; Stollery Children's Hospital; University of Toronto; University
Health Network Toronto; Toronto General Hospital; University of Toronto;
University Health Network Toronto; Toronto General Hospital; University
of Toronto; University Health Network Toronto; Toronto General Hospital;
BC Childrens Hospital; University of British Columbia; University of
Calgary; Dalhousie University; University of Calgary; Universite de
Montreal; University of Toronto; Hospital for Sick Children (SickKids);
University of Toronto; University Health Network Toronto; University of
Toronto
RP Montano-Loza, AJ (corresponding author), Univ Alberta, Zeidler Ledcor Ctr, Div Gastroenterol, 8540 112 St NW, Edmonton, AB T6G 2X8, Canada.; Montano-Loza, AJ (corresponding author), Univ Alberta, Zeidler Ledcor Ctr, Liver Unit, 8540 112 St NW, Edmonton, AB T6G 2X8, Canada.
EM montanol@ualberta.ca
RI Ricciuto, Amanda/JUF-0278-2023; Montano-Loza, Aldo/B-3092-2013;
Hirschfield, Gideon/M-2143-2015
OI , Susan/0000-0003-2432-1549
FU MRC [MR/L001489/1] Funding Source: UKRI
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NR 127
TC 1
Z9 1
U1 0
U2 2
PU UNIV TORONTO PRESS INC
PI TORONTO
PA JOURNALS DIVISION, 5201 DUFFERIN ST, DOWNSVIEW, TORONTO, ON M3H 5T8,
CANADA
EI 2561-4444
J9 CAN LIVER J
JI Can. Liver J.
PD NOV 1
PY 2021
VL 4
IS 4
BP 401
EP 425
DI 10.3138/canlivj-2021-0006
PG 25
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA XL2QO
UT WOS:000727994100007
PM 35989897
OA Green Published
DA 2025-01-07
ER
PT J
AU Liu, SS
Wu, F
Jin, YM
Chang, WQ
Xu, TM
AF Liu, Shan-Shan
Wu, Fei
Jin, Yue-Mei
Chang, Wei-Qin
Xu, Tian-Min
TI HDAC11: a rising star in epigenetics
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE HDAC11; epigenetics; pathophysiological; disease; cancer
ID HISTONE DEACETYLASE 11; GENE-EXPRESSION; LYSINE DEACETYLASES; B-CELLS;
CANCER; REGULATOR; INTERLEUKIN-10; ACETYLATION; PROGNOSIS; LYMPHOMA
AB Epigenetic mechanisms, such as acetylation, methylation, and succinylation, play pivotal roles in the regulation of multiple normal biological processes, including neuron regulation, hematopoiesis, bone cell maturation, and metabolism. In addition, epigenetic mechanisms are closely associated with the pathological processes of various diseases, such as metabolic diseases, autoimmune diseases and cancers. Epigenetic changes may precede genetic mutation, so research on epigenetic changes and regulation may be important for the early detection and diagnosis of disease. Histone deacetylase11 (HDAC11) is the newest member of the histone deacetylase (HDAC) family and the only class IV histone deacetylase. HDAC11 has different expression levels and biological functions in different systems of the human body and is among the top 1 to 4% of genes overexpressed in cancers, such as breast cancer, hepatocellular carcinoma and renal pelvis urothelial carcinoma. This article analyzes the role and mechanism of HDAC11 in disease, especially in tumorigenesis, in an attempt to provide new ideas for clinical and basic research.
C1 [Liu, Shan-Shan; Wu, Fei; Jin, Yue-Mei; Xu, Tian-Min] Second Hosp Jilin Univ, Dept Obstet & Gynecol, Changchun 130041, Jilin, Peoples R China.
[Chang, Wei-Qin] Second Hosp Jilin Univ, Dept Surg, 218 Ziqiang Rd, Changchun 130041, Jilin, Peoples R China.
C3 Jilin University; Jilin University
RP Xu, TM (corresponding author), Second Hosp Jilin Univ, Dept Obstet & Gynecol, Changchun 130041, Jilin, Peoples R China.; Chang, WQ (corresponding author), Second Hosp Jilin Univ, Dept Surg, 218 Ziqiang Rd, Changchun 130041, Jilin, Peoples R China.
EM coralcoralreef@163.com; 15526856915@163.com; 67590282@163.com;
weiqinchang@126.com; xutianmin@126.com
RI Liu, shanshan/AAT-3465-2020
FU Department of Science and Technology of Jilin Province [20190101014JH,
20190905004SF, 20180203032YY]
FX This work was supported by grants from the Department of Science and
Technology of Jilin Province [grant number 20190101014JH, 20190905004SF,
20180203032YY]
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NR 99
TC 76
Z9 80
U1 4
U2 36
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD NOV
PY 2020
VL 131
AR 110607
DI 10.1016/j.biopha.2020.110607
PG 7
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA OH6KI
UT WOS:000582699600013
PM 32841898
OA gold
DA 2025-01-07
ER
PT S
AU Morel, E
Mehrpour, M
Botti, J
Dupont, N
Hamaï, A
Nascimbeni, AC
Codogno, P
AF Morel, Etienne
Mehrpour, Maryam
Botti, Joelle
Dupont, Nicolas
Hamai, Ahmed
Nascimbeni, Anna Chiara
Codogno, Patrice
BE Insel, PA
TI Autophagy: A Druggable Process
SO ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, VOL 57
SE Annual Review of Pharmacology and Toxicology
LA English
DT Review; Book Chapter
DE macroautophagy; autophagosome; lysosome; activators; inhibitors; disease
ID HEPATOCELLULAR-CARCINOMA; LYSOSOMAL BIOGENESIS; PROTEIN-DEGRADATION;
PROMOTES AUTOPHAGY; BLOCKS AUTOPHAGY; CYTOSOLIC FOXO1; CROSS-TALK;
INHIBITION; COMPLEX; DISEASE
AB Macroautophagy (hereafter called autophagy) is a vacuolar, lysosomal pathway for catabolism of intracellular material that is conserved among eukaryotic cells. Autophagy plays a crucial role in tissue homeostasis, adaptation to stress situations, immune responses, and the regulation of the inflammatory response. Blockade or uncontrolled activation of autophagy is associated with cancer, diabetes, obesity, cardiovascular disease, neurodegenerative disease, autoimmune disease, infection, and chronic inflammatory disease. During the past decade, researchers have made major progress in understanding the three levels of regulation of autophagy in mammalian cells: signaling, autophagosome formation, and autophagosome maturation and lysosomal degradation. As we discuss in this review, each of these levels is potentially druggable, and, depending on the indication, may be able to stimulate or inhibit autophagy. We also summarize the different modulators of autophagy and their potential and limitations in the treatment of life-threatening diseases.
C1 [Morel, Etienne; Mehrpour, Maryam; Botti, Joelle; Dupont, Nicolas; Hamai, Ahmed; Nascimbeni, Anna Chiara; Codogno, Patrice] INEM, CNRS UMR 8253, INSERM U1151, F-75993 Paris, France.
[Morel, Etienne; Mehrpour, Maryam; Dupont, Nicolas; Hamai, Ahmed; Nascimbeni, Anna Chiara; Codogno, Patrice] Univ Paris 05, Sorbonne Paris Cite, F-75012 Paris, France.
[Botti, Joelle] Univ Paris Diderot, Sorbonne Paris Cite, F-75993 Paris, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
Universite Paris Cite; Centre National de la Recherche Scientifique
(CNRS); CNRS - National Institute for Biology (INSB); Universite Paris
Cite; Universite Paris Cite
RP Codogno, P (corresponding author), INEM, CNRS UMR 8253, INSERM U1151, F-75993 Paris, France.; Codogno, P (corresponding author), Univ Paris 05, Sorbonne Paris Cite, F-75012 Paris, France.
EM patrice.codogno@inserm.fr
RI Nascimbeni, Anna/AAG-4782-2021; Mehrpour, Maryam/D-8640-2017; DUPONT,
NICOLAS/AAJ-7192-2021; Codogno, Patrice/G-1384-2013; MOREL,
Etienne/N-2194-2014
OI Hamai, Ahmed/0000-0002-7921-4014; DUPONT, NICOLAS/0000-0002-3056-9906;
Codogno, Patrice/0000-0002-5492-3180; MOREL, Etienne/0000-0002-4763-4954
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NR 97
TC 128
Z9 145
U1 0
U2 74
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0897 USA
SN 0362-1642
EI 1545-4304
BN 978-0-8243-0457-7
J9 ANNU REV PHARMACOL
JI Annu. Rev. Pharmacol. Toxicol.
PY 2017
VL 57
BP 375
EP 398
DI 10.1146/annurev-pharmtox-010716-104936
PG 24
WC Pharmacology & Pharmacy; Toxicology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA BH0QN
UT WOS:000396044800019
PM 28061686
OA Bronze
DA 2025-01-07
ER
PT J
AU Yuan, YG
Wang, JL
Zhang, YX
Li, L
Reza, AMT
Gurunathan, S
AF Yuan, Yu-Guo
Wang, Jia-Lin
Zhang, Ya-Xin
Li, Ling
Reza, Abu Musa Md Talimur
Gurunathan, Sangiliyandi
TI Biogenesis, Composition and Potential Therapeutic Applications of
Mesenchymal Stem Cells Derived Exosomes in Various Diseases
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Review
DE extracellular vesicle; biogenesis; mesenchymal stem cells; exosomes;
autoimmune disease; angiogenesis
ID HUMAN BONE-MARROW; INFLAMMATORY-BOWEL-DISEASE; TRAUMATIC BRAIN-INJURY;
NF-KAPPA-B; EXTRACELLULAR VESICLES; STROMAL CELLS; RHEUMATOID-ARTHRITIS;
PROMOTE ANGIOGENESIS; FUNCTIONAL RECOVERY; SIGNALING PATHWAY
AB Exosomes are nanovesicles with a wide range of chemical compositions used in many different applications. Mesenchymal stem cell-derived exosomes (MSCs-EXOs) are spherical vesicles that have been shown to mediate tissue regeneration in a variety of diseases, including neurological, autoimmune and inflammatory, cancer, ischemic heart disease, lung injury, and liver fibrosis. They can modulate the immune response by interacting with immune effector cells due to the presence of anti-inflammatory compounds and are involved in intercellular communication through various types of cargo. MSCs-EXOs exhibit cytokine storm-mitigating properties in response to COVID-19. This review discussed the potential function of MSCs-EXOs in a variety of diseases including neurological, notably epileptic encephalopathy and Parkinson's disease, cancer, angiogenesis, autoimmune and inflammatory diseases. We provided an overview of exosome biogenesis and factors that regulate exosome biogenesis. Additionally, we highlight the functions and potential use of MSCs-EXOs in the treatment of the inflammatory disease COVID-19. Finally, we covered a strategies and challenges of MSCs-EXOs. Finally, we discuss conclusion and future perspectives of MSCs-EXOs.
C1 [Yuan, Yu-Guo; Wang, Jia-Lin; Zhang, Ya-Xin; Li, Ling] Yangzhou Univ, Coll Vet Med, Dept Clin Vet Med, Yangzhou, Jiangsu, Peoples R China.
[Yuan, Yu-Guo; Wang, Jia-Lin; Zhang, Ya-Xin; Li, Ling] Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou, Jiangsu, Peoples R China.
[Reza, Abu Musa Md Talimur] Gebze Tech Univ, Fac Sci, Dept Mol Biol & Genet, Gebze, Kocaeli, Turkiye.
[Gurunathan, Sangiliyandi] Rathinam Coll Arts & Sci, Dept Biotechnol, Coimbatore, Tamil Nadu, India.
C3 Yangzhou University; Yangzhou University; Gebze Technical University
RP Yuan, YG (corresponding author), Yangzhou Univ, Coll Vet Med, Dept Clin Vet Med, Yangzhou, Jiangsu, Peoples R China.; Yuan, YG (corresponding author), Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou, Jiangsu, Peoples R China.; Gurunathan, S (corresponding author), Rathinam Coll Arts & Sci, Dept Biotechnol, Coimbatore, Tamil Nadu, India.
EM yyg9776430@163.com; gsangiliyandi@yahoo.com
RI Reza, Abu Musa/AAY-7828-2020
OI Gurunathan, Sangiliyandi/0000-0001-9924-8433
FU Priority Academic Program Development of Jiangsu Higher Education
Institutions (PAPD) [JBGS (2021) 025]; 111 Project; Yangzhou University
corporation [D18007]; [YZ2021161/YZ2022187]
FX This study was supported by Development of a new precise cytosine base
editor (JBGS (2021) 025) , the Priority Academic Program Development of
Jiangsu Higher Education Institutions (PAPD) , the 111 Project D18007,
and Yangzhou city and Yangzhou University corporation
(YZ2021161/YZ2022187) .
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NR 412
TC 25
Z9 25
U1 3
U2 29
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2023
VL 18
BP 3177
EP 3210
DI 10.2147/IJN.S407029
PG 34
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA K0DA3
UT WOS:001013227700001
PM 37337578
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Fricker, ZP
Lichtenstein, DR
AF Fricker, Zachary P.
Lichtenstein, David R.
TI Primary Sclerosing Cholangitis: A Concise Review of Diagnosis and
Management
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Review
DE Primary sclerosing cholangitis (PSC); Cholangiocarcinoma;
Cholangiopathy; Cholestasis
ID INFLAMMATORY-BOWEL-DISEASE; DOSE URSODEOXYCHOLIC ACID; PRIMARY
BILIARY-CIRRHOSIS; NATURAL-HISTORY MODEL; ULCERATIVE-COLITIS;
LIVER-TRANSPLANTATION; COLORECTAL NEOPLASIA; AUTOIMMUNE HEPATITIS;
PROGNOSTIC-FACTORS; ALKALINE-PHOSPHATASE
AB Primary sclerosing cholangitis is a rare, chronic cholestatic liver disease characterized by progressive idiopathic stricturing of the biliary system, typically leading to cirrhosis, end-stage liver disease, and colonic or hepatobiliary malignancy. Its presentation is often that of asymptomatic alkaline phosphatase elevation. When symptoms are present, they typically include fatigue, pruritus, or jaundice. The diagnosis can be confirmed via cholangiography, either magnetic resonance cholangiography (MRCP) or endoscopic retrograde cholangiography if the former is inconclusive. The clinical course is marked by progressive liver disease leading to cirrhosis with its attendant complications of portal hypertension, often including recurrent episodes of cholangitis. Greater elevation in alkaline phosphatase or liver stiffness is associated with worse clinical outcomes. Management includes endoscopic treatment of symptomatic biliary strictures and evaluation of dominant strictures as no adequate medical treatment is available. Multiple medical therapies are under evaluation. Ultimately, liver transplantation may be necessary for management of decompensated cirrhosis or disabling symptoms. There is also a markedly increased risk of cancer, notably including cholangiocarcinoma and gallbladder and colorectal cancers (particularly in patients with colitis). Cancer screening can be done with semi-annual liver imaging (MRCP or ultrasound) and colonoscopy every 1-2years in those with colitis.
C1 [Fricker, Zachary P.] Univ Penn, Perelman Sch Med, Div Gastroenterol, PCAM South Pavil, 7th Floor,3400 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
[Fricker, Zachary P.; Lichtenstein, David R.] Boston Univ, Sch Med, Evans Dept Med, Gastroenterol Sect, Suite 7717,85 E Concord St, Boston, MA 02118 USA.
C3 University of Pennsylvania; Boston University
RP Fricker, ZP (corresponding author), Univ Penn, Perelman Sch Med, Div Gastroenterol, PCAM South Pavil, 7th Floor,3400 Civ Ctr Blvd, Philadelphia, PA 19104 USA.; Fricker, ZP (corresponding author), Boston Univ, Sch Med, Evans Dept Med, Gastroenterol Sect, Suite 7717,85 E Concord St, Boston, MA 02118 USA.
EM zfricker@bu.edu; David.Lichtenstein@bmc.org
FU Boston University Clinical and Translational Science Institute
[UL1-TR000157]
FX Dr. Fricker was supported in part by the Boston University Clinical and
Translational Science Institute (Grant UL1-TR000157).
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NR 116
TC 17
Z9 21
U1 1
U2 16
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD MAR
PY 2019
VL 64
IS 3
BP 632
EP 642
DI 10.1007/s10620-019-05484-y
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HM3ZW
UT WOS:000459414300008
PM 30725292
DA 2025-01-07
ER
PT J
AU Huang, YQ
Liang, W
Li, K
Liao, XL
Chen, JW
Qiu, XS
Liu, KP
Qiu, DB
Qin, YF
AF Huang, Yingqi
Liang, Wei
Li, Kun
Liao, Xialin
Chen, Jiawen
Qiu, Xiusheng
Liu, Kunpeng
Qiu, Dongbo
Qin, Yunfei
TI Sorafenib suppresses the activation of type I interferon pathway induced
by RLR-MAVS and cGAS-STING signaling
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Sorafenib; Type I IFN pathway; Autophagy
ID STRUCTURAL BASIS; DEGRADATION; AUTOPHAGY
AB Type I interferon pathway is a crucial component of innate immune signaling upon pathogen infection or endogenous instability. An imbalance of type I interferon can lead to many diseases, such as autoimmune diseases and inflammatory diseases. Meanwhile, the side effects of clinical drugs on type I interferon signaling may result in impaired outcomes in clinical treatment, especially in cancer immunotherapy which is associated with type I interferon signaling. Here, we found that sorafenib, an FDA-approved drug for HCC chemotherapy, suppresses both DNA- and RNA-sensing mediated type I interferon pathway. Mechanistically, sorafenib treatment induces the autophagic degradation of MAVS, cGAS, TBK1, and IRF3, and attenuates the signaling transduction. In addition, sorafenib also inhibits the recruiting of STING or MAVS with TBK1 and IRF3. This work reveals the negative role of sorafenib in the regulation of type I interferon pathway. Sorafenib treatment is not only a potential drug for autoimmune disease and inflammation diseases, but also needs to be noticed in HCC chemotherapy. (C) 2022 Elsevier Inc. All rights reserved.
C1 [Huang, Yingqi; Liang, Wei; Liao, Xialin; Chen, Jiawen; Liu, Kunpeng; Qin, Yunfei] SunYat Sen Univ, Affiliated Hosp 3, Biotherapy Ctr, Guangzhou, Peoples R China.
[Huang, Yingqi; Qin, Yunfei] SunYat Sen Univ, Affiliated Hosp 3, Cell Gene Therapy Translat Med Res Ctr, Guangzhou, Peoples R China.
[Huang, Yingqi; Qin, Yunfei] Guangdong Prov Key Lab Liver Dis Res, Guangzhou, Peoples R China.
[Li, Kun] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Hepat Surg, Guangzhou, Peoples R China.
[Li, Kun] Sun Yat Sen Univ, Affiliated Hosp 3, Liver Transplantat Ctr, Guangzhou, Peoples R China.
[Qiu, Xiusheng; Qiu, Dongbo] Sun Yat Sen Univ, Affiliated Hosp 3, Vaccine Res Inst, Guangzhou, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
Sun Yat Sen University; Sun Yat Sen University
RP Liu, KP; Qin, YF (corresponding author), SunYat Sen Univ, Affiliated Hosp 3, Biotherapy Ctr, Guangzhou, Peoples R China.; Qiu, DB (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 3, Vaccine Res Inst, Guangzhou, Peoples R China.
EM liukp5@mail.sysu.edu; qiudb3@mail.sysu.edu.cn; qinyf6@mail.sysu.edu.cn
RI Liu, Kunpeng/IAP-6799-2023; Qiu, Dongbo/KPB-2114-2024
OI Qiu, Dongbo/0000-0002-1469-4571; Liu, Kunpeng/0000-0003-3452-880X
FU National Natural Science Foundation of China [81970509, 81800559];
Natural Science Foundation of Guangdong Province [2022A1515012223];
Fundamental Research Funds for the Central Universities [20ykzd03]
FX This work was supported by the National Natural Science Foundation of
China (81970509, 81800559), the Natural Science Foundation of Guangdong
Province (2022A1515012223), Yunfei Qin is partially supported by the
Fundamental Research Funds for the Central Universities (20ykzd03).
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NR 31
TC 6
Z9 6
U1 2
U2 12
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD OCT 1
PY 2022
VL 623
BP 181
EP 188
DI 10.1016/j.bbrc.2022.07.028
EA JUL 2022
PG 8
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 5W9DW
UT WOS:000878209100007
PM 35921710
DA 2025-01-07
ER
PT J
AU Axley, P
Mudumbi, S
Sarker, S
Kuo, YF
Singal, A
AF Axley, Page
Mudumbi, Sandhya
Sarker, Shabnam
Kuo, Yong-Fang
Singal, Ashwani
TI Patients with stage 3 compared to stage 4 liver fibrosis have lower
frequency of and longer time to liver disease complications
SO PLOS ONE
LA English
DT Article
ID CHRONIC HEPATITIS-C; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
PROGNOSTIC VALUE; SCORING SYSTEMS; FOLLOW-UP; MORTALITY; FEATURES;
OUTCOMES; DEATH
AB Background and aims
Advanced liver fibrosis is an important predictor of liver disease progression and mortality, and current guidelines recommend screening for complications of cirrhosis once patients develop F3 fibrosis. Our study compared liver disease progression and survival in patients with stage 3 (F3) and stage 4 (F4) fibrosis on liver biopsy.
Methods
Retrospective study of patients with F3 or F4 on liver biopsy followed for development of liver disease complications (variceal bleeding, ascites, and hepatic encephalopathy); hepatocellular carcinoma, and survival (overall and transplant free survival).
Results
Of 2488 patients receiving liver biopsy between 01/02 and 12/12, a total of 294 (171 F3) were analyzed. Over a median follow up period of 3 years, patients with F4 (mean age 53 years, 63% male) compared to F3 (mean age 49 years, 43% male) had higher five year cumulative probability of any decompensation (38% vs. 14%, p<0.0001), including variceal bleed (10% vs. 4%, p = 0.014), ascites (21% vs. 9%, p = 0.0014), and hepatic encephalopathy (14% vs. 5%, p = 0.003). F4 patients also had lower overall 5-year survival (80% vs. 93%, p = 0.003) and transplant free survival (80% vs. 93%, p = 0.002). Probability of hepatocellular carcinoma in 5 years after biopsy was similar between F3 and F4 (1.2% vs. 2%, p = 0.54).
Conclusions
Compared to F4 stage, patients with F3 fibrosis have decreased risk for development of liver disease complications and better survival. Prospective well designed studies are suggested with large sample size and overcoming the limitations identified in this study, to confirm and validate these findings, as basis for modifying guidelines and recommendations on follow up of patients with advanced fibrosis and stage 3 liver fibrosis.
C1 [Axley, Page; Mudumbi, Sandhya; Sarker, Shabnam] Univ Alabama Birmingham, Dept Internal Med, Birmingham, AL USA.
[Kuo, Yong-Fang] Univ Texas Med Branch, Dept Biostat, Galveston, TX 77555 USA.
[Singal, Ashwani] Univ Alabama Birmingham, Div Gastroenterol & Hepatol, Birmingham, AL 35294 USA.
C3 University of Alabama System; University of Alabama Birmingham;
University of Texas System; University of Texas Medical Branch
Galveston; University of Alabama System; University of Alabama
Birmingham
RP Singal, A (corresponding author), Univ Alabama Birmingham, Div Gastroenterol & Hepatol, Birmingham, AL 35294 USA.
EM ashwanisingal.com@gmail.com
RI Singal, Ashwani/H-6181-2019
OI Singal, Ashwani/0000-0003-1207-3998
FU American College of Gastroenterology
FX A Faculty Development Grant from the American College of
Gastroenterology supported our work.
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NR 21
TC 17
Z9 20
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 10
PY 2018
VL 13
IS 5
AR e0197117
DI 10.1371/journal.pone.0197117
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GF3JM
UT WOS:000431851700072
PM 29746540
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Wang, X
Luo, JN
Wu, XY
Zhang, QX
Wu, B
AF Wang, Xing
Luo, Jin-Ni
Wu, Xiao-Ying
Zhang, Qi-Xian
Wu, Bin
TI Study of liver cirrhosis over twenty consecutive years in adults in
Southern China
SO WORLD JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Liver cirrhosis; Epidemiology; Etiology; Upper gastrointestinal
bleeding; Hepatocellular carcinoma; In-hospital mortality
ID GLOBAL BURDEN; DISEASE; MORTALITY; COMPLICATIONS; TRENDS; IMPACT; TIME
AB BACKGROUNDLiver cirrhosis (LC) is a prevalent and severe disease in China. The burden of LC is changing with widespread vaccination of hepatitis B virus (HBV) and antiviral therapy. However, the recent transition in etiologies and clinical features of LC cases requiring hospitalization is unclear.AIMTo identify the transition in etiologies and clinical characteristics of hospitalized LC patients in Southern China.METHODSIn this retrospective, cross-sectional study we included LC inpatients admitted between January 2001 and December 2020. Medical data indicating etiological diagnosis and LC complications, and demographic, laboratory, and imaging data were collected from our hospital-based dataset. The etiologies of LC were mainly determined according to the discharge diagnosis, and upper gastrointestinal bleeding, ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatocellular carcinoma (HCC), portal vein thrombosis, hepatorenal syndrome, and acute-on-chronic liver failure (ACLF) were considered LC-related complications in our study. Changing trends in the etiologies and clinical characteristics were investigated using logistic regression, and temporal trends in proportions of separated years were investigated using the Cochran-Armitage test. In-hospital prognosis and risk factors associated with in-hospital mortality were also investigated.RESULTSA total of 33143 patients were included in the study [mean (SD) age, 51.7 (11.9) years], and 82.2% were males. The mean age of the study population increased from 51.0 years in 2001-2010 to 52.0 years in 2011-2020 (P < 0.001), and the proportion of female patients increased from 16.7% in 2001-2010 to 18.2% in 2011-2020 (P = 0.003). LC patients in the decompensated stage at diagnosis decreased from 68.1% in 2001-2010 to 64.6% in 2011-2020 (P < 0.001), and the median score of model for end-stage liver disease also decreased from 14.0 to 11.0 (P < 0.001). HBV remained the major etiology of LC (75.0%) and the dominant cause of viral hepatitis-LC (94.5%) during the study period. However, the proportion of HBV-LC decreased from 82.4% in 2001-2005 to 74.2% in 2016-2020, and the proportion of viral hepatitis-LC decreased from 85.2% in 2001-2005 to 78.1% in 2016-2020 (both P for trend < 0.001). Meanwhile, the proportions of LC caused by alcoholic liver disease, autoimmune hepatitis and mixed etiology increased by 2.5%, 0.8% and 4.5%, respectively (all P for trend < 0.001). In-hospital mortality was stable at 1.0% in 2011-2020, whereas HCC and ACLF manifested the highest increases in prevalence among all LC complications (35.8% to 41.0% and 5.7% to 12.4%, respectively) and were associated with 6-fold and 4-fold increased risks of mortality (odds ratios: 6.03 and 4.22, respectively).CONCLUSIONLC inpatients have experienced changes in age distribution and etiologies of cirrhosis over the last 20 years in Southern China. HCC and ACLF are associated with the highest risk of in-hospital mortality among LC complications.
C1 [Wang, Xing; Luo, Jin-Ni; Wu, Xiao-Ying; Wu, Bin] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Gastroenterol, 600 Tianhe Rd, Guangzhou 510630, Guangdong, Peoples R China.
[Wang, Xing; Luo, Jin-Ni; Wu, Xiao-Ying; Wu, Bin] Sun Yat sen Univ, Affiliated Hosp 3, Guangdong Prov Key Lab Liver Dis Res, Guangzhou 510630, Guangdong, Peoples R China.
[Zhang, Qi-Xian] Sun Yat sen Univ, Affiliated Hosp 3, Patient Case Management Div, Guangzhou 510630, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University
RP Wu, B (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 3, Dept Gastroenterol, 600 Tianhe Rd, Guangzhou 510630, Guangdong, Peoples R China.
EM wubin6@mail.sysu.edu.cn
RI wang, xl/Y-8251-2019; Zhang, Qixian/AAD-7646-2020; Wu,
Xiaoying/ABD-8904-2020
FU National Natural Science Foundation of China [82070574]; Natural Science
Foundation of Guangdong Province Team Project [2018B030312009]
FX Supported by National Natural Science Foundation of China, No. 82070574;
Natural Science Foundation of Guangdong Province Team Project, No.
2018B030312009.
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NR 34
TC 3
Z9 3
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5182
J9 WORLD J HEPATOL
JI World J. Hepatol.
PD DEC 27
PY 2023
VL 15
IS 12
DI 10.4254/wjh.v15.i12.1294
PG 14
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA FB0V1
UT WOS:001143179400002
PM 38223413
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Czaja, AJ
AF Czaja, Albert J.
TI Global Disparities and Their Implications in the Occurrence and Outcome
of Autoimmune Hepatitis
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Review
DE Autoimmune hepatitis; Epidemiology; Incidence; Prevalence; Mortality
ID PRIMARY BILIARY-CIRRHOSIS; CHRONIC ACTIVE HEPATITIS; PRIMARY SCLEROSING
CHOLANGITIS; SOLUBLE LIVER ANTIGEN; ANTINEUTROPHIL CYTOPLASMIC
ANTIBODIES; SYSTEMIC-LUPUS-ERYTHEMATOSUS; BILE-DUCT INJURY;
UNITED-STATES; GUT MICROBIOTA; HEPATOCELLULAR-CARCINOMA
AB Autoimmune hepatitis has a variable occurrence, clinical phenotype, and outcome, and the factors contributing to this variability are uncertain. The goals of this review are to examine the global disparities in the occurrence and outcome of autoimmune hepatitis, suggest bases for these disparities, and encourage investigations that extend beyond single-center experiences. Disparities in the incidence and prevalence of autoimmune hepatitis in different age groups, genders, ethnicities, and geographical regions suggest that factors other than genetic predisposition are involved. Age- and gender-related antigen exposures from the external (infections, toxins, and medications) and internal (intestinal microbiome) environment may affect the incidence of the disease, and the timeliness and nature of treatment may influence its prevalence. The increasing incidence of autoimmune hepatitis in Spain, Denmark, and the Netherlands suggests that a new etiological trigger has been introduced or that the susceptible population has changed. Variations in mortality between Western and Asian-Pacific countries may result from differences in disease detection or management, and variations in gender predilection, peak age of onset, frequency of concurrent immune diseases, and serological profile may reflect gender-biased and age-related antigen exposures and genetic predispositions. Global collaborations, population-based epidemiological studies that identify case clustering, and controlled interview-based surveys are mechanisms by which to understand these disparities and improve management. In conclusion, autoimmune hepatitis has a rising incidence in some countries and variable occurrence, phenotype, and outcome between countries and subgroups within countries. These disparities suggest that unrecognized population-based environmental, infectious, or socioeconomic factors are affecting its character.
C1 [Czaja, Albert J.] Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, Med, 200 First St SW, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Czaja, AJ (corresponding author), Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, Med, 200 First St SW, Rochester, MN 55905 USA.
EM czaja.albert@mayo.edu
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NR 192
TC 52
Z9 56
U1 0
U2 14
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD SEP
PY 2017
VL 62
IS 9
BP 2277
EP 2292
DI 10.1007/s10620-017-4675-y
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FD9LZ
UT WOS:000407845200012
PM 28710658
DA 2025-01-07
ER
PT J
AU Zhou, ZY
Gong, L
Wang, XY
Hu, Z
Wu, GJ
Tang, XJ
Peng, XB
Tang, S
Meng, M
Feng, H
AF Zhou, Zhenyu
Gong, Lei
Wang, Xiaoyun
Hu, Zhen
Wu, Gaojue
Tang, Xuejun
Peng, Xiaobin
Tang, Shuan
Meng, Miao
Feng, Hui
TI The role of regulatory B cells in digestive system diseases
SO INFLAMMATION RESEARCH
LA English
DT Review
DE Regulatory B cells; IL-10; Digestive system diseases; Adaptive immunity
ID TYPE-1 AUTOIMMUNE PANCREATITIS; B10 CELLS; HEPATOCELLULAR-CARCINOMA;
ESOPHAGEAL CANCER; T-CELLS; SUPPRESSIVE ROLE; HBV INFECTION; TNF-ALPHA;
MICE; PROGRESSION
AB The past decade has provided striking insights into a newly identified subset of B cells known as regulatory B cells (Bregs). In addition to producing antibody, Bregs also regulate diseases via cytokine production and antigen presentation. This subset of B cells has protective and potentially therapeutic effects. However, the particularity of Bregs has caused some difficulties in conducting research on their roles. Notably, human B10 cells, which are Bregs that produce interleukin 10, share phenotypic characteristics with other previously defined B cell subsets, and currently, there is no known surface phenotype that is unique to B10 cells.
An online search was performed in the PubMed and Web of Science databases for articles published providing evidences on the role of regulatory B cells in digestive system diseases.
Abundant evidence has demonstrated that Bregs play a regulatory role in inflammatory, autoimmune, and tumor diseases, and regulatory B cells play different roles in different diseases, but future work needs to determine the mechanisms by which Bregs are activated and how these cells affect their target cells.
C1 [Zhou, Zhenyu; Gong, Lei; Wang, Xiaoyun; Hu, Zhen; Wu, Gaojue; Tang, Xuejun; Peng, Xiaobin; Tang, Shuan; Meng, Miao; Feng, Hui] Nanjing Med Univ, Wuxi Hosp 2, Div Gastroenterol, Zhong Shan Rd 68, Wuxi, Jiangsu, Peoples R China.
C3 Nanjing Medical University
RP Wang, XY (corresponding author), Nanjing Med Univ, Wuxi Hosp 2, Div Gastroenterol, Zhong Shan Rd 68, Wuxi, Jiangsu, Peoples R China.
EM xiaoyunwang68@aliyun.com
RI wang, lili/HDL-7210-2022
FU Wuxi Hospital Management Center [YGZXZ1504]; General project of Health
Bureau of Wuxi City [MS201414]
FX The National Natural Science Foundation of China (81500467). The
National Natural Science Foundation of Jiangsu Province (BK20151116).
Major project of Wuxi Hospital Management Center (YGZXZ1504). General
project of Health Bureau of Wuxi City (MS201414).
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NR 41
TC 0
Z9 1
U1 0
U2 10
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1023-3830
EI 1420-908X
J9 INFLAMM RES
JI Inflamm. Res.
PD APR
PY 2017
VL 66
IS 4
BP 303
EP 309
DI 10.1007/s00011-016-1007-1
PG 7
WC Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Immunology
GA EN9OV
UT WOS:000396330400003
PM 27878329
DA 2025-01-07
ER
PT J
AU Kadasah, SF
Radwan, MO
AF Kadasah, Sultan F.
Radwan, Mohamed O.
TI Overview of Ursolic Acid Potential for the Treatment of Metabolic
Disorders, Autoimmune Diseases, and Cancers via Nuclear Receptor
Pathways
SO BIOMEDICINES
LA English
DT Review
DE ursolic acid; nuclear receptors; NASH; metabolic disorders; autoimmune
diseases
ID FARNESOID-X-RECEPTOR; PPAR-GAMMA AGONIST; OLEANOLIC ACID; PENTACYCLIC
TRITERPENE; INDUCED APOPTOSIS; NATURAL-PRODUCTS; STRUCTURAL BASIS; MOUSE
MODEL; LXR-ALPHA; IN-VITRO
AB Nuclear receptors (NRs) form a family of druggable transcription factors that are regulated by ligand binding to orchestrate multifaceted physiological functions, including reproduction, immunity, metabolism, and growth. NRs represent attractive and valid targets for the management and treatment of a vast array of ailments. Pentacyclic triterpenes (PTs) are ubiquitously distributed natural products in medicinal and aromatic plants, of which ursolic acid (UA) is an extensively studied member, due to its diverse bio-pertinent activities against different cancers, inflammation, aging, obesity, diabetes, dyslipidemia, and liver injury. In fact, PTs share a common lipophilic structure that resembles NRs' endogenous ligands. Herein, we present a review of the literature on UA's effect on NRs, showcasing the resulting health benefits and potential therapeutic outcomes. De facto, UA exhibited numerous pharmacodynamic effects on PPAR, LXR, FXR, and PXR, resulting in remarkable anti-inflammatory, anti-hyperlipidemic, and hepatoprotective properties, by lowering lipid accumulation in hepatocytes and mitigating non-alcoholic steatohepatitis (NASH) and its subsequent liver fibrosis. Furthermore, UA reversed valproate and rifampicin-induced hepatic lipid accumulation. Additionally, UA showed great promise for the treatment of autoimmune inflammatory diseases such as multiple sclerosis and autoimmune arthritis by antagonizing ROR gamma. UA exhibited antiproliferative effects against skin, prostate, and breast cancers, partially via PPAR alpha and ROR gamma pathways. Herein, for the first time, we explore and provide insights into UA bioactivity with respect to NR modulation.
C1 [Kadasah, Sultan F.] Univ Bisha, Fac Sci, Dept Biol, POB 551, Bisha 61922, Saudi Arabia.
[Radwan, Mohamed O.] Kumamoto Univ, Fac Life Sci, Med & Biol Chem Sci Farm Joint Res Lab, Kumamoto 8620973, Japan.
C3 University of Bisha; Kumamoto University
RP Kadasah, SF (corresponding author), Univ Bisha, Fac Sci, Dept Biol, POB 551, Bisha 61922, Saudi Arabia.; Radwan, MO (corresponding author), Kumamoto Univ, Fac Life Sci, Med & Biol Chem Sci Farm Joint Res Lab, Kumamoto 8620973, Japan.
EM sukadasah@ub.edu.sa; mohamedradwan@kumamoto-u.ac.jp
RI Kadasah, Sultan/JJE-7102-2023; , Mohamed/AAX-3535-2021
OI , Mohamed/0000-0002-9220-2659; Kadasah, Sultan F/0000-0001-8077-3668
FU The authors are thankful to the Deanship of Scientific Research at the
University of Bisha for supporting this work through the Fast-Track
Research Support Program.; Deanship of Scientific Research at the
University of Bisha
FX The authors are thankful to the Deanship of Scientific Research at the
University of Bisha for supporting this work through the Fast-Track
Research Support Program.
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NR 152
TC 11
Z9 11
U1 2
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD OCT
PY 2023
VL 11
IS 10
AR 2845
DI 10.3390/biomedicines11102845
PG 19
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA W5ZR2
UT WOS:001092411100001
PM 37893218
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Keyvani, H
Fazlalipour, M
Monavari, SHR
Mollaie, HR
AF Keyvani, Hossein
Fazlalipour, Mehdi
Monavari, Seyed Hamid Reza
Mollaie, Hamid Reza
TI Hepatitis C Virus - Proteins, Diagnosis, Treatment and New Approaches
for Vaccine Development
SO ASIAN PACIFIC JOURNAL OF CANCER PREVENTION
LA English
DT Review
DE Hepatitis C Virus; treatment; vaccine; virus like particle
ID HCV-CORE PROTEIN; PRIME-BOOST IMMUNIZATION; CYTOTOXIC T-LYMPHOCYTES;
METHYLOTROPHIC YEAST; STRUCTURAL PROTEINS; IMMUNE-RESPONSES; DENDRITIC
CELLS; ANTI-HCV; MULTICENTER EVALUATION; INTERFERON THERAPY
AB Background: Hepatitis C virus (HCV) causes acute and chronic human hepatitis infection and as such is an important global health problem. The virus was discovered in the USA in 1989 and it is now known that three to four million people are infected every year, WHO estimating that 3 percent of the 7 billion people worldwide being chronically infected. Humans are the natural hosts of HCV and this virus can eventually lead to permanent liver damage and carcinoma. HCV is a member of the Flaviviridae family and Hepacivirus genus. The diameter of the virus is about 50-60 nm and the virion contains a single-stranded positive RNA approximately 10,000 nucleotides in length and consisting of one ORF which is encapsulated by an external lipid envelope and icosahedral capsid. HCV is a heterogeneous virus, classified into 6 genotypes and more than 50 subtypes. Because of the genome variability, nucleotide sequences of genotypes differ by approximately 31-34%, and by 20-23% among subtypes. Quasi-species of mixed virus populations provide a survival advantage for the virus to create multiple variant genomes and a high rate of generation of variants to allow rapid selection of mutants for new environmental conditions. Direct contact with infected blood and blood products, sexual relationships and availability of injectable drugs have had remarkable effects on HCV epidemiology. Hundreds of thousands of people die each year from hepatitis and liver cancer caused by HCV virus infection. Approximately 80% of patients with acute hepatitis C progress into a chronic disease state leading to serious hepatic disorders, 10-20% of which develop chronic liver cirrhosis and hepatocellular carcinoma. The incubation period of HCV is 6-8 weeks and the infection is often asymptomatic so it is very hard to detect at early stages, making early treatment very difficult. Therefore, hepatitis C is called a "silent disease". Neutralizing antibodies are produced against several HCV proteins during infection but the virus mutates to escape from antibodies. Some patients with chronic hepatitis C may have some symptoms such as fatigue, muscle aches, nausea and pain. Autoimmune and immunecomplex-mediated diseases have also been reported with chronic HCV infection.
C1 [Keyvani, Hossein; Monavari, Seyed Hamid Reza] Univ Tehran Med Sci, Dept Clin Virol, Tehran, Iran.
[Fazlalipour, Mehdi; Mollaie, Hamid Reza] Univ Tehran Med Sci, Dept Med Virol, Tehran, Iran.
C3 Tehran University of Medical Sciences; Tehran University of Medical
Sciences
RP Fazlalipour, M (corresponding author), Univ Tehran Med Sci, Dept Med Virol, Tehran, Iran.
EM mfp.virology@gmail.com
RI Keyvani, Hossein/LRT-8288-2024; SeyedAlinaghi, SeyedAhmad/M-2938-2017;
Fazlalipour, Mehdi/K-9621-2017; Mollaei, Hamid Reza/AAA-4051-2019
OI Mollaei, Hamid Reza/0000-0001-6874-0011
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NR 186
TC 20
Z9 20
U1 0
U2 8
PU ASIAN PACIFIC ORGANIZATION CANCER PREVENTION
PI GYEONGGI-DO
PA APJCP HEAD OFFICE, KOREAN NATL CANCER CENTER, 323 ILAN -RO,
ILSANDONG-GU, GOYANG-SI, GYEONGGI-DO, 410-769, SOUTH KOREA
SN 1513-7368
J9 ASIAN PAC J CANCER P
JI Asian Pac. J. Cancer Prev.
PY 2012
VL 13
IS 12
BP 5917
EP 5935
DI 10.7314/APJCP.2012.13.12.5917
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 244RE
UT WOS:000326406300001
OA gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Libra, M
Indelicato, M
De Re, V
Zignego, AL
Chiocchetti, A
Malaponte, G
Dianzani, U
Nicoletti, F
Stivala, F
McCubrey, JA
Mazzarino, MC
AF Libra, M
Indelicato, M
De Re, V
Zignego, AL
Chiocchetti, A
Malaponte, G
Dianzani, U
Nicoletti, F
Stivala, F
McCubrey, JA
Mazzarino, MC
TI Elevated serum levels of osteopontin in HCV-associated
lymphoproliferative disorders
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE ostepontin; type II mixed cryoglobulinemia syndrome; HCV; NHL
ID HEPATITIS-C VIRUS; MIXED CRYOGLOBULINEMIA; EXTRAHEPATIC MANIFESTATIONS;
TRANSGENIC MICE; CELLULAR BASIS; INFECTION; AUTOIMMUNE; GENE;
AUTOANTIBODIES; HEPATOCYTES
AB Hepatitis C virus ( HCV) infection is associated with chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Recent evidences have also suggested that HCV infection contributes to development of autoimmune disorders and B-cell nonHodgkin's lymphoma ( NHL). Mechanisms by which HCV infection promotes B-cell NHL development remain unclear. Increased serum osteopontin ( OPN) levels have been associated with several autoimmune diseases as well as a variety of cancers. However, the association between OPN and B-cell NHL or HCV-associated B-cell proliferation has not previously been reported. In the present study, we determined whether serum OPN differences were associated with HCV infection, type II mixed cryglobulinemia ( MC) syndrome and B-cell NHL. Serum OPN levels were measured by capture enzyme-linked immunosorbent assay. Our results show that high serum OPN levels are associated with B-cell NHL and HCV infection. Interestingly, highest serum OPN concentrations were found among HCV-infected patients with concomitant type II MC syndrome with and without B-cell NHL. These data indicate that OPN is involved in the lymphomagenesis, especially, in the context of HCV infection and autoimmune diseases.
C1 Univ Catania, Dept Biomed Sci, I-95124 Catania, Italy.
Natl Canc Inst, IRCCS, Ctr Riferimento Oncol, Aviano, Italy.
Univ Florence, Dept Internal Med, Florence, Italy.
Avogadro Univ Eastern Piedmont, Interdisciplinary Res Ctr Autoimmune Dis, Dept Med Sci, Novara, Italy.
E Carolina Univ, Dept Microbiol & Immunol, Greenville, NC USA.
E Carolina Univ, Leo W Jenkins Canc Ctr, Brody Sch Med, Greenville, NC USA.
C3 University of Catania; IRCCS Aviano (CRO); University of Florence;
University of Eastern Piedmont Amedeo Avogadro; University of North
Carolina; East Carolina University; University of North Carolina; East
Carolina University
RP Univ Catania, Dept Biomed Sci, Via Androne,83, I-95124 Catania, Italy.
EM clomazza@unict.it
RI Zignego, Anna/AAL-8205-2021; Dianzani, Umberto/K-1952-2016; Libra,
Massimo/ABF-6654-2020; De Re, Valli/K-4121-2016; Libra,
Massimo/L-8241-2018; NICOLETTI, Ferdinando/M-4428-2016; DE RE,
VALLI/AAA-1374-2019
OI MALAPONTE, Grazia/0000-0001-6595-1198; Libra,
Massimo/0000-0002-7232-7737; Chiocchetti, Annalisa/0000-0002-4349-1087;
Zignego, Anna Linda/0000-0002-8552-4166; NICOLETTI,
Ferdinando/0000-0002-4570-8462; DE RE, VALLI/0000-0001-6100-9373;
DIANZANI, Umberto/0000-0001-6723-3931; McCubrey,
James/0000-0001-6027-3156
FU NCI NIH HHS [CA098195] Funding Source: Medline
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NR 35
TC 25
Z9 26
U1 0
U2 3
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4047
EI 1555-8576
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD NOV
PY 2005
VL 4
IS 11
BP 1192
EP 1194
DI 10.4161/cbt.4.11.2087
PG 3
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 022GS
UT WOS:000236044100012
PM 16177564
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Liu, GY
Zhang, Y
Han, SS
Zhuang, W
Lv, J
Han, MY
Xie, L
Jiang, XR
Wang, C
Saimaier, K
Shen, JS
Du, CS
AF Liu, Guangyu
Zhang, Yan
Han, Sansheng
Zhuang, Wei
Lv, Jie
Han, Mengyao
Xie, Ling
Jiang, Xiangrui
Wang, Chun
Saimaier, Kaidireya
Shen, Jingshan
Du, Changsheng
TI TPN10466 ameliorates Concanavalin A-induced autoimmune hepatitis in mice
via inhibiting ERK/JNK/p38 signaling pathway
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE Artemisinin derivatives; Concanavalin A-induced hepatitis; IFN-gamma;
MAPK signaling pathway
ID LIVER-INJURY; INTERFERON-GAMMA; T-CELLS; TH1; JNK
AB Autoimmune hepatitis (AIH) eventually progresses to liver fibrosis, cirrhosis, and even hepatocellular carcinoma, causing irreversible damage to the liver. Concanavalin A-induced hepatitis in mice is a well-established model with pathophysiology similar to that of immune-mediated liver injury in human viral and autoimmune hepatitis, and it has been widely used to explore the pathogenesis and clinical treatment of human immune hepatitis. Artemisinin has been shown to exhibit anti-inflammatory effects through unclear mechanisms. In this study, we aimed to assess the effect of the artemisinin derivative TPN10466 on AIH. In vitro studies showed that TPN10466 dose dependently inhibited the percentage of IFN-gamma-producing T cells. Further studies showed that TPN10466 attenuated the disease severity of AIH by downregulating the ability of lymphocytes to secrete IFN-gamma and by reducing lymphocyte number in the liver. In addition, we found that TPN10466 treatment reduced T-cell responses by inhibiting JNK, ERK, and p38 pathways. In conclusion, our work suggests that TPN10466 provides protection against the autoimmune disease AIH by suppressing the inflammatory response of T cells, suggesting that TPN10466 may be a promising potential agent for the treatment of AIH.
C1 [Liu, Guangyu; Han, Sansheng; Zhuang, Wei; Lv, Jie; Han, Mengyao; Xie, Ling; Wang, Chun; Saimaier, Kaidireya; Du, Changsheng] Tongji Univ, Orthopaed Dept Tongji Hosp, Sch Life Sci & Technol, Key Lab Spine & Spinal Cord Injury Repair & Regene, Shanghai, Peoples R China.
[Zhang, Yan; Zhuang, Wei; Jiang, Xiangrui; Shen, Jingshan] Univ Chinese Acad Sci, Beijing, Peoples R China.
[Zhang, Yan] Chinese Acad Sci, Xinjiang Tech Inst Phys & Chem, Urumqi, Peoples R China.
[Zhuang, Wei] Chinese Acad Sci, Inst Biophys, Beijing, Peoples R China.
[Jiang, Xiangrui; Shen, Jingshan] Chinese Acad Sci, Shanghai Inst Mat, CAS Key Lab Receptor Res, Med, Shanghai, Peoples R China.
[Du, Changsheng] Tongji Univ, Orthopaed Dept Tongji Hosp, Sch Life Sci & Technol, Key Lab Spine & Spinal Cord Injury Repair & Regene, Shanghai 200092, Peoples R China.
C3 Tongji University; Chinese Academy of Sciences; University of Chinese
Academy of Sciences, CAS; Chinese Academy of Sciences; Xinjiang
Technical Institute of Physics & Chemistry, CAS; Chinese Academy of
Sciences; Institute of Biophysics, CAS; Chinese Academy of Sciences;
Tongji University
RP Du, CS (corresponding author), Tongji Univ, Orthopaed Dept Tongji Hosp, Sch Life Sci & Technol, Key Lab Spine & Spinal Cord Injury Repair & Regene, Shanghai 200092, Peoples R China.
EM ducs2015@163.com
RI Zhang, Yanbing/AAX-8387-2020; Du, Changsheng/E-1552-2011
FU National Natural Science Foundation of China [32070768, 31871404,
31900658, 32270754]
FX Acknowledgements This work was supported by the National Natural Science
Foundation of China (grant number: 32070768, 31871404, 31900658,
32270754). Graphical image was drawn by Figdraw.
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NR 33
TC 4
Z9 4
U1 1
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD APR
PY 2023
VL 53
IS 4
DI 10.1002/eji.202250100
EA FEB 2023
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA D4WS6
UT WOS:000930063100001
PM 36648433
DA 2025-01-07
ER
PT J
AU Prasidthrathsint, K
Stapleton, JT
AF Prasidthrathsint, Kunatum
Stapleton, Jack T.
TI Laboratory Diagnosis and Monitoring of Viral Hepatitis
SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Viral hepatitis; Viral diagnostics; Hepatitis A; Hepatitis B; Hepatitis
C; Hepatitis D; Hepatitis E
ID B-VIRUS-INFECTION; C VIRUS; SURFACE-ANTIGEN; DELTA-VIRUS;
NATURAL-HISTORY; PERFORMANCE-CHARACTERISTICS; ANTIBODY-RESPONSE;
SEROLOGIC ASSAYS; HCV INFECTION; CORE ANTIGEN
AB Many microbes, toxins, autoimmune diseases, and neoplastic diseases may cause liver inflammation; however, 5 viruses whose main pathogenesis is liver disease are referred to as hepatitis A, B, C, D, and E viruses. These viruses cause a significant burden of global illness. With the exception of hepatitis A virus, all may cause chronic infection potentially leading to cirrhosis and hepatocellular carcinoma. Excellent serologic and nucleic acid detection methods are available for determining the precise cause and, in some cases, the duration of infection. Diagnostics are critical for identifying individuals needing treatment and for monitoring the treatment success.
C1 [Prasidthrathsint, Kunatum; Stapleton, Jack T.] Univ Iowa, Carver Coll Med, Dept Internal Med, Div Infect Dis, Iowa City, IA 52242 USA.
[Prasidthrathsint, Kunatum] Univ Iowa, Carver Coll Med, Dept Pathol, Div Clin Microbiol, Iowa City, IA USA.
[Prasidthrathsint, Kunatum; Stapleton, Jack T.] Univ Iowa, Carver Coll Med, Dept Microbiol & Immunol, Iowa City, IA 52242 USA.
[Prasidthrathsint, Kunatum; Stapleton, Jack T.] Univ Iowa Hosp & Clin, SW54,GH,200 Hawkins Dr, Iowa City, IA 52242 USA.
[Prasidthrathsint, Kunatum; Stapleton, Jack T.] Iowa City Vet Adm Hlth Care Ctr, Med & Res Serv, Iowa City, IA 52242 USA.
C3 University of Iowa; University of Iowa; University of Iowa; University
of Iowa
RP Stapleton, JT (corresponding author), Univ Iowa, Carver Coll Med, Dept Internal Med, Div Infect Dis, Iowa City, IA 52242 USA.; Stapleton, JT (corresponding author), Univ Iowa, Carver Coll Med, Dept Microbiol & Immunol, Iowa City, IA 52242 USA.; Stapleton, JT (corresponding author), Univ Iowa Hosp & Clin, SW54,GH,200 Hawkins Dr, Iowa City, IA 52242 USA.; Stapleton, JT (corresponding author), Iowa City Vet Adm Hlth Care Ctr, Med & Res Serv, Iowa City, IA 52242 USA.
EM jack-stapleton@uiowa.edu
RI Stapleton, John/I-6550-2012
OI Stapleton, Jack/0000-0002-2302-9055; Prasidthrathsint,
Kunatum/0000-0001-7920-6738
FU Department of Veterans Affairs Merit Review Grants [BX000207]; NIAID
[R56A1126493]
FX Department of Veterans Affairs Merit Review Grants BX000207 (J.T.
Stapleton), and NIAID R56A1126493
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NR 100
TC 6
Z9 7
U1 0
U2 14
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8553
EI 1558-1942
J9 GASTROENTEROL CLIN N
JI Gastroenterol. Clin. North Am.
PD JUN
PY 2019
VL 48
IS 2
BP 259
EP +
DI 10.1016/j.gtc.2019.02.007
PG 22
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IA1HZ
UT WOS:000469311300007
PM 31046974
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Miklossy, G
Hilliard, TS
Turkson, J
AF Miklossy, Gabriella
Hilliard, Tyvette S.
Turkson, James
TI Therapeutic modulators of STAT signalling for human diseases
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Review
ID HUMAN MULTIPLE-MYELOMA; HUMAN HEPATOCELLULAR-CARCINOMA; SMALL-MOLECULE
INHIBITOR; DNA-BINDING ACTIVITY; SELECTIVELY INDUCES APOPTOSIS;
GROWTH-SUPPRESSIVE ACTIVITY; TYROSINE-PHOSPHATASE SHP-1; LUNG-CANCER
CELLS; NF-KAPPA-B; TRANSCRIPTION 3
AB The signal transducer and activator of transcription (STAT) proteins have important roles in biological processes. The abnormal activation of STAT signalling pathways is also implicated in many human diseases, including cancer, autoimmune diseases, rheumatoid arthritis, asthma and diabetes. Over a decade has passed since the first inhibitor of a STAT protein was reported and efforts to discover modulators of STAT signalling as therapeutics continue. This Review discusses the outcomes of the ongoing drug discovery research endeavours against STAT proteins, provides perspectives on new directions for accelerating the discovery of drug candidates, and highlights the noteworthy candidate therapeutics that have progressed to clinical trials.
C1 [Miklossy, Gabriella; Hilliard, Tyvette S.; Turkson, James] Univ Hawaii, Ctr Canc, Canc Biol Program, Honolulu, HI 96813 USA.
[Miklossy, Gabriella; Hilliard, Tyvette S.; Turkson, James] Univ Hawaii, Ctr Canc, Nat Prod & Expt Therapeut Program, Honolulu, HI 96813 USA.
C3 Cancer Research Center of Hawaii; University of Hawaii System;
University of Hawaii System; Cancer Research Center of Hawaii
RP Turkson, J (corresponding author), Univ Hawaii, Ctr Canc, Canc Biol Program, 701 Ilalo St, Honolulu, HI 96813 USA.
EM jturkson@cc.hawaii.edu
FU National Cancer Institute [CA128865, CA161931]; University of Hawaii
FX The authors thank all their colleagues and members of their laboratory
for the stimulating discussions related to this work. The authors also
thank A. Chelsky for the art work for figure 3. This work was supported
by grants from the National Cancer Institute (CA128865 and CA161931) and
from the University of Hawaii to J.T.
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HEPATOCELLULAR-CARCINOMA; STELLATE CELLS; MIR-200 FAMILY; NONALCOHOLIC
STEATOHEPATITIS; HEPATOCYTE PROLIFERATION
AB Small, noncoding microRNAs (miRNAs) regulate diverse biological functions in the liver and increasing evidence suggests that they have a role in liver pathology. This Review summarizes advances in the field of miRNAs in liver diseases, inflammation and cirrhosis. MicroRNA-122, the most abundant miRNA in hepatocytes, has well-defined roles in HCV replication, and data indicate that it also serves as a viable therapeutic target. The role of miR-122 is also emerging in other liver diseases. Ample evidence exists for the important regulatory potential of other miRNAs in conditions associated with liver inflammation related to alcohol use, the metabolic syndrome or autoimmune processes. In addition, a broad array of miRNAs have been associated with the development of liver fibrosis both in animal models and human studies. The significance of the function and cellular distribution of miRNAs in the liver and the potential of miRNAs as a means of communication between cells and organs is discussed as well as the emerging utility of circulating miRNAs as biomarkers of different forms of liver damage and as early markers of disease and progression in hepatocellular carcinoma. Importantly, miRNA modulation in the liver represents a new therapeutic approach in the treatment armamentarium of hepatologists in the future.
C1 [Szabo, Gyongyi; Bala, Shashi] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA 01605 USA.
C3 University of Massachusetts System; University of Massachusetts
Worcester
RP Szabo, G (corresponding author), Univ Massachusetts, Sch Med, Dept Med, LRB208,364 Plantat St, Worcester, MA 01605 USA.
EM gyongyi.szabo@umassmed.edu
FU NIAAA [RO1-AA020744]
FX The work of the authors is supported by NIAAA grant RO1-AA020744 (to G.
Szabo).
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NR 140
TC 480
Z9 509
U1 3
U2 207
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5045
EI 1759-5053
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD SEP
PY 2013
VL 10
IS 9
BP 542
EP 552
DI 10.1038/nrgastro.2013.87
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 214HZ
UT WOS:000324124300009
PM 23689081
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Fiore, M
Leone, S
Maraolo, AE
Berti, E
Damiani, G
AF Fiore, Marco
Leone, Sebastiano
Maraolo, Alberto Enrico
Berti, Emilio
Damiani, Giovanni
TI Liver Illness and Psoriatic Patients
SO BIOMED RESEARCH INTERNATIONAL
LA English
DT Review
ID HEPATITIS-B-VIRUS; GENERALIZED PUSTULAR PSORIASIS; PRIMARY
BILIARY-CIRRHOSIS; FACTOR-ALPHA INHIBITORS; C VIRUS;
RHEUMATOID-ARTHRITIS; IMMUNOSUPPRESSED PATIENTS;
HEPATOCELLULAR-CARCINOMA; RETROSPECTIVE ANALYSIS; CLINICAL-PRACTICE
AB Psoriasis is a chronic inflammatory disease of the skin affecting approximately 2% of the world's population. Systemic treatments, including methotrexate and cyclosporin, are associated with potential hepatotoxicity, due to either direct liver damage or immunosuppression or both immunomediated and a direct liver injury; therefore, treatment of patients with psoriasis poses a therapeutic challenge. The aim of this minireview is to help clinicians in the management of psoriatic patients who develop signs of liver dysfunction. To find relevant articles, a comprehensive search was performed on PubMed, EMBASE, and Cochrane with appropriate combinations of the following keywords being considered: viral hepatitis, nonalcoholic fatty liver disease, psoriasis, hepatotoxicity, drug toxicity, cholestasis, and autoimmune liver diseases.
C1 [Fiore, Marco] Univ Campania Luigi Vanvitelli, Dept Anaesthesiol Surg & Emergency Sci, Naples, Italy.
[Leone, Sebastiano] San Giuseppe Moscati Hosp, Dept Med, Div Infect Dis, Avellino, Italy.
[Maraolo, Alberto Enrico] Univ Naples Federico II, Dept Clin Med & Surg, Sect Infect Dis, Naples, Italy.
[Berti, Emilio; Damiani, Giovanni] Univ Milan, IRCCS Ca Granda, Dept Pathophysiol & Transplantat, Dermatol Unit, Milan, Italy.
[Damiani, Giovanni] Study Ctr Young Dermatologists Italian Network YD, Bergamo, Italy.
C3 Universita della Campania Vanvitelli; San Giuseppe Moscati Hospital;
University of Naples Federico II; University of Milan; IRCCS Ca Granda
Ospedale Maggiore Policlinico
RP Fiore, M (corresponding author), Univ Campania Luigi Vanvitelli, Dept Anaesthesiol Surg & Emergency Sci, Naples, Italy.; Leone, S (corresponding author), San Giuseppe Moscati Hosp, Dept Med, Div Infect Dis, Avellino, Italy.
EM marco.fiore@hotmail.it; sebastianoleone@yahoo.it
RI Berti, Emilio/F-5256-2012; Chavshin, Alireza/B-1944-2009; Maraolo,
Alberto Enrico/K-3953-2018; Fiore, Marco/I-1343-2017
OI Damiani, Giovanni/0000-0002-2390-6505; Berti,
Emilio/0000-0001-6753-4910; Maraolo, Alberto Enrico/0000-0002-7218-7762;
Fiore, Marco/0000-0001-7263-0229
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NR 129
TC 56
Z9 59
U1 0
U2 4
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-6133
EI 2314-6141
J9 BIOMED RES INT
JI Biomed Res. Int.
PY 2018
VL 2018
AR 3140983
DI 10.1155/2018/3140983
PG 12
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA FV7FE
UT WOS:000424748100001
PM 29546055
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Torbenson, MS
Arnold, CA
Graham, RP
Jain, D
Kakar, S
Lam-Himlin, DM
Naini, BV
Wu, TT
Yeh, M
AF Torbenson, Michael S.
Arnold, Christina A.
Graham, Rondell P.
Jain, Dhanpat
Kakar, Sanjay
Lam-Himlin, Dora M.
Naini, Bita V.
Wu, Tsung-Teh
Yeh, Matthew
TI Identification of key challenges in liver pathology: data from a
multicenter study of extramural consults
SO HUMAN PATHOLOGY
LA English
DT Article
DE Liver pathology consultation; Autoimmune hepatitis; Primary biliary
cirrhosis; Fatty liver disease; Hepatocellular carcinoma
ID SURGICAL PATHOLOGY; 2ND OPINION; IMPACT
AB Extramural consultation for challenging pathology cases is an important part of patient care. The specific reasons why liver cases are submitted in consultation are poorly understood. To study patterns in extramural consultation, data were gathered from 1360 liver/Glipancreatobiliary consults submitted to 7 academic centers. Liver cases comprised 40% of consults and are the focus of this paper. They were submitted for questions on medical (61%) and tumor pathology (39%). A preliminary diagnosis was provided by the referring pathologist in 65% of cases. The most common questions in medical liver pathology were on general classification of a hepatitic pattern of injury (37%), primary biliary cirrhosis (14%), fatty liver disease (13%), autoimmune hepatitis (12%), and etiology of cirrhosis (10%). Most tumor consults were submitted for classification (83%). The most common final tumor consultant diagnoses for benign tumors were hepatic adenoma or focal nodular hyperplasia (52%) and for malignant tumors were metastatic malignancies (47%), hepatocellular carcinoma (32%), or cholangiocarcinoma (8%). For cases submitted with a diagnosis of malignancy, the diagnosis was concordant (43% of cases), concordant but with a generic diagnosis for which a more specific diagnosis could be rendered (37%), or discordant with a major change in diagnosis from malignant to benign or change in tumor type (17%). In conclusion, analysis of consult patterns identifies challenging areas in medical and tumor liver pathology, areas that benefit from consult services and can be focused on by continuing medical educational activities. (C) 2019 Elsevier Inc. All rights reserved.
C1 [Torbenson, Michael S.; Graham, Rondell P.; Wu, Tsung-Teh] Mayo Clin Rochester, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
[Arnold, Christina A.] Ohio State Univ, Med Ctr, Dept Pathol, Columbus, OH 43210 USA.
[Jain, Dhanpat] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA.
[Kakar, Sanjay] Univ Calif San Francisco, Med Ctr, Dept Anat Pathol, San Francisco, CA 94143 USA.
[Lam-Himlin, Dora M.] Univ Calif Los Angeles, Med Ctr, Dept Pathol & Lab Med, Los Angeles, CA 90024 USA.
[Naini, Bita V.] Mayo Clin Scottsdale, Dept Lab Med & Pathol, Scottsdale, AZ USA.
[Yeh, Matthew] Univ Washington, Med Ctr, Dept Pathol, Seattle, WA 98195 USA.
C3 Mayo Clinic; University System of Ohio; Ohio State University; Yale
University; University of California System; University of California
San Francisco; University of California System; University of California
Los Angeles; University of California Los Angeles Medical Center; Mayo
Clinic; Mayo Clinic Phoenix; University of Washington; University of
Washington Seattle
RP Torbenson, MS (corresponding author), Mayo Clin Rochester, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
EM torbenson.michael@mayo.edu
OI Graham, Rondell/0000-0002-8686-4867
CR Ahmed Z., 2004, JPMA Journal of the Pakistan Medical Association, V54, P306
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NR 10
TC 7
Z9 7
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD MAY
PY 2019
VL 87
BP 75
EP 82
DI 10.1016/j.humpath.2019.03.001
PG 8
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA IA4GX
UT WOS:000469523100010
PM 30857968
DA 2025-01-07
ER
PT J
AU Maheshwari, A
Thuluvath, PJ
AF Maheshwari, A
Thuluvath, PJ
TI Cryptogenic cirrhosis and NAFLD: Are they related?
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
ID CHRONIC LIVER-DISEASE; HEPATITIS-B-VIRUS; HETEROZYGOUS
ALPHA(1)-ANTITRYPSIN DEFICIENCY; MZ ALPHA-1-ANTITRYPSIN DEFICIENCY;
HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC STEATOHEPATITIS; NATURAL-HISTORY;
UNITED-STATES; TRANSPLANTATION; ADULTS
AB Cryptogenic cirrhosis (CC), literally meaning cirrhosis of obscure or unknown origin, is a diagnosis of exclusion. The circumstantial evidence indicates that nonalcoholic fatty liver disease (NAFLD) is perhaps one of the important causes of CC. There is also evidence, especially from the European literature, that some patients with CC may have undiagnosed or burnt-out autoimmune hepatitis (AIH). Other rare causes may include "unknown" viral (non-A, non-B, non-C) hepatitis, and occult alcoholism. In this review, we examine the role of NAFLD and other causes in the pathogenesis of CC, and the impact of obesity on patients with chronic liver disease.
C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
C3 Johns Hopkins University
RP Thuluvath, PJ (corresponding author), Johns Hopkins Univ Hosp, 1830 E Monument St, Baltimore, MD 21205 USA.
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NR 36
TC 67
Z9 75
U1 0
U2 3
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD MAR
PY 2006
VL 101
IS 3
BP 664
EP 668
DI 10.1111/j.1572-0241.2006.00478.x
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 016YD
UT WOS:000235659500037
PM 16464222
DA 2025-01-07
ER
PT J
AU Michalak, TI
AF Michalak, Tomasz I.
TI Diverse Virus and Host-Dependent Mechanisms Influence the Systemic and
Intrahepatic Immune Responses in the Woodchuck Model of Hepatitis B
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE woodchuck model of hepatitis B; virus-hepatocyte interaction; major
histocompatibility complex presentation; asialoglycoprotein receptor;
hepatocyte as cytotoxic immune effector; intrahepatic innate and
adaptive immune responses; pre-acute infection; toll-like receptors
ID BLOOD MONONUCLEAR-CELLS; HEPATOCYTE PLASMA-MEMBRANE; HISTOCOMPATIBILITY
COMPLEX PRESENTATION; CD8(+) T-CELLS; ASIALOGLYCOPROTEIN RECEPTOR;
SURFACE-ANTIGEN; LYMPHOID-CELLS; HEPADNAVIRAL INFECTION;
HEPATOCELLULAR-CARCINOMA; REVERSE TRANSCRIPTION
AB Woodchuck infected with woodchuck hepatitis virus (WHV) represents the pathogenically nearest model of hepatitis B and associated hepatocellular carcinoma (HCC). This naturally occurring animal model also is highly valuable for development and preclinical evaluation of new anti-HBV agents and immunotherapies against chronic hepatitis (CH) B and HCC. Studies in this system uncovered a number of molecular and immunological processes which contribute or likely contribute to the immunopathogenesis of liver disease and modulation of the systemic and intrahepatic innate and adaptive immune responses during hepadnaviral infection. Among them, inhibition of presentation of the class I major histocompatibility complex on chronically infected hepatocytes and a role of WHV envelope proteins in this process, as well as augmented hepatocyte cytotoxicity mediated by constitutively expressed components of CD95 (Fas) ligand- and perforin-dependent pathways, capable of eliminating cells brought to contact with hepatocyte surface, including activated T lymphocytes, were uncovered. Other findings pointed to a role of autoimmune response against hepatocyte asialoglycoprotein receptor in augmenting severity of liver damage in hepadnaviral CH. It was also documented that WHV in the first few hours activates intrahepatic innate immunity that transiently decreases hepatic virus load. However, this activation is not translated in a timely manner to induction of virus-specific T cell response which appears to be hindered by defective activation of antigen presenting cells and presentation of viral epitopes to T cells. The early WHV infection also induces generalized polyclonal activation of T cells that precedes emergence of virus-specific T lymphocyte reactivity. The combination of these mechanisms hinder recognition of virus allowing its dissemination in the initial, asymptomatic stages of infection before adaptive cellular response became apparent. This review will highlight a range of diverse mechanisms uncovered in the woodchuck model which affect effectiveness of the anti-viral systemic and intrahepatic immune responses, and modify liver disease outcomes. Further exploration of these and other mechanisms, either already discovered or yet unknown, and their interactions should bring more comprehensive understanding of HBV pathogenesis and help to identify novel targets for therapeutic and preventive interventions. The woodchuck model is uniquely positioned to further contribute to these advances.
C1 [Michalak, Tomasz I.] Mem Univ Newfoundland, Mol Virol & Hepatol Res Grp, Div Biomed Sci, Fac Med,Hlth Sci Ctr, St John, NF, Canada.
C3 Memorial University Newfoundland
RP Michalak, TI (corresponding author), Mem Univ Newfoundland, Mol Virol & Hepatol Res Grp, Div Biomed Sci, Fac Med,Hlth Sci Ctr, St John, NF, Canada.
EM timich@mun.ca
FU Canadian Institutes of Health Research (CIHR) [MA-9256, MT-11262,
MT-14818, RO-15174, MOP-14818, PJT-153001]; Senior (Tier 1) Canada
Research Chair in Viral Hepatitis/Immunology - Canada Research Chair
Program; CIHR; Canada Foundation for Innovation; Memorial University,
St. John's, NL, Canada
FX The studies from the author's laboratory summarized in this review were
supported by operating grants MA-9256, MT-11262, MT-14818, RO-15174,
MOP-14818, and PJT-153001 from the Canadian Institutes of Health
Research (CIHR), formerly the Medical Research Council of Canada,
Ottawa, Canada awarded to TM. TMwas a recipient of the Senior (Tier 1)
Canada Research Chair in Viral Hepatitis/Immunology sponsored by the
Canada Research Chair Program and funds from the CIHR, the Canada
Foundation for Innovation, and Memorial University, St. John's, NL,
Canada.
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NR 170
TC 14
Z9 15
U1 0
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAY 27
PY 2020
VL 11
AR 853
DI 10.3389/fimmu.2020.00853
PG 21
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA LZ0RS
UT WOS:000540939500001
PM 32536912
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kaushik, P
Kumar, A
AF Kaushik, Pankhuri
Kumar, Arun
TI Emerging role and function of miR-198 in human health and diseases
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Review
DE MicroRNAs; MiRNAs; MiR-198; LncRNAs; Circular RNAs; Cancer
ID MICRORNA EXPRESSION PROFILES; SQUAMOUS-CELL CARCINOMA;
COLORECTAL-CANCER; LUNG-CANCER; HEPATOCELLULAR-CARCINOMA;
OVARIAN-CANCER; PROSTATE-CANCER; DOWN-REGULATION; GASTRIC-CANCER;
PROLIFERATION
AB Ever since their discovery, microRNAs (miRNAs/miRs) have astonished us by the plethora of processes they regulate, and thus adding another dimension to the gene regulation. They have been implicated in several diseases affecting cardiovascular, neurodegenerative, hepatic, autoimmune and inflammatory functions. A primate specific exonic miRNA, miR-198 has been vastly studied during the past decade, and shown to have a critical role in wound healing. The aberrant expression of miR-198 was first reported in schizophrenia, linking it to neural development. Later, its dysregulation and tumor suppressive role was reported in hepatocellular carcinoma. However, this was just a beginning, and after which there was an explosion of reports linking miR-198 deregulation to cancers and other ailments. The first target to be identified for miR-198 was Cyclin T1 in monocytes affecting HIV1 replication. Depending on the type of cancer, miR-198 has been shown to function either as a tumor suppressor or an oncomir. Interestingly, miR-198 is not only known to regulate multiple targets and pathways, but also is itself regulated by several circular RNAs and long-non-coding RNAs, highlighting a complex regulatory network. This review highlights the currently understood mechanism and regulation of miR198 in different diseases, and its possible diagnostic and therapeutic potential.
C1 [Kaushik, Pankhuri; Kumar, Arun] Indian Inst Sci, Dept Mol Reprod Dev & Genet, Bangalore 560012, Karnataka, India.
C3 Indian Institute of Science (IISC) - Bangalore
RP Kumar, A (corresponding author), Indian Inst Sci, Dept Mol Reprod Dev & Genet, Bangalore 560012, Karnataka, India.
EM arunk@iisc.ac.in
FU Department of Biotechnology, New Delhi [BT/PR33054/MED/30/2210/2020]
FX The financial support from Department of Biotechnology
(BT/PR33054/MED/30/2210/2020) , New Delhi is gratefully acknowledged.
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NR 135
TC 4
Z9 4
U1 0
U2 7
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD JAN
PY 2022
VL 229
AR 153741
DI 10.1016/j.prp.2021.153741
EA DEC 2021
PG 13
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA XW0UA
UT WOS:000735344000003
PM 34952425
DA 2025-01-07
ER
PT J
AU Montiel, MDM
Herce, BC
AF Martinez Montiel, Maria del Pilar
Casis Herce, Begone
TI Inflammatory bowel disease and solid organ transplantation
SO REVISTA ESPANOLA DE ENFERMEDADES DIGESTIVAS
LA English
DT Review
DE Inflammatory bowel disease; Transplantation; Solid organs; Biologics;
Colorectal cancer
ID PRIMARY SCLEROSING CHOLANGITIS; LIVER-TRANSPLANTATION;
COLORECTAL-CANCER; DE-NOVO; IMMUNOSUPPRESSION; RECIPIENTS; RISK;
MANAGEMENT; SAFETY; IMPACT
AB The population of patients with inflammatory bowel disease (IBD) and solid organ transplant (SOT) is increasing. Two clinical scenarios exist, recurrence of pre-existing IBD, which is more common, and de novo development of IBD, with a much higher incidence than in the general population. Their clinical course differs and may have a negative impact on the graft in both cases. The pathophysiological mechanisms remain unknown and no specific treatment recommendations are available. The combined effect of biologic therapy against IBD and immunosuppressive therapy against a potential rejection means that close monitoring is mandatory to identify infection, autoimmune events and malignancies. The colorectal cancer (CRC) rate is higher in this population. The group at greatest risk are patients with IBD undergoing liver transplantation (LT) for primary sclerosing cholangitis (PSC).
C1 [Martinez Montiel, Maria del Pilar; Casis Herce, Begone] Hosp Univ 12 Octubre, Digest Dis Dept, Av Cordoba S-N, Madrid 28041, Spain.
C3 Hospital Universitario 12 de Octubre
RP Montiel, MDM (corresponding author), Hosp Univ 12 Octubre, Digest Dis Dept, Av Cordoba S-N, Madrid 28041, Spain.
EM pilarmarmon123@telefonica.net
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NR 30
TC 5
Z9 5
U1 0
U2 1
PU ARAN EDICIONES, S A
PI MADRID
PA CASTELLO, 128, 28006 MADRID, SPAIN
SN 1130-0108
EI 2340-4167
J9 REV ESP ENFERM DIG
JI Rev. Esp. Enferm. Dig.
PY 2021
VL 113
IS 1
BP 60
EP 64
DI 10.17235/reed.2020.7361/2020
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA PR2GH
UT WOS:000607059300012
PM 33233912
OA gold
DA 2025-01-07
ER
PT J
AU Syed, H
Penner, T
Mason, AL
AF Syed, Hussain
Penner, Tara
Mason, Andrew L.
TI Linking Human Betaretrovirus with Autoimmunity and Liver Disease in
Patients with Primary Biliary Cholangitis
SO VIRUSES-BASEL
LA English
DT Review
DE biliary epithelial cells (BEC); Bradford Hill criteria; human
betaretrovirus (HBRV); Koch's postulates; mouse mammary tumor virus
(MMTV); primary biliary cholangitis (PBC)
ID MAMMARY-TUMOR VIRUS; COMBINATION ANTIRETROVIRAL THERAPY; HUMAN
BREAST-CANCER; PYRUVATE-DEHYDROGENASE; ANTIMITOCHONDRIAL ANTIBODIES;
MOLECULAR MIMICRY; EPITHELIAL-CELLS; RISK-FACTORS; CIRRHOSIS; MOUSE
AB Primary biliary cholangitis (PBC) is an autoimmune liver disease characterized by the production of diagnostic antimitochondrial antibodies (AMA) reactive to the pyruvate dehydrogenase complex. A human betaretrovirus (HBRV) resembling mouse mammary tumor virus has been characterized in patients with PBC. However, linking the viral infection with the disease is not a straight-forward process because PBC is a complex multifactorial disease influenced by genetic, hormonal, autoimmune, environmental, and other factors. Currently, PBC is assumed to have an autoimmune etiology, but the evidence is lacking to support this conjecture. In this review, we describe different approaches connecting HBRV with PBC. Initially, we used co-cultivation of HBRV with biliary epithelial cells to trigger the PBC-specific phenotype with cell surface expression of cryptic mitochondrial autoantigens linked with antimitochondrial antibody expression. Subsequently, we have derived layers of proof to support the role of betaretrovirus infection in mouse models of autoimmune biliary disease with spontaneous AMA production and in patients with PBC. Using Hill's criteria, we provide an overview of how betaretrovirus infection may trigger autoimmunity and propagate biliary disease. Ultimately, the demonstration that disease can be cured with antiviral therapy may sway the argument toward an infectious disease etiology in an analogous fashion that was used to link H. pylori with peptic ulcer disease.
C1 [Syed, Hussain; Mason, Andrew L.] Univ Alberta, Dept Med, Edmonton, AB T6G 2E1, Canada.
[Syed, Hussain; Penner, Tara; Mason, Andrew L.] Univ Alberta, Ctr Excellence Gastrointestinal Inflammat & Immun, Edmonton, AB T6G 2E1, Canada.
[Syed, Hussain; Mason, Andrew L.] Univ Alberta, Li Ka Shing Inst Virol, Edmonton, AB T6G 2E1, Canada.
C3 University of Alberta; University of Alberta; University of Alberta
RP Mason, AL (corresponding author), Univ Alberta, Dept Med, Edmonton, AB T6G 2E1, Canada.; Mason, AL (corresponding author), Univ Alberta, Ctr Excellence Gastrointestinal Inflammat & Immun, Edmonton, AB T6G 2E1, Canada.; Mason, AL (corresponding author), Univ Alberta, Li Ka Shing Inst Virol, Edmonton, AB T6G 2E1, Canada.
EM andrew.mason@ualberta.ca
RI Mason, Andrew/D-2938-2013
OI Mason, Andrew/0000-0002-0470-9522
FU Canadian Institutes for Health Research [MOP 114998]
FX The study was supported by the Canadian Institutes for Health Research
(MOP 114998).
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TC 3
Z9 3
U1 2
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD SEP
PY 2022
VL 14
IS 9
AR 1941
DI 10.3390/v14091941
PG 25
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA 4R7MR
UT WOS:000856943700001
PM 36146750
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhang, HR
Jiang, ZZ
Zhang, LY
AF Zhang, Haoran
Jiang, Zhenzhou
Zhang, Luyong
TI Dual effect of T helper cell 17 (Th17) and regulatory T cell (Treg) in
liver pathological process: From occurrence to end stage of disease
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE Liver disease; CD4(+) T cell; Th17; Treg
ID HEPATOCELLULAR-CARCINOMA; TH17/TREG IMBALANCE; VIRUS-INFECTION;
HEPATITIS-A; PROGRESSION; EXPRESSION; INJURY; FIBROSIS; BALANCE;
INFLAMMATION
AB Liver disease is a complicated pathological status with acute or chronic progressions, causing a series of damages to liver and massive burden to public health and society. Th17 and Treg, two subsets of CD4(+) T helper cells, seem to keep a subtle balance in the maintenance of organic immune homeostasis including liver. The dysfunction of Th17/Treg balance in liver has been proved associated with hepatic injury and disease. Herein, we summarized the research advance of Th17 and Treg cells in different phenotypes of liver diseases in the past decade. It is known to all that hepatic diseases start from stimulations or infections like virus, autoimmune, alcohol and so on in the early stage, which would cause inflammation. With the disease consistently existed, severe outcomes like cirrhosis and hepatocellular carcinoma appear finally. In conclusion, it is found that Th17 and Treg cells serve as an important role in the immune response imbalance of liver diseases from the beginning to the end stage. However, the effect of these two subsets of CD4(+) T helper cells is not a stereotype. Pathological role which exacerbates the disease and protective character which inhibits damage to liver are co-existed in the effect of Th17 and Treg cells. Still, more studies should be carried out to enrich the understandings of liver disease and Th17/Treg immune balance in the future.
C1 [Zhang, Haoran; Jiang, Zhenzhou; Zhang, Luyong] China Pharmaceut Univ, Jiangsu Key Lab Drug Screening, 24 Tong Jia Xiang, Nanjing 210009, Jiangsu, Peoples R China.
[Zhang, Luyong] Guangdong Pharmaceut Univ, Sch Pharm, Ctr Drug Screening & Pharmacodynam Evaluat, Guangzhou 510006, Guangdong, Peoples R China.
[Jiang, Zhenzhou] China Pharmaceut Univ, Jiangsu Ctr Pharmacodynam Res & Evaluat, Nanjing 210009, Jiangsu, Peoples R China.
C3 China Pharmaceutical University; Guangdong Pharmaceutical University;
China Pharmaceutical University
RP Jiang, ZZ (corresponding author), China Pharmaceut Univ, Jiangsu Key Lab Drug Screening, 24 Tong Jia Xiang, Nanjing 210009, Jiangsu, Peoples R China.; Zhang, LY (corresponding author), Guangdong Pharmaceut Univ, Ctr Drug Screening & Pharmacodynam Evaluat, 280 Wai Huan Dong Rd, Guangzhou 510006, Guangdong, Peoples R China.
EM beaglejiang@cpu.edu.cn; lyzhang@cpu.edu.cn
FU National Natural Science Foundation of China [81773995, 81320108029,
81573690, 81573514, 81773827]; Natural Science Foundation of Jiangsu
Province [BK20151439]; National "Major Scientific and Technological
Special Project for Significant New Drugs" project
[2015ZX09501004-002-004]; Specific Fund for Public Interest Research of
Traditional Chinese Medicine, Ministry of Finance [201507004-002];
Priority Academic Program Development of Jiangsu Higher Education
Institutions (PAPD)
FX This study was supported by the National Natural Science Foundation of
China (81773995, 81320108029, 81573690, 81573514, 81773827), the Natural
Science Foundation of Jiangsu Province (BK20151439), the National "Major
Scientific and Technological Special Project for Significant New Drugs"
project (2015ZX09501004-002-004), Specific Fund for Public Interest
Research of Traditional Chinese Medicine, Ministry of Finance
(201507004-002), and the Priority Academic Program Development of
Jiangsu Higher Education Institutions (PAPD).
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Z9 39
U1 0
U2 24
PU ELSEVIER
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SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
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PY 2019
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BP 50
EP 59
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PG 10
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA HR4OG
UT WOS:000463125200006
PM 30669025
DA 2025-01-07
ER
PT J
AU King, B
Pezalla, E
Fung, S
Tran, H
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AF King, Brett
Pezalla, Edmund
Fung, Selwyn
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Takiya, Liza
Napatalung, Lynne
TI Overview of alopecia areata for managed care and payer stakeholders in
the United States
SO JOURNAL OF MANAGED CARE & SPECIALTY PHARMACY
LA English
DT Article
ID QUALITY-OF-LIFE; COMORBIDITY PROFILES; ADULTS; EPIDEMIOLOGY; PREVALENCE;
AUTOIMMUNE; GUIDELINES; BURDEN; ONSET; HAIR
AB Alopecia areata (AA) is an autoimmune disease with a complex pathophysiology resulting in nonscarring hair loss in genetically susceptible individuals. We aim to provide health care decision makers an overview of the pathophysiology of AA, its causes and diagnosis, disease burden, costs, comorbidities, and information on current and emerging treatment options to help inform payer benefit design and prior authorization decisions.
Literature searches for AA were conducted using PubMed between 2016 and 2022 inclusive, using search terms covering the causes and diagnosis of AA, pathophysiology, comorbidities, disease management, costs, and impact on quality of life (QoL).
AA is a polygenic autoimmune disease that significantly impacts QoL. Patients with AA face economic burden and an increased prevalence of psychiatric disease, as well as numerous systemic comorbidities. AA is predominantly treated using corticosteroids, systemic immunosuppressants, and topical immunotherapy. Currently, there are limited data to reliably inform effective treatment decisions, particularly for patients with extensive disease. However, several novel therapies that specifically target the immunopathology of AA have emerged, including Janus kinase (JAK) 1/2 inhibitors such as baricitinib and deuruxolitinib, and the JAK3/ tyrosine kinase expressed in hepatocellular carcinoma (TEC) family kinase inhibitor ritlecitinib. To support disease management, a disease severity classification tool, the Alopecia Areata Severity Scale, was recently developed that evaluates patients with AA holistically (extent of hair loss and other factors).
AA is an autoimmune disease often associated with comorbidities and poor QoL, which poses a significant economic burden for payers and patients. Better treatments are needed for patients, and JAK inhibitors, among other approaches, may address this tremendous unmet medical need.
C1 [King, Brett] Yale Univ, Dept Dermatol, Sch Med, New Haven, CT 06510 USA.
[Pezalla, Edmund] Enlightenment Bioconsult LLC, Daytona Beach, FL USA.
[Fung, Selwyn; Tran, Helen; Bourret, Jeffrey A.; Peeples-Lamirande, Kathleen; Takiya, Liza] Pfizer, Med Affairs, New York, NY USA.
[Napatalung, Lynne] Icahn Sch Med Mt Sinai, Dept Dermatol, New York, NY USA.
C3 Yale University; Pfizer; Icahn School of Medicine at Mount Sinai
RP King, B (corresponding author), Yale Univ, Dept Dermatol, Sch Med, New Haven, CT 06510 USA.
EM brett.king@yale.edu
OI Tran, Helen/0009-0007-6053-6703
FU Pfizer
FX & nbsp;Medical writing support for the article was provided by Katy
Beck, PhD, and David Sunter, PhD, of Engage Scientific Solutions and
Nicola Gillespie, DVM, of Health Interactions and was funded by Pfizer.
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NR 72
TC 2
Z9 2
U1 1
U2 4
PU ACAD MANAGED CARE PHARMACY
PI ALEXANDRIA
PA 100 N PITT ST, 400, ALEXANDRIA, VA 22314-3134 USA
SN 2376-0540
EI 2376-1032
J9 J MANAG CARE SPEC PH
JI J. Manag. Care Spec. Pharm.
PD JUL
PY 2023
VL 29
IS 7
BP 848
EP 856
PG 9
WC Health Care Sciences & Services; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; Pharmacology & Pharmacy
GA O0HC5
UT WOS:001040707800015
PM 37219075
OA Green Published
DA 2025-01-07
ER
PT J
AU Mieli-Vergani, G
Vergani, D
Czaja, AJ
Manns, MP
Krawitt, EL
Vierling, JM
Lohse, AW
Montano-Loza, AJ
AF Mieli-Vergani, Giorgina
Vergani, Diego
Czaja, Albert J.
Manns, Michael P.
Krawitt, Edward L.
Vierling, John M.
Lohse, Ansgar W.
Montano-Loza, Aldo J.
TI Autoimmune hepatitis
SO NATURE REVIEWS DISEASE PRIMERS
LA English
DT Article
ID REGULATORY T-CELLS; QUALITY-OF-LIFE; CHRONIC ACTIVE HEPATITIS; PRIMARY
SCLEROSING CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE; MICROSOME ANTIBODY
TYPE-1; FATTY LIVER-DISEASE; TERM-FOLLOW-UP; HEPATOCELLULAR-CARCINOMA;
WILSONS-DISEASE
AB Autoimmune hepatitis (AIH) is a severe liver disease that affects children and adults worldwide. The diagnosis of AIH relies on increased serum transaminase and immunoglobulin G levels, presence of autoantibodies and interface hepatitis on liver histology. AIH arises in genetically predisposed individuals when a trigger, such as exposure to a virus, leads to a T cell-mediated autoimmune response directed against liver autoantigens; this immune response is permitted by inadequate regulatory immune control leading to a loss of tolerance. AIH responds favourably to immunosuppressive treatment, which should be started as soon as the diagnosis is made. Standard regimens include fairly high initial doses of corticosteroids (prednisone or prednisolone), which are tapered gradually as azathioprine is introduced. For those patients who do not respond to standard treatment, second-line drugs should be considered, including mycophenolate mofetil, calcineurin inhibitors, mechanistic target of rapamycin (mTOR) inhibitors and biologic agents, which should be administered only in specialized hepatology centres. Liver transplantation is a life-saving option for those who progress to end-stage liver disease, although AIH can recur or develop de novo after transplantation. In-depth investigation of immune pathways and analysis of changes to the intestinal microbiota should advance our knowledge of the pathogenesis of AIH and lead to novel, tailored and better tolerated therapies.
C1 [Mieli-Vergani, Giorgina] Kings Coll Hosp London, Paediat Liver GI & Nutr Ctr, MowatLabs, Denmark Hill, London SE5 9RS, England.
[Vergani, Diego] Kings Coll Hosp London, Inst Liver Studies, MowatLabs, Denmark Hill, London SE5 9RS, England.
[Czaja, Albert J.] Mayo Clin, Div Gastroenterol & Hepatol, Coll Med, Rochester, MN USA.
[Manns, Michael P.] Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Hannover, Germany.
[Manns, Michael P.] Helmholtz Ctr Infect Res HZI, Braunschweig, Germany.
[Krawitt, Edward L.] Univ Vermont, Dept Med, Burlington, VT USA.
[Krawitt, Edward L.] Dartmouth Coll, Dept Med, Geisel Sch Med, Hanover, NH 03755 USA.
[Vierling, John M.] Baylor Coll Med, Dept Med, Div Abdominal Transplantat, Houston, TX 77030 USA.
[Vierling, John M.] Baylor Coll Med, Dept Surg, Div Abdominal Transplantat, Houston, TX 77030 USA.
[Vierling, John M.] Baylor Coll Med, Dept Med, Sect Gastroenterol & Hepatol, Houston, TX 77030 USA.
[Vierling, John M.] Baylor Coll Med, Dept Surg, Sect Gastroenterol & Hepatol, Houston, TX 77030 USA.
[Lohse, Ansgar W.] Univ Med Ctr Hamburg Eppendorf, Dept Med, Hamburg, Germany.
[Montano-Loza, Aldo J.] Univ Alberta, Div Gastroenterol, Edmonton, AB, Canada.
[Montano-Loza, Aldo J.] Univ Alberta, Liver Unit, Edmonton, AB, Canada.
C3 King's College Hospital NHS Foundation Trust; King's College Hospital;
King's College Hospital NHS Foundation Trust; King's College Hospital;
Mayo Clinic; Hannover Medical School; Helmholtz Association;
Helmholtz-Center for Infection Research; University of Vermont;
Dartmouth College; Baylor College of Medicine; Baylor College of
Medicine; Baylor College of Medicine; Baylor College of Medicine;
University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Alberta; University of Alberta
RP Mieli-Vergani, G (corresponding author), Kings Coll Hosp London, Paediat Liver GI & Nutr Ctr, MowatLabs, Denmark Hill, London SE5 9RS, England.; Vergani, D (corresponding author), Kings Coll Hosp London, Inst Liver Studies, MowatLabs, Denmark Hill, London SE5 9RS, England.
EM giorgina.vergani@kcl.ac.uk; diego.vergani@kcl.ac.uk
RI Manns, Michael/AFG-3063-2022; Montano-Loza, Aldo/B-3092-2013; Vergani,
Diego/H-7610-2019; Mieli-Vergani, Giorgina/G-5616-2011
OI Montano-Loza, Aldo J./0000-0002-2511-7980; Mieli-Vergani,
Giorgina/0000-0002-8215-4489
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NR 235
TC 288
Z9 300
U1 5
U2 108
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2056-676X
J9 NAT REV DIS PRIMERS
JI Nat. Rev. Dis. Primers
PD APR 12
PY 2018
VL 4
AR 18017
DI 10.1038/nrdp.2018.17
PG 21
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA GC9VX
UT WOS:000430148000001
PM 29644995
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Badshah, A
Atif, D
AF Badshah, Aliena
Atif, Durkho
TI Potential Candidacy for Liver Transplantation among Chronic Liver
Disease Patients Presenting to Khyber Teaching Hospital, Peshawar
SO JOURNAL OF THE LIAQUAT UNIVERSITY OF MEDICAL AND HEALTH SCIENCES
LA English
DT Article
DE liver transplant; chronic liver disease; MELD-Na score.
ID SCORE
AB OBJECTIVE: To determine the frequency of potential candidates for liver transplantation among decompensated chronic liver parenchymal disease patients.
METHODOLOGY: This cross-sectional descriptive study was conducted in the Department of Medicine at Khyber Teaching Hospital, Peshawar, from September 2021 to February 2022. The study included 200 patients with decompensated chronic liver parenchymal disease. Their eligibility for liver transplantation was determined by calculating the MELD-Na score for each of them. Eligibility for liver transplant was correlated with a higher MELD-Na score (> 25). Data were collected and entered in SPSS 25.
RESULTS: 168 of the 200 patients comprised those with viral hepatitis B or C (84%); 73.21% of these were hepatitis C positive, and 26.8% were hepatitis B positive; this was followed by patients with hepatocellular carcinoma (8%). 62.5% (5% of the total sample size) were HBV positive, and 37.5% (3% of the entire sample size) were HCV positive; however, HCC secondary to viral hepatitis was taken as an independent indication for a liver transplant. 4% of the patients had autoimmune hepatitis, 2% had NAFLD, and 2% were attributed to other causes. Of the 200 patients, 5% had MELD-Na score <= 9; 19% had MELD-Na score 10-19; 36% had MELD-Na score 20-29; 39% had MELD-Na score 30-39; 1% had MELD-Na score >= 40.
CONCLUSION: Many patients with DCLPD are potential candidates for liver transplantation. Hence, measures are needed to establish a liver transplant centre in Khyber Pakhtunkhwa.
C1 [Badshah, Aliena; Atif, Durkho] Khyber Teaching Hosp, Peshawar, Kpk, Pakistan.
RP Badshah, A (corresponding author), Khyber Teaching Hosp, Peshawar, Kpk, Pakistan.
EM alienabadshah@yahoo.com
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NR 16
TC 0
Z9 0
U1 0
U2 0
PU LIAQUAT UNIV MEDICAL & HEALTH SCIENCES - LUMHS
PI JAMSHORO
PA LIAQUAT UNIV MEDICAL & HEALTH SCIENCES, JAMSHORO, 00000, PAKISTAN
SN 1729-0341
J9 J LIAQUAT UNIV MED H
JI J. Liaquat Univ. Med. Health Sci.
PD OCT-DEC
PY 2023
VL 22
IS 4
BP 256
EP 259
DI 10.22442/jlumhs.2023.01007
PG 4
WC Health Care Sciences & Services
WE Emerging Sources Citation Index (ESCI)
SC Health Care Sciences & Services
GA IO8J4
UT WOS:001167359900007
OA gold
DA 2025-01-07
ER
PT J
AU Carbone, M
Neuberger, JM
AF Carbone, Marco
Neuberger, James M.
TI Autoimmune liver disease, autoimmunity and liver transplantation
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Autoimmunity; Primary biliary cirrhosis; Primary sclerosing cholangitis;
Autoimmune hepatitis; Genome-wide association studies; Recurrence;
Rejection; De novo autoimmune hepatitis
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY-CIRRHOSIS; GENOME-WIDE
ASSOCIATION; INFLAMMATORY-BOWEL-DISEASE; NOVO IMMUNE HEPATITIS; KILLER
T-CELLS; RISK-FACTORS; URSODEOXYCHOLIC ACID; HEPATOCELLULAR-CARCINOMA;
SUSCEPTIBILITY LOCI
AB Primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and autoimmune hepatitis (AIH) represent the three major autoimmune liver diseases (AILD). PBC, PSC, and AIH are all complex disorders in that they result from the effects of multiple genes in combination with as yet unidentified environmental factors. Recent genome-wide association studies have identified numerous risk loci for PBC and PSC that host genes involved in innate or acquired immune responses. These loci may provide a clue as to the immune-based pathogenesis of AILD. Moreover, many significant risk loci for PBC and PSC are also risk loci for other autoimmune disorders, such type I diabetes, multiple sclerosis and rheumatoid arthritis, suggesting a shared genetic basis and possibly similar molecular pathways for diverse autoimmune conditions. There is no curative treatment for all three disorders, and a significant number of patients eventually progress to end-stage liver disease requiring liver transplantation (LT). LT in this context has a favourable overall outcome with current patient and graft survival exceeding 80% at 5 years. Indications are as for other chronic liver disease although recent data suggest that while lethargy improves after transplantation, the effect is modest and variable so lethargy alone is not an indication. In contrast, pruritus rapidly responds. Cholangiocarcinoma, except under rigorous selection criteria, excludes LT because of the high risk of recurrence. All three conditions may recur after transplantation and are associated with a greater risk of both acute cellular and chronic ductopenic rejection. It is possible that a crosstalk between alloimmune and autoimmune response perpetuate each other. An immunological response toward self- or alloantigens is well recognised after LT in patients transplanted for non-autoimmune indications and sometimes termed "de novo autoimmune hepatitis". Whether this is part of the spectrum of rejection or an autoimmune process is not clear.
In this manuscript, we review novel findings about disease processes and mechanisms that lead to autoimmunity in the liver and their possible involvement in the immune response vs. the graft after LT. (C) 2013 European Association for the Study of the Liver. Published by Elsevier B. V. All rights reserved.
C1 [Carbone, Marco] Addenbrookes Hosp, Dept Med, Div Gastroenterol & Hepatol, Cambridge CB2 2QQ, England.
[Neuberger, James M.] Queen Elizabeth Hosp, Liver Unit, Birmingham B15 2TH, W Midlands, England.
[Carbone, Marco; Neuberger, James M.] NHSBT, Bristol, Avon, England.
C3 University of Cambridge; Cambridge University Hospitals NHS Foundation
Trust; Addenbrooke's Hospital; University of Birmingham
RP Neuberger, JM (corresponding author), NHSBT, Bristol, Avon, England.
EM James.Neuberger@nhsbt.nhs.uk
RI Neuberger, James/ABG-3010-2020
OI CARBONE, MARCO/0000-0003-1445-0443
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NR 159
TC 151
Z9 168
U1 0
U2 30
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD JAN
PY 2014
VL 60
IS 1
BP 210
EP 223
DI 10.1016/j.jhep.2013.09.020
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 276GI
UT WOS:000328736400031
PM 24084655
OA hybrid
DA 2025-01-07
ER
PT J
AU Saggau, C
Bacher, P
Esser, D
Rasa, M
Meise, S
Mohr, N
Kohlstedt, N
Hutloff, A
Schacht, SS
Dargvainiene, J
Martini, GR
Stürner, KH
Schröder, I
Markewitz, R
Hartl, J
Hastermann, M
Duchow, A
Schindler, P
Becker, M
Bautista, C
Gottfreund, J
Walter, J
Polansky, JK
Yang, MX
Naghavian, R
Wendorff, M
Schuster, EM
Dahl, A
Petzold, A
Reinhardt, S
Franke, A
Wieczorek, M
Henschel, L
Berger, D
Heine, G
Holtsche, M
Häussler, V
Peters, C
Schmidt, E
Fillatreau, S
Busch, DH
Wandinger, KP
Schober, K
Martin, R
Paul, F
Leypoldt, F
Scheffold, A
AF Saggau, Carina
Bacher, Petra
Esser, Daniela
Rasa, Mahdi
Meise, Silja
Mohr, Nicola
Kohlstedt, Nora
Hutloff, Andreas
Schacht, Sarah-Sophie
Dargvainiene, Justina
Martini, Gabriela Rios
Stuerner, Klarissa H.
Schroeder, Ina
Markewitz, Robert
Hartl, Johannes
Hastermann, Maria
Duchow, Ankelien
Schindler, Patrick
Becker, Mareike
Bautista, Carolin
Gottfreund, Judith
Walter, Joem
Polansky, Julia K.
Yang, Mingxing
Naghavian, Reza
Wendorff, Mareike
Schuster, Ev-Marie
Dahl, Andras
Petzold, Andreas
Reinhardt, Susanne
Franke, Andre
Wieczorek, Marek
Henschel, Lea
Berger, Daniel
Heine, Guido
Holtsche, Maike
Haeussler, Vivien
Peters, Christian
Schmidt, Enno
Fillatreau, Simon
Busch, Dirk H.
Wandinger, Klaus-Peter
Schober, Kilian
Martin, Roland
Paul, Friedemann
Leypoldt, Frank
Scheffold, Alexander
TI Autoantigen-specific CD4+T cells acquire an exhausted phenotype and
persist in human antigen-specific autoimmune diseases
SO IMMUNITY
LA English
DT Article
ID OPTICA SPECTRUM DISORDER; CONVENTIONAL T-CELLS; NEUROMYELITIS-OPTICA;
HIGH-RESOLUTION; METHYLATION; EXPRESSION; TOLERANCE; EFFICACY; MEMORY;
SAFETY
AB Pro-inflammatory autoantigen-specific CD4+ T helper (auto-Th) cells are central orchestrators of autoimmune diseases (AIDs). We aimed to characterize these cells in human AIDs with defined autoantigens by combining human leukocyte antigen (HLA)-tetramer-based and activation-based multidimensional ex vivo analyses. In aquaporin4-antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD) patients, auto-Th cells expressed CD154, but proliferative capacity and pro-inflammatory cytokines were strongly reduced. Instead, exhaustion-associated co-inhibitory receptors were expressed together with FOXP3, the canonical regulatory T cell (Treg) transcription factor. Auto-Th cells responded in vitro to checkpoint inhibition and provided potent B cell help. Cells with the same exhaustion-like (ThEx) phenotype were identified in soluble liver antigen (SLA)-antibody-autoimmune hepatitis and BP180-antibody-positive bullous pemphigoid, AIDs of the liver and skin, respectively. While originally described in cancer and chronic infection, our data point to T cell exhaustion as a common mechanism of adaptation to chronic (self-)stimulation across AID types and link exhausted CD4+ T cells to humoral autoimmune responses, with implications for therapeutic targeting.
C1 [Bacher, Petra; Hutloff, Andreas; Martini, Gabriela Rios; Peters, Christian; Scheffold, Alexander] Christian Albrechts Univ Kiel, Inst Immunol, Kiel, Germany.
[Bacher, Petra; Hutloff, Andreas; Martini, Gabriela Rios; Peters, Christian; Wandinger, Klaus-Peter; Scheffold, Alexander] Univ Hosp Schleswig Holstein UKSH, Kiel, Germany.
[Esser, Daniela; Dargvainiene, Justina; Stuerner, Klarissa H.; Schroeder, Ina; Franke, Andre; Leypoldt, Frank] Christian Albrechts Univ Kiel, Inst Clin Mol Biol, Kiel, Germany.
[Rasa, Mahdi; Leypoldt, Frank] Univ Hosp Schleswig Holstein, Inst Clin Chem, Kiel, Germany.
[Stuerner, Klarissa H.; Wendorff, Mareike] Fritz Lipmann Inst FLI, Leibniz Inst Aging, Jena, Germany.
[Hartl, Johannes; Leypoldt, Frank] Univ Hosp Schleswig Holstein, Dept Neurol, Kiel, Germany.
[Hastermann, Maria; Duchow, Ankelien; Schindler, Patrick] Univ Med Ctr Hamburg Eppendorf, Dept Med, D-20246 Hamburg, Germany.
[Becker, Mareike; Paul, Friedemann] Max Delbrueck Ctr Mol Med, Expt & Clin Res Ctr, Berlin, Germany.
[Becker, Mareike] Charite Univ Med Berlin, Berlin, Germany.
[Becker, Mareike] Inst Expt Dermatol, Lubeck, Germany.
[Bautista, Carolin] Catholic Childrens Hosp Wilhelmstift, Dept Pediat Dermatol, Hamburg, Germany.
[Gottfreund, Judith; Walter, Joem] Univ Hosp Schleswig Holstein, Dept Dermatol Allergy & Venerol, Campus Lubeck, Lubeck, Germany.
[Polansky, Julia K.; Yang, Mingxing] BIH Charite Univ Med Berlin, Berlin Inst Hlth BIH, Berlin Inst Hlth, Augustenburger Pl 1, D-13353 Berlin, Germany.
[Naghavian, Reza] Leibniz Inst DRFZ, German Rheumatism Res Ctr, Charite Pl 1, D-10117 Berlin, Germany.
[Naghavian, Reza; Martin, Roland] Univ Zurich, Univ Hosp Zurich, Neurol Clin, Neuroimmunol & MS Res Sect NIMS, Zurich, Switzerland.
[Naghavian, Reza; Wendorff, Mareike; Martin, Roland] Cellerys AG, Wagistr 21, CH-8952 Schlieren, Switzerland.
[Wendorff, Mareike; Schuster, Ev-Marie] Leibniz Inst Sci & Math Educ, Kiel, Germany.
[Schuster, Ev-Marie; Petzold, Andreas; Reinhardt, Susanne; Schober, Kilian] Univ Klinikum Erlangen, Mikrobiol Inst Klin Mikrobiol Immunol & Hyg, Wasserturmstr 3-5, D-91054 Erlangen, Germany.
[Schuster, Ev-Marie; Dahl, Andras; Petzold, Andreas; Reinhardt, Susanne] Friedrich Alexander Univ FAU Erlangen Nurnberg, Wasserturmstr 3-5, D-91054 Erlangen, Germany.
[Dahl, Andras; Wieczorek, Marek; Henschel, Lea; Berger, Daniel] Tech Univ Dresden, DRESDEN Concept Genome Ctr, Technol Platform Ctr Mol & Cellular Bioengn CMCB, Dresden, Germany.
[Esser, Daniela; Wieczorek, Marek; Henschel, Lea; Heine, Guido] Miltenyi Botec BV & Co KG, Friedrich Ebert Str 68, D-51429 Bergisch Gladbach, Germany.
[Heine, Guido; Holtsche, Maike; Schmidt, Enno] Univ Hosp Schleswig Holstein, Dept Dermatol & Allergy, Kiel, Germany.
[Holtsche, Maike; Schmidt, Enno] Univ Lubeck, Univ Hosp Schleswig Holstein, Inst Expt Dermatol, Dept Dermatol, Lubeck, Germany.
[Haeussler, Vivien] Univ Med Ctr Hamburg Eppendorf, Clin & Polyclin Neurol, D-20246 Hamburg, Germany.
[Fillatreau, Simon] Univ Paris Cite CNRS, Inst Necker Enfants Malad INEM, INSERM, F-75015 Paris, France.
[Fillatreau, Simon] Univ Paris Cite, Fac Med, Paris, France.
[Fillatreau, Simon] Hosp Necker Enfants Malad, AP HP, Paris, France.
[Busch, Dirk H.] Tech Univ Munich, Inst Med Microbiol Immunol & Hyg, Munich, Germany.
[Schober, Kilian] Friedrich Alexander Univ FAU Erlangen Nurnberg, Med Immunol, Campus Erlangen,Schlosspl 1, D-91054 Erlangen, Germany.
[Martin, Roland] Univ Zurich, Inst Expt Immunol, Wintherturerstr 190, CH-8057 Zurich, Switzerland.
[Martin, Roland] Karolinska Inst, Karolinska Univ Hosp, Ctr Mol Med, Dept Clin Neurosci, Stockholm, Sweden.
C3 University of Kiel; University of Kiel; Schleswig Holstein University
Hospital; University of Kiel; University of Kiel; Schleswig Holstein
University Hospital; Leibniz Association; Leibniz Institut fur
Alternsforschung - Fritz-Lipmann-Institut (FLI); University of Kiel;
Schleswig Holstein University Hospital; University of Hamburg;
University Medical Center Hamburg-Eppendorf; Helmholtz Association; Max
Delbruck Center for Molecular Medicine; Berlin Institute of Health; Free
University of Berlin; Humboldt University of Berlin; Charite
Universitatsmedizin Berlin; University of Kiel; Schleswig Holstein
University Hospital; Berlin Institute of Health; Leibniz Association;
Deutsches Rheuma-Forschungszentrum (DRFZ); University of Zurich;
University Zurich Hospital; Leibniz Association; Leibniz Institut fur
die Padagogik der Naturwissenschaften und Mathematik an der Universitat
Kiel (IPN); University of Erlangen Nuremberg; University of Erlangen
Nuremberg; Technische Universitat Dresden; University of Kiel; Schleswig
Holstein University Hospital; University of Kiel; Schleswig Holstein
University Hospital; University of Lubeck; University of Hamburg;
University Medical Center Hamburg-Eppendorf; Institut National de la
Sante et de la Recherche Medicale (Inserm); Universite Paris Cite;
Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
Universite Paris Cite; Hopital Universitaire Necker-Enfants Malades -
APHP; Technical University of Munich; University of Erlangen Nuremberg;
University of Zurich; Karolinska Institutet; Karolinska University
Hospital
RP Scheffold, A (corresponding author), Christian Albrechts Univ Kiel, Inst Immunol, Kiel, Germany.; Scheffold, A (corresponding author), Univ Hosp Schleswig Holstein UKSH, Kiel, Germany.
EM alexander.scheffold@uksh.de
RI Paul, Friedemann/ABF-9415-2020; Naghavian, Reza/JBS-0869-2023; Yang,
Mingxing/JJE-8560-2023; Esser, Daniela/ABB-9383-2020; Heine,
Guido/G-1656-2018; Leypoldt, Frank/ABC-3186-2021; Bacher,
Petra/AAF-1565-2021; Hutloff, Andreas/D-1781-2014; Scheffold,
Alexander/S-2090-2016
OI Rasa, Seyed Mohammad Mahdi/0000-0001-6850-8909; Hutloff,
Andreas/0000-0002-0572-8151; Schindler, Patrick/0000-0002-8846-121X;
Schuster, Ev-Marie/0000-0002-2469-9501; Scheffold,
Alexander/0000-0002-0626-343X; Yang, Mingxing/0009-0004-9582-0294;
Schacht, Sarah-Sophie/0000-0003-2512-1741
FU German Federal Ministry of Education and Science (BMBF); European Joint
Program for Rare Diseases [01GM1923A]; BMBF [01KI2013, 01EO2106,
CONNECT-GENERATE 01GM1908A, 01GM22088]; Deutsche Forschungsgemeinschaft
(DFG) under Germany's Excellence Strategy [2167-390884018]; DFG [SCHE
670 3-1, 433038070, TRR241, 375876048, TRR355, 490846870, CRC1526,
454193335, HU 1294/8-1, HA 8440/3-1, SFB1309, CRC1309, 325871075];
European Union [LE3064/2-1]; ERC [803992]; Clinical Research Priority
Program MS (CRPPMS) of the University of Zurich (UZH); Suisse SNF
[32ER30_187509]; Swiss National Science Foundation (SNF) [32ER30_187509]
Funding Source: Swiss National Science Foundation (SNF); European
Research Council (ERC) [803992] Funding Source: European Research
Council (ERC)
FX This research was supported by the German Federal Ministry of Education
and Science (BMBF) and the European Joint Program for Rare Diseases
(EJPRD) grant AspecT-NMO (01GM1923A) (to A.S., S.F., R.M., and M.W.) ;
BMBF projects 01KI2013 and 01EO2106 (to E.S., K.S., and J.H.) ;
CONNECT-GENERATE 01GM1908A and 01GM22088 (to F.L.) ; the Deutsche
Forschungsgemeinschaft (DFG) under Germany's Excellence Strategy-EXC
2167-390884018 (to A.S., P.B., and A.F.) ; DFG grant SCHE 670 3-1
project no. 433038070, TRR241 project ID 375876048, and TRR355 project
no. 490846870 (to A.S. and P.B.) ; CRC1526 (SFB1526/01, project no.
454193335) (to A.S., E.S., M.H., and M.B.) ; HU 1294/8-1 (to A.H.) ; HA
8440/3-1 (to J.H.) ; SFB1309 (DFG program CRC1309, ID: 325871075) (to
J.W.) ; the European Union via E-Rare Joint Transnational research
support (ERA-Net, UltraAIE, LE3064/2-1 to F.L.) ; HORIZON MSCA 2022
Doctoral Network 101119457-IgG4-TREAT (to F.L.) ; the ERC starting grant
EpiTune (803992) (to J.K.P.) ; the Clinical Research Priority Program MS
(CRPPMS) of the University of Zurich (UZH) and the Suisse SNF grant
32ER30_187509 (to R.M.) ; and the Stiftung Pathobiochemie of the German
Society for Laboratory Medicine (to F.L.) . We thank Anne Schulze for
expert technical assistance. We thank Beate Schmitt and Christina
LoPorto for sequencing assistance, Abdulrahman Salhab for bio-informatic
assistance, and Lucia Bernhardt for establishment of the hairpin
construct. We thank Johannes Herkel for his valuable scientific advice.
The graphical abstract was created with BioRender.com .
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NR 97
TC 5
Z9 5
U1 5
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 1074-7613
EI 1097-4180
J9 IMMUNITY
JI Immunity
PD OCT 8
PY 2024
VL 57
IS 10
DI 10.1016/j.immuni.2024.08.005
EA OCT 2024
PG 26
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA L4D4T
UT WOS:001350240600001
PM 39226901
DA 2025-01-07
ER
PT J
AU Jiang, XX
Huang, JF
Huo, Z
Zhang, QQ
Jiang, Y
Wu, XP
Li, YW
Jiang, GM
Zeng, LP
Yan, XX
Yu, P
Cao, RX
AF Jiang, Xiaoxin
Huang, Ju-Fang
Huo, Zhi
Zhang, Qiuqui
Jiang, Yan
Wu, Xiaoping
Li, Yanwen
Jiang, Guanmin
Zeng, Leping
Yan, Xiao-Xin
Yu, Ping
Cao, Renxian
TI Elevation of soluble major histocompatibility complex class I related
chain A protein in malignant and infectious diseases in Chinese patients
SO BMC IMMUNOLOGY
LA English
DT Article
DE MHC; sMICA/B; NKG2D; Cancer diagnosis; Serum
ID CHLAMYDIA-TRACHOMATIS INFECTION; MICA GENE POLYMORPHISMS; SQUAMOUS-CELL
CARCINOMA; SERUM-LEVELS CORRELATE; NKG2D LIGANDS; MULTIPLE-MYELOMA;
DOWN-REGULATION; T-CELLS; HEPATOCELLULAR-CARCINOMA; ULCERATIVE-COLITIS
AB Background: Elevation of soluble major histocompatibility complex class I chain-related gene A (sMICA) products in serum has been linked to tissue/organ transplantation, autoimmune diseases and some malignant disorders. Cells infected by microbiological pathogens may release sMICA, whereas less is known whether and to what extent serum sMICA levels may change in infectious diseases.
Methods: The present study determined serum sMICA levels by enzyme-linked immunosorbent assay (ELISA) in a southern China population, including patients (n = 1041) suffering from several types of malignant and infectious diseases and healthy controls (n = 141).
Results: Relative to controls, serum sMICA elevation was significant in patients of hepatic cancer, and was approaching statistical significance in patients with lung, gastric and nasopharyngeal cancers. sMICA elevation was also associated with some bacterial (Enterobacteriaceae, Mycobacterium tuberculosis, non-fermenting Gram-negative bacteria and Gram-positive cocci), viral (hepatitis B and C) and the Microspironema pallidum infections.
Conclusion: Serum sMICA levels may be informative for the diagnosis of some malignant and infectious diseases. The results also indicate that microbiological infections should be considered as a potential confounding clinical condition causing serum sMICA elevation while using this test to evaluate the status of other disorders, such as cancers, host-graft response and autoimmune diseases.
C1 [Jiang, Xiaoxin; Huo, Zhi; Zhang, Qiuqui; Jiang, Yan; Wu, Xiaoping; Li, Yanwen; Jiang, Guanmin; Cao, Renxian] Nanhua Univ, Affiliated Hosp 1, Hengyang 421001, Peoples R China.
[Jiang, Xiaoxin; Yu, Ping] Cent S Univ, Xiangya Sch Med, Dept Immunol, Changsha 410078, Hunan, Peoples R China.
[Jiang, Xiaoxin; Huang, Ju-Fang; Zeng, Leping; Yan, Xiao-Xin] Cent S Univ, Xiangya Sch Med, Dept Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China.
C3 University of South China; Central South University; Central South
University
RP Yan, XX (corresponding author), Cent S Univ, Xiangya Sch Med, Dept Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China.
EM yanxiaoxin@csu.edu.cn; caorenxian@hotmail.com
RI Jufang, Huang/AAW-1847-2020; Yu, Ping/B-1205-2008; JIANG,
xx/KHV-3752-2024
FU National Natural Science Foundation of China [81172542, 30870135];
Central South University
FX The authors appreciate the patients for their blood donation, the stuff
of the in- and out-patient laboratory units of the First Affiliated
Hospital of Nanhua University for sample collection. We thank Dr. Zou
Yizhou for kindly providing the anti-MICA 6B3 antibody and the
recombinant human MICA*008 protein, and Ye Cao for secretary assistance.
This work was supported in part by the National Natural Science
Foundation of China (general programs #81172542 and #30870135) and a
postdoctoral fund from Central South University.
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TC 11
Z9 13
U1 0
U2 14
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2172
J9 BMC IMMUNOL
JI BMC Immunol.
PD NOV 26
PY 2012
VL 13
AR 62
DI 10.1186/1471-2172-13-62
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 078HX
UT WOS:000314090500001
PM 23181907
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhang, Z
Schluesener, HJ
AF Zhang, Zhiren
Schluesener, Hermann J.
TI FTY720: A most promising immunosuppressant modulating immune cell
functions
SO MINI-REVIEWS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE FTY720; lymphocytes; monocytes; dendritic cells; endothelial cells;
transplantation; autoimmune diseases; tumors
ID SPHINGOSINE 1-PHOSPHATE RECEPTORS; CIRCULATING MATURE LYMPHOCYTES;
INDEPENDENT PROSTATE-CANCER; PROTEIN-COUPLED RECEPTORS; IN-VIVO;
TUMOR-GROWTH; SPHINGOSINE-1-PHOSPHATE RECEPTORS;
HEPATOCELLULAR-CARCINOMA; AKT DEPHOSPHORYLATION; BIOLOGICAL EVALUATION
AB FTY720, the pharmacological analog of S I P, acts as an agonist of sphingosine-1-phosphate receptors, resulting in the inhibition of lymphocyte egress from secondary lymphoid tissues and thymocytes from the thymus, peripheral lymphopenia and interfering with normal functions of several other cell types. FTY720 has been clinically tried for transplantation and multiple sclerosis, showing promising protective effects. This review will summarize potential applications and effects of FTY720.
C1 Univ Tubingen, Inst Brain Res, D-72076 Tubingen, Germany.
C3 Eberhard Karls University of Tubingen
RP Zhang, Z (corresponding author), Univ Tubingen, Inst Brain Res, Calwer Str 3, D-72076 Tubingen, Germany.
EM zhangzhiren@yahoo.com
RI Zhang, Zhiren/O-1012-2019; Zhang, Zhiren/I-1046-2014
OI Zhang, Zhiren/0000-0002-5238-2835
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NR 75
TC 26
Z9 37
U1 0
U2 3
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-5575
EI 1875-5607
J9 MINI-REV MED CHEM
JI Mini-Rev. Med. Chem.
PD AUG
PY 2007
VL 7
IS 8
BP 845
EP 850
PG 6
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 200CZ
UT WOS:000248742800008
PM 17692046
DA 2025-01-07
ER
PT J
AU Hartmann, P
Chu, HK
Duan, Y
Schnabl, B
AF Hartmann, Phillipp
Chu, Huikuan
Duan, Yi
Schnabl, Bernd
TI Gut microbiota in liver disease: too much is harmful, nothing at all is
not helpful either
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Review
DE antibiotics; germ-free; humanized rodents; liver disease; microbiota
ID PRIMARY SCLEROSING CHOLANGITIS; GERM-FREE STATUS; INTESTINAL MICROBIOTA;
INSULIN-RESISTANCE; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
CELLULAR SENESCENCE; RECEPTOR-ALPHA; POTENTIAL ROLE; MOUSE MODEL
AB The intestinal microbiome plays a major role in the pathogenesis of liver disease, with a hallmark event being dysbiosis, or an imbalance of pathobionts and beneficial bacteria with the associated deleterious effects on their host. Reducing the number of intestinal bacteria with antibiotic treatment is generally advantageous in experimental liver diseases. Complete absence of intestinal microbiota as in germ-free rodents can be protective in autoimmune hepatitis and hepatic tumors induced by chemicals, or it can exacerbate disease as in acute toxic liver injury and liver fibrosis/cirrhosis. In alcoholic liver disease, nonalcoholic fatty liver disease, and autoimmune cholangiopathies, germ-free status can be associated with worsened or improved hepatic phenotype depending on the experimental model and type of rodent. Some of the unexpected outcomes can be explained by the limitations of rodents raised in a germ-free environment including a deficient immune system and an altered metabolism of lipids, cholesterol, xenobiotics/toxins, and bile acids. Given these limitations and to advance understanding of the interactions between host and intestinal microbiota, simplified model systems such as humanized gnotobiotic mice, or gnotobiotic mice monoassociated with a single bacterial strain or colonized with a defined set of microbes, are unique and useful models for investigation of liver disease in a complex ecosystem.
C1 [Hartmann, Phillipp] Univ Calif San Diego, Dept Pediat, La Jolla, CA 92093 USA.
[Chu, Huikuan] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Div Gastroenterol, Wuhan, Hubei, Peoples R China.
[Chu, Huikuan; Duan, Yi; Schnabl, Bernd] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Duan, Yi; Schnabl, Bernd] Vet Affairs San Diego Healthcare Syst, Dept Med, San Diego, CA USA.
C3 University of California System; University of California San Diego;
Huazhong University of Science & Technology; University of California
System; University of California San Diego; US Department of Veterans
Affairs; Veterans Health Administration (VHA); VA San Diego Healthcare
System
RP Schnabl, B (corresponding author), Univ Calif San Diego, Dept Med, Biomed Res Facil 2, Rm 4A22,9500 Gilman Dr,MC0063, La Jolla, CA 92093 USA.
EM beschnabl@ucsd.edu
RI Schnabl, Bernd/HCH-3471-2022
OI Duan, Yi/0000-0002-6229-9461
FU National Institutes of Health [R01-AA-020703, R01-AA-24726,
U01-AA-021856, U01-AA-026939, I01BX002213]; Biomedical Laboratory
Research & Development Service of the Veterans Affairs Office of
Research Development
FX This study was supported in part by National Institutes of Health Grants
R01-AA-020703, R01-AA-24726, U01-AA-021856, and U01-AA-026939 and by
Award I01BX002213 from the Biomedical Laboratory Research & Development
Service of the Veterans Affairs Office of Research & Development (to B.
Schnabl).
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NR 121
TC 56
Z9 60
U1 0
U2 42
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1857
EI 1522-1547
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD MAY
PY 2019
VL 316
IS 5
BP G563
EP G573
DI 10.1152/ajpgi.00370.2018
PG 11
WC Gastroenterology & Hepatology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Physiology
GA HY5WK
UT WOS:000468199100001
PM 30767680
OA Bronze, Green Published
DA 2025-01-07
ER
PT J
AU Takaya, H
Kawaratani, H
Nakanishi, K
Takeyama, S
Morioka, C
Sawai, M
Toyohara, M
Fujimoto, M
Yoshiji, H
Yamao, J
Fukui, H
AF Takaya, Hiroaki
Kawaratani, Hideto
Nakanishi, Keisuke
Takeyama, Shinya
Morioka, Chie
Sawai, Masayoshi
Toyohara, Masahisa
Fujimoto, Masao
Yoshiji, Hitoshi
Yamao, Junichi
Fukui, Hiroshi
TI Development of Nodular Regenerative Hyperplasia (NRH) with Portal
Hypertension Following the Administration of Oxaliplatin for the
Recurrence of Colon Cancer
SO INTERNAL MEDICINE
LA English
DT Article
DE nodular regenerative hyperplasia (NRH); esophageal varices; oxaliplatin;
colon cancer
ID LIVER; CHEMOTHERAPY
AB Nodular regenerative hyperplasia (NRH) is associated with autoimmune and hematologic diseases and may lead to portal hypertension. We herein report a case of NRH diagnosed based on a liver biopsy. A 63-year-old woman developed esophageal varices and splenomegaly. She had undergone surgery for transverse colon cancer 24 years earlier and received systemic chemotherapy (FOLFOX4 including oxaliplatin) to treat lymph node metastasis 21 years after the operation. The present liver biopsy confirmed NRH, and, after two years, she received endoscopic injection sclerotherapy. Oxaliplatin was suspected to be the causative agent of NRH in this case. Therefore, physicians must consider the possibility of NRH in patients who receive chemotherapy.
C1 [Takaya, Hiroaki; Kawaratani, Hideto; Nakanishi, Keisuke; Takeyama, Shinya; Morioka, Chie; Sawai, Masayoshi; Toyohara, Masahisa; Fujimoto, Masao; Yoshiji, Hitoshi; Yamao, Junichi; Fukui, Hiroshi] Nara Med Univ, Dept Internal Med 3, Kashihara, Nara, Japan.
C3 Nara Medical University
RP Kawaratani, H (corresponding author), Nara Med Univ, Dept Internal Med 3, Kashihara, Nara, Japan.
EM kawara@naramed-u.ac.jp
OI Yoshiji, Hitoshi/0000-0002-5243-8544
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NR 16
TC 5
Z9 5
U1 0
U2 0
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
EI 1349-7235
J9 INTERNAL MED
JI Intern. Med.
PY 2015
VL 54
IS 4
BP 383
EP 387
DI 10.2169/internalmedicine.54.2461
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA CB7WT
UT WOS:000349840000004
PM 25748953
OA gold
DA 2025-01-07
ER
PT J
AU Tam, C
Wong, JH
Tsui, SKW
Zuo, T
Chan, TF
Ng, TB
AF Tam, Chit
Wong, Jack Ho
Tsui, Stephen Kwok Wing
Zuo, Tao
Chan, Ting Fung
Ng, Tzi Bun
TI LncRNAs with miRNAs in regulation of gastric, liver, and colorectal
cancers: updates in recent years
SO APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
LA English
DT Review
DE lncRNA; miRNA; Epigenetic alteration; Microbiota meditation; Tumor
proliferation; Metastasis; Targeted therapy design
ID LONG NONCODING RNA; PROMOTES CELL-PROLIFERATION; EPITHELIAL-MESENCHYMAL
TRANSITION; HEPATOCELLULAR-CARCINOMA CELLS; PREDICTS POOR-PROGNOSIS;
HELICOBACTER-PYLORI INFECTION; WNT/BETA-CATENIN PATHWAY; FACILITATES
TUMOR-GROWTH; GENOME-WIDE ANALYSIS; COLON-CANCER
AB Long noncoding RNA (lncRNA) is a kind of RNAi molecule composed of hundreds to thousands of nucleotides. There are several major types of functional lncRNAs which participate in some important cellular pathways. LncRNA-RNA interaction controls mRNA translation and degradation or serves as a microRNA (miRNA) sponge for silencing. LncRNA-protein interaction regulates protein activity in transcriptional activation and silencing. LncRNA guide, decoy, and scaffold regulate transcription regulators of enhancer or repressor region of the coding genes for alteration of expression. LncRNA plays a role in cellular responses including the following activities: regulation of chromatin structural modification and gene expression for epigenetic and cell function control, promotion of hematopoiesis and maturation of immunity, cell programming in stem cell and somatic cell development, modulation of pathogen infection, switching glycolysis and lipid metabolism, and initiation of autoimmune diseases. LncRNA, together with miRNA, are considered the critical elements in cancer development. It has been demonstrated that tumorigenesis could be driven by homeostatic imbalance of lncRNA/miRNA/cancer regulatory factors resulting in biochemical and physiological alterations inside the cells. Cancer-driven lncRNAs with other cellular RNAs, epigenetic modulators, or protein effectors may change gene expression level and affect the viability, immortality, and motility of the cells that facilitate cancer cell cycle rearrangement, angiogenesis, proliferation, and metastasis. Molecular medicine will be the future trend for development. LncRNA/miRNA could be one of the potential candidates in this category. Continuous studies in lncRNA functional discrepancy between cancer cells and normal cells and regional and rational genetic differences of lncRNA profiles are critical for clinical research which is beneficial for clinical practice.
C1 [Tam, Chit; Wong, Jack Ho; Tsui, Stephen Kwok Wing; Ng, Tzi Bun] Chinese Univ Hong Kong, Sch Biomed Sci, Fac Med, Shatin, Lo Kwee Seong Integrated Biomed Sci Bldg,Area 39, Hong Kong, Peoples R China.
[Zuo, Tao] Chinese Univ Hong Kong, Dept Med & Therapeut, Fac Med, Shatin, Hong Kong, Peoples R China.
[Chan, Ting Fung] Chinese Univ Hong Kong, Sch Life Sci, Fac Sci, Shatin, Run Run Shaw Sci Bldg, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong; Chinese University of Hong Kong;
Chinese University of Hong Kong
RP Tam, C; Ng, TB (corresponding author), Chinese Univ Hong Kong, Sch Biomed Sci, Fac Med, Shatin, Lo Kwee Seong Integrated Biomed Sci Bldg,Area 39, Hong Kong, Peoples R China.; Chan, TF (corresponding author), Chinese Univ Hong Kong, Sch Life Sci, Fac Sci, Shatin, Run Run Shaw Sci Bldg, Hong Kong, Peoples R China.
EM 1155059540@link.cuhk.edu.hk; tf.chan@cuhk.edu.hk; tzibunng@cuhk.edu.hk
RI Zuo, Tao/AAB-9328-2020; Chan, TingFung/A-6161-2013; Tsui, Stephen
Kwok-Wing/E-4385-2015; TAM, Chit/IQU-3939-2023
OI Chan, TingFung/0000-0002-0489-3884; Tsui, Stephen
Kwok-Wing/0000-0003-0686-4259; Zuo, Tao/0000-0001-8450-5281; TAM,
Chit/0000-0002-8719-1190; WONG, Jack/0000-0002-9732-986X
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NR 406
TC 109
Z9 117
U1 1
U2 51
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0175-7598
EI 1432-0614
J9 APPL MICROBIOL BIOT
JI Appl. Microbiol. Biotechnol.
PD JUN
PY 2019
VL 103
IS 12
BP 4649
EP 4677
DI 10.1007/s00253-019-09837-5
PG 29
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA HZ9QN
UT WOS:000469192100001
PM 31062053
DA 2025-01-07
ER
PT J
AU Ramadan, HKA
El-Raey, F
Zaky, S
Bakr, A
Meghezel, EM
Bazeed, SES
Badawi, R
Abd-Elsalam, S
Elbadry, M
Hagag, M
Abu Rahma, MZ
AF Ramadan, Haidi Karam-Allah
El-Raey, Fathiya
Zaky, Samy
Bakr, Asmaa
Meghezel, El-Zahraa M.
Bazeed, Shamardan Ezzeldin S.
Badawi, Rehab
Abd-Elsalam, Sherief
Elbadry, Mohamed
Hagag, Mahmoud
Abu Rahma, Mohamed Zakaria
TI A paradigm shift in non-viral liver cirrhosis: a multicenter study on
clinicoepidemiological characteristics and outcome of non-B non-C
cirrhosis
SO EGYPTIAN LIVER JOURNAL
LA English
DT Article
DE Non-B non-C cirrhosis; Non-viral cirrhosis; Cryptogenic;
Clinicoepidemiological; Mortality
ID HEPATOCELLULAR-CARCINOMA; CRYPTOGENIC CIRRHOSIS; VIRAL-HEPATITIS;
NATURAL-HISTORY; VIRUS-INFECTION; WILSON DISEASE; RISK-FACTORS;
EPIDEMIOLOGY; ALCOHOL; CARCINOGENESIS
AB BackgroundChronic hepatitis C (HCV) and B viruses (HBV) represent the commonest global causes of liver cirrhosis. Other etiologies of non-viral cirrhosis such as autoimmune, metabolic, vascular, or biliary diseases are underestimated. The study aimed to identify causes, clinicoepidemiological characteristics, and outcome of non-B non-C liver cirrhosis. This Egyptian multicenter study recruited patients with liver cirrhosis excluding HCV and HBV. Clinical evaluation and the mortality were recorded. Laboratory, radiological, and histopathological assessment to diagnose the etiology was performed.ResultsOne hundred eighty-eight patients were included: 54.3% were males. Autoimmune hepatitis (AIH) was the most common cause of cirrhosis (28.2%), followed by Budd-Chiari syndrome (BCS) in 25%, and cryptogenic in 23.9%. Metabolic causes such as Wilson's disease, non-alcoholic steatohepatitis (NASH), and hemochromatosis were reported in 7.4%, 3.2%, and 1.1%, respectively. Biliary and cardiac cirrhosis were less frequent. Older age was prevalent in hemochromatosis (67.5 & PLUSMN; 17.7 years) and NASH (60.7 & PLUSMN; 11), while young age in Wilson's disease (29.5 & PLUSMN; 14.8) and secondary biliary cirrhosis (14.8 & PLUSMN; 4.8). Rural residence was common (60.6%). Mortality was reported in BCS (40.4%), cryptogenic (28.9%), cardiac (25%), Wilson's disease (21.4%), AIH (17%), and NASH (16.7%). Hepatocellular carcinoma complicated 10.6% of cases. A significantly high percentage of patients had decompensated cirrhosis. Child-Pugh class and rural residence were significant predictors of mortality.ConclusionThis first report on non-B non-C cirrhosis in Egypt revealed a high prevalence of AIH, BCS, and cryptogenic cirrhosis. Advanced Child class and rural residence were the predictors of mortality.
C1 [Ramadan, Haidi Karam-Allah; Abu Rahma, Mohamed Zakaria] Assiut Univ, Fac Med, Dept Trop Med & Gastroenterol, Assiut 71515, Egypt.
[El-Raey, Fathiya] Al Azhar Univ, Fac Med, Dept Hepatogastroenterol & Infect Dis, Dumyat, Egypt.
[Zaky, Samy; Bakr, Asmaa] Al Azhar Univ, Fac Med, Dept Hepatogastroenterol & Infect Dis, Cairo, Egypt.
[Meghezel, El-Zahraa M.] Sohag Univ, Fac Med, Dept Trop Med & Gastroenterol, Sohag, Egypt.
[Bazeed, Shamardan Ezzeldin S.] South Valley Univ, Fac Med, Dept Trop Med & Gastroenterol, Qena, Egypt.
[Badawi, Rehab; Abd-Elsalam, Sherief] Tanta Univ, Fac Med, Dept Trop Med & Infect Dis, Tanta, Egypt.
[Elbadry, Mohamed] Helwan Univ, Fac Med, Dept Endem Med, Cairo, Egypt.
[Hagag, Mahmoud] Minist Hlth Cairo, Dept Gastroenterol & Hepatol, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); Assiut University; Egyptian Knowledge
Bank (EKB); Al Azhar University; Egyptian Knowledge Bank (EKB); Al Azhar
University; Egyptian Knowledge Bank (EKB); Sohag University; Egyptian
Knowledge Bank (EKB); South Valley University Egypt; Egyptian Knowledge
Bank (EKB); Tanta University; Egyptian Knowledge Bank (EKB); Helwan
University; Egyptian Knowledge Bank (EKB); Ministry of Health &
Population - Egypt
RP Ramadan, HKA (corresponding author), Assiut Univ, Fac Med, Dept Trop Med & Gastroenterol, Assiut 71515, Egypt.
EM haidikaram@aun.edu.eg
RI badawi, rehab/AAW-2512-2020; Zaky, Samy/AAB-6469-2021; Elbadry,
Mohamed/ABD-3435-2020; EL-Raey, Fathiya/AAU-6534-2020; Ramadan,
Haidi/ABA-9666-2020; Abd-Elsalam, sherief/L-3274-2018
OI Zaky, Samy/0000-0003-4123-9221; Elbadry, Mohamed/0000-0002-9020-8870;
Ramadan, Haidi Karam-Allah/0000-0003-0627-3985
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NR 47
TC 0
Z9 0
U1 2
U2 3
PU SPRINGEROPEN
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, GWENT N1 9XW, ENGLAND
SN 2090-6218
EI 2090-6226
J9 EGYPT LIVER J
JI Egypt. Liver J.
PD JUL 11
PY 2023
VL 13
IS 1
AR 35
DI 10.1186/s43066-023-00270-y
PG 10
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA L9NF3
UT WOS:001026454300002
OA gold
DA 2025-01-07
ER
PT J
AU Mei, Y
Zhu, Y
Teo, HY
Liu, YH
Song, Y
Lim, HY
Hanafi, ZB
Angeli, V
Liu, HY
AF Mei, Yu
Zhu, Ying
Teo, Huey Yee
Liu, Yonghao
Song, Yuan
Lim, Hwee Ying
Binte Hanafi, Zuhairah
Angeli, Veronique
Liu, Haiyan
TI The indirect antiangiogenic effect of IL-37 in the tumor
microenvironment
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE angiogenesis; HCC; IL-37; tumor microenvironment
ID BEVACIZUMAB PLUS IRINOTECAN; GROWTH-FACTOR RECEPTOR; MATRIX
METALLOPROTEINASES; ANGIOGENIC SWITCH; CARCINOMA CELLS; BREAST-CANCER;
COLON-CANCER; EXPRESSION; INHIBITOR; ANGIOPOIETIN-1
AB IL-37, a newly identified IL-1 family cytokine, has been shown to play an important role in inflammatory diseases, autoimmune diseases, and carcinogenesis. IL-37 has been suggested to suppress tumoral angiogenesis, whereas some publications showed that IL-37 promoted angiogenesis through TGF-beta signaling in both physiologic and pathologic conditions. Therefore, the function of IL-37 in tumoral angiogenesis is not clear and the underlying mechanism is not known. In this current study, we investigated the direct role of IL-37 on endothelial cells, as well as its indirect effect on angiogenesis through functioning on tumor cells both in vitro and in vivo. We found that IL-37 treatment directly promoted HUVEC migration and tubule formation, indicating IL-37 as a proangiogenic factor. Surprisingly, the supernatants from IL-37 overexpressing tumor cell line promoted HUVEC apoptosis and inhibited its migration and tubule formation. Furthermore, we demonstrated that IL-37 suppressed tumor angiogenesis in a murine orthotopic hepatocellular carcinoma model, suggesting its dominant antiangiogenesis role in vivo. Moreover, microarray and qPCR analysis demonstrated that IL-37 reduced the expressions of proangiogenic factors and increased the expressions of antiangiogenic factors by tumor cells. Matrix metalloproteinase (MMP)2 expression was significantly decreased by IL-37 in both cell lines and murine tumor models. MMP9 and vascular endothelial growth factor expressions were also reduced in murine tumors overexpressing IL-37, as well as in cell lines overexpressing IL-37 under hypoxic conditions. In conclusion, although IL-37 could exert direct proangiogenic effects on endothelial cells, it plays an antiangiogenic role via modulating proangiogenic and antiangiogenic factor expressions by tumor cells in the tumor microenvironment.
C1 [Mei, Yu; Zhu, Ying; Teo, Huey Yee; Liu, Yonghao; Song, Yuan; Lim, Hwee Ying; Binte Hanafi, Zuhairah; Angeli, Veronique; Liu, Haiyan] Natl Univ Singapore, Immunol Programme, Inst Life Sci, Singapore 117456, Singapore.
[Mei, Yu; Zhu, Ying; Teo, Huey Yee; Liu, Yonghao; Song, Yuan; Lim, Hwee Ying; Binte Hanafi, Zuhairah; Angeli, Veronique; Liu, Haiyan] Natl Univ Singapore, Dept Microbiol & Immunol, Singapore 117456, Singapore.
C3 National University of Singapore; National University of Singapore
RP Liu, HY (corresponding author), Natl Univ Singapore, Immunol Programme, Inst Life Sci, Singapore 117456, Singapore.; Liu, HY (corresponding author), Natl Univ Singapore, Dept Microbiol & Immunol, Singapore 117456, Singapore.
EM micliuh@nus.edu.sg
RI Liu, Haiyan/ABD-8689-2021
OI Lim, Hwee Ying/0000-0003-3991-7855; Liu, Haiyan/0000-0002-4652-469X
FU MOE Tier 2 funding from Singapore Ministry of Education
[MOE2018-T2-1-072]
FX We thank Dr. Paul Hutchinson and Mr. Teo Guo Hui for assistance in flow
cytometry. We thank Dr. Esther Koh and Miss Tan Qi Hui for assistance
with immunofluorescent and immunohistochemistry staining. This study is
supported by MOE Tier 2 funding from Singapore Ministry of Education
(MOE2018-T2-1-072).
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NR 65
TC 12
Z9 12
U1 0
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-5400
EI 1938-3673
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD MAY
PY 2020
VL 107
IS 5
SI SI
BP 783
EP 796
DI 10.1002/JLB.3MA0220-207RR
EA MAR 2020
PG 14
WC Cell Biology; Hematology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Hematology; Immunology
GA LI2GZ
UT WOS:000517639600001
PM 32125036
DA 2025-01-07
ER
PT J
AU Smolka, V
Karaskova, E
Tkachyk, O
Aiglova, K
Ehrmann, J
Michalkova, K
Konecny, M
Volejnikova, J
AF Smolka, Vratislav
Karaskova, Eva
Tkachyk, Oksana
Aiglova, Kvetoslava
Ehrmann, Jiri
Michalkova, Kamila
Konecny, Michal
Volejnikova, Jana
TI Long-term follow-up of children and adolescents with primary sclerosing
cholangitis and autoimmune sclerosing cholangitis
SO HEPATOBILIARY & PANCREATIC DISEASES INTERNATIONAL
LA English
DT Article
DE autoimmune sclerosing cholangitis; childhood; inflammatory bowel
disease; primary sclerosing cholangitis; prognosis
ID SURVIVAL ANALYSIS; OVERLAP SYNDROME; HEPATITIS; EPIDEMIOLOGY;
METAANALYSIS; CHILDHOOD; ADULTS
AB BACKGROUND: Sclerosing cholangitis (SC) is a chronic cholestatic hepatobiliary disease with uncertain long-term prognosis in pediatric patients. This study aimed to evaluate long-term results in children with SC according to the types of SC.
METHODS: We retrospectively followed up 25 children with SC over a period of 4-17 years (median 12). The diagnosis of SC was based on biochemical, histological and cholangiographic findings. Patients fulfilling diagnostic criteria for probable or definite autoimmune hepatitis at the time of diagnosis were defined as having autoimmune sclerosing cholangitis (ASC); other patients were included in a group of primary sclerosing cholangitis (PSC). The incidence of the following complications was studied: obstructive cholangitis, portal hypertension, advanced liver disease and death associated with the primary disease.
RESULTS: Fourteen (56%) patients had PSC and 11 (44%) had ASC. Patients with ASC were significantly younger at the time of diagnosis (12.3 vs 15.4 years, P=0.032) and had higher IgG levels (22.7 vs 17.2 g/L, P=0.003). The mentioned complications occurred in 4 (16%) patients with SC, exclusively in the PSC group: one patient died from colorectal cancer, one patient underwent liver transplantation and two patients, in whom severe bile duct stenosis was present at diagnosis, were endoscopically treated for acute cholangitis. Furthermore, two other children with ASC and 2 children with PSC had elevated aminotransferase levels. The 10-year overall survival was 95.8% in all patients, 100% in patients without complicated liver disease, and 75.0% in patients with complications.
CONCLUSION: In children, ASC is a frequent type of SC, whose prognosis may be better than that in patients with PSC.
C1 [Smolka, Vratislav; Karaskova, Eva; Tkachyk, Oksana; Volejnikova, Jana] Palacky Univ, Fac Med & Dent, Dept Pediat, IP Pavlova 6, Olomouc 77900, Czech Republic.
[Aiglova, Kvetoslava; Konecny, Michal] Palacky Univ, Fac Med & Dent, Dept Internal Med, IP Pavlova 6, Olomouc 77900, Czech Republic.
[Ehrmann, Jiri] Palacky Univ, Fac Med & Dent, Dept Clin & Mol Pathol, IP Pavlova 6, Olomouc 77900, Czech Republic.
[Michalkova, Kamila] Palacky Univ, Fac Med & Dent, Dept Radiol, IP Pavlova 6, Olomouc 77900, Czech Republic.
[Michalkova, Kamila] Univ Hosp Olomouc, IP Pavlova 6, Olomouc 77900, Czech Republic.
C3 Palacky University Olomouc; Palacky University Olomouc; Palacky
University Olomouc; Palacky University Olomouc; University Hospital
Olomouc
RP Smolka, V (corresponding author), Palacky Univ, Fac Med & Dent, Dept Pediat, IP Pavlova 6, Olomouc 77900, Czech Republic.; Smolka, V (corresponding author), Univ Hosp Olomouc, IP Pavlova 6, Olomouc 77900, Czech Republic.
EM vratislav.smolka@fnol.cz
RI Ehrmann, Jiri/C-9074-2009; Konečný, Michal/HKE-0581-2023
FU Czech Ministry of Education, Youth and Sports [NPU LO 1304]
FX This study was supported by a grant from the Czech Ministry of
Education, Youth and Sports (NPU LO 1304).
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NR 27
TC 21
Z9 23
U1 0
U2 7
PU ZHEJIANG UNIV SCH MEDICINE
PI HANGZHOU
PA FIRST AFFILIATED HOSPITAL, 79 QINGCHUN ROAD, HANGZHOU, 310003, PEOPLES R
CHINA
SN 1499-3872
EI 2352-9377
J9 HEPATOB PANCREAT DIS
JI Hepatob. Pancreatic. Dis. Int.
PD AUG 15
PY 2016
VL 15
IS 4
BP 412
EP 418
DI 10.1016/S1499-3872(16)60088-7
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DY0QW
UT WOS:000384802300010
PM 27498582
DA 2025-01-07
ER
PT J
AU Cao, HJ
Zhou, J
Wang, MD
Li, SG
Zhu, L
Zheng, JH
AF Cao, Haijun
Zhou, Jun
Wang, Mudan
Li, Shangao
Zhu, Ling
Zheng, Jianhao
TI Comparison of LncRNA profile in mouse models of drug-induced liver
injury and autoimmnue hepatitis
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Article
DE lncRNAs; lncRNA microarray; differential diagnosis; drug-induced liver
injury; autoimmune hepatitis
ID LONG NONCODING RNAS; MICE; EXPRESSION; PROLIFERATION; CANCER; NEAT1
AB Aim: To analyze and compare the expression profile of long non-coding RNA (lncRNA) in the liver tissue of drug-induced liver injury (DILI) and autoimmune hepatitis (AIH). Methods: Mouse models of DILI and AIH were constructed, with non-treated mice as healthy controls. lncRNA microarray was used to detect the lncRNA expression profile in mice liver tissues. Defferentially expressed lncRNAs with the most meaningful fold changes were further validated by real-time PCR. Results: Compared with normal hepatic tissues, 8 lncRNAs were simultaneously upregulated in both DILI and AIH, and 28 were simultaneously down-regulated in both diseases. Notably, among these simultaneously dysregulated lncRNAs, some had quite different fold changes in the two disease models. Besides, 32 dysregulated lncRNAs (13 up-regulated ones and 19 down-regulated ones) were observed only in DILI models, while 24 dysregulated lncRNAs (9 up-regulated ones and 15 down-regulated ones) were restrictedly expressed in AIH models. RT-PCR validation was consistent with the results of microarray analysis. Conclusion: Some of the dysregulated lncRNAs were differentially expressed between AIH and DILI, and the detection of lncRNA profile or of differentially expressed lncRNAs may help distinguish between the two diseases.
C1 [Cao, Haijun; Li, Shangao; Zhu, Ling; Zheng, Jianhao] Zhejiang Chinese Med Univ, Dept Gastrointestinal Med, Affiliated Hosp 1, Hangzhou, Zhejiang, Peoples R China.
[Wang, Mudan] Zhejiang Chinese Med Univ, Dept Emergency, Affiliated Hosp 1, Hangzhou 310018, Zhejiang, Peoples R China.
[Wang, Mudan] Zhejiang Chinese Med Univ, Ctr Trauma, Affiliated Hosp 1, Hangzhou 310018, Zhejiang, Peoples R China.
[Zhou, Jun] Shaoxing Shangyu Peoples Hosp, Dept Gastrointestinal Med, Shaoxing, Peoples R China.
C3 Zhejiang Chinese Medical University; Zhejiang Chinese Medical
University; Zhejiang Chinese Medical University
RP Wang, MD (corresponding author), Zhejiang Chinese Med Univ, Dept Emergency, Affiliated Hosp 1, Hangzhou 310018, Zhejiang, Peoples R China.; Wang, MD (corresponding author), Zhejiang Chinese Med Univ, Ctr Trauma, Affiliated Hosp 1, Hangzhou 310018, Zhejiang, Peoples R China.
EM wang-mudan_md@163.com
RI zheng, jianhao/KFB-4624-2024; cao, haijun/H-6045-2011
FU Zhejiang Provincial Natural Science Foundation of China [LY14H030007]
FX This research was supported by Zhejiang Provincial Natural Science
Foundation of China (No. LY14H030007).
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NR 23
TC 0
Z9 0
U1 0
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1940-5901
J9 INT J CLIN EXP MED
JI Int. J. Clin. Exp. Med.
PY 2016
VL 9
IS 7
BP 14345
EP 14352
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA EA2MT
UT WOS:000386428400233
DA 2025-01-07
ER
PT J
AU Hemminki, K
Li, X
Sundquist, J
Sundquist, K
AF Hemminki, K.
Li, X.
Sundquist, J.
Sundquist, K.
TI Cancer risks in Crohn disease patients
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE age at onset; autoimmunity; cancer risk; inflammatory bowel disease;
subsequent cancer
ID INFLAMMATORY-BOWEL-DISEASE; GENOME-WIDE ASSOCIATION;
RHEUMATOID-ARTHRITIS; CLINICAL CHARACTERISTICS; ULCERATIVE-COLITIS;
COLORECTAL-CANCER; NORDIC COUNTRIES; POPULATION; TRANSPLANTATION;
SUSCEPTIBILITY
AB Background: Patients diagnosed with Crohn disease (CD) are known to be at an increased risk of bowel cancers and lymphoma. CD is an autoimmune disease and we hypothesize that the patients are predisposed to a wider spectrum of cancers.
Patients and methods: A CD research database was constructed by identifying hospitalized CD patients from the Hospital Discharge Register and cancer patients from the Swedish Cancer Registry. Follow-up of 21 788 CD patients first hospitalized during the years 1964-2004 identified 1424 cancer cases. Standardized incidence ratios (SIRs) were calculated by comparing cancers in CD patients with subjects without CD.
Results: In addition to the known sites, many additional sites were in excess in CD patients. These included liver, pancreatic, lung, prostate, testicular, kidney and skin (squamous cell) cancers; nonthyroid endocrine tumors and leukemia. The previously established sites showed the highest SIRs; however, SIRs > 2.0 were noted for the novel sites of the liver, testis and kidney. For testicular cancer, the SIR of seminoma was 2.74. Cancer risks were influences by age at first hospitalization for CD but whether the age effects were increasing or decreasing depending on the cancer type.
Conclusions: This large study identified many novel subsequent cancers in CD patients.
C1 [Hemminki, K.] German Canc Res Ctr, Div Mol Genet Epidemiol, D-69120 Heidelberg, Germany.
[Hemminki, K.; Li, X.; Sundquist, J.; Sundquist, K.] Karolinska Inst, Ctr Family & Community Med, Huddinge, Sweden.
C3 Helmholtz Association; German Cancer Research Center (DKFZ); Karolinska
Institutet
RP Hemminki, K (corresponding author), German Canc Res Ctr, Div Mol Genet Epidemiol, Neuenheimer Feld 580, D-69120 Heidelberg, Germany.
EM k.hemminki@dkfz.de
OI Li, Xinjun/0000-0002-5559-4657
FU Swedish Cancer Society; Swedish Council for Working Life and Social
Research; European Union [LSHC-CT-2004-503465]
FX Deutsche Krebshilfe; the Bundesministerium fu r r Bildung und Forschung
(BMBF) for the National Genome Research Network plus (NGFN+); the
Swedish Cancer Society; the Swedish Council for Working Life and Social
Research; the European Union (LSHC-CT-2004-503465).
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NR 32
TC 98
Z9 112
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD MAR
PY 2009
VL 20
IS 3
BP 574
EP 580
DI 10.1093/annonc/mdn595
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 413ZU
UT WOS:000263834500029
PM 18765463
DA 2025-01-07
ER
PT J
AU Muratori, L
Lohse, AW
Lenzi, M
AF Muratori, Luigi
Lohse, Ansgar W.
Lenzi, Marco
TI Diagnosis and management of autoimmune hepatitis
SO BMJ-BRITISH MEDICAL JOURNAL
LA English
DT Review
ID PRIMARY SCLEROSING CHOLANGITIS; LIVER ANTIGEN/LIVER PANCREAS; PRIMARY
BILIARY-CIRRHOSIS; CHRONIC ACTIVE HEPATITIS; TERM-FOLLOW-UP;
CLINICAL-FEATURES; HEPATOCELLULAR-CARCINOMA; CLINICOPATHOLOGICAL
FEATURES; ANTIMITOCHONDRIAL ANTIBODY; IMMUNOSUPPRESSIVE THERAPY
AB Autoimmune hepatitis is an inflammatory disease of the liver of unknown cause that may progress to liver cirrhosis and end stage liver failure if diagnosis is overlooked and treatment delayed. The clinical presentation is often that of acute hepatitis, sometimes very severe; less frequently, it can be insidious or completely asymptomatic. The disease can affect people of any age and is more common in women; its incidence and prevalence seem to be on the rise worldwide. An abnormal immune response targeting liver autoantigens and inducing persistent and self-perpetuating liver inflammation is the pathogenic mechanism of the disease. A specific set of autoantibodies, increased IgG concentrations, and histological demonstration of interface hepatitis and periportal necrosis are the diagnostic hallmarks of autoimmune hepatitis. Prompt response to treatment with corticosteroids and other immunomodulatory drugs is almost universal and supports the diagnosis. The aims of treatment are to induce and maintain long term remission of liver inflammation. Treatment can often even reverse liver fibrosis, thus preventing progression to advanced cirrhosis and its complications. Most patients need lifelong maintenance therapy, and repeated follow-up in experienced hands improves the quality of care and quality of life for affected patients.
C1 [Muratori, Luigi; Lenzi, Marco] Univ Bologna, DIMEC, Bologna, Italy.
[Muratori, Luigi; Lenzi, Marco] IRCCS Policlin St Orsola, Bologna, Italy.
[Lohse, Ansgar W.] Univ Med Ctr Hamburg Eppendorf, Dept Med, Hamburg, Germany.
[Muratori, Luigi; Lohse, Ansgar W.; Lenzi, Marco] European Reference Network Hepatol Dis ERN RARE LI, Hamburg, Germany.
C3 University of Bologna; University of Hamburg; University Medical Center
Hamburg-Eppendorf
RP Muratori, L (corresponding author), Univ Bologna, DIMEC, Bologna, Italy.; Muratori, L (corresponding author), IRCCS Policlin St Orsola, Bologna, Italy.; Muratori, L (corresponding author), European Reference Network Hepatol Dis ERN RARE LI, Hamburg, Germany.
EM luigi.muratori@unibo.it
RI Muratori, Luigi/I-3181-2012
FU German Research Foundation [SFB841, KFO306]; European Commission
FX Financial support from the German Research Foundation (SFB841 and
KFO306) and the European Commission (ERN RARE-LIVER) is gratefully
acknowledged.
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NR 200
TC 75
Z9 78
U1 18
U2 54
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0959-535X
EI 1756-1833
J9 BMJ-BRIT MED J
JI BMJ-British Medical Journal
PD FEB 6
PY 2023
VL 380
AR e070201
DI 10.1136/bmj-2022-070201
PG 18
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 9I1HC
UT WOS:000939269100003
PM 36746473
OA Bronze
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Buzzetti, E
Parikh, PM
Gerussi, A
Tsochatzis, E
AF Buzzetti, Elena
Parikh, Pathik M.
Gerussi, Alessio
Tsochatzis, Emmanuel
TI Gender differences in liver disease and the drug-dose gender gap
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Gender; Liver toxicity; Liver disease; Systematic review
ID HEPATITIS-B-VIRUS; PRIMARY BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA
DEVELOPMENT; AUTOIMMUNE HEPATITIS; ORAL-CONTRACEPTIVES; SERUM
TESTOSTERONE; NATURAL-HISTORY; FEMALE SEX; HEREDITARY HEMOCHROMATOSIS;
SPONTANEOUS CLEARANCE
AB Although gender-based medicine is a relatively recent concept, it is now emerging as an important field of research, supported by the finding that many diseases manifest differently in men and women and therefore, might require a different treatment.
Sex-related differences regarding the epidemiology, progression and treatment strategies of certain liver diseases have long been known, but most of the epidemiological and clinical trials still report results only about one sex, with consequent different rate of response and adverse reactions to treatment between men and women in clinical practice.
This review reports the data found in the literature concerning the gender -related differences for the most representative hepatic diseases. (C) 2017 Elsevier Ltd. All rights reserved.
C1 [Buzzetti, Elena; Parikh, Pathik M.; Gerussi, Alessio; Tsochatzis, Emmanuel] Royal Free Hosp, UCL Inst Liver & Digest Hlth, London, England.
[Gerussi, Alessio] Univ Udine, Dept Expt & Clin Med Sci, Internal Med Unit, Udine, Italy.
C3 University of London; University College London; UCL Medical School;
Royal Free London NHS Foundation Trust; University of Udine
RP Buzzetti, E (corresponding author), Royal Free Hosp, UCL Inst Liver & Digest Hlth, London, England.
EM buzzetti.elena@gmail.com
RI Gerussi, Alessio/AAM-5199-2020; Buzzetti, Elena/AAC-1975-2019;
Tsochatzis, Emmanuel/A-1651-2012
OI Tsochatzis, Emmanuel/0000-0001-5069-2461; Gerussi,
Alessio/0000-0002-5086-0514; Buzzetti, Elena/0000-0002-4462-7935
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NR 174
TC 60
Z9 65
U1 3
U2 16
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD JUN
PY 2017
VL 120
BP 97
EP 108
DI 10.1016/j.phrs.2017.03.014
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EV6MI
UT WOS:000401883100010
PM 28336373
OA Green Submitted, Green Accepted
DA 2025-01-07
ER
PT J
AU Hirose, K
Toshima, T
Tobo, T
Kai, S
Hirakawa, M
Higuchi, S
Ofuchi, T
Hosoda, K
Yonemura, Y
Hisamatsu, Y
Masuda, T
Aishima, S
Mimori, K
AF Hirose, Kosuke
Toshima, Takeo
Tobo, Taro
Kai, Satohiro
Hirakawa, Masakazu
Higuchi, Satoshi
Ofuchi, Takashi
Hosoda, Kiyotaka
Yonemura, Yusuke
Hisamatsu, Yuichi
Masuda, Takaaki
Aishima, Shinichi
Mimori, Koshi
TI A rare case of liver regenerative and non-neoplastic lesion resembling a
well-differentiated hepatocellular carcinoma
SO SURGICAL CASE REPORTS
LA English
DT Article
DE Regenerative lesion; Nodular regenerative hyperplasia; NRH-like lesion;
Laparoscopic partial resection; Fatty liver
ID PORTAL-HYPERTENSION; HYPERPLASIA; RESECTION; DISEASE
AB BackgroundNodular regenerative hyperplasia (NRH) is a rare disease that presents pathologically as diffuse hepatic nodules without fibrous septa. It is believed to be caused by vasculopathy against a background of various systemic diseases, such as hematologic, autoimmune, and drug-induced diseases, with various symptoms. In spite of the recent imaging advances, various atypical cases of nodular lesions are observed in daily clinical practice. Cases that do not completely meet these criteria are referred to as -like or -similar lesions in clinical situations, making it difficult to understand their pathogenesis. We present a case in which two hepatic nodular lesions were noted and difficult to differentiate from malignancy preoperatively. The lesions were laparoscopically resected and a pathological diagnosis with non-neoplastic liver regenerative nodules resembling NRH was made.Case presentationA 49-year-old man with no alcohol or drug intake and no past medical history was identified as having liver tumors on screening examination without any symptoms. Contrast-enhanced computed tomography (CT) showed two hepatic tumors; approximately 2-cm tumors at S7 and S8. Gadolinium-ethoxybenzyl-diethylenetriamine-pentaacetic acid (Gd-EOB-DTPA)-enhanced magnetic resonance imaging (MRI) revealed fat inclusions in their contents. Ethoxybenzyl (EOB) uptake was also observed during the hepatobiliary phase. Based on preoperative examinations, we suspected well-differentiated hepatocellular carcinoma (HCC) and performed laparoscopic S7/8 partial resection for these lesions. Macroscopically, the resected specimens showed a non-cirrhotic yellowish-cut surface containing brownish, ill-defined lesions with irregular borders. Microscopically, these lesions showed zonal necrosis, congestion, and aggregation of hemosiderin-laden macrophages around the central vein. In these areas, the fatty deposition of hepatocytes was lower than that in the surrounding background hepatocytes. Histopathologically, neither neoplastic nor hyperplastic lesions were observed, and he was diagnosed as regenerative hepatic change with centrilobular necrosis.ConclusionsConsidering the pathological results, these lesions were thought to be a type of NRH-like lesion with possible hepatic vessel disorder. However, the lesion's cause and classification was difficult to determine. The accumulation of these regenerative changes accompanying fatty liver is needed to clarify the mechanism and its clinical significance.
C1 [Hirose, Kosuke; Toshima, Takeo; Higuchi, Satoshi; Ofuchi, Takashi; Hosoda, Kiyotaka; Yonemura, Yusuke; Hisamatsu, Yuichi; Masuda, Takaaki; Mimori, Koshi] Kyushu Univ, Beppu Hosp, Dept Surg, 4546 Shoen, Beppu, Oita 8740838, Japan.
[Tobo, Taro] Kyushu Univ, Beppu Hosp, Dept Pathol, 4546 Shoen, Beppu, Oita 8740838, Japan.
[Kai, Satohiro; Hirakawa, Masakazu] Kyushu Univ, Beppu Hosp, Dept Radiol, 4546 Shoen, Beppu, Oita 8740838, Japan.
[Aishima, Shinichi] Saga Univ, Dept Pathol & Microbiol, Nabeshima 5-1-1, Saga 8498501, Japan.
C3 Kyushu University; Kyushu University; Kyushu University; Saga University
RP Mimori, K (corresponding author), Kyushu Univ, Beppu Hosp, Dept Surg, 4546 Shoen, Beppu, Oita 8740838, Japan.
EM mimori.koshi.791@m.kyushu-u.ac.jp
RI Higuchi, Satoshi/AAT-6748-2021; Hirose, Kosuke/HOF-1663-2023
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NR 20
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2198-7793
J9 SURG CASE REP
JI SURG. CASE REP.
PD FEB 1
PY 2024
VL 10
IS 1
AR 30
DI 10.1186/s40792-024-01820-1
PG 6
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA GP2F4
UT WOS:001153799600001
PM 38300348
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Chen, YY
Cui, SS
Guo, YF
Chen, DH
AF Chen, Yuanyuan
Cui, Shuaishuai
Guo, Yunfei
Chen, Dahu
TI Co-regulator NCOA5 and cancer
SO BIOCELL
LA English
DT Article
DE NCOA5; Co-regulator; Structure and function; Nuclear receptors; Cancer
ID NF-KAPPA-B; RECEPTOR COACTIVATOR; ANDROGEN RECEPTOR; ROR-ALPHA; GENE;
ACTIVATION; EXPRESSION; POLYMORPHISM; PROGRESSION; PROGNOSIS
AB NCOA5 encodes a co-regulator for estrogen receptors (ER alpha and ER beta), orphan nuclear receptors (REV-ERB alpha and REV-ERB beta) and liver X receptor. It can influence many cellular processes by either promoting or inhibiting gene expression through its two important functional motifs: LxxLL (co-activator) and Phi xx Phi Phi (co-repressor). Many reports have revealed the important roles of NCOA5 in diseases, such as diabetes, reproductive defects and autoimmune disease. In this review, we focus on its function in cancers and summary the current research progresses regarding its different roles in various cancers.
C1 [Chen, Yuanyuan; Cui, Shuaishuai; Guo, Yunfei; Chen, Dahu] Shandong Univ Technol, Sch Life Sci, Zibo 225000, Peoples R China.
C3 Shandong University of Technology
RP Chen, DH (corresponding author), Shandong Univ Technol, Sch Life Sci, Zibo 225000, Peoples R China.
EM dahuchen@outlook.com
FU National Natural Science Foundation of China [81872005]
FX This study was supported by the National Natural Science Foundation of
China (81872005) to DC.
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NR 61
TC 0
Z9 0
U1 0
U2 6
PU TECH SCIENCE PRESS
PI HENDERSON
PA 871 CORONADO CENTER DR, SUTE 200, HENDERSON, NV 89052 USA
SN 0327-9545
EI 1667-5746
J9 BIOCELL
JI Biocell
PY 2022
VL 46
IS 7
BP 1643
EP 1650
DI 10.32604/biocell.2022.019142
EA JAN 2022
PG 8
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA 0D3IA
UT WOS:000755191800001
OA gold
DA 2025-01-07
ER
PT J
AU Ozaki, T
Yumita, S
Ogasawara, S
Fujiya, M
Tsuchiya, T
Yoshino, R
Sawada, M
Akatsuka, T
Izai, R
Miwa, C
Yonemoto, T
Fujimoto, K
Unozawa, H
Fujiwara, K
Kojima, R
Kanzaki, H
Koroki, K
Inoue, M
Kobayashi, K
Nakamura, M
Kiyono, S
Kanogawa, N
Kondo, T
Nakagawa, R
Nakamoto, S
Kato, N
AF Ozaki, Tomomi
Yumita, Sae
Ogasawara, Sadahisa
Fujiya, Makoto
Tsuchiya, Takahiro
Yoshino, Ryohei
Sawada, Midori
Akatsuka, Teppei
Izai, Ryo
Miwa, Chihiro
Yonemoto, Takuya
Fujimoto, Kentaro
Unozawa, Hidemi
Fujiwara, Kisako
Kojima, Ryuta
Kanzaki, Hiroaki
Koroki, Keisuke
Inoue, Masanori
Kobayashi, Kazufumi
Nakamura, Masato
Kiyono, Soichiro
Kanogawa, Naoya
Kondo, Takayuki
Nakagawa, Ryo
Nakamoto, Shingo
Kato, Naoya
TI Cytokine release syndrome following durvalumab and tremelimumab in
advanced hepatocellular carcinoma: A case report with cytokine and
damage-associated molecular pattern analysis
SO HEPATOLOGY RESEARCH
LA English
DT Article; Early Access
DE cytokine release syndrome; damage-associated molecular patterns;
hepatocellular carcinoma; immune checkpoint inhibitors; immune-related
adverse events
AB Cytokine release syndrome (CRS) is a systemic inflammatory syndrome that causes fatal circulatory failure due to hypercytokinemia, and subsequent immune cell hyperactivation caused by therapeutic agents, pathogens, cancers, and autoimmune diseases. In recent years, CRS has emerged as a rare, but significant, immune-related adverse event linked to immune checkpoint inhibitor therapy. Furthermore, several previous studies suggested that damage-associated molecular patterns (DAMPs) could be involved in malignancy-related CRS. In this study, we present a case of severe CRS following combination therapy with durvalumab and tremelimumab for advanced hepatocellular carcinoma, which recurred during treatment, as well as an analysis of cytokine and DAMPs trends. A 35-year-old woman diagnosed with hepatocellular carcinoma underwent a partial hepatectomy. Due to cancer recurrence, she started a combination of durvalumab and tremelimumab. Then, 29 days post-administration, she developed fever and headache, initially suspected as sepsis. Despite antibiotics, her condition worsened, leading to disseminated intravascular coagulation and hemophagocytic syndrome. The clinical course and elevated serum interleukin-6 levels led to a CRS diagnosis. Steroid pulse therapy was administered, resulting in temporary improvement. However, she relapsed with increased interleukin-6, prompting tocilizumab treatment. Her condition improved, and she was discharged on day 22. Measurements of inflammatory cytokines interferon-gamma, tumor necrosis factor-alpha, and DAMPs, along with interleukin-6, using preserved serum samples, confirmed marked elevation at CRS onset. CRS can occur after the administration of any immune checkpoint inhibitor, with the most likely trigger being the release of DAMPs associated with tumor collapse.
Cytokine release syndrome has emerged as a rare, but significant, immune-related adverse event associated with immune checkpoint inhibitor therapy. Several previous studies have suggested that damage-associated molecular patterns could be involved in malignancy-related cytokine release syndrome. In this study, we present a case of severe cytokine release syndrome following combination therapy with durvalumab and tremelimumab for advanced hepatocellular carcinoma, which recurred during treatment. We also provide an analysis of cytokine and damage-associated molecular pattern trends. image
C1 [Ozaki, Tomomi; Yumita, Sae; Ogasawara, Sadahisa; Fujiya, Makoto; Tsuchiya, Takahiro; Yoshino, Ryohei; Sawada, Midori; Akatsuka, Teppei; Izai, Ryo; Miwa, Chihiro; Yonemoto, Takuya; Fujimoto, Kentaro; Unozawa, Hidemi; Fujiwara, Kisako; Kojima, Ryuta; Kanzaki, Hiroaki; Koroki, Keisuke; Inoue, Masanori; Kobayashi, Kazufumi; Nakamura, Masato; Kiyono, Soichiro; Kanogawa, Naoya; Kondo, Takayuki; Nakagawa, Ryo; Nakamoto, Shingo; Kato, Naoya] Chiba Univ, Grad Sch Med, Dept Gastroenterol, 1-8-1 Inohana,Chuo Ku, Chiba 2608670, Japan.
C3 Chiba University
RP Ogasawara, S (corresponding author), Chiba Univ, Grad Sch Med, Dept Gastroenterol, 1-8-1 Inohana,Chuo Ku, Chiba 2608670, Japan.
EM ogasawaras@chiba-u.jp
RI Nakagawa, Ryo/AAC-7066-2022; Ogasawara, Sadahisa/GRF-7061-2022
OI Ogasawara, Sadahisa/0000-0002-6540-9064
FX We thank Risa Kakiuchi for her assistance with data analysis. The
authors thank Enago for their English language review. This study
received no external funding.
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NR 22
TC 1
Z9 1
U1 1
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD 2024 JUN 29
PY 2024
DI 10.1111/hepr.14088
EA JUN 2024
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WV0I5
UT WOS:001257526700001
PM 38943555
DA 2025-01-07
ER
PT J
AU Ravi, S
Shoreibah, M
Raff, E
Bloomer, J
Kakati, D
Rasheed, K
Singal, AK
AF Ravi, Sujan
Shoreibah, Mohamed
Raff, Evan
Bloomer, Joseph
Kakati, Donny
Rasheed, Khalid
Singal, Ashwani K.
TI Autoimmune Markers Do Not Impact Clinical Presentation or Natural
History of Steatohepatitis-Related Liver Disease
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE NAFLD; ALD; NASH; Fatty liver; Autoimmunity
ID ORGAN-SPECIFIC AUTOANTIBODIES; NONALCOHOLIC STEATOHEPATITIS; PREVALENCE
AB Autoimmune (AI) markers are reported in patients with steatohepatitis-related liver disease. However, their clinical significance is unclear.
Charts of patients due to alcoholic liver disease (ALD) or nonalcoholic fatty liver disease (NAFLD) were stratified for antinuclear antigen (ANA > 1:80), antismooth muscle antibody (ASMA > 1:40), or antimitochondrial antibody (AMA > 1:20). Study outcomes were patient survival and complications of liver disease.
Of 607 patients (401 NAFLD), information about AI markers was available for 398 (mean age 50 +/- A 15 year; 52 % males; median body mass index (BMI) 38; 44 % diabetic; 62 % nonalcoholic steatohepatitis (NASH) as type of steatohepatitis; median MELD score 9). A total of 78 (19.6 %) patients were positive for AI markers without differences for ALD versus NAFLD, cirrhosis versus no cirrhosis, and NASH versus no NASH. There were no differences for age, gender, BMI, cirrhosis at presentation, MELD score, endoscopic findings, and histology based on AI markers. Serum ALT was higher among patients with AI markers (65 +/- A 46 vs. 59 +/- A 66 IU/l; P = 0.048). Data remained unchanged on analyzing NAFLD patients. None of the 11 ANA-positive patients (1:640 in 4) showed findings of AI hepatitis. Biopsy in three AMA-positive patients showed mild bile duct damage in one patient. On median follow-up of about 3 years, there were no differences in liver disease outcomes (ascites, encephalopathy, variceal bleeding), hepatocellular carcinoma, transplantation, and survival.
Autoimmune markers are frequently present in steatohepatitis-related liver disease patients. Their presence is an epiphenomenon without histological changes of autoimmune hepatitis. Further, their presence does not impact clinical presentation and follow-up outcomes.
C1 [Ravi, Sujan; Raff, Evan; Kakati, Donny] Univ Alabama Birmingham, Dept Internal Med, Birmingham, AL 35294 USA.
[Shoreibah, Mohamed; Bloomer, Joseph; Singal, Ashwani K.] Univ Alabama Birmingham, Div Gastroenterol & Hepatol, Birmingham, AL 35294 USA.
[Rasheed, Khalid] Univ Alabama Birmingham, Dept Internal Med, Montgomery Program, Montgomery, AL USA.
C3 University of Alabama System; University of Alabama Birmingham;
University of Alabama System; University of Alabama Birmingham;
University of Alabama System; University of Alabama Birmingham
RP Singal, AK (corresponding author), Univ Alabama Birmingham, Div Gastroenterol & Hepatol, Birmingham, AL 35294 USA.
EM aksingal@uab.edu
RI Singal, Ashwani/H-6181-2019
FU NIAAA NIH HHS [R21 AA023273] Funding Source: Medline
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NR 16
TC 30
Z9 30
U1 3
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD DEC
PY 2015
VL 60
IS 12
BP 3788
EP 3793
DI 10.1007/s10620-015-3795-5
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CV8UO
UT WOS:000364563600038
PM 26173506
OA Green Accepted
DA 2025-01-07
ER
PT J
AU El-Masry, M
Gilbert, CP
Saab, S
AF El-Masry, Monica
Gilbert, Carlos Puig
Saab, Sammy
TI Recurrence of non-viral liver disease after orthotopic liver
transplantation
SO LIVER INTERNATIONAL
LA English
DT Review
DE cirrhosis; clinical trials; hepatocellular carcinoma; radionuclide
studies; stem cells
ID PRIMARY SCLEROSING CHOLANGITIS; PRIMARY BILIARY-CIRRHOSIS;
TERM-FOLLOW-UP; FATTY LIVER; AUTOIMMUNE HEPATITIS; RISK-FACTORS;
NONALCOHOLIC STEATOHEPATITIS; ALCOHOLIC CIRRHOSIS; CRYPTOGENIC
CIRRHOSIS; MEDICAL PROGRESS
AB Liver transplant remains the ultimate treatment for decompensated liver disease. However, many diseases do recur after orthotopic liver transplant, which may affect recipients' quality of life and survival rate. We performed a systematic review of relevant epidemiological studies available on Medline that provided information on the recurrence of non-viral hepatitis after orthotopic liver transplantation in adult patients published until August 2010. All data were compiled from either review articles or retrospective studies. Primary sclerosing cholangitis, primary biliary cirrhosis, autoimmune hepatitis, non-alcoholic steatohepatitis, alcoholic steatohepatitis and haemochromatosis can recur after liver transplantation. The rates for disease recurrence varied according to the indication for transplantation, and ranged from 7 to 50%. Although the survival rate of patients with liver disease has increased with the advent of liver transplantation and novel immunosuppressive protocols, recurrence of the primary liver disease remains a concern. The recurrence rates differ not only according to the cause of underlying liver disease but also vary within the indication for transplant. Further studies are needed to elucidate the risk factors for varied disease recurrence.
C1 [Saab, Sammy] Univ Calif Los Angeles, Med Ctr, Pfleger Liver Inst, Dept Med,David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Saab, Sammy] Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Los Angeles, CA 90095 USA.
[El-Masry, Monica] Olive View UCLA Med Ctr, Dept Med, Sylmar, CA USA.
[Gilbert, Carlos Puig] Univ Catolica Santiago Guayaquil, Dept Cirugia & Med, Guayaquil, Ecuador.
C3 University of California System; University of California Los Angeles;
University of California Los Angeles Medical Center; David Geffen School
of Medicine at UCLA; University of California System; University of
California Los Angeles; University of California Los Angeles Medical
Center; David Geffen School of Medicine at UCLA; University of
California System; University of California Los Angeles
RP Saab, S (corresponding author), Univ Calif Los Angeles, Med Ctr, Pfleger Liver Inst, Dept Med,David Geffen Sch Med, 200 Med Plaza,Suite 214, Los Angeles, CA 90095 USA.
EM SSaab@mednet.ucla.edu
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[Anonymous], ANN REP US ORG PROC
[Anonymous], LIVER TRANSPL
[Anonymous], DISEASES LIVER
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NR 142
TC 26
Z9 26
U1 1
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD MAR
PY 2011
VL 31
IS 3
BP 291
EP 302
DI 10.1111/j.1478-3231.2010.02434.x
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 714VK
UT WOS:000286836900004
PM 21281429
OA Bronze
DA 2025-01-07
ER
PT J
AU Liberal, R
Mieli-Vergani, G
Vergani, D
AF Liberal, R.
Mieli-Vergani, G.
Vergani, D.
TI Autoimmune hepatitis: From mechanisms to therapy
SO REVISTA CLINICA ESPANOLA
LA English
DT Review
DE Autoimmune hepatitis; Pathogenesis; Autoantibodies; Diagnosis;
Immunosuppressive treatment
ID REGULATORY T-CELLS; PRIMARY BILIARY-CIRRHOSIS; SMOOTH-MUSCLE ANTIBODIES;
ACTIVE CHRONIC HEPATITIS; LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA;
SCLEROSING CHOLANGITIS; CLINICAL-FEATURES; ANTIGENIC TARGETS;
CONTROLLED-TRIAL
AB Autoimmune hepatitis (AIH) is a progressive inflammatory hepatopathy and an important cause of end-stage liver disease. Its aetiology remains unknown, though both genetic and environmental factors are involved in its development. The major mechanism of autoimmune liver damage involves immune reactions against host liver antigens. Numerical and functional defects of regulatory T-cells play a permissive role enabling autoimmune liver injury to occur and persist. The most typical features of AIH are female preponderance, hypergammaglobulinaemia, seropositivity for circulating autoantibodies and a picture of interface hepatitis on histology. Two types of AIH are distinguished according to serological profile: AIH type 1 patients are positive for anti-nuclear and/or anti-smooth muscle antibodies, whereas AIH type 2 patients are defined by the positivity for anti-liver kidney microsomal type 1 antibody and/or for anti-liver cytosol type 1 antibody. Clinical manifestations are variable, and AIH onset is often ill-defined, frequently mimicking acute hepatitis; its course may be fluctuating. AIH responds to immunosuppressive treatment in the majority of cases. Steroids with or without azathioprine should be instituted promptly upon diagnosis. Remission is achieved in some 80% of patients. For the remaining 20% of patients, alternative immunosuppressive agents such as mycophenolate mofetil and calcineurin inhibitors are an option. Liver transplantation should be considered for those patients who progress to cirrhosis and develop complications of end-stage liver disease, as well as for those presenting with acute liver failure; outcomes are excellent, although the disease may recur in the allograft. (C) 2016 Elsevier Espana, S.L.U. and Sociedad Espanola de Medicina Interna (SEMI). All rights reserved.
C1 [Liberal, R.; Mieli-Vergani, G.; Vergani, D.] Kings Coll London, Inst Liver Studies, Fac Life Sci & Med, London, England.
[Liberal, R.] Ctr Hosp Sao Joao, Dept Gastroenterol, Oporto, Portugal.
[Liberal, R.] Univ Porto, Fac Med, Oporto, Portugal.
[Mieli-Vergani, G.] Kings Coll Hosp London, Paediat Liver GI & Nutr Ctr, London, England.
C3 University of London; King's College London; Sao Joao Hospital;
Universidade do Porto; King's College Hospital NHS Foundation Trust;
King's College Hospital
RP Vergani, D (corresponding author), Kings Coll London, Inst Liver Studies, Fac Life Sci & Med, London, England.
EM diego.vergani@kcl.ac.uk
RI Vergani, Diego/H-7610-2019; Mieli-Vergani, Giorgina/G-5616-2011
OI Mieli-Vergani, Giorgina/0000-0002-8215-4489
FU Rosetree Foundation, UK; PSC Partners Seeking a Cure, USA
FX R. Liberal, D. Vergani and G. Mieli-Vergani are supported by grants from
the Rosetree Foundation, UK, and PSC Partners Seeking a Cure, USA.
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NR 79
TC 8
Z9 9
U1 0
U2 13
PU EDICIONES DOYMA S A
PI BARCELONA
PA TRAV DE GRACIA 17-21, 08021 BARCELONA, SPAIN
SN 0014-2565
EI 1578-1860
J9 REV CLIN ESP
JI Rev. Clin. Esp.
PD OCT
PY 2016
VL 216
IS 7
BP 372
EP 383
DI 10.1016/j.rce.2016.04.003
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DX6TT
UT WOS:000384516700006
PM 27161382
DA 2025-01-07
ER
PT J
AU Malakar, S
Mohindra, S
Mishra, P
Kothalkar, S
Shirol, VV
Borah, G
Hoda, US
Shah, NS
Balankhe, K
Pande, G
Ghoshal, UC
AF Malakar, Sayan
Mohindra, Samir
Mishra, Piyush
Kothalkar, Srikanth
Shirol, Vivek V.
Borah, Gourav
Hoda, Umair Shamsul
Shah, Nishant
Balankhe, Kartik
Pande, Gaurav
Ghoshal, Uday C.
TI Implications of Gender on the Outcome in Patients With Autoimmune
Hepatitis
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE autoimmune flare up; seronegative autoimmune hepatitis; chronic liver
disease (cld); live cirrhosis; acute on chronic liver disease;
aih-autoimmune hepatitis
ID CRITERIA; FAILURE
AB Background: Autoimmune hepatitis (AIH) is uncommon and predominantly affects females. Data on AIH from India are scanty. We retrospectively analyzed the spectrum and outcome of adults with AIH and compared it between male and female patients. Methods: AIH was diagnosed using a simplified AIH score. For suspected seronegative AIH, the revised score was used. Standard therapies for AIH and portal hypertension were administered and response was assessed at six months. Relapse rates and five-year mortality were also evaluated. Results: Of the 157 patients with AIH, 85 (male: female 25: 60) were included in the study. The median age at diagnosis was 46 (interquartile range (IQR) 32-55.5) years in males vs 45 (IQR 34.2-54) years in females (p=0.91). A similar proportion of male and female patients presented with cirrhosis, acute severe AIH, or AIH-related acute on chronic liver failure (ACLF); Extra -hepatic autoimmune diseases were less common in male patients (16% vs 35.5% p=0.02). Other laboratory and histological features were comparable in both groups. During the median follow-up period of 51 months (IQR 45-67 months). The biochemical and clinical response at six months were seen in 64% of male patients and 63.3% of female patients (p= 0.57). Of patients, 75% relapsed in the male AIH group (12 of 16 patients) after initial remission compared to 42% in the female group (p=0.02). Five-year mortality was 14.1%, and no patient developed hepatocellular carcinoma. Conclusion: Male and female patients with AIH have similar clinical, biochemical, and histological profiles. More male patients relapsed after an initial response to therapy.
C1 [Malakar, Sayan; Mohindra, Samir; Mishra, Piyush; Kothalkar, Srikanth; Shirol, Vivek V.; Borah, Gourav; Hoda, Umair Shamsul; Shah, Nishant; Balankhe, Kartik; Pande, Gaurav; Ghoshal, Uday C.] Sanjay Gandhi Postgrad Inst Med Sci, Dept Gastroenterol, Lucknow, India.
C3 Sanjay Gandhi Postgraduate Institute of Medical Sciences
RP Ghoshal, UC (corresponding author), Sanjay Gandhi Postgrad Inst Med Sci, Dept Gastroenterol, Lucknow, India.
EM udayghoshal@gmail.com
OI Shamsul Hoda, Umair/0009-0005-6286-5274
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Xue M, 2021, CAN J GASTROENTEROL, V2021, DOI 10.1155/2021/6692511
NR 26
TC 2
Z9 2
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD MAR 4
PY 2024
VL 16
IS 3
AR e55477
DI 10.7759/cureus.55477
PG 11
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA NM1I1
UT WOS:001200774600009
PM 38571851
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Yatsuji, S
Hashimoto, E
Kaneda, H
Taniai, M
Tokushige, K
Shiratori, K
AF Yatsuji, S
Hashimoto, E
Kaneda, H
Taniai, M
Tokushige, K
Shiratori, K
TI Diagnosing autoimmune hepatitis in nonalcoholic fatty liver disease: is
the International Autoimmune Hepatitis Group scoring system useful?
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE nonalcoholic steatohepatitis; nonalcoholic fatty liver disease;
autoimmune hepatitis; autoimmune hepatitis scoring system; antinuclear
antibody
ID HEPATOCELLULAR-CARCINOMA; STEATOHEPATITIS; AUTOANTIBODIES; PREVALENCE;
CIRRHOSIS; F1-MICE
AB Background. There are no surrogate serum markers for autoimmune hepatitis (AIH) and nonalcoholic fatty liver disease (NAFLD). An AIH scoring system was reported by the International Autoimmune Hepatitis Group; however, the criteria did not focus on making the distinction between AIH and NAFLD. We examined the effectiveness of using the AIH score for diagnosing AIH in NAFLD patients. We also identified the prevalence of autoimmune phenomena, in terms of various auto-antibodies, including antinuclear antibodies (ANA), to determine whether these markers had any clinicopathological significance, and whether they were related to the patients' clinical courses. Methods. We studied 212 patients ( 103 males and 109 females) with biopsy-proven NAFLD. The AIH score of each patient was calculated without including the liver biopsy results. The patients were divided into three groups based on their clinicopathological features: the overlap group (those with clinical and histological features of both NAFLD and AIH), the systemic group (those with systemic antoimmune disease other than AIH), and the "other" group (patients with no antoimmune disease). To evaluate the clinicopathological significance of ANA in NAFLD patients, those without autoimmune diseases (the "others" group) were classified according to their ANA positivity and ANA titer. Results. Seventy patients (33.0%) were positive for ANA. Among the female patients, 106 patients (97.2%) had an AIH score of 10 or more. Of the 103 male patients, 21 (20.4%) had an AIH score of 10 or more. However, after liver biopsy, only 1 patient (0.5%) could be classified as "definite AIH." In the NAFLD patients without autoimmune diseases ("other" group), multivariate logistic regression analysis found that female sex was an independent predictor of the presence of ANA (P = 0.029). In contrast, multivariate logistic regression analysis found that severe obesity (body mass index [BMI], >= 30kg/m(2)) was the only independent predictor of the presence of an ANA titer of 1:80 or more (P = 0.026). Conclusions. The AIH score without liver biopsy findings was not useful for diagnosing AIH in NAFLD patients. In patients with elevated ANA titers and risk factors for NAFLD, it is very important to perform a liver biopsy to make a definitive diagnosis before treatment.
C1 Tokyo Womens Med Univ, Dept Internal Med & Gastroenterol, Shinjuku Ku, Tokyo 1628666, Japan.
C3 Tokyo Women's Medical University
RP Tokyo Womens Med Univ, Dept Internal Med & Gastroenterol, Shinjuku Ku, 8-1 Kawada Cho, Tokyo 1628666, Japan.
RI taniai, makiko/HZH-7431-2023
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NR 25
TC 63
Z9 71
U1 0
U2 2
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD DEC
PY 2005
VL 40
IS 12
BP 1130
EP 1138
DI 10.1007/s00535-005-1711-z
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 996XG
UT WOS:000234208400006
PM 16378177
DA 2025-01-07
ER
PT J
AU Grant, RK
Brindle, WM
Donnelly, MC
McConville, PM
Stroud, TG
Bandieri, L
Plevris, JN
AF Grant, Rebecca K.
Brindle, William M.
Donnelly, Mhairi C.
McConville, Pauline M.
Stroud, Thomas G.
Bandieri, Lorenzo
Plevris, John N.
TI Gastrointestinal and liver disease in patients with schizophrenia: A
narrative review
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Schizophrenia; Gastrointestinal disease; Liver disease; Mental health
ID SEVERE MENTAL-ILLNESS; CELIAC-DISEASE; HEPATITIS-C; CANCER-MORTALITY;
RISK-FACTORS; RELAPSED SCHIZOPHRENICS; PSYCHIATRIC-PATIENTS;
HELICOBACTER-PYLORI; AUTOIMMUNE-DISEASES; METABOLIC SYNDROME
AB Schizophrenia is a severe mental illness which can have a devastating impact on an individual's quality of life. Comorbidities are high amongst patients and life expectancy is approximately 15 years less than the general population. Despite the well-known increased mortality, little is known about the impact of gastrointestinal and liver disease on patients with schizophrenia. We aimed to review the literature and to make recommendations regarding future care. Literature searches were performed on PubMed to identify studies related to gastrointestinal and liver disease in patients with schizophrenia. High rates of chronic liver disease were reported, with Non-Alcoholic Fatty Liver Disease being of particular concern; antipsychotics and metabolic syndrome were contributing factors. Rates of acute liver failure were low but have been associated with antipsychotic use and paracetamol overdose. Coeliac disease has historically been linked to schizophrenia; however, recent research suggests that a causal link is yet to be proven. Evidence is emerging regarding the relationships between schizophrenia and peptic ulcer disease, inflammatory bowel disease and irritable bowel syndrome; clinical vigilance regarding these conditions should be high. Patients with schizophrenia poorly engage with bowel cancer screening programmes, leading to late diagnosis and increased mortality. Clozapine induced constipation is a significant issue for many patients and requires close monitoring. There is a significant burden of gastrointestinal and liver disease amongst patients with schizophrenia. Better levels of support from all members of the medical team are essential to ensure that appropriate, timely care is provided.
C1 [Grant, Rebecca K.; Brindle, William M.; Donnelly, Mhairi C.; Plevris, John N.] Royal Infirm Edinburgh NHS Trust, Ctr Liver & Digest Disorders, Edinburgh EH164SA, Scotland.
[McConville, Pauline M.; Stroud, Thomas G.; Bandieri, Lorenzo] Royal Edinburgh & Associated Hosp, Gen Adult Psychiat, Edinburgh EH105HF, Scotland.
[Grant, Rebecca K.] Royal Infirm Edinburgh NHS Trust, Ctr Liver & Digest Disorders, 51 Little France Cres,Old Dalkeith Rd, Edinburgh EH164SA, Scotland.
C3 Royal Infirmary of Edinburgh; Royal Infirmary of Edinburgh; Royal
Infirmary of Edinburgh
RP Grant, RK (corresponding author), Royal Infirm Edinburgh NHS Trust, Ctr Liver & Digest Disorders, 51 Little France Cres,Old Dalkeith Rd, Edinburgh EH164SA, Scotland.
EM rebecca.x.grant@nhs.scot
RI Plevris, John/O-3517-2014; Grant, Rebecca/JZD-6885-2024
OI Grant, Rebecca/0000-0002-9440-1192
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NR 102
TC 13
Z9 14
U1 2
U2 13
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD OCT 14
PY 2022
VL 28
IS 38
BP 5515
EP 5529
DI 10.3748/wjg.v28.i38.5515
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 5U4OK
UT WOS:000876528000001
PM 36304087
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Xu, BY
Yang, Q
Tang, YZ
Tan, ZX
Fu, HY
Peng, J
Xiang, XM
Gan, LL
Deng, GH
Mao, Q
Xu, PX
Jiang, Y
Ding, JQ
AF Xu, Baoyan
Yang, Qiao
Tang, Yingzi
Tan, Zhaoxia
Fu, Haiyan
Peng, Jing
Xiang, Xiaomei
Gan, Linlin
Deng, Guohong
Mao, Qing
Xu, Pin-Xian
Jiang, Yi
Ding, Jianqiang
TI SIX1/EYA1 are novel liver damage biomarkers in chronic hepatitis B and
other liver diseases
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Sine oculis homeobox homolog 1 (SIX1); eyes absent 1 (EYA1); liver
damage; chronic hepatitis B (CHB); liver disease
ID HEPATOCELLULAR-CARCINOMA; SIX1; HEPATOTOXICITY; MICRORNA-122;
METASTASIS; CELLS
AB Background: This study aimed to investigate the clinicopathological significance of sine oculis homeobox homolog 1 (SIX1) and eyes absent 1 (EYA1) in patients with chronic hepatitis B (CHB) and other liver diseases. Methods: SIX1 and EYA1 levels were detected in human serum and liver tissues by enzyme linked immunosorbent assay (ELISA) and immunofluorescent staining method, respectively. Results: The serum SIX1 and EYA1 levels in 313 CHB patients were 7.24 +/- 0.11 and 25.21 +/- 0.51 ng/mL, respectively, and these values were significantly higher than those in 33 healthy controls (2.84 +/- 0.15 and 13.11 +/- 1.01 ng/mL, respectively; P<0.05). Serum SIX1 and EYA1 levels were also markedly increased in patients with numerous other liver diseases, including liver fibrosis, hepatocellular carcinoma, fatty liver disease, alcoholic liver disease, fulminant hepatic failure, autoimmune liver disease, and hepatitis C, compared to the healthy controls (P<0.05). Dynamic observation of these proteins over time in 35 selected CHB patients revealed that SIX1 and EYA1 serum levels increased over an interval. Immunofluorescent staining revealed that both SIX1 and EYA1 were only expressed in hepatic stellate cells (HSCs), and their increased expression was evident in CHB liver tissue. Conclusions: SIX1 and EYA1 are novel biomarkers of liver damage in patients of CHB and other liver diseases, with potential clinical utility. Keywords: Sine oculis homeobox homolog 1 (SIX1); eyes absent 1 (EYA1); liver damage; chronic hepatitis B
Background: This study aimed to investigate the clinicopathological significance of sine oculis homeobox homolog 1 (SIX1) and eyes absent 1 (EYA1) in patients with chronic hepatitis B (CHB) and other liver diseases. Methods: SIX1 and EYA1 levels were detected in human serum and liver tissues by enzyme linked immunosorbent assay (ELISA) and immunofluorescent staining method, respectively. Results: The serum SIX1 and EYA1 levels in 313 CHB patients were 7.24 +/- 0.11 and 25.21 +/- 0.51 ng/mL, respectively, and these values were significantly higher than those in 33 healthy controls (2.84 +/- 0.15 and 13.11 +/- 1.01 ng/mL, respectively; P<0.05). Serum SIX1 and EYA1 levels were also markedly increased in patients with numerous other liver diseases, including liver fibrosis, hepatocellular carcinoma, fatty liver disease, alcoholic liver disease, fulminant hepatic failure, autoimmune liver disease, and hepatitis C, compared to the healthy controls (P<0.05). Dynamic observation of these proteins over time in 35 selected CHB patients revealed that SIX1 and EYA1 serum levels increased over an interval. Immunofluorescent staining revealed that both SIX1 and EYA1 were only expressed in hepatic stellate cells (HSCs), and their increased expression was evident in CHB liver tissue. Conclusions: SIX1 and EYA1 are novel biomarkers of liver damage in patients of CHB and other liver diseases, with potential clinical utility.
C1 [Xu, Baoyan; Tang, Yingzi; Tan, Zhaoxia; Peng, Jing; Xiang, Xiaomei; Gan, Linlin; Deng, Guohong; Mao, Qing; Ding, Jianqiang] Third Mil Med Univ, Southwest Hosp, Dept Infect Dis, Army Med Univ, Chongqing, Peoples R China.
[Yang, Qiao; Jiang, Yi] Chongqing Univ, Chongqing Emergency Med Ctr, Dept Gen Med, Cent Hosp, 1 Hlth Rd, Chongqing 400014, Peoples R China.
[Fu, Haiyan] Third Mil Med Univ, Southwest Hosp, Hlth Management Ctr, Army Med Univ, Chongqing, Peoples R China.
[Xu, Pin-Xian] Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
C3 Army Medical University; Chongqing University; Army Medical University;
Icahn School of Medicine at Mount Sinai
RP Jiang, Y (corresponding author), Chongqing Univ, Chongqing Emergency Med Ctr, Dept Gen Med, Cent Hosp, 1 Hlth Rd, Chongqing 400014, Peoples R China.; Ding, JQ (corresponding author), Third Mil Med Univ, Dept Infect Dis, Army Med Univ, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.
EM jiangyi0115@163.com; jding18@foxmail.com
RI jiang, jun/GWC-9329-2022; Ding, Jianqiang/LXU-5124-2024
FU Talent Start-up Fund [4174DG]; Southwest Hospital, Third Military
Medical University [SWH2016BZGFKJ-40]
FX The present study was financially supported by the Talent Start-up Fund
4174DG (to JD) and the Clinical Innovation Project SWH2016BZGFKJ-40 (to
BX) from Southwest Hospital, Third Military Medical University.
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NR 32
TC 0
Z9 0
U1 1
U2 3
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD JUN
PY 2021
VL 9
IS 12
AR 992
DI 10.21037/atm-21-2526
PG 8
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA TD7KZ
UT WOS:000669502300006
PM 34277792
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Zhu, LJ
Chen, DZ
Zhu, Y
Pan, TT
Xia, DC
Cai, TC
Lin, HW
Lin, J
Jin, XZ
Wu, FL
Yu, SJ
Zhu, KL
Xu, LM
Chen, YP
AF Zhu, Lujian
Chen, Dazhi
Zhu, Yin
Pan, Tongtong
Xia, Dingchao
Cai, Tingchen
Lin, Hongwei
Lin, Jing
Jin, Xiaozhi
Wu, Faling
Yu, Sijie
Zhu, Kailu
Xu, Lanman
Chen, Yongping
TI GPX4-Regulated Ferroptosis Mediates S100-Induced Experimental Autoimmune
Hepatitis Associated with the Nrf2/HO-1 Signaling Pathway
SO OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
LA English
DT Article
ID CELL-DEATH; IRON; MECHANISMS; CANCER; LIVER; INACTIVATION; STRESS;
ROLES; ACSL4; TNF
AB Autoimmune hepatitis (AIH) is an inflammatory autoimmune disease of the liver. Oxidative stress triggered by reactive oxygen radicals is a common pathophysiological basis for the pathogenesis of many liver diseases, and ferroptosis is associated with the toxic accumulation of reactive oxygen species. The signaling transduction pathways responsible for iron processing and lipid-peroxidation mechanisms are believed to drive ferroptosis. However, the specific mechanisms regulating ferroptosis remain unclear. The aims of this investigation were to identify the possible effector functions of ferroptosis, based on glutathione peroxidase 4 (GPX4) regulation in an S100-induced autoimmune hepatitis mouse model and hepatocyte injury models. The S100 liver antigen-induced AIH mouse model was used to detect ferroptotic biomarkers using western blotting. Upregulated levels of cyclooxygenase2 (COX2) and Acyl-Coenzyme A synthase long-chain family member 4 (ACSL4) were observed in the S100-induced AIH model group, while levels of GPX4 and ferritin heavy chain 1 (FTH1) were downregulated (P<0.05). The expression profiles of COX2, ACSL4, GPX4, and FTH1 were restored following the administration of ferrostatin-1. In addition, Nrf2 and HO-1 levels in the S100-induced AIH model mice after treatment with ferrostatin-1 were downregulated compared to the nonferrostatin-1-treated S100-induced AIH model mice (P<0.05). Moreover, COX2 and ACSL4 levels were significantly upregulated, with significant FTH1 downregulation, in the AIH model mice when liver-specific GPX4 was silenced using AAV8 constructs. These data indicate that inhibition of ferroptosis significantly ameliorated the influence of AIH on the Nuclear factor E2-related factor 2 (Nrf2)/Heme oxygenase-1 (HO-1) signaling pathway, and that ferroptosis may act as an initiator or intermediate mediator leading to AIH.
C1 [Zhu, Lujian; Zhu, Yin; Pan, Tongtong; Xia, Dingchao; Cai, Tingchen; Lin, Hongwei; Lin, Jing; Jin, Xiaozhi; Wu, Faling; Yu, Sijie; Zhu, Kailu; Xu, Lanman; Chen, Yongping] Wenzhou Med Univ, Zhejiang Prov Key Lab Accurate Diag & Treatment C, Affiliated Hosp 1,Dept Infect Dis, Wenzhou Key Lab Hepatol,Hepatol Inst, Wenzhou, Peoples R China.
[Chen, Dazhi] Peking Univ First Hosp, Dept Gastroenterol, Beijing, Peoples R China.
[Xu, Lanman] Ningbo Univ, Ningbo Inst Innovat Combined Med & Engn, Ningbo Med Ctr Lihuili Hosp, Dept Infect Dis & Liver Dis,Affiliated Lihuili Ho, Ningbo, Peoples R China.
C3 Wenzhou Medical University; Ningbo University
RP Xu, LM; Chen, YP (corresponding author), Wenzhou Med Univ, Zhejiang Prov Key Lab Accurate Diag & Treatment C, Affiliated Hosp 1,Dept Infect Dis, Wenzhou Key Lab Hepatol,Hepatol Inst, Wenzhou, Peoples R China.; Xu, LM (corresponding author), Ningbo Univ, Ningbo Inst Innovat Combined Med & Engn, Ningbo Med Ctr Lihuili Hosp, Dept Infect Dis & Liver Dis,Affiliated Lihuili Ho, Ningbo, Peoples R China.
EM zhulj_brave@163.com; dazhichen@126.com; zhuyin19950827@163.com;
ptt_wmu@163.com; qiubear@163.com; 602545182@qq.com;
linhw_strive@163.com; linjing137999@163.com; xzjin@wmu.edu.cn;
543429199wfl@sina.com; 623019592@qq.com; 448159091@qq.com;
13587646315@163.com; cyp@wmu.edu.cn
RI lin, jing/HND-8168-2023
FU Wenzhou Science and Technology Bureau major scientific and technological
innovation to attack health care projects [ZY2019008]; Wenzhou Science
and Technology Bureau basic medical and health science and technology
projects [Y20210147]; Zhejiang Provincial Natural Science Foundation of
China [LD21H030002]; National Natural Science Foundation of China
[81770585, 82070593]
FX AcknowledgmentsThis research was supported by Wenzhou Science and
Technology Bureau major scientific and technological innovation to
attack health care projects (no. ZY2019008), Wenzhou Science and
Technology Bureau basic medical and health science and technology
projects (no. Y20210147), Zhejiang Provincial Natural Science Foundation
of China (no. LD21H030002), and the National Natural Science Foundation
of China (no. 81770585 and no. 82070593).
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NR 44
TC 40
Z9 43
U1 2
U2 35
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1942-0900
EI 1942-0994
J9 OXID MED CELL LONGEV
JI Oxidative Med. Cell. Longev.
PD DEC 20
PY 2021
VL 2021
AR 6551069
DI 10.1155/2021/6551069
PG 16
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA YB6XT
UT WOS:000739153300001
PM 34966478
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Saich, R
Chapman, R
AF Saich, Rebecca
Chapman, Roger
TI Primary sclerosing cholangitis, autoimmune hepatitis and overlap
syndromes in inflammatory bowel disease
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE primary sclerosing cholangitis; autoimmune hepatitis; liver disease;
inflammatory bowel disease; Crohns disease; ulcerative colitis
ID CHRONIC ULCERATIVE-COLITIS; ORTHOTOPIC LIVER-TRANSPLANTATION; DOSE
URSODEOXYCHOLIC ACID; NATURAL-HISTORY; PROGNOSTIC VARIABLES; INCREASED
FREQUENCY; COLORECTAL-CANCER; SWEDISH PATIENTS; CLINICAL-COURSE;
INCREASED RISK
AB Primary sclerosing cholangitis (PSC) is a chronic progressive disorder of unknown aetiology characterised by chronic inflammation and stricture formation of the biliary tree. Symptoms include itch and lethargy and in advanced cases cholangitis and end-stage liver disease, however increasing numbers of asymptomatic individuals are being identified. The disease is rare in the general population but is strongly associated with inflammatory bowel disease (IBD) affecting up to 5% of patients with Ulcerative Colitis, with a slightly lower prevalence (up to 3.6%) in Crohns disease. The strength of this association means that the vast majority (> 90%) of patients with PSC also have IBD, although many may have only mild gastro-intestinal symptoms. Usually IBD presents before PSC, although vice-versa can occur and the onset of both conditions can be separated in some cases by many years. Mean age of diagnosis of PSC is in the fifth decade of life with a strong male predominance. Risk is increased in those with a family history of PSC, suggesting a genetic predisposition and the disease is almost exclusive to non-smokers. The ulcerative colitis associated with PSC is characteristically mild, runs a quiescent course, is associated with rectal sparing, more severe right sided disease, backwash ilieitis and has a high risk of pouchitis post-colectomy. Most worrisome is the high risk of colorectal malignancy which necessitates routine colonoscopic surveillance. Cholangiocarcinoma is also a frequent complication of PSC with a 10%-15% lifetime risk of developing this condition. Treatment with high dose ursodeoxycholic acid offers some chemoprotective effects against colorectal malignancy and may decrease symptoms, biochemical and histological progression of liver disease. Small duct PSC patients characteristically have normal cholangiography, and liver biopsy is required for diagnosis, it appears to have a more favourable prognosis. Autoimmune Hepatitis (AIH) is also more prevalent in patients with IBD, with up to 16% of patients with Autoimmune Hepatitis also having ulcerative colitis. A small subgroup of patients have a AIH-PSC overlap syndrome and the management of these patients depends on liver histology, serum IgM levels, autoantibodies, degree of biochemical cholestasis and cholangiography as some of these patients may respond to immunosupression. (c) 2008 WJG. All rights reserved.
C1 [Saich, Rebecca; Chapman, Roger] John Radcliffe Hosp, Dept Gastroenterol, Oxford OX3 9DU, England.
C3 University of Oxford
RP Saich, R (corresponding author), John Radcliffe Hosp, Dept Gastroenterol, Headley Way, Oxford OX3 9DU, England.
EM r.saich@medsch.ucl.ac.uk
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NR 93
TC 88
Z9 94
U1 0
U2 8
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JAN 21
PY 2008
VL 14
IS 3
BP 331
EP 337
DI 10.3748/wjg.14.331
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 255TE
UT WOS:000252679500002
PM 18200656
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Uzdzicki, AW
Wawrzynowicz-Syczewska, M
AF Uzdzicki, Artur W.
Wawrzynowicz-Syczewska, Marta
TI Characteristic features of ulcerative colitis with concomitant primary
sclerosing cholangitis
SO GASTROENTEROLOGY REVIEW-PRZEGLAD GASTROENTEROLOGICZNY
LA English
DT Review
DE ulcerative colitis; primary sclerosing cholangitis; inflammatory bowel
disease
ID INFLAMMATORY-BOWEL-DISEASE; COLORECTAL-CANCER; CLINICAL-COURSE; RISK;
EPIDEMIOLOGY; AUTOIMMUNE; MANAGEMENT; OUTCOMES
AB Ulcerative colitis is a chronic inflammatory bowel disease of the colon. The most frequent symptoms include bloody diarrhoea with rectal urgency and tenesmus. It is often complicated by the presence of primary sclerosing cholangitis, a chronic, cholestatic liver disease, characterised by the inflammation and fibrosis of bile ducts. The presence of primary sclerosing cholangitis seems to alter the course of ulcerative colitis, changing its natural course.
C1 [Uzdzicki, Artur W.; Wawrzynowicz-Syczewska, Marta] Pomeranian Med Univ, Dept Infect Dis Hepatol & Liver Transplantat, 4 Arkonska St, PL-71455 Szczecin, Poland.
C3 Pomeranian Medical University
RP Uzdzicki, AW (corresponding author), Pomeranian Med Univ, Dept Infect Dis Hepatol & Liver Transplantat, 4 Arkonska St, PL-71455 Szczecin, Poland.
EM arturuzdzicki@gmail.com
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NR 45
TC 6
Z9 6
U1 0
U2 3
PU TERMEDIA PUBLISHING HOUSE LTD
PI POZNAN
PA KLEEBERGA ST 2, POZNAN, 61-615, POLAND
SN 1895-5770
EI 1897-4317
J9 GASTROENTEROL REV
JI Gastroenterol. Rev.
PY 2021
VL 16
IS 3
BP 184
EP 187
DI 10.5114/pg.2021.108983
PG 4
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA YM8PE
UT WOS:000746830100002
PM 34584578
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Wu, Q
Yang, QR
Sun, HS
AF Wu, Qian
Yang, Qingrui
Sun, Hongsheng
TI Role of collagen triple helix repeat containing-1 in tumor and
inflammatory diseases
SO JOURNAL OF CANCER RESEARCH AND THERAPEUTICS
LA English
DT Review
DE Bone mass; collagen triple helix repeat containing-1;
dermatofibrosarcoma protuberans; keloid fibroblasts; myelination;
rheumatoid arthritis; tumors
ID TRANSFORMING-GROWTH-FACTOR; CTHRC1 EXPRESSION; CANCER; PROGNOSIS;
PROTEIN; OVEREXPRESSION; INVASIVENESS; METASTASIS; CARCINOMA; MIGRATION
AB Initially, collagen triple helix repeat containing-1 (CTHRC1) is expressed mainly in adventitial fibroblasts and neointimal smooth muscle cells of balloon-injured vessels, and increases cell migration, promotes tissue repair in response to injury. A variety of studies demonstrated that over-expression of CTHRC1 in solid tumors results in enhancement of migration and invasion of tumor cells, and is associated with decreased overall survival and disease-free survival. CTHRC1 expression is elevated in hepatitis B virus-infected patients and highly correlated with hepatocellular carcinoma progression as well. Furthermore, CTHRC1 plays a pivotal role in a great many fields, including increases bone mass, prevents myelination, reverses collagen synthesis in keloid fibroblasts, and increases fibroblast-like synoviocytes migration speed and abundant production of arthritic pannus in rheumatoid arthritis. Therefore, it will provide new insight into the pathogenesis of tumor and autoimmune diseases, and will shed new light on the therapy of related clinical diseases.
C1 [Wu, Qian; Yang, Qingrui; Sun, Hongsheng] Shandong Univ, Dept Rheumatol & Immunol, Shandong Prov Hosp, 324 Jing Wu Rd, Jinan 250021, Shandong, Peoples R China.
C3 Shandong University; Shandong First Medical University & Shandong
Academy of Medical Sciences
RP Yang, QR; Sun, HS (corresponding author), Shandong Univ, Dept Rheumatol & Immunol, Shandong Prov Hosp, 324 Jing Wu Rd, Jinan 250021, Shandong, Peoples R China.
EM qryang720@163.com; 13869192509@126.com
RI Yin, Qing/HNC-6727-2023
FU National Natural Science Foundation of China (CN) [81501399/H1008]
FX The study was supported by the National Natural Science Foundation of
China (CN) (No. 81501399/H1008).
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NR 41
TC 19
Z9 21
U1 1
U2 9
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S NO 1498A-2
VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 0973-1482
EI 1998-4138
J9 J CANCER RES THER
JI J. Canc. Res. Ther.
PY 2017
VL 13
IS 4
BP 621
EP 624
DI 10.4103/jcrt.JCRT_410_17
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FG9PN
UT WOS:000410771500004
PM 28901303
OA gold
DA 2025-01-07
ER
PT J
AU Vidal-Castiñeira, JR
López-Vázquez, A
Diaz-Bulnes, P
Díaz-Coto, S
Márquez-Kisinousky, L
Martínez-Borra, J
Navascues, CA
Sanz-Cameno, P
de la Vega, J
Astudillo, A
Rodríguez, M
López-Larrea, C
AF Ramon Vidal-Castineira, Jose
Lopez-Vazquez, Antonio
Diaz-Bulnes, Paula
Diaz-Coto, Susana
Marquez-Kisinousky, Leonardo
Martinez-Borra, Jess
Navascues, Carmen A.
Sanz-Cameno, Paloma
de la Vega, Juan
Astudillo, Aurora
Rodriguez, Manuel
Lopez-Larrea, Carlos
TI Genetic contribution of endoplasmic reticulum aminopeptidase 1
polymorphisms to liver fibrosis progression in patients with HCV
infection
SO JOURNAL OF MOLECULAR MEDICINE-JMM
LA English
DT Article
DE Endoplasmic reticulum aminopeptidase-1; Hepatitis C virus; Fibrosis
development; Polymorphisms; Immune modulators
ID GENOME-WIDE ASSOCIATION; CHRONIC HEPATITIS-C; HEPATOCELLULAR-CARCINOMA;
ANKYLOSING-SPONDYLITIS; SUSCEPTIBILITY LOCI; VIRUS-INFECTION; RECEPTORS;
HLA-B27
AB The endoplasmic reticulum aminopeptidase ERAP1 regulates innate and adaptive immune responses, trimming peptides and loading onto HLA class I molecules. Coding single nucleotide polymorphisms within ERAP1 are associated with autoimmune diseases, viral infections, and cancer development. Our purpose was to analyze the influence of ERAP1 variants on fibrogenesis in hepatitis C virus (HCV)-infected patients. A range of ERAP1 polymorphisms were genotyped in 722 unrelated Caucasian patients diagnosed with chronic HCV from two Spanish cohorts. Patients were classified according to their fibrosis stage. Paraffin-embedded tissue microarrays were constructed to assess ERAP1 expression (HCV = 38; alcoholic = 20) by immunohistochemistry. A statistical algorithm was applied to derive a fibrogenesis prediction model. The ERAP1 variants rs30187/T (K528,p(c) < 0.001) and rs27044/G (Q730,p(c) < 0.001) were related with severe fibrosis. These results were validated in the two independent cohorts. Furthermore, patients with the rs30187/T allele had stronger ERAP1 protein expression than those with the rs30187/C (p < 0.05). The statistical model showed that patients with rs30187 C/T and T/T genotypes took 15.58 years (median) to develop advanced fibrosis, but this value was 32.08 years in patients carrying C/C genotype (p < 0.005). ERAP1 variants may influence the clinical course of fibrogenesis in HCV-infected patients. These polymorphisms could be exploited as constitutive new markers of fibrosis evolution. The results highlight the possibility of using modulators of ERAP1 to generate a protective immune response against chronic HCV infection. Key messages What is known Several ERAP1 polymorphisms are associated with autoimmune diseases and cancer. ERAP1 trims peptides to HLA class I presentation. What is new here ERAP1 polymorphisms are associated with fibrogenesis. The ERAP1 polymorphisms genotype could help us in clinical management of patients. Potential translational impact The use of modulators of ERAP1 could generate a protective response depending on SNPs.
C1 [Ramon Vidal-Castineira, Jose; Lopez-Vazquez, Antonio; Diaz-Bulnes, Paula; Marquez-Kisinousky, Leonardo; Martinez-Borra, Jess; Lopez-Larrea, Carlos] Hosp Univ Cent Asturias, Hlth Res Inst Principal Asturias ISPA, Translat Immunol Lab, Oviedo, Spain.
[Lopez-Vazquez, Antonio; Martinez-Borra, Jess; Lopez-Larrea, Carlos] Hosp Univ Cent Asturias, Immunol Serv, Av Roma S-N, Oviedo 33011, Spain.
[Diaz-Coto, Susana] Univ Oviedo, Stat Dept, Oviedo, Spain.
[Navascues, Carmen A.; Rodriguez, Manuel] Hosp Univ Cent Asturias, Gastroenterol Serv, Oviedo, Spain.
[Sanz-Cameno, Paloma] Univ Autonoma Madrid, Hosp Univ La Princcsa, Inst Invest Sanitaria Princesa IIS IP, Liver Unit,Gastroenterol Serv, Madrid, Spain.
[Sanz-Cameno, Paloma] Inst Salud Carlos III, CIBERehd, Madrid, Spain.
[de la Vega, Juan] Hosp San Agustin, Gastroenterol Serv, Aviles, Spain.
[Astudillo, Aurora] Hosp Univ Cent Asturias, Pathol Serv, Oviedo, Spain.
C3 Central University Hospital Asturias; Instituto de Investigacion
Sanitaria del Principado de Asturias (ISPA); Central University Hospital
Asturias; University of Oviedo; Central University Hospital Asturias;
Autonomous University of Madrid; CIBER - Centro de Investigacion
Biomedica en Red; CIBEREHD; Instituto de Salud Carlos III; Hospital San
Agustin; Central University Hospital Asturias
RP López-Larrea, C (corresponding author), Hosp Univ Cent Asturias, Hlth Res Inst Principal Asturias ISPA, Translat Immunol Lab, Oviedo, Spain.; López-Larrea, C (corresponding author), Hosp Univ Cent Asturias, Immunol Serv, Av Roma S-N, Oviedo 33011, Spain.
EM inmuno@hca.es
RI Astudillo, Aurora/AAA-5487-2022; Rodriguez, Manuel/AAH-9936-2020
OI Vidal-Castineira, Jose Ramon/0000-0003-4877-3566; Rodriguez,
Manuel/0000-0001-5763-7668; Marquez, Leonardo/0000-0002-5019-5753;
Astudillo Gonzalez, Maria Aurora/0000-0001-8947-8809; Lopez-Vazquez,
Antonio/0000-0002-5065-6513
FU Plan Nacional de I + D + I 2013-2016 ISCIII (Spanish Institute of Health
Carlos III) [PI16/01318, PI17/01244, PI19/00184]; Gobierno del
Principado de Asturias, PCTI-Plan de Ciencia, Tecnologia e Innovacion
2013-2017 [IDI/2018/144]; FEDER "Funding Program of the European Union";
Red Espanola de Investigacion Renal (REDinREN) [RD16/0009/0020]
FX This work was supported by the Plan Nacional de I + D + I 2013-2016
ISCIII (Spanish Institute of Health Carlos III; grant numbers
PI16/01318, PI17/01244, and PI19/00184); Gobierno del Principado de
Asturias, PCTI-Plan de Ciencia, Tecnologia e Innovacion 2013-2017 (grant
number IDI/2018/144); FEDER "Funding Program of the European Union"; and
the Red Espanola de Investigacion Renal (REDinREN, grant number
RD16/0009/0020).
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NR 38
TC 2
Z9 2
U1 0
U2 4
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0946-2716
EI 1432-1440
J9 J MOL MED
JI J. Mol. Med.
PD SEP
PY 2020
VL 98
IS 9
BP 1245
EP 1254
DI 10.1007/s00109-020-01948-1
EA JUL 2020
PG 10
WC Genetics & Heredity; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Research & Experimental Medicine
GA NH9QM
UT WOS:000546889800001
PM 32647953
DA 2025-01-07
ER
PT J
AU Zhang, W
Rho, JH
Roehrl, MW
Roehrl, MH
Wang, JY
AF Zhang, Wei
Rho, Jung-hyun
Roehrl, Michael W.
Roehrl, Michael H.
Wang, Julia Y.
TI A repertoire of 124 potential autoantigens for autoimmune kidney
diseases identified by dermatan sulfate affinity enrichment of kidney
tissue proteins
SO PLOS ONE
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; PRIMARY BILIARY-CIRRHOSIS;
HEPATOCELLULAR-CARCINOMA; SERUM ANTIBODIES; CELL ANTIBODIES; TARGET
ANTIGEN; AUTOANTIBODIES; EPITOPE; ONSET; ASSOCIATION
AB Autoantigens are the molecular targets in autoimmune diseases. They are a cohort of seemingly unrelated self-molecules present in different parts of the body, yet they can trigger a similar chain of autoimmune responses such as autoantibody production. We previously reported that dermatan sulfate (DS) can bind self-molecules of dying cells to stimulate autoreactive CD5+ B cells to produce autoantibodies. The formation of autoantigen-DS complexes converts the normally non-antigenic self-molecules to none-self antigens, and thus DS-affinity represents a common underlying biochemical property for autoantigens. This study sought to apply this property to identify potential autoantigens in the kidney. Total proteins were extracted from mouse kidney tissues and loaded onto DS-Sepharose resins. Proteins without affinity were washed off the resins, whereas those with increasing DS-affinity were eluted with step gradients of increasing salt strength. Fractions with strong and moderate DS-affinity were sequenced by mass spectrometry and yielded 25 and 99 proteins, respectively. An extensive literature search was conducted to validate whether these had been previously reported as autoantigens. Of the 124 proteins, 79 were reported autoantigens, and 19 out of 25 of the strong-DS-binding ones were well-known autoantigens. Moreover, these proteins largely fell into the two most common autoantibody categories in autoimmune kidney diseases, including 40 ANA (anti-nuclear autoantibodies) and 25 GBM (glomerular basement membrane) autoantigens. In summary, this study compiles a large repertoire of potential autoantigens for autoimmune kidney diseases. This autoantigen-ome sheds light on the molecular etiology of autoimmunity and further supports our hypothesis DS-autoantigen complexes as a unifying principle of autoantigenicity.
C1 [Zhang, Wei] Guizhou Med Univ, Affiliated Hosp, Dept Gastroenterol, Guiyang, Guizhou, Peoples R China.
[Rho, Jung-hyun] MP Biomed, Auckland, New Zealand.
[Roehrl, Michael W.; Wang, Julia Y.] Curandis, Scarsdale, NY 10583 USA.
[Roehrl, Michael H.] Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.
[Roehrl, Michael H.] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, 1275 York Ave, New York, NY 10021 USA.
C3 Guizhou Medical University; Memorial Sloan Kettering Cancer Center;
Memorial Sloan Kettering Cancer Center
RP Wang, JY (corresponding author), Curandis, Scarsdale, NY 10583 USA.; Roehrl, MH (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.; Roehrl, MH (corresponding author), Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, 1275 York Ave, New York, NY 10021 USA.
EM roehrlm@mskcc.org; julia@curandis.com
RI Roehrl, Michael/AAU-8506-2020; Zhang, Wei/ABD-4849-2021
OI Wang, Julia Y./0000-0002-9458-5825; Roehrl, Michael/0000-0003-4892-1098
FU Nation Institutes of Health [NIH R01 AI068826]; Curandis; NIH
FX This study was partially funded by the Nation Institutes of Health (NIH
R01 AI068826 to JYW) and Curandis. Wei Zhang (WZ) and Junghyun Rho (JHR)
were supported by the NIH during the course of this study. MP
Biomedicals is the current employer of JHR but has neither relation to
nor made any contribution, financial or otherwise, to the study.
Curandis provided support in the form of salary to Julia Y. Wang who is
a co-founder and shareholder of Curandis. None of the other authors
received remuneration from Curandis. The funders did not have any
additional role in the study design, data collection and analysis,
decision to publish, or preparation of the manuscript. The specific
roles of the authors are articulated in the 'author contributions'
section.
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NR 83
TC 10
Z9 10
U1 3
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD JUN 25
PY 2019
VL 14
IS 6
AR e0219018
DI 10.1371/journal.pone.0219018
PG 16
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA IW3BT
UT WOS:000484856000058
PM 31237920
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Lin, TA
Chen, TC
Tseng, JH
Yeh, TS
AF Lin, Tien-An
Chen, Tse-Ching
Tseng, Jeng-Hwei
Yeh, Ta-Sen
TI Autoimmune pancreatitis type 2: Mimicking pancreatic cancer
SO FORMOSAN JOURNAL OF SURGERY
LA English
DT Article
DE Autoimmune pancreatitis type 1; autoimmune pancreatitis type 2;
pancreatic tumor; IgG4 antibody; pancreatectomy
ID INTERNATIONAL CONSENSUS
AB Autoimmune pancreatitis (AIP) is a rare disease, which comprises two distinct forms of steroid response chronic pancreatitis. AIP type 2 with no association to IgG level and more confined to the pancreas makes it hard to differentiate with pancreatic cancer preoperatively. Here, we present two cases that were preoperatively diagnosed as pancreatic cancer but turn out to be AIP type 2. The first case is a 55-year-old male with epigastric pain, body weight loss and obstructive jaundice. He also had elevated liver enzyme, but tumor marker and IgG4 level were within normal range. The image studies showed the pancreatic head mass. The pylorus-preserving pancreaticoduodenectomy was performed. The second case is a 35-year-old female with epigastric pain and fever. The laboratory data were within the normal range except elevated C-reactive protein level. The magnetic resonance cholangiopancreatography showed a lobulated mass at the pancreatic tail with regional lymphadenopathy. The laparoscopic distal pancreatectomy with splenectomy was arranged for suspect pancreatic neoplasm. In summary, we had reviewed several studies and concluded several steps to help differential AIP to pancreatic cancer. This may help reduce the unnecessary pancreatic resection in the future.
C1 [Lin, Tien-An; Yeh, Ta-Sen] Chang Gung Mem Hosp, Dept Gen Surg, Taipei, Taiwan.
[Chen, Tse-Ching] Chang Gung Mem Hosp, Dept Anat Pathol, Taipei, Taiwan.
[Tseng, Jeng-Hwei] Chang Gung Mem Hosp, Dept Med Imaging & Intervent, Taipei, Taiwan.
Chang Gung Univ, Coll Med, Taipei, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung Memorial Hospital; Chang Gung
Memorial Hospital; Chang Gung University
RP Yeh, TS (corresponding author), 5 Fu Hsing St, Taoyuan, Taiwan.
EM tsy471027@cgmh.org.tw
CR Dickerson LD, 2019, WORLD J SURG, V43, P1604, DOI 10.1007/s00268-019-04928-w
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NR 10
TC 1
Z9 1
U1 0
U2 1
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S NO 1498A-2
VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 1682-606X
EI 2213-5413
J9 FORMOS J SURG
JI Formos. J. Surg.
PD MAY-JUN
PY 2020
VL 53
IS 3
BP 113
EP 116
DI 10.4103/fjs.fjs_104_19
PG 4
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA LU9IK
UT WOS:000538060100006
OA gold
DA 2025-01-07
ER
PT J
AU Ramos-Casals, M
De Vita, S
Tzioufas, AG
AF Ramos-Casals, M
De Vita, S
Tzioufas, AG
TI Hepatitis C virus, Sjogren's syndrome and B-cell lymphoma: linking
infection, autoimmunity and cancer
SO AUTOIMMUNITY REVIEWS
LA English
DT Article
DE hepatitis C virus; Sjogren's syndrome; cryoglobulinemia; B-cell lymphoma
ID NON-HODGKINS-LYMPHOMAS; MIXED CRYOGLOBULINEMIA; SALIVARY-GLANDS;
SIALADENITIS; DISEASE; MANIFESTATIONS; MULTICENTER; LIVER; RNA
AB An increased prevalence of hematologic malignancies is often described in patients with Sjogren's syndrome (SS). Viruses have been proposed as possible etiologic or triggering agents of systemic autoimmune diseases (SADs), with hepatitis C virus (HCV) being one of the viruses most frequently associated with autoimmune features and with systemic autoinumme diseases such as mixed cryoglobulinemia or SS. Moreover, the association between HCV infection and hematologic malignancies, mainly non-Hodgkin's lymphoma (NHL), is supported by several studies. For these reasons, the recognized association of specific systemic autoimmune diseases (mainly SS and mixed cryoglobulinemia) with HCV infection, added to the possible evolution of any one of these entities into a B-cell NHL, suggests the possibility of a close relationship among SS, HCV and B-cell lymphoproliferative disorders, especially in patients with type 11 mixed cryoglobulinemia. (C) 2004 Elsevier B.V. All rights reserved.
C1 Univ Barcelona, Sch Med, Dept Autoimmune Dis, Hosp Clin,IDIBAPS, Barcelona, Spain.
Univ Udine, Dept Rheumatol, DPMSC, I-33100 Udine, Italy.
Univ Athens, Sch Med, Dept Pathophysiol, GR-11527 Athens, Greece.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS;
University of Udine; Athens Medical School; National & Kapodistrian
University of Athens
RP Univ Barcelona, Hosp Clin, Serv Malaties Autoimmunes, CVillarroel 170, E-08036 Barcelona, Spain.
EM mramos@clinic.ub.es
RI Ramos-Casals, Manuel/IUQ-6082-2023; TZIOUFAS, ATHANASIOS/A-1690-2008
OI Tzioufas, Athanasios/0000-0001-6666-8642; Ramos-Casals,
Manuel/0000-0001-5709-6734
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NR 32
TC 71
Z9 77
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD JAN
PY 2005
VL 4
IS 1
BP 8
EP 15
DI 10.1016/j.autrev.2004.04.004
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 897DY
UT WOS:000226985400002
PM 15652773
DA 2025-01-07
ER
PT J
AU Moon, SH
Kim, MH
Park, DH
AF Moon, Sung-Hoon
Kim, Myung-Hwan
Park, Do Hyun
TI Treatment and Relapse of Autoimmune Pancreatitis
SO GUT AND LIVER
LA English
DT Review
DE Autoimmune pancreatitis; Treatment; Relapse
ID SERUM IGG4 CONCENTRATIONS; LONG-TERM PROGNOSIS; STEROID-THERAPY;
CHOLANGITIS; MOLECULES; CANCER; ACID
AB Autoimmune pancreatitis (AIP) is a peculiar type of chronic pancreatitis whose pathogenesis involves autoimmune mechanisms. The steroid responsiveness has a significant impact on the diagnosis of AIP because patients with AIP and pancreatic cancer share many clinical features. This review focuses on the treatment and relapse of AIR The goal of AIP treatment is remission of symptoms, serology, radiologic changes, or histology, which also applies to relapse. Although it is generally agreed that steroids should be offered to AIP patients with active disease, there is no standardized steroid regimen for AIP and no consensus on the dose and duration of steroid induction and tapering schedule, and optimal duration and dose of maintenance therapy. Obtaining a consensus on the optimal treatment regimen is very important to reducing the relapse rate. In this review, we discuss the treatment regimens used in many centers. (Gut and Liver 2008;2:1-7)
C1 [Moon, Sung-Hoon; Kim, Myung-Hwan; Park, Do Hyun] Univ Ulsan, Dept Internal Med, Coll Med, Asan Med Ctr, Seoul 138736, South Korea.
C3 University of Ulsan
RP Kim, MH (corresponding author), Univ Ulsan, Dept Internal Med, Coll Med, Asan Med Ctr, 388-1 Pungnap 2 Dong, Seoul 138736, South Korea.
EM mhkim@amc.seoul.kr
RI Kim, Soo-Jong/JCP-3527-2023
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NR 38
TC 22
Z9 23
U1 0
U2 2
PU EDITORIAL OFFICE GUT & LIVER
PI SEOUL
PA 305 LOTTE GOLD ROSE II, 890-59, DAECHI 4-DONG, GANGNAM-GU, SEOUL,
135-839, SOUTH KOREA
SN 1976-2283
EI 2005-1212
J9 GUT LIVER
JI Gut Liver
PD JUN
PY 2008
VL 2
IS 1
BP 1
EP 7
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 422OX
UT WOS:000264438700001
PM 20485603
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Fattizzo, B
Giannotta, JA
Serpenti, F
Barcellini, W
AF Fattizzo, Bruno
Giannotta, Juri Alessandro
Serpenti, Fabio
Barcellini, Wilma
TI Difficult Cases of Autoimmune Hemolytic Anemia: A Challenge for the
Internal Medicine Specialist
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE warm autoimmune hemolytic anemia; cold agglutinin disease; intensive
care unit; transplant; immunodeficiencies
ID IMMUNE; MANAGEMENT; PREGNANCY; CYTOPENIAS; MANIFESTATIONS; DIAGNOSIS
AB Autoimmune hemolytic anemia (AIHA) is diagnosed in the presence of anemia, hemolysis, and direct antiglobulin test (DAT) positivity with monospecific antisera. Many confounders of anemia and hemolytic markers should be included in the initial workup (i.e., nutrients deficiencies, chronic liver or kidney diseases, infections, and cancers). Besides classical presentation, there are difficult cases that may challenge the treating physician. These include DAT negative AIHA, diagnosed after the exclusion of other causes of hemolysis, and supported by the response to steroids, and secondary cases (infections, drugs, lymphoproliferative disorders, immunodeficiencies, etc.) that should be suspected and investigated through careful anamnesis physical examination, and specific tests in selected cases. The latter include autoantibody screening in patients with signs/symptoms of systemic autoimmune diseases, immunoglobulins (Ig) levels in case of frequent infections or suspected immunodeficiency, and ultrasound/ computed tomography (CT) studies and bone marrow evaluation to exclude hematologic diseases. AIHA occurring in pregnancy is a specific situation, usually manageable with steroids and intravenous (iv) Ig, although refractory cases have been described. Finally, AIHA may complicate specific clinical settings, including intensive care unit (ICU) admission, reticulocytopenia, treatment with novel anti-cancer drugs, and transplant. These cases are often severe, more frequently DAT negative, and require multiple treatments in a short time.
C1 [Fattizzo, Bruno; Giannotta, Juri Alessandro; Serpenti, Fabio; Barcellini, Wilma] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Hematol Unit, Via Francesco Sforza 35, I-20100 Milan, Italy.
[Fattizzo, Bruno; Giannotta, Juri Alessandro; Serpenti, Fabio] Univ Milan, Dept Oncol & Oncohematol, Via Festa Perdono 7, I-20100 Milan, Italy.
C3 IRCCS Ca Granda Ospedale Maggiore Policlinico; University of Milan
RP Fattizzo, B (corresponding author), Fdn IRCCS Ca Granda Osped Maggiore Policlin, Hematol Unit, Via Francesco Sforza 35, I-20100 Milan, Italy.; Fattizzo, B (corresponding author), Univ Milan, Dept Oncol & Oncohematol, Via Festa Perdono 7, I-20100 Milan, Italy.
EM bruno.fattizzo@unimi.it; jurigiann@gmail.com; fabio.serpenti@unimi.it;
wilma.barcellini@policlinico.mi.it
RI Fattizzo, Bruno/AAB-6816-2022; Giannotta, Juri/AAB-8331-2021
OI Fattizzo, Bruno/0000-0003-0857-8379
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NR 49
TC 10
Z9 12
U1 1
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD DEC
PY 2020
VL 9
IS 12
AR 3858
DI 10.3390/jcm9123858
PG 14
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA PJ9HS
UT WOS:000602069600001
PM 33261016
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU El Dirani, M
Nagaratnam, JM
Kholoki, S
AF El Dirani, Mirna
Nagaratnam, Julius M.
Kholoki, Samer
TI Factors Explaining the Coincidence of Smoldering Multiple Myeloma and
Primary Biliary Cholangitis: A Case Report
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE autoimmune cirrhosis; autoimmune disease and cancer; multiple myeloma
prognosis; smoldering multiple myeloma; primary biliary cirrhosis (pbc)
ID AUTOIMMUNE HEPATITIS; CIRRHOSIS; OVERLAP
AB To date, there have been nine reported instances of coinciding smoldering multiple myeloma (SMM) and primary biliary cholangitis (PBC). The term SMM was coined in 1980 to describe low-severity multiple myeloma cases, a hematologic neoplasia that involves the malignant proliferation of plasma cells. PBC is an autoimmune disorder targeting the intrahepatic bile ducts and is characterized by elevated anti-mitochondrial antibodies and often resulting in autoimmune liver cirrhosis. Currently, there is no plausible rationale for the coincidence of SMM and PBC in patients. This report investigates the relationship between SMM and PBC in a Hispanic 49-year-old female residing in the United States and attempts to determine the possible genetic and biochemical causes of this coincidence.
C1 [El Dirani, Mirna] St James Sch Med, Internal Med, Chicago, IL USA.
[Nagaratnam, Julius M.] Avalon Univ, Internal Med, Sch Med, Chicago, IL USA.
[Kholoki, Samer] La Grange Mem Hosp, Internal Med, Chicago, IL USA.
RP Nagaratnam, JM (corresponding author), Avalon Univ, Internal Med, Sch Med, Chicago, IL USA.
EM juliusnagaratnam@gmail.com
CR Bonder A, 2011, CLIN GASTROENTEROL H, V9, P609, DOI 10.1016/j.cgh.2011.03.019
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NR 19
TC 0
Z9 0
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD JUL 13
PY 2022
VL 14
IS 7
DI 10.7759/cureus.26830
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 3X3TC
UT WOS:000842965000003
PM 35974869
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Deneau, M
Jensen, MK
Holmen, J
Williams, MS
Book, LS
Guthery, SL
AF Deneau, Mark
Jensen, M. Kyle
Holmen, John
Williams, Marc S.
Book, Linda S.
Guthery, Stephen L.
TI Primary Sclerosing Cholangitis, Autoimmune Hepatitis, and Overlap in
Utah Children: Epidemiology and Natural History
SO HEPATOLOGY
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; PRIMARY BILIARY-CIRRHOSIS; TERM-FOLLOW-UP;
COLORECTAL-CANCER; ULCERATIVE-COLITIS; EXTRAINTESTINAL MANIFESTATIONS;
PREVALENCE; POPULATION; DIAGNOSIS; RISK
AB The epidemiology and natural history of pediatric primary sclerosing cholangitis (PSC), autoimmune sclerosing cholangitis (ASC), and autoimmune hepatitis (AIH) are not well characterized. Using multiple, overlapping search strategies followed by a detailed records review, we identified all cases of pediatric PSC, ASC, AIH, and inflammatory bowel disease (IBD) in a geographically isolated region of the United States. We identified 607 cases of IBD, 29 cases of PSC, 12 cases of ASC, and 44 cases of AIH. The mean age at diagnosis was 13.0 years for PSC, 11.3 years for ASC, and 9.8 years for AIH. The incidence and prevalence of PSC, ASC, and AIH were 0.2 and 1.5 cases, 0.1 and 0.6 cases, and 0.4 and 3.0 cases per 100,000 children, respectively. The mean duration of follow-up was 5.9 years. The probability of developing complicated liver disease within 5 years of the diagnosis of liver disease was 37% [95% confidence interval (CI)=21%-58%] for PSC, 25% (95% CI=7%-70%) for ASC, and 15% (95% CI=7%-33%) for AIH. The 5-year survival rates with the native liver were 78% (95% CI=54%-91%) for PSC, 90% (95% CI=47%-99%) for ASC, and 87% (95% CI=71%-95%) for AIH. Cholangiocarcinoma developed in 2 of the 29 PSC patients (6.9%). PSC occurred in 9.9% of patients with ulcerative colitis (UC) and in 0.6% of patients with Crohn's disease (CD). ASC occurred in 2.3% of UC patients and 0.9% of CD patients. AIH occurred in 0.4% of UC patients and in 0.3% of CD patients. Liver disease occurred in 39 of 607 IBD patients (6.4%) overall. Conclusion: Immune-mediated liver diseases are important sources of morbidity in children. Using a population-based design, this study quantifies the burden and natural history of immune-mediated liver disease in children. (Hepatology 2013;58:1392-1400)
C1 [Deneau, Mark; Jensen, M. Kyle; Book, Linda S.; Guthery, Stephen L.] Univ Utah, Dept Pediat, Div Pediat Gastroenterol Hepatol & Nutr, Salt Lake City, UT 84113 USA.
[Holmen, John] Intermt Healthcare, Homer Warner Ctr Informat Res, Salt Lake City, UT USA.
[Williams, Marc S.] Geisinger Hlth Syst, Genom Med Inst, Danville, PA USA.
C3 Utah System of Higher Education; University of Utah; Intermountain
Healthcare; Intermountain Medical Center; Geisinger Health System
RP Deneau, M (corresponding author), Univ Utah, Dept Pediat, Div Pediat Gastroenterol Hepatol & Nutr, 100 North Mario Capecchi Dr,Suite 2650, Salt Lake City, UT 84113 USA.
EM mark.deneau@hsc.utah.edu; stephen.guthery@hsc.utah.edu
OI Williams, Marc/0000-0001-6165-8701
FU National Center for Research Resources; National Center for Advancing
Translational Sciences (National Institutes of Health) [8UL1TR000105]
FX The project described in this article was supported by the National
Center for Research Resources and the National Center for Advancing
Translational Sciences (National Institutes of Health) through grant
8UL1TR000105 (formerly UL1RR025764). The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Institutes of Health.
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NR 45
TC 141
Z9 155
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2013
VL 58
IS 4
BP 1392
EP 1400
DI 10.1002/hep.26454
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 227XX
UT WOS:000325150100025
PM 23686586
OA Bronze
DA 2025-01-07
ER
PT J
AU Simula, MP
De Re, V
AF Simula, Maria Paola
De Re, Valli
TI Hepatitis C virus-induced oxidative stress and mitochondrial
dysfunction: A focus on recent advances in proteomics
SO PROTEOMICS CLINICAL APPLICATIONS
LA English
DT Review
DE ER stress; Hepatitis C virus; Oxidative stress; ROS
ID NF-KAPPA-B; ANTIVIRAL SIGNALING PROTEIN; NECROSIS-FACTOR-ALPHA; LOW-IRON
DIET; HEPATOCELLULAR-CARCINOMA; CORE PROTEIN; HCV INFECTION;
ENDOPLASMIC-RETICULUM; LIPID-PEROXIDATION; HEPATOMA-CELLS
AB The natural history of chronic hepatitis C virus (HCV) infection presents two major aspects. On one side, the illness is by itself benign, whereas, on the other side, epidemiological evidence clearly identifies chronic HCV infection as the principal cause of cirrhosis, hepatocellular carcinoma, and extrahepatic diseases, such as autoimmune type II mixed cryoglobulinemia and some B cell non-Hodgkin's lymphomas. The mechanisms responsible for the progression of liver disease to severe liver injury are still poorly understood. Nonetheless, considerable biological data and studies from animal models suggest that oxidative stress contributes to steatohepatitis and that the increased generation of reactive oxygen and nitrogen species, together with the decreased antioxidant defense, promotes the development of hepatic and extrahepatic complications of HCV infection. The principal mechanisms causing oxidative stress in HCV-positive subjects have only been partially elucidated and have identified chronic inflammation, iron overload, ER stress, and a direct activity of HCV proteins in increasing mitochondrial ROS production, as key events. This review summarizes current knowledge regarding mechanisms of HCV-induced oxidative stress with its long-term effects in the context of HCV-related diseases, and includes a discussion of recent contributions from proteomics studies.
C1 [Simula, Maria Paola; De Re, Valli] IRCCS Natl Canc Inst, Expt & Clin Pharmacol Unit, CRO, I-33081 Aviano, PN, Italy.
C3 IRCCS Aviano (CRO)
RP De Re, V (corresponding author), IRCCS Natl Canc Inst, Expt & Clin Pharmacol Unit, CRO, Via F Gallini 2, I-33081 Aviano, PN, Italy.
EM vdere@cro.it
RI De Re, Valli/K-4121-2016; DE RE, VALLI/AAA-1374-2019
OI DE RE, VALLI/0000-0001-6100-9373
FU Associazione Italiana per la Ricerca sul Cancro'' (AIRC); Programma
Integrato Oncologia, Tematica 2
FX This study was supported by Programma Integrato Oncologia, Tematica 2
and "Associazione Italiana per la Ricerca sul Cancro'' (AIRC).
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NR 126
TC 36
Z9 41
U1 0
U2 9
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1862-8346
EI 1862-8354
J9 PROTEOM CLIN APPL
JI Proteom. Clin. Appl.
PD NOV
PY 2010
VL 4
IS 10-11
BP 782
EP 793
DI 10.1002/prca.201000049
PG 12
WC Biochemical Research Methods; Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 678BU
UT WOS:000284044300001
PM 21137022
DA 2025-01-07
ER
PT J
AU Davis, MR
Zhu, ZW
Hansen, DM
Bai, Q
Fang, YJ
AF Davis, Matthew R.
Zhu, Ziwen
Hansen, Dwayne M.
Bai, Qian
Fang, Yujiang
TI The role of IL-21 in immunity and cancer
SO CANCER LETTERS
LA English
DT Review
DE IL-21; Immune response; Cancer
ID B-CELL DIFFERENTIATION; NATURAL-KILLER-CELL; CD8(+) T-CELLS; HUMAN
NAIVE; METASTATIC MELANOMA; CUTTING EDGE; PHASE-I; HOMEOSTATIC
PROLIFERATION; STAT3 ACTIVATION; LIVER-CANCER
AB Interleukin-21 (IL-21), produced predominantly by CD4+ T cells and natural killer T (NKT) cells, is a newly discovered member of the common gamma-chain family of cytokines. It has been implicated in many immunological processes and has been linked to autoimmune diseases, allergies and other inflammatory diseases. In recent years, the role for IL-21 in the pathogenesis of cancer has also been extensively studied. In this review, we will discuss recent advances concerning the role of IL-21 in immunological processes and the pathogenesis of cancer. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Davis, Matthew R.; Hansen, Dwayne M.; Fang, Yujiang] Des Moines Univ, Dept Microbiol & Immunol, Des Moines, IA 50312 USA.
[Zhu, Ziwen; Bai, Qian; Fang, Yujiang] Univ Missouri, Sch Med, Dept Surg, Columbia, MO 65212 USA.
C3 University of Missouri System; University of Missouri Columbia
RP Fang, YJ (corresponding author), Des Moines Univ, Dept Microbiol & Immunol, Des Moines, IA 50312 USA.
EM yujiang.fang@dmu.edu
RI Zhu, Ziwen/I-1895-2014
FU Des Moines University [IOER 05-14-01, IOER 112-3749, IOER 112-3113]
FX This study was supported by grants from Des Moines University (IOER
05-14-01 and IOER 112-3749) for Yujiang Fang. Matthew R. Davis and
Dwayne M. Hansen were supported by Mentored Research Promgram from Des
Moines University (IOER 112-3113).
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NR 91
TC 114
Z9 131
U1 1
U2 26
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD MAR 28
PY 2015
VL 358
IS 2
BP 107
EP 114
DI 10.1016/j.canlet.2014.12.047
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CB8KG
UT WOS:000349877900003
PM 25575696
DA 2025-01-07
ER
PT J
AU Katsumi, T
Ueno, Y
AF Katsumi, Tomohiro
Ueno, Yoshiyuki
TI Epidemiology and surveillance of autoimmune hepatitis in Asia
SO LIVER INTERNATIONAL
LA English
DT Review
DE autoimmune hepatitis; epidemiology; human leukocyte antigen; incidence;
prevalence
ID HEPATOCELLULAR-CARCINOMA; CLINICAL-FEATURES; TYPE-1; NATIONWIDE;
DIAGNOSIS; JAPAN; PREVALENCE; CIRRHOSIS; CRITERIA; TAIWAN
AB Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease that mainly injures the hepatocytes. The autoimmune disease might be involved in its aetiology, but this remains to be confirmed. Recently epidemiological studies of AIH in Asia have been broadly conducted, revealing characteristics and management of AIH patients in Asia. In East Asia, most AIH patients are type 1, and type 2 AIH is very rare. However, type 2 AIH in South Asia is as frequent as in Europe and the USA. HLA-DR4 is associated with the characteristics of type 1 AIH in East Asia, whereas HLA-DR3 occurs in AIH patients from South Asia. AIH prevalence worldwide is increasing, and several studies have reported a prevalence of 19.44, 22.80 and 12.99 per 100 000 people in Europe, the USA and Asia respectively. A meta-analysis of studies on AIH showed similar annual incidence rates for all regions, with 1.31, 1.37 and 1.00 per 100 000 people in Asia, Europe and the USA respectively. The increase in the rates could be attributable to the increased awareness of disease concepts and diagnosis. In South Asia, most cases were diagnosed as AIH only after having progressed to cirrhosis, which may cause a higher mortality rate in South Asia than in East Asia. Therefore, the early diagnosis and treatment of AIH patients can improve the current situation in Asia.
C1 [Katsumi, Tomohiro; Ueno, Yoshiyuki] Yamagata Univ, Fac Med, Dept Gastroenterol, 2-2-2 Iida Nishi, Yamagata 9909585, Japan.
C3 Yamagata University
RP Katsumi, T (corresponding author), Yamagata Univ, Fac Med, Dept Gastroenterol, 2-2-2 Iida Nishi, Yamagata 9909585, Japan.
EM t-katsumi@med.id.yamagata-u.ac.jp
RI Ueno, Yoshiyuki/R-9242-2019
OI Ueno, Yoshiyuki/0000-0001-5623-4250; Katsumi,
Tomohiro/0000-0001-5670-7505
FU Japan Society for the Promotion of Science (JSPS) [19H03632, 20K17010];
Grants-in-Aid for Scientific Research [20K17010, 19H03632] Funding
Source: KAKEN
FX Grant-in-Aid for Scientific Research C (19H03632) and Grant-in-Aid for
Early-Career Scientists (20K17010) from Japan Society for the Promotion
of Science (JSPS).
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NR 50
TC 17
Z9 18
U1 0
U2 15
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD AUG
PY 2022
VL 42
IS 9
SI SI
BP 2015
EP 2022
DI 10.1111/liv.15155
EA JAN 2022
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 3C8NQ
UT WOS:000740662000001
PM 34990076
DA 2025-01-07
ER
PT J
AU Mieli-Vergani, G
Vergani, D
AF Mieli-Vergani, Giorgina
Vergani, Diego
TI Autoimmune hepatitis
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
ID CHRONIC ACTIVE HEPATITIS; REGULATORY T-CELLS; SOLUBLE LIVER ANTIGEN;
PRIMARY SCLEROSING CHOLANGITIS; FOLLOW-UP; DISEASE-ACTIVITY;
MYCOPHENOLATE-MOFETIL; CONTROLLED-TRIAL; HEPATOCELLULAR-CARCINOMA;
RISK-FACTORS
AB Autoimmune hepatitis (AIH) is an inflammatory liver disease that mainly affects females. It is characterized histologically by interface hepatitis, biochemically by increased aspartate and alanine aminotransferase levels, and serologically by the presence of autoantibodies and increased levels of immunoglobulin G. AIH affects both adults and children, and is particularly aggressive in the latter group. It is a relatively rare but devastating disease, which progresses rapidly unless immunosuppressive treatment is started promptly. With appropriate treatment 80% of patients achieve remission and long-term survival. Those patients who progress to end-stage liver disease because they are unresponsive or nonadherent to treatment, and those with fulminant liver failure (encephalopathy grade II-IV) at diagnosis, require liver transplantation. Seropositivity for smooth muscle and/or antinuclear antibodies defines type 1 AIH, while positivity for liver kidney microsomal type 1 antibodies defines type 2 AIH. The primary cause of AIH is unknown; however, considerable knowledge about the mechanisms of liver damage involved has been gathered over the past 30 years, which is likely to provide the basis for specific modes of treatment and a possible cure.
C1 [Mieli-Vergani, Giorgina; Vergani, Diego] Kings Coll Hosp London, Kings Coll London Sch Med, Inst Liver Studies, London SE5 9RS, England.
C3 University of London; King's College London; King's College Hospital NHS
Foundation Trust; King's College Hospital
RP Mieli-Vergani, G (corresponding author), Kings Coll Hosp London, Kings Coll London Sch Med, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
EM giorgina.vergani@kcl.ac.uk
RI Vergani, Diego/H-7610-2019; Mieli-Vergani, Giorgina/G-5616-2011
OI Mieli-Vergani, Giorgina/0000-0002-8215-4489
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NR 112
TC 99
Z9 110
U1 0
U2 14
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5045
EI 1759-5053
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD JUN
PY 2011
VL 8
IS 6
BP 320
EP 329
DI 10.1038/nrgastro.2011.69
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 773JC
UT WOS:000291301800006
PM 21537351
DA 2025-01-07
ER
PT J
AU Li, C
Ni, YQ
Xu, H
Xiang, QY
Zhao, Y
Zhan, JK
He, JY
Li, S
Liu, YS
AF Li, Chen
Ni, Yu-Qing
Xu, Hui
Xiang, Qun-Yan
Zhao, Yan
Zhan, Jun-Kun
He, Jie-Yu
Li, Shuang
Liu, You-Shuo
TI Roles and mechanisms of exosomal non-coding RNAs in human health and
diseases
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID MESENCHYMAL STEM-CELLS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; ACUTE
MYOCARDIAL-INFARCTION; GASTRIC-CANCER PROGRESSION; AMYLOID PRECURSOR
PROTEIN; TYPE-2 DIABETES-MELLITUS; ISLET BETA-CELL;
HEPATOCELLULAR-CARCINOMA; EXTRACELLULAR VESICLES; BREAST-CANCER
AB Exosomes play a role as mediators of cell-to-cell communication, thus exhibiting pleiotropic activities to homeostasis regulation. Exosomal non-coding RNAs (ncRNAs), mainly microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), are closely related to a variety of biological and functional aspects of human health. When the exosomal ncRNAs undergo tissue-specific changes due to diverse internal or external disorders, they can cause tissue dysfunction, aging, and diseases. In this review, we comprehensively discuss the underlying regulatory mechanisms of exosomes in human diseases. In addition, we explore the current knowledge on the roles of exosomal miRNAs, lncRNAs, and circRNAs in human health and diseases, including cancers, metabolic diseases, neurodegenerative diseases, cardiovascular diseases, autoimmune diseases, and infectious diseases, to determine their potential implication in biomarker identification and therapeutic exploration.
C1 [Li, Chen; Ni, Yu-Qing; Xu, Hui; Xiang, Qun-Yan; Zhao, Yan; Zhan, Jun-Kun; He, Jie-Yu; Li, Shuang; Liu, You-Shuo] Cent South Univ, Xiangya Hosp 2, Dept Geriatr, Changsha 410011, Hunan, Peoples R China.
[Li, Chen; Ni, Yu-Qing; Xu, Hui; Xiang, Qun-Yan; Zhao, Yan; Zhan, Jun-Kun; He, Jie-Yu; Li, Shuang; Liu, You-Shuo] Cent South Univ, Inst Aging & Age Related Dis Res, Changsha 410011, Hunan, Peoples R China.
C3 Central South University; Central South University
RP Liu, YS (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Geriatr, Changsha 410011, Hunan, Peoples R China.; Liu, YS (corresponding author), Cent South Univ, Inst Aging & Age Related Dis Res, Changsha 410011, Hunan, Peoples R China.
EM liuyoushuo@csu.edu.cn
OI Liu, Youshuo/0000-0001-9835-4074; Xiang, Qunyan/0009-0009-0315-2740
FU National Natural Science Foundation of China [82071593, 81770833,
81974223, 82101663]; Fundamental Research Funds For the Central
Universities of Central South University [2019zzts354]
FX This work was supported by the National Natural Science Foundation of
China (No. 82071593, 81770833, 81974223, and 82101663); the Fundamental
Research Funds For the Central Universities of Central South University
(NO. 2019zzts354).
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NR 575
TC 201
Z9 209
U1 20
U2 87
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD NOV 10
PY 2021
VL 6
IS 1
AR 383
DI 10.1038/s41392-021-00779-x
PG 31
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA WU3FJ
UT WOS:000716433900001
PM 34753929
OA gold, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Umemura, T
Katsuyama, Y
Yoshizawa, K
Kimura, T
Joshita, S
Komatsu, M
Matsumoto, A
Tanaka, E
Ota, M
AF Umemura, Takeji
Katsuyama, Yoshihiko
Yoshizawa, Kaname
Kimura, Takefumi
Joshita, Satoru
Komatsu, Michiharu
Matsumoto, Akihiro
Tanaka, Eiji
Ota, Masao
TI Human Leukocyte Antigen Class II Haplotypes Affect Clinical
Characteristics and Progression of Type 1 Autoimmune Hepatitis in Japan
SO PLOS ONE
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; MAJOR HISTOCOMPATIBILITY COMPLEX;
HEPATOCELLULAR-CARCINOMA; BERYLLIUM DISEASE; PEPTIDE BINDING;
AMINO-ACIDS; HLA-C; HLA-DPB1; SUSCEPTIBILITY; ALLELES
AB Although we earlier demonstrated that the human leukocyte antigen (HLA) DRB1*04:05 allele was associated with susceptibility to autoimmune hepatitis (AIH) in Japan, the precise relationship of HLA haplotype and the role of amino acid alignment with disease susceptibility and progression has not been fully clarified. We reinvestigated HLA class I A, B, and C and HLA class II DRB1, DQB1, and DPB1 alleles and haplotypes in a larger new cohort of 156 Japanese patients with type 1 AIH and compared them with the published data of 210 healthy subjects. The DRB1*04: 05-DQB1*04:01 haplotype was significantly associated with AIH susceptibility (30% vs. 11%, P = 1.2x10(-10); odds ratio [OR] = 3.51) and correlated with elevated serum IgG (3042 vs. 2606 mg/dL, P = 0.041) and anti-smooth muscle antigen positivity (77% vs. 34%, P = 0.000006). No associations with HLA-DPB1 alleles were found. The HLA A*24:02 and C*01:02 alleles were associated with disease susceptibility (corrected P = 0.0053 and 0.036, respectively), but this likely constituents of a long ranged haplotype including DRB1*04:05-DQB1*04:01 haplotype. Conversely, the DRB1*15:01-DQB1*06:02 haplotype was associated with protection from both disease onset (5% vs. 13%, P = 0.00057; OR = 0.38) and the development of hepatocellular carcinoma (25% vs. 5%, P = 0.017; OR = 6.81). The frequency of the DRB1*08:03-DQB1*06:01 haplotype was significantly higher in patients who developed hepatic failure (22% vs. 6%, P = 0.034; OR = 4.38). In conclusion, this study established the role of HLA haplotypes in determining AIH susceptibility and progression in the Japanese population. Additional sequencing of the entire HLA region is required to more precisely identify the genetic components of AIH.
C1 [Umemura, Takeji; Yoshizawa, Kaname; Kimura, Takefumi; Joshita, Satoru; Komatsu, Michiharu; Matsumoto, Akihiro; Tanaka, Eiji] Shinshu Univ, Sch Med, Dept Med, Div Gastroenterol & Hepatol, Matsumoto, Nagano 390, Japan.
[Katsuyama, Yoshihiko] Shinshu Univ Hosp, Dept Pharm, Matsumoto, Nagano, Japan.
[Ota, Masao] Shinshu Univ, Sch Med, Dept Legal Med, Matsumoto, Nagano 390, Japan.
[Yoshizawa, Kaname] NHO Ueda Med Ctr, Dept Gastroenterol, Ueda, Nagano, Japan.
C3 Shinshu University; Shinshu University; Shinshu University
RP Umemura, T (corresponding author), Shinshu Univ, Sch Med, Dept Med, Div Gastroenterol & Hepatol, Matsumoto, Nagano 390, Japan.
EM tumemura@shinshu-u.ac.jp; otamasao@shinshu-u.ac.jp
RI Joshita, Satoru/K-5679-2019; Kimura, Takefumi/D-3412-2011
OI Ota, Masao/0000-0002-6400-5658; Kimura, Takefumi/0000-0002-1481-1029
FU Ministry of Health, Labor and Welfare of Japan; Ministry of Education,
Culture, Sports, Science, and Technology of Japan [23590969];
Grants-in-Aid for Scientific Research [22133002, 26460996, 23590969]
Funding Source: KAKEN
FX This research was supported in part by a research grant from the
Ministry of Health, Labor and Welfare of Japan and the Ministry of
Education, Culture, Sports, Science, and Technology of Japan (23590969).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 40
TC 47
Z9 48
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD JUN 23
PY 2014
VL 9
IS 6
AR e100565
DI 10.1371/journal.pone.0100565
PG 6
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AL1WV
UT WOS:000338917900068
PM 24956105
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU He, MM
Lo, CH
Wang, K
Polychronidis, G
Wang, L
Zhong, R
Knudsen, MD
Fang, Z
Song, MY
AF He, Ming-ming
Lo, Chun-Han
Wang, Kai
Polychronidis, Georgios
Wang, Liang
Zhong, Rong
Knudsen, Markus D.
Fang, Zhe
Song, Mingyang
TI Immune-Mediated Diseases Associated With Cancer Risks
SO JAMA ONCOLOGY
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASES;
ULCERATIVE-COLITIS; ORAL MICROBIOME; MORTALITY; COHORT; MALIGNANCIES;
LYMPHOMA; THERAPY
AB IMPORTANCE Immune regulation is important for carcinogenesis; however, the cancer risk profiles associated with immune-mediated diseases need further characterization.
OBJECTIVE To assess the prospective association of 48 immune-mediated diseases with the risk of total and individual cancers and the prospective association of organ-specific immune-mediated diseases with the risk of local and extralocal cancers.
DESIGN, SETTING, AND PARTICIPANTS This prospective cohort study used data from the UK Biobank cohort study on adults aged 37 to 73 years who were recruited at 22 assessment centers throughout the UK between January 1, 2006, and December 31, 2010, with follow-up through February 28, 2019.
EXPOSURES Immune-mediated diseases.
MAIN OUTCOMES AND MEASURES The association of immune-mediated diseases with risk of cancer was assessed with multivariable hazard ratios (HRs) and 95% CIs after adjusting for various potential confounders using time-varying Cox proportional hazards regression. Heterogeneity in the associations of organ-specific immune-mediated diseases with local and extralocal cancers was assessed using the contrast testmethod.
RESULTS A total of 478 753 participants (mean [SD] age, 56.4 [8.1] years; 54% female) were included in the study. During 4 600 460 person-years of follow-up, a total of 2834 cases of cancer were documented in 61 496 patients with immune-mediated diseases and 26 817 cases of cancer in 417 257 patients without any immune-mediated diseases (multivariable HR, 1.08; 95% CI, 1.04-1.12). Five of the organ-specific immune-mediated diseases were significantly associated with higher risk of local but not extralocal cancers: asthma (HR, 1.34; 95% CI, 1.14-1.56), celiac disease (HR, 6.89; 95% CI, 2.18-21.75), idiopathic thrombocytopenic purpura (HR, 6.94; 95% CI, 3.94-12.25), primary biliary cholangitis (HR, 42.12; 95% CI, 20.76-85.44), and autoimmune hepatitis (HR, 21.26; 95% CI, 6.79-66.61) (P <.002 for heterogeneity). Nine immune-mediated diseases were associated with an increased risk of cancers in the involved organs (eg, asthma with lung cancer [HR, 1.34; 95% CI, 1.14-1.57; P <.001] and celiac disease with small intestine cancer [HR, 6.89; 95% CI, 2.18-21.75; P =.001]); 13 immune-mediated diseases were associated with an increased risk of cancer in the near organs (eg, Crohn disease with liver cancer: [HR, 4.01; 95% CI, 1.65-9.72; P =.002]) or distant organs (eg, autoimmune hepatitis with tongue cancer [HR, 27.75; 95% CI, 3.82-199.91; P =.001]) or in different systems (eg, idiopathic thrombocytopenic purpura with liver cancer [HR, 11.96; 95% CI, 3.82-37.42; P <.001]).
CONCLUSIONS AND RELEVANCE In this cohort study, immune-mediated diseaseswere associated with an increased risk of total cancer. Organ-specific immune-mediated diseases had stronger associations with risk of local cancers than extralocal cancers. The associations for individual immune-mediated diseases were largely organ specific but were also observed for some cancers in the near and distant organs or different systems. Our findings support the role of local and systemic immunoregulation in cancer development.
C1 [He, Ming-ming] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, Dept Med Oncol, State Key Lab Oncol South China,Canc Ctr, Guangzhou, Peoples R China.
[He, Ming-ming; Lo, Chun-Han; Wang, Kai; Polychronidis, Georgios; Wang, Liang; Zhong, Rong; Knudsen, Markus D.; Fang, Zhe; Song, Mingyang] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, 667 Huntington Ave,Kresge 906A, Boston, MA 02115 USA.
[Lo, Chun-Han; Song, Mingyang] Harvard Med Sch, Massachusetts Gen Hosp, Clin & Translat Epidemiol Unit, Boston, MA 02115 USA.
[Lo, Chun-Han; Song, Mingyang] Harvard Med Sch, Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02115 USA.
[Polychronidis, Georgios] Heidelberg Univ, Dept Gen Visceral & Transplantat Surg, Heidelberg, Germany.
[Polychronidis, Georgios] Heidelberg Univ, Study Ctr German Surg Soc, Heidelberg, Germany.
[Wang, Liang] Sun Yat Sen Univ, Affiliated Hosp 1, Ctr Gastrointestinal Surg, Guangzhou, Peoples R China.
[Knudsen, Markus D.] Canc Registry Norway, Sect Colorectal Canc Screening, Oslo, Norway.
[Knudsen, Markus D.] Oslo Univ Hosp, Norwegian PSC Res Ctr, Dept Transplantat Med Inflammatory Dis & Transpla, Div Surg, Oslo, Norway.
[Song, Mingyang] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
C3 State Key Lab Oncology South China; Sun Yat Sen University; Harvard
University; Harvard T.H. Chan School of Public Health; Harvard
University; Harvard Medical School; Massachusetts General Hospital;
Harvard University; Harvard Medical School; Massachusetts General
Hospital; Ruprecht Karls University Heidelberg; Ruprecht Karls
University Heidelberg; Sun Yat Sen University; University of Oslo;
University of Oslo; Harvard University; Harvard T.H. Chan School of
Public Health
RP Song, MY (corresponding author), Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, 667 Huntington Ave,Kresge 906A, Boston, MA 02115 USA.
EM mis911@mail.harvard.edu
RI Lo, Chun-Han/AAT-4992-2020; Fang, Zhe/HSF-1902-2023; Zhong,
Rong/HSA-9353-2023; Song, Mingyang/M-6701-2013; Wang, Kai/O-7754-2019
OI Polychronidis, Georgios/0000-0002-9819-8179; Knudsen, Markus
Dines/0000-0001-9306-8327; He, Ming-ming/0000-0003-4706-6093; Wang,
Kai/0000-0002-5614-5618
FU American Cancer Society [MRSG-17-220-01-NEC]; US National Institutes of
Health [R00 CA215314]; German Research Foundation [DFG 426308975]; UK
Department of Health; Scottish Government; Wellcome Trust; Welsh
Assembly Government; British Heart Foundation; Diabetes UK
FX This work was supported by grant MRSG-17-220-01-NEC from the American
Cancer Society (Dr Song), grant R00 CA215314 from the US National
Institutes of Health (Dr Song), and grant DFG 426308975 from the German
Research Foundation (Dr Polychronidis). The UK Biobank was primarily
funded by theWellcome Trust and the Medical Research Council. Other
areas of funding include the UK Department of Health, the Scottish
Government, theWelsh Assembly Government, the British Heart Foundation,
and Diabetes UK.
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NR 62
TC 57
Z9 61
U1 1
U2 18
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2374-2437
EI 2374-2445
J9 JAMA ONCOL
JI JAMA Oncol.
PD FEB
PY 2022
VL 8
IS 2
BP 209
EP 219
DI 10.1001/jamaoncol.2021.5680
EA DEC 2021
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZC4TN
UT WOS:000725722400004
PM 34854871
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Mostafa, NR
Ali, AAM
Alkaphoury, MG
Marzo, RR
AF Mostafa, Neveen Rashad
Ali, Abeer A. M.
Alkaphoury, Mona Gamalludin
Marzo, Roy Rillera
TI Helicobacter Pylori infection and non-alcoholic fatty liver disease. Is
there a relationship?
SO HEALTHCARE IN LOW-RESOURCE SETTINGS
LA English
DT Article
DE Helicobacter Pylori; lipid; non-alcoholic fatty liver
ID CARDIOVASCULAR-DISEASE; NAFLD; PATHOGENESIS; PROGRESSION; PREVALENCE;
FIBROSIS
AB The most prevalent infection that causes chronic gastritis, gas-tric ulcers, and gastric cancer is Helicobacter pylori infection. Recent research has implicated H. pylori in the pathogenesis of non-gastrointestinal diseases such as cardiovascular, autoimmune, and metabolic disorders. In addition, since H. pylori is believed to be implicated in insulin resistance, numerous studies have been conducted to determine the relationship between H. pylori infec-tion and nonalcoholic fatty liver diseases (NAFLD), but the results have been contested. The purpose of this study is to determine the relationship between H. Pylori infection and nonalcoholic fatty liver diseases. One hundred patients were examined via urea breath test for the presence of H. pylori infection and vibration-controlled transient elastography for the diagnosis of non-alcoholic fatty liver disease. After adjusting for other variables, age, body mass index (BMI), and H. pylori infection were associated with elastography 248dB/m. Infection with H. pylori contributes to the development of NAFLD, and its eradication may influence prognosis.
C1 [Mostafa, Neveen Rashad] Alexandria Univ, Med Res Inst, Dept Expt & Clin Internal Med, Alexandria, Egypt.
[Ali, Abeer A. M.] Alexandria Univ, Med Res Inst, Dept Chem Pathol, Alexandria, Egypt.
[Alkaphoury, Mona Gamalludin] Ain Shams Univ, Dept Diagnost Radiol, Cairo, Egypt.
[Marzo, Roy Rillera] Management & Sci Univ, Int Med Sch, Dept Community Med, Shah Alam, Malaysia.
[Marzo, Roy Rillera] Monash Univ Malaysia, Jeffrey Cheah Sch Med & Hlth Sci, Global Publ Hlth, Kuala Lumpur, Malaysia.
C3 Egyptian Knowledge Bank (EKB); Alexandria University; Egyptian Knowledge
Bank (EKB); Alexandria University; Egyptian Knowledge Bank (EKB); Ain
Shams University; Management Science University; Monash University;
Monash University Malaysia
RP Mostafa, NR (corresponding author), Alexandria Univ, Med Res Inst, Dept Expt & Clin Internal Med, Alexandria, Egypt.
EM doctor.aj.2000@gmail.com
RI MARZO, ROY/ABA-4304-2020
OI MARZO, ROY/0000-0001-9414-4010
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NR 34
TC 1
Z9 1
U1 3
U2 8
PU PAGEPRESS PUBL
PI PAVIA
PA MEDITGROUP, VIA G BELLI, 4, PAVIA, 27100, ITALY
EI 2281-7824
J9 HEALTHC LOW-RESOUR S
JI Healthc. Low-resource Settings
PY 2023
VL 11
SU 2
AR 11379
DI 10.4081/hls.2023.11379
PG 6
WC Health Care Sciences & Services
WE Emerging Sources Citation Index (ESCI)
SC Health Care Sciences & Services
GA K7GT0
UT WOS:001018093900001
OA gold
DA 2025-01-07
ER
PT J
AU Valizadeh, A
Sanaei, R
Rezaei, N
Azizi, G
Fekrvand, S
Aghamohammadi, A
Yazdani, R
AF Valizadeh, Amir
Sanaei, Roozbeh
Rezaei, Nima
Azizi, Gholamreza
Fekrvand, Saba
Aghamohammadi, Asghar
Yazdani, Reza
TI Potential role of regulatory B cells in immunological diseases
SO IMMUNOLOGY LETTERS
LA English
DT Review
DE Regulatory B cells; Autoimmunity; Chronic infectious disease;
Malignancies; Allergies; Primary immunodeficiencies
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; BREAST-CANCER METASTASIS;
PLACEBO-CONTROLLED TRIAL; EFFECTOR T-CELLS; MULTIPLE-SCLEROSIS;
HEPATOCELLULAR-CARCINOMA; B10 CELLS; ULCERATIVE-COLITIS; AUTOIMMUNE
INFLAMMATION; PROTECTIVE IMMUNITY
AB Regulatory B cells (Bregs) are immune-modulating cells that affect the immune system by producing cytokines or cellular interactions. These cells have immunomodulatory effects on the immune system by cytokine production. The abnormalities in Bregs could be involved in various disorders such as autoimmunity, chronic infectious disease, malignancies, allergies, and primary immunodeficiencies are immune-related scenarios. Ongoing investigation could disclose the biology and the exact phenotype of these cells and also the assigned mechanisms of action of each subset, as a result, potential therapeutic strategies for treating immune-related anomalies. In this review, we collect the findings of human and mouse Bregs and the therapeutic efforts to change the pathogenicity of these cells in diverse disease.
C1 [Valizadeh, Amir; Rezaei, Nima; Fekrvand, Saba; Aghamohammadi, Asghar; Yazdani, Reza] Univ Tehran Med Sci, Res Ctr Immunodeficiencies, Pediat Ctr Excellence, Childrens Med Ctr, Tehran, Iran.
[Sanaei, Roozbeh] Iran Univ Med Sci, Immunol Res Ctr, Inst Immunol & Infect Dis, Tehran, Iran.
[Sanaei, Roozbeh; Rezaei, Nima] USERN, NIIMA, Tehran, Iran.
[Azizi, Gholamreza] Alborz Univ Med Sci, Noncommunicable Dis Res Ctr, Karaj, Iran.
C3 Tehran University of Medical Sciences; Iran University of Medical
Sciences
RP Yazdani, R (corresponding author), Childrens Med Ctr Hosp, 62 Qarib St,Keshavarz Blvd, Tehran 14194, Iran.
EM reza_yazdani86@yahoo.com
RI Sanaei, Roozbeh/GQH-3488-2022; Yazdani, Reza/LEM-2441-2024; Azizi,
Gholamreza/B-9477-2018; Aghamohammadi, Asghar/B-4167-2009; Rezaei,
Nima/B-4245-2008; Valizadeh, Amir/ABE-3424-2020
OI Valizadeh, Amir/0000-0001-5983-8527; Yazdani, Reza/0000-0002-5578-6595;
Fekrvand, Saba/0000-0001-7091-9651
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NR 207
TC 10
Z9 12
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0165-2478
EI 1879-0542
J9 IMMUNOL LETT
JI Immunol. Lett.
PD NOV
PY 2019
VL 215
BP 48
EP 59
DI 10.1016/j.imlet.2019.08.004
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA JP5XW
UT WOS:000498338300009
PM 31442542
DA 2025-01-07
ER
PT J
AU Loria, P
Carulli, L
Bertolotti, M
Lonardo, A
AF Loria, Paola
Carulli, Lucia
Bertolotti, Marco
Lonardo, Amedeo
TI Endocrine and liver interaction: the role of endocrine pathways in NASH
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
ID POLYCYSTIC-OVARY-SYNDROME; C VIRUS-INFECTION; GLUCOCORTICOID-RECEPTOR
AGONISTS; GROWTH-HORMONE DEFICIENCY; PRIMARY BILIARY-CIRRHOSIS;
HIGH-DENSITY-LIPOPROTEIN; FATTY LIVER; AUTOIMMUNE HEPATITIS;
THYROID-HORMONE; ADRENAL INSUFFICIENCY
AB This article reviews evidence that causally links hormonal disorders with hepatobiliary disease, and gives particular focus to nonalcoholic steatohepatitis (NASH). The downstream mechanisms by which endocrine disturbances cause liver disease might be similar to those involved in the development of primary liver disease. Hypothyroidism, for example, might lead to NASH, cirrhosis and potentially liver cancer via the development of hyperlipidemia and obesity. Patients with growth hormone deficiency have a metabolic-syndrome-like phenotype that is also associated with the development of NASH. Polycystic ovary syndrome is a common endocrine disorder that is often associated with insulin resistance, the metabolic syndrome, altered levels of liver enzymes and the development of NASH. recent findings support a role of dehydroepiandrosterone sulfate deficiency in the development of advanced NASH. in addition, adrenal failure is increasingly reported in patients with end stage liver disease and in patients who have received a liver transplant, which suggests a bidirectional relationship between liver and endocrine functions. Clinicians should, therefore, be aware of the potential role of endocrine disorders in patients with cryptogenic liver disease and of the effects of liver function on the endocrine system.
C1 [Loria, Paola; Carulli, Lucia; Bertolotti, Marco; Lonardo, Amedeo] Univ Modena & Reggio Emilia, Dipartimento Endocrinol Metab & Geriatria, NOCSAE Baggiovara, Modena, MO, Italy.
C3 Universita di Modena e Reggio Emilia
RP Loria, P (corresponding author), Univ Modena & Reggio Emilia, Dipartimento Endocrinol Metab & Geriatria, NOCSAE Baggiovara, Via Giardini 1355, Modena, MO, Italy.
EM paola.loria@unimore.it
RI Carulli, Lucia/AAA-4358-2019; Carulli, Lucia/G-3783-2016; Lonardo,
Amedeo/I-5911-2019; Bertolotti, Marco/P-6040-2015
OI Carulli, Lucia/0000-0001-7792-8542; Lonardo, Amedeo/0000-0001-9886-0698;
Bertolotti, Marco/0000-0001-6908-1820
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EP 247
DI 10.1038/nrgastro.2009.33
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 442PX
UT WOS:000265854200011
PM 19347015
DA 2025-01-07
ER
PT J
AU Fujita, K
Oura, K
Tadokoro, T
Nakahara, M
Tani, J
Morishita, A
Kobara, H
Tsutsui, K
Himoto, T
Masaki, T
AF Fujita, Koji
Oura, Kyoko
Tadokoro, Tomoko
Nakahara, Mai
Tani, Joji
Morishita, Asahiro
Kobara, Hideki
Tsutsui, Kunihiko
Himoto, Takashi
Masaki, Tsutomu
TI Prognosis of probable autoimmune hepatitis patients: a single-center
study in Japan
SO INTERNAL AND EMERGENCY MEDICINE
LA English
DT Article
DE Autoimmune hepatitis; Diagnoses; Prognoses; Cirrhosis; Hepatocellular
carcinoma; Biomarkers
AB Autoimmune hepatitis (AIH) is an idiopathic inflammatory liver disease with genetic susceptibility and unknown environmental triggers. The gold standard for diagnosis, International Autoimmune Hepatitis Group (IAIHG) scoring system, classifies AIH as definite or probable. Conventional research on probable AIH has focused on the Caucasian population and there is little data pertaining to the Asian population. This study aimed to assess and compare the prognosis of Japanese patients with probable and definite AIH. In the current study, patients with probable and definite AIH diagnosed based on IAIHG scores between 1987 and 2018 were enrolled. As a result, 72 patients with definite AIH and 49 patients with probable AIH were evaluated. Univariate analysis revealed age, fibrosis stage 4, and the fibrosis-4 index were prognostic factors for overall survival. Multivariate analysis indicated that age and liver cirrhosis significantly affected the overall survival. When the cut off albumin-bilirubin score was set appropriately, cirrhosis was differentially diagnosed using albumin-bilirubin score with 100% sensitivity and 70.5% specificity. Classification of probable or definite disease did not alter overall survival with statistical significance. In conclusion, our findings suggest that probable AIH should be managed as definite AIH is managed in Japanese population. The albumin-bilirubin score helps identify liver cirrhosis and is a prognostic biomarker for overall survival.
C1 [Fujita, Koji; Oura, Kyoko; Tadokoro, Tomoko; Nakahara, Mai; Tani, Joji; Morishita, Asahiro; Kobara, Hideki; Tsutsui, Kunihiko; Masaki, Tsutomu] Kagawa Univ, Dept Gastroenterol & Neurol, Fac Med, Kita Ku, 1750-1 Ikenobe, Miki, Kagawa 7610793, Japan.
[Himoto, Takashi] Kagawa Prefectural Univ Hlth Sci, Dept Med Technol, 281-1 Hara, Takamatsu, Kagawa 7610123, Japan.
C3 Kagawa University
RP Fujita, K (corresponding author), Kagawa Univ, Dept Gastroenterol & Neurol, Fac Med, Kita Ku, 1750-1 Ikenobe, Miki, Kagawa 7610793, Japan.; Himoto, T (corresponding author), Kagawa Prefectural Univ Hlth Sci, Dept Med Technol, 281-1 Hara, Takamatsu, Kagawa 7610123, Japan.
EM 92m7v9@med.kagawa-u.ac.jp; himoto@chs.pref.kagawa.jp
RI Fujita, Koji/X-4478-2019
OI Kobara, Hideki/0000-0002-8508-827X; Tadokoro, Tomoko/0000-0001-9975-386X
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NR 38
TC 1
Z9 2
U1 0
U2 1
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 1828-0447
EI 1970-9366
J9 INTERN EMERG MED
JI Intern. Emerg. Med.
PD NOV
PY 2021
VL 16
IS 8
BP 2155
EP 2162
DI 10.1007/s11739-021-02720-0
EA MAR 2021
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA WQ8XR
UT WOS:000635067600001
PM 33783693
DA 2025-01-07
ER
PT J
AU Xu, J
Chen, DZ
Jin, LL
Chen, ZK
Tu, YL
Huang, XZ
Xue, FB
Xu, JL
Chen, MZ
Wang, XD
Chen, YP
AF Xu, Jie
Chen, Dazhi
Jin, Lanling
Chen, Zhengkang
Tu, Yulu
Huang, Xiaozhe
Xue, Feiben
Xu, Jialu
Chen, Mingzhuan
Wang, Xiaodong
Chen, Yongping
TI Ubiquitously specific protease 4 inhibitor-Vialinin A attenuates
inflammation and fibrosis in S100-induced hepatitis mice through
Rheb/mTOR signalling
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE autoimmune hepatitis; mTOR; USP4; Vialinin A
ID HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; CELLS
AB Inflammation and fibrosis are major consequences of autoimmune hepatitis, however, the therapeutic mechanism remains to be investigated. USP4 is a deubiquitinating enzyme and plays an important role in tissue fibrosis and immune disease. Vialinin A is an extract from mushroom and is a specific USP4 inhibitor. However, there is lack of evidences that Vialinin A plays a role in autoimmune hepatitis. By employing S100-induced autoimmune hepatitis in mice and AML12 cell line, therapeutic mechanism of Vialinin A was examined. Inflammation was documented by liver histological staining and inflammatory cytokines. Fibrosis was demonstrated by Masson, Sirius red staining and fibrotic cytokines with western blot and real-time RT-PCR. In experimental animal, there were increases in inflammation and fibrosis as well as USP4, and which were reduced after treatment of Vialinin A. Vialinin A also reduced Rheb and phosphorylated mTOR. Moreover, in LPS-treated AML12 cells, LPS-induced USP4, inflammatory and fibrotic cytokines, phosphorylated mTOR and Rheb. Specific inhibitory siRNA of USP4 reduced USP4 level and the parameters mentioned above. In conclusion, USP4 was significantly elevated in autoimmune hepatitis mice and Vialinin A reduced USP4 level and attenuate inflammation and fibrosis in the liver. The mechanism may be related to regulation of Rheb/mTOR signalling.
C1 [Xu, Jie; Jin, Lanling; Chen, Zhengkang; Tu, Yulu; Huang, Xiaozhe; Xue, Feiben; Xu, Jialu; Chen, Mingzhuan; Wang, Xiaodong; Chen, Yongping] Wenzhou Med Univ, Dept Infect Dis, Zhejiang Prov Key Lab Accurate Diag & Treatment C, Wenzhou Key Lab Hepatol,Hepatol Inst,Affiliated H, Wenzhou 325025, Zhejiang, Peoples R China.
[Chen, Dazhi] Peking Univ First Hosp, Dept Gastroenterol, Beijing, Peoples R China.
C3 Wenzhou Medical University
RP Chen, YP (corresponding author), Wenzhou Med Univ, Dept Infect Dis, Zhejiang Prov Key Lab Accurate Diag & Treatment C, Wenzhou Key Lab Hepatol,Hepatol Inst,Affiliated H, Wenzhou 325025, Zhejiang, Peoples R China.
EM did@wzhospital.cn
OI xu, jie/0000-0002-7758-7597
FU National Natural Science Foundation of China (NSFC) [81570514, 81770585,
81600466]; National Science and Technology Major Project
[2017ZX10202201, 2017ZX10203201, 2018ZX10725506-001]; Scientific
Research Seed Fund of Peking University First Hospital [BMU2020PYB005]
FX National Natural Science Foundation of China (NSFC), Grant/Award Number:
81570514, 81770585 and 81600466; National Science and Technology Major
Project, Grant/Award Number: 2017ZX10202201, 2017ZX10203201 and
2018ZX10725506-001; Scientific Research Seed Fund of Peking University
First Hospital, Grant/Award Number: BMU2020PYB005
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NR 27
TC 12
Z9 12
U1 0
U2 17
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1582-1838
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD JAN
PY 2021
VL 25
IS 2
BP 1140
EP 1150
DI 10.1111/jcmm.16180
EA DEC 2020
PG 11
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA PS9MN
UT WOS:000596571000001
PM 33295107
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Jiang, XJ
Karlsen, TH
AF Jiang, Xiaojun
Karlsen, Tom H.
TI Genetics of primary sclerosing cholangitis and pathophysiological
implications
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
ID GENOME-WIDE ASSOCIATION; INFLAMMATORY-BOWEL-DISEASE; MUCOSA-ASSOCIATED
MICROBIOTA; PRIMARY BILIARY-CIRRHOSIS; CD4(+) T-CELLS; NF-KAPPA-B;
ULCERATIVE-COLITIS PATIENTS; EVIDENCE-BASED CONSENSUS; CRIGLER-NAJJAR
SYNDROME; INDUCED LIVER-INJURY
AB Primary sclerosing cholangitis (PSC) is a chronic disease leading to fibrotic scarring of the intrahepatic and extrahepatic bile ducts, causing considerable morbidity and mortality via the development of cholestatic liver cirrhosis, concurrent IBD and a high risk of bile duct cancer. Expectations have been high that genetic studies would determine key factors in PSC pathogenesis to support the development of effective medical therapies. Through the application of genome-wide association studies, a large number of disease susceptibility genes have been identified. The overall genetic architecture of PSC shares features with both autoimmune diseases and IBD. Strong human leukocyte antigen gene associations, along with several susceptibility genes that are critically involved in T-cell function, support the involvement of adaptive immune responses in disease pathogenesis, and position PSC as an autoimmune disease. In this Review, we survey the developments that have led to these gene discoveries. We also elaborate relevant interpretations of individual gene findings in the context of established disease models in PSC, and propose relevant translational research efforts to pursue novel insights.
C1 [Jiang, Xiaojun; Karlsen, Tom H.] Oslo Univ Hosp, Rikshosp, Div Canc Med Surg & Transplantat, Norwegian PSC Res Ctr,Dept Transplantat Med, Postbox 4950, N-0424 Oslo, Norway.
[Jiang, Xiaojun; Karlsen, Tom H.] Univ Oslo, Fac Med, Inst Clin Med, Postbox 1171 Blindern, N-0318 Oslo, Norway.
[Jiang, Xiaojun; Karlsen, Tom H.] Oslo Univ Hosp, Rikshosp, Div Canc Med Surg & Transplantat, Res Inst Internal Med, Postbox 4950 Nydalen, N-0424 Oslo, Norway.
[Jiang, Xiaojun; Karlsen, Tom H.] Univ Oslo, Fac Med, Inst Clin Med, KG Jebsen Inflammat Res Ctr, Postbox 1171 Blindern, N-0318 Oslo, Norway.
C3 University of Oslo; National Hospital Norway; University of Oslo;
University of Oslo; National Hospital Norway; University of Oslo
RP Karlsen, TH (corresponding author), Oslo Univ Hosp, Rikshosp, Div Canc Med Surg & Transplantat, Norwegian PSC Res Ctr,Dept Transplantat Med, Postbox 4950, N-0424 Oslo, Norway.
EM t.h.karlsen@medisin.uio.no
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NR 253
TC 93
Z9 96
U1 1
U2 18
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5045
EI 1759-5053
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD MAY
PY 2017
VL 14
IS 5
BP 279
EP 295
DI 10.1038/nrgastro.2016.154
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ET1AF
UT WOS:000399997400005
PM 28293027
DA 2025-01-07
ER
PT J
AU Williamson, KD
Chapman, RW
AF Williamson, Kate D.
Chapman, Roger W.
TI Primary sclerosing cholangitis: a clinical update
SO BRITISH MEDICAL BULLETIN
LA English
DT Article
DE primary sclerosing cholangitis; sclerosing cholangitis;
cholangiocarcinoma; cholestasis; inflammatory bowel disease;
ursodeoxycholic acid; CCR9; colorectal cancer; genetics
ID INFLAMMATORY-BOWEL-DISEASE; GENOME-WIDE ASSOCIATION; IMMUNOGLOBULIN
G4-ASSOCIATED CHOLANGITIS; THYMUS-EXPRESSED CHEMOKINE; DOSE
URSODEOXYCHOLIC ACID; POUCH-ANAL ANASTOMOSIS; LIVER-TRANSPLANTATION;
ULCERATIVE-COLITIS; ALKALINE-PHOSPHATASE; RISK LOCI
AB Primary sclerosing cholangitis (PSC) is a progressive cholestatic disorder that ultimately can lead to cirrhosis, liver failure, malignancy and death. It is strongly associated with inflammatory bowel disease (IBD), and though a rare disease, its incidence is increasing. There are no proven medical therapies for PSC.
Ovid Medline was utilised to search for articles with keywords 'sclerosing cholangitis' and 'cholangiocarcinoma' and containing titles 'primary sclerosing cholangitis', and references of these papers were cross-referenced for further relevant manuscripts.
PSC is a rare disease, and there is a strong association with risk loci within the major histocompatibility complex and other genes common to other autoimmune diseases. PSC is a premalignant condition, associated with higher rates of hepatobiliary and colorectal cancer in patients with ulcerative colitis (UC).
The pathogenesis is unclear, and competing theories exist surrounding toxic bile acids, enhanced homing of particular T cells from the gut to the liver and increased passage of toxins to the liver through a permeable bowel wall. It is unclear whether the higher rate of colonic cancer in PSC/UC occurs in PSC/Crohn's disease. Ursodeoxycholic acid therapy reduces liver enzymes but has not been shown to improve survival. It may reduce the prevalence of bowel cancer.
Recent genetic studies have revealed new risk loci, pointing to the importance of the immune system and its interaction with the biome.
On the basis of the genetic studies discussed earlier, novel agents are being developed and trialled in the treatment of PSC.
C1 [Williamson, Kate D.; Chapman, Roger W.] Univ Oxford, Nuffield Dept Clin Med, Oxford, England.
[Williamson, Kate D.; Chapman, Roger W.] John Radcliffe Hosp, Translat Gastroenterol Unit, Oxford OX3 9DU, England.
C3 University of Oxford; University of Oxford
RP Chapman, RW (corresponding author), John Radcliffe Hosp, Translat Gastroenterol Unit, Level 5,Headley Way, Oxford OX3 9DU, England.
EM roger.chapman@ndm.ox.ac.uk
OI Lynch, Kate/0000-0001-7748-2165
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Williamson KD, 2010, OXFORD TXB MED
NR 78
TC 36
Z9 44
U1 0
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0007-1420
EI 1471-8391
J9 BRIT MED BULL
JI Br. Med. Bull.
PD JUN
PY 2015
VL 114
IS 1
BP 53
EP 64
DI 10.1093/bmb/ldv019
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA CJ7HG
UT WOS:000355664800006
PM 25981516
OA Bronze
DA 2025-01-07
ER
PT J
AU He, RJ
Yu, ZH
Zhang, RY
Zhang, ZY
AF He, Rong-jun
Yu, Zhi-hong
Zhang, Ruo-yu
Zhang, Zhong-yin
TI Protein tyrosine phosphatases as potential therapeutic targets
SO ACTA PHARMACOLOGICA SINICA
LA English
DT Review
DE drug target; protein tyrosine phosphatases; PTP1B; Src homology
phosphotyrosyl phosphatase 2; lymphoid-specific tyrosine phosphatase;
Fas associated phosphatase-1; CD45 antigen; striatal enriched tyrosine
phosphatases; mitogen-activated protein kinase phosphatases;
phosphatases of regenerating liver-1; low molecular weight PTPs; CDC25
ID INSULIN-RECEPTOR SUBSTRATE-1; NEGATIVE REGULATORY TYROSINE;
SMALL-MOLECULE INHIBITOR; HUMAN COLORECTAL-CANCER; TUMOR-SUPPRESSOR
GENE; LIVER 2 PRL2; KINASE PHOSPHATASE-1; REGENERATING LIVER; IN-VIVO;
LMW-PTP
AB Protein tyrosine phosphorylation is a key regulatory process in virtually all aspects of cellular functions. Dysregulation of protein tyrosine phosphorylation is a major cause of human diseases, such as cancers, diabetes, autoimmune disorders, and neurological diseases. Indeed, protein tyrosine phosphorylation-mediated signaling events offer ample therapeutic targets, and drug discovery efforts to date have brought over two dozen kinase inhibitors to the clinic. Accordingly, protein tyrosine phosphatases (PTPs) are considered next-generation drug targets. For instance, PTP1B is a well-known targets of type 2 diabetes and obesity, and recent studies indicate that it is also a promising target for breast cancer. SHP2 is a bona-fide oncoprotein, mutations of which cause juvenile myelomonocytic leukemia, acute myeloid leukemia, and solid tumors. In addition, LYP is strongly associated with type 1 diabetes and many other autoimmune diseases. This review summarizes recent findings on several highly recognized PTP family drug targets, including PTP1B, Src homology phosphotyrosyl phosphatase 2 (SHP2), lymphoid-specific tyrosine phosphatase (LYP), CD45, Fas associated phosphatase-1 (FAP-1), striatal enriched tyrosine phosphatases (STEP), mitogen-activated protein kinase/dual-specificity phosphatase 1 (MKP-1), phosphatases of regenerating liver-1 (PRL), low molecular weight PTPs (LMWPTP), and CDC25. Given that there are over 100 family members, we hope this review will serve as a road map for innovative drug discovery targeting PTPs.
C1 [He, Rong-jun; Yu, Zhi-hong; Zhang, Ruo-yu; Zhang, Zhong-yin] Indiana Univ, Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA.
C3 Indiana University System; Indiana University Indianapolis
RP Zhang, ZY (corresponding author), Indiana Univ, Sch Med, Dept Biochem & Mol Biol, 635 Barnhill Dr, Indianapolis, IN 46202 USA.
EM zyzhang@iu.edu
RI He, Rongjun/H-5791-2011; zhang, ruoyu/LCD-4543-2024; yu,
zhihong/KRO-4146-2024
FU National Institutes of Health [CA69202, CA126937]
FX This work was supported in part by National Institutes of Health Grants
CA69202 and CA126937.
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NR 277
TC 264
Z9 307
U1 17
U2 253
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1671-4083
EI 1745-7254
J9 ACTA PHARMACOL SIN
JI Acta Pharmacol. Sin.
PD OCT
PY 2014
VL 35
IS 10
BP 1227
EP 1246
DI 10.1038/aps.2014.80
PG 20
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA AQ4AO
UT WOS:000342734800001
PM 25220640
OA Bronze, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Czaja, AJ
AF Czaja, Albert J.
TI Animal models of autoimmune hepatitis
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE genetic engineering; humanization; models; preconditioning; transgenic
ID MAJOR HISTOCOMPATIBILITY COMPLEX; CHRONIC ACTIVE HEPATITIS; REGULATORY
T-CELLS; SINUSOIDAL ENDOTHELIAL-CELLS; NATURAL-KILLER-CELLS; MOLECULAR
MIMICRY; LIVER-DISEASE; MURINE MODEL; HEPATOCELLULAR-CARCINOMA;
CYTOCHROMES P450
AB Animal models of autoimmune hepatitis have been important in defining pathogenic mechanisms, and they promise to aid in the evaluation of new molecular and cellular treatments. They have evolved from models based on crude liver homogenates that produced a transient hepatitis to models that express antibodies to human antigens, manifest liver-infiltrating T cells, persist for at least 3 months and develop fibrosis. Animal models allow the study of autoimmune hepatitis from its inception, and they can detail the progression of pathological events. Key imbalances in counter-regulatory mechanisms can be isolated and manipulated. Models can be humanized by the insertion of human genetic promoters and the expression of human antigens. Genetic engineering and preconditioning have been milestones in the evolution of animal models. Vaccination or infection of murine models with viral vectors carrying human antigens are the most recent developments. Animal models promise to extend the knowledge of etiological agents and improve treatment algorithms.
C1 Mayo Clin, Coll Med, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Czaja, AJ (corresponding author), Mayo Clin, Coll Med, 200 1st St SW, Rochester, MN 55905 USA.
EM czaja.albert@mayo.edu
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NR 184
TC 21
Z9 24
U1 0
U2 9
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD AUG
PY 2010
VL 4
IS 4
BP 429
EP 443
DI 10.1586/EGH.10.42
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 860YA
UT WOS:000297983200012
PM 20678017
DA 2025-01-07
ER
PT J
AU Zhang, YF
Wang, YR
Ding, J
Liu, P
AF Zhang, Yifan
Wang, Yiru
Ding, Jie
Liu, Ping
TI Efferocytosis in multisystem diseases
SO MOLECULAR MEDICINE REPORTS
LA English
DT Review
DE efferocytosis; cardiovascular diseases; respiratory diseases; liver and
intestine diseases; autoimmune diseases; neurodegenerative diseases
ID RECEPTOR TYROSINE KINASE; SYSTEMIC-LUPUS-ERYTHEMATOSUS; APOPTOTIC CELL
ACCUMULATION; MACROPHAGE PHAGOCYTIC FUNCTION;
INFLAMMATORY-BOWEL-DISEASE; COLLAGEN-INDUCED ARTHRITIS; ACUTE LUNG
INJURY; EAT ME SIGNAL; OXIDATIVE STRESS; UP-REGULATION
AB Efferocytosis, the phagocytosis of apoptotic cells performed by both specialized phagocytes (such as macrophages) and non-specialized phagocytes (such as epithelial cells), is involved in tissue repair and homeostasis. Effective efferocytosis prevents secondary necrosis, terminates inflammatory responses, promotes self-tolerance and activates pro-resolving pathways to maintain homeostasis. When efferocytosis is impaired, apoptotic cells that could not be cleared in time aggregate, resulting in the necrosis of apoptotic cells and release of pro-inflammatory factors. In addition, defective efferocytosis inhibits the intracellular cholesterol reverse transportation pathways, which may lead to atherosclerosis, lung damage, non-alcoholic fatty liver disease and neurodegenerative diseases. The uncleared apoptotic cells can also release autoantigens, which can cause autoimmune diseases. Cancer cells escape from phagocytosis via efferocytosis. Therefore, new treatment strategies for diseases related to defective efferocytosis are proposed. This review illustrated the mechanisms of efferocytosis in multisystem diseases and organismal homeostasis and the pathophysiological consequences of defective efferocytosis. Several drugs and treatments available to enhance efferocytosis are also mentioned in the review, serving as new evidence for clinical application.
C1 [Zhang, Yifan; Wang, Yiru; Ding, Jie; Liu, Ping] Shanghai Univ Tradit Chinese Med, Longhua Hosp, 725 South Wan Ping Rd, Shanghai 200032, Peoples R China.
[Zhang, Yifan; Wang, Yiru; Ding, Jie] Shanghai Univ Tradit Chinese Med, Shanghai 201203, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine; Shanghai University
of Traditional Chinese Medicine
RP Liu, P (corresponding author), Shanghai Univ Tradit Chinese Med, Longhua Hosp, 725 South Wan Ping Rd, Shanghai 200032, Peoples R China.
EM liuping0207@126.com
RI Wang, Yiru/JMB-2281-2023
FU Natural Science Foundation of China [81873117]
FX The present review was supported by the Natural Science Foundation of
China (grant nos. 81873117).
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NR 217
TC 11
Z9 13
U1 10
U2 41
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD JAN
PY 2022
VL 25
IS 1
AR 13
DI 10.3892/mmr.2021.12529
PG 15
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA XA0MN
UT WOS:000720352600001
PM 34779503
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Björnsson, ES
AF Bjornsson, Einar Stefan
TI The Epidemiology of Newly Recognized Causes of Drug-Induced Liver
Injury: An Update
SO PHARMACEUTICALS
LA English
DT Review
DE drug-induced liver injury; checkpoint inhibitors; COVID vaccination;
AIH; DI-ALH; green tea extract
ID IDIOPATHIC AUTOIMMUNE HEPATITIS; GREEN TEA; SARS-COV-2 VACCINATION;
COMBINED NIVOLUMAB; COVID-19 VACCINE; HEPATOTOXICITY; POPULATION;
CAUSALITY; DISEASE; RISK
AB The incidence and prevalence of drug-induced liver injury appear to be increasing globally, for example, with the introduction of checkpoint inhibitors. Several reviews have been published in the last decade on the epidemiology of DILI, both among hospitalized patients and in the general population, as well as from retrospective and prospective studies on DILI. Most of these reviews have not focused on newly recognized agents that have recently changed the landscape of DILI. Apart from liver injury associated with antibiotics, oncological agents, particularly checkpoint inhibitors, are increasingly being recognized as causing liver injury. The type of liver injury associated with these agents is not idiosyncratic but rather an indirect type of injury. Furthermore, recently, COVID-19 vaccines and green tea extract have been found to lead to liver injury. Checkpoint inhibitors have revolutionized the treatment of many malignancies, such as malignant melanoma, lung cancer, and renal cancer. Via the activation of T cells, they can increase immune activity against malignant cells, but at the same time, they can decrease immune tolerance and therefore lead to immune-related adverse effects in many organs. The most common adverse effect in clinical practice is liver injury. A recent prospective study demonstrated an 8% frequency of DILI due to the use of checkpoint inhibitors among patients with malignant melanoma and renal cancer. This rate is much higher than observed with drugs, leading to idiosyncratic liver injury. Shortly after the implementation of the worldwide vaccination program against COVID-19, several case reports were published on suspected vaccination-induced autoimmune-like hepatitis occurring shortly after the vaccination. At first, these reports were met with skepticism, but currently, around 100 reports have been published, and cases of positive recurrence have been reported. The clinical, biochemical, immunological, and histological features are indistinguishable from classic autoimmune hepatitis (AIH). These reactions are very similar to drug-induced autoimmune-like hepatitis (DI-ALH) due to drugs such as nitrofurantoin, minocycline, and infliximab, which do not relapse after a short course of corticosteroids, which is the general rule in classic autoimmune hepatitis (AIH). Green tea extract has been found to be a well-documented cause of acute hepatocellular liver injury with jaundice. A strong HLA association has been reported, showing a high prevalence of HLA-B*35:01 among patients suffering from green tea-induced liver injury. Overall, 3% of patients recruited in the DILIN study were supplemented with green tea extract as one of the ingredients. In a prospective population-based study from Iceland, green tea was implicated in approximately 8% of patients with DILI.
C1 [Bjornsson, Einar Stefan] Univ Iceland, Natl Univ Hosp Iceland, Fac Med, Dept Internal Med,Div Gastroenterol & Hepatol, IS-101 Reykjavik, Iceland.
C3 Landspitali National University Hospital; University of Iceland
RP Björnsson, ES (corresponding author), Univ Iceland, Natl Univ Hosp Iceland, Fac Med, Dept Internal Med,Div Gastroenterol & Hepatol, IS-101 Reykjavik, Iceland.
EM einarsb@landspitali.is
OI Bjornsson, Einar Stefan/0000-0002-8392-0632
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NR 85
TC 0
Z9 0
U1 1
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1424-8247
J9 PHARMACEUTICALS-BASE
JI Pharmaceuticals
PD APR
PY 2024
VL 17
IS 4
AR 520
DI 10.3390/ph17040520
PG 11
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA OX7L4
UT WOS:001210640800001
PM 38675480
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kulkarni, AA
Soni, P
Sharma, VK
Bal, A
Rana, SS
Gupta, R
AF Kulkarni, Aditya A.
Soni, Praveen
Sharma, Vipan K.
Bal, Amanjit
Rana, Surinder S.
Gupta, Rajesh
TI Immunoglobulin G4-related disease mimicking gallbladder cancer with
associated choledochal cyst: A case report of a malignant masquerade
SO JGH OPEN
LA English
DT Article
DE autoimmune disease; gallbladder mass; cholecystitis; case report;
immunoglobulin4-related sclerosing disease
AB Immunoglobulin G4 (IgG4)-related disease is a recently described autoimmune disease that can involve diverse organ systems, causing pancreatitis, cholangitis, retroperitoneal fibrosis, and thyroiditis to name a few. Key histological features include storiform fibrosis, obliterative venulitis, and intense inflammatory infiltrate composed of lymphoplasmacytic cells. The disease has a tendency to present with mass-forming lesions, often difficult to differentiate from malignant processes. We report the case of a 48-year-old male from an area endemic for gallbladder cancer (north India). He presented with a short history of abdominal pain and was found to have asymmetric thickening of the gallbladder wall with a soft-tissue mass invading the adjacent liver. In addition, the bile duct was dilated throughout its extent. A clinical and radiological diagnosis of gallbladder cancer with choledochal cyst was made, and the patient underwent radical cholecystectomy with bile duct excision. Histopathology surprisingly demonstrated IgG4-related disease with no evidence of malignancy. Notably, serum levels of immunoglobulins were found to be normal. Preoperative diagnosis was challenging due to the absence of other manifestations. IgG4-related disease is a possible diagnostic pitfall and should be included as a possible differential diagnosis for gallbladder masses.
C1 [Kulkarni, Aditya A.; Soni, Praveen; Sharma, Vipan K.; Gupta, Rajesh] Postgrad Inst Med Educ & Res, Div Surg Gastroenterol, Dept Gen Surg, Chandigarh 160012, India.
[Bal, Amanjit] Postgrad Inst Med Educ & Res, Dept Histopathol, Chandigarh, India.
[Rana, Surinder S.] Postgrad Inst Med Educ & Res, Dept Gastroenterol, Chandigarh, India.
C3 Post Graduate Institute of Medical Education & Research (PGIMER),
Chandigarh; Post Graduate Institute of Medical Education & Research
(PGIMER), Chandigarh; Post Graduate Institute of Medical Education &
Research (PGIMER), Chandigarh
RP Gupta, R (corresponding author), Postgrad Inst Med Educ & Res, Div Surg Gastroenterol, Dept Gen Surg, Chandigarh 160012, India.
EM rajsarakshi@gmail.com
RI Kulkarni, Aditya/AAC-1487-2022; , Praveen Soni/KLC-7640-2024
OI , Praveen Soni/0009-0004-3795-1683; Kulkarni, Aditya/0000-0002-3432-2484
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Z9 6
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2397-9070
J9 JGH OPEN
JI JGH Open
PD DEC
PY 2019
VL 3
IS 6
BP 536
EP 539
DI 10.1002/jgh3.12154
PG 4
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA JT9FQ
UT WOS:000501287500016
PM 31832557
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Streeter, HB
Wraith, DC
AF Streeter, Heather B.
Wraith, David C.
TI Manipulating antigen presentation for antigen-specific immunotherapy of
autoimmune diseases
SO CURRENT OPINION IN IMMUNOLOGY
LA English
DT Review
ID MYELIN BASIC-PROTEIN; DENDRITIC CELLS; MULTIPLE-SCLEROSIS; T-CELLS;
PEPTIDE; INDUCTION; TOLERANCE; THERAPY
AB Current treatments for autoimmune diseases do not address the immune pathology underlying their initiation and progression and too often rely on non-specific immunosuppressive drugs for control of symptoms. Antigenspecific immunotherapy aims to induce tolerance selectively among the cells causing the disease while leaving the rest of the adaptive immune system capable of protecting against infectious diseases and cancers. Here we describe how novel approaches for antigen-specific immunotherapy are designed to manipulate antigen presentation and promote tolerance to specific self-antigens. This analysis points to liver antigen presenting cells, targeted by carrier particles, and steady-state dendritic cells, to which antigen-processing independent T-cell epitopes (apitopes) bind directly, as the principal targets for antigen-specific immunotherapy. Delivery of antigens to these cells holds great promise for effective control of this rapidly expanding group of diseases.
C1 [Streeter, Heather B.; Wraith, David C.] Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham B15 2TT, W Midlands, England.
C3 University of Birmingham
RP Wraith, DC (corresponding author), Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham B15 2TT, W Midlands, England.
EM d.wraith@bham.ac.uk
FU University of Birmingham, Medical Research Council [MR/K007645/1,
MR/K015990/1]; Wellcome Trust [204565/Z/16/Z]; EU-IMI; Diabetes UK;
Helmsley Trust; Children's Liver Disease Foundation; Wellcome Trust
[204565/Z/16/Z] Funding Source: Wellcome Trust
FX The authors acknowledge support from the University of Birmingham,
Medical Research Council (MR/K007645/1, MR/K015990/1) , Wellcome Trust
(204565/Z/16/Z) , EU-IMI (RTCure consortium) , Diabetes UK, Helmsley
Trust & Children's Liver Disease Foundation.
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NR 54
TC 17
Z9 18
U1 0
U2 5
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0952-7915
EI 1879-0372
J9 CURR OPIN IMMUNOL
JI Curr. Opin. Immunol.
PD JUN
PY 2021
VL 70
SI SI
BP 75
EP 81
DI 10.1016/j.coi.2021.03.019
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA UA1NH
UT WOS:000684932100012
PM 33878516
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Chen, CC
Chang, YT
Liu, HN
Chen, YJ
AF Chen, Chih-Chiang
Chang, Yun-Ting
Liu, Han-Nan
Chen, Yi-Ju
TI Cancer risk in patients with alopecia areata: a nationwide
population-based matched cohort study
SO CANCER MEDICINE
LA English
DT Article
DE Alopecia areata; autoimmune disorder; breast cancer; cancer risk; kidney
cancer; lymphoma; urinary bladder cancer
ID T-CELL LYMPHOMA; HODGKINS-DISEASE; NK CELLS; ASSOCIATION; UNIVERSALIS;
PREVALENCE; EXPRESSION; PROGNOSIS; IMMUNITY; RECEPTOR
AB Alopecia areata (AA) is an organ-specific autoimmune disorder. Defective immune system related disorders are prone to increase the risk of cancer formation. However, the association among AA and variety of cancer types had never been studied. A nationwide population-based matched cohort study was conducted to evaluate the cancer risk in patients with AA. Records from Taiwan National Health Insurance Research Database were analyzed. Cases of AA from 1997 to 2013 and cancers registered in the catastrophic illness profile from the same time period were collected. The standard incidence ratio (SIR) of each cancer was calculated. In total, 2099 cancers among 162,499 patients with AA and without prior cancers were identified. The overall cancer risks in AA patients were slightly decreased, especially among male subjects (SIR: 0.89). Refer to individual cancer, the cancer risk of nonmelanoma skin cancer (NMSC) (SIR: 0.59), upper GI cancer (SIR: 0.70), liver cancer (SIR: 0.82), uterine, and cervix cancer (SIR: 0.84) were significantly lower in patients with AA. In contrast, AA patients were inclined to have lymphoma, breast cancer, kidney, and urinary bladder cancer with the SIR of 1.55, 2.93, and 2.95, respectively. Age stratified analyses revealed female AA patients younger than 50 years old have even higher risk of breast cancer (SIR: 3.37). Further sensitivity analysis showed similar results after excluding major autoimmune disorders. Cancer risk in AA patients is organ specific, and it is not associated with the underlying autoimmune disorders in patients with AA.
C1 [Chen, Chih-Chiang; Chen, Yi-Ju] Natl Yang Ming Univ, Inst Clin Med, Taipei, Taiwan.
[Chen, Chih-Chiang; Chang, Yun-Ting; Liu, Han-Nan; Chen, Yi-Ju] Natl Yang Ming Univ, Dept Dermatol, Taipei, Taiwan.
[Chen, Chih-Chiang; Chang, Yun-Ting; Liu, Han-Nan] Taipei Vet Gen Hosp, Dept Dermatol, Taipei, Taiwan.
[Chen, Yi-Ju] Taichung Vet Gen Hosp, Dept Dermatol, Taichung, Taiwan.
C3 National Yang Ming Chiao Tung University; National Yang Ming Chiao Tung
University; Taipei Veterans General Hospital; Taichung Veterans General
Hospital
RP Chen, YJ (corresponding author), Taichung Vet Gen Hosp, Dept Dermatol, Taichung, Taiwan.; Chen, YJ (corresponding author), Natl Yang Ming Univ, Sch Med, Fac Med, 1650,Sec 4,Taiwan Blvd, Taichung 407, Taiwan.
EM yjchenmd@vghtc.gov.tw
OI Chen, Yi-Ju/0000-0001-8932-5095
FU Taipei Veterans General Hospital [VN104-12, VN106-13, VN107-10,
V104C-055, V105C-033, V106C-030, V106D25-002-MY3, V107C-124,
VGHUST104-G1-1-1, VGHUST105-G1-4-1]; [NSC MOST 104-2314-B-010-051 MY3];
[TCVGH-1046802]; [MOST 104-2314-B-075-054-MY3]; [MOST
105-2628-B-010-016-MY3]
FX Yi-Ju Chen is funded by grants NSC MOST 104-2314-B-010-051 MY3, and
TCVGH-1046802. Chih-Chiang Chen, Yun-Ting Chang, and Han-Nan Liu are
funded by MOST 104-2314-B-075-054-MY3, MOST 105-2628-B-010-016-MY3,
Taipei Veterans General Hospital (VN104-12, VN106-13, VN107-10,
V104C-055, V105C-033, V106C-030, V106D25-002-MY3, V107C-124,
VGHUST104-G1-1-1, VGHUST105-G1-4-1).
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NR 40
TC 15
Z9 15
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD MAY
PY 2018
VL 7
IS 5
BP 2153
EP 2159
DI 10.1002/cam4.1448
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GF4ZG
UT WOS:000431972900054
PM 29577672
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Karlsen, TH
Lammert, F
Thompson, RJ
AF Karlsen, Tom H.
Lammert, Frank
Thompson, Richard J.
TI Genetics of liver disease: From pathophysiology to clinical practice
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Human genetics; Mendelian disease; Multifactorial disease
ID GENOME-WIDE ASSOCIATION; SALT EXPORT PUMP; FAMILIAL INTRAHEPATIC
CHOLESTASIS; CRIGLER-NAJJAR SYNDROME; CHRONIC HEPATITIS-B;
HEPATOCELLULAR-CARCINOMA; IDENTIFIES VARIANTS; MDR3 GENE; SPONTANEOUS
CLEARANCE; AUTOIMMUNE HEPATITIS
AB Paralleling the first 30 years of the Journal of Hepatology we have witnessed huge advances in our understanding of liver disease and physiology. Genetic advances have played no small part in that. Initial studies in the 1970s and 1980s identified the strong major histocompatibility complex associations in autoimmune liver diseases. During the 1990s, developments in genomic technologies drove the identification of genes responsible for Mendelian liver diseases. Over the last decade, genome-wide association studies have allowed for the dissection of the genetic susceptibility to complex liver disorders, in which also environmental co-factors play important roles. Findings have allowed the identification and elaboration of pathophysiological processes, have indicated the need for reclassification of liver diseases and have already pointed to new disease treatments. In the immediate future genetics will allow further stratification of liver diseases and contribute to personalized medicine. Challenges exist with regard to clinical implementation of rapidly developing technologies and interpretation of the wealth of accumulating genetic data. The historical perspective of genetics in liver diseases illustrates the opportunities for future research and clinical care of our patients. (C) 2015 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Karlsen, Tom H.] Oslo Univ Hosp, Rigshosp, Norwegian PSC Res Ctr, Oslo, Norway.
[Karlsen, Tom H.] Oslo Univ Hosp, Rigshosp, Gastroenterol Sect, Dept Transplantat Med,Div Canc Med Surg & Transpl, Oslo, Norway.
[Karlsen, Tom H.] Univ Oslo, Inst Clin Med, Oslo, Norway.
[Lammert, Frank] Univ Saarland, Med Ctr, Dept Med 2, Kirrberger Str, D-66421 Homburg, Germany.
[Lammert, Frank] Univ Saarland, D-66123 Saarbrucken, Germany.
[Thompson, Richard J.] Kings Coll London, Inst Liver Studies, Div Transplantat Immunol & Mucosal Biol, London WC2R 2LS, England.
C3 University of Oslo; National Hospital Norway; University of Oslo;
National Hospital Norway; University of Oslo; Saarland University;
Saarland University; University of London; King's College London
RP Lammert, F (corresponding author), Univ Saarland, Med Ctr, Dept Med 2, Kirrberger Str, D-66421 Homburg, Germany.
EM frank.lammert@uks.eu
RI Thompson, Richard/B-7954-2009
OI Thompson, Richard/0000-0001-5652-0150
FU Medical Research Council [MR/J006742/1] Funding Source: Medline
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NR 109
TC 61
Z9 66
U1 1
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2015
VL 62
SU 1
BP S6
EP S14
DI 10.1016/j.jhep.2015.02.025
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CG6JE
UT WOS:000353405400003
PM 25920091
OA hybrid
DA 2025-01-07
ER
PT J
AU Wörns, MA
Teufel, A
Kanzler, S
Shrestha, A
Victor, A
Otto, G
Lohse, AW
Galle, PR
Höhler, T
AF Woerns, Marcus A.
Teufel, Andreas
Kanzler, Stephan
Shrestha, Annette
Victor, Anja
Otto, Gerd
Lohse, Ansgar W.
Galle, Peter R.
Hoehler, Thomas
TI Incidence of HAV and HBV infections and vaccination rates in patients
with autoimmune liver diseases
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID HEPATITIS-B-VACCINE; PRIMARY BILIARY-CIRRHOSIS; CHRONIC ACTIVE
HEPATITIS; C VIRUS-INFECTION; A-VIRUS; HEPATOCELLULAR-CARCINOMA;
FULMINANT-HEPATITIS; RISK-FACTORS; TRANSPLANTATION; IMMUNOGENICITY
AB OBJECTIVES: Hepatitis A virus (HAV) or hepatitis B virus (HBV) superinfection is associated with an increased mortality in patients with chronic liver diseases (CLD). Despite official recommendations, it was reported that the vaccination rate against HAV is low in patients with chronic hepatitis C infection. To evaluate the situation in patients with autoimmune liver diseases, we conducted a retrospective cohort study.
METHODS: Susceptibility to HAV and HBV infections, course of HAV and HBV infections, vaccination rates against HAV and HBV, and efficacy of hepatitis A/B vaccines were evaluated by antibody testing in 225 patients with autoimmune liver diseases during 1,677 person-years.
RESULTS: Susceptibility to HAV/HBV infection was 51/86%. Incidence of HAV/HBV infection was 1.3/1.4 per 1,000 person-years. One HAV infection occurred, but the patient recovered spontaneously. Two patients were HBV-infected after receiving an anti-HBc-positive (antibody to hepatitis B core antigen) donor graft during orthotopic liver transplantation, and one of them developed chronic HBV infection. Vaccination rates were 11% (HBV) and 13% (HAV), respectively. Seventy-six percent of the vaccinated patients (HBV vaccine) developed anti-HBs (antibody to hepatitis surface antigen) >= 10 UI/L. Ten out of 13 vaccinated patients, showing a low or nonresponse to hepatitis B vaccine, had concomitant immunosuppressive therapy. Anti-HAV was detectable in all patients after administration of HAV vaccine.
CONCLUSIONS: Patients with autoimmune liver diseases have a high susceptibility to HAV and HBV infections. Vaccination rates are low in this patient cohort and efficacy of hepatitis B vaccine is reduced due to immunosuppressive therapy. Improving adherence to vaccine recommendations is essential to prevent HAV and HBV infections in patients with autoimmune liver diseases.
C1 [Woerns, Marcus A.; Teufel, Andreas; Kanzler, Stephan; Shrestha, Annette; Galle, Peter R.] Johannes Gutenberg Univ Mainz, Dept Internal Med 1, D-55101 Mainz, Germany.
[Victor, Anja] Johannes Gutenberg Univ Mainz, Inst Med Biometry Epidemiol & Informat, D-55101 Mainz, Germany.
[Otto, Gerd] Johannes Gutenberg Univ Mainz, Dept Transplantat & Hepatobiliopancreat Surg, D-55101 Mainz, Germany.
[Lohse, Ansgar W.] Univ Med Ctr Hamburg Eppendorf, Dept Internal Med 1, Hamburg, Germany.
[Hoehler, Thomas] Prosper Hosp, Dept Internal Med 1, Recklinghausen, Germany.
C3 Johannes Gutenberg University of Mainz; Johannes Gutenberg University of
Mainz; Johannes Gutenberg University of Mainz; University of Hamburg;
University Medical Center Hamburg-Eppendorf
RP Wörns, MA (corresponding author), Johannes Gutenberg Univ Mainz, Dept Internal Med 1, Langenbeckstr 1, D-55101 Mainz, Germany.
RI Galle, Peter/ABE-2872-2021; Teufel, Andreas/ABD-8000-2021; ,
Thomas/AAD-4757-2020
OI Galle, Peter Robert/0000-0001-8294-0992
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NR 47
TC 46
Z9 48
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD JAN
PY 2008
VL 103
IS 1
BP 138
EP 146
DI 10.1111/j.1572-0241.2007.01609.x
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 247UP
UT WOS:000252108400022
PM 17970833
DA 2025-01-07
ER
PT J
AU Duclos-Vallée, JC
Yilmaz, F
Johanet, C
Roque-Afonso, AM
Gigou, M
Trichet, C
Féray, C
Ballot, E
Dussaix, E
Castaing, D
Bismuth, H
Samuel, D
Guettier, C
AF Duclos-Vallée, JC
Yilmaz, F
Johanet, C
Roque-Afonso, AM
Gigou, M
Trichet, C
Féray, C
Ballot, E
Dussaix, E
Castaing, D
Bismuth, H
Samuel, D
Guettier, C
TI Could post-liver transplantation course be helpful for the diagnosis of
so called cryptogenic cirrhosis?
SO CLINICAL TRANSPLANTATION
LA English
DT Article
DE autoimmune liver disease; cryptogenic cirrhosis; liver transplantation
ID INCOMPLETE SEPTAL CIRRHOSIS; AUTOIMMUNE HEPATITIS; NONALCOHOLIC
STEATOHEPATITIS; HEPATOCELLULAR-CARCINOMA; PORTAL-HYPERTENSION; DISEASE;
OBESITY
AB Cryptogenic cirrhosis (CC) is diagnosed in 5-30% of cirrhotic patients overall and 7% of patients who undergo liver transplantation for cirrhosis. In our series of patients transplanted for CC, pre-transplant clinical and histological data and the post-transplant course were reexamined in an attempt to identify the aetiology. Among the 881 patients transplanted in our centre between 1987 and 2000, 28 patients with a median age of 46 yr (range: 18-69) at transplantation were initially classified as having CC. Two patients were excluded because of intense ischaemic lesions caused by chemoembolization prevented histological analysis of the native liver (n = 1) and because of cryptic HBV infection (n = 1). Among the remaining 26 patients, four groups were individualized: (i) patients with chronic inflammatory liver disease with autoimmune features (n = 14, 54%); (ii) patients with features suggestive of non-alcoholic fatty liver disease (n = 3, 11.5%); (iii); patients with incomplete septal cirrhosis (ISC) and vascular liver disease (n = 3), and (iv) patients with unresolved CC (n = 6, 23%). In the autoimmune liver disease group, the median International Autoimmune Hepatitis score was 12.5 (range: 11-19) after reevaluation and review of the post-transplantation course was helpful to confirm the diagnosis with the occurrence of active graft hepatitis in nine patients, with autoantibodies in five patients. The vascular group was characterized by lesions of obliterative portal venopathy and ISC in all native livers. Diagnosis of NAFLD was based on the clinical background of obesity and/or type 2 diabetes and the presence of steatosis or steatohepatitis in native livers and graft biopsies. A definite aetiological diagnosis can be achieved in the majority of patients initially diagnosed with CC. Autoimmune liver disease emerged as the main aetiology (14 of 26 patients, 54%) and frequently recurred on the grafted liver (nine cases). In all cases a precise diagnosis is obviously of practical interest for better management of post-transplant survey and treatment.
C1 Assistance Publ Hop Paris, Hop Paul Brousse, Ctr Hepatobiliaire, Villejuif, France.
Hop Paul Brousse, Lab Anatomopathol, Villejuif, France.
Hop St Antoine, Immunol Lab, F-75571 Paris, France.
Hop Paul Brousse, Virol Lab, Villejuif, France.
Hop Bicetre, Hematol Lab, Le Kremlin Bicetre, France.
Univ Paris 11, Fac Med Paris Sud, UPRES EA 3541, Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
Hopital Universitaire Saint-Louis - APHP; Hopital Universitaire
Paul-Brousse - APHP; Assistance Publique Hopitaux Paris (APHP); Hopital
Universitaire Paul-Brousse - APHP; Assistance Publique Hopitaux Paris
(APHP); Sorbonne Universite; Hopital Universitaire Saint-Antoine - APHP;
Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
Paul-Brousse - APHP; Assistance Publique Hopitaux Paris (APHP); Hopital
Universitaire Bicetre - APHP; Hopital Universitaire Antoine-Beclere -
APHP; Universite Paris Saclay; Universite Paris Saclay
RP Assistance Publ Hop Paris, Hop Paul Brousse, Ctr Hepatobiliaire, Villejuif, France.
EM jean-charles.duclos-vallee@pbr.ap-hop-paris.fr
RI Roque-Afonso, Anne-Marie/AAF-9706-2021; FERAY, Cyrille/T-7370-2018;
Yılmaz, Funda/O-9646-2018; Samuel, Didier/U-5265-2018
OI Samuel, Didier/0000-0001-9481-3616; cyrille, feray/0000-0002-8627-9676
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NR 28
TC 17
Z9 19
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0902-0063
EI 1399-0012
J9 CLIN TRANSPLANT
JI Clin. Transplant.
PD OCT
PY 2005
VL 19
IS 5
BP 591
EP 599
DI 10.1111/j.1399-0012.2004.00323.x
PG 9
WC Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery; Transplantation
GA 961RG
UT WOS:000231678900004
PM 16146549
DA 2025-01-07
ER
PT J
AU Haag, A
Huffman, D
Peterson, C
Shankar, K
Alnimer, L
Samhouri, Y
Greenberg, L
AF Haag, Aaron
Huffman, Deanna
Peterson, Chelsea
Shankar, Karthik
Alnimer, Lynna
Samhouri, Yazan
Greenberg, Larisa
TI Cutaneous Lesion of the Nose as Initial Presentation of Esophageal
Adenocarcinoma
SO ANTICANCER RESEARCH
LA English
DT Article
DE Adenocarcinoma; esophageal cancer; chemotherapy; cutaneous lesion;
metastatic disease
ID METASTASES; CARCINOMA; CANCER
AB Background/Aim: Cutaneous manifestations of disease are exceedingly rare and commonly overlooked in clinical practice. Allergies or contact dermatitis, autoimmune disease or skin cancer are the most common conditions typically associated with skin lesions. Rarely, cutaneous lesions may be the first sign of internal malignancy, or even resemble recurrent disease in those with history of cancer. Case Report: Herein, we report a case of an otherwise healthy male who presented to his primary care provider (PCP) with a skin lesion misdiagnosed as a furuncle, which eventually led to diagnosis of metastatic esophageal cancer. The patient was a 64-year-old male, presenting with a fungating lesion on the tip of his nose which was biopsied, confirming adenocarcinoma likely from a gastrointestinal source. Staging imaging showed extensive lung, liver, and boney metastatic disease. He was initially treated with chemotherapy and trastuzumab. Conclusion: Cutaneous lesions are a rare presenting sign of malignancy, but rapidly growing lesions should be evaluated for possible metastatic disease.
C1 [Haag, Aaron; Huffman, Deanna; Peterson, Chelsea; Shankar, Karthik] Allegheny Gen Hosp, Dept Med, Pittsburgh, PA 15212 USA.
[Alnimer, Lynna] Michigan State Univ, Coll Human Med, Ascens Providence Hosp, Dept Internal Med, Southfield, MI USA.
[Samhouri, Yazan; Greenberg, Larisa] Allegheny Gen Hosp, Div Med Oncol, Pittsburgh, PA 15212 USA.
C3 Allegheny General Hospital; Michigan State University; Michigan State
University College of Human Medicine; Allegheny General Hospital
RP Haag, A (corresponding author), Allegheny Gen Hosp, Dept Internal Med, 320 E North Ave, Pittsburgh, PA 15212 USA.
EM Aaron.Haag@ahn.org
RI Shankar, Karthik/ABB-9636-2020; Peterson, Chelsea/KOM-7523-2024
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NR 19
TC 0
Z9 0
U1 0
U2 1
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD MAY
PY 2021
VL 41
IS 5
BP 2485
EP 2488
DI 10.21873/anticanres.15025
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RZ5VV
UT WOS:000648665800017
PM 33952475
DA 2025-01-07
ER
PT J
AU Hilliard, A
Hilliard, B
Zheng, SJ
Sun, H
Miwa, T
Song, W
Göke, R
Chen, YH
AF Hilliard, Anja
Hilliard, Brendan
Zheng, Shi-Jun
Sun, Honghong
Miwa, Takashi
Song, Wenchao
Goeke, Rudiger
Chen, Youhai H.
TI Translational regulation of autoimmune inflammation and lymphoma genesis
by programmed cell death 4
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID DEPENDENT DIABETES-MELLITUS; BINDING PROTEIN EIF4E; INITIATION-FACTOR
4G; TRANSCRIPTIONAL REGULATION; P53-DEFICIENT MICE; CELL-DEATH;
RAPAMYCIN; ENCEPHALOMYELITIS; TUMORIGENESIS; EXPRESSION
AB Both inflammatory diseases and cancer are associated with heightened protein translation. However, the mechanisms of translational regulation and the roles of translation factors in these diseases are not clear. Programmed cell death 4 (PDCD4) is a newly described inhibitor of protein translation. To determine the roles of PDCD4 in vivo, we generated PDCD4-deficient mice by gene targeting. We report here that mice deficient in PDCD4 develop spontaneous lymphomas and have a significantly reduced life span. Most tumors are of the B lymphoid origin with frequent metastasis to liver and kidney. However, PDCD4-deficient mice are resistant to inflammatory diseases such as autoimmune encephalomyelitis and diabetes. Mechanistic studies reveal that upon activation, PDCD4-deficient lymphocytes preferentially produce cytokines that promote oncogenesis but inhibit inflammation. These results establish that PDCD4 controls lymphoma genesis and autoimmune inflammation by selectively inhibiting protein translation in the immune system.
C1 Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
Univ Penn, Sch Med, Dept Pharmacol, Philadelphia, PA 19104 USA.
Univ Marburg, Marburg, Germany.
C3 University of Pennsylvania; University of Pennsylvania; Philipps
University Marburg
RP Chen, YH (corresponding author), Univ Penn, Sch Med, Dept Pathol & Lab Med, 614 BRB 2-3,421 Curie Blvd, Philadelphia, PA 19104 USA.
EM yhc@mail.med.upenn.edu
RI ZHENG, John/ACC-5580-2022; Chen, Youhai/AAJ-4031-2021
FU NIAID NIH HHS [AI 55934, AI 50059] Funding Source: Medline
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NR 36
TC 148
Z9 176
U1 0
U2 8
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD DEC 1
PY 2006
VL 177
IS 11
BP 8095
EP 8102
DI 10.4049/jimmunol.177.11.8095
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 108TJ
UT WOS:000242261800071
PM 17114484
OA Bronze
DA 2025-01-07
ER
PT J
AU van Gerven, NMF
de Boer, YS
Mulder, CJJ
van Nieuwkerk, CMJ
Bouma, G
AF van Gerven, Nicole M. F.
de Boer, Ynto S.
Mulder, Chris J. J.
van Nieuwkerk, Carin M. J.
Bouma, Gerd
TI Auto immune hepatitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Auto immune hepatitis; Diagnosis; Liver; Epidemiology; Treatment
ID TYPE-1 AUTOIMMUNE HEPATITIS; PRIMARY BILIARY-CIRRHOSIS; ACTIVE
LIVER-DISEASE; REGULATORY T-CELLS; HEPATOCELLULAR-CARCINOMA;
CLINICAL-FEATURES; MYCOPHENOLATE-MOFETIL; SCLEROSING CHOLANGITIS;
INTERNATIONAL CRITERIA; INITIAL PRESENTATION
AB To provide an update of the latest trends in epidemiology, clinical course, diagnostics, complications and treatment of auto immune hepatitis (AIH). A search of the MEDLINE database was performed using the search terms: "auto immune hepatitis", "clinical presentation", "symptoms", "signs", "diagnosis", "auto antibodies", "laboratory values", "serology", "histopathology", "histology", "genetics", "HLA genes", "non-HLA genes", "environment", "epidemiology", "prevalence", "incidence", "demographics", "complications", "HCC", "PBC", "PSC", "corticosteroid", "therapy", "treatment", "alternative treatment". English-language full-text articles and abstracts were considered. Articles included reviews, meta-analysis, prospective retrospective studies. No publication date restrictions were applied. AIH is an immune meditated progressive inflammatory liver disease that predominantly affects middle-aged females but may affect people of all ages. The clinical spectrum of AIH is wide, ranging from absent or mild symptoms to fulminant hepatic failure. The aetiology of AIH is still unknown, but is believed to occur as the consequence of an aberrant immune response towards an un-known trigger in a genetically susceptible host. In the absence of a gold standard, diagnosis is based on the combination of clinical, biochemical and histopathological criteria. Immunosuppressive treatment has been the cornerstone of treatment since the earliest description of the disease in 1950 by Waldenstrom. Such treatment is often successful at inducing remission and generally leads to normal life expectancy. Nevertheless, there remain significant areas of unmet aetiological a clinical needs including fundamental insight in disease pathogenesis, optimal therapy, duration of treatment and treatment alternatives in those patients unresponsive to standard treatment regimens.
C1 [van Gerven, Nicole M. F.; de Boer, Ynto S.; Mulder, Chris J. J.; van Nieuwkerk, Carin M. J.; Bouma, Gerd] Vrije Univ Amsterdam Med Ctr, Dept Gastroenterol & Hepatol, De Boelelaan 1118, NL-1081 HV Amsterdam, Netherlands.
C3 Vrije Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER
RP Mulder, CJJ (corresponding author), Vrije Univ Amsterdam Med Ctr, Dept Gastroenterol & Hepatol, De Boelelaan 1118, NL-1081 HV Amsterdam, Netherlands.
EM cjmulder@vumc.nl
RI bouma, gerd/E-2520-2013; Kluin-Nelemans, Johanna/F-8658-2018; de Boer,
Ynto/D-9242-2013
OI de Boer, Ynto/0000-0002-4066-7593
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NR 127
TC 34
Z9 38
U1 1
U2 13
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAY 21
PY 2016
VL 22
IS 19
BP 4651
EP 4661
DI 10.3748/wjg.v22.i19.4651
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DN4ZH
UT WOS:000377075200005
PM 27217697
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Li, BA
Liu, J
Hou, J
Tang, J
Zhang, J
Xu, J
Song, YJ
Liu, AX
Zhao, J
Guo, JX
Chen, L
Wang, H
Yang, LH
Lu, J
Mao, YL
AF Li, Bo-An
Liu, Jia
Hou, Jun
Tang, Jie
Zhang, Jian
Xu, Jun
Song, Yong-Ji
Liu, Ai-Xia
Zhao, Jing
Guo, Jing-Xia
Chen, Lin
Wang, Han
Yang, Li-Hua
Lu, Jie
Mao, Yuan-Li
TI Autoantibodies in Chinese patients with chronic hepatitis B: Prevalence
and clinical associations
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoantibodies; Chronic hepatitis B; Autoimmune hepatitis; Primary
biliary cirrhosis; Cirrhosis; Hepatocellular carcinoma
ID PRIMARY BILIARY-CIRRHOSIS; C VIRUS-INFECTION; ORGAN-SPECIFIC
AUTOANTIBODIES; ANTIMITOCHONDRIAL ANTIBODIES; ANTINUCLEAR ANTIBODIES;
LIVER-DISEASE; MANIFESTATIONS; AUTOIMMUNITY; PROFILE; HBV
AB AIM: To investigate the prevalence of autoantibodies and their associations with clinical features in Chinese patients with chronic hepatitis B (CHB).
METHODS: A total of 325 Chinese patients with CHB were enrolled in this retrospective, hospitalbased study. Patients with chronic hepatitis C (CHC), autoimmune hepatitis (AIH), or primary biliary cirrhosis (PBC) were included, with healthy donors acting as controls. A panel of autoantibodies that serologically define AIH and PBC was tested by indirect immunofluorescence assay and line immunoassay. The AIH-related autoantibody profile included homogeneous anti-nuclear antibodies (ANA-H), smooth-muscle antibodies, anti-liver kidney microsome type 1, antiliver cytosolic antigen type 1, and anti-soluble liver antigen/liver pancreas; the PBC-related antibodies were characterized by ANA-nuclear dots/membranous rimlike, anti-mitochondrial antibodies-M2 (AMA-M2), antiBPO (recombinant antigen targeted by AMA-M2), antiSp100, anti-promyelocytic leukemia protein (anti-PML), and anti-gp210. The dichotomization of clustering was used to unequivocally designate the AIH or PBC profiles for each case. Anti-Ro52 antibodies were also tested.
RESULTS: The prevalence of any autoantibody in CHB amounted to 58.2%, which was similar to the 66.2% prevalence in CHC, significantly higher than the 6.7% in the healthy controls (P < 0.001), and lower than the 100% found in AIH and PBC (P = 0.004 and P < 0.001, respectively). There were more anti-PML and anti-gp210 antibodies among the CHB patients than the CHC patients (11.1% vs 0%, P = 0.003; 12.6% vs 0%, P < 0.001, respectively). The prevalence and titer of AMA, anti-BPO, anti-PML, and anti-gp210 were higher in PBC than in those with CHB. Among the CHB patients, the prevalence of ANA, especially ANA-H, was significantly lower in patients with compensated and decompensated cirrhosis compared with patients without cirrhosis. Thirty-eight cases of hepatocellular carcinoma (HCC) in CHB showed a significant difference compared with non-HCC patients in the prevalence of anti-PML (0% vs 12.5%, P = 0.013). Dichotomization of the autoantibodies revealed that the PBC profile was more prevalent in patients with CHB than in those with CHC, and that it was strongly correlated with both compensated and decompensated cirrhosis. In contrast, the prevalence of the AIH profile was significantly higher in non-cirrhosis patients with CHB than in those with compensated cirrhosis (18.5% vs 8.2%, P = 0.039). Moreover, the AIH profile was also closely associated with hepatitis B e-antigen positivity.
CONCLUSION: ANA-H could be an indicator of earlystage CHB. Dichotomizing the autoantibody profiles revealed that the PBC profile is strongly associated with cirrhosis in CHB.
C1 [Li, Bo-An; Liu, Jia; Hou, Jun; Zhang, Jian; Xu, Jun; Song, Yong-Ji; Liu, Ai-Xia; Zhao, Jing; Guo, Jing-Xia; Chen, Lin; Wang, Han; Yang, Li-Hua; Mao, Yuan-Li] 302 Mil Hosp China, Ctr Clin Lab Med, Beijing 100039, Peoples R China.
[Tang, Jie; Lu, Jie] EUROIMMUN Med Diagnost China Co Ltd, Beijing 100101, Peoples R China.
C3 Fifth Medical Center of Chinese PLA General Hospital
RP Mao, YL (corresponding author), 302 Mil Hosp China, Ctr Clin Lab Med, 100 W 4th Ring Middle Rd, Beijing 100039, Peoples R China.
EM maoyuanli2013@163.com
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NR 32
TC 17
Z9 21
U1 0
U2 3
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JAN 7
PY 2015
VL 21
IS 1
BP 283
EP 291
DI 10.3748/wjg.v21.i1.283
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AY3CG
UT WOS:000347461500029
PM 25574103
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Nagai, K
Nagai, K
Iwaki, M
Kobayashi, T
Nogami, A
Oka, M
Saito, S
Yoneda, M
AF Nagai, Koki
Nagai, Kazuki
Iwaki, Michihiro
Kobayashi, Takashi
Nogami, Asako
Oka, Masanao
Saito, Satoru
Yoneda, Masato
TI Frontiers of Collaboration between Primary Care and Specialists in the
Management of Metabolic Dysfunction-Associated Steatotic Liver Disease:
A Review
SO LIFE-BASEL
LA English
DT Review
DE nonalcoholic fatty liver disease; metabolic dysfunction-associated
steatotic liver disease; review; management of MASLD; hepatologists;
primary care physicians
ID NONALCOHOLIC FATTY LIVER; INSULIN-RESISTANCE; CONFERS SUSCEPTIBILITY;
AUTOIMMUNE HEPATITIS; FOLLOW-UP; STEATOHEPATITIS; FIBROSIS; NAFLD;
CONSUMPTION; PROGRESSION
AB Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), is the most common liver disease. It has a rapidly growing patient population owing to the increasing prevalence of obesity and type 2 diabetes. Patients with MASLD are primarily treated by family physicians when fibrosis is absent or mild and by gastroenterologists/hepatologists when fibrosis is more advanced. It is imperative that a system for the appropriate treatment and surveillance of hepatocellular carcinoma be established in order to ensure that highly fibrotic cases are not overlooked among the large number of MASLD patients. Family physicians should check for viral hepatitis, autoimmune hepatitis, alcoholic liver disease, and drug-induced liver disease, and should evaluate fibrosis using NIT; gastroenterologists/hepatologists should perform liver biopsy, ultrasound elastography (260 units in Japan as of October 2023), and MR elastography (35 units in Japan as of October 2023). This review presents the latest findings in MASLD and the role, accuracy, and clinical use of NIT. It also describes the collaboration between Japanese primary care and gastroenterologists/hepatologists in Japan in the treatment of liver diseases, including MASLD.
C1 [Nagai, Koki; Yoneda, Masato] Natl Hosp Org Yokohama Med Ctr, Gastroenterol Div, 3-60-2 Harajyuku,Totsuka Ku, Yokohama 2458575, Japan.
[Nagai, Kazuki] Nagai Clin, 1-7-25 Yokodai,Isogo Ku, Yokohama 2350045, Japan.
[Iwaki, Michihiro; Kobayashi, Takashi; Nogami, Asako] Yokohama City Univ Med, Dept Gastroenterol & Hepatol, 3-9 Fuku Ura,Kanazawa Ku, Yokohama 2360004, Japan.
[Oka, Masanao] OkaMedical, 1-19-18-3F Kamiookanishi,Kounan Ku, Yokohama 2330002, Japan.
[Saito, Satoru] Sanno Hosp, 8-10-16 Akasaka,Minato Ku, Tokyo 1070052, Japan.
RP Yoneda, M (corresponding author), Natl Hosp Org Yokohama Med Ctr, Gastroenterol Div, 3-60-2 Harajyuku,Totsuka Ku, Yokohama 2458575, Japan.
EM k78naga@gmail.com; k-nagai@mtj.biglobe.ne.jp;
michihir@yokohama-cu.ac.jp; tkbys@yokohama-cu.ac.jp;
nogamia@yokohama-cu.ac.jp; okam@clinics.jp; ssai1423@iuhw.ac.jp;
yoneda@yokohama-cu.ac.jp
RI Nogami, Asako/HLP-4920-2023; KOBAYASHI, Takashi/AAM-7549-2021
OI Yoneda, Masato/0000-0001-7815-549X; Saito, Satoru/0000-0002-5666-5218;
Nogami, Asako/0000-0002-6923-365X
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NR 71
TC 3
Z9 3
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-1729
J9 LIFE-BASEL
JI Life-Basel
PD NOV
PY 2023
VL 13
IS 11
AR 2144
DI 10.3390/life13112144
PG 13
WC Biology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microbiology
GA Z7FP8
UT WOS:001113697800001
PM 38004284
OA gold
DA 2025-01-07
ER
PT J
AU Shi, RF
Yang, F
Wu, HL
Liu, YG
AF Shi, Ruifang
Yang, Fan
Wu, Hongli
Liu, Yonggang
TI The Diagnostic Value of Liver Biopsy for Unexplained Liver Dysfunction:
A Retrospective Study
SO JOURNAL OF MULTIDISCIPLINARY HEALTHCARE
LA English
DT Article
DE unexplained abnormal liver function; clinical manifestations; liver
biopsy; pathology
AB Objective: To analyse clinical manifestations of unexplained abnormal liver function and perform hepatobiliary histopathology procedures on patients to evaluate the value of liver biopsy in diagnosing the aetiology of unexplained abnormal liver function. Methods: A convenience sampling method was used to retrospectively collect the data of patients who were diagnosed with unexplained abnormal liver function and who received liver biopsy in the Pathology Department of Tianjin Second People's Hospital, China, between March 2022 and July 2023 to analyse liver pathology and clinical manifestations. Results: A total of 1302 patients were included in this study, which mainly included 11 diseases: autoimmune liver disease (74 cases, 5.68%), drug-induced liver injury (DILI) (204 cases, 15.67%), cancer (237 cases, 18.20%), non-alcoholic fatty liver disease (104 cases, 7.99%), non-alcoholic steatohepatitis (74 cases, 5.68%), viral hepatitis (490 cases, 37.63%), other types of hepatitis (30 cases, 2.30%), cholestatic liver disease (17 cases, 1.31%), alcoholic liver disease (15 cases, 1.15%), hepatic cyst (5 cases, 0.38%) and Gilbert syndrome (4 cases, 0.31%). The success rate of liver biopsy sampling was 100%, and (1.52 +/- 0.130) tissue strips were sampled. The average operating time was 11.52 minutes. The percutaneous liver biopsy did not significantly increase short -term liver function index values (serum gamma-glutamyl transpeptidase, total bilirubin, alanine transaminase, aspartate aminotransferase, alkaline phosphatase). Ninety-two patients had a small amount of liver subcapsular fluid, but there was no progress after medical treatment. Conclusion: Ultrasound-guided percutaneous liver biopsy has value in the diagnosis of unexplained abnormal liver function. Viral hepatitis, cancer and DILI are the most common causes of unexplained abnormal liver function. Liver biopsy does not aggravate the organic and functional impairment of the liver.
C1 [Shi, Ruifang; Yang, Fan; Liu, Yonggang] Tianjin Second Peoples Hosp, Tianjin Inst Hepatol, Dept Pathol, 7 Sudi South Rd, Tianjin 300192, Peoples R China.
[Wu, Hongli] Tianjin Second Peoples Hosp, Tianjin Inst Hepatol, Dept Clin Lab, Tianjin 300192, Peoples R China.
RP Liu, YG (corresponding author), Tianjin Second Peoples Hosp, Tianjin Inst Hepatol, Dept Pathol, 7 Sudi South Rd, Tianjin 300192, Peoples R China.
EM liuyonggang_2023@163.com
RI Wu, Hongli/J-1674-2015; Yang, Fan/CAH-5460-2022
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NR 39
TC 1
Z9 1
U1 1
U2 2
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2390
J9 J MULTIDISCIP HEALTH
JI J. Multidiscip. Healthc.
PY 2024
VL 17
BP 2399
EP 2407
DI 10.2147/JMDH.S460338
PG 9
WC Health Care Sciences & Services
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services
GA RU3D4
UT WOS:001230125100001
PM 38779307
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Purde, MT
Niederer, R
Wagner, NB
Diem, S
Berner, F
Ali, OH
Hillmann, D
Bergamin, I
Joerger, M
Risch, M
Niederhauser, C
Lenz, TL
Früh, M
Risch, L
Semela, D
Flatz, L
AF Purde, Mette-Triin
Niederer, Rebekka
Wagner, Nikolaus B.
Diem, Stefan
Berner, Fiamma
Hasan Ali, Omar
Hillmann, Dorothea
Bergamin, Irina
Joerger, Markus
Risch, Martin
Niederhauser, Christoph
Lenz, Tobias L.
Fruh, Martin
Risch, Lorenz
Semela, David
Flatz, Lukas
TI Presence of autoantibodies in serum does not impact the occurrence of
immune checkpoint inhibitor-induced hepatitis in a prospective cohort of
cancer patients
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Autoantibodies; Checkpoint inhibitors; Drug-induced liver injury;
Drug-related side effects and adverse reactions
ID ADVERSE EVENTS; LIVER-INJURY
AB Purpose Immune checkpoint inhibitor (ICI)-induced hepatitis belongs to the frequently occurring immune-related adverse events (irAEs), particularly with the combination therapy involving ipilimumab and nivolumab. However, predisposing factors predicting the occurrence of ICI-induced hepatitis are barely known. We investigated the association of preexisting autoantibodies in the development of ICI-induced hepatitis in a prospective cohort of cancer patients. Methods Data from a prospective biomarker cohort comprising melanoma and non-small cell lung cancer (NSCLC) patients were used to analyze the incidence of ICI-induced hepatitis, putatively associated factors, and outcome. Results 40 patients with melanoma and 91 patients with NSCLC received ICI between July 2016 and May 2019. 11 patients developed ICI-induced hepatitis (8.4%). Prior to treatment, 45.5% of patients in the hepatitis cohort and 43.8% of the control cohort showed elevated titers of autoantibodies commonly associated with autoimmune liver diseases (p = 0.82). We found two nominally significant associations between the occurrence of ICI-induced hepatitis and HLA alleles associated with autoimmune liver diseases among NSCLC patients. Of note, significantly more patients with ICI-induced hepatitis developed additional irAEs in other organs (p = 0.0001). Neither overall nor progression-free survival was affected in the hepatitis group. Conclusion We found nominally significant associations of ICI-induced hepatitis with two HLA alleles. ICI-induced hepatitis showed no correlation with liver-specific autoantibodies, but frequently co-occurred with irAEs affecting other organs. Unlike other irAEs, ICI-induced hepatitis is not associated with a better prognosis.
C1 [Purde, Mette-Triin; Niederer, Rebekka; Diem, Stefan; Berner, Fiamma; Hasan Ali, Omar; Flatz, Lukas] Kantonsspital St Gallen, Inst Immunobiol, Rorschacher Str 95, CH-9007 St Gallen, Switzerland.
[Wagner, Nikolaus B.; Flatz, Lukas] Kantonsspital St Gallen, Dept Dermatol Venereol & Allergol, Rorschacher Str 95, CH-9007 St Gallen, Switzerland.
[Diem, Stefan; Joerger, Markus; Fruh, Martin; Flatz, Lukas] Kantonsspital St Gallen, Dept Oncol & Hematol, Rorschacher Str 95, CH-9007 St Gallen, Switzerland.
[Diem, Stefan] Hosp Grabs, Dept Hematol & Oncol, Spitalstr 44, CH-9472 Grabs, Switzerland.
[Hasan Ali, Omar] Univ Hosp Zurich, Dept Dermatol, Ramistr 100, CH-8091 Zurich, Switzerland.
[Hillmann, Dorothea; Risch, Martin; Risch, Lorenz] Labormed Zentrum Dr Risch Ostschweiz AG, Brauerstr 95, CH-9016 St Gallen, Switzerland.
[Bergamin, Irina; Semela, David] Kantonsspital St Gallen, Dept Gastroenterol & Hepatol, Rorschacher Str 95, CH-9007 St Gallen, Switzerland.
[Niederhauser, Christoph] Interreg Blood Transfus SRC, Murtenstr 137A, CH-3008 Bern, Switzerland.
[Niederhauser, Christoph] Univ Lausanne, CH-1015 Lausanne, Switzerland.
[Niederhauser, Christoph; Fruh, Martin] Univ Bern, Hochschulstr 6, CH-3012 Bern, Switzerland.
[Lenz, Tobias L.] Max Planck Inst Evolutionary Biol, Res Grp Evolutionary Immunogenom, August Thienemann Str 2, D-24306 Plon, Germany.
[Flatz, Lukas] Univ Hosp Tubingen, Dept Dermatol, D-72016 Tubingen, Germany.
C3 Kantonsspital St. Gallen; Kantonsspital St. Gallen; Kantonsspital St.
Gallen; University of Zurich; University Zurich Hospital; Kantonsspital
St. Gallen; University of Lausanne; University of Bern; Max Planck
Society; Eberhard Karls University of Tubingen; Eberhard Karls
University Hospital
RP Flatz, L (corresponding author), Kantonsspital St Gallen, Inst Immunobiol, Rorschacher Str 95, CH-9007 St Gallen, Switzerland.; Flatz, L (corresponding author), Kantonsspital St Gallen, Dept Dermatol Venereol & Allergol, Rorschacher Str 95, CH-9007 St Gallen, Switzerland.; Flatz, L (corresponding author), Kantonsspital St Gallen, Dept Oncol & Hematol, Rorschacher Str 95, CH-9007 St Gallen, Switzerland.; Flatz, L (corresponding author), Univ Hosp Tubingen, Dept Dermatol, D-72016 Tubingen, Germany.
EM mette-triin.purde@kssg.ch; rebekka.niederer@kssg.ch;
nikolaus.wagner@kssg.ch; stefan.diem@kssg.ch; fiamma.berner@kssg.ch;
omar.hasanali@kssg.ch; dorothea.hillmann@risch.ch;
irina.bergamin@kssg.ch; markus.joerger@kssg.ch; martin.risch@risch.ch;
christoph.niederhauser@itransfusion.ch; lenz@evolbio.mpg.de;
martin.frueh@kssg.ch; lorenz.risch@risch.ch; david.semela@kssg.ch;
lukas.flatz@med.uni-tuebingen.de
RI Lenz, Tobias/D-1387-2009; joerger, markus/B-7230-2011; Semela,
David/D-1988-2010; Ali, Md Hasan/GZH-1120-2022; Wagner,
Nikolaus/AAB-9027-2021; Risch, Lorenz/D-4629-2011
OI Risch, Lorenz/0000-0003-2692-6699; Purde,
Mette-Triin/0000-0002-2631-9736; Hasan Ali, Omar/0000-0001-5185-7520;
Flatz, Lukas/0000-0001-9683-8390; Lenz, Tobias/0000-0002-7203-0044
FU Swiss National Science Foundation [PP00P3_157448]; Swiss Cancer League
[KLS-4409-02-2018]; Forschungsforderung of the Kantonsspital St. Gallen;
Swiss National Science Foundation (SNF) [PP00P3_157448] Funding Source:
Swiss National Science Foundation (SNF)
FX Open Access funding enabled and organized by Projekt DEAL. This project
was supported by the Swiss National Science Foundation grant
PP00P3_157448 and the Swiss Cancer League grant KLS-4409-02-2018 (both
to LF). Study coordination of this patient cohort was supported by a
grant from the Forschungsforderung of the Kantonsspital St. Gallen.
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NR 41
TC 10
Z9 10
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD MAR
PY 2022
VL 148
IS 3
BP 647
EP 656
DI 10.1007/s00432-021-03870-6
EA DEC 2021
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZH8XM
UT WOS:000727755600001
PM 34874490
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Plaza-Díaz, J
Solís-Urra, P
Rodríguez-Rodríguez, F
Olivares-Arancibia, J
Navarro-Oliveros, M
Abadía-Molina, F
Alvarez-Mercado, AI
AF Plaza-Diaz, Julio
Solis-Urra, Patricio
Rodriguez-Rodriguez, Fernando
Olivares-Arancibia, Jorge
Navarro-Oliveros, Miguel
Abadia-Molina, Francisco
Alvarez-Mercado, Ana, I
TI The Gut Barrier, Intestinal Microbiota, and Liver Disease: Molecular
Mechanisms and Strategies to Manage
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE liver disease; intestinal barrier; intestinal permeability; microbiota
ID NONALCOHOLIC-FATTY-LIVER; LIFE-STYLE MODIFICATION; BACTERIAL
TRANSLOCATION; AUTOIMMUNE HEPATITIS; OXIDATIVE STRESS; MEDICAL PROGRESS;
PERMEABILITY; ALCOHOL; CIRRHOSIS; INFLAMMATION
AB Liver disease encompasses pathologies as non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, alcohol liver disease, hepatocellular carcinoma, viral hepatitis, and autoimmune hepatitis. Nowadays, underlying mechanisms associating gut permeability and liver disease development are not well understood, although evidence points to the involvement of intestinal microbiota and their metabolites. Animal studies have shown alterations in Toll-like receptor signaling related to the leaky gut syndrome by the action of bacterial lipopolysaccharide. In humans, modifications of the intestinal microbiota in intestinal permeability have also been related to liver disease. Some of these changes were observed in bacterial species belonging Roseburia, Streptococcus, and Rothia. Currently, numerous strategies to treat liver disease are being assessed. This review summarizes and discusses studies addressed to determine mechanisms associated with the microbiota able to alter the intestinal barrier complementing the progress and advancement of liver disease, as well as the main strategies under development to manage these pathologies. We highlight those approaches that have shown improvement in intestinal microbiota and barrier function, namely lifestyle changes (diet and physical activity) and probiotics intervention. Nevertheless, knowledge about how such modifications are beneficial is still limited and specific mechanisms involved are not clear. Thus, further in-vitro, animal, and human studies are needed.
C1 [Plaza-Diaz, Julio] Childrens Hosp, Eastern Ontario Res Inst, Ottawa, ON K1H 8L1, Canada.
[Plaza-Diaz, Julio; Alvarez-Mercado, Ana, I] Univ Granada, Sch Pharm, Dept Biochem & Mol Biol 2, Granada 18071, Spain.
[Plaza-Diaz, Julio; Alvarez-Mercado, Ana, I] Complejo Hosp Univ Granada, Inst Invest Biosanitaria IBS GRANADA, Granada 18071, Spain.
[Solis-Urra, Patricio] Univ Andres Bello, Fac Educ & Social Sci, Vina Del Mar 2531015, Chile.
[Rodriguez-Rodriguez, Fernando; Olivares-Arancibia, Jorge] Pontificia Univ Catolica Valparaiso, Sch Phys Educ, IRyS Res Grp, Valparaiso 2374631, Chile.
[Olivares-Arancibia, Jorge] Univ Amer, Fac Educ, Escuela Pedag Educ Fis, Santiago 8370035, Chile.
[Navarro-Oliveros, Miguel] BioCrit Grp Biomed Res Crit Care Med, Valladolid 47005, Spain.
[Abadia-Molina, Francisco; Alvarez-Mercado, Ana, I] Univ Granada, Ctr Biomed Res, Inst Nutr & Food Technol Jose Mataix, Avda Conocimiento S-N, Granada 18016, Spain.
[Abadia-Molina, Francisco] Univ Granada, Sch Sci, Dept Cell Biol, Granada 18071, Spain.
C3 University of Ottawa; Children's Hospital of Eastern Ontario; University
of Granada; Instituto de Investigacion Biosanitaria IBS Granada;
University of Granada; Universidad Andres Bello; Pontificia Universidad
Catolica de Valparaiso; Universidad de Las Americas - Chile; University
of Granada; University of Granada
RP Alvarez-Mercado, AI (corresponding author), Univ Granada, Sch Pharm, Dept Biochem & Mol Biol 2, Granada 18071, Spain.; Alvarez-Mercado, AI (corresponding author), Complejo Hosp Univ Granada, Inst Invest Biosanitaria IBS GRANADA, Granada 18071, Spain.; Alvarez-Mercado, AI (corresponding author), Univ Granada, Ctr Biomed Res, Inst Nutr & Food Technol Jose Mataix, Avda Conocimiento S-N, Granada 18016, Spain.
EM jrplaza@ugr.es; patricio.solis.u@gmail.com; fernando.rodriguez@pucv.cl;
jorge.olivares.ar@gmail.com; miguelno@ugr.es; fmolina@ugr.es;
alvarezmercado@ugr.es
RI Solis-Urra, Patricio/ABH-5748-2022; Alvarez, Ana/GXW-0690-2022;
Navarro-Oliveros, Miguel/V-5841-2019; Plaza-Diaz, Julio/C-8094-2016;
Abadia Molina, Francisco/T-6439-2017; Alvarez-Mercado, Ana
I./C-3466-2019; RODRIGUEZ, FERNANDO/F-2842-2016
OI Solis-Urra, Patricio/0000-0002-2493-9528; Plaza-Diaz,
Julio/0000-0002-5171-9408; Olivares-Arancibia,
Jorge/0000-0002-7186-3941; Abadia Molina, Francisco/0000-0002-0995-2572;
Navarro-Oliveros, Miguel/0000-0001-8745-4985; Alvarez-Mercado, Ana
I./0000-0002-8476-9970; RODRIGUEZ, FERNANDO/0000-0002-4999-4857
FU National Agency for Research and Development (ANID) BECAS Chile
[72180543]
FX Julio Plaza-Diaz is part of the "UGR Plan Propio de Investigacion 2016"
and the "Excellence actions: Unit of Excellence on Exercise and Health
(UCEES), University of Granada". Patricio Solis-Urra was supported by a
grant from the National Agency for Research and Development (ANID) BECAS
Chile/72180543. We are grateful to Belen Vazquez-Gonzalez for her
assistance with the illustration service.
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2016, OBESITY FACTS, V9, P65, DOI DOI 10.1007/S00125-016-3902-Y
NR 170
TC 72
Z9 78
U1 2
U2 29
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD NOV
PY 2020
VL 21
IS 21
AR 8351
DI 10.3390/ijms21218351
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA OQ8EW
UT WOS:000589010400001
PM 33171747
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Cuomo, F
Altucci, L
Cobellis, G
AF Cuomo, Francesca
Altucci, Lucia
Cobellis, Gilda
TI Autophagy Function and Dysfunction: Potential Drugs as Anti-Cancer
Therapy
SO CANCERS
LA English
DT Review
DE autophagy; cancer; apoptosis; chloroquine; mTOR inhibitors; drugs
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ADVANCED BREAST-CANCER; PHASE-II TRIAL;
MTOR INHIBITION; DOUBLE-BLIND; CELL-DEATH; ESTROGEN-RECEPTOR;
THYROID-CANCER; ADVANCED NSCLC; DUAL ROLE
AB Autophagy is a highly conserved catabolic and energy-generating process that facilitates the degradation of damaged organelles or intracellular components, providing cells with components for the synthesis of new ones. Autophagy acts as a quality control system, and has a pro-survival role. The imbalance of this process is associated with apoptosis, which is a "positive" and desired biological choice in some circumstances. Autophagy dysfunction is associated with several diseases, including neurodegenerative disorders, cardiomyopathy, diabetes, liver disease, autoimmune diseases, and cancer. Here, we provide an overview of the regulatory mechanisms underlying autophagy, with a particular focus on cancer and the autophagy-targeting drugs currently approved for use in the treatment of solid and non-solid malignancies.
C1 [Cuomo, Francesca; Altucci, Lucia; Cobellis, Gilda] Univ Campania L Vanvitelli, Dept Precis Med, Via L De Crecchio 7, I-80138 Naples, Italy.
C3 Universita della Campania Vanvitelli
RP Altucci, L; Cobellis, G (corresponding author), Univ Campania L Vanvitelli, Dept Precis Med, Via L De Crecchio 7, I-80138 Naples, Italy.
EM francesca.cuomo@unicampania.it; lucia.altucci@unicampania.it;
g.cobellis@unicampania.it
RI Altucci, Lucia/S-8031-2019; Cobellis, Gilda/F-7668-2012
OI Cobellis, Gilda/0000-0003-2687-2272; Cuomo,
Francesca/0000-0002-8600-3071
FU PROGRAMMA VALERE: Vanvitelli per la Ricerca; Regione Campania lotta alle
patologie oncologiche: iCURE; Regione Campania FASE2: IDEAL;
[AIRC-17217]
FX We are grateful to AIRC-17217; PROGRAMMA VALERE: Vanvitelli per la
Ricerca; Regione Campania lotta alle patologie oncologiche: iCURE;
Regione Campania FASE2: IDEAL.
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Zhao JX, 2014, EUR REV MED PHARMACO, V18, P2428
NR 141
TC 52
Z9 53
U1 0
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD OCT
PY 2019
VL 11
IS 10
AR 1465
DI 10.3390/cancers11101465
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JQ3CF
UT WOS:000498826000062
PM 31569540
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Komaki, Y
Komaki, F
Micic, D
Ido, A
Sakuraba, A
AF Komaki, Yuga
Komaki, Fukiko
Micic, Dejan
Ido, Akio
Sakuraba, Atsushi
TI Risk of colorectal cancer in chronic liver diseases: a systematic review
and meta-analysis
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Review
ID PRIMARY SCLEROSING CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE; DE-NOVO
MALIGNANCIES; EXTRAHEPATIC MALIGNANCIES; ULCERATIVE-COLITIS;
SINGLE-CENTER; FOLLOW-UP; TRANSPLANTATION; MORTALITY; NEOPLASMS
AB Background and Aims: The risk of colorectal cancer (CRC) in various chronic liver diseases compared with the general population remains unclear. We performed a systematic review and meta-analysis to assess the risk of CRC in patients with chronic liver diseases before and after liver transplantation.
Methods: Electronic databases were searched for studies assessing the risk of CRC in patients with chronic liver diseases. The primary outcome was the pooled risk of CRC among studies that reported the risk as standardized incidence rate (SIR).
Results: Fifty studies that included 55,991 patients were identified. Among studies that included hepatitis and cirrhotic patients, the pooled SIR was 2.06 (P<.0001; 95% confidence interval (CI), 1.46-2.90) with moderate heterogeneity (I-2 = 49.2%), which appeared to be because of the difference between subgroup of diseases and the power of studies. Three studies reported an increased risk of CRC in primary sclerosing cholangitis patients (pooled SIR 6.70; P<.0001; 95% CI, 3.48-12.91) with moderate heterogeneity (I-2 = 36.3%), which appeared to be because of the difference between the power of studies. Among studies that included post-transplant patients, the pooled SIR was 2.16 (P<.0001; 95% CI, 1.59-2.94) with moderate heterogeneity (I-2 = 56.4%). Meta-regression showed a correlation between the proportion of autoimmune-related liver diseases and the risk of CRC.
Conclusions: Patients with chronic liver diseases had an increased risk of CRC compared with the general population, which persisted after liver transplantation. A more intensive surveillance for CRC is warranted in this population.
C1 [Komaki, Yuga; Komaki, Fukiko; Sakuraba, Atsushi] Univ Chicago Med, Sect Gastroenterol Hepatol & Nutr, Dept Med, 5841 S Maryland Ave,MC 4076, Chicago, IL 60637 USA.
[Micic, Dejan] Northwestern Univ, Dept Med, Div Gastroenterol & Hepatol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Ido, Akio] Kagoshima Univ, Grad Sch Med & Dent Sci, Digest & Lifestyle Dis, Kagoshima, Japan.
C3 Northwestern University; Feinberg School of Medicine; Kagoshima
University
RP Sakuraba, A (corresponding author), Univ Chicago Med, Sect Gastroenterol Hepatol & Nutr, Dept Med, 5841 S Maryland Ave,MC 4076, Chicago, IL 60637 USA.
EM asakurab@medicine.bsd.uchicago.edu
RI Sakuraba, Atsushi/ABD-6796-2020
OI Sakuraba, Atsushi/0000-0003-2519-6129; Komaki, Yuga/0000-0001-8807-0895
FU Pediatric Oncology Research Fellowship of the Children's Cancer
Association of Japan
FX The following author received research support for this study from the
Pediatric Oncology Research Fellowship of the Children's Cancer
Association of Japan: Y. Komaki. All other authors disclosed no
financial relationships relevant to this publication.
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NR 52
TC 32
Z9 33
U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
EI 1097-6779
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD JUL
PY 2017
VL 86
IS 1
BP 93
EP +
DI 10.1016/j.gie.2016.12.009
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EX1KE
UT WOS:000402980700010
PM 28011280
DA 2025-01-07
ER
PT J
AU Peng, B
Huang, XY
Nakayasu, ES
Petersen, JR
Qiu, SM
Almeida, IC
Zhang, JY
AF Peng, Bo
Huang, Xueyong
Nakayasu, Ernesto S.
Petersen, John R.
Qiu, Suimin
Almeida, Igor C.
Zhang, Jian-Ying
TI Using Immunoproteomics to Identify Alpha-enolase as an Autoantigen in
Liver Fibrosis
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE liver fibrosis; autoantigen; autoimmune response; immunoproteomics;
alpha-enolase
ID TUMOR-ASSOCIATED ANTIGENS; AUTOANTIBODIES; PROTEINS; ANTIBODIES;
CATALASE
AB Liver fibrosis results from extracellular matrix accumulation during the wound healing process when the liver is insulted with chronic viral infection, inflammation, or alcoholic diseases. The current diagnosis of liver fibrosis is mainly dependent on biopsy, which is an invasive approach. Identification of serological biomarkers has been considered as the most promising way for early detection of the disease. Although several biomarkers in liver fibrosis have been identified, the problem is that these markers can be also detected in fibrogenesis that occurred in other organs. In this study, we have identified and characterized some cellular proteins that can be recognized by autoantibodies in the sera from patients with precirrhotic stage of liver fibrosis. Among 180 sera from patients with liver fibrosis, 144% (26/180) of sera contained autoantibody against a protein migrating around 47 kDa on SDS-PAGE gel Indirect immunofluorescence assay using purified autoantibody against the 47-kDa protein showed that this protein mainly localized in the cytoplasm. Using immunoproteomic approach, the 47-kDa protein was identified as alpha-enolase. In further study, the frequency of antialpha-enolase antibody in sera from patients with precirrhotic stage of liver fibrosis (21.6%, 27/125) was significantly higher than that in sera from patients with cirrhosis (9.1%, 5/55) and liver cancer (14.3%, 12/84), as well as in sera from healthy individuals (4.1%, 3/74). Therefore, alpha-enolase is an autoantigen that elicits autoimmune response in liver fibrosis and can be a potential prognostic factor for liver fibrosis diagnosis.
C1 [Peng, Bo; Huang, Xueyong; Nakayasu, Ernesto S.; Almeida, Igor C.; Zhang, Jian-Ying] Univ Texas El Paso, Dept Biol Sci, Border Biomed Res Ctr, El Paso, TX 79968 USA.
[Petersen, John R.; Qiu, Suimin] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA.
C3 University of Texas System; University of Texas El Paso; University of
Texas System; University of Texas Medical Branch Galveston
RP Zhang, JY (corresponding author), Univ Texas El Paso, Dept Biol Sci, Border Biomed Res Ctr, El Paso, TX 79968 USA.
EM icalmeida@utep.edu; jzhang@utep.edu
RI Nakayasu, Ernesto/AAJ-8374-2020; Zhang, Jianying/F-3798-2010; Almeida,
Igor/AAF-9409-2019
OI Nakayasu, Ernesto/0000-0002-4056-2695; Almeida, Igor/0000-0002-2443-8213
FU NIH [SC1CA166016, 5G12MD007592, 5G12RR008124-16A1, 5G12RR008124-16A1S1]
FX This work was supported by grants from NIH (SC1CA166016 and
5G12MD007592). We thank the Biomolecule Analysis Core Facility and
Analytical Cytology Core Facility of Border Biological Research Center
(BBRC) at The University of Texas at El Paso (UTEP), funded by NIH
grants 5G12RR008124-16A1, 5G12RR008124-16A1S1, and 5G12MD007592, for
their support.
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NR 34
TC 33
Z9 38
U1 1
U2 13
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
EI 1535-3907
J9 J PROTEOME RES
JI J. Proteome Res.
PD APR
PY 2013
VL 12
IS 4
BP 1789
EP 1796
DI 10.1021/pr3011342
PG 8
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 122ON
UT WOS:000317327500023
PM 23458688
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Liberal, R
Krawitt, EL
Vierling, JM
Manns, MP
Mieli-Vergani, G
Vergani, D
AF Liberal, Rodrigo
Krawitt, Edward L.
Vierling, John M.
Manns, Michael P.
Mieli-Vergani, Giorgina
Vergani, Diego
TI Cutting edge issues in autoimmune hepatitis
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Review
DE Autoimmune hepatitis; Pathogenesis; Immunosuppression; International
Autoimmune Hepatitis Group
ID REGULATORY T-CELLS; PRIMARY BILIARY-CIRRHOSIS; LIVER-DISEASE; SCLEROSING
CHOLANGITIS; MYCOPHENOLATE-MOFETIL; DE-NOVO; HEPATOCELLULAR-CARCINOMA;
CLINICAL CHARACTERISTICS; OVERLAP SYNDROME; CONTROLLED-TRIAL
AB Autoimmune hepatitis (AIH) is a severe liver disease affecting all age groups worldwide. Novel basic and clinical aspects of AIH, addressed at a Monothematic Conference in London in September 2015, are highlighted in this review. The diagnosis of AIH relies upon detection of characteristic autoantibodies, hypergammaglobulinemia, and interface hepatitis on liver histology. The International Autoimmune Hepatitis Group (IAIHG) has devised diagnostic scoring systems to help in comparative studies and clinical practice. AIH arises in a genetically predisposed host, when yet unknown triggers such an encounter with a pathogen lead to a T cell-mediated immune response targeting liver autoantigens. This immune response is inadequately controlled because regulatory mechanisms are impaired. The mainstay of treatment for AIH is immunosuppression, which should be instituted as soon as the diagnosis is made. Standard treatment regimens include relatively high doses of predniso(lo)ne, which are tapered gradually as azathioprine is introduced. Recent guidelines have described newer treatment regimens and have tightened the goal of therapy to complete normalization of biochemical, serological and histological parameters. Mycophenolate mofetil, calcineurin inhibitors, mTOR inhibitors and biological agents are potential salvage therapies, but should be reserved for selected non-responsive patients and administered only in experienced centers. Liver transplantation is a life-saving option for those patients who progress to end-stage liver disease. Further dissection of cellular and molecular pathways involved in AIH pathogenesis is likely to lead to the discovery of novel, tailored and better tolerated therapies. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Liberal, Rodrigo; Mieli-Vergani, Giorgina; Vergani, Diego] Kings Coll Hosp London, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
[Krawitt, Edward L.] Dartmouth Coll, Dept Med, Hanover, NH 03755 USA.
[Krawitt, Edward L.] Univ Vermont, Dept Med, Burlington, VT USA.
[Vierling, John M.] Baylor Coll Med, Baylor St Lukes Med Ctr, Dept Med, Houston, TX 77030 USA.
[Vierling, John M.] Baylor Coll Med, Baylor St Lukes Med Ctr, Dept Surg, Houston, TX 77030 USA.
[Mieli-Vergani, Giorgina] Hannover Med Sch, Hannover, Germany.
[Mieli-Vergani, Giorgina] Kings Coll Hosp London, GI & Nutr Ctr, Paediat Liver, London, England.
C3 King's College Hospital NHS Foundation Trust; King's College Hospital;
Dartmouth College; University of Vermont; Baylor College of Medicine;
Baylor College of Medicine; Hannover Medical School; King's College
Hospital NHS Foundation Trust; King's College Hospital
RP Vergani, D (corresponding author), Kings Coll Hosp London, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
EM diego.vergani@kcl.ac.uk
RI Vergani, Diego/H-7610-2019; Manns, Michael/AFG-3063-2022; Mieli-Vergani,
Giorgina/G-5616-2011
OI Mieli-Vergani, Giorgina/0000-0002-8215-4489
FU Roche-Genentech; TaiwanJ; Falk Pharma GmbH, Freiburg, Germany
FX JMV: Novartis, global advisory board; Roche-Genentech, research grant
funding, scientific advisory board; TaiwanJ, research grant funding;
Biolncept, consultant; MM: received research funding and trial support
from Falk Pharma GmbH, Freiburg, Germany; RL, ELK, GMV and DV: none.
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NR 143
TC 81
Z9 86
U1 0
U2 13
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD DEC
PY 2016
VL 75
BP 6
EP 19
DI 10.1016/j.jaut.2016.07.005
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA EE6OD
UT WOS:000389731200002
PM 27502148
DA 2025-01-07
ER
PT J
AU Liaskos, C
Rigopoulou, EI
Orfanidou, T
Bogdanos, DP
Papandreou, CN
AF Liaskos, Christos
Rigopoulou, Eirini I.
Orfanidou, Timoklia
Bogdanos, Dimitrios P.
Papandreou, Christos N.
TI CUZD1 and Anti-CUZD1 Antibodies as Markers of Cancer and Inflammatory
Bowel Diseases
SO CLINICAL & DEVELOPMENTAL IMMUNOLOGY
LA English
DT Review
ID DOMAIN-CONTAINING PROTEIN-1; PARANEOPLASTIC NEUROLOGICAL DISORDERS;
TUMOR-ASSOCIATED ANTIGENS; GRANULE MEMBRANE-PROTEIN; CELL LUNG-CANCER;
HEPATOCELLULAR-CARCINOMA; CUB-DOMAIN; EXOCRINE PANCREAS; SEROLOGIC
MARKERS; CROHNS-DISEASE
AB CUZD1, the CUB, and zona pellucida-like domains-containing protein 1, is a newly identified antigen of pancreatic autoantibodies (PAB) giving a reticulogranular pattern in patients with inflammatory bowel diseases, and in particular Crohn's disease. The exact mechanisms by which this pancreatic antigen becomes the target of IBD-specific pancreatic autoantibodies are unclear. At the same time, evolving data strongly support a role for CUZD1 in carcinogenesis. Human CUZD1 is mapped at chromosome 10q26.13 and the loss of this region is a frequent event in various malignant tumours. mRNA overexpression of CUZD1 has been noted in ovarian cancer and serum levels of CUZD1 are elevated in women with ovarian cancer and patients suffering from pancreatic cancer. CUZD1 appears to be one of the relatively few biomarkers that serve as both cancer biomarker and autoantigen of autoantibodies in an autoimmune disease unrelated to cancerous organs. This review discusses the role of CUZD1 in cancer and autoimmunity. We anticipate that a better understanding of the function of CUZD1 will help us to understand how it becomes the focus of an autoimmune attack specifically targeting the intestine and its enigmatic role in carcinogenesis.
C1 [Liaskos, Christos; Orfanidou, Timoklia; Bogdanos, Dimitrios P.] Inst Res & Technol Thessaly, Larisa 41222, Greece.
[Rigopoulou, Eirini I.; Bogdanos, Dimitrios P.] Univ Thessaly, Fac Med, Sch Hlth Sci, Dept Med, Biopolis 41110, Larissa, Greece.
[Bogdanos, Dimitrios P.] Kings Coll London, Univ London Kings Coll Hosp, Sch Med, Div Transplantat Immunol & Mucosal Biol, London SE5 9RS, England.
[Papandreou, Christos N.] Univ Thessaly, Univ Hosp Larissa, Fac Med, Dept Med Oncol,Sch Hlth Sci, Biopolis 41110, Larissa, Greece.
C3 University of Thessaly; King's College Hospital NHS Foundation Trust;
King's College Hospital; University of London; King's College London;
General University Hospital of Larissa; University of Thessaly
RP Bogdanos, DP (corresponding author), Inst Res & Technol Thessaly, Larisa 41222, Greece.
EM dimitrios.bogdanos@kcl.ac.uk
RI Bogdanos, Dimitrios/AAF-8620-2020; Liaskos, Christos/Q-7351-2017
OI Liaskos, Christos/0000-0002-1271-8613; Bogdanos,
Dimitrios/0000-0002-9697-7902
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NR 105
TC 12
Z9 17
U1 0
U2 5
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1740-2522
EI 1740-2530
J9 CLIN DEV IMMUNOL
JI Clin. Dev. Immunol.
PY 2013
AR 968041
DI 10.1155/2013/968041
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 141LO
UT WOS:000318726900001
PM 23710207
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Yazbeck, R
Jaenisch, SE
Abbott, CA
AF Yazbeck, Roger
Jaenisch, Simone E.
Abbott, Catherine A.
TI Potential disease biomarkers: dipeptidyl peptidase 4 and fibroblast
activation protein
SO PROTOPLASMA
LA English
DT Review
DE Dipeptidyl peptidase; Fibroblast activation protein; Cancer; Biomarker;
Inflammation
ID SQUAMOUS-CELL CARCINOMA; COLLAGENASE-LIKE PEPTIDASE; FATTY
LIVER-DISEASE; IV DPP IV; RHEUMATOID-ARTHRITIS; MULTIPLE-SCLEROSIS;
SYNOVIAL-FLUID; PANCREATIC ADENOCARCINOMA; CLINICAL-IMPLICATIONS;
COLORECTAL-CANCER
AB The importance of the dipeptidyl peptidase 4 (DPP4) gene family in regulating critical biochemical pathways continues to emerge. The two most well-studied members of the family, DPP4 and fibroblast activation protein (FAP), have been investigated both as therapeutic targets for disease and as diagnostic biomarkers. The interest in DPP4 and FAP as potential disease biomarkers has been driven primarily by observations of altered expression profiles in inflammatory diseases and cancer. Furthermore, the stability and persistence of soluble DPP4 and FAP in the serum make them attractive candidate serology markers. This review summarises investigations into DPP4 and FAP as biomarkers of autoimmune disease, gut inflammation, psychosomatic disorders and malignancy and discusses their potential likelihood as clinically useful tools.
C1 [Yazbeck, Roger; Jaenisch, Simone E.] Flinders Univ S Australia, Coll Med & Publ Hlth, Dept Surg, GPO Box 2100, Adelaide, SA 5001, Australia.
[Yazbeck, Roger; Jaenisch, Simone E.; Abbott, Catherine A.] Flinders Univ S Australia, Flinders Ctr Innovat Canc, Adelaide, SA, Australia.
[Abbott, Catherine A.] Flinders Univ S Australia, Coll Sci & Engn, GPO Box 2100, Adelaide, SA 5001, Australia.
C3 Flinders University South Australia; Flinders University South
Australia; Flinders University South Australia
RP Abbott, CA (corresponding author), Flinders Univ S Australia, Flinders Ctr Innovat Canc, Adelaide, SA, Australia.; Abbott, CA (corresponding author), Flinders Univ S Australia, Coll Sci & Engn, GPO Box 2100, Adelaide, SA 5001, Australia.
EM cathy.abbott@flinders.edu.au
RI Yazbek, Roger/AAX-1750-2020; Abbott, Catherine/A-9121-2008
OI Abbott, Catherine/0000-0001-8215-4406; Yazbeck,
Roger/0000-0002-1038-4998
FU Catherine Marie Enright Kelly cancer research fellowship within the
Flinders University Department of Surgery
FX Dr. Yazbeck is supported by the Catherine Marie Enright Kelly cancer
research fellowship within the Flinders University Department of
Surgery.
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NR 110
TC 36
Z9 40
U1 0
U2 26
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0033-183X
EI 1615-6102
J9 PROTOPLASMA
JI Protoplasma
PD JAN
PY 2018
VL 255
IS 1
BP 375
EP 386
DI 10.1007/s00709-017-1129-5
PG 12
WC Plant Sciences; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Cell Biology
GA FS0JY
UT WOS:000419461400027
PM 28620698
DA 2025-01-07
ER
PT J
AU Gronbaek, L
Otete, H
Ban, L
Crooks, C
Card, T
Jepsen, P
West, J
AF Gronbaek, Lisbet
Otete, Harmony
Ban, Lu
Crooks, Colin
Card, Timothy
Jepsen, Peter
West, Joe
TI Incidence, prevalence and mortality of autoimmune hepatitis in England
1997-2015. A population-based cohort study
SO LIVER INTERNATIONAL
LA English
DT Article
DE cohort study; epidemiology; hepatitis; autoimmune; incidence;
prevalence; prognosis; registry
ID CHRONIC ACTIVE HEPATITIS; PRIMARY SCLEROSING CHOLANGITIS;
LIVER-DISEASES; CIRRHOSIS; EPIDEMIOLOGY; PROGNOSIS; DIAGNOSIS; CRITERIA;
TIME; AIH
AB Background & Aims There are few population-based studies of the incidence and mortality of autoimmune hepatitis. The burden of the disease and how it has changed over time have not been fully explored. We conducted a population-based cohort study on the incidence and mortality of autoimmune hepatitis in England, 1997-2015.
Methods From the Clinical Practice Research Datalink we included 882 patients diagnosed with autoimmune hepatitis in England, 1997-2015. The patients were followed through 2015, and we calculated the sex- and age-standardized incidence and prevalence of autoimmune hepatitis. We examined variation in incidence by sex, age, calendar year, geographical region and socioeconomic status, and incidence rate ratios were calculated with Poisson regression. We calculated all-cause and cause-specific mortality.
Results The overall standardized incidence rate of autoimmune hepatitis was 2.08 (95% confidence interval 1.94-2.22) per 100,000 population per year, higher in women, higher in older age and independent of region and socioeconomic status. From 1997 to 2015 the incidence doubled from 1.27 (95% confidence interval 0.51-2.02) to 2.56 (95% confidence interval 1.79-3.33) per 100,000 population per year. The 10-year cumulative all-cause mortality was 31.9% (95% confidence interval 27.6-36.5), and the 10-year cumulative liver-related mortality, including hepatocellular carcinoma was similar to 10.5%.
Conclusions This population-based study showed that the incidence of autoimmune hepatitis doubled over an eighteen-year period. The incidence was particularly high in older women and was similar across all regions of England and independent of socioeconomic status. Patients with autoimmune hepatitis had a high mortality.
C1 [Gronbaek, Lisbet; Jepsen, Peter] Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Palle Juul Jensens Blvd 99, Aarhus 8200 N, Denmark.
[Gronbaek, Lisbet; Jepsen, Peter] Aarhus Univ Hosp, Dept Clin Epidemiol, Aarhus N, Denmark.
[Gronbaek, Lisbet; Otete, Harmony; Card, Timothy; Jepsen, Peter; West, Joe] Univ Nottingham, Sch Med, Div Epidemiol & Publ Hlth, Nottingham, England.
[Gronbaek, Lisbet] Reg Hosp Horsens, Dept Med, Horsens, Denmark.
[Otete, Harmony] Univ Cent Lancashire, Sch Med & Dent, Preston, Lancs, England.
[Ban, Lu; Crooks, Colin; Card, Timothy; West, Joe] Nottingham Univ Hosp NHS Trust, Nottingham Biomed Res Ctr, NIHR, Nottingham, England.
[Ban, Lu; Crooks, Colin; Card, Timothy; West, Joe] Univ Nottingham, Nottingham, England.
[Ban, Lu; Crooks, Colin] Univ Nottingham, Nottingham Digest Dis Ctr, Sch Med, Nottingham, England.
C3 Aarhus University; Aarhus University; University of Nottingham;
University of Central Lancashire; University of Nottingham; Nottingham
University Hospital NHS Trust; University of Nottingham; University of
Nottingham
RP Gronbaek, L (corresponding author), Aarhus Univ Hosp, Dept Hepatol & Gastroenterol, Palle Juul Jensens Blvd 99, Aarhus 8200 N, Denmark.
EM groenbaek.lisbet@gmail.com
RI Crooks, Colin/I-1130-2016; West, Joe/I-6637-2012; Card,
Timothy/J-8651-2013
OI Crooks, Colin/0000-0002-6794-6621; Gronbaek, Lisbet/0000-0003-0626-179X;
Jepsen, Peter/0000-0002-6641-1430; West, Joe/0000-0002-1135-9356; Card,
Timothy/0000-0003-2555-2250
FU Danish foundation
FX Lisbet Gronbaek received funding from the Danish foundation of
17.12.1981 and the Danish Foundation of AP Moller. The funding sources
were not involved in the conduct of the research or preparation of the
article.
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NR 58
TC 43
Z9 44
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD JUL
PY 2020
VL 40
IS 7
BP 1634
EP 1644
DI 10.1111/liv.14480
EA MAY 2020
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA MA2LS
UT WOS:000529694400001
PM 32304617
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Zhang, Z
Xu, L
Qin, NS
Zhang, JX
Xiang, Q
Liu, Q
Cheng, YJ
Bai, YG
Liu, QX
Liu, YH
Duan, XN
Cui, YM
AF Zhang, Zhuo
Xu, Ling
Qin, Naishan
Zhang, Jixin
Xiang, Qian
Liu, Qian
Cheng, Yuanjia
Bai, Yuge
Liu, Qianxin
Liu, Yinhua
Duan, Xuening
Cui, Yimin
TI Case report: Secondary sclerosing cholangitis induced by lapatinib and
vinorelbine in a metastasis breast cancer patient
SO THORACIC CANCER
LA English
DT Article
DE case report; cholestatic drug‐ induced liver injury; lapatinib;
secondary sclerosing cholangitis; vinorelbine
AB Secondary sclerosing cholangitis (SSC) is a rare cholestatic liver disease that may have a severe clinical course. A 61-year-old woman with a history of metastasis breast cancer was admitted to our hospital for the second cycle of chemotherapy with lapatinib and vinorelbine. The patient had no reports of elevated liver function tests (LFTs) in the previous multiple chemotherapies or history of liver disease. However, the admission laboratory results showed severe cholestatic liver injury with the possibility of SSC by magnetic resonance cholangiopancreatography. Although chemotherapy was discontinued and patient was treated with hepatoprotective drugs, the LFTs did not improve and liver biopsy indicated mild injury of intrahepatic bile duct epithelium and hepatocyte. We added ursodeoxycholic acid and prednisolone to protect the liver, and laboratory data showed a response. To prevent the progression, lapatinib and vinorelbine were reintroduced and transient increases in alanine aminotransferase and gamma-glutamyl transpeptidase were observed. With no evidence of viral or autoimmune liver disease, SSC induced by lapatinib and vinorelbine was diagnosed. This is the first case report of tyrosine kinase inhibitors and vinorelbine induced SSC and clinicians should be aware of the possibility of it. More case reports about this adverse drug reaction are needed to delineate optimal management.
C1 [Zhang, Zhuo; Xiang, Qian; Liu, Qianxin; Cui, Yimin] Peking Univ First Hosp, Dept Pharm, 6 Dahongluochang St, Beijing 100034, Peoples R China.
[Xu, Ling; Liu, Qian; Cheng, Yuanjia; Bai, Yuge; Liu, Yinhua; Duan, Xuening] Peking Univ First Hosp, Breast Dis Ctr, 8 Xishiku St, Beijing 10034, Peoples R China.
[Qin, Naishan] Peking Univ First Hosp, Dept Radiol, Beijing, Peoples R China.
[Zhang, Jixin] Peking Univ First Hosp, Dept Pathol, Beijing, Peoples R China.
C3 Peking University
RP Cui, YM (corresponding author), Peking Univ First Hosp, Dept Pharm, 6 Dahongluochang St, Beijing 100034, Peoples R China.; Xu, L (corresponding author), Peking Univ First Hosp, Breast Dis Ctr, 8 Xishiku St, Beijing 10034, Peoples R China.
EM xuling_en@126.com; cui.pharm@pkufh.com
RI Xu, Ling/ITR-8242-2023; Zhang, Jixin/JDV-9635-2023; xiang,
qian/F-2024-2018; cui, yimin/JCE-0464-2023
OI Xiang, Qian/0000-0002-8245-2611
FU National Key R&D Program of China [2016YFC0901302]; National Natural
Science Foundation of China [81673509, 81573504]; National Science and
Technology Major Projects for 'Major New Drugs Innovation and
Development' [2017ZX09101001, 2017ZX09304028, 2018ZX09201014]; Natural
Science Foundation of Beijing Municipality [7171012]; China-Japan
Friendship Hospital
FX National Key R&D Program of China, Grant/Award Number: 2016YFC0901302;
National Natural Science Foundation of China, Grant/Award Numbers:
81673509, 81573504; National Science and Technology Major Projects for `
Major New Drugs Innovation and Development', Grant/Award Numbers:
2017ZX09101001, 2017ZX09304028, 2018ZX09201014; Natural Science
Foundation of Beijing Municipality, Grant/Award Number: 7171012;
China-Japan Friendship Hospital
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NR 18
TC 2
Z9 3
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1759-7706
EI 1759-7714
J9 THORAC CANCER
JI Thorac. Cancer
PD JUN
PY 2021
VL 12
IS 12
BP 1912
EP 1916
DI 10.1111/1759-7714.13986
EA MAY 2021
PG 5
WC Oncology; Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Respiratory System
GA SR6BK
UT WOS:000647846100001
PM 33957015
OA Green Published
DA 2025-01-07
ER
PT J
AU Ngu, JH
Gearry, RB
Wright, AJ
Stedman, CAM
AF Ngu, Jing Hieng
Gearry, Richard Blair
Wright, Andrew Jeffrey
Stedman, Catherine Ann Malcolm
TI Inflammatory Bowel Disease Is Associated With Poor Outcomes of Patients
With Primary Sclerosing Cholangitis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Inflammation; Cancer Risk; Mortality; Autoimmune Liver Disease; Biliary
Duct; Fibrosis
ID NATURAL-HISTORY; PROGNOSTIC VARIABLES; AUTOIMMUNE HEPATITIS;
NEW-ZEALAND; POPULATION; EPIDEMIOLOGY; PREVALENCE; JAPAN
AB BACKGROUND & AIMS: Little is known about the exact etiology of primary sclerosing cholangitis (PSC); epidemiologic data are scarce. We performed a population-based epidemiologic study of PSC in Canterbury, New Zealand. METHODS: By using multiple case-finding methods, we searched public and private adult and pediatric outpatient clinics, hospital discharge summaries, and radiology and pathology reports to identify all cases of PSC in the region. Cases were included if PSC was identified by endoscopic retrograde cholangiography, magnetic resonance cholangiography, or liver biopsy analysis (n = 79). RESULTS: The incidence of PSC in 2008 was 1.6 per 100,000 persons (95% confidence interval [CI], 0.5-2.7). The point prevalence on December 31, 2008, was 11.7 per 100,000 persons (95% CI, 8.7-14.8). The mean and median ages at diagnosis were 50 years (95% CI, 46-53 years) and 49 years (range, 17-80 years), respectively. Patients who had inflammatory bowel disease (IBD) presented with PSC earlier than those without IBD (P = .003), were more likely to develop serious malignant complications (P = .017), and were more likely to require liver transplantation or die (P = .03). CONCLUSIONS: In a population-based epidemiology study of PSC in Canterbury, New Zealand, we observed large differences between PSC patients with or without concurrent IBD in age at diagnosis, development of cancer, mortality, and requirement for liver transplantation. IBD therefore affects outcomes of patients with PSC, an important observation that requires further study.
C1 [Ngu, Jing Hieng; Gearry, Richard Blair; Stedman, Catherine Ann Malcolm] Christchurch Hosp, Dept Gastroenterol, Christchurch, New Zealand.
[Ngu, Jing Hieng; Gearry, Richard Blair; Wright, Andrew Jeffrey; Stedman, Catherine Ann Malcolm] Univ Otago, Canterbury, New Zealand.
C3 Christchurch Hospital New Zealand; University of Otago
RP Stedman, CAM (corresponding author), Christchurch Hosp, Dept Gastroenterol, Private Bag 4710, Christchurch, New Zealand.
EM catherine.stedman@cdhb.govt.nz
RI Wright, Andrew/HDM-9615-2022; Stedman, Catherine/AFM-4210-2022; Gearry,
Richard/H-3959-2019
OI Gearry, Richard/0000-0002-2298-5141
FU Health Research Council of New Zealand; Ferring/New Zealand Society of
Gastroenterology; Canterbury Medical Research Foundation; Royal
Australasia College of Physicians
FX Dr Ngu's stipend is supported by Clinical Research Training Fellowship
from the Health Research Council of New Zealand (2011-2013), Ferring/New
Zealand Society of Gastroenterology Fellowship, and Canterbury Medical
Research Foundation Fellowship (2010). Research-related expenses were
supported by a grant from the Royal Australasia College of Physicians.
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NR 38
TC 66
Z9 69
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD DEC
PY 2011
VL 9
IS 12
BP 1092
EP 1097
DI 10.1016/j.cgh.2011.08.027
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 857WJ
UT WOS:000297754100023
PM 21893134
OA Bronze
DA 2025-01-07
ER
PT J
AU Villeneuve, JP
Pichette, V
AF Villeneuve, JP
Pichette, V
TI Cytochrome P450 and liver diseases
SO CURRENT DRUG METABOLISM
LA English
DT Review
DE liver disease; cirrhosis; cholestasis; hepatitis; cytochrome P450;
isoforms; drug metabolism; hepatotoxicity
ID AMINOPYRINE BREATH TEST; HEPATIC STELLATE CELLS; SERUM BILE-ACIDS;
NONALCOHOLIC STEATOHEPATITIS; HEPATOCELLULAR-CARCINOMA; PROGNOSTIC
VALUE; IN-VITRO; GENETIC POLYMORPHISMS; ANTIPYRINE CLEARANCE; HEPATOCYTE
APOPTOSIS
AB Cytochrome P-450 (CYPs) are involved in the metabolism of drugs. Chemicals and endogonous Substrates. The hepatic CYPs arc also involved in the pathogenesis of several liver diseases. CYP-mediated activation of drugs to toxic metabolites induces hepatotoxicity. Well-known examples include acetaminophen and halothane. In some instances,, covalent binding of the toxic metabolite to CYP leads to the formation of anti-CYP antibodies and immune-mediated hepatotoxicity (hydralazine. tienilic acid). Anti-CYP2D6 antibodies are also present in the serum of patients with type II autoimmune hepatitis, but the mechanism leading to their presence and their pathogenic significance remains unclear. Several studies Support a role for CYP2E1 in the pathogenesis of alcoholic liver disease and non-alcoholic steatohepatitis. In these conditions, enhanced CYP2E1 activity is associated with lipid peroxidation and the production of reactivc oxygen species with secondary damage to cellular membranes and mitochondria. Because of its ability to activate carcinogens, a role for CYP2E1 as a cofactor for hepatocellular carcinoma has also been postulated.
On the other hand, drug metabolism is impaired in patients with liver disease, particularly that mediated by CYPs. The content and activity of CYP1A, 2C19 and 3A appear to be particularly vulnerable to the effect of liver disease while CYP2D6, 2C9 and 2E1 are less affected. The pattern of CYPs isoenzymes alterations also differs according to the etiology of liver disease. A strong relationship between the activity of CYPs and the severity of cirrhosis has been demonstrated, but the usefulness of measuring CYP activity to assess hepatic functional reserve remains uncertain.
C1 CHUM, Hop St Luc, Ctr Rech, Montreal, PQ H2X 1P1, Canada.
Univ Montreal, Hop Maison Neuve Rosemont, Div Nephrol, Montreal, PQ, Canada.
C3 Universite de Montreal; Universite de Montreal
RP CHUM, Hop St Luc, Ctr Rech, 264 Rene Levesque Blvd E, Montreal, PQ H2X 1P1, Canada.
EM villej@sympatico.ca
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NR 116
TC 148
Z9 166
U1 0
U2 26
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-2002
EI 1875-5453
J9 CURR DRUG METAB
JI Curr. Drug Metab.
PD JUN
PY 2004
VL 5
IS 3
BP 273
EP 282
DI 10.2174/1389200043335531
PG 10
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 822VZ
UT WOS:000221570000007
PM 15180496
DA 2025-01-07
ER
PT J
AU Zhou, JM
Zheng, QX
Chen, Z
AF Zhou, Jiaming
Zheng, Qiuxian
Chen, Zhi
TI The Nrf2 Pathway in Liver Diseases
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE reactive oxygen species; nuclear factor-erythroid 2-related factor 2;
kelch-like ECH-associated protein 1; oxidative stress; liver diseases
ID TRANSCRIPTION FACTOR NRF2; OXIDATIVE STRESS; HEME OXYGENASE-1;
ACETAMINOPHEN HEPATOTOXICITY; NF-E2-RELATED FACTOR-2;
SIGNAL-TRANSDUCTION; HO-1 EXPRESSION; KNOCKOUT MICE; CORE PROTEIN;
ACTIVATION
AB Oxidative stress is the leading cause of most liver diseases, such as drug-induced liver injury, viral hepatitis, and alcoholic hepatitis caused by drugs, viruses, and ethanol. The Kelch-like ECH-associated protein 1-NFE2-related factor 2 (Keap1-Nrf2) system is a critical defense mechanism of cells and organisms in response to oxidative stress. Accelerating studies have clarified that the Keap1-Nrf2 axis are involved in the prevention and attenuation of liver injury. Nrf2 up-regulation could alleviate drug-induced liver injury in mice. Moreover, many natural Nrf2 activators can regulate lipid metabolism and oxidative stress of liver cells to alleviate fatty liver disease in mice. In virus hepatitis, the increased Nrf2 can inhibit hepatitis C viral replication by up-regulating hemeoxygenase-1. In autoimmune liver diseases, the increased Nrf2 is essential for mice to resist liver injury. In liver cirrhosis, the enhanced Nrf2 reduces the activation of hepatic stellate cells by reducing reactive oxygen species levels to prevent liver fibrosis. Nrf2 plays a dual function in liver cancer progression. At present, a Nrf2 agonist has received clinical approval. Therefore, activating the Nrf2 pathway to induce the expression of cytoprotective genes is a potential option for treating liver diseases. In this review, we comprehensively summarized the relationships between oxidative stress and liver injury, and the critical role of the Nrf2 pathway in multiple liver diseases.
C1 [Zhou, Jiaming; Zheng, Qiuxian; Chen, Zhi] Zhejiang Univ, Collaborat Innovat Ctr Diag & Treatment Infect Di, State Key Lab Diag & Treatment Infect Dis,Sch Med, Natl Clin Res Ctr Infect Dis,Affiliated Hosp 1,Na, Hangzhou, Peoples R China.
C3 Zhejiang University; Collaborative Innovation Center for Diagnosis &
Treatment of Infectious Diseases
RP Chen, Z (corresponding author), Zhejiang Univ, Collaborat Innovat Ctr Diag & Treatment Infect Di, State Key Lab Diag & Treatment Infect Dis,Sch Med, Natl Clin Res Ctr Infect Dis,Affiliated Hosp 1,Na, Hangzhou, Peoples R China.
EM zjuchenzhi@zju.edu.cn
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NR 101
TC 101
Z9 107
U1 2
U2 51
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD FEB 10
PY 2022
VL 10
AR 826204
DI 10.3389/fcell.2022.826204
PG 14
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA ZH2ZX
UT WOS:000760813500001
PM 35223849
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Park, HS
Jang, KY
Kim, YK
Cho, BH
Moon, WS
AF Park, Ho Sung
Jang, Kyu Yun
Kim, Young Kon
Cho, Baik Hwan
Moon, Woo Sung
TI Histiocyte-rich reactive hyperplasia of the liver: Unusual morphologic
features
SO JOURNAL OF KOREAN MEDICAL SCIENCE
LA English
DT Article
DE pseudolymphoma; liver neoplasms; lymphoid hyperplasia; reactive
ID NODULAR LYMPHOID LESION; PSEUDOLYMPHOMA; PATIENT; DISORDER
AB Reactive lymphoid hyperplasia (RLH) of the liver is a rare entity and has also been termed nodular lymphoid lesion or pseudolymphoma of the liver. We report a case of hepatic RLH exhibiting unusual histiocyte-rich histologic features in a 47-yr-old woman in conjunction with a renal cell carcinoma, A follow-up computed tomography scan was done 14 months after a right radical nephrectomy for renal cell carcinoma revealed a nodular lesion in segment 5 of the liver. The lesion was interpreted as metastatic renal cell carcinoma or hepatocellular carcinoma based on the history of the patient and radiologic findings. Wedge resection of segment 5 was done with sufficient distance from the mass. Microscopically, the lesion was composed predominantly of peculiar histiocytic proliferation and was characterized by lymphoid aggregates forming a lymphoid follicle with germinal centers. The present case and prior cases reported in the literature suggest that RLH of the liver appear to be a heterogenous group of reactive inflammatory lesions that are often associated with autoimmune disease or malignant tumors.
C1 [Park, Ho Sung; Jang, Kyu Yun; Moon, Woo Sung] Chonbuk Natl Univ, Sch Med, Dept Pathol, Inst Med Sci, Jeonju 561180, South Korea.
[Kim, Young Kon] Chonbuk Natl Univ, Sch Med, Dept Radiol, Inst Med Sci, Jeonju 561180, South Korea.
[Cho, Baik Hwan] Chonbuk Natl Univ, Sch Med, Dept Surg, Inst Med Sci, Jeonju 561180, South Korea.
Ctr Healthcare Technol Dev, Jeonju, South Korea.
C3 Jeonbuk National University; Jeonbuk National University; Jeonbuk
National University
RP Moon, WS (corresponding author), Chonbuk Natl Univ, Sch Med, Dept Pathol, Inst Med Sci, San 2-20 Geumam Dong, Jeonju 561180, South Korea.
EM mws@chonbuk.ac.kr
RI Kim, Sung Hwan/GQQ-1731-2022; KIM, KYUN/Q-3070-2018
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PU KOREAN ACAD MEDICAL SCIENCES
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PA 302 75 DONG DU ICHON, DONG YONGSAN KU, SEOUL 140 031, SOUTH KOREA
SN 1011-8934
EI 1598-6357
J9 J KOREAN MED SCI
JI J. Korean Med. Sci.
PD FEB
PY 2008
VL 23
IS 1
BP 156
EP 160
DI 10.3346/jkms.2008.23.1.156
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 271XZ
UT WOS:000253823300030
PM 18303220
OA Green Submitted, gold, Green Published
DA 2025-01-07
ER
PT J
AU Alhebbi, H
Peer-Zada, AA
Al-Hussaini, AA
Algubaisi, S
Albassami, A
AlMasri, N
Alrusayni, Y
Alruzug, IM
Alharby, E
Samman, MA
Ayoub, SZ
Maddirevula, S
Peake, RWA
Alkuraya, FS
Wali, S
Almontashiri, NAM
AF Alhebbi, Hamoud
Peer-Zada, Abdul Ali
Al-Hussaini, Abdulrahman A.
Algubaisi, Sara
Albassami, Awad
AlMasri, Nasser
Alrusayni, Yasir
Alruzug, Ibrahim M.
Alharby, Essa
Samman, Manar A.
Ayoub, Syed Zubair
Maddirevula, Sateesh
Peake, Roy W. A.
Alkuraya, Fowzan S.
Wali, Sami
Almontashiri, Naif A. M.
TI New paradigms ofUSP53disease: normal GGT cholestasis, BRIC,
cholangiopathy, and responsiveness to rifampicin
SO JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID FAMILIAL INTRAHEPATIC CHOLESTASIS; HEPATOCELLULAR-CARCINOMA; MUTATIONS;
ATP8B1; DISEASE; ABCB11; TJP2; STIMULATION; EXPRESSION; TRANSPORT
AB Biallelic variants in theUSP53gene have recently been reported to segregate with normal gamma glutamyltransferase (GGT) cholestasis. Using whole-exome sequencing (WES), we detected two USP53homozygous variants (c.951delT; p. Phe317fs and c.1744C>T; p. Arg582*) in five additional cases, including an unpublished cousin of a previously described family with intractable itching and normal GGT cholestasis. Three patients, a child and two adults, presented with recurrent episodes of normal GGT cholestasis, consistent with a diagnosis of benign recurrent intrahepatic cholestasis (BRIC). Cholangiopathic changes, possibly autoimmune in origin, were recognized in some patients. Additional phenotypic details in one patient included an enlarged left kidney, and speech/developmental delay. Notably, two patients exhibited a complete response to rifampicin, and one responded to ursodeoxycholic acid (UDCA). Two adult patients were suspected to have autoimmune liver disease and treated with steroids. This report describes new cases of USP53 disease presenting with normal GGT cholestasis or BRIC in three children and two adults. We also describe the novel finding of a dramatic response to rifampicin. The association of cholangiopathy with normal GGT cholestasis provides a diagnostic challenge and remains poorly understood.
C1 [Alhebbi, Hamoud; Algubaisi, Sara; Albassami, Awad; Wali, Sami] Prince Sultan Mil Med City, Div Gastroenterol & Hepatol, Dept Pediat, Riyadh, Saudi Arabia.
[Peer-Zada, Abdul Ali; Samman, Manar A.; Ayoub, Syed Zubair] King Fahad Med City, Mol Pathol Pathol & Clin Lab Med Adm, Riyadh, Saudi Arabia.
[Al-Hussaini, Abdulrahman A.] Childrens Specialized Hosp King Fahad Med City, Pediat Gastroenterol Div, Riyadh, Saudi Arabia.
[Al-Hussaini, Abdulrahman A.; Alkuraya, Fowzan S.] Alfaisal Univ, Coll Med, Riyadh, Saudi Arabia.
[AlMasri, Nasser] Prince Sultan Mil Med City, Dept Adult Gastroenterol & Hepatol, Riyadh, Saudi Arabia.
[Alrusayni, Yasir] Prince Sultan Mil Med City, Dept Pathol, Riyadh, Saudi Arabia.
[Alruzug, Ibrahim M.] King Saud Med City, Dept Adult Gastroenterol & Hepatol, Riyadh, Saudi Arabia.
[Alharby, Essa; Almontashiri, Naif A. M.] Taibah Univ, Ctr Genet & Inherited Dis, Almadinah Almunwarah, Saudi Arabia.
[Maddirevula, Sateesh; Alkuraya, Fowzan S.] King Faisal Specialist Hosp & Res Ctr, Dept Genet, Riyadh, Saudi Arabia.
[Peake, Roy W. A.] Boston Childrens Hosp, Dept Lab Med, 300 Longwood Ave, Boston, MA 02115 USA.
[Almontashiri, Naif A. M.] Taibah Univ, Fac Appl Med Sci, Almadinah Almunwarah, Saudi Arabia.
C3 Prince Sultan Military Medical City; King Fahad Medical City; Alfaisal
University; Prince Sultan Military Medical City; Prince Sultan Military
Medical City; King Saud Medical City; Taibah University; King Faisal
Specialist Hospital & Research Center; Harvard University; Boston
Children's Hospital; Taibah University
RP Wali, S (corresponding author), Prince Sultan Mil Med City, Div Gastroenterol & Hepatol, Dept Pediat, Riyadh, Saudi Arabia.; Almontashiri, NAM (corresponding author), Taibah Univ, Ctr Genet & Inherited Dis, Almadinah Almunwarah, Saudi Arabia.; Almontashiri, NAM (corresponding author), Taibah Univ, Fac Appl Med Sci, Almadinah Almunwarah, Saudi Arabia.
EM swali@psmmc.med.sa; nmontashri@taibahu.edu.sa
RI Almontashiri, Naif/AAR-3806-2020; Alharby, Essa/HPG-0450-2023;
Maddirevula, Sateesh/ABE-3655-2021; Peer Zada, Abdul Ali/HJJ-0800-2023;
Alkuraya, Fowzan/A-1542-2009
OI Maddirevula, Sateesh/0000-0003-2999-2229; Almontashiri,
Naif/0000-0003-3607-395X; Alkuraya, Fowzan/0000-0003-4158-341X
FU Deputyship for Research and Innovation, Ministry of Education in Saudi
Arabia [821]
FX The authors extend their appreciation to the Deputyship for Research and
Innovation, Ministry of Education in Saudi Arabia for funding this
research work through the project number 821.
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NR 50
TC 24
Z9 25
U1 2
U2 6
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1434-5161
EI 1435-232X
J9 J HUM GENET
JI J. Hum. Genet.
PD FEB
PY 2021
VL 66
IS 2
BP 151
EP 159
DI 10.1038/s10038-020-0811-1
EA AUG 2020
PG 9
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA PO1XK
UT WOS:000556182700001
PM 32759993
DA 2025-01-07
ER
PT J
AU Ilan, Y
AF Ilan, Yaron
TI Oral tolerance: Can we make it work?
SO HUMAN IMMUNOLOGY
LA English
DT Review
DE Oral tolerance; Dendritic cells; NKT cells; Mucosal immunity
ID REGULATORY T-CELLS; MYELIN BASIC-PROTEIN; GROWTH-FACTOR-BETA; TOXIN
B-SUBUNIT; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
HEPATOCELLULAR-CARCINOMA GROWTH; INFLAMMATORY-BOWEL-DISEASE; INTESTINAL
DENDRITIC CELLS; LATENCY-ASSOCIATED PEPTIDE; TGF-BETA
AB Mucosal tolerance remains an attractive approach for the treatment of autoimmune and inflammatory diseases. The agents used in these treatments lack toxicity, can be easily administered, and enable the promotion of antigen-specific immune responses. The limited success of clinical trials over the past 2 decades has led to the fear that the beneficial effect observed in animal models cannot be repeated in humans. Successful application of mucosal tolerance for the treatment of human diseases will depend on strategies that target the correct cells in the gut-liver axis, improve antigen presentation, alter the administered dose and formulations, utilize potent mucosal adjuvants, develop immune biomarkers enabling follow-up of the effect, utilize combination therapies with other immune modulatory agents, and target the right patient populations. Here, we discuss 12 of the major questions related to oral tolerance and its clinical application to humans with immune-mediated disorders. (C) 2009 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
C1 [Ilan, Yaron] Hadassah Hebrew Univ, Dept Med, Gastroenterol Unit, Med Ctr, Jerusalem, Israel.
[Ilan, Yaron] Hadassah Hebrew Univ, Dept Med, Liver Unit, Med Ctr, Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hadassah University Medical Center;
Hebrew University of Jerusalem; Hadassah University Medical Center
RP Ilan, Y (corresponding author), Hadassah Hebrew Univ, Dept Med, Gastroenterol Unit, Med Ctr, Jerusalem, Israel.
EM ilan@hadassah.org.il
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NR 134
TC 24
Z9 30
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD OCT
PY 2009
VL 70
IS 10
BP 768
EP 776
DI 10.1016/j.humimm.2009.06.018
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 503YI
UT WOS:000270577900002
PM 19559742
DA 2025-01-07
ER
PT J
AU Parikh-Patel, A
White, RH
Allen, M
Cress, R
AF Parikh-Patel, Arti
White, Richard H.
Allen, Mark
Cress, Rosemary
TI Cancer risk in a cohort of patients with systemic lupus erythematosus
(SLE) in California
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE cancer; systemic lupus erythematosus; malignancy; autoimmune diseases;
hematologic neoplasms
ID CORONARY-ARTERY-DISEASE; NON-HODGKINS-LYMPHOMA; ACUTE NONLYMPHOCYTIC
LEUKEMIA; CYCLOPHOSPHAMIDE TREATMENT; AUTOIMMUNE-DISEASES; SOUTHERN
SWEDEN; BLADDER-CANCER; MALIGNANCY; NEPHRITIS; PREVALENCE
AB Objective We conducted a retrospective cohort study to examine cancer risk in a large cohort of systemic lupus erythematosus (SLE) patients in California.
Methods The cohort consisted of individuals with SLE derived from statewide patient discharge data during the period 1991-2002. SLE patients were followed using cancer registry data to examine patterns of cancer development. Standardized incidence ratios (SIRs) and 95% CI were calculated to compare the observed to expected numbers of cancers based on age-, race-, and sex-specific incidence rates in the California population.
Results The 30,478 SLE patients were observed for 157,969 person-years. A total of 1,273 cancers occurred within the observation interval. Overall cancer risk was significantly elevated (SIR = 1.14, 95% CI = 1.07-1.20). SLE patients had higher risks of vagina/vulva (SIR = 3.27, 95% CI = 2.41-4.31) and liver cancers (SIR = 2.70, 95% CI = 1.54-4.24). Elevated risks of lung, kidney, and thyroid cancers and several hematopoietic malignancies were also observed. Individuals had significantly lower risks of several screenable cancers, including breast, cervix, and prostate.
Conclusions These data suggest that risks of several cancer types are elevated among SLE patients. Detailed studies of endogenous and exogenous factors that drive these associations are needed.
C1 [Parikh-Patel, Arti; Allen, Mark; Cress, Rosemary] Calif Canc Registry, Inst Publ Hlth, Sacramento, CA 95815 USA.
[White, Richard H.] Univ Calif Davis, Sch Med, Dept Internal Med, Sacramento, CA 95817 USA.
[Cress, Rosemary] Univ Calif Davis, Dept Publ Hlth Sci, Davis, CA 95616 USA.
C3 Public Health Institute; University of California System; University of
California Davis; University of California System; University of
California Davis
RP Parikh-Patel, A (corresponding author), Calif Canc Registry, Inst Publ Hlth, 1700 Tribute Rd,Suite 100, Sacramento, CA 95815 USA.
EM aparikh@ccr.ca.gov
FU National Cancer Institute [1R21CA100759-01A2]; California Department of
Health Services; National Cancer Institute's Surveillance, Epidemiology
[N01-PC-35136]; Northern California Cancer Center
FX This work was funded by grant 1R21CA100759-01A2 (A. Parikh-Patel) from
the National Cancer Institute. The collection of cancer incidence data
used in this study was supported by the California Department of Health
Services as part of the statewide cancer reporting program mandated by
California Health and Safety Code Section 103885; the National Cancer
Institute's Surveillance, Epidemiology, and End Results Program under
contract N01-PC-35136 awarded to the Northern California Cancer Center,
contract N01-PC-35139 awarded to the University of Southern California,
and contract N02-PC-15105 awarded to the Public Health Institute; and
the Centers for Disease Control and Prevention's National Program of
Cancer Registries, under agreement # U55/CCR921930-02 awarded to the
Public Health Institute. The ideas and opinions expressed herein are
those of the author(s) and endorsement by the State of California,
Department of Health Services, the National Cancer Institute, and the
Centers for Disease Control and Prevention or their Contractors and
Subcontractors is not intended nor should be inferred.
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PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
EI 1573-7225
J9 CANCER CAUSE CONTROL
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WE Science Citation Index Expanded (SCI-EXPANDED)
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GA 350QL
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PM 18386139
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Zhang, LL
Hou, CF
Chen, C
Guo, YX
Yuan, WT
Yin, DT
Liu, JB
Sun, ZQ
AF Zhang, Lele
Hou, Chaofeng
Chen, Chen
Guo, Yaxin
Yuan, Weitang
Yin, Detao
Liu, Jinbo
Sun, Zhenqiang
TI The role of N6-methyladenosine (m6A) modification
in the regulation of circRNAs
SO MOLECULAR CANCER
LA English
DT Review
DE M(6)A; CircRNA; M(6)A modified circRNA; Innate immunity; Tumour
ID MESSENGER-RNA METHYLATION; CIRCULAR RNAS; HEPATOCELLULAR-CARCINOMA;
NUCLEAR-RNA; CERVICAL-CANCER; PROMOTES; TRANSLATION; PROGRESSION;
N6-METHYLADENOSINE; IDENTIFICATION
AB N-6-methyladenosine (m(6)A), the most abundant modification in eukaryotic cells, regulates RNA transcription, processing, splicing, degradation, and translation. Circular RNA (circRNA) is a class of covalently closed RNA molecules characterized by universality, diversity, stability and conservatism of evolution. Accumulating evidence shows that both m(6)A modification and circRNAs participate in the pathogenesis of multiple diseases, such as cancers, neurological diseases, autoimmune diseases, and infertility. Recently, m(6)A modification has been identified for its enrichment and vital biological functions in regulating circRNAs. In this review, we summarize the role of m(6)A modification in the regulation and function of circRNAs. Moreover, we discuss the potential applications and possible future directions in the field.
C1 [Zhang, Lele; Yuan, Weitang; Liu, Jinbo; Sun, Zhenqiang] Zhengzhou Univ, Dept Colorectal Surg, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China.
[Zhang, Lele; Hou, Chaofeng] Zhengzhou Univ, Zhengzhou Cent Hosp, Dept Colorectal Surg, Zhengzhou 450007, Henan, Peoples R China.
[Zhang, Lele; Yin, Detao] Zhengzhou Univ, Dept Thyroid Surg, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China.
[Zhang, Lele; Chen, Chen; Guo, Yaxin] Zhengzhou Univ, Acad Med Sci, Zhengzhou 450052, Henan, Peoples R China.
[Chen, Chen] Zhengzhou Univ, Sch Life Sci, Zhengzhou 450001, Henan, Peoples R China.
[Guo, Yaxin; Sun, Zhenqiang] Zhengzhou Univ, Sch Basic Med Sci, Zhengzhou 450002, Henan, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Zhengzhou University;
Zhengzhou University; Zhengzhou University; Zhengzhou University
RP Liu, JB; Sun, ZQ (corresponding author), Zhengzhou Univ, Dept Colorectal Surg, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China.; Yin, DT (corresponding author), Zhengzhou Univ, Dept Thyroid Surg, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China.; Sun, ZQ (corresponding author), Zhengzhou Univ, Sch Basic Med Sci, Zhengzhou 450002, Henan, Peoples R China.
EM detaoyin@zzu.edu.cn; 1999liujb@163.com; zqsun82@csu.edu.cn
RI zhang, lele/IWM-4398-2023
OI Sun, Zhenqiang/0000-0002-9098-7296
FU National Natural Science Foundation of China [81972663, 81560385]; Key
Scientific Research Projects of Institutions of Higher Education in
Henan Province [19A310024]; Medical Scientific and Technological
Research Project of Henan Province [201702027]; China Postdoctoral
Science Foundation [2019 T120648, 2017 M610462]; National Natural
Science Foundation of Henan Province [182300410342]; Health Commission
Technology Talents Overseas Training Project of Henan Province
[2018140]; Key Scientific Research Project of Henan Higher Education
Institutions [20A310024]
FX This study was supported by The National Natural Science Foundation of
China (81972663, 81560385), Key Scientific Research Projects of
Institutions of Higher Education in Henan Province (19A310024), The
Medical Scientific and Technological Research Project of Henan Province
(201702027), The China Postdoctoral Science Foundation (2019 T120648,
2017 M610462), The National Natural Science Foundation of Henan Province
(182300410342), The Health Commission Technology Talents Overseas
Training Project of Henan Province (2018140) and The Key Scientific
Research Project of Henan Higher Education Institutions (20A310024).
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NR 109
TC 207
Z9 227
U1 5
U2 51
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD JUN 10
PY 2020
VL 19
IS 1
AR 105
DI 10.1186/s12943-020-01224-3
PG 11
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA MA9KF
UT WOS:000542228400001
PM 32522202
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Rizvi, S
Gawrieh, S
AF Rizvi, Syed
Gawrieh, Samer
TI Autoimmune Hepatitis in the Elderly: Diagnosis and Pharmacologic
Management
SO DRUGS & AGING
LA English
DT Article
ID ACTIVE LIVER-DISEASE; ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES;
TERM-FOLLOW-UP; PRIMARY SCLEROSING CHOLANGITIS; MYCOPHENOLATE-MOFETIL;
CORTICOSTEROID-THERAPY; ANTIMITOCHONDRIAL-ANTIBODIES; PROGNOSTIC
IMPLICATIONS; CLINICAL-FEATURES; SUSTAINED REMISSION
AB Autoimmune hepatitis (AIH) may present as acute or chronic hepatitis in the elderly. Advanced hepatic fibrosis and cirrhosis are common on first presentation in this population. In this review, we discuss the presentation, approach to diagnosis and management of AIH in the elderly. As polypharmacy is common in the elderly, careful medication use history is essential for detecting drug-induced AIH-like hepatitis. Steroid-sparing or minimizing therapeutic regimens are preferred to treat AIH in the elderly. For the purpose of induction, budesonide or lower dose prednisone in combination with azathioprine (AZA) regimens are preferred over high-dose prednisone monotherapy due to the higher risk of side effects of the later in the elderly. The goal of maintenance therapy should be to achieve full biochemical and histologic remission. Bone density monitoring and interventions to prevent steroid-related bone disease should be implemented throughout the course of the disease. Liver transplantation should be considered in the elderly patient with liver failure or early hepatocellular carcinoma if there are no significant comorbidities or compromise in functional status.
C1 [Rizvi, Syed] Med Coll Wisconsin, Gastroenterol & Hepatol Div, 9200 West Wisconsin Ave, Milwaukee, WI 53226 USA.
[Gawrieh, Samer] Indiana Univ Sch Med, Gastroenterol & Hepatol Div, 702 Rotary Cir, Indianapolis, IN 46202 USA.
C3 Medical College of Wisconsin; Indiana University System; Indiana
University Bloomington
RP Rizvi, S (corresponding author), Med Coll Wisconsin, Gastroenterol & Hepatol Div, 9200 West Wisconsin Ave, Milwaukee, WI 53226 USA.; Gawrieh, S (corresponding author), Indiana Univ Sch Med, Gastroenterol & Hepatol Div, 702 Rotary Cir, Indianapolis, IN 46202 USA.
EM srizvi@mcw.edu; sgawrieh@iu.edu
RI Gawrieh, Samer/AAS-8904-2020
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NR 128
TC 11
Z9 11
U1 1
U2 3
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 1170-229X
EI 1179-1969
J9 DRUG AGING
JI Drugs Aging
PD JUL
PY 2018
VL 35
IS 7
BP 589
EP 602
DI 10.1007/s40266-018-0556-0
PG 14
WC Geriatrics & Gerontology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Geriatrics & Gerontology; Pharmacology & Pharmacy
GA GO2RJ
UT WOS:000439824000002
PM 29971609
DA 2025-01-07
ER
PT J
AU Drescher, HK
Bartsch, LM
Weiskirchen, S
Weiskirchen, R
AF Drescher, Hannah K.
Bartsch, Lea M.
Weiskirchen, Sabine
Weiskirchen, Ralf
TI Intrahepatic TH17/TRegCells in Homeostasis and
Disease-It's All About the Balance
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE T(H)17 cells; T(Reg)cells; T(H)17; T(Reg)balance; liver; autoimmune
diseases; viral infection
ID REGULATORY T-CELLS; LOW-DOSE INTERLEUKIN-2; RHEUMATOID-ARTHRITIS
PATIENTS; COLLAGEN-INDUCED ARTHRITIS; GERMINAL CENTER REACTION;
TGF-BETA; TH17 CELLS; AUTOIMMUNE ENCEPHALOMYELITIS;
HEPATOCELLULAR-CARCINOMA; IMMUNE DYSREGULATION
AB Both acute and chronic hepatic inflammation likely result from an imbalance in the T(H)1/T(H)2 cell response and can lead to liver fibrosis and end-stage liver disease. More recently, a novel CD4+ T helper cell subset was described, characterized by the production of IL-17 and IL-22. These T(H)17 cells 50were predominantly implicated in host defense against infections and in autoimmune diseases. Interestingly, studies over the last 10 years revealed that the development of T(H)17 cells favors pro-inflammatory responses in almost all tissues and there is a reciprocal relationship between T(H)17 and T(Reg)cells. The balance between T(H)17and T(Reg)cells is critical for immune reactions, especially in injured liver tissue and the return to immune homeostasis. The pathogenic contribution of T(H)17 and T(Reg)cells in autoimmunity, acute infection, and chronic liver injury is diverse and varies among disease etiologies. Understanding the mechanisms underlying T(H)17 cell development, recruitment, and maintenance, along with the suppression of T(Reg)cells, will inform the development of new therapeutic strategies in liver diseases. Active manipulation of the balance between pathogenic and regulatory processes in the liver may assist in the restoration of homeostasis, especially in hepatic inflammation.
C1 [Drescher, Hannah K.; Bartsch, Lea M.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Drescher, Hannah K.; Bartsch, Lea M.] Harvard Med Sch, Boston, MA 02115 USA.
[Weiskirchen, Sabine; Weiskirchen, Ralf] Rhein Westfal TH Aachen, Univ Hosp, Inst Mol Pathobiochem Expt Gene Therapy & Clin Ch, Aachen, Germany.
C3 Harvard University; Massachusetts General Hospital; Harvard University;
Harvard Medical School; RWTH Aachen University; RWTH Aachen University
Hospital
RP Drescher, HK; Bartsch, LM (corresponding author), Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.; Drescher, HK; Bartsch, LM (corresponding author), Harvard Med Sch, Boston, MA 02115 USA.
EM hdrescher@mgh.harvard.edu; lbartsch1@mgh.harvard.edu
RI Weiskirchen, Ralf/O-1734-2018
OI Weiskirchen, Ralf/0000-0003-3888-0931; Bartsch, Lea/0000-0003-4456-3430;
Drescher, Hannah/0000-0001-9945-1239
FU German Research Foundation [SFB/TRR57, DR 1161/1-1, BA 7175/1-1]
FX The research was funded by the German Research Foundation (RW:
SFB/TRR57, HD: DR 1161/1-1 LB: BA 7175/1-1).
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NR 186
TC 26
Z9 27
U1 0
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD OCT 2
PY 2020
VL 11
AR 588436
DI 10.3389/fphar.2020.588436
PG 19
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA OA8BR
UT WOS:000578005200001
PM 33123017
OA Green Published
DA 2025-01-07
ER
PT J
AU Li, JY
Fong, DYT
Lok, KYW
Wong, JYH
Ho, MM
Choi, EPH
Pandian, V
Davidson, PM
Duan, WJ
Tarrant, M
Lee, JJ
Lin, CC
Akingbade, O
Alabdulwahhab, KM
Ahmad, MS
Alboraie, M
Alzahrani, MA
Bilimale, AS
Boonpatcharanon, S
Byiringiro, S
Hasan, MKC
Schettini, LC
Corzo, W
De Leon, JM
De Leon, AS
Deek, H
Efficace, F
El Nayal, MA
El-Raey, F
Ensaldo-Carrasco, E
Escotorin, P
Fadodun, OA
Fawole, IO
Goh, YSS
Irawan, D
Khan, NE
Koirala, B
Krishna, A
Kwok, C
Le, TT
Leal, DG
Lezana-Fernández, MA
Manirambona, E
Mantoani, LC
Meneses-González, F
Mohamed, IE
Mukeshimana, M
Nguyen, CTM
Nguyen, HTT
Nguyen, KT
Nguyen, ST
Nurumal, MS
Nzabonimana, A
Omer, NAMA
Ogungbe, O
Poon, ACY
Reséndiz-Rodríguez, A
Puang-Ngern, B
Sagun, CG
Shaik, RA
Shankar, NG
Sommer, K
Toro, E
Tran, HTH
Urgel, EL
Uwiringiyimana, E
Vanichbuncha, T
Youssef, N
AF Li, Jiaying
Fong, Daniel Yee Tak
Lok, Kris Yuet Wan
Wong, Janet Yuen Ha
Ho, Mandy Man
Choi, Edmond Pui Hang
Pandian, Vinciya
Davidson, Patricia M.
Duan, Wenjie
Tarrant, Marie
Lee, Jung Jae
Lin, Chia-Chin
Akingbade, Oluwadamilare
Alabdulwahhab, Khalid M.
Ahmad, Mohammad Shakil
Alboraie, Mohamed
Alzahrani, Meshari A.
Bilimale, Anil S.
Boonpatcharanon, Sawitree
Byiringiro, Samuel
Hasan, Muhammad Kamil Che
Schettini, Luisa Clausi
Corzo, Walter
De Leon, Josephine M.
De Leon, Anjanette S.
Deek, Hiba
Efficace, Fabio
El Nayal, Mayssah A.
El-Raey, Fathiya
Ensaldo-Carrasco, Eduardo
Escotorin, Pilar
Fadodun, Oluwadamilola Agnes
Fawole, Israel Opeyemi
Goh, Yong-Shian Shawn
Irawan, Devi
Khan, Naimah Ebrahim
Koirala, Binu
Krishna, Ashish
Kwok, Cannas
Le, Tung Thanh
Leal, Daniela Giambruno
Lezana-Fernandez, Miguel Angel
Manirambona, Emery
Mantoani, Leandro Cruz
Meneses-Gonzalez, Fernando
Mohamed, Iman Elmahdi
Mukeshimana, Madeleine
Nguyen Chinh Thi Minh
Nguyen Huong Thi Thanh
Nguyen Khanh Thi
Nguyen Son Truong
Nurumal, Mohd Said
Nzabonimana, Aimable
Omer, Nagla Abdelrahim Mohamed Ahmed
Ogungbe, Oluwabunmi
Poon, Angela Chiu Yin
Resendiz-Rodriguez, Areli
Puang-Ngern, Busayasachee
Sagun, Ceryl G.
Shaik, Riyaz Ahmed
Shankar, Nikhil Gauri
Sommer, Kathrin
Toro, Edgardo
Tran Hanh Thi Hong
Urgel, Elvira L.
Uwiringiyimana, Emmanuel
Vanichbuncha, Tita
Youssef, Naglaa
TI Key lifestyles and health outcomes across 16 prevalent chronic diseases:
A network analysis of an international observational study
SO JOURNAL OF GLOBAL HEALTH
LA English
DT Article
ID SUGAR-SWEETENED BEVERAGES; SEDENTARY BEHAVIOR; PHYSICAL-ACTIVITY; US
ADULTS; EXERCISE; IMPACT; RISK
AB Background Central and bridge nodes can drive significant overall improvements within their respective networks. We aimed to identify them in 16 prevalent chronic diseases during the coronavirus disease 2019 (COVID-19) pandemic to guide effective intervention strategies and appropriate resource allocation for most significant holistic lifestyle and health improvements. Methods We surveyed 16 512 adults from July 2020 to August 2021 in 30 territories. Participants self-reported their medical histories and the perceived impact of COVID-19 on 18 lifestyle factors and 13 health outcomes. For each disease subgroup, we generated lifestyle, health outcome, and bridge networks. Variables with the highest centrality indices in each were identified central or bridge. We validated these networks using nonparametric and case-dropping subset bootstrapping and confirmed central and bridge variables' significantly higher indices through a centrality difference test. Findings Among the 48 networks, 44 were validated (all correlation -stability coefficients >0.25). Six central lifestyle factors were identified: less consumption of snacks (for the chronic disease: anxiety), less sugary drinks (cancer, gastric ulcer, hypertension, insomnia, and pre -diabetes), less smoking tobacco (chronic obstructive pulmonary disease), frequency of exercise (depression and fatty liver disease), duration of exercise (irritable bowel syndrome), and overall amount of exercise (autoimmune disease, diabetes, eczema, heart attack, and high cholesterol). Two central health outcomes emerged: less emotional distress (chronic obstructive pulmonary disease, eczema, fatty liver disease, gastric ulcer, heart attack, high cholesterol, hypertension, insomnia, and pre -diabetes) and quality of life (anxiety, autoimmune disease, cancer, depression, diabetes, and irritable bowel syndrome). Four bridge lifestyles were identified: consumption of fruits and vegetables (diabetes, high cholesterol, hypertension, and insomnia), less duration of sitting (eczema, fatty liver disease, and heart attack), frequency of exercise (autoimmune disease, depression, and heart attack), and overall amount of exercise (anxiety, gastric ulcer, and insomnia). The centrality difference test showed the central and bridge variables had significantly higher centrality indices than others in their networks (P < 0.05). Conclusion To effectively manage chronic diseases during the COVID-19 pandemic, enhanced interventions and optimised resource allocation toward central lifestyle factors, health outcomes, and bridge lifestyles are paramount. The key variables shared across chronic diseases emphasise the importance of coordinated intervention strategies.
C1 [Li, Jiaying; Fong, Daniel Yee Tak; Lok, Kris Yuet Wan; Ho, Mandy Man; Choi, Edmond Pui Hang; Lee, Jung Jae; Lin, Chia-Chin] Univ Hong Kong, Li Ka Shing Fac Med, Sch Nursing, Pokfulam, 5-F Acad Bldg,3 Sassoon Rd, Hong Kong, Peoples R China.
[Wong, Janet Yuen Ha] Hong Kong Metropolitan Univ, Sch Nursing & Hlth Studies, Hong Kong, Peoples R China.
[Pandian, Vinciya; Byiringiro, Samuel; Koirala, Binu; Ogungbe, Oluwabunmi] Johns Hopkins Univ, Sch Nursing, Baltimore, MD USA.
[Davidson, Patricia M.] Univ Wollongong, Wollongong, NSW, Australia.
[Duan, Wenjie] East China Univ Sci & Technol, Dept Social Work, Shanghai, Peoples R China.
[Tarrant, Marie] Univ British Columbia, Sch Nursing, Kelowna, BC, Canada.
[Akingbade, Oluwadamilare] Chinese Univ Hong Kong, Nethersole Sch Nursing, Hong Kong, Peoples R China.
[Akingbade, Oluwadamilare] Inst Nursing Res, Osogbo, Osun, Nigeria.
[Alabdulwahhab, Khalid M.] Majmaah Univ, Coll Med, Al Majmaah, Saudi Arabia.
[Ahmad, Mohammad Shakil; Shaik, Riyaz Ahmed] Majmaah Univ, Coll Med, Dept Family & Community Med, Al Majmaah, Saudi Arabia.
[Alboraie, Mohamed] Al Azhar Univ, Dept Internal Med, Cairo, Egypt.
[Alzahrani, Meshari A.] Majmaah Univ, Coll Med, Dept Urol, Al Majmaah, Saudi Arabia.
[Bilimale, Anil S.] JSS AHER, Sch Publ Hlth, JSS Med Coll, Mysuru, India.
[Boonpatcharanon, Sawitree; Puang-Ngern, Busayasachee; Vanichbuncha, Tita] Chulalongkorn Business Sch, Dept Stat, Bangkok, Thailand.
[Hasan, Muhammad Kamil Che; Nurumal, Mohd Said] Int Islamic Univ Malaysia, Kulliyyah Nursing, Kuantan, Malaysia.
[Schettini, Luisa Clausi] Italian Assoc Leukaemia Lymphoma & Myeloma AIL, Rome, Italy.
[Corzo, Walter] Dialogos Guatemala, Guatemala City, Guatemala.
[De Leon, Josephine M.; De Leon, Anjanette S.; Sagun, Ceryl G.; Urgel, Elvira L.] Ctr Escolar Univ, Sch Nursing, Manila, Philippines.
[Deek, Hiba] Beirut Arab Univ, Fac Hlth Sci, Nursing Dept, Beirut, Lebanon.
[Efficace, Fabio] Italian Grp Adult Hematol Dis GIMEMA, Data Ctr & Hlth Outcomes Res Unit, Rome, Italy.
[El Nayal, Mayssah A.; Sommer, Kathrin] Beirut Arab Univ, Dept Psychol, Beirut, Lebanon.
[El-Raey, Fathiya] Al Azhar Univ, Damietta Fac Med, Dept Hepatogastroenterol & Infect Dis, Cairo, Egypt.
[Ensaldo-Carrasco, Eduardo] Univ Guadalajara, Ergon Res Ctr ECR, Guadalajara, Jalisco, Mexico.
[Escotorin, Pilar] Autonomous Univ Barcelona, Dept Basic Dev & Educ Psychol, Lab Appl Prosocial Res, Barcelona, Spain.
[Fadodun, Oluwadamilola Agnes] Univ Lethbridge, Fac Hlth Sci, Lethbridge, AB, Canada.
[Fawole, Israel Opeyemi] Ladoke Akintola Univ Technol, Fac Nursing, Ogbomosho, Nigeria.
[Goh, Yong-Shian Shawn] Natl Univ Singapore, Alice Lee Ctr Nursing Studies, Singapore, Singapore.
[Irawan, Devi] Wijaya Husada Hlth Inst, Sch Nursing, Bogor, Indonesia.
[Khan, Naimah Ebrahim] Univ KwaZulu Natal, Dept Optometry, Durban, South Africa.
[Krishna, Ashish] Ecove, Ghaziabad, India.
[Kwok, Cannas] Charles Sturt Univ, Sch Nursing Paramed & Hlth Care Sci, Sydney, NSW, Australia.
[Le, Tung Thanh; Nguyen Chinh Thi Minh; Nguyen Huong Thi Thanh; Nguyen Khanh Thi; Nguyen Son Truong; Tran Hanh Thi Hong] Nam Dinh Univ Nursing, Nam Dinh, Vietnam.
[Leal, Daniela Giambruno; Toro, Edgardo] Pontificia Univ Catolica Valparaiso, Sch Social Work, Valparaiso, Chile.
[Lezana-Fernandez, Miguel Angel; Meneses-Gonzalez, Fernando] Natl Commiss Med Arbitrat, Res Dept, Mexico City, Mexico.
[Manirambona, Emery; Uwiringiyimana, Emmanuel] Univ Rwanda, Coll Med & Hlth Sci, Kigali, Rwanda.
[Mantoani, Leandro Cruz] Sao Paulo State Univ UNESP, Dept Physiotherapy, Fac Sci & Technol, Presidente Prudente, Brazil.
[Mohamed, Iman Elmahdi] Benghazi Univ, Fac Pharm, Pharmacol & Toxicol Dept, Benghazi, Libya.
[Mukeshimana, Madeleine] Univ Rwanda, Coll Med & Hlth Sci, Sch Nursing & Midwifery, Kigali, Rwanda.
[Nzabonimana, Aimable] Univ Rwanda, Coll Arts & Social Sci, Ctr Language Enhancement, Huye, Rwanda.
[Omer, Nagla Abdelrahim Mohamed Ahmed] Alzaiem Alazhari Univ, Fac Med, Khartoum, Sudan.
[Poon, Angela Chiu Yin] Macao Polytech Univ, Fac Hlth Sci & Sports, Taipa, Macao, Peoples R China.
[Resendiz-Rodriguez, Areli] Univ Nacl Autonoma Mexico, Mexico City, Mexico.
[Shankar, Nikhil Gauri] Wrexham Maelor Hosp, Mental Hlth & Learning Div, Wrexham, Wales.
[Youssef, Naglaa] Cairo Univ, Fac Nursing, Med Surg Nursing Dept, Cairo, Egypt.
C3 University of Hong Kong; Hong Kong Metropolitan University; Johns
Hopkins University; University of Wollongong; East China University of
Science & Technology; University of British Columbia; Chinese University
of Hong Kong; Majmaah University; Majmaah University; Egyptian Knowledge
Bank (EKB); Al Azhar University; Majmaah University; JSS Academy of
Higher Education & Research; JSS Medical College, Mysuru; Chulalongkorn
University; International Islamic University Malaysia; Centro Escolar
University; Beirut Arab University; Fondazione GIMEMA; American
University of Beirut; Beirut Arab University; Egyptian Knowledge Bank
(EKB); Al Azhar University; Universidad de Guadalajara; Autonomous
University of Barcelona; University of Lethbridge; National University
of Singapore; University of Kwazulu Natal; Charles Sturt University;
Pontificia Universidad Catolica de Valparaiso; University of Rwanda;
Universidade Estadual Paulista; University of Benghazi; University of
Rwanda; University of Rwanda; Macao Polytechnic University; Universidad
Nacional Autonoma de Mexico; Egyptian Knowledge Bank (EKB); Cairo
University
RP Fong, DYT (corresponding author), Univ Hong Kong, Li Ka Shing Fac Med, Sch Nursing, Pokfulam, 5-F Acad Bldg,3 Sassoon Rd, Hong Kong, Peoples R China.
EM dytfong@hku.hk
RI Lee, Jeong/V-3429-2019; Duan, Wenjie/C-8722-2016; Akingbade,
Oluwadamilare/ACH-6708-2022; EbrahimKhan, Naimah/KIG-2113-2024;
Byiringiro, Samuel/ABF-6161-2021; Tarrant, Agnes/C-4413-2009; Kwok,
Cannas/AGZ-4949-2022; EL-Raey, Fathiya/AAU-6534-2020; Le,
Tung/AAD-7494-2020; Ho, Mandy/P-8821-2019; Pandian,
Vinciya/AAM-1218-2020; Deek, Hiba/Y-9356-2019; Lin,
Cheng-Hui/AAV-7085-2021; Alboraie, Mohamed/F-5688-2011; Nguyen,
Son/AAG-4274-2020; Youssef, Naglaa/GQP-7870-2022; Choi,
Edmond/H-4187-2019; Ogungbe, Bunmi/AAD-5945-2022; Ensaldo-Carrasco,
Eduardo/C-4774-2018; Lok, Kris Yuet Wan/P-8814-2019; Fong,
Daniel/C-4269-2009; Manirambona, Emery/ADF-0353-2022
OI Ensaldo-Carrasco, Eduardo/0000-0002-5474-7500; Lok, Kris Yuet
Wan/0000-0002-3227-0799; Youssef, Naglaa/0000-0002-0368-1759; Krishna,
Ashish/0000-0003-2325-6183; Fong, Daniel/0000-0001-7365-9146;
Manirambona, Emery/0000-0002-0579-3607; Davidson, Patricia
M./0000-0003-2050-1534; Lee, Jay Jung Jae/0000-0001-9704-2116; Li,
Jiaying/0000-0002-5473-4320; Uwiringiyimana,
Emmanuel/0000-0001-5092-6109; , cannas/0000-0002-6296-1144
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NR 42
TC 2
Z9 2
U1 8
U2 13
PU INT SOC GLOBAL HEALTH
PI EDINBURGH
PA CALEDONIAN EXCHANGE, 19A CANNING ST, EDINBURGH, Lothian, ENGLAND
SN 2047-2978
EI 2047-2986
J9 J GLOB HEALTH
JI J. Glob. Health
PY 2024
VL 14
AR 04068
DI 10.7189/jogh.14.04068
PG 15
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA OR3Z8
UT WOS:001208974600001
PM 38606605
DA 2025-01-07
ER
PT J
AU Chen, RC
Hou, W
Zhang, QH
Kang, R
Fan, XG
Tang, DL
AF Chen, Ruochan
Hou, Wen
Zhang, Qiuhong
Kang, Rui
Fan, Xue-Gong
Tang, Daolin
TI Emerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases
SO MOLECULAR MEDICINE
LA English
DT Review
ID ISCHEMIA-REPERFUSION INJURY; HEPATIC ISCHEMIA/REPERFUSION INJURY;
CHROMATIN PROTEIN HMGB1; END-PRODUCTS RAGE; RECEPTOR 4;
HEPATOCELLULAR-CARCINOMA; LETHAL SEPSIS; CLINICOPATHOLOGICAL FEATURES;
STERILE INFLAMMATION; THERAPEUTIC TARGET
AB Damage-associated molecular pattern (DAMP) molecules are essential for the initiation of innate inflammatory responses to infection and injury. The prototypic DAMP molecule, high-mobility group box 1 (HMGB1), is an abundant architectural chromosomal protein that has location-specific biological functions: within the nucleus as a DNA chaperone, within the cytosol to sustain autophagy and outside the cell as a DAMP molecule. Recent research indicates that aberrant activation of HMGB1 signaling can promote the onset of inflammatory and autoimmune diseases, raising interest in the development of therapeutic strategies to control their function. The importance of HMGB1 activation in various forms of liver disease in relation to liver damage, steatosis, inflammation, fibrosis, tumorigenesis and regeneration is discussed in this review.
C1 [Chen, Ruochan; Hou, Wen; Zhang, Qiuhong; Kang, Rui; Tang, Daolin] Univ Pittsburgh, Dept Surg, Pittsburgh, PA USA.
[Chen, Ruochan; Fan, Xue-Gong] Cent South Univ, Xiangya Hosp, Dept Infect Dis, Changsha, Hunan, Peoples R China.
[Chen, Ruochan; Fan, Xue-Gong] Cent South Univ, Xiangya Hosp, State Key Lab Viral Hepatitis, Changsha, Hunan, Peoples R China.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Central South University; Central South University
RP Tang, DL (corresponding author), Hillman Canc Ctr, 5117 Ctr Ave, Pittsburgh, PA 15213 USA.
EM xgfan@hotmail.com; tangd2@upmc.edu
RI Tang, Daolin/B-2905-2010; Kang, Rui/ABD-5291-2021
OI Tang, Daolin/0000-0002-1903-6180
FU National Institutes of Health [R01CA160417]; National Natural Sciences
Foundation of China [81272253]
FX We apologize to the researchers who were not referenced because of space
limitations. We thank Christine Heiner (Department of Surgery,
University of Pittsburgh) for her critical reading of the manuscript.
This work was supported by the National Institutes of Health (grant
R01CA160417 to D Tang) and the National Natural Sciences Foundation of
China (grant 81272253 to X-G Fan).
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NR 118
TC 89
Z9 102
U1 0
U2 31
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1076-1551
EI 1528-3658
J9 MOL MED
JI Mol. Med.
PD JUL-DEC
PY 2013
VL 19
BP 357
EP 366
DI 10.2119/molmed.2013.00099
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 274KH
UT WOS:000328604700024
PM 24306421
OA Green Accepted, gold
DA 2025-01-07
ER
PT J
AU Tota, M
Baron, V
Musial, K
Derrough, B
Konieczny, A
Krajewska, M
Turkmen, K
Kusztal, M
AF Tota, Maciej
Baron, Vanessa
Musial, Katie
Derrough, Bouchra
Konieczny, Andrzej
Krajewska, Magdalena
Turkmen, Kultigin
Kusztal, Mariusz
TI Secondary IgA Nephropathy and IgA-Associated Nephropathy: A Systematic
Review of Case Reports
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE IgA-associated; gastrointestinal; infection; dermatological; cancer;
liver; autoimmune; drug-induced; treatment; pathophysiology
ID IMMUNOGLOBULIN-A NEPHROPATHY; HENOCH-SCHONLEIN PURPURA;
IMMUNODEFICIENCY-VIRUS-INFECTION; DYSTROPHIC EPIDERMOLYSIS-BULLOSA;
ACUTE-RENAL-FAILURE; CELIAC-DISEASE; GLOMERULAR-DISEASES;
ULCERATIVE-COLITIS; TRANSGLUTAMINASE 2; CELL CARCINOMA
AB Primary (pIgAN), secondary IgA nephropathy (sIgAN), and IgA-associated nephropathy can be distinguished. While pIgAN has been thoroughly studied, information about the etiology of sIgAN remains scarce. As concerns sIgAN, several studies suggest that different etiologic factors play a role and ultimately lead to a pathophysiologic process similar to that of pIgAN. In this article, we review a vast number of cases in order to determine the novel putative underlying diseases of sIgAN. Moreover, updates on the common pathophysiology of primary disorders and sIgAN are presented. We identified liver, gastrointestinal, oncological, dermatological, autoimmune, and respiratory diseases, as well as infectious, iatrogenic, and environmental factors, as triggers of sIgAN. As novel biological therapies for listed underlying diseases emerge, we suggest implementing drug-induced sIgAN as a new significant category. Clinicians should acknowledge the possibility of sIgAN progression in patients treated with TNF-a inhibitors, IL-12/IL-23-inhibitors, immune checkpoint inhibitors, CTLA-4, oral anticoagulants, thioureylene derivatives, and anti-vascular endothelial growth factor drugs.
C1 [Tota, Maciej; Baron, Vanessa; Musial, Katie; Derrough, Bouchra] Wroclaw Med Univ, Fac Med, PL-50367 Wroclaw, Poland.
[Baron, Vanessa] Wroclaw Med Univ, Fac Dent, PL-50435 Wroclaw, Poland.
[Konieczny, Andrzej; Krajewska, Magdalena; Kusztal, Mariusz] Wroclaw Med Univ, Dept Nephrol & Transplantat Med, PL-50556 Wroclaw, Poland.
[Turkmen, Kultigin] Necmettin Erbakan Univ, Meram Med Fac, Dept Internal Med, Div Nephrol, TR-42090 Konya, Turkiye.
C3 Wroclaw Medical University; Wroclaw Medical University; Wroclaw Medical
University; Necmettin Erbakan University
RP Krajewska, M (corresponding author), Wroclaw Med Univ, Dept Nephrol & Transplantat Med, PL-50556 Wroclaw, Poland.
EM magdalena.krajewska@umw.edu.pl; mariusz.kusztal@umw.edu.pl
RI Konieczny, Andrzej/ABD-6492-2021; Turkmen, Kultigin/AFR-4244-2022;
Kusztal, Mariusz/AAY-5669-2020; Tota, Maciej/IAP-6442-2023
OI Turkmen, Kultigin/0000-0002-1667-7716; Konieczny,
Andrzej/0000-0002-4966-9771; Baron, Vanessa/0000-0003-4602-3024;
Krajewska, Magdalena/0000-0002-2632-2409; Kusztal,
Mariusz/0000-0002-6502-0374; Derrough, Bouchra/0000-0003-1545-9511
FU Wroclaw Medical University [SUBZ.C160.23.046]
FX This work was supported by Wroclaw Medical University subvention no
SUBZ.C160.23.046.
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NR 151
TC 4
Z9 4
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD APR
PY 2023
VL 12
IS 7
AR 2726
DI 10.3390/jcm12072726
PG 30
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA D6IJ6
UT WOS:000969744300001
PM 37048809
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Sierra, L
Barba, R
Ferrigno, B
Goyes, D
Diaz, W
Patwardhan, VR
Saberi, B
Bonder, A
AF Sierra, Leandro
Barba, Romelia
Ferrigno, Bryan
Goyes, Daniela
Diaz, Wilfor
Patwardhan, Vilas R.
Saberi, Behnam
Bonder, Alan
TI Living-Donor Liver Transplant and Improved Post-Transplant Survival in
Patients with Primary Sclerosing Cholangitis
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE primary sclerosing cholangitis; autoimmune liver diseases; liver
transplant; graft survival
ID LONG-TERM OUTCOMES; MODEL
AB Primary sclerosing cholangitis (PSC) is the leading indication of liver transplantation (LT) among autoimmune liver disease patients. There is a scarcity of studies comparing survival outcomes between living-donor liver transplants (LDLT)s and deceased-donor liver transplants (DDLTs) in this population. Using the United Network for Organ Sharing database, we compared 4679 DDLTs and 805 LDLTs. Our outcome of interest was post-LT patient survival and post-LT graft survival. A stepwise multivariate analysis was performed, adjusting for recipient age, gender, diabetes mellitus, ascites, hepatic encephalopathy, cholangiocarcinoma, hepatocellular carcinoma, race, and the model for end-stage liver disease (MELD) score; donor' age and sex were also included to the analysis. According to univariate and multivariate analysis, LDLT had a patient and graft survival benefit compared to DDLT (HR, 0.77, 95% CI 0.65-0.92; p < 0.002). LDLT patient survival (95.2%, 92.6%, 90.1%, and 81.9%) and graft survival (94.1%, 91.1%, 88.5%, and 80.5%) at 1, 3, 5, and 10 years were significantly better than DDLT patient survival (93.2%, 87.6%, 83.3%, and 72.7%) and graft survival (92.1%, 86.5%, 82.1%, and 70.9%) (p < 0.001) in the same interval. Variables including donor and recipient age, male recipient gender, MELD score, diabetes mellitus, hepatocellular carcinoma, and cholangiocarcinoma were associated with mortality and graft failure in PSC patients. Interestingly, Asians were more protected than Whites (HR, 0.61; 95% CI, 0.35-0.99; p < 0.047), and cholangiocarcinoma was associated with the highest hazard of mortality (HR, 2.07; 95% CI, 1.71-2.50; p < 0.001) in multivariate analysis. LDLT in PSC patients were associated with greater post-transplant patient and graft survival compared to DDLT patients.
C1 [Sierra, Leandro; Barba, Romelia; Patwardhan, Vilas R.; Saberi, Behnam; Bonder, Alan] Beth Israel Deaconess Med Ctr, Div Gastroenterol Hepatol & Nutr, Boston, MA 02215 USA.
[Ferrigno, Bryan; Diaz, Wilfor] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Goyes, Daniela] Loyola Med MacNeal Hosp, Dept Med, Berwyn, IL 60402 USA.
C3 Harvard University; Beth Israel Deaconess Medical Center; Harvard
University; Beth Israel Deaconess Medical Center
RP Bonder, A (corresponding author), Beth Israel Deaconess Med Ctr, Div Gastroenterol Hepatol & Nutr, Boston, MA 02215 USA.
EM lsierrac@bidmc.harvard.edu; rbarbabe@bidmc.harvard.edu;
bwferrig@bidmc.harvard.edu; daniela.goyesvaca@luhs.org;
wdiazfer@bidmc.harvard.edu; vpatward@bidmc.harvard.edu;
bsaberi@bidmc.harvard.edu; abonder@bidmc.harvard.edu
OI Ferrigno, Bryan/0000-0002-3319-9664; Barba, Romelia/0000-0003-4158-9264;
Sierra Carrero, Leandro Luis/0000-0002-7148-5450; BONDER,
ALAN/0000-0001-6821-0416
CR [Anonymous], CLIN OUTC LIV VERS D
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NR 27
TC 7
Z9 7
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD APR
PY 2023
VL 12
IS 8
AR 2807
DI 10.3390/jcm12082807
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA E7NF1
UT WOS:000977360800001
PM 37109144
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Yimam, KK
Bowlus, CL
AF Yimam, Kidist K.
Bowlus, Christopher L.
TI Diagnosis and classification of primary sclerosing cholangitis
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE Primary sclerosis cholangitis; Clinical manifestation; Etiopathogenesis
inflammatory bowel disease; Liver transplantation
ID INFLAMMATORY-BOWEL-DISEASE; PRIMARY BILIARY-CIRRHOSIS; DOSE
URSODEOXYCHOLIC ACID; LIVER-TRANSPLANTATION; NATURAL-HISTORY; AUTOIMMUNE
HEPATITIS; MYCOPHENOLATE-MOFETIL; PROGNOSTIC VARIABLES; 1ST-DEGREE
RELATIVES; INCREASED PREVALENCE
AB Primary sclerosing cholangitis (PSC) is a chronic cholestatic disease of the liver and that is characterized by progressive inflammation, fibrosis, and stricturing of the intrahepatic and extrahepatic bile ducts. It is progressive in most patients and leads to cirrhosis. It is a rare disease, mostly affecting people of northern European descent, males greater than females. The diagnosis is best established by contrast cholangiography, which reveals a characteristic picture of diffuse, multifocal strictures and focal dilation of the bile ducts, leading to a beaded appearance. Inflammatory bowel disease (IBD) is present in similar to 75% of the patients with PSC, mostly ulcerative colitis (similar to 85% of the cases). In addition to biliary cirrhosis, complications of PSC include dominant strictures of the bile ducts, cholangitis, cholangiocarcinoma, colon dysplasia and cancer in patients with IBD, gallbladder polyps and cancer, and hepatic osteodystrophy. The etiology of PSC is not clear, but studies are ongoing. The median survival without liver transplantation is 12 to 15 years after diagnosis. Currently there are no effective treatments except liver transplantation. Immunosuppressive medications have not been shown to be effective but antibiotics and anti-fibrotic agents seem promising. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Yimam, Kidist K.] Calif Pacific Med Ctr, Div Hepatol & Liver Transplant, San Francisco, CA USA.
[Bowlus, Christopher L.] Univ Calif Davis, Div Gastroenterol & Hepatol, Sacramento, CA 95817 USA.
C3 California Pacific Medical Center; University of California System;
University of California Davis
RP Bowlus, CL (corresponding author), 4150 V St,PSSB 3500, Sacramento, CA 95817 USA.
EM clbowlus@ucdavis.edu
RI Bowlus, Christopher/N-9276-2016
OI Bowlus, Christopher/0000-0002-3906-6811
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NR 87
TC 38
Z9 44
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD APR-MAY
PY 2014
VL 13
IS 4-5
SI SI
BP 445
EP 450
DI 10.1016/j.autrev.2014.01.040
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AE2AM
UT WOS:000333775700024
PM 24424180
DA 2025-01-07
ER
PT J
AU Nakano, M
Saeki, C
Takahashi, H
Homma, S
Tajiri, H
Zeniya, M
AF Nakano, M.
Saeki, C.
Takahashi, H.
Homma, S.
Tajiri, H.
Zeniya, M.
TI Activated natural killer T cells producing interferon-gamma elicit
promoting activity to murine dendritic cell-based autoimmune hepatic
inflammation
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Article
DE alpha-GalCer; autoimmune hepatic inflammation; cytotoxic T lymphocyte;
interferon-gamma; natural killer T cell
ID NONOBESE DIABETIC MICE; MEDIATED LIVER-INJURY; INVARIANT NKT CELLS;
ADAPTIVE IMMUNITY; PROTECTS MICE; ALPHA; ENCEPHALOMYELITIS;
INTERLEUKIN-12; ANTIGEN
AB As natural killer (NK) T cells play an important role in the development of autoimmune diseases, they should have significant roles for the pathogenesis of autoimmune liver disease. Implication of the NK T cells in the generation of autoimmune-related hepatic inflammation was investigated using a novel mouse model. Immunization of mice with dendritic cells (DCs) loaded with hepatocyte-mimicking hepatocellular carcinoma cells (DC/Hepa1-6) induces cytotoxic T lymphocytes (CTL) capable of killing hepatocytes. Subsequent administration of interleukin (IL)-12, a potent interferon-gamma (IFN-gamma) inducer, to the immunized mice generates autoimmune hepatic inflammation (AHI), as reported previously. Upon onset of the AHI response, the number of intrahepatic CD3(+)NK1 center dot 1(+) NK T cells increased markedly, along with a decrease in the number of splenic NK T cells, augmented expression of CXCR6 on intrahepatic NK T cells and CXCL16 in hepatic tissue, suggesting that NK T cells were recruited into the inflamed liver. The NK T cells were strongly positive for CD69 and produced IFN-gamma, but not IL-4. AHI activity was attenuated markedly in CD1d(-/-) NK T cell-deficient mice, indicating that NK T cells play a pivotal role in the development of AHI. Mice treated with DC/Hepa1-6 and alpha-galactosylceramide, a potent NK T cell activator, also exhibited similar hepatic inflammation, in which activated NK T cells producing IFN-gamma and CD8(+) T cells cytotoxic to hepatocytes were induced in liver-infiltrating mononuclear cells. Activated NK T cells producing IFN-gamma potentiate DC-based AHI in the mouse model.
C1 [Homma, S.] Jikei Univ, Sch Med, Inst DNA Med, Dept Oncol,Minato Ku, Tokyo 1058461, Japan.
[Nakano, M.; Saeki, C.; Takahashi, H.; Tajiri, H.] Jikei Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol, Tokyo 1058461, Japan.
C3 Jikei University; Jikei University
RP Homma, S (corresponding author), Jikei Univ, Sch Med, Inst DNA Med, Dept Oncol,Minato Ku, 3-25-8 Nishi Shimbashi, Tokyo 1058461, Japan.
EM sahya@jikei.ac.jp
FU Ministry of Health, Labor and welfare of Japan; Grants-in-Aid for
Scientific Research [22590748, 24501334] Funding Source: KAKEN
FX This work was supported by Health Labor Science Research on Measures for
intractable disease (Intractable Hepato-Biliary Disease Study Group)
founded by the Ministry of Health, Labor and welfare of Japan.
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NR 37
TC 10
Z9 11
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD DEC
PY 2012
VL 170
IS 3
SI SI
BP 274
EP 282
DI 10.1111/j.1365-2249.2012.04664.x
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 030DZ
UT WOS:000310550500004
PM 23121668
OA Green Published
DA 2025-01-07
ER
PT J
AU Cicalese, L
Westra, JR
O'Connor, CM
Kuo, YF
AF Cicalese, Luca
Westra, Jordan R.
O'Connor, Casey M.
Kuo, Yong-Fang
TI Increased Risk of Malignancy with Immunosuppression: A Population-Based
Analysis of Texas Medicare Beneficiaries
SO CANCERS
LA English
DT Article
DE immunosuppressive drugs; immunosuppression; cancer; liver cancer; skin
cancer; lymphoma; kidney cancer; transplantation
ID KIDNEY-TRANSPLANTATION; RENAL-TRANSPLANTATION; CANCER; RECIPIENTS
AB Simple Summary This study analyzed patients receiving immunosuppressive drugs (IMD) for the prevention of organ transplant rejection or treatment of other conditions (rheumatoid arthritis, lupus, myasthenia gravis, interstitial lung disease, fibromyalgia, and other autoimmune diseases). This retrospective study utilized Medicare claims data from all Texas Medicare beneficiaries between 2007 and 2018. In these patients, the risk of developing cancer was evaluated. We found an increased risk of cancer for all patients using IMD, regardless of its indication or duration, with a distribution of the types of cancer different from that previously described and with a higher risk for liver cancer. We also observed a higher risk of cancer in younger patients and ethnic minorities. Immunosuppressive drugs (IMD) are widely utilized to treat many autoimmune conditions and to prevent rejection in organ transplantation. Cancer has been associated with prolonged use of IMD in transplant patients. However, no detailed, systematic analysis of the risk of cancer has been performed in patients receiving IMD for any condition and duration. We analyzed Medicare data from Texas Medicare beneficiaries, regardless of their age, between 2007 and 2018, from the Texas Cancer Registry. We analyzed the data for the risk of cancer after IMD use associated with demographic characteristics, clinical conditions, and subsequent cancer type. Of 29,196 patients who used IMD for a variety of indications, 5684 developed cancer. The risk of cancer (standardized incidence ratio) was particularly high for liver (9.10), skin (7.95), lymphoma (4.89), and kidney (4.39). Patients receiving IMD had a four fold greater likelihood of developing cancer than the general population. This risk was higher within the first 3 years of IMD utilization and in patients younger than 65 years and minorities. This study shows that patients receiving IMD for any indications have a significantly increased risk of cancer, even with short-term use. Caution is needed for IMD use; in addition, an aggressive neoplastic diagnostic screening is warranted.
C1 [Cicalese, Luca; O'Connor, Casey M.] Univ Texas Med Branch, Dept Surg, Div Transplant Surg, Galveston, TX 77555 USA.
[Westra, Jordan R.; Kuo, Yong-Fang] Univ Texas Med Branch, Off Biostat, Galveston, TX 77555 USA.
[Westra, Jordan R.] Univ Texas Med Branch, Dept Biostat & Data Sci, Galveston, TX 77555 USA.
[Kuo, Yong-Fang] Univ Texas Med Branch, Sealy Ctr Aging, Galveston, TX 77555 USA.
C3 University of Texas System; University of Texas Medical Branch
Galveston; University of Texas System; University of Texas Medical
Branch Galveston; University of Texas System; University of Texas
Medical Branch Galveston; University of Texas System; University of
Texas Medical Branch Galveston
RP Cicalese, L (corresponding author), Univ Texas Med Branch, Dept Surg, Div Transplant Surg, Galveston, TX 77555 USA.
EM lucicale@utmb.edu
OI Westra, Jordan/0000-0002-1473-1766
FU Cancer Prevention Research Institute of Texas (CPRIT) [RP210130]
FX This work was supported by the Cancer Prevention Research Institute of
Texas (CPRIT) (grant RP210130).
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NR 33
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2023
VL 15
IS 12
AR 3144
DI 10.3390/cancers15123144
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA K1PZ4
UT WOS:001014247200001
PM 37370754
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Li, YH
Zhang, Y
Pan, G
Xiang, LX
Luo, DC
Shao, JZ
AF Li, Yuan-hui
Zhang, Yu
Pan, Gang
Xiang, Li-xin
Luo, Ding-cun
Shao, Jian-zhong
TI Occurrences and Functions of Ly6Chi and Ly6Clo
Macrophages in Health and Disease
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE Ly6C(hi) and Ly6C(lo) macrophages; differentiation; inflammation;
autoimmune disease; cancer
ID LEUKEMIA-ASSOCIATED MACROPHAGES; SYSTEMIC-LUPUS-ERYTHEMATOSUS; TISSUE
MACROPHAGE; FETAL MONOCYTES; DENDRITIC CELLS; LIVER FIBROSIS;
BONE-MARROW; EXPRESSION; ACTIVATION; SURVIVAL
AB Macrophages originating from the yolk sac or bone marrow play essential roles in tissue homeostasis and disease. Bone marrow-derived monocytes differentiate into Ly6C(hi) and Ly6C(lo) macrophages according to the differential expression of the surface marker protein Ly6C. Ly6C(hi) and Ly6C(lo) cells possess diverse functions and transcriptional profiles and can accelerate the disease process or support tissue repair and reconstruction. In this review, we discuss the basic biology of Ly6C(hi) and Ly6C(lo) macrophages, including their origin, differentiation, and phenotypic switching, and the diverse functions of Ly6C(hi) and Ly6C(lo) macrophages in homeostasis and disease, including in injury, chronic inflammation, wound repair, autoimmune disease, and cancer. Furthermore, we clarify the differences between Ly6C(hi) and Ly6C(lo) macrophages and their connections with traditional M1 and M2 macrophages. We also summarize the limitations and perspectives for Ly6C(hi) and Ly6C(lo) macrophages. Overall, continued efforts to understand these cells may provide therapeutic approaches for disease treatment.
C1 [Li, Yuan-hui; Zhang, Yu; Pan, Gang; Luo, Ding-cun] Zhejiang Univ, Affiliated Hangzhou Peoples Hosp 1, Dept Oncol Surg, Sch Med, Hangzhou, Peoples R China.
[Xiang, Li-xin; Shao, Jian-zhong] Zhejiang Univ, Coll Life Sci, Key Lab Cell & Gene Engn Zhejiang Prov, Hangzhou, Peoples R China.
[Shao, Jian-zhong] Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao, Peoples R China.
C3 Zhejiang University; Zhejiang University; Laoshan Laboratory
RP Luo, DC (corresponding author), Zhejiang Univ, Affiliated Hangzhou Peoples Hosp 1, Dept Oncol Surg, Sch Med, Hangzhou, Peoples R China.; Xiang, LX; Shao, JZ (corresponding author), Zhejiang Univ, Coll Life Sci, Key Lab Cell & Gene Engn Zhejiang Prov, Hangzhou, Peoples R China.; Shao, JZ (corresponding author), Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao, Peoples R China.
EM xianglx@zju.edu.cn; ldc65@163.com; shaojz@zju.edu.cn
FU Stem Cell and Translational Research; National Key Research and
Development Program of China [2016YFA0101001, 2018YFD0900503,
2018YFD0900505]; National Natural Science Foundation of China [32173003,
31630083]
FX This work was supported by grants from Stem Cell and Translational
Research, the National Key Research and Development Program of China
(2016YFA0101001, 2018YFD0900503, 2018YFD0900505), the National Natural
Science Foundation of China (32173003, 31630083).
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NR 98
TC 35
Z9 39
U1 1
U2 25
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAY 30
PY 2022
VL 13
AR 901672
DI 10.3389/fimmu.2022.901672
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 2B4ZI
UT WOS:000810197700001
PM 35707538
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Goodstein, T
Goldberg, I
Acikgoz, Y
Hasanov, E
Srinivasan, R
Singer, EA
AF Goodstein, Taylor
Goldberg, Ilana
Acikgoz, Yusuf
Hasanov, Elshad
Srinivasan, Ramaprasad
Singer, Eric A.
TI Special populations in metastatic renal cell carcinoma
SO CURRENT OPINION IN ONCOLOGY
LA English
DT Review
DE autoimmune disease; elderly; immunotherapy; metastatic renal cell
carcinoma; sarcomatoid features; tyrosine kinase inhibitors
ID CABOZANTINIB; EVEROLIMUS; NIVOLUMAB; SUNITINIB; EFFICACY; CANCER; BONE
AB Purpose of reviewThis review focuses on special populations poorly represented in current evidence-based practice for metastatic renal cell carcinoma (mRCC). This includes the elderly and frail, patients on immunosuppression or with autoimmune diseases, patients with brain, liver, and/or bone metastases, and RCC with sarcomatoid features.Recent findingsCertain populations are poorly represented in current trials for mRCC. Patients with central nervous system (CNS) metastases are often excluded from first-line therapy trials. Modern doublet systemic therapy appears to benefit patients with bone or liver metastases, but data supporting this conclusion is not robust. Post-hoc analyses on patients with sarcomatoid differentiation have shown improved response to modern doublet therapy over historical treatments. The elderly are underrepresented in current clinical trials, and most trials exclude all but high-performing (nonfrail) patients, though true frailty is likely poorly captured using the current widely adopted indices. It is difficult to make conclusions about the efficacy of modern therapy in these populations from subgroup analyses. Data from trials on other malignancies in patients with autoimmune diseases or solid organ transplant recipients on immunosuppression suggest that immune checkpoint inhibitors (ICIs) may still have benefit, though at the risk of disease flare or organ rejection. The efficacy of ICIs has not been demonstrated specifically for RCC in this group of patients.SummaryThe elderly, frail, and immunosuppressed, those with tumors having aggressive histologic features, and patients with brain, bone, and/or liver metastases represent the populations least understood in the modern era of RCC treatment.
C1 [Goodstein, Taylor; Singer, Eric A.] Ohio State Univ, Comprehens Canc Ctr, Div Urol Oncol, Columbus, OH USA.
[Goldberg, Ilana] Thomas Jefferson Univ Hosp, Div Internal Med, Philadelphia, PA USA.
[Acikgoz, Yusuf; Hasanov, Elshad] Ohio State Univ, Div Med Oncol, Comprehens Canc Ctr, Columbus, OH USA.
[Srinivasan, Ramaprasad] NCI, NIH, Ctr Canc Res, Urol Oncol Branch,Mol Therapeut Sect, Bethesda, MD USA.
[Singer, Eric A.] Ohio State Univ, Comprehens Canc Ctr, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University; James Cancer Hospital
& Solove Research Institute; Jefferson University; James Cancer Hospital
& Solove Research Institute; University System of Ohio; Ohio State
University; National Institutes of Health (NIH) - USA; NIH National
Cancer Institute (NCI); James Cancer Hospital & Solove Research
Institute; University System of Ohio; Ohio State University
RP Singer, EA (corresponding author), Ohio State Univ, Comprehens Canc Ctr, Columbus, OH 43210 USA.
EM eric.singer@osumc.edu
RI Hasanov, Elshad/AAO-8340-2021; Acikgoz, Yusuf/V-1147-2019
OI Goodstein, Taylor/0000-0001-5062-5461
FU National Institutes of Health (National Cancer Institute, Center for
Cancer Research, Bethesda, Maryland, USA); National Cancer Institute
[2P30CA016058]; Center for Cancer Research, National Cancer Institute,
National Institutes of Health Intramural Research Program [ZIA BC
011648]; National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX This work is supported by the Intramural Research Program of the
National Institutes of Health (National Cancer Institute, Center for
Cancer Research, Bethesda, Maryland, USA) and a grant from the National
Cancer Institute (2P30CA016058).R.S. - This Research was supported in
part by the Center for Cancer Research, National Cancer Institute,
National Institutes of Health Intramural Research Program project number
ZIA BC 011648 and federal funds from the National Cancer Institute,
National Institutes of Health, under contract HHSN261200800001E. The
content of this publication does not necessarily reflect the views or
policies of the Department of Health and Human Services, nor does
mention of trade names, commercial products or organizations imply
endorsement by the US Government.
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Zhou J, 2022, Report No.: NCT03966209
NR 69
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-8746
EI 1531-703X
J9 CURR OPIN ONCOL
JI Curr. Opin. Oncol.
PD MAY
PY 2024
VL 36
IS 3
BP 186
EP 194
DI 10.1097/CCO.0000000000001028
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SI1E2
UT WOS:001233725900003
PM 38573208
DA 2025-01-07
ER
PT J
AU Ekstrand, C
Bahmanyar, S
Cherif, H
Kieler, H
Linder, M
AF Ekstrand, Charlotta
Bahmanyar, Shahram
Cherif, Honar
Kieler, Helle
Linder, Marie
TI Cancer risk in patients with primary immune thrombocytopenia - A Swedish
nationwide register study
SO CANCER EPIDEMIOLOGY
LA English
DT Article
DE Primary immune thrombocytopenia; Sweden; Nationwide; Hematologic
neoplasms; Liver neoplasms
ID NON-HODGKIN-LYMPHOMA; AUTOIMMUNE-DISEASES; ASSOCIATIONS; MALIGNANCIES;
MANAGEMENT; INDEX; CELL
AB Background: Immune thrombocytopenia (ITP) is an autoimmune disease treated with immunosuppressive agents, thrombopoietin receptor agonists, immunomodulation drugs and/or splenectomy. Patients with ITP have been found to have increased risk ofhematological malignancies. Studies investigating stomach/liver cancer are contradictory and the risk of developing other solid tumors is largely unknown. We aimed at estimating risk of overall and organ-specific cancers in patients with primary ITP.
Methods: The study population was Swedish patients with at least one ITP diagnosis recorded in the National Patient Register and a 1:10 matched comparison cohort from the population. The study period covers 1997-2016. The Cancer Register and the Cause of Death Register provided data on malignancies and deaths, respectively. Primary ITP was identified using an established algorithm. We used time-split Cox models to estimate hazard ratios (HRs) with 95 % confidence intervals (CIs), adjusted for age, sex, index-year, county, income, education, Charlson score and number of inand outpatient contacts.
Results: In total 66,134 individuals were included in the study. Patients with ITP had higher risk of gastrointestinal, skin (all morphologies), lymphoid and hematological cancers. Adjusted HR (95 % CI) for cancer was 1.37 (1.27-1.48), with highest risk during the first year, but with increased risk remaining for up to 20 years for men. For women, the overall risk was increased during the first year, HR (95 % CI) 2.00 (1.55-2.60). A significantly increased liver cancer risk was seen up to 9 years after diagnosis.
Conclusion: Patients with primary ITP have higher risk of cancer than the population. The observed increased risk does not seem to be solely due to surveillance bias, but might be associated with ITP or its treatments. Treating hematologists need to have high index of suspicion for cancer.
C1 [Ekstrand, Charlotta; Bahmanyar, Shahram; Kieler, Helle; Linder, Marie] Karolinska Inst, Dept Med, Ctr Pharmacoepidemiol, Solna, Sweden.
[Cherif, Honar] Uppsala Univ, Dept Med Sci Haematol, Uppsala, Sweden.
[Kieler, Helle] Karolinska Inst, Dept Lab Med, Huddinge, Sweden.
C3 Karolinska Institutet; Uppsala University; Karolinska Institutet
RP Linder, M (corresponding author), Karolinska Inst, Dept Med, Ctr Pharmacoepidemiol, SE-17176 Stockholm, Sweden.
EM marie.linder@ki.se
OI Cherif, Honar/0000-0001-7582-4002; Linder, Marie/0000-0003-2619-2189
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Statistics Sweden, 2020, LONG INT DAT HLTH IN
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NR 45
TC 8
Z9 8
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1877-7821
EI 1877-783X
J9 CANCER EPIDEMIOL
JI Cancer Epidemiol.
PD DEC
PY 2020
VL 69
AR 101806
DI 10.1016/j.canep.2020.101806
PG 8
WC Oncology; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Public, Environmental & Occupational Health
GA PB8IZ
UT WOS:000596559500020
PM 32947155
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Subleski, JJ
Jiang, Q
Weiss, JM
Wiltrout, RH
AF Subleski, Jeff J.
Jiang, Qun
Weiss, Jonathan M.
Wiltrout, Robert H.
TI The split personality of NKT cells in malignancy, autoimmune and
allergic disorders
SO IMMUNOTHERAPY
LA English
DT Review
DE autoimmunity; cancer; inflammation; NAFLD; type I NKT cells; type II NKT
cells
ID KILLER T-CELLS; FATTY LIVER-DISEASE; INDUCED JOINT INFLAMMATION;
NONOBESE DIABETIC MICE; INNATE IMMUNE-SYSTEM; INDUCED AIRWAY
HYPERREACTIVITY; ANTIGEN-PRESENTING CELLS; PHASE I/II TRIAL;
NATURAL-KILLER; DENDRITIC CELLS
AB NKT cells are a heterogeneous subset of specialized, self-reactive T cells, with innate and adaptive immune properties, which allow them to bridge innate and adaptive immunity and profoundly influence autoimmune and malignant disease outcomes. NKT cells mediate these activities through their ability to rapidly express pro- and anti-inflammatory cytokines that influence the type and magnitude of the immune response. Not only do NKT cells regulate the functions of other cell types, but experimental evidence has found NKT cell subsets can modulate the functions of other NKT subsets. Depending on underlying mechanisms, NKT cells can inhibit or exacerbate autoimmunity and malignancy, making them potential targets for disease intervention. NKT cells can respond to foreign and endogenous antigenic glycolipid signals that are expressed during pathogenic invasion or ongoing inflammation, respectively, allowing them to rapidly react to and influence a broad array of diseases. In this article we review the unique development and activation pathways of NKT cells and focus on how these attributes augment or exacerbate autoimmune disorders and malignancy. We also examine the growing evidence that NKT cells are involved in liver inflammatory conditions that can contribute to the development of malignancy.
C1 [Subleski, Jeff J.; Jiang, Qun; Weiss, Jonathan M.; Wiltrout, Robert H.] NCI, Lab Expt Immunol, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI)
RP Wiltrout, RH (corresponding author), NCI, Lab Expt Immunol, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
EM wiltrour@mail.nih.gov
RI Jiang, Qun/A-1358-2014
OI Subleski, Jeff/0000-0002-7442-1807
FU National Cancer Institute (NCI)/NIH
FX This work was supported by the Intramural Research Program of the
National Cancer Institute (NCI)/NIH. The authors have no other relevant
affiliations or financial involvement with any organization or entity
with a financial interest in or financial conflict with the subject
matter or materials discussed in the manuscript apart from those
disclosed.
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NR 210
TC 34
Z9 46
U1 0
U2 4
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1750-743X
EI 1750-7448
J9 IMMUNOTHERAPY-UK
JI Immunotherapy
PD OCT
PY 2011
VL 3
IS 10
BP 1167
EP 1184
DI 10.2217/IMT.11.117
PG 18
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 843XX
UT WOS:000296711800007
PM 21995570
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Naftaly, JP
Feldman, ECH
Greenley, RN
AF Naftaly, Jessica P.
Feldman, Estee C. H.
Greenley, Rachel N.
TI Perceived Stigma in Patients with Autoimmune Hepatitis
SO JOURNAL OF CLINICAL PSYCHOLOGY IN MEDICAL SETTINGS
LA English
DT Article
DE Autoimmune hepatitis; Disease impact and burden; Primary biliary
cholangitis; Stigma; Psychosocial
ID QUALITY-OF-LIFE; POSTTRAUMATIC STRESS SYMPTOMS; BREAST-CANCER;
DEPRESSIVE SYMPTOMS; GROWTH; TRAJECTORIES; INTERVENTION; METAANALYSIS;
ACCEPTANCE; PREDICTORS
AB Perceived stigma (PS) adversely impacts psychosocial and disease outcomes in patients with chronic liver diseases (CLD), and those with autoimmune hepatitis (AIH) may be at risk for PS given inaccurate assumptions about the origin of their diagnosis. The aims of the current study are to describe the frequency of PS in patients with AIH, compare rates of PS in AIH to rates of PS in primary biliary cholangitis (PBC) and CLD, and examine demographic correlates of PS. 262 adults with AIH (95% female, Mage = 51.53 years) completed online questionnaires on demographics, disease information, and PS. 54-68% reported PS with themes of selective disclosure, non-disclosure, or hiding diagnosis. PS was higher in those with AIH compared to those with PBC, but lower than those with various CLD. Age was inversely related to PS. Given the results, provider screening of PS and integration of clinical health psychologists may be helpful for identifying PS in patients with AIH.
C1 [Naftaly, Jessica P.] Univ Michigan, Dept Internal Med Gastroenterol, Michigan Med, 1500 E Med Ctr Dr,Floor 3,Recept D, Ann Arbor, MI 48109 USA.
[Naftaly, Jessica P.; Greenley, Rachel N.] Rosalind Franklin Univ Med & Sci, Dept Psychol, 3333 Green Bay Rd, N Chicago, IL 60064 USA.
[Feldman, Estee C. H.] Cincinnati Childrens Hosp Med Ctr, 3333 Burnet Ave, Cincinnati, OH 45229 USA.
C3 University of Michigan System; University of Michigan; Rosalind Franklin
University of Medicine & Science; Cincinnati Children's Hospital Medical
Center
RP Naftaly, JP (corresponding author), Univ Michigan, Dept Internal Med Gastroenterol, Michigan Med, 1500 E Med Ctr Dr,Floor 3,Recept D, Ann Arbor, MI 48109 USA.; Naftaly, JP (corresponding author), Rosalind Franklin Univ Med & Sci, Dept Psychol, 3333 Green Bay Rd, N Chicago, IL 60064 USA.
EM jnaftaly@med.umich.edu; Estee.feldman@cchmc.org;
rachel.greenley@rosalindfranklin.edu
FU Rosalind Franklin University of Medicine and Science
FX The authors would like to thank the patients with autoimmune hepatitis
who participated in this research study. The authors would also like to
thank Craig Lammert, MD for his assistance.
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NR 49
TC 0
Z9 0
U1 2
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9583
EI 1573-3572
J9 J CLIN PSYCHOL MED S
JI J. Clin. Psychol. Med. Settings
PD JUN
PY 2024
VL 31
IS 2
BP 455
EP 464
DI 10.1007/s10880-023-09983-z
EA DEC 2023
PG 10
WC Psychology, Clinical
WE Social Science Citation Index (SSCI)
SC Psychology
GA RI4G2
UT WOS:001130101400002
PM 38127091
DA 2025-01-07
ER
PT J
AU Connelly, MA
Gruppen, EG
Otvos, JD
Dullaart, RPF
AF Connelly, Margery A.
Gruppen, Eke G.
Otvos, James D.
Dullaart, Robin P. F.
TI Inflammatory glycoproteins in cardiometabolic disorders, autoimmune
diseases and cancer
SO CLINICA CHIMICA ACTA
LA English
DT Review
DE Biomarker; Inflammation; Glycan; Glycomics; Glycoproteins; Glycosylation
ID C-REACTIVE PROTEIN; ACUTE-PHASE GLYCOPROTEINS;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; TYPE-2 DIABETES-MELLITUS; SERUM
SIALIC-ACID; RHEUMATOID-ARTHRITIS; MASS-SPECTROMETRY; PROSTATE-CANCER;
LIVER FIBROSIS; N-GLYCOME
AB The physiological function initially attributed to the oligosaccharide moieties or glycans on inflammatory glycoproteins was to improve protein stability. However, it is now clear that glycans play a prominent role in glycoprotein structure and function and in some cases contribute to disease states. In fact, glycan processing contributes to pathogenicity not only in autoimmune disorders but also in atherosclerotic cardiovascular disease, diabetes and malignancy. While most clinical laboratory tests measure circulating levels of inflammatory proteins, newly developed diagnostic and prognostic tests are harvesting the information that can be gleaned by measuring the amount or structure of the attached glycans, which may be unique to individuals as well as various diseases. As such, these newer glycan-based tests may provide future means for more personalized approaches to patient stratification and improved patient care.
Here we will discuss recent progress in high-throughput laboratory methods for glycomics (Le. the study of glycan structures) and glycoprotein quantification by methods such as mass spectrometry and nuclear magnetic resonance spectroscopy. We will also review the clinical utility of glycoprotein and glycan measurements in the prediction of common low-grade inflammatory disorders including cardiovascular disease, diabetes and cancer, as well as for monitoring autoimmune disease activity. (C) 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
C1 [Connelly, Margery A.; Otvos, James D.] Lab Corp Amer Holdings, LipoSci, Raleigh, NC USA.
[Gruppen, Eke G.; Dullaart, Robin P. F.] Univ Groningen, Univ Med Ctr Groningen, Dept Endocrinol, POB 30-001, NL-9700 RB Groningen, Netherlands.
[Gruppen, Eke G.] Univ Groningen, Univ Med Ctr Groningen, Dept Nephrol, Groningen, Netherlands.
C3 LipoScience, Inc; University of Groningen; University of Groningen
RP Dullaart, RPF (corresponding author), Univ Groningen, Univ Med Ctr Groningen, Dept Endocrinol, POB 30-001, NL-9700 RB Groningen, Netherlands.
EM r.p.f.dullaart@umcg.nl
RI Connelly, Margery/IZP-5440-2023
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NR 116
TC 67
Z9 76
U1 0
U2 31
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0009-8981
EI 1873-3492
J9 CLIN CHIM ACTA
JI Clin. Chim. Acta
PD AUG 1
PY 2016
VL 459
BP 177
EP 186
DI 10.1016/j.cca.2016.06.012
PG 10
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA DS6CO
UT WOS:000380869500029
PM 27312321
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Rigopoulou, EI
Gatselis, N
Arvaniti, P
Koukoulis, GK
Dalekos, GN
AF Rigopoulou, Eirini I.
Gatselis, Nikolaos
Arvaniti, Pinelopi
Koukoulis, George K.
Dalekos, George N.
TI Alcoholic liver disease and autoimmune hepatitis: Sometimes a closer
look under the surface is needed
SO EUROPEAN JOURNAL OF INTERNAL MEDICINE
LA English
DT Article
DE Alcoholic liver disease; Autoimmune hepatitis; Liver autoimmune
serology; Alcohol-use disorder; Cirrhosis; Outcome
ID HEPATOCELLULAR-CARCINOMA; LARGE COHORT; RISK; MANAGEMENT; DIAGNOSIS;
CIRRHOSIS; MYCOPHENOLATE; PREDICTION; EFFICACY
AB Aims: Differential diagnosis of autoimmune hepatitis (AIH) incorporates various liver diseases, including alcoholic liver disease (ALD). We report on clinical, laboratory and outcome characteristics of AIH patients who were initially referred as ALD based on increased alcohol consumption (AIH/ALD). Methods: From 2000-2019, we retrospectively identified 12 AIH/ALD patients [9 males, age: 61 (30-73) years] in our prospective data base of 317 AIH patients. Results: AIH diagnosis was based on aminotransferases elevation in 10 patients, high IgG in 8, compatible autoantibody profile in all and typical/compatible histology in all 9 with available biopsy. There were no significant differences of baseline demographics, presentation, cirrhosis at diagnosis, response to treatment and simplified score compared to 45 ageand sex-matched AIH patients without alcohol consumption and 44 age and sex-matched ALD patients. However, the AIH/ALD cohort was characterized by more frequent progression to cirrhosis, higher liver-related deaths and overall mortality compared to AIH, though similar to the ALD group. AST/ALT ratio>1 seems to bear a good positive (0.84) and negative predictive value (0.88) for ALD and AIH diagnosis, respectively, but cannot help in discriminating the AIH/ALD variant. Conclusions: AIH should not be forgotten in patients with alcohol use when clinical and laboratory features hint towards the diagnosis of AIH/ALD variant as this group seems to have worse outcome compared to those with AIH alone suggesting the need for closer follow-up and surveillance. Reliable autoantibody testing and cautious interpretation of liver histology appear mandatory for AIH diagnosis in these difficult to diagnose cases.
C1 [Rigopoulou, Eirini I.; Gatselis, Nikolaos; Dalekos, George N.] Inst Internal Med & Hepatol, Larisa 41447, Greece.
[Rigopoulou, Eirini I.; Gatselis, Nikolaos; Arvaniti, Pinelopi; Dalekos, George N.] Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Dept Med & Res Lab Internal Med, Larisa 41110, Greece.
[Koukoulis, George K.] Univ Thessaly, Med Sch, Dept Pathol, Larisa 41110, Greece.
C3 General University Hospital of Larissa; University of Thessaly
RP Dalekos, GN (corresponding author), Inst Internal Med & Hepatol, Larisa 41447, Greece.; Dalekos, GN (corresponding author), Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Dept Med & Res Lab Internal Med, Larisa 41110, Greece.
EM dalekos@med.uth.gr
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NR 46
TC 13
Z9 14
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0953-6205
EI 1879-0828
J9 EUR J INTERN MED
JI Eur. J. Intern. Med.
PD MAR
PY 2021
VL 85
BP 86
EP 91
DI 10.1016/j.ejim.2020.12.024
EA MAR 2021
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA QQ5MK
UT WOS:000624567600013
PM 33451888
DA 2025-01-07
ER
PT J
AU Kunovsky, L
Dite, P
Hornakova, L
Dolina, J
Uvirova, M
Kojecky, V
Martinek, A
Jabandziev, P
AF Kunovsky, Lumir
Dite, Petr
Hornakova, Lubomira
Dolina, Jiri
Uvirova, Magdalena
Kojecky, Vladimir
Martinek, Arnost
Jabandziev, Petr
TI Differentiating Primary Sclerosing Cholangitis from Similar Diseases of
Autoimmune Origin
SO JOURNAL OF GASTROINTESTINAL AND LIVER DISEASES
LA English
DT Review
DE autoimmune diseases; IgG4-related sclerosing cholangitis;
primary sclerosing cholangitis; primary sclerosing cholangitis
with increased IgG4
ID DIAGNOSTIC-CRITERIA; PANCREATITIS; MANAGEMENT
AB Background & Aims: Primary sclerosing cholangitis (PSC) is a rare cholestatic liver disease. Differential diagnostics can confuse it with immunoglobulin (Ig) G4-related sclerosing cholangitis (SC), an IgG4-related disease with clearly proven autoimmune origin. Differential diagnosis is made even more challenging because PSC with increased IgG4 levels (PSC-increased IgG4) also occurs. In order to facilitate their differential diagnosis, we reviewed recent literature regarding the etiologies, identifying characteristics, the most useful diagnostics, treatment, and the progression of these partially similar diseases. It is clear that PSC's pathogenesis differs from that of IgG4-related SC. In any differential diagnosis between PSC and PSC-increased IgG4, high IgG1 and low or normal IgG2 levels are characteristic for patients with PSC. Histological examination of the biliary tree wall in patients with IgG4-related SC typically reveals such changes as storiform fibrosis, obliterative phlebitis, and venulitis. These are absent in PSC-increased IgG4, which is characterized by a typical circular thickness in different parts of the biliary ducts. Finally, PSC is associated with inflammatory bowel disease, which is rare in IgG4-related SC, and more frequently is associated with cholangiocarcinomas and colon cancers. As distinct from IgG4-related SC, PSC is not a primary autoimmune disease.
C1 [Kunovsky, Lumir; Dite, Petr; Hornakova, Lubomira; Dolina, Jiri] Univ Hosp Brno, Dept Gastroenterol & Internal Med, Brno, Czech Republic.
[Kunovsky, Lumir] Univ Hosp Brno, Dept Surg, Brno, Czech Republic.
[Kunovsky, Lumir; Hornakova, Lubomira; Dolina, Jiri; Kojecky, Vladimir; Jabandziev, Petr] Masaryk Univ, Fac Med, Brno, Czech Republic.
[Dite, Petr; Martinek, Arnost] Univ Hosp Ostrava, Dept Internal Med, Dept Gastroenterol, Ostrava, Czech Republic.
[Dite, Petr; Martinek, Arnost] Univ Ostrava, Fac Med, Ostrava, Czech Republic.
[Uvirova, Magdalena] CGB Lab AS, Ostrava, Czech Republic.
[Kojecky, Vladimir] Hosp Zlin, Dept Internal Med, Zlin, Czech Republic.
[Jabandziev, Petr] Univ Hosp Brno, Dept Pediat, Brno, Czech Republic.
[Jabandziev, Petr] Masaryk Univ, Cent European Inst Technol, Brno, Czech Republic.
C3 University Hospital Brno; University Hospital Brno; Masaryk University
Brno; University Hospital Ostrava; University of Ostrava; Tomas Bata
Hospital in Zlin; University Hospital Brno; Masaryk University Brno
RP Kunovsky, L (corresponding author), Masaryk Univ, Univ Hosp Brno, Fac Med, Dept Gastroenterol & Internal Med, Jihlavska 20, Brno 62500, Czech Republic.
EM lumir.kunovsky@gmail.com
RI Kunovsky, Lumir/HCI-3910-2022; Martinek, Arnost/R-6518-2019
OI Martinek, Arnost/0000-0001-7597-3235
FU Ministry of Health, Czech Republic - conceptual development of research
organization (FNBr) [65269705]
FX This work was supported by the Ministry of Health, Czech Republic -
conceptual development of research organization (FNBr, 65269705) and by
the Ministry of Health, Czech Republic - conceptual development of
research organization (FNBr, 65269705, Sup 15/21) .
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NR 34
TC 0
Z9 0
U1 0
U2 17
PU MEDICAL UNIV PRESS
PI CLUJ-NAPOCA
PA 3RD MEDICAL CLINIC, STR CROITORILOR NO 19-21, CLUJ-NAPOCA, 400162,
ROMANIA
SN 1841-8724
EI 1842-1121
J9 J GASTROINTEST LIVER
JI J. Gastrointest. Liver Dis.
PD SEP
PY 2021
VL 30
IS 3
BP 398
EP 403
DI 10.15403/jgld-3849
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA UY1HJ
UT WOS:000701282100014
PM 34551027
OA gold
DA 2025-01-07
ER
PT J
AU Stokkeland, K
Lageborn, CT
Ekbom, A
Höijer, J
Bottai, M
Stål, P
Söderberg-Löfdal, K
AF Stokkeland, Knut
Lageborn, Christine Takami
Ekbom, Anders
Hoijer, Jonas
Bottai, Matteo
Stal, Per
Soderberg-Lofdal, Karin
TI Statins and Angiotensin-Converting Enzyme Inhibitors are Associated with
Reduced Mortality and Morbidity in Chronic Liver Disease
SO BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY
LA English
DT Article
ID ATTENUATES HEPATIC-FIBROSIS; NONALCOHOLIC STEATOHEPATITIS; PORTAL
PRESSURE; C VIRUS; ATORVASTATIN; CANCER; SIMVASTATIN; REDUCTION;
METFORMIN; CIRRHOSIS
AB Liver fibrosis is a common response to many chronic liver diseases. The aim of our study was to explore whether pharmacotherapy for concurrent diseases affects overall mortality, liver-related mortality and liver-related morbidity in patients with chronic liver disease. We performed a register-based cohort study of all patients with a first-time diagnosis of chronic liver disease between 2005 and 2012 in Sweden (n=70546). Data from the Patient Register, the Prescribed Drug Register and the Death Certificate Register were linked. We studied whether the use of statins, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and antibiotics affected the risk of total mortality, liver-specific mortality and morbidity. We found a reduction in mortality risk for statin users (n=11,245) with hazard ratios from 0.57 (95% CI: 0.32-0.99) for patients with autoimmune hepatitis to 0.84 (95% CI: 0.75-0.95) for patients with alcoholic liver disease. There was a significantly reduced liver-related mortality for patients with alcoholic liver disease who used angiotensin-converting enzyme inhibitors, 0.85 (95% CI: 0.65-0.96). There were increased overall mortality risks for antibiotic users (n=44,572), with hazard ratios up to 1.67 (95% CI, 1.55-1.80) for viral hepatitis. Statin use was associated with decreased risks of liver-specific mortality and morbidity, and reduced total mortality foremost among patients with alcoholic liver disease. Angiotensin -converting enzyme inhibitors was associated with reduced liver-related mortality among patients with alcoholic liver disease.
C1 [Stokkeland, Knut] Visby Hosp, Dept Med, St Gorans Str 8, SE-62184 Visby, Sweden.
[Stokkeland, Knut; Stal, Per] Karolinska Inst, Dept Med Huddinge, Unit Gastroenterol & Rheumatol, Stockholm, Sweden.
[Lageborn, Christine Takami] Karolinska Inst, Stockholm, Sweden.
[Ekbom, Anders] Karolinska Inst, Unit Clin Epidemiol, Dept Med, Stockholm, Sweden.
[Hoijer, Jonas; Bottai, Matteo] Karolinska Inst, Unit Biostat, IMM, Stockholm, Sweden.
[Stal, Per] Karolinska Univ Hosp, Unit Hepatol, Ctr Digest Dis, Stockholm, Sweden.
[Soderberg-Lofdal, Karin] Karolinska Inst, Div Clin Pharmacol, Dept Lab Med, Stockholm, Sweden.
[Soderberg-Lofdal, Karin] Karolinska Univ Hosp, Dept Clin Pharmacol, Stockholm, Sweden.
C3 Karolinska Institutet; Karolinska Institutet; Karolinska Institutet;
Karolinska Institutet; Karolinska Institutet; Karolinska University
Hospital; Karolinska Institutet; Karolinska Institutet; Karolinska
University Hospital
RP Stokkeland, K (corresponding author), Visby Hosp, Dept Med, St Gorans Str 8, SE-62184 Visby, Sweden.
EM knut.stokkeland@gotland.se
RI Stål, Per/J-2154-2019; Stokkeland, Knut/AFW-7014-2022
OI Soderberg Lofdal, Karin/0000-0002-3494-9535; Stal,
Per/0000-0003-2915-1964; Stokkeland, Knut/0000-0002-5705-2069
FU Department of Medicine, Visby Hospital; Karolinska Institute; Ruth and
Richard Julins Foundation; Swedish Society of Medicine; Stockholm County
Council (ALF) [20130084, 20150403]
FX This work was supported by the Department of Medicine, Visby Hospital;
funds from the Karolinska Institute, Ruth and Richard Julins Foundation,
and the Swedish Society of Medicine; and grants provided by the
Stockholm County Council (ALF projects, nos. 20130084 and 20150403).
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NR 53
TC 12
Z9 12
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1742-7835
EI 1742-7843
J9 BASIC CLIN PHARMACOL
JI Basic Clin. Pharmacol. Toxicol.
PD JAN
PY 2018
VL 122
IS 1
BP 104
EP 110
DI 10.1111/bcpt.12844
PG 7
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA FQ9BK
UT WOS:000418657100013
PM 28691216
OA Bronze
DA 2025-01-07
ER
PT J
AU Elli, L
Discepolo, V
Bardella, MT
Guandalini, S
AF Elli, Luca
Discepolo, Valentina
Bardella, Maria T.
Guandalini, Stefano
TI Does Gluten Intake Influence the Development of Celiac
Disease-associated Complications?
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Review
DE celiac disease; gluten-free diet; autoimmune disease; malignancy;
lymphoma; gluten
ID DEPENDENT DIABETES-MELLITUS; POPULATION-BASED COHORT; AUTOIMMUNE
THYROID-DISEASE; PRIMARY BILIARY-CIRRHOSIS; FREE DIET;
DERMATITIS-HERPETIFORMIS; LIVER-DISEASE; HIGH PREVALENCE; SWEDISH
COHORT; CANCER-RISK
AB Celiac disease (CD) is regarded as the most common autoimmune enteropathy in western countries. Epidemiological studies indicate that approximately 1:100 individuals may present with histologically proven CD. CD develops in genetically predisposed subjects after gluten ingestion. It usually subsides after gluten is withdrawn from their diet. Gluten is the only known environmental factor that affects the progression/regression of the intestinal villous atrophy, which is the hallmark of this disease. CD generally follows a benign course after gluten elimination. However, it is also associated with the development of other autoimmune disorders or of intestinal malignancies. The issue of whether such complications, sometimes of significant clinical and prognostic impact, are or are not the result of ongoing gluten ingestion, is an important one that has been investigated over the recent years with conflicting results. In terms of practical implications, the presence of a positive correlation between gluten intake and the development of severe complications would lead to the need for early diagnosis and mass screening. The lack of such correlation would instead suggest a less aggressive diagnostic strategy. This review aims at critically summarizing the evidence supporting either hypothesis.
C1 [Elli, Luca; Bardella, Maria T.] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Ctr Prevent & Diag Celiac Dis Gastroenterol 2, Milan, Italy.
[Discepolo, Valentina] Univ Naples Federico II, Dept Translat Med, Sect Pediat, Naples, Italy.
[Guandalini, Stefano] Univ Chicago, Dept Pediat, Sect Pediat Gastroenterol Hepatol & Nutr, Celiac Dis Ctr, Chicago, IL 60637 USA.
C3 IRCCS Ca Granda Ospedale Maggiore Policlinico; University of Naples
Federico II; University of Chicago
RP Guandalini, S (corresponding author), Univ Chicago, Dept Pediat, Sect Pediat Gastroenterol Hepatol & Nutr, Celiac Dis Ctr, 5841S Maryland Ave, Chicago, IL 60637 USA.
EM sguandalini@peds.bsd.uchicago.edu
RI Discepolo, Valentina/AAC-7665-2022; Guandalini, Stefano/G-8084-2011;
Elli, Luca/K-6084-2016
OI Discepolo, Valentina/0000-0001-6158-0545; Elli, Luca/0000-0002-0873-0759
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NR 101
TC 20
Z9 22
U1 0
U2 19
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD JAN
PY 2014
VL 48
IS 1
BP 13
EP 20
DI 10.1097/MCG.0b013e3182a9f898
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 274UA
UT WOS:000328630500006
PM 24072075
DA 2025-01-07
ER
PT J
AU Ghumman, NA
Qamar, MA
Khurrum, N
Khan, ZA
Ul Mustafa, Z
Irshad, F
AF Ghumman, Nasim Aslam
Qamar, Muhammad Adeel
Khurrum, Nosheen
Khan, Zahid Ahmad
Ul Mustafa, Zia
Irshad, Faiza
TI Clinical Symptomatology and Laboratory Diagnosis of Nonalcoholic Chronic
Fatty Liver Disease
SO PAKISTAN JOURNAL OF MEDICAL & HEALTH SCIENCES
LA English
DT Article
DE NAFLD; hepatocellular carcinoma; cirrhosis
ID METABOLIC SYNDROME; PREVALENCE; STEATOHEPATITIS; EPIDEMIOLOGY;
MANAGEMENT; FRUCTOSE; DIFFERS; INSULIN
AB Background: One of the leading causes for hepatocellular carcinoma is Nonalcoholic fatty liver diseases (NAFLD) that also increases incidence of mortality rates.
Aim: To understand alterations biochemically and clinically in patients suffering from NAFLD since they are at stake of cirrhosis as well as nonalcoholic steatohepatitis (NASH) in case of Pakistani population.
Methods: Patients suffering from NAFLD were selected for these case reaches that were all confirmed via ultrasonography. Candidates were tested negative for autoimmune or viral hepatitis serologic markers, no record was found with respect to liver disease related to metabolism, moreover candidates were also not administer any medication that has its impact on liver like Ursobil. Clinically and biochemically all the patients were tested for history, signs and symptoms and they depicted variables.
Results: A enrollment of 80 candidates was carried out that included 38 female and 42 male, owing mean age of 40.4 years. The candidates with no diabetes and obesity were 26.4% and 18.3%, respectively. Late dinner sleep disorders and delayed sleep were the most detectable reasons in patients suffering from NAFLD. Moreover, thirst sensation, anxiety, bloating, and upper abdominal pain, warming sensation and defecation disturbances, were seen common in case of patients suffering from NAFLD.
Conclusion: NAFLD is regarded as heterogeneous pathology with variety of clinical findings. It has been experienced that gastrointestinal problems as well as anxiety are most frequently seen in patients suffering from NAFLD.
C1 [Ghumman, Nasim Aslam; Khurrum, Nosheen] Rashid Latif Med Coll, LHR 37Km Ferozpur Rd, Lhr, Pakistan.
[Qamar, Muhammad Adeel] Sahara Md Coll Narowal, Gastroenterol, Narowal, Pakistan.
[Khan, Zahid Ahmad] Mohtarma Benazir Bhutto Shaheed Med Coll, Mirpur, Ajk, Pakistan.
[Ul Mustafa, Zia] Sahara Med Coll Narowal, Narowal, Pakistan.
[Irshad, Faiza] Anatom M Islam Med & Dent Coll, Gujranwala, Pakistan.
RP Qamar, MA (corresponding author), Sahara Md Coll Narowal, Gastroenterol, Narowal, Pakistan.
EM dradeel176@gmail.com
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NR 20
TC 1
Z9 1
U1 0
U2 0
PU LAHORE MEDICAL RESEARCH CENTER LLP
PI LAHORE
PA 590, Karim Block, Allama Iqbal Town, LAHORE, 00000, PAKISTAN
SN 1996-7195
J9 PAK J MED HEALTH SCI
JI Pak. J. Med. Health Sci.
PD SEP
PY 2021
VL 15
IS 9
BP 2371
EP 2372
DI 10.53350/pjmhs211592371
PG 2
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA XN1WE
UT WOS:000729302200075
DA 2025-01-07
ER
PT J
AU Erker, C
Moellmann, M
Valencia, MIB
Schwartz, IVD
AF Erker, Christian
Moellmann, Michael
Berrio Valencia, Marta Ines
Doederlein Schwartz, Ida Vanessa
TI Anaesthesia recommendations for patients suffering from Glycogen storage
disease type I
SO ANASTHESIOLOGIE & INTENSIVMEDIZIN
LA English
DT Article
ID CONTINUOUS GLUCOSE THERAPY; TERM CLINICAL-COURSE; MANAGEMENT; PREGNANCY
AB Disease summary: Glycogen storage disease type I is a rare autosomal recessive inherited disorder with an annual incidence of approximately 1:100,000 [1]. Due to a deficiency of glucose-6-phosphatase [2], glycogen stored in the liver cannot be metabolized. This leads to poor tolerance to fasting and increased risk of hypoglycemia and lactate acidosis. The accumulation of glycogen [3] in liver tissue leads to hepatomegaly, and later in life to an increased risk of hepatocellular adenoma and/or carcinoma. The clinical presentation is accompanied by growth retardation. Renal affection, hyperlipidemia [4], and platelet dysfunctions [5] are common. Perioperative management has to focus on metabolic homeostasis by adequate glucose supply and prevention of lactate acidosis exacerbation. Platelet dysfunction poses a challenge to regional anaesthesia techniques, and haemostasis throughout an operation. Subtype Ib is caused by deficiency of glucose-6-phosphatasetranslocase and is accompanied by neutrophil dysfunction, recurrent infections, autoimmune thyreoid disease, and inflammatory bowel disease.
C1 [Erker, Christian; Moellmann, Michael] St Franziskus Hosp Muenster, Munster, Germany.
[Berrio Valencia, Marta Ines] Hosp Pablo Tobon Uribe, Medellin, Colombia.
[Doederlein Schwartz, Ida Vanessa] Univ Fed Rio Grande do Sul UFRGS, Dept Genet, Porto Alegre, RS, Brazil.
C3 St. Franziskus-Hospital; Universidade Federal do Rio Grande do Sul
RP Erker, C (corresponding author), St Franziskus Hosp Muenster, Munster, Germany.
EM Christian.Erker@sfh-muenster.de; michael.moellmann@sfh-muenster.de;
martaberrio@gmail.com; ischwartz@hcpa.ufrgs.br
RI Schwartz, Ida/M-1422-2015
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NR 29
TC 0
Z9 0
U1 0
U2 0
PU AKTIV DRUCK & VERLAG GMBH
PI EBELSBACH
PA AN DER LOHWIESE 36, EBELSBACH, 97500, GERMANY
SN 0170-5334
EI 1439-0256
J9 ANASTH INTENSIVMED
JI Anasthesiol. Intensivmed.
PD MAR
PY 2017
VL 58
SU 4
BP S90
EP S98
PG 9
WC Anesthesiology; Critical Care Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anesthesiology; General & Internal Medicine
GA VK9BV
UT WOS:000765809100002
DA 2025-01-07
ER
PT J
AU Furuta, K
Sato, S
Yamauchi, T
Ozawa, T
Harada, M
Kakumu, S
AF Furuta, Keiko
Sato, Sayaka
Yamauchi, Taeko
Ozawa, Takuya
Harada, Manabu
Kakumu, Shinichi
TI Intrahepatic gene expression profiles in chronic hepatitis B and
autoimmune liver disease
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE chronic hepatitis B; autoimmune liver disease; intrahepatic gene
expression; pathogenesis
ID PRIMARY BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; CDNA MICROARRAY;
IDENTIFICATION; METALLOTHIONEIN; CLASSIFICATION; FIBROSIS
AB DNA microarray technology has enabled genomewide analysis of gene transcript levels, yielding insight into the molecular nature of liver disease.
We compared gene expression of liver biopsy specimens in 16 patients with different stages of chronic hepatitis B, five with autoimmune hepatitis (AIH), five with primary biliary cirrhosis (PBC), and six with druginduced hepatitis.
Of 21 073 genes, 424 showed different expression in a particular disease group on analysis of variance. Genes associated with extracellular matrix, cell growth, and DNA repair were noted in the advanced fibrotic stage of chronic hepatitis B (B-3), while gene expression regarding complement activation and the innate immune response decreased. When we compared gene expression at the relatively early stage in each disease group with pathway analysis, pathways relating to chemotaxis and cell homeostasis were selected in chronic hepatitis B. In PBC, gene expression relating to structural constituents and contractions of muscle such as actin and myosin were enhanced, in contrast to the downregulation of genes relating to protein binding in AIH. A hierarchical clustering analysis of hepatitis B genes defined five clusters. Generally, the transcripts upregulated according to disease progression were associated with signaling pathway/transcription, including tumor-associated calcium signal transducer 1 and chemokine ligand 19, and with cell communication, such as collagen. In two groups, all transcripts were downregulated; transcripts related to chemokine ligands and metallothionein were further depressed in B-3.
Analysis of gene expression in liver may be useful for understanding features of distinct liver diseases and for guiding disease progression, particularly in chronic hepatitis B.
C1 [Furuta, Keiko; Sato, Sayaka; Yamauchi, Taeko; Kakumu, Shinichi] Aichi Med Univ, Sch Med, Dept Internal Med, Div Gastroenterol, Aichi, Japan.
[Ozawa, Takuya; Harada, Manabu] Filgen Inc, Dept Biosci, Nagoya, Aichi, Japan.
C3 Aichi Medical University
RP Kakumu, S (corresponding author), 5-2104 Uedayama,Tenpaku Ku, Nagoya, Aichi 4680001, Japan.
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NR 22
TC 10
Z9 11
U1 0
U2 4
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD NOV
PY 2008
VL 43
IS 11
BP 866
EP 874
DI 10.1007/s00535-008-2237-y
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 374BU
UT WOS:000261018100007
PM 19012040
DA 2025-01-07
ER
PT J
AU Qin, LS
Tian, S
Yang, L
Fan, J
Zhang, JC
AF Qin, Lisha
Tian, Shan
Yang, Lian
Fan, Jun
Zhang, Jianchu
TI Liver failure as the initial presentation in cancer of unknown primary:
a case report
SO BMC INFECTIOUS DISEASES
LA English
DT Article
DE Liver failure; cancer of unknown primary; Malignant infiltration;
Polymyositis; Case report
ID HEPATIC INFILTRATION; SECONDARY
AB BackgroundLiver failure is severe hepatic cellular damage caused by multiple factors that leads to clinical manifestations. Hepatic infiltration by malignancy is rarely reported as a cause of liver failure.Case presentationA 51-year-old male patient was admitted to the Wuhan Union Hospital complaining of bloating and jaundice. He had been diagnosed with polymyositis ten prior and was taking oral glucocorticoids. Physical examination revealed seroperitoneum and icteric sclera; laboratory tests revealed liver dysfunction, a coagulopathy, and negative results for the common causes of liver failure. Moreover, an ascitic tap and bone marrow aspirate and trephine confirmed a metastatic, poorly differentiated adenocarcinoma. These findings indicate that malignant infiltration is the most likely cause of liver failure. Regrettably, the patient refused complete liver and lymph node biopsies and was discharged on day 31.ConclusionClinicians should consider the possibility of malignant infiltration when approaching a case of liver failure with prodromal symptoms or imaging abnormalities, especially in patients with autoimmune diseases, such as polymyositis.
C1 [Qin, Lisha; Zhang, Jianchu] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Resp & Crit Care Med, Wuhan 430022, Peoples R China.
[Tian, Shan] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Infect Dis, Wuhan 430022, Peoples R China.
[Yang, Lian] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Radiol, Wuhan 430022, Peoples R China.
[Fan, Jun] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Pathol, Wuhan 430022, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
Science & Technology; Huazhong University of Science & Technology;
Huazhong University of Science & Technology
RP Zhang, JC (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Resp & Crit Care Med, Wuhan 430022, Peoples R China.
EM zsn0928@163.com
RI Fan, Jun/D-3853-2013
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NR 16
TC 0
Z9 0
U1 2
U2 6
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2334
J9 BMC INFECT DIS
JI BMC Infect. Dis.
PD MAY 30
PY 2023
VL 23
IS 1
AR 363
DI 10.1186/s12879-023-08274-0
PG 5
WC Infectious Diseases
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases
GA I0NY1
UT WOS:000999840300002
PM 37254054
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Yu, MQ
Zhu, Y
Cong, QW
Wu, CY
AF Yu, Mengqian
Zhu, Ying
Cong, Qingwei
Wu, Chunyan
TI Metabonomics Research Progress on Liver Diseases
SO CANADIAN JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
ID CHROMATOGRAPHY-MASS SPECTROMETRY; PRIMARY BILIARY-CIRRHOSIS;
HEPATOCELLULAR-CARCINOMA; H-1-NMR SPECTROSCOPY; POTENTIAL BIOMARKERS;
SERUM; HEPATITIS; METABOLOMICS; DISCOVERY; FAILURE
AB Metabolomics as the new omics technique develops after genomics, transcriptomics, and proteomics and has rapid development at present. Liver diseases are worldwide public health problems. In China, chronic hepatitis B and its secondary diseases are the common liver diseases. They can be diagnosed by the combination of history, virology, liver function, and medical imaging. However, some patients seldom have relevant physical examination, so the diagnosis may be delayed. Many other liver diseases, such asdrug- induced liver injury (DILI), alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD), and autoimmune liver diseases, still do not have definite diagnostic markers; the diagnosis consists of history, medical imaging, and the relevant score. As a result, the clinical work becomes very complex. So it has broad prospects to explore the specific and sensitive biomarkers of liver diseases with metabolomics. In this paper, there are several summaries which are related to the current research progress and application of metabolomics on biomarkers of liver diseases.
C1 [Yu, Mengqian; Zhu, Ying; Cong, Qingwei; Wu, Chunyan] Dalian Med Univ, Affiliated Hosp 1, Dept Infect Dis, Dalian 116000, Liaoning, Peoples R China.
C3 Dalian Medical University
RP Zhu, Y (corresponding author), Dalian Med Univ, Affiliated Hosp 1, Dept Infect Dis, Dalian 116000, Liaoning, Peoples R China.
EM zhuyingsh52@126.com
RI WU, CHUNYAN/HMO-6771-2023
FU National Natural Science Foundation of China [81673728]
FX This paper was financially supported by the National Natural Science
Foundation of China (no. 81673728).
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NR 62
TC 51
Z9 59
U1 1
U2 60
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2291-2789
EI 2291-2797
J9 CAN J GASTROENTEROL
JI Can. J. Gastroenterol. Hepatol.
PY 2017
VL 2017
AR 8467192
DI 10.1155/2017/8467192
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EN6YM
UT WOS:000396149300001
PM 28321390
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Efe, C
Torgutalp, M
Henriksson, I
Alalkim, F
Lytvyak, E
Trivedi, H
Eren, F
Fischer, J
Chayanupatkul, M
Coppo, C
Purnak, T
Muratori, L
Werner, M
Muratori, P
Rorsman, F
Onnerhag, K
Nilsson, E
Heurgué-Berlot, A
Demir, N
Semela, D
Kiyici, M
Schiano, TD
Montano-Loza, AJ
Berg, T
Ozaslan, E
Yoshida, EM
Bonder, A
Marschall, HU
Beretta-Piccoli, BT
Wahlin, S
AF Efe, Cumali
Torgutalp, Murat
Henriksson, Ida
Alalkim, Fatema
Lytvyak, Ellina
Trivedi, Hirsh
Eren, Fatih
Fischer, Janett
Chayanupatkul, Maneerat
Coppo, Claudia
Purnak, Tugrul
Muratori, Luigi
Werner, Marten
Muratori, Paolo
Rorsman, Fredrik
Onnerhag, Kristina
Nilsson, Emma
Heurgue-Berlot, Alexandra
Demir, Nurhan
Semela, David
Kiyici, Murat
Schiano, Thomas D.
Montano-Loza, Aldo J.
Berg, Thomas
Ozaslan, Ersan
Yoshida, Eric M.
Bonder, Alan
Marschall, Hanns-Ulrich
Beretta-Piccoli, Benedetta Terziroli
Wahlin, Staffan
TI Extrahepatic autoimmune diseases in primary biliary cholangitis:
Prevalence and significance for clinical presentation and disease
outcome
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Ankylosing spondylitis; Anti-phospholipid syndrome; Autoimmune hemolytic
anemia; Idiopathic thrombocytopenic purpura; IgA nephropathy; Multiple
sclerosis; Polyarteritis nodosa; Polymyositis; Sarcoidosis; Temporal
arteritis
ID BIOCHEMICAL RESPONSE; URSODEOXYCHOLIC ACID; RISK-FACTORS; CIRRHOSIS;
PROGNOSIS; SARCOIDOSIS; MANAGEMENT; PBC
AB Background and Aim The prevalence and clinical significance of extrahepatic autoimmune diseases (EHAIDs) have not been evaluated in a large cohort of primary biliary cholangitis (PBC). Methods The medical records of 1554 patients with PBC from 20 international centers were retrospectively reviewed. Development of decompensated cirrhosis (ascites, variceal bleeding, and/or hepatic encephalopathy) and hepatocellular carcinoma were considered clinical endpoints. Results A total of 35 different EHAIDs were diagnosed in 440 (28.3%) patients with PBC. Patients with EHAIDs were more often female (92.5%vs86.1%,P < 0.001) and seropositive for anti-mitochondrial antibodies (88%vs84%,P = 0.05) and antinuclear antibodies and/or smooth muscle antibodies (53.8%vs43.6%,P = 0.005). At presentation, patients with EHAIDs had significantly lower levels of alkaline phosphatase (1.76vs1.98 x upper limit of normal [ULN],P = 0.006), aspartate aminotransferase (1.29vs1.50 x ULN,P < 0.001), and total bilirubin (0.53vs0.58 x ULN,P = 0.002). Patients with EHAIDs and without EHAIDs had similar rates of GLOBE high-risk status (12.3%vs16.1%,P = 0.07) and Paris II response (71.4%vs69.4%,P = 0.59). Overall, event-free survival was not different in patients with and without EHAIDs (90.8%vs90.7%,P = 0.53, log rank). Coexistence of each autoimmune thyroid diseases (10.6%), Sjogren disease (8.3%), systemic sclerosis (2.9%), rheumatoid arthritis (2.7%), systemic lupus erythematosus (1.7%), celiac disease (1.7%), psoriasis (1.5%), and inflammatory bowel diseases (1.3%) did not influence the outcome. Conclusions Our study confirms that EHAIDs are frequently diagnosed in patients with PBC. The presence of EHAIDs may influence the clinical phenotype of PBC at presentation but has no impact on PBC outcome.
C1 [Efe, Cumali; Demir, Nurhan] Gazi Yasargil Educ & Res Hosp, Dept Gastroenterol, Diyarbakir, Turkey.
[Torgutalp, Murat] Ankara Univ Hosp, Dept Rheumatol, Ankara, Turkey.
[Purnak, Tugrul] Hacettepe Univ, Dept Gastroenterol, Ankara, Turkey.
[Ozaslan, Ersan] Ankara City Hosp, Dept Gastroenterol, Ankara, Turkey.
[Eren, Fatih; Kiyici, Murat] Uludag Univ, Med Fac, Dept Gastroenterol, Bursa, Turkey.
[Henriksson, Ida] Orebro Univ, Fac Med & Hlth, Dept Gastroenterol, Orebro, Sweden.
[Werner, Marten] Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden.
[Rorsman, Fredrik] Uppsala Univ Hosp, Dept Gastroenterol & Hepatol, Uppsala, Sweden.
[Onnerhag, Kristina] Skane Univ Hosp, Dept Gastroenterol & Hepatol, Malmo, Sweden.
[Nilsson, Emma] Skane Univ Hosp, Dept Clin Sci, Gastroenterol Div, Lund, Sweden.
[Marschall, Hanns-Ulrich] Univ Gothenburg, Sahlgrenska Acad, Dept Mol & Clin Med, Gothenburg, Sweden.
[Wahlin, Staffan] Karolinska Inst, Ctr Digest Dis, Hepatol Div, Stockholm, Sweden.
[Wahlin, Staffan] Karolinska Univ Hosp, Stockholm, Sweden.
[Alalkim, Fatema; Yoshida, Eric M.] Univ British Columbia, Div Gastroenterol, Vancouver, BC, Canada.
[Alalkim, Fatema; Yoshida, Eric M.] Vancouver Gen Hosp, Vancouver, BC, Canada.
[Lytvyak, Ellina; Montano-Loza, Aldo J.] Univ Alberta, Div Gastroenterol, Edmonton, AB, Canada.
[Lytvyak, Ellina; Montano-Loza, Aldo J.] Univ Alberta, Liver Unit, Edmonton, AB, Canada.
[Trivedi, Hirsh; Bonder, Alan] Harvard Med Sch, Beth Israel Med Ctr, Div GI & Hepatol, Boston, MA 02115 USA.
[Schiano, Thomas D.] Mt Sinai Med Ctr, Div Liver Dis, New York, NY 10029 USA.
[Fischer, Janett; Berg, Thomas] Univ Clin Leipzig, Div Gastroenterol, Clin & Polyclin Oncol Hepatol Infect Dis & Pneumo, Leipzig, Germany.
[Chayanupatkul, Maneerat] Chulalongkorn Univ, Fac Med, Bangkok, Thailand.
[Coppo, Claudia; Muratori, Luigi; Muratori, Paolo] Univ Bologna, Ctr Study & Treatment Autoimmune Dis Liver & Bina, Bologna, Italy.
[Heurgue-Berlot, Alexandra] CHU Reims, Dept Hepatogastroenterol, Reims, France.
[Semela, David] Kantonsspital St Gallen, Div Gastroenterol & Hepatol, St Gallen, Switzerland.
[Beretta-Piccoli, Benedetta Terziroli] Epatoctr Ticino, Lugano, Switzerland.
C3 Diyarbakir Training & Research Hospital; Ankara University; Hacettepe
University; City Hospital Ankara; Uludag University; Orebro University;
Umea University; Uppsala University; Uppsala University Hospital; Lund
University; Skane University Hospital; Lund University; Skane University
Hospital; University of Gothenburg; Karolinska Institutet; Karolinska
Institutet; Karolinska University Hospital; University of British
Columbia; University of British Columbia; University of Alberta;
University of Alberta; Harvard University; Beth Israel Deaconess Medical
Center; Harvard Medical School; Icahn School of Medicine at Mount Sinai;
Leipzig University; Chulalongkorn University; University of Bologna; CHU
de Reims; Universite de Reims Champagne-Ardenne; Kantonsspital St.
Gallen
RP Efe, C (corresponding author), Gazi Yasargil Educ & Res Hosp, Dept Gastroenterol, Diyarbakir, Turkey.
EM drcumi21@hotmail.com
RI Efe, Cumali/AAE-4127-2021; Wahlin, Staffan/B-5486-2012; Muratori,
Luigi/I-3181-2012; Chayanupatkul, Maneerat/AAX-1797-2020; Torgutalp,
Murat/ABA-3372-2021; KIYICI, Murat/AAI-4213-2021; Beretta-Piccoli,
Benedetta/U-8460-2019; Marschall, Hanns-Ulrich/K-8842-2017; Semela,
David/D-1988-2010
OI TORGUTALP, MURAT/0000-0003-4600-9484; Marschall,
Hanns-Ulrich/0000-0001-7347-3085; KIYICI, Murat/0000-0002-3208-6211;
Lytvyak, Ellina/0000-0001-5651-9010; efe, cumali/0000-0001-6593-5702;
Trivedi, Hirsh/0000-0002-8328-9211; chayanupatkul,
maneerat/0000-0002-1649-5373; Demir, Nurhan/0000-0003-0037-7775; Wahlin,
Staffan/0000-0002-5985-9464; Terziroli Beretta-Piccoli,
Benedetta/0000-0001-5004-5029
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NR 39
TC 43
Z9 44
U1 3
U2 20
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD APR
PY 2021
VL 36
IS 4
SI SI
BP 936
EP 942
DI 10.1111/jgh.15214
EA AUG 2020
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA RP3YJ
UT WOS:000561706700001
PM 32790935
DA 2025-01-07
ER
PT J
AU Liu, X
Han, Z
Yang, C
AF Liu, X.
Han, Z.
Yang, C.
TI Associations of microRNA single nucleotide polymorphisms and disease
risk and pathophysiology
SO CLINICAL GENETICS
LA English
DT Review
DE diseases; microRNAs; physiological and pathological processes; single
nucleotide polymorphisms
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; FUNCTIONAL POLYMORPHISM;
HEPATOCELLULAR-CARCINOMA; GENETIC-VARIATION; ISCHEMIC-STROKE;
BREAST-CANCER; RS3746444 POLYMORPHISM; TURKISH POPULATION; NEGATIVE
SYMPTOMS; SCHIZOPHRENIA
AB Single nucleotide polymorphisms (SNPs) are genetic variations that contribute to human phenotypes associated with various diseases. SNPs are involved in the regulation of a broad range of physiological and pathological processes, such as cellular senescence, apoptosis, inflammation, and immune response, by upregulating the expression of classical inflammation markers. Recent studies have suggested that SNPs located in gene-encoding microRNAs (miRNAs) affect various aspects of diseases by regulating the expression or activity of miRNAs. In the last few years, miRNA polymorphisms that increase and/or reduce the risk of developing many diseases, such as cancers, autoimmune diseases, and cardiovascular diseases, have attracted increasing attention not only because of their involvement in the pathophysiology of diseases but also because they can be used as prognostic biomarkers for a variety of diseases. In this review, we summarize the relationships between miRNA SNPs and the pathophysiology and risk of diseases.
C1 [Liu, X.; Yang, C.] Nanjing Med Univ, Wuxi Peoples Hosp 2, Dept Cardiol, Wuxi 214002, Peoples R China.
[Han, Z.] Nanjing Med Univ, Wuxi Peoples Hosp 2, Dept Lab Med, Wuxi 214002, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University
RP Yang, C (corresponding author), Nanjing Med Univ, Wuxi Peoples Hosp 2, Dept Cardiol, Wuxi 214002, Peoples R China.; Han, Z (corresponding author), Nanjing Med Univ, Wuxi Peoples Hosp 2, Dept Lab Med, Wuxi 214002, Peoples R China.
EM zjhan1125@163.com; doctory2071@sina.com
FU Clinical Technology Foundation of Jiangsu Province [BL2012042]; National
Natural Science Foundation of China [81301503]; Science and Technology
Projects of Wuxi City [YGZXM1501]
FX This work was supported by the Clinical Technology Foundation of Jiangsu
Province (BL2012042), the National Natural Science Foundation of China
(81301503), and the Science and Technology Projects of Wuxi City
(YGZXM1501).
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NR 97
TC 16
Z9 16
U1 2
U2 18
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9163
EI 1399-0004
J9 CLIN GENET
JI Clin. Genet.
PD SEP
PY 2017
VL 92
IS 3
BP 235
EP 242
DI 10.1111/cge.12950
PG 8
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA FE0LL
UT WOS:000407911700001
PM 27925170
DA 2025-01-07
ER
PT J
AU Gelsomino, F
Vitale, G
Ardizzoni, A
AF Gelsomino, Francesco
Vitale, Giovanni
Ardizzoni, Andrea
TI A case of nivolumab-related cholangitis and literature review: how to
look for the right tools for a correct diagnosis of this rare
immune-related adverse event
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Review
DE Nivolumab; Cholangitis; Non-small cell lung cancer; Immunotherapy
ID DOCETAXEL; SAFETY
AB Anti-programmed cell death-1 (PD-1) monoclonal antibodies, such as nivolumab, used for the treatment of several tumors, can trigger effector T-cells against tumor- and self-antigens, leading to the occurrence of different immune-related adverse events. Among them, liver injuries are rare and usually transient. To date, only four cases of immune-related cholangitis in non-small cell lung cancer (NSCLC) patients have been described during nivolumab treatment. Here, we describe laboratory tests, imaging and liver biopsy features that confirm this diagnosis as opposed to other forms of autoimmune liver disease; nevertheless, we also provide evidence of the presence of different clinical-pathological patterns of immune-related cholangitis.
C1 [Gelsomino, Francesco] Univ Hosp Parma, Med Oncol Unit, Parma, Italy.
[Vitale, Giovanni] Univ Bologna, Dept Med & Surg Sci, Policlin S Orsola Malpighi, Bologna, Italy.
[Ardizzoni, Andrea] Univ Bologna, Med Oncol Unit, Policlin S Orsola Malpighi, Bologna, Italy.
C3 University of Parma; University Hospital of Parma; University of
Bologna; IRCCS Azienda Ospedaliero-Universitaria di Bologna; IRCCS
Azienda Ospedaliero-Universitaria di Bologna; University of Bologna
RP Gelsomino, F (corresponding author), Univ Hosp Parma, Med Oncol Unit, Parma, Italy.
EM fgelsomino@ao.pr.it
RI ardizzoni, andrea/AAC-4337-2021; Vitale, Giovanni/K-6322-2016;
Gelsomino, Francesco/J-8292-2018
OI Vitale, Giovanni/0000-0003-2603-8245; Gelsomino,
Francesco/0000-0002-9204-1728; ardizzoni, andrea/0000-0003-2678-0714
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NR 11
TC 36
Z9 37
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD FEB
PY 2018
VL 36
IS 1
BP 144
EP 146
DI 10.1007/s10637-017-0484-6
PG 3
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA FV5SE
UT WOS:000424641900016
PM 28631096
DA 2025-01-07
ER
PT J
AU Cai, XY
Zha, HY
Yang, ZX
Du, YW
Dai, XY
Yang, B
Wang, JJ
He, QJ
Weng, QJ
AF Cai, Xuanyan
Zha, Huiyan
Yang, Zhaoxu
Du, Yiwen
Dai, Xiaoyang
Yang, Bo
Wang, Jiajia
He, Qiaojun
Weng, Qinjie
TI Genetic dominance of transforming growth factor-β1 polymorphisms in
chronic liver disease
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE transforming growth factor-beta 1; polymorphisms; susceptibility;
chronic liver disease; cirrhosis
ID GROWTH-FACTOR-BETA; TGF-BETA; HEPATOCELLULAR-CARCINOMA; TRANSCRIPTION
FACTORS; ASSOCIATION; ACTIVATION; RISK; MECHANISMS; EXPRESSION;
PREDICTION
AB Chronic liver disease (CLD) is an extremely common clinical condition accompanied by sustained inflammatory response leading to tissue damage. Transforming growth factor-beta 1 (TGF-beta 1) is known as a master immune regulator in CLDs, but the association between TGF-beta 1 polymorphisms and CLD risk is controversial and inconclusive, and the genetic dominance of CLDs remains unknown. In this study, the relationship between TGF-beta 1 polymorphisms and CLD susceptibility is systematically analyzed based on 35 eligible studies. Individuals with the TGF-beta 1-509 allele (TT or CT) or codon 10 allele (Pro/Pro) show an increased risk of CLDs. Subgroup analyses indicate TGF-beta 1-509C/T has a significant correlation with cirrhosis and chronic hepatitis C, codon 10 is associated with chronic hepatitis B occurrence, and codon 25 exhibits a relationship with autoimmune hepatitis risk. Missense mutations in G29E, A105S, D191N, and F321L of TGF-beta 1 are the genetic factors of HCC susceptibility. Furthermore, the TGF-beta 1 gene expression is significantly elevated in CLD patients, and the TGF-beta 1 codon 263 is located close to the region where the TGF-beta 1 dimerization interacts, indicating the TGF-beta 1 codon 263 variant may affect the secretion of TGF-beta 1 by altering its dimerization. Together, our findings provide new insights into the immune regulator gene TGF-beta 1 polymorphisms as susceptibility factors for CLD occurrence and regulators for TGF-beta 1 expression, which have implications for the regulation of immune factors during CLD development.
C1 [Cai, Xuanyan; Zha, Huiyan; Yang, Zhaoxu; Du, Yiwen; Dai, Xiaoyang; Yang, Bo; Wang, Jiajia; He, Qiaojun; Weng, Qinjie] Zhejiang Univ, Coll Pharmaceut Sci, Ctr Drug Safety Evaluat & Res, Hangzhou, Peoples R China.
[Cai, Xuanyan; Zha, Huiyan; Yang, Zhaoxu; Du, Yiwen; Dai, Xiaoyang; Yang, Bo; Wang, Jiajia; He, Qiaojun; Weng, Qinjie] Zhejiang Univ, Coll Pharmaceut Sci, Zhejiang Prov Key Lab Anticanc Drug Res, Hangzhou, Peoples R China.
[He, Qiaojun; Weng, Qinjie] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University
RP Wang, JJ; He, QJ; Weng, QJ (corresponding author), Zhejiang Univ, Coll Pharmaceut Sci, Ctr Drug Safety Evaluat & Res, Hangzhou, Peoples R China.; Wang, JJ; He, QJ; Weng, QJ (corresponding author), Zhejiang Univ, Coll Pharmaceut Sci, Zhejiang Prov Key Lab Anticanc Drug Res, Hangzhou, Peoples R China.; He, QJ; Weng, QJ (corresponding author), Zhejiang Univ, Affiliated Hosp 2, Sch Med, Hangzhou, Peoples R China.
EM wangjiajia3301@zju.edu.cn; qiaojunhe@zju.edu.cn; wengqinjie@zju.edu.cn
RI Wang, Jiajia/HCI-5717-2022
FU Zhejiang Provincial Natural Science Foundation; Fundamental Research
Funds for the Central Universities; [LY22H310001]; [LR21H310001]
FX Funding This research was funded by the Zhejiang Provincial Natural
Science Foundation (No. LY22H310001, No. LR21H310001) and the
Fundamental Research Funds for the Central Universities.
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NR 64
TC 1
Z9 1
U1 2
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD NOV 16
PY 2022
VL 13
AR 1058532
DI 10.3389/fimmu.2022.1058532
PG 20
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 6R0WH
UT WOS:000892028100001
PM 36466817
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Lefkowitch, JH
AF Lefkowitch, JH
TI Hepatobiliary pathology
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Review
DE fatty liver; chronic hepatitis; liver biopsy; hepatitis C virus;
hemochromatosis
ID NONALCOHOLIC FATTY LIVER; PRIMARY BILIARY-CIRRHOSIS;
BUDD-CHIARI-SYNDROME; HEPATITIS-C VIRUS; PRIMARY SCLEROSING CHOLANGITIS;
FOCAL NODULAR HYPERPLASIA; CHRONIC VIRAL-HEPATITIS;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; PORTAL-HYPERTENSION
AB Purpose of review Liver biopsy continues to be an essential component in the evaluation of many widely prevalent liver diseases, including chronic hepatitis C, fatty liver, and liver tumors. This annual review of publications in hepatobiliary pathology highlights recent pathologic studies that can be applied to the daily practice of interpreting liver biopsy, explant, and postmortem specimens.
Recent findings The problem of the fatty liver was the subject of many studies. In chronic hepatitis C, genotype 3 infection results in moderate to marked fat that is ameliorated with successful antiviral therapy. In nonalcoholic steatohepatitis, in which the metabolic syndrome is often operative, gene microarray analysis showed altered expression of genes involved in insulin sensitivity and maintenance of mitochondrial function. Pathologic changes affecting centrilobular regions were described in the context of heart disease, Budd-Chiari syndrome, and the sinusoidal obstruction syndrome (veno-occlusive disease). A mutation in ferroportin 1 produced a form of hemochromatosis with excessive iron in hepatocytes and also in Kupffer cells and macrophages. Immunostains for Hep Par 1 and polyclonal carcinoembryonic antigen remain important cornerstones in the immunohistochemical diagnosis of hepatocellular carcinoma and its distinction from metastatic adenocarcinoma and cholangiocarcinoma.
Summary This report reviews recent articles addressing hepatobiliary pathology. In the areas of viral and drug hepatitis, fatty liver, hemochromatosis, Wilson disease, several biliary tract disorders, and pathology of liver tumors, the emerging data have important diagnostic applications.
C1 Columbia Univ Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA.
C3 Columbia University
RP Columbia Univ Coll Phys & Surg, Dept Pathol, 630 W 168th St, New York, NY 10032 USA.
EM jhl3@columbia.edu
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NR 102
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0267-1379
EI 1531-7056
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD MAY
PY 2004
VL 20
IS 3
BP 188
EP 197
DI 10.1097/00001574-200405000-00003
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 815EZ
UT WOS:000221026900002
PM 15703643
DA 2025-01-07
ER
PT J
AU Jain, M
Venkataraman, J
Varghese, J
Vij, M
Reddy, MS
Rela, M
AF Jain, Mayank
Venkataraman, Jayanthi
Varghese, Joy
Vij, Mukul
Reddy, Mettu S.
Rela, Mohamed
TI Explant liver evaluation decodes the mystery of cryptogenic cirrhosis!
SO JGH OPEN
LA English
DT Article
DE liver; transplantation; histology; cryptogenic
ID NONALCOHOLIC STEATOHEPATITIS; HEPATOCELLULAR-CARCINOMA; TRANSPLANTATION;
DISEASE
AB Background and AimTo determine the concordance of liver explants with the pretransplant diagnosis.
MethodsThis was a retrospective analysis of 251 liver explants. Patient information included demography, comorbidity, and etiological diagnosis. Final diagnosis was based on morphological and histological findings. For non-alcoholic steatohepatitis (NASH) and cryptogenic cirrhosis, we investigated comorbid states such as obesity, hypertension, and diabetes. Chi square test and Cohen's Kappa value were used. A P value of <0.05 was considered significant.
ResultsA total of 192 patients (76.5%) were males. A significant concordance of explant diagnosis with pretransplant diagnosis was present in 225 (89.6%) patients. It was 100% for alcohol-related disease, hepatitis B, hepatitis C, autoimmune (AI) liver disease, biliary cirrhosis, and Budd-Chiari syndrome. Of 37 patients with a pretransplant diagnosis of cryptogenic cirrhosis, major discordance was observed in 23 (62.1%). On explant, seven patients each had hemochromatosis 5 (13.5%), AI hepatitis, and NASH (18.9%); two had noncirrhotic fibrosis (5.4%); and one each had Wilson's disease and congenital hepatic fibrosis (2.7%). Of the 20 explants, 3 with pretransplant diagnosis of NASH had a diagnosis of cryptogenic cirrhosis on explant specimens. Cohen's Kappa for the concordance of pretransplant diagnosis and explant diagnosis in NASH and cryptogenic cirrhosis patients was 0.75 and 0.47, respectively. An incidental hepatocellular carcinoma was picked up in 16 explants, and 18 had granulomas.
ConclusionConcordance between pretransplant and explant diagnosis is lower for NASH and cryptogenic cirrhosis. The true prevalence of cryptogenic cirrhosis in our study was 5.6%.
C1 [Jain, Mayank; Venkataraman, Jayanthi; Varghese, Joy; Vij, Mukul; Reddy, Mettu S.; Rela, Mohamed] Gleneagles Global Hlth City, Inst GI Sci & Liver Transplantat, Chennai 100, Tamil Nadu, India.
RP Jain, M (corresponding author), Gleneagles Global Hlth City, Inst GI Sci & Liver Transplantat, Chennai 100, Tamil Nadu, India.
EM mayank4670@rediffmail.com
RI vij, mukul/Y-9635-2019
OI Vij, Mukul/0000-0003-0149-0294; Varghese, Joy/0000-0003-3107-4216
CR [Anonymous], GASTROENTEROL HEPATO
[Anonymous], EUR J GASTROENTEROL
[Anonymous], J CANC THER
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NR 25
TC 8
Z9 8
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2397-9070
J9 JGH OPEN
JI JGH Open
PD FEB
PY 2020
VL 4
IS 1
BP 39
EP 43
DI 10.1002/jgh3.12200
PG 5
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA KM7BU
UT WOS:000514295500006
PM 32055695
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Guo, XY
Cen, Y
Wang, JX
Jiang, HX
AF Guo, Xiaoyun
Cen, Yu
Wang, Jiaxu
Jiang, Haixing
TI CXCL10-induced IL-9 promotes liver fibrosis via Raf/MEK/ERK signaling
pathway
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Liver fibrosis; Interleukin-9; CXCL10; Raf/MEK/ERK
ID HEPATIC STELLATE CELLS; T-LYMPHOCYTES; DISEASE; MECHANISMS; EXPRESSION;
CHEMOKINE; CXCR3; INTERLEUKIN-9; FIBROGENESIS; CANCER
AB Liver fibrosis is a typical complication of chronic liver diseases resulting in cirrhosis that remains a major public health problem. The aim of the present study was to identify the role of interleukin-9 (IL-9), an important regulator of inflammation and autoimmune diseases, in hepatic fibrosis progression. It was found that the expression of IL-9 was significantly increased in liver tissues of liver cirrhosis patients compared with that in healthy controls. Moreover, CXCL10, not CXCL9 or CXCL11, induced IL-9 expression in the liver tissue. Overexpression of IL-9 enhanced the severity of liver fibrosis in the carbon tetrachloride (CCl4)-induced liver fibrosis model. Western Blotting analysis revealed that this pro-fibrosis bioactivity of IL-9 was attributed to its selective activation of Raf/MEK/ERK signaling. Finally, administration of neutralizing anti-IL-9 antibody ameliorated liver fibrosis and attenuated the activation of hepatic stellate cells in mice. All these findings indicate that IL-9 plays a deleterious role in the development and progression of liver fibrosis, and IL-9 based immunotherapy may prove to be a promising strategy for the treatment of liver fibrosis.
C1 [Guo, Xiaoyun] Guangxi Med Univ, Tumor Hosp, Dept Comprehens Internal Med, 71 Hedi Rd, Nanning 530021, Guangxi Zhuang, Peoples R China.
[Cen, Yu; Wang, Jiaxu; Jiang, Haixing] Guangxi Med Univ, Affiliated Hosp 1, Dept Gastroenterol, 22 Shuang Yong Rd, Nanning 530021, Peoples R China.
C3 Guangxi Medical University; Guangxi Medical University
RP Guo, XY (corresponding author), Guangxi Med Univ, Tumor Hosp, Dept Comprehens Internal Med, 71 Hedi Rd, Nanning 530021, Guangxi Zhuang, Peoples R China.; Jiang, HX (corresponding author), Guangxi Med Univ, Affiliated Hosp 1, Dept Gastroenterol, 22 Shuang Yong Rd, Nanning 530021, Peoples R China.
EM W154192158@163.com; w1808588161@163.com; peerlw@163.com; jihaxi@163.com
FU University Science Foundation of Guangxi Zhuang Autonomous Region
[KY2015YB069]; National Natural Science Foundation of China [81260083]
FX This work was supported by the University Science Foundation of Guangxi
Zhuang Autonomous Region (No. KY2015YB069), and National Natural Science
Foundation of China (No. 81260083).
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NR 48
TC 27
Z9 33
U1 1
U2 21
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD SEP
PY 2018
VL 105
BP 282
EP 289
DI 10.1016/j.biopha.2018.05.128
PG 8
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA GM6UT
UT WOS:000438312600032
PM 29860220
DA 2025-01-07
ER
PT J
AU Tatour, M
Neeman, Z
Aviv, A
Hazzan, R
AF Tatour, Mifleh
Neeman, Ziv
Aviv, Ariel
Hazzan, Rawi
TI Increased Risk of Non-Hodgkin Lymphoma in Autoimmune Hepatitis: A Large
Retrospective Cohort Study
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE autoimmune hepatitis; non-hodgkin lymphoma; azathioprine;
6-mercaptopurine; mycophenolate mofetil
ID INFLAMMATORY-BOWEL-DISEASE; RHEUMATOID-ARTHRITIS; AZATHIOPRINE;
DIAGNOSIS; CANCER; MANAGEMENT; SURVIVAL; 6-MERCAPTOPURINE; MALIGNANCIES;
GUIDELINES
AB Background/Objectives: Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease caused by an autoimmune attack on hepatocytes. The first-line treatment for AIH comprises two core components: glucocorticoids and thiopurine analog inhibitors and mycophenolate mofetil (MMF). Numerous studies have suggested an increased risk for lymphoma among patients with either rheumatoid arthritis or inflammatory bowel disease (IBD) who are treated with azathioprine/6-mercaptopurine (6-MP). The relative risk of non-Hodgkin lymphoma (NHL) among autoimmune hepatitis patients treated with these immunosuppressive drugs remains unclear. We aimed at investigating the risk of NHL across a large retrospective AIH cohort after a long-term follow-up. Methods: This retrospective, population-based study comprised approximately 2.7 million adults over two decades. It included adult patients aged 20 years or older at the time of autoimmune hepatitis diagnosis who had initiated treatment with azathioprine, 6-MP, or MMF. The primary outcome was the development of non-Hodgkin lymphoma. Results: The study initially included 834 patients diagnosed with AIH. A total of 685 patients remained in the research cohort after matching the data to the local cancer registry. Compared to the predicted NHL rate in the general population, NHL incidence was considerably higher in AIH patients (Standardized Incidence Ratio, SIR = 36.5). Subgroup studies showed that lymphoma mainly affected patients 45 years of age and over and was detected primarily during the first seven years following the AIH diagnosis. No correlation was found between the incidence of NHL and the treatment drug used. Conclusions: Patients with AIH exhibit a markedly higher risk of NHL compared to the general population.
C1 [Tatour, Mifleh; Hazzan, Rawi] Clalit Hlth Serv, IL-1710601 Nof Hagalil, Israel.
[Tatour, Mifleh] Clalit Hlth Serv, Dept Family Med, IL-1710601 Afula, Israel.
[Neeman, Ziv] Clalit Hlth Serv, Emek Med Ctr, Imaging Inst & Nucl Med, IL-183411 Afula, Israel.
[Neeman, Ziv; Aviv, Ariel] Technion Israel Inst Technol, Fac Med, Ruth & Bruce Rappaport, IL-3109601 Haifa, Israel.
[Aviv, Ariel] HaEmek Med Ctr, Hematol Unit, IL-183411 Afula, Israel.
[Hazzan, Rawi] Bar Ilan Univ, Azrieli Fac Med, IL-1311502 Safed, Israel.
[Hazzan, Rawi] Emek Med Ctr, 21 Yitzhak Rabin Blvd, IL-183411 Afula, Israel.
C3 Clalit Health Services; Clalit Health Services; Emek Medical Center;
Clalit Health Services; Technion Israel Institute of Technology; Bar
Ilan University; Emek Medical Center
RP Tatour, M (corresponding author), Clalit Hlth Serv, IL-1710601 Nof Hagalil, Israel.; Tatour, M (corresponding author), Clalit Hlth Serv, Dept Family Med, IL-1710601 Afula, Israel.
EM mifleh.rt.1989@gmail.com; zivneeman@gmail.com; ariel_av@clalit.org.il;
rawihazzan1@gmail.com
RI hazzan, rawi/JOZ-9699-2023
OI Aviv, Ariel/0000-0002-6024-1100; Hazzan, Rawi/0000-0001-7731-118X;
Tatour, Mifleh/0009-0005-9865-0785
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NR 47
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD OCT
PY 2024
VL 13
IS 20
AR 6258
DI 10.3390/jcm13206258
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA K1C1E
UT WOS:001341322200001
PM 39458208
OA gold
DA 2025-01-07
ER
PT J
AU Mells, G
Mann, C
Hubscher, S
Neuberger, J
AF Mells, George
Mann, Caroline
Hubscher, Stefan
Neuberger, James
TI Late Protocol Liver Biopsies in the Liver Allograft: A Neglected
Investigation?
SO LIVER TRANSPLANTATION
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; CHRONIC HEPATITIS; HISTOLOGICAL FEATURES;
CRYPTOGENIC CIRRHOSIS; AUTOIMMUNE HEPATITIS; DISEASE RECURRENCE;
TRANSPLANTATION; RECIPIENTS; ORGAN; DYSFUNCTION
AB As outcomes from liver transplantation have improved, attention has focused on long-term outcomes: patient and graft survival is affected by many factors, including the consequences of both overimmunosuppression (eg, renal failure and cancer) and underimmunosuppression (eg, rejection). The use of protocol (rather than event-driven) biopsies of the liver allograft, except for those grafted for HCV infection, has been largely abandoned. The aim of this study was to determine if protocol biopsies can improve the management of liver allograft recipients. A retrospective analysis of liver allograft recipients who had undergone protocol liver biopsies between 2000 and 2006 was performed. One hundred seventy-eight patients with normal liver tests (alcoholic liver disease, 49; autoimmune hepatitis, 20; and primary biliary cirrhosis, 107) who had undergone 235 protocol biopsies were identified. No significant complication from the biopsy was recorded. Liver histology was reported as normal or nearly normal in only 57 (24%). Chronic hepatitis (not obviously related to disease recurrence) was present in 78 (33%). Interpreted in the light of the calculated creatinine clearance, the biopsy findings indicated that overall immunosuppression (IMS) should be maintained or increased with standard calcineurin inhibitor (CNI)-based IMS in 25% of cases, that overall IMS should be reduced in 15% of cases, and that overall IMS should be maintained or increased by the substitution of non-nephrotoxic agents for CNIs in 9% of cases. The histological findings led to a documented change in IMS in 76 (32%) (increased IMS, 11; decreased IMS, 58; and switch from CNI, 7). In conclusion, protocol liver biopsy provides important histological information about graft function that is not available from standard liver tests and safely allows modification of IMS to ensure that long-term side effects of drug therapy (eg, renal failure) are minimized while graft function is sustained. Liver Transpl 15:931-938, 2009. (C) 2009 AASLD.
C1 [Mells, George; Mann, Caroline; Neuberger, James] Queen Elizabeth Hosp, Liver Unit, Univ Hosp, Birmingham NHS Fdn Trust, Birmingham B15 2TH, W Midlands, England.
[Hubscher, Stefan] Univ Birmingham, Dept Pathol, Birmingham, W Midlands, England.
C3 University of Birmingham; University of Birmingham
RP Neuberger, J (corresponding author), Queen Elizabeth Hosp, Liver Unit, Univ Hosp, Birmingham NHS Fdn Trust, Birmingham B15 2TH, W Midlands, England.
EM j.m.neuberger@bham.ac.uk
RI Neuberger, James/ABG-3010-2020
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NR 29
TC 58
Z9 61
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6465
EI 1527-6473
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD AUG
PY 2009
VL 15
IS 8
BP 931
EP 938
DI 10.1002/lt.21781
PG 8
WC Gastroenterology & Hepatology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA 480MO
UT WOS:000268739200014
PM 19642126
DA 2025-01-07
ER
PT J
AU Almashhrawi, AA
Ahmed, KT
Rahman, RN
Hammoud, GM
Ibdah, JA
AF Almashhrawi, Ashraf A.
Ahmed, Khulood T.
Rahman, Rubayat N.
Hammoud, Ghassan M.
Ibdah, Jamal A.
TI Liver diseases in pregnancy: Diseases not unique to pregnancy
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Liver; Pregnancy; Viral hepatitis; Autoimmune; Cirrhosis; Gallstones;
Adenoma
ID HEPATITIS-C VIRUS; TO-CHILD TRANSMISSION; PRIMARY BILIARY-CIRRHOSIS;
BUDD-CHIARI-SYNDROME; PERINATAL TRANSMISSION; B-VIRUS; AUTOIMMUNE
HEPATITIS; INFANT TRANSMISSION; VIRAL LOAD; VERTICAL TRANSMISSION
AB Pregnancy is a special clinical state with several normal physiological changes that influence body organs including the liver. Liver disease can cause significant morbidity and mortality in both pregnant women and their infants. Few challenges arise in reaching an accurate diagnosis in light of such physiological changes. Laboratory test results should be carefully interpreted and the knowledge of what normal changes to expect is prudent to avoid clinical misjudgment. Other challenges entail the methods of treatment and their safety for both the mother and the baby. This review summarizes liver diseases that are not unique to pregnancy. We focus on viral hepatitis and its mode of transmission, diagnosis, effect on the pregnancy, the mother, the infant, treatment, and breast-feeding. Autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, Wilson's disease, Budd Chiari and portal vein thrombosis in pregnancy are also discussed. Pregnancy is rare in patients with cirrhosis because of the metabolic and hormonal changes associated with cirrhosis. Variceal bleeding can happen in up to 38% of cirrhotic pregnant women. Management of portal hypertension during pregnancy is discussed. Pregnancy increases the pathogenicity leading to an increase in the rate of gallstones. We discuss some of the interventions for gallstones in pregnancy if symptoms arise. Finally, we provide an overview of some of the options in managing hepatic adenomas and hepatocellular carcinoma during pregnancy. (C) 2013 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Almashhrawi, Ashraf A.; Ahmed, Khulood T.; Rahman, Rubayat N.; Hammoud, Ghassan M.; Ibdah, Jamal A.] Univ Missouri, Div Gastroenterol & Hepatol, Columbia, MO 65212 USA.
C3 University of Missouri System; University of Missouri Columbia
RP Ibdah, JA (corresponding author), Univ Missouri, Div Gastroenterol & Hepatol, 319 Jesse Hall, Columbia, MO 65212 USA.
EM ibdahj@health.missouri.edu
OI Ibdah, Jamal/0000-0002-5646-9014; Hammoud, Ghassan/0000-0003-3551-0652
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NR 99
TC 10
Z9 14
U1 0
U2 6
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 21
PY 2013
VL 19
IS 43
BP 7630
EP 7638
DI 10.3748/wjg.v19.i43.7630
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 259HW
UT WOS:000327519000015
PM 24282352
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Zhong, WT
Wang, QY
Shen, XF
Du, JF
AF Zhong, Wentao
Wang, Qianyu
Shen, Xiaofei
Du, Junfeng
TI The emerging role of neutrophil extracellular traps in cancer: from lab
to ward
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE cancer; therapeutics; tumor microenvironment; neutrophil extracellular
traps; metastasis (cancer metastasis)
ID CIRCULATING TUMOR-CELLS; MICROENVIRONMENTAL REGULATION; THERAPEUTIC
TARGET; DNA TRAPS; PROMOTE; METASTASIS; PROGRESSION; LIVER; SURGERY;
NETOSIS
AB Neutrophil extracellular traps (NETs) are web-like structures derived from neutrophils, which typically consist of DNA, released from the nucleus or mitochondria, and decorated with histones and granule proteins. They are well known as an important structure in innate immunity to eliminate pathogenic bacteria, similar to neutrophils. Initially, NETs are reported to take part in the progression of inflammatory diseases; now, they have also been implicated in the progression of sterile inflammation such as autoimmune disease, diabetes, and cancer. In this review, we will describe the recent studies which have investigated the role of NETs in the development of cancer, especially metastasis. We also prescribe the strategies for targeting NETs in the multiple cancer types, which suggest that NETs are a promising treatment for cancer patients.
C1 [Zhong, Wentao; Du, Junfeng] Southern Med Univ, Sch Clin Med 2, Guangzhou, Peoples R China.
[Wang, Qianyu] Shanxi Med Univ, Sch Clin Med 2, Taiyuan, Peoples R China.
[Shen, Xiaofei] Nanjing Univ, Drum Tower Hosp, Dept Gen Surg, Med Sch, Nanjing, Peoples R China.
[Du, Junfeng] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 1, Med Dept Gen Surg, Beijing, Peoples R China.
[Du, Junfeng] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 7, Dept Gen Surg, Beijing, Peoples R China.
C3 Southern Medical University - China; Shanxi Medical University; Nanjing
University; Chinese People's Liberation Army General Hospital; Chinese
People's Liberation Army General Hospital; Seventh Medical Center of
Chinese PLA General Hospital
RP Du, JF (corresponding author), Southern Med Univ, Sch Clin Med 2, Guangzhou, Peoples R China.; Shen, XF (corresponding author), Nanjing Univ, Drum Tower Hosp, Dept Gen Surg, Med Sch, Nanjing, Peoples R China.; Du, JF (corresponding author), Chinese Peoples Liberat Army Gen Hosp, Med Ctr 1, Med Dept Gen Surg, Beijing, Peoples R China.; Du, JF (corresponding author), Chinese Peoples Liberat Army Gen Hosp, Med Ctr 7, Dept Gen Surg, Beijing, Peoples R China.
EM dg1535058@smail.nju.edu.cn; dujf66@126.com
RI Shen, Xiaofei/HDL-7300-2022
OI du, junfeng/0000-0002-8482-4271; Shen, Xiaofei/0000-0002-5816-1814;
Zhong, Wentao/0000-0002-6268-1898; Wang, Qianyu/0000-0001-7048-8847
FU National Natural Science Foundation of China [81870393, 81970500]
FX Funding This work was supported by the National Natural Science
Foundation of China (81870393, JD and No.81970500, XS).
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NR 131
TC 7
Z9 8
U1 1
U2 14
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD APR 28
PY 2023
VL 13
AR 1163802
DI 10.3389/fonc.2023.1163802
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA F9AH1
UT WOS:000985195400001
PM 37188184
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Hirschfield, GM
Karlsen, TH
Lindor, KD
Adams, DH
AF Hirschfield, Gideon M.
Karlsen, Tom H.
Lindor, Keith D.
Adams, David H.
TI Primary sclerosing cholangitis
SO LANCET
LA English
DT Article
ID DOSE URSODEOXYCHOLIC ACID; GENOME-WIDE ASSOCIATION; PRIMARY
BILIARY-CIRRHOSIS; ULCERATIVE-COLITIS; LIVER-TRANSPLANTATION; COLORECTAL
NEOPLASIA; RISK-FACTORS; BILE-DUCTS; NORURSODEOXYCHOLIC ACID; AUTOIMMUNE
HEPATITIS
AB Primary sclerosing cholangitis is the classic hepatobiliary manifestation of infl ammatory bowel disease and is generally chronic and progressive. Patients frequently present with asymptomatic, anicteric cholestasis, but many develop progressive biliary strictures with time, leading to recurrent cholangitis, biliary cirrhosis, and end-stage liver disease. Medical treatment does not slow the progression of disease, and many patients need liver transplantation, after which recurrent disease is a risk. The increased incidence of hepatobiliary cancer, which is not related to the underlying severity of biliary fi brosis, is of particular concern. Risk of colorectal cancer is also increased in patients with coexistent infl ammatory bowel disease. Mechanistic insights have arisen from studies of secondary sclerosing cholangitis, in which a similar clinical profi le is associated with a specifi c cause, and genomic studies have elucidated potential disease-initiating pathways in the primary form. The close association between infl ammatory bowel disease and primary sclerosing cholangitis underscores the need to further understand the role of environmental factors in generation of lymphocytes that are postulated to be retargeted, deleteriously, to the biliary tree. Treatment of primary sclerosing cholangitis is confi ned to supportive measures, but advances in pathobiology suggest that new stratifi ed approaches will soon be available.
C1 [Hirschfield, Gideon M.; Adams, David H.] Univ Birmingham, Liver Res Ctr, Natl Inst Hlth Res, Biomed Res Unit, Birmingham B15 2TT, W Midlands, England.
[Karlsen, Tom H.] Univ Oslo, Rikshosp,Oslo Univ Hosp, Norwegian Primary Sclerosing Cholangitis Res Ctr, Dept Transplantat Med,Div Canc Med Surg & Transpl, N-0027 Oslo, Norway.
[Karlsen, Tom H.] Univ Bergen, Dept Clin Med, Fac Med & Dent, Bergen, Norway.
[Lindor, Keith D.] Arizona State Univ, Phoenix, AZ USA.
C3 University of Birmingham; University of Oslo; National Hospital Norway;
University of Bergen; Arizona State University; Arizona State
University-Downtown Phoenix
RP Hirschfield, GM (corresponding author), Univ Birmingham, Liver Res Ctr, Natl Inst Hlth Res, Biomed Res Unit, Birmingham B15 2TT, W Midlands, England.
EM g.hirschfield@bham.ac.uk
RI Adams, David/C-9092-2009; Hirschfield, Gideon/M-2143-2015
OI Hirschfield, Gideon/0000-0002-6736-2255; ADAMS,
David/0000-0001-6776-0336
FU Medical Research Council [G0700301, G0400496, G0300101] Funding Source:
Medline; MRC [G0400496, G0700301, G0300101] Funding Source: UKRI
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NR 141
TC 420
Z9 450
U1 0
U2 59
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD NOV 9
PY 2013
VL 382
IS 9904
BP 1587
EP 1599
DI 10.1016/S0140-6736(13)60096-3
PG 13
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 247NE
UT WOS:000326623900030
PM 23810223
DA 2025-01-07
ER
PT J
AU Reshetnyak, VI
AF Reshetnyak, Vasiliy Ivanovich
TI Primary biliary cirrhosis: Clinical and laboratory criteria for its
diagnosis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Primary biliary cirrhosis; Clinical criteria; Laboratory criteria;
Immunological signs; Biochemical signs; Morphological signs
ID PYRUVATE-DEHYDROGENASE COMPLEX; BONE-MINERAL DENSITY; CHRONIC
HEPATITIS-C; T-CELL RESPONSES; BILE-DUCT CELLS; AUTOIMMUNE HEPATITIS;
ANTIMITOCHONDRIAL ANTIBODIES; URSODEOXYCHOLIC ACID;
HEPATOCELLULAR-CARCINOMA; OVERLAP SYNDROME
AB Primary biliary cirrhosis (PBC) is a chronic progressive cholestatic granulomatous, and destructive inflammatory lesion of small intralobular and septal bile ducts, which is likely to be caused by an autoimmune mechanism with a the presence of serum antimitochondrial antibodies and a potential tendency to progress to cirrhosis. Despite the fact that the etiology of this disease has been unknown so far, there has been a considerable body of scientific evidence that can reveal the clinical and laboratory signs of PBC and the individual components of its pathogenesis and elaborate diagnostic criteria for the disease and its symptomatic therapy. Deficiencies in autoimmune tolerance are critical factors for the initiation and perpetuation of the disease. The purpose of this review is to summarize the data available in the literature and the author's findings on clinical and laboratory criteria for the diagnosis of PBC. This review describes the major clinical manifestations of the disease and the mechanisms of its development. It presents the immunological, biochemical, and morphological signs of PBC and their significance for its diagnosis. A great deal of novel scientific evidence for the problem of PBC has been accumulated. However, the inadequate efficiency of therapy for the disease lends impetus to the quest for its etiological factors and to further investigations of its pathogenetic mechanisms and, on this basis, to searches for new methods for its early diagnosis.
C1 [Reshetnyak, Vasiliy Ivanovich] VA Negovsky Res Inst Gen Reanimatol, Moscow 107031, Russia.
C3 Federal Research & Clinical Center of Intensive Care Medicine &
Rehabilitology
RP Reshetnyak, VI (corresponding author), VA Negovsky Res Inst Gen Reanimatol, Acad Secretary, 25-2 Petrovka St, Moscow 107031, Russia.
EM vasiliy.reshetnyak@yandex.ru
RI Reshetnyak, Vasiliy/A-5999-2016
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NR 262
TC 50
Z9 64
U1 0
U2 12
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUL 7
PY 2015
VL 21
IS 25
BP 7683
EP 7708
DI 10.3748/wjg.v21.i25.7683
PG 26
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CM3LW
UT WOS:000357584700007
PM 26167070
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Prado, LG
Nagy, LE
AF Prado, Luan G.
Nagy, Laura E.
TI Role of Complement in Liver Diseases
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE alcohol-associated liver disease; metabolic-associated steatotic liver
disease; liver fibrosis; cirrhosis
ID MANNAN-BINDING LECTIN; FATTY LIVER; C4B-BINDING PROTEIN; HUMAN
MONOCYTES; ACTIVATION; HEPATITIS; SYSTEM; INJURY; CELLS; INFLAMMATION
AB This review aims to summarize recent research using animal models, cell models, and human data regarding the role of complement in liver disease. Complement is part of the innate immune system and was initially characterized for its role in control of pathogens. However, evidence now indicates that complement also plays an important role in the response to cellular injury that is independent of pathogens. The liver is the main organ responsible for producing circulating complement. In response to liver injury, complement is activated and likely plays a dual role, both contributing to and protecting from injury. In uncontrolled complement activation, cell injury and liver inflammation occur, contributing to progression of liver disease. Complement activation is implicated in the pathogenesis of multiple liver diseases, including alcohol- associated liver disease, metabolic dysfunction-associated steatotic liver disease, fibrosis and cirrhosis, hepatocellular carcinoma, and autoimmune hepatitis. However, the mechanisms by which complement is overactivated in liver diseases are still being unraveled.
C1 [Prado, Luan G.; Nagy, Laura E.] Cleveland Clin, Dept Inflammat & Immun, Cleveland, OH USA.
[Nagy, Laura E.] Case Western Reserve Univ, Dept Mol Med, Cleveland, OH USA.
C3 Cleveland Clinic Foundation; University System of Ohio; Case Western
Reserve University
RP Nagy, LE (corresponding author), Cleveland Clin, Lerner Res Inst NE40, 9500 Euclid Ave, Cleveland, OH 44195 USA.
EM nagyL3@ccf.org
RI Gavião Prado, Luan/AHA-8446-2022
FU National Institutes of Health [P50AA024333, U01AA026398]
FX This work was supported in part by grants from the National Institutes
of Health: P50AA024333 and U01AA026398 (L.E.N.).
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NR 117
TC 0
Z9 0
U1 2
U2 2
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD NOV
PY 2024
VL 44
IS 04
BP 510
EP 522
DI 10.1055/s-0044-1795143
EA NOV 2024
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA O3Y7K
UT WOS:001366940900001
PM 39608405
DA 2025-01-07
ER
PT J
AU Kountouras, J
Zavos, C
Chatzopoulos, D
AF Kountouras, J
Zavos, C
Chatzopoulos, D
TI Induction of apoptosis as a proposed pathophysiological link between
glaucoma and Helicobacter pylori infection
SO MEDICAL HYPOTHESES
LA English
DT Article
ID OPEN-ANGLE GLAUCOMA; HEPATOCELLULAR-CARCINOMA; CEREBROSPINAL-FLUID;
ANTIGENIC MIMICRY; GASTRIC-MUCOSA; AQUEOUS-HUMOR; EXPRESSION; DISEASE;
ERADICATION; HEPATECTOMY
AB Although apoptosis is equally important both for the development and for the maintenance of homeostasis in some adult tissues, it, can also be associated with disease processes. Current studies indicate that apoptosis is a mechanism of cell death in several important ocular and gastrointestinal diseases including glaucoma, and Helicobacter pylori (H. pylori)-induced upper gastrointestinal disorders and/or extraintestinal diseases, including autoimmune and neurodegenerative ones (Sjogren's syndrome, Guillain-Barre syndrome or Parkinson's disease). Glaucoma is also associated with similar autoimmune and neurodegenerative disorders, characterized by apoptotic loss of specific populations of neurons. Recently, a high prevalence of H. pylori infection has been recognized in patients with chronic open-angle glaucoma,. In addition, H. pylori eradication may positively influence glaucoma parameters, thereby suggesting a possible causal link between H. pylori and glaucoma. H. pylori infection may influence the pathophysiology of glaucoma by releasing various proinflammatory and vasoactive substances, as well as by influencing apoptotic process; parameters that may also exert their own effects in the induction and/or progression of glaucomatous neuropathy. Importantly, H. pylori infection and glaucoma share the Fas/FasL and the mitochondria-mediated apoptotic pathways, thereby proposing an apoptotic link in the pathophysiology of both diseases. (C) 2003 Elsevier Ltd. All rights reserved.
C1 Aristotle Univ Thessaloniki, Ippokrat Hosp, Med Clin 2, Dept Gastroenterol, GR-54006 Thessaloniki, Greece.
C3 Aristotle University of Thessaloniki
RP 8 Fanariou St, Thessaloniki 55133, Macedonia, Greece.
EM jannis@med.auth.gr
RI Zavos, Christos/N-8618-2015
OI Zavos, Christos/0000-0002-3443-7791
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NR 34
TC 47
Z9 50
U1 0
U2 4
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0306-9877
EI 1532-2777
J9 MED HYPOTHESES
JI Med. Hypotheses
PY 2004
VL 62
IS 3
BP 378
EP 381
DI 10.1016/j.mehy.2003.11.013
PG 4
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 805UR
UT WOS:000220391700011
PM 14975507
DA 2025-01-07
ER
PT J
AU Chen, Y
Hua, XW
Huang, BY
Karsten, S
You, ZR
Li, B
Li, Y
Li, YK
Liang, JB
Zhang, J
Wei, YR
Chen, RL
Lyu, ZW
Xiao, X
Lian, M
Wei, J
Fang, JY
Miao, Q
Wang, QX
Berglung, UW
Tang, RQ
Helleday, T
Ma, X
AF Chen, Yong
Hua, Xiangwei
Huang, Bingyuan
Karsten, Stella
You, Zhengrui
Li, Bo
Li, You
Li, Yikang
Liang, Jubo
Zhang, Jun
Wei, Yiran
Chen, Ruiling
Lyu, Zhuwan
Xiao, Xiao
Lian, Min
Wei, Jue
Fang, Jingyuan
Miao, Qi
Wang, Qixia
Berglung, Ulrika Warpman
Tang, Ruqi
Helleday, Thomas
Ma, Xiong
TI MutT Homolog 1 Inhibitor Karonudib Attenuates Autoimmune Hepatitis by
Inhibiting DNA Repair in Activated T Cells
SO HEPATOLOGY COMMUNICATIONS
LA English
DT Article
ID MUTAGENIC SUBSTRATE; MTH1; DIAGNOSIS; EXPRESSION; GENE; ASSOCIATION;
MANAGEMENT; CANCER; ENZYME; POOL
AB Autoimmune hepatitis (AIH) is an inflammatory liver disease driven by the hyperactivation of various intrahepatic antigen-specific T cells due to a breach of immune tolerance. Studies in immunometabolism demonstrate that activated T cells harbor increased levels of reactive oxygen species that cause oxidative DNA damage. In this study, we assessed the potential of DNA damage repair enzyme MutT homolog 1 (MTH1) as a therapeutic target in AIH and karonudib as a novel drug for patients with AIH. We report herein that MTH1 expression was significantly increased in liver samples from patients with AIH compared to patients with chronic hepatitis B and nonalcoholic fatty liver disease and from healthy controls. In addition, the expression of MTH1 was positively correlated with AIH disease severity. We further found abundant T cells that expressed MTH1 in AIH. Next, we found that karonudib significantly altered T-cell receptor signaling in human T cells and robustly inhibited proliferation of human T cells in vitro. Interestingly, our data reflected a preferential inhibition of DNA damage repair in activated T cells by karonudib. Moreover, MTH1 was required to develop liver inflammation and damage because specific deletion of MTH1 in T cells ameliorated liver injury in the concanavalin A (Con A)-induced hepatitis model by inhibiting T-cell activation and proliferation. Lastly, we validated the protective effect of karonudib on the Con A-induced hepatitis model. Conclusion: MTH1 functions as a critical regulator in the development of AIH, and its inhibition in activated T cells reduces liver inflammation and damage.
C1 [Chen, Yong; Huang, Bingyuan; You, Zhengrui; Li, Bo; Li, You; Li, Yikang; Liang, Jubo; Zhang, Jun; Wei, Yiran; Chen, Ruiling; Lyu, Zhuwan; Xiao, Xiao; Lian, Min; Fang, Jingyuan; Miao, Qi; Wang, Qixia; Tang, Ruqi; Ma, Xiong] Shanghai Jiao Tong Univ, Shanghai Inst Digest Dis, Key Lab Gastroenterol & Hepatol,Div Gastroenterol, Minist Hlth,Renji Hosp,Sch Med,State Key Lab Onco, Shanghai, Peoples R China.
[Hua, Xiangwei] Tongji Univ, Dept Thyroid Breast Oncol, Sch Med, Shanghai East Hosp, Shanghai, Peoples R China.
[Hua, Xiangwei; Karsten, Stella; Berglung, Ulrika Warpman; Helleday, Thomas] Karolinska Inst, Dept Oncol & Pathol, Sci Life Lab, Stockholm, Sweden.
[Hua, Xiangwei] Renji Hosp, Sch Med, Dept Liver Surg, Shanghai, Peoples R China.
[Hua, Xiangwei] Renji Hosp, Sch Med, Liver Transplantat Ctr, Shanghai, Peoples R China.
[Wei, Jue] Shanghai Jiao Tong Univ, Sch Med, Shanghai Tongren Hosp, Dept Gastroenterol, Shanghai, Peoples R China.
[Helleday, Thomas] Univ Sheffield, Dept Oncol & Metab, Weston Pk Canc Ctr, Sheffield, S Yorkshire, England.
C3 Shanghai Jiao Tong University; Tongji University; Karolinska Institutet;
Shanghai Jiao Tong University; University of Sheffield
RP Ma, X (corresponding author), Shanghai Jiao Tong Univ, Shanghai Inst Digest Dis, Renji Hosp, Sch Med, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.; Helleday, T (corresponding author), Karolinska Inst, Dept Oncol Pathol, Sci Life Lab, S-17176 Stockholm, Sweden.
EM thomas.helleday@scilifelab.se; maxiongmd@hotmail.com
RI you, zhengrui/JYP-7419-2024; Helleday, Thomas/D-5224-2013; Chen,
Yong/JXM-0078-2024; FANG, Jing-Yuan/JOZ-1388-2023; Zhang,
Jun/U-2902-2018; Li, Bo/AAA-8968-2020
OI you, zhengrui/0000-0003-0765-5141; Ma, Xiong/0000-0001-9616-4672; Zhang,
Jun/0000-0003-1706-1611
FU National Natural Science Foundation of China [81830016, 81771732,
81620108002, 81800504, 81922010, 81873561, 81570469, 81421001, 81790634,
81300299, 81500435]; Shanghai Sailing Program [18YF1412900]; Shanghai
Municipal Health Commission [201840233]; Shanghai Committee of Science
and Technology [21ZR1458700]; Municipal Human Resources Development
Program for Outstanding Young Talents in Medical and Health Sciences in
Shanghai [2017YQ037]; Shanghai Rising-Star Program [18QA1402700]
FX Supported by the National Natural Science Foundation of China (grants
#81830016, 81771732, and 81620108002 to X.M.; #81800504 to M.L.;
#81922010, 81873561, and 81570469 to R.T.; #81421001 to J.F.; #81790634
to Q.W.; #81300299 to Z.Y.; and #81500435 to X.X.), Shanghai Sailing
Program (No. 18YF1412900 to M. L.), Shanghai Municipal Health Commission
(No. 201840233 to J.W.), Shanghai Committee of Science and Technology
(No. 21ZR1458700 to J.W.), the Municipal Human Resources Development
Program for Outstanding Young Talents in Medical and Health Sciences in
Shanghai (No. 2017YQ037 to Q.W.), and Shanghai Rising--Star Program (No.
18QA1402700 to Q.W.).
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NR 42
TC 3
Z9 3
U1 4
U2 21
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2471-254X
J9 HEPATOL COMMUN
JI Hepatol. Commun.
PD MAY
PY 2022
VL 6
IS 5
BP 1016
EP 1031
DI 10.1002/hep4.1862
EA DEC 2021
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 0S7GP
UT WOS:000728996900001
PM 34894107
OA Green Accepted, gold, Green Published
DA 2025-01-07
ER
PT J
AU Oppenheimer, AP
Koh, C
McLaughlin, M
Williamson, JC
Norton, TD
Laudadio, J
Heller, T
Kleiner, DE
High, KP
Morse, CG
AF Oppenheimer, Ana Paula
Koh, Christopher
McLaughlin, Mary
Williamson, John C.
Norton, Thomas D.
Laudadio, Jennifer
Heller, Theo
Kleiner, David E.
High, Kevin P.
Morse, Caryn G.
TI Vanishing bile duct syndrome in human immunodeficiency virus infected
adults: A report of two cases
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Human immunodeficiency virus; Antiretroviral therapy; Vanishing bile
duct syndrome; Ductopenia; Liver biopsy
ID LIVER-TRANSPLANTATION; HEPATITIS-C; CYTOMEGALOVIRUS-INFECTION;
DUCTOPENIC REJECTION; HODGKINS LYMPHOMA; ADVANCED AIDS; PATIENT;
DISEASE; PANCREATITIS; CHOLESTASIS
AB Vanishing bile duct syndrome (VBDS) is a group of rare disorders characterized by ductopenia, the progressive destruction and disappearance of intrahepatic bile ducts leading to cholestasis. Described in association with medications, autoimmune disorders, cancer, transplantation, and infections, the specific mechanisms of disease are not known. To date, only 4 cases of VBDS have been reported in human immunodeficiency virus (HIV) infected patients. We report 2 additional cases of HIV-associated VBDS and review the features common to the HIV-associated cases. Presentation includes hyperbilirubinemia, normal liver imaging, and negative viral and autoimmune hepatitis studies. In HIV-infected subjects, VBDS occurred at a range of CD4+ T-cell counts, in some cases following initiation or change in antiretroviral therapy. Lymphoma was associated with two cases; nevirapine, antibiotics, and viral co-infection were suggested as etiologies in the other cases. In HIV-positive patients with progressive cholestasis, early identification of VBDS and referral for transplantation may improve outcomes. (C) 2013 Baishideng. All rights reserved.
C1 [Oppenheimer, Ana Paula; Williamson, John C.; High, Kevin P.] Wake Forest Sch Med, Infect Dis Sect, Dept Med, Winston Salem, NC 27109 USA.
[Koh, Christopher; Heller, Theo] NIDDKD, Liver Dis Branch, NIH, Ctr Clin, Bethesda, MD 20892 USA.
[McLaughlin, Mary] NIAID, Immunoregulat Lab, NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Norton, Thomas D.] NYU, Div Infect Dis & Immunol, Dept Med, Sch Med, New York, NY 10016 USA.
[Laudadio, Jennifer] Wake Forest Sch Med, Pathol Lab, Winston Salem, NC 27109 USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Morse, Caryn G.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
C3 Wake Forest University; National Institutes of Health (NIH) - USA; NIH
National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK);
NIH Clinical Center (CC); National Institutes of Health (NIH) - USA; NIH
Clinical Center (CC); NIH National Institute of Allergy & Infectious
Diseases (NIAID); New York University; Wake Forest University; National
Institutes of Health (NIH) - USA; NIH Clinical Center (CC); NIH National
Cancer Institute (NCI); National Institutes of Health (NIH) - USA; NIH
Clinical Center (CC)
RP Morse, CG (corresponding author), NIH, Dept Crit Care Med, Ctr Clin, 9000 Rockville Pike,Bldg 10,5A06,MSC 1403, Bethesda, MD 20892 USA.
EM cmorse@mail.nih.gov
RI Williamson, John/AAU-6302-2021; Kleiner, David/N-2770-2013
OI Heller, Theo/0000-0002-2643-6289; Kleiner, David/0000-0003-3442-4453;
Morse, Caryn/0000-0002-1177-4365; Norton, Thomas/0009-0004-5896-9057;
Williamson, John/0000-0002-3840-7143
FU National Institutes of Health Clinical Center; National Institute of
Allergy and Infectious Diseases
FX Supported by The Intramural Research Programs of the National Institutes
of Health Clinical Center and the National Institute of Allergy and
Infectious Diseases
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NR 40
TC 12
Z9 13
U1 0
U2 1
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JAN 7
PY 2013
VL 19
IS 1
BP 115
EP 121
DI 10.3748/wjg.v19.i1.115
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 066DH
UT WOS:000313199800018
PM 23326172
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Huang, DF
Shen, HB
Xie, FF
Hu, D
Jin, Q
Hu, YX
Zhong, TY
AF Huang, Defa
Shen, Haibin
Xie, Fangfang
Hu, Die
Jin, Qing
Hu, Yuexin
Zhong, Tianyu
TI Role of mesenchymal stem cell-derived exosomes in the regeneration of
different tissues
SO JOURNAL OF BIOLOGICAL ENGINEERING
LA English
DT Review
DE Mesenchymal stem cell; Exosomes; Tissue regeneration
ID STROMAL CELLS; EXTRACELLULAR VESICLES; AUTOPHAGY; DISEASE; MODEL;
ACTIVATION; MECHANISMS; THERAPY; ENHANCE; BIOLOGY
AB Exosomes are nanovesicles with multiple components used in several applications. Mesenchymal stem cells (MSCs) are well known for their great potential in clinical applications. MSC-derived exosomes (MSC-Exos) have been shown to mediate tissue regeneration in various diseases, including neurological, autoimmune, and inflammatory diseases, cancer, ischemic heart disease, lung injury, and liver fibrosis. They can modulate the immune response by interacting with immune effector cells in the presence of anti-inflammatory compounds and are involved in intercellular communication through various types of cargo. This review summarizes the MSC-Exos-mediated tissue regeneration in various diseases, including neurological, cardiovascular, liver, kidney, articular cartilage, and oral tissue applications. In addition, we discuss the challenges and prospects of MSC-Exos in tissue regeneration.
C1 [Huang, Defa; Shen, Haibin; Xie, Fangfang; Hu, Die; Jin, Qing; Hu, Yuexin; Zhong, Tianyu] Gannan Med Univ, Lab Med, Affiliated Hosp 1, Ganzhou, Peoples R China.
[Zhong, Tianyu] Gannan Med Univ, Precis Med Ctr, Affiliated Hosp 1, Ganzhou, Peoples R China.
C3 Gannan Medical University; Gannan Medical University
RP Zhong, TY (corresponding author), Gannan Med Univ, Lab Med, Affiliated Hosp 1, Ganzhou, Peoples R China.; Zhong, TY (corresponding author), Gannan Med Univ, Precis Med Ctr, Affiliated Hosp 1, Ganzhou, Peoples R China.
EM zhongtianyu@gmail.com
RI Zhong, Tianyu/A-7936-2016
FU Ganzhou Science and Technology Plan Project
FX Not applicable.
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NR 91
TC 1
Z9 1
U1 5
U2 7
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1754-1611
J9 J BIOL ENG
JI J. Biol. Eng.
PD JUN 6
PY 2024
VL 18
IS 1
AR 36
DI 10.1186/s13036-024-00431-6
PG 11
WC Biochemical Research Methods; Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA TR8H6
UT WOS:001243073600001
PM 38845032
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kerkar, N
Lakhole, A
AF Kerkar, Nanda
Lakhole, Arathi
TI Pediatric liver transplantation: a North American perspective
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE Children; organ allocation; outcomes; biomarkers; machine perfusion
ID ANTIBODY-MEDIATED REJECTION; HEPATIC-ARTERY THROMBOSIS; BILIARY
COMPLICATIONS; PRACTICE GUIDELINE; GRAFT FAILURE; UNITED-STATES; LIVING
DONOR; CHILDREN; OUTCOMES; DISEASE
AB Liver transplantation (LT) is an important component in the therapeutic armamentarium of managing end-stage liver disease. In North American children, biliary atresia remains the most common indication for LT compared to hepatitis C in adults, while hepatoblastoma is the most common liver tumor requiring LT, versus Hepatocellular carcinoma in adults. Rejection, lymphoproliferative disease, renal insufficiency, metabolic syndrome, recurrent disease, de novo' autoimmune hepatitis and malignancy require careful surveillance and prompt action in adults and children after LT. In children, specific attention to EBV viremia, growth, development, adherence and transition to the adult services is also required. Antibody mediated rejection and screening for donor specific antibodies is becoming important in managing liver graft dysfunction. Biomarkers to identify and predict tolerance are being developed. Machine perfusion and stem cells (iPS) to synthesize organs are generating interest and are a focus for research.
C1 [Kerkar, Nanda] Univ Southern Calif, Childrens Hosp Los Angeles, Keck Sch Med, Liver Intestinal & Hepatol Transplant Program, 4650 Sunset Blvd 147, Los Angeles, CA 90027 USA.
[Lakhole, Arathi] Univ Southern Calif, Childrens Hosp Los Angeles, Div Gastroenterol Hepatol & Nutr, Los Angeles, CA USA.
C3 Children's Hospital Los Angeles; University of Southern California;
University of Southern California; Children's Hospital Los Angeles
RP Kerkar, N (corresponding author), Univ Southern Calif, Childrens Hosp Los Angeles, Keck Sch Med, Liver Intestinal & Hepatol Transplant Program, 4650 Sunset Blvd 147, Los Angeles, CA 90027 USA.
EM nkerkar@chla.usc.edu
RI Lakhole, Arathi/AAV-5475-2021
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U1 1
U2 11
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD AUG
PY 2016
VL 10
IS 8
BP 949
EP 959
DI 10.1586/17474124.2016.1166951
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DT2OE
UT WOS:000381319000009
PM 26982346
DA 2025-01-07
ER
PT J
AU Denk, G
Omary, AJ
Reiter, FP
Hohenester, S
Wimmer, R
Holdenrieder, S
Rust, C
AF Denk, Gerald
Omary, Ahmed-Jawid
Reiter, Florian Paul
Hohenester, Simon
Wimmer, Ralf
Holdenrieder, Stefan
Rust, Christian
TI Soluble intracellular adhesion molecule, M30 and M65 as serum markers of
disease activity and prognosis in cholestatic liver diseases
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE M30; M65; primary biliary cirrhosis; primary sclerosing cholangitis;
soluble Fas; soluble intracellular adhesion molecule
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; BREAST-CANCER
PATIENTS; CYTOKERATIN-18 FRAGMENTS; AUTOIMMUNE HEPATITIS; NONALCOHOLIC
STEATOHEPATITIS; NEOADJUVANT CHEMOTHERAPY; PLASMINOGEN-ACTIVATOR;
APOPTOSIS; FAS
AB AimHepatic apoptosis is involved in the pathogenesis of immune-mediated liver diseases such as autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). The aim of our study was to quantify distinct markers of apoptosis in sera of patients with AIH, PBC and PSC, and to evaluate correlation with markers of disease activity and prognosis.
MethodsSera of patients with AIH, PBC and PSC, and of healthy controls were collected and distinct cell death markers were quantified using a bead-based multiplex enzyme linked immunosorbent assay (soluble intracellular adhesion molecule [sICAM], macrophage migration inhibitory factor [MIF], soluble Fas [sFas], plasminogen activator inhibitor 1 [PAI-1]) or single enzyme-linked immunosorbent assays (DNAse, M30, M65).
ResultsIn comparison with healthy controls, the apoptotic markers sFas, sICAM (only in PSC patients), M30 and the cell death marker M65 were substantially elevated in sera of patients with immune-mediated liver diseases, whereas DNAse activity was reduced. Interestingly, patients with advanced PSC presented with higher levels of sICAM, M30 and M65 than patients with mild PSC. Regression analysis revealed correlations between serum levels of sICAM, M30 and M65 with the Mayo Risk Score for PSC, and of M65 with the Mayo Risk Score for PBC.
ConclusionConcentrations of the serum markers of apoptosis sFas and M30 and of the marker of total cell death M65 are elevated in patients with immune-mediated liver diseases, whereas activity of DNAse is reduced. In patients with PSC, sICAM, M30 and M65 may serve as indicators for disease activity and prognosis.
C1 [Denk, Gerald; Omary, Ahmed-Jawid; Reiter, Florian Paul; Hohenester, Simon; Wimmer, Ralf] Univ Munich, Dept Med Grosshadern 2, D-81377 Munich, Germany.
[Rust, Christian] Krankenhaus Barmherzige Bruder, Dept Med 1, Munich, Germany.
[Holdenrieder, Stefan] Univ Hosp Bonn, Inst Clin Chem & Clin Pharmacol, Bonn, Germany.
C3 University of Munich; University of Bonn
RP Denk, G (corresponding author), Univ Munich, Klinikum Grosshadern, Dept Med 2, Marchioninistr 15, D-81377 Munich, Germany.
EM gerald.denk@med.uni-muenchen.de
RI OMARY, AREEN/C-4188-2016; Reiter, Florian/KIB-0399-2024; Holdenrieder,
Stefan/JCO-7468-2023
OI Dr. Reiter, Florian/0000-0003-3807-1456; Omary,
Areen/0000-0002-3985-2011; Hohenester, Simon/0000-0002-9982-6317
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NR 37
TC 19
Z9 22
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD DEC
PY 2014
VL 44
IS 13
BP 1286
EP 1298
DI 10.1111/hepr.12304
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AU1DX
UT WOS:000345362300004
PM 24451045
DA 2025-01-07
ER
PT J
AU Halász, T
Horváth, G
Pár, G
Werling, K
Kiss, A
Schaff, Z
Lendvai, G
AF Halasz, Tuende
Horvath, Gabor
Par, Gabriella
Werling, Klara
Kiss, Andras
Schaff, Zsuzsa
Lendvai, Gabor
TI miR-122 negatively correlates with liver fibrosis as detected by
histology and FibroScan
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Expression; FibroScan; Liver fibrosis; METAVIR; microRNA; miR-122
ID CHRONIC HEPATITIS-C; HEPATOCELLULAR-CARCINOMA; TRANSIENT ELASTOGRAPHY;
MOLECULAR PATHOGENESIS; NONINVASIVE MARKERS; STELLATE CELLS; EXPRESSION;
MICRORNAS; DISEASE; INFECTION
AB AIM: To investigate whether expression of selected miRNAs obtained from fibrotic liver biopsies correlate with fibrosis stage.
METHODS: Altogether, 52 patients were enrolled in the study representing various etiologic backgrounds of fibrosis: 24 cases with chronic hepatitis infections (types B, C), 19 with autoimmune liver diseases (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, overlapping syndrome cases), and 9 of mixed etiology (alcoholic and nonalcoholic steatosis, cryptogenic cases). Severity of fibrosis was determined by both histologic staging using the METAVIR scoring system and noninvasive transient elastography. Following RNA isolation, expression levels of miR-21, miR-122, miR-214, miR-221, miR-222, and miR-224 were determined using TaqMan MicroRNA Assays applying miR-140 as the reference. Selection of miRNAs was based on their characteristic up- or down-regulation observed in hepatocellular carcinoma. Relative expression of miRNAs was correlated with fibrosis stage and liver stiffness (LS) value measured by transient elastography, as well as with serum alanine aminotransferase (ALT) level.
RESULTS: The expression of individual miRNAs showed deregulated patterns in stages F1-F4 as compared with stage F0, but only the reduced level of miR-122 in stage F4 was statistically significant (P < 0.04). When analyzing miRNA expression in relation to fibrosis, levels of miR-122 and miR-221 showed negative correlations with fibrosis stage, and miR-122 was found to correlate negatively and miR-224 positively with LS values (all P < 0.05). ALT levels displayed a positive correlation with miR-21 (P < 0.04). Negative correlations were observed in the fibrosis samples of mixed etiology between miR-122 and fibrosis stage and LS values (P < 0.05), and in the samples of chronic viral hepatitis, between miR-221 and fibrosis stage (P < 0.01), whereas miR-21 showed positive correlation with ALT values in the samples of autoimmune liver diseases (P < 0.03). The results also revealed a strong correlation between fibrosis stage and LS values (P < 0.01) when etiology of fibrosis was not taken into account.
CONCLUSION: Reduced expression of miR-122 in advanced fibrosis and its correlation with fibrosis stage and LS values seem to be characteristic of hepatic fibrosis of various etiologies.
C1 [Halasz, Tuende; Kiss, Andras; Schaff, Zsuzsa; Lendvai, Gabor] Semmelweis Univ, Dept Pathol 2, H-1091 Budapest, Hungary.
[Halasz, Tuende] Mil Hosp, Dept Pathol, H-1134 Budapest, Hungary.
[Horvath, Gabor] Hepatol Ctr Buda, H-1111 Budapest, Hungary.
[Par, Gabriella] Univ Pecs, Dept Med 1, H-7624 Pecs, Hungary.
[Werling, Klara] Semmelweis Univ, Dept Internal Med 2, H-1088 Budapest, Hungary.
[Schaff, Zsuzsa; Lendvai, Gabor] Semmelweis Univ, MTA SE Tumor Progress Res Grp, H-1091 Budapest, Hungary.
C3 Semmelweis University; University of Pecs; Semmelweis University;
Semmelweis University
RP Lendvai, G (corresponding author), Semmelweis Univ, Dept Pathol 2, Ulloi 93, H-1091 Budapest, Hungary.
EM lendvai.gabor@med.semmelweis-univ.hu
RI Lendvai, Gabor/GZL-5723-2022; Kiss, András/K-5649-2017; Schaff,
Zsuzsa/K-5613-2017
FU National Scientific Research Fund, OTKA [K101435, K108548]
FX Supported by Grant from the National Scientific Research Fund, OTKA
K101435 and K108548.
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NR 52
TC 54
Z9 60
U1 1
U2 20
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUL 7
PY 2015
VL 21
IS 25
BP 7814
EP 7823
DI 10.3748/wjg.v21.i25.7814
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CM3LW
UT WOS:000357584700018
PM 26167081
OA Green Published, hybrid, Green Submitted, Green Accepted
DA 2025-01-07
ER
PT J
AU Hsieh, CC
Hung, CH
Lu, LN
Qian, SG
AF Hsieh, Ching-Chuan
Hung, Chien-Hui
Lu, Lina
Qian, Shiguang
TI Hepatic immune tolerance induced by hepatic stellate cells
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Hepatic stellate cells; Myeloid-derived; suppressor cells; Hepatic
tolerance; Immunotherapy
ID SINUSOIDAL ENDOTHELIAL-CELLS; NITRIC-OXIDE SYNTHASE; REGULATORY T-CELLS;
SUPPRESSOR-CELLS; DENDRITIC CELLS; AUTOIMMUNE HEPATITIS;
CANCER-PATIENTS; MYELOID CELLS; LIVER; MICE
AB The liver, which is a metabolic organ, plays a pivotal role in tolerance induction. Hepatic stellate cells (HpSCs), which are unique non-parenchymal cells, exert potent immunoregulatory activity during cotransplantation with allogeneic islets effectively protecting the islet allografts from rejection. Multiple mechanisms participate in the immune tolerance induced by HpSCs, including the marked expansion of myeloid-derived suppressor cells (MDSCs), attenuation of effector T cell functions and augmentation of regulatory T cells. HpSC conditioned MDSC-based immunotherapy has been conducted in mice with autoimmune disease and the results show that this technique may be promising. This article demonstrates how HpSCs orchestrate both innate immunity and adaptive immunity to build a negative network that leads to immune tolerance.
C1 [Hsieh, Ching-Chuan] Chang Gung Mem Hosp, Dept Surg, Chiayi 613, Taiwan.
[Hsieh, Ching-Chuan; Hung, Chien-Hui] Chang Gung Univ, Grad Inst Clin Med Sci, Taoyuan 333, Taiwan.
[Lu, Lina; Qian, Shiguang] Cleveland Clin, Inst Digest Dis, Transplantat Ctr, Dept Immunol,Lerner Res Inst, Cleveland, OH 44195 USA.
[Lu, Lina; Qian, Shiguang] Cleveland Clin, Inst Digest Dis, Transplantat Ctr, Dept Gen Surg, Cleveland, OH 44195 USA.
C3 Chang Gung Memorial Hospital; Chang Gung University; Cleveland Clinic
Foundation; Cleveland Clinic Foundation
RP Hsieh, CC (corresponding author), Chang Gung Mem Hosp, Dept Surg, 6 Sect West Chia Pu Rd, Chiayi 613, Taiwan.
EM jeffrey570404@gmail.com
RI Wu, Chun-Ying/AAX-5077-2021; Li, Tsai-Chung/P-2052-2015
OI Hung, Chien-Hui/0000-0002-3887-6679
FU National Science Council [NSC 101-2314-B-182A-040-MY2, CMRPG6A0523]
FX Supported by National Science Council, No. NSC 101-2314-B-182A-040-MY2
and No. CMRPG6A0523.
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NR 39
TC 24
Z9 29
U1 1
U2 13
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 14
PY 2015
VL 21
IS 42
BP 11887
EP 11892
DI 10.3748/wjg.v21.i42.11887
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CW5HC
UT WOS:000365025300001
PM 26576077
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Peng, WF
Xu, BJ
Zhou, HP
Du, J
Ge, XX
Huang, S
AF Peng, Wenfang
Xu, Bojin
Zhou, Haiping
Du, Juan
Ge, Xiaoxu
Huang, Shan
TI Causal effects of autoimmune diseases on thyroid cancer: a two-sample
Mendelian randomization study
SO FRONTIERS IN ENDOCRINOLOGY
LA English
DT Article
DE autoimmune disease; thyroid cancer; Mendelian randomization; causality;
systemic lupus erythematosus; primary biliary cirrhosis
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; PRIMARY BILIARY-CIRRHOSIS;
HEPATOCELLULAR-CARCINOMA; RISK; MALIGNANCIES; LUNG
AB Background Although numerous studies had revealed associations between autoimmune diseases (AIDs) and thyroid cancer (TC), the potential causal associations between the two remain poorly defined.Methods Using five approaches, two-sample Mendelian randomization (MR) analyses were carried out to determine the causal effects of 12 major AIDs on risk of TC. The sensitivity analyses were conducted to verify the reliability of the analysis. The reverse MR analysis was performed to evaluate the possibility of reverse causation.Results The results showed a significant causal association of systemic lupus erythematosus (SLE) and primary biliary cirrhosis (PBC) on the risk of TC. Genetically predicted PBC elevated the risk of TC (OR = 1.46, 95% CI = 1.06-2.02, p = 0.021). The risk of TC was also increased by genetically predicted SLE (OR = 6.52, 95% CI = 1.38-30.84, p = 0.018) with heterogeneity. After outlier-corrected analyses, the results still suggested that genetically predicted SLE increased the risk of TC (p = 0.019). No evidence of a causal relationship between the remaining 10 AIDs and TC was observed. No reverse causal effects of TC on AIDs were found in reverse MR analysis.Conclusion These findings support a significant causal association of SLE/PBC on the increased risk of TC, indicating that patients with SLE/PBC should be under a close monitoring of TC.
C1 [Peng, Wenfang; Xu, Bojin; Zhou, Haiping; Du, Juan; Ge, Xiaoxu; Huang, Shan] Shanghai Jiao Tong Univ, Tongren Hosp, Sch Med, Dept Endocrinol, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University
RP Huang, S (corresponding author), Shanghai Jiao Tong Univ, Tongren Hosp, Sch Med, Dept Endocrinol, Shanghai, Peoples R China.
EM hs1147@126.com
FU Talent Program of Tongren Hospital, Shanghai Jiao Tong University School
of Medicine [TRKYRC-yc202202]; Master and Doctor innovation talent base
for endocrine and metabolic diseases [RCJD2021S03]
FX The author(s) declare financial support was received for the research,
authorship, and/or publication of this article. This study was supported
by Talent Program of Tongren Hospital, Shanghai Jiao Tong University
School of Medicine (TRKYRC-yc202202) and Master and Doctor innovation
talent base for endocrine and metabolic diseases (RCJD2021S03).
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NR 46
TC 0
Z9 0
U1 2
U2 2
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-2392
J9 FRONT ENDOCRINOL
JI Front. Endocrinol.
PD AUG 8
PY 2024
VL 15
AR 1401458
DI 10.3389/fendo.2024.1401458
PG 9
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA D3T6F
UT WOS:001295446800001
PM 39175579
OA Green Published
DA 2025-01-07
ER
PT J
AU Ates, I
Yilmaz, AD
Buttari, B
Arese, M
Saso, L
Suzen, S
AF Ates, Ilker
Yilmaz, Ayse Didem
Buttari, Brigitta
Arese, Marzia
Saso, Luciano
Suzen, Sibel
TI A Review of the Potential of Nuclear Factor [Erythroid-Derived 2]-like 2
Activation in Autoimmune Diseases
SO BRAIN SCIENCES
LA English
DT Review
DE Nrf2 activation; autoimmune diseases; inflammation; autoimmunity;
immunoregulatory
ID TRANSCRIPTION FACTOR NRF2; NF-KAPPA-B; INNATE IMMUNE-RESPONSE; HEME
OXYGENASE SYSTEM; OXIDATIVE STRESS; MOLECULAR-MECHANISMS; REACTIVE
OXYGEN; INCREASED SUSCEPTIBILITY; DIABETIC-NEPHROPATHY; NRF2-DEFICIENT
MICE
AB An autoimmune disease is the consequence of the immune system attacking healthy cells, tissues, and organs by mistake instead of protecting them. Inflammation and oxidative stress (OS) are well-recognized processes occurring in association with acute or chronic impairment of cell homeostasis. The transcription factor Nrf2 (nuclear factor [erythroid-derived 2]-like 2) is of major importance as the defense instrument against OS and alters anti-inflammatory activities related to different pathological states. Researchers have described Nrf2 as a significant regulator of innate immunity. Growing indications suggest that the Nrf2 signaling pathway is deregulated in numerous diseases, including autoimmune disorders. The advantageous outcome of the pharmacological activation of Nrf2 is an essential part of Nrf2-based chemoprevention and intervention in other chronic illnesses, such as neurodegeneration, cardiovascular disease, autoimmune diseases, and chronic kidney and liver disease. Nevertheless, a growing number of investigations have indicated that Nrf2 is already elevated in specific cancer and disease steps, suggesting that the pharmacological agents developed to mitigate the potentially destructive or transformative results associated with the protracted activation of Nrf2 should also be evaluated. The activators of Nrf2 have revealed an improvement in the progress of OS-associated diseases, resulting in immunoregulatory and anti-inflammatory activities; by contrast, the depletion of Nrf2 worsens disease progression. These data strengthen the growing attention to the biological properties of Nrf2 and its possible healing power on diseases. The evidence supporting a correlation between Nrf2 signaling and the most common autoimmune diseases is reviewed here. We focus on the aspects related to the possible effect of Nrf2 activation in ameliorating pathologic conditions based on the role of this regulator of antioxidant genes in the control of inflammation and OS, which are processes related to the progression of autoimmune diseases. Finally, the possibility of Nrf2 activation as a new drug development strategy to target pathogenesis is proposed.
C1 [Ates, Ilker] Ankara Univ, Fac Pharm, Dept Pharmaceut Toxicol, Degol Str 4, TR-06560 Ankara, Turkiye.
[Yilmaz, Ayse Didem; Suzen, Sibel] Ankara Univ, Fac Pharm, Dept Pharmaceut Chem, Degol Str 4, TR-06560 Ankara, Turkiye.
[Buttari, Brigitta] Italian Natl Inst Hlth, Dept Cardiovasc & Endocrine, Metab Dis & Aging, I-00161 Rome, Italy.
[Arese, Marzia] Sapienza Univ Rome, Dept Biochem Sci A Rossi Fanelli, Piazzae Aldo Moro 5, I-00185 Rome, Italy.
[Saso, Luciano] Sapienza Univ Rome, Dept Physiol & Pharmacol Vittorio Erspamer, Piazzale Aldo Moro 5, I-00185 Rome, Italy.
C3 Ankara University; Ankara University; Istituto Superiore di Sanita
(ISS); Sapienza University Rome; Sapienza University Rome
RP Ates, I (corresponding author), Ankara Univ, Fac Pharm, Dept Pharmaceut Toxicol, Degol Str 4, TR-06560 Ankara, Turkiye.
EM ilkerates976@gmail.com; aysedidemyilmaz@gmail.com;
brigitta.buttari@iss.it; marzia.arese@uniroma1.it;
luciano.saso@uniroma1.it; sibel.suzen@pharmacy.ankara.edu.tr
RI Ateş, İlker/W-4563-2017; Buttari, Brigitta/I-3030-2014; saso,
luciano/F-6306-2012
OI Buttari, Brigitta/0000-0002-0575-4106; saso,
luciano/0000-0003-4530-8706; ARESE, Marzia/0000-0002-6140-2287; SUZEN,
Sibel/0000-0003-3413-6152; ATES, ILKER/0000-0001-5791-7694
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NR 212
TC 2
Z9 2
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-3425
J9 BRAIN SCI
JI Brain Sci.
PD NOV
PY 2023
VL 13
IS 11
AR 1532
DI 10.3390/brainsci13111532
PG 30
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA AP1K7
UT WOS:001119573500001
PM 38002492
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Meyerson, C
Naini, BV
AF Meyerson, Cherise
Naini, Bita, V
TI Something old, something new: liver injury associated with total
parenteral nutrition therapy and immune checkpoint inhibitors
SO HUMAN PATHOLOGY
LA English
DT Article
DE Total parenteral nutrition (TPN); Intestinal failure- associated liver
disease (IFALD); Liver injury; Cholestasis; Steatosis; Immune checkpoint
inhibitor (ICI); ICI-induced hepatitis
ID INTESTINAL-FAILURE; INDUCED CHOLESTASIS; LIPID EMULSION; HEPATOBILIARY
COMPLICATIONS; HEPATOCELLULAR-CARCINOMA; GRANULOMATOUS HEPATITIS; ADULT
PATIENTS; DISEASE; IPILIMUMAB; NIVOLUMAB
AB Drug-induced liver injury (DILI) is a challenging and constantly changing field. The pathologist plays a key role in interpreting liver biopsies by classifying the pattern of injury, grading the severity of injury, and evaluating for other possible causes. Reports of iatrogenic liver injury are reviewed here with a focus on total parenteral nutrition (ie, intestinal failure-associated liver disease [IFALD]) and immune checkpoint inhibitors (ICIs). The hallmark features of IFALD are cholestasis and steatosis. Cholestasis is more common in infants, whereas steatosis and steatohepatitis are more commonly seen in older children and adults. Infants tend to have a faster progression to fibrosis and cirrhosis. Perivenular fibrosis and ductopenia may also be seen in IFALD. Although fish oil-based lipid emulsions can reverse cholestasis, recent studies have shown persistent or progressive fibrosis. ICI-induced liver injury usually presents as an acute hepatitis with features similar to those seen in idiopathic autoimmune hepatitis and drug-induced autoimmune hepatitis. However, it lacks a prominent plasma cell infiltrate and serological markers of autoimmune hepatitis. Other features such as fibrin ring granulomas and cholangitis have also been reported in association with ICIs. Treatment for ICI-induced liver injury includes corticosteroids and other immunosuppressants. (C) 2019 Elsevier Inc. All rights reserved.
C1 [Meyerson, Cherise; Naini, Bita, V] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
C3 University of California System; University of California Los Angeles;
University of California Los Angeles Medical Center; David Geffen School
of Medicine at UCLA
RP Naini, BV (corresponding author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
EM bnaini@mednet.ucla.edu
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NR 88
TC 14
Z9 17
U1 1
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD FEB
PY 2020
VL 96
BP 39
EP 47
DI 10.1016/j.humpath.2019.10.007
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA KX8QA
UT WOS:000522138200005
PM 31669893
DA 2025-01-07
ER
PT J
AU Farhangnia, P
Ghomi, SM
Mollazadehghomi, S
Nickho, H
Akbarpour, M
Delbandi, AA
AF Farhangnia, Pooya
Ghomi, Shamim Mollazadeh
Mollazadehghomi, Shabnam
Nickho, Hamid
Akbarpour, Mahzad
Delbandi, Ali-Akbar
TI SLAM-family receptors come of age as a potential molecular target in
cancer immunotherapy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE SLAM; cancer immunotherapy; elotuzumab; CD150; CD84; CD229; SLAMF7; CS1
ID LYMPHOCYTIC ACTIVATION MOLECULE; LINKED LYMPHOPROLIFERATIVE-DISEASE;
NATURAL-KILLER-CELLS; CD8(+) T-CELLS; LOW-DOSE DEXAMETHASONE; CUTTING
EDGE; CD150 SLAM; DIFFERENTIAL EXPRESSION; MEASLES-VIRUS;
MULTIPLE-MYELOMA
AB The signaling lymphocytic activation molecule (SLAM) family receptors were discovered in immune cells for the first time. The SLAM-family receptors are a significant player in cytotoxicity, humoral immune responses, autoimmune diseases, lymphocyte development, cell survival, and cell adhesion. There is growing evidence that SLAM-family receptors have been involved in cancer progression and heralded as a novel immune checkpoint on T cells. Previous studies have reported the role of SLAMs in tumor immunity in various cancers, including chronic lymphocytic leukemia, lymphoma, multiple myeloma, acute myeloid leukemia, hepatocellular carcinoma, head and neck squamous cell carcinoma, pancreas, lung, and melanoma. Evidence has deciphered that the SLAM-family receptors may be targeted for cancer immunotherapy. However, our understanding in this regard is not complete. This review will discuss the role of SLAM-family receptors in cancer immunotherapy. It will also provide an update on recent advances in SLAM-based targeted immunotherapies.
C1 [Farhangnia, Pooya; Nickho, Hamid; Delbandi, Ali-Akbar] Iran Univ Med Sci, Inst Immunol & Infect Dis, Immunol Res Ctr, Tehran, Iran.
[Farhangnia, Pooya; Nickho, Hamid; Delbandi, Ali-Akbar] Iran Univ Med Sci, Sch Med, Dept Immunol, Tehran, Iran.
[Farhangnia, Pooya; Ghomi, Shamim Mollazadeh; Mollazadehghomi, Shabnam; Akbarpour, Mahzad] Universal Sci Educ & Res Network USERN, Immunol Board Transplantat & Cell Based Therapeut, Tehran, Iran.
[Akbarpour, Mahzad] Univ Chicago, Dept Med, Sect Hematol & Oncol,Med Ctr, Adv Cellular Therapeut Facil ACTF,Hematopoiet Cell, Chicago, IL 60637 USA.
C3 Iran University of Medical Sciences; Iran University of Medical
Sciences; Universal Scientific Education & Research Network (USERN);
University of Chicago; University of Chicago Medical Center
RP Delbandi, AA (corresponding author), Iran Univ Med Sci, Inst Immunol & Infect Dis, Immunol Res Ctr, Tehran, Iran.; Delbandi, AA (corresponding author), Iran Univ Med Sci, Sch Med, Dept Immunol, Tehran, Iran.; Akbarpour, M (corresponding author), Universal Sci Educ & Res Network USERN, Immunol Board Transplantat & Cell Based Therapeut, Tehran, Iran.; Akbarpour, M (corresponding author), Univ Chicago, Dept Med, Sect Hematol & Oncol,Med Ctr, Adv Cellular Therapeut Facil ACTF,Hematopoiet Cell, Chicago, IL 60637 USA.
EM Makbarpour@medicine.bsd.uchicago.edu; Delbandi.ak@Iums.ac.ir
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NR 201
TC 20
Z9 21
U1 2
U2 19
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAY 11
PY 2023
VL 14
AR 1174138
DI 10.3389/fimmu.2023.1174138
PG 16
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA H3FH6
UT WOS:000994852900001
PM 37251372
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Urbanski, G
Hamel, JF
Prouveur, B
Annweiler, C
Ghali, A
Cassereau, J
Lozac'h, P
Lavigne, C
Lacombe, V
AF Urbanski, Geoffrey
Hamel, Jean-Francois
Prouveur, Benoit
Annweiler, Cedric
Ghali, Alaa
Cassereau, Julien
Lozac'h, Pierre
Lavigne, Christian
Lacombe, Valentin
TI Strength of the Association of Elevated Vitamin B12 and Solid Cancers:
An Adjusted Case-Control Study
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE vitamin B12; neoplasms; neoplasm metastasis; case-control study;
biomarkers
ID PLASMA; FOLATE; DEFICIENCY
AB The association between elevated plasma vitamin B12 (B12) level and solid cancers has been documented by two national registries. However, their design did not allow for the adjustment for other conditions associated with elevated B12. The objectives of this study were to confirm this association after the adjustment for all causes of elevated B12, and to study the variations according to the increasing B12 level, the type of cancers, and the presence of metastases. We compared 785 patients with B12 >= 1000 ng/L with 785 controls matched for sex and age with B12 < 1000 ng/L. Analyses were adjusted for the causes of elevated B12: myeloid blood malignancies, acute or chronic liver diseases, chronic kidney failure, autoimmune or inflammatory diseases, and excessive B12 supplementation. A B12 >= 1000 ng/L was associated with the presence of solid cancer without metastases (OR 1.96 [95%CI: 1.18 to 3.25]) and with metastases (OR 4.21 [95%CI: 2.67 to 6.64]) after adjustment for all elevated B12-related causes. The strength of the association rose with the increasing B12 level, in particular in cases of metastases. No association between liver cancers and elevated B12 level was found after adjustment for chronic liver diseases. In conclusion, unexplained elevated B12 levels should be examined as a possible marker of solid cancer.
C1 [Urbanski, Geoffrey; Prouveur, Benoit; Ghali, Alaa; Lozac'h, Pierre; Lavigne, Christian; Lacombe, Valentin] Angers Univ Hosp, Dept Internal Med, F-49933 Angers, France.
[Hamel, Jean-Francois] Angers Univ Hosp, Dept Biostat & Methodol, F-49933 Angers, France.
[Annweiler, Cedric] Angers Univ Hosp, Dept Geriatr Med, F-49933 Angers, France.
[Annweiler, Cedric] Angers Univ Hosp, Memory Clin, F-49933 Angers, France.
[Cassereau, Julien] Angers Univ Hosp, Dept Neurol, F-49933 Angers, France.
C3 Universite d'Angers; Centre Hospitalier Universitaire d'Angers;
Universite d'Angers; Centre Hospitalier Universitaire d'Angers;
Universite d'Angers; Centre Hospitalier Universitaire d'Angers;
Universite d'Angers; Centre Hospitalier Universitaire d'Angers;
Universite d'Angers; Centre Hospitalier Universitaire d'Angers
RP Urbanski, G (corresponding author), Angers Univ Hosp, Dept Internal Med, F-49933 Angers, France.
EM urbanskigeoffrey@gmail.com; jeanfrancois.hamel@chu-angers.fr;
benoit.prouveur@laposte.net; ceannweiler@chu-angers.fr;
alghali@chu-angers.fr; jucassereau@chu-angers.fr;
pierre.lozac@gmail.com; chlavigne@chu-angers.fr;
lacombe.valentin31@gmail.com
RI Urbanski, Geoffrey/AAO-8343-2021
OI Annweiler, Cedric/0000-0002-7199-8109; Lavigne,
Christian/0000-0002-2538-0076; Urbanski, Geoffrey/0000-0001-5719-8423
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NR 31
TC 19
Z9 19
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD FEB
PY 2020
VL 9
IS 2
AR 474
DI 10.3390/jcm9020474
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA KT2DG
UT WOS:000518823000186
PM 32050436
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Yan, J
Zhang, Y
Zhang, JP
Liang, J
Li, L
Zheng, LM
AF Yan, Jing
Zhang, Yi
Zhang, Jing-Ping
Liang, Jing
Li, Lian
Zheng, Limin
TI Tim-3 Expression Defines Regulatory T Cells in Human Tumors
SO PLOS ONE
LA English
DT Article
ID INTERFERON-GAMMA PRODUCTION; ACTIVATED MONOCYTES; PERITUMORAL STROMA;
POOR-PROGNOSIS; UP-REGULATION; PATHWAY; GALECTIN-9; IMMUNITY; CANCER;
EXHAUSTION
AB Tim-3, a member of the novel Tim (T cell immunoglobulin and mucin domain) family, has been reported to negatively regulate the immune responses against viral infection and had implications for autoimmune disease. However, the nature and role of Tim-3(+) CD4 T cells in human tumors remain largely unknown. In the present study, we characterized Tim-3(+) CD4 T cells in 100 specimens from human hepatocellular, cervical, colorectal and ovarian carcinoma patients. Compared with peripheral blood and nontumor-infiltrating lymphocytes, the lymphocytes isolated from the corresponding tumor tissues of hepatocellular, cervical, colorectal and ovarian carcinoma patients contained significantly greater proportion of Tim-3(+) CD4 T cells. The majority of tumor-derived Tim-3(+) CD4 T cells exhibited an impaired capacity to produce IFN-gamma and IL-2, but expressed higher levels of CD25, Foxp3, CTLA-4 and GITR than their Tim-3 2 CD4 T cell counterparts. In contrast, most Tim-3(+) CD4 T cells isolated from the paired nontumor tissues and peripheral blood did not express these molecules. Moreover, tumor-derived Tim-3(+) CD4 T cells, but not tumor-derived Tim-3(+) CD4 T cells, significantly suppressed the proliferation of autologous CD8(+) T cells in vitro. Notably, multi-color immunofluorescence and confocal microscopy demonstrated that Tim-3(+) Foxp3(+) CD4(+) cells were preferentially distributed in the tumor nest rather than the peritumoral stroma of hepatocellular carcinoma. Together, our data indicate that Tim-3-expressing CD4 T cells in human tumors could represent the functional regulatory T cells which contribute to the formation of the immune-suppressive tumor micromilieu.
C1 [Yan, Jing; Zhang, Jing-Ping; Zheng, Limin] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol S China, Guangzhou 510275, Guangdong, Peoples R China.
[Zhang, Yi; Liang, Jing; Li, Lian; Zheng, Limin] Sun Yat Sen Univ, State Key Lab Biocontrol, Sch Life Sci, Guangzhou 510275, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University
RP Zheng, LM (corresponding author), Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol S China, Guangzhou 510275, Guangdong, Peoples R China.
EM zhenglm@mail.sysu.edu.cn
RI zheng, limin/HGB-2510-2022; ZHANG, JINGPING/AAT-8229-2021
OI Zheng, Limin/0000-0002-8281-1450; Zhang, Jingping/0000-0003-0090-6710
FU National Basic Research Program of China [2010CB529904, 2011CB811305];
National Natural Science Foundation of China [81230073, 91029737];
Ministry of Health of China [2012ZX10002-011]
FX This work was supported by project grants from the National Basic
Research Program of China (2010CB529904 and 2011CB811305;
http://www.973.gov.cn/Default_3.aspx), the National Natural Science
Foundation of China (81230073 and 91029737;
http://www.nsfc.gov.cn/Portal0/default152.htm), and the Ministry of
Health of China (2012ZX10002-011;
http://www.moh.gov.cn/publicfiles//business/htmlfiles/wsb/index.htm).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 56
TC 147
Z9 173
U1 1
U2 21
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAR 5
PY 2013
VL 8
IS 3
AR e58006
DI 10.1371/journal.pone.0058006
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 099RC
UT WOS:000315637900072
PM 23526963
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Dong, G
Huang, XQ
Chen, RX
Wu, L
Jiang, SY
Chen, SY
AF Dong, Gang
Huang, Xiaoquan
Chen, Rongxin
Wu, Ling
Jiang, Siyu
Chen, Shiyao
TI Increased PD-L1 Restricts Liver Injury in Nonalcoholic Fatty Liver
Disease
SO OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
LA English
DT Article
ID CHECKPOINT; EXPRESSION; PATHWAYS; THERAPY; BINDING; CANCER
AB PD-L1 is a critical checkpoint that protects tissues from autoimmune injury. Nevertheless, the role of PD-L1 in nonalcoholic fatty liver disease- (NAFLD-) induced liver damage is still unclear. In this study, we examined the role and mechanism of PD-L1 expression on NAFLD-induced liver damage in vitro and in vivo. PD-L1 expression in the livers from patients with NAFLD, and LO2 cells treated by FFA, was significantly increased. FFA triggers a large amount of ROS (generated from NOX4 and damaged mitochondria), promoting the ZNF24 expression and suppressing ZN24 sumoylation, both of which enhance the PD-L1 transcription and expression. The knockdown of PD-L1 increases CD8 + T cells' damage to FFA-treated LO2 cells, while its upregulation limits the liver injury in NAFLD models. Collectively, we demonstrate that FFA promotes PD-L1 expression through the ROS/ZNF24 pathway and suppresses UBE2I-mediated ZNF24 sumoylation to enhance its transcriptional activity of PD-L1. PD-L1 upregulation limits FFA-induced injury of hepatocytes in vitro and in vivo.
C1 [Dong, Gang; Huang, Xiaoquan; Wu, Ling; Jiang, Siyu; Chen, Shiyao] Fudan Univ, Zhongshan Hosp, Dept Gastroenterol & Hepatol, Shanghai 200032, Peoples R China.
[Chen, Rongxin] Fudan Univ, Zhongshan Hosp, Liver Canc Inst, Key Lab Carcinogenesis & Canc Invas,Minist Educ, Shanghai 200032, Peoples R China.
[Chen, Shiyao] Fudan Univ, Zhongshan Hosp, Endoscopy Res Inst, Endoscopy Ctr, Shanghai 200032, Peoples R China.
[Chen, Shiyao] Fudan Univ, Ctr Evidence Based Med, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Fudan University
RP Chen, SY (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gastroenterol & Hepatol, Shanghai 200032, Peoples R China.; Chen, SY (corresponding author), Fudan Univ, Zhongshan Hosp, Endoscopy Res Inst, Endoscopy Ctr, Shanghai 200032, Peoples R China.; Chen, SY (corresponding author), Fudan Univ, Ctr Evidence Based Med, Shanghai 200032, Peoples R China.
EM 18111210010@fudan.edu.cn; huang.xiaoquan@zs-hospital.sh.cn;
chen.rongxin@zs-hospital.sh.cn; 18211210016@fudan.edu.cn;
643313428@qq.com; chen.shiyao@zs-hospital.sh.cn
RI JIANG, Siyu/IZP-6407-2023
OI Wu, Ling/0000-0001-6574-6493
FU National Natural Science Foundation of China [81900511]; Shanghai
Sailing Program [19YF1406500]
FX AcknowledgmentsThis work was supported by the National Natural Science
Foundation of China (No. 81900511) and Shanghai Sailing Program (No.
19YF1406500).
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Z9 9
U1 1
U2 14
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1942-0900
EI 1942-0994
J9 OXID MED CELL LONGEV
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PY 2022
VL 2022
AR 5954437
DI 10.1155/2022/5954437
PG 18
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 1W9YQ
UT WOS:000807122500001
PM 35615575
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Frith, J
Newton, JL
AF Frith, James
Newton, Julia L.
TI Liver disease in older women
SO MATURITAS
LA English
DT Review
DE Liver disease; Ageing; Menopause
ID PRIMARY BILIARY-CIRRHOSIS; BONE-MINERAL DENSITY; HORMONE REPLACEMENT
THERAPY; PLACEBO-CONTROLLED TRIAL; CHRONIC HEPATITIS-C; AUTOIMMUNE
HEPATITIS; HEPATOCELLULAR-CARCINOMA; CLINICAL-FEATURES;
ELDERLY-PATIENTS; VIRUS-INFECTION
AB Clinicians are seeing increasing number of patients with chronic liver disease (CLD). The prevalence of diseases such as nonalcoholic fatty liver disease is increasing dramatically, our population is ageing and people with CLD are surviving into old age. Signs and symptoms of CLD in the older patient are often subtle and non-specific and a high index of suspicion is required in order to investigate. A number of diseases, which are predominate in women, tend to present in middle to older age. The menopause may render the liver more susceptible to disease progression and although hormone replacement appears safe in CLD but it is not recommended for liver protection. Osteoporosis is common in CLD but robust evidence is lacking on fracture prevention. Vigilance is required when interpreting investigations as there are no age-associated changes in clinical liver function testing. Management strategies are similar irrespective of age or gender, but evidence is lacking specific to older populations. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
C1 [Frith, James; Newton, Julia L.] Univ Newcastle, UK NIHR Biomed Res Ctr Ageing & Age Related Dis, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
C3 Newcastle University - UK
RP Frith, J (corresponding author), Univ Newcastle, UK NIHR Biomed Res Ctr Ageing & Age Related Dis, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
EM james.frith@ncl.ac.uk
OI Frith, James/0000-0002-6491-3701; Newton, Julia/0000-0002-1249-5253
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NR 59
TC 9
Z9 11
U1 0
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0378-5122
EI 1873-4111
J9 MATURITAS
JI Maturitas
PD MAR
PY 2010
VL 65
IS 3
BP 210
EP 214
DI 10.1016/j.maturitas.2009.11.010
PG 5
WC Geriatrics & Gerontology; Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Geriatrics & Gerontology; Obstetrics & Gynecology
GA 574MG
UT WOS:000275992900007
PM 19962256
DA 2025-01-07
ER
PT J
AU Licata, A
Russo, GT
Giandalia, A
Cammilleri, M
Asero, C
Cacciola, I
AF Licata, Anna
Russo, Giuseppina T.
Giandalia, Annalisa
Cammilleri, Marcella
Asero, Clelia
Cacciola, Irene
TI Impact of Sex and Gender on Clinical Management of Patients with
Advanced Chronic Liver Disease and Type 2 Diabetes
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Review
DE cirrhosis; type 2 diabetes; gender; sex
ID GLP-1 RECEPTOR AGONISTS; FATTY LIVER; HEPATITIS-C;
HEPATOCELLULAR-CARCINOMA; DIPEPTIDYL PEPTIDASE-4; INSULIN-RESISTANCE;
STATIN USE; AUTOIMMUNE HEPATITIS; DNA METHYLATION; VIRUS-INFECTION
AB Gender differences in the epidemiology, pathophysiological mechanisms and clinical features in chronic liver diseases that may be associated with type 2 diabetes (T2D) have been increasingly reported in recent years. This sexual dimorphism is due to a complex interaction between sex- and gender-related factors, including biological, hormonal, psychological and socio-cultural variables. However, the impact of sex and gender on the management of T2D subjects with liver disease is still unclear. In this regard, sex-related differences deserve careful consideration in pharmacology, aimed at improving drug safety and optimising medical therapy, both in men and women with T2D; moreover, low adherence to and persistence of long-term drug treatment is more common among women. A better understanding of sex- and gender-related differences in this field would provide an opportunity for a tailored diagnostic and therapeutic approach to the management of T2D subjects with chronic liver disease. In this narrative review, we summarized available data on sex- and gender-related differences in chronic liver disease, including metabolic, autoimmune, alcoholic and virus-related forms and their potential evolution towards cirrhosis and/or hepatocarcinoma in T2D subjects, to support their appropriate and personalized clinical management.
C1 [Licata, Anna; Cammilleri, Marcella] Univ Palermo, Univ Hosp Palermo, Internal Med & Hepatol Unit, PROMISE, I-90127 Palermo, Italy.
[Russo, Giuseppina T.] Univ Messina, Internal Med & Diabetol Unit, I-98125 Messina, Italy.
[Giandalia, Annalisa; Asero, Clelia; Cacciola, Irene] Univ Hosp Messina, Internal Med & Hepatol Unit, I-98124 Messina, Italy.
[Giandalia, Annalisa; Asero, Clelia; Cacciola, Irene] Univ Messina, Dept Clin & Expt Med, I-98124 Messina, Italy.
C3 University of Palermo; Policlinico Paolo Giaccone; University of
Messina; AOU Policlinico Gaetano Martino; University of Messina
RP Licata, A (corresponding author), Univ Palermo, Univ Hosp Palermo, Internal Med & Hepatol Unit, PROMISE, I-90127 Palermo, Italy.
EM anna.licata@unipa.it
RI Licata, Anna/ADF-0000-2022; Cacciola, Irene/K-1174-2019; Giandalia,
Annalisa/HLQ-2632-2023
OI Licata, Anna/0000-0003-0383-6121; CACCIOLA, Irene/0000-0001-7721-6799;
Asero, Clelia/0000-0003-0427-6963; Giandalia,
Annalisa/0000-0002-0778-4130
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NR 182
TC 1
Z9 1
U1 2
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4426
J9 J PERS MED
JI J. Pers. Med.
PD MAR
PY 2023
VL 13
IS 3
AR 558
DI 10.3390/jpm13030558
PG 24
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA C0LC1
UT WOS:000958928100001
PM 36983739
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Mishima, S
Mizuta, Y
Yamao, T
Yamakawa, M
Akazawa, Y
Mishima, R
Ohba, K
Masuda, JI
Ohnita, K
Isomoto, H
Shikuwa, S
Omagari, K
Kohno, S
AF Mishima, Shiho
Mizuta, Yohei
Yamao, Takuji
Yamakawa, Masaki
Akazawa, Yuko
Mishima, Ryosuke
Ohba, Kazuo
Masuda, Jun-ich
Ohnita, Ken
Isomoto, Hajime
Shikuwa, Saburo
Omagari, Katsuhisa
Kohno, Shigeru
TI Autoimmune pancreatitis with extreme elevation of DUPAN-2
SO INTERNAL MEDICINE
LA English
DT Article
DE autoimmune pancreatitis; DUPAN-2; IgG4; steroid
ID IGG4 CONCENTRATIONS; SERUM LEVELS; ANTIGEN; FEATURES; DU-PAN-2;
DISEASES; CANCER; CA19-9; CT
AB An 80-year-old woman was admitted to our hospital with complaints of jaundice and liver dysfunction. She was found to have a high titer of serum IgG4, positive rheumatoid factor and marked elevation of DUPAN-2 (11,148 U/ml). Computed tomography showed swelling of the pancreas, and endoscopic retrograde cholangiopancreatography revealed diffuse irregular narrowing of the main pancreatic duct, which are typical findings of autoimmune pancreatitis. There was no evidence of malignancy. Administration of 30 mg/day of prednisolone was started. Computed tomography showed significant regression in the size of the pancreas, and the stenosis of the main pancreatic duct was improved on ERCP. The serum level of DUPAN-2 was also markedly decreased after the treatment.
C1 [Mishima, Shiho; Yamao, Takuji; Yamakawa, Masaki] Nagasaki Municipal Hosp, Dept Internal Med, Nagasaki, Japan.
[Mishima, Shiho; Mizuta, Yohei; Akazawa, Yuko; Mishima, Ryosuke; Ohba, Kazuo; Masuda, Jun-ich; Ohnita, Ken; Isomoto, Hajime; Shikuwa, Saburo; Omagari, Katsuhisa; Kohno, Shigeru] Nagasaki Univ, Sch Med, Dept Internal Med 2, Nagasaki 852, Japan.
C3 Nagasaki University
RP Mizuta, Y (corresponding author), Nagasaki Municipal Hosp, Dept Internal Med, Nagasaki, Japan.
EM ymizuta@net.nagasaki-u.ac.jp
RI Ichimura-Shimizu, Mayuko/KFT-1304-2024
OI Ichimura-Shimizu, Mayuko/0000-0003-4030-1249
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NR 26
TC 3
Z9 3
U1 0
U2 3
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
J9 INTERNAL MED
JI Intern. Med.
PY 2007
VL 46
IS 7
BP 373
EP 377
DI 10.2169/internalmedicine.46.6184
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 342QB
UT WOS:000258797500009
PM 17409601
OA hybrid, Green Submitted
DA 2025-01-07
ER
PT J
AU Bayoumy, AB
Simsek, M
Seinen, ML
Mulder, CJJ
Ansari, A
Peters, GJ
De Boer, NK
AF Bayoumy, Ahmed B.
Simsek, Melek
Seinen, Margien L.
Mulder, Chris J. J.
Ansari, Azhar
Peters, Godefridus J.
De Boer, Nanne K.
TI The continuous rediscovery and the benefit-risk ratio of thioguanine, a
comprehensive review
SO EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY
LA English
DT Review
DE Thioguanine; thiopurines; gastroenterology; hematology; rheumatology;
dermatology; drug Rediscovery; drug-induced liver injury; inflammatory
Bowel Disease
ID INFLAMMATORY-BOWEL-DISEASE; NODULAR REGENERATIVE HYPERPLASIA; ACUTE
LYMPHOBLASTIC-LEUKEMIA; LOW-DOSE 6-THIOGUANINE; LOW-GRADE GLIOMAS; CELL
LUNG-CANCER; PHASE-II TRIAL; INTRAVENOUS 6-THIOGUANINE; MULTIAGENT
CHEMOTHERAPY; PORTAL-HYPERTENSION
AB Introduction: In the 1950s, thioguanine (TG), a thiopurine-derivative together with azathioprine (AZA) and mercaptopurine (MP), were developed for the treatment of childhood leukemia. Over the years, the use of TG was also explored for other, mainly immune-mediated and inflammatory, diseases such as in the field of dermatology and rheumatology (e.g. psoriasis, systemic lupus erythematosus (SLE)) and gastroenterology and hepatology (e.g. inflammatory bowel diseases (IBD), autoimmune hepatitis). Areas covered: This review provides a comprehensive overview of all the clinical uses of TG and describes its mechanism of action, pharmacokinetic/pharmacodynamic features, and toxicity. Expert opinion: Thioguanine has shown beneficial clinical effects in hematological (particularly leukemia) and several immune-inflammatory diseases including psoriasis, SLE, polycythemia vera, Churg-Strauss syndrome, IBD, collagenous sprue, refractory celiac disease, and autoimmune hepatitis. Thioguanine is not effective in treating solid-cancers. At relatively low dosages, i.e. 0.2- 0.3mg/kg/day or 20 mg/day, TG has a favorable risk-benefit ratio and is a safe and effective drug in the long-term treatment of amongst other IBD patients. Thioguanine toxicity, especially myelotoxicity, and hepatotoxicity, including nodular regenerative hyperplasia (NRH) of the liver, is limited when dosed adequately. The occurrence of NRH appears dose-dependent and has been especially described during high dose TG above 40 mg/day.
C1 [Bayoumy, Ahmed B.; Seinen, Margien L.; Mulder, Chris J. J.] Vrije Univ Amsterdam, Med Ctr, Dept Gastroenterol & Hepatol, Amsterdam UMC, Amsterdam, Netherlands.
[Simsek, Melek; De Boer, Nanne K.] Vrije Univ Amsterdam, Med Ctr, Dept Gastroenterol & Hepatol, Amsterdam UMC,AG&M Res Inst, Amsterdam, Netherlands.
[Ansari, Azhar] Easy Surrey Hosp, Surrey & Sussex NHS, Dept Gastroenterol, Surrey, England.
[Peters, Godefridus J.] Vrije Univ Amsterdam, Med Ctr, Amsterdam UMC, Lab Med Oncol,Canc Ctr Amsterdam, Amsterdam, Netherlands.
[Peters, Godefridus J.] Med Univ Gdansk, Dept Biochem, Gdansk, Poland.
C3 University of Amsterdam; Vrije Universiteit Amsterdam; University of
Amsterdam; Vrije Universiteit Amsterdam; Vrije Universiteit Amsterdam;
University of Amsterdam; Fahrenheit Universities; Medical University
Gdansk
RP Bayoumy, AB (corresponding author), Vrije Univ Amsterdam, Amsterdam UMC, Dept Gastroenterol & Hepatol, Boelelaan 1118, NL-1081 HZ Amsterdam, Netherlands.
EM a.b.bayoumy@amsterdamumc.nl
RI Bayoumy, Ahmed/HLG-2626-2023; Kluin-Nelemans, Johanna/F-8658-2018; de
Boer, Nanne/AAE-8731-2022; Peters, Godefridus J/C-7562-2013
OI de Boer, Nanne/0000-0001-8357-9887; Bayoumy, Ahmed
Bayoumy/0000-0002-5302-9312; Peters, Godefridus J/0000-0002-5447-2877
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NR 125
TC 37
Z9 37
U1 0
U2 8
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1742-5255
EI 1744-7607
J9 EXPERT OPIN DRUG MET
JI Expert Opin. Drug Metab. Toxicol.
PD FEB 1
PY 2020
VL 16
IS 2
BP 111
EP 123
DI 10.1080/17425255.2020.1719996
PG 13
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA KP7XI
UT WOS:000516444800004
PM 32090622
OA hybrid
DA 2025-01-07
ER
PT J
AU Abdollahi, E
Momtazi, AA
Johnston, TP
Sahebkar, A
AF Abdollahi, Elham
Momtazi, Amir Abbas
Johnston, Thomas P.
Sahebkar, Amirhossein
TI Therapeutic effects of curcumin in inflammatory and immune-mediated
diseases: A nature-made jack-of-all-trades?
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Review
DE autoimmune disease; curcumin; immune system; inflammation
ID NF-KAPPA-B; NITRIC-OXIDE SYNTHASE; REGULATORY T-CELLS;
NECROSIS-FACTOR-ALPHA; ACID-INDUCED COLITIS; FATTY LIVER-DISEASE;
BREAST-CANCER CELLS; GENE-EXPRESSION; DOUBLE-BLIND; DENDRITIC CELLS
AB Curcumin is a dietary polyphenol from turmeric with numerous pharmacological activities. Novel animal and human studies indicate that curcumin can affect different immune cells, such as various T lymphocyte subsets, macrophages, dendritic cells, B lymphocytes and natural killer cells, which results in decreasing severity of various diseases with immunological etiology. The present review provides a comprehensive overview of the effects of curcumin on different immune cells and immune system-related diseases.
C1 [Abdollahi, Elham; Sahebkar, Amirhossein] Mashhad Univ Med Sci, Sch Med, Dept Med Immunol, POB 91779-48564, Mashhad, Iran.
[Abdollahi, Elham] Mashhad Univ Med Sci, Student Res Comm, Mashhad, Iran.
[Momtazi, Amir Abbas] Mashhad Univ Med Sci, Sch Med, Dept Med Biotechnol, Student Res Comm,Nanotechnol Res Ctr, Mashhad, Iran.
[Johnston, Thomas P.] Univ Missouri, Sch Pharm, Div Pharmaceut Sci, Kansas City, MO 64110 USA.
[Sahebkar, Amirhossein] Mashhad Univ Med Sci, Biotechnol Res Ctr, Mashhad, Iran.
[Sahebkar, Amirhossein] Mashhad Univ Med Sci, Neurogen Inflammat Res Ctr, Mashhad, Iran.
C3 Mashhad University of Medical Sciences; Mashhad University of Medical
Sciences; Mashhad University of Medical Sciences; University of Missouri
System; University of Missouri Kansas City; Mashhad University of
Medical Sciences; Mashhad University of Medical Sciences
RP Sahebkar, A (corresponding author), Mashhad Univ Med Sci, Sch Med, Dept Med Immunol, POB 91779-48564, Mashhad, Iran.
EM sahebkara@mums.ac.ir
RI Sahebkar, Amirhossein/B-5124-2018; Momtazi-Borojeni, Amir/AAC-6972-2019;
Abdollahi, Elham/AAA-2731-2020
OI Momtazi-Borojeni, Amir Abaas/0000-0002-4376-1083; Abdollahi,
Elham/0000-0002-8176-3557
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NR 189
TC 187
Z9 198
U1 5
U2 134
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD FEB
PY 2018
VL 233
IS 2
BP 830
EP 848
DI 10.1002/jcp.25778
PG 19
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA FL9RB
UT WOS:000414593500012
PM 28059453
OA Bronze
DA 2025-01-07
ER
PT J
AU Wacker, M
Holick, MF
AF Wacker, Matthias
Holick, Michael F.
TI Vitamin D-Effects on Skeletal and Extraskeletal Health and the Need for
Supplementation
SO NUTRIENTS
LA English
DT Review
DE vitamin D; 25-hydroxyvitamin D; vitamin D deficiency; osteoporosis;
fractures; cancer; type 2 diabetes mellitus; cardiovascular diseases;
autoimmune diseases; infectious diseases
ID SERUM 25-HYDROXYVITAMIN D; RESPIRATORY-TRACT INFECTION; D-RECEPTOR
POLYMORPHISMS; COD-LIVER OIL; D DEFICIENCY; CALCIUM SUPPLEMENTATION;
RHEUMATOID-ARTHRITIS; HYPOVITAMINOSIS-D; DOUBLE-BLIND;
1,25-DIHYDROXYVITAMIN-D3 RECEPTORS
AB Vitamin D, the sunshine vitamin, has received a lot of attention recently as a result of a meteoric rise in the number of publications showing that vitamin D plays a crucial role in a plethora of physiological functions and associating vitamin D deficiency with many acute and chronic illnesses including disorders of calcium metabolism, autoimmune diseases, some cancers, type 2 diabetes mellitus, cardiovascular disease and infectious diseases. Vitamin D deficiency is now recognized as a global pandemic. The major cause for vitamin D deficiency is the lack of appreciation that sun exposure has been and continues to be the major source of vitamin D for children and adults of all ages. Vitamin D plays a crucial role in the development and maintenance of a healthy skeleton throughout life. There remains some controversy regarding what blood level of 25-hydroxyvitamin D should be attained for both bone health and reducing risk for vitamin D deficiency associated acute and chronic diseases and how much vitamin D should be supplemented.
C1 [Wacker, Matthias; Holick, Michael F.] Boston Univ, Med Ctr, Vitamin Skin & Bone Res Lab D, Sect Endocrinol Nutr & Diabet,Dept Med, Boston, MA 02118 USA.
C3 Boston University
RP Holick, MF (corresponding author), Boston Univ, Med Ctr, Vitamin Skin & Bone Res Lab D, Sect Endocrinol Nutr & Diabet,Dept Med, 85 E Newton St,M-1013, Boston, MA 02118 USA.
EM mwacker@bu.edu; mfholick@bu.edu
RI Holick, Michael/AFG-9586-2022
OI Holick, Michael/0000-0001-6023-9062
FU UV Foundation (San Jose, CA, USA); Mushroom Council (McLean, VA, USA)
FX This work was supported in part by the UV Foundation (2880 Zanker Road,
Suite 203, San Jose, CA 95134, USA) and the Mushroom Council (6620
Fletcher Lane, McLean, VA, USA).
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NR 243
TC 459
Z9 537
U1 1
U2 196
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD JAN
PY 2013
VL 5
IS 1
BP 111
EP 148
DI 10.3390/nu5010111
PG 38
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA 077KN
UT WOS:000314026700008
PM 23306192
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Vásquez-Garzón, VR
Ramírez-Cosmes, A
Reyes-Jiménez, E
Carrasco-Torres, G
Hernández-García, S
Aguilar-Ruiz, SR
Torres-Aguilar, H
Alpuche, J
Mayoral, LPC
Pina-Canseco, S
Arellanes-Robledo, J
Villa-Treviño, S
Baltiérrez-Hoyos, R
AF Vasquez-Garzon, V. R.
Ramirez-Cosmes, A.
Reyes-Jimenez, E.
Carrasco-Torres, G.
Hernandez-Garcia, S.
Aguilar-Ruiz, S. R.
Torres-Aguilar, H.
Alpuche, J.
Mayoral, L. Perez-Campos
Pina-Canseco, S.
Arellanes-Robledo, J.
Villa-Trevino, S.
Baltierrez-Hoyos, R.
TI Liver damage in bleomycin-induced pulmonary fibrosis in mice
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Article
DE Liver damage; Bleomycin; Multiorgan disease; Reactive oxygen species;
Proliferation
ID SYSTEMIC-SCLEROSIS; OXIDATIVE STRESS; MOLECULAR-MECHANISMS;
ANIMAL-MODEL; LUNG; SCLERODERMA; CELLS; ELECTROCHEMOTHERAPY;
REGENERATION; HYDROLASE
AB Pulmonary fibrosis is an emerging disease with a poor prognosis and high mortality rate that is even surpassing some types of cancer. This disease has been linked to the concomitant appearance of liver cirrhosis. Bleomycin-induced pulmonary fibrosis is a widely used mouse model that mimics the histopathological and biochemical features of human systemic sclerosis, an autoimmune disease that is associated with inflammation and expressed in several corporal systems as fibrosis or other alterations. To determine the effects on proliferation, redox and inflammation protein expression markers were analyzed by immunohistochemistry. Analyses showed a significant increase in protein oxidation levels by lipoperoxidation bio-products and in proliferation and inflammation processes. These phenomena were associated with the induction of the redox status in mice subjected to 100 U/kg bleomycin. These findings clearly show that the bleomycin model induces histopathological alterations in the liver and partially reproduces the complexity of systemic sclerosis. Our results using the bleomycin-induced pulmonary fibrosis model provide a protocol to investigate the mechanism underlying the molecular alteration found in the liver linked to systemic sclerosis.
C1 [Vasquez-Garzon, V. R.; Alpuche, J.; Baltierrez-Hoyos, R.] Univ Autonoma Benito Juarez Oaxaca, Fac Med & Cirugia, CONACYT, Oaxaca, Oax, Mexico.
[Ramirez-Cosmes, A.; Reyes-Jimenez, E.; Aguilar-Ruiz, S. R.] Univ Autonoma Benito Juarez Oaxaca, Fac Med & Cirugia, Oaxaca, Oax, Mexico.
[Carrasco-Torres, G.] CINVESTAV, Programa Nanociencias & Nanotecnol, Mexico City, DF, Mexico.
[Hernandez-Garcia, S.; Villa-Trevino, S.] CINVESTAV, Dept Biol Celular, Mexico City, DF, Mexico.
[Torres-Aguilar, H.] Univ Autonoma Benito Juarez Oaxaca, Fac Ciencias Quim, Oaxaca, Oax, Mexico.
[Mayoral, L. Perez-Campos; Pina-Canseco, S.] UNAM, UABJO, Fac Med, Ctr Invest, Oaxaca, Oax, Mexico.
[Arellanes-Robledo, J.] Inst Nacl Med Genom, CONACYT, Mexico City, DF, Mexico.
C3 Universidad Autonoma Benito Juarez de Oaxaca; Universidad Autonoma
Benito Juarez de Oaxaca; CINVESTAV - Centro de Investigacion y de
Estudios Avanzados del Instituto Politecnico Nacional; CINVESTAV -
Centro de Investigacion y de Estudios Avanzados del Instituto
Politecnico Nacional; Universidad Autonoma Benito Juarez de Oaxaca;
Universidad Nacional Autonoma de Mexico; Universidad Autonoma Benito
Juarez de Oaxaca; Instituto Nacional de Medicina Genomica
RP Baltiérrez-Hoyos, R (corresponding author), Univ Autonoma Benito Juarez Oaxaca, Fac Med & Cirugia, CONACYT, Oaxaca, Oax, Mexico.
EM rbaltierrez@hotmail.com
RI VILLA, SAUL/AAU-3346-2020; Baltierrez-Hoyos, Rafael/G-8884-2019;
Torres-Aguilar, HonorioTorresAguilar/AAF-8405-2020; Alpuche,
Juan/IYS-3565-2023; CARRASCO TORRES, GABRIELA/IWM-2710-2023; Ruiz,
Sergio/AAH-2741-2020; Vásquez-Garzón, Verónica/T-9939-2019; Perez-Campos
Mayoral, Laura/G-2014-2018; Arellanes-Robledo, Jaime/P-3926-2017
OI Alpuche, Juan/0000-0002-8532-6717; Villa-Trevino,
Saul/0000-0002-8292-8157; Perez-Campos Mayoral,
Laura/0000-0003-4140-4661; Reyes-Jimenez, Edilburga/0000-0001-9077-2159;
Torres-Aguilar, Honorio/0000-0003-2853-4891; Arellanes-Robledo,
Jaime/0000-0001-7363-4870; Aguilar Ruiz, Sergio
Roberto/0000-0002-2412-0360; BALTIERREZ HOYOS,
RAFAEL/0000-0003-3416-6917; /0000-0002-9486-5093
FU Consejo Nacional de Ciencia y Tecnologia (CONACYT) [270189-2016, 178558,
287162, 290194]; Catedra-CONACYT [2499-2014]
FX The authors want to express their gratitude to the UPEAL-CINVESTAV staff
and American Journal Experts (AJE). This work was supported by the
Consejo Nacional de Ciencia y Tecnologia (CONACYT), 270189-2016; from
RBH, 178558 from SVT, 287162 from RBH, 290194 from VRVG, and
Catedra-CONACYT 2499-2014 (Molecular studies for the treatment of
scleroderma) from RBH, VRVG, and JA.
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NR 55
TC 6
Z9 8
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0028-1298
EI 1432-1912
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD DEC
PY 2019
VL 392
IS 12
BP 1503
EP 1513
DI 10.1007/s00210-019-01690-7
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JL8UB
UT WOS:000495801700003
PM 31312848
DA 2025-01-07
ER
PT J
AU Yang, XL
Jiang, S
Liu, YH
Zhang, P
Xie, SL
Wang, GY
AF Yang, Xueliang
Jiang, Shuang
Liu, Yahui
Zhang, Ping
Xie, Shuli
Wang, Guangyi
TI Recombinant VAA-I from Viscum album Induces Apoptotic Cell Death
of Hepatocellular Carcinoma SMMC7721 Cells
SO MOLECULES
LA English
DT Article
DE Viscum album; rVAA-I; apoptosis; phosphoinositide 3-kinase
ID GALACTOSIDE-SPECIFIC LECTIN; NECROSIS-FACTOR-ALPHA; FILAMIN-A;
INDUCTION; CASPASES; CYTOTOXICITY; ACTIVATION
AB Researchers have proposed that VAA-I, a specific plant lectin found in Viscum album, has therapeutic effects on cancer and autoimmune diseases. VAA-I has shown some promising treatment results in some types of tumor cell lines, especially SMMC-7721 cells (human hepatocellular carcinoma cells). However, few details are known about the mechanism and process of cell death induced by VAA-I in tumor cells. In this study, the cell morphology results showed that SMMC-7721 cells treated with VAA-I exhibited several features typical of apoptotic cell death, which was confirmed by the Caspase inhibition assay. Fluo-3-acetoxymethyl ester (AM) fluorescence imaging techniques showed that rVAA-I significantly elevated the intracellular calcium level ([Ca2+](i)) in SMMC-7721 cells. These findings suggest that apoptosis may play the most important role in SMMC-7721 cell death induced by rVAA-I. Finally, in the SMMC-7721 cells treated with rVAA-I, a series of genes in the p38 mitogen-activated protein kinase (MAPK) signaling pathway were expressed differentially, and further found that PI 3-kinase pathway is involved in rVAA-I signal transduction in SMMC-7721 cells.
C1 [Yang, Xueliang; Liu, Yahui; Zhang, Ping; Xie, Shuli; Wang, Guangyi] Jilin Univ, Dept Hepatobiliary & Pancreat Surg, Clin Hosp 1, Changchun 130021, Peoples R China.
[Yang, Xueliang] Beihua Univ, Dept Gen Surg, Affiliated Hosp, Jilin 132000, Peoples R China.
[Jiang, Shuang] Beihua Univ, Coll Pharm, Jilin 132013, Peoples R China.
C3 Jilin University; Beihua University; Beihua University
RP Wang, GY (corresponding author), Jilin Univ, Dept Hepatobiliary & Pancreat Surg, Clin Hosp 1, Changchun 130021, Peoples R China.
EM ibiocc0431@gmail.com
RI li, Yaojie/JDD-5749-2023
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NR 22
TC 10
Z9 10
U1 0
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1420-3049
J9 MOLECULES
JI Molecules
PD OCT
PY 2012
VL 17
IS 10
BP 11435
EP 11446
DI 10.3390/molecules171011435
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 029OO
UT WOS:000310505400010
PM 23014500
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Ferre-Aracil, C
Riveiro-Barciela, M
Trapero-Marugán, M
Rodríguez-Perálvarez, M
Llovet, LP
Téllez, L
Sánchez-Torrijos, Y
Díaz-Fontenla, F
Salcedo-Plaza, M
Alvarez-López, P
de la Mata, M
Londoño, MC
Bañares-Cañizares, R
Calleja, JL
AF Ferre-Aracil, Carlos
Riveiro-Barciela, Mar
Trapero-Marugan, Maria
Rodriguez-Peralvarez, Manuel
Llovet, Laura-Patricia
Tellez, Luis
Sanchez-Torrijos, Yolanda
Diaz-Fontenla, Fernando
Salcedo-Plaza, Magdalena
Alvarez-Lopez, Patricia
de la Mata, Manuel
Londono, Maria-Carlota
Banares-Canizares, Rafael
Luis Calleja, Jose
TI Tacrolimus as an Effective and Durable Second-Line Treatment for Chronic
Autoimmune Hepatitis: A Multicentric Study
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Autoimmune hepatitis; Tacrolimus; Therapy
ID MYCOPHENOLATE-MOFETIL; EFFICACY; THERAPY
AB Background Autoimmune hepatitis (AIH) is a chronic liver disease able to progress to acute liver failure, cirrhosis, and liver cancer. A significant proportion of patients fail to first-line therapy or develop severe toxicity. Aims To assess safety and effectiveness of tacrolimus as a second-line therapy in AIH patients. Methods Multicentric retrospective study of AIH patients treated with tacrolimus for at least 3 months as a second-line therapy. Effectiveness was defined as complete normalization of transaminases and IgG. Results A total of 23 AIH patients were included in the final analysis. In 13% of patients tacrolimus was initiated because of toxicity to previous first-line treatments and the rest were switched because of previous non-efficacy. Tacrolimus was effective in 18 patients (78%; 95%CI: 55.20-91.92%). The median time receiving tacrolimus was 16 months (IQR 20). There was a sustained response with a significant improvement in all liver enzymes and IgG on last follow-up. Only one patient discontinued tacrolimus at the third month because of severe neuropathy, and ototoxicity. Responders were significantly older at diagnosis of AIH (41 +/- 13vs.27 +/- 10 years old;p = 0.0496). Conclusion Tacrolimus is effective and well tolerated as a second-line therapy in patients with AIH.
C1 [Ferre-Aracil, Carlos; Trapero-Marugan, Maria; Luis Calleja, Jose] Hosp Univ Puerta de Hierro Majadahonda, Gastroenterol & Hepatol Unit, Joaquin Rodrigo 1, Madrid 28888, Spain.
[Riveiro-Barciela, Mar; Alvarez-Lopez, Patricia] Hosp Univ Vall dHebron, Hepatol Internal Med Unit, Barcelona, Spain.
[Rodriguez-Peralvarez, Manuel; de la Mata, Manuel] Hosp Univ Reina Sofia, IMBIC, CIBERehd, Hepatol & Liver Transplantat Unit, Cordoba, Spain.
[Llovet, Laura-Patricia; Londono, Maria-Carlota] Hosp Clin Barcelona, Liver Unit, CIBERehd, IDIBAPS, Barcelona, Spain.
[Tellez, Luis] Univ Alcala, Gastroenterol & Hepatol Unit, Hosp Univ Ramon y Cajal, IRYCIS,CIBERehd, Madrid, Spain.
[Sanchez-Torrijos, Yolanda] Hosp Univ Virgen del Rocio, UGC Aparato Digest, Seville, Spain.
[Diaz-Fontenla, Fernando; Salcedo-Plaza, Magdalena; Banares-Canizares, Rafael] Hosp Univ Gregorio Maranon, Gastroenterol & Hepatol Unit, Madrid, Spain.
[Riveiro-Barciela, Mar] CIBERehd, Barcelona, Spain.
C3 Hospital Puerta de Hierro-Majadahonda; Hospital Universitari Vall
d'Hebron; CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD;
University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; CIBER -
Centro de Investigacion Biomedica en Red; CIBEREHD; Universidad de
Alcala; CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD;
Hospital Universitario Ramon y Cajal; Virgen del Rocio University
Hospital; General University Gregorio Maranon Hospital; CIBER - Centro
de Investigacion Biomedica en Red; CIBEREHD
RP Ferre-Aracil, C (corresponding author), Hosp Univ Puerta de Hierro Majadahonda, Gastroenterol & Hepatol Unit, Joaquin Rodrigo 1, Madrid 28888, Spain.
EM c_ferre_a@hotmail.com
RI Londono, Maria/KMA-4581-2024; López, Patricia/AAG-1921-2021;
Rodríguez-Perálvarez, Manuel/AAO-8616-2021; Panero, Jose/A-5351-2010;
Banares, Rafael/J-1460-2012; Téllez, Luis/AAF-7220-2021
OI Rodriguez-peralvarez, Manuel/0000-0002-1795-2919; Tellez,
Luis/0000-0002-9254-3891; Banares, Rafael/0000-0002-0412-8437; Ferre
Aracil, Carlos/0000-0002-5547-2801; Londono,
Maria-Carlota/0000-0002-6533-1586; Diaz Fontenla,
Fernando/0000-0002-4700-0281; Riveiro-Barciela, Mar/0000-0001-9309-2052
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NR 19
TC 6
Z9 6
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD AUG
PY 2021
VL 66
IS 8
BP 2826
EP 2832
DI 10.1007/s10620-020-06569-9
EA AUG 2020
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA TR0YK
UT WOS:000564285100001
PM 32860579
DA 2025-01-07
ER
PT J
AU Chen, K
Shao, LH
Wang, F
Shen, XF
Xia, XF
Kang, X
Song, P
Wang, M
Lu, XF
Wang, C
Hu, QY
Liu, S
Guan, WX
AF Chen, Kai
Shao, Li-Hua
Wang, Feng
Shen, Xiao-Fei
Xia, Xue-Feng
Kang, Xing
Song, Peng
Wang, Meng
Lu, Xiao-Feng
Wang, Chao
Hu, Qiong-Yuan
Liu, Song
Guan, Wen-Xian
TI Netting Gut Disease: Neutrophil Extracellular Trap in Intestinal
Pathology
SO OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
LA English
DT Review
ID CIRCULATING TUMOR-CELLS; PROCOAGULANT ACTIVITY; DNA TRAPS; IN-VITRO;
CANCER; LIVER; PLATELETS; RELEASE; METASTASIS; CONTRIBUTE
AB Many gut disease etiologies are attributed to the presence of robust inflammatory cell recruitment. The recruitment of neutrophils plays a vital role in inflammatory infiltration. Neutrophils have various antimicrobial effector mechanisms, including phagocytosis, oxidative burst, and degranulation. It is suggested that neutrophils could release neutrophil extracellular traps (NETs) to kill pathogens. However, recent evidence indicates that neutrophil infiltration within the gut is associated with disrupted local immunological microenvironment and impaired epithelial barrier. Growing evidence implies that NETs are involved in the progression of many diseases, including cancer, diabetes, thrombosis, and autoimmune disease. Increased NET formation was found in acute or chronic conditions, including infection, sterile inflammation, cancer, and ischemia/reperfusion injury (IRI). Here, we present a comprehensive review of recent advances in the understanding of NETs, focusing on their effects in gut disease. We also discuss NETs as a potential therapeutic target in gut disease.
C1 [Chen, Kai; Shao, Li-Hua; Wang, Feng; Shen, Xiao-Fei; Xia, Xue-Feng; Kang, Xing; Song, Peng; Wang, Meng; Lu, Xiao-Feng; Wang, Chao; Hu, Qiong-Yuan; Liu, Song; Guan, Wen-Xian] Nanjing Univ, Dept Gastrointestinal Surg, Med Sch, Affiliated Hosp,Nanjing Drum Tower Hosp, Nanjing, Peoples R China.
[Chen, Kai; Hu, Qiong-Yuan] Nanjing Univ, Med Sch, Nanjing, Peoples R China.
C3 Nanjing University; Nanjing University
RP Hu, QY; Liu, S; Guan, WX (corresponding author), Nanjing Univ, Dept Gastrointestinal Surg, Med Sch, Affiliated Hosp,Nanjing Drum Tower Hosp, Nanjing, Peoples R China.; Hu, QY (corresponding author), Nanjing Univ, Med Sch, Nanjing, Peoples R China.
EM qiongyuan_hu@foxmail.com; medical.lis@gmail.com; guan_wenxian@sina.com
RI Liu, Song/GMW-4362-2022; Shen, Xiaofei/HDL-7300-2022
FU National Natural Science Foundation of China [81602103, 82102294]
FX This work was supported by grants from the National Natural Science
Foundation of China (81602103 (to S.L.) and 82102294 (to Q. -Y. H.)).
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NR 101
TC 16
Z9 18
U1 2
U2 10
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1942-0900
EI 1942-0994
J9 OXID MED CELL LONGEV
JI Oxidative Med. Cell. Longev.
PD OCT 19
PY 2021
VL 2021
AR 5541222
DI 10.1155/2021/5541222
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 1Y7YR
UT WOS:000808356200004
PM 34712384
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Moss, P
Berenbaum, F
Curigliano, G
Grupper, A
Berg, T
Pather, S
AF Moss, Paul
Berenbaum, Francis
Curigliano, Giuseppe
Grupper, Ayelet
Berg, Thomas
Pather, Shanti
TI Benefit-risk evaluation of COVID-19 vaccination in special population
groups of interest
SO VACCINE
LA English
DT Review
DE COVID-19; Oncology; Kidney disease; Liver disease; Immunocompromised;
Vaccination; Special populations
ID BNT162B2 MESSENGER-RNA; TRANSPLANT RECIPIENTS; LIVER-TRANSPLANTATION;
SARS-COV-2; VACCINES; IMMUNOGENICITY; SAFETY; EFFICACY; CANCER;
INFECTION
AB Several population groups display an increased risk of severe disease and mortality following SARS-CoV-2 infection. These include those who are immunocompromised (IC), have a cancer diagnosis, human immunodeficiency virus (HIV) infection or chronic inflammatory disease including autoimmune disease, primary immunodeficiencies, and those with kidney or liver disease. As such, improved understanding of the course of COVID-19 disease, as well as the efficacy, safety, and benefit-risk profiles of COVID-19 vac-cines in these vulnerable groups is paramount in order to inform health policy makers and identify evidence-based vaccination strategies. In this review, we seek to summarize current data, including rec-ommendations by national health authorities, on the impact and benefit-risk profiles of COVID-19 vacci-nation in these populations. Moving forward, although significant efforts have been made to elucidate and characterize COVID-19 disease course and vaccine responses in these groups, further larger-scale and longer-term evaluation will be instrumental to help further guide management and vaccination strategies, particularly given concerns about waning of vaccine-induced immunity and the recent surge of transmission with SARS-CoV-2 variants of concern. (c) 2022 Elsevier Ltd. All rights reserved.
C1 [Moss, Paul] Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham B15 2TT, W Midlands, England.
[Moss, Paul] Univ Hosp Birmingham, Queen Elizabeth Hosp, Birmingham B15 2TH, W Midlands, England.
[Berenbaum, Francis] Sorbonne Univ, St Antoine Hosp, AP HP, INSERM, Paris, France.
[Curigliano, Giuseppe] IRCCS, Ist Europeo Oncol, Milan, Italy.
[Curigliano, Giuseppe] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
[Grupper, Ayelet] Tel Aviv Univ, Sackler Fac Med, Tel Aviv Sourasky Med Ctr, Dept Nephrol, Tel Aviv, Israel.
[Berg, Thomas] Univ Leipzig, Dept Med 2, Div Hepatol, Med Ctr, D-04103 Leipzig, Germany.
[Pather, Shanti] BioNTech SE, Mainz, Germany.
C3 University of Birmingham; University of Birmingham; Institut National de
la Sante et de la Recherche Medicale (Inserm); Assistance Publique
Hopitaux Paris (APHP); Sorbonne Universite; Hopital Universitaire
Saint-Antoine - APHP; IRCCS European Institute of Oncology (IEO);
University of Milan; Tel Aviv University; Tel Aviv Sourasky Medical
Center; Leipzig University; BioNTech SE
RP Pather, S (corresponding author), BioNTech SE, Mainz, Germany.
EM shanti.pather@biontech.de
RI Berenbaum, Francis/AAO-5690-2020; Curigliano, Giuseppe/D-3371-2018;
Moss, Paul/D-1728-2009
OI Grupper, Ayelet/0000-0002-5590-9428; Moss, Paul/0000-0002-6895-1967
FU BioNTech SE; COVID [MC_PC_20060] Funding Source: UKRI
FX Medical writing support, including assisting authors with the
development of the outline and initial draft and incorporation comments
was provided by Prime Global, and Camilla West, PhD, from BioNTech SE,
according to Good Publication Practice guidelines. BioNTech SE provided
funding to Prime Global for the development of the initial outline and
literature search.
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NR 161
TC 8
Z9 8
U1 0
U2 3
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD JUL 30
PY 2022
VL 40
IS 32
BP 4348
EP 4360
DI 10.1016/j.vaccine.2022.05.067
EA JUL 2022
PG 13
WC Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Research & Experimental Medicine
GA 3S4UV
UT WOS:000839593900013
PM 35718592
OA Green Published
DA 2025-01-07
ER
PT J
AU Guo, T
Qian, JM
Zhu, LM
Zhou, WX
Zhu, F
Sun, G
Fang, XC
AF Guo, Tao
Qian, Jiaming
Zhu, Liming
Zhou, Weixun
Zhu, Feng
Sun, Gang
Fang, Xiucai
TI Clinical Analysis of 15 Cases of Liver Nodular Regenerative Hyperplasia
SO CELL BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Article
DE Nodular regenerative hyperplasia; Non-cirrhotic intrahepatic portal
hypertension; Idiopathic portal hypertension; Splenomegaly;
Hypersplenism; Esophageal varices
ID NONCIRRHOTIC PORTAL-HYPERTENSION; HEPATOCELLULAR-CARCINOMA;
LUPUS-ERYTHEMATOSUS; DISORDERS; FEATURES; AUTOPSY; SERIES
AB Nodular regenerative hyperplasia (NRH) of liver may be one of the leading causes of non-cirrhotic intrahepatic portal hypertension (NCIPH), although the exact relationship is currently unknown. Diagnosis of NRH is relatively difficult and involves surgical pathology, and thus it is necessary to improve the preoperative recognition of NRH. Here, we analyze 15 cases of NRH to better understand this disease. All the liver specimens were microscopically examined by hematoxylin-eosin staining and reticulin and Masson trichrome staining. Diagnoses of NRH were confirmed by pathological examination. Clinically, NRH presents as diffused liver lesions with mildly increased liver enzymes. Portal hypertension is the most common clinical manifestation presenting prominently as splenomegaly, hypersplenism, and esophageal varices bleeding. NRH is often associated with autoimmune or collagen vascular diseases, and such patients often present with a variety of positive autoantibodies and increased erythrocyte sedimentation rate (ESR), Ig and gamma %. Pathological examination of the liver showed diffuse small regenerative nodules without fibrous septa and obstructive portal venopathy. For those patients with portal hypertension of unknown cause and preserved liver function, especially, those combined with autoimmune diseases, NRH should be considered.
C1 [Guo, Tao; Qian, Jiaming; Zhu, Liming; Zhu, Feng; Sun, Gang; Fang, Xiucai] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gastroenterol, Peking Union Med Coll, Beijing 100730, Peoples R China.
[Zhou, Weixun] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Pathol, Beijing 100730, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Peking Union Medical College; Peking Union Medical College Hospital;
Chinese Academy of Medical Sciences - Peking Union Medical College;
Peking Union Medical College Hospital
RP Qian, JM (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gastroenterol, Peking Union Med Coll, Beijing 100730, Peoples R China.
EM qjiaming57@gmail.com
RI Zhu, Li/GWV-0143-2022; guo, tao/HGE-4503-2022
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NR 25
TC 9
Z9 10
U1 0
U2 3
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1085-9195
J9 CELL BIOCHEM BIOPHYS
JI Cell Biochem. Biophys.
PD NOV
PY 2012
VL 64
IS 2
BP 115
EP 121
DI 10.1007/s12013-012-9379-5
PG 7
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 021DM
UT WOS:000309865500008
PM 22707296
DA 2025-01-07
ER
PT J
AU Romo, EM
Muñoz-Robles, JA
Castillo-Rama, M
Meneu, JC
Moreno-Elola, A
Pérez-Saborido, B
Mancebo, E
Calleja-Antolín, SM
Bernardo, I
Allende, LM
Paz-Artal, E
AF Romo, Eva M.
Munoz-Robles, Jorge A.
Castillo-Rama, Mareela
Meneu, Juan C.
Moreno-Elola, Almudena
Perez-Saborido, Baltasar
Mancebo, Esther
Calleja-Antolin, Sara M.
Bernardo, Ivan
Allende, Luis M.
Paz-Artal, Estela
TI Peripheral blood lymphocyte populations in end-stage liver diseases
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE lymphocyte subpopulations; viral hepatitis; alcoholic cirrhosis;
hepatocellular carcinoma; autoimmune liver diseases
ID HEPATITIS-B-VIRUS; T-CELLS; MONONUCLEAR-CELLS; IMMUNE-SYSTEM;
ACTIVATION; ETHANOL; HCV; INFECTION
AB Goals/Background: The aim of this study was to decipher whether end-stage liver failure modifies peripheral blood lymphocytes (PBL) in a homogeneous manner, independently of the base pathology, or, if on the contrary, PBL subsets show a different profile in each hepatic disease.
Methods: We studied PBL subsets in 71 patients with end-stage liver disease, before liver transplant, and 74 healthy controls by flow cytometry. The results were statistically compared between patients and controls, and cohorts of patients classified according to their base pathology.
Results: We observed lower absolute numbers in all lymphocyte populations in patients compared with controls. We found an increment of CD3 + activated cells (p < 10(-5)) and CD45RO + CD4 + (p < 10(-5)) in chronic hepatitis C virus versus controls; hepatitis B virus showed high TCR gamma delta+ and CD8 + T cells with respect to controls (P = 0.008 and P = 0.029, respectively); alcoholic cirrhotic patients showed low CD8 +, mainly CD45RA + CD8 + (P = 0.007) and high CD45RO + CD4 + (p < 10(-5)) compared with the normal population; autoimmune diseases showed lower CD3 + and TCR alpha beta + (P = 0.002 and P = 0.0001) than controls.
Conclusions: Regardless of the base pathology, patients with end-stage liver disease show a low absolute number of lymphocyte populations compared with controls. However, PBL profiles are different, characteristic, and specific of every disease causing chronic liver failure.
C1 Hosp 12 Octubre, Serv Immunol, Dept Immunol, E-28041 Madrid, Spain.
Hosp 12 Octubre, Surg Dept Gen Digest & Abdominal Organ Transplant, E-28041 Madrid, Spain.
C3 Hospital Universitario 12 de Octubre; Hospital Universitario 12 de
Octubre
RP Romo, EM (corresponding author), Hosp 12 Octubre, Serv Immunol, Dept Immunol, Avda Andalucia S-N, E-28041 Madrid, Spain.
EM eromop.hdoc@salud.madrid.org
RI Mancebo, Esther/KVB-9132-2024; Calleja, Sara/X-9928-2019
OI PEREZ-SABORIDO, BALTASAR/0000-0003-0842-1654; Mancebo,
Esther/0000-0002-1535-9062; , Marcela/0000-0003-2052-2773; Meneu-Diaz,
Juan Carlos/0000-0002-7853-4016; Paz-Artal, Estela/0000-0002-0646-2375;
Bernardo, Ivan/0000-0002-9452-0079; /0000-0001-9586-8539
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NR 36
TC 15
Z9 16
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD AUG
PY 2007
VL 41
IS 7
BP 713
EP 721
DI 10.1097/01.mcg.0000248000.42581.35
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 197IY
UT WOS:000248549400013
PM 17667057
DA 2025-01-07
ER
PT J
AU Li, CX
Peng, KX
Xiao, SQ
Long, YY
Yu, Q
AF Li, Congxin
Peng, Kaixin
Xiao, Siqi
Long, Yuanyuan
Yu, Qin
TI The role of Lactobacillus in inflammatory bowel disease: from
actualities to prospects
SO CELL DEATH DISCOVERY
LA English
DT Review
ID GUT MICROBIOTA; HEPATITIS-B; MOUSE MODEL; VITAMIN-D; T-CELLS;
EXPRESSION; COLITIS; BACTERIA; STRAINS; LIVER
AB Inflammatory Bowel Disease (IBD), a chronic nonspecific intestinal inflammatory disease, is comprised of Ulcerative Colitis (UC) and Crohn's Disease (CD). IBD is closely related to a systemic inflammatory reaction and affects the progression of many intestinal and extraintestinal diseases. As one of the representative bacteria for probiotic-assisted therapy in IBD, multiple strains of Lactobacillus have been proven to alleviate intestinal damage and strengthen the intestinal immunological barrier, epithelial cell barrier, and mucus barrier. Lactobacillus also spares no effort in the alleviation of IBD-related diseases such as Colitis-associated Colorectal cancer (CAC), Alzheimer's Disease (AD), Depression, Anxiety, Autoimmune Hepatitis (AIH), and so on via gut-brain axis and gut-liver axis. This article aims to discuss the role of Lactobacillus in IBD and IBD-related diseases, including its underlying mechanisms and related curative strategies from the present to the future.
C1 [Li, Congxin; Peng, Kaixin; Xiao, Siqi; Long, Yuanyuan; Yu, Qin] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Gastroenterol, Wuhan, Peoples R China.
[Li, Congxin; Peng, Kaixin; Xiao, Siqi; Long, Yuanyuan; Yu, Qin] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Inst Liver & Gastrointestinal Dis, Wuhan, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
Science & Technology
RP Yu, Q (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Gastroenterol, Wuhan, Peoples R China.; Yu, Q (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Inst Liver & Gastrointestinal Dis, Wuhan, Peoples R China.
EM yuqin@tjh.tjmu.edu.cn
OI Li, Congxin/0009-0000-1383-7852; Yu, Qin/0000-0002-4342-9398
FU National Natural Science Foundation of China [8197032978]
FX This work was supported by the [National Natural Science Foundation of
China],[8197032978].
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NR 108
TC 36
Z9 36
U1 12
U2 29
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PD SEP 29
PY 2023
VL 9
IS 1
AR 361
DI 10.1038/s41420-023-01666-w
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA U0SR8
UT WOS:001081997200001
PM 37773196
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Kuo, PC
Brown, DA
Scofield, BA
Yu, IC
Chang, FL
Wang, PY
Yen, JH
AF Kuo, Ping-Chang
Brown, Dennis A.
Scofield, Barbara A.
Yu, I-Chen
Chang, Fen-Lei
Wang, Pei-Yu
Yen, Jui-Hung
TI 3H-1,2-dithiole-3-thione as a novel therapeutic agent for the treatment
of experimental autoimmune encephalomyelitis
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE MS/EAE; D3T; Th1/Th17; Dendritic cells; Microglia
ID TRANSCRIPTION FACTOR NRF2; LIVER ISCHEMIA/REPERFUSION INJURY;
MULTIPLE-SCLEROSIS; HEME OXYGENASE-1; CANCER CHEMOPREVENTION;
ELECTROPHILIC STRESS; PHASE-2 ENZYMES; T-CELLS; KAPPA-B; GM-CSF
AB 3H-1,2-dithiole-3-thione (D3T), the simplest member of the sulfur-containing dithiolethiones, is found in cruciferous vegetables, and has been previously reported to be a potent inducer of antioxidant genes and glutathione biosynthesis by activation of the transcription factor Nrf2. D3T is a cancer chemopreventive agent and possesses anti-inflammatory properties. Although D3T has been shown to protect against neoplasia, the effect of D3T in the autoimmune inflammatory disease multiple sclerosis/experimental autoimmune encephalomyelitis (EAE) is unknown. The present study is the first report of the therapeutic effect of D3T in EAE. Our results show D3T, administered post immunization, not only delays disease onset but also dramatically reduces disease severity in EAE. Strikingly, D3T, administered post disease onset of EAE, effectively prevents disease progression and exacerbation. Mechanistic studies revealed that D3T suppresses dendritic cell activation and cytokine production, inhibits pathogenic Th1 and Th17 differentiation, represses microglia activation and inflammatory cytokine expression, and promotes microglia phase II enzyme induction. In summary, these results indicate that D3T affects both innate and adaptive immune cells, and the protective effect of D3T in EAE might be attributed to its effects on modulating dendritic cell and microglia activation and pathogenic Th1/Th17 cell differentiation. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Kuo, Ping-Chang; Scofield, Barbara A.; Yen, Jui-Hung] Indiana Univ Sch Med, Dept Microbiol & Immunol, Ft Wayne, IN 46805 USA.
[Brown, Dennis A.] Univ Manchester, Coll Pharm, Dept Pharmaceut Sci, Ft Wayne, IN USA.
[Yu, I-Chen] Indiana Univ Sch Med, Dept Anat & Cell Biol, Ft Wayne, IN USA.
[Chang, Fen-Lei] Indiana Univ Sch Med, Dept Neurol, Ft Wayne, IN USA.
[Wang, Pei-Yu] Natl Taiwan Univ, Coll Med, Grad Inst Brain & Mind Sci, Taipei, Taiwan.
C3 Purdue University System; Indiana University Purdue University Fort
Wayne; Purdue University System; Indiana University Purdue University
Fort Wayne; Purdue University System; Indiana University Purdue
University Fort Wayne; National Taiwan University
RP Yen, JH (corresponding author), Indiana Univ Sch Med, Dept Microbiol & Immunol, Ft Wayne, IN 46805 USA.
EM yenj@ipfw.edu
RI Yen, Jui-Hung/AAV-3455-2020; Kuo, Ping-Chang/AAR-8920-2021
OI Yen, Jui-Hung Jimmy/0000-0002-7325-9756; Yu, I-Chen/0000-0001-5270-9888;
WANG, PEI-YU/0000-0002-1792-8935
FU Anna Yoder MS fund; American Heart Association [12SDG8170005]; American
Heart Association (AHA) [12SDG8170005] Funding Source: American Heart
Association (AHA)
FX This work was supported by grants from Anna Yoder MS fund and American
Heart Association 12SDG8170005 to J-H. Yen.
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NR 41
TC 32
Z9 33
U1 0
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0889-1591
EI 1090-2139
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD OCT
PY 2016
VL 57
BP 173
EP 186
DI 10.1016/j.bbi.2016.03.015
PG 14
WC Immunology; Neurosciences; Psychiatry
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Neurosciences & Neurology; Psychiatry
GA DW0BP
UT WOS:000383306200020
PM 27013356
DA 2025-01-07
ER
PT J
AU Yu, Z
Nian, CN
Sun, WM
Liu, XH
Nian, XY
AF Yu, Zhi
Nian, Caina
Sun, Wenmei
Liu, Xinhua
Nian, Xueyuan
TI Elevated serum HE4 levels as a novel biomarker of disease severity and
hepatic fibrosis in autoimmune hepatitis
SO CLINICA CHIMICA ACTA
LA English
DT Article
DE Human epididymis protein 4; Autoimmune hepatitis; Hepatic fibrosis;
Cirrhosis
ID EPIDIDYMIS PROTEIN 4; TUMOR-MARKER; OVARIAN-CANCER; ANTIGEN 125;
DIAGNOSIS; MECHANISMS; GUIDELINES; MANAGEMENT; STIFFNESS
AB Background: Human epididymis protein 4 (HE4) has been identified as a biomarker for renal fibrosis. This study aimed to evaluate the role of HE4 in the diagnosis and determination of disease severity and hepatic fibrosis in autoimmune hepatitis (AIH). Methods: Serum HE4 levels were determined via electrochemiluminescence immunoassays in 60 healthy controls and 109 AIH patients (43 without liver cirrhosis and 66 with liver cirrhosis). Liver biopsy was performed on 56 of 109 enrolled patients. We conducted a 5-year follow-up survey of 53 enrolled patients. All continuous variables were reported as median (25th-75th percentile). Results: Serum HE4 levels were significantly elevated in autoimmune hepatitis with liver cirrhosis (AIH-LC) patients compared with AIH patients and healthy controls [98.60 (74.15-139.08) vs 73.50 (59.88-82.00) vs 48.75 (43.38-52.93) pmol/L, p = 0.004]. The serum HE4 levels showed a positive correlation with the METAVIR scoring system in patients with liver biopsy (r = 0.711, p < 0.001). Serum HE4 levels were significantly elevated in Child-Pugh class C patients compared with Child-Pugh class B patients and Child-Pugh class A patients [106.50 (83.46-151.25) vs 110.00 (73.83-166.75) vs 77.03 (72.35-83.33) pmol/L, p = 0.006]. The diagnostic sensitivity and specificity of serum HE4 for evaluating liver cirrhosis were 69.7 % and 79.07 %, respectively, with a cutoff value of 82.34 pmol/L in enrolled patients. The logistic regression analysis showed that high levels of HE4 (>= 82.34 pmol/L) were associated with AIH-LC (OR = 8.751, 95 % CI = 1.412-54.225, p = 0.020). The Kaplan-Meier curves demonstrated that high levels of serum HE4 (>= 82.34 pmol/L) were associated with poor outcome (log-rank p = 0.037, HR = 0.372, 95 % CI = 0.146-0.946). Conclusions: Serum HE4 levels were found to be elevated in AIH-LC patients and exhibited a strong correlation with the severity of hepatic fibrosis, thus supporting their potential clinical value as a novel biomarker of disease severity and hepatic fibrosis in AIH.
C1 [Yu, Zhi; Sun, Wenmei; Liu, Xinhua; Nian, Xueyuan] Med Coll Qingdao, Yantai Yuhuangding Hosp, Dept Gastroenterol, Yantai 264200, Shandong, Peoples R China.
[Nian, Caina] Yantai Municipal Laiyang Cent Hosp, Dept Intervent Therapy, Yantai 265200, Shandong, Peoples R China.
RP Liu, XH; Nian, XY (corresponding author), Med Coll Qingdao, Yantai Yuhuangding Hosp, Dept Gastroenterol, Yantai 264200, Shandong, Peoples R China.
EM liuxinhua_yhd@163.com; nianxueyuan12345@163.com
FU Science and Technology Program of Yantai City [2019YD026]
FX This work was supported by the Science and Technology Program of Yantai
City, Grant/Award Number: 2019YD026.
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NR 41
TC 1
Z9 1
U1 2
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0009-8981
EI 1873-3492
J9 CLIN CHIM ACTA
JI Clin. Chim. Acta
PD JUN 1
PY 2024
VL 559
AR 119682
DI 10.1016/j.cca.2024.119682
EA APR 2024
PG 8
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA SQ6K0
UT WOS:001235954100001
PM 38643819
OA hybrid
DA 2025-01-07
ER
PT J
AU Zheng, ZH
Huang, G
Gao, T
Huang, TY
Zou, MS
Zou, YH
Duan, SW
AF Zheng, Zhonghua
Huang, Gang
Gao, Tong
Huang, Tianyi
Zou, Mengsha
Zou, Yuhao
Duan, Shiwei
TI Epigenetic Changes Associated With Interleukin-10
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE DNA methylation; epigenetics; interleukin-10; immune inflammatory
disease; histone modification; microRNA; lncRNA
ID PERIPHERAL B-CELLS; BLOOD MONONUCLEAR-CELLS; DNA METHYLATION;
HEPATOCELLULAR-CARCINOMA; IL-10 EXPRESSION; T-CELLS; PROMOTER
POLYMORPHISM; GASTRIC-CANCER; BREAST-CANCER; GENE
AB IL-10 is a regulator of inflammation and immunosuppression. IL-10 regulates a variety of immune cells to limit and stop the inflammatory response, and thus plays an important role in autoimmune diseases, inflammatory diseases and cancer. IL-10 is closely related to epigenetic modification, in which changes in DNA methylation of IL-10 gene can affect mRNA and protein levels of IL-10. In addition, changes in histone modifications, especially histone acetylation, can also lead to abnormal expression of IL-10 mRNA. At the same time, a handful of IL-10 related microRNAs (miRNAs) are found to be aberrantly expressed in multiple diseases. Besides, long non-coding RNA (lncRNA) growth arrest specific transcript 5 (GAS5) also inhibits IL-10 expression. Here, we reviewed the epigenetic changes related to IL-10 in various diseases, as well as the regulation of IL-10 gene expression in various diseases by epigenetic modifications such as DNA methylation, histone modification, miRNA, and lncRNA.
C1 [Zheng, Zhonghua; Huang, Gang; Gao, Tong; Huang, Tianyi; Zou, Mengsha; Zou, Yuhao; Duan, Shiwei] Ningbo Univ, Sch Med, Ctr Med Genet, Ningbo, Peoples R China.
C3 Ningbo University
RP Duan, SW (corresponding author), Ningbo Univ, Sch Med, Ctr Med Genet, Ningbo, Peoples R China.
EM duanshiwei@nbu.edu.cn
RI Duan, Shiwei/AAA-4782-2022; Zou, Mengsha/GQR-2114-2022
OI Duan, Shiwei/0000-0001-7682-2877
FU K. C. Wong Magna Fund in Ningbo University
FX This research was supported by the grants from K. C. Wong Magna Fund in
Ningbo University.
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NR 79
TC 26
Z9 31
U1 3
U2 16
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUN 4
PY 2020
VL 11
AR 1105
DI 10.3389/fimmu.2020.01105
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA MC2YW
UT WOS:000543160000001
PM 32582189
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Carambia, A
Schuran, FA
AF Carambia, Antonella
Schuran, Fenja Amrei
TI The aryl hydrocarbon receptor in liver inflammation
SO SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Review
DE Aryl hydrocarbon receptor; AHR ligands; Hepatic immune response; Hepatic
tolerance; Liver inflammation; Therapy
ID PLAYS PROTECTIVE ROLES; REGULATORY T-CELLS; DIOXIN RECEPTOR;
HEPATIC-FIBROSIS; FATTY LIVER; INJURY; AHR; HEPATOCYTES; INDUCTION;
IMMUNITY
AB The aryl hydrocarbon receptor (AHR) is a ubiquitously expressed ligand-activated transcription factor with multifaceted physiological functions. In the immune system, AHR has been unequivocally identified as a key regulatory factor that can integrate environmental, dietary, or microbial signals into innate and adaptive immune responses. Correspondingly, AHR activity seems to be most important at barrier organs, such as the gut, skin, and lung. The liver is likewise prominently exposed to gut-derived dietary or microbial AHR ligands and, moreover, generates plenty of AHR ligands itself. Yet, surprisingly little is known about the role of AHR in the regulation of hepatic immune responses, which are normally biased towards tolerance, preventing harmful inflammation in response to innocuous stimuli. In this review, we summarize the current knowledge about the role of AHR in hepatic immune responses in the healthy liver as well as in inflammatory liver disease. Moreover, we discuss AHR as a potential therapeutic target in hepatic disorders, including autoimmune liver disease, liver fibrosis, and liver cancer.
C1 [Carambia, Antonella; Schuran, Fenja Amrei] Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Martinistr 52, D-20246 Hamburg, Germany.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf
RP Carambia, A (corresponding author), Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Martinistr 52, D-20246 Hamburg, Germany.
EM a.carambia@uke.de
FU Projekt DEAL; Deutsche Forschungsgemeinschaft - DFG [SFB841]
FX Open Access funding enabled and organized by Projekt DEAL. The authors
received funding from the Deutsche Forschungsgemeinschaft - DFG
(SFB841).
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NR 80
TC 27
Z9 30
U1 1
U2 30
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1863-2297
EI 1863-2300
J9 SEMIN IMMUNOPATHOL
JI Semin. Immunopathol.
PD AUG
PY 2021
VL 43
IS 4
SI SI
BP 563
EP 575
DI 10.1007/s00281-021-00867-8
EA JUN 2021
PG 13
WC Immunology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pathology
GA UQ6YR
UT WOS:000656795300001
PM 34075438
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Shaker, M
Mansour, N
John, BV
AF Shaker, Mina
Mansour, Natalie
John, Binu V.
TI Primary Biliary Cholangitis in Males Pathogenesis, Clinical
Presentation, and Prognosis
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Primary biliary cholangitis; Autoimmune hepatitis; Men; Epidemiology;
Clinical presentation; Prognosis
ID HEPATOCELLULAR-CARCINOMA; RISK-FACTORS; 1ST-DEGREE RELATIVES; INCREASED
PREVALENCE; FOLLOW-UP; CIRRHOSIS; EPIDEMIOLOGY; PBC; AUTOANTIBODIES;
SPECIFICITY
AB PBC remains a female predominant disease, but the disease is more prevalent in males than previously believed, with contemporary studies showing a 4-6:1 female-to-male ratio. Men present later in disease process, as evidenced by older age, higher bilirubin, lower platelet count, higher model for end-stage liver disease -Na, and lower UDCA exposure-time in several studies. Although males present at a more advanced stage of disease at diagnosis than females, male sex has been shown to be associated with a higher death or transplantation, or liver-related death or transplantation in PBC cirrhosis, even after adjusting for age, comorbidities, UDCA response, and the stage of disease.
A diagnosis of PBC is often delayed among males because of the myth that PBC is extremely rare in males. Greater research and education are needed to raise awareness, so that PBC is suspected and diagnosed at an earlier stage among males.
C1 [Shaker, Mina; Mansour, Natalie; John, Binu V.] Miami VA Med Ctr, Div Hepatol, 1201 NW 16th St, Miami, FL 33125 USA.
[John, Binu V.] Univ Miami, Dept Med, Miller Sch Med, Miami, FL USA.
C3 University of Miami
RP Shaker, M (corresponding author), Miami VA Med Ctr, Div Hepatol, 1201 NW 16th St, Miami, FL 33125 USA.
EM Mina.Shaker@va.gov
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NR 61
TC 4
Z9 4
U1 1
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
EI 1557-8224
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD NOV
PY 2022
VL 26
IS 4
BP 643
EP 655
DI 10.1016/j.cld.2022.06.008
EA OCT 2022
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 5V4EJ
UT WOS:000877183600007
PM 36270721
DA 2025-01-07
ER
PT J
AU Antonelli, A
Ferri, C
Galeazzi, M
Giannitti, C
Manno, D
Mieli-Vergani, G
Menegatti, E
Olivieri, I
Puoti, M
Palazzi, C
Roccatello, D
Vergani, D
Sarzi-Puttini, P
Atzeni, F
AF Antonelli, A.
Ferri, C.
Galeazzi, M.
Giannitti, C.
Manno, D.
Mieli-Vergani, G.
Menegatti, E.
Olivieri, I.
Puoti, M.
Palazzi, C.
Roccatello, D.
Vergani, D.
Sarzi-Puttini, P.
Atzeni, F.
TI HCV infection: pathogenesis, clinical manifestations and therapy
SO CLINICAL AND EXPERIMENTAL RHEUMATOLOGY
LA English
DT Article
DE hepatitis C virus; mixed cryoglobulinemia; autoimmune endocrine
diseases; chronic arthritis; rituximab
ID HEPATITIS-C VIRUS; MONOCLONAL-ANTIBODY TREATMENT; MIXED
CRYOGLOBULINEMIA; RHEUMATOID-ARTHRITIS; THYROID-DISORDERS;
CYCLOSPORINE-A; EXTRAHEPATIC MANIFESTATIONS; DIFFERENTIAL-DIAGNOSIS;
RITUXIMAB; SAFETY
AB Chronic hepatitis C virus (HCV) infection is a worldwide public health problem with a global prevalence of 2-3%. It is believed that about 170 million people are currently infected (about 3% of the world's population), and a further 3-4 million are infected each year. HCV is the main reason for liver transplantation in the developed world, and the main cause of liver-related morbidity and mortality in a number of countries, including Italy. It is not only a frequent cause of chronic liver diseases such as hepatitis, cirrhosis and hepatocellular carcinoma, but is also involved in the pathogenesis of various autoimmune and rheumatic disorders (arthritis, vasculitis, sicca syndrome, porphyria cutanea tarda, lichen planus, nephropathies, thyroid diseases, and lung fibrosis), as well as in the development of B-cell lymphoproliferative diseases. Furthermore, patients suffering from C hepatitis tend to produce rheumatoid factor, cryoglobulins and a large series of autoantibodies (ANA, anti-SSA/SSB, SAM, ATG, aCL). The use of glucocorticoids or immunosuppressant agents in HCV infected individuals, which are needed to treat autoimmune and rheumatic disorders, leads to a risk of worsening the clinical outcome of HCV Under these conditions, the viral infection often needs to be treated with antiviral agents, mainly pegylated interferon combined with ribavirin. However, cyclosporine A seems to be safe and effective in patients with autoimmune disease (AD) and concomitant chronic HCV infection as is documented by the reduction in viremia and transaminases, particularly in patients with high baseline levels. Finally, HCV is the main trigger of mixed cryoglobulinemia. An attempt at viral eradication is therefore indicated in most patients, and is particularly effective in the case of mild or moderate manifestations. In severe cases, rituximab is an apparently safe and effective alternative to conventional immunosuppression and, specifically, it controls B-cell proliferation.
C1 [Antonelli, A.] Univ Pisa, Sch Med, Dept Internal Med, I-56100 Pisa, Italy.
[Ferri, C.] Univ Modena & Reggio Emilia, Emilia Sch Med, Dept Internal Med, Rheumatol Unit, Modena, Italy.
[Galeazzi, M.; Giannitti, C.] Univ Siena, Rheumatol Sect, Dept Clin Med & Immunol Sci, I-53100 Siena, Italy.
[Manno, D.; Puoti, M.] Univ Brescia, Dept Infect Dis, I-25121 Brescia, Italy.
[Mieli-Vergani, G.] Kings Coll London, Kings Coll Hosp, Inst Liver Studies, Sch Med, London WC2R 2LS, England.
[Menegatti, E.; Roccatello, D.; Vergani, D.] Univ Turin, Multidisciplinary Ctr Immunopathol Res & Document, SG Bosco Hosp, I-10124 Turin, Italy.
[Menegatti, E.; Roccatello, D.; Vergani, D.] Univ Turin, Clin Pathol Sect, Dept Med & Expt Oncol, I-10124 Turin, Italy.
[Olivieri, I.] S Carlo Hosp Potenza, Rheumatol Dept Lucania, Potenza, Italy.
[Olivieri, I.] Madonna Grazie Hosp Matera, Matera, Italy.
[Palazzi, C.] Villa Pini Clin, Div Rheumatol, Chieti, Italy.
[Sarzi-Puttini, P.; Atzeni, F.] Univ Milan, Rheumatol Unit, L Sacco Hosp, I-20122 Milan, Italy.
C3 University of Pisa; Universita di Modena e Reggio Emilia; University of
Siena; University of Brescia; University of London; King's College
London; King's College Hospital NHS Foundation Trust; King's College
Hospital; University of Turin; University of Turin; University of Milan;
Luigi Sacco Hospital
RP Atzeni, F (corresponding author), L Sacco Univ Hosp, Rheumatol Unit, Via GB Grassi 74, I-20157 Milan, Italy.
EM atzenifabiola@hotmail.com
RI Puoti, Massimo/AAA-6580-2020; Vergani, Diego/H-7610-2019; Antonelli,
Alessandro/AAU-2291-2020; Mieli-Vergani, Giorgina/G-5616-2011;
Menegatti, Elisa/G-9038-2011; Sarzi-Puttini, Piercarlo/S-6457-2017
OI Mieli-Vergani, Giorgina/0000-0002-8215-4489; Puoti,
Massimo/0000-0003-3278-7138; MENEGATTI, Elisa/0000-0001-7849-6323;
Sarzi-Puttini, Piercarlo/0000-0002-8673-5133
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NR 59
TC 80
Z9 95
U1 0
U2 3
PU CLINICAL & EXPER RHEUMATOLOGY
PI PISA
PA VIA SANTA MARIA 31, 56126 PISA, ITALY
SN 0392-856X
EI 1593-098X
J9 CLIN EXP RHEUMATOL
JI Clin. Exp. Rheumatol.
PD JAN-FEB
PY 2008
VL 26
IS 1
SU 48
BP S39
EP S47
PG 9
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 292TN
UT WOS:000255289100007
PM 18570753
DA 2025-01-07
ER
PT J
AU Jeong, SH
AF Jeong, Sook-Hyang
TI Current epidemiology and clinical characteristics of autoimmune liver
diseases in South Korea
SO CLINICAL AND MOLECULAR HEPATOLOGY
LA English
DT Review
DE Autoimmune hepatitis; Primary biliary cholangitis; Simplified scoring
system; Autoantibody; Liver transplantation
ID PRIMARY BILIARY-CIRRHOSIS; LONG-TERM OUTCOMES; HEPATOCELLULAR-CARCINOMA;
URSODEOXYCHOLIC ACID; CONTROLLED-TRIAL; SCORING SYSTEM; HEPATITIS;
TRANSPLANTATION; MULTICENTER; DIAGNOSIS
AB Autoimmune liver diseases including autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC) are rare diseases. The aim of this review is to examine the epidemiology and clinical characteristics of AIH and PBC in South Korea. There were 4,085 patients registered as AIH in the Rare Intractable Disease Registry of Korea between 2009-2013, with a median age of 56 years and female-to male ratio of 6.4. The age-adjusted incidence and prevalence of AIH were 1.07/100,000/year and 4.82/100,000 persons, respectively. Among the patients, 1.1% underwent liver transplantation, and case fatality was 2.18%. Liver cirrhosis at diagnosis was accompanied in 23%; liver biopsy was performed in 75.2%, and prednisolone therapy or prednisolone and azathioprine combination therapy was done in 73% with a remission rate of 86%. There were 2,824 patients with PBC (>= 20 years) registered in Korea between 2009-2013 with a median age of 57 years and female-to male ratio of 6.2. The age-adjusted incidence and prevalence of PBC were 0.86/100,000/year and 4.75/100,000 persons, respectively. Among the patients, 2.5% underwent liver transplantation, and case fatality was 2.2% with a 5-year transplantation-free survival of 95.4%. Ursodeoxycholic acid (UDCA) was prescribed in 90% of the patients with a UDCA inadequate response rate of 30%. In conclusion, AIH and PBC are rare but mostly treatable diseases if diagnosed in the early stages. However, scarce data, low awareness, delayed diagnosis and non-availability of 2nd line therapeutics are important issues to be solved. Therefore, governmental support for research and drug development and nationwide cooperative studies are warranted.
C1 [Jeong, Sook-Hyang] Seoul Natl Univ, Coll Med, Bundang Hosp, Dept Internal Med, Seongnam, South Korea.
C3 Seoul National University (SNU)
RP Jeong, SH (corresponding author), Seoul Natl Univ, Bundang Hosp, Dept Internal Med, 82,Gumi Ro 173 Beon Gil, Seongnam 13620, South Korea.
EM jsh@snubh.org
RI Jeong, Sook-Hyang/J-5642-2012
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NR 40
TC 18
Z9 19
U1 0
U2 1
PU KOREAN ASSOC STUDY LIVER
PI SEOUL
PA RM A1210, 53 MAPO-DAERO, MAPOTRAPALACE, DOWHA-DONG, MAPO-GU, SEOUL,
04158, SOUTH KOREA
SN 2287-2728
EI 2287-285X
J9 CLIN MOL HEPATOL
JI Clin. Mol. Hepatol.
PD MAR
PY 2018
VL 24
IS 1
BP 10
EP 19
DI 10.3350/cmh.2017.0066
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GK6VR
UT WOS:000436329800002
PM 29307132
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Zen, Y
Yeh, MM
AF Zen, Yoh
Yeh, Matthew M.
TI Checkpoint inhibitor-induced liver injury: A novel form of liver disease
emerging in the era of cancer immunotherapy
SO SEMINARS IN DIAGNOSTIC PATHOLOGY
LA English
DT Review
DE Nivolumab; Ipilimumab; Liver biopsy; Hepatitis; Cholangitis
ID IPILIMUMAB; NIVOLUMAB; SAFETY; MONOTHERAPY; HEPATITIS; ANTIBODY;
MELANOMA; PEMBROLIZUMAB; CTLA-4
AB Liver injury triggered by immune checkpoint inhibitors has been increasingly seen in clinical practice, and the incidence is likely to rise further in the next several years because of expanded indications for cancer immunotherapy. Tissue damage driven by disrupted immune tolerance against self-antigens is called an immune-related adverse event (irAE). irAEs in the liver histologically presents panlobular hepatitis (similar to 70%), isolated central zonal necrosis (similar to 20%), primarily granulomatous hepatitis (similar to 5%), and other minor forms of tissue injury (similar to 5%). Infiltrating cells are mainly lymphocytes and occasional eosinophils. Unlike classic autoimmune hepatitis (AIH), plasma cell infiltration is not conspicuous. Immunostaining reveals a large number of CD8+ T lymphocytes and a markedly smaller number of CD4+ cells or CD20+ B lymphocytes. The unique CD3+ / CD20+ and CD4+ /CD8+ ratios shifted in favor of CD8+ cytotoxic T lymphocytes are helpful to discriminate irAEs from other conditions (e.g., AIH, idiosyncratic drug-induced liver injury). Another hepatobiliary manifestation of irAEs is sclerosing cholangitis clinically characterized by elevations of biliary enzymes, diffuse duct wall thickening, and duct dilatation. Lymphocytic infiltration can be observed by endoscopic biopsies from the thick extrahepatic bile ducts, and liver needle biopsies may also show severe lymphocytic cholangitis resembling primary biliary cholangitis. An important differential diagnosis of irAEs is previously asymptomatic or subclinical liver disease unmasked by cancer immunotherapy, which is often challenging and requires close dinicopathological correlations.
C1 [Zen, Yoh] Kings Coll Hosp London, Inst Liver Studies, London, England.
[Yeh, Matthew M.] Univ Washington, Dept Pathol, Sch Med, Seattle, WA 98195 USA.
[Yeh, Matthew M.] Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA.
C3 University of London; King's College London; King's College Hospital NHS
Foundation Trust; King's College Hospital; University of Washington;
University of Washington Seattle; University of Washington; University
of Washington Seattle
RP Yeh, MM (corresponding author), Univ Washington, Dept Pathol, Sch Med, Seattle, WA 98195 USA.
EM yoh.zen@nhs.net; myeh@uw.edu
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NR 34
TC 53
Z9 56
U1 2
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0740-2570
EI 1930-1111
J9 SEMIN DIAGN PATHOL
JI Semin. Diagn. Pathol.
PD NOV
PY 2019
VL 36
IS 6
BP 434
EP 440
DI 10.1053/j.semdp.2019.07.009
PG 7
WC Medical Laboratory Technology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Pathology
GA JM2FL
UT WOS:000496036100008
PM 31358424
DA 2025-01-07
ER
PT J
AU Nawaz, A
Zaib, S
Khan, I
Ahmed, A
Shahzadi, K
Riaz, H
AF Nawaz, Aisha
Zaib, Sumera
Khan, Imtiaz
Ahmed, Abrar
Shahzadi, Kiran
Riaz, Huma
TI Silybum marianum: An Overview of its Phytochemistry and
Pharmacological Activities with Emphasis on Potential Anticancer
Properties
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Flavonolignans; silymarin; STAT3 pathway; anticancer; cardioprotective;
nephroprotective; antimicrobial; neuroprotective
ID MILK THISTLE; HEPATIC DAMAGE; L. GAERTN.; IN-VITRO; SILYMARIN;
SILIBININ; CANCER; APOPTOSIS; EXTRACT; LIVER
AB Silybum marianum (SM) belongs to the family Asteraceae, which holds therapeutic significance in medicinal chemistry. Phytochemistry analysis revealed an abundance of active constituents, particularly silymarin, composed of polyphenols and flavonolignans. Silymarin is majorly found in leaves, seeds, and fruits and is comprised of seven flavonolignans. Silymarin derivatives, specifically silybin, were reported for their medicinal properties. This review summarizes the studies conducted to evaluate SM's pharmacological properties and proposed mechanisms. SM exhibited anticancer properties due to being capable of modifying the induction of apoptosis, inhibiting the STAT3 pathway, decreasing the transcription of various growth factors, impeding the growth of 4T1 cells and inducing cell cycle arrest in various types of cancers, i.e., skin cancer, liver cancer, breast cancer, ovarian cancer etc. Silymarin and its derivatives protect the liver and ameliorate various immune-mediated and autoimmune hepatic diseases. Moreover, antimicrobial, antidiabetic, cardioprotective, nephroprotective, and neuroprotective activities were also reported. Based on testified in vitro and in vivo studies, SM can serve as an alternative to cure various pathological ailments.
C1 [Nawaz, Aisha; Zaib, Sumera; Shahzadi, Kiran; Riaz, Huma] Univ Cent Punjab, Fac Sci & Technol, Dept Basic & Appl Chem, Lahore 54590, Pakistan.
[Khan, Imtiaz] Univ Manchester, Dept Chem, 131 Princess St, Manchester M1 7DN, England.
[Khan, Imtiaz] Univ Manchester, Manchester Inst Biotechnol, 131 Princess St, Manchester M1 7DN, England.
[Ahmed, Abrar] Univ Punjab, Univ Coll Pharm, Lahore, Pakistan.
C3 University of Central Punjab; University of Manchester; University of
Manchester; University of Punjab
RP Zaib, S (corresponding author), Univ Cent Punjab, Fac Sci & Technol, Dept Basic & Appl Chem, Lahore 54590, Pakistan.; Khan, I (corresponding author), Univ Manchester, Dept Chem, 131 Princess St, Manchester M1 7DN, England.; Khan, I (corresponding author), Univ Manchester, Manchester Inst Biotechnol, 131 Princess St, Manchester M1 7DN, England.
EM sumera.zaib@ucp.edu.pk; kimtiaz@hotmail.co.uk
RI Zaib, Sumera/AAF-6879-2021
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NR 111
TC 5
Z9 5
U1 4
U2 10
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PY 2023
VL 23
IS 13
BP 1519
EP 1534
DI 10.2174/1871520623666230412111152
PG 16
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA P4PH0
UT WOS:001050477300005
PM 37055902
DA 2025-01-07
ER
PT J
AU Oberholzer, J
Al-Saghier, M
Kneteman, NM
AF Oberholzer, Jose
Al-Saghier, Mohammed
Kneteman, Norman M.
TI Steroid avoidance in liver transplantation
SO CANADIAN JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Immunosuppression; Liver transplantation; Mycophenolate mofetil;
Steroids
ID POSTTRANSPLANT DIABETES-MELLITUS; CHRONIC ACTIVE HEPATITIS; C
VIRUS-REPLICATION; LONG-TERM; HEPATOCELLULAR-CARCINOMA;
MYCOPHENOLATE-MOFETIL; VIRAL REPLICATION; PROSPECTIVE TRIAL;
IMMUNOSUPPRESSION; WITHDRAWAL
AB Corticosteroids have always played a Valuable role in transplantation. Unfortunately, they are Subject to a wide range of side effects, such as hyperlipidemia, hypertension, diabetes mellitus, osteoporosis, growth retardation and Cushingoid appearance. Steroids may also exacerbate problems that existed before Surgery, including malignancy, hepatitis B and hepatitis C. New, powerful immunosuppressants have allowed steroid use to be reduced or avoided altogether, but use of these regimens is not simple and may be associated with late acute rejection and recurrence of autoimmune disease. The present review examines the rationale for steroid avoidance in liver transplantation and assesses the new regimens that are currently being developed.
C1 [Oberholzer, Jose; Al-Saghier, Mohammed; Kneteman, Norman M.] Univ Alberta, Edmonton, AB, Canada.
C3 University of Alberta
RP Kneteman, NM (corresponding author), 2D4 Walter C Mackenzie Ctr, Edmonton, AB T6G 2B7, Canada.
EM nkneteman@cha.ab.ca
RI Alharthi, Mohammed/AAY-3275-2020
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NR 84
TC 2
Z9 2
U1 0
U2 0
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2291-2789
EI 2291-2797
J9 CAN J GASTROENTEROL
JI Can. J. Gastroenterol. Hepatol.
PD OCT
PY 2004
VL 18
SU C
BP 5C
EP 11C
DI 10.1155/2004/412135
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA V05FO
UT WOS:000207112100002
PM 16807621
OA Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Schelbert, S
Schindeldecker, M
Drebber, U
Witzel, HR
Weinmann, A
Dries, V
Schirmacher, P
Roth, W
Straub, BK
AF Schelbert, Selina
Schindeldecker, Mario
Drebber, Uta
Witzel, Hagen Roland
Weinmann, Arndt
Dries, Volker
Schirmacher, Peter
Roth, Wilfried
Straub, Beate Katharina
TI Lipid Droplet-Associated Proteins Perilipin 1 and 2: Molecular Markers
of Steatosis and Microvesicular Steatotic Foci in Chronic Hepatitis C
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE PAT proteins; hepatitis C virus (HCV); hepatitis B virus (HBV);
non-alcoholic steatohepatitis (NASH); focal fatty change
ID FATTY LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA; VIRUS-REPLICATION;
EXPRESSION; STORAGE; DIAGNOSIS; PATHOLOGY; ADIPOPHILIN; MECHANISM;
ALCOHOL
AB Chronic infection with hepatitis C (HCV) is a major risk factor in the development of cirrhosis and hepatocellular carcinoma. Lipid metabolism plays a major role in the replication and deposition of HCV at lipid droplets (LDs). We have demonstrated the importance of LD-associated proteins of the perilipin family in steatotic liver diseases. Using a large collection of 231 human liver biopsies with HCV, perilipins 1 and 2 have been localized to LDs of hepatocytes that correlate with the degree of steatosis and specific HCV genotypes, but not significantly with the HCV viral load. Perilipin 1- and 2-positive microvesicular steatotic foci were observed in 36% of HCV liver biopsies, and also in chronic hepatitis B, autoimmune hepatitis and mildly steatotic or normal livers, but less or none were observed in normal livers of younger patients. Microvesicular steatotic foci did not frequently overlap with glycogenotic/clear cell foci as determined by PAS stain in serial sections. Steatotic foci were detected in all liver zones with slight architectural disarrays, as demonstrated by immunohistochemical glutamine synthetase staining of zone three, but without elevated Ki67-proliferation rates. In conclusion, microvesicular steatotic foci are frequently found in chronic viral hepatitis, but the clinical significance of these foci is so far not clear.
C1 [Schelbert, Selina; Schindeldecker, Mario; Witzel, Hagen Roland; Roth, Wilfried; Straub, Beate Katharina] Univ Med Ctr Mainz, Inst Pathol, D-55131 Mainz, Germany.
[Schelbert, Selina] Univ Hosp Wuerzburg, Inst Pathol, D-97080 Wurzburg, Germany.
[Drebber, Uta; Dries, Volker] Univ Clin Cologne, Inst Pathol, D-50931 Cologne, Germany.
[Weinmann, Arndt] Univ Med Ctr, Dept Internal Med, D-55131 Mainz, Germany.
[Schirmacher, Peter] Univ Med Ctr Heidelberg, Inst Pathol, D-69120 Heidelberg, Germany.
C3 Johannes Gutenberg University of Mainz; University of Wurzburg;
University of Cologne; Johannes Gutenberg University of Mainz; Ruprecht
Karls University Heidelberg
RP Straub, BK (corresponding author), Univ Med Ctr Mainz, Inst Pathol, D-55131 Mainz, Germany.
EM beate.straub@unimedizin-mainz.de
OI Schindeldecker, Mario/0000-0003-4843-7992; Straub,
Beate/0000-0002-4857-1561
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NR 90
TC 6
Z9 6
U1 1
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD DEC
PY 2022
VL 23
IS 24
AR 15456
DI 10.3390/ijms232415456
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 7E7PP
UT WOS:000901355200001
PM 36555099
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Tannapfel, A
Dienes, HP
Lohse, AW
AF Tannapfel, Andrea
Dienes, Hans-Peter
Lohse, Ansgar W.
TI The Indications for Liver Biopsy
SO DEUTSCHES ARZTEBLATT INTERNATIONAL
LA English
DT Review
ID AUTOIMMUNE HEPATITIS; SCLEROSING CHOLANGITIS; DIAGNOSIS; MANAGEMENT;
THERAPY; PATHOGENESIS; PROPHYLAXIS; INFECTION; DISEASE; CANCER
AB Background: Despite improvements in serological and radiological techniques, liver biopsy remains the most reliable way to diagnose diffuse hepatic disease and hepatic nodules. The indications for this invasive technique must be weighed against the small, but not negligible, risk of a complication.
Methods: The indications for liver biopsy are summarized on the basis of a selective review of the literature, including the published recommendations and position statements of specialty societies in Germany and abroad. The conclusions are supplemented with an evaluation of the authors' own experience.
Results: The success of liver biopsy depends not only on the selection of the puncture method and on due attention to the relative and absolute contraindications, but also on the experience of the person carrying out the procedure. For patients with hepatitis of various etiologies, liver biopsy is used not only to establish the cause of the disorder, but also to assess the degree of inflammatory activity (grading) and the extent of fibrosis (staging).
Conclusion: Liver biopsy enables the reliable diagnosis of hepatic lesions and is an important aid to treatment planning and prognostication.
C1 [Tannapfel, Andrea] Ruhr Univ Bochum, Inst Pathol, D-44789 Bochum, Germany.
[Dienes, Hans-Peter] Univ Cologne, Dept Pathol, Cologne, Germany.
[Lohse, Ansgar W.] Univ Med Ctr Hamburg Eppendorf, Dept Internal Med 1, Hamburg, Germany.
C3 Ruhr University Bochum; University of Cologne; University of Hamburg;
University Medical Center Hamburg-Eppendorf
RP Tannapfel, A (corresponding author), Ruhr Univ Bochum, Inst Pathol, Burkle de la Camp Pl 1, D-44789 Bochum, Germany.
EM Andrea.Tannapfel@rub.de
FU Boehringer Ingelheim; Roche companies
FX Prof. Lohse has received lecture honoraria from the Falk Foundation,
MSD, and Roche. He has received research funding from the Boehringer
Ingelheim and Roche companies, among others.
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NR 29
TC 42
Z9 44
U1 0
U2 7
PU DEUTSCHER AERZTE-VERLAG GMBH
PI COLOGNE
PA DIESELSTRABE 2, POSTFACH 400265, D-50859 COLOGNE, GERMANY
SN 1866-0452
J9 DTSCH ARZTEBL INT
JI Dtsch. Arztebl. Int.
PD JUL 9
PY 2012
VL 109
IS 27-28
BP 477
EP U14
DI 10.3238/arztebl.2012.0477
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 986AW
UT WOS:000307312700001
PM 22833761
OA Green Published
DA 2025-01-07
ER
PT J
AU Bhakuni, GS
Bedi, O
Bariwal, J
Deshmukh, R
Kumar, P
AF Bhakuni, Ganesh Singh
Bedi, Onkar
Bariwal, Jitender
Deshmukh, Rahul
Kumar, Puneet
TI Animal models of hepatotoxicity
SO INFLAMMATION RESEARCH
LA English
DT Review
DE Animal models; Drug targets; Hepatotoxicity; Liver diseases;
Pathogenesis
ID INDUCED HEPATIC-INJURY; LIVER FIBROSIS; HEPATOCELLULAR-CARCINOMA;
MACROLIDE ANTIBIOTICS; ETHANOLIC EXTRACT; BINDING-SITE; CIRRHOSIS;
MECHANISM; ALCOHOL; DAMAGE
AB Liver is the largest and important organ in the body, involved in the metabolism of food and drugs. Liver diseases are potentially life threatening for humans. The etiology of liver disorder varied due to different reasons like autoimmune disorder, viral infection, toxic chemical, and due to changing diet style. Liver injury produces pathological changes like increase level of SGOT, SGPT, TB and generation of free radical radicals.
A better understanding of primary mechanisms is mandatory for designing of new therapeutic drugs. Therefore, animal models are being developed to mimic human liver diseases. Animal models are being used for several decades to study the pathogenesis of liver disorders and related toxicities.
In this review, we revealed various animal models with their merits and demerits. Our main focus is to explore all new and traditional animal models under broad classification like non-invasive, invasive and genetic models which directly or indirectly produce hepatotoxicity.
C1 [Bhakuni, Ganesh Singh; Bedi, Onkar; Bariwal, Jitender; Deshmukh, Rahul; Kumar, Puneet] ISF Coll Pharm, Dept Pharmacol, Moga 142001, Punjab, India.
C3 ISF College of Pharmacy
RP Kumar, P (corresponding author), ISF Coll Pharm, Dept Pharmacol, Moga 142001, Punjab, India.
EM punnubansal79@gmail.com
RI Bariwal, Jitender/N-4102-2018; Bedi, Onkar/AAZ-5394-2020; Deshmukh,
Rahul/T-1333-2019; kumar, puneet/ABH-2313-2020
OI kumar, puneet/0000-0002-7978-1043; Hameed, Linda/0000-0003-4414-3778;
Bedi, Onkar/0000-0003-4724-366X; Deshmukh, Rahul/0000-0001-5834-0962
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NR 111
TC 29
Z9 34
U1 1
U2 21
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1023-3830
EI 1420-908X
J9 INFLAMM RES
JI Inflamm. Res.
PD JAN
PY 2016
VL 65
IS 1
BP 13
EP 24
DI 10.1007/s00011-015-0883-0
PG 12
WC Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Immunology
GA DA6MG
UT WOS:000367918300002
PM 26427493
DA 2025-01-07
ER
PT J
AU Cooper, KM
Delk, M
Devuni, D
Sarkar, M
AF Cooper, Katherine M.
Delk, Molly
Devuni, Deepika
Sarkar, Monika
TI Sex differences in chronic liver disease and benign liver lesions
SO JHEP REPORTS
LA English
DT Review
DE Gender; Liver; Epidemiology; Sex disparities
ID PRIMARY SCLEROSING CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE; FOCAL
NODULAR HYPERPLASIA; C VIRUS-INFECTION; HEPATITIS-B; FIBROSIS
PROGRESSION; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
INSULIN-RESISTANCE; GENDER DISPARITY
AB The epidemiology, natural history, and therapeutic responses of chronic liver diseases and liver lesions often vary by sex. In this review, we summarize available clinical and translational data on these aspects of the most common liver conditions encountered in clinical practice, including the potential contributions of sex hormones to the underlying pathophysiology of observed differences. We also highlight areas of notable knowledge gaps and discuss sex disparities in access to liver transplant and potential strategies to address these barriers. Given established sex differences in immune response, drug metabolism, and response to liver-related therapies, emerging clinical trials and epidemiological studies should prioritize dedicated analyses by sex to inform sex-specific approaches to liver-related care.(c) 2023 The Authors. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver (EASL).
C1 [Cooper, Katherine M.; Devuni, Deepika] UMass Chan Med Sch, Dept Med, Div Gastroenterol Hepatol, Worcester, MA USA.
[Delk, Molly; Sarkar, Monika] Univ Calif San Francisco, Dept Med, Div Gastroenterol Hepatol, San Francisco, CA USA.
[Sarkar, Monika] Univ Calif San Francisco, Dept Med, Div Gastroenterol Hepatol, 513 Parnassus Ave,Room S 357, San Francisco, CA 94143 USA.
C3 University of Massachusetts System; UMass Chan Medical School;
University of California System; University of California San Francisco;
University of California System; University of California San Francisco
RP Sarkar, M (corresponding author), Univ Calif San Francisco, Dept Med, Div Gastroenterol Hepatol, 513 Parnassus Ave,Room S 357, San Francisco, CA 94143 USA.
EM monika.sarkar@ucsf.edu
RI Cooper, Katherine/HTM-4574-2023
OI Devuni, Deepika/0000-0002-1011-9414; Cooper,
Katherine/0000-0002-6030-4773
FU NIDDK [DK111944/DK131238]; NIAAA [AA017986]
FX Financial support MS receives grant support from the NIDDK
(DK111944/DK131238) . DD receives grant support from the NIAAA
(AA017986) .
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NR 150
TC 4
Z9 4
U1 3
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2589-5559
J9 JHEP REP
JI JHEP Rep.
PD NOV
PY 2023
VL 5
IS 11
AR 100870
DI 10.1016/j.jhepr.2023.100870
EA SEP 2023
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA U5LJ8
UT WOS:001085212500001
PM 37791378
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Sánchez-Martín, L
Sánchez-Mateos, P
Cabañas, C
AF Sanchez-Martin, Lorena
Sanchez-Mateos, Paloma
Cabanas, Carlos
TI CXCR7 impact on CXCL12 biology and disease
SO TRENDS IN MOLECULAR MEDICINE
LA English
DT Review
DE chemokines; CXCL12; G-protein-coupled receptors (GPCRs);
seven-transmembrane spanning receptors (7-TMRs); CXCR7; RDC1
ID CHEMOKINE RECEPTOR CXCR7; PROTEIN-COUPLED RECEPTOR; COLLECTIVE
CELL-MIGRATION; POSTERIOR LATERAL-LINE; HEMATOPOIETIC STEM;
BETA-ARRESTIN; BONE-MARROW; ORPHAN RECEPTOR; FACTOR-I;
HEPATOCELLULAR-CARCINOMA
AB It is known that the chemokine receptor CXCR7 (RDC1) can be engaged by both chemokines CXCL12 (SDF-1) and CXCL11 (I-TAC), but the exact expression pattern and function of CXCR7 is controversial. CXCR7 expression seems to be enhanced during pathological inflammation and tumor development, and emerging data suggest this receptor is an attractive therapeutic target for autoimmune diseases and cancer. CXCR7/CXCR4 heterodimerization, beta-arrestin-mediated signaling, and modulation of CXCL12 responsiveness by CXCR7 suggest that the monogamous CXCR4/CXCL12 signaling axis is an oversimplified model that needs to be revisited. Consequently, research into CXCR7 biology is of great interest and further studies are warranted. This review summarizes recent findings about the CXCR7 receptor and analyses its impact on understanding the roles of CXCL12 biology in health and disease.
C1 [Sanchez-Martin, Lorena; Cabanas, Carlos] UAM, CSIC, Ctr Biol Mol Severo Ochoa, Dept Biol Celular & Inmunol, Madrid 28049, Spain.
[Sanchez-Mateos, Paloma] Hosp Gen Univ Gregorio Maranon, Serv Inmunol, Madrid 28007, Spain.
C3 Consejo Superior de Investigaciones Cientificas (CSIC); CSIC - Centro de
Biologia Molecular Severo Ochoa (CBM); Autonomous University of Madrid;
General University Gregorio Maranon Hospital
RP Sánchez-Martín, L (corresponding author), UAM, CSIC, Ctr Biol Mol Severo Ochoa, Dept Biol Celular & Inmunol, Madrid 28049, Spain.
EM lorena_s@cbm.uam.es; ccabanas@cbm.uam.es
RI Sanchez-Mateos, Paloma/E-8931-2013; Sanchez-Martin, Lorena/A-3926-2012;
CABANAS, CARLOS/J-4595-2012
OI Sanchez-Martin, Lorena/0000-0003-4087-0636; Sanchez-Mateos,
Paloma/0000-0001-6589-4445; CABANAS, CARLOS/0000-0002-8767-060X
FU Ministerio de Ciencia e Innovacion [BFU2010-19144]; Instituto de Salud
Carlos III-Redes Tematicas de Investigacion Cooperativa en Salud
(ISCIII-RETICS) [RD08/0075/0002]
FX We especially thank Dr Jose Luis Rodriguez-Fernandez for his critical
reading of this manuscript and all the comments and suggestions. This
work was supported by grants from Ministerio de Ciencia e Innovacion
BFU2010-19144 (to C.C.) and by Instituto de Salud Carlos III-Redes
Tematicas de Investigacion Cooperativa en Salud (ISCIII-RETICS)
RD08/0075/0002 (to L.S-M and C.C.).
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NR 125
TC 170
Z9 192
U1 1
U2 67
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4914
EI 1471-499X
J9 TRENDS MOL MED
JI Trends Mol. Med
PD JAN
PY 2013
VL 19
IS 1
BP 12
EP 22
DI 10.1016/j.molmed.2012.10.004
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 077BU
UT WOS:000314003700003
PM 23153575
DA 2025-01-07
ER
PT J
AU Vipperla, K
O'Keefe, SJ
AF Vipperla, Kishore
O'Keefe, Stephen J.
TI The Microbiota and Its Metabolites in Colonic Mucosal Health and Cancer
Risk
SO NUTRITION IN CLINICAL PRACTICE
LA English
DT Review
DE colon; metagenome; fatty acids; inflammation; colonic neoplasms;
irritable bowel syndrome; inflammatory bowel diseases; autoimmune
diseases; allergy and immunology; obesity
ID CHAIN FATTY-ACIDS; INFLAMMATORY-BOWEL-DISEASE; SULFATE-REDUCING
BACTERIA; HUMAN LARGE-INTESTINE; DIET-INDUCED OBESITY;
COLORECTAL-CANCER; GUT MICROBIOTA; PROPIONIC-ACID; BILE-ACIDS; RAT COLON
AB Recent advances in our ability to identify and characterize the human microbiota have transformed our appreciation of the function of the colon from an organ principally involved in the reabsorption of secretory fluids to a metabolic organ on a par with the liver. High-throughput technology has been applied to the identification of specific differences in microbial DNA, allowing the identification of trillions of microbes belonging to more than 1000 different species, with a metabolic mass of approximately 1.5 kg. The close proximity of these microbes with the mucosa and gut lymphoid tissue helps explain why a balanced microbiota is likely to preserve mucosal health, whereas an unbalanced composition, as seen in dysbiosis, may increase the prevalence of diseases not only of the mucosa but also within the body due to the strong interactions with the gut immune system, the largest immune organ of the body. Such abnormalities have been pinpointed as etiological factors in a wide range of diseases, including autoimmune disorders, allergy, irritable bowel syndrome, inflammatory bowel disease, obesity, and colon cancer. Recognition of the strong potential for food to manipulate microbiota composition has opened up new therapeutic strategies against these diseases based on dietary intervention. (Nutr Clin Pract. 2012;27:624-635)
C1 [O'Keefe, Stephen J.] Univ Pittsburgh, Sch Med, Div Gastroenterol Hepatol & Nutr, PUH, Pittsburgh, PA 15213 USA.
[Vipperla, Kishore] Univ Pittsburgh, Med Ctr, Div Gen Internal Med, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh
RP O'Keefe, SJ (corresponding author), Univ Pittsburgh, Sch Med, Div Gastroenterol Hepatol & Nutr, PUH, 200 Lothrop St,Mezzanine Level C Wing, Pittsburgh, PA 15213 USA.
EM sjokeefe@pitt.edu
RI O'Keefe, Stephen/A-6734-2013
OI O'Keefe, Stephen/0000-0003-4422-3145
FU NCI NIH HHS [R01 CA135379] Funding Source: Medline
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NR 109
TC 91
Z9 104
U1 2
U2 61
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0884-5336
EI 1941-2452
J9 NUTR CLIN PRACT
JI Nutr. Clin. Pract.
PD OCT
PY 2012
VL 27
IS 5
BP 624
EP 635
DI 10.1177/0884533612452012
PG 12
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA 000UC
UT WOS:000308413300007
PM 22868282
DA 2025-01-07
ER
PT J
AU Hassan, N
Siddiqui, AR
Abbas, Z
Hassan, SM
Soomro, GB
Mubarak, M
Anis, S
Muzaffar, R
Zafar, MN
AF Hassan, Nasir
Siddiqui, Adeelur Rehman
Abbas, Zaigham
Hassan, Syed Mujahid
Soomro, Ghous Bux
Mubarak, Muhammed
Anis, Sabiha
Muzaffar, Rana
Zafar, Mirza Naqi
TI Clinical Profile and HLA Typing of Autoimmune Hepatitis From Pakistan
SO HEPATITIS MONTHLY
LA English
DT Article
DE Hepatitis, Autoimmune; Histocompatibility Testing; Alleles, HLA-DR6
Antigen; Pakistan
ID LIVER-DISEASE; CELIAC-DISEASE; DIAGNOSIS; CRITERIA; SUSCEPTIBILITY;
PREVALENCE; CIRRHOSIS; FORMS; CORTICOSTEROIDS; CHOLANGITIS
AB Background: Human leukocyte antigen (HLA) typing in autoimmune hepatitis (AIH) has been investigated in different populations and ethnic groups, but no such data is available from Pakistan.
Objectives: The aim of this study was to evaluate the clinical profile of autoimmune hepatitis (AIH), and determine the associated antigens and alleles by performing HLA typing.
Patients and Methods: A total of 58 patients, diagnosed and treated as AIH in the last 10 years were reviewed. Diagnosis was based on International AIH Group criteria. Forty one patients underwent liver biopsy. HLA typing was performed in 44 patients and 912 controls by serological method for HLA A and B, and by PCR technique using sequence specific primers for DR alleles.
Results: Of 58 cases, 35 were females (60.3%). The median age was 14.5 (range 4-70 years), and AIH score was 14 (10-22). Thirty-six (62.0%) patients had type 1 AIH, 10 (17.2%) type 2, and the remaining 12 were seronegative with biopsy proven AIH. Forty-nine patients (84.4%) had cirrhosis. Twenty-four (41.4%) patients had ascites at the time of presentation. Among 41 patients who underwent liver biopsy, thirty-two had advance stages III and IV disease, and twenty had severe grade of inflammation. Fifteen patients had other associated autoimmune diseases and one developed hepatocellular carcinoma. HLA A2 (P = 0.036), HLA A9 (23) (P = 0.018), HLA A10 (25) (P = 0.000), HLA A19 (33) (P = 0.000), HLA B15 (63) (P = 0.007), HLA B40 (61) (P = 0.002), HLA DR6 (P = 0.001) with its subtypes HLA-DRB1*13 (P = 0.032) and HLA-DRB1*14 (p = 0.017) were more prevalent in AIH with statistical significance than controls.
Conclusions: AIH in our region presents with advanced disease affecting predominantly children and adolescents. There is a genetic association of HLA DR6 along with other alleles and antigens in our patients with AIH.
C1 [Hassan, Nasir; Siddiqui, Adeelur Rehman; Abbas, Zaigham; Hassan, Syed Mujahid; Soomro, Ghous Bux] Sindh Inst Urol & Transplantat, Dept Hepatogastroenterol, Karachi 74200, Pakistan.
[Mubarak, Muhammed; Zafar, Mirza Naqi] Sindh Inst Urol & Transplantat, Dept Pathol, Karachi 74200, Pakistan.
[Anis, Sabiha; Muzaffar, Rana] Sindh Inst Urol & Transplantat, Karachi 74200, Pakistan.
C3 Dow University of Health Sciences; Dow University of Health Sciences;
Dow University of Health Sciences
RP Abbas, Z (corresponding author), Sindh Inst Urol & Transplantat, Dept Hepatogastroenterol, Karachi 74200, Pakistan.
EM drzabbas@gmail.com
RI Hassan, Saif/AAO-6969-2020; Anis, Sabiha/IZP-6316-2023; Mubarak,
Muhammed/I-1164-2013
OI Mubarak, Muhammed/0000-0001-6120-5884
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NR 61
TC 22
Z9 23
U1 0
U2 2
PU KOWSAR PUBL
PI HOENSBROEK
PA PATERSWEG 22,, HOENSBROEK, LIMBURG 6431 GC, NETHERLANDS
SN 1735-143X
EI 1735-3408
J9 HEPAT MON
JI Hepat. Mon.
PD DEC
PY 2013
VL 13
IS 12
AR e13598
DI 10.5812/hepatmon.13598
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 273LO
UT WOS:000328536500003
PM 24358040
OA Green Submitted, hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Cacoub, P
Gragnani, L
Comarmond, C
Zignego, AL
AF Cacoub, Patrice
Gragnani, Laura
Comarmond, Cloe
Zignego, Anna Linda
TI Extrahepatic manifestations of chronic hepatitis C virus infection
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Review
DE Extra hepatic manifestations; HCV; Treatment
ID QUALITY-OF-LIFE; NON-HODGKINS-LYMPHOMA; MIXED CRYOGLOBULINEMIA
VASCULITIS; MONOCLONAL-ANTIBODY TREATMENT; RANDOMIZED CONTROLLED-TRIAL;
PEGYLATED INTERFERON-ALPHA; CHRONIC HCV INFECTION; B-CELL; ANTIVIRAL
TREATMENT; INSULIN-RESISTANCE
AB Hepatitis C virus (HCV) infected patients are known to be at risk of developing liver complications i.e. cirrhosis and liver cancer. However, the risks of morbidity and mortality are underestimated because they do not take into account non-liver consequences of chronic hepatitis C virus infection. Numerous extrahepatic manifestations have been reported in up to 74% of patients, from perceived to disabling conditions. The majority of data concern hepatitis C virus-related autoimmune and/or lymphoproliferative disorders, from mixed cryoglobulinaemia vasculitis to frank lymphomas. More recently, other hepatitis C virus-associated disorders have been reported including cardiovascular, renal, metabolic, and central nervous system diseases. This review aims to outline most of the extrahepatic manifestations that are currently being investigated, including some of autoimmune and/or lymphoproliferative nature, and others in which the role of immune mechanisms appears less clear.
Beyond the liver, hepatitis C virus chronic infection should be analyzed as a multifaceted systemic disease leading to heavy direct and indirect costs. The accurate consideration of extrahepatic consequences of such a systemic infection significantly increases the weight of its pathological burden. The need for effective viral eradication measures is underlined. (C) 2014 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Cacoub, Patrice; Comarmond, Cloe] Univ Paris 06, Sorbonne Univ, UMR 7211, Paris, France.
[Cacoub, Patrice; Comarmond, Cloe] Univ Paris 06, Sorbonne Univ, Inflammat Immunopathol Biotherapy Dept DHU i2B, Paris, France.
[Cacoub, Patrice; Comarmond, Cloe] INSERM, UMR S 959, Paris, France.
[Cacoub, Patrice; Comarmond, Cloe] CNRS, FRE3632, Paris, France.
[Cacoub, Patrice; Comarmond, Cloe] Grp Hosp Pitie Salpetriere, AP HP, Dept Internal Med & Clin Immunol, F-75634 Paris, France.
[Gragnani, Laura; Zignego, Anna Linda] Univ Florence, Dept Expt & Clin Med, Interdept Ctr Syst Manifestat Hepatitis Viruses M, Florence, Italy.
C3 Sorbonne Universite; Sorbonne Universite; Institut National de la Sante
et de la Recherche Medicale (Inserm); Centre National de la Recherche
Scientifique (CNRS); Sorbonne Universite; Assistance Publique Hopitaux
Paris (APHP); Hopital Universitaire Pitie-Salpetriere - APHP; University
of Florence
RP Cacoub, P (corresponding author), Hop La Pitie Salpetriere, Dept Internal Med & Clin Immunol, 47-83 Blvd Hop, F-75651 Paris 13, France.
EM patrice.cacoub@psl.aphp.fr
RI COMARMOND, Chloé/AAN-1192-2021; Gragnani, Laura/H-7755-2019; Zignego,
Anna/AAL-8205-2021; Gragnani, Laura/K-7751-2013
OI Cacoub, Patrice/0000-0002-6727-4992; Gragnani, Laura/0000-0001-6800-9149
FU "Fondazione Umberto Veronesi"; Fondation pour la Recherche Medicale
(FRM); Gilead Sciences Europe Ltd.
FX L.G. was supported by "Fondazione Umberto Veronesi". C.C. has received a
grant from the Fondation pour la Recherche Medicale (FRM).This article
is part of a supplement supported by an unrestricted educational grant
from Gilead Sciences Europe Ltd. Gilead has had no editorial control or
involvement in the content of this article. The views and opinions
within this supplement are those of the authors and not necessarily
those of Gilead.
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NR 181
TC 209
Z9 223
U1 0
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD DEC 15
PY 2014
VL 46
SU 5
BP S165
EP S173
DI 10.1016/j.dld.2014.10.005
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CA2MR
UT WOS:000348743000003
PM 25458776
OA hybrid, Green Submitted
DA 2025-01-07
ER
PT J
AU Nakazawa, T
Naitoh, I
Hayashi, K
Miyabe, K
Simizu, S
Joh, T
AF Nakazawa, Takahiro
Naitoh, Itaru
Hayashi, Kazuki
Miyabe, Katsuyuki
Simizu, Shuya
Joh, Takashi
TI Diagnosis of IgG4-related sclerosing cholangitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE IgG4-related sclerosing cholangitis; Primary sclerosing cholangitis;
IgG4; Sclerosing cholangitis
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; AUTOIMMUNE PANCREATITIS;
EXTRAPANCREATIC LESIONS; IGG4-ASSOCIATED CHOLANGITIS; LIVER-BIOPSY;
PLASMA-CELLS; CHOLANGIOGRAPHY; INVOLVEMENT; SPECTRUM; DISEASE
AB IgG4-related sclerosing cholangitis (IgG4-SC) is often associated with autoimmune pancreatitis. However, the diffuse cholangiographic abnormalities observed in IgG4-SC may resemble those observed in primary sclerosing cholangitis (PSC), and the presence of segmental stenosis suggests cholangiocarcinoma (CC). IgG4-SC responds well to steroid therapy, whereas PSC is only effectively treated with liver transplantation and CC requires surgical intervention. Since IgG4-SC was first described, it has become a third distinct clinical entity of sclerosing cholangitis. The aim of this review was to introduce the diagnostic methods for IgG4-SC. IgG4-SC should be carefully diagnosed based on a combination of characteristic clinical, serological, morphological, and histopathological features after cholangiographic classification and targeting of a disease for differential diagnosis. When intrapancreatic stenosis is detected, pancreatic cancer or CC should be ruled out. If multiple intrahepatic stenoses are evident, PSC should be distinguished on the basis of cholangiographic findings and liver biopsy with IgG4 immunostaining. Associated inflammatory bowel disease is suggestive of PSC. If stenosis is demonstrated in the hepatic hilar region, CC should be discriminated by ultrasonography, intraductal ultrasonography, bile duct biopsy, and a higher cutoff serum IgG4 level of 182 mg/dL. (C) 2013 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Nakazawa, Takahiro; Naitoh, Itaru; Hayashi, Kazuki; Miyabe, Katsuyuki; Simizu, Shuya; Joh, Takashi] Nagoya City Univ, Dept Gastroenterol & Metab, Grad Sch Med Sci, Nagoya, Aichi 4678601, Japan.
C3 Nagoya City University
RP Nakazawa, T (corresponding author), Nagoya City Univ, Dept Gastroenterol & Metab, Grad Sch Med Sci, Mizuho Ku, 1 Kawasumi,Mizuho Cho, Nagoya, Aichi 4678601, Japan.
EM tnakazaw@med.nagoya-cu.ac.jp
RI Naitoh, Itaru/AAB-7252-2020
OI Naitoh, Itaru/0000-0001-8342-886X; Miyabe, Katsuyuki/0000-0002-4915-9835
FU Grants-in-Aid for Scientific Research [23790803, 23591015] Funding
Source: KAKEN
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NR 55
TC 73
Z9 83
U1 0
U2 8
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 21
PY 2013
VL 19
IS 43
BP 7661
EP 7670
DI 10.3748/wjg.v19.i43.7661
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 259HW
UT WOS:000327519000019
PM 24282356
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Muiesan, P
Vergani, D
Mieli-Vergani, G
AF Muiesan, Paolo
Vergani, Diego
Mieli-Vergani, Giorgina
TI Liver transplantation in children
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
ID IDIOPATHIC THROMBOCYTOPENIC PURPURA; EPSTEIN-BARR-VIRUS; SOLID-ORGAN
TRANSPLANTATION; AUTOIMMUNE HEMOLYTIC-ANEMIA; PARVOVIRUS B19 INFECTION;
LIVING-RELATED DONORS; LYMPHOPROLIFERATIVE-DISEASE; HEPATOCYTE
TRANSPLANTATION; CYTOMEGALOVIRUS-INFECTION; VASCULAR COMPLICATIONS
AB Liver transplantation (LT) is now a standard treatment for children with end-stage liver disease with excellent 1- and 5-year survival. This has been achieved through improvement of surgical techniques and anti-rejection treatment and management. The donor pool for children has been extended by the use of cut-down, split, living-related and, recently, non-heart-beating donor and isolated hepatocyte transplantation. Though the majority of transplanted children enjoy an excellent quality of life, there remain a high number of possible complications, including short-term primary non-function, vascular and biliary problems, bowel perforation, severe rejection, infection, hypertension and long-term renal impairment, chronic rejection, de novo autoimmunity, lymphoproliferative disease and cancer, most of which are related to anti-rejection drug toxicity. Hence, the focus of research for paediatric LT should be induction of tolerance, avoiding long-term immunosuppression and its toxicity. (c) 2006 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 Kings Coll Hosp London, Sch Med, Inst Liver Studies, London SE5 9RS, England.
C3 King's College Hospital NHS Foundation Trust; King's College Hospital;
University of London; King's College London
RP Mieli-Vergani, G (corresponding author), Kings Coll Hosp London, Sch Med, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
EM giorgina.vergani@kcl.ac.uk
RI Vergani, Diego/H-7610-2019; Muiesan, Maria/C-1111-2011; Mieli-Vergani,
Giorgina/G-5616-2011; Muiesan, Paolo/H-3900-2018
OI Muiesan, Paolo/0000-0002-7389-6691; Mieli-Vergani,
Giorgina/0000-0002-8215-4489
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NR 70
TC 50
Z9 55
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD FEB
PY 2007
VL 46
IS 2
BP 340
EP 348
DI 10.1016/j.jhep.2006.11.006
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 130QC
UT WOS:000243813100020
PM 17161491
OA Bronze
DA 2025-01-07
ER
PT J
AU Domerecka, W
Kowalska-Kepczynska, A
Homa-Mlak, I
Michalak, A
Mlak, R
Mazurek, M
Cichoz-Lach, H
Malecka-Massalska, T
AF Domerecka, Weronika
Kowalska-Kepczynska, Anna
Homa-Mlak, Iwona
Michalak, Agata
Mlak, Radoslaw
Mazurek, Marcin
Cichoz-Lach, Halina
Malecka-Massalska, Teresa
TI The Usefulness of Extended Inflammation Parameters and Systemic
Inflammatory Response Markers in the Diagnostics of Autoimmune Hepatitis
SO CELLS
LA English
DT Article
DE autoimmune hepatitis; inflammation; extended inflammation parameters;
systemic inflammatory response markers
ID TO-LYMPHOCYTE RATIO; NEUTROPHIL; PLATELET; PATHOGENESIS; SEVERITY;
SEPSIS; CANCER
AB (1) Introduction: Autoimmune hepatitis (AIH) is a chronic disease. A persistent autoimmune reaction in the liver is significantly related to the systemic inflammatory response. Extended Inflammation Parameters (EIP) can be used to assess the activation of immune cells such as activated neutrophils (NEUT-RI and NEUT-GI) and activated lymphocytes (RE-LYMP and AS-LYMP) in the phase of active inflammation. The role of the systemic inflammatory response markers should also be emphasised, especially: NLR, PLR, and RLR, which have recently been widely studied as markers in autoimmune skin diseases or liver diseases. (2) Materials and Methods: The study included 30 patients with AIH and 30 healthy volunteers. The parameters of the EIP group (RE-LYMP, AS-LYMP, NEUT-RI, NEUT-GI), calculated haematological indices Red Blood Cell Distribution Width-to-Platelet Ratio (RPR), Mean Platelet Volume-to-Platelet Ratio (MPR), Neutrophil-to-Lymphocyte Ratio (NLR), Platelet-to-Lymphocyte Ratio (PLR), Red Blood Cell Distribution Width-to-Lymphocyte Ratio (RLR), and selected blood morphological and biochemical indices were analysed. The aim of the study was to assess the usefulness of the EIP and systemic inflammatory response markers in the diagnostics of AIH. (3) Results: Compared to the controls, the patients with AIH showed significantly higher EIP values: NEUT-RI (48.05 vs. 43.30), NEUT-GI (152.65 vs. 147.40), RE-LYMP (0.07 vs. 0.03), and the inflammatory response markers: MPR (0.05 vs. 0.04), RPR (0.07 vs. 0.05), and NLR (2.81 vs. 1.42. Among the examined markers, EIP has significant diagnostic potential: NEUT-RI (AUC = 0.86), NEUT-GI (AUC = 0.80), and RE-LYMP (AUC = 0.78), and so do calculated haematological indices, i.e., MPR (AUC = 0.75), PLR (AUC = 1.00), and RLR (AUC = 1.00) Moreover, the importance of NEUT-GI (AUC = 0.89), MPR (AUC = 0.93), PLR (AUC = 0.86), RPR (AUC = 0.91), and FIB-4 (AUC = 0.83) in the detection of liver fibrosis in the course of AIH has also been proven. (4) Conclusions: EIP and systemic inflammatory response markers may turn out to be useful in detecting AIH and in looking for features of already developed liver cirrhosis in its course.
C1 [Domerecka, Weronika; Homa-Mlak, Iwona; Mlak, Radoslaw; Mazurek, Marcin; Malecka-Massalska, Teresa] Med Univ Lublin, Chair & Dept Human Physiol, 11 Radziwillowska Str, PL-20080 Lublin, Poland.
[Kowalska-Kepczynska, Anna] Med Univ Lublin, Dept Biochem Diagnost, Chair Lab Diagnost, PL-20081 Lublin, Poland.
[Michalak, Agata; Cichoz-Lach, Halina] Dept Gastroenterol Endoscopy Unit, 8 Jaczewskiego Str, PL-20090 Lublin, Poland.
C3 Medical University of Lublin; Medical University of Lublin
RP Domerecka, W (corresponding author), Med Univ Lublin, Chair & Dept Human Physiol, 11 Radziwillowska Str, PL-20080 Lublin, Poland.
EM weronikakasprzycka2@gmail.com
RI Homa-Mlak, Iwona/ADM-2116-2022; Kowalska-Kępczyńska, Anna/AAT-3961-2020;
Miak, Radoslaw/I-9994-2019; Michalak, Agata/HBQ-1569-2022;
Kowalska-Kepczynska, Anna/S-7324-2018
OI Kowalska-Kepczynska, Anna/0000-0002-6018-9437; Mazurek,
Marcin/0000-0002-4040-0450; Michalak, Agata/0000-0003-4426-6321;
Cichoz-Lach, Halina/0000-0002-7337-835X; Domerecka,
Weronika/0000-0002-7654-2573; Mlak, Radoslaw/0000-0001-7399-8340
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NR 40
TC 7
Z9 7
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD AUG
PY 2022
VL 11
IS 16
AR 2554
DI 10.3390/cells11162554
PG 18
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 4B9EU
UT WOS:000846071700001
PM 36010631
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Wei, HW
Zhao, T
Liu, XL
Ding, QT
Yang, JR
Bi, XY
Cheng, ZQ
Ding, CB
Liu, WC
AF Wei, Hewei
Zhao, Ting
Liu, Xinglong
Ding, Qiteng
Yang, Junran
Bi, Xiaoyu
Cheng, Zhiqiang
Ding, Chuanbo
Liu, Wencong
TI Mechanism of Action of Dihydroquercetin in the Prevention and Therapy of
Experimental Liver Injury
SO MOLECULES
LA English
DT Review
DE dihydroquercetin; liver injury; biological availability; mechanism
ID AUTOIMMUNE HEPATITIS; OXIDATIVE STRESS; TAXIFOLIN; CISPLATIN;
EXPRESSION; EPIDEMIOLOGY; DISEASE; HEPATOTOXICITY; PREVALENCE;
FLAVONOIDS
AB Liver disease is a global health problem that affects the well-being of tens of thousands of people. Dihydroquercetin (DHQ) is a flavonoid compound derived from various plants. Furthermore, DHQ has shown excellent activity in the prevention and treatment of liver injury, such as the inhibition of hepatocellular carcinoma cell proliferation after administration, the normalization of oxidative indices (like SOD, GSH) in this tissue, and the down-regulation of pro-inflammatory molecules (such as IL-6 and TNF-alpha). DHQ also exerts its therapeutic effects by affecting molecular pathways such as NF-kappa B and Nrf2. This paper discusses the latest research progress of DHQ in the treatment of various liver diseases (including viral liver injury, drug liver injury, alcoholic liver injury, non-alcoholic liver injury, fatty liver injury, and immune liver injury). It explores how to optimize the application of DHQ to improve its effectiveness in treating liver diseases, which is valuable for preparing potential therapeutic drugs for human liver diseases in conjunction with DHQ.
C1 [Wei, Hewei; Ding, Qiteng; Yang, Junran; Bi, Xiaoyu; Cheng, Zhiqiang; Ding, Chuanbo] Jilin Agr Univ, Coll Tradit Chinese Med, Changchun 130118, Peoples R China.
[Zhao, Ting; Liu, Xinglong; Ding, Qiteng; Liu, Wencong] Wuzhou Univ, Sch Food & Pharmaceut Engn, Wuzhou 543002, Peoples R China.
[Ding, Chuanbo] Jilin Agr Sci & Technol Coll, Coll Tradit Chinese Med, Jilin 132101, Peoples R China.
C3 Jilin Agricultural University; Wuzhou University
RP Ding, CB (corresponding author), Jilin Agr Univ, Coll Tradit Chinese Med, Changchun 130118, Peoples R China.; Liu, WC (corresponding author), Wuzhou Univ, Sch Food & Pharmaceut Engn, Wuzhou 543002, Peoples R China.; Ding, CB (corresponding author), Jilin Agr Sci & Technol Coll, Coll Tradit Chinese Med, Jilin 132101, Peoples R China.
EM www03211@126.com; lyguiwandingding@163.com; xinglongliu1221@126.com;
ding152778@163.com; junran231201@163.com; bxy123163@163.com;
czq5974@163.com; chuanboding0506@163.com; jwlw6803@126.com
RI liu, wencong/KAM-2858-2024; Xinglong, LIU/IUN-7675-2023
FU Jilin College of Agricultural Science and Technology Projects [20230049]
FX This work was supported by the Jilin College of Agricultural Science and
Technology Projects (20230049).
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NR 105
TC 0
Z9 0
U1 13
U2 13
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD AUG
PY 2024
VL 29
IS 15
AR 3537
DI 10.3390/molecules29153537
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA C1G7A
UT WOS:001286921000001
PM 39124941
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Yin, H
Cheng, LL
Agarwal, C
Agarwal, R
Ju, C
AF Yin, Hao
Cheng, Linling
Agarwal, Chapla
Agarwal, Rajesh
Ju, Cynthia
TI Lactoferrin protects against concanavalin A-induced liver injury in mice
SO LIVER INTERNATIONAL
LA English
DT Article
DE concanavalin A; IFN-gamma; IL-4; lactoferrin; liver
ID RECOMBINANT HUMAN INTERLEUKIN-4; LANGERHANS CELL-MIGRATION; MEDIATED
HEPATIC-INJURY; BOVINE LACTOFERRIN; T-CELLS; INTERFERON-GAMMA;
IFN-GAMMA; APOPTOSIS; MODEL; IL-4
AB Background
Liver diseases, caused by viral infection, autoimmune conditions, alcohol ingestion or the use of certain drugs, are a significant health issue, as many can develop into liver failure. Lactoferrin (Lac) is an iron-binding glycoprotein that belongs to the transferrin family. Owing to its multiple biological functions, Lac has been evaluated in a number of clinical trials to treat infections, inflammation and cancer.
Aim
The present study aims to reveal a profound hepatoprotective effect of Lac, using a mouse model of Concanavalin A (Con A)-induced hepatitis, which mimics the pathophysiology of human viral and autoimmune hepatitis.
Method
C57Bl/6J mice were injected with bovine Lac following Con A challenge. The effects of Lac on interferon (IFN)-gamma and interleukin (IL)-4 expression were determined. The roles of Lac on T-cell apoptosis and activation, and leukocytes infiltration were examined.
Result
The data demonstrated that the protective effect of Lac was attributed to its ability to inhibit T-cell activation and production of IFN-gamma, as well as to suppress IL-4 production by hepatic natural killer T cells.
Conclusion
These findings indicate a great therapeutic potential of Lac in treating in treating inflammatory hepatitis and possibly other inflammatory diseases.
C1 [Yin, Hao; Cheng, Linling; Agarwal, Chapla; Agarwal, Rajesh; Ju, Cynthia] Univ Colorado Denver, Dept Pharmaceut Sci, Aurora, CO 80045 USA.
[Agarwal, Chapla; Agarwal, Rajesh] Univ Colorado Denver, Ctr Canc, Aurora, CO 80045 USA.
[Ju, Cynthia] Univ Colorado Denver, Integrated Dept Immunol, Aurora, CO 80045 USA.
C3 University of Colorado System; University of Colorado Anschutz Medical
Campus; Children's Hospital Colorado; Children's Hospital Colorado;
University of Colorado System; University of Colorado Anschutz Medical
Campus; University of Colorado System; University of Colorado Anschutz
Medical Campus; Children's Hospital Colorado
RP Ju, C (corresponding author), Univ Colorado Denver, Dept Pharmaceut Sci, Res Complex 2,C-238,12700 E 19th Ave, Aurora, CO 80045 USA.
EM cynthia.ju@ucdenver.edu
FU US National Institutes of Health [RO1 ES012914]
FX This work was supported by US National Institutes of Health grant RO1
ES012914 (to Cynthia Ju).
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NR 38
TC 16
Z9 18
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD APR
PY 2010
VL 30
IS 4
BP 623
EP 632
DI 10.1111/j.1478-3231.2009.02199.x
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 559FU
UT WOS:000274809200019
PM 20136718
DA 2025-01-07
ER
PT J
AU Rashidi, S
Farhadi, L
Ghasemi, F
Sheikhesmaeili, F
Mohammadi, A
AF Rashidi, Saadyeh
Farhadi, Leila
Ghasemi, Faezeh
Sheikhesmaeili, Farshad
Mohammadi, Asadollah
TI The potential role of HLA-G in the pathogenesis of HBV infection:
Immunosuppressive or immunoprotective?
SO INFECTION GENETICS AND EVOLUTION
LA English
DT Review
DE Hepatitis B virus; HLA-G; Pathogenesis; Protection
ID HEPATITIS-B-VIRUS; 14-BP INSERTION/DELETION POLYMORPHISM; ANTIGEN-G
EXPRESSION; IFN-GAMMA; G GENE; INTERFERON-GAMMA; IMMUNE ESCAPE; G
MOLECULES; G ISOFORMS; SHLA-G
AB The non-classical human leukocyte antigens (HLA)-G could be generally considered as a potent tolerogenic molecule, which modulates immune responses. HLA-G due to the immunosuppressive properties may play an important role in the pathogenesis of infections related to the liver. HLA-G may display two distinct activities in the pathological conditions so that it could be protective in the autoimmune and inflammatory diseases or could be suppressive of the immune system in the infections or cancers. HLA-G might be used as a novel therapeutic target for liver diseases in the future. Indeed, new therapeutic agents targeting HLA-G expression or antibodies which block HLA-G activity are being developed and tested. However, further consideration of the HLA-G function in liver disease is required. This review aims to summarize the role of HLA-G in the liver of patients with HBV infection.
C1 [Rashidi, Saadyeh; Farhadi, Leila; Mohammadi, Asadollah] Kurdistan Univ Med Sci, Res Inst Hlth Dev, Cellular & Mol Res Ctr, Sanandaj, Iran.
[Ghasemi, Faezeh] High Inst Res & Educ Transfus Med, Blood Transfus Res Ctr, Tehran, Iran.
[Sheikhesmaeili, Farshad] Kurdistan Univ Med Sci, Res Inst Hlth Dev, Liver & Digest Res Ctr, Sanandaj, Iran.
C3 Kurdistan University of Medical Sciences; Kurdistan University of
Medical Sciences
RP Mohammadi, A (corresponding author), Kurdistan Univ Med Sci, Res Inst Hlth Dev, Cellular & Mol Res Ctr, Sanandaj, Iran.
EM amohammadi.kani@yahoo.com
RI Rashidi, Saadyeh/KXR-7664-2024; Mohammadi, Asadollah/E-1411-2018
OI Mohammadi, Asadollah/0000-0002-6695-0506
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NR 112
TC 9
Z9 9
U1 0
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-1348
EI 1567-7257
J9 INFECT GENET EVOL
JI Infect. Genet. Evol.
PD NOV
PY 2020
VL 85
AR 104580
DI 10.1016/j.meegid.2020.104580
PG 8
WC Infectious Diseases
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases
GA OY0BO
UT WOS:000593919700001
PM 33022425
DA 2025-01-07
ER
PT J
AU Cianci, R
Franza, L
Schinzari, G
Rossi, E
Ianiro, G
Tortora, G
Gasbarrini, A
Gambassi, G
Cammarota, G
AF Cianci, Rossella
Franza, Laura
Schinzari, Giovanni
Rossi, Ernesto
Ianiro, Gianluca
Tortora, Giampaolo
Gasbarrini, Antonio
Gambassi, Giovanni
Cammarota, Giovanni
TI The Interplay between Immunity and Microbiota at Intestinal
Immunological Niche: The Case of Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE gut microbiota; immunological niche; dysbiosis; cancer; immune system
ID ENTEROTOXIGENIC BACTEROIDES-FRAGILIS; FATTY LIVER-DISEASE; TOLL-LIKE
RECEPTORS; REGULATORY T-CELLS; GUT MICROBIOTA; HELICOBACTER-PYLORI;
COLORECTAL-CANCER; INFILTRATING LYMPHOCYTES; PANCREATIC-CANCER; ADAPTER
PROTEIN
AB The gut microbiota is central to the pathogenesis of several inflammatory and autoimmune diseases. While multiple mechanisms are involved, the immune system clearly plays a special role. Indeed, the breakdown of the physiological balance in gut microbial composition leads to dysbiosis, which is then able to enhance inflammation and to influence gene expression. At the same time, there is an intense cross-talk between the microbiota and the immunological niche in the intestinal mucosa. These interactions may pave the way to the development, growth and spreading of cancer, especially in the gastro-intestinal system. Here, we review the changes in microbiota composition, how they relate to the immunological imbalance, influencing the onset of different types of cancer and the impact of these mechanisms on the efficacy of traditional and upcoming cancer treatments.
C1 [Cianci, Rossella; Franza, Laura; Gambassi, Giovanni] Univ Cattolica Sacro Cuore, Dept Internal Med, Fdn Policlin Univ A Gemelli IRCCS, Largo A Gemelli 8, I-00168 Rome, Italy.
[Schinzari, Giovanni; Rossi, Ernesto; Tortora, Giampaolo] Univ Cattolica Sacro Cuore, Dept Med Oncol, Fdn Policlin Univ A Gemelli IRCCS, Largo A Gemelli 8, I-00168 Rome, Italy.
[Ianiro, Gianluca; Gasbarrini, Antonio; Cammarota, Giovanni] Univ Cattolica Sacro Cuore, Dept Gastroenterol, Fdn Policlin Univ A Gemelli IRCCS, Largo A Gemelli 8, I-00168 Rome, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli
RP Cianci, R (corresponding author), Univ Cattolica Sacro Cuore, Dept Internal Med, Fdn Policlin Univ A Gemelli IRCCS, Largo A Gemelli 8, I-00168 Rome, Italy.
EM rossellacianci@gmail.com; laura.franza01@icatt.it;
giovanni.gambassi@unicatt.it; ernestorossi.rm@gmail.com;
gianluca.ianiro@hotmail.it; giampaolo.tortora@policlinicogemelli.it;
antonio.gasbarrini@unicatt.it; giovanni.gambassi@unicatt.it;
giovanni.cammarota@unicatt.it
RI Gambassi, Giovanni/AAC-3612-2020; Rossi, Ernesto/AAB-7519-2022; Tortora,
Giampaolo/AAA-1252-2019; cianci, rossella/AAH-7896-2021; Cammarota,
Giovanni/AAD-1732-2022; Franza, Laura/W-6071-2018; Gasbarrini,
Antonio/AAB-8487-2019; Schinzari, Giovanni/AAC-1547-2019; Ianiro,
Gianluca/K-5578-2016
OI Ianiro, Gianluca/0000-0002-8318-0515; Cianci,
Rossella/0000-0001-5378-8442; Tortora, Giampaolo/0000-0002-1378-4962;
Gambassi, Giovanni/0000-0002-7030-9359; Rossi,
Ernesto/0000-0002-6442-1707; Gasbarrini, Antonio/0000-0003-4863-6924;
Gasbarrini, Antonio/0000-0002-6230-1779; Cammarota,
Giovanni/0000-0002-3626-6148; Franza, Laura/0000-0001-8638-7565
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NR 145
TC 36
Z9 37
U1 1
U2 14
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB 1
PY 2019
VL 20
IS 3
AR 501
DI 10.3390/ijms20030501
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA HQ4WR
UT WOS:000462412500045
PM 30682772
OA Green Submitted, gold, Green Published
DA 2025-01-07
ER
PT J
AU Gao, MX
Li, XL
He, LL
Yang, JR
Ye, XH
Xiao, F
Wei, HS
AF Gao, Meixin
Li, Xiulan
He, Lingling
Yang, Junru
Ye, Xiaohui
Xiao, Fan
Wei, Hongshan
TI Diammonium Glycyrrhizinate Mitigates Liver Injury Via Inhibiting
Proliferation Of NKT Cells And Promoting Proliferation Of Tregs
SO DRUG DESIGN DEVELOPMENT AND THERAPY
LA English
DT Article
DE autoimmune hepatitis; concanavalin A; diammonium glycyrrhizinate; NKT
cells; regulatory T-cell
ID REGULATORY T-CELLS; AUTOIMMUNE HEPATITIS; MOUSE MODEL; ACTIVATION; ACID;
ASSOCIATION; EXPRESSION; SYSTEM; CANCER; MICE
AB Purpose: Diammonium glycyrrhizinate (DG) is a replacement for glycyrrhizic acid, which is used as a hepatic protector in clinical practice for most liver diseases. The potential role of immune response during autoimmune hepatitis-induced by concanavalin A (Con A)-remains to be elucidated.
Methods: C57BL/6J mice were treated with two different doses of DG (75 and 200 mg/kg) 2 hrs before administering Con A. The mice were sacrificed after administering Con A for 0, 6, and 24 hrs. Liver damage grade and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin levels were evaluated. The expression level of cleaved-caspase 3 in liver was detected by Western blotting. Inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and interferon gamma (IFN-gamma) in liver were detected by RT-PCR. Thymus, peripheral blood, spleen, and liver tissues were collected to analyze the percentages of NKT cells, subsets of CD4(+)CD25(-)CD69(+) and CD8(+)CD69(+) T cells, and subsets of regulatory T cells (Tregs).
Results: Our results revealed that DG pre-treatment significantly decreased the serum ALT and AST levels and improved the histological damage in Con A-induced autoimmune liver injury. Pre-treatment with DG down-regulated the inflammatory cytokines upon challenge with Con A. The DG pre-treatment inhibited the apoptosis of T lymphocytes in the thymus. Further, it effectively suppressed the proliferation of CD4(+)CD25(-)CD69(+) and CD8(+)CD69(+) subsets in the peripheral blood and spleen. In addition, the DG pretreatment significantly downregulated the frequency of NKT cells, while upregulating the frequency of Tregs in the liver.
Conclusion: We believe that the potential protective effect of DG against Con A-induced hepatitis may be partially attributed to its inhibitory activities on inflammatory cytokines in the livers, lymphocyte apoptosis in the thymus, NKT cells proliferation, and activation of CD8(+) T cells; further, there may also be a possibility of DC promoting Tregs proliferation.
C1 [Gao, Meixin; Wei, Hongshan] Peking Univ, Dept Gastroenterol, Ditan Teaching Hosp, Beijing 100015, Peoples R China.
[Li, Xiulan; Wei, Hongshan] Capital Med Univ, Beijing Ditan Hosp, Ctr Liver Dis, Beijing 100015, Peoples R China.
[He, Lingling; Yang, Junru; Ye, Xiaohui; Wei, Hongshan] Capital Med Univ, Beijing Ditan Hosp, Dept Gastroenterol, 8 Jingshun East St, Beijing 100015, Peoples R China.
[Xiao, Fan] Capital Med Univ, Beijing Ditan Hosp, Inst Infect Dis, Beijing 100015, Peoples R China.
C3 Peking University; Capital Medical University; Capital Medical
University; Capital Medical University
RP Wei, HS (corresponding author), Capital Med Univ, Beijing Ditan Hosp, Dept Gastroenterol, 8 Jingshun East St, Beijing 100015, Peoples R China.
EM drwei@ccmu.edu.cn
RI yang, Junru/IST-1525-2023
OI He, Lingling/0000-0001-8082-8788; Yang, Junru/0000-0003-4030-7560
FU Capital Foundation for Clinical Characteristic Applied Research Projects
[Z181100001718084]; Digestive Medical Coordinated Development Center of
Beijing Hospitals Authority [XXZ0404]; National Natural Science
Foundation of China [81271901]; Beijing Natural Science Foundation
[7152073]
FX This work was supported by the Capital Foundation for Clinical
Characteristic Applied Research Projects [Number Z181100001718084]; the
Digestive Medical Coordinated Development Center of Beijing Hospitals
Authority [Number XXZ0404]; National Natural Science Foundation of China
[Number 81271901]; and Beijing Natural Science Foundation [Number
7152073].
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NR 41
TC 27
Z9 29
U1 0
U2 18
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1177-8881
J9 DRUG DES DEV THER
JI Drug Des. Dev. Ther.
PY 2019
VL 13
BP 3579
EP 3589
DI 10.2147/DDDT.S220030
PG 11
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JE5BL
UT WOS:000490706100002
PM 31802846
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Sun, LM
Liang, JA
Lin, CL
Lin, MC
Chang, NJ
Kao, CH
AF Sun, Li-Min
Liang, Ji-An
Lin, Cheng-Li
Lin, Ming-Chia
Chang, Nai-Jen
Kao, Chia-Hung
TI Cancer risk in patients with osteoporosis: a population-based cohort
study
SO CURRENT MEDICAL RESEARCH AND OPINION
LA English
DT Article
DE Cohort study; malignancy; osteoporosis; population-based
ID BONE-MINERAL DENSITY; PROSTATE-CANCER; BREAST-CANCER;
AUTOIMMUNE-DISEASES; COLORECTAL-CANCER; THYROID-HORMONES;
GRAVES-DISEASE; REDUCED RISK; WOMEN; MEN
AB Background: Osteoporosis has been associated with cancer development. We conducted a nationwide population-based cohort study in Taiwan to evaluate this possible association of osteoporosis with subsequent cancer development.
Methods: A total of 35,979 patients diagnosed with osteoporosis between 2000 and 2010 identified from the National Health Insurance Research Database comprised the osteoporosis cohort, and each patient was randomly frequency matched with one individual from the general population (without osteoporosis) based on age, sex, and year of osteoporosis diagnosis to form the non-osteoporosis (control) cohort. Cox proportional hazard regression analysis was used to calculate adjusted hazard ratios and 95% confidence intervals and determine the effect of osteoporosis on cancer risk.
Results: Patients with osteoporosis showed a significantly higher risk of developing liver and thyroid cancers and lower risk of colorectal cancer than did individuals without osteoporosis. Male patients with osteoporosis had a significantly increased risk for liver cancer, whereas female patients with osteoporosis had a significantly increased risk for thyroid cancer, but a significantly decreased risk for overall and colorectal cancers. In addition, more significant findings were observed when age 64 years or the follow-up duration was 5 years; however, a significantly lower risk for colorectal cancer was observed when follow-up duration was >5 years. Study limits including lack of data for some health-related behaviors, inclusion criteria of osteoporosis and potential selection bias have been discussed.
Conclusion: Patients with osteoporosis showed a higher risk for liver and thyroid cancers and a lower risk for colorectal cancer than did control individuals. Stratified analyses by sex, age, and follow-up duration showed various patterns in different cancers.
C1 [Sun, Li-Min] Kaohsiung Armed Forces Gen Hosp, Dept Radiat Oncol, Zuoying Branch, Kaohsiung, Taiwan.
[Liang, Ji-An; Kao, Chia-Hung] China Med Univ, Coll Med, Sch Med, Grad Inst Clin Med Sci, Taichung, Taiwan.
[Liang, Ji-An] China Med Univ Hosp, Dept Radiat Oncol, Taichung, Taiwan.
[Lin, Cheng-Li] China Med Univ Hosp, Management Off Hlth Data, Taichung, Taiwan.
[Lin, Cheng-Li] China Med Univ, Coll Med, Taichung, Taiwan.
[Lin, Ming-Chia] I Shou Univ, Dept Nucl Med, Kaohsiung, Taiwan.
[Lin, Ming-Chia] E Da Hosp, Kaohsiung, Taiwan.
[Chang, Nai-Jen] Kaohsiung Armed Forces Gen Hosp, Dept Pathol, Zuoying Branch, Kaohsiung, Taiwan.
[Kao, Chia-Hung] China Med Univ Hosp, Dept Nucl Med, Taichung, Taiwan.
[Kao, Chia-Hung] China Med Univ Hosp, PET Ctr, Taichung, Taiwan.
[Kao, Chia-Hung] Asia Univ, Dept Bioinformat & Med Engn, Taichung, Taiwan.
C3 China Medical University Taiwan; China Medical University Taiwan; China
Medical University Hospital - Taiwan; China Medical University Taiwan;
China Medical University Hospital - Taiwan; China Medical University
Taiwan; I Shou University; E-Da Hospital; China Medical University
Taiwan; China Medical University Hospital - Taiwan; China Medical
University Taiwan; China Medical University Hospital - Taiwan; Asia
University Taiwan
RP Kao, CH (corresponding author), China Med Univ, Coll Med, Grad Inst Clin Med Sci, 2 Yuh Der Rd, Taichung 40447, Taiwan.
EM d10040@mail.cmuh.org.tw
RI Lin, Cheng-Li/AAU-1138-2021; liang, jian/HNI-8846-2023; Chang,
Nai-Jen/L-5777-2019
OI Lin, Cheng-Li/0000-0001-9926-3668
FU Taiwan Ministry of Health and Welfare Clinical Trial and Research Center
of Excellence [MOHW105-TDU-B-212-133019]; China Medical University
Hospital; Academia Sinica Taiwan Biobank Stroke Biosignature Project
[BM10501010037]; NRPB Stroke Clinical Trial Consortium
[MOST105-2325-B-039-003]; Tseng-Lien Lin Foundation, Taichung, Taiwan;
Taiwan Brain Disease Foundation, Taipei, Taiwan; Katsuzo and Kiyo
Aoshima Memorial Funds, Japan; CMU under the Aim for Top University Plan
of the Ministry of Education, Taiwan, and Health and welfare surcharge
of tobacco products; China Medical University Hospital Cancer Research
Center of Excellence (Taiwan) [MOHW105-TDU-B-212-134003]
FX This study is supported in part by Taiwan Ministry of Health and Welfare
Clinical Trial and Research Center of Excellence
(MOHW105-TDU-B-212-133019), China Medical University Hospital, Academia
Sinica Taiwan Biobank Stroke Biosignature Project (BM10501010037), NRPB
Stroke Clinical Trial Consortium (MOST105-2325-B-039-003), Tseng-Lien
Lin Foundation, Taichung, Taiwan, Taiwan Brain Disease Foundation,
Taipei, Taiwan, and Katsuzo and Kiyo Aoshima Memorial Funds, Japan; and
CMU under the Aim for Top University Plan of the Ministry of Education,
Taiwan, and Health and welfare surcharge of tobacco products, and China
Medical University Hospital Cancer Research Center of Excellence
(MOHW105-TDU-B-212-134003, Taiwan). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript. No additional external funding received
for this study.
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NR 46
TC 5
Z9 5
U1 0
U2 13
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0300-7995
EI 1473-4877
J9 CURR MED RES OPIN
JI Curr. Med. Res. Opin.
PD APR
PY 2017
VL 33
IS 4
BP 733
EP 739
DI 10.1080/03007995.2017.1278681
PG 7
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA ES4KX
UT WOS:000399504200015
PM 28044464
DA 2025-01-07
ER
PT J
AU Sharif, K
Watad, A
Bragazzi, NL
Adawi, M
Amital, H
Shoenfeld, Y
AF Sharif, Kassem
Watad, Abdulla
Bragazzi, Nicola Luigi
Adawi, Mohammad
Amital, Howard
Shoenfeld, Yehuda
TI Coffee and autoimmunity: More than a mere hot beverage!
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE Autoimmune diseases; Rheumatology; Clinical nutrition; Coffee; Caffeine;
Autoimmunity; Rheumatoid arthritis
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; INFLAMMATORY-BOWEL-DISEASE; PRIMARY
SCLEROSING CHOLANGITIS; PRIMARY BILIARY-CIRRHOSIS; GLUTEN-FREE DIET;
RHEUMATOID-ARTHRITIS; MULTIPLE-SCLEROSIS; CELIAC-DISEASE; CAFFEINE
CONSUMPTION; ENVIRONMENTAL-FACTORS
AB Coffee is one of the world's most consumed beverage. In the last decades, coffee consumption has attracted a huge body of research due to its impact on health. Recent scientific evidences showed that coffee intake could be associated with decreased mortality from cardiovascular and neurological diseases, diabetes type II, as well as from endometrial and liver cancer, among others.
In this review, on the basis of available data in the literature, we aimed to investigate the association between coffee intake and its influence on the immune systemand the insurgence of themost relevant autoimmune diseases. While some studies reported conflicting results, general trends have been identified. Coffee consumption seems to increase the risk of developing rheumatoid arthritis (RA) and type 1 diabetesmellitus (T1DM). By contrast, coffee consumption may exert a protective role against multiple sclerosis, primary sclerosing cholangitis, and ulcerative colitis. Concerning other autoimmune diseases such as systemic lupus erythematosus, psoriasis, primary biliary cholangitis and Crohn's disease, no significant associationwas found. In other studies, coffee consumption was shown to influence disease course and management options. Coffee intake led to a decrease in insulin sensitivity in T1DM, inmethotrexate efficacy in RA, and in levothyroxine absorption in Hashimoto's disease. Further, coffee consumptionwas associated with cross reactivitywith gliadin antibodies in celiac patients. Data on certain autoimmune diseases like systemic sclerosis, Sjogren's syndrome, and Behcet's disease, among others, are lacking in the existent literature. As such, further research is warranted. (C) 2017 Elsevier B.V. All rights reserved.
C1 [Sharif, Kassem; Watad, Abdulla; Amital, Howard] Sheba Med Ctr, Dept Med B, Tel Hashomer, Israel.
[Sharif, Kassem; Watad, Abdulla; Amital, Howard; Shoenfeld, Yehuda] Sheba Med Ctr, Zabludowicz Ctr Autoimmune Dis, Tel Hashomer, Israel.
[Sharif, Kassem; Watad, Abdulla; Amital, Howard; Shoenfeld, Yehuda] Tel Aviv Univ, Sackler Fac Med, Tel Aviv, Israel.
[Bragazzi, Nicola Luigi] Univ Genoa, Dept Hlth Sci DISSAL, Sch Publ Hlth, Genoa, Italy.
[Adawi, Mohammad] Bar Ilan Fac Med, Padeh Hosp, Safed, Israel.
[Adawi, Mohammad] Bar Ilan Fac Med, Ziv Hosp, Safed, Israel.
C3 Chaim Sheba Medical Center; Chaim Sheba Medical Center; Tel Aviv
University; University of Genoa; Ziv Medical Center
RP Shoenfeld, Y (corresponding author), Tel Aviv Univ, Sheba Med Ctr, Zabludowicz Ctr Autoimmune Dis, IL-5265601 Tel Hashomer, Israel.
EM shoenfel@post.tau.ac.il
RI Adawi, Mohammad/ABG-4428-2021; Bragazzi, Nicola/G-1672-2011; sharif,
kassem/K-5663-2019; Schoenfeld, Yehuda/I-1525-2016
OI Sharif, Kassem/0000-0003-3905-3313; watad, abdulla/0000-0002-1404-8027
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NR 135
TC 73
Z9 78
U1 1
U2 61
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD JUL
PY 2017
VL 16
IS 7
BP 712
EP 721
DI 10.1016/j.autrev.2017.05.007
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA EX1JI
UT WOS:000402978300006
PM 28479483
DA 2025-01-07
ER
PT J
AU Hemminki, K
Li, XJ
Sundquist, J
Sundquist, K
AF Hemminki, Kari
Li, Xinjun
Sundquist, Jan
Sundquist, Kristina
TI Cancer risks in ulcerative colitis patients
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE autoimmunity; cancer risk; inflammatory bowel disease; age at
hospitalization
ID INFLAMMATORY-BOWEL-DISEASE; CLINICAL CHARACTERISTICS;
RHEUMATOID-ARTHRITIS; NORDIC COUNTRIES; CROHNS-DISEASE; POPULATION;
SUSCEPTIBILITY; TRANSPLANTATION; AUTOIMMUNITY; CONCORDANCE
AB Patients diagnosed with ulcerative colitis (UC) are known to be at an increased risk of colorectal and liver cancers and leukemia. UC is an autoimmune disease, which may present a wider spectrum of cancers. We wanted to examine the risk of cancer in a large population of UC patients in order to reach high statistical power. A UC research database was constructed by identifying UC patients from the Swedish Hospital Discharge Register and cancer patients from the Cancer Registry. Follow-up of 27,606 UC patients hospitalized for the first time during the years 1964-2004 identified 2,058 patients with cancer. Standardized incidence ratios were calculated for cancer in UC patients by comparing to subjects without hospitalization for UC. The novel tumor sites in UC patients included small intestinal (carcinoid), pancreatic, breast and prostate cancers, nonthyroid endocrine gland tumors, non-Hodgkin lymphoma and multiple myeloma. A total of 11 sites showed an increased risk, which remained at 6 sites when tumors diagnosed in the year of UC hospitalization were excluded; even chronic myeloid leukemia was in excess. Cancer risks depended on the age at first hospitalization for UC. The SIRs for colon, rectal, liver and pancreatic cancers declined by age at hospitalization for UC, while for endocrine tumors the older patients were at higher risk. Our large study identified novel subsequent cancers in UC patients. However, some of these, including small intestinal carcinoids, prostate cancers and nonthyroid endocrine tumors, may be in excess because of intensified medical surveillance of the patients. (C) 2008 Wiley-Liss, Inc.
C1 [Hemminki, Kari] DKFZ, German Canc Res Ctr, Div Mol Genet Epidemiol, D-69120 Heidelberg, Germany.
[Hemminki, Kari; Li, Xinjun; Sundquist, Jan; Sundquist, Kristina] Karolinska Inst, Ctr Family & Community Med, S-14183 Huddinge, Sweden.
C3 Helmholtz Association; German Cancer Research Center (DKFZ); Karolinska
Institutet
RP Hemminki, K (corresponding author), DKFZ, German Canc Res Ctr, Div Mol Genet Epidemiol, Neuenheimer Feld 580, D-69120 Heidelberg, Germany.
EM k.hemminki@dk.fz.de
OI Li, Xinjun/0000-0002-5559-4657
FU EU [LSHC-CT-2004-503465]; Deutsche Krebshilfe; NGFN Plus; Swedish Cancer
Society; Swedish Council for Working Life and Social Research
FX Grant sponsor: EU; Grant number: LSHC-CT-2004-503465; Grant sponsors:
Deutsche Krebshilfe, NGFN Plus, Swedish Cancer Society, The Swedish
Council for Working Life and Social Research.
CR [Anonymous], CANC INC SWED 2005
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Wolfe F, 2007, ARTHRITIS RHEUM, V56, P2886, DOI 10.1002/art.22864
NR 26
TC 67
Z9 69
U1 0
U2 4
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD SEP 15
PY 2008
VL 123
IS 6
BP 1417
EP 1421
DI 10.1002/ijc.23666
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 338BO
UT WOS:000258480100026
PM 18561319
OA Bronze
DA 2025-01-07
ER
PT J
AU Aedma, SK
Chidharla, A
Kelting, S
Kasi, A
AF Aedma, Surya Kiran
Chidharla, Anusha
Kelting, Sarah
Kasi, Anup
TI Oxaliplatin-associated sarcoid-like reaction masquerading as recurrent
colon cancer
SO BMJ CASE REPORTS
LA English
DT Article
DE oncology; cancer intervention; contraindications and precautions
ID ADVANCED COLORECTAL-CANCER; ORGANIZING PNEUMONIA; CHEMOTHERAPY; DISEASE
AB A 54-year-old man with stage IV B metastatic colorectal cancer with liver and peritoneal metastasis was treated with cytoreductive surgery (extended left colectomy, right partial hepatectomy, resection of right diaphragm nodule) and perioperative oxaliplatin-based chemotherapy. The patient was cancer-free for 6months, at which point a surveillance positron emission tomography-CT scan showed metabolically active hepatosplenic lesions and mediastinal and bilateral hilar lymph nodes. An endobronchial ultrasound bronchoscopy-guided fine needle aspiration of the mediastinal and hilar lymph nodes revealed non-necrotising granulomas. The workup was negative for bacterial, fungal or mycobacterial infection, cancer or autoimmune disease. Carcinoembryonic antigen and COLVERA (a circulating tumour DNA liquid biopsy test for the detection of recurrent colon cancer) tests were negative. Subsequently the rare diagnosis of a sarcoidosis-like reaction from oxaliplatin-based chemotherapy was made. Repeat imaging after 3months showed resolution of the hepatosplenic lesions and lymphadenopathy, alike.
C1 [Aedma, Surya Kiran] Carle Fdn Hosp, Internal Med, Urbana, IL USA.
[Chidharla, Anusha] Univ Illinois, Coll Med Peoria, Internal Med, Peoria, IL USA.
[Kelting, Sarah; Kasi, Anup] Univ Kansas, Med Ctr, Med Oncol, Kansas City, KS 66103 USA.
C3 University of Illinois System; University of Illinois Peoria; University
of Kansas; University of Kansas Medical Center
RP Kasi, A (corresponding author), Univ Kansas, Med Ctr, Med Oncol, Kansas City, KS 66103 USA.
EM anupdoc@gmail.com
CR Axel Grothey DS., 2005, OVERALL SURVIV PATIE
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NR 16
TC 4
Z9 4
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 1757-790X
J9 BMJ CASE REP
JI BMJ Case Rep.
PD SEP
PY 2020
VL 13
IS 9
AR e229548
DI 10.1136/bcr-2019-229548
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA SS1ZA
UT WOS:000661540300001
PM 32907862
OA Green Published
DA 2025-01-07
ER
PT J
AU Frith, J
Jones, D
Newton, JL
AF Frith, James
Jones, David
Newton, Julia L.
TI Chronic liver disease in an ageing population
SO AGE AND AGEING
LA English
DT Review
ID C VIRUS-INFECTION; AUTOIMMUNE HEPATITIS; WILSONS-DISEASE;
CLINICAL-FEATURES; HEPATOCELLULAR-CARCINOMA; ELDERLY-PATIENTS;
PROGNOSIS; PREDICTORS; DIAGNOSIS; CIRRHOSIS
AB The prevalence of chronic liver disease is increasing in the elderly population. With a mostly asymptomatic or non-specific presentation, these diseases may easily go undiagnosed. Abnormal liver function tests of unknown cause are a common reason for referral to secondary care. Investigating the older person with abnormal liver function is important; even with mild abnormalities, the same vigilance should be applied to an older person as in a young person. Liver biopsy is safe but often overlooked in this age group and may provide useful information to diagnose, direct therapy and prognosticate. Treatment options are similar for all age groups, with a few subtle differences, although further evidence is frequently required for the older population. Morbidity and age-adjusted mortality are often more severe in older people, and therefore early diagnosis and intervention is important. Presented here are the most common chronic liver diseases that geriatricians are likely to encounter in clinical practise. Their epidemiology, clinical features, investigation, treatment and mortality are described with a particular focus on the elderly population.
C1 [Frith, James; Jones, David; Newton, Julia L.] Univ Newcastle, Liver Theme & Inst Cellular Med, Biomed Res Ctr Ageing, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
C3 Newcastle University - UK
RP Newton, JL (corresponding author), Univ Newcastle, Liver Theme & Inst Cellular Med, Biomed Res Ctr Ageing, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
EM Julia.newton@nuth.nhs.uk
OI Newton, Julia/0000-0002-1249-5253; Frith, James/0000-0002-6491-3701
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NR 30
TC 72
Z9 79
U1 1
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0002-0729
EI 1468-2834
J9 AGE AGEING
JI Age Ageing
PD JAN
PY 2009
VL 38
IS 1
BP 11
EP 18
DI 10.1093/ageing/afn242
PG 8
WC Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Geriatrics & Gerontology
GA 395IP
UT WOS:000262518100005
PM 19029099
OA Bronze
DA 2025-01-07
ER
PT J
AU Antonelli, A
Ferrari, SM
Ruffilli, I
Fallahi, P
AF Antonelli, Alessandro
Ferrari, Silvia Martina
Ruffilli, Ilaria
Fallahi, Poupak
TI Cytokines and HCV-related autoimmune disorders
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Chronic hepatitis C; Cryoglobulinemia; Thyroiditis; Diabetes; CXCL10;
Cytokines
ID HEPATITIS-C VIRUS; NATURAL-KILLER-CELLS; CCL2 SERUM-LEVELS; MOTIF LIGAND
9; MIXED CRYOGLOBULINEMIA; IFN-GAMMA; THYROID-CANCER; GRAVES-DISEASE;
T-CELLS; CIRCULATING CXCL11
AB Cytokines are intercellular mediators involved in viral control and liver damage being induced by infection with hepatitis C virus (HCV). The complex cytokine network operating during initial infection allows a coordinated, effective development of both innate and adaptive immune responses. However, HCV interferes with cytokines at various levels and escapes immune response by inducing a T-helper (Th)2/T cytotoxic 2 cytokine profile. Inability to control infection leads to the recruitment of inflammatory infiltrates into the liver parenchyma by interferon (IFN)-gamma-inducible CXC chemokine ligand (CXCL)9, -10, and -11 chemokines, which results in sustained liver damage and eventually in liver cirrhosis. The most important systemic HCV-related extrahepatic diseases-mixed cryoglobulinemia, lymphoproliferative disorders, thyroid autoimmune disorders, and type 2 diabetes-are associated with a complex dysregulation of the cytokine/chemokine network, involving proinflammatory and Th1 chemokines. The therapeutical administration of cytokines such as IFN-alpha may result in viral clearance during persistent infection and revert this process. Theoretically agents that selectively neutralize CXCL10 could increase patient responsiveness to traditional IFN-based HCV therapy. Several studies have reported IL-28B polymorphisms and circulating CXCL10 may be a prognostic markers for HCV treatment efficacy in HCV genotype 1 infection.
C1 [Antonelli, Alessandro; Ferrari, Silvia Martina; Ruffilli, Ilaria; Fallahi, Poupak] Univ Pisa, Dept Clin & Expt Med, I-56126 Pisa, Italy.
C3 University of Pisa
RP Antonelli, A (corresponding author), Univ Pisa, Dept Clin & Expt Med, Via Savi 10, I-56126 Pisa, Italy.
EM alessandro.antonelli@med.unipi.it
RI Fallahi, Poupak/AAC-6041-2022; Antonelli, Alessandro/AAU-2291-2020
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NR 98
TC 24
Z9 27
U1 0
U2 6
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD DEC
PY 2014
VL 60
IS 2-3
SI SI
BP 311
EP 319
DI 10.1007/s12026-014-8569-1
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AW6YT
UT WOS:000346412300019
PM 25381483
DA 2025-01-07
ER
PT J
AU Shi, YZ
Dong, H
Sun, SW
Wu, XQ
Fang, JS
Zhao, JB
Han, JM
Li, ZY
Wu, HX
Liu, LA
Wu, WH
Tian, Y
Yuan, GD
Fan, XD
Xu, C
AF Shi, Yingzhou
Dong, Hang
Sun, Shiwei
Wu, Xiaoqin
Fang, Jiansong
Zhao, Jianbo
Han, Junming
Li, Zongyue
Wu, Huixiao
Liu, Luna
Wu, Wanhong
Tian, Yang
Yuan, Guandou
Fan, Xiude
Xu, Chao
TI Protein-centric omics analysis reveals circulating complements linked to
non-viral liver diseases as potential therapeutic targets
SO CLINICAL AND MOLECULAR HEPATOLOGY
LA English
DT Article
DE Liver diseases; Complement system proteins; Mendelian randomization
analysis; Drug repositioning
ID FATTY LIVER; HEPATOCELLULAR-CARCINOMA; THALIDOMIDE; CIRRHOSIS
AB Background/Aims: To evaluate the causal correlation between complement components and non -viral liver diseases and their potential use as druggable targets. Methods: We conducted Mendelian randomization (MR) to assess the causal role of circulating complements in the risk of non -viral liver diseases. A complement -centric protein interaction network was constructed to explore biological functions and identify potential therapeutic options. Results: In the MR analysis, genetically predicted levels of complement C1q C chain (C1QC) were positively associated with the risk of autoimmune hepatitis (odds ratio 1.125, 95% confidence interval 1.018-1.244), while complement factor -related protein 5 (CFHR5) was positively associated with the risk of primary sclerosing cholangitis (PSC;1.193, 1.048- 1.357). On the other hand, CFHR1 (0.621, 0.497-0.776) and CFHR2 (0.824, 0.703-0.965) were inversely associated with the risk of alcohol -related cirrhosis. There were also significant inverse associations between C8 gamma chain (C8G) and PSC (0.832, 0.707-0.979), as well as the risk of metabolic dysfunction -associated steatotic liver disease (1.167, 1.036-1.314). Additionally, C1S (0.111, 0.018-0.672), C7 (1.631, 1.190-2.236), and CFHR2 (1.279, 1.059-1.546) were significantly associated with the risk of hepatocellular carcinoma. Proteins from the complement regulatory networks and various liver diseaserelated proteins share common biological processes. Furthermore, potential therapeutic drugs for various liver diseases were identified through drug repurposing based on the complement regulatory network. Conclusions: Our study suggests that certain complement components, including C1S, C1QC, CFHR1, CFHR2, CFHR5, C7, and C8G, might play a role in non -viral liver diseases and could be potential targets for drug development. (Clin Mol Hepatol 2024;30:80-97)
C1 [Shi, Yingzhou; Dong, Hang; Liu, Luna; Tian, Yang; Xu, Chao] Shandong Univ, Shandong Prov Hosp, Dept Endocrinol, Jinan, Shandong, Peoples R China.
[Shi, Yingzhou; Dong, Hang; Sun, Shiwei; Zhao, Jianbo; Han, Junming; Li, Zongyue; Wu, Huixiao; Liu, Luna; Wu, Wanhong; Tian, Yang; Fan, Xiude; Xu, Chao] Minist Educ, Key Lab Endocrine Glucose & Lipids Metab & Brain A, Jinan, Shandong, Peoples R China.
[Shi, Yingzhou; Dong, Hang; Sun, Shiwei; Zhao, Jianbo; Han, Junming; Li, Zongyue; Wu, Huixiao; Liu, Luna; Wu, Wanhong; Tian, Yang; Fan, Xiude; Xu, Chao] Shandong First Med Univ, Shandong Prov Hosp, Dept Endocrinol, Jinan, Shandong, Peoples R China.
[Shi, Yingzhou; Dong, Hang; Sun, Shiwei; Zhao, Jianbo; Han, Junming; Li, Zongyue; Wu, Huixiao; Liu, Luna; Wu, Wanhong; Tian, Yang; Fan, Xiude; Xu, Chao] Shandong Clin Res Ctr Diabet & Metab Dis, Jinan, Shandong, Peoples R China.
[Shi, Yingzhou; Dong, Hang; Sun, Shiwei; Zhao, Jianbo; Han, Junming; Li, Zongyue; Wu, Huixiao; Liu, Luna; Wu, Wanhong; Tian, Yang; Fan, Xiude; Xu, Chao] Shandong Inst Endocrine & Metab Dis, Jinan, Shandong, Peoples R China.
[Shi, Yingzhou; Dong, Hang; Sun, Shiwei; Zhao, Jianbo; Han, Junming; Li, Zongyue; Wu, Huixiao; Liu, Luna; Wu, Wanhong; Tian, Yang; Fan, Xiude; Xu, Chao] Chuangxin China Innovat Base Stem Cell & Gene Ther, Jinan, Shandong, Peoples R China.
[Shi, Yingzhou; Dong, Hang; Sun, Shiwei; Zhao, Jianbo; Han, Junming; Li, Zongyue; Wu, Huixiao; Liu, Luna; Wu, Wanhong; Tian, Yang; Fan, Xiude; Xu, Chao] Shandong Engn Lab Prevent & Control Endocrine & Me, Jinan, Shandong, Peoples R China.
[Shi, Yingzhou; Dong, Hang; Sun, Shiwei; Zhao, Jianbo; Han, Junming; Li, Zongyue; Wu, Huixiao; Liu, Luna; Wu, Wanhong; Tian, Yang; Fan, Xiude; Xu, Chao] Shandong Engn Res Ctr Stem Cell & Gene Therapy End, Jinan, Shandong, Peoples R China.
[Wu, Xiaoqin] Cleveland Clin, Northern Ohio Alcohol Ctr, Dept Inflammat & Immun, Cleveland, OH USA.
[Fang, Jiansong] Guangzhou Univ Chinese Med, Sci & Technol Innovat Ctr, Guangzhou, Guangdong, Peoples R China.
[Zhao, Jianbo] Ningxia Med Univ, Clin Med Coll, Yinchuan, Ningxia, Peoples R China.
[Yuan, Guandou] Guangxi Med Univ, Affiliated Hosp 1, Div Hepatobiliary Surg, Nanning, Guangxi, Peoples R China.
[Xu, Chao] Shandong Univ, Shandong Prov Hosp, Jinan 250021, Shandong, Peoples R China.
[Fan, Xiude] Shandong First Med Univ, Shandong Prov Hosp, Jinan 250021, Shandong, Peoples R China.
[Yuan, Guandou] Guangxi Med Univ, Affiliated Hosp 1, Div Hepatobiliary Surg, Nanning 530021, Guangxi, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
Sciences; Shandong University; Shandong First Medical University &
Shandong Academy of Medical Sciences; Cleveland Clinic Foundation;
Guangzhou University of Chinese Medicine; Ningxia Medical University;
Guangxi Medical University; Shandong First Medical University & Shandong
Academy of Medical Sciences; Shandong University; Shandong First Medical
University & Shandong Academy of Medical Sciences; Guangxi Medical
University
RP Xu, C (corresponding author), Shandong Univ, Shandong Prov Hosp, Jinan 250021, Shandong, Peoples R China.; Fan, XD (corresponding author), Shandong First Med Univ, Shandong Prov Hosp, Jinan 250021, Shandong, Peoples R China.; Yuan, GD (corresponding author), Guangxi Med Univ, Affiliated Hosp 1, Div Hepatobiliary Surg, Nanning 530021, Guangxi, Peoples R China.
EM dr_yuangd@gxmu.edu.cn; fanxiudexjtu@163.com; doctorxuchao@163.com
RI ryan, Shrink/GVU-8630-2022
OI Liu, Luna/0009-0004-4209-0718
FU National Natural Science Foundation [82200659]; Natural Science
Foundation of Shandong Province [ZR20220H002]
FX This work was supported by the National Natural Science Foundation
(Grants No. 82200659) , and the Natural Science Foundation of Shandong
Province (Grant No. ZR20220H002) .
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NR 45
TC 6
Z9 6
U1 2
U2 8
PU KOREAN ASSOC STUDY LIVER
PI SEOUL
PA RM A1210, 53 MAPO-DAERO, MAPOTRAPALACE, DOWHA-DONG, MAPO-GU, SEOUL,
04158, SOUTH KOREA
SN 2287-2728
EI 2287-285X
J9 CLIN MOL HEPATOL
JI Clin. Mol. Hepatol.
PD JAN
PY 2024
VL 30
IS 1
DI 10.3350/cmh.2023.0343
PG 19
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA LK4M4
UT WOS:001186681200010
PM 38061333
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kamada, Y
Sumida, Y
Takahashi, H
Fujii, H
Miyoshi, E
Nakajima, A
AF Kamada, Yoshihiro
Sumida, Yoshio
Takahashi, Hirokazu
Fujii, Hideki
Miyoshi, Eiji
Nakajima, Atsushi
CA Japan Study Grp NAFLD JSG NAFLD
TI Utility of Mac-2 binding protein glycosylation isomer as an excellent
biomarker for the prediction of liver fibrosis, activity, and
hepatocellular carcinoma onset: an expert review
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review; Early Access
DE MASLD/MASH; Chronic hepatitis type C; Chronic hepatitis type B;
Autoimmune hepatitis; Primary biliary cholangitis
ID POSITIVE MAC-2-BINDING PROTEIN; CHRONIC HEPATITIS-B; ELEVATED
SERUM-LEVELS; DISEASE; ASSOCIATION; LEVEL; GLYCOPROTEIN; SUPERFAMILY;
PROGRESSION; WFA(+)-M2BP
AB Mac-2 binding protein glycosylation isomer (M2BPGi) is a liver fibrosis biomarker that originated in Japan and has been covered by health insurance for 10 years. M2BPGi is useful not only for liver fibrosis stage prediction but also for assessment of the degree of liver inflammation and prediction of hepatocellular carcinoma development. The usefulness of M2BPGi for assessing disease progression in patients with various chronic liver diseases has been demonstrated over the past decade in a large number of patients. Recently, there have been many reports from outside Japan, including reports from South Korea, Taiwan, Hong Kong, and China. These studies demonstrated that M2BPGi is an excellent biomarker that can evaluate the progression of liver fibrosis in chronic liver disease. It is also an excellent indicator of liver activity. Recently, a quantitative M2BPGi (M2BPGi-Qt) assay was developed, and future validation in real-world settings is expected. This will enable diagnosis of the progression of liver fibrosis based on more precise test results and is expected to contribute to the early detection and follow-up of diseases caused by chronic hepatitis, as well as post-treatment monitoring. The significance of the M2BPGi-Qt assay will likely become clearer as real-world data accumulate. If new cutoff values for each chronic liver disease stage and activity level using the M2BPGi-Qt assay are set based on real-world data, it is expected that this will become a useful tool to identify cases of liver fibrosis and monitor the progression of chronic liver disease.
C1 [Kamada, Yoshihiro] Osaka Univ, Dept Adv Metab Hepatol, Grad Sch Med, 1-7 Yamadaoka, Suita, Osaka 5650871, Japan.
[Sumida, Yoshio] Int Univ Healthcare & Welf, Grad Sch Healthcare Management, 4-1-26 Akasaka,Minato Ku, Tokyo 1078402, Japan.
[Takahashi, Hirokazu] Saga Univ Hosp, Liver Ctr, 5-1-1 Nabeshima, Saga 8498501, Japan.
[Fujii, Hideki] Osaka Metropolitan Univ, Grad Sch Med, Dept Hepatol, 1-4-3 Asahimachi, Osaka 5458585, Japan.
[Miyoshi, Eiji] Osaka Univ, Grad Sch Med, Dept Mol Biochem & Clin Invest, Suita, Osaka 5650871, Japan.
[Nakajima, Atsushi] Yokohama City, Dept Gastroenterol & Hepatol, Grad Sch Med, Univ Grad Sch Med, 3-9 Fukuura,Kanazawa Ku, Yokohama 2360004, Japan.
C3 Osaka University; Saga University; Osaka Metropolitan University; Osaka
University
RP Sumida, Y (corresponding author), Int Univ Healthcare & Welf, Grad Sch Healthcare Management, 4-1-26 Akasaka,Minato Ku, Tokyo 1078402, Japan.
EM ykamada@sahs.med.osaka-u.ac.jp; sumida19701106@yahoo.co.jp;
takahas2@cc.saga-u.ac.jp; fujiirola@yahoo.co.jp;
emiyoshi@sahs.med.osaka-u.ac.jp; nakajima-tky@umin.ac.jp
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NR 105
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD 2024 DEC 9
PY 2024
DI 10.1007/s00535-024-02179-8
EA DEC 2024
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA O7F9W
UT WOS:001372752500001
PM 39652103
DA 2025-01-07
ER
PT J
AU Barreiros, AP
Chiorean, L
Braden, B
Dietrich, CF
AF Barreiros, A. P.
Chiorean, L.
Braden, B.
Dietrich, C. F.
TI Ultrasound in Rare Diffuse Liver Disease
SO ZEITSCHRIFT FUR GASTROENTEROLOGIE
LA English
DT Article
DE guidelines; Wilson's disease; schistosomiasis; PSC; PBC; viral
hepatitis; autoimmune hepatitis
ID CONTRAST-ENHANCED ULTRASOUND; CLINICAL-PRACTICE RECOMMENDATIONS; FOCAL
FATTY INFILTRATION; PERIHEPATIC LYMPH-NODES; IMAGING FINDINGS;
HEPATOCELLULAR-CARCINOMA; SONOGRAPHIC DETECTION; ABDOMINAL ULTRASOUND;
ANTIVIRAL RESPONSE; EFSUMB GUIDELINES
AB Ultrasound is often the first imaging procedure performed in the evaluation of individuals with suspected or known liver disease. Despite technical advances in ultrasound techniques, sonographic detection and evaluation of diffuse liver disease still remains difficult. This is due to the fact that diffuse liver disease does not always cause distortion of the liver parenchymal texture, internal liver architecture, or shape of the liver. On the other hand, the size of the liver, the echo pattern of the hepatic parenchyma, the analysis of intrahepatic vessels and alterations in perihepatic structures and lymph nodes can be helpful sonographic parameters of diffuse liver disease. Until now, the sonographic appearance of some rare diffuse liver diseases is not well known. However, there are some typical sonomorphological signs that, once identified, can facilitate the differentiation between various diseases. The aim of this paper is to highlight some typical ultrasound findings of liver parenchyma and perihepatic lymph node structures in rare diffuse liver diseases based on a review of published data.
C1 [Barreiros, A. P.] Univ Regensburg, Univ Hosp, Dept Med 1, D-93053 Regensburg, Germany.
[Chiorean, L.] Octavian Fodor Inst Gastroenterol & Hepatol, Dept Ultrasonog, Cluj Napoca, Romania.
[Braden, B.] Oxford Univ Hosp, Translat Gastroenterol Unit, Oxford, England.
[Dietrich, C. F.] Caritaskrankenhaus, Med Dept 2, Bad Mergentheim, Germany.
C3 University of Regensburg; Regional Institute of Gastroenterology &
Hepatology; Caritas Hospital Bad Mergentheim
RP Dietrich, CF (corresponding author), Caritaskrankenhaus Bad Mergentheim, Med Klin, Uhlandstr 7, D-97980 Bad Mergentheim, Germany.
EM christoph.dietrich@ckbm.de
RI Dietrich, Christoph/AAB-7514-2020; Braden, Barbara/AAH-8693-2021
OI Braden, Barbara/0000-0002-8534-6873; Dietrich, Christoph
FDiet/0000-0001-6015-6347
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NR 79
TC 19
Z9 19
U1 0
U2 5
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0044-2771
EI 1439-7803
J9 Z GASTROENTEROL
JI Z. Gastroent.
PD NOV
PY 2014
VL 52
IS 11
BP 1247
EP 1256
DI 10.1055/s-0034-1384996
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AT4WZ
UT WOS:000344944100001
PM 25390211
DA 2025-01-07
ER
PT J
AU Wen, GX
Zhou, T
Gu, WJ
AF Wen, Guoxia
Zhou, Tong
Gu, Wanjun
TI The potential of using blood circular RNA as liquid biopsy biomarker for
human diseases
SO PROTEIN & CELL
LA English
DT Review
DE peripheral blood circular RNA; liquid biopsy; human diseases;
translational biomarkers
ID NONINVASIVE DIAGNOSTIC BIOMARKER; MICROARRAY EXPRESSION PROFILE; LONG
NONCODING RNAS; CELL LUNG-CANCER; PERIPHERAL-BLOOD; EXTRACELLULAR
VESICLES; MONONUCLEAR-CELLS; HEPATOCELLULAR-CARCINOMA; PROGNOSTIC
BIOMARKER; PROMISING BIOMARKER
AB Circular RNA (circRNA) is a novel class of single-stranded RNAs with a closed loop structure. The majority of circRNAs are formed by a back-splicing process in pre-mRNA splicing. Their expression is dynamically regulated and shows spatiotemporal patterns among cell types, tissues and developmental stages. CircRNAs have important biological functions in many physiological processes, and their aberrant expression is implicated in many human diseases. Due to their high stability, circRNAs are becoming promising biomarkers in many human diseases, such as cardiovascular diseases, autoimmune diseases and human cancers. In this review, we focus on the translational potential of using human blood circRNAs as liquid biopsy biomarkers for human diseases. We highlight their abundant expression, essential biological functions and significant correlations to human diseases in various components of peripheral blood, including whole blood, blood cells and extracellular vesicles. In addition, we summarize the current knowledge of blood circRNA biomarkers for disease diagnosis or prognosis.
C1 [Wen, Guoxia; Gu, Wanjun] Southeast Univ, Sch Biol Sci & Med Engn, State Key Lab Bioelect, Nanjing 210096, Peoples R China.
[Zhou, Tong] Univ Nevada, Reno Sch Med, Dept Physiol & Cell Biol, Reno, NV 89557 USA.
C3 Southeast University - China; Nevada System of Higher Education (NSHE);
University of Nevada Reno
RP Gu, WJ (corresponding author), Southeast Univ, Sch Biol Sci & Med Engn, State Key Lab Bioelect, Nanjing 210096, Peoples R China.; Zhou, T (corresponding author), Univ Nevada, Reno Sch Med, Dept Physiol & Cell Biol, Reno, NV 89557 USA.
EM tongz@med.unr.edu; wanjungu@seu.edu.cn
RI Gu, Wanjun/B-3998-2010; Wen, Autumn/JUF-0854-2023
OI Zhou, Tong/0000-0003-2361-1931; Wen, Guoxia/0000-0001-6544-8242
FU National Key R&D Program of China [2018YFC1314900, 2018YFC1314902];
National Natural Science Foundation of China [61571109]; Fundamental
Research Funds for the Central Universities [2242017K3DN04]
FX We thank Ms. Aiping Zhang for editing the figures. This work was funded
by Grants from National Key R&D Program of China (2018YFC1314900,
2018YFC1314902), National Natural Science Foundation of China
(61571109), and the Fundamental Research Funds for the Central
Universities (2242017K3DN04).
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TC 123
Z9 130
U1 5
U2 51
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1674-800X
EI 1674-8018
J9 PROTEIN CELL
JI Protein Cell
PD DEC
PY 2021
VL 12
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BP 911
EP 946
DI 10.1007/s13238-020-00799-3
EA NOV 2020
PG 36
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA XP0OA
UT WOS:000583640700001
PM 33131025
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Dombrowski, F
Mathieu, C
Evert, M
AF Dombrowski, F
Mathieu, C
Evert, M
TI Hepatocellular neoplasms induced by low-number pancreatic islet
transplants in autoimmune diabetic BB/Pfd rats
SO CANCER RESEARCH
LA English
DT Article
ID PRENEOPLASTIC HEPATIC FOCI; INSULIN-RECEPTOR SUBSTRATE-1; BB RAT;
N-NITROSOMORPHOLINE; EDMONTON PROTOCOL; TRANSGENIC MICE; UNITED-STATES;
LIVER-DISEASE; STREPTOZOTOCIN; HEPATOCARCINOGENESIS
AB It has been shown that combined high local hyperinsulinism and hyperglycemia after low-number islet transplantation into the livers of streptozotocin-diabetic rats lead to the development of hepatocellular neoplasms but a substantial cocarcinogenic effect of genotoxic streptozotocin could not be ruled out completely. Thus, we herein investigated this model in BB/Pfd rats (n = 805; nine experimental groups), which develop spontaneous autoimmune diabetes similar to human type 1 diabetes. After low-number islet transplantation (n = 450), the liver acini downstream of the islets show insulin-induced alterations: massive glycogen and/or fat accumulation, translocation of the insulin receptor, decrease in glucose-6-phosphatase activity, increase in expression of insulin-like growth factor (IGF)-I, IGF-II/mannose-6-phosphate receptor, insulin receptor substrate-1, Raf-1, and Mck-1, corresponding to clear cell preneoplastic foci of altered hepatocytes known from chemical hepatocarcinogenesis and identical to that in streptozotocin-diabetic Lewis rats. After 6 months, many altered liver acini progressed to other types of preneoplasias often accompanied by an overexpression of the glutathione-S transferase (placental form), IGF-I receptor, and transforming growth factor (TGF)-alpha. After 12 to 15 and 15 to 18 months, 52% and 100% of the animals showed one or multiple hepatocellular adenomas or hepatocellular carcinomas (HCCs), respectively. Conclusively, this study identifies combined hyperinsulinism and hyperglycemia as a carcinogenic mechanism for the development of HCCs in diabetic rats. Hepatocarcinogenesis is independent from additional genotoxic compounds (i.e., streptozotocin), but is primarily triggered by increased intracellular insulin signaling via pathways associated with cell growth and proliferation, such as the Ras-Raf-mitogen-activated protein kinase pathway and the IGF system, and secondarily involves other growth factors, such as TGF-alpha.
C1 Univ Magdeburg, Inst Pathol, D-39120 Magdeburg, Germany.
Katholieke Univ Leuven, Rega Inst, Lab Expt Med & Endocrinol, B-3000 Louvain, Belgium.
C3 Otto von Guericke University; KU Leuven
RP Univ Magdeburg, Inst Pathol, Leipziger Str 44, D-39120 Magdeburg, Germany.
EM Frank.Dombrowski@medizin.uni-magdeburg.de
RI mathieu, chantal/ABD-5505-2021
OI Mathieu, Chantal/0000-0002-4055-5233
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[No title captured]
NR 51
TC 55
Z9 58
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD FEB 1
PY 2006
VL 66
IS 3
BP 1833
EP 1843
DI 10.1158/0008-5472.CAN-05-2787
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 009FD
UT WOS:000235095900072
PM 16452245
DA 2025-01-07
ER
PT J
AU Iwamoto, S
Kido, M
Aoki, N
Nishiura, H
Maruoka, R
Ikeda, A
Okazaki, T
Chiba, T
Watanabe, N
AF Iwamoto, Satoru
Kido, Masahiro
Aoki, Nobuhiro
Nishiura, Hisayo
Maruoka, Ryutaro
Ikeda, Aki
Okazaki, Taku
Chiba, Tsutomu
Watanabe, Norihiko
TI TNF-α is essential in the induction of fatal autoimmune hepatitis in
mice through upregulation of hepatic CCL20 expression
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE Mouse model; Autoimmune hepatitis; TNF-alpha; CCL20; TNF-alpha
antagonist
ID IFN-GAMMA; T-CELLS; HEPATOCELLULAR-CARCINOMA; LIVER-TRANSPLANTATION;
CONCANAVALIN-A; HUMAN-DISEASES; MOUSE MODEL; MECHANISMS; BLOCKADE;
INJURY
AB It is unclear what roles TNF-alpha has in the development of autoimmune hepatitis (AIH) and whether AIH is responsive to anti-TNF-alpha. We recently developed a mouse model of fatal AIH that develops in PD-1-deficient mice thymectomized three days after birth, finding that CCR6-CCL20 axis-dependent migration of dysregulated splenic T cells is crucial to induce AIH. In this study, we show the indispensable role of TNF-alpha in the development of AIH. Administering anti-TNF-alpha prevented the induction, but treatment by anti-TNF-alpha after the induction did not suppress progression. Administering anti-TNF-alpha did not prevent splenic T-cell activation, but did suppress hepatic CCL20 expression. In contrast, administering anti-CCL20 suppressed AIH but not elevated serum TNF-alpha levels. TNF-alpha stimulation enhanced CCL20 expression in hepatocytes. These findings suggest that TNF-alpha is essential in the induction of AIH through upregulation of hepatic CCL20 expression, which allows migration of dysregulated splenic T cells. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Iwamoto, Satoru; Kido, Masahiro; Aoki, Nobuhiro; Nishiura, Hisayo; Maruoka, Ryutaro; Ikeda, Aki; Watanabe, Norihiko] Kyoto Univ, Grad Sch Med, Ctr Innovat Immunoregulat Technol & Therapeut, Kyoto 6068501, Japan.
[Iwamoto, Satoru; Kido, Masahiro; Aoki, Nobuhiro; Nishiura, Hisayo; Maruoka, Ryutaro; Ikeda, Aki; Chiba, Tsutomu; Watanabe, Norihiko] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Kyoto 6068501, Japan.
[Okazaki, Taku] Univ Tokushima, Inst Genome Res, Div Immune Regulat, Tokushima 7708503, Japan.
C3 Kyoto University; Kyoto University; Tokushima University
RP Watanabe, N (corresponding author), Kyoto Univ, Grad Sch Med, Ctr Innovat Immunoregulat Technol & Therapeut, Kyoto 6068501, Japan.
EM norihiko@kuhp.kyoto-u.ac.jp
OI Okazaki, Taku/0000-0003-4790-1925
FU Special Coordination Funds for Promoting Science and Technology of the
Japanese Government; Astellas Pharma Inc. in the Formation of Innovation
Center for the Fusion of Advanced Technologies Program; Japan Society
for the Promotion of Science (JSPS) [21229009, 23590973]; Ministry of
Health, Labour and Welfare, Japan; Kato Memorial Trust for Nambyo
Research; Waksman Foundation of Japan; Grants-in-Aid for Scientific
Research [23590973, 24659151] Funding Source: KAKEN
FX We thank Dr. Dovie Wylie for assistance in preparation of the
manuscript; Ms. Chigusa Tanaka for excellent technical assistance; Drs.
Tasuku Honjo, Shuh Narumiya, Nagahiro Minato, Shimon Sakaguchi, Takeshi
Watanabe, and Ichiro Aramori for critical discussion and suggestions.
Funding: The Center for Innovation in Immunoregulative Technology and
Therapeutics is supported in part by the Special Coordination Funds for
Promoting Science and Technology of the Japanese Government and in part
by Astellas Pharma Inc. in the Formation of Innovation Center for the
Fusion of Advanced Technologies Program. This work is partially
supported by Grants-in-aid for Scientific Research 21229009 and 23590973
from the Japan Society for the Promotion of Science (JSPS), a Health and
Labour Sciences Research Grant for Research on Intractable Diseases, and
Research on Hepatitis from the Ministry of Health, Labour and Welfare,
Japan, Grants-in-Aid for Research by The Kato Memorial Trust for Nambyo
Research, and The Waksman Foundation of Japan.
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NR 33
TC 37
Z9 39
U1 1
U2 12
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD JAN
PY 2013
VL 146
IS 1
BP 15
EP 25
DI 10.1016/j.clim.2012.10.008
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 143AP
UT WOS:000318839000004
PM 23178752
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Zhao, XY
Rakhda, MIA
Wang, TI
Jia, JD
AF Zhao, X. -Y.
Rakhda, M. I. A.
Wang, T. -I.
Jia, J. -D.
TI Immunoglobulin G4-Associated De Novo Autoimmune Hepatitis After Liver
Transplantation for Chronic Hepatitis B- and C-Related Cirrhosis and
Hepatocellular Carcinoma: A Case Report With Literature Review
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Review
ID PLASMA-CELL HEPATITIS; REJECTION; DIAGNOSIS; VARIANT
AB Immunoglobulin G4 (IgG4)-associated autoimmune hepatitis (AIH) was recognized as a new disease entity; however, IgG4-associated de novo AIH after the liver transplantation had not been reported yet. Herein we have described a 56-year-old man who developed IgG4 de novo All as 1 year post liver transplantation after receiving pegylated interferon alpha-2a and ribavirin therapy for hepatitis C virus recurrence. The histopathologic evidence showed an aggressive lymphoplasmacytic interface hepatitis with centrilobular necrosis (plasma cells > 30%) and IgG4-positive plasma cells (>10 per high power field). Serum IgG (9220 mg/dL) and IgG4 (3289 mg/dL) were also elevated. Improvement of liver function tests (LFTs) by prednisone and azathioprine therapy are manifested as normalized alanine aminotransferase and IgG levels. IgG4 relates to more severe histological activity; however, it is believed to be a good prognostic predictor of a response to prednisone plus azathioprine therapy especially with early diagnosis and timely management.
C1 [Zhao, X. -Y.; Jia, J. -D.] Capital Med Univ, Beijing Friendship Hosp, Liver Res Ctr, Beijing, Peoples R China.
[Rakhda, M. I. A.] Capital Med Univ, Int Sch, Beijing, Peoples R China.
[Wang, T. -I.] China Japan Friendship Hosp, Dept Pathol, Beijing, Peoples R China.
C3 Capital Medical University; Capital Medical University; China-Japan
Friendship Hospital
RP Zhao, XY (corresponding author), Beijing Friendship Hosp, Liver Res Ctr, 95 Yong An Rd, Beijing, Peoples R China.
EM Zhao_xinyan@ccmu.edu.cn
OI zhao, xinyan/0000-0002-8016-4368
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NR 19
TC 10
Z9 14
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0041-1345
EI 1873-2623
J9 TRANSPL P
JI Transplant. Proc.
PD MAR
PY 2013
VL 45
IS 2
BP 824
EP 827
DI 10.1016/j.transproceed.2012.02.049
PG 4
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA 114WA
UT WOS:000316772500065
PM 23498828
DA 2025-01-07
ER
PT J
AU Shah, P
Choi, SW
Kim, HJ
Cho, SK
Thulstrup, PW
Bjerrum, MJ
Bhang, YJ
Ahn, JC
Yang, SW
AF Shah, Pratik
Choi, Suk Won
Kim, Ho-jin
Cho, Seok Keun
Thulstrup, Peter Waaben
Bjerrum, Morten Jannik
Bhang, Yong-Joo
Ahn, Jong Cheol
Yang, Seong Wook
TI DNA/RNA chimera templates improve the emission intensity and target the
accessibility of silver nanocluster-based sensors for human microRNA
detection
SO ANALYST
LA English
DT Article
ID PANCREATIC-CANCER CELLS; TO-MESENCHYMAL TRANSITION; BREAST-CANCER;
RNA/DNA OLIGONUCLEOTIDES; COLORECTAL-CANCER; EXPRESSION; RNA; MIR-200;
LET-7A; PROBES
AB In recent years microRNAs (miRNAs) have been established as important biomarkers in a variety of diseases including cancer, diabetes, cardiovascular disease, aging, Alzheimer's disease, asthma, autoimmune disease and liver diseases. As a consequence, a variety of monitoring methods for miRNAs have been developed, including a fast and simple method for miRNA detection by exploitation of the unique photoluminescence of DNA-templated silver nanoclusters (DNA/AgNCs). To increase the versatility of the AgNC-based method, we have adopted DNA/RNA chimera templates for AgNC-based probes, allowing response from several human miRNAs which are hardly detectable with DNA-based probes. Here, we demonstrate in detail the power of DNA/RNA chimera/AgNC probes in detecting two human miRNAs, let-7a and miR-200c. The DNA/RNA chimera-based probes are highly efficient to determine the level of miRNAs in several human cell lines.
C1 [Shah, Pratik; Cho, Seok Keun; Yang, Seong Wook] Univ Copenhagen, UNIK Ctr Synthet Biol, DK-1871 Copenhagen C, Denmark.
[Choi, Suk Won; Kim, Ho-jin; Bhang, Yong-Joo; Ahn, Jong Cheol] Seoulin Biosci Co Ltd, Seongnam Si, Gyeonggi Do, South Korea.
[Thulstrup, Peter Waaben; Bjerrum, Morten Jannik] Univ Copenhagen, Dept Chem, DK-2100 Copenhagen, Denmark.
C3 University of Copenhagen; University of Copenhagen
RP Yang, SW (corresponding author), Univ Copenhagen, UNIK Ctr Synthet Biol, Thorvaldsensvej 40, DK-1871 Copenhagen C, Denmark.
EM swyang@life.ku.dk
RI Thulstrup, Peter/V-6371-2019; Shah, Pratik/J-3557-2015; Thulstrup, Peter
Waaben/C-5598-2013
OI Choi, Suk Won/0000-0001-9372-1947; Shah, Pratik/0000-0003-4755-1267;
Thulstrup, Peter Waaben/0000-0002-9241-4352
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NR 53
TC 20
Z9 20
U1 2
U2 73
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 0003-2654
EI 1364-5528
J9 ANALYST
JI Analyst
PY 2015
VL 140
IS 10
BP 3422
EP 3430
DI 10.1039/c5an00093a
PG 9
WC Chemistry, Analytical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA CH7CF
UT WOS:000354192500017
PM 25759134
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Schmidtmann, I
Kraus, D
Weinmann, A
Pütz, K
Classen, P
Schleicher, EM
Boedecker-Lips, SC
Weinmann-Menke, J
AF Schmidtmann, Irene
Kraus, Daniel
Weinmann, Arndt
Puetz, Katharina
Classen, Paul
Schleicher, Eva Maria
Boedecker-Lips, Simone Cosima
Weinmann-Menke, Julia
TI Validation of the 2019 EULAR/ACR classification criteria for systemic
lupus erythematosus in an academic tertiary care centre
SO RMD OPEN
LA English
DT Article
DE Systemic Lupus Erythematosus; Lupus Erythematosus; Systemic; Autoimmune
Diseases
ID REVISED CRITERIA
AB ObjectivesTo assess the sensitivity and specificity of the 2019 EULAR/American College of Rheumatology (ACR) classification criteria for systemic lupus erythematosus (SLE) in outpatients at an academic tertiary care centre and to compare them to the 1997 ACR and the 2012 Systemic Lupus International Collaborating Clinics criteria. MethodsProspective and retrospective observational cohort study. Results3377 patients were included: 606 with SLE, 1015 with non-SLE autoimmune-mediated rheumatic diseases (ARD) and 1756 with non-ARD diseases (hepatocellular carcinoma, primary biliary cirrhosis, autoimmune hepatitis). The 2019 criteria were more sensitive than the 1997 criteria (87.0% vs 81.8%), but less specific (98.1% vs 99.5% in the entire cohort and 96.5% vs 98.8% in patients with non-SLE ARD), resulting in Youden Indexes for patients with SLE/non-SLE ARD of 0.835 and 0.806, respectively. The most sensitive items were history of antinuclear antibody (ANA) positivity and detection of anti-double-stranded deoxyribonucleic acid (dsDNA) antibodies. These were also the least specific items. The most specific items were class III/IV lupus nephritis and the combination of low C3 and low C4 complement levels, followed by class II/V lupus nephritis, either low C3 or low C4 complement levels, delirium and psychosis, when these were not attributable to non-SLE causes. ConclusionsIn this cohort from an independent academic medical centre, the sensitivity and specificity of the 2019 lupus classification criteria were confirmed. Overall agreement of the 1997 and the 2019 criteria was very good.
C1 [Schmidtmann, Irene] Johannes Gutenberg Univ Mainz, Inst Med Biostat Epidemiol & Informat IMBEI, Univ Med Ctr, Mainz, Germany.
[Kraus, Daniel; Weinmann, Arndt; Puetz, Katharina; Classen, Paul; Schleicher, Eva Maria; Boedecker-Lips, Simone Cosima; Weinmann-Menke, Julia] Johannes Gutenberg Univ Mainz, Dept Med 1, Univ Med Ctr, Mainz, Germany.
[Weinmann-Menke, Julia] Johannes Gutenberg Univ Mainz, Res Ctr Immunotherapy FZI, Univ Med Ctr, Mainz, Germany.
C3 Johannes Gutenberg University of Mainz; Johannes Gutenberg University of
Mainz; Johannes Gutenberg University of Mainz
RP Weinmann-Menke, J (corresponding author), Johannes Gutenberg Univ Mainz, Dept Med 1, Univ Med Ctr, Mainz, Germany.; Weinmann-Menke, J (corresponding author), Johannes Gutenberg Univ Mainz, Res Ctr Immunotherapy FZI, Univ Med Ctr, Mainz, Germany.
EM Julia.Weinmann-Menke@unimedizinmainz.de
RI Weinmann-Menke, Julia/ABC-3559-2021; Kraus, Daniel/AAD-4592-2021; Kraus,
Daniel/N-7631-2013
OI Weinmann-Menke, Julia/0000-0001-7344-8381; Kraus,
Daniel/0000-0002-6351-3706; Classen, Paul/0000-0002-9410-0525
FU Deutsche Forschungsgemeinschaft (DFG) [WE5779/2-3]; Clinician Scientist
Fellowship 'Else Kroener Research College' [2018_Kolleg.05]; Else Kroner
Fresenius Foundation [2019_A72]
FX This work was supported by the Deutsche Forschungsgemeinschaft (DFG),
grant no. WE5779/2-3, to JW-M. EMS is supported by the Clinician
Scientist Fellowship 'Else Kroener Research College: 2018_Kolleg.05'.
SCB-L is supported by the Clinician Scientist Fellowship 'TransMed
Jumpstart Program: 2019_A72' which is funded by the Else Kroner
Fresenius Foundation.
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NR 14
TC 6
Z9 6
U1 2
U2 3
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 2056-5933
J9 RMD OPEN
JI RMD Open
PD JUL
PY 2023
VL 9
IS 3
AR e003037
DI 10.1136/rmdopen-2023-003037
PG 6
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA M9SF3
UT WOS:001033532600003
PM 37419524
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Park, MK
Park, JS
Park, EM
Lim, MA
Kim, SM
Lee, DG
Baek, SY
Yang, EJ
Woo, JW
Lee, J
Kwok, SK
Kim, HY
Cho, ML
Park, SH
AF Park, Mi-Kyung
Park, Jin-Sil
Park, Eun-Mi
Lim, Mi-Ae
Kim, Sung-Min
Lee, Dong-Gun
Baek, Seung-Ye
Yang, Eun-Ji
Woo, Jung-Won
Lee, Jennifer
Kwok, Seung-Ki
Kim, Ho-Youn
Cho, Mi-La
Park, Sung-Hwan
TI Halofuginone Ameliorates Autoimmune Arthritis in Mice by Regulating the
Balance Between Th17 and Treg Cells and Inhibiting Osteoclastogenesis
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Article
ID T-CELLS; RHEUMATOID-ARTHRITIS; MEDIATED REGULATION; INDOLEAMINE
2,3-DIOXYGENASE; HEPATOCELLULAR-CARCINOMA; TRANSCRIPTION FACTOR;
DIFFERENTIATION; RANKL; KINASE; INFLAMMATION
AB Objective. The small molecule halofuginone has been shown to inhibit fibrosis, angiogenesis, and tumor progression. This study was undertaken to evaluate the effects of halofuginone in preventing autoimmune arthritis in mice.
Methods. The effects of halofuginone on joint diseases were assessed by clinical scoring and histologic analysis. Protein expression levels were confirmed by immunohistochemistry, enzyme-linked immunosorbent assay, flow cytometry, and/or Western blotting. The expression levels of messenger RNA (mRNA) for various molecules were determined by real-time polymerase chain reaction (PCR). Proliferation of osteoclast precursors was assessed by bromodeoxyuridine uptake. Osteoclast differentiation and activity were determined by quantifying tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells and area of re-sorbed bone.
Results. Treatment with halofuginone suppressed the development of autoimmune arthritis and reciprocally regulated Th17 cells and FoxP3+ Treg cells. These effects of halofuginone on Th17 differentiation involved increased signaling of ERK and reduction of STAT-3 and NF-ATc1 expression. Furthermore, halofuginone induced the expression of indoleamine 2,3-dioxygenase (IDO) in dendritic cells, leading to reduced production of Th17 cells. In addition, halofuginone prevented the formation and activity of osteoclasts through suppression of transcription factors, such as activator protein 1 and NF-ATc1, and inhibited cell cycle arrest by the committed osteoclast precursors via expression of Ccnd1 encoding cyclin D1.
Conclusion. Taken together, our results suggest that halofuginone is a promising therapeutic agent for the treatment of Th17 cell-mediated inflammatory diseases and bone diseases.
C1 [Park, Mi-Kyung; Park, Jin-Sil; Park, Eun-Mi; Lim, Mi-Ae; Kim, Sung-Min; Lee, Dong-Gun; Baek, Seung-Ye; Yang, Eun-Ji; Lee, Jennifer; Kwok, Seung-Ki; Kim, Ho-Youn; Cho, Mi-La; Park, Sung-Hwan] Catholic Univ Korea, Seoul 137701, South Korea.
[Woo, Jung-Won; Cho, Mi-La] Seoul St Marys Hosp, Seoul, South Korea.
C3 Catholic University of Korea; Seoul St. Mary's Hospital
RP Cho, ML (corresponding author), Catholic Univ Korea, Rheumatism Res Ctr, 222 Banpo Daero, Seoul 137701, South Korea.
EM iammila@catholic.ac.kr; rapark@catholic.ac.kr
RI Jung, SeungHyun/HTS-1049-2023; Park, Mi-Kyung/J-9643-2017; Lee,
Dong-Gun/IWD-9833-2023; Lee, Jeonghwan/C-5214-2011
FU Ministry of Education, Science, and Technology, Republic of Korea
[2005-0048480]; Ministry for Health, Welfare, and Family Affairs,
Republic of Korea [A092258]
FX Supported by the Ministry of Education, Science, and Technology,
Republic of Korea through funding to the National Research Foundation of
Korea (Basic Science Research Program grant number 2005-0048480) and by
the Ministry for Health, Welfare, and Family Affairs, Republic of Korea
(Korea Health Technology R&D Project grant number A092258).
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TC 25
Z9 31
U1 2
U2 19
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2326-5191
EI 2326-5205
J9 ARTHRITIS RHEUMATOL
JI Arthritis Rheumatol.
PD MAY
PY 2014
VL 66
IS 5
BP 1195
EP 1207
DI 10.1002/art.38313
PG 13
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA AJ0RM
UT WOS:000337363400016
PM 24782183
DA 2025-01-07
ER
PT J
AU Shizuru, JA
Negrin, RS
Weissman, IL
AF Shizuru, JA
Negrin, RS
Weissman, IL
TI Hematopoietic stem and progenitor cells: Clinical and preclinical
regeneration of the hematolymphoid system
SO ANNUAL REVIEW OF MEDICINE
SE Annual Review of Medicine
LA English
DT Review; Book Chapter
DE bone marrow; embryonic stem cell; transplantation; cancer; autoimmune
ID COLONY-STIMULATING FACTOR; BONE-MARROW-CELLS; COMMON LYMPHOID
PROGENITORS; VERSUS-HOST-DISEASE; ACUTE MYELOID-LEUKEMIA; SCID-HU MOUSE;
NATURAL-KILLER; FETAL LIVER; T-CELLS; AUTOIMMUNE-DISEASES
AB A vast literature exists on the biology of blood formation and regeneration under experimental and clinical conditions. The field of hematopoiesis was recently advanced by the capacity to purify to homogeneity primitive hematopoietic stem and progenitor cells. Isolation of cells at defined maturational stages has enhanced the understanding of the fundamental nature of stem cells, including how cell fate decisions are made, and this understanding is relevant to the development of other normal as well as malignant tissues. This review updates the basic biology of hematopoietic stem cells (HSC) and progenitors, the evolving use of purified HSC as grafts for clinical hematopoietic cell transplantation (HCT) including immune tolerance induction, and the application of HSC biology to other stem cell fields.
C1 Stanford Univ, Med Ctr, Div Blood & Marrow Transplantat, Stanford, CA 94305 USA.
Stanford Univ, Med Ctr, Dept Pathol, Stanford, CA 94305 USA.
C3 Stanford University; Stanford University
RP Stanford Univ, Med Ctr, Div Blood & Marrow Transplantat, Stanford, CA 94305 USA.
EM jshizuru@stanford.edu; negrs@stanford.edu; irv@stanford.edu
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NR 188
TC 266
Z9 322
U1 0
U2 20
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA
SN 0066-4219
J9 ANNU REV MED
JI Annu. Rev. Med.
PY 2005
VL 56
BP 509
EP 538
DI 10.1146/annurev.med.54.101601.152334
PG 30
WC Medicine, Research & Experimental
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 904ND
UT WOS:000227504100028
PM 15660525
DA 2025-01-07
ER
PT J
AU Österreicher, CH
Trauner, M
AF Oesterreicher, Christoph H.
Trauner, Michael
TI Animal models of biliary tract injury
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Review
DE biliary fibrosis; cholangiocyte; cholestasis; hepatic stellate cells;
inflammation; portal fibroblasts
ID EPITHELIAL-MESENCHYMAL TRANSITION; NF-KAPPA-B; SCLEROSING CHOLANGITIS;
LIVER FIBROSIS; MOUSE MODEL; BILE-ACIDS; PROLIFERATION; INFLAMMATION;
AUTOIMMUNE; MICE
AB Purpose of review
Cholestatic liver diseases with bile duct injury and biliary fibrosis account for a significant percentage of patients with end-stage liver disease and undergoing liver transplantation. A number of different animal models have been established and have added substantially to our understanding of the molecular mechanisms underlying this group of chronic liver diseases. In the present review, we discuss recent findings and new insight derived from different animal models of biliary tract injury and fibrosis.
Recent findings Cholangiocytes do not undergo epithelial to mesenchymal transition and do not contribute to the pool of biliary fibroblasts involved in extracellular matrix deposition. Rather cholangiocytes can acquire a reactive phenotype activating fibrogenesis through secretion of proinflammatory and profibrogenic mediators. Bile acid homeostasis is controlled by a gut-liver axis playing a crucial role in the adaptive response to bile duct injury and cholestasis. The nuclear factor-kappa B and hedgehog signaling pathways play a critical role in cholestatic liver injury and the emergence of liver cancer. Nuclear receptors are key mediators of adaptive response mechanisms in cholestasis and potential therapeutical targets.
Summary
Recent progress and mechanistic insights from mouse models have added to our understanding of the molecular mechanisms underlying cholestatic liver and biliary tract injury and pointed to new therapeutic options.
C1 [Trauner, Michael] Med Univ Vienna, Div Gastroenterol & Hepatol, Dept Internal Med 3, A-1090 Vienna, Austria.
[Oesterreicher, Christoph H.] Med Univ Vienna, Ctr Physiol & Pharmacol, Inst Pharmacol, A-1090 Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna
RP Trauner, M (corresponding author), Med Univ Vienna, Div Gastroenterol & Hepatol, Dept Internal Med 3, Waehringer Guer Tel 18-20, A-1090 Vienna, Austria.
EM michael.trauner@meduniwien.ac.at
RI Trauner, Michael/HCH-4032-2022
OI Trauner, Michael/0000-0002-1275-6425
FU Austrian Academy of Sciences; Austrian Science Foundation [P19118-B05,
F3008-B05]; Austrian Academy of Sciences at the Institute of
Pharmacology, Center for Physiology and Pharmacology, Medical University
Vienna; Austrian Science Fund (FWF) [P19118] Funding Source: Austrian
Science Fund (FWF)
FX The authors acknowledge funding from the Austrian Academy of Sciences
(APART-fellowship to C.H.O.) and the Austrian Science Foundation (grants
P19118-B05 and F3008-B05 to M.T.). C.H.O. is recipient of an
APART-fellowship of the Austrian Academy of Sciences at the Institute of
Pharmacology, Center for Physiology and Pharmacology, Medical University
Vienna. This work was supported by grants P19118-B05 and F3008-B05 from
the Austrian Science Foundation (to M. T.). There are no conflicts of
interest.
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NR 32
TC 8
Z9 10
U1 1
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0267-1379
EI 1531-7056
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD MAY
PY 2012
VL 28
IS 3
BP 239
EP 243
DI 10.1097/MOG.0b013e32835264d9
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 927YE
UT WOS:000302945700010
PM 22450892
DA 2025-01-07
ER
PT J
AU Hsu, YC
Ho, HJ
Huang, YT
Wang, HH
Wu, MS
Lin, JT
Wu, CY
AF Hsu, Yao-Chun
Ho, Hsiu J.
Huang, Yen-Tsung
Wang, Hsi-Hao
Wu, Ming-Shiang
Lin, Jaw-Town
Wu, Chun-Ying
TI Association between antiviral treatment and extrahepatic outcomes in
patients with hepatitis C virus infection
SO GUT
LA English
DT Article
ID SUSTAINED VIROLOGICAL RESPONSE; PLUS RIBAVIRIN;
HEPATOCELLULAR-CARCINOMA; INCREASED RISK; HCV INFECTION; B-VIRUS;
MORTALITY; THERAPY; DISEASE; SEROPOSITIVITY
AB Objective To elucidate the association between antiviral therapy and extrahepatic outcomes in individuals infected with HCV.
Methods This nationwide cohort study screened 293 480 Taiwanese residents with HCV infection and excluded those with substantial comorbidity. A total of 12 384 eligible patients who had received pegylated interferon plus ribavirin between 1 October 2003 and 31 December 2010 were enrolled in the treated cohort; they were matched 1 : 2 with 24 768 untreated controls in the propensity score and post-diagnosis treatment-free period. The incidences of end-stage renal disease (ESRD), acute coronary syndrome (ACS), ischaemic stroke and catastrophic autoimmune diseases were calculated after adjustment for competing mortality.
Results The treated and untreated cohorts were followed up for a mean (+/- SD) duration of 3.3 (+/- 2.5) and 3.2 (+/- 2.4) years, respectively, until 31 December 2011. The calculated 8-year cumulative incidences of ESRD, ACS, ischaemic stroke and autoimmune catastrophes between treated and untreated patients were 0.15% vs 1.32% (p<0.001), 2.21% vs 2.96% (p=0.027), 1.31% vs 1.76% (p=0.001) and 0.57% vs 0.49% (p=0.816), respectively. Multivariate-adjusted Cox regression revealed that antiviral treatment was associated with lower risks of ESRD (HR 0.15; 95% CI 0.07 to 0.31; p<0.001), ACS (HR 0.77; 95% CI 0.62 to 0.97; p=0.026) and ischaemic stroke (HR 0.62; 95% CI 0.46 to 0.83; p=0.001), but unrelated to autoimmune catastrophes. These favourable associations were invalid in incompletely treated patients with duration <16 weeks.
Conclusions Antiviral treatment for HCV is associated with improved renal and circulatory outcomes, but unrelated to catastrophic autoimmune diseases.
C1 [Hsu, Yao-Chun; Wu, Chun-Ying] China Med Univ, Grad Inst Clin Med, Taichung, Taiwan.
[Hsu, Yao-Chun; Wang, Hsi-Hao] E Da Hosp, Dept Internal Med, Kaohsiung, Taiwan.
[Hsu, Yao-Chun] E Da Hosp, Ctr Database Res, Kaohsiung, Taiwan.
[Hsu, Yao-Chun] I Shou Univ, Sch Med, Kaohsiung, Taiwan.
[Ho, Hsiu J.; Wu, Chun-Ying] Taichung Vet Gen Hosp, Div Gastroenterol, Taichung 40705, Taiwan.
[Huang, Yen-Tsung] Brown Univ, Dept Epidemiol, Providence, RI 02912 USA.
[Wu, Ming-Shiang] Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 100, Taiwan.
[Lin, Jaw-Town] Fu Jen Catholic Univ, Sch Med, New Taipei, Taiwan.
[Lin, Jaw-Town; Wu, Chun-Ying] Natl Hlth Res Inst, Ctr Hlth Policy Res & Dev, Miaoli, Taiwan.
[Wu, Chun-Ying] Natl Yang Ming Univ, Sch Med, Taipei 112, Taiwan.
[Wu, Chun-Ying] China Med Univ, Coll Publ Hlth, Taichung, Taiwan.
[Wu, Chun-Ying] Natl Chung Hsing Univ, Dept Life Sci, Taichung 40227, Taiwan.
C3 China Medical University Taiwan; E-Da Hospital; E-Da Hospital; I Shou
University; Taichung Veterans General Hospital; Brown University;
National Taiwan University; National Taiwan University Hospital; Fu Jen
Catholic University; National Health Research Institutes - Taiwan;
National Yang Ming Chiao Tung University; China Medical University
Taiwan; National Chung Hsing University
RP Wu, CY (corresponding author), Taichung Vet Gen Hosp, Div Gastroenterol, 1650,Sec 4,Taiwan Ave, Taichung 40705, Taiwan.
EM chun@vghtc.gov.tw
RI Huang, Yen-Tsung/AAQ-3919-2021; Wu, Chun-Ying/AAX-5077-2021
OI Huang, Yen-Tsung/0000-0001-7657-0040; Wu,
Ming-Shiang/0000-0002-1940-6428; Wu, Chun-Ying/0000-0001-5053-1801
FU Taiwan National Science Council [NSC 102-2314-B-650-008]; National
Health Research Institute [PH-101-PP-23]; E-Da Hospital [EDAHP102006]
FX This work was supported in part by the Taiwan National Science Council
(NSC 102-2314-B-650-008), National Health Research Institute
(PH-101-PP-23) and the E-Da Hospital (EDAHP102006).
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NR 43
TC 177
Z9 184
U1 0
U2 16
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD MAR
PY 2015
VL 64
IS 3
BP 495
EP 503
DI 10.1136/gutjnl-2014-308163
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CB1GZ
UT WOS:000349376600018
PM 25398770
OA Bronze
DA 2025-01-07
ER
PT J
AU Elkoshi, Z
AF Elkoshi, Zeev
TI "High Treg" Inflammations Promote (Most) Non-Hematologic Cancers While
"Low Treg" Inflammations Promote Lymphoid Cancers
SO JOURNAL OF INFLAMMATION RESEARCH
LA English
DT Article
DE regulatory T cells; lymphoma; cancer; alcohol consumption; cigarette
smoking; checkpoint inhibitors; high Treg; low Treg; inflammation;
autoimmune diseases; immune escape
ID REGULATORY T-CELLS; GROWTH-FACTOR-BETA; TGF-BETA;
HEPATOCELLULAR-CARCINOMA; ALCOHOL-CONSUMPTION; IMMUNE DYSFUNCTION;
IMPROVED SURVIVAL; TOBACCO SMOKING; HODGKIN; RISK
AB In an earlier publication, a binary classification of chronic diseases has been proposed. Chronic diseases were classified as "high Treg" or "low Treg" diseases depending on whether the pro-inflammatory or the anti-inflammatory arms of the immune response are deficient. The present work uses this model to analyze the interplay between cancer and the immune system, based on published literature. The work leans upon the etiology of alcohol and tobacco-related malignancies. The main conclusions are: triggers of specific "high Treg" immune reaction promote most non-hematologic cancers, whereas triggers of "low Treg" immune reaction promote lymphomas. The opposite is also true: triggers of specific "high Treg" immune reaction suppress lymphoma, whereas triggers of "low Treg" immune reaction suppress non-hematologic cancers. Both lymphoma and autoimmune diseases are "low Treg" conditions. For this reason, both are promoted by the same panel of "low Treg" bacteria and parasites and are inhibited by "high Treg" triggers. For example, alcohol consumption, a "high Treg" trigger, protects against lymphoma and autoimmune hypothyroidism. In addition, the same immune-modulatory drugs are effective in the treatment of both lymphoma and autoimmune diseases. Like other cancers, lymphoma transforms from a "low Treg" type at early stage of the disease into a "high Treg" type at advanced stages. However, lymphoma is distinguished from most other cancers by the length of time it dwells at an indolent "low Treg" state (many years) before lymphoma cells sensitivity to transforming growth factor-beta is impaired. This impairment stimulates the switch from "low Treg" into "high Treg" response and results in immune escape. The application of this analysis to the pharmacological activity of checkpoint inhibitors forecasts that checkpoint inhibitors would not be effective in low-grade, indolent lymphomas. As of now, checkpoint inhibitors are approved for the treatment of advanced lymphoma only.
C1 [Elkoshi, Zeev] Taro Pharmaceut Ind Ltd, Res & Dev Dept, Haifa, Israel.
RP Elkoshi, Z (corresponding author), Taro Pharmaceut Ind Ltd, Res & Dev Dept, Haifa, Israel.
EM zeev.elkoshi@gmail.com
OI Elkoshi, Zeev/0000-0001-6873-9619
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NR 86
TC 6
Z9 6
U1 0
U2 1
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-7031
J9 J INFLAMM RES
JI J. Inflamm. Res.
PY 2020
VL 13
BP 209
EP 221
DI 10.2147/JIR.S249384
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA LR3DU
UT WOS:000535574900001
PM 32547153
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Cuadrado, A
Rojo, AI
Wells, G
Hayes, JD
Cousins, SP
Rumsey, WL
Attucks, OC
Franklin, S
Levonen, AL
Kensler, TW
Dinkova-Kostova, AT
AF Cuadrado, Antonio
Rojo, Ana, I
Wells, Geoffrey
Hayes, John D.
Cousins, Sharon P.
Rumsey, William L.
Attucks, Otis C.
Franklin, Stephen
Levonen, Anna-Liisa
Kensler, Thomas W.
Dinkova-Kostova, Albena T.
TI Therapeutic targeting of the NRF2 and KEAP 1 partnership in chronic
diseases
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Review
ID TRANSCRIPTION FACTOR NRF2; NF-KAPPA-B; PROTEIN-PROTEIN INTERACTION;
SMOKE-INDUCED EMPHYSEMA; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
ANTIOXIDANT RESPONSE ELEMENT; REMITTING MULTIPLE-SCLEROSIS; GENE
PROMOTER POLYMORPHISM; FRATAXIN DEFICIENCY LEADS; RELEASE DIMETHYL
FUMARATE
AB The transcription factor NF-E2 p45-related factor 2 (NRF2; encoded by NFE2L2) and its principal negative regulator, the E3 ligase adaptor Kelch-like ECH-associated protein 1 (KEAP1), are critical in the maintenance of redox, metabolic and protein homeostasis, as well as the regulation of inflammation. Thus, NRF2 activation provides cytoprotection against numerous pathologies including chronic diseases of the lung and liver; autoimmune, neurodegenerative and metabolic disorders; and cancer initiation. One NRF2 activator has received clinical approval and several electrophilic modifiers of the cysteine-based sensor KEAP1 and inhibitors of its interaction with NRF2 are now in clinical development. However, challenges regarding target specificity, pharmacodynamic properties, efficacy and safety remain.
C1 [Cuadrado, Antonio; Rojo, Ana, I] Autonomous Univ Madrid, Fac Med, Dept Biochem, Inst Invest Sanitaria Paz Idi Paz,Ctr Invest Biom, Madrid, Spain.
[Cuadrado, Antonio; Rojo, Ana, I] Autonomous Univ Madrid, Fac Med, Inst Invest Biomed Alberto Sols UAM CSIC, Madrid, Spain.
[Cuadrado, Antonio] Victor Babes Natl Inst Pathol, Bucharest, Romania.
[Wells, Geoffrey] UCL, UCL Sch Pharm, London, England.
[Hayes, John D.; Dinkova-Kostova, Albena T.] Univ Dundee, Sch Med, Div Cellular Med, Jacqui Wood Canc Ctr, Dundee, Scotland.
[Cousins, Sharon P.] Reata Pharmaceut, Irving, TX USA.
[Rumsey, William L.] GlaxoSmithKline, Collegeville, PA USA.
[Attucks, Otis C.] vTv Therapeut, High Point, NC USA.
[Franklin, Stephen] Evgen Pharma, Wilmslow, Cheshire, England.
[Levonen, Anna-Liisa] Univ Eastern Finland, AI Virtanen Inst Mol Sci, Kuopio, Finland.
[Kensler, Thomas W.] Fred Hutchinson Canc Res Ctr, Translat Res Program, 1124 Columbia St, Seattle, WA 98104 USA.
[Dinkova-Kostova, Albena T.] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA.
[Dinkova-Kostova, Albena T.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
C3 Autonomous University of Madrid; Autonomous University of Madrid;
Consejo Superior de Investigaciones Cientificas (CSIC); CSIC - Instituto
de Investigaciones Biomedicas Alberto Sols (IIBM); Victor Babes National
Institute of Pathology; University of London; University College London;
University of Dundee; GlaxoSmithKline; University of Eastern Finland;
Fred Hutchinson Cancer Center; Johns Hopkins University; Johns Hopkins
University
RP Dinkova-Kostova, AT (corresponding author), Univ Dundee, Sch Med, Div Cellular Med, Jacqui Wood Canc Ctr, Dundee, Scotland.; Dinkova-Kostova, AT (corresponding author), Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA.; Dinkova-Kostova, AT (corresponding author), Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
EM a.dinkovakostova@dundee.ac.uk
RI Rojo, Ana/AAA-5203-2019; Dinkova-Kostova, Albena/AEB-8168-2022; Hayes,
John/GVT-0789-2022; Kensler, Thomas/D-8686-2014
OI Wells, Geoffrey/0000-0002-0253-911X; Rojo, Ana I/0000-0002-0312-5867;
Kensler, Thomas/0000-0002-6676-261X; Cuadrado,
Antonio/0000-0002-4039-7140; Levonen, Anna-Liisa/0000-0002-6575-2137;
Dinkova-Kostova, Albena/0000-0003-0316-9859; Hayes,
John/0000-0002-2927-5548
FU Spanish Ministry of Economy and Competitiveness [SAF2015-71304-REDT,
SAF2016-76520-R]; European Regional Development Fund [P_37_732/2016
REDBRAIN]; Competitiveness Operational Program 2014-2020; US National
Institutes of Health [R35 CA197222]; Cancer Research UK [C20953/A18644];
Medical Research Council [MR/N009851/1]; Biotechnology and Biological
Sciences Research Council [BB/L01923X/1]; Tenovus Scotland grant
[T17/14]; Academy of Finland [275147]; Sigrid Juselius Foundation;
Finnish Cancer Foundation; BBSRC [BB/L01923X/1] Funding Source: UKRI;
MRC [MR/N009851/1] Funding Source: UKRI
FX This work was supported by grants SAF2015-71304-REDT and SAF2016-76520-R
from the Spanish Ministry of Economy and Competitiveness; P_37_732/2016
REDBRAIN from the European Regional Development Fund; Competitiveness
Operational Program 2014-2020; US National Institutes of Health grant
R35 CA197222; Cancer Research UK grant C20953/A18644; Medical Research
Council grant MR/N009851/1; Biotechnology and Biological Sciences
Research Council grant BB/L01923X/1; Tenovus Scotland grant T17/14; and
grant 275147 from the Academy of Finland, Sigrid Juselius Foundation and
Finnish Cancer Foundation.
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NR 328
TC 898
Z9 959
U1 11
U2 386
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
EI 1474-1784
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD APR
PY 2019
VL 18
IS 4
BP 295
EP 317
DI 10.1038/s41573-018-0008-x
PG 23
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA HR1AX
UT WOS:000462861500018
PM 30610225
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Asano, J
Watanabe, T
Oguchi, T
Kanai, K
Maruyama, M
Ito, T
Muraki, T
Hamano, H
Arakura, N
Matsumoto, A
Kawa, S
AF Asano, Junpei
Watanabe, Takayuki
Oguchi, Takaya
Kanai, Keita
Maruyama, Masahiro
Ito, Tetsuya
Muraki, Takashi
Hamano, Hideaki
Arakura, Norikazu
Matsumoto, Akihiro
Kawa, Shigeyuki
TI Association Between Immunoglobulin G4-related Disease and Malignancy
within 12 Years after Diagnosis: An Analysis after Longterm Followup
SO JOURNAL OF RHEUMATOLOGY
LA English
DT Article
DE IMMUNOGLOBULIN G4-RELATED DISEASE; AUTOIMMUNE PANCREATITIS;
MALIGNANCIES; ACTIVITY MARKER
ID PANCREATIC DUCTAL ADENOCARCINOMA; AUTOIMMUNE PANCREATITIS;
HEPATOCELLULAR-CARCINOMA; CANCER; RISK; CRITERIA; IMMUNOSURVEILLANCE;
GUIDELINES; INFECTION
AB Objective. Because it is uncertain whether immunoglobulin G4-related disease (IgG4-RD) is associated with malignancy, we evaluated the incidence of cancer development in a large cohort of patients with IgG4-RD.
Methods. The study enrolled 158 patients diagnosed as having IgG4-RD between 1992 and 2012. We calculated the standardized incidence ratio (SIR) and cumulative rate of malignancies in this group and searched for risk factors associated with the occurrence of tumors.
Results. A total of 34 malignancies were observed in the patients with IgG4-RD over a mean followup period of 5.95 +/- 4.48 years. The overall SIR of malignancies was 2.01 (95% CI 1.34-2.69). The SIR of patients who exhibited a tumor within 1 year after IgG4-RD diagnosis was 3.53 (95% CI 1.23-5.83), while that of subjects forming a malignancy in subsequent years was 1.48 (95% CI 0.99-1.98). The cumulative rate of malignancy development was significantly higher in patients with IgG4-RD within 12 years after diagnosis than in the Japanese general population. Comparable results were obtained for an autoimmune pancreatitis subgroup. The serum concentrations of several disease activity markers at diagnosis were significantly higher in patients with malignancies than in those without.
Conclusion. We identified a close association between IgG4-RD and malignancy formation within 12 years after diagnosis, particularly during the first year. An active IgG4-RD state is presumed to be a strong risk factor for malignancy development.
C1 [Asano, Junpei; Watanabe, Takayuki; Oguchi, Takaya; Kanai, Keita; Maruyama, Masahiro; Ito, Tetsuya; Muraki, Takashi; Hamano, Hideaki; Matsumoto, Akihiro] Shinshu Univ, Sch Med, Dept Gastroenterol, Matsumoto, Nagano 3908621, Japan.
[Arakura, Norikazu] Shinshu Univ, Sch Med, Endoscop Examinat Ctr, Matsumoto, Nagano 3908621, Japan.
Shinshu Univ, Sch Med, Ctr Hlth Safety & Environm Management, Matsumoto, Nagano 3908621, Japan.
[Kawa, Shigeyuki] Shinshu Univ, Ctr Hlth Safety & Environm Management, Matsumoto, Nagano 3908621, Japan.
C3 Shinshu University; Shinshu University; Shinshu University; Shinshu
University
RP Kawa, S (corresponding author), Shinshu Univ, Ctr Hlth Safety & Environm Management, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan.
EM skawapc@shinshu-u.ac.jp
FU Ministry of Health, Labor, and Welfare of Japan; Ministry of Education,
Science, Sports, and Culture of Japan [23591012]; Grants-in-Aid for
Scientific Research [15K09045] Funding Source: KAKEN
FX Supported partially by the Research Program of Intractable Disease
provided by the Ministry of Health, Labor, and Welfare of Japan and in
part by Grants-in-aid for Scientific Research from the Ministry of
Education, Science, Sports, and Culture of Japan (23591012).
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NR 41
TC 102
Z9 109
U1 0
U2 6
PU J RHEUMATOL PUBL CO
PI TORONTO
PA 365 BLOOR ST E, STE 901, TORONTO, ONTARIO M4W 3L4, CANADA
SN 0315-162X
EI 1499-2752
J9 J RHEUMATOL
JI J. Rheumatol.
PD NOV
PY 2015
VL 42
IS 11
BP 2135
EP 2142
DI 10.3899/jrheum.150436
PG 8
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA CW8AS
UT WOS:000365221400019
PM 26472416
OA Green Submitted, Bronze
DA 2025-01-07
ER
PT J
AU Atalay, C
Atalay, G
Yilmaz, KB
Altinok, Y
AF Atalay, C
Atalay, G
Yilmaz, KB
Altinok, Y
TI The role of anti-CENP-B and anti-SS-B antibodies in breast cancer
SO NEOPLASMA
LA English
DT Article
DE anti-SS-B; anti-CENP-B; autoimmunity; breast cancer
ID HEPATOCELLULAR-CARCINOMA; HUMAN KERATINOCYTES; CELL-LINE;
AUTOANTIBODIES; PROTEIN; PROLIFERATION; AUTOANTIGENS; MALIGNANCIES;
AUTOIMMUNITY; RESPONSES
AB A close relationship between autoimmunity and malignant diseases has been supposed for a long time. In clinical practice, anti-SS-B and anti-CENP-B antibodies are used as serologic markers for autoimmune diseases. In this study, anti-SS-B and anti-CENP-B autoantibodies were studied in breast cancer patients and compared to a control group surgically treated due to benign diseases. These antibodies were evaluated by enzyme linked immunoassay and serum values >10 U/ml were accepted as positive. Fifty-five patients with breast cancer and 25 patients with benign diseases were prospectively included in the study. In the breast cancer group, both anti-CENP-B (33% vs. 8%) and anti-SS-B (44% vs. 24%) autoantibodies had higher positivity compared to the control group, but this difference reached statistical significance only for anti-CENP-B antibodies (p=0.02). Besides, anti-SS-beta positivity was detected more frequently in breast cancer patients with axillary involvement (63% vs. 24%) (p=0.006) and increased as the number of involved lymph nodes increased in the axilla (p=0.03). Although the clinical significance of autoantibody detection in cancer patients is still not clear, autoantibodies especially detected in individuals without proven autoimmune diseases needs to be thoroughly evaluated for early diagnosis and treatment of various cancers.
C1 Ankara Oncol Hosp, Dept Gen Surg, Ankara, Turkey.
Med Lab Labs, Ankara, Turkey.
C3 Dr. Abdurrahman Yurtaslan Oncology Hospital
RP Atalay, C (corresponding author), Ankara Oncol Hosp, Dept Gen Surg, Ankara, Turkey.
EM atalay_can@hotmail.com
RI Yilmaz, Kerim Bora/HJI-8568-2023; Atik-Altınok, Yasemin/A-5858-2019
OI Yilmaz, Kerim Bora/0000-0002-5514-4103
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NR 19
TC 27
Z9 28
U1 1
U2 3
PU VEDA, SLOVAK ACADEMY SCIENCES
PI BRASTISLAVA
PA DUBRAVSKA CESTA 9, 842 34 BRASTISLAVA, SLOVAKIA
SN 0028-2685
J9 NEOPLASMA
JI Neoplasma
PY 2005
VL 52
IS 1
BP 32
EP 35
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 901OF
UT WOS:000227291100005
PM 15739023
DA 2025-01-07
ER
PT J
AU Reddy, HG
Schneider, BJ
Tai, AW
AF Reddy, Haritha G.
Schneider, Bryan J.
Tai, Andrew W.
TI Immune Checkpoint Inhibitor-Associated Colits and Hepatitis
SO CLINICAL AND TRANSLATIONAL GASTROENTEROLOGY
LA English
DT Review
ID ADVANCED MELANOMA; ADVERSE EVENTS; IPILIMUMAB; CANCER; NIVOLUMAB;
IMMUNOTHERAPY; MONOTHERAPY; BLOCKADE; FEATURES; THERAPY
AB Immune checkpoint inhibitors (ICPIs) are monoclonal antibodies that target downregulators of the anti-cancer immune response: cytotoxic T-lymphocyte antigen-4, programmed cell death protein-1, and its ligand PD-L1. ICPIs are now approved for the treatment of a wide array of malignancies, with rates of durable responses in the metastatic setting far exceeding what would be expected from conventional chemotherapy. ICPIs have also been associated with rare but serious immune-related adverse events due to over-activation of the immune system that can affect any organ, including the gastrointestinal tract and liver. As the use of ICPIs in oncology continues to increase, ICPI-associated colitis and hepatitis will be encountered frequently by gastroenterologists and hepatologists. This review will focus on the diagnosis and management of ICPI-associated colitis and hepatitis. We will also compare these ICPI-related toxicities with sporadic inflammatory bowel disease and autoimmune liver disease.
C1 [Reddy, Haritha G.; Schneider, Bryan J.] Univ Michigan, Dept Internal Med, Div Hematol Oncol, Rogel Canc Ctr, Ann Arbor, MI 48109 USA.
[Tai, Andrew W.] Univ Michigan, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Tai, Andrew W.] Univ Michigan, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
[Tai, Andrew W.] VA Ann Arbor Healthcare Syst, Med Serv, Ann Arbor, MI 48105 USA.
C3 University of Michigan System; University of Michigan; University of
Michigan System; University of Michigan; University of Michigan System;
University of Michigan; US Department of Veterans Affairs; Veterans
Health Administration (VHA); VA Ann Arbor Healthcare System
RP Tai, AW (corresponding author), Univ Michigan, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.; Tai, AW (corresponding author), Univ Michigan, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
EM andrewwt@umich.edu
RI Schneider, Bryan/KWV-1027-2024; Tai, Andrew/M-8380-2017
OI Tai, Andrew/0000-0002-6877-450X
FU National Institutes of Health [R01DK097374]
FX This work was supported by the National Institutes of Health grant
R01DK097374 (AWT). The funders had no role in the study design, data
collection and interpretation, or the decision to submit the work for
publication.
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NR 37
TC 73
Z9 79
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2155-384X
J9 CLIN TRANSL GASTROEN
JI Clin. Transl. Gastroenterol.
PD SEP 19
PY 2018
VL 9
AR 180
DI 10.1038/s41424-018-0049-9
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GX2HQ
UT WOS:000447540200001
PM 30228268
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Gu, XY
Chu, QF
Ma, X
Wang, J
Chen, C
Guan, J
Ren, YL
Wu, SS
Zhu, HH
AF Gu, Xinyu
Chu, Qingfei
Ma, Xiao
Wang, Jing
Chen, Chao
Guan, Jun
Ren, Yanli
Wu, Shanshan
Zhu, Haihong
TI New insights into iNKT cells and their roles in liver diseases
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE NKT cells; cytokine; chemokine; liver diseases; immune
ID KILLER T-CELLS; HEPATIC NKT CELLS; ORAL IMMUNE REGULATION;
HEPATOCELLULAR-CARCINOMA GROWTH; PERIPHERAL NATURAL-KILLER;
B-VIRUS-REPLICATION; ALPHA-GALACTOSYLCERAMIDE; NONALCOHOLIC
STEATOHEPATITIS; CYTOKINE PRODUCTION; INSULIN-RESISTANCE
AB Natural killer T cells (NKTs) are an important part of the immune system. Since their discovery in the 1990s, researchers have gained deeper insights into the physiology and functions of these cells in many liver diseases. NKT cells are divided into two subsets, type I and type II. Type I NKT cells are also named iNKT cells as they express a semi-invariant T cell-receptor (TCR) alpha chain. As part of the innate immune system, hepatic iNKT cells interact with hepatocytes, macrophages (Kupffer cells), T cells, and dendritic cells through direct cell-to-cell contact and cytokine secretion, bridging the innate and adaptive immune systems. A better understanding of hepatic iNKT cells is necessary for finding new methods of treating liver disease including autoimmune liver diseases, alcoholic liver diseases (ALDs), non-alcoholic fatty liver diseases (NAFLDs), and liver tumors. Here we summarize how iNKT cells are activated, how they interact with other cells, and how they function in the presence of liver disease.
C1 [Gu, Xinyu; Chu, Qingfei; Wang, Jing; Chen, Chao; Guan, Jun; Ren, Yanli; Wu, Shanshan; Zhu, Haihong] Zhejiang Univ, Affiliated Hosp 1, Natl Clin Res Ctr Infect Dis, Natl Med Ctr Infect Dis,Sch Med,Collaborat Innovat, Hangzhou, Peoples R China.
[Ma, Xiao] Zhejiang Univ, Sch Med, Hangzhou, Zhejiang, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Zhu, HH (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Natl Clin Res Ctr Infect Dis, Natl Med Ctr Infect Dis,Sch Med,Collaborat Innovat, Hangzhou, Peoples R China.
EM zhuhh72@zju.edu.cn
RI Zhu, Haihong/A-1769-2017; Gu, Xinyu/JDD-9651-2023; Wang,
Jingya/HZM-1570-2023; REN, CHAO/KRO-9616-2024
OI Ma, Xiao/0000-0002-1891-3815
FU National Science and Technology Major Project of China; Science and
Technology Major Projects of Zhejiang Province; Science and Technology
Major Projects of Ningbo; [2018ZX10302206]; [2018C04016];
[2016C51008]
FX Funding This study was supported by grants awarded by the National
Science and Technology Major Project of China (NO 2018ZX10302206),
Science and Technology Major Projects of Zhejiang Province (NO
2018C04016), and the Science and Technology Major Projects of Ningbo (NO
2016C51008).
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NR 199
TC 18
Z9 19
U1 3
U2 25
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD OCT 26
PY 2022
VL 13
AR 1035950
DI 10.3389/fimmu.2022.1035950
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 6C5TC
UT WOS:000882075400001
PM 36389715
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Jia, DL
Yang, H
Wan, L
Cheng, JQ
Lu, XF
AF Jia, Dianlong
Yang, Hao
Wan, Lin
Cheng, Jingqiu
Lu, Xiaofeng
TI Production of bioactive, SUMO-modified, and native-like TNF-α of the
rhesus monkey, Macaca mulatta, in Escherichia coli
SO APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
LA English
DT Article
DE Tumor necrosis factor; Autoimmune disease; Rhesus monkey; Small
ubiquitin-like modifier
ID TUMOR-NECROSIS-FACTOR; ISOLATED LIMB PERFUSION; MOLECULAR-CLONING;
CANCER CELLS; PROTEIN; EXTREMITIES; HOMOLOGY; THERAPY; DISEASE; MODELS
AB Biotechnologically produced tumor necrosis factor alpha (TNF-alpha) neutralizing agents have proven efficient in patients suffering from disparate autoimmune diseases. The rhesus monkey (Macaca mulatta) could be developed as a model for human autoimmune disease. Consequently, a large amount of M. mulatta TNF-alpha (mmTNF alpha) is required to further understand TNF-alpha-related pathogenesis and evaluate novel human TNF-alpha (hTNF alpha) neutralizing agents. We therefore attempted to express mmTNF alpha by using a small ubiquitin-like modifier (SUMO) fusion system. The synthetic gene, encoding the fusion protein SUMO-mmTNF alpha, was inserted into a pQE30 plasmid and was transformed into Escherichia coli M15. The fusion protein was expressed as both soluble and insoluble protein in E. coli. Approximately 10-12 mg of SUMO-mmTNF alpha was obtained from the soluble fraction of 1 L of bacterial culture. Cleavage of the fusion protein with SUMO protease produced native-like mmTNF alpha. Both native-like and SUMO-modified mmTNF alpha formed functional trimers and showed excellent cytotoxicity (ED50, 0.05-0.1 ng/ml) in standard L929 cells. In addition, SUMO-mmTNF alpha and mmTNF alpha also exhibited cytotoxicity in human cancer cell types, such as, breast, lung, and liver cancer cells. The hTNF alpha neutralizing agents, including soluble receptors of hTNF alpha and antibodies against hTNF alpha, interacted with the mmTNF alpha. These results demonstrate that the bioactive mmTNF alpha produced with the SUMO fusion system is useful for further research, especially for the in vitro preclinical evaluation of biological hTNF alpha neutralizing agents.
C1 [Jia, Dianlong; Yang, Hao; Wan, Lin; Cheng, Jingqiu; Lu, Xiaofeng] Sichuan Univ, W China Hosp, Minist Hlth, Key Lab Transplant Engn & Immunol, Chengdu 610041, Peoples R China.
[Jia, Dianlong] Sichuan Univ, W China Hosp, Regenerat Med Res Ctr, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University
RP Lu, XF (corresponding author), Sichuan Univ, W China Hosp, Minist Hlth, Key Lab Transplant Engn & Immunol, Chengdu 610041, Peoples R China.
EM xiaofenglu@yahoo.com
RI Chen, Yi/HPD-0595-2023; Lu, Xiaofeng/ABD-9075-2021
OI Yang, Hao/0000-0003-2214-9474
FU Natural Science Fund of China [81072566]; Key Program for Natural
Science Fund of China [30930088]
FX This project was supported by the Natural Science Fund of China 81072566
and Key Program for Natural Science Fund of China 30930088.
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NR 36
TC 5
Z9 5
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0175-7598
EI 1432-0614
J9 APPL MICROBIOL BIOT
JI Appl. Microbiol. Biotechnol.
PD MAR
PY 2012
VL 93
IS 6
BP 2345
EP 2355
DI 10.1007/s00253-011-3794-1
PG 11
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA 904GF
UT WOS:000301181600010
PM 22207214
DA 2025-01-07
ER
PT J
AU Vitek, L
Tiribelli, C
AF Vitek, Libor
Tiribelli, Claudio
TI Gilbert's syndrome revisited
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
DE benign hyperbilirubinemia; civilization diseases; Gilbert's syndrome
ID BILIRUBIN
AB Gilbert's syndrome, also known as benign hyperbilirubinaemia, was described more than 100 years ago. It has usually been considered a physiological abnormality characterised by a mild elevation of the systemic level of unconjugated bilirubin, in the absence of any underlying liver or overt haemolytic disease. However, since the re-discovery of the potent antioxidant effects of bilirubin in the late 1980s, as well as multiple intracellular signalling pathways affected by bilirubin, an ever-increasing body of evidence suggests that individuals with Gilbert's syndrome may benefit from the mild hyperbilirubinaemia and are actually pro-tected from the development of a wide variety of "diseases of civilisation" such as cardiovascular diseases, certain cancers, and autoimmune or neurodegenerative diseases. This review analyses the current state of medical knowledge given recent discoveries in this rapidly developing field, as well as their possible clinical significance, and provides a new perspective on this condition. (c) 2023 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Vitek, Libor] Charles Univ Prague, Inst Med Biochem, Fac Med 1, Lab Diagnost, Prague, Czech Republic.
[Vitek, Libor] Gen Univ, Hosp Prague, Katerinska 32, Prague 2, Czech Republic.
[Tiribelli, Claudio] Fdn Italiana Fegato, AREA Sci Pk-Blgd Q, Campus Basovizza, I-34140 Trieste, Italy.
C3 Charles University Prague; General University Hospital Prague
RP Vitek, L (corresponding author), Charles Univ Prague, Inst Med Biochem, Fac Med 1, Lab Diagnost, Prague, Czech Republic.; Vitek, L (corresponding author), Gen Univ, Hosp Prague, Katerinska 32, Prague 2, Czech Republic.; Tiribelli, C (corresponding author), Fdn Italiana Fegato, AREA Sci Pk-Blgd Q, Campus Basovizza, I-34140 Trieste, Italy.
EM vitek@cesnet.cz; ctliver@fegato.it
RI Vitek, Libor/A-2645-2008; Tiribelli, Claudio/A-4716-2014
OI Vitek, Libor/0000-0002-5318-0151; Tiribelli, Claudio/0000-0001-6596-7595
FU Czech Ministry of Health [MH CZ-DRO-VFN64165]; National Institute for
Research of Metabolic and Cardiovascular Diseases (Programme EXCELES) -
European Union-Next Generation EU [LX22NPO5104]; Fondazione Italiana
Fegato
FX This work was supported by a grant MH CZ-DRO-VFN64165 from the Czech
Ministry of Health and National Institute for Research of Metabolic and
Cardiovascular Diseases (Programme EXCELES, ID Project No. LX22NPO5104)
funded by the European Union-Next Generation EU (LV) and by an
intramural grant from Fondazione Italiana Fegato (CT). The funding
bodies had no role in collecting, managing, analyzing, and interpreting
the data. They also had no role in the manuscript's preparation, review,
or approval; and the decision to submit the manuscript for publication.
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NR 54
TC 14
Z9 14
U1 9
U2 15
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD OCT
PY 2023
VL 79
IS 4
BP 1049
EP 1055
DI 10.1016/j.jhep.2023.06.004
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IG7N6
UT WOS:001165242800001
PM 37390966
OA Bronze
DA 2025-01-07
ER
PT J
AU Culver, EL
Chapman, RW
AF Culver, E. L.
Chapman, R. W.
TI Systematic review: management options for primary sclerosing cholangitis
and its variant forms-IgG4-associated cholangitis and overlap with
autoimmune hepatitis
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
ID DOSE URSODEOXYCHOLIC ACID; INFLAMMATORY-BOWEL-DISEASE;
ULCERATIVE-COLITIS PATIENTS; CHOLESTATIC LIVER-DISEASE; NATURAL-HISTORY
MODEL; DOUBLE-BLIND; RISK-FACTORS; MYCOPHENOLATE-MOFETIL;
CHEMOPREVENTIVE AGENT; COLORECTAL NEOPLASIA
AB P>Background
Primary sclerosing cholangitis (PSC) remains a challenging disease to manage. The main goals are prevention of disease progression and reduction of the increased cancer risk.
Aims
To review the management strategies for PSC and its variant forms based on published studies.
Methods
Publications were identified using Pubmed, Medline and Ovid search engines.
Results
Distinguishing PSC from variants, such as IgG4-associated cholangitis, and overlap with autoimmune hepatitis is essential to guide treatment decisions. There is no proven efficacious medical treatment for PSC. Ursodeoxycholic acid has been disappointing in low and moderate doses, and potentially dangerous in higher doses, although its role and optimal dose in chemoprevention requires investigation. The novel bile acid, 24-norursodeoxycholic acid, has shown promise in mouse models; human trials are in progress. Dominant strictures are optimally managed by dilatation and stenting to relieve obstructive complications, although exclusion of biliary malignancy is essential. Liver transplantation is the only proven therapy for those with advanced disease. Cholangiocarcinoma remains the most unpredictable and feared complication. In highly selected groups, neo-adjuvant chemoradiation with liver transplantation seems promising, but requires further validation. Screening for inflammatory bowel disease and surveillance for colorectal carcinoma should not be overlooked.
Conclusions
The effective management of PSC and its variants is hindered by uncertainties regarding pathogenesis of disease and factors responsible for its progression. Genome studies may help to identify further targets for drug therapy and factors leading to malignant transformation.
C1 [Culver, E. L.; Chapman, R. W.] John Radcliffe Hosp, Oxford OX3 9DU, England.
C3 University of Oxford
RP Chapman, RW (corresponding author), John Radcliffe Hosp, Oxford OX3 9DU, England.
EM roger.chapman@ndm.ox.ac.uk
OI Culver, Emma/0000-0001-9644-8392
FU Oxford Merck Academic Fellowship Program
FX Declaration of personal interests: Emma Culver has received research
funding from the Oxford Merck Academic Fellowship Program. Declaration
of funding interests: None.
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NR 206
TC 37
Z9 41
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD JUN 15
PY 2011
VL 33
IS 12
BP 1273
EP 1291
DI 10.1111/j.1365-2036.2011.04658.x
PG 19
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 764JV
UT WOS:000290626700002
PM 21501198
OA Bronze, Green Submitted
DA 2025-01-07
ER
PT J
AU Georgiadou, SP
Zachou, K
Liaskos, C
Gabeta, S
Rigopoulou, EI
Dalekos, GN
AF Georgiadou, Sarah P.
Zachou, Kalliopi
Liaskos, Christos
Gabeta, Stella
Rigopoulou, Eirini I.
Dalekos, George N.
TI Occult hepatitis B virus infection in patients with autoimmune liver
diseases
SO LIVER INTERNATIONAL
LA English
DT Article
DE autoimmune hepatitis; HBV-DNA; liver autoimmunity; occult HBV infection;
primary biliary cirrhosis; primary sclerosing cholangitis
ID PRIMARY BILIARY-CIRRHOSIS; HBSAG-NEGATIVE PATIENTS;
HEPATOCELLULAR-CARCINOMA; CYTOTOXIC CHEMOTHERAPY; HBV INFECTION;
RISK-FACTORS; ANTICARDIOLIPIN ANTIBODIES; CLINICAL-SIGNIFICANCE;
SEROLOGICAL MARKERS; INTERFERON-ALPHA
AB Occult hepatitis B virus (HBV) infection is characterized by undetectable serum HBV surface antigen (HBsAg) but detectable HBV-DNA in serum or liver.
To determine the prevalence and clinical impact of occult HBV in autoimmune liver diseases as similar data are missing.
One hundred and ninety-six sera samples from HBsAg-negative patients, including 66 autoimmune hepatitis (AIH), 93 primary biliary cirrhosis (PBC) and 37 primary sclerosing cholangitis (PSC), were investigated for HBV-DNA using the polymerase chain reaction (PCR) before treatment initiation. One hundred and three serial samples from 38 AIH patients under immunosuppression and 282 selected blood donors (HBsAg negative; antibodies to HBV-core antigen positive) were also investigated. Fourteen available paraffin-embedded AIH liver samples were also investigated for HBV-DNA by nested-PCR.
Hepatitis B virus DNA was detected in the serum of 24/196 patients (12.2%) and 0/282 donors (P=0.0000). Nine patients had AIH (13.6%), eight had PBC (8.6%) and seven had PSC (18.9%) (P=0.0000 vs healthy). HBV-DNA detection in AIH livers was higher than in serum. HBV-DNA was associated neither with HBV markers nor with epidemiological, laboratory and clinical data. Serial testing of AIH patients revealed two HBV-DNA-negative patients before treatment becoming positive during treatment, while all HBV-DNA-positive patients before immunosuppression became negative.
Based mainly on serum HBV-DNA, we found a significant proportion of autoimmune liver disease patients with occult HBV compared with donors. However, taking into account our results in a small number of liver tissues, it should be emphasized that occult HBV could be even higher when both serum and liver specimens are investigated. Occult HBV does not seem to affect the clinical and laboratory features of the diseases, while AIH patients with occult HBV under immunosuppression do not deteriorate during follow-up.
C1 [Georgiadou, Sarah P.; Zachou, Kalliopi; Liaskos, Christos; Gabeta, Stella; Rigopoulou, Eirini I.; Dalekos, George N.] Univ Thessaly, Sch Med, Dept Med, Res Lab Internal Med,Acad Liver Unit, Larisa 41222, Greece.
[Liaskos, Christos; Gabeta, Stella; Dalekos, George N.] Ctr Res & Technol Thessaly CE RE TE TH, Inst Biomed Res & Technol, Res Grp Invest Med, Larisa, Greece.
C3 University of Thessaly
RP Dalekos, GN (corresponding author), Univ Thessaly, Sch Med, Dept Med, Res Lab Internal Med,Acad Liver Unit, Papakiriazi 22 Str, Larisa 41222, Greece.
EM dalekos@med.uth.gr
RI Gabeta, Stella/IXW-9909-2023; Liaskos, Christos/Q-7351-2017
OI Liaskos, Christos/0000-0002-1271-8613
FU Gilead Sciences Hellas Ltd.; Research Committee of the University of
Thessaly, Greece [2446]; CE.RE.TE.TH; Alexander S. Onassis Public
Benefit Foundation
FX The authors would like to thank Ms Paraskevi Mina for technical
assistance in determining the HBV-DNA by PCR. This work was supported in
part by Gilead Sciences Hellas Ltd. and a research grant from the
Research Committee of the University of Thessaly, Greece (Code no:
2446); S. G. and C. L. were supported by CE.RE.TE.TH, and E. I. R. was
supported by the Alexander S. Onassis Public Benefit Foundation.
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NR 67
TC 42
Z9 50
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD MAR
PY 2009
VL 29
IS 3
BP 434
EP 442
DI 10.1111/j.1478-3231.2008.01851.x
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 402XO
UT WOS:000263046600019
PM 18694399
DA 2025-01-07
ER
PT J
AU Liu, J
Wang, FP
Luo, FM
AF Liu, Jia
Wang, Faping
Luo, Fengming
TI The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and
Cellular Mechanisms
SO BIOMOLECULES
LA English
DT Review
DE Janus kinases (JAK); signal transducer and activator of transcription
(STAT); cytokines; fibrosis; fibroblast; inhibitor
ID JAK-STAT PATHWAY; IL-12 GENE-THERAPY; GROWTH-FACTOR-BETA; SIGNAL
TRANSDUCER; TGF-BETA; LIVER FIBROSIS; INTERFERON-GAMMA; TRANSCRIPTION 3;
HEPATOCELLULAR-CARCINOMA; INTERSTITIAL FIBROSIS
AB There are four members of the JAK family and seven of the STAT family in mammals. The JAK/STAT molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT signaling pathway extensively mediates various biological processes such as cell proliferation, differentiation, migration, apoptosis, and immune regulation. JAK/STAT activation is closely related to growth and development, homeostasis, various solid tumors, inflammatory illness, and autoimmune diseases. Recently, with the deepening understanding of the JAK/STAT pathway, the relationship between JAK/STAT and the pathophysiology of fibrotic diseases was noticed, including the liver, renal, heart, bone marrow, and lung. JAK inhibitor has been approved for myelofibrosis, and subsequently, JAK/STAT may serve as a promising target for fibrosis in other organs. Therefore, this article reviews the roles and mechanisms of the JAK/STAT signaling pathway in fibrotic diseases.
C1 [Liu, Jia; Wang, Faping; Luo, Fengming] Sichuan Univ, West China Hosp, Dept Pulm & Crit Care Med, Chengdu 610041, Peoples R China.
[Liu, Jia; Wang, Faping; Luo, Fengming] Sichuan Univ, West China Hosp, Lab Pulm Immunol & Inflammat, Frontiers Sci Ctr Dis,Related Mol Network, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University
RP Luo, FM (corresponding author), Sichuan Univ, West China Hosp, Dept Pulm & Crit Care Med, Chengdu 610041, Peoples R China.; Luo, FM (corresponding author), Sichuan Univ, West China Hosp, Lab Pulm Immunol & Inflammat, Frontiers Sci Ctr Dis,Related Mol Network, Chengdu 610041, Peoples R China.
EM fengmingluo@outlook.com
OI Luo, Fengming/0000-0001-9267-3437; Wang, Faping/0000-0002-4473-1169
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NR 137
TC 52
Z9 53
U1 16
U2 65
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD JAN
PY 2023
VL 13
IS 1
AR 119
DI 10.3390/biom13010119
PG 15
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 7Y1AT
UT WOS:000914621900001
PM 36671504
OA Green Published, gold
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Nadeem, A
Hussain, MM
Aslam, M
Hussain, T
AF Nadeem, Amina
Hussain, Muhammad Mazhar
Aslam, Muhammad
Hussain, Tassawar
TI Interferon-Alpha Induced and Ribavirin Induced Thyroid Dysfunction in
Patients with Chronic Hepatitis C
SO HEPATITIS MONTHLY
LA English
DT Review
DE Chronic Hepatitis C; Interferon; Ribavirin; Thyroid Disease
ID CHRONIC VIRAL-HEPATITIS; VIRUS-INFECTION; PEGYLATED INTERFERON;
AUTOANTIBODY PATTERN; NATURAL-HISTORY; THERAPY; HYPOTHYROIDISM; DISEASE;
DISORDERS; RISK
AB Chronic hepatitis C (CHC) is one of the commonest infectious diseases of the liver and may lead to cirrhosis or hepatocellular carcinoma. Combination therapy with pegylated interferon (PEG-IFN) and Ribavirin is the treatment of choice for CHC. Combination therapy is thought to act by means of antiviral mechanisms and immunomodulation. Thyroid dysfunction is the most common autoimmune adverse effect associated with combination therapy; hypothyroidism is more common than hyperthyroidism. Antithyroid antibodies and female sex have a predictive value in the development of interferon induced thyroid disease (IITD). Patients with CHC should be informed of the possibility of side effects on the thyroid gland. Screening for antithyroid antibodies and thyroid function tests should be performed in patients with CHC before the commencement of antiviral treatment, and during and after it. This article reviews different aspects of IITD, including its pathogenesis, clinical manifestations, association with treatment regimens and treatment response and the outcome of thyroid dysfunction.
C1 [Nadeem, Amina; Hussain, Muhammad Mazhar] Army Med Coll, Dept Physiol, Rawalpindi, Pakistan.
[Aslam, Muhammad] Shifa Coll Med, Dept Physiol, Islamabad, Pakistan.
[Hussain, Tassawar] Hearts Int Hosp, Islamabad, Pakistan.
C3 National University of Sciences & Technology - Pakistan; Shifa College
of Medicine
RP Nadeem, A (corresponding author), Army Med Coll, Dept Physiol, Abid Majeed Rd, Islamabad, Pakistan.
EM nadeemamina@yahoo.com
OI Aslam, Muhammad/0000-0001-9418-3714
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NR 46
TC 10
Z9 10
U1 0
U2 6
PU KOWSAR PUBL
PI HOENSBROEK
PA PATERSWEG 22,, HOENSBROEK, LIMBURG 6431 GC, NETHERLANDS
SN 1735-143X
EI 1735-3408
J9 HEPAT MON
JI Hepat. Mon.
PD SPR
PY 2010
VL 10
IS 2
BP 132
EP 140
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 589JX
UT WOS:000277144600010
PM 22312386
DA 2025-01-07
ER
PT J
AU Mohammadzadeh, M
Derafshi, H
Ghari, T
AF Mohammadzadeh, Mehdi
Derafshi, Hamid
Ghari, Tayebeh
TI The Estimation of Economic Burden of Hepatitis C Virus Infection in Iran
SO IRANIAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
DE Hepatitis C; Economic burden of disease; Direct and indirect costs;
DALYs; Iran
ID MEDICAL PROGRESS; EPIDEMIOLOGY; DISEASE; DISABILITY
AB Background: One of the major causes of liver-related mortality and morbidity is Hepatitis C Virus (HCV) infection. It is also one of the reasons behinds of chronic liver disease and related complications such as cirrhosis and hepatocellular carcinoma. This autoimmune liver disease imposes a high economic burden on individuals and the society. This study aimed to estimate burden of HCV in Iran.
Methods: Overall, 200 patients with HCV infection, referred to hospitals in three cities of Tehran, Karaj and Tabriz, Iran during year 2015, were randomly enrolled. To estimate the total burden of hepatitis, direct and indirect costs, costs of DALYs and social welfare were calculated.
Results: Economic burden of HCV infection was obtained 26242.8 purchasing power parity (PPP$). Intangible costs of HCV was calculated 207421.6 PPP$.
Conclusion: Total direct costs of HCV for each patient are more than household consumption expenditure. Therefore, it is a reasonable policy to control and increase insurance coverage of HCV patients in order to decrease their costs.
C1 [Mohammadzadeh, Mehdi] Shahid Beheshti Univ Med Sci, Sch Pharm, Dept Pharmacoecon & Adm Pharm, Tehran, Iran.
[Mohammadzadeh, Mehdi; Ghari, Tayebeh] Pharmacoecon & Med Pharma Management Res Ctr, Tehran, Iran.
[Derafshi, Hamid] Alborz Univ Med Sci, Sch Med, Dept Ophthalmol, Karaj, Iran.
[Derafshi, Hamid] Iran Univ Med Sci, Sch Med, Dept Ophthalmol, Tehran, Iran.
[Ghari, Tayebeh] Alborz Univ Med Sci, Sch Pharm, Dept Pharmaceut, Karaj, Iran.
C3 Shahid Beheshti University Medical Sciences; Iran University of Medical
Sciences
RP Ghari, T (corresponding author), Pharmacoecon & Med Pharma Management Res Ctr, Tehran, Iran.; Ghari, T (corresponding author), Alborz Univ Med Sci, Sch Pharm, Dept Pharmaceut, Karaj, Iran.
EM tayebehghari@gmail.com
RI Ghari, Tayebeh/S-4812-2017
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NR 23
TC 3
Z9 3
U1 1
U2 7
PU IRANIAN SCIENTIFIC SOCIETY MEDICAL ENTOMOLOGY
PI TEHRAN
PA SCHOOL PUBLIC HEALTH & INST HEALTH RESEARCH, TEHRAN UNIV MEDICAL
SCIENCES, P O BOX 6446-14155, TEHRAN, 00000, IRAN
SN 2251-6085
EI 2251-6093
J9 IRAN J PUBLIC HEALTH
JI Iran J. Public Health
PD OCT
PY 2018
VL 47
IS 10
BP 1575
EP 1582
PG 8
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA GW0IU
UT WOS:000446547800017
PM 30524989
DA 2025-01-07
ER
PT J
AU Cappelli, F
Mengozzi, A
AF Cappelli, Federica
Mengozzi, Alessandro
TI Liver DE(HP)toxification: luteolin as "phthalates-cleaner" to protect
from environmental pollution
SO EMBO MOLECULAR MEDICINE
LA English
DT Article
AB Environmental pollution is a major health problem that affects the health of individuals worldwide and is cumulative with other environmental stressors, contributing to the increasing prevalence of cancer, cardiometabolic, neurological and autoimmune diseases (Fav & eacute; et al, 2018). Although being extensively studied, therapeutic strategies still rely primarily on exposure prevention, often with no option available to allow pollutant detoxification. In this issue of EMBO Molecular Medicine, Wang et al (Wang et al, 2024) investigated potential pharmacological strategies to allow the direct removal of phthalates, major environmental pollutants, from the liver.
A Mengozzi and F Cappelli discuss a potential pharmacological strategy for phthalate detoxification of the liver as reported by S Chen, C Liu, W Zhang and colleagues, in this issue of EMBO Mol Med.
C1 [Cappelli, Federica; Mengozzi, Alessandro] Univ Pisa, Dept Clin & Expt Med, Pisa, Italy.
[Mengozzi, Alessandro] Univ Zurich, Univ Hosp Zurich, Ctr Translat & Expt Cardiol CTEC, Dept Cardiol, Schlieren, Switzerland.
C3 University of Pisa; University of Zurich; University Zurich Hospital
RP Mengozzi, A (corresponding author), Univ Pisa, Dept Clin & Expt Med, Pisa, Italy.; Mengozzi, A (corresponding author), Univ Zurich, Univ Hosp Zurich, Ctr Translat & Expt Cardiol CTEC, Dept Cardiol, Schlieren, Switzerland.
EM alessandro.mengozzi@unipi.it
RI Mengozzi, Alessandro/JSK-7085-2023
OI Mengozzi, Alessandro/0000-0003-2834-9725
CR Favé MJ, 2018, NAT COMMUN, V9, DOI 10.1038/s41467-018-03202-2
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Mengozzi A, 2019, J CLIN ENDOCR METAB, V104, P1491, DOI 10.1210/jc.2018-01797
Wang HT, 2024, EMBO MOL MED, V16, P2699, DOI 10.1038/s44321-024-00160-9
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Zhang Y, 2022, ENVIRON POLLUT, V313, DOI 10.1016/j.envpol.2022.120173
NR 10
TC 0
Z9 0
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1757-4676
EI 1757-4684
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD NOV 11
PY 2024
VL 16
IS 11
BP 2655
EP 2656
DI 10.1038/s44321-024-00158-3
EA OCT 2024
PG 2
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA L8D4Y
UT WOS:001344733400002
PM 39472513
OA gold
DA 2025-01-07
ER
PT J
AU Shah, RA
Kowdley, KV
AF Shah, Raj A.
Kowdley, Kris V.
TI IgG4-related Sclerosing Cholangitis
SO PRACTICAL GASTROENTEROLOGY
LA English
DT Article
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; LONG-TERM OUTCOMES; AUTOIMMUNE
PANCREATITIS; BILE-DUCT; DIAGNOSIS; DISEASE; FEATURES; CANCER; CELLS
AB IgG4-related disease, characterized by IgG4-rich inflammatory infiltrates and variable degrees of fibrosis, encompasses a variety of disorders involving multiple organs. IgG4-related sclerosing cholangitis (IgG4-SC) is frequently associated with autoimmune pancreatitis. The disease is associated with a clinical presentation of obstruction, jaundice, weight loss and abdominal pain. IgG4-SC is typically diagnosed in middleaged and older men and therefore may lead to a suspicion of cholangiocarcinoma or primary sclerosing cholangitis. The association with autoimmune pancreatitis and an elevated IgG4 level (>135 mg/dl) should increase the clinical suspicion of IgG4-SC. There are typical histological features of an IgG4-rich plasma cell infiltrate on liver histology as well as storiform fibrosis and obstructive phlebitis. Cholangiographic changes in IgG4-SC are distinct from PSC and four types of IgG4-SC have been described. All diagnostic modalities should be used to evaluate patients with suspected IgG4-SC including imaging, endoscopic methods and biopsy as well as a thorough history, physical examination and laboratory assessment to evaluate for extrahepatic disease. Corticosteroids are the mainstay of therapy, with a starting dose of prednisone of 0.6 mg/kg/day. Other immunosuppressive therapies can be used for steroid-intolerant or refractory patients. This review describes the epidemiology, diagnosis and management of IgG4-SC.
C1 [Shah, Raj A.; Kowdley, Kris V.] Swedish Med Ctr, Liver Care Network & Organ Care Res, Seattle, WA 98122 USA.
C3 Swedish Medical Center
RP Shah, RA (corresponding author), Swedish Med Ctr, Liver Care Network & Organ Care Res, Seattle, WA 98122 USA.
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Zhang LL, 2018, WORLD J GASTROENTERO, V24, P2047, DOI 10.3748/wjg.v24.i19.2047
NR 36
TC 0
Z9 0
U1 0
U2 0
PU SHUGAR PUBLISHING INC
PI WESTHAMPTON BEACH
PA 32 MILL ROAD, WESTHAMPTON BEACH, NY 11978 USA
SN 0277-4208
J9 PRACT GASTROENTEROL
JI Pract. Gasterontol.
PD JUL
PY 2019
VL 43
IS 7
BP 26
EP 31
PG 5
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA ML0UG
UT WOS:000549191500002
DA 2025-01-07
ER
PT J
AU Li, M
Chen, L
Gao, Y
Li, MY
Wang, XS
Qiang, L
Wang, XP
AF Li, Min
Chen, Liu
Gao, Yue
Li, Mengyuan
Wang, Xiaosheng
Qiang, Lei
Wang, Xiaoping
TI Recent advances targeting C-C chemokine receptor type 2 for liver
diseases in monocyte/macrophage
SO LIVER INTERNATIONAL
LA English
DT Review
DE CCR2; cenicriviroc; liver; macrophage
ID MONOCYTE CHEMOATTRACTANT PROTEIN-1; PROMOTES HEPATIC-FIBROSIS;
NONALCOHOLIC STEATOHEPATITIS; INSULIN-RESISTANCE; INFLAMMATORY
MONOCYTES; GENE POLYMORPHISMS; IMMUNE-RESPONSES; KUPFFER CELLS; CCR2;
RECRUITMENT
AB Liver plays a critical role in metabolism, nutrient storage and detoxification. Emergency signals or appropriate immune response leads to pathological inflammation and breaks the steady state when liver dysfunction appears, which makes body more susceptible to chronic liver infection, autoimmune diseases and tumour. Compelling proof has illustrated the non-redundant importance of C-C chemokine receptor type 2 (CCR2), one of G-protein-coupled receptors, in different diseases. Selectively expressed on the surface of cells, CCR2 is involved in various signalling pathways and regulates the migration of cells. Especially, a peculiar role of CCR2 has been identified within decades in the onset and progression of hepatic diseases, which led to particular focusing on CCR2 as a new therapeutic and diagnostic target for non-alcoholic fatty liver disease and hepatocellular carcinoma. In this review, we discuss the effect of CCR2 in monocytes/macrophages on liver diseases. The application and translation of the decades of discoveries into therapies promise novel approaches in the treatment of liver disease.
C1 [Li, Min; Chen, Liu; Gao, Yue; Qiang, Lei; Wang, Xiaoping] China Pharmaceut Univ, Sch Basic Med & Clin Pharm, State Key Lab Nat Med, Nanjing, Peoples R China.
[Li, Mengyuan; Wang, Xiaosheng] China Pharmaceut Univ, Sch Basic Med & Clin Pharm, Biomed Informat Res Lab, Nanjing, Peoples R China.
[Li, Mengyuan; Wang, Xiaosheng] China Pharmaceut Univ, Big Data Res Inst, Nanjing, Peoples R China.
C3 China Pharmaceutical University; China Pharmaceutical University; China
Pharmaceutical University
RP Qiang, L; Wang, XP (corresponding author), China Pharmaceut Univ, Sch Basic Med & Clin Pharm, State Key Lab Nat Med, Nanjing, Peoples R China.
EM lqiang@cpu.edu.cn; cpuwxp@163.com
RI Wang, Xiaosheng/AAN-6410-2020; qiang, lei/B-2763-2012; Li,
Mengyuan/GZM-6335-2022
OI qiang, lei/0000-0002-7164-3164; Wang, Xiaosheng/0000-0002-7199-7093; Li,
Min/0000-0001-7536-8828; Li, Mengyuan/0000-0001-6856-6463
FU China Postdoctoral Science Foundation [2019M652035]; General Program of
National Natural Science Foundation of China [81772911, 81974425,
81903648]; Natural Science Foundation of Jiangsu Province [BK20170744];
Six Talent Peaks Project in Jiangsu Province [SWYY-095]
FX This work was supported by the China Postdoctoral Science Foundation
Grant (2019M652035); the General Program of National Natural Science
Foundation of China (81772911, 81974425 and 81903648); the Natural
Science Foundation of Jiangsu Province (BK20170744) and the Six Talent
Peaks Project in Jiangsu Province (SWYY-095).
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NR 90
TC 12
Z9 13
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD DEC
PY 2020
VL 40
IS 12
BP 2928
EP 2936
DI 10.1111/liv.14687
EA OCT 2020
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA OY1EV
UT WOS:000580411800001
PM 33025657
OA Bronze
DA 2025-01-07
ER
PT J
AU Poggioli, R
Hirani, K
Jogani, VG
Ricordi, C
AF Poggioli, R.
Hirani, K.
Jogani, V. G.
Ricordi, C.
TI Modulation of inflammation and immunity by Omega-3 fatty acids: a
possible role for prevention and to halt disease progression in
autoimmune, viral, and age-related disorders
SO EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
LA English
DT Article
DE Omega-3 fatty acids; Inflammation; Autoimmune diseases; Age-related
disease; Viral diseases
ID POLYUNSATURATED FATTY-ACIDS; EICOSAPENTAENOIC ACID; FISH-OIL; MARINE
OMEGA-3-FATTY-ACIDS; DIETARY SUPPLEMENTATION; RHEUMATOID-ARTHRITIS;
MACULAR DEGENERATION; NUTRITIONAL FACTORS; COGNITIVE FUNCTION;
CLINICAL-OUTCOMES
AB Omega-3 polyunsaturated fatty acids (PUFA) have demonstrated anti-inflammatory properties, while Omega-6 have pro-inflammatory effects, and the balance between the two is an important aspect of healthy nutrition. Over the last 30 years, however, the Western diet has shifted largely from Omega-3 to Omega-6 consumption. Uncontrolled aberrant and chronic inflammation is a leading component of many common diseases, including arthritis, cardiovascular diseases, neurodegenerative diseases, cancer, obesity, autoimmune diseases, and infective diseases. Eicosanoids derived from Omega-6 participate in the inflammatory process, while Omega-3 PUFA have the opposite effect. Many favorable effects of Omega-3 are believed to result from their anti-inflammatory properties, but eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) also have inhibitory effects on immune cells and reduce proinflammatory cytokine release. All these mechanisms can be beneficial in autoimmunity. No effective preventions or definite cures for autoimmune diseases are yet known because pathophysiology is also unclear. Omega-3 fatty acid supplementation is associated with a significant reduction in disease activity in several autoimmune diseases, like type 1 diabetes (T1D), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and multiple sclerosis (MS). Studies of viral diseases, including COVID-19, show improvement in symptom severity, recovery prognosis, and probability of survival with the use of Omega-3. Finally, the evidence of the beneficial effect of Omega-3 on metabolic diseases associated with aging is persuasive; various studies have demonstrated that their consumption improves lipids, fatty liver disease, obesity, cognitive function, and cardiovascular complications of chronic kidney disease (CKD). Omega-3 PUFA have also been shown to support an anti-inflammatory effect in older age and to have favorable effects on age-related disease's complications, frailty, and mortality. A healthy Omega-6/3 PUFA ratio should be targeted for the modulation of low-grade inflammation, as well as for the prevention of immune dysregulation and complications of uncontrolled inflammation triggered by infections, development, and progression of autoimmune disorders, and the consequences of oxidative stress due to aging. There is still a need for randomized clinical studies to validate current evidence supporting supplementation with correct doses of Omega-3 PUFA in autoimmune and chronic disease prevention.
C1 [Poggioli, R.; Hirani, K.; Jogani, V. G.; Ricordi, C.] Univ Miami, Miller Sch Med, Diabet Res Inst, Miami, FL 33136 USA.
C3 University of Miami
RP Ricordi, C (corresponding author), Univ Miami, Miller Sch Med, Diabet Res Inst, Miami, FL 33136 USA.
EM cricordi@med.miami.edu
FU Diabetes Research Institute Foundation
FX The work was supported in part by the Diabetes Research Institute
Foundation.
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NR 150
TC 19
Z9 19
U1 5
U2 11
PU VERDUCI PUBLISHER
PI ROME
PA VIA GREGORIO VII, ROME, 186-00165, ITALY
SN 1128-3602
J9 EUR REV MED PHARMACO
JI Eur. Rev. Med. Pharmacol. Sci.
PD AUG
PY 2023
VL 27
IS 15
BP 7380
EP 7400
PG 21
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA ES8M9
UT WOS:001141008100025
PM 37606147
DA 2025-01-07
ER
PT J
AU Okazaki, K
Uchida, K
Koyabu, M
Miyoshi, H
Ikeura, T
Takaoka, M
AF Okazaki, Kazuichi
Uchida, Kazushige
Koyabu, Masanori
Miyoshi, Hideaki
Ikeura, Tsukasa
Takaoka, Makoto
TI IgG4 cholangiopathy - Current concept, diagnosis, and pathogenesis
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE IgG4-related disease; IgG4-cholangiopathy; IgG4-related sclerosing
cholangitis; Autoimmune pancreatitis
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; AUTOIMMUNE PANCREATITIS;
SCLEROSING PANCREATITIS; IGG4-RELATED DISEASE; RITUXIMAB; THERAPY;
SYSTEM
AB IgG4 related cholangiopathy, a distinctive type of cholangitis of unknown origin, is characterized by increased serum levels of IgG4, massive infiltration of IgG4-positive plasma cells with storiform fibrosis and/or obliterative phlebitis in the thickened bile duct wall, and good response to steroids. Patients with IgG4-cholangiopathy are frequently associated with autoimmune pancreatitis; IgG4-cholangiopathy is recognized as a biliary manifestation of IgG4-related disease. This condition can be diagnosed by a combination of imaging, serology, histopathology, and steroid responsiveness; however, cholangiographic features are often difficult to differentiate from primary sclerosing cholangitis, pancreatic cancer, or cholangiocarcinoma. The Japanese clinical diagnostic criteria for IgG4-related sclerosing cholangitis established in 2012 are useful in the diagnosis of IgG4-cholangiopathy. Although the precise pathogenic mechanism remains unclear, the development of IgG4-cholangiopathy may involve: susceptible genetic factors, abnormal innate and acquired immunity, decreased naive regulatory T cells, and specific B cell responses.
Further studies on genetic backgrounds, disease specific antigens, and the role of IgG4 are necessary to clarify the pathogenesis. (C) 2014 Published by Elsevier B.V. on behalf of the European Association for the Study of the Liver.
C1 [Okazaki, Kazuichi; Uchida, Kazushige; Koyabu, Masanori; Miyoshi, Hideaki; Ikeura, Tsukasa; Takaoka, Makoto] Kansai Med Univ, Div Gastroenterol & Hepatol, Dept Internal Med 3, Hirakata, Osaka 5731197, Japan.
C3 Kansai Medical University
RP Okazaki, K (corresponding author), Kansai Med Univ, Div Gastroenterol & Hepatol, Dept Internal Med 3, Shinmachi, Hirakata, Osaka 5731197, Japan.
EM okazaki@hirakata.kmu.ac.jp
RI Uchida, Kazushige/AAD-4966-2020
OI Uchida, Kazushige/0000-0002-3160-3184
FU Ministry of Culture and Science of Japan [20590810, 24591020, 12008507,
26461038]; Research Program on Intractable Diseases, from the Ministry
of Labor and Welfare of Japan; Ministry of Education, Culture, Sports,
Science and Technology of Japan, from CREST Japan Science, and
Technology Agency; Grants-in-Aid for Scientific Research [26461038,
23591017, 24591020] Funding Source: KAKEN
FX This study was partially supported by (1) Grant-in-Aid for Scientific
Research (C) of the Ministry of Culture and Science of Japan (20590810,
24591020, 12008507, 26461038), (2) the Research Program on Intractable
Diseases, from the Ministry of Labor and Welfare of Japan, and (3)
grants-in-aid from the Ministry of Education, Culture, Sports, Science
and Technology of Japan, from CREST Japan Science, and Technology
Agency.
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NR 21
TC 50
Z9 58
U1 0
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD SEP
PY 2014
VL 61
IS 3
BP 690
EP 695
DI 10.1016/j.jhep.2014.04.016
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AN8QI
UT WOS:000340868300035
PM 24768756
OA hybrid
DA 2025-01-07
ER
PT J
AU Zhang, CS
Yang, GS
Ling, Y
Chen, GH
Zhou, TB
AF Zhang, Changsong
Yang, Guangshun
Ling, Yang
Chen, Guihua
Zhou, Tianbao
TI Graft versus host disease following liver transplantation: A case report
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE graft versus host disease; liver transplantation
ID BONE-MARROW-TRANSPLANTATION
AB Graft versus host disease (GVHD) is an uncommon complication following liver transplantation. In the present case report, a 53-year-old male hepatitis B virus carrier was diagnosed with primary liver cancer with post-hepatitis cirrhosis. Preoperative cytomegalovirus (CMV), Epstein-Barr virus, coxsackievirus, herpes simplex virus and autoimmune antibody series were negative. Preoperative human leukocyte antigen type was also negative. Following classic orthotropic liver transplantation, postoperative treatment included immunosuppression therapy, infection protection, anti-human immunodeficiency virus therapy and CMV infection protection therapy. Chemotherapy was initiated at day 16 following surgery. At day 26 following the transplantation, the patient developed a fever of unknown cause, and a scattered red rash was observed behind the left ear and on the neck. The patient presented with a fever of unknown cause, rash, symptoms of the digestive tract, leukocytopenia and pancytopenia. A diagnosis of GVHD was confirmed following a skin biopsy. Symptomatic therapies, including antivirals, anti-anaphylaxis drugs and steroids were administered. However, the patient succumbed to infection, acute respiratory distress syndrome and multiple organ failure at day 46 following surgery. Therefore, an effective therapeutic strategy for the treatment of GVHD following liver transplantation is yet to be established, and further research is required prior to such a regimen being developed.
C1 [Zhang, Changsong; Ling, Yang] Soochow Univ, Coll Med, Changzhou Tumor Hosp, Clin Oncol Lab, Changzhou 213002, Jiangsu, Peoples R China.
[Yang, Guangshun] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Hepat Surg Ctr, Shanghai 200438, Peoples R China.
[Chen, Guihua] Sun Yat Sen Univ, Affiliated Hosp 3, Hepat Surg Ctr, Guangzhou 510630, Guangdong, Peoples R China.
[Zhou, Tianbao] Ningbo Univ, Sch Med, Affiliated Ningbo Hosp 2, Hepatobiliary Surg Ctr, Ningbo 315010, Zhejiang, Peoples R China.
C3 Soochow University - China; Naval Medical University; Sun Yat Sen
University; Ningbo University
RP Zhou, TB (corresponding author), Ningbo Univ, Sch Med, Affiliated Ningbo Hosp 2, Hepatobiliary Surg Ctr, 41 Northwest St, Ningbo 315010, Zhejiang, Peoples R China.
EM hbzcs@126.com
FU China Postdoctoral Science Foundation [201003380]; Natural Science
Foundation of Ningbo [2011A610057]; Natural Science Foundation of China
[81372212]; Natural Science Foundation of Jiangsu [BK2011251]; Jiangsu
Provincial Special Program of Medical Science [BL2013012]; Health
Talents Project for Jiangsu, China [LJ201157, RC2011038, BRA2011038]
FX The study was supported by grants from the China Postdoctoral Science
Foundation Specific funded project (no. 201003380), the Natural Science
Foundation of Ningbo (no. 2011A610057), the Natural Science Foundation
of China (no. 81372212), the Natural Science Foundation of Jiangsu (no.
BK2011251), the Jiangsu Provincial Special Program of Medical Science
(no. BL2013012), the Health Talents Project for Jiangsu, China (nos.
LJ201157, RC2011038 and BRA2011038) and the Natural Science Foundation
of Ningbo (no. 2011A610057).
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TC 5
Z9 5
U1 0
U2 6
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD OCT
PY 2014
VL 8
IS 4
BP 1164
EP 1166
DI 10.3892/etm.2014.1850
PG 3
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA AQ4AN
UT WOS:000342734700025
PM 25187816
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Seki, S
Nakashima, H
Nakashima, M
Kinoshita, M
AF Seki, Shuhji
Nakashima, Hiroyuki
Nakashima, Masahiro
Kinoshita, Manabu
TI Antitumor Immunity Produced by the Liver Kupffer Cells, NK Cells, NKT
Cells, and CD8+ CD122+ T Cells
SO CLINICAL & DEVELOPMENTAL IMMUNOLOGY
LA English
DT Review
ID NATURAL-KILLER-CELLS; TUMOR-NECROSIS-FACTOR; HEMATOPOIETIC STEM-CELLS;
LIGAND-MEDIATED FUNCTION; C-REACTIVE PROTEIN; ALPHA-GALACTOSYLCERAMIDE;
HEPATIC METASTASIS; HEPATOCELLULAR-CARCINOMA; SHWARTZMAN REACTION;
CYTOKINE PRODUCTION
AB Mouse and human livers contain innate immune leukocytes, NK cells, NKT cells, and macrophage-lineage Kupffer cells. Various bacterial components, including Toll-like receptor (TLR) ligands and an NKT cell ligand (alpha-galactocylceramide), activate liver Kupffer cells, which produce IL-1, IL-6, IL-12, and TNF. IL-12 activates hepatic NK cells and NKT cells to produce IFN-gamma, which further activates hepatic T cells, in turn activating phagocytosis and cytokine production by Kupffer cells in a positive feedback loop. These immunological events are essentially evoked to protect the host from bacterial and viral infections; however, these events also contribute to antitumor and antimetastatic immunity in the liver by activated liver NK cells and NKT cells. Bystander CD8(+)CD122(+) T cells, and tumor-specific memory CD8(+)T cells, are also induced in the liver by a-galactocylceramide. Furthermore, adoptive transfer experiments have revealed that activated liver lymphocytes may migrate to other organs to inhibit tumor growth, such as the lungs and kidneys. The immunological mechanism underlying the development of hepatocellular carcinoma in cirrhotic livers in hepatitis C patients and liver innate immunity as a double-edged sword (hepatocyte injury/regeneration, septic shock, autoimmune disease, etc.) are also discussed.
C1 [Seki, Shuhji; Nakashima, Hiroyuki; Nakashima, Masahiro; Kinoshita, Manabu] Natl Def Med Coll, Dept Immunol & Microbiol, Tokorozawa, Saitama 3588513, Japan.
C3 National Defense Medical College - Japan
RP Seki, S (corresponding author), Natl Def Med Coll, Dept Immunol & Microbiol, Namiki 3-2, Tokorozawa, Saitama 3588513, Japan.
EM btraums@ndmc.ac.jp
OI Nakashima, Hiroyuki/0000-0001-6066-3031
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NR 85
TC 60
Z9 68
U1 0
U2 11
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1740-2522
EI 1740-2530
J9 CLIN DEV IMMUNOL
JI Clin. Dev. Immunol.
PY 2011
AR 868345
DI 10.1155/2011/868345
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 870XW
UT WOS:000298703200001
PM 22190974
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Koike, K
Miyoshi, H
AF Koike, K
Miyoshi, H
TI Oxidative stress and hepatitis C viral infection
SO HEPATOLOGY RESEARCH
LA English
DT Review
DE oxidative stress; hepatitis C virus; hepatocarcinogenesis; lipid
peroxidation; steatosis; insulin resistance
ID VIRUS CORE PROTEIN; TYPE-2 DIABETES-MELLITUS; FAS-MEDIATED APOPTOSIS;
NITRIC-OXIDE; HEPATOCELLULAR-CARCINOMA; LIPID-PEROXIDATION; DNA-DAMAGE;
SERUM AMINOTRANSFERASE; THIOREDOXIN LEVELS; ACTIVATES ERK
AB The involvement of oxidative stress in the pathogenesis of hepatitis and hepatocellular carcinoma has been strongly suggested. Oxidative stress is produced by inflammatory processes that occur in hepatitis via immunological mechanisms. In addition, in hepatitis C virus (HCV) infectious disease, some role has been assigned to viral proteins in the induction of oxidative stress. In the presence of hepatic steatosis, insulin resistance and increased levels of some cytokines, all of which are also induced by viral protein expression, oxidative stress is enhanced in HCV infection. In this sense, the role of oxidative stress in the progression of chronic hepatitis and hepatocarcinogenesis is greater in hepatitis C than in other types of hepatitis such as hepatitis B or autoimmune hepatitis. The additive effects of oxidative stress caused by the inflammatory process and that induced by HCV proteins may, furthermore, exert synergistic effects with alterations in intracellular signaling systems such as mitogen-activated protein kinases (MAPK), which are also induced by HCV proteins. These synergistic effects may be responsible for rare characteristics, that is, the high incidence and multicentric nature of hepatocarcinogenesis in HCV infection. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
C1 Univ Tokyo, Grad Sch Med, Dept Internal Med, Tokyo 1138655, Japan.
C3 University of Tokyo
RP Univ Tokyo, Grad Sch Med, Dept Infect Dis, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
EM kkoike-tky@umin.ac.jp
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NR 94
TC 44
Z9 49
U1 2
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD FEB
PY 2006
VL 34
IS 2
BP 65
EP 73
DI 10.1016/j.hepres.2005.11.001
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 014TK
UT WOS:000235502800001
PM 16364681
DA 2025-01-07
ER
PT J
AU Lu, Y
Ye, P
Chen, SL
Tan, EM
Chan, EKL
AF Lu, Y
Ye, P
Chen, SL
Tan, EM
Chan, EKL
TI Identification of kinectin as a novel Behcet's disease autoantigen
SO ARTHRITIS RESEARCH & THERAPY
LA English
DT Article
ID TUMOR-ASSOCIATED ANTIGENS; KINESIN-BINDING PROTEIN; GOLGI-COMPLEX;
MOLECULAR CHARACTERIZATION; HEPATOCELLULAR-CARCINOMA; SS-A/RO; HUMAN
AUTOANTIBODIES; ALPHA-TROPOMYOSIN; APLASTIC-ANEMIA; TARGET ANTIGEN
AB There has been some evidence that Behcet's disease ( BD) has a significant autoimmune component but the molecular identity of putative autoantigens has not been well characterized. In the initial analysis of the autoantibody profile in 39 Chinese BD patients, autoantibodies to cellular proteins were uncovered in 23% as determined by immunoblotting. We have now identified one of the major autoantibody specificities using expression cloning. Serum from a BD patient was used as a probe to immunoscreen lambda ZAP expression cDNA library. Candidate autoantigen cDNAs were characterized by direct nucleotide sequencing and their expressed products were examined for reactivity to the entire panel of BD sera using immunoprecipitation. Reactivity was also examined with normal control sera and disease control sera from patients with lupus and Sjogren's syndrome. Six independent candidate clones were isolated from the cDNA library screen and were identified as overlapping partial human kinectin cDNAs. The finding that kinectin was an autoantigen was verified in 9 out of 39 (23%) BD patient sera by immunoprecipitation of the in vitro translation products. Sera from controls showed no reactivity. The significance of kinectin as a participant in autoimmune pathogenesis in BD and the potential use of autoantibody to kinectin in serodiagnostics are discussed.
C1 Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA.
Shanghai Med Univ 2, Dept Rheumatol, Shanghai, Peoples R China.
Univ Florida, Dept Oral Biol, Gainesville, FL USA.
C3 Scripps Research Institute; Shanghai Jiao Tong University; State
University System of Florida; University of Florida
RP Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA.
EM luyu100@sina.com; echan@ufl.edu
RI Chan, Edward/B-5671-2009
OI Chan, Edward/0000-0003-3938-9503
FU NCI NIH HHS [R01 CA056956, CA56956] Funding Source: Medline; NIAID NIH
HHS [R01 AI039645, R01 AI047859, AI39645, AI47859, R21 AI047859] Funding
Source: Medline; NIAMS NIH HHS [R01 AR042455, AR42455, R37 AR042455]
Funding Source: Medline
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NR 52
TC 28
Z9 31
U1 0
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1478-6354
EI 1478-6362
J9 ARTHRITIS RES THER
JI Arthritis Res. Ther.
PY 2005
VL 7
IS 5
BP R1133
EP R1139
DI 10.1186/ar1798
PG 7
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 952QI
UT WOS:000231020200024
PM 16207330
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Powell, LW
AF Powell, Lawrie W.
TI Overview: Liver disease and transplantation
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE Australia; liver disease; transplantation
ID ACTIVE CHRONIC HEPATITIS; DIFFERENTIAL GENE-EXPRESSION; HEREDITARY
HEMOCHROMATOSIS; NATURAL-HISTORY; C-VIRUS; NONALCOHOLIC STEATOHEPATITIS;
HEPATOCELLULAR-CARCINOMA; DIPEPTIDYL PEPTIDASE; DIAGNOSTIC-CRITERIA;
HEPCIDIN REGULATION
AB Australia has had a proud and enviable record of seminal contributions to hepatology, with many contributors. Thus, any attempt to summarize these contributions ab initio in a brief review article is a significant challenge, primarily because it is so easy to overlook or underestimate particular aspects. In this article, I have confined my comments primarily to the areas where the contributions have had a significant global impact and have clearly been recognized internationally. This means that many worthwhile Australian additions will be omitted if there was less apparent international impact. The first significant interest in liver disease in Australia was from the Melbourne group at the Walter and Eliza Hall Institute (WEHI) and Royal Melbourne Hospital, leading to seminal contributions to the description, diagnosis, aetiopathogenesis and therapy of autoimmune hepatitis and primary biliary cirrhosis. Others from Royal Prince Alfred Hospital in Sydney contributed substantially to the effects of immunosuppression of autoimmune hepatitis and to early descriptions of primary sclerosing cholangitis. Other areas where Australians have contributed significantly include steatohepatitis, iron metabolism (and in particular hemochromatosis), viral hepatitis (both at the molecular and clinical level), portal hypertension, and transplant immunology. The remarkable contribution of Professor Dame Sheila Sherlock to Australian hepatology is also summarized.
C1 [Powell, Lawrie W.] Royal Brisbane & Womens Hosp, Ctr Adv Clin Res, UQ Ctr Clin Res, Brisbane, Qld 4029, Australia.
[Powell, Lawrie W.] Univ Queensland, Brisbane, Qld, Australia.
C3 Royal Brisbane & Women's Hospital; University of Queensland; University
of Queensland
RP Powell, LW (corresponding author), Royal Brisbane & Womens Hosp, Ctr Adv Clin Res, UQ Ctr Clin Res, Level 4, Brisbane, Qld 4029, Australia.
EM lawrie.powell@qimr.edu.au
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NR 75
TC 1
Z9 3
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD OCT
PY 2009
VL 24
SU 3
BP S97
EP S104
DI 10.1111/j.1440-1746.2009.06079.x
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 502AG
UT WOS:000270425600017
PM 19799707
OA Bronze
DA 2025-01-07
ER
PT J
AU Lu, JJG
Ji, P
French, SW
AF Lu, Jiajie G.
Ji, Ping
French, Samuel W.
TI The Major Histocompatibility Complex Class II-CD4 Immunologic Synapse in
Alcoholic Hepatitis and Autoimmune Liver Pathology The Role of
Aberrant Major Histocompatibility Complex Class II in Hepatocytes
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Review
ID MHC CLASS-II; INTERCELLULAR-ADHESION MOLECULE-1; MONONUCLEAR CELL
INFILTRATE; PRIMARY BILIARY-CIRRHOSIS; CD4(+) T-CELLS; DIFFERENTIAL
EXPRESSION; PIECEMEAL NECROSIS; EPITHELIAL-CELLS; HLA-DQ; ANTIGEN
AB The major histocompatibility complex class II (MHC II)-CD4 immunologic synapse is classically described between the T-cell receptor of CD4-positive lymphocytes and MHC II on antigen-presenting cells. This interaction and others between surrounding costimulatory and checkpoint molecules promote differentiation of naive CD4 T lymphocytes into helper T cells subtypes, including types 1, 2, and 17 helper T cells, that have more tailored immunologic responses. Although MHC II is mainly produced by professional antigen-presenting cells, it can be aberrantly produced by other cell types, including hepatocytes in various Liver pathologies, such as autoimmune hepatitis and alcoholic hepatitis. This can lead to direct targeting of hepatocytes by CD4-positive lymphocytes, which form an immunologic synapse with the hepatocyte. The lymphocytes internalize the MHC II-CD4 complexes in a phagocytosis-like mechanism and in the process eat the hepatocyte piece by piece. We review the evidence for this mechanism and the role of these autoimmune responses in various liver diseases, including alcoholic hepatitis, autoimmune hepatitis, and primary biliary cirrhosis. The role of aberrant MHC II in malignancy, including hepatocellular carcinoma, is also reviewed. Further understanding of this mechanism can lead to better understanding of the immune mechanisms involved in these liver pathologies, with potential diagnostic and therapeutic applications.
C1 [Lu, Jiajie G.; Ji, Ping; French, Samuel W.] Harbor UCLA Med Ctr, Dept Pathol, 1000 W Carson St, Torrance, CA 90502 USA.
C3 University of California System; University of California Los Angeles;
University of California Los Angeles Medical Center
RP Lu, JJG (corresponding author), Harbor UCLA Med Ctr, Dept Pathol, 1000 W Carson St, Torrance, CA 90502 USA.
EM j1u3@dhs.lacounty.gov
FU NIH/National Institute on Alcohol Abuse and Alcoholism [UO-21898-05]
FX Supported by NIH/National Institute on Alcohol Abuse and Alcoholism
grant UO-21898-05 (S.W.F.).
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NR 72
TC 8
Z9 9
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0002-9440
EI 1525-2191
J9 AM J PATHOL
JI Am. J. Pathol.
PD JAN
PY 2020
VL 190
IS 1
BP 25
EP 32
DI 10.1016/j.ajpath.2019.09.019
PG 8
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA JZ7FS
UT WOS:000505274700003
PM 31669415
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Wolkersdörfer, GW
Marx, C
Brown, J
Schröder, S
Füssel, M
Rieber, EP
Kuhlisch, E
Ehninger, G
Bornstein, SR
AF Wolkersdörfer, GW
Marx, C
Brown, J
Schröder, S
Füssel, M
Rieber, EP
Kuhlisch, E
Ehninger, G
Bornstein, SR
TI Prevalence of HLA-DRB1 genotype and altered Fas/Fas ligand expression in
adrenocortical carcinoma
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID COMPLEX CLASS-II; AUTOIMMUNE ADDISONS-DISEASE; TUMOR IMMUNE PRIVILEGE;
INDUCED CELL-DEATH; HLA CLASS-I; FAS LIGAND; COLON-CANCER; INFILTRATING
LYMPHOCYTES; HEPATOCELLULAR-CARCINOMA; ADRENAL MASSES
AB A distinctive feature of malignant adrenocortical neoplasms is decreased major histocompatibility complex (MHC) class II molecule expression. However, it is unknown whether there exists a restriction to certain MHC genotypes and whether this involves alterations of the Fas/Fas ligand system and thereby affects tissue homeostasis.
Therefore, MHC class II phenotype and genotype and expression patterns of the Fas/Fas ligand system were investigated in 24 adrenocortical tumors (n(Adenomas) = 14, n(Carcinomas) = 10) and an adrenal cancer cell line (NCI-H295). No MHC class II antigen expression was detected in carcinomas. The DRB1*01 genotype was found in 54.5% of patients with carcinoma ( P = 0.046). No prevalence of any genotype could be detected in patients with adenomas, which exhibited varying levels of antigen expression. Fas receptor expression was 75.0% in adenomas compared with 20.0% in carcinomas ( P = 0.0196), whereas ligand expression was 37.7% in adenomas and reached almost 100% in the carcinomas investigated in this study ( P = 0.0033).
In summary, the DRB1* 01 genotype may be correlated to a higher risk for malignancy. Additional studies on MHC class II genotype and phenotype and the altered Fas/Fas ligand system in adrenal neoplasms may help to identify mechanisms of immune escape and suggest new diagnostic approaches.
C1 Tech Univ Dresden, Dept Internal Med 1, D-01307 Dresden, Germany.
Tech Univ Dresden, Dept Internal Med 3, D-01307 Dresden, Germany.
Tech Univ Dresden, Dept Immunol, D-01307 Dresden, Germany.
Tech Univ Dresden, Inst Med Informat & Biometry, D-01307 Dresden, Germany.
Vet Affairs Med Ctr, Miami, FL 33149 USA.
Univ Leipzig, Dept Immunol, D-04129 Leipzig, Germany.
C3 Technische Universitat Dresden; Technische Universitat Dresden;
Technische Universitat Dresden; Technische Universitat Dresden; US
Department of Veterans Affairs; Veterans Health Administration (VHA);
Leipzig University
RP Tech Univ Dresden, Fac Med Carl Gustav Carus, Dept Med 1, Fetscherstr 74, D-01307 Dresden, Germany.
EM wolkersdoerfer@mk1.med.tu-dresden.de
OI Kuhlisch, Eberhard/0000-0003-2777-6522
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NR 69
TC 16
Z9 16
U1 0
U2 1
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD MAR
PY 2005
VL 90
IS 3
BP 1768
EP 1774
DI 10.1210/jc.2004-1406
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 904UQ
UT WOS:000227523600075
PM 15585555
OA Bronze
DA 2025-01-07
ER
PT J
AU Carlino, MS
Larkin, J
Long, GV
AF Carlino, Matteo S.
Larkin, James
Long, Georgina V.
TI Immune checkpoint inhibitors in melanoma
SO LANCET
LA English
DT Review
ID PREEXISTING AUTOIMMUNE DISORDERS; NIVOLUMAB PLUS IPILIMUMAB; INDIVIDUAL
PATIENT DATA; METASTATIC MELANOMA; BRAIN METASTASES; POOLED ANALYSIS;
ADVERSE EVENTS; DOUBLE-BLIND; OPEN-LABEL; DISEASE PROGRESSION
AB Immune checkpoint inhibitors target the dysfunctional immune system, to induce cancer-cell killing by CD8-positive T cells. Immune checkpoint inhibitors, specifically anti-CTLA4 and anti-PD-1 antibodies, have revolutionised the management of many cancers, particularly advanced melanoma, for which tumour regression and long-term durable cancer control is possible in nearly 50% of patients, compared with less than 10% historically. Despite the absence of adequately powered trial data, combined anti-CTLA4 and anti-PD-1 checkpoint inhibition has the highest 5-year overall survival rate of all therapies in advanced melanoma, and has high activity in melanoma brain metastases. A phase 3 study has shown the addition of an anti-LAG3 antibody to nivolumab improves progression-free survival, but its effect on overall survival and how this combination compares to combined anti-CTLA4 and anti-PD-1 checkpoint inhibition is unknown. At present, there are no highly sensitive and specific biomarkers of response to immune checkpoint inhibitors, and clinical factors, such as volume and sites of disease, serum lactate dehydrogenase, and BRAF mutation status, are used to select initial therapy for patients with advanced melanoma. Immune checkpoint inhibitors can induce autoimmune toxicities by virtue of their mechanism of action. These toxicities, termed immune-related adverse events, occur most frequently with combined anti-CTLA4 and anti-PD-1 checkpoint inhibition; can have a variety of presentations; can affect any organ system (most often the skin, colon, endocrine system, and liver); and appear to mimic classic autoimmune diseases. Immune-related adverse events require prompt recognition and management, which may be different from the autoimmune disease it mimics. Immune checkpoint inhibitors appear to be safe for use in patients with HIV, viral hepatitis, and patients with mild-to-moderate pre-existing autoimmune diseases. Patients with organ transplants can respond to immune checkpoint inhibitors but have a high chance of transplant loss. PD-1 inhibitors are now an established standard of care as adjuvant therapy in high-risk resected stage III or IV melanoma. Neoadjuvant checkpoint inhibition for resectable stage III melanoma, which is currently limited to clinical trials, is emerging as a highly effective therapy.
C1 [Carlino, Matteo S.; Long, Georgina V.] Univ Sydney, Melanoma Inst Australia, Sydney, NSW, Australia.
[Carlino, Matteo S.] Blacktown Hosp, Dept Med Oncol, Sydney, NSW, Australia.
[Carlino, Matteo S.] Westmead Hosp, Dept Med Oncol, Sydney, NSW, Australia.
[Larkin, James] Royal Marsden NHS Fdn Trust, London, England.
[Long, Georgina V.] Royal North Shore & Mater Hosp, Sydney, NSW, Australia.
C3 Melanoma Institute Australia; University of Sydney; NSW Health;
Blacktown & Mount Druitt Hospital; University of Sydney; NSW Health;
Westmead Hospital; Royal Marsden NHS Foundation Trust; Royal North Shore
Hospital
RP Long, GV (corresponding author), Univ Sydney, Melanoma Inst Australia, Sydney, NSW 2060, Australia.
EM georgina.long@sydney.edu.au
RI Carlino, Matteo/GRS-7198-2022; Long, Georgina/C-1771-2013
OI Carlino, Matteo S/0000-0002-7861-4104; Long,
Georgina/0000-0001-8894-3545; Larkin, James/0000-0001-5569-9523
FU National Institute of Health Research/Institute of Cancer Research
Biomedical Research Centre for cancer; NHMRC Practitioner Fellowship;
Melanoma Institute Australia; University of Sydney Medical Foundation
FX JL is supported by National Institute of Health Research/Institute of
Cancer Research Biomedical Research Centre for cancer. GVL is supported
by NHMRC Practitioner Fellowship, Melanoma Institute Australia, and the
University of Sydney Medical Foundation.
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NR 98
TC 633
Z9 669
U1 25
U2 213
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD SEP 11
PY 2021
VL 398
IS 10304
BP 1002
EP 1014
PG 13
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA UP1FQ
UT WOS:000695130500026
PM 34509219
OA Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Poschke, I
Kiessling, R
AF Poschke, Isabel
Kiessling, Rolf
TI On the armament and appearances of human myeloid-derived suppressor
cells
SO CLINICAL IMMUNOLOGY
LA English
DT Review
DE MDSC; Cancer; Autoimmunity; Transplantation
ID CD4(+) T-CELLS; DENDRITIC CELL; IMMUNE SUPPRESSION; CANCER-PATIENTS;
ARGINASE-I; IMMUNOSUPPRESSIVE ACTIVITY; HEPATOCELLULAR-CARCINOMA;
HEMATOPOIETIC STEM; ANTITUMOR IMMUNITY; HYDROGEN-PEROXIDE
AB Myeloid-derived suppressor cells (MDSC) have frequently been observed in patients with cancer. This heterogeneous population of myeloid cells can exert potent suppression of lymphocyte function and thereby poses a significant hurdle to natural or therapeutically induced anti-tumor immunity. On the other hand, the natural function of MDSC is not yet well understood and their role in infection, inflammation and autoimmune disease is still puzzling.
Understanding MDSC biology will provide the tools necessary for therapeutic targeting of this population, but also permit exploitation of their strong tolerogenic function in the treatment of inflammatory conditions and the prevention of graft rejection. (C) 2012 Elsevier Inc. All rights reserved.
C1 Karolinska Inst, Dept Pathol & Oncol, Canc Ctr Karolinska R8 01, Stockholm, Sweden.
C3 Karolinska Institutet
RP Poschke, I (corresponding author), Karolinska Inst, Dept Pathol & Oncol, Canc Ctr Karolinska R8 01, Stockholm, Sweden.
EM Isabel.Poschke@ki.se
FU Karolinska Institutet; Cancerfonden; Cancerforeningen; Lars Hiertas
memorial foundation; Robert Lundberg fund; Sigurd och Elsa Goljes
memorial foundation; Jubileumsfonden
FX This work has been supported by Karolinska Institutet, Jubileumsfonden,
Cancerfonden, Cancerforeningen, the Lars Hiertas memorial foundation,
the Robert Lundberg fund and the Sigurd och Elsa Goljes memorial
foundation.
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NR 149
TC 151
Z9 163
U1 0
U2 20
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
EI 1521-7035
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD SEP
PY 2012
VL 144
IS 3
BP 250
EP 268
DI 10.1016/j.clim.2012.06.003
PG 19
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 995XR
UT WOS:000308049100007
PM 22858650
DA 2025-01-07
ER
PT J
AU Floreani, A
Tanaka, A
Bowlus, C
Gershwin, ME
AF Floreani, Annarosa
Tanaka, Atsushi
Bowlus, Christopher
Gershwin, Merrill Eric
TI Geoepidemiology and changing mortality in primary biliary cholangitis
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Ursodeoxycholic acid; Obeticholic acid; Cirrhosis; Etiology; Precision
medicine
ID MURINE AUTOIMMUNE CHOLANGITIS; URSODEOXYCHOLIC ACID THERAPY;
POPULATION-BASED COHORT; NATURAL-HISTORY; LIVER FIBROSIS; FOLLOW-UP;
TRANSIENT ELASTOGRAPHY; RISK-FACTORS; HEPATOCELLULAR-CARCINOMA;
NONINVASIVE MARKERS
AB Primary biliary cholangitis (PBC), formerly called primary biliary cirrhosis, is a chronic cholestatic disease characterized by an autoimmune-mediated destruction of small and medium-sized intrahepatic bile ducts. Originally PBC was considered to be rare and almost invariably fatal, mainly because the diagnosis was made in patients presenting with advanced symptomatic disease (jaundice and decompensated cirrhosis). However, the development of a reproducible indirect immunofluorescence assay for antimitochondrial antibody made it possible to diagnose the disease at an earlier stage, and introduction of ursodeoxycholic acid therapy as the first-line therapy for PBC drastically changed PBC-related mortality. At present, patients with an early histological stage have survival rates similar to those of an age- and sex-matched control population. Although 30% of patients treated with ursodeoxycholic acid may exhibit incomplete responses, obeticholic acid and drugs currently in development are expected to be effective for these patients and improve outcomes. Meanwhile, more etiology and immunopathology studies using new technologies and novel animal models are needed to dissect variances of clinical course, treatment response, and outcome in each patient with PBC. Precision medicine that is individualized for each patient on the basis of the cause identified is eagerly awaited.
C1 [Floreani, Annarosa] Univ Padua, Dept Surg Oncol & Gastroenterol, Via Giustiniani 2, Padua, Italy.
[Tanaka, Atsushi] Teikyo Univ, Dept Med, Sch Med, Tokyo, Japan.
[Bowlus, Christopher] Univ Calif Davis, Sch Med, Div Gastroenterol & Hepatol, Davis, CA 95616 USA.
[Gershwin, Merrill Eric] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
C3 University of Padua; Teikyo University; University of California System;
University of California Davis; University of California System;
University of California Davis
RP Gershwin, ME (corresponding author), Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
EM megershwin@ucdavis.edu
RI Bowlus, Christopher/N-9276-2016
OI Bowlus, Christopher/0000-0002-3906-6811
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NR 72
TC 17
Z9 17
U1 0
U2 11
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JUN
PY 2017
VL 52
IS 6
BP 655
EP 662
DI 10.1007/s00535-017-1333-2
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EV5FP
UT WOS:000401788200001
PM 28365879
OA Bronze
DA 2025-01-07
ER
PT J
AU Letchumanan, P
Thumboo, J
AF Letchumanan, Pagalavan
Thumboo, Julian
TI Danazol in the Treatment of Systemic Lupus Erythematosus: A Qualitative
Systematic Review
SO SEMINARS IN ARTHRITIS AND RHEUMATISM
LA English
DT Review
DE systemic lupus erythematosus; danazol; androgens; autoimmune
thrombocytopenia
ID REFRACTORY AUTOIMMUNE THROMBOCYTOPENIA; KLINEFELTERS-SYNDROME; C1
INHIBITOR; HEPATOCELLULAR-CARCINOMA; EVANS-SYNDROME; SEX-HORMONES;
MURINE LUPUS; DEFICIENCY; THERAPY; DISEASE
AB Objectives: To review and summarize published information on the use, effectiveness, and adverse effects of danazol in patients with systemic lupus erythematosus (SLE).
Methods: A MEDLINE search from January 1950 to July 2009 was conducted using 2 search strategies retrieving 51 and 62 references, respectively. We also searched 2 standard reference textbooks and bibliographies of the 38 articles selected.
Results: Of the 38 articles selected, there were 19 case series/reports with a total of 153 patients, including 2 prospective trials of 7 and 16 patients, respectively, and 1 randomized controlled trial of 40 patients. Danazol has been used successfully in the treatment of hematologic manifestations of SLE such as thrombocytopenia, Evan's syndrome, autoimmune hemolytic anemia, and a case of red cell aplasia. Thirteen patients responded to danazol after failing splenectomy. There is limited information on the use of danazol in nonhematologic manifestations of SLE. Adverse effects were generally tolerable but high doses may produce undesirable side effects for female patients.
Conclusions: Danazol is a useful drug in the treatment of SLE patients, especially in patients with refractory thrombocytopenia, autoimmune hemolytic anemia, and premenstrual flares, and in some mild nonhematologic manifestations of SLE. It appears to be relatively well tolerated, safe, and efficacious. (C) 2011 Elsevier Inc. All rights reserved. Semin Arthritis Rheum 40:298-306
C1 [Letchumanan, Pagalavan] Monash Univ, Sch Med & Hlth Sci, Bukit Azah 80100, Johor Bahru, Malaysia.
[Thumboo, Julian] Singapore Gen Hosp, Dept Rheumatol & Immunol, Singapore 0316, Singapore.
[Thumboo, Julian] Natl Univ Singapore, Yong Loo Lin Sch Med, Singapore 117595, Singapore.
[Thumboo, Julian] Natl Univ Singapore, Duke NUS Grad Med Sch, Singapore 117595, Singapore.
C3 Monash University; Monash University Malaysia; Singapore General
Hospital; National University of Singapore; National University of
Singapore
RP Letchumanan, P (corresponding author), Monash Univ, Sch Med & Hlth Sci, Sunway Campus,JKR 1235, Bukit Azah 80100, Johor Bahru, Malaysia.
EM pagal72@gmail.com
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NR 59
TC 23
Z9 24
U1 1
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0049-0172
EI 1532-866X
J9 SEMIN ARTHRITIS RHEU
JI Semin. Arthritis Rheum.
PD FEB
PY 2011
VL 40
IS 4
BP 298
EP 306
DI 10.1016/j.semarthrit.2010.03.005
PG 9
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 717AL
UT WOS:000287014500003
PM 20541792
DA 2025-01-07
ER
PT J
AU Zignego, AL
Gragnani, L
Piluso, A
Sebastiani, M
Giuggioli, D
Fallahi, P
Antonelli, A
Ferri, C
AF Zignego, Anna Linda
Gragnani, Laura
Piluso, Alessia
Sebastiani, Marco
Giuggioli, Dilia
Fallahi, Poupak
Antonelli, Alessandro
Ferri, Clodoveo
TI Virus-driven autoimmunity and lymphoproliferation: the example of HCV
infection
SO EXPERT REVIEW OF CLINICAL IMMUNOLOGY
LA English
DT Review
DE autoimmunity; B-cell NHL; cancer; cryoglobulinemia; cryoglobulinemic
vasculitis; diabetes; hepatitis C virus; lymphoma; mixed
cryoglobulinemia; thyroid
ID HEPATITIS-C-VIRUS; NON-HODGKINS-LYMPHOMA; B-CELL LYMPHOMA; HLA-CLASS-II;
MIXED CRYOGLOBULINEMIA SYNDROME; PEGYLATED INTERFERON-ALPHA; MARGINAL
ZONE LYMPHOMA; SERUM-LEVELS; ANTIVIRAL TREATMENT; SPLENIC LYMPHOMA
AB HCV chronic infection is characterized by possible development of both hepatic and extrahepatic manifestations. The infection by this both hepatotropic and lymphotropic virus is responsible for polyoligoclonal B-lymphocyte expansion, leading to several immune-mediated disorders. Mixed cryoglobulinemia syndrome that in some cases may evolve to frank B-cell non-Hodgkin's lymphoma is the prototype of HCV-driven autoimmune and lymphoproliferative disorders. The HCV oncogenic potential has been suggested by several clinicoepidemiological and laboratory studies; it includes hepatocellular carcinoma, B-cell non-Hodgkin's lymphoma and papillary thyroid cancer. The definition HCV syndrome refers to the complex of HCV-driven diseases; these latter are characterized by heterogeneous geographical distribution, suggesting a role of other important genetic and/or environmental cofactors. The natural history of HCV syndrome is the result of a multifactorial and multistep pathogenetic process, which may evolve from mild manifestations to systemic autoimmune disorders, and less frequently to malignant neoplasias. The present updated review analyzes the clinical and pathogenetic aspects of the main HCV-associated diseases.
C1 [Zignego, Anna Linda; Gragnani, Laura; Piluso, Alessia] Univ Florence, Ctr Syst Manifestat Hepatitis Viruses MASVE, Dept Expt & Clin Med, Florence, Italy.
[Sebastiani, Marco; Giuggioli, Dilia; Ferri, Clodoveo] Univ Modena & Reggio Emilia, Sch Med, Azienda Ospedaliero Univ, Policlin Modena,Chair & Rheumatol Unit, Modena, Italy.
[Fallahi, Poupak] Univ Pisa, Sch Med, Dept Internal Med, I-56100 Pisa, Italy.
[Antonelli, Alessandro] Univ Pisa, Dept Clin & Expt Med, I-56126 Pisa, Italy.
C3 University of Florence; Universita di Modena e Reggio Emilia; University
of Pisa; University of Pisa
RP Ferri, C (corresponding author), Univ Modena & Reggio Emilia, Sch Med, Azienda Ospedaliero Univ, Policlin Modena,Chair & Rheumatol Unit, Modena, Italy.
EM clferri@unimore.it
RI Fallahi, Poupak/AAC-6041-2022; Antonelli, Alessandro/AAU-2291-2020;
Zignego, Anna/AAL-8205-2021; Gragnani, Laura/H-7755-2019; Giuggioli,
Dilia/AAQ-8865-2020; Gragnani, Laura/K-7751-2013; Sebastiani,
Marco/Q-7557-2016
OI Giuggioli, Dilia/0000-0002-0041-3695; Gragnani,
Laura/0000-0001-6800-9149; Sebastiani, Marco/0000-0002-1294-6421
FU Fondazione Umberto Veronesi
FX L Gragnani is supported by a 2014 fellowship 'Fondazione Umberto
Veronesi.' The authors have no other relevant affiliations or financial
involvement with any organization or entity with a financial interest in
or financial conflict with the subject matter or materials discussed in
the manuscript apart from those disclosed.
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NR 192
TC 88
Z9 92
U1 0
U2 15
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1744-666X
EI 1744-8409
J9 EXPERT REV CLIN IMMU
JI Expert Rev. Clin. Immunol.
PD JAN
PY 2015
VL 11
IS 1
SI SI
BP 15
EP 31
DI 10.1586/1744666X.2015.997214
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AX2GE
UT WOS:000346760700003
PM 25534977
DA 2025-01-07
ER
PT J
AU De Keukeleire, S
Vermassen, T
De Schoenmakere, G
Kruse, V
Vermaelen, K
Rottey, S
AF De Keukeleire, Stijn
Vermassen, Tijl
De Schoenmakere, Gert
Kruse, Vibeke
Vermaelen, Karim
Rottey, Sylvie
TI To treat or not to treat? Managing comorbidities in cancer patients
under immune checkpoint inhibition
SO ACTA CLINICA BELGICA
LA English
DT Review
DE Immune checkpoint inhibition; organ failure; elderly; autoimmune
disease; brain metastasis; organ transplant patients
ID METASTATIC UROTHELIAL CARCINOMA; ADVERSE EVENTS; PREEXISTING AUTOIMMUNE;
NIVOLUMAB NIVO; EFFICACY; ATEZOLIZUMAB; IPILIMUMAB; SAFETY;
COMPLICATIONS; MULTICENTER
AB Objectives: Assessing the safety and efficacy of immune checkpoint inhibition in risky cancer patient subgroups: pre-existing organ failure, elderly, presence of auto-immune disease, transplanted patients and brain metastasis treated with immune checkpoint inhibitors. Methods: PubMed, Web of Science and Google scholar databases were searched for English articles published prior to February 2019. Search terms used were organ failure, dialysis, elderly, organ transplant, liver disease, auto-immune disease, immunosuppression, and brain metastasis. Results: Our literature data indicate that immune checkpoint inhibition in the majority of these subpopulations can be administered safely without any loss of efficacy. These data are mostly based on case-reports as only a minority of high-risk patients were included in (the earliest) clinical trials. Validation of these results is necessary on a larger scale. Conclusion: Future trials should not automatically exclude aforementioned patient groups but alter the study design and make their inclusion possible, since more data are needed to answer several remaining questions in these populations. Especially since ICI appears to be safe to administer in these patients.
C1 [De Keukeleire, Stijn; Vermassen, Tijl; Kruse, Vibeke; Rottey, Sylvie] Ghent Univ Hosp, Dept Med Oncol, Ghent, Belgium.
[Vermassen, Tijl; Rottey, Sylvie] Ghent Univ Hosp, Drug Res Unit Ghent, Ghent, Belgium.
[De Schoenmakere, Gert] AZ Delta Hosp, Dept Nephrol, Roeselare, Belgium.
[Vermaelen, Karim] Ghent Univ Hosp, Dept Lung Diseases Thorac Oncol, Ghent, Belgium.
C3 Ghent University; Ghent University Hospital; Ghent University; Ghent
University Hospital; Ghent University; Ghent University Hospital
RP De Keukeleire, S (corresponding author), Ghent Univ Hosp, Dept Med Oncol, Ghent, Belgium.
EM Stijn.dekeukeleire@uzgent.be
RI Vermassen, Tijl/AHA-6274-2022
OI Vermassen, Tijl/0000-0002-1335-9966; Kruse, Vibeke/0000-0002-8840-3298;
De Keukeleire, Stijn/0000-0001-8380-0414
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[Anonymous], J CLIN ONCOL S
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NR 45
TC 2
Z9 2
U1 0
U2 11
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1784-3286
EI 2295-3337
J9 ACTA CLIN BELG
JI Acta Clin. Belg.
PD NOV 1
PY 2020
VL 75
IS 6
BP 434
EP 441
DI 10.1080/17843286.2019.1646516
EA JUL 2019
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OI6AA
UT WOS:000480135400001
PM 31357914
DA 2025-01-07
ER
PT J
AU Das, T
Khatun, S
Jha, T
Gayen, S
AF Das, Totan
Khatun, Samima
Jha, Tarun
Gayen, Shovanlal
TI HDAC9 as a Privileged Target: Reviewing its Role in Different Diseases
and Structure-activity Relationships (SARs) of its Inhibitors
SO MINI-REVIEWS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Epigenetic; cancer; HDAC9 inhibitor; selectivity; structure-activity
relationships; SARs
ID HISTONE DEACETYLASE 9; CLASS IIA HDACS; HEPATIC STELLATE CELLS;
IN-VITRO; BIOLOGICAL EVALUATION; ISCHEMIC-STROKE; GENE-REGULATION;
POOR-PROGNOSIS; BREAST-CANCER; PROMOTES
AB HDAC9 is a histone deacetylase enzyme belonging to the class IIa of HDACs which catalyses histone deacetylation. HDAC9 inhibit cell proliferation by repairing DNA, arresting the cell cycle, inducing apoptosis, and altering genetic expression. HDAC9 plays a significant part in human physiological system and are involved in various type of diseases like cancer, diabetes, atherosclerosis and CVD, autoimmune response, inflammatory disease, osteoporosis and liver fibrosis. This review discusses the role of HDAC9 in different diseases and structure-activity relationships (SARs) of various hydroxamate and non-hydroxamate-based inhibitors. SAR of compounds containing several scaffolds have been discussed in detail. Moreover, structural requirements regarding the various components of HDAC9 inhibitor (cap group, linker and zinc-binding group) has been highlighted in this review. Though, HDAC9 is a promising target for the treatment of a number of diseases including cancer, a very few research are available. Thus, this review may provide useful information for designing novel HDAC9 inhibitors to fight against different diseases in the future.
C1 [Das, Totan; Khatun, Samima; Gayen, Shovanlal] Jadavpur Univ, Dept Pharmaceut Technol, Lab Drug Design & Discovery, Kolkata 700032, India.
[Jha, Tarun] Jadavpur Univ, Dept Pharmaceut Technol, Div Med & Pharmaceut Chem, Nat Sci Lab, Kolkata 700032, India.
C3 Jadavpur University; Jadavpur University
RP Gayen, S (corresponding author), Jadavpur Univ, Dept Pharmaceut Technol, Lab Drug Design & Discovery, Kolkata 700032, India.; Jha, T (corresponding author), Jadavpur Univ, Dept Pharmaceut Technol, Div Med & Pharmaceut Chem, Nat Sci Lab, Kolkata 700032, India.
EM tjupharm@yahoo.com; shovanlal.gayen@gmail.com
RI gayen, shovanlal/B-7409-2013
OI Das, Totan/0009-0007-7509-1356; Gayen, Shovanlal/0000-0002-3367-578X;
KHATUN, SAMIMA/0000-0002-3322-9915
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Zhou XB, 2001, P NATL ACAD SCI USA, V98, P10572, DOI 10.1073/pnas.191375098
Zhou X, 2017, SCI REP-UK, V7, DOI 10.1038/srep41538
Zou YK, 2015, J BIOL CHEM, V290, P30607, DOI 10.1074/jbc.M115.681627
NR 129
TC 2
Z9 2
U1 4
U2 12
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-5575
EI 1875-5607
J9 MINI-REV MED CHEM
JI Mini-Rev. Med. Chem.
PY 2024
VL 24
IS 7
BP 767
EP 784
DI 10.2174/0113895575267301230919165827
PG 18
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA MB4K8
UT WOS:001191151700007
PM 37818566
DA 2025-01-07
ER
PT J
AU Gonzalez-Quintela, A
Mallo, N
Mella, C
Campos, J
Perez, LF
Lopez-Rodriguez, R
Tome, S
Otero, E
AF Gonzalez-Quintela, Arturo
Mallo, Nieves
Mella, Carmen
Campos, Joaquin
Perez, Luis-Fernando
Lopez-Rodriguez, Raimundo
Tome, Santiago
Otero, Esteban
TI Serum levels of cytokeratin-18 (tissue polypeptide-specific antigen) in
liver diseases
SO LIVER INTERNATIONAL
LA English
DT Article
DE alcohol; cytokeratin; cytokeratin-18; hepatitis virus; hepatitis; liver;
tissue polypeptide-specific antigen
ID HEPATOCELLULAR-CARCINOMA; TPS; HEPATITIS; KERATIN-18; ALCOHOLICS;
APOPTOSIS; EPITOPE; MARKER
AB Objective: The tissue polypeptide-specific antigen (TPS, cytokeratin-18, a normal constituent of the hepatocyte cytoskeleton) is a standard tumour marker. This study aimed to evaluate serum TPS levels in patients with liver disease. Methods: Serum TPS was measured with a commercial immunoassay in 884 individuals (753 outpatients from a liver disease clinic, 131 patients admitted to the hospital with acute liver disease). Results: Abnormally high (> 80 U/l) TPS levels were found in 57.7% (95% CI 54.0-61.3%) of outpatients with liver disease. Elevated TPS levels were observed for all liver diseases, including fatty liver, alcoholic disease, chronic viral hepatitis, autoimmune hepatitis, cholestasis, transplantation, and hepatocarcinoma. TPS levels correlated with liver markers, particularly serum AST. In addition, TPS levels correlated with Knodell's score in patients with chronic hepatitis. TPS was increased in one-third of patients with normal liver enzyme values. Serum TPS levels decreased after specific therapy in patients with hepatitis C and autoimmune hepatitis. Abnormally high TPS levels were found in the vast majority of patients admitted to the hospital, with markedly high (> 800 U/l) values being observed in 47.5% (95% CI 36.1-55.7%) of patients with alcoholic liver disease and in 80.8% (95% CI 60.0-92.7%) of patients with acute hepatitis. Conclusions: Serum TPS (cytokeratin-18) is elevated in patients with non-malignant liver diseases, particularly in those with prominent cytolysis. Further studies are needed to evaluate the use of TPS as a marker of liver disease.
C1 Hosp Clin Univ, Dept Internal Med, Santiago De Compostela 15706, Spain.
Complejo Hosp Univ Santiago, Dept Biochem, Santiago De Compostela 15706, Spain.
C3 Complexo Hospitalario Universitario de Santiago de Compostela; Complexo
Hospitalario Universitario de Santiago de Compostela
RP Gonzalez-Quintela, A (corresponding author), Hosp Clin Univ, Dept Internal Med, Santiago De Compostela 15706, Spain.
EM mearturo@usc.es
RI Campos, Joaquin/A-9206-2009; Lucey, Michael/AAR-4571-2020
OI Campos-Franco, Joaquin/0000-0003-1629-5424; Gonzalez-Quintela,
Arturo/0000-0002-6909-1807
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NR 24
TC 28
Z9 31
U1 0
U2 2
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 1478-3223
J9 LIVER INT
JI Liver Int.
PD DEC
PY 2006
VL 26
IS 10
BP 1217
EP 1224
DI 10.1111/j.1478-3231.2006.01380.x
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 103WI
UT WOS:000241917500008
PM 17105587
DA 2025-01-07
ER
PT J
AU Asghar, K
Ashiq, MT
Zulfiqar, B
Mahroo, A
Nasir, K
Murad, S
AF Asghar, Kashif
Ashiq, M. Taimour
Zulfiqar, Bilal
Mahroo, Amnah
Nasir, Kaenat
Murad, Sheeba
TI Indoleamine 2,3-dioxygenase expression and activity in patients with
hepatitis C virus-induced liver cirrhosis
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE indoleamine 2,3-dioxygenase; hepatitis C virus; liver cirrhosis
ID REGULATORY T-LYMPHOCYTES; DENDRITIC CELLS; HEPATOCELLULAR-CARCINOMA;
TRYPTOPHAN DEGRADATION; INFECTION; CD4(+); IDO; TOLERANCE; RESPONSES;
PROLIFERATION
AB Indoleamine 2,3-dioxygenase (IDO) is an immunoregulatory enzyme. It plays a key role in various malignancies, infection and autoimmune diseases. IDO induces immunosuppression through the depletion of tryptophan and its downstream metabolites. Hepatitis C virus (HCV) has infected more than 12 million individuals in Pakistan. The aim of the present study was to assess the expression and activity of IDO in HCV-infected patients. The functional enzymatic activity of IDO was measured by colorimetric assay. Serum samples from 100 HCV-infected patients were taken to examine IDO activity and samples from 100 healthy volunteers were used as controls. Liver sections from patients with HCV (n=35) and healthy controls (n=5) were used for immunohistochemical studies. Immunohistochemical analysis revealed that IDO was overexpressed in 28 of 35 (80%) cirrhotic liver Samples, whereas 5 of 35 (14.2%) cases presented moderate and 2 of 35 (5.7%) cases presented mild expression of IDO. The enzymatic activity of IDO was significantly higher in the serum samples of HCV-infected patients as compared with those in the control. These data indicate that the expression of IDO correlated with the pathogenesis of disease. In summary, it is suggested that the high expression of IDO in the progressively cirrhotic livers of HCV-infected patients might contribute to the development of hepatocellular carcinoma. IDO may characterize a novel therapeutic target against HCV.
C1 [Asghar, Kashif; Ashiq, M. Taimour; Zulfiqar, Bilal; Mahroo, Amnah; Nasir, Kaenat; Murad, Sheeba] Natl Univ Sci & Technol, Atta Ur Rahman Sch Appl Biosci ASAB, Mol Immunol Res Grp, Islamabad 44000, Pakistan.
C3 National University of Sciences & Technology - Pakistan
RP Asghar, K (corresponding author), Natl Univ Sci & Technol, Atta Ur Rahman Sch Appl Biosci ASAB, Mol Immunol Res Grp, Acad Block 1,Main NUST Campus,Sect H-12, Islamabad 44000, Pakistan.
EM drkashifasghar@gmail.com; sheebamall@yahoo.com
RI Mahroo, Amnah/GSM-7706-2022
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NR 36
TC 17
Z9 27
U1 0
U2 0
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD MAR
PY 2015
VL 9
IS 3
BP 901
EP 904
DI 10.3892/etm.2014.2146
PG 4
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA CD2OC
UT WOS:000350917900043
PM 25667650
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Patil, A
Shaikh, IM
Kadam, VJ
Jadhav, KR
AF Patil, Anuja
Shaikh, I. M.
Kadam, V. J.
Jadhav, K. R.
TI Nanotechnology in Therapeutics - Current Technologies and Applications
SO CURRENT NANOSCIENCE
LA English
DT Article
DE Nanomedicine; cancer therapy; dendrimers; neurodegenerative disorders;
osteoporosis
ID LOW-MOLECULAR-WEIGHT; BLOOD-BRAIN-BARRIER; DRUG-DELIVERY; GENE-DELIVERY;
TRANSFECTION EFFICIENCY; POLYMERIC MICELLES; DNA DELIVERY; POLY(ETHYLENE
GLYCOL); SURFACE MODIFICATION; TUMOR VASCULATURE
AB Nanotechnology is an area of science devoted to the design, construction and utilization of functional structures on the nanometer scale (often 100nm or smaller). Therapeutic applications of nanotechnologies include the treatment of cancer liver diseases. Avoiding the recognition by the liver is also possible by developing long circulating polymeric colloidal carriers ("stealth" systems) able to avoid the opsonisation process and the recognition by the macrophages. The design of such carriers is based on the physico-chemical concept of the "steric repulsion" by grafting polyethylene glycol chains at the surface of nanoparticles, the adsorption of steric proteins may be dramatically reduced due to steric hindrance. Such an approach allows maintaining the drug carrier for a longer time into the circulation and the resulting extravasation towards non reticuloendothelial-located cancers may become possible. Now, new applications and exciting perspectives are proposed for the delivery of drugs to previously non-accessible diseased sanctuaries, like the brain (treatment of glioma and autoimmune diseases of the brain) or the ocular tissues (treatment of the autoimmune uveitis). Ocular autoimmunity is especially intriguing because of the unique immunological characteristics of the eye. On the basis of laboratory data, the feeding of ocular antigens, has been proposed as a safe and efficacious therapy for uveitis. This review highlights how these obstacles can be overcome by polymer science and nanotechnology. New developments in polymer science coupled with cell-based delivery strategies support the notion that diseases that now have limited therapeutic options can show improved outcomes by advances in nanomedicine.
C1 [Patil, Anuja; Kadam, V. J.; Jadhav, K. R.] Bharati Vidyapeeths Coll Pharm, Dept Pharmaceut, CBD, Belapur 400614, Navi Mumbai, India.
[Shaikh, I. M.] Natl Univ Singapore, Dept Pharm, Singapore 117543, Singapore.
C3 National University of Singapore
RP Jadhav, KR (corresponding author), Bharati Vidyapeeths Coll Pharm, Dept Pharmaceut, CBD, Sector 8, Belapur 400614, Navi Mumbai, India.
EM krj24@rediffmail.com
RI KADAM, VILASRAO/AAS-6745-2021; Jadhav, Kisan/AAS-6733-2021
OI Jadhav, Kisan/0000-0001-7563-3935
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MAT USED NANOTECHNOL
NR 71
TC 7
Z9 7
U1 0
U2 20
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1573-4137
EI 1875-6786
J9 CURR NANOSCI
JI Curr. Nanosci.
PD MAY
PY 2009
VL 5
IS 2
BP 141
EP 153
DI 10.2174/157341309788185532
PG 13
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology;
Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
Topics; Materials Science
GA 440JU
UT WOS:000265697400003
DA 2025-01-07
ER
PT J
AU Ardesjö, B
Hansson, CM
Bruder, CEG
Rorsman, F
Betterle, C
Dumanski, JP
Kämpe, O
Ekwall, O
AF Ardesjo, Brita
Hansson, Caisa M.
Bruder, Carl E. G.
Rorsman, Fredrik
Betterle, Corrado
Dumanski, Jan P.
Kampe, Olle
Ekwall, Olov
TI Autoantibodies to glutathione S-transferase theta 1 in patients with
primary sclerosing cholangitis and other autoimmune diseases
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE autoantibodies; copy number variation; glutathione S-transferase theta
1; PCR product based array-CGH; primary sclerosing cholangitis
ID PRIMARY BILIARY-CIRRHOSIS; S-TRANSFERASE T1; CANCER-RISK; GLUTATHIONE;
GSTT1; POLYMORPHISMS; MICROARRAY; HEPATITIS; GENOTYPES; LIVER
AB Primary sclerosing cholangitis (PSC) is an enigmatic disorder with a suggested autoimmune basis. A variety of autoantigens have been suggested but no specific or highly directed epitope has been identified. To address this issue, we constructed a cDNA library from normal human choledochus and screened expressing clones with serum from a patient with PSC and inflammatory bowel disease (IBD). Based on this screening, glutathione S-transferase theta 1 (GSTT1) was identified as a potential autoantigenic target. To study the specificity of GSTT1, we determined immunoreactivity using a panel of 58 patients with PSC, with and without IBD, 57 patients with IBD, 31 patients with Hashimoto's thyroiditis, 30 patients with primary biliary cirrhosis (PBC), 20 patients with insulin dependent diabetes mellitus, 22 patients with autoimmune polyendocrine syndrome type 1, 10 patients with systemic lupus erythematosus (SLE), 20 patients with Sjogren's syndrome, 12 patients with autoimmune pancreatitis, 28 patients with Addison's disease, 27 patients with Grave's disease, 17 with myasthenia gravis, and 118 healthy controls. Reactivity against GSTT1 was found with PSC and IBD as well as some patients with other autoimmune pathology, indicating that this population of antibodies is neither specific nor a sensitive serologic marker for PSC, but the frequency was clearly higher in autoimmune patients than controls. GSTT1-antibodies have been described in persons with GSTT1-null genotype and are suggested to develop as an alloimmune response to blood transfusions from GSTT1-positive donors or pregnancies with GSTT1-positive children. Therefore, two IBD patients with and 15 PSC patients without GSTT1-antibodies were genotyped for GSTT1 to investigate if the presence of GSTT1-antibodies was associated with the GSTT1-null genotype and possibly caused by an alloimmune response. Both IBD patients and three of the PSC patients were of the GSTT1-null genotype. We note that the frequency of GSTT1-antibodies in this study is more than 100-fold higher than the frequency described earlier in patients with autoimmune diseases. We also observe an increased frequency of GSTT1-antibodies in patients with autoimmune diseases compared to healthy controls. This increased frequency can be explained by an autoimmune phenotype which increases susceptibility to such autoantibodies, or by a high frequency of the GSTT1-null genotype in autoimmune disease. (C) 2007 Elsevier Ltd. All rights reserved.
C1 [Ardesjo, Brita; Rorsman, Fredrik; Kampe, Olle; Ekwall, Olov] Uppsala Univ, Univ Uppsala Hosp, Dept Med Sci, Res Dept 2,Lab 21, SE-75185 Uppsala, Sweden.
[Hansson, Caisa M.; Dumanski, Jan P.] Uppsala Univ, Dept Genet & Pathol, Rudbeck Lab, S-75185 Uppsala, Sweden.
[Bruder, Carl E. G.; Dumanski, Jan P.] Univ Alabama, Dept Genet, Birmingham, AL 35294 USA.
[Betterle, Corrado] Univ Padua, Sch Med, Dept Med & Surg Sci, I-35128 Padua, Italy.
[Ekwall, Olov] Univ Gothenburg, Sahlgrenska Inst, Dept Paediat, Gothenburg, Sweden.
C3 Uppsala University; Uppsala University Hospital; Uppsala University;
University of Alabama System; University of Alabama Birmingham;
University of Padua; University of Gothenburg
RP Ardesjö, B (corresponding author), Uppsala Univ, Univ Uppsala Hosp, Dept Med Sci, Res Dept 2,Lab 21, Entrance 70,3rd Floor, SE-75185 Uppsala, Sweden.
EM brita.ardesjo@medsci.uu.se
OI Dumanski, Jan Piotr/0000-0002-1489-1452; Ekwall,
Olov/0000-0002-4506-9955; Kampe, Olle/0000-0001-6091-9914
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NR 42
TC 14
Z9 14
U1 0
U2 3
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
J9 J AUTOIMMUN
JI J. Autoimmun.
PD JUN
PY 2008
VL 30
IS 4
BP 273
EP 282
DI 10.1016/j.jaut.2007.11.008
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 300OO
UT WOS:000255834500010
PM 18242955
DA 2025-01-07
ER
PT J
AU Budigi, B
Oliphant, M
Itri, J
AF Budigi, Bhavana
Oliphant, Michael
Itri, Jason
TI , Ph no: 336-716-1066
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Pancreatic ductal adenocarcinoma; Diagnostic errors; Staging
ID PANCREATIC DUCTAL ADENOCARCINOMA; AUTOIMMUNE PANCREATITIS; CANCER; CT;
RESECTABILITY; INVASION; LIVER
AB The purpose of this article is to review diagnostic errors in preoperative and post-operative imaging for pancreatic ductal adenocarcinoma (PDAC), discuss contributing factors, and provide solutions that minimize errors. Accurate radiological staging and restaging of PDAC dictates surgical management and errors can have significant negative effects on patient care, such as missed vessel involvement or metastatic disease that would preclude surgery. Familiarity with these errors and their contributing factors improves diagnostic accuracy and ultimately leads to improved patient outcomes.
C1 [Budigi, Bhavana; Oliphant, Michael; Itri, Jason] Wake For est Baptist Med Ctr, Dept Radiol, Div Abdominal Imaging, 1 Med Ctr Blvd, Winston Salem, NC 27157 USA.
[Budigi, Bhavana] Wake Forest Baptist Med Ctr, Dept Radiol, Div Neuro Radiol, 1 Med Ctr Blvd, Winston Salem, NC 27157 USA.
C3 Wake Forest University; Wake Forest Baptist Medical Center
RP Budigi, B (corresponding author), Wake Forest Baptist Med Ctr, Dept Radiol, Div Neuro Radiol, 1 Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM bbudigi@wakehealth.edu
OI budigi, bhavana/0000-0002-6200-335X
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NR 46
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1076-6332
EI 1878-4046
J9 ACAD RADIOL
JI Acad. Radiol.
PD JUL
PY 2022
VL 29
IS 7
BP 967
EP 976
DI 10.1016/j.acra.2021.10.025
EA MAY 2022
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 1Z1RG
UT WOS:000808609500003
PM 34838452
DA 2025-01-07
ER
PT J
AU Nakazawa, T
Ando, T
Hayashi, K
Naitoh, I
Ohara, H
Joh, T
AF Nakazawa, Takahiro
Ando, Tomoaki
Hayashi, Kazuki
Naitoh, Itaru
Ohara, Hirotaka
Joh, Takashi
TI Diagnostic procedures for IgG4-related sclerosing cholangitis
SO JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
LA English
DT Review
DE IgG4-related sclerosing cholangitis (IgG4-SC); Primary sclerosing
cholangitis (PSC)
ID AUTOIMMUNE PANCREATITIS; EXTRAPANCREATIC LESIONS; PLASMA-CELLS; LIVER;
PSEUDOTUMOR; PATHOLOGY; SPECTRUM; CRITERIA; THERAPY; DISEASE
AB IgG4-related sclerosing cholangitis (IgG4-SC) is one of several diseases associated with autoimmune pancreatitis (AIP). However, diffuse cholangraphic abnormalities seen in association with AIP may resemble those seen in primary sclerosing cholangitis (PSC), and the presence of segmental stenosis suggests cholangiocarcinoma. IgG4-SC responds well to steroid therapy, whereas in contrast, liver transplantation is the only effective therapy for PSC, and surgical intervention is also needed for cholangiocarcinoma. The aim of this review was to establish the diagnostic procedures for IgG4-SC.
A literature search was conducted, covering English-language articles dealing with IgG4-SC published between 1991 and March 2010. As clinical data on IgG4-SC are limited, the author also took into consideration his own clinical experience with the treatment of IgG4-SC over a period of more than 19 years.
When intrapancreatic stenosis is detected, pancreatic cancer should be ruled out. If multiple intrahepatic stenosis is evident, PSC should be discriminated on the basis of cholangiographic findings and liver biopsy with IgG4 immunostaining. An association with inflammatory bowel disease (IBD) is suggestive of PSC. If stenosis is demonstrated in the hepatic hilar region, cholangiocarcinoma should be discriminated by US, EUS, IDUS, and bile duct biopsy.
For diagnosis of IgG4-SC, coexistence of AIP is the most useful finding. However, the most important consideration for clinicians is to be aware of IgG4-SC when encountering patients with obstructive jaundice.
C1 [Nakazawa, Takahiro; Ando, Tomoaki; Hayashi, Kazuki; Naitoh, Itaru; Joh, Takashi] Nagoya City Univ, Dept Gastroenterol & Metab, Grad Sch Med Sci, Mizuho Ku, Nagoya, Aichi 4678601, Japan.
[Ohara, Hirotaka] Nagoya City Univ, Dept Community Based Med Educ, Grad Sch Med Sci, Nagoya, Aichi 4678601, Japan.
C3 Nagoya City University; Nagoya City University
RP Nakazawa, T (corresponding author), Nagoya City Univ, Dept Gastroenterol & Metab, Grad Sch Med Sci, Mizuho Ku, 1 Kawasumi,Mizuho Cho, Nagoya, Aichi 4678601, Japan.
EM tnakazaw@med.nagoya-cu.ac.jp
RI Naitoh, Itaru/AAB-7252-2020
OI Naitoh, Itaru/0000-0001-8342-886X
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NR 50
TC 23
Z9 28
U1 0
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1868-6974
EI 1868-6982
J9 J HEPATO-BIL-PAN SCI
JI J. Hepato-Biliary-Pancreat. Sci.
PD MAR
PY 2011
VL 18
IS 2
BP 127
EP 136
DI 10.1007/s00534-010-0320-2
PG 10
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 737HQ
UT WOS:000288560200001
PM 20814701
DA 2025-01-07
ER
PT J
AU Ilyas, SZ
Tabassum, R
Hamed, H
Rehman, SU
Qadri, I
AF Ilyas, Syeda Zainab
Tabassum, Rabia
Hamed, Haroon
Rehman, Shafiq Ur
Qadri, Ishtiaq
TI Hepatitis C Virus-Associated Extrahepatic Manifestations in Lung and
Heart and Antiviral Therapy-Related Cardiopulmonary Toxicity
SO VIRAL IMMUNOLOGY
LA English
DT Review
DE chronic hepatitis C virus; extrahepatic manifestations; cardiac and
pulmonary manifestations; pathogenesis; mixed cryoglobulinemia;
antiviral treatment
ID PERIPHERAL ARTERIAL-DISEASE; NECROSIS-FACTOR-ALPHA; INTERFERON THERAPY;
MIXED CRYOGLOBULINEMIA; DILATED CARDIOMYOPATHY; BRONCHOALVEOLAR LAVAGE;
PULMONARY FIBROSIS; HCV INFECTION; CORE PROTEIN; LIVER
AB Besides liver cirrhosis and hepatocellular carcinoma, chronic hepatitis C virus (HCV) infection is associated with many extrahepatic manifestations (EHMs). HCV exhibits lymphotropism that is responsible for various EHM. An important characteristic of HCV is escape from the immune system, which enables it to produce chronic infections and autoimmune disorders along with accumulation of circulating immune complexes. These EHMs have large spectrum, because they affect many organs such as heart, lungs, kidney, brain, thyroid, and skin. HCV-related cardiac and pulmonary manifestations include myocarditis, cardiomyopathies, cardiovascular diseases (i.e., Stroke, ischemic heart disease), chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, asthma, and interstitial lung diseases. This review discusses etiology and pathogenesis of HCV-associated cardiac and pulmonary manifestations and how different genes, immune system, indirectly linked factors (mixed cryo-globulinemia), liver cirrhosis, and antiviral treatment are involved in HCV-related heart and lung diseases, however, their exact mechanism is not clear.
C1 [Ilyas, Syeda Zainab; Tabassum, Rabia; Rehman, Shafiq Ur] Univ Punjab, Dept Microbiol & Mol Genet, Lahore, Pakistan.
[Hamed, Haroon; Qadri, Ishtiaq] King Abdulaziz Univ, Dept Biol Sci, Jeddah 110809, Saudi Arabia.
C3 University of Punjab; King Abdulaziz University
RP Qadri, I (corresponding author), King Abdulaziz Univ, Dept Biol Sci, Jeddah 110809, Saudi Arabia.
EM ishtiaq80262@yahoo.com
RI Rehman, shafiq/AAE-9102-2019; Qadri, Ishtiaq/I-6889-2013
OI Rehman, Shafiq ur/0000-0002-1265-3442; Qadri,
Ishtiaq/0000-0003-4334-0585
FU KACST large grant [162-34]
FX IQ received funding from KACST large grant #162-34.
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NR 94
TC 18
Z9 18
U1 0
U2 7
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0882-8245
EI 1557-8976
J9 VIRAL IMMUNOL
JI Viral Immunol.
PD NOV
PY 2017
VL 30
IS 9
BP 633
EP 641
DI 10.1089/vim.2017.0009
PG 9
WC Immunology; Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Virology
GA FL6ZE
UT WOS:000414394200003
PM 28953449
DA 2025-01-07
ER
PT J
AU Philips, CA
Schnabl, B
Bajaj, JS
AF Philips, Cyriac A.
Schnabl, Bernd
Bajaj, Jasmohan S.
TI Gut Microbiome and Alcohol-associated Liver Disease
SO JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
LA English
DT Review
DE ALD; ACLF; microbiome; FMT; cirrhosis
ID INTESTINAL DYSBIOSIS; TRANSPLANTATION; HEPATITIS; INJURY;
SUSCEPTIBILITY; CIRRHOSIS; ACIDS
AB Changes in gut microbiota (GM) maybe associated with the causation and progression of multiple liver diseases such as metabolic-associated liver disease, alcohol-associated liver disease (ALD), alcohol-associated hepatitis (AH), primary biliary cholangitis, primary sclerosing cholangitis, autoimmune liver disease, and most impor-tantly, complications of cirrhosis and portal hypertension such as hepatic encephalopathy (HE), infection, and hepatocellular carcinoma. ALD includes simple steatosis, steatohepatitis, AH, cirrhosis, and acute-on -chronic liver failure. Alcohol consumption is associated with GM changes even before ALD development, and continued alcohol intake results in progressive dysbiosis and development of clinical events such as AH, infec-tion, and HE. The composition and function of GM, specific changes in bacterial communities, and the func-tional metabolism of GM are affected in the spectrum of ALD, as revealed using high-throughput sequencing. It was reported in preliminary studies that modulation of disrupted GM improves adverse clinical events and ameliorates disease progression in ALD. In this review, we exhaustively discuss the preclinical and clinical studies on GM in ALD and critically discuss GM modulation and its effects based on various human and animal models of ALD. ( J CLIN EXP HEPATOL 2022;12:1349-1359)
C1 [Philips, Cyriac A.] Rajagiri Hosp, Liver Inst, Ctr Excellence Gastrointestinal Sci, Dept Clin & Translat Hepatol, Aluva, Kerala, India.
[Philips, Cyriac A.] Rajagiri Hosp, Liver Inst, Ctr Excellence Gastrointestinal Sci, Monarch Liver Lab, Aluva, Kerala, India.
[Schnabl, Bernd] Univ Calif San Diego, Dept Med, La Jolla, CA USA.
[Bajaj, Jasmohan S.] Virginia Commonwealth Univ, Dept Internal Med, Div Gastroenterol Hepatol & Nutr, Richmond, VA USA.
[Bajaj, Jasmohan S.] Cent Virginia Vet Healthcare Syst, Richmond, VA USA.
[Philips, Cyriac A.] Rajagiri Hosp, Liver Inst, Ctr Excellence GI Sci, Ground Floor,Phase 2, Ernakulam 683112, Kerala, India.
C3 University of California System; University of California San Diego;
Virginia Commonwealth University
RP Philips, CA (corresponding author), Rajagiri Hosp, Liver Inst, Ctr Excellence GI Sci, Ground Floor,Phase 2, Ernakulam 683112, Kerala, India.
EM abbyphilips@theliverinst.in
RI Schnabl, Bernd/HCH-3471-2022
OI Philips, Cyriac Abby/0000-0002-9587-336X
FU NIH funded San Diego Digestive Diseases Research Center (SDDRC) [P30
DK120515]; VA Merit Review [2IOCX001076]; NIH [R21TR003095]
FX B.S. is supported by NIH funded San Diego Digestive Dis-eases Research
Center (SDDRC) P30 DK120515. JSB is supported by VA Merit Review
2IOCX001076 and NIH R21TR003095.
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NR 56
TC 16
Z9 16
U1 2
U2 11
PU ELSEVIER - DIVISION REED ELSEVIER INDIA PVT LTD
PI NEW DELHI
PA 17-A/1 MAIN RING ROAD, LAJPAT NAGAR IV, NEW DELHI, 110024, INDIA
SN 0973-6883
EI 2213-3453
J9 J CLIN EXP HEPATOL
JI J. Clin. Exp. Hepatol.
PD SEP-OCT
PY 2022
VL 12
IS 5
BP 1349
EP 1359
DI 10.1016/j.jceh.2021.12.016
EA SEP 2022
PG 11
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA 8Z6EO
UT WOS:000933469400011
PM 36157139
OA Green Published
DA 2025-01-07
ER
PT J
AU Chen, N
Zhou, JQ
Wang, K
Li, XY
Li, ZB
AF Chen, Ning
Zhou, Jingqi
Wang, Kai
Li, Xiaoying
Li, Zhibin
TI Non-obese or lean non-alcoholic fatty liver disease was associated with
increased risk of cancer in patients with type 2 diabetes mellitus
SO BMJ OPEN DIABETES RESEARCH & CARE
LA English
DT Article
DE cancer; obesity; diabetes mellitus; type 2; non-alcoholic fatty liver
disease
ID PREVALENCE; OBESITY; ADULTS; INDEX
AB IntroductionRisk of non-obese or lean non-alcoholic fatty liver disease (NAFLD) for cancer in patients with type 2 diabetes mellitus (T2DM) is less known. We aimed to evaluate independent associations of NAFLD, especially non-obese or lean NAFLD, and body mass index (BMI) on risks of cancer in patients with T2DM.Research design and methodsCross-sectional analyses of baseline information on a cohort of 233 patients with T2DM were conducted in Xiamen, China. NAFLD was identified by hepatic ultrasonography diagnosis of hepatic steatosis without excessive alcohol consumption, viral or autoimmune liver disease. Fibrosis-4 (FIB-4) score was calculated to quantify severity of hepatic fibrosis.ResultsAll types of cancers were diagnosed on 19 (8.2%) patients. Prevalence of cancer was significantly higher in those with NAFLD than those without (15.5% vs 4.0%, p=0.002), but were not significantly different among BMI categories (6.8%, 13.7% and 6.5% for those with underweight or normal weight (n=74), overweight (n=51) and obesity (n=108), respectively, p=0.258). With adjustment for potential confounding factors in the multivariable logistic regression models, NAFLD was significantly associated with increased risk of cancer with the adjusted OR (95% CI) of 5.969 (1.349 to 26.413, p=0.019). Stratified analyses across BMI categories found similar association of NAFLD with risk of cancer for those non-obese or lean (the adjusted OR (95% CI) 17.446 (1.690 to 180.095, p=0.016)) but not for those with either overweight (OR (95% CI) 11.642 (0.832 to 162.963, p=0.068) or obesity (OR (95% CI) 0.917 (0.170 to 4.954, p=0.920). FIB-4 score was not significantly associated with risk of cancer for all subjects or stratified across BMI categories. BMI was not significantly associated with risk of cancer for all patients or stratified by NAFLD.ConclusionsNAFLD, even non-obese or lean NAFLD, was independently associated with increased risk of cancer in patients with T2DM. Screening and management of NAFLD, especially for those with underweight or normal weight, should be strengthened from the perspective of improving prevention and management of cancer in patients with T2DM.
C1 [Chen, Ning; Zhou, Jingqi; Wang, Kai] Fudan Univ, Zhongshan Hosp, Dept Endocrinol, Xiamen Branch, Xiamen, Fujian, Peoples R China.
[Li, Xiaoying] Fudan Univ, Dept Endocrinol, Xiamen Branch, Xiamen, Fujian, Peoples R China.
[Li, Xiaoying] Fudan Univ Shanghai, Dept Endocrinol, Shanghai, Peoples R China.
[Li, Zhibin] Xiamen Univ, Affiliated Hosp 1, Translat Med Res Ctr, Epidemiol Res Unit, Xiamen, Fujian, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Xiamen University
RP Li, XY (corresponding author), Fudan Univ, Dept Endocrinol, Xiamen Branch, Xiamen, Fujian, Peoples R China.; Li, XY (corresponding author), Fudan Univ Shanghai, Dept Endocrinol, Shanghai, Peoples R China.; Li, ZB (corresponding author), Xiamen Univ, Affiliated Hosp 1, Translat Med Res Ctr, Epidemiol Res Unit, Xiamen, Fujian, Peoples R China.
EM li.xiaoying@zs-hospital.sh.cn; zhibinli33@hotmail.com
RI wang, kaijing/ABG-9934-2021; Li, Xianzhi/IUO-5698-2023; Li,
xiaolong/GRS-9148-2022
OI Li, Zhibin/0000-0001-6642-9780
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NR 36
TC 7
Z9 8
U1 1
U2 5
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 2052-4897
J9 BMJ OPEN DIAB RES CA
JI BMJ Open Diab. Res. Care
PD FEB
PY 2023
VL 11
IS 1
AR e003066
DI 10.1136/bmjdrc-2022-003066
PG 9
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 9I3FG
UT WOS:000939400300001
PM 36792168
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Federico, S
Pozzetti, L
Papa, A
Carullo, G
Gemma, S
Butini, S
Campiani, G
Relitti, N
AF Federico, Stefano
Pozzetti, Luca
Papa, Alessandro
Carullo, Gabriele
Gemma, Sandra
Butini, Stefania
Campiani, Giuseppe
Relitti, Nicola
TI Modulation of the Innate Immune Response by Targeting Toll-like
Receptors: A Perspective on Their Agonists and Antagonists
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID NF-KAPPA-B; HEPATOCELLULAR-CARCINOMA CELLS; PATTERN-RECOGNITION
RECEPTORS; SIGNALING PATHWAY; TLR3 AGONIST; CPG ODN; INFLAMMATORY
RESPONSE; RETINAL DEGENERATION; VACCINE ADJUVANTS; PROTECTS MICE
AB Toll-like receptors (TLRs) are a class of proteins that recognize pathogen-associated molecular patterns (PAMPs) and damaged-associated molecular patterns (DAMPs), and they are involved in the regulation of innate immune system. These transmembrane receptors, localized at the cellular or endosomal membrane, trigger inflammatory processes through either myeloid differentiation primary response 88 (MyD88) or TIR-domain-containing adapter-inducing interferon-beta (TRIF) signaling pathways. In the last decades, extensive research has been performed on TLR modulators and their therapeutic implication under several pathological conditions, spanning from infections to cancer, from metabolic disorders to neurodegeneration and autoimmune diseases. This Perspective will highlight the recent discoveries in this field, emphasizing the role of TLRs in different diseases and the therapeutic effect of their natural and synthetic modulators, and it will discuss insights for the future exploitation of TLR modulators in human health.
C1 [Federico, Stefano; Pozzetti, Luca; Papa, Alessandro; Carullo, Gabriele; Gemma, Sandra; Butini, Stefania; Campiani, Giuseppe; Relitti, Nicola] Univ Siena, Dept Biotechnol Chem & Pharm, Dept Excellence 2018 2022, I-53100 Siena, Italy.
C3 University of Siena
RP Butini, S; Campiani, G (corresponding author), Univ Siena, Dept Biotechnol Chem & Pharm, Dept Excellence 2018 2022, I-53100 Siena, Italy.
EM butini3@unisi.it; campiani@unisi.it
RI Pozzetti, Luca/KHT-2236-2024; Butini, Stefania/D-9954-2015; Gemma,
Sandra/D-3568-2009
OI Federico, Stefano/0000-0002-7478-6128; Carullo,
Gabriele/0000-0002-1619-3295; Butini, Stefania/0000-0002-8471-0880;
PAPA, ALESSANDRO/0000-0001-8141-3648; Gemma, Sandra/0000-0002-8313-2417;
Pozzetti, Luca/0000-0002-0035-4621; Relitti, Nicola/0000-0001-9783-8966;
Campiani, Giuseppe/0000-0001-5295-9529
FU MIUR Grant Dipartimento di Eccellenza [2018-2022(l. 232/2016), POR-FSE
2014, POR-FSE 2015, POR-FSE 2016, POR-FSE 2017, POR-FSE 2018, POR-FSE
2019, POR-FSE 2020]; Ministero dell'Istruzione, dell'Universita e della
Ricerca (MIUR) PRIN Project [20154JRJPP]
FX We acknowledge MIUR Grant Dipartimento di Eccellenza (No. 2018-2022(l.
232/2016)) to the Department of Biotechnology, Chemistry and Pharmacy,
University of Siena and the Tuscany strategic project (No. POR-FSE 2014
to 2020), "Medicina di Precisione e Malattie Rare" (MePreMaRe),
(ACE-ESCC). This work was supported by Ministero dell'Istruzione,
dell'Universita e della Ricerca (MIUR) PRIN Project No. 20154JRJPP.
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NR 320
TC 79
Z9 86
U1 2
U2 60
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 25
PY 2020
VL 63
IS 22
BP 13466
EP 13513
DI 10.1021/acs.jmedchem.0c01049
PG 48
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA PA3NV
UT WOS:000595545900015
PM 32845153
DA 2025-01-07
ER
PT J
AU Flerova, E
Ambilil, M
Civan, JM
Sass, DA
Maley, WR
Pulinthanathu, R
Huang, JL
AF Flerova, Elizaveta
Ambilil, Manju
Civan, Jesse M.
Sass, David A.
Maley, Warren R.
Pulinthanathu, Rajiv
Huang, Jialing
TI Striking Cholestatic Giant Cell Hepatitis Resulting in Fulminant Liver
Failure After Garcinia Cambogia Use
SO INTERNATIONAL JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE drug-induced liver injury (DILI); garcinia cambogia; giant cell
hepatitis; liver transplantation; liver failure
ID DIETARY-SUPPLEMENTS; INJURY; CYTOMEGALOVIRUS; EXPERIENCE; PATIENT
AB Garcinia cambogia, a weight control herbal, can cause mild liver toxicity with nonspecific histologic changes. Herein, we reported a case of herbal-induced fulminant cholestatic giant cell hepatitis due to garcinia cambogia use. A 65-year-old woman with breast cancer treated 18 years earlier was admitted for obstructive jaundice for 2 weeks. She started using garcinia cambogia 3 months ago for weight loss. Physical exam showed scleral icterus. Serum studies excluded Wilson's disease, systemic infection including COVID-19 (coronavirus disease 2019), autoimmune hepatitis, and metabolic or toxicologic causes. An urgent liver biopsy showed severe giant cell hepatitis in absence of HSV-1/2, cytomegalovirus, HBsAg and HBcAg (immunostain), and EBV (in situ hybridization). Despite supportive therapy, the patient developed grade 2-3 hepatic encephalopathy and necessitated liver transplant. The explanted liver was markedly atrophy, in which the most striking histologic finding was diffuse distribution of multinucleated giant hepatocytes with syncytial pattern in a background of extensive zone-1 accentuated, geographic, hemorrhagic, confluent hepatocytic necrosis, along with remarkable hepatocytic and canalicular cholestasis. Marked hepatocellular and sinusoidal iron orverload present. The patient recovered uneventfully.
C1 [Flerova, Elizaveta; Ambilil, Manju] Thomas Jefferson Univ Hosp, Dept Pathol, Philadelphia, PA USA.
[Civan, Jesse M.; Sass, David A.] Thomas Jefferson Univ Hosp, Div Gastroenterol & Hepatol, Philadelphia, PA USA.
[Maley, Warren R.] Thomas Jefferson Univ Hosp, Div Transplant Surg, Philadelphia, PA USA.
[Pulinthanathu, Rajiv] Cooperman St Barnabas Med Ctr, Dept Pathol, Livingston, NJ USA.
[Huang, Jialing] Geisinger Med Ctr, Dept Pathol, Danville, PA USA.
[Huang, Jialing] Geisinger Med Ctr, Dept Pathol, 100N Acad Ave, Danville, PA 17822 USA.
C3 Jefferson University; Jefferson University; Jefferson University;
Geisinger Medical Center; Geisinger Medical Center
RP Huang, JL (corresponding author), Geisinger Med Ctr, Dept Pathol, 100N Acad Ave, Danville, PA 17822 USA.
EM jhuang1@geisinger.edu
OI Huang, Jialing/0000-0003-4406-7293
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NR 39
TC 2
Z9 2
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1066-8969
EI 1940-2465
J9 INT J SURG PATHOL
JI Int. J. Surg. Pathol.
PD MAY
PY 2024
VL 32
IS 3
BP 619
EP 624
DI 10.1177/10668969231186926
EA JUL 2023
PG 6
WC Pathology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA NZ5I3
UT WOS:001030718700001
PM 37461217
DA 2025-01-07
ER
PT J
AU Baggio, G
Corsini, A
Floreani, A
Giannini, S
Zagonel, V
AF Baggio, Giovannella
Corsini, Alberto
Floreani, Annarosa
Giannini, Sandro
Zagonel, Vittorina
TI Gender medicine: a task for the third millennium
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Review
DE cancer; cardiovascular diseases; liver diseases; osteoporosis;
pharmacology
ID CORONARY-ARTERY-DISEASE; CARDIOVASCULAR-DISEASE; CANCER SUSCEPTIBILITY;
INTERVENTION TRIAL; PRIMARY PREVENTION; COLORECTAL-CANCER;
FEMALE-PATIENTS; SEX-DIFFERENCES; LUNG-CANCER; FATTY LIVER
AB Gender-specific medicine is the study of how diseases differ between men and women in terms of prevention, clinical signs, therapeutic approach, prognosis, psychological and social impact. It is a neglected dimension of medicine. In this review we like to point out some major issues in five enormous fields of medicine: cardiovascular diseases (CVDs), pharmacology, oncology, liver diseases and osteoporosis.
CVDs have been studied in the last decades mainly in men, but they are the first cause of mortality and disability in women. Risk factors for CVD have different impacts in men and women; clinical manifestations of CVD and the influence of drugs on CVD have lot of gender differences. Sex-related differences in pharmacokinetics and pharmacodynamics are also emerging. These differences have obvious relevance to the efficacy and side effect profiles of various medications in the two sexes. This evidence should be considered for drug development as well as before starting any therapy. Gender disparity in cancer incidence, aggressiveness and prognosis has been observed for a variety of cancers and, even if partially known, is underestimated in clinical practice for the treatment of the major types of cancer. It is necessary to systematize and encode all the known data for each type of tumor on gender differences, to identify where this variable has to be considered for the purposes of the prognosis, the choice of treatment and possible toxicity. Clinical data suggest that men and women exhibit differences regarding the epidemiology and the progression of certain liver diseases, i.e., autoimmune conditions, genetic hemochromatosis, non-alcoholic steatohepatitis and chronic hepatitis C. Numerous hypotheses have been formulated to justify this sex imbalance including sex hormones, reproductive and genetic factors. Nevertheless, none of these hypothesis has thus far gathered enough convincing evidence and in most cases the evidence is conflicting. Osteoporosis is an important public health problem both in women and men. On the whole, far more epidemiologic, diagnostic and therapeutic studies have been carried out in women than in men. In clinical practice, if this disease remains underestimated in women, patients' and physicians' awareness is even lower for male osteoporosis, for which diagnostic and therapeutic strategies are at present less defined.
In conclusion this review emphasizes the urgency of basic science and clinical research to increase our understanding of the gender differences of diseases.
C1 [Baggio, Giovannella] Azienda Osped Padova, Internal Med Unit, I-35125 Padua, Italy.
[Baggio, Giovannella; Corsini, Alberto; Floreani, Annarosa; Giannini, Sandro; Zagonel, Vittorina] Natl Ctr Gender Hlth & Med, Milan, Italy.
[Corsini, Alberto] Univ Milan, Dept Pharmacol & Biomol Sci, Milan, Italy.
[Floreani, Annarosa] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
[Giannini, Sandro] Univ Padua, Dept Med, Padua, Italy.
[Zagonel, Vittorina] IRCCS, Med Oncol Unit 1, Ist Oncol Veneto, Padua, Italy.
C3 University of Padua; Azienda Ospedaliera - Universita di Padova;
University of Milan; University of Padua; University of Padua; IRCCS
Istituto Oncologico Veneto (IOV)
RP Baggio, G (corresponding author), Azienda Osped Padova, Internal Med Unit, Via Giustiniani 2, I-35125 Padua, Italy.
EM giovannella.baggio@sanita.padova.it
RI Corsini, Alessandro/JAC-6765-2023; zagonel, vittorina/F-4226-2014
OI GIANNINI, SANDRO/0000-0003-0796-9749; zagonel,
vittorina/0000-0002-0829-2525
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NR 98
TC 158
Z9 168
U1 0
U2 36
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
EI 1437-4331
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD APR
PY 2013
VL 51
IS 4
BP 713
EP 727
DI 10.1515/cclm-2012-0849
PG 15
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA 111VC
UT WOS:000316548000014
PM 23515103
OA Bronze
DA 2025-01-07
ER
PT J
AU Nagpal, S
Na, SQ
Rathnachalam, R
AF Nagpal, S
Na, SQ
Rathnachalam, R
TI Noncalcemic actions of vitamin D receptor ligands
SO ENDOCRINE REVIEWS
LA English
DT Review
ID RETINOID-X-RECEPTOR; PROSTATE-CANCER CELLS; D RESPONSE ELEMENT;
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; 1,25-DIHYDROXYVITAMIN D-3
RECEPTOR; T-LYMPHOCYTE PROLIFERATION; KERATINOCYTE GROWTH-FACTOR;
COLLAGEN-INDUCED ARTHRITIS; THYROID-HORMONE RECEPTORS;
COLONY-STIMULATING FACTOR
AB 1 alpha,25-Dihydroxyvitamin D-3 [1,25-(OH)(2)D-3], the active metabolite of vitamin D-3, is known for the maintenance of mineral homeostasis and normal skeletal architecture. However, apart from these traditional calcium-related actions, 1,25-(OH)(2)D-3 and its synthetic analogs are being increasingly recognized for their potent antiproliferative, prodifferentiative, and immunomodulatory activities. These actions of 1,25-(OH)(2)D-3 are mediated through vitamin D receptor (VDR), which belongs to the superfamily of steroid/thyroid hormone nuclear receptors. Physiological and pharmacological actions of 1,25-(OH)(2)D-3 in various systems, along with the detection of VDR in target cells, have indicated potential therapeutic applications of VDR ligands in inflammation (rheumatoid arthritis, psoriatic arthritis), dermatological indications (psoriasis, actinic keratosis, seborrheic dermatitis, photoaging), osteoporosis (postmenopausal and steroid-induced osteoporosis), cancers (prostate, colon, breast, myelodysplasia, leukemia, head and neck squamous cell carcinoma, and basal cell carcinoma), secondary hyperparathyroidism, and autoimmune-diseases (systemic lupus erythematosus, type I diabetes, multiple sclerosis, and organ transplantation). As a result, VDR ligands have been developed for the treatment of psoriasis, osteoporosis, and secondary hyperparathyroidism. Furthermore, encouraging results have been obtained with VDR ligands in clinical trials of prostate cancer and hepatocellular carcinoma. This review deals with the molecular aspects of noncalcemic actions of vitamin D analogs that account for the efficacy of VDR ligands in the above-mentioned indications.
C1 Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA.
C3 Eli Lilly
RP Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA.
EM nagpal_sunil@lilly.com
RI Nagpal, Sunil/A-8007-2009
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NR 285
TC 730
Z9 861
U1 0
U2 77
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0163-769X
EI 1945-7189
J9 ENDOCR REV
JI Endocr. Rev.
PD AUG
PY 2005
VL 26
IS 5
BP 662
EP 687
DI 10.1210/er.2004-0002
PG 26
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 950HP
UT WOS:000230848500004
PM 15798098
OA Bronze
DA 2025-01-07
ER
PT J
AU Gui, Z
Zhang, Y
Zhang, AH
Xia, WW
Jia, ZJ
AF Gui, Zhen
Zhang, Yan
Zhang, Aihua
Xia, Weiwei
Jia, Zhanjun
TI CARMA3: A potential therapeutic target in non-cancer diseases
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE CARMA3; BCL10; MALT1; NF-kappa B; non-cancer diseases
ID NF-KAPPA-B; RECRUITMENT DOMAIN FAMILY; CELL-PROLIFERATION; SIGNALING
CONTRIBUTES; AUTOIMMUNE HEPATITIS; CARD11 MUTATIONS; GENE-EXPRESSION;
ACTIVATION; CANCER; MIGRATION
AB Caspase recruitment domain and membrane-associated guanylate kinase-like protein 3 (CARMA3) is a scaffold protein widely expressed in non-hematopoietic cells. It is encoded by the caspase recruitment domain protein 10 (CARD10) gene. CARMA3 can form a CARMA3-BCL10-MALT1 complex by recruiting B cell lymphoma 10 (BCL10) and mucosa- associated lymphoid tissue lymphoma translocation protein 1 (MALT1), thereby activating nuclear factor- kappa B (NF-kappa B), a key transcription factor that involves in various biological responses. CARMA3 mediates different receptors-dependent signaling pathways, including G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs). Inappropriate expression and activation of GPCRs and/or RTKs/CARMA3 signaling lead to the pathogenesis of human diseases. Emerging studies have reported that CARMA3 mediates the development of various types of cancers. Moreover, CARMA3 and its partners participate in human non-cancer diseases, including atherogenesis, abdominal aortic aneurysm, asthma, pulmonary fibrosis, liver fibrosis, insulin resistance, inflammatory bowel disease, and psoriasis. Here we provide a review on its structure, regulation, and molecular function, and further highlight recent findings in human non-cancerous diseases, which will provide a novel therapeutic target.
C1 [Gui, Zhen; Zhang, Yan; Xia, Weiwei] Nanjing Med Univ, Childrens Hosp, Dept Clin Lab, Nanjing, Peoples R China.
[Zhang, Aihua; Xia, Weiwei; Jia, Zhanjun] Nanjing Med Univ, Childrens Hosp, Dept Nephrol, Nanjing, Peoples R China.
[Zhang, Aihua; Xia, Weiwei; Jia, Zhanjun] Nanjing Med Univ, Jiangsu Key Lab Pediat, Nanjing, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing Medical
University
RP Xia, WW (corresponding author), Nanjing Med Univ, Childrens Hosp, Dept Clin Lab, Nanjing, Peoples R China.; Xia, WW; Jia, ZJ (corresponding author), Nanjing Med Univ, Childrens Hosp, Dept Nephrol, Nanjing, Peoples R China.; Xia, WW; Jia, ZJ (corresponding author), Nanjing Med Univ, Jiangsu Key Lab Pediat, Nanjing, Peoples R China.
EM xiawwpku@163.com; jiazj72@hotmail.com
FU National Natural Science Foundation of China; Nanjing National
Commission on Health and Family Planning; [82070760]; [82070701];
[81600352]; [ZKX19042]
FX Funding This study was supported by a grant from the National Natural
Science Foundation of China (no. 82070760, 82070701, 81600352), grants
from the Nanjing National Commission on Health and Family Planning (no.
ZKX19042).
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NR 94
TC 5
Z9 5
U1 3
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD DEC 22
PY 2022
VL 13
AR 1057980
DI 10.3389/fimmu.2022.1057980
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 7O9YF
UT WOS:000908369800001
PM 36618379
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Weber, M
Nair, VP
Bauer, T
Sprinzl, MF
Protzer, U
Vincendeau, M
AF Weber, Melanie
Padmanabhan Nair, Vidya
Bauer, Tanja
Sprinzl, Martin F.
Protzer, Ulrike
Vincendeau, Michelle
TI Increased HERV-K(HML-2) Transcript Levels Correlate with Clinical
Parameters of Liver Damage in Hepatitis C Patients
SO CELLS
LA English
DT Article
DE hepatitis C virus; human endogenous retroviruses; liver cirrhosis;
albumin; viral clearance; direct-acting antivirals
AB Chronic hepatitis C virus (HCV) infection is closely associated with a plethora of diseases, including cancers and autoimmune disorders. However, the distinct triggers and cellular networks leading to such HCV-derived diseases are poorly understood. Around 8% of the human genome consists of human endogenous retroviruses. They are usually silenced but can be reactivated by environmental conditions, including viral infections. Our current understanding indicates that the activation of one specific family-namely, HERV-K(HML-2)-is linked to distinct pathologies, including cancer and autoimmunity. In this study, we analyzed the transcription levels of HERV-K(HML-2) in 42 HCV-infected patients receiving direct-acting antiviral therapies. Samples from the start of treatment until 12 weeks post-treatment were investigated. Our results show increased HERV-K(HML-2) transcript levels in patients with HCV-derived liver cirrhosis throughout the observation period. Several clinical parameters specifying poor liver function are positively correlated with HERV-K(HML-2) expression. Of note, patients without a sustained viral clearance showed a drastic increase in HERV-K(HML-2) transcript levels. Together, our data suggest that increased HERV-K(HML-2) expression is correlated with reduced liver function as well as therapy success in HCV-infected patients.
C1 [Weber, Melanie; Padmanabhan Nair, Vidya; Bauer, Tanja; Protzer, Ulrike; Vincendeau, Michelle] HelmholtzZentrum Munchen, Inst Virol, D-85764 Neuherberg, Germany.
[Bauer, Tanja; Protzer, Ulrike] Tech Univ Munich, Inst Virol, D-81675 Munich, Germany.
[Bauer, Tanja; Protzer, Ulrike] German Ctr Infect Res DZIF, Partner Site, D-81675 Munich, Germany.
[Sprinzl, Martin F.] Univ Hosp Mainz, Med Dept, D-55131 Mainz, Germany.
C3 Helmholtz Association; Helmholtz-Center Munich - German Research Center
for Environmental Health; Technical University of Munich; German Center
for Infection Research; University Hospital Mainz
RP Protzer, U; Vincendeau, M (corresponding author), HelmholtzZentrum Munchen, Inst Virol, D-85764 Neuherberg, Germany.; Protzer, U (corresponding author), Tech Univ Munich, Inst Virol, D-81675 Munich, Germany.; Protzer, U (corresponding author), German Ctr Infect Res DZIF, Partner Site, D-81675 Munich, Germany.
EM weber.m.melanie@gmail.com; vidya.padmanabhan@helmholtz-muenchen.de;
tanja.bauer@helmholtz-muenchen.de; Martin.Sprinzl@unimedizin-mainz.de;
Protzer@tum.de; michelle.vincendeau@helmholtz-muenchen.de
RI Vincendeau, Michelle/AAD-4320-2022; Prabakaran, Vidya/HHY-8233-2022;
Protzer, Ulrike/D-5915-2015
OI Sprinzl, Martin/0000-0002-4544-9560; Weber, Melanie/0000-0003-4232-4807;
Protzer, Ulrike/0000-0002-9421-1911; Padmanabhan Nair,
Vidya/0000-0002-8865-6404
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NR 44
TC 5
Z9 6
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD APR
PY 2021
VL 10
IS 4
AR 774
DI 10.3390/cells10040774
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA RR1WG
UT WOS:000642896300001
PM 33807462
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Seela, S
Sheela, H
Boyer, JL
AF Seela, S
Sheela, H
Boyer, JL
TI Autoimmune hepatitis type 1: safety and efficacy of prolonged medical
therapy
SO LIVER INTERNATIONAL
LA English
DT Article
DE autoimmune hepatitis; prednisone therapy; azathio prine;
transplantation; chronic liver disease
ID CHRONIC ACTIVE HEPATITIS; LIVER-TRANSPLANTATION; CORTICOSTEROID-THERAPY;
FOLLOW-UP; RECURRENCE; DISEASE; AZATHIOPRINE; REJECTION; REMISSION
AB Studies on the long-term outcome of immunosuppression in patients with autoimmune hepatitis (AIH) type 1 are limited. Aim: To assess the efficacy and safety of prolonged medical therapy for up to four decades in a cohort of patients with AIH. Methods: Forty-two patients were followed long term in the Yale Liver Clinics who met the criteria of 'definite autoimmune hepatitis' as defined by the International Autoimmune Hepatitis Group. Records were reviewed for the dosage of immunosuppression, rate of relapse, steroid side effects, current status of liver function tests and evidence for cirrhosis and its complications. Results: Mean follow-up was 16 years and ranged from 7 to 43 years. The median follow-up was 13.5 years. Steroid withdrawal resulted in a mean of 1.78 relapses/patient (range, 0-8). All but six patients responded well to prednisone and azathioprine and alanine aminotransferases were completely normal in 29 (81%) at last exam. Five patients have discontinued medication. Steroid side effects have been minimal (weight gain in eight, osteoporosis in three) except for one patient who recovered successfully from cryptococcal meningitis and another with aseptic necrosis of the hip. Progression to cirrhosis occurred in 54% with evidence of esophageal varices in 37% but none developed hepatocellular carcinoma. Only one patient has received a liver transplant, while five others are currently listed because of symptoms of ascites, encephalopathy or bleeding from esophageal varices. Conclusions: AIH can be managed effectively over three to four decades with low-dose immunosuppression resulting in essentially normal lifestyles and minimal side effects. Liver transplantation with an increased risk of rejection and graft failure in this group can be avoided for long periods in most of these patients.
C1 Yale Univ, Sch Med, Ctr Liver, New Haven, CT 06520 USA.
C3 Yale University
RP Seela, S (corresponding author), Yale Univ, Sch Med, Ctr Liver, POB 208019,333 Cedar St, New Haven, CT 06520 USA.
EM james.boyer@yale.edu
FU NIDDK NIH HHS [DK P3034989] Funding Source: Medline
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NR 27
TC 45
Z9 48
U1 0
U2 1
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
SN 1478-3223
J9 LIVER INT
JI Liver Int.
PD AUG
PY 2005
VL 25
IS 4
BP 734
EP 739
DI 10.1111/j.1478-3231.2005.01141.x
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 942SO
UT WOS:000230302900008
PM 15998423
DA 2025-01-07
ER
PT J
AU Santos, GR
Boin, IFSF
Pereira, MIW
Bonato, TCMP
Silva, RCMA
Stucchi, RSB
da Silva, RF
AF Santos, G. R.
Boin, I. F. S. F.
Pereira, M. I. W.
Bonato, T. C. M. P.
Silva, R. C. M. A.
Stucchi, R. S. B.
da Silva, R. F.
TI Anxiety Levels Observed in Candidates for Liver Transplantation
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article
AB Introduction. Anxiety can be considered an emotional state that does not present itself at the same intensity in all patients, and can be classified into 3 levels: mild, moderate, and severe. The patient, upon entering the waiting list for transplantation, reflects on the decision taken, which leaves him constantly anxious about the idea of possible death.
Objective. This study had the aim of evaluating the degree of anxiety observed in orthotopic liver transplantation (OLT) candidates and whether there was a correlation between anxiety and etiologic diagnosis.
Methods. This study was a prospective study where the patients underwent psychological evaluation by Beck Anxiety Inventory (BAT). The anxiety level was minimal, mild, moderate, or severe. The Model for End-Stage Liver Disease (MELD) score and etiology were recorded.
Results. The level of anxiety found were as follows: 55% minimal, 27% mild, 12% moderate, and 7% severe. The correlation between level of anxiety and etiologic diagnosis showed that 71% of patients with alcoholic cirrhosis and 60% of those with liver cancer showed a minimal degree of anxiety and 27% of patients with autoimmune cirrhosis had severe anxiety.
Conclusion. We found that in patients with autoimmune hepatitis, the degree of anxiety was more pronounced. It is believed that the absence of physical symptoms is an important factor when observing anxiety in OLT candidates.
C1 Univ Estadual Campinas, Fac Med Sci, Psychol Serv, Unit Liver Transplantat,Gastroctr, Campinas, SP, Brazil.
Hosp Base Sao Jose do Rio Preto, Liver Transplantat Unit, Sao Jose Do Rio Preto, SP, Brazil.
C3 Universidade Estadual de Campinas
RP Boin, IFSF (corresponding author), Rua Aldo Oliveira Barbosa 184, BR-13086030 Campinas, SP, Brazil.
EM ilkaboin@yahoo.com
RI da Silva, Renato/A-3016-2019; Silva, Rita/KGM-6226-2024; Boin,
Ilka/M-7184-2019
CR ABRUNHEIRO LMM, 2005, SAUDE DOENCA, V6, P139
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NR 20
TC 16
Z9 17
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0041-1345
EI 1873-2623
J9 TRANSPL P
JI Transplant. Proc.
PD MAR
PY 2010
VL 42
IS 2
BP 513
EP 516
DI 10.1016/j.transproceed.2010.01.009
PG 4
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA 575FD
UT WOS:000276051400031
PM 20304181
OA hybrid
DA 2025-01-07
ER
PT J
AU Carlé, A
Pedersen, IB
Knudsen, N
Perrild, H
Ovesen, L
Rasmussen, LB
Jorgensen, T
Laurberg, P
AF Carle, Allan
Pedersen, Inge Bulow
Knudsen, Nils
Perrild, Hans
Ovesen, Lars
Rasmussen, Lone Banke
Jorgensen, Torben
Laurberg, Peter
TI Moderate alcohol consumption may protect against overt autoimmune
hypothyroidism: a population-based case-control study
SO EUROPEAN JOURNAL OF ENDOCRINOLOGY
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; THYROGLOBULIN AUTOANTIBODIES;
RHEUMATOID-ARTHRITIS; THYROID PEROXIDASE; WINE CONSUMPTION;
BREAST-CANCER; DISEASE; RISK; SMOKING; LIVER
AB Objective: Alcohol consumption is an important protective risk factor for many autoimmune diseases. We wished to study the association between alcohol consumption and autoimmune hypothyroidism.
Design: Population-based, case-control study, 1997-2001, Denmark.
Methods: Patients with newly diagnosed autoimmune overt hypothyroidism (n = 140) were prospectively identified in a population (2 027 208 person-years of observation), and their matched controls with normal thyroid function (n = 560) were recruited simultaneously from the same population. Participants gave information on alcohol intake, smoking, previous diseases, education, and family history of hypothyroidism. The association between alcohol intake and development of hypothyroidism was analyzed in conditional regression models.
Results: Hypothyroid cases had reported a lower alcohol consumption than controls (median units of alcohol (12 g) per week: 3 vs 5, P = 0.002). In a multivariate regression model, alcohol consumption was associated with a reduction in risk for development of overt autoimmune hypothyroidism. Odds ratios (95% confidence interval) compared with the reference group with a recent (last year) consumption of 1-10 units of alcohol per week were as follows: 0 units/week, 1.98 (1.21-3.33); 11-20 units/week, 0.41 (0.20-0.83); and >= 21 units/week, 0.90 (0.41-2.00). Similar results were found for maximum previous alcohol consumption during a calendar year. No interaction was found with type of alcohol consumed (wine vs beer), sex, or region of inhabitancy.
Conclusions: Alcohol consumption seems to confer considerable protection against development of overt autoimmune hypothyroidism irrespective of sex and type of alcohol consumed.
C1 [Carle, Allan; Pedersen, Inge Bulow; Laurberg, Peter] Aarhus Univ Hosp, Aalborg Hosp, Dept Endocrinol & Med, DK-9000 Aalborg, Denmark.
[Knudsen, Nils; Perrild, Hans] Bispebjerg Hosp, Med Clin 1, Endocrine Unit, DK-2400 Copenhagen, Denmark.
[Ovesen, Lars] Slagelse Hosp, Dept Internal Med, Slagelse, Denmark.
[Rasmussen, Lone Banke] Tech Univ Denmark, Natl Food Inst, Minist Food Agr & Fisheries, Copenhagen, Denmark.
[Jorgensen, Torben] Res Ctr Dis Prevent & Hlth, Copenhagen, Denmark.
C3 Aalborg University; Aalborg University Hospital; Aarhus University;
University of Copenhagen; Bispebjerg Hospital; Technical University of
Denmark
RP Carlé, A (corresponding author), Aarhus Univ Hosp, Aalborg Hosp, Dept Endocrinol & Med, DK-9000 Aalborg, Denmark.
EM carle@dadlnet.dk
RI Jørgensen, Torben/Z-1335-2018
OI Jorgensen, Torben/0000-0001-9453-2830
FU IMK General Foundation; Danish Council for Independent Research;
Ministry of Food, Agriculture and Fisheries; Danish Agency for Science,
Technology and Innovation, Institute for Clinical Medicine, University
of Aarhus; Aase og Ejnar Danielsens Foundation
FX This study was part of DanThyr, and it was supported by the following
grants: IMK General Foundation; The Danish Council for Independent
Research; Ministry of Food, Agriculture and Fisheries; the Danish Agency
for Science, Technology and Innovation, Institute for Clinical Medicine,
University of Aarhus; and Aase og Ejnar Danielsens Foundation.
CR Carlé A, 2006, EUR J ENDOCRINOL, V154, P21, DOI 10.1530/eje.1.02068
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NR 41
TC 74
Z9 80
U1 0
U2 7
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 0804-4643
J9 EUR J ENDOCRINOL
JI Eur. J. Endocrinol.
PD OCT
PY 2012
VL 167
IS 4
BP 483
EP 490
DI 10.1530/EJE-12-0356
PG 8
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Endocrinology & Metabolism
GA 009BF
UT WOS:000308999600004
PM 22802427
OA Bronze
DA 2025-01-07
ER
PT J
AU Herrmann, J
Petit, P
Grabhorn, E
Lenz, A
Jürgens, J
Franchi-Albella, S
AF Herrmann, Jochen
Petit, Philippe
Grabhorn, Enke
Lenz, Alexander
Jurgens, Julian
Franchi-Albella, Stephanie
TI Liver cirrhosis in children - the role of imaging in the diagnostic
pathway
SO PEDIATRIC RADIOLOGY
LA English
DT Article
DE Children; Cirrhosis; Computed tomography; Elastography; Imaging; Liver;
Magnetic resonance imaging; Ultrasound
ID SHEAR-WAVE ELASTOGRAPHY; MAGNETIC-RESONANCE ELASTOGRAPHY;
HEPATOCELLULAR-CARCINOMA; HEPATIC-FIBROSIS; TRANSIENT ELASTOGRAPHY;
BILIARY ATRESIA; ULTRASOUND ELASTOGRAPHY; BIOCHEMICAL REMISSION;
PORTAL-HYPERTENSION; HEALTHY-CHILDREN
AB Liver cirrhosis in children is a rare disease with multifactorial causes that are distinct from those in adults. Underlying reasons include cholestatic, viral, autoimmune, hereditary, metabolic and cardiac disorders. Early detection of fibrosis is important as clinical stabilization or even reversal of fibrosis can be achieved in some disorders with adequate treatment. This article focuses on the longitudinal evaluation of children with chronic liver disease with noninvasive imaging tools, which play an important role in detecting cirrhosis, defining underlying causes, grading fibrosis and monitoring patients during follow-up. Ultrasound is the primary imaging modality and it is used in a multiparametric fashion. Magnetic resonance imaging and computed tomography are usually applied second line for refined tissue characterization, clarification of nodular lesions and full delineation of abdominal vessels, including portosystemic communications.
C1 [Herrmann, Jochen; Jurgens, Julian] Univ Med Ctr Hamburg Eppendorf, Dept Diagnost & Intervent Radiol & Nucl Med, Sect Pediat Radiol, Martinistr 52, D-20251 Hamburg, Germany.
[Petit, Philippe] Aix Marseille Univ, Hop Timone Enfants, Marseille, France.
[Grabhorn, Enke] Univ Med Ctr Hamburg, Dept Pediat Gastroenterol & Hepatol, Hamburg, Germany.
[Lenz, Alexander] Univ Med Ctr, Dept Diagnost & Intervent Radiol & Nucl Med, Hamburg, Germany.
[Franchi-Albella, Stephanie] Hop Bicetre, Dept Pediat Radiol, Natl Reference Ctr Rare Pediat Liver Dis, Paris, France.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf;
Aix-Marseille Universite; Assistance Publique-Hopitaux de Marseille;
University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Hamburg; University Medical Center Hamburg-Eppendorf;
Universite Paris Saclay; Assistance Publique Hopitaux Paris (APHP);
Hopital Universitaire Bicetre - APHP
RP Herrmann, J (corresponding author), Univ Med Ctr Hamburg Eppendorf, Dept Diagnost & Intervent Radiol & Nucl Med, Sect Pediat Radiol, Martinistr 52, D-20251 Hamburg, Germany.
EM j.herrmann@uke.de
OI Jurgens, Julian H.W./0009-0004-7982-6303
FU Projekt DEAL
FX Open Access funding enabled and organized by Projekt DEAL.
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NR 116
TC 4
Z9 4
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0301-0449
EI 1432-1998
J9 PEDIATR RADIOL
JI Pediatr. Radiol.
PD APR
PY 2023
VL 53
IS 4
SI SI
BP 714
EP 726
DI 10.1007/s00247-022-05480-x
EA AUG 2022
PG 13
WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging
GA M6XC2
UT WOS:000847633900002
PM 36040526
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Zandvakili, I
Lazaridis, KN
AF Zandvakili, Inuk
Lazaridis, Konstantinos N.
TI Cell-free DNA testing: future applications in gastroenterology and
hepatology
SO THERAPEUTIC ADVANCES IN GASTROENTEROLOGY
LA English
DT Review
DE cell-free DNA; gastroenterology and hepatology; individualized medicine
ID METASTATIC COLORECTAL-CANCER; GASTRIC-CANCER; METHYLATION CHANGES;
CLINICAL-RELEVANCE; PANCREATIC-CANCER; PROGNOSTIC MARKER;
PERIPHERAL-BLOOD; CIRCULATING DNA; PLASMA DNA; SERUM DNA
AB The application of next-generation sequencing in clinical practice is increasing as accuracy and interpretation have improved and the cost continues to decline rapidly. Cell-free DNA is a unique source for next-generation sequencing that could change routine clinical practice in gastroenterology and hepatology. Testing of cell-free DNA in blood and fecal samples is an easy, rapid, and noninvasive method to assess for premalignant, malignant, metabolic, infectious, inflammatory, and autoimmune gastrointestinal and liver diseases. In this review, we describe cell-free DNA technologies, current applications of cell-free DNA testing, and proposed cell-free DNA targets for gastrointestinal and hepatic diseases, with a specific focus on malignancy. In addition, we provide commentary on how cell-free DNA can be integrated into clinical practice and help guide diagnosis, prognosis, disease management, and therapeutic response.
C1 [Lazaridis, Konstantinos N.] Mayo Clin, Div Gastroenterol & Hepatol, 200 First St SW, Rochester, MN 55905 USA.
[Zandvakili, Inuk] Mayo Clin, Div Internal Med, Rochester, MN 55905 USA.
C3 Mayo Clinic; Mayo Clinic
RP Lazaridis, KN (corresponding author), Mayo Clin, Div Gastroenterol & Hepatol, 200 First St SW, Rochester, MN 55905 USA.
EM lazaridis.konstantinos@mayo.edu
RI Zandvakili, Inuk/C-8496-2011
OI Zandvakili, Inuk/0000-0003-3409-0019; Lazaridis,
Konstantinos/0000-0002-0437-681X
FU Catharine Nicole Jockisch Carlos Endowment Fund in Primary Sclerosing
Cholangitis (PSC)
FX Chris M. Carlos and Catharine Nicole Jockisch Carlos Endowment Fund in
Primary Sclerosing Cholangitis (PSC).
CR [Anonymous], EARL ONS INFL BOW DI
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NR 90
TC 8
Z9 8
U1 5
U2 11
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1756-283X
EI 1756-2848
J9 THER ADV GASTROENTER
JI Ther. Adv. Gastroenterol.
PD APR
PY 2019
VL 12
AR 1756284819841896
DI 10.1177/1756284819841896
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IN7MG
UT WOS:000478865900001
PM 31019553
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Yamamoto, M
Tabeya, T
Naishiro, Y
Yajima, H
Ishigami, K
Shimizu, Y
Obara, M
Suzuki, C
Yamashita, K
Yamamoto, H
Hayashi, T
Sasaki, S
Sugaya, T
Ishida, T
Takano, K
Himi, T
Suzuki, Y
Nishimoto, N
Honda, S
Takahashi, H
Imai, K
Shinomura, Y
AF Yamamoto, Motohisa
Tabeya, Tetsuya
Naishiro, Yasuyoshi
Yajima, Hidetaka
Ishigami, Keisuke
Shimizu, Yui
Obara, Mikiko
Suzuki, Chisako
Yamashita, Kentaro
Yamamoto, Hiroyuki
Hayashi, Toshiaki
Sasaki, Shigeru
Sugaya, Toshiaki
Ishida, Tadao
Takano, Ken-ichi
Himi, Tetsuo
Suzuki, Yasuo
Nishimoto, Norihiro
Honda, Saho
Takahashi, Hiroki
Imai, Kohzoh
Shinomura, Yasuhisa
TI Value of serum IgG4 in the diagnosis of IgG4-related disease and in
differentiation from rheumatic diseases and other diseases
SO MODERN RHEUMATOLOGY
LA English
DT Article
DE Autoimmune pancreatitis; Churg-Strauss syndrome; IgG4; Mikulicz's
disease; Rheumatoid arthritis
ID COLLEGE-OF-RHEUMATOLOGY; SKIN THICKNESS SCORE; AUTOIMMUNE PANCREATITIS;
AMERICAN-COLLEGE; CLASSIFICATION CRITERIA; SUBCLASS CONCENTRATIONS;
SYSTEMIC-SCLEROSIS; MIKULICZS-DISEASE; SJOGRENS-SYNDROME; LIVER-DISEASE
AB IgG4-related disease (IgG4-RD) is a novel disease entity that includes Mikulicz's disease, autoimmune pancreatitis (AIP), and many other conditions. It is characterized by elevated serum IgG4 levels and abundant IgG4-bearing plasmacyte infiltration of involved organs. We postulated that high levels of serum IgG4 would comprise a useful diagnostic tool, but little information is available about IgG4 in conditions other than IgG4-RD, including rheumatic diseases. Several reports have described cutoff values for serum IgG4 when diagnosing IgG4-RD, but these studies mostly used 135 mg/dL in AIP to differentiate from pancreatic cancer instead of rheumatic and other common diseases. There is no evidence for a cutoff serum IgG4 level of 135 mg/dL for rheumatic diseases and common diseases that are often complicated with rheumatic diseases. The aim of this work was to re-evaluate the usual cutoff serum IgG4 value in AIP (135 mg/dL) that is used to diagnose whole IgG4-RD in the setting of a rheumatic clinic by measuring serum IgG4 levels in IgG4-RD and various disorders. We therefore constructed ROC curves of serum IgG4 levels in 418 patients who attended Sapporo Medical University Hospital due to IgG4-RD and various rheumatic and common disorders. The optimal cut-off value of serum IgG4 for a diagnosis of IgG4-RD was 144 mg/dL, and the sensitivity and specificity were 95.10 and 90.76%, respectively. Levels of serum IgG4 were elevated in IgG4-RD, Churg-Strauss syndrome, multicentric Castleman's disease, eosinophilic disorders, and in some patients with rheumatoid arthritis, systemic sclerosis, chronic hepatitis, and liver cirrhosis. The usual cut-off value of 135 mg/dL in AIP is useful for diagnosing whole IgG4-RD, but high levels of serum IgG4 are sometimes observed in not only IgG4-RD but also other rheumatic and common diseases.
C1 [Yamamoto, Motohisa; Tabeya, Tetsuya; Naishiro, Yasuyoshi; Yajima, Hidetaka; Ishigami, Keisuke; Shimizu, Yui; Obara, Mikiko; Suzuki, Chisako; Yamashita, Kentaro; Yamamoto, Hiroyuki; Hayashi, Toshiaki; Sasaki, Shigeru; Sugaya, Toshiaki; Ishida, Tadao; Takahashi, Hiroki; Imai, Kohzoh; Shinomura, Yasuhisa] Sapporo Med Univ, Sch Med, Dept Internal Med 1, Chuo Ku, Sapporo, Hokkaido 0608543, Japan.
[Takano, Ken-ichi; Himi, Tetsuo] Sapporo Med Univ, Sch Med, Dept Otolaryngol, Sapporo, Hokkaido 0608543, Japan.
[Suzuki, Yasuo] Teine Keijinkai Hosp, Dept Ophthalmol, Sapporo, Hokkaido, Japan.
[Nishimoto, Norihiro] Wakayama Med Univ, Lab Immune Regulat, Osaka, Japan.
[Honda, Saho] JR Sapporo Hosp, Dept Internal Med & Rheumatol, Sapporo, Hokkaido, Japan.
[Imai, Kohzoh] Univ Tokyo, Inst Med Sci, Adv Clin Res Ctr, Tokyo, Japan.
C3 Sapporo Medical University; Sapporo Medical University; Teine Keijinkai
Hospital; Wakayama Medical University; University of Tokyo
RP Yamamoto, M (corresponding author), Sapporo Med Univ, Sch Med, Dept Internal Med 1, Chuo Ku, South 1,West 16, Sapporo, Hokkaido 0608543, Japan.
EM mocha@cocoa.plala.or.jp
FU Grants-in-Aid for Scientific Research [23390398, 21390299, 24659750]
Funding Source: KAKEN
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NR 49
TC 81
Z9 97
U1 0
U2 12
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1439-7595
EI 1439-7609
J9 MOD RHEUMATOL
JI Mod. Rheumatol.
PD JUN
PY 2012
VL 22
IS 3
BP 419
EP 425
DI 10.1007/s10165-011-0532-6
PG 7
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 958XW
UT WOS:000305275300013
PM 21953287
DA 2025-01-07
ER
PT J
AU Singh, R
Kaul, R
Kaul, A
Khan, K
AF Singh, Rashmi
Kaul, Rashmi
Kaul, Anil
Khan, Khalid
TI A comparative review of HLA associations with hepatitis B and C viral
infections across global populations
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE human leukocyte antigen; HBV persistence; HCV persistence; interferon
response to HBV and HCV; HBV vaccination response
ID HUMAN-LEUKOCYTE ANTIGEN; CLASS-II ALLELES; NECROSIS-FACTOR-ALPHA; GENE
PROMOTER POLYMORPHISMS; T-CELL RESPONSE; MHC CLASS-I; VIRUS-INFECTION;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; INTERFERON THERAPY
AB Hepatitis B (HBV) and hepatitis C (HCV) viral infection or co-infection leads to risk of development of chronic infection, cirrhosis and hepatocellular carcinoma (HCC). Immigration and globalization have added to the challenges of public health concerns regarding chronic HBV and HCV infections worldwide. The aim of this study is to review existing global literature across ethnic populations on HBV and HCV related human leukocyte antigen (HLA) associations in relation to susceptibility, viral persistence and treatment. Extensive literature search was conducted to explore the HLA associations in HBV and HCV infections reported across global populations over the past decade to understand the knowledge status, weaknesses and strengths of this information in different ethnic populations. HLA DR13 is consistently associated with HBV clearance globally. HLADRB1*11/*12 alleles and DQB1*0301 are associated with HBV persistence but with HCV clearance worldwide. Consistent association of DRB1*03 and *07 is observed with HCV susceptibility and non-responsiveness to HBV vaccination across the population. HLA DR13 is protective for vertical HBV and HCV transmission in Chinese and Italian neonates, but different alleles are associated with their susceptibility in these populations. HLA class I molecule interactions with Killer cell immunoglobulin like receptors (KIR) of natural killer (NK) cells modulate HCV infection outcome via regulating immune regulatory cells and molecules. HLA associations with HBV vaccination, interferon therapy in HBV and HCV, and with extra hepatic manifestations of viral hepatitis are also discussed. Systematic studies in compliance with global regulatory standards are required to identify the HLA specific viral epitope, stage specific T cell populations interacting with different HLA alleles during disease progression and viral clearance of chronic HBV or HCV infections among different ethnic populations. These studies would facilitate stage specific therapeutic strategies for clearance of HBV and HCV infections or co-infections across global populations and aid in identification of HBV-HCV combined vaccine. HLA associations of chronic HBV or HCV development with confounding host factors including alcohol, drug abuse, insulin resistance, age and gender are lacking and warrant detailed investigation across global populations.
(C) 2007 The WJG Press. All rights reserved.
C1 Oklahoma State Univ, Ctr Hlth Sci, Dept Biochem & Microbiol, Tulsa, OK 74107 USA.
Univ Minnesota, Dept Pediat, Div Gastroenterol, Minneapolis, MN 55455 USA.
C3 Oklahoma State University System; Oklahoma State University Center for
Health Sciences; University of Minnesota System; University of Minnesota
Twin Cities
RP Kaul, R (corresponding author), Oklahoma State Univ, Ctr Hlth Sci, Dept Biochem & Microbiol, 1111 W 17th St, Tulsa, OK 74107 USA.
EM rashmi.kaul10@okstate.edu
RI Kaul, Anil/B-2075-2016; kaul, Rashmi/A-3374-2008
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NR 159
TC 177
Z9 191
U1 0
U2 15
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 28
PY 2007
VL 13
IS 12
BP 1770
EP 1787
DI 10.3748/wjg.v13.i12.1770
PG 18
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 162LX
UT WOS:000246090000002
PM 17465466
OA Green Published
DA 2025-01-07
ER
PT J
AU Wang, X
Wang, XP
Sun, J
Fu, SO
AF Wang, Xin
Wang, Xueping
Sun, Jin
Fu, Shiou
TI An enhanced RRM2 siRNA delivery to rheumatoid arthritis fibroblast-like
synoviocytes through a liposome-protamine-DNA-siRNA complex with cell
permeable peptides
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Article
DE ribonucleotide reductase M2; fibroblast-like synoviocytes; small
interfering RNA; liposomes; rheumatoid arthritis
ID HEPATOCELLULAR-CARCINOMA; PEGYLATED IMMUNOLIPOSOMES; RNA INTERFERENCE;
KAPPA-B
AB Rheumatoid arthritis (RA) is considered to be a systemic autoimmune disease that induces systemic complications and progressive disability. It affects a large number of people. RA fibroblast-like synoviocytes (RA-FLS) promote the progression of RA through the secretion of proinflammatory cytokines and increasing invasiveness into the extracellular matrix. Therefore, targeting RA-FLS represents a potential approach for the treatment of RA. Ribonucleotide reductase M2 (RRM2), a critical protein for DNA synthesis and repair, may promote the proliferation of cells and inhibit cellular apoptosis. In previous studies it has been confirmed that the suppression of RRM2 markedly suppressed the proliferation of liver cancer cells. In the present study, a cell permeable peptide-conjugated liposome-polycation-DNA (LPD) complex loaded with RRM2 small interfering RNA (siRNA) (CCP-LPDR) was developed, aiming to increase the levels of apoptosis and inhibit the proliferation of RA-FLS. CCP-LPDR is a small-sized molecule (similar to 130 nm) with high encapsulation efficiency of siRNA (>90%) and high stability. Furthermore, it was verified that CCP-LPDR markedly suppressed RRM2 gene and protein expression by similar to 80%. Notably, CCP-LPDR efficiently targeted RA-FLS, resulting in a marked decrease in the proliferation and increase in the level of apoptosis in RA-FLS. In addition, the levels of proinflammatory cytokines tumor necrosis factor- and interleukin-6 were markedly decreased in RA-FLS following CCP-LPDR treatment. Therefore, CCP-LPDR may efficiently deliver RRM2 to RA-FLS and represent a potential treatment for RA.
C1 [Wang, Xin] Qingdao Municipal Hosp, Dept Pain Management 1, Qingdao 2660011, Shandong, Peoples R China.
[Wang, Xueping; Fu, Shiou] Qingdao Municipal Hosp, Dept Pain Management 2, 1 Jiaozhou Rd, Qingdao 2660011, Shandong, Peoples R China.
[Sun, Jin] Second Mil Med Univ, Int Joint Canc Inst, Shanghai 200433, Peoples R China.
C3 Qingdao Municipal Hospital; Qingdao Municipal Hospital; Naval Medical
University
RP Fu, SO (corresponding author), Qingdao Municipal Hosp, Dept Pain Management 2, 1 Jiaozhou Rd, Qingdao 2660011, Shandong, Peoples R China.
EM bhyxouou@163.com
FU National Natural Science Foundation of China [81771964, 81472829]
FX The present study was funded by the National Natural Science Foundation
of China (grant nos. 81771964 and 81472829).
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Zhang KQ, 2009, MOL CANCER, V8, DOI 10.1186/1476-4598-8-11
NR 28
TC 19
Z9 19
U1 2
U2 33
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD NOV
PY 2018
VL 42
IS 5
BP 2393
EP 2402
DI 10.3892/ijmm.2018.3815
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA GX4LA
UT WOS:000447702700008
PM 30106091
OA Green Published, Green Submitted, hybrid
DA 2025-01-07
ER
PT J
AU Minezaki, D
Endo, M
Saito, T
Tokumaru, T
Iwao, M
Arakawa, M
Honda, K
Mizukami, K
Kodama, M
Murakami, K
AF Minezaki, Daisuke
Endo, Mizuki
Saito, Tomoko
Tokumaru, Tomoko
Iwao, Masao
Arakawa, Mie
Honda, Koichi
Mizukami, Kazuhiro
Kodama, Masaaki
Murakami, Kazunari
TI A case of hepatosplenic cat scratch disease with hemophagocytic
lymphohistiocytosis
SO CLINICAL JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Hepatosplenic cat scratch disease; Hemophagocytic lymphohistiocytosis;
Bartonella henselae
ID BARTONELLA-HENSELAE INFECTION; GRANULOMATOUS HEPATITIS; LYMPHOMA
AB Cat scratch disease (CSD) is associated with Bartonella henselae (B. henselae) infection caused by cat scratches or bites. It typically presents with lymphadenitis and fever. However, there are atypical cases such as hepatosplenic CSD, which presents with specific lesions in the liver and spleen. Hemophagocytic lymphohistiocytosis (HLH) is a rare and severe multisystem disorder triggered by infections, cancers, or autoimmune diseases. We experienced a rare case of hepatosplenic CSD with HLH in a non-immunocompromised adult. A 78-year-old woman complained of fever and fatigue. Laboratory tests revealed anemia and liver dysfunction; abdominal contrast-enhanced computed tomography (CT) revealed splenomegaly and nodular hypodense areas in the spleen. In addition, the levels of ferritin and serum soluble IL-2R were markedly elevated, so clinical diagnosis of HLH was made. Positron emission tomography/CT revealed diffuse fluorodeoxyglucose uptake in the liver and spleen suggesting malignant lymphoma, while the pathological findings from liver biopsy suggested infectious diseases. Although she had no cat bites and scratches, she had many cats; therefore, serum B. henselae antibody titers were measured. The B. henselae IgG and IgM titer were 1:128 and 1:20; thus, she was diagnosed with hepatosplenic CSD. Patients with hepatosplenic nodular lesions and contact with cats should be considered for this disease.
C1 [Minezaki, Daisuke; Endo, Mizuki; Saito, Tomoko; Tokumaru, Tomoko; Iwao, Masao; Arakawa, Mie; Honda, Koichi; Mizukami, Kazuhiro; Kodama, Masaaki; Murakami, Kazunari] Oita Univ, Dept Gastroenterol, 1-1 Idaigaoka, Yufu, Oita 8795593, Japan.
C3 Oita University
RP Endo, M (corresponding author), Oita Univ, Dept Gastroenterol, 1-1 Idaigaoka, Yufu, Oita 8795593, Japan.
EM emizuki@oita-u.ac.jp
OI Minezaki, Daisuke/0000-0002-0429-4814
CR ADAL KA, 1994, NEW ENGL J MED, V330, P1509, DOI 10.1056/NEJM199405263302108
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NR 22
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 1865-7257
EI 1865-7265
J9 CLIN J GASTROENTEROL
JI Clin. J. Gastroenterol.
PD DEC
PY 2023
VL 16
IS 6
BP 871
EP 876
DI 10.1007/s12328-023-01840-8
EA AUG 2023
PG 6
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA Y5NC4
UT WOS:001048371200001
PM 37581719
DA 2025-01-07
ER
PT J
AU Askari, F
Innis, D
Dick, RB
Hou, GQ
Marrero, J
Greenson, J
Brewer, GJ
AF Askari, Fred
Innis, Dawna
Dick, Robert B.
Hou, Guoqing
Marrero, Jorge
Greenson, Joel
Brewer, George J.
TI Treatment of primary biliary cirrhosis with tetrathiomolybdate: results
of a double-blind trial
SO TRANSLATIONAL RESEARCH
LA English
DT Article
ID PHASE-II TRIAL; MOUSE MODEL; AMMONIUM TETRATHIOMOLYBDATE;
PULMONARY-FIBROSIS; WILSON-DISEASE; CANCER; PROTECTS; THERAPY; STRATEGY;
AGENT
AB The results of a double-blind trial of tetrathiomolybdate therapy and standard of care, versus placebo and standard of care treatment, in primary biliary cirrhosis patients are presented. Baseline studies of liver function, various safety variables, ceruloplasmin, a liver biopsy for histologic analysis, and for various cytokine analyses were carried out. Patients were observed every 4 months for up to 2 years of treatment by a hepatologist for clinical evaluation and repeat of all the baseline studies except liver biopsy, which was repeated at 2 years. The primary end points were improvement in 2 liver function tests and in 1 inflammatory cytokine. Fifteen placebo patients were followed for an average of 13 months, and 13 tetrathiomolybdate patients were followed for an average of 14 months. The predefined primary end points for efficacy were met. Tetrathiomolybdate was well tolerated. Because tetrathiomolybdate has been shown in numerous animal studies to inhibit autoimmune and inflammatory processes, and because primary biliary cirrhosis is an autoimmune attack on bile ducts, these positive findings on efficacy of tetrathiomolybdate therapy in primary biliary cirrhosis fit with the animal studies and suggest the need for a longer clinical trial to examine transplant-free survival. (Translational Research 2010; 155:123-130)
C1 [Brewer, George J.] Univ Michigan, Sch Med, Dept Human Genet, Ann Arbor, MI 48109 USA.
Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA.
Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan; University of
Michigan System; University of Michigan; University of Michigan System;
University of Michigan
RP Brewer, GJ (corresponding author), Univ Michigan, Sch Med, Dept Human Genet, G061X MBNI, Ann Arbor, MI 48109 USA.
EM brewergj@umich.edu
FU U.S. Food and Drug Administration's Orphan Products Office
[FD-02590-02]; General Clinical Research Center of the University of
Michigan Hospitals; National Institutes of Health [MO1-RR000042];
Clinical and Translational Science Awards [U11-RR024986]
FX Supported by Grant FD-02590-02 from the U.S. Food and Drug
Administration's Orphan Products Office, the General Clinical Research
Center of the University of Michigan Hospitals, Grant MO1-RR000042 from
the National Institutes of Health, and Grant U11-RR024986 Clinical and
Translational Science Awards.
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NR 25
TC 21
Z9 21
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1931-5244
J9 TRANSL RES
JI Transl. Res.
PD MAR
PY 2010
VL 155
IS 3
BP 123
EP 130
DI 10.1016/j.trsl.2009.09.009
PG 8
WC Medical Laboratory Technology; Medicine, General & Internal; Medicine,
Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; General & Internal Medicine; Research &
Experimental Medicine
GA 593GK
UT WOS:000277440800004
PM 20171597
DA 2025-01-07
ER
PT J
AU Dalekos, GN
Koskinas, J
Papatheodoridis, GV
AF Dalekos, George N.
Koskinas, John
Papatheodoridis, George V.
TI Hellenic Association for the Study of the Liver Clinical Practice
Guidelines: Autoimmune hepatitis
SO ANNALS OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune hepatitis; autoantibodies; clinical practice guidelines;
corticosteroids; azathioprine
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; ALPHA-ACTININ
ANTIBODIES; REGULATORY T-CELLS; TERM-FOLLOW-UP; MYCOPHENOLATE-MOFETIL;
ANTIMITOCHONDRIAL-ANTIBODIES; HEPATOCELLULAR-CARCINOMA; OVERLAP
SYNDROME; VIRUS-INFECTION
AB Autoimmune hepatitis (AIH) is a relatively rare acute or chronic liver disease of unknown etiology characterized by large heterogeneity. Its distribution is global, covering all ages, both sexes and all ethnic groups. The aim of the present Clinical Practice Guidelines (CPG) of the Hellenic Association for the Study of the Liver was to provide updated guidance and help to gastroenterologists, hepatologists, internists and general practitioners for AIH diagnosis and management. AIH diagnosis is based on clinicopathological characteristics: namely, polyclonal hypergammaglobulinemia, particularly of immunoglobulin G (IgG), circulating autoantibodies, interface hepatitis on liver histology, absence of viral hepatitis, and a favorable response to immunosuppression. Clinical manifestations at disease onset are variable, ranging from asymptomatic to the acute/severe form. Aminotransferase and bilirubin levels vary, while the presence of hepatitis at the histological level is a prerequisite for diagnosis. Autoantibodies are the hallmark for AIH diagnosis; therefore, the CPG describe the appropriate serological algorithm for their detection. AIH therapy should aim to achieve complete biochemical (normalization of IgG and aminotransferases) and histological remission. All patients who have active disease, even those with cirrhosis, should be treated with individualized and response-guided induction therapy using prednisolone in combination with azathioprine or mycophenolate mofetil as first-line therapy. Immunosuppression should be given for at least 3 years and for at least 2 years after the achievement of complete biochemical response, while a liver biopsy should be recommended before treatment discontinuation. Current CPG are also provided for several specific conditions and difficult-to-treat patients.
C1 [Dalekos, George N.] Inst Internal Med & Hepatol, Larisa, Greece.
[Dalekos, George N.] Univ Hosp Larissa, Dept Med, Larisa 41110, Greece.
[Dalekos, George N.] Univ Hosp Larissa, Res Lab Internal Med, Larisa 41110, Greece.
[Koskinas, John] Natl & Kapodistrian Univ Athens, Hippokratio Gen Hosp Athens, Dept Internal Med 2, Athens, Greece.
[Papatheodoridis, George V.] Natl & Kapodistrian Univ Athens, Laiko Gen Hosp Athens, Med Sch, Dept Gastroenterol, Athens, Greece.
C3 General University Hospital of Larissa; General University Hospital of
Larissa; National & Kapodistrian University of Athens; Laiko General
Hospital; National & Kapodistrian University of Athens
RP Dalekos, GN (corresponding author), Univ Hosp Larissa, Dept Med, Larisa 41110, Greece.; Dalekos, GN (corresponding author), Univ Hosp Larissa, Res Lab Internal Med, Larisa 41110, Greece.; Dalekos, GN (corresponding author), Inst Internal Med & Hepatol, Med, Larisa 41110, Greece.
EM georgedalekos@gmail.com
RI Papatheodoridis, George/A-4603-2008
OI Papatheodoridis, George/0000-0002-3518-4060
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NR 223
TC 43
Z9 47
U1 0
U2 5
PU HELLENIC SOC GASTROENTEROLOGY
PI ATHENS
PA DEMOKRATIAS AVE 67, ATHENS, 15451, GREECE
SN 1108-7471
EI 1792-7463
J9 ANN GASTROENTEROL
JI Ann. Gastroenterol.
PY 2019
VL 32
IS 1
BP 1
EP +
DI 10.20524/aog.2018.0330
PG 24
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA HF5KB
UT WOS:000454270100001
PM 30598587
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Baudin, B
Bruneel, A
Poupon, R
Vaubourdolle, M
AF Baudin, Bruno
Bruneel, Arnaud
Poupon, Raoul
Vaubourdolle, Michel
TI Serum proteomic signatures as biomarkers of primary biliary cirrhosis
diagnosis and prognosis
SO ANNALES DE BIOLOGIE CLINIQUE
LA English
DT Article
DE primary biliary cirrhosis; surface-enhanced laser desorption/ionization
time-of-flight mass spectrometry; ursodeoxycholic acid; chronic
cholestatic hepatic diseases
ID HEPATOCELLULAR-CARCINOMA; LIVER-DISEASES; IDENTIFICATION; MARKER
AB Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease considered as an autoimmune disease. To identify new biomarkers of PBC, serum profiling analysis using Surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) was employed. Twelve patients with either asymptomatic PBC (group 1, n=6) or PBC with a poor response to UDCA (group 2, n=6), were compared to healthy controls (group 3, n=6). Analysing the 18 sera by using four SELDI-TOF arrays under various conditions, we found four biomarkers of PBC at 5.9, 8.6, 8.9 and 9.0 kDa. The combination of the two arrays IMAC-40/Zn2+ and CM-10/pH 7 improved the positive diagnosis of this disease. We also found a biomarker of severity of PBC at 95.2 kDa on LSAX-30 array which characterized patients with a bad prognosis. In conclusion, our study identified several serum proteomics signatures as potential biomarkers of PBC for its diagnosis or prognosis.
C1 [Baudin, Bruno; Bruneel, Arnaud; Vaubourdolle, Michel] St Antoine Hosp, AP HP, Biochem Lab, Paris, France.
[Poupon, Raoul] St Antoine Hosp, Ctr Reference Malad Inflammatoires Voies Biliaire, AP HP, Paris, France.
[Baudin, Bruno; Poupon, Raoul] St Antoine Hosp, AP HP, UPMC UMRS 893, CdR St Antoine, Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
Universitaire Saint-Antoine - APHP; Assistance Publique Hopitaux Paris
(APHP); Sorbonne Universite; Hopital Universitaire Saint-Antoine - APHP;
Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
Universitaire Saint-Antoine - APHP
RP Baudin, B (corresponding author), St Antoine Hosp, AP HP, Biochem Lab, Paris, France.; Baudin, B (corresponding author), St Antoine Hosp, AP HP, UPMC UMRS 893, CdR St Antoine, Paris, France.
EM bruno.baudin@aphp.fr
RI Baudin, Bruno/T-6728-2018; Bruneel, Arnaud/AAD-1338-2021
OI BRUNEEL, ARNAUD/0000-0001-8411-3309
CR Alempijevic T, 2009, WORLD J GASTROENTERO, V15, P591, DOI 10.3748/wjg.15.591
Baudin P. B., 2003, Recent Research Developments in Biophysics & Biochemistry, Vol. 3, Part II, P977
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NR 16
TC 4
Z9 4
U1 0
U2 5
PU JOHN LIBBEY EUROTEXT LTD
PI MONTROUGE
PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE
SN 0003-3898
EI 1950-6112
J9 ANN BIOL CLIN-PARIS
JI Ann. Biol. Clin.
PD SEP-OCT
PY 2016
VL 74
IS 5
BP 607
EP 612
DI 10.1684/abc.2016.1182
PG 6
WC Medical Laboratory Technology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Research & Experimental Medicine
GA DZ9KL
UT WOS:000386193900011
PM 27707675
DA 2025-01-07
ER
PT J
AU Sim, KK
Fernando, T
Tarquinio, L
Navadgi, S
AF Sim, Kwang Kiat
Fernando, Tarini
Tarquinio, Lorenzo
Navadgi, Suresh
TI Hepatic reactive lymphoid hyperplasia-associated primary biliary
cholangitis masquerading as a neoplastic liver lesion
SO BMJ CASE REPORTS
LA English
DT Article
DE hepatic cancer; liver disease; gastrointestinal surgery
ID PSEUDOLYMPHOMA; CIRRHOSIS; LYMPHADENOPATHY; FEATURES
AB Hepatic reactive lymphoid hyperplasia is an uncommon benign condition, often found incidentally as a solitary liver lesion. The chronic inflammatory reaction associated with autoimmune conditions and malignancies has been postulated as a possible aetiology. The diagnosis is challenging as it often mimics various malignancies radiologically and histologically, hence the diagnosis being made only after surgical resection. Lymphadenopathy is common with primary biliary cholangitis, though rarely reported with reactive lymphoid hyperplasia. We report a case of hepatic reactive lymphoid hyperplasia associated with portacaval lymphadenopathy in a patient with primary biliary cholangitis, diagnosed after surgical resection. We propose lesional biopsy be considered in patients with primary biliary cholangitis found to have a solitary lesion with supporting low-risk clinical and radiological features.
C1 [Sim, Kwang Kiat] Fiona Stanley Hosp, Gen Surg, Murdoch, WA, Australia.
[Fernando, Tarini] Australian Clin Labs, Anat Pathol, Clayton, Vic, Australia.
[Tarquinio, Lorenzo] Univ Notre Dame Australia, Sch Med, Fremantle, WA, Australia.
[Navadgi, Suresh] Royal Perth Hosp, Upper GI HPB Surg, Perth, WA, Australia.
C3 South Metropolitan Health Service; Fiona Stanley Fremantle Hospitals
Group; Fiona Stanley Hospital; The University of Notre Dame Australia;
East Metropolitan Health Service; Royal Perth Hospital
RP Sim, KK (corresponding author), Fiona Stanley Hosp, Gen Surg, Murdoch, WA, Australia.
EM kkwang.sim@health.wa.gov.au
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NR 26
TC 2
Z9 2
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 1757-790X
J9 BMJ CASE REP
JI BMJ Case Rep.
PD NOV
PY 2023
VL 16
IS 11
AR e254963
DI 10.1136/bcr-2023-254963
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA Y7WN0
UT WOS:001107326700019
PM 37967929
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Casswall, TH
Németh, A
Nilsson, I
Wadström, T
Nilsson, HO
AF Casswall, Thomas H.
Nemeth, Antal
Nilsson, Ingrid
Wadstrom, Torkel
Nilsson, Hans-Olof
TI Helicobacter species DNA in liver and gastric tissues in children
and adolescents with chronic liver disease
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune hepatitis; children; enterohepatic Helicobacter species;
Helicobacter pylori; inflammatory bowel disease; liver tissue;
polymerase chain reaction; primary sclerosing cholangitis; ulcerative
colitis
ID PRIMARY SCLEROSING CHOLANGITIS; PYLORI INFECTION;
HEPATOCELLULAR-CARCINOMA; HEPATOBILIARY DISEASES; CHRONIC CHOLECYSTITIS;
GALLBLADDER TISSUE; SERUM ANTIBODIES; BILE SAMPLES; HEPATITIS;
IDENTIFICATION
AB Objective. Enterohepatic Helicobacter species (EHS) have previously been found in adults with hepatobiliary diseases. Here, we report the prevalence of Helicobacter pylori and EHS in liver and gastric tissue in children and adolescents with chronic liver disease (CLD). Material and methods. Seventy-seven consecutive children and adolescents with CLD with or without ulcerative colitis or Crohn's disease (UC/CD) were investigated. Tissue samples were analysed using a Helicobacter genus specific 16S rDNA polymerase chain reaction (PCR) assay and DNA-sequence analysis. Sera from 61 subjects were also analysed using enzyme immunoassay and immunoblotting. Results. The Helicobacter PCR was positive in 3/23 (13%) livers from patients with primary sclerosing cholangitis and UC, and in 1/2 livers from patients with autoimmune hepatitis (AIH) and UC. Sequenced PCR products matched the 16S rDNA of H. hepaticus, H. muridarum, H. canis, and H. pylori, respectively. H. ganmani and H. bilis were detected in gastric tissues from two AIH patients. H. hepaticus and H. pullorum were found in livers from two patients with acute liver failure and intrahepatic cholestasis. Antibody reactivity to Helicobacter cell-surface proteins was negative. Conclusions. H. pylori and EHS can be detected in the livers of some patients with UC and concomitant liver disease, as well as in other children with liver diseases. Multicentre studies from different locations are needed to find out whether these bacteria play a pathogenetic role or whether their presence is an epiphenomenon.
C1 [Casswall, Thomas H.; Nemeth, Antal] Karolinska Univ Hosp, Dept Pediat Gastroenterol Hepatol & Nutr, Astrid Lindgrens Childrens Hosp, CLINTEC,Karolinska Inst, SE-14186 Stockholm, Sweden.
[Nilsson, Ingrid; Wadstrom, Torkel; Nilsson, Hans-Olof] Lund Univ, Dept Med Microbiol, Lund, Sweden.
C3 Karolinska Institutet; Karolinska University Hospital; Lund University
RP Casswall, TH (corresponding author), Karolinska Univ Hosp, Div Pediat Gastroenterol Hepatol & Nutr, Astrid Lindgrens Childrens Hosp B57, SE-14186 Stockholm, Sweden.
EM thomas.casswall@ki.se
OI Nemeth, Antal/0000-0002-6229-5882
FU Karolinska University Hospital, Stockholm; Lund University Hospital
(ALF); The Royal Physiographic Society in Lund; Swedish order of
Freemasons
FX This study was supported by the Karolinska University Hospital,
Stockholm, Lund University Hospital (ALF grant), The Royal Physiographic
Society in Lund and the Swedish order of Freemasons.
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NR 45
TC 30
Z9 34
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PY 2010
VL 45
IS 2
BP 160
EP 167
DI 10.3109/00365520903426915
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 547GI
UT WOS:000273874200005
PM 20095882
DA 2025-01-07
ER
PT J
AU Cheng, HS
Tan, WR
Low, ZS
Marvalim, C
Lee, JYH
Tan, NS
AF Cheng, Hong Sheng
Tan, Wei Ren
Low, Zun Siong
Marvalim, Charlie
Lee, Justin Yin Hao
Tan, Nguan Soon
TI Exploration and Development of PPAR Modulators in Health and Disease: An
Update of Clinical Evidence
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE clinical trials; metabolic syndrome; type 2 diabetes mellitus; cancer;
non-alcoholic fatty liver diseases; cardiovascular diseases;
neurological disorders
ID ACTIVATED-RECEPTOR-GAMMA; PLACEBO-CONTROLLED TRIAL; PRIMARY
BILIARY-CIRRHOSIS; TYPE-2 DIABETES-MELLITUS; IMPAIRED GLUCOSE-TOLERANCE;
POLYCYSTIC-OVARY-SYNDROME; INTIMA-MEDIA THICKNESS; PROOF-OF-CONCEPT;
VENTRICULAR DIASTOLIC FUNCTION; ADVERSE CARDIOVASCULAR EVENTS
AB Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that govern the expression of genes responsible for energy metabolism, cellular development, and differentiation. Their crucial biological roles dictate the significance of PPAR-targeting synthetic ligands in medical research and drug discovery. Clinical implications of PPAR agonists span across a wide range of health conditions, including metabolic diseases, chronic inflammatory diseases, infections, autoimmune diseases, neurological and psychiatric disorders, and malignancies. In this review we aim to consolidate existing clinical evidence of PPAR modulators, highlighting their clinical prospects and challenges. Findings from clinical trials revealed that different agonists of the same PPAR subtype could present different safety profiles and clinical outcomes in a disease-dependent manner. Pemafibrate, due to its high selectivity, is likely to replace other PPAR alpha agonists for dyslipidemia and cardiovascular diseases. PPAR gamma agonist pioglitazone showed tremendous promises in many non-metabolic disorders like chronic kidney disease, depression, inflammation, and autoimmune diseases. The clinical niche of PPAR beta/delta agonists is less well-explored. Interestingly, dual- or pan-PPAR agonists, namely chiglitazar, saroglitazar, elafibranor, and lanifibranor, are gaining momentum with their optimistic outcomes in many diseases including type 2 diabetes, dyslipidemia, non-alcoholic fatty liver disease, and primary biliary cholangitis. Notably, the preclinical and clinical development for PPAR antagonists remains unacceptably deficient. We anticipate the future design of better PPAR modulators with minimal off-target effects, high selectivity, superior bioavailability, and pharmacokinetics. This will open new possibilities for PPAR ligands in medicine.
C1 [Cheng, Hong Sheng; Marvalim, Charlie; Tan, Nguan Soon] Nanyang Technol Univ Singapore, Sch Biol Sci, 60 Nanyang Dr, Singapore 637551, Singapore.
[Tan, Wei Ren; Low, Zun Siong; Lee, Justin Yin Hao; Tan, Nguan Soon] Nanyang Technol Univ Singapore, Lee Kong Chian Sch Med, 11 Mandalay Rd, Singapore 308232, Singapore.
C3 Nanyang Technological University; Nanyang Technological University
RP Cheng, HS; Tan, NS (corresponding author), Nanyang Technol Univ Singapore, Sch Biol Sci, 60 Nanyang Dr, Singapore 637551, Singapore.; Tan, NS (corresponding author), Nanyang Technol Univ Singapore, Lee Kong Chian Sch Med, 11 Mandalay Rd, Singapore 308232, Singapore.
EM hscheng@ntu.edu.sg; WTAN074@e.ntu.edu.sg; ZUNSIONG001@e.ntu.edu.sg;
CMARVALI001@e.ntu.edu.sg; lee.yinhao@ntu.edu.sg; nstan@ntu.edu.sg
RI Sheng, Cheng/AAD-6121-2019; TAN, WEI REN/KHZ-3186-2024; Tan, Nguan
Soon/A-2220-2011
OI Marvalim, Charlie/0000-0003-3287-1794; Low, Zun
Siong/0000-0001-5335-6826; TAN, WEI REN/0000-0002-5076-0206; Tan, Nguan
Soon/0000-0003-0136-7341; Cheng, Hong Sheng/0000-0001-9745-7872
FU Nanyang Technological University Start-Up Grant [M4082040]
FX N.S.T.'s work was supported by Nanyang Technological University Start-Up
Grant, grant number M4082040.
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NR 331
TC 167
Z9 180
U1 3
U2 43
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT 2
PY 2019
VL 20
IS 20
AR 5055
DI 10.3390/ijms20205055
PG 69
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Biochemistry & Molecular Biology; Chemistry
GA JQ3AZ
UT WOS:000498822800087
PM 31614690
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Mehtani, R
Rathi, S
AF Mehtani, Rohit
Rathi, Sahaj
TI Recurrence of Primary Disease After Adult Liver Transplant - Risk
Factors, Early Diagnosis, Management, and Prevention
SO JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
LA English
DT Review
DE liver transplant; recurrence; posttransplant metabolic syndrome;
non-alcoholic fatty liver disease
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS; LONG-TERM
SURVIVAL; EN-Y CHOLEDOCHOJEJUNOSTOMY; BUDD-CHIARI-SYNDROME;
DUCT-TO-DUCT; AUTOIMMUNE HEPATITIS; FOLLOW-UP; NONALCOHOLIC
STEATOHEPATITIS; WEIGHT-GAIN
AB Liver transplantation offers a new lease of life to patients with end -stage liver disease and hepatocellular carcinoma. However, the implantation of an exogenous allograft and the accompanying immunosuppression bring their own challenges. Moreover, the persistence of risk factors for the initial liver insult place the new graft at a higher risk of damage. With the increasing number of liver transplants along with the improvement in survival posttransplant, the recurrence of primary disease in liver grafts has become more common. Pre -2015, the most common disease to recur after transplant was hepatitis C. However, directly acting antivirals have nearly eliminated this problem. The greatest challenge of disease recurrence we now face are those of nonalcoholic steatohepatitis, alcohol -related liver disease, and primary sclerosing cholangitis. We focus on the epidemiology and pathophysiology of the recurrence of primary disease after transplant. We also discuss means of early identifi- cation, risk stratification, prevention, and management of recurrent primary disease after liver transplantation. ( J CLIN EXP HEPATOL 2024;14:101432)
C1 [Mehtani, Rohit] Amrita Inst Med Sci & Res, Dept Hepatol, Faridabad, Haryana, India.
[Rathi, Sahaj] Post Grad Inst Med Educ & Res, Dept Hepatol, Chandigarh, India.
C3 Amrita Vishwa Vidyapeetham; Post Graduate Institute of Medical Education
& Research (PGIMER), Chandigarh
RP Rathi, S (corresponding author), Post Grad Inst Med Educ & Res, Dept Hepatol, Chandigarh, India.
EM sahajrathi@gmail.com
RI Mehtani, Rohit/AGZ-3983-2022; Rathi, Sahaj/P-9277-2016
OI Rathi, Sahaj/0000-0001-6529-9080; Mehtani, Rohit/0000-0002-0007-0063
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NR 119
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER - DIVISION REED ELSEVIER INDIA PVT LTD
PI NEW DELHI
PA 17-A/1 MAIN RING ROAD, LAJPAT NAGAR IV, NEW DELHI, 110024, INDIA
SN 0973-6883
EI 2213-3453
J9 J CLIN EXP HEPATOL
JI J. Clin. Exp. Hepatol.
PD NOV-DEC
PY 2024
VL 14
IS 6
AR 101432
DI 10.1016/j.jceh.2024.101432
EA JUN 2024
PG 16
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA WF3X5
UT WOS:001253427100001
PM 38975605
DA 2025-01-07
ER
PT J
AU Asuri, S
McIntosh, S
Taylor, V
Rokeby, A
Kelly, J
Shumansky, K
Field, LL
Yoshida, EM
Arbour, L
AF Asuri, Sirisha
McIntosh, Sarah
Taylor, Valerie
Rokeby, Andrew
Kelly, James
Shumansky, Karey
Field, Lanora Leigh
Yoshida, Eric M.
Arbour, Laura
TI Primary Biliary Cholangitis in British Columbia First Nations: Clinical
features and discovery of novel genetic susceptibility loci
SO LIVER INTERNATIONAL
LA English
DT Article
DE First Nations; genetic linkage; Indigenous; Primary Biliary Cholangitis
ID HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; CIRRHOSIS; LIVER;
EPIGENETICS; DISEASE; PIN1; DNA; RECRUITMENT; PREVALENCE
AB Background & Aims: Primary Biliary Cholangitis (PBC) is a chronic autoimmune liver disease characterized by destruction of intrahepatic bile ducts, portal inflammation and cirrhosis. Although rare in most populations, it is prevalent and often familial in British Columbia First Nations. We hypothesized that major genetic factors increased the risk in First Nations.
Methods: In all, 44 individuals with Primary Biliary Cholangitis and 61 unaffected relatives from 32 First Nations families participated. Family history and co-morbidities were documented. Medical records were reviewed and available biopsies were re-reviewed by our team pathologist. Genotyping was performed on DNA from 36 affected persons and 27 unaffected relatives using the Affymetrix Human Mapping 500K Array Set. MERLIN software was used to carry out multipoint parametric and nonparametric linkage analysis. Candidate genes were identified and entered into InnateDB and KEGG software to identify potential pathways affecting pathogenesis.
Results: In all, 34% of families were multiplex. Fifty per cent of cases and 33% of unaffected relatives reported other autoimmune disease. Three genomic regions (9q21, 17p13 and 19p13) produced LOD scores of 2.3 or greater suggestive of linkage, but no single linkage peak reached statistical significance. Candidate genes identified in the three regions suggested involvement of IL17, NF kappa B, IL6, JAK-STAT, IFN gamma and TGF beta immune signalling pathways. Specifically, four genes-ACT1, PIN1, DNMT1 and NTN1-emerged as having roles in these pathways that may influence Primary Biliary Cholangitis pathogenesis.
Conclusions: Our whole genome linkage study results reflect the multifactorial nature of Primary Biliary Cholangitis, support previous studies suggesting signalling pathway involvement and identify new candidate genes for consideration.
C1 [Asuri, Sirisha; McIntosh, Sarah; Shumansky, Karey; Field, Lanora Leigh; Arbour, Laura] Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada.
[Taylor, Valerie; Rokeby, Andrew; Arbour, Laura] Univ Victoria, Div Med Sci, Victoria, BC, Canada.
[Kelly, James] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC, Canada.
[Yoshida, Eric M.] Univ British Columbia, Div Gastroenterol, Vancouver, BC, Canada.
C3 University of British Columbia; University of Victoria; University of
British Columbia; University of British Columbia
RP Arbour, L (corresponding author), Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada.
EM larbour@uvic.ca
RI Kelly, James/JFJ-3378-2023
OI Arbour, Laura/0000-0002-9589-0880
FU Canadian Liver Foundation; Kloshe Tillicum; BC Clinical Genomics
Network; Michael Smith Foundation for Health Research Scholar Award in
Population Health
FX Funding for this study was provided by an Operating Grant from the
Canadian Liver Foundation. Student funding to VT was provided by Kloshe
Tillicum and the BC Clinical Genomics Network. LA was the recipient of a
Michael Smith Foundation for Health Research Scholar Award in Population
Health.
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NR 54
TC 13
Z9 14
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD MAY
PY 2018
VL 38
IS 5
BP 940
EP 948
DI 10.1111/liv.13686
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GK1EA
UT WOS:000435855300022
PM 29297981
DA 2025-01-07
ER
PT J
AU Bannu, SM
Lomada, D
Gulla, S
Chandrasekhar, T
Reddanna, P
Reddy, MC
AF Bannu, Saira M.
Lomada, Dakshayani
Gulla, Surendra
Chandrasekhar, Thummala
Reddanna, Pallu
Reddy, Madhava C.
TI Potential Therapeutic Applications of C-Phycocyanin
SO CURRENT DRUG METABOLISM
LA English
DT Review
DE C-Phycocyanin; therapeutic agent; cancer; inflammation; cell death;
public health
ID BLUE-GREEN-ALGA; SELENIUM-CONTAINING PHYCOCYANIN; ZYMOSAN-INDUCED
ARTHRITIS; TRANS-RETINOIC ACID; IN-VITRO; ANTIINFLAMMATORY ACTIVITY;
SPIRULINA-PLATENSIS; ARTHRONEMA-AFRICANUM; OXIDATIVE STRESS; ANTIOXIDANT
PROPERTIES
AB Background: Cancer and other disorders such as inflammation, autoimmune diseases and diabetes are the major health problems observed all over the world. Therefore, identifying a therapeutic target molecule for the treatment of these diseases is urgently needed to benefit public health. C-Phycocyanin (C-PC) is an important light yielding pigment intermittently systematized in the cyanobacterial species along with other algal species. It has numerous applications in the field of biotechnology and drug industry and also possesses antioxidant, anticancer, anti-inflammatory, enhanced immune function, including liver and kidney protection properties. The molecular mechanism of action of C-PC for its anticancer activity could be the blockage of cell cycle progression, inducing apoptosis and autophagy in cancer cells.
Objectives: The current review summarizes an update on therapeutic applications of C-PC, its mechanism of action and mainly focuses on the recent development in the field of C-PC as a drug that exhibits beneficial effects against various human diseases including cancer and inflammation.
Conclusion: The data from various studies suggest the therapeutic applications of C-PC such as anti-cancer activity, anti-inflammation, anti-angiogenic activity and healing capacity of certain autoimmune disorders. Mechanism of action of C-PC for its anticancer activity is the blockage of cell cycle progression, inducing apoptosis and autophagy in cancer cells. The future perspective of C-PC is to identify and define the molecular mechanism of its anti-cancer, anti-inflammatory and antioxidant activities, which would shed light on our knowledge on therapeutic applications of C-PC and may contribute significant benefits to global public health.
C1 [Bannu, Saira M.; Gulla, Surendra; Reddy, Madhava C.] Yogi Vemana Univ, Dept Biotechnol & Bioinformat, Kadapa 516005, Andhra Pradesh, India.
[Lomada, Dakshayani] Yogi Vemana Univ, Dept Genet & Genom, Kadapa 516005, Andhra Pradesh, India.
[Chandrasekhar, Thummala] Yogi Vemana Univ, Dept Environm Sci, Kadapa 516005, Andhra Pradesh, India.
[Reddanna, Pallu] Univ Hyderabad, Dept Anim Sci, Hyderabad 500046, Telangana, India.
C3 Yogi Vemana University; Yogi Vemana University; Yogi Vemana University;
University of Hyderabad
RP Reddy, MC (corresponding author), Yogi Vemana Univ, Dept Biotechnol & Bioinformat, Kadapa 516005, Andhra Pradesh, India.
EM cmadhavareddy@gmail.com
RI reddy, malllu/H-6461-2014; Gulla, Surendra/LSK-5520-2024
OI Gulla, Surendra/0000-0003-1555-2046; Reddy, Madhava/0000-0003-4885-0437
FU Science and Engineering Research Board (SERB) [EMR/2016/007208]
FX This work was partially supported in part by the grants from the Science
and Engineering Research Board (SERB) (No: EMR/2016/007208).
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NR 123
TC 36
Z9 39
U1 3
U2 67
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-2002
EI 1875-5453
J9 CURR DRUG METAB
JI Curr. Drug Metab.
PY 2019
VL 20
IS 12
BP 967
EP 976
DI 10.2174/1389200220666191127110857
PG 10
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA KE0GA
UT WOS:000508238700006
PM 31775595
DA 2025-01-07
ER
PT J
AU Arsenijevic, A
Stojanovic, B
Milovanovic, J
Arsenijevic, D
Arsenijevic, N
Milovanovic, M
AF Arsenijevic, Aleksandar
Stojanovic, Bojana
Milovanovic, Jelena
Arsenijevic, Dragana
Arsenijevic, Nebojsa
Milovanovic, Marija
TI Galectin-3 in Inflammasome Activation and Primary Biliary Cholangitis
Development
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE primary biliary cholangitis (PBC); galectin-3; NLRP3; inflammasome
ID FOLLICULAR HELPER-CELLS; GENOME-WIDE ASSOCIATION; NLRP3 INFLAMMASOME;
T-CELL; IMMUNE-RESPONSES; EPITHELIAL-CELLS; INNATE IMMUNITY;
HEPATOCELLULAR-CARCINOMA; DENDRITIC CELLS; KUPFFER CELLS
AB Primary biliary cholangitis (PBC) is a chronic inflammatory autoimmune liver disease characterized by inflammation and damage of small bile ducts. The NLRP3 inflammasome is a multimeric complex of proteins that after activation with various stimuli initiates an inflammatory process. Increasing data obtained from animal studies implicate the role of NLRP3 inflammasome in the pathogenesis of various diseases. Galectin-3 is a beta-galactoside-binding lectin that plays important roles in various biological processes including cell proliferation, differentiation, transformation and apoptosis, pre-mRNA splicing, inflammation, fibrosis and host defense. The multilineage immune response at various stages of PBC development includes the involvement of Gal-3 in the pathogenesis of this disease. The role of Galectin-3 in the specific binding to NLRP3, and inflammasome activation in models of primary biliary cholangitis has been recently described. This review provides a brief pathogenesis of PBC and discusses the current knowledge about the role of Gal-3 in NLRP3 activation and PBC development.
C1 [Arsenijevic, Aleksandar; Stojanovic, Bojana; Milovanovic, Jelena; Arsenijevic, Nebojsa; Milovanovic, Marija] Univ Kragujevac, Fac Med Sci, Ctr Mol Med & Stem Cell Res, Kragujevac 34000, Serbia.
[Stojanovic, Bojana] Univ Kragujevac, Fac Med Sci, Dept Pathophysiol, Kragujevac 34000, Serbia.
[Milovanovic, Jelena] Univ Kragujevac, Fac Med Sci, Dept Histol, Kragujevac 34000, Serbia.
[Arsenijevic, Dragana] Univ Kragujevac, Fac Med Sci, Dept Pharm, Kragujevac 34000, Serbia.
C3 University of Kragujevac; University of Kragujevac; University of
Kragujevac; University of Kragujevac
RP Milovanovic, M (corresponding author), Univ Kragujevac, Fac Med Sci, Ctr Mol Med & Stem Cell Res, Kragujevac 34000, Serbia.
EM aleksandar@medf.kg.ac.rs; bojana.stojanovic04@gmail.com;
jelenamilovanovic205@gmail.com; menki@hotmail.rs; arne@medf.kg.ac.rs;
marijaposta@gmail.com
RI Milovanovic, Marija/HPB-6090-2023
OI Arsenijevic, Nebojsa/0000-0002-2107-3490; Stojanovic,
Bojana/0000-0002-2385-0126; Arsenijevic, Aleksandar/0000-0003-2742-8165;
Milovanovic, Jelena/0000-0002-6422-5423; Milovanovic,
Marija/0000-0002-6894-1275
FU Serbian Ministry of Science and Technological Development, Serbia,
bilateral project with PR China [ON175069, 06/2018]; Faculty of Medical
Sciences, University of Kragujevac [MP 01/19]
FX This work was funded by grant from the Serbian Ministry of Science and
Technological Development, Grants No. ON175069, Serbia, bilateral
project with PR China (06/2018) and the Faculty of Medical Sciences,
University of Kragujevac (MP 01/19).
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NR 173
TC 24
Z9 25
U1 2
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2020
VL 21
IS 14
AR 5097
DI 10.3390/ijms21145097
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA MW9OY
UT WOS:000557361700001
PM 32707678
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Buechter, M
Klein, CG
Kloeters, C
Schlaak, JF
Canbay, A
Gerken, G
Kahraman, A
AF Buechter, M.
Klein, C. Georg
Kloeters, C.
Schlaak, J. F.
Canbay, A.
Gerken, G.
Kahraman, A.
TI Tacrolimus as a Reasonable Alternative in a Patient with
Steroid-Dependent and Thiopurine-Refractory Autoimmune Pancreatitis with
IgG4-Associated Cholangitis
SO ZEITSCHRIFT FUR GASTROENTEROLOGIE
LA English
DT Article
DE autoimmune hepatitis; autoimmune pancreatitis; IgG4-associated
cholangitis
ID SCLEROSING DISEASE; DIAGNOSIS; MAINTENANCE; GUIDELINES; CONSENSUS;
FEATURES; THERAPY; CANCER
AB Background: More recently, autoimmune pancreatitis (AIP) in association with IgG4-positive cholangitis (IAC) has been recognised as a new and challenging entity. Currently, initiation of high dose steroids (e.g., prednisolone 0.5 - 1 mg/kg/day) followed by a steroid dose taper in combination with purine antagonists (e.g., azathioprine or 6-mercaptopurine) after resolution has been recommended as standard therapy.
Case Report: A 68-year-old male patient was referred to our institution in February 2012 for therapy evaluation of a steroid-dependent course of autoimmune pancreatitis type 1 with IgG4-associated cholangitis. Since the first diagnosis in March 2011, the patient was treated with high-dose steroids with good response. Whenever steroids were tapered down to a daily dose <20mg, cholestatic liver enzymes increased dramatically despite concurrent immunosuppressive therapy primarily with azathioprine and 6-MP thereafter. Therefore, we restarted steroid therapy (1 mg/kg/day) in combination with tacrolimus achieving a target level of 5 - 7 ng/mL. During the down-tapering phase, follow-up examinations presented a patient in good general condition without jaundice. Moreover, liver and pancreatic enzymes and also immunoglobulins returned to normal values without any evidence of relapse up today (66 weeks).
Conclusion: In this case, the combination of steroids with tacrolimus seems to be a reasonable alternative in a patient with steroid-dependent and thiopurine-refractory autoimmune pancreatitis with IgG4-associated cholangitis. To date, this is the first description of such a therapeutic approach for this entity.
C1 [Buechter, M.; Canbay, A.; Gerken, G.; Kahraman, A.] Univ Hosp Essen, Dept Gastroenterol & Hepatol, D-45147 Essen, Germany.
[Klein, C. Georg] Univ Hosp Essen, Dept Gen Visceral & Transplantat Surg, D-45147 Essen, Germany.
[Kloeters, C.; Schlaak, J. F.] Univ Hosp Essen, Dept Radiol, D-45147 Essen, Germany.
C3 University of Duisburg Essen; University of Duisburg Essen; University
of Duisburg Essen
RP Kahraman, A (corresponding author), Univ Hosp Essen, Hufelandstr 55, D-45147 Essen, Germany.
EM alisan.kahraman@uk-essen.de
RI Canbay, Ali/AAL-9620-2020
OI Canbay, Ali/0000-0001-6069-7899
CR Bateman AC, 2009, HISTOPATHOLOGY, V55, P373, DOI 10.1111/j.1365-2559.2008.03217.x
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NR 25
TC 17
Z9 20
U1 0
U2 5
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0044-2771
EI 1439-7803
J9 Z GASTROENTEROL
JI Z. Gastroent.
PD JUN
PY 2014
VL 52
IS 6
BP 564
EP 568
DI 10.1055/s-0034-1366331
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AJ8KJ
UT WOS:000337952400013
PM 24905108
DA 2025-01-07
ER
PT J
AU Abu Tailakh, M
Poupko, L
Kayyal, N
Alsana, A
Estis-Deaton, A
Etzion, O
Fich, A
Yardni, D
Abu-Freha, N
AF Abu Tailakh, Muhammad
Poupko, Liat
Kayyal, Najwan
Alsana, Ali
Estis-Deaton, Asia
Etzion, Ohad
Fich, Alexander
Yardni, David
Abu-Freha, Naim
TI Liver Cirrhosis, Etiology and Clinical Characteristics Disparities Among
Minority Population
SO JOURNAL OF IMMIGRANT AND MINORITY HEALTH
LA English
DT Article
DE Cirrhosis; Arab Bedouin; Jews; Complications; Mortality
ID C VIRUS-INFECTION; RISK-FACTORS; HEPATOCELLULAR-CARCINOMA; PREVALENCE;
EPIDEMIOLOGY; PREVENTION; TRANSITION; MORTALITY; BEDOUINS; DISEASE
AB Liver cirrhosis (LC) is a common disease with varied primary causes and ethnic disparities. Clinical characteristics and outcomes of Arab Bedouin (AB) and Jewish patients with LC were retrospective collected and compared. We included 1048 patients, 95 (9%) Arab Bedouin and 953 (91%) Jewish patients. The incidence of cirrhosis was much lower among AB. Age at diagnosis was 47 +/- 18 years among Bedouins compared to 61 +/- 13 years (p < 0.001) among Jews. The most frequent causes of cirrhosis among Bedouin patients were fatty liver 21.1%, cryptogenic 20%, hepatitis B 17.9% and autoimmune hepatitis 15.8%, while hepatitis C (39.2%), fatty liver (17.2%) and alcoholic liver disease (14.4%) were most common among Jewish patients. An all-cause mortality of 48.4% was observed in AB patients compared to 66.4% in Jewish patients (p < 0.001). Significant disparities regarding incidence, clinical characteristics and outcomes of cirrhosis among Arab Bedouin compared with Jewish population were found.
C1 [Abu Tailakh, Muhammad] Ben Gurion Univ Negev, Fac Hlth Sci, Recanati Sch Community Hlth Profess, Dept Nursing, Beer Sheva, Israel.
[Abu Tailakh, Muhammad] Soroka Univ, Med Ctr, Beer Sheva, Israel.
[Poupko, Liat] Ben Gurion Univ Negev, Med Sch Int Hlth, Beer Sheva, Israel.
[Kayyal, Najwan; Alsana, Ali; Estis-Deaton, Asia] Soroka Univ, Div Internal Med, Med Ctr, Beer Sheva, Israel.
[Etzion, Ohad; Fich, Alexander; Yardni, David; Abu-Freha, Naim] Soroka Univ, Inst Gastroenterol & Hepatol, Med Ctr, POB 151, IL-84101 Beer Sheva, Israel.
[Etzion, Ohad; Fich, Alexander; Yardni, David; Abu-Freha, Naim] Ben Gurion Univ Negev, Fac Hlth Sci, Beer Sheva, Israel.
C3 Ben Gurion University; Ben Gurion University; Soroka Medical Center; Ben
Gurion University; Ben Gurion University; Soroka Medical Center; Ben
Gurion University; Soroka Medical Center; Ben Gurion University
RP Abu-Freha, N (corresponding author), Soroka Univ, Inst Gastroenterol & Hepatol, Med Ctr, POB 151, IL-84101 Beer Sheva, Israel.; Abu-Freha, N (corresponding author), Ben Gurion Univ Negev, Fac Hlth Sci, Beer Sheva, Israel.
EM abufreha@yahoo.de
RI Abu Freha, Naim/AAJ-9585-2020; Abu Tailakh, Muhammad/Z-4608-2019
OI Abu Tailakh, Muhammad/0000-0003-3770-0927
CR Abo Rabia Y, 2016, AR MED ASS ANN M 30
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[Anonymous], HIGHL HLTH ISR 2016
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NR 26
TC 5
Z9 5
U1 2
U2 8
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1557-1912
EI 1557-1920
J9 J IMMIGR MINOR HEALT
JI J. Immigr. Minor. Health
PD OCT
PY 2022
VL 24
IS 5
BP 1122
EP 1128
DI 10.1007/s10903-021-01263-y
EA AUG 2021
PG 7
WC Public, Environmental & Occupational Health
WE Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA 3W5DE
UT WOS:000690728100002
PM 34453643
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Lee, NK
Kim, S
Kim, DU
Seo, HI
Kim, HS
Jo, HJ
Kim, TU
AF Lee, Nam Kyung
Kim, Suk
Kim, Dong Uk
Seo, Hyung I. I.
Kim, Hyun Sung
Jo, Hong Jae
Kim, Tae Un
TI Diffusion-weighted magnetic resonance imaging for non-neoplastic
conditions in the hepatobiliary and pancreatic regions: pearls and
potential pitfalls in imaging interpretation
SO ABDOMINAL IMAGING
LA English
DT Article
DE Diffusion-weighted magnetic resonance imaging; Liver diseases; Bile
tract diseases; Pancreatic diseases
ID FORMING CHRONIC-PANCREATITIS; INTRAPANCREATIC ACCESSORY SPLEEN; FOCAL
EOSINOPHILIC INFILTRATION; XANTHOGRANULOMATOUS CHOLECYSTITIS; AUTOIMMUNE
PANCREATITIS; GALLBLADDER CANCER; HEPATIC-ABSCESS; MRI FINDINGS;
PORTAL-VEIN; DIFFERENTIATION
AB Potentially, diffusion-weighted magnetic resonance imaging (DWI) can assess the functional information on concerning the status of tissue cellularity, because increased cellularity is associated with impeded diffusion. DWI in the hepatobiliary and pancreatic regions has demonstrated the usefulness to detect malignant lesions and differentiate them from benign lesions. However, it has been shown more recently that there is some overlap in ADC values for benign and malignant neoplasms. Moreover, some non-neoplastic lesions in the hepatobiliary and pancreatic regions exhibit restricted diffusion on DWI, because of pus, inflammation, or high cellularity. Focal eosinophilic liver disease, hepatic inflammatory myofibroblastic tumor, granulomatous liver disease, acute cholecystitis, xanthogranulomatous cholecystitis, focal pancreatitis, or autoimmune pancreatitis frequently exhibit restricted diffusion on DWI, which may be confused with malignancy in the hepatobiliary and pancreatic regions. Thus, DWI should not be interpreted in isolation, but in conjunction with other conventional images, to avoid the diagnostic pitfalls of DWI. Nevertheless, the presence of diffusion restriction in the non-neoplastic lesions sometimes provides additional information regarding the diagnosis, in problematic patients where conventional images have yielded equivocal findings. DWI may help differentiate hepatic abscess from malignant necrotic tumors, gallbladder empyema from dense bile or sludge in the gallbladder, and pylephlebitis from bland thrombosis in the portal vein. Therefore, knowledge of DWI findings to conventional imaging findings of diffusion-restricted non-neoplastic conditions in the hepatobiliary and pancreatic regions helps establishing a correct diagnosis.
C1 [Lee, Nam Kyung; Kim, Suk] Pusan Natl Univ, Pusan Natl Univ Hosp, Dept Radiol, Biomed Res Inst,Sch Med, Pusan 602739, South Korea.
[Kim, Dong Uk] Pusan Natl Univ, Dept Internal Med, Biomed Res Inst, Pusan Natl Univ Hosp,Sch Med, Pusan 602739, South Korea.
[Seo, Hyung I. I.; Kim, Hyun Sung; Jo, Hong Jae] Pusan Natl Univ, Pusan Natl Univ Hosp, Dept Surg, Biomed Res Inst,Sch Med, Pusan 602739, South Korea.
[Kim, Tae Un] Pusan Natl Univ, Dept Radiol, Yangsan Pusan Natl Univ Hosp, Sch Med, Yangsan 626770, South Korea.
C3 Pusan National University; Pusan National University Hospital; Pusan
National University; Pusan National University Hospital; Pusan National
University; Pusan National University Hospital; Pusan National
University; Pusan National University Hospital
RP Kim, S (corresponding author), Pusan Natl Univ, Pusan Natl Univ Hosp, Dept Radiol, Biomed Res Inst,Sch Med, 179 Gudeok Ro, Pusan 602739, South Korea.
EM kimsuk@medimail.co.kr
RI Kim, Ik-Sang/J-5425-2012
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NR 52
TC 24
Z9 25
U1 0
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-8925
EI 1432-0509
J9 ABDOM IMAGING
JI Abdom. Imaging
PD MAR
PY 2015
VL 40
IS 3
BP 643
EP 662
DI 10.1007/s00261-014-0235-5
PG 20
WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
GA CB1CJ
UT WOS:000349363900023
PM 25216848
DA 2025-01-07
ER
PT J
AU Seki, E
Schwabe, RF
AF Seki, Ekihiro
Schwabe, Robert F.
TI Hepatic Inflammation and Fibrosis: Functional Links and Key Pathways
SO HEPATOLOGY
LA English
DT Review
ID NF-KAPPA-B; STELLATE CELL ACTIVATION; SINUSOIDAL ENDOTHELIAL-CELLS;
CHRONIC VIRAL-HEPATITIS; CHRONIC LIVER-INJURY; GROWTH-FACTOR-BETA;
NONALCOHOLIC STEATOHEPATITIS; NATURAL-KILLER; INTERFERON-GAMMA; T-CELLS
AB Inflammation is one of the most characteristic features of chronic liver disease of viral, alcoholic, fatty, and autoimmune origin. Inflammation is typically present in all disease stages and associated with the development of fibrosis, cirrhosis, and hepatocellular carcinoma. In the past decade, numerous studies have contributed to improved understanding of the links between hepatic inflammation and fibrosis. Here, we review mechanisms that link inflammation with the development of liver fibrosis, focusing on the role of inflammatory mediators in hepatic stellate cell (HSC) activation and HSC survival during fibrogenesis and fibrosis regression. We will summarize the contributions of different inflammatory cells, including hepatic macrophages, T and B lymphocytes, natural killer cells and platelets, as well as key effectors, such as cytokines, chemokines, and damage-associated molecular patterns. Furthermore, we will discuss the relevance of inflammatory signaling pathways for clinical liver disease and for the development of antifibrogenic strategies. (Hepatology 2015;61:1066-1079)
C1 [Seki, Ekihiro] Univ Calif San Diego, Sch Med, Dept Med, La Jolla, CA 92093 USA.
[Seki, Ekihiro] Univ Calif San Diego, Sch Med, Dept Surg, La Jolla, CA 92093 USA.
[Schwabe, Robert F.] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
[Schwabe, Robert F.] Columbia Univ Coll Phys & Surg, Inst Human Nutr, New York, NY 10032 USA.
C3 University of California System; University of California San Diego;
University of California System; University of California San Diego;
Columbia University; Columbia University
RP Schwabe, RF (corresponding author), Columbia Univ Coll Phys & Surg, Dept Med, Russ Berrie Pavil,Room 415,1150 St Nicholas Ave, New York, NY 10032 USA.
EM ekseki@ucsd.edu; rfs2102@cumc.columbia.edu
RI Schwabe, Robert/AAY-6506-2021; Seki, Ekihiro/K-2481-2016
FU National Institutes of Health (NIH) [5R01AA02017204, 5R01DK085252,
5P42ES010337]; NIH [5R01AA020211, 1U01AA021912, 5R01DK076920]
FX E.S. was supported by National Institutes of Health (NIH) grants
5R01AA02017204, 5R01DK085252, and 5P42ES010337. R.F.S. was supported by
NIH grants 5R01AA020211, 1U01AA021912, and 5R01DK076920.
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NR 109
TC 700
Z9 752
U1 6
U2 280
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD MAR
PY 2015
VL 61
IS 3
BP 1066
EP 1079
DI 10.1002/hep.27332
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CC2BS
UT WOS:000350150300036
PM 25066777
OA Green Accepted
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Gupta, SC
Kismali, G
Aggarwal, BB
AF Gupta, Subash C.
Kismali, Gorkem
Aggarwal, Bharat B.
TI Curcumin, a component of turmeric: From farm to pharmacy
SO BIOFACTORS
LA English
DT Review
DE autophagy; cancer stem cells; curcumin; microRNA
ID CANCER STEM-CELLS; ADVANCED PANCREATIC-CANCER; EPITHELIAL
OVARIAN-CANCER; LUNG ADENOCARCINOMA CELLS; I CLINICAL-TRIAL;
COLORECTAL-CANCER; BRAIN-TUMORS; ORAL BIOAVAILABILITY; MIR-21
EXPRESSION; MOLECULAR TARGETS
AB Curcumin, an active polyphenol of the golden spice turmeric, is a highly pleiotropic molecule with the potential to modulate the biological activity of a number of signaling molecules. Traditionally, this polyphenol has been used in Asian countries to treat such human ailments as acne, psoriasis, dermatitis, and rash. Recent studies have indicated that curcumin can target newly identified signaling pathways including those associated with microRNA, cancer stem cells, and autophagy. Extensive research from preclinical and clinical studies has delineated the molecular basis for the pharmaceutical uses of this polyphenol against cancer, pulmonary diseases, neurological diseases, liver diseases, metabolic diseases, autoimmune diseases, cardiovascular diseases, and numerous other chronic diseases. Multiple studies have indicated the safety and efficacy of curcumin in numerous animals including rodents, monkeys, horses, rabbits, and cats and have provided a solid basis for evaluating its safety and efficacy in humans. To date, more than 65 human clinical trials of curcumin, which included more than 1000 patients, have been completed, and as many as 35 clinical trials are underway. Curcumin is now used as a supplement in several countries including the United States, India, Japan, Korea, Thailand, China, Turkey, South Africa, Nepal, and Pakistan. In this review, we provide evidence for the pharmaceutical uses of curcumin for various diseases. (c) 2013 BioFactors, 39(1):213, 2013
C1 [Gupta, Subash C.; Kismali, Gorkem; Aggarwal, Bharat B.] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Cytokine Res Lab, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Aggarwal, BB (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Cytokine Res Lab, Houston, TX 77030 USA.
EM aggarwal@mdanderson.org
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NR 128
TC 300
Z9 326
U1 2
U2 150
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0951-6433
EI 1872-8081
J9 BIOFACTORS
JI Biofactors
PD JAN-FEB
PY 2013
VL 39
IS 1
SI SI
BP 2
EP 13
DI 10.1002/biof.1079
PG 12
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 093RX
UT WOS:000315210600002
PM 23339055
DA 2025-01-07
ER
PT J
AU Bergers, LIJC
Reijnders, CMA
van den Broek, LJ
Spiekstra, SW
de Gruijl, TD
Weijers, EM
Gibbs, S
AF Bergers, Lambert I. J. C.
Reijnders, Christianne M. A.
van den Broek, Lenie J.
Spiekstra, Sander W.
de Gruijl, Tanja D.
Weijers, Ester M.
Gibbs, Susan
TI Immune-competent human skin disease models
SO DRUG DISCOVERY TODAY
LA English
DT Review
ID REGULATORY T-CELLS; IN-VITRO; EPIDERMOLYSIS-BULLOSA; ANIMAL-MODELS;
MELANOMA-CELLS; MICROFLUIDIC PLATFORM; LANGERHANS CELLS; MOUSE MODELS;
HUMAN LIVER; VITILIGO
AB All skin diseases have an underlying immune component. Owing to differences in animal and human immunology, the majority of drugs fail in the preclinical or clinical testing phases. Therefore animal alternative methods that incorporate human immunology into in vitro skin disease models are required to move the field forward. This review summarizes the progress, using examples from fibrosis, autoimmune diseases, psoriasis, cancer and contact allergy. The emphasis is on co-cultures and 3D organotypic models. Our conclusion is that current models are inadequate and future developments with immune-competent skin-on-chip models based on induced pluripotent stem cells could provide a next generation of skin models for drug discovery and testing.
C1 [Bergers, Lambert I. J. C.; Reijnders, Christianne M. A.; van den Broek, Lenie J.; Spiekstra, Sander W.; Weijers, Ester M.; Gibbs, Susan] Vrije Univ Amsterdam Med Ctr, Dept Dermatol, Amsterdam, Netherlands.
[de Gruijl, Tanja D.] Vrije Univ Amsterdam Med Ctr, Dept Med Oncol, Amsterdam, Netherlands.
[Gibbs, Susan] Univ Amsterdam, Dept Oral Cell Biol, Acad Ctr Dent Amsterdam, Amsterdam, Netherlands.
[Gibbs, Susan] Vrije Univ Amsterdam, Amsterdam, Netherlands.
C3 Vrije Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER; Vrije
Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER; University of
Amsterdam; Vrije Universiteit Amsterdam; Academic Center for Dentistry
Amsterdam; Vrije Universiteit Amsterdam
RP Gibbs, S (corresponding author), Vrije Univ Amsterdam Med Ctr, Dept Dermatol, Amsterdam, Netherlands.; Gibbs, S (corresponding author), Univ Amsterdam, Dept Oral Cell Biol, Acad Ctr Dent Amsterdam, Amsterdam, Netherlands.; Gibbs, S (corresponding author), Vrije Univ Amsterdam, Amsterdam, Netherlands.
EM s.gibbs@vumc.nl
RI Bergers, Lambert/J-2734-2019; spiekstra, sw/J-8957-2012
OI spiekstra, sw/0000-0002-8178-5318; Bergers, Lambert/0000-0001-7411-3014
FU Dutch Government ZonMW (MKMD project) [40-42600-98-010]; Netherlands
Initiative for Regenerative Medicine (NIRM); EuroStars project [8855]
FX This study was in part supported by: the Dutch Government ZonMW (MKMD
project number 40-42600-98-010); by a grant of The Netherlands
Initiative for Regenerative Medicine (NIRM); and by a EuroStars project
(8855).
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NR 115
TC 35
Z9 37
U1 1
U2 63
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6446
EI 1878-5832
J9 DRUG DISCOV TODAY
JI Drug Discov. Today
PD SEP
PY 2016
VL 21
IS 9
BP 1479
EP 1488
DI 10.1016/j.drudis.2016.05.008
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DY1OE
UT WOS:000384863500015
PM 27265772
DA 2025-01-07
ER
PT J
AU Jiang, P
Li, XP
AF Jiang, Ping
Li, Xiaopeng
TI Regulatory Mechanism of lncRNAs in M1/M2 Macrophages Polarization in the
Diseases of Different Etiology
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE long noncoding RNAs; regulation; macrophages; polarization; diseases
ID TUMOR-ASSOCIATED MACROPHAGES; LONG NONCODING RNAS; M2 POLARIZATION;
HEPATOCELLULAR-CARCINOMA; CELL-PROLIFERATION; IN-VIVO; CANCER;
INFLAMMATION; METASTASIS; ACTIVATION
AB Precise expression and regulation of genes in the immune system is important for organisms to produce strong immunity towards pathogens and limit autoimmunity. In recent years, an increasing number of studies has shown that long noncoding RNAs (lncRNAs) are closely related to immune function and can participate in regulating immune responses by regulating immune cell differentiation, development, and function. As immune cells, the polarization response of macrophages (M phi s) plays an important role in immune function and inflammation. LncRNAs can regulate the phenotypic polarization of M phi s to M1 or M2 through various mechanisms; promote pro-inflammatory or anti-inflammatory effects; and participate in the pathogenesis of cancers, inflammatory diseases, infections, metabolic diseases, and autoimmune diseases. In addition, it is important to explore the regulatory mechanisms of lncRNAs on the dynamic transition between different M phi s phenotypes. Thus, the regulatory role of lncRNAs in the polarization of M phi s and their mechanism are discussed in this review.
C1 [Jiang, Ping] Shanghai Univ Tradit Chinese Med, Guanghua Clin Med Coll, Shanghai, Peoples R China.
[Jiang, Ping] Shanghai Univ Tradit Chinese Med, Shanghai Guanghua Hosp Integrated Tradit Chinese, Dept Rheumatol, Shanghai, Peoples R China.
[Li, Xiaopeng] Rizhao Hosp Tradit Chinese Med, Dept Neurol, Rizhao, Peoples R China.
[Li, Xiaopeng] Shandong Univ Tradit Chinese Med, Integrated Tradit Chinese & Western Med, Jinan, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine; Shanghai University
of Traditional Chinese Medicine; Shandong University of Traditional
Chinese Medicine
RP Li, XP (corresponding author), Rizhao Hosp Tradit Chinese Med, Dept Neurol, Rizhao, Peoples R China.; Li, XP (corresponding author), Shandong Univ Tradit Chinese Med, Integrated Tradit Chinese & Western Med, Jinan, Peoples R China.
EM 1150635695@qq.com
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NR 131
TC 12
Z9 13
U1 4
U2 17
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 25
PY 2022
VL 13
AR 835932
DI 10.3389/fimmu.2022.835932
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA YV3WR
UT WOS:000752662000001
PM 35145526
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Medina, J
Moreno-Otero, R
AF Medina, J
Moreno-Otero, R
TI Pathophysiological basis for antioxidant therapy in chronic liver
disease
SO DRUGS
LA English
DT Review
ID NITRIC-OXIDE SYNTHASE; TUMOR-NECROSIS-FACTOR; CHRONIC HEPATITIS-C;
PRIMARY BILIARY-CIRRHOSIS; ADENOSYL-L-METHIONINE; HUMAN
HEPATOCELLULAR-CARCINOMA; URSODEOXYCHOLIC ACID PROTECTS; VITAMIN-E
SUPPLEMENTATION; INDUCED OXIDATIVE STRESS; CHRONIC VIRAL-HEPATITIS
AB Oxidative stress is a common pathogenetic mechanism contributing to initiation and progression of hepatic damage in a variety of liver disorders. Cell damage occurs when there is an excess of reactive species derived from oxygen and nitrogen, or a defect of antioxidant molecules. Experimental research on the delicately regulated molecular strategies whereby cells control the balance between oxidant and antioxidant molecules has progressed in recent years. On the basis of this evidence, antioxidants represent a logical therapeutic strategy for the treatment of chronic liver disease. Clinical studies with large numbers of patients have not yet been performed. However, results from several pilot trials support this concept and indicate that it may be worth performing multicentre studies, particularly combining antioxidants with anti-inflammatory and/or antiviral therapy. Oxidative stress plays a pathogenetic role in liver diseases such as alcoholic liver disease, chronic viral hepatitis, autoimmune liver diseases and non-alcoholic steatohepatitis. The use of antioxidants (e.g. S-adenosylmethionine [SAMe; ademetionine], tocopherol [vitamin E], polyenylphosphatidylcholine or silymarin) has already shown promising results in some of these pathologies.
C1 Univ Autonoma Madrid, Hosp Univ Princesa, Unidad Hepatol Planta 3, E-28006 Madrid, Spain.
C3 Autonomous University of Madrid; Hospital de La Princesa
RP Univ Autonoma Madrid, Hosp Univ Princesa, Unidad Hepatol Planta 3, Diego Leon 62, E-28006 Madrid, Spain.
EM rmoreno.hlpr@salud.madrid.org
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NR 137
TC 148
Z9 173
U1 1
U2 15
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 0012-6667
EI 1179-1950
J9 DRUGS
JI Drugs
PY 2005
VL 65
IS 17
BP 2445
EP 2461
DI 10.2165/00003495-200565170-00003
PG 17
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA 998EL
UT WOS:000234301300003
PM 16296871
DA 2025-01-07
ER
PT J
AU Filková, M
Haluzík, M
Gay, S
Senolt, L
AF Filkova, Maria
Haluzik, Martin
Gay, Steffen
Senolt, Ladislav
TI The role of resistin as a regulator of inflammation: Implications for
various human pathologies
SO CLINICAL IMMUNOLOGY
LA English
DT Review
DE Resistin; Inflammation; Obesity; Cancer; Molecular pathway
ID FATTY LIVER-DISEASE; HEPATIC INSULIN-RESISTANCE; CHRONIC KIDNEY-DISEASE;
SERUM RESISTIN; ADIPOSE-TISSUE; RHEUMATOID-ARTHRITIS; BOWEL-DISEASE;
IN-VITRO; RECOMBINANT RESISTIN; SYNOVIAL-FLUID
AB Resistin was originally described as an adipocyte-secreted peptide that induced insulin resistance in rodents. Increasing evidence indicates its important regulatory roles in various biological processes, including several inflammatory diseases. Further studies have shown that resistin in humans, in contrast to its production by adipocytes in mice, is synthesized predominantly by mononuclear cells both within and outside adipose tissue. Possible roles for resistin in obesity-related subclinical. inflammation, atherosclerosis and cardiovascular disease, non-alcoholic fatty liver disease, rheumatic diseases, malignant tumors, asthma, inflammatory bowel disease, and chronic kidney disease have already been demonstrated. In addition, resistin can modulate several molecular pathways involved in metabolic, inflammatory, and autoimmune diseases. In this review, current knowledge about the functions and pathophysiological implications of resistin in different human pathologies is summarized, although there is a significant lack of firm evidence regarding the specific role resistin plays in the "orchestra" of the numerous mediators of inflammation. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Filkova, Maria; Senolt, Ladislav] Charles Univ Prague, Fac Med 1, Dept Rheumatol, Inst Rheumatol, Slupi 4, Prague 12850 2, Czech Republic.
[Filkova, Maria; Senolt, Ladislav] Charles Univ Prague, Fac Med 1, Dept Rheumatol, Connect Tissue Res Lab, Prague 12850 2, Czech Republic.
[Haluzik, Martin] Charles Univ Prague, Fac Med 1, Dept Med 3, Prague 12850 2, Czech Republic.
[Gay, Steffen] Univ Zurich Hosp, Ctr Expt Rheumatol, CH-8091 Zurich, Switzerland.
C3 Charles University Prague; Institute of Rheumatology; Charles University
Prague; Charles University Prague; University of Zurich; University
Zurich Hospital
RP Senolt, L (corresponding author), Charles Univ Prague, Fac Med 1, Dept Rheumatol, Inst Rheumatol, Slupi 4, Prague 12850 2, Czech Republic.
EM seno@revma.cz
RI Filkova, Maria/M-9307-2017; Haluzik, Martin/I-8190-2017; Senolt,
Ladislav/O-6097-2017
OI Filkova, Maria/0000-0002-8488-9227; Haluzik, Martin/0000-0002-0201-6888;
Senolt, Ladislav/0000-0001-5500-7312
FU MH CR [00023728, NS/10614-3]
FX This work was supported by MH CR - research project No. 00023728 and
grant project No. NS/10614-3.
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NR 142
TC 331
Z9 360
U1 2
U2 23
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
EI 1521-7035
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD NOV
PY 2009
VL 133
IS 2
BP 157
EP 170
DI 10.1016/j.clim.2009.07.013
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 511LX
UT WOS:000271167800002
PM 19740705
DA 2025-01-07
ER
PT J
AU Vinay, DS
Kwon, BS
AF Vinay, Dass S.
Kwon, Byoung S.
TI Therapeutic potential of anti-CD137 (4-1BB) monoclonal antibodies
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
DE 4-1BB; autoimmune disease; cancer; T cells; therapy
ID REGULATORY T-CELLS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
MERCURY-INDUCED AUTOIMMUNITY; IL-12 GENE-THERAPY; IN-VIVO; COMBINATION
THERAPY; ANTITUMOR IMMUNITY; CLONAL EXPANSION; TUMOR XENOGRAFTS;
ANTI-4-1BB SCFV
AB Introduction: 4-1BB (CD137) is an important T-cell stimulating molecule. The 4-1BB mAb or its variants have shown remarkable therapeutic activity against autoimmunity, viral infections, and cancer. Antibodies to 4-1BB have recently entered clinical trials for the treatment of cancer with favorable toxicity profile. In this article, we present a review documenting the efficacy and pitfalls of 4-1BB therapy.Areas covered: An extensive literature search has been made on 4-1BB, spanning two decades, and a comprehensive report is presented here highlighting the origins, biological effects, therapeutic potential, and mechanistic basis of targeting 4-1BB as well as the side effects associated with such therapy.Expert opinion: Research so far indicates that 4-1BB is highly protective against various pathological conditions including cancer. However, a few important side effects of 4-1BB therapy such as liver toxicity, thrombocytopenia, anemia, and suppressive effects on certain immune competent cells should be taken into consideration before it is used for human therapy.
C1 [Vinay, Dass S.; Kwon, Byoung S.] Tulane Univ, Dept Med, Sect Clin Immunol Allergy & Rheumatol, New Orleans, LA 70112 USA.
[Kwon, Byoung S.] Natl Canc Ctr, Cell & Immunobiol, Goyang 410769, South Korea.
[Kwon, Byoung S.] Natl Canc Ctr, R&D Ctr Canc Therapeut, Goyang 410769, South Korea.
C3 Tulane University; National Cancer Center - Korea (NCC); National Cancer
Center - Korea (NCC)
RP Kwon, BS (corresponding author), Tulane Univ, Dept Med, Sect Clin Immunol Allergy & Rheumatol, New Orleans, LA 70112 USA.; Kwon, BS (corresponding author), Natl Canc Ctr, Cell & Immunobiol, Goyang 410769, South Korea.; Kwon, BS (corresponding author), Natl Canc Ctr, R&D Ctr Canc Therapeut, Goyang 410769, South Korea.
EM bskwon@ncc.re.kr
FU National Cancer Center, Korea [NCC-1310430-2]; National Research
Foundation of Korea [NRF-2005-0093837]; Korea Drug Development Fund
[KDDF-201408-11]; Korea Institute for Advancement of Technology under
their International Collaborative Research and Development Program
[KIAT-N0000901]
FX The authors were supported by grants from the National Cancer Center,
Korea (NCC-1310430-2), the National Research Foundation of Korea
(NRF-2005-0093837), the Korea Drug Development Fund (KDDF-201408-11),
and the Korea Institute for Advancement of Technology under their
International Collaborative Research and Development Program
(KIAT-N0000901). The authors have no other relevant affiliations or
financial involvement with any organization or entity with a financial
interest in or financial conflict with the subject matter or materials
discussed in the manuscript apart from those disclosed.
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NR 109
TC 29
Z9 42
U1 0
U2 21
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1472-8222
EI 1744-7631
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD MAR 3
PY 2016
VL 20
IS 3
BP 361
EP 373
DI 10.1517/14728222.2016.1091448
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DD8GU
UT WOS:000370165000001
PM 26428392
DA 2025-01-07
ER
PT J
AU Brito-Zerón, P
Acar-Denizli, N
Sisó-Almirall, A
Bosch, X
Hernández, F
Vilanova, S
Villalta, M
Kostov, B
Paradela, M
Sanchez, M
Ramírez, J
Muxí, A
Berruezo, A
Galceran-Chaves, C
Xaubet, A
Agustí, C
Sellarés, J
Ramos-Casals, M
AF Brito-Zeron, Pilar
Acar-Denizli, Nihan
Siso-Almirall, Antoni
Bosch, Xavier
Hernandez, Fernanda
Vilanova, Sergi
Villalta, Mireia
Kostov, Belchin
Paradela, Marina
Sanchez, Marcelo
Ramirez, Jose
Muxi, Africa
Berruezo, Antonio
Galceran-Chaves, Celeste
Xaubet, Antoni
Agusti, Carles
Sellares, Jacobo
Ramos-Casals, Manuel
TI The Burden of Comorbidity and Complexity in Sarcoidosis: Impact of
Associated Chronic Diseases
SO LUNG
LA English
DT Article
DE Sarcoidosis; Comorbidity; Complexity; Clinical Risk Groups
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; CANCER-RISK; MORTALITY; COHORT;
HOSPITALIZATION; METAANALYSIS; INVOLVEMENT; PHENOTYPES; MORBIDITY;
HEPATITIS
AB To evaluate comorbidity, complexity and poor outcomes in patients with sarcoidosis and to compare those scores with a control group.
218 consecutive patients were diagnosed with sarcoidosis according to the ATS/ERS/WASOG criteria; extrathoracic involvement was evaluated using the 2014 WASOG organ assessment instrument. Sarcoidosis patients were compared with an age- and gender-matched control group of primary care outpatients without sarcoidosis. Comorbidities were assessed retrospectively using the Charlson Comorbidity Index (CCI); complexity was evaluated according to the classification into Clinical Risk Groups (CRG) and severity levels.
The cohort included 142 women and 76 men; the mean age was 47.1 years at diagnosis of sarcoidosis and 55.9 years at the last visit. Patients with a CCI > 1 had a higher frequency of calcium/vitamin D abnormalities (p < 0.001), kidney involvement (p = 0.005) and a higher mortality rate (p < 0.001) compared with patients with a CCI <= 1. Patients with a CRG >= 6 had a higher frequency of extrathoracic involvement (p = 0.039), calcium/vitamin D abnormalities (p = 0.019) and treatment with glucocorticoids (p = 0.032) compared with patients with a CRG < 6. 11% patients died after a mean follow-up of 102.3 months. Country of birth, kidney involvement and extrathoracic disease were significantly associated with death. Patients with sarcoidosis had a higher frequency of liver (p < 0.001), pulmonary (p = 0.002) and autoimmune disease (p = 0.011) and cancer (p = 0.007) compared with the control group.
We found higher rates of comorbidity and complexity in patients with sarcoidosis compared with a control group. Liver, pulmonary, autoimmune and neoplastic diseases were the main comorbidities found in patients with sarcoidosis.
C1 [Brito-Zeron, Pilar; Ramos-Casals, Manuel] Hosp Clin Barcelona, Inst Invest Biomed August Pi & Sunyer IDIBAPS, Dept Syst Autoimmune Dis, Lab Syst Autoimmune Dis Josep Font,CELLEX,ICMID, C Villarroel 170, Barcelona 08036, Spain.
[Brito-Zeron, Pilar] Hosp CIMA Sanitas, Dept Internal Med, Autoimmune Dis Unit, Barcelona, Spain.
[Acar-Denizli, Nihan] Mimar Sinan Fine Arts Univ, Fac Sci & Letters, Dept Stat, Istanbul, Turkey.
[Siso-Almirall, Antoni; Vilanova, Sergi; Villalta, Mireia; Kostov, Belchin] CAPSBE, Primary Healthcare Transversal Res Grp, Primary Care Ctr Les Corts, IDIBAPS, Barcelona, Spain.
[Bosch, Xavier] Hosp Clin Barcelona, Dept Internal Med, Quick Diag Unit, ICMID, Barcelona, Spain.
[Hernandez, Fernanda; Xaubet, Antoni; Agusti, Carles; Sellares, Jacobo] Hosp Clin Barcelona, Dept Pneumol, ICR, Barcelona, Spain.
[Paradela, Marina] Hosp Clin Barcelona, Dept Thorac Surg, Barcelona, Spain.
[Sanchez, Marcelo] Hosp Clin Barcelona, Dept Radiol, Barcelona, Spain.
[Ramirez, Jose] Hosp Clin Barcelona, Dept Pathol, Barcelona, Spain.
[Muxi, Africa] Hosp Clin Barcelona, Dept Nucl Med, Barcelona, Spain.
[Berruezo, Antonio] Hosp Clin Barcelona, Dept Cardiol, ICCV, Barcelona, Catalonia, Spain.
[Galceran-Chaves, Celeste] Hosp Clin Barcelona, Dept Child & Adolescent Psychiat & Psychol, Barcelona, Spain.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; Mimar
Sinan Guzel Sanatlar University; University of Barcelona; Hospital
Clinic de Barcelona; IDIBAPS; University of Barcelona; Hospital Clinic
de Barcelona; University of Barcelona; Hospital Clinic de Barcelona;
University of Barcelona; Hospital Clinic de Barcelona; University of
Barcelona; Hospital Clinic de Barcelona; University of Barcelona;
Hospital Clinic de Barcelona; University of Barcelona; Hospital Clinic
de Barcelona; University of Barcelona; Hospital Clinic de Barcelona;
University of Barcelona; Hospital Clinic de Barcelona
RP Ramos-Casals, M (corresponding author), Hosp Clin Barcelona, Inst Invest Biomed August Pi & Sunyer IDIBAPS, Dept Syst Autoimmune Dis, Lab Syst Autoimmune Dis Josep Font,CELLEX,ICMID, C Villarroel 170, Barcelona 08036, Spain.
EM mramos@clinic.ub.es
RI Ramos-Casals, Manuel/IUQ-6082-2023; Acar-Denizli, Nihan/JBJ-7729-2023;
Sellares, Jacobo/AAN-3250-2020; Bosch Genover, Xavier/E-7890-2014;
Acar-Denizli, Nihan/D-5954-2019
OI Ramirez, Jose/0000-0002-7833-1374; Sellares, Jacobo/0000-0001-6047-1670;
Siso Almirall, Antoni/0000-0001-9832-2689; Bosch Genover,
Xavier/0000-0002-0133-1587; Acar-Denizli, Nihan/0000-0002-0012-8632;
Ramos-Casals, Manuel/0000-0001-5709-6734; Vilanova Rotllan,
Sergi/0000-0003-4050-7335; Kostov, Belchin/0000-0002-2126-3892
FU Grants Fondo de Investigaciones Sanitarias (MRC) [INT15/00085]; "Ajut
per a la Recerca Josep Font" (PBZ, Hospital Clinic-Barcelona)
FX This study was supported by Grants Fondo de Investigaciones Sanitarias
(MRC, INT15/00085) and "Ajut per a la Recerca Josep Font" (PBZ, Hospital
Clinic-Barcelona 2012). The authors wish to thank David Buss for his
editorial assistance.
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NR 46
TC 41
Z9 42
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0341-2040
EI 1432-1750
J9 LUNG
JI Lung
PD APR
PY 2018
VL 196
IS 2
BP 239
EP 248
DI 10.1007/s00408-017-0076-4
PG 10
WC Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Respiratory System
GA FZ5JT
UT WOS:000427629200015
PM 29230534
DA 2025-01-07
ER
PT J
AU Silva, LD
Rocha, AMC
Rocha, GA
de Moura, SB
Rocha, MMNP
Dani, R
de Melo, FF
Guerra, JB
de Castro, LPF
Mendes, GS
Ferrari, TCD
Lima, AS
Queiroz, DMM
AF Silva, Luciana Diniz
Camargos Rocha, Andreia Maria
Rocha, Gifone Aguiar
de Moura, Silvia Beleza
Negreiros Pinto Rocha, Marcia Maria
Dani, Renato
de Melo, Fabricio Freire
Guerra, Juliana Becattini
Fonseca de Castro, Lucia Porto
Mendes, Guilherme Santiago
de Abreu Ferrari, Teresa Cristina
Lima, Agnaldo Soares
Magalhaes Queiroz, Dulciene Maria
TI The presence of Helicobacter pylori in the liver depends on the
Th1, Th17 and Treg cytokine profile of the patient
SO MEMORIAS DO INSTITUTO OSWALDO CRUZ
LA English
DT Article
DE Helicobacter pylori; liver diseases; IL-10; IL-17; IFN-gamma
ID HEPATOCELLULAR-CARCINOMA; CHRONIC HEPATITIS; DISEASE; INFECTION;
ASSOCIATION; CIRRHOSIS
AB The hypothesis that Helicobacter might be a risk factor for human liver diseases has arisen after the detection of Helicobacter DNA in hepatic tissue of patients with hepatobiliary diseases. Nevertheless, no explanation that justifies the presence of the bacterium in the human liver has been proposed. We evaluated the presence of Helicobacter in the liver of patients with hepatic diseases of different aetiologies. We prospectively evaluated 147 patients (106 with primary hepatic diseases and 41 with hepatic metastatic tumours) and 20 liver donors as controls. Helicobacter species were investigated in the liver by culture and specific 16S rDNA nested-polymerase chain reaction followed by sequencing. Serum and hepatic levels of representative cytokines of T regulatory cell, T helper (Th) 1 and Th17 cell lineages were determined using enzyme linked immunosorbent assay. The data were evaluated using logistic models. Detection of Helicobacter pylori DNA in the liver was independently associated with hepatitis B virus/hepatitis C virus, pancreatic carcinoma and a cytokine pattern characterised by high interleukin (IL)-10, low/absent interferon-gamma and decreased IL-17A concentrations (p < 10(-3)). The bacterial DNA was never detected in the liver of patients with alcoholic cirrhosis and autoimmune hepatitis that are associated with Th1/Th17 polarisation. H. pylori may be observed in the liver of patients with certain hepatic and pancreatic diseases, but this might depend on the patient cytokine profile.
C1 [Silva, Luciana Diniz; Camargos Rocha, Andreia Maria; Rocha, Gifone Aguiar; Negreiros Pinto Rocha, Marcia Maria; de Melo, Fabricio Freire; Guerra, Juliana Becattini; Magalhaes Queiroz, Dulciene Maria] Univ Fed Minas Gerais, Lab Pesquisa Bacteriol, Belo Horizonte, MG, Brazil.
[Fonseca de Castro, Lucia Porto] Univ Fed Minas Gerais, Dept Anat Patol, Belo Horizonte, MG, Brazil.
[de Abreu Ferrari, Teresa Cristina; Lima, Agnaldo Soares] Univ Fed Minas Gerais, Fac Med, Hosp Clin, Serv Transplante, Belo Horizonte, MG, Brazil.
[de Moura, Silvia Beleza; de Melo, Fabricio Freire] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Microbiol, Belo Horizonte, MG, Brazil.
[Dani, Renato; Mendes, Guilherme Santiago] Hosp Governador Israel Pinheiro, Inst Previdencia Servidores Estado Minas Gerais, Belo Horizonte, MG, Brazil.
C3 Universidade Federal de Minas Gerais; Universidade Federal de Minas
Gerais; Universidade Federal de Minas Gerais; Universidade Federal de
Minas Gerais
RP Queiroz, DMM (corresponding author), Univ Fed Minas Gerais, Lab Pesquisa Bacteriol, Belo Horizonte, MG, Brazil.
EM dqueiroz@medicina.ufmg.br
RI Silva, LD/N-2047-2019; de Melo, Fabrício/AAN-5517-2020; Queiroz,
Dulciene/AAU-9386-2020; Lima, Agnaldo/F-7452-2011; Ferrari, Teresa
Cristina de Abreu/D-5530-2014; Rocha, Gifone/N-6913-2018; silva, luciana
diniz silva/O-1867-2013
OI Ferrari, Teresa Cristina de Abreu/0000-0001-9459-2294; Queiroz,
Dulciene/0000-0003-1334-9423; Freire de Melo,
Fabricio/0000-0002-5680-2753; Rocha, Gifone/0000-0002-1858-3166; Lima,
Agnaldo Soares/0000-0001-6421-3062; silva, luciana diniz
silva/0000-0003-0061-7361
FU CNPq; FAPEMIG; CAPES; European Union [INCO-CT-2006-032136]
FX Financial support: CNPq, FAPEMIG, CAPES, Sixth Framework Program of the
European Union (Project CONTENT; INCO-CT-2006-032136) (to DMMQ)
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NR 22
TC 12
Z9 15
U1 0
U2 5
PU FUNDACO OSWALDO CRUZ
PI RIO DE JANEIRO, RJ
PA AV BRASIL 4365, 21045-900 RIO DE JANEIRO, RJ, BRAZIL
SN 0074-0276
J9 MEM I OSWALDO CRUZ
JI Mem. Inst. Oswaldo Cruz
PD SEP
PY 2011
VL 106
IS 6
BP 748
EP 754
DI 10.1590/S0074-02762011000600016
PG 7
WC Parasitology; Tropical Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Parasitology; Tropical Medicine
GA 835FY
UT WOS:000296022400016
PM 22012231
OA Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Liu, J
Xing, XM
Huang, HY
Jiang, YZ
He, HW
Xu, XY
Yuan, JH
Zhou, L
Yang, LQ
Zhuang, ZX
AF Liu, Jianjun
Xing, Xiumei
Huang, Haiyan
Jiang, Yingzhi
He, Haowei
Xu, Xinyun
Yuan, Jianhui
Zhou, Li
Yang, Linqing
Zhuang, Zhixiong
TI Identification of antigenic proteins associated with
trichloroethylene-induced autoimmune disease by serological proteome
analysis
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Trichloroethylene; Autoimmune disease; L-02 cell line; Sera; Serological
proteome analysis
ID NUCLEOSIDE DIPHOSPHATE KINASE; SYSTEMIC-LUPUS-ERYTHEMATOSUS; GENERALIZED
SKIN DISORDERS; HUMORAL IMMUNE-RESPONSE; T-CELL-ACTIVATION; OCCUPATIONAL
EXPOSURE; LUNG-CANCER; SCLERODERMA; HEPATITIS; CHEMICALS
AB Although many studies indicated that trichloroethylene (TCE) could induce autoimmune diseases and some protein adducts were detected, the proteins were not identified and mechanisms remain unknown. To screen and identify autoantigens which might be involved in TCE-induced autoimmune diseases, three groups of sera were collected from healthy donors (I), patients suffering from TCE-induced exfoliative dermatitis (ED) (II), and the healed ones (III). Serological proteome analysis (SERPA) was performed with total proteins of TCE-treated L-02 liver cells as antigen sources and immunoglobins of the above sera as probes. Highly immunogenic spots (2-fold or above increase compared with group I) in group II and III were submitted to matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS) and tandem mass spectrometry sequencing. Western blot analysis was followed using commercial antibodies and individual serum. Six proteins were identified. Among them, Enoyl Coenzyme A hydratase peroxisoma 1 and lactate dehydrogenase B only showed stronger immunogenicity for group II sera, while Purine nucleoside phosphorylase, ribosomal protein PO and proteasome activator subunit1 isoform1 also showed stronger immunogenicity for group III sera. Noteworthy, NM23 reacted only with group II sera. Western blot analysis of NM23 expression indicated that all of the individual serum of group II showed immune activity, which confirmed the validity of SERPA result. These findings revealed that there exist autoantibodies in group II and III sera. Besides, autoantibodies of the two stages of disease course were different. These autoantigens might serve as biomarkers to elucidate mechanisms underlying TCE toxicity and are helpful for diagnosis, therapy and prognosis of TCE-induced autoimmune diseases. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Liu, Jianjun; Xing, Xiumei; Huang, Haiyan; Jiang, Yingzhi; He, Haowei; Xu, Xinyun; Yuan, Jianhui; Zhou, Li; Yang, Linqing; Zhuang, Zhixiong] Shenzhen Ctr Dis Control & Prevent, Key Lab Modern Toxicol Shenzhen, Shenzhen 518020, Peoples R China.
C3 Shenzhen Center for Disease Control & Prevention (SZCDC)
RP Zhuang, ZX (corresponding author), Shenzhen Ctr Dis Control & Prevent, Key Lab Modern Toxicol Shenzhen, 21 Rd 1st Tianbei, Shenzhen 518020, Peoples R China.
EM bio-research@hotmail.com
RI yuan, jianhui/GQA-4825-2022
FU National Natural Science Foundation of China [30571557]; National Key
Basic Research and Development Program (973) [2002CB512903]; Guangdong
Natural Science Foundation [5009153]; Shenzhen Science Technology Plan
Key Project [200801010]
FX This work was supported by the National Natural Science Foundation of
China [30571557]; National Key Basic Research and Development Program
(973) [2002CB512903]; Guangdong Natural Science Foundation [5009153];
and Shenzhen Science Technology Plan Key Project [200801010]. We would
like to thank Dr. Ge Yue (US Environmental Protection Agency) for his
help in proof reading of the article.
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NR 50
TC 15
Z9 20
U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD NOV 1
PY 2009
VL 240
IS 3
BP 393
EP 400
DI 10.1016/j.taap.2009.07.031
PG 8
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA 507TC
UT WOS:000270876800009
PM 19647757
DA 2025-01-07
ER
PT J
AU Wang, PY
Chan, WK
Wang, JM
Yang, ZX
Wang, YW
AF Wang, Peiying
Chan, Wing Keung
Wang, Jiming
Yang, Zhouxin
Wang, Youwei
TI Role of IL-22 in intestinal microenvironment and potential targeted
therapy through diet
SO IMMUNOLOGIC RESEARCH
LA English
DT Review
DE Innate lymphoid cells; Cytokines; Intestinal immunity; Interleukin-22
ID INNATE LYMPHOID-CELLS; INTERLEUKIN 22; COLORECTAL-CANCER; STEM-CELLS;
BINDING-PROTEIN; HOST-DEFENSE; LIVER-INJURY; RECEPTOR; EXPRESSION;
PROMOTES
AB IL-22 is a type 2 receptor cytokine in IL-10 family. IL-22 is usually secreted by innate and adaptive immune cells and takes its effects on non-hematopoietic cells. Through activate STAT3 pathway, IL-22 plays an important role in infection clearance and tissue regeneration, which is critical for barrier integrate and homeostasis. Abnormal activation of IL-22 signal was observed in inflammation diseases, autoimmune diseases, and cancers. We review the recent discoveries about the mechanism and regulation of IL-22 signal pathway from the perspective of intestinal micro-environment. Diet-based IL-22 target therapeutic strategies and their potential clinical significance will also be discussed.
C1 [Wang, Peiying; Wang, Youwei] Tianjin Univ, Inst Med Engn & Translat Med, 92 Weijin Rd, Tianjin 300072, Peoples R China.
[Chan, Wing Keung] Ohio State Univ, Dept Internal Med, Div Hematol, 400 W 12th Ave, Columbus, OH 43210 USA.
[Wang, Jiming] Tianjin Econ Technol Dev Area TEDA Hosp, 65 3rd Ave, Tianjin 300451, Peoples R China.
[Yang, Zhouxin] Zhejiang Hosp, Dept Crit Care Med, 1229 Gudun Rd, Hangzhou 310030, Peoples R China.
C3 Tianjin University; University System of Ohio; Ohio State University
RP Wang, YW (corresponding author), Tianjin Univ, Inst Med Engn & Translat Med, 92 Weijin Rd, Tianjin 300072, Peoples R China.; Yang, ZX (corresponding author), Zhejiang Hosp, Dept Crit Care Med, 1229 Gudun Rd, Hangzhou 310030, Peoples R China.
EM yangzhouxin@hotmail.com; youwei.wang@tju.edu.cn
RI Li, Xiaoli/JVZ-4089-2024
FU National Key Research and Development Program of China [2021YFF1200800];
Natural Science Foundation of Tianjin [21JCZDJC00430]
FX This project was supported by grants from National Key Research and
Development Program of China (2021YFF1200800) and Natural Science
Foundation of Tianjin (21JCZDJC00430).
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NR 90
TC 0
Z9 0
U1 3
U2 16
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD APR
PY 2023
VL 71
IS 2
BP 121
EP 129
DI 10.1007/s12026-022-09325-5
EA SEP 2022
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA C3JE7
UT WOS:000863143500001
PM 36173554
DA 2025-01-07
ER
PT J
AU Wang, X
Zhou, Y
Min, JX
Wang, FD
AF Wang, Xue
Zhou, Ye
Min, Junxia
Wang, Fudi
TI Zooming in and out of ferroptosis in human disease
SO FRONTIERS OF MEDICINE
LA English
DT Review
DE ferroptosis; human disease; iron metabolism; lipid peroxidation;
antioxidation
ID ERASTIN-INDUCED FERROPTOSIS; ACUTE KIDNEY INJURY; CELL-DEATH; PROMOTES
FERROPTOSIS; CANCER-CELLS; ISCHEMIA-REPERFUSION; INHIBITS FERROPTOSIS;
LIPID-PEROXIDATION; PHYSIOLOGICAL FUNCTIONS; OVERCOMES RESISTANCE
AB Ferroptosis is defined as an iron-dependent regulated form of cell death driven by lipid peroxidation. In the past decade, it has been implicated in the pathogenesis of various diseases that together involve almost every organ of the body, including various cancers, neurodegenerative diseases, cardiovascular diseases, lung diseases, liver diseases, kidney diseases, endocrine metabolic diseases, iron-overload-related diseases, orthopedic diseases and autoimmune diseases. Understanding the underlying molecular mechanisms of ferroptosis and its regulatory pathways could provide additional strategies for the management of these disease conditions. Indeed, there are an expanding number of studies suggesting that ferroptosis serves as a bona-fide target for the prevention and treatment of these diseases in relevant pre-clinical models. In this review, we summarize the progress in the research into ferroptosis and its regulatory mechanisms in human disease, while providing evidence in support of ferroptosis as a target for the treatment of these diseases. We also discuss our perspectives on the future directions in the targeting of ferroptosis in human disease.
C1 [Wang, Xue; Min, Junxia; Wang, Fudi] Zhejiang Univ, Affiliated Hosp 2, Affiliated Hosp 1, Inst Translat Med,Sch Publ Hlth,State Key Lab Expt, Hangzhou 310058, Peoples R China.
[Wang, Xue; Wang, Fudi] Univ South China, Affiliated Hosp 1, Sch Publ Hlth, Hengyang Med Sch,Basic Med Sci, Hengyang 421001, Peoples R China.
[Zhou, Ye] Ningbo First Hosp, Dept Endocrinol & Metab, Ningbo 315000, Peoples R China.
C3 Zhejiang University; University of South China; Ningbo University
RP Min, JX; Wang, FD (corresponding author), Zhejiang Univ, Affiliated Hosp 2, Affiliated Hosp 1, Inst Translat Med,Sch Publ Hlth,State Key Lab Expt, Hangzhou 310058, Peoples R China.; Wang, FD (corresponding author), Univ South China, Affiliated Hosp 1, Sch Publ Hlth, Hengyang Med Sch,Basic Med Sci, Hengyang 421001, Peoples R China.
EM junxiamin@zju.edu.cn; fwang@zju.edu.cn
RI Wang, Fudi/L-7888-2018
OI Wang, Fudi/0000-0001-8730-0003
FU National Natural Science Foundation of China [31930057, 31970689];
National Key RD Program [2018YFA0507801, 2018YFA0507802]; China
Postdoctoral Science Foundation [2022M712733]
FX AcknowledgementsThe authors receive support from the National Natural
Science Foundation of China (No. 31930057 to Fudi Wang and No. 31970689
to Junxia Min), the National Key R&D Program (No. 2018YFA0507801 to
Junxia Min and No. 2018YFA0507802 to Fudi Wang) and the China
Postdoctoral Science Foundation (No. 2022M712733 to Xue Wang). The
authors thank Hao Wang (Zhengzhou University School of Public Health,
China), Xuexian Fang (Hangzhou Normal University School of Public
Health, China), Yingying Yu, Enjun Xie, and Xinquan Yang (Zhejiang
University School of Medicine, China) for their contribution to the
discussion for this review.
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NR 339
TC 43
Z9 47
U1 25
U2 97
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2095-0217
EI 2095-0225
J9 FRONT MED-PRC
JI Front. Med.
PD APR
PY 2023
VL 17
IS 2
BP 173
EP 206
DI 10.1007/s11684-023-0992-z
EA MAY 2023
PG 34
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA H5DK2
UT WOS:000978562100003
PM 37121959
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Dias, FC
Castelli, EC
Collares, CVA
Moreau, P
Donadil, EA
AF Dias, Fabricio C.
Castelli, Erick C.
Collares, Cristhianna V. A.
Moreau, Philippe
Donadil, Eduardo A.
TI The role of HLA-G molecule and HLA-G gene polymorphisms in
tumors, viral hepatitis, and parasitic diseases
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE HLA-G; tumors; viral hepatitis; parasitic disorders; polymorphism
ID LEUKOCYTE-ANTIGEN-G; CHRONIC LYMPHOCYTIC-LEUKEMIA; SQUAMOUS-CELL
CARCINOMA; B-VIRUS INFECTION; 14-BP INSERTION/DELETION POLYMORPHISM; 3'
UNTRANSLATED REGION; BREAST-CANCER PATIENTS; CLASS-I ANTIGENS; G
EXPRESSION; HEPATOCELLULAR-CARCINOMA
AB Considering that the non-classical HLA-G molecule has well-recognized tolerogenic properties, HLA-G expression is expected to be deleterious when present in tumor cells and in cells chronically infected by viruses, whereas HLA-G expression is expected to be advantageous in autoimmune disorders. The expression of HLA-G on tissue or peripheral blood cells, the levels of soluble HLA-G and polymorphic sites along the gene have been studied in several disorders. In this study, we revised the role of the molecule and polymorphic sites along the HLA-G gene in tumors, viral hepatitis, and parasitic disorders. Overall, several lines of evidence clearly show that the induction of HLA-G expression in tumors has been associated with worse disease outcome and disease spread. In addition, the few studies conducted on hepatitis and parasitic disorders indicate that HLA-G may contribute to disease pathogenesis. Few isolated polymorphic sites, primarily located at the coding or 3' untranslated HLA-G region, have been evaluated in these disorders, and a complete HLA-G typing together with the study of gene regulatory elements may further help on the understanding of the influence of the genetic background on disease susceptibility.
C1 [Dias, Fabricio C.; Collares, Cristhianna V. A.; Donadil, Eduardo A.] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Med, Div Clin Immunol, BR-14049 Ribeirao Preto, Brazil.
[Castelli, Erick C.] Univ Estadual Paulista, Sch Med Botucatu, Dept Pathol, Botucatu, SP, Brazil.
[Moreau, Philippe] Hop St Louis, CEA, Inst Emerging Dis & Innovat Therapies, Res Div Hematol & Immunol, Paris, France.
C3 Universidade de Sao Paulo; Universidade Estadual Paulista; CEA;
Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
Hopital Universitaire Saint-Louis - APHP
RP Donadil, EA (corresponding author), Univ Sao Paulo, Ave Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP, Brazil.
EM eadonadi@fmrp.usp.br
RI Moreau, Philippe/HKN-2799-2023; Collares, Cristhianna/H-8521-2013;
Castelli, Erick/B-4250-2010; donadi, eduardo/H-7080-2013
OI Castelli, Erick/0000-0003-2142-7196; Moreau,
Philippe/0000-0002-2868-7401; donadi, eduardo/0000-0002-9457-9601
FU Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior
[CAPES/COFECUB 653/09]; Conselho Nacional de Desenvolvimento Cientifico
e Tecnologico [CNPq] [236754/2012-2, 406594/2013-9, 401641/2013-9,
66036/2013-5, 31/2014, 467157/2014-6]; Nucleo de Apoio a Pesquisa em
Doencas Inflamatorias (NAP-DIN)
FX This work was supported by Coordenacao de Aperfeicoamento de Pessoal de
Nivel Superior [grant number CAPES/COFECUB 653/09], Conselho Nacional de
Desenvolvimento Cientifico e Tecnologico [CNPq Science Without Borders
Program, grant number 236754/2012-2; Special Visiting Researcher, grant
number 406594/2013-9; Young Talents, grant number 401641/2013-9; CNPq
edital 71/2013, grant number 406594/2013-9; CNPq Universal, grant number
466036/2013-5; CNPq/MS/SCTIE/DECIT No. 31/2014 - Pesquisas sobre Doenca
de Chagas, grant number 467157/2014-6], and Nucleo de Apoio a Pesquisa
em Doencas Inflamatorias (NAP-DIN).
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NR 107
TC 52
Z9 58
U1 1
U2 7
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD FEB 2
PY 2015
VL 6
AR 9
DI 10.3389/fimmu.2015.00009
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CI4YC
UT WOS:000354758800001
PM 25699038
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Stirnimann, G
Ebadi, M
Czaja, AJ
Montano-Loza, AJ
AF Stirnimann, Guido
Ebadi, Maryam
Czaja, Albert J.
Montano-Loza, Aldo J.
TI Recurrent and De Novo Autoimmune Hepatitis
SO LIVER TRANSPLANTATION
LA English
DT Review
ID PRIMARY BILIARY-CIRRHOSIS; DONOR LIVER-TRANSPLANTATION;
GLUTATHIONE-S-TRANSFERASE; CHRONIC ACTIVE HEPATITIS; LATE GRAFT
DYSFUNCTION; PLASMA-CELL HEPATITIS; RISK-FACTORS; CLINICAL-RELEVANCE;
DISEASE; DIAGNOSIS
AB Clinical indications for liver transplantation (LT) in patients with autoimmune hepatitis (AIH) are identical to those of patients with other chronic liver diseases that end in acute or semiacute liver failure, decompensated cirrhosis, or hepatocellular carcinoma. Recurrent disease after LT has been reported in 10%-50% of patients with AIH, and the frequency of detection is influenced in part by the use of protocol or clinically indicated liver biopsy. De novo AIH connotes the development of AIH in patients transplanted for liver diseases other than AIH, and it has been reported in 5%-10% of pediatric and 1%-2% of adult recipients. Recurrent disease can negatively impact on graft and patient survival, and retransplantation has been required in 8%-23%. De novo AIH is within the spectrum of graft dysfunction that includes plasma cell-rich rejection, and it can also progress to cirrhosis and graft failure. Treatment for recurrent or de novo disease is based on the conventional regimens for AIH, and corticosteroid therapy alone or combined with azathioprine is standard. Better control of disease activity prior to LT has been associated with less recurrence, and maintenance corticosteroid treatment after LT can reduce its frequency. In conclusion, recurrent AIH is far more frequent than de novo AIH. Both may have negative impacts on graft and patient survival, and early detection and treatment are key objectives. Future investigations must codify the diagnostic criteria for each graft dysfunction, seek diagnostic biomarkers, and evaluate treatments that improve outcomes without increasing the risk of pre- and post-LT infections.
C1 [Stirnimann, Guido] Bern Univ Hosp, Inselspital Bern, Dept Visceral Surg & Med, Bern, Switzerland.
[Stirnimann, Guido] Univ Bern, Bern, Switzerland.
[Stirnimann, Guido; Ebadi, Maryam; Montano-Loza, Aldo J.] Univ Alberta Hosp, Div Gastroenterol, Edmonton, AB, Canada.
[Stirnimann, Guido; Ebadi, Maryam; Montano-Loza, Aldo J.] Univ Alberta Hosp, Liver Unit, Edmonton, AB, Canada.
[Czaja, Albert J.] Mayo Clin, Coll Med & Sci, Div Gastroenterol & Hepatol, Rochester, MN USA.
C3 University of Bern; University Hospital of Bern; University of Bern;
University of Alberta; University of Alberta; Mayo Clinic
RP Montano-Loza, AJ (corresponding author), Zeidler Ledcor Ctr, Div Gastroenterol, 8540 112 St NW,Room 1-20B, Edmonton, AB T6G 2X8, Canada.; Montano-Loza, AJ (corresponding author), Zeidler Ledcor Ctr, Liver Unit, 8540 112 St NW,Room 1-20B, Edmonton, AB T6G 2X8, Canada.
EM montanol@ualberta.ca
RI Montano-Loza, Aldo/B-3092-2013
OI Montano-Loza, Aldo J./0000-0002-2511-7980
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NR 80
TC 38
Z9 39
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6465
EI 1527-6473
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD JAN
PY 2019
VL 25
IS 1
BP 152
EP 166
DI 10.1002/lt.25375
PG 15
WC Gastroenterology & Hepatology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA HG4QI
UT WOS:000454959600018
PM 30375180
OA Green Published
DA 2025-01-07
ER
PT J
AU Ejam, SS
Saleh, RO
Opulencia, MJC
Najm, MA
Makhmudova, A
Jalil, AT
Abdelbasset, WK
Al-Gazally, ME
Hammid, AT
Mustafa, YF
Sergeevna, SE
Karampoor, S
Mirzaei, R
AF Ejam, Sura Salman
Saleh, Raed Obaid
Catalan Opulencia, Maria Jade
Najm, Mazin A. A.
Makhmudova, Aziza
Jalil, Abduladheem Turki
Abdelbasset, Walid Kamal
Al-Gazally, Moaed E.
Hammid, Ali Thaeer
Mustafa, Yasser Fakri
Sergeevna, Sergushina Elena
Karampoor, Sajad
Mirzaei, Rasoul
TI Pathogenic role of 25-hydroxycholesterol in cancer development and
progression
SO FUTURE ONCOLOGY
LA English
DT Review
DE cancer; immunity; immunometabolism; inflammation; 25-HC
ID HUMAN COLON-CANCER; ELEMENT-BINDING PROTEIN; POSITIVE BREAST-CANCER;
RANDOMIZED PHASE-III; B-CELL MIGRATION; NF-KAPPA-B;
HEPATOCELLULAR-CARCINOMA; STATIN USE; CHOLESTEROL 25-HYDROXYLASE;
LEYDIG-CELLS
AB Cholesterol is an essential lipid that serves several important functions, including maintaining the homeostasis of cells, acting as a precursor to bile acid and steroid hormones and preserving the stability of membrane lipid rafts. 25-hydroxycholesterol (25-HC) is a cholesterol derivative that may be formed from cholesterol. 25-HC is a crucial component in various biological activities, including cholesterol metabolism. In recent years, growing evidence has shown that 25-HC performs a critical function in the etiology of cancer, infectious diseases and autoimmune disorders. This review will summarize the latest findings regarding 25-HC, including its biogenesis, immunomodulatory properties and role in innate/adaptive immunity, inflammation and the development of various types of cancer.
C1 [Ejam, Sura Salman] Univ Babylon, Coll Med, Babylon, Iraq.
[Saleh, Raed Obaid] Al Maarif Univ Coll, Dept Pharm, Al Anbar, Iraq.
[Catalan Opulencia, Maria Jade] Ajman Univ, Coll Business Adm, Ajman, U Arab Emirates.
[Najm, Mazin A. A.] Al Ayen Univ, Coll Pharm, Pharmaceut Chem Dept, Thi Qar, Iraq.
[Makhmudova, Aziza] Samarkand State Med Inst, Dept Social Sci & Humanities, Samarkand, Uzbekistan.
[Makhmudova, Aziza] Tashkent State Dent Inst, Dept Sci Affairs, Makhtumkuli St 103, Tashkent 100047, Uzbekistan.
[Jalil, Abduladheem Turki] Al Mustaqbal Univ Coll, Med Labs Tech Dept, Babylon 51001, Hilla, Iraq.
[Abdelbasset, Walid Kamal] Prince Sattam bin Abdulaziz Univ, Coll Appl Med Sci, Dept Hlth & Rehabil Sci, Al Kharj, Saudi Arabia.
[Abdelbasset, Walid Kamal] Cairo Univ, Kasr Al Aini Hosp, Dept Phys Therapy, Giza, Egypt.
[Al-Gazally, Moaed E.] Univ Al Ameed, Coll Med, Karbala, Iraq.
[Hammid, Ali Thaeer] Imam Jaafar Al Sadiq Univ, Fac Informat Technol, Comp Engn Tech Dept, Baghdad, Iraq.
[Mustafa, Yasser Fakri] Univ Mosul, Coll Pharm, Dept Pharmaceut Chem, Mosul 41001, Iraq.
[Sergeevna, Sergushina Elena] Natl Res Ogarev Mordovia State Univ, 68 Bolshevitskaya St, Saransk 430005, Russia.
[Karampoor, Sajad] Iran Univ Med Sci, Gastrointestinal & Liver Dis Res Ctr, Tehran, Iran.
[Mirzaei, Rasoul] Pasteur Inst Iran, Biotechnol Res Ctr, Med Biotechnol Dept, Venom & Biotherapeut Mol Lab, Tehran, Iran.
C3 University of Babylon; Al-Maarif University; Ajman University; Al-Ayen
University; Samarkand State Medical University; Al-Mustaqbal University
College; Prince Sattam Bin Abdulaziz University; Egyptian Knowledge Bank
(EKB); Cairo University; University of Al-Ameed; Imam Jaa'far al-Sadiq
University; University of Mosul; Mordovian State University; Iran
University of Medical Sciences; Pasteur Network; Pasteur Institute of
Iran
RP Karampoor, S (corresponding author), Iran Univ Med Sci, Gastrointestinal & Liver Dis Res Ctr, Tehran, Iran.; Mirzaei, R (corresponding author), Pasteur Inst Iran, Biotechnol Res Ctr, Med Biotechnol Dept, Venom & Biotherapeut Mol Lab, Tehran, Iran.
EM sajadkarampour1987@gmail.com; rasul.micro92@gmail.com
RI Saleh, Raed/AAM-3803-2020; Ejam, Sura/JGI-1252-2023; Mirzaei,
Rasoul/GQZ-2348-2022; Karampoor, Sajad/AAY-7072-2021; Mustafa, Yasser
Fakri/D-1589-2019; , Walid Kamal/T-8648-2017; AL-Attabi,
Abduladheem/AAD-1741-2021; Al-Gazally, Moaed/T-2395-2017
OI Obaid, Raed/0000-0003-3873-3181; , Walid Kamal/0000-0003-4703-661X;
Raed, Saleh/0009-0004-1238-378X; Mustafa, Yasser
Fakri/0000-0002-0926-7428; AL-Attabi, Abduladheem/0000-0001-8403-7465;
Saleh, Raed/0009-0007-5402-922X; Al-Gazally, Moaed/0000-0002-5325-5280
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NR 286
TC 5
Z9 5
U1 0
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD DEC
PY 2022
VL 18
IS 39
BP 4415
EP 4442
DI 10.2217/fon-2022-0819
EA JAN 2023
PG 28
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C9BL6
UT WOS:000913999200001
PM 36651359
DA 2025-01-07
ER
PT J
AU Nana, K
Satsuki, I
Noritaka, H
Akira, H
Daisuke, T
Teruhide, Y
AF Nana, Kawasaki
Satsuki, Itoh
Noritaka, Hashii
Akira, Harazono
Daisuke, Takakura
Teruhide, Yamaguchi
TI Mass spectrometric analysis of carbohydrate heterogeneity for the
characterization of glycoprotein-based products
SO TRENDS IN GLYCOSCIENCE AND GLYCOTECHNOLOGY
LA English
DT Review
DE liquid chromatography/mass spectrometry; glycoprotem; oligosaccharide;
glycopeptide
ID N-LINKED OLIGOSACCHARIDES; LIQUID CHROMATOGRAPHY/MASS SPECTROMETRY;
TISSUE PLASMINOGEN-ACTIVATOR; HEPATOCELLULAR-CARCINOMA; GLYCOSYLATION
ANALYSIS; PROTEIN GLYCOSYLATION; QUANTITATIVE-ANALYSIS;
RHEUMATOID-ARTHRITIS; SERUM GLYCOPROTEINS; AUTOIMMUNE-DISEASE
AB Analysis of the carbohydrate heterogeneity of glycoprotein-based substances is crucial for establishing the nomenclature and definition of biological substances, ensuring consistency in the quality of these products, comparatively assessing the products obtained after the implementation of changes in the manufacturing process, and developing biosimilar or follow-on biological products. Liquid chromatography/mass spectrometry is recognized as one of the most useful techniques for analyzing the carbohydrate heterogeneity of glycoprotein substances. Here, we demonstrate the utility of LC/MS for analyzing the carbohydrate heterogeneity by using some representative glycoproteins such as tissue-plasminogen activator, a monoclonal antibody, the follicle-stimulating hormone, and human chorionic gonadotropin. Further, we demonstrate that MS-based glycoprotein analysis has potential applications in glycomics.
C1 [Nana, Kawasaki; Satsuki, Itoh; Noritaka, Hashii; Akira, Harazono; Daisuke, Takakura; Teruhide, Yamaguchi] Natl Inst Hlth Sci, Setagaya Ku, Tokyo 1588501, Japan.
C3 National Institute of Health Sciences - Japan
RP Nana, K (corresponding author), Natl Inst Hlth Sci, Setagaya Ku, 1-18-1 Kamiyoga, Tokyo 1588501, Japan.
EM nana@nihs.go.jp
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U1 0
U2 18
PU GAKUSHIN PUBL CO
PI TOKYO
PA YUSHOKAIN7F, 1-38-12 NIHONBASHIKAKIGARACHO, CHUO-KU, TOKYO, 103-0014,
JAPAN
SN 0915-7352
J9 TRENDS GLYCOSCI GLYC
JI Trends Glycosci. Glycotechnol.
PD MAY
PY 2008
VL 20
IS 112
BP 97
EP 116
PG 20
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 335DR
UT WOS:000258271500004
DA 2025-01-07
ER
PT J
AU Pan, W
Yang, B
He, DX
Chen, LX
Fu, CX
AF Pan, Wei
Yang, Bo
He, Dongxiu
Chen, Linxi
Fu, Chengxiao
TI Functions and targets of miRNAs in pharmacological and toxicological
effects of major components of Tripterygium wilfordii Hook F
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Review
DE MicroRNA; Triptolide; Celastrol; Pharmacological effect; Toxicological
effect
ID LUNG ADENOCARCINOMA CELLS; MOUSE LEYDIG-CELLS; HEPATOCELLULAR-CARCINOMA;
DOWN-REGULATION; CANCER CELLS; KNOCKDOWN INCREASES; REGULATING MIR-21;
TRIPTOLIDE; CELASTROL; PROLIFERATION
AB Tripterygium wilfordii Hook F (TwHF) has a long history of use as a traditional Chinese medicine and has been widely administered to treat various inflammatory and autoimmune diseases. MicroRNAs (miRNAs) are endogenous, short, non-coding RNAs that regulate gene expression post-transcriptionally. They participate in the efficacies and even toxicities of the components of TwHF, rendering miRNAs an appealing therapeutic strategy. This review summarizes the recent literature related to the roles and mechanisms of miRNAs in the pharmacological and toxicological effects of main components of TwHF, focusing on two active compounds, triptolide (TP) and celastrol (CEL). Additionally, the prospects for the "You Gu Wu Yun" theory regarding TwHF nephrotoxicity are presented.
C1 [Pan, Wei; He, Dongxiu; Chen, Linxi; Fu, Chengxiao] Univ South China, Hengyang Med Sch, Inst Pharm & Pharmacol, Coll Basic Med Sci, Hengyang 421200, Peoples R China.
[Pan, Wei; Yang, Bo; Fu, Chengxiao] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Pharm, Hengyang 421001, Hunan, Peoples R China.
C3 University of South China; University of South China
RP Fu, CX (corresponding author), Univ South China, Hengyang Med Sch, Inst Pharm & Pharmacol, Coll Basic Med Sci, Hengyang 421200, Peoples R China.; Fu, CX (corresponding author), Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Pharm, Hengyang 421001, Hunan, Peoples R China.
EM paulfcx@126.com
RI Yang, Bo/D-2691-2012
FU Hunan Provincial Natural Science Foundation of China [2021JJ80072,
2020JJ8099]; Medical Technology Innovation Guidance Project of Hunan
Province Science and Technology Department [2021SK51806]; Science and
Technology Innovation Project of Hengyang City [202250045225]
FX This study was supported by grants of the Hunan Provincial Natural
Science Foundation of China (No. 2021JJ80072, 2020JJ8099), Medical
Technology Innovation Guidance Project of Hunan Province Science and
Technology Department (No. 2021SK51806), and Science and Technology
Innovation Project of Hengyang City (202250045225)
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NR 118
TC 0
Z9 0
U1 6
U2 16
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0028-1298
EI 1432-1912
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD APR
PY 2024
VL 397
IS 4
BP 1997
EP 2019
DI 10.1007/s00210-023-02764-3
EA OCT 2023
PG 23
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA LG4P0
UT WOS:001084814300001
PM 37831113
DA 2025-01-07
ER
PT J
AU Hench, LL
AF Hench, Larry L.
TI Glass and Glass-Ceramic Technologies to Transform the World
SO INTERNATIONAL JOURNAL OF APPLIED GLASS SCIENCE
LA English
DT Article
ID ANGIOGENIC GROWTH-FACTORS; BIOACTIVE GLASS; IN-VITRO;
HEPATOCELLULAR-CARCINOMA; DISSOLUTION PRODUCTS; EXTRACELLULAR-MATRIX;
Y-90 MICROSPHERES; HUMAN OSTEOBLASTS; IONIC PRODUCTS; SOFT-TISSUE
AB This presentation is an overview of the findings from June 21 to 22, 2010 American Ceramic Society Leadership Summit and a personal perspective on the economic issues and technical feasibility of achieving breakthrough technologies in the business segments of Energy and Healthcare. The top 10 rankings from an extensive listing of 100 potentially important ceramic, glass and glass-ceramic technologies were all in the Energy and Healthcare Sectors of business. Innovative technologies that have the potential for being world-changing are discussed, including Transforming Technology for Energy No. 1: Innovative Energy Storage Devices; Transforming Technology for Healthcare No. 1: Bioactive Materials for Regeneration of Tissues; No. 2: Localized Therapies for Cancer and Autoimmune Diseases; No. 3: Tissue Engineering of Soft Tissues; No. 4: Stem Cell Engineering; No. 5: Preventative Medicine.
C1 [Hench, Larry L.] Univ Florida, Dept Mat Sci & Engn, Gainesville, FL 32605 USA.
[Hench, Larry L.] Univ Cent Florida, Off Vice President, Orlando, FL 32826 USA.
[Hench, Larry L.] Kings Coll London, Sch Dent, Guys Hosp, London, England.
C3 State University System of Florida; University of Florida; State
University System of Florida; University of Central Florida; University
of London; King's College London; Guy's & St Thomas' NHS Foundation
Trust
RP Hench, LL (corresponding author), Univ Florida, Dept Mat Sci & Engn, Gainesville, FL 32605 USA.
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NR 93
TC 25
Z9 25
U1 1
U2 54
PU WILEY PERIODICALS, INC
PI SAN FRANCISCO
PA ONE MONTGOMERY ST, SUITE 1200, SAN FRANCISCO, CA 94104 USA
SN 2041-1286
EI 2041-1294
J9 INT J APPL GLASS SCI
JI Int. J. Appl. Glass Sci.
PD SEP
PY 2011
VL 2
IS 3
SI SI
BP 162
EP 176
DI 10.1111/j.2041-1294.2011.00056.x
PG 15
WC Materials Science, Ceramics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science
GA 034CT
UT WOS:000310848400002
DA 2025-01-07
ER
PT J
AU Liu, XZ
Wang, LF
Tan, SW
Chen, ZB
Wu, B
Wu, XY
AF Liu, Xianzhi
Wang, Lifu
Tan, Siwei
Chen, Zebin
Wu, Bin
Wu, Xiaoying
TI Therapeutic Effects of Berberine on Liver Fibrosis are associated With
Lipid Metabolism and Intestinal Flora
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE cirrhosis; liver fibrosis; lipid metabolism; intestinal flora; berberine
ID ACTIVATED PROTEIN-KINASE; HEPATIC STELLATE CELLS; DE-NOVO LIPOGENESIS;
CHAIN FATTY-ACIDS; JIE-DU-TANG; GUT MICROBIOTA; IN-VITRO; INDUCED
HEPATOTOXICITY; UP-REGULATION; BILE-ACIDS
AB Liver cirrhosis is a form of liver fibrosis resulting from chronic hepatitis caused by various liver diseases, such as viral hepatitis, alcoholic liver damage, nonalcoholic steatohepatitis, autoimmune liver disease, and by parasitic diseases such as schistosomiasis. Liver fibrosis is the common pathological base and precursors of cirrhosis. Inflammation and disorders of lipid metabolism are key drivers in liver fibrosis. Studies have determined that parts of the arachidonic acid pathway, such as its metabolic enzymes and biologically active products, are hallmarks of inflammation, and that aberrant peroxisome proliferator-activated receptor gamma (PPAR gamma)-mediated regulation causes disorders of lipid metabolism. However, despite the ongoing research focus on delineating the mechanisms of liver fibrosis that underpin various chronic liver diseases, effective clinical treatments have yet to be developed. Berberine (BBR) is an isoquinoline alkaloid with multiple biological activities, such as anti-inflammatory, anti-bacterial, anti-cancer, and anti-hyperlipidemic activities. Many studies have also found that BBR acts via multiple pathways to alleviate liver fibrosis. Furthermore, the absorption of BBR is increased by nitroreductase-containing intestinal flora, and is strengthened via crosstalk with bile acid metabolism. This improves the oral bioavailability of BBR, thereby enhancing its clinical utility. The production of butyrate by intestinal anaerobic bacteria is dramatically increased by BBR, thereby amplifying butyrate-mediated alleviation of liver fibrosis. In this review, we discuss the effects of BBR on liver fibrosis and lipid metabolism, particularly the metabolism of arachidonic acid, and highlight the potential mechanisms by which BBR relieves liver fibrosis through lipid metabolism related and intestinal flora related pathways. We hope that this review will provide insights on the BBR-based treatment of liver cirrhosis and related research in this area, and we encourage further studies that increase the ability of BBR to enhance liver health.
C1 [Liu, Xianzhi; Tan, Siwei; Wu, Bin; Wu, Xiaoying] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Gastroenterol, Guangzhou, Peoples R China.
[Liu, Xianzhi; Tan, Siwei; Wu, Bin; Wu, Xiaoying] Guangdong Prov Key Lab Liver Dis Res, Guangzhou, Peoples R China.
[Liu, Xianzhi; Tan, Siwei; Wu, Bin; Wu, Xiaoying] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Lab Med, Guangdong, Peoples R China.
[Wang, Lifu] Guangzhou Med Univ, King Med Sch Lab Med, Guangzhou, Peoples R China.
[Chen, Zebin] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Hepat Surg, Guangzhou, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Guangzhou Medical
University; Sun Yat Sen University
RP Wu, B; Wu, XY (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 3, Dept Gastroenterol, Guangzhou, Peoples R China.; Wu, B; Wu, XY (corresponding author), Guangdong Prov Key Lab Liver Dis Res, Guangzhou, Peoples R China.; Wu, B; Wu, XY (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 3, Dept Lab Med, Guangdong, Peoples R China.; Chen, ZB (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 1, Dept Hepat Surg, Guangzhou, Peoples R China.
EM chzbin@mail3.sysu.edu.cn; wubin6@mail.sysu.edu.cn;
wuxy227@mail.sysu.edu.cn
RI Wu, Xiaoying/ABD-8904-2020
FU National Natural Science Foundation of China [82170569]; Science and
Technology Planning Projects of Guangzhou City [201804010026]
FX Funding This work was supported by the National Natural Science
Foundation of China (No. 82170569); the Science and Technology Planning
Projects of Guangzhou City (201804010026).
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PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD MAR 2
PY 2022
VL 13
AR 814871
DI 10.3389/fphar.2022.814871
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA ZX0QC
UT WOS:000771605800001
PM 35308208
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Pongracz, T
Biewenga, M
Stoelinga, AEC
Bladergroen, MR
Nicolardi, S
Trouw, LA
Wuhrer, M
de Haan, N
van Hoek, B
AF Pongracz, Tamas
Biewenga, Maaike
Stoelinga, Anna Eva Charlotte
Bladergroen, Marco Rene
Nicolardi, Simone
Trouw, Leendert Adrianus
Wuhrer, Manfred
de Haan, Noortje
van Hoek, Bart
TI Autoimmune hepatitis displays distinctively high multi-antennary
sialylation on plasma N-glycans compared to other liver diseases
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Autoimmune hepatitis; Liver inflammation; Plasma N-glycosylation; IgG
glycosylation; Tetraantennary glycans; Glycome; Biomarker
ID ALPHA-1-ACID GLYCOPROTEIN; GLYCOSYLATION CHANGES; RHEUMATOID-ARTHRITIS;
FC-GLYCOSYLATION; IGG; DIAGNOSIS; CRITERIA; GALACTOSYLATION;
GLYCOPEPTIDES; ASSOCIATION
AB Background Changes in plasma protein glycosylation are known to functionally affect proteins and to associate with liver diseases, including cirrhosis and hepatocellular carcinoma. Autoimmune hepatitis (AIH) is a liver disease characterized by liver inflammation and raised serum levels of IgG, and is difficult to distinguish from other liver diseases. The aim of this study was to examine plasma and IgG-specific N-glycosylation in AIH and compare it with healthy controls and other liver diseases. Methods In this cross-sectional cohort study, total plasma N-glycosylation and IgG Fc glycosylation analysis was performed by mass spectrometry for 66 AIH patients, 60 age- and sex-matched healthy controls, 31 primary biliary cholangitis patients, 10 primary sclerosing cholangitis patients, 30 non-alcoholic fatty liver disease patients and 74 patients with viral or alcoholic hepatitis. A total of 121 glycans were quantified per individual. Associations between glycosylation traits and AIH were investigated as compared to healthy controls and other liver diseases. Results Glycan traits bisection (OR: 3.78 [1.88-9.35], p-value: 5.88 x 10(- 3)), tetraantennary sialylation per galactose (A4GS) (OR: 2.88 [1.75-5.16], p-value: 1.63 x 10(- 3)), IgG1 galactosylation (OR: 0.35 [0.2-0.58], p-value: 3.47 x 10(- 5)) and hybrid type glycans (OR: 2.73 [1.67-4.89], p-value: 2.31 x 10(- 3)) were found as discriminators between AIH and healthy controls. High A4GS differentiated AIH from other liver diseases, while bisection associated with cirrhosis severity. Conclusions Compared to other liver diseases, AIH shows distinctively high A4GS levels in plasma, with potential implications on glycoprotein function and clearance. Plasma-derived glycosylation has potential to be used as a diagnostic marker for AIH in the future. This may alleviate the need for a liver biopsy at diagnosis. Glycosidic changes should be investigated further in longitudinal studies and may be used for diagnostic and monitoring purposes in the future.
C1 [Pongracz, Tamas; Bladergroen, Marco Rene; Nicolardi, Simone; Wuhrer, Manfred; de Haan, Noortje] Leiden Univ, Ctr Prote & Metabol, Med Ctr, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
[Biewenga, Maaike; Stoelinga, Anna Eva Charlotte; van Hoek, Bart] Leiden Univ, Dept Gastroenterol & Hepatol, Med Ctr, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
[Trouw, Leendert Adrianus] Leiden Univ, Dept Immunol, Med Ctr, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
C3 Leiden University; Leiden University Medical Center (LUMC); Leiden
University - Excl LUMC; Leiden University - Excl LUMC; Leiden
University; Leiden University Medical Center (LUMC); Leiden University;
Leiden University Medical Center (LUMC); Leiden University - Excl LUMC
RP de Haan, N (corresponding author), Leiden Univ, Ctr Prote & Metabol, Med Ctr, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
EM n.de_haan@lumc.nl
RI Wuhrer, Manfred/ABE-9168-2020; Trouw, Leendert/AGK-5202-2022; van Hoek,
Bart/AAU-8953-2020; Pongracz, Tamas/HNJ-5146-2023; Bladergroen,
Marco/GWD-1457-2022; Nicolardi, Simone/K-1698-2013
OI Bladergroen, Marco/0000-0003-4434-4799; de Haan,
Noortje/0000-0001-7026-6750; Wuhrer, Manfred/0000-0002-0814-4995;
Pongracz, Tamas/0000-0002-8089-4352; Nicolardi,
Simone/0000-0001-8393-1625; Trouw, Leendert/0000-0001-5186-2290; van
Hoek, Bart/0000-0001-6527-764X
FU Horizon 2020 Framework Programme
FX We thank Carolien Koeleman for her kind support with sample preparation.
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TC 1
Z9 1
U1 2
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD MAY 14
PY 2024
VL 22
IS 1
AR 456
DI 10.1186/s12967-024-05173-z
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA QS0G2
UT WOS:001222735700001
PM 38745252
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Li, SY
Li, N
Yang, SR
Deng, HY
Li, YG
Wang, YX
Yang, JQ
Lv, JX
Dong, L
Yu, GS
Hou, X
Wang, G
AF Li, Siyu
Li, Na
Yang, Shanru
Deng, Haiyan
Li, Yanguo
Wang, Yixuan
Yang, Jiaqiang
Lv, Jiaxin
Dong, Lan
Yu, Guansen
Hou, Xin
Wang, Geng
TI The study of immune checkpoint inhibitors in chronic hepatitis B virus
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SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE Hepatitis B virus; Chronic hepatitis B; Immune checkpoint inhibitors
ID CD8 T-CELLS; UP-REGULATION; THERAPEUTIC VACCINATION;
AUTOIMMUNE-DISEASES; VIRAL-HEPATITIS; TIM-3; EXPRESSION; PD-1;
ACTIVATION; BLOCKADE
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[Li, Yanguo] Ningbo Univ, Inst Drug Discovery Technol, Ningbo, Peoples R China.
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RP Wang, G (corresponding author), Ningbo Univ, Sch Med, Ningbo 315211, Peoples R China.
EM wanggeng@nbu.edu.cn
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NR 103
TC 6
Z9 6
U1 1
U2 15
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD AUG
PY 2022
VL 109
AR 108842
DI 10.1016/j.intimp.2022.108842
EA MAY 2022
PG 9
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA 1Q8DX
UT WOS:000802913800003
PM 35569306
DA 2025-01-07
ER
PT J
AU Ajdacic-Gross, V
Rodgers, S
Aleksandrowicz, A
Mutsch, M
Steinemann, N
Von Wyl, V
von Kanel, R
Bopp, M
AF Ajdacic-Gross, Vladeta
Rodgers, Stephanie
Aleksandrowicz, Aleksandra
Mutsch, Margot
Steinemann, Nina
Von Wyl, Viktor
von Kanel, Roland
Bopp, Matthias
TI Cancer co-occurrence patterns in Parkinson's disease and multiple
sclerosis-Do they mirror immune system imbalances?
SO CANCER EPIDEMIOLOGY
LA English
DT Article
DE Cancer; Multiple sclerosis; Parkinson's disease; Comorbidity;
Epidemiology
ID EPSTEIN-BARR-VIRUS; 1ST-DEGREE RELATIVES; AUTOIMMUNE-DISEASES;
LUNG-CANCER; RISK; SMOKING; SCHIZOPHRENIA; INFLAMMATION; MELANOMA;
HYPOTHESIS
AB Background: To examine the site-specific cancer mortality among deaths registered with Parkinson's disease (PD) and multiple sclerosis (MS). We focused on the patterns related to the most frequent cancers.
Methods: We analyzed Swiss mortality data over a 39-year period (1969-2007), using a statistical approach applicable to unique daabases, i.e. when no linkage with morbidity databases or disease registries is possible. It was based on a case-control design with bootstrapping to derive standardized mortality ratios (SMR). The cases were defined by the cancer-PD or cancer-MS co-registrations, whereas the controls were drawn from the remaining records with cancer deaths (matching criteria: sex, age, language region of Switzerland, subperiods 1969-1981, 1982-1994, 1995-2007).
Results: For PD we found lower SMRs in lung and liver cancer and higher SMRs in melanoma/skin cancer, and in cancers of breast and prostate. As for MS, the SMR in lung cancer was lower than expected, whereas SMRs in colorectal, breast and bladder cancer were higher.
Conclusions: A common pattern of associations can be observed in PD and MS, with a lower risk of lung cancer and higher risk of breast cancer than expected. Thus, PD and MS resemble other conditions with similar (schizophrenia) or reversed patterns (rheumatoid arthritis, immunosuppression after organ transplantation). (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Ajdacic-Gross, Vladeta; Rodgers, Stephanie; Mutsch, Margot; Steinemann, Nina; Von Wyl, Viktor; Bopp, Matthias] Univ Zurich, Swiss MS Registry, Epidemiol Biostat & Prevent Inst, Hirschengraben 84, CH-8001 Zurich, Switzerland.
[Ajdacic-Gross, Vladeta; Rodgers, Stephanie; Aleksandrowicz, Aleksandra] Univ Zurich, Hosp Psychiat, Zurich, Switzerland.
[von Kanel, Roland] Univ Hosp Bern, Dept Neurol, Bern, Switzerland.
[von Kanel, Roland] Clin Barmelweid, Barmelweid, Switzerland.
C3 University of Zurich; University of Zurich; University of Bern;
University Hospital of Bern
RP Ajdacic-Gross, V (corresponding author), Univ Zurich, Swiss MS Registry, Epidemiol Biostat & Prevent Inst, Hirschengraben 84, CH-8001 Zurich, Switzerland.
EM vladeta.ajdacic-gross@uzh.ch
RI ; von Kanel, Roland/B-1811-2019
OI Steinemann, Nina/0009-0009-2780-6948; Mutsch,
Margot/0000-0003-0620-5376; von Wyl, Viktor/0000-0002-8754-9797; Bopp,
Matthias/0000-0003-0766-3723; Rodgers, Stephanie/0000-0003-2811-7991;
von Kanel, Roland/0000-0002-8929-5129
FU Swiss National Science Foundation [32-042345.94/1]; Swiss Multiple
Sclerosis Society; Swiss Federal Statistical Office in Neuchatel,
Switzerland
FX This study was supported by the Swiss National Science Foundation (grant
#32-042345.94/1) and by the Swiss Multiple Sclerosis Society. The data
was extracted from the Swiss mortality statistics with authorization
granted by the Swiss Federal Statistical Office in Neuchatel,
Switzerland. We thank Heather Murray for helping us improve the language
and the readability of this paper.
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NR 66
TC 15
Z9 16
U1 1
U2 8
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1877-7821
EI 1877-783X
J9 CANCER EPIDEMIOL
JI Cancer Epidemiol.
PD OCT
PY 2016
VL 44
BP 167
EP 173
DI 10.1016/j.canep.2016.08.018
PG 7
WC Oncology; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Oncology; Public, Environmental & Occupational Health
GA EE3RU
UT WOS:000389515700028
PM 27612279
OA Bronze
DA 2025-01-07
ER
PT J
AU Chang, CSP
AF Chang, Christopher
TI Immunodysregulation in immunodeficiency
SO ALLERGY AND ASTHMA PROCEEDINGS
LA English
DT Article
ID IMMUNE DYSREGULATION; AUTOIMMUNITY; DISEASE
AB The primary immunodeficiency fi ciency diseases are often accompanied by autoimmunity, autoinflammatory, fl ammatory, or aberrant lymphoproliferation. The paradoxical nature of this association can be explained by the multiple cells and molecules involved in immune networks that interact with each other in synergistic, redundant, antagonistic, and parallel arrangements. Because progressively more immunodeficiencies fi ciencies are found to have a genetic etiology, in many cases, a monogenic pathology, an understanding of why immunodeficiency fi ciency is really an immune dysfunction becomes evident. Understanding the role of specific fi c genes allows us to better understand the complete nature of the inborn error of immunity (IEI); the latter is a term generally used when a clear genetic etiology can be discerned. Autoimmune cytopenias, inflammatory fl ammatory bowel disease, autoimmune thyroiditis, and autoimmune liver diseases as well as lymphomas and cancers frequently accompany primary immunodeficiencies, fi ciencies, and it is important that the practitioner be aware of this association and to expect that this is more common than not. The treatment of autoimmune or immunodysregulation in primary immunodeficiencies fi ciencies often involves further immunosuppression, which places the patient at even greater risk of infection. Mitigating measures to prevent such an infection should be considered as part of the treatment regimen. Treatment of immunodysregulation should be mechanism based, as much as we understand the pathways that lead to the dysfunction. Focusing on abnormalities in specific fi c cells or molecules, e.g., cytokines, will become increasingly used to provide a targeted approach to therapy, a prelude to the success of personalized medicine in the treatment of IEIs.
C1 [Chang, Christopher] Mem Healthcare Syst, Div Immunol Allergy & Pediat Rheumatol, 1311 N 35th Ave, Hollywood, FL 33021 USA.
[Chang, Christopher] Joe DiMaggio Childrens Hosp, 1311 N 35th Ave, Hollywood, FL 33021 USA.
RP Chang, CSP (corresponding author), Mem Healthcare Syst, Div Immunol Allergy & Pediat Rheumatol, 1311 N 35th Ave, Hollywood, FL 33021 USA.; Chang, CSP (corresponding author), Joe DiMaggio Childrens Hosp, 1311 N 35th Ave, Hollywood, FL 33021 USA.
EM chrchang@mhs.net
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NR 33
TC 3
Z9 3
U1 0
U2 0
PU OCEAN SIDE PUBLICATIONS INC
PI PROVIDENCE
PA 95 PITMAN ST, PROVIDENCE, RI 02906 USA
SN 1088-5412
EI 1539-6304
J9 ALLERGY ASTHMA PROC
JI Allergy Asthma Proc.
PD SEP 1
PY 2024
VL 45
IS 5
BP 340
EP 346
DI 10.2500/aap.2024.45.240058
PG 7
WC Allergy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy
GA J7Y1N
UT WOS:001339170200010
PM 39294914
DA 2025-01-07
ER
PT J
AU Yang, F
Fan, XL
Liu, YF
Shen, Y
Zhao, SL
Zheng, YY
Men, R
Xie, Y
Yang, L
AF Yang, Fan
Fan, Xiaoli
Liu, Yifeng
Shen, Yi
Zhao, Shenglan
Zheng, Yanyi
Men, Ruoting
Xie, Yan
Yang, Li
TI Long Noncoding RNA and Circular RNA Expression Profiles of
Monocyte-Derived Dendritic Cells in Autoimmune Hepatitis
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE monocyte-derived dendritic cells (MoDCs); autoimmune hepatitis (AIH);
long noncoding RNA (IncRNA); circular RNA (circRNA); microRNA; mRNA
ID ACTIVATION; MECHANISMS; PHENOTYPE; CRITERIA; CANCER; CERNA
AB Autoimmune hepatitis (AIH) is a chronic liver disease caused by disruption of liver immune homeostasis. The effect of dendritic cells (DCs) on the pathogenesis of AIH is not fully understood. Long noncoding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs) have been shown to play critical roles in the regulation of cell function. In this study, we analyzed the immunophenotypic characteristics of DCs in the peripheral blood. The percentage of mature DCs was higher in AIH patients than in healthy controls (HCs), and the proportion of mature DCs decreased after treatment. We isolated monocyte-derived DCs (moDCs) from the peripheral blood, obtained whole RNA-sequencing (RNA-seq) data for the moDCs from the two groups, and identified differentially expressed (DE) lncRNAs, circRNAs, miRNAs and mRNAs. In addition, we performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses for the DE mRNAs and constructed competing endogenous RNA (ceRNA) networks. ENST00000543334, hsa_circ_0000279, and hsa_circ_0005076 were selected and validated by RT-qPCR. These results provide a possible molecular mechanism of DCs in the pathogenesis of AIH and identify some potential therapeutic targets.
C1 [Yang, Fan; Fan, Xiaoli; Liu, Yifeng; Shen, Yi; Zhao, Shenglan; Zheng, Yanyi; Men, Ruoting; Xie, Yan; Yang, Li] Sichuan Univ, Univ Oxford Huaxi Joint Ctr Gastrointestinal Canc, West China Hosp, Dept Gastroenterol & Hepatol, Chengdu, Peoples R China.
C3 Sichuan University
RP Xie, Y; Yang, L (corresponding author), Sichuan Univ, Univ Oxford Huaxi Joint Ctr Gastrointestinal Canc, West China Hosp, Dept Gastroenterol & Hepatol, Chengdu, Peoples R China.
EM xieyan@wchscu.cn; yangli_hx@scu.edu.cn
RI Zheng, Yanyi/GYU-9344-2022; Liu, Yifeng/G-5833-2017; Yang,
Fan/LQK-8676-2024
OI Yang, Fan/0009-0008-5468-4782
FU National Natural Science Foundation of China [81770568]; 1.3.5 project
for disciplines of excellence-Clinical Research Incubation Project, West
China Hospital, Sichuan University [2019HXFH025]
FX This work was supported by grants from the National Natural Science
Foundation of China (No. 81770568) and 1 center dot 3 center dot 5
project for disciplines of excellence-Clinical Research Incubation
Project, West China Hospital, Sichuan University (No. 2019HXFH025).
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NR 55
TC 4
Z9 4
U1 1
U2 17
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD DEC 6
PY 2021
VL 12
AR 792138
DI 10.3389/fphar.2021.792138
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XR1PK
UT WOS:000732010100001
PM 34938195
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Aljohani, MSA
Alshammari, MRA
Alhafi, AMA
Alsharari, ANS
Alruwayeh, SKAA
Alanazi, SAH
Alshammari, FHH
Alsharari, KSS
Alzahrani, FMA
Alaleet, WAM
AF Aljohani, Mohammed Saud Ali
Alshammari, Muteb Radhi A.
Alhafi, Alhumaidi Mohammed A.
Alsharari, Abdullah Nafea S.
Alruwayeh, Salma Kh A. A.
Alanazi, Sami Ahmed H.
Alshammari, Fahad Hamdan H.
Alsharari, Khalid Saleh S.
Alzahrani, Fahad Matar Abdulaziz
Alaleet, Walied Abdulaziz M.
TI LIVER TRANSPLANT SURGERY-AN OVERVIEW
SO INDO AMERICAN JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Article
DE Surgery; liver transplant; an overview; recent advances
ID DONATION; DISEASE; ADULT; LIFE
AB Introduction: The amazing work of Thomas Starzl, et al and other researchers in the 1950s led to the first ever successful liver transplant in 1963 by Starzl in Denver, et al. 5 years later, Sir Roy Calne, conducted the first European liver transplant programme in Cambridge, UK. In the beginning, the progress was very gradual and the death rates of recipients were very high. It is due to the tribute to the early pioneers that they stayed persistent in overcoming the many challenges and obstacles; advances in surgical and anaesthetic techniques, greater understanding of the physiological, haematological, biochemical, microbiological and immunological variations in liver disease and transplantation led to a multidisciplinary approach that led to better outcomes. The progress made, together with more effective immunosuppressive and anti-microbial agents and enhancements in patient and donor selection, has made liver replacement as a routine surgery with very good long term results Aim of work: In this review, we will discuss the most recent evidence regarding liver transplant surgery. Methodology: We did a systematic search for liver transplant surgery-an overview using PubMed search engine (http://www.ncbi.nlm.nih.gov/) and Google Scholar search engine (https://scholar.google.com). All relevant studies were retrieved and discussed. We only included full articles. Conclusions: Liver transplantation, though currently considered a routine procedure, with known indications and usually excellent results, still has many difficulties. Donor shortage continues to be a major drawback. Transplanted organs are full of risk and could transmit malignancy, infections, metabolic or autoimmune diseases. Methods to solve the donor shortage problem consist of using of organs from donors after circulatory death, from living donors and from those previously infected with Hepatitis B and C and even HIV for selected recipients. Normothermic regional and/or machine perfusion, whether static or pulsatile, normo- or hypothermic, are being studied and will be probably have an essential role in enhancing donation rates and results. The main indications for liver replacement are alcoholic liver disease, HCV, non-alcoholic liver disease and liver cancer. New research have concluded that selected patients with severe alcoholic hepatitis could also get advantages from liver transplant. The advent of new and highly effective treatments for HCV, whether given before or aftertransplant will have a major impact on outcomes. The role of transplantation for those with liver cell cancer continues to evolve as other interventions become more efficient. Immunosuppression is often needed for life-long and adherence continues to be a huge difficulty, particularly in young adolescents. Immunosuppression with calcineurin inhibitors (primarily tacrolimus), antimetabolites (azathioprine or mycophenolate) and corticosteroids remains standard. Results after transplantation are good but not normal in quality or quantity. Premature death may be due to increased risk of cardiovascular disease, de novo cancer, recurrent disease or late technical problems
C1 [Aljohani, Mohammed Saud Ali; Alshammari, Muteb Radhi A.; Alhafi, Alhumaidi Mohammed A.; Alsharari, Abdullah Nafea S.; Alruwayeh, Salma Kh A. A.; Alanazi, Sami Ahmed H.; Alshammari, Fahad Hamdan H.; Alsharari, Khalid Saleh S.; Alzahrani, Fahad Matar Abdulaziz; Alaleet, Walied Abdulaziz M.] Jordan Univ Sci & Technol, Irbid, Jordan.
C3 Jordan University of Science & Technology
RP Aljohani, MSA (corresponding author), Jordan Univ Sci & Technol, Irbid, Jordan.
RI Alshammari, Maha/JGM-7078-2023
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NR 14
TC 0
Z9 0
U1 0
U2 2
PU SSJ COLL PHARMACY-SSJCP
PI NAGPUR
PA 125B-125 SANTRANJIPURA, TLIPHONE EXCHANGE RD, NAGPUR, 440001, INDIA
SN 2349-7750
J9 INDO AM J PHARM SCI
JI Indo Am. J. Pharm. Sci.
PD JAN
PY 2019
VL 6
IS 1
BP 1531
EP 1535
DI 10.5281/zenodo.2545847
PG 5
WC Chemistry, Medicinal
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA HI3WK
UT WOS:000456382000239
DA 2025-01-07
ER
PT J
AU Li, S
Fan, GF
Li, XJY
Cai, YJ
Liu, RP
AF Li, Shuo
Fan, Guifang
Li, Xiaojiaoyang
Cai, Yajie
Liu, Runping
TI Modulation of type I interferon signaling by natural products in the
treatment of immune-related diseases
SO CHINESE JOURNAL OF NATURAL MEDICINES
LA English
DT Review
DE [KEY WORDS] Type I interferons; Natural products; Infection; Cancer;
Autoimmune diseases
ID RESPIRATORY SYNCYTIAL VIRUS; JANUS KINASE/SIGNAL TRANSDUCER;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; TOLL-LIKE RECEPTORS; RIG-I; DNA SENSOR;
HEPATOCELLULAR-CARCINOMA; INFLAMMATORY MEDIATORS; TBK1/IRF3 PATHWAYS;
ANTIVIRAL ACTIVITY
AB Type I interferon (IFN) is considered as a bridge between innate and adaptive immunity. Proper activation or inhibi-tion of type I IFN signaling is essential for host defense against pathogen invasion, tumor cell proliferation, and overactive immune re-sponses. Due to intricate and diverse chemical structures, natural products and their derivatives have become an invaluable source in-spiring innovative drug discovery. In addition, some natural products have been applied in clinical practice for infection, cancer, and autoimmunity over thousands of years and their promising curative effects and safety have been well-accepted. However, whether these natural products are primarily targeting type I IFN signaling and specific molecular targets involved are not fully elucidated. In the current review, we thoroughly summarize recent advances in the pharmacology researches of natural products for their type I IFN activity, including both agonism/activation and antagonism/inhibition, and their potential application as therapies. Furthermore, the source and chemical nature of natural products with type I IFN activity are highlighted and their specific molecular targets in the type I IFN pathway and mode of action are classified. In conclusion, natural products possessing type I IFN activity represent promising therapeutic strategies and have a bright prospect in the treatment of infection, cancer, and autoimmune diseases.
C1 [Li, Shuo; Fan, Guifang; Cai, Yajie; Liu, Runping] Beijing Univ Chinese Med, Sch Chinese Mat Med, Beijing 100029, Peoples R China.
[Li, Xiaojiaoyang] Beijing Univ Chinese Med, Sch Life Sci, Beijing 102488, Peoples R China.
C3 Beijing University of Chinese Medicine; Beijing University of Chinese
Medicine
RP Liu, RP (corresponding author), Beijing Univ Chinese Med, Sch Chinese Mat Med, Beijing 100029, Peoples R China.
EM liurun-ping@bucm.edu.cn
RI liu, runping/V-2733-2018; Li, Xiaojiaoyang/CAG-6603-2022
FU Beijing Nova Pro- gram of Science Technology [Z201100006820025,
Z211100002121167]; Young Elite Scientists Sponsorship Pro- gram from
CACM [CACM-2020-QNRC2-04]; National Natural Science Foundation of China
[82004029]
FX [Received on] 17 -Aug. -2022 [Research funding] This work was supported
by Beijing Nova Pro- gram of Science & Technology (Nos. Z201100006820025
and Z211100002121167) , the Young Elite Scientists Sponsorship Pro- gram
from CACM (No. CACM-2020-QNRC2-04) and the National Natural Science
Foundation of China (No. 82004029) . [* Corresponding author] Tel:
86-10-53912122, E-mail: liurun- ping@bucm.edu.cn These authors have no
conflict of interest to declare.
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NR 160
TC 4
Z9 4
U1 3
U2 16
PU CHINESE JOURNAL NATURAL MEDICINES
PI NANJING
PA 24, TONGJIA XIANG, NANJING, 210009, PEOPLES R CHINA
SN 2095-6975
EI 1875-5364
J9 CHIN J NAT MEDICINES
JI Chin. J. Nat. Med.
PD JAN
PY 2023
VL 21
IS 1
BP 3
EP 18
DI 10.1016/S1875-5364(23)60381-4
EA JAN 2023
PG 16
WC Integrative & Complementary Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine; Pharmacology & Pharmacy
GA E5RS3
UT WOS:000976118700002
PM 36641230
OA Bronze
DA 2025-01-07
ER
PT J
AU Cai, QY
Gan, C
Tang, CW
Wu, H
Gao, JH
AF Cai, Qiuyu
Gan, Can
Tang, Chengwei
Wu, Hao
Gao, Jinhang
TI Mechanism and Therapeutic Opportunities of Histone Modifications in
Chronic Liver Disease
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE histone acetylation; histone methylation; histone phosphorylation;
alcoholic liver disease; metabolic associated fatty liver disease; viral
hepatitis; liver fibrosis; liver cirrhosis
ID HEPATIC STELLATE CELLS; B-VIRUS REPLICATION; S-ADENOSYLMETHIONINE;
IN-VITRO; HEPATOCELLULAR-CARCINOMA; UP-REGULATION; EPIGENETIC MECHANISM;
SECONDARY STRUCTURE; CHROMATIN-STRUCTURE; P300/CBP INHIBITOR
AB Chronic liver disease (CLD) represents a global health problem, accounting for the heavy burden of disability and increased health care utilization. Epigenome alterations play an important role in the occurrence and progression of CLD. Histone modifications, which include acetylation, methylation, and phosphorylation, represent an essential part of epigenetic modifications that affect the transcriptional activity of genes. Different from genetic mutations, histone modifications are plastic and reversible. They can be modulated pharmacologically without changing the DNA sequence. Thus, there might be chances to establish interventional solutions by targeting histone modifications to reverse CLD. Here we summarized the roles of histone modifications in the context of alcoholic liver disease (ALD), metabolic associated fatty liver disease (MAFLD), viral hepatitis, autoimmune liver disease, drug-induced liver injury (DILI), and liver fibrosis or cirrhosis. The potential targets of histone modifications for translation into therapeutics were also investigated. In prospect, high efficacy and low toxicity drugs that are selectively targeting histone modifications are required to completely reverse CLD and prevent the development of liver cirrhosis and malignancy.
C1 [Cai, Qiuyu; Gan, Can; Tang, Chengwei; Gao, Jinhang] Sichuan Univ, West China Hosp, Lab Gastroenterol & Hepatol, Chengdu, Peoples R China.
[Cai, Qiuyu; Gan, Can; Tang, Chengwei; Wu, Hao; Gao, Jinhang] Sichuan Univ, West China Hosp, Dept Gastroenterol, Chengdu, Peoples R China.
C3 Sichuan University; Sichuan University
RP Gao, JH (corresponding author), Sichuan Univ, West China Hosp, Lab Gastroenterol & Hepatol, Chengdu, Peoples R China.; Wu, H; Gao, JH (corresponding author), Sichuan Univ, West China Hosp, Dept Gastroenterol, Chengdu, Peoples R China.
EM Gao.jinhang@scu.edu.cn; Gao.jinhang@qq.com
RI Gao, Jinhang/KXN-7503-2024; Chen, Tony Hsiu-Hsi/JPY-2493-2023
FU National Natural Science Fund of China [82170623, 82170625, U1702281,
81873584, 82000613, 82000574]; National Key R&D Program of China
[2017YFA0205404]; Sichuan Science and Technology Program [2020YJ0084,
2021YFS0147]; 135 projects for disciplines of excellence of West China
Hospital, Sichuan University [ZYGD18004]
FX Funding This work was supported by the National Natural Science Fund of
China (82170623, 82170625, U1702281, 81873584, 82000613, and 82000574),
National Key R&D Program of China (2017YFA0205404), Sichuan Science and
Technology Program (2020YJ0084 and 2021YFS0147), and the 135 projects
for disciplines of excellence of West China Hospital, Sichuan University
(ZYGD18004).
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NR 221
TC 19
Z9 20
U1 6
U2 39
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD NOV 23
PY 2021
VL 12
AR 784591
DI 10.3389/fphar.2021.784591
PG 20
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XK7NA
UT WOS:000727646300001
PM 34887768
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Pines, M
Spector, I
AF Pines, Mark
Spector, Itai
TI Halofuginone - The Multifaceted Molecule
SO MOLECULES
LA English
DT Review
DE malaria; fibrosis; inflammation; autoimmunity; Th-17; apoptosis
ID VERSUS-HOST-DISEASE; GROWTH-FACTOR-BETA; T(H)17 CELL-DIFFERENTIATION;
INDUCED LIVER FIBROSIS; TGF-BETA; I SYNTHESIS; FEBRIFUGINE DERIVATIVES;
COLLAGEN-SYNTHESIS; T-CELL; CRYPTOSPORIDIUM-PARVUM
AB Halofuginone is an analog of febrifugine-an alkaloid originally isolated from the plant Dichroa febrifuga. During recent years, halofuginone has attracted much attention because of its wide range of beneficial biological activities, which encompass malaria, cancer, and fibrosis-related and autoimmune diseases. At present two modes of halofuginone actions have been described: (1) Inhibition of Smad3 phosphorylation downstream of the TGF beta signaling pathway results in inhibition of fibroblasts-to-myofibroblasts transition and fibrosis. (2) Inhibition of prolyl-tRNA synthetase (ProRS) activity in the blood stage of malaria and inhibition of Th17 cell differentiation thereby inhibiting inflammation and the autoimmune reaction by activation of the amino acid starvation and integrated stress responses. This review deals with the history and origin of this natural product, its synthesis, its known modes of action, and it's various biological activities in pre-clinical animal models and in humans.
C1 [Pines, Mark; Spector, Itai] Agr Res Org, Volcani Ctr, Inst Anim Sci, IL-50250 Bet Dagan, Israel.
[Spector, Itai] Hebrew Univ Jerusalem, Dept Anim Sci, IL-76100 Rehovot, Israel.
C3 VOLCANI INSTITUTE OF AGRICULTURAL RESEARCH; Hebrew University of
Jerusalem
RP Pines, M (corresponding author), Agr Res Org, Volcani Ctr, Inst Anim Sci, POB 6, IL-50250 Bet Dagan, Israel.
EM mark.pines@mail.huji.ac.il; itais222@gmail.com
FU Legacy Heritage Bio-Medical Program of the Israel Science Foundation
[1315/10]
FX We thank the Legacy Heritage Bio-Medical Program of the Israel Science
Foundation grant (No. 1315/10) for financial support.
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NR 126
TC 97
Z9 111
U1 0
U2 43
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1420-3049
J9 MOLECULES
JI Molecules
PD JAN
PY 2015
VL 20
IS 1
BP 573
EP 594
DI 10.3390/molecules20010573
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA AZ6HB
UT WOS:000348319000034
PM 25569515
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Frankson, R
Yu, ZH
Bai, YP
Li, QL
Zhang, RY
Zhang, ZY
AF Frankson, Rochelle
Yu, Zhi-Hong
Bai, Yunpeng
Li, Qinglin
Zhang, Ruo-Yu
Zhang, Zhong-Yin
TI Therapeutic Targeting of Oncogenic Tyrosine Phosphatases
SO CANCER RESEARCH
LA English
DT Review
ID NEGATIVE BREAST-CANCER; LIVER 2 PRL2; REGENERATING LIVER; SHP2
PHOSPHATASE; PROTEIN; INHIBITOR; GROWTH; PROGRESSION; PTPN11; CELLS
AB Protein tyrosine phosphatases (PTP) are exciting and novel targets for cancer drug discovery that work in concert with protein tyrosine kinases (PTK) in controlling cellular homeostasis. Given the activating role that some PTKs play in initiating growth factor-mediated cellular processes, PTPs are usually perceived as the negative regulators of these events and therefore tumor suppressive in nature. However, mounting evidence indicate that PTPs do not always antagonize the activity of PTKs in regulating tyrosine phosphorylation, but can also play dominant roles in the initiation and progression of signaling cascades that regulate cell functions. It follows, therefore, that PTP malfunction can actively contribute to a host of human disorders, in particular, cancer, metabolic syndromes, and autoimmune diseases. The Src homology domain containing phosphatase 2 (SHP2) and the three-membered family of phosphatases of regenerating liver (PRL) are infamously oncogenic members of the PTP superfamily. Both are established regulators of major cancer pathways such as Ras/ERK1/2, Src, JAK/STAT, JNK, NF-kappa B, and PTEN/PI3K/AKT. Furthermore, upregulation, mutation, or other dysregulation of these PTPs has been positively correlated with cancer initiation and progression. This review will provide topical coverage of target validation and drug discovery efforts made in targeting these oncogenic PTPs as compelling candidates for cancer therapy. (C) 2017 AACR.
C1 Purdue Univ, Dept Med Chem, W Lafayette, IN 47907 USA.
Purdue Univ, Dept Mol Pharmacol & Chem, Ctr Canc Res, W Lafayette, IN 47907 USA.
Purdue Univ, Inst Drug Discovery, W Lafayette, IN 47907 USA.
C3 Purdue University System; Purdue University; Purdue University System;
Purdue University; Purdue University System; Purdue University
RP Zhang, ZY (corresponding author), Purdue Univ, 575 Stadium Mall Dr,RHPH 202A, W Lafayette, IN 47907 USA.
EM zhang-zy@purdue.edu
RI Bai, Yunpeng/M-8396-2014; yu, zhihong/KRO-4146-2024
OI Bai, Yunpeng/0000-0002-5879-3555
FU NIH [RO1 CA69202, RO1 CA207288]
FX We gratefully acknowledge the financial support of NIH grants RO1
CA69202 and RO1 CA207288.
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NR 43
TC 136
Z9 160
U1 1
U2 55
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2017
VL 77
IS 21
BP 5701
EP 5705
DI 10.1158/0008-5472.CAN-17-1510
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FL5CI
UT WOS:000414248300032
PM 28855209
OA Bronze, Green Accepted
DA 2025-01-07
ER
PT J
AU Lee, WS
Karthik, SV
Ng, RT
Ong, SY
Ong, C
Chiou, FK
Wong, SY
Quak, SH
Aw, MM
AF Lee, Way Seah
Karthik, Sivaramakrishnan Venkatesh
Ng, Ruey Terng
Ong, Sik Yong
Ong, Christina
Chiou, Fang K.
Wong, Shin Yee
Quak, Seng Hock
Aw, Marion Margaret
TI Characteristics and outcome of primary sclerosing cholangitis associated
with inflammatory bowel disease in Asian children
SO PEDIATRICS AND NEONATOLOGY
LA English
DT Article
DE sclerosing cholangitis; ulcerative colitis; progressive
ID ULCERATIVE-COLITIS; NATURAL-HISTORY; PSC-IBD; DIAGNOSIS; PHENOTYPE;
EPIDEMIOLOGY; FEATURES
AB Background: Current knowledge on the clinical features and natural history of childhood primary sclerosing cholangitis - inflammatory bowel disease in Asia is limited. We described the presenting features and natural history of primary sclerosing cholangitis-inflammatory bowel disease seen in a cohort of Southeast Asian children.
Methods: We conducted a retrospective review of childhood primary sclerosing cholangitis-inflammatory bowel disease from three tertiary centers in Singapore and Malaysia.
Results: Of 24 patients (boys, 58%; median age at diagnosis: 6.3 years) with primary sclerosing cholangitis-inflammatory bowel disease (ulcerative colitis, n = 21; Crohn's disease, n = 1; undifferentiated, n = 2), 63% (n = 15) were diagnosed during follow-up for colitis, and 21% (n = 5) presented with acute or chronic hepatitis, 17% (n = 4) presented simultaneously. Disease phenotype of liver involvement showed 79% had sclerosing cholangitis-autoimmune hepatitis overlap, 54% large duct disease, and 46% small duct disease. All patients received immunosuppression therapy. At final review after a median [+/- S.D.] duration follow-up of 4.7 [+/- 3.8] years, 12.5% patients had normal liver enzymes, 75% persistent disease, and 12.5% liver failure. The proportion of patients with liver cirrhosis increased from 13% at diagnosis to 29%; 21% had portal hypertension, and 17% had liver dysfunction. One patient required liver transplant. Transplant-free survival was 95%. For colitis, 95% had pancolitis, 27% rectal sparing, and 11% backwash ileitis at initial presentation. At final review, 67% patients had quiescent bowel disease with immunosuppression. One patient who had UC with pancolitis which was diagnosed at 3 years old developed colorectal cancer at 22 years of age. All patients survived.
Conclusions: Liver disease in primary sclerosing cholangitis-inflammatory bowel disease in Asian children has variable severity. With immunosuppression, two-thirds of patients have quiescent bowel disease but the majority have persistent cholangitis and progressive liver disease. Copyright (C) 2018, Taiwan Pediatric Association. Published by Elsevier Taiwan LLC.
C1 [Lee, Way Seah; Ng, Ruey Terng; Ong, Sik Yong; Wong, Shin Yee] Univ Malaya, Med Ctr, Dept Paediat, Kuala Lumpur 59100, Malaysia.
[Lee, Way Seah] Univ Malaya, Paediat & Child Hlth Res Grp, Kuala Lumpur, Malaysia.
[Karthik, Sivaramakrishnan Venkatesh; Quak, Seng Hock; Aw, Marion Margaret] Natl Univ Singapore Hosp, Khoo Teck Puat Natl Univ Childrens Med Inst, Singapore, Singapore.
[Ong, Christina; Chiou, Fang K.] KK Womens & Childrens Hosp, Gastroenterol Serv, Dept Paediat Med, Bukit Timah Rd, Singapore, Singapore.
[Quak, Seng Hock; Aw, Marion Margaret] Natl Univ Singapore, Dept Paediat, Kent Ridge Rd, Singapore, Singapore.
C3 Universiti Malaya; Universiti Malaya; National University of Singapore;
KK Women's & Children's Hospital; National University of Singapore
RP Lee, WS (corresponding author), Univ Malaya, Med Ctr, Dept Paediat, Kuala Lumpur 59100, Malaysia.
EM leews@ummc.edu.my
RI NG, RUEY/T-1761-2017; Lee, Way Seah/B-8844-2010
OI Lee, Way Seah/0000-0001-9163-2828; Chiou, Fang Kuan/0000-0003-4777-0267
FU University Malaya High Impact Research, Ministry of Higher Education,
Malaysia [UM.C/625/HIR/MOHE/CHAN/13/1]
FX WS Lee and SY Wong are supported by a research grant from University
Malaya High Impact Research, Ministry of Higher Education, Malaysia
(UM.C/625/HIR/MOHE/CHAN/13/1).
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NR 31
TC 5
Z9 5
U1 0
U2 2
PU ELSEVIER TAIWAN
PI TAIPEI
PA RM N-412, 4F, CHIA HSIN BUILDING 11, NO 96, ZHONG SHAN N ROAD SEC 2,
TAIPEI, 10449, TAIWAN
SN 1875-9572
EI 2212-1692
J9 PEDIATR NEONATOL
JI Pediatr. Neonatol.
PD AUG
PY 2019
VL 60
IS 4
BP 396
EP 404
DI 10.1016/j.pedneo.2018.09.007
PG 9
WC Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics
GA IQ0CV
UT WOS:000480419100008
PM 31409456
DA 2025-01-07
ER
PT J
AU Zhao, HF
Du, WT
Gu, DS
Wang, DH
Xue, F
Ge, J
Sui, T
Yang, RC
AF Zhao, Haifeng
Du, Weiting
Gu, Dongsheng
Wang, Donghai
Xue, Feng
Ge, Jing
Sui, Tao
Yang, Renchi
TI DNMT3B 579G>T Promoter Polymorphism and the Risk for Idiopathic
Thrombocytopenic Purpura in a Chinese Population
SO ACTA HAEMATOLOGICA
LA English
DT Article
DE DNA methyltransferase 3B; Polymorphism; Idiopathic thrombocytopenic
purpura
ID MAMMALIAN DNA METHYLTRANSFERASES; SQUAMOUS-CELL CARCINOMA; LUNG-CANCER;
HEPATOCELLULAR CARCINOMAS; PERIPHERAL-BLOOD; IMMUNE-SYSTEM;
BREAST-CANCER; MESSENGER-RNA; EXPRESSION; METHYLATION
AB Epigenetics may influence the expression of numerous genes, which might contribute to autoimmune diseases. DNA methylation is mediated by DNA methyltransferases, especially DNA methyltransferase 3B (DNMT3B). Polymorphisms of the DNMT3B gene may influence DNMT3B activity on DNA methylation and increase the susceptibility to several diseases. The current study investigated the association between DNMT3B 579G > T and the risk for idiopathic thrombocytopenic purpura (ITP). The DNMT3B 579G > T polymorphisms were analyzed by PCR-RFLP. There was no significant difference in genotype and allele distribution between the ITP patient and the controls (p = 0.722 and 0.667, respectively). Similar results were observed between the 2 groups when stratified by age and disease course, including acute in childhood, chronic in childhood, acute in adult and chronic in adult. Importantly, this study showed a statistical difference in the distribution of SNP of DNMT3B between Chinese and Koreans or Americans. It is shown that the SNP of DNMT3B 579G > T may not be used on its own as a marker to predict the susceptibility to ITP in a Chinese population and that DNMT3B 579G > T promoter SNP varies from one ethnic population to another. Copyright (C) 2009 S. Karger AG, Basel
C1 [Zhao, Haifeng; Du, Weiting; Gu, Dongsheng; Xue, Feng; Ge, Jing; Sui, Tao; Yang, Renchi] Chinese Acad Med Sci, Inst Hematol, State Key Lab Expt Hematol, Tianjin 300020, Peoples R China.
[Zhao, Haifeng; Du, Weiting; Gu, Dongsheng; Xue, Feng; Ge, Jing; Sui, Tao; Yang, Renchi] Chinese Acad Med Sci, Blood Dis Hosp, Tianjin 300020, Peoples R China.
[Zhao, Haifeng; Du, Weiting; Gu, Dongsheng; Xue, Feng; Ge, Jing; Sui, Tao; Yang, Renchi] Peking Union Med Coll, Tianjin 300020, Peoples R China.
[Wang, Donghai] Albert Einstein Coll Med, Albert Einstein Canc Ctr, Montefiore Med Ctr, Bronx, NY USA.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Institute of Hematology & Blood Diseases Hospital - CAMS; Chinese
Academy of Medical Sciences - Peking Union Medical College; Institute of
Hematology & Blood Diseases Hospital - CAMS; Chinese Academy of Medical
Sciences - Peking Union Medical College; Peking Union Medical College;
Montefiore Medical Center; Albert Einstein College of Medicine; Yeshiva
University
RP Yang, RC (corresponding author), Chinese Acad Med Sci, Inst Hematol, State Key Lab Expt Hematol, 288 Nanjing Rd, Tianjin 300020, Peoples R China.
EM rcyang65@yahoo.com
RI zhao, haifeng/JNX-7170-2023; wang, zhe/JNE-3510-2023; Du,
Weiting/C-9971-2014
FU National Natural Science Foundation of China [30670900]; Ministry of
Education of China [20060023038]; Ministry of Health [200802031]
FX This work was supported in part by grants from the National Natural
Science Foundation of China (30670900), the Ministry of Education of
China (20060023038) and the Ministry of Health (200802031).
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NR 27
TC 12
Z9 13
U1 2
U2 8
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0001-5792
EI 1421-9662
J9 ACTA HAEMATOL-BASEL
JI Acta Haematol.
PY 2009
VL 122
IS 1
BP 31
EP 35
DI 10.1159/000235616
PG 5
WC Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology
GA 503SS
UT WOS:000270560600008
PM 19696477
DA 2025-01-07
ER
PT J
AU Lee, JJ
Schindera, ST
Jang, HJ
Fung, S
Kim, TK
AF Lee, Jonghun John
Schindera, Sebastian T.
Jang, Hyun-Jung
Fung, Scott
Kim, Tae Kyoung
TI Cholangiocarcinoma and its mimickers in primary sclerosing cholangitis
SO ABDOMINAL RADIOLOGY
LA English
DT Article
DE Cholangiocarcinoma; Primary sclerosing cholangitis; Mass-forming;
Perihilar; Imaging
ID CONTRAST-ENHANCED ULTRASOUND; RADIOLOGIC-PATHOLOGICAL CORRELATION;
IN-SITU HYBRIDIZATION; INTRAHEPATIC CHOLANGIOCARCINOMA;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE PANCREATITIS; HILAR
CHOLANGIOCARCINOMA; LIVER-TRANSPLANTATION; PERIPHERAL
CHOLANGIOCARCINOMA; NATURAL-HISTORY
AB Cholangiocarcinoma (CCA) is the most common malignancy in primary sclerosing cholangitis (PSC). Approximately half of CCA are diagnosed within two years of initial diagnosis and often have a poor prognosis because of advanced tumor stage at the time of diagnosis. Thus, rigorous initial imaging evaluation for detecting CCA is important. CCA in PSC usually manifests as intrahepatic mass-forming or perihilar periductal-infiltrating type. Imaging diagnosis is often challenging due to pre-existing biliary strictures and heterogeneous liver. Multimodality imaging approach and careful comparison with prior images are often helpful in detecting small CCA. Ultrasound is widely used as an initial test, but has a limited ability to detect small tumors in the heterogeneous liver with PSC. MRI combined with MRCP is excellent to demonstrate focal biliary abnormalities as well as subtle liver masses. Contrast-enhanced ultrasound is useful to demonstrate CCA by demonstrating rapid and marked washout. In addition, there are other disease entities that mimic CCA including hepatocellular carcinoma, confluent hepatic fibrosis, IgG4-related sclerosing cholangitis, inflammatory mass, and focal fat deposition. In this pictorial essay, imaging findings of CCA in PSC is described and discuss the challenges in imaging surveillance for CCA in the patients with PSC. Imaging findings of the mimickers of CCA in PSC and their differentiating features are also discussed.
C1 [Lee, Jonghun John; Jang, Hyun-Jung; Kim, Tae Kyoung] Univ Toronto, Toronto Gen Hosp, Dept Med Imaging, 585 Univ Ave, Toronto, ON M5G 2N2, Canada.
[Schindera, Sebastian T.] Kantonsspital Aarau AG, Dept Radiol, Aarau, Switzerland.
[Fung, Scott] Univ Toronto, Dept Gastroenterol, Toronto, ON, Canada.
C3 University of Toronto; University Health Network Toronto; Toronto
General Hospital; Kantonsspital Aarau AG (KSA); University of Toronto
RP Kim, TK (corresponding author), Univ Toronto, Toronto Gen Hosp, Dept Med Imaging, 585 Univ Ave, Toronto, ON M5G 2N2, Canada.
EM taekyoung.kim@uhn.on.ca
RI Kim, Tae Kyoung/O-4252-2015
OI Kim, Tae Kyoung/0000-0001-5193-1428
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NR 61
TC 15
Z9 17
U1 1
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 2366-004X
EI 2366-0058
J9 ABDOM RADIOL
JI Abdom. Radiol.
PD DEC
PY 2017
VL 42
IS 12
BP 2898
EP 2908
DI 10.1007/s00261-017-1328-8
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA FN3ZT
UT WOS:000415942900015
PM 28951947
DA 2025-01-07
ER
PT J
AU Wang, ZY
Luo, HJ
Wang, HP
Xiao, M
Jia, HX
Ren, CH
Liu, JF
AF Wang, Zhongyan
Luo, Hongjing
Wang, Heping
Xiao, Meng
Jia, Haixue
Ren, Chunhua
Liu, Jianfeng
TI Peptide-Based Supramolecular Therapeutics for Fighting Major Diseases
SO ADVANCED FUNCTIONAL MATERIALS
LA English
DT Review
DE major disease; nanomedicine; peptide; self-assembly; supramolecular
therapeutics
ID SELF-ASSEMBLED PEPTIDE; FATTY LIVER; FUNCTIONAL RECOVERY; CANCER-CELLS;
HYDROGELS; DELIVERY; MODEL; IMMUNOTHERAPY; NANOMEDICINE; FENOFIBRATE
AB Peptide-based supramolecular therapeutics (PST) refer to those theranostic nanomedicines based on peptide or peptide derivatives self-assembly that are constructed in vitro or in vivo. Benefiting from the inherent advantages of peptides, such as good biocompatibility, high bioactivity, and flexible tunability, the reported PST have shown excellent application prospects in combating many major diseases including cancer, cardiovascular disease, infectious disease, autoimmune disease, metabolic disease, and so on. Through thoughtful design, the PST can be fabricated in various forms, including self-assembled precursor molecules, functional nano-assemblies, and macroscopic large-scale hydrogels. The involved peptides in the PST can play different roles, such as serving drug carriers for effective delivery, acting as scaffold materials for cell culture, and functioning as bioactive sequences for treating diseases. In this review, a comprehensive overview of traditional strategies is provided to build PST and emphasize their therapeutic applications for fighting major diseases that pose a threat to human life and health. Moreover, the main challenges of PST in systems design, therapeutic application, and clinical translation are also briefly discussed. It is hoped that this review can arouse much more attention to be paid for PST and promote its practical application in the biomedical field.
In this review, a comprehensive overview of traditional strategies is provided to build PST and emphasize their therapeutic applications for fighting major diseases that pose a threat to human life and health including cancer, cardiovascular and cerebrovascular diseases, infectious diseases, autoimmune diseases, etc. The main challenges of PST in systems design, therapeutic application, and clinical translation are also briefly discussed. It is hoped that this review can arouse much more attention to be paid for PST and promote its practical application in the biomedical field. image
C1 [Wang, Zhongyan; Luo, Hongjing; Wang, Heping; Xiao, Meng; Jia, Haixue; Ren, Chunhua; Liu, Jianfeng] Chinese Acad Med Sci & Peking Union Med Coll, Tianjin Key Lab Radiat Med & Mol Nucl Med, Key Lab Radiopharmacokinet Innovat Drugs, Chinese Acad Med Sci,Inst Radiat Med, Tianjin 300192, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Institute of Radiation Medicine - CAMS; Peking Union Medical College
RP Ren, CH; Liu, JF (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Tianjin Key Lab Radiat Med & Mol Nucl Med, Key Lab Radiopharmacokinet Innovat Drugs, Chinese Acad Med Sci,Inst Radiat Med, Tianjin 300192, Peoples R China.
EM renchunhua@irm-cams.ac.cn; liujianfeng@irm-cams.ac.cn
RI wang, heping/AAX-7194-2020; Ren, Chunhua/LQJ-6189-2024; liu,
jianfeng/I-8577-2015
OI luo, hong jing/0009-0009-1723-6363; Ren, chunhua/0009-0001-9662-7769;
liu, jianfeng/0000-0003-0541-5072
FU National Science Fund for Distinguished Young Scholars; National Natural
Science Foundation of China [32271465, 32371462, 81971731]; CAMS
Innovation Fund for Medical Sciences [2021-I2M-1-042, 2023-I2MQJ-016];
Non-Profit Central Research Institute Fund of the Chinese Academy of
Medical Sciences [2022-RC350-06]; [82225026]
FX This work was supported by the National Science Fund for Distinguished
Young Scholars (82225026), the National Natural Science Foundation of
China (32271465, 32371462, 81971731), CAMS Innovation Fund for Medical
Sciences (2021-I2M-1-042, 2023-I2MQJ-016), Non-Profit Central Research
Institute Fund of the Chinese Academy of Medical Sciences
(2022-RC350-06)
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Zhou L, 2022, STEM CELL RES THER, V13, DOI 10.1186/s13287-022-02876-2
Zhou P, 2023, MATTER-US, V6, P1945, DOI 10.1016/j.matt.2023.03.029
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NR 187
TC 7
Z9 7
U1 24
U2 42
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1616-301X
EI 1616-3028
J9 ADV FUNCT MATER
JI Adv. Funct. Mater.
PD JUN
PY 2024
VL 34
IS 25
DI 10.1002/adfm.202314492
EA FEB 2024
PG 28
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
Physics, Condensed Matter
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
Physics
GA WC1S3
UT WOS:001171191300001
DA 2025-01-07
ER
PT J
AU Nakanishi, Y
Tsuneyama, K
Fujimoto, M
Salunga, TL
Nomoto, K
An, JL
Takano, Y
Iizuka, S
Nagata, M
Suzuki, W
Shimada, T
Aburada, M
Nakano, M
Selmi, C
Gershwin, ME
AF Nakanishi, Yuko
Tsuneyama, Koichi
Fujimoto, Makoto
Salunga, Thucydides L.
Nomoto, Kazuhiro
An, Jun-Ling
Takano, Yasuo
Iizuka, Seiichi
Nagata, Mitsunobu
Suzuki, Wataru
Shimada, Tsutomu
Aburada, Masaki
Nakano, Masayuki
Selmi, Carlo
Gershwin, M. Eric
TI Monosodium glutamate (MSG): A villain and promoter of liver inflammation
and dysplasia
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article; Proceedings Paper
CT Symposium on the Mosaic of Autoimmunity held in honor of Yehuda
Shoenfelds 60th Birthday
CY FEB 10-11, 2005
CL Tel Aviv, ISRAEL
DE liver steatosis; nonalcoholic steatohepatitis; obesity; diabetes
mellitus
ID AUTOIMMUNE HEPATITIS; NONALCOHOLIC STEATOHEPATITIS; SCORING SYSTEM;
DISEASE; PATHOGENESIS; STEATOSIS; CELLS; MODEL; EPIDEMIOLOGY; PREVALENCE
AB Chronic inflammation is a common theme in a variety of disease pathways, including autoimmune diseases. The pathways of chronic inflammation are well illustrated by nonalcoholic steatohepatitis (NASH), which is of a serious concern due to its increasing prevalence in the westernized world and its direct correlation with lifestyle factors, particularly diet. Importantly, NASH may ultimately lead to the development of hepatocellular carcinoma. We previously reported that injection of monosodium glutamate (MSG) in ICR mice leads to the development of significant inflammation, central obesity, and type 2 diabetes. To directly address the long-term consequences of MSG on inflammation, we have performed serial analysis of MSG-injected mice and focused in particular on liver pathology. By 6 and 12 months of age, all MSG-treated mice developed NAFLD and NASH-like histology, respectively. In particular, the murine steatohepatitis at 12 months was virtually undistinguishable from human NASH. Further, dysplastic nodular lesions were detected in some cases within the fibrotic liver parenchyma. We submit that MSG treatment of mice induces obesity and diabetes with steatosis and steatohepatitis resembling human NAFLD and NASH with pre-neoplastic lesions. These results take on considerable significance in light of the widespread usage of dietary MSG and we suggest that MSG should have its safety profile re-examined and be potentially withdrawn from the food chain. (C) 2007 Elsevier Ltd. All rights reserved.
C1 [Nakanishi, Yuko; Tsuneyama, Koichi; Salunga, Thucydides L.; Nomoto, Kazuhiro; An, Jun-Ling; Takano, Yasuo] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Diagnost Pathol, Toyama 9300194, Japan.
[Tsuneyama, Koichi; Salunga, Thucydides L.] Toyama Univ, 21st Century COE Program, Toyama 9300194, Japan.
[Fujimoto, Makoto] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Japanese Oriental Med, Toyama 9300194, Japan.
[Salunga, Thucydides L.] Univ Philippines, Inst Biol, Quezon City 1101, Philippines.
[Iizuka, Seiichi; Nagata, Mitsunobu; Suzuki, Wataru; Shimada, Tsutomu; Aburada, Masaki] Musashino Univ, Res Inst Pharmaceut Sci, Tokyo, Japan.
[Nakano, Masayuki] Natl Hosp Org Chiba Med Ctr, Div Clin Invest, Chiba, Japan.
[Selmi, Carlo] Univ Milan, San Paolo Hosp, Sch Med, I-20122 Milan, Italy.
[Selmi, Carlo; Gershwin, M. Eric] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA USA.
C3 University of Toyama; University of Toyama; University of Toyama;
University of the Philippines System; University of the Philippines
Diliman; San Paolo-Polo Universitaria Hospital; University of Milan;
University of California System; University of California Davis
RP Tsuneyama, K (corresponding author), Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Diagnost Pathol, 2630 Sugitani, Toyama 9300194, Japan.
EM ktsune@med.u-toyama.ac.jp; cfselmi@ucdavis.edu
RI An, Junling/AAV-6885-2020; Selmi, Carlo/ABG-4899-2021
OI Tsuneyama, Koichi/0000-0002-0670-9868; Selmi, Carlo/0000-0002-0323-0376
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NR 47
TC 97
Z9 105
U1 1
U2 12
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD FEB-MAR
PY 2008
VL 30
IS 1-2
BP 42
EP 50
DI 10.1016/j.jaut.2007.11.016
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Immunology
GA 255QD
UT WOS:000252671600007
PM 18178378
DA 2025-01-07
ER
PT J
AU Liu, ZC
Yu, MS
Zhao, F
Zhu, CF
AF Liu, Zichang
Yu, Maosheng
Zhao, Feng
Zhu, Chenfang
TI Anlotinib combined with Sintilimab is win-win cooperation for primary
squamous cell carcinoma of the thyroid: A case report and literature
review
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE primary squamous cell carcinoma of the thyroid; tyrosine kinase
inhibitors; immune checkpoint inhibitors; Anlotinib; Sintilimab;
immune-related adverse reactions; autoimmune liver disease
ID ENDOTHELIAL GROWTH-FACTOR; SIGNALING PATHWAYS; ADVERSE EVENTS;
TUMOR-CELLS; CANCER; GLAND; IMMUNOTHERAPY; PEMBROLIZUMAB; IPILIMUMAB;
DIAGNOSIS
AB BackgroundPrimary squamous cell carcinoma of the thyroid (PSCCT) is a rare malignant tumor. The incidence rate of PSCCT is less than 1%. However, the diagnosis and treatment of PSCCT are limited. Surgical resection is considered to be one of the few effective intervention methods. In this article, we reported a case of taking tyrosine kinase inhibitors (TKIs) combined with immune checkpoint inhibitors (ICIs) for PSCCT. Case summaryAn 80-year-old male was admitted to our hospital with dyspnea, cough, wheezing, and hoarseness for a giant thyroid mass. He underwent bronchoscopy and tracheal stent implantation to alleviate the respiratory obstruction. Then he accepted right partial thyroid and right lymph node biopsy. Postoperative pathology revealed squamous cell carcinoma. Subsequently, he underwent an endoscopy to exclude upper gastrointestinal squamous cell carcinoma. Finally, he was diagnosed with PSCCT. The patient was tentatively treated with a combination of Anlotinib and Sintilimab. After two courses, the tumor volume significantly reduced in MRI images and shrank further after five courses of combined treatment. Unfortunately, the patient died of fulminant liver failure and autoimmune liver disease after 5-month-treatment. ConclusionTKIs combined with ICIs may be an effective and novel way for PSCCT treatment, but immune-related complications, especially liver damage, should be cared.
C1 [Liu, Zichang; Yu, Maosheng; Zhao, Feng; Zhu, Chenfang] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Gen Surg, Sch Med, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University
RP Zhao, F; Zhu, CF (corresponding author), Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Gen Surg, Sch Med, Shanghai, Peoples R China.
EM phillip_zhao@126.com; sammizz1977@126.com
RI Zhang, Baocai/AFW-3565-2022
FU Clinical Research Program of 9th People's Hospital, Shanghai Jiao Tong
University School of Medicine [JYLJ202016]
FX This study was supported by Clinical Research Program of 9th People's
Hospital, Shanghai Jiao Tong University School of Medicine (JYLJ202016).
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NR 71
TC 3
Z9 3
U1 1
U2 2
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD MAR 16
PY 2023
VL 13
AR 976415
DI 10.3389/fonc.2023.976415
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C4IL1
UT WOS:000961568400001
PM 37007162
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Jhaveri, MA
Kowdley, KV
AF Jhaveri, Manan A.
Kowdley, Kris V.
TI New developments in the treatment of primary biliary cholangitis - role
of obeticholic acid
SO THERAPEUTICS AND CLINICAL RISK MANAGEMENT
LA English
DT Review
DE primary biliary cholangitis; obeticholic acid; ursodeoxycholic acid
ID HEPATITIS OVERLAP SYNDROME; URSODEOXYCHOLIC ACID; BIOCHEMICAL RESPONSE;
LIVER-DISEASES; END-POINTS; CIRRHOSIS; PROGNOSIS; EPIDEMIOLOGY;
FREQUENCY; DIAGNOSIS
AB Primary biliary cholangitis (PBC) is a chronic autoimmune cholestatic liver disease that predominantly affects women in early to middle age. It is typically associated with autoantibodies to mitochondrial antigens and results in immune-mediated destruction of small and medium-sized intrahepatic bile ducts leading to cholestasis, hepatic fibrosis and may progress to cirrhosis or hepatic failure and, in some cases, hepatocellular carcinoma. The clinical presentation and the natural history of PBC have improved over the years due to recognition of earlier widespread use of ursodeoxycholic acid (UDCA); about one-third of patients show suboptimal biochemical response to UDCA with poor prognosis. Until recently, UDCA was the only US Food and Drug Administration approved agent for this disease for more than two decades; obeticholic acid was approved in 2016 for treatment of patients with PBC with a suboptimal response or intolerance to UDCA. Currently, liver transplantation is the most effective treatment modality for PBC patients with end-stage liver disease. This review will focus on the recent advances in therapy of primary biliary cholangitis, with emphasis on obeticholic acid.
C1 [Jhaveri, Manan A.; Kowdley, Kris V.] Swedish Med Ctr, Liver Care Network, 1124 Columbia St,Suite 600, Seattle, WA 98104 USA.
C3 Swedish Medical Center
RP Kowdley, KV (corresponding author), Swedish Med Ctr, Liver Care Network, 1124 Columbia St,Suite 600, Seattle, WA 98104 USA.
EM kris.kowdley@swedish.org
RI Kowdley, Kris/AAF-5202-2019
FU Evidera; Gilead; Immuron; Intercept; Tobira
FX KVK: Grants/Research: Evidera, Gilead, Immuron, Intercept, Tobira.
Advisory Board: Abbvie, Achillion, BMS, Evidera, Gilead, Merck,
Novartis. MAJ reports no conflicts of interest in this work.
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NR 57
TC 27
Z9 28
U1 0
U2 5
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-203X
J9 THER CLIN RISK MANAG
JI Therap. Clin. Risk Manag.
PY 2017
VL 13
BP 1053
EP 1060
DI 10.2147/TCRM.S113052
PG 8
WC Health Care Sciences & Services
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services
GA FE2OQ
UT WOS:000408056000001
PM 28860789
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Rachisan, AL
Hrusca, A
Stefanescu, A
Pop, TL
AF Rachisan, A. L.
Hrusca, A.
Stefanescu, A.
Pop, T. L.
TI ROLE OF 8-ISO-PROSTAGLANDIN F2α IN EVOLUTION OF CHRONIC LIVER DISEASES
IN CHILDREN
SO JOURNAL OF ENVIRONMENTAL PROTECTION AND ECOLOGY
LA English
DT Article
DE hepatitis; oxidative stress; isoprostane; autoimmunity
ID CHRONIC HEPATITIS-C; OXIDATIVE DNA-DAMAGE; HEPATOCELLULAR-CARCINOMA;
FIBROSIS; STRESS; RISK
AB The oxidative stress (OS) appears to play an important role in the clinical evolution of chronic liver diseases. The aim of this study was to determine the activity of serum 8-iso-prostaglandin F2 alpha (8iPGF2 alpha), as an in vivo oxidative stress marker, in paediatric patients with chronic liver disease and in a control group. Fifty-one children (30 males) aged 7.68 +/- 7.46 years with chronic hepatitis were enrolled in the study. Twenty healthy children, age- and gender-matched, were enrolled as controls. Patients and controls underwent the 8iPGF2 alpha assessment through an ELISA serum method. The mean 8iPGF2 alpha value was 650.62 +/- 139.20 in the study patient group versus 305.85 +/- 204.61 in controls (p = 0.001). The mean value for the 8iPGF2 alpha activity was 670.85 +/- 135.78 in viral hepatitis patients (n = 41) versus 612.8 +/- 130.36 in autoimmune hepatitis patients (n = 10), p = 0.44. Oxidative stress reactions are more intense in patients with chronic liver disease than in healthy patients.
C1 [Rachisan, A. L.; Stefanescu, A.; Pop, T. L.] Univ Med & Pharm Iuliu Hatieganu Cluj Napoca, Dept Pediat 2, Cluj Napoca, Romania.
[Hrusca, A.] Univ Med & Pharm Iuliu Hatieganu Cluj Napoca, Dept Med Biophys, Cluj Napoca, Romania.
C3 Iuliu Hatieganu University of Medicine & Pharmacy; Iuliu Hatieganu
University of Medicine & Pharmacy
RP Rachisan, AL (corresponding author), Univ Med & Pharm Iuliu Hatieganu Cluj Napoca, Dept Pediat 2, Cluj Napoca, Romania.
EM andreea_rachisan@yahoo.com
RI RACHISAN, ANDREEA/M-9731-2013; Pop, Tudor Lucian/I-4155-2015
OI Pop, Tudor Lucian/0000-0002-4931-1219
FU Romanian National Authority for Scientific Research, CNDI-UEFISCDI
[PN-II-PT-PCCA-2011-3.2-0917]
FX Ana Stefanescu and Tudor Lucian Pop acknowledged the support work
supported by a grant from the Romanian National Authority for Scientific
Research, CNDI-UEFISCDI, Project Number PN-II-PT-PCCA-2011-3.2-0917.
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NR 15
TC 0
Z9 0
U1 0
U2 4
PU SCIBULCOM LTD
PI SOFIA
PA PO BOX 249, 1113 SOFIA, BULGARIA
SN 1311-5065
J9 J ENVIRON PROT ECOL
JI J. Environ. Prot. Ecol.
PY 2018
VL 19
IS 1
BP 400
EP 406
PG 7
WC Environmental Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology
GA GD2HA
UT WOS:000430319500043
DA 2025-01-07
ER
PT J
AU Alzahrani, N
AF Alzahrani, Nabeel
TI Hepatitis C virus, insulin resistance, and diabetes: A review
SO MICROBIOLOGY AND IMMUNOLOGY
LA English
DT Review
DE HCV; insulin resistance; metabolic disease; type 1 diabetes mellitus;
type 2 diabetes mellitus
ID HCV GENOTYPE 1; DIRECT-ACTING ANTIVIRALS; ALPHA-2A PLUS RIBAVIRIN;
HEPATOCELLULAR-CARCINOMA; RECEPTOR SUBSTRATE-1; INTERFERON-ALPHA;
GLYCEMIC CONTROL; SIGNALING PATHWAY; CORE PROTEIN; INFECTION
AB Hepatitis C virus (HCV) infection and diabetes mellitus (DM) are two chronic diseases that are a cause of significant health and economic burdens worldwide. HCV is associated with the development of insulin resistance (IR) and DM. The mechanisms through which HCV induces IR and DM include direct viral effects, proinflammatory cytokines, and other immune-mediated processes. Type 1 DM (T1DM) and type 2 DM (T2DM) are both chronic diseases that involve impaired glucose homeostasis, albeit through different mechanisms. T1DM is an autoimmune disease that leads to the destruction of pancreatic beta cells resulting in insulin deficiency. In T2DM, a combination of peripheral IR and irregular production of insulin eventually leads to beta-cell destruction and insulin insufficiency. Both T1DM and T2DM etiologies involve a combination of genetic and environmental factors. The data on HCV and T1DM association remain limited, unlike T2DM, where a large body of evidence linking HCV to T2DM is available. Here, we intend to outline the current state of knowledge on HCV, IR, and DM.
C1 [Alzahrani, Nabeel] King Saud bin Abdulaziz Univ Hlth Sci, Coll Appl Med Sci, Dept Clin Lab Sci, POB 3660, Riyadh 14611, Saudi Arabia.
C3 King Saud Bin Abdulaziz University for Health Sciences
RP Alzahrani, N (corresponding author), King Saud bin Abdulaziz Univ Hlth Sci, Coll Appl Med Sci, Dept Clin Lab Sci, POB 3660, Riyadh 14611, Saudi Arabia.
EM Alzahranin@ksau-hs.edu.sa
RI Alzahrani, Nabeel/GQI-4234-2022
OI Alzahrani, Nabeel/0000-0002-1077-0872
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NR 93
TC 7
Z9 9
U1 1
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0385-5600
EI 1348-0421
J9 MICROBIOL IMMUNOL
JI Microbiol. Immunol.
PD OCT
PY 2022
VL 66
IS 10
BP 453
EP 459
DI 10.1111/1348-0421.13023
EA AUG 2022
PG 7
WC Immunology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology
GA 5C8KC
UT WOS:000842820200001
PM 35941761
DA 2025-01-07
ER
PT J
AU Liu, Y
Chen, H
Hao, JH
Li, ZC
Hou, TZ
Hao, HQ
AF Liu, Yang
Chen, Hao
Hao, Jian-heng
Li, Zhen-cheng
Hou, Tiezheng
Hao, Hui-qin
TI Microarray-based transcriptional profiling of a mouse model of
autoimmune hepatitis
SO FEBS OPEN BIO
LA English
DT Article
DE autoimmune hepatitis; concanavalin A; Gene Ontology; KEGG; lncRNA;
microarray
ID LONG NONCODING RNAS; REGULATORY T-CELLS; LIVER-INJURY; GENE-EXPRESSION;
EMERGING ROLE; KUPFFER CELLS; FACTOR FOXP1; IL-10; ASSOCIATION;
DIFFERENTIATION
AB Long noncoding RNAs (lncRNAs) are RNA molecules longer than 200 nucleotides that do not typically code for a protein. lncRNAs have regulatory roles in many physiological processes, and their dysregulation can contribute to cancer, cardiovascular and neurodegenerative diseases, as well as the onset of autoimmune diseases, including systemic lupus erythematosus and rheumatoid arthritis. However, lncRNA expression changes in autoimmune hepatitis (AIH), a form of inflammation induced by immunological tolerance disorders, are poorly understood. Here, for the first time to our knowledge, we used microarrays to profile 1161 differentially expressed lncRNAs (DELs; 608 up- and 553 down-regulated) and 11 512 differentially expressed mRNAs (DEMs; 5189 up- and 6323 down- regulated) in a concanavalin A-induced AIH mouse model. We used quantitative real-time PCR to confirm the expression of eight DELs and DEMs, and analyzed the coexpression relationship between them. Potential biological functions of screened DELs and DEMs were predicted with Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. DEL-DEM interaction networks were also constructed. Our study revealed the roles of DELs and DEMs in the pathogenesis of AIH. We also provided potential candidate biomarkers that may have potential for future development into possible diagnostics or as a treatment for this disorder.
C1 [Liu, Yang; Chen, Hao; Hao, Jian-heng; Li, Zhen-cheng; Hou, Tiezheng; Hao, Hui-qin] Shanxi Univ Chinese Med, Coll Basic Med Sci, Jinzhong 030619, Peoples R China.
[Liu, Yang; Chen, Hao; Hao, Jian-heng; Li, Zhen-cheng; Hou, Tiezheng; Hao, Hui-qin] Shanxi Univ Chinese Med, Basic Lab Integrated Tradit Chinese & Western Med, Jinzhong, Peoples R China.
C3 Shanxi University of Chinese Medicine; Shanxi University of Chinese
Medicine
RP Hou, TZ; Hao, HQ (corresponding author), Shanxi Univ Chinese Med, Coll Basic Med Sci, Jinzhong 030619, Peoples R China.
EM th@sxtcm.edu.cn; th@sxtcm.edu.cn
OI Liu, Yang/0000-0002-6627-5002
FU Natural Science Foundation of Shanxi Province [201901D111333,
201801D121228]; Shanxi Provincial Key Research and Development Project
[201803D31084]; Shanxi Key Laboratory of Innovative Drug for the
Treatment of Serious Diseases Basing on the Chronic Inflammation (Shanxi
University of Chinese Medicine) [SXIDL-2018-07]; research projects of
Health Commission of Shanxi Province [2018002]; Science and Technology
Innovation Program of Shanxi University of Chinese Medicine
[2020PY-JC-07]; Basic Laboratory of Integrated Traditional Chinese and
Western Medicine, Shanxi University of Chinese Medicine
FX We are grateful to Haiguang Liu (OE Biotech. Co., Ltd., Shanghai, China)
for providing help with data analysis. We thank the animal facility for
breeding and maintaining the mice. This study was funded by Natural
Science Foundation of Shanxi Province (Grant Number: Basic applied study
of Shanxi Province 201901D111333 to YL; Grant Number: Basic applied
study of Shanxi Province: 201801D121228 to H-qH), Shanxi Provincial Key
Research and Development Project (Grant Number: 201803D31084 to H-qH),
Shanxi Key Laboratory of Innovative Drug for the Treatment of Serious
Diseases Basing on the Chronic Inflammation (Shanxi University of
Chinese Medicine) (Grant Number: SXIDL-2018-07 to YL), research projects
of Health Commission of Shanxi Province (Grant Number: 2018002 to YL),
Science and Technology Innovation Program of Shanxi University of
Chinese Medicine (Grant Number: 2020PY-JC-07 to YL), and The Basic
Laboratory of Integrated Traditional Chinese and Western Medicine,
Shanxi University of Chinese Medicine.
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NR 57
TC 5
Z9 5
U1 1
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2211-5463
J9 FEBS OPEN BIO
JI FEBS Open Bio
PD OCT
PY 2020
VL 10
IS 10
BP 2040
EP 2054
DI 10.1002/2211-5463.12953
EA SEP 2020
PG 15
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA NV2WM
UT WOS:000570877700001
PM 32808463
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Lim, DH
Kim, YG
Lee, D
Ahn, SM
Hong, S
Lee, CK
Yoo, B
AF Lim, Doo-Ho
Kim, Yong-Gil
Lee, Danbi
Ahn, Soo Min
Hong, Seokchan
Lee, Chang-Keun
Yoo, Bin
TI Immunoglobulin G Levels as a Prognostic Factor for Autoimmune Hepatitis
Combined With Systemic Lupus Erythematosus
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID LIVER-DISEASE; CRITERIA; CLASSIFICATION; EPIDEMIOLOGY; DYSFUNCTION;
POPULATION; DIAGNOSIS; PATIENT
AB ObjectiveAutoimmune hepatitis (AIH) is a chronic progressive liver disease characterized by circulating autoantibodies and hyperglobulinemia. This study was conducted to identify the features of AIH accompanied by systemic lupus erythematosus (SLE-AIH) that differ from those of primary AIH (P-AIH), and to evaluate factors that affect the outcome for SLE-AIH patients.
MethodsFrom May 1995 to April 2014, clinical data (including liver pathology) from 164 patients with P-AIH and 23 patients with SLE-AIH were collected from an electronic database at a tertiary referral center. AIH was diagnosed according to the diagnostic scoring system for AIH (revised in 1999). SLE patients fulfilled at least 4 of the 1997 revised American College of Rheumatology criteria. Progression was defined as occurrence of cirrhosis, hepatocellular carcinoma, liver transplantation, or death from hepatic failure.
ResultsThe age at the time of AIH diagnosis was lower and initial levels of serum IgG were higher in SLE-AIH than in P-AIH patients. Progression was more common in P-AIH, and hepatocellular carcinoma, liver transplantation, or death occurred only in P-AIH patients. Among 23 patients with SLE-AIH, 8 with cirrhosis had higher levels of serum IgG than 15 patients without cirrhosis (meanSD 4,077.4 +/- 1,641.0 mg/dl and 2,560.7 +/- 932.2 mg/dl, respectively; P=0.017). Moreover, a serum IgG level more than 2-fold the upper normal limit was associated with a high risk of cirrhosis in SLE-AIH (odds ratio 11.00 [95% confidence interval 1.420-85.201]; P=0.026).
ConclusionInitially high levels of serum IgG are a poor prognostic factor for SLE-AIH. Additionally, the long-term outcome for SLE-AIH might be better than for P-AIH.
C1 [Lim, Doo-Ho; Kim, Yong-Gil; Lee, Danbi; Ahn, Soo Min; Hong, Seokchan; Lee, Chang-Keun; Yoo, Bin] Univ Ulsan, Coll Med, AsanMed Ctr, Seoul, South Korea.
C3 University of Ulsan
RP Kim, YG (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Div Rheumatol,Dept Internal Med, 88 Olymp Ro 43 Gil, Seoul 138736, South Korea.
EM bestmd2000@amc.seoul.kr
RI Kim, Hyung/ABW-5643-2022
OI Lim, Doo-Ho/0000-0002-8012-7364; Hong, Seokchan/0000-0001-8722-3124
FU Asan Institute for Life Science [15-463]
FX Supported by the Asan Institute for Life Science (grant 15-463).
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NR 36
TC 11
Z9 11
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2151-464X
EI 2151-4658
J9 ARTHRIT CARE RES
JI Arthritis Care Res.
PD JUL
PY 2016
VL 68
IS 7
BP 995
EP 1002
DI 10.1002/acr.22800
PG 8
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA DR1OB
UT WOS:000379673700014
PM 27338104
OA Bronze
DA 2025-01-07
ER
PT J
AU Thuluvath, PJ
Kantsevoy, S
Thuluvath, AJ
Savva, Y
AF Thuluvath, Paul J.
Kantsevoy, Sergey
Thuluvath, Avesh J.
Savva, Yulia
TI Is cryptogenic cirrhosis different from NASH cirrhosis?
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE UNOS; Autoimmune hepatitis; Alcoholic cirrhosis; Age and gender matched
ID FATTY LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC
STEATOHEPATITIS; RISK-FACTORS; NATURAL-HISTORY; TRANSPLANTATION;
OBESITY; ASSOCIATION; PREVALENCE; HEPATITIS
AB Background & Aims: We hypothesized that patients currently diagnosed with cryptogenic cirrhosis (CC) have truly 'cryptogenic' liver disease, which is unlikely to have evolved from NASH. The aim of this study is to characterize patients with CC, and compare their characteristics to patients with cirrhosis of other etiologies.
Methods: To investigate this, we compared the clinical characteristics of adults with CC (n = 7,999) to those with cirrhosis caused by non-alcoholic steatohepatitis (NASH) (n = 11,302), alcohol (n = 21,714) and autoimmune hepatitis (n = 3,447), using the UNOS database from 2002-16. We performed an age, gender and year of listing matched comparison of CC and NASH (n = 7,201 in each group), and also stratified patients by the presence of obesity or diabetes mellitus (DM).
Results: From 2002 to 2016, patients listed with a diagnosis of NASH increased from about 1% to 16% while CC decreased from 8% to 4%. A logistic regression model using the entire United Network for Organ Sharing data (n = 138,021) suggested that the strongest predictors of NASH were type 2 DM, obesity, age >= 60 years, female gender and white race. Type 2 DM was more common in patients with NASH (53%) than those with CC (29%), alcoholic cirrhosis (16%) and autoimmune hepatitis (16%), and obesity was more common in NASH (65.3%) compared to the other three groups (33-42%). There were more white individuals (82.3%) in the NASH group and a lower prevalence of black, Hispanic and Asian individuals, compared to the other three groups. Hepatocellular carcinoma was more commonly seen in NASH (19% vs. 9-13% in the other groups) and this is not influenced by obesity and type 2 DM. The differences between CC and NASH remained unchanged even when two groups were matched for age, gender and year of listing, or when stratified by the presence or absence of obesity or type 2DM.
Conclusions: Based on risk perspectives, CC should not be equated with the term 'NASH cirrhosis'.
Lay summary: We hypothesized that cryptogenic cirrhosis is a distinct condition from cirrhosis caused by non-alcoholic steatohepatitis (NASH). By comparing cryptogenic cirrhosis with cirrhosis of other causes, we found clear clinical differences. Therefore, cryptogenic cirrhosis should not be considered the same as NASH cirrhosis. Further investigations are required to identify unknown causes of cirrhosis. (C) 2017 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Thuluvath, Paul J.; Kantsevoy, Sergey; Savva, Yulia] Mercy Med Ctr, Inst Digest Hlth & Liver Dis, Baltimore, MD 21202 USA.
[Thuluvath, Paul J.; Kantsevoy, Sergey] Univ Maryland, Sch Med, Dept Surg, Baltimore, MD 21201 USA.
[Thuluvath, Paul J.; Kantsevoy, Sergey] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
[Thuluvath, Avesh J.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
C3 Mercy Medical Center - Maryland; University System of Maryland;
University of Maryland Baltimore; University System of Maryland;
University of Maryland Baltimore; Johns Hopkins University
RP Thuluvath, PJ (corresponding author), Mercy Med Ctr, Inst Digest Hlth & Liver Dis, Baltimore, MD 21202 USA.
EM thuluvath@gmail.com
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NR 33
TC 48
Z9 50
U1 1
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD MAR
PY 2018
VL 68
IS 3
BP 519
EP 525
DI 10.1016/j.jhep.2017.11.018
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FW4JK
UT WOS:000425279100021
PM 29162389
DA 2025-01-07
ER
PT J
AU Feuerlein, S
Pauls, S
Juchems, MS
Stuber, T
Hoffmann, MHK
Brambs, HJ
Ernst, AS
AF Feuerlein, Sebastian
Pauls, Sandra
Juchems, Markus S.
Stuber, Tina
Hoffmann, Martin H. K.
Brambs, Hans-Juergen
Ernst, Andrea S.
TI Pitfalls in Abdominal Diffusion-Weighted Imaging: How Predictive is
Restricted Water Diffusion for Malignancy
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE abdominal MRI; apparent diffusion coefficient; diffusion-weighted
imaging
ID ROSAI-DORFMAN-DISEASE; BILATERAL RENAL HISTIOCYTOSIS; VASCULAR TARGETING
AGENT; LYMPH-NODES; AUTOIMMUNE PANCREATITIS; EXTRANODAL VARIANT; BRAIN
ABSCESSES; LIVER-LESIONS; MRI; CANCER
AB OBJECTIVE. As diffusion-weighted imaging is increasingly implemented into routine protocols of abdominal MRI, abnormal findings in expected and unexpected locations become more common. The aim of our retrospective study was to investigate the specificity of restricted diffusion in differentiation of benign from malignant abdominal disease.
MATERIALS AND METHODS. Two hundred thirty consecutively registered patients underwent abdominal MRI including diffusion-weighted imaging (single-shot spin-echo echo-planar sequence) with b values of 0, 150, 500, and 1,000 s/mm(2). Lesions were detected by two blinded readers using only the images with a b value of 1,000 s/mm(2), and representative apparent diffusion coefficients were measured. Lymph nodes were not documented.
RESULTS. Fifty-two of the 230 patients had a total of 55 lesions with restricted diffusion (23.9%). The mean apparent diffusion coefficient was 809 mm(2)/s. Forty-three lesions (78.2%) were malignant. The 12 benign lesions were liver hemangioma, liver adenoma, autoimmune pancreatitis, pancreatic teratoma, two abscesses, three cases of inflammatory bowel wall thickening due to Crohn's disease, Bartholin cyst, hemorrhagic ovarian cyst, and renal Rosai-Dorfman disease.
CONCLUSION. Restricted diffusion is generally considered to be associated with malignant tumors because of the high cellularity of these tumors. However, in interpretation of diffusion-weighted images, it should be kept in mind that a number of benign lesions, as many as 22% in our cohort, can exhibit restricted diffusion on images with high b values, thus mimicking malignant lesions.
C1 [Feuerlein, Sebastian; Pauls, Sandra; Juchems, Markus S.; Stuber, Tina; Hoffmann, Martin H. K.; Brambs, Hans-Juergen; Ernst, Andrea S.] Univ Ulm, Dept Diagnost & Intervent Radiol, D-89075 Ulm, Germany.
C3 Ulm University
RP Feuerlein, S (corresponding author), Univ Ulm, Dept Diagnost & Intervent Radiol, Steinhoevelstr 9, D-89075 Ulm, Germany.
EM sfeuerlein@yahoo.com
RI Juchems, Markus/C-7110-2011
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NR 35
TC 76
Z9 89
U1 0
U2 7
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
EI 1546-3141
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD OCT
PY 2009
VL 193
IS 4
BP 1070
EP 1076
DI 10.2214/AJR.08.2093
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 497CZ
UT WOS:000270033300022
PM 19770331
DA 2025-01-07
ER
PT J
AU Bax, CE
Maddukuri, S
Ravishankar, A
Pappas-Taffer, L
Werth, VP
AF Bax, Christina E.
Maddukuri, Spandana
Ravishankar, Adarsh
Pappas-Taffer, Lisa
Werth, Victoria P.
TI Environmental triggers of dermatomyositis: a narrative review
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Dermatomyositis (DM); triggers; herbal supplements; drugs; infections;
ultraviolet irradiation (UV irradiation); air pollution
ID ANTITUMOR NECROSIS FACTOR; IDIOPATHIC INFLAMMATORY MYOPATHIES; JUVENILE
DERMATOMYOSITIS; OCCUPATIONAL-EXPOSURE; HEPATOCELLULAR-CARCINOMA;
LUPUS-ERYTHEMATOSUS; RHEUMATIC-DISEASES; INFLUENZA VACCINE; ADVERSE
EVENTS; AIR-POLLUTANTS
AB Dermatomyositis (DM) is an autoimmune disease that affects the skin, lungs, and muscle. Although the pathogenesis of DM is not completely understood, several environmental triggers have been linked to DM onset or flare. This article specifically examines the effects of herbal supplements, drugs, infections, ultraviolet (UV) radiation, and environmental pollutants on the onset or exacerbation of DM. Herbal supplements such as Spirulina platensis, Aphanizomenon flos-aquae, Chlorella, Echinacea, and Alfalfa have been implicated and are frequently used in health foods. Medications such as hydroxyurea, TNF-alpha inhibitors, immune checkpoint inhibitors (ICI), and penicillamine, as well as certain viral infections, such as parvovirus B19, coxsackie virus, polyomavirus, Epstein-Barr virus (EBV), hepatitis, influenza, and human immunodeficiency viruses (HIV) have been associated with DM onset. Bacterial infections and vaccinations have also been linked to the development of DM. Additional environmental factors, including UV radiation and air pollutants, such as silica, biological/mineral dust, and particulate air matter from vehicle and industrial emissions, may also play a role in DM pathogenesis. Overall, there is general agreement that an autoimmune attack of the skin, muscle, and lungs in DM can be triggered by various environmental factors and warrants further investigation.
C1 [Bax, Christina E.; Maddukuri, Spandana; Ravishankar, Adarsh; Pappas-Taffer, Lisa; Werth, Victoria P.] Corporal Michael J Crescenz VAMC, Philadelphia, PA USA.
[Bax, Christina E.; Maddukuri, Spandana; Ravishankar, Adarsh; Pappas-Taffer, Lisa; Werth, Victoria P.] Univ Penn, Dept Dermatol, Philadelphia, PA 19104 USA.
C3 University of Pennsylvania
RP Werth, VP (corresponding author), Perelman Ctr Adv Med, Dept Dermatol, Suite 1-330A,3400 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM werth@pennmedicine.upenn.edu
FU NIH [R01AR071653]; United States Department of Veterans Affairs
(Veterans Health Administration, Office of Research and Development and
Biomedical Laboratory Research and Development); National Center for
Advancing Translational Sciences of the National Institutes of Health
[TL1TR001880]
FX NIH R01AR071653. This work was supported by the United States Department
of Veterans Affairs (Veterans Health Administration, Office of Research
and Development and Biomedical Laboratory Research and Development). One
of us (CEB) was supported by the National Center for Advancing
Translational Sciences of the National Institutes of Health under award
number TL1TR001880.
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NR 133
TC 31
Z9 32
U1 1
U2 5
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD MAR
PY 2021
VL 9
IS 5
AR 434
DI 10.21037/atm-20-3719
PG 14
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA RB3TT
UT WOS:000632037900013
PM 33842655
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wu, YR
Lee, YC
Li, WM
Hsu, WC
Lin, HH
Chang, LL
Huang, AM
Jhan, JH
Wu, WJ
Li, CC
Lee, HY
Yeh, HC
Ke, HL
AF Wu, Yi-Ru
Lee, Yi-Chen
Li, Wei-Ming
Hsu, Wei-Chi
Lin, Hui-Hui
Chang, Lin-Li
Huang, A-Mei
Jhan, Jhen-Hao
Wu, Wen-Jeng
Li, Ching-Chia
Lee, Hsiang-Ying
Yeh, Hsin-Chih
Ke, Hung-Lung
TI High Transaldolase 1 expression predicts poor survival of patients with
upper tract urothelial carcinoma
SO PATHOLOGY INTERNATIONAL
LA English
DT Article
DE immunohistochemistry; prognosis; Transaldolase 1; upper tract urothelial
carcinoma
ID PENTOSE-PHOSPHATE PATHWAY; HEPATOCELLULAR-CARCINOMA; CANCER; NRF2;
ASSOCIATION; METASTASIS; BIOMARKER; GLUCOSE
AB Upper tract urothelial carcinoma (UTUC) is a rare tumor with an incidence that varies greatly between Eastern and Western countries. Transaldolase 1 (TALDO1) is a rate-limiting enzyme of the pentose phosphate pathway. In humans, aberrant TALDO1 activity has been implicated in various autoimmune diseases and malignancies; however, the function of TALDO1 in UTUC has not been previously investigated. Here we evaluated the clinical significance of TALDO1 expression in 115 paraffin-embedded tumor samples from patients with UTUC using immunohistochemistry. Our results demonstrated that there was an association between high TALDO1 expression and advanced stage (P = 0.011), tumor size (P = 0.005), tumor location (P = 0.047), distant metastases (P = 0.023), local recurrence (P = 0.002), and cancer death (P = 0.003). Using univariate and multivariate analyses, we found that chemotherapy was an independent factor for bladder recurrence-free survival. Late stage (III/IV) and high TALDO1 expression were independent prognostic factors for progression-free and cancer-specific survival. In summary, increased TALDO1 expression in UTUC was significantly correlated with late stage, tumor size, tumor location, distant metastases, local recurrence, and cancer death. Therefore, high TALDO1 expression could be a predictor of poor survival in patients with UTUC. Further studies are necessary to investigate the role of TALDO1 in UTUC development.
C1 [Wu, Yi-Ru] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Gen Div, Kaohsiung, Taiwan.
[Lee, Yi-Chen] Kaohsiung Med Univ, Sch Med, Dept Anat, Coll Med, Kaohsiung, Taiwan.
[Li, Wei-Ming; Lin, Hui-Hui; Jhan, Jhen-Hao; Wu, Wen-Jeng; Li, Ching-Chia; Lee, Hsiang-Ying; Yeh, Hsin-Chih; Ke, Hung-Lung] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Urol, Kaohsiung, Taiwan.
[Li, Wei-Ming; Wu, Wen-Jeng; Li, Ching-Chia; Lee, Hsiang-Ying; Yeh, Hsin-Chih; Ke, Hung-Lung] Kaohsiung Med Univ, Sch Med, Dept Urol, Coll Med, 100 Shih Chuan 1st Rd, Kaohsiung 80708, Taiwan.
[Li, Wei-Ming] Pingtung Hosp, Dept Urol, Minist Hlth & Welf, Pingtung, Taiwan.
[Hsu, Wei-Chi; Lin, Hui-Hui; Chang, Lin-Li; Huang, A-Mei; Wu, Wen-Jeng; Ke, Hung-Lung] Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.
[Chang, Lin-Li] Kaohsiung Med Univ, Sch Med, Dept Microbiol, Coll Med, Kaohsiung, Taiwan.
[Huang, A-Mei; Jhan, Jhen-Hao; Lee, Hsiang-Ying] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.
[Huang, A-Mei] Kaohsiung Med Univ, Sch Med, Dept Biochem, Coll Med, Kaohsiung, Taiwan.
[Jhan, Jhen-Hao] Kaohsiung Municipal Siaogang Hosp, Dept Urol, Kaohsiung, Taiwan.
[Lee, Hsiang-Ying; Yeh, Hsin-Chih] Kaohsiung Municipal Tatung Hosp, Dept Urol, Kaohsiung, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
Kaohsiung Medical University; Kaohsiung Medical University; Kaohsiung
Medical University Hospital; Kaohsiung Medical University; Kaohsiung
Medical University; Kaohsiung Medical University; Kaohsiung Medical
University; Kaohsiung Medical University; Kaohsiung Medical University;
Kaohsiung Municipal Siao-Gang Hospital; Kaohsiung Medical University;
Kaohsiung Municipal Ta-Tung Hospital
RP Ke, HL (corresponding author), Kaohsiung Med Univ, Sch Med, Dept Urol, Coll Med, 100 Shih Chuan 1st Rd, Kaohsiung 80708, Taiwan.
EM hunglungke@gmail.com
RI Wu, Wen-Jeng/C-7267-2009; Chang, Lin-Li/D-5472-2009; Li,
Ching-Chia/D-5024-2009; Yeh, Hsin-Chih/ABI-1268-2020; Ke,
Hung-Lung/HCH-9079-2022; Hsu, Wei-Chi/ITV-5471-2023
OI Lin, Hui-Hui/0000-0002-3514-0391; Hsu, Wei-Chi/0000-0001-8184-6945; Ke,
Hung-Lung/0000-0002-4208-3858; Yeh, Hsin-Chih/0000-0003-4113-629X; Jhan,
Jhen-Hao/0000-0003-3239-0712
FU Ministry of Science and Technology [MOST106-2314-B-037-092,
MOST107-2314-B-037-014]; Kaohsiung Medical University Hospital
[KMUH-105-5R70, KMUH-106-6R59, KMUH-108-8R52]
FX This study was supported by grants from the Ministry of Science and
Technology (MOST106-2314-B-037-092, MOST107-2314-B-037-014) and
Kaohsiung Medical University Hospital (KMUH-105-5R70, KMUH-106-6R59, and
KMUH-108-8R52).
CR [Anonymous], 2018, CA Cancer J Clin, DOI DOI 10.3322/CANJCLIN.49.1.33
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NR 25
TC 7
Z9 7
U1 0
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1320-5463
EI 1440-1827
J9 PATHOL INT
JI Pathol. Int.
PD JUL
PY 2021
VL 71
IS 7
BP 463
EP 470
DI 10.1111/pin.13101
EA APR 2021
PG 8
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA TP7JY
UT WOS:000639587300001
PM 33848380
DA 2025-01-07
ER
PT J
AU Wang, BH
Yao, MF
Lv, LX
Ling, ZX
Li, LJ
AF Wang, Baohong
Yao, Mingfei
Lv, Longxian
Ling, Zongxin
Li, Lanjuan
TI The Human Microbiota in Health and Disease
SO ENGINEERING
LA English
DT Review
DE Microbiome; Health; Infectious disease; Liver diseases; Gastrointestinal
malignancy; Metabolic disorder; Microbiota technology; Probiotics
ID HUMAN GUT MICROBIOME; INTESTINAL BACTERIAL OVERGROWTH; METAGENOME-WIDE
ASSOCIATION; CHAIN FATTY-ACIDS; HELICOBACTER-PYLORI; FECAL MICROBIOTA;
LIVER-DISEASE; GASTROINTESTINAL MICROBIOTA; CLOSTRIDIUM-DIFFICILE;
BACTEROIDES-FRAGILIS
AB Trillions of microbes have evolved with and continue to live on and within human beings. A variety of environmental factors can affect intestinal microbial imbalance, which has a close relationship with human health and disease. Here, we focus on the interactions between the human microbiota and the host in order to provide an overview of the microbial role in basic biological processes and in the development and progression of major human diseases such as infectious diseases, liver diseases, gastrointestinal cancers, metabolic diseases, respiratory diseases, mental or psychological diseases, and autoimmune diseases. We also review important advances in techniques associated with microbial research, such as DNA sequencing, metabonomics, and proteomics combined with computation-based bioinformatics. Current research on the human microbiota has become much more sophisticated and more comprehensive. Therefore, we propose that research should focus on the host-microbe interaction and on cause-effect mechanisms, which could pave the way to an understanding of the role of gut microbiota in health and disease, and provide new therapeutic targets and treatment approaches in clinical practice. (C) 2017 THE AUTHORS. Published by Elsevier LTD on behalf of the Chinese Academy of Engineering and Higher Education Press Limited Company. This is an open access article under the CC BY-NC-ND license (http://creativecommons. org/licenses/by-nc-nd/4.0/).
C1 [Wang, Baohong; Yao, Mingfei; Lv, Longxian; Ling, Zongxin; Li, Lanjuan] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Natl Collaborat Innovat Ctr Diag & Treatment Infe, Hangzhou 310003, Peoples R China.
C3 Collaborative Innovation Center for Diagnosis & Treatment of Infectious
Diseases; Zhejiang University
RP Li, LJ (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 1, Natl Collaborat Innovat Ctr Diag & Treatment Infe, Hangzhou 310003, Peoples R China.
EM ljli@zju.edu.cn
RI Yao, Mingfei/GWN-1600-2022; li, li/HJY-8663-2023; Ling,
Zongxin/M-1657-2018
OI Ling, Zongxin/0000-0001-9662-099X
FU National Basic Research Program of China (973 Program) [2013CB531401];
Major Science and Technology Program of Zhejiang Province [2014C03039];
Natural Science Foundation of Zhejiang Province [R16H260001]
FX This study was supported by grants from the National Basic Research
Program of China (973 Program, 2013CB531401), the Major Science and
Technology Program of Zhejiang Province (2014C03039), and the Natural
Science Foundation of Zhejiang Province (R16H260001). We acknowledge
Doctors Chunlei Chen, Bo Li, Jing Guo, Ding Shi, Qiongling Bao, Silan
Gu, Yanfei Chen, Kai Zhou, Qixiang Luo, Ruiqi Tang, and Xiangyang Jiang
for the literature search and the preparation for the manuscript. We
also thank the reviewers for their thoughtful and helpful comments.
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TC 520
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U1 11
U2 211
PU ELSEVIER
PI AMSTERDAM
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VL 3
IS 1
BP 71
EP 82
DI 10.1016/J.ENG.2017.01.008
PG 12
WC Engineering, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering
GA EQ4IS
UT WOS:000398040300010
OA gold
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Wang, XM
Zhang, YY
Wang, S
Ni, HY
Zhao, P
Chen, GY
Xu, BL
Yuan, L
AF Wang, Xiaoming
Zhang, Yangyang
Wang, Sen
Ni, Hongyan
Zhao, Peng
Chen, Guangyu
Xu, Benling
Yuan, Long
TI The role of CXCR3 and its ligands in cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE CXCR3; CXCR3 and its ligands; CXCL9; CXCL10; CXCL11
ID CHEMOKINE RECEPTOR CXCR3; CELL ALPHA-CHEMOATTRACTANT; T-CELLS;
BREAST-CANCER; IFN-GAMMA; TUMOR-GROWTH; HEPATOCELLULAR-CARCINOMA;
INTERFERON-GAMMA; MURINE MODEL; GENE-THERAPY
AB Chemokines are a class of small cytokines or signaling proteins that are secreted by cells. Owing to their ability to induce directional chemotaxis of nearby responding cells, they are called chemotactic cytokines. Chemokines and chemokine receptors have now been shown to influence many cellular functions, including survival, adhesion, invasion, and proliferation, and regulate chemokine levels. Most malignant tumors express one or more chemokine receptors. The CXC subgroup of chemokine receptors, CXCR3, is mainly expressed on the surface of activated T cells, B cells, and natural killer cells, and plays an essential role in infection, autoimmune diseases, and tumor immunity by binding to specific receptors on target cell membranes to induce targeted migration and immune responses. It is vital to treat infections, autoimmune diseases, and tumors. CXCR3 and its ligands, CXCL9, CXCL10, and CXCL11, are closely associated with the development and progression of many tumors. With the elucidation of its mechanism of action, CXCR3 is expected to become a new indicator for evaluating the prognosis of patients with tumors and a new target for clinical tumor immunotherapy. This article reviews the significance and mechanism of action of the chemokine receptor CXCR3 and its specific ligands in tumor development.
C1 [Wang, Xiaoming; Zhang, Yangyang; Wang, Sen; Zhao, Peng; Yuan, Long] Zhengzhou Univ, Affiliated Canc Hosp, Dept Surg, Zhengzhou, Peoples R China.
[Wang, Xiaoming; Zhang, Yangyang; Wang, Sen; Zhao, Peng; Xu, Benling; Yuan, Long] Henan Canc Hosp, Zhengzhou, Peoples R China.
[Ni, Hongyan] Henan 3 Prov Peoples Hosp, Dept Surg, Zhengzhou, Peoples R China.
[Chen, Guangyu; Xu, Benling] Zhengzhou Univ, Affiliated Canc Hosp, Dept Immunotherapy, Zhengzhou, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Zhengzhou University
RP Yuan, L (corresponding author), Zhengzhou Univ, Affiliated Canc Hosp, Dept Surg, Zhengzhou, Peoples R China.; Xu, BL; Yuan, L (corresponding author), Henan Canc Hosp, Zhengzhou, Peoples R China.; Xu, BL (corresponding author), Zhengzhou Univ, Affiliated Canc Hosp, Dept Immunotherapy, Zhengzhou, Peoples R China.
EM zlyyxbl1267@zzu.edu.cn; zlyyyuanlong1255@zzu.edu.cn
RI Yuan, Long/H-9552-2013
FU National Cancer Center Climbing Fund; Provincial-ministerial
Co-construction Project of Henan Province Science and Technology Key
Point Tackling Plan; Henan Provincial Scientific and Technological
Project; [NCC201916B03]; [SBGJ202102064]; [222102310363];
[222102310677]
FX Funding This project was supported by National Cancer Center Climbing
Fund (NCC201916B03), Provincial-ministerial Co-construction Project of
Henan Province Science and Technology Key Point Tackling Plan
(SBGJ202102064), and Henan Provincial Scientific and Technological
Project (222102310363, 222102310677).
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NR 146
TC 25
Z9 26
U1 2
U2 20
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 21
PY 2022
VL 12
AR 1022688
DI 10.3389/fonc.2022.1022688
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6T6TS
UT WOS:000893810900001
PM 36479091
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Cleary, J
Sitwala, KV
Khodadoust, MS
Kwok, RPS
Mor-Vaknin, N
Cebrat, M
Cole, PA
Markovitz, DM
AF Cleary, J
Sitwala, KV
Khodadoust, MS
Kwok, RPS
Mor-Vaknin, N
Cebrat, M
Cole, PA
Markovitz, DM
TI p300/CBP-associated factor drives DEK into interchromatin granule
clusters
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; POSTTRANSLATIONAL PROTEIN MODIFICATIONS;
SCAFFOLD ATTACHMENT FACTOR; EXON JUNCTION COMPLEX; BREAST-CANCER CELLS;
MESSENGER-RNA; REVERSIBLE ACETYLATION; GENE-EXPRESSION; HUMAN
SPLICEOSOME; NUCLEAR SPECKLES
AB DEK is a mammalian protein that has been implicated in the pathogenesis of autoimmune diseases and cancer, including acute myeloid leukemia, melanoma, glioblastoma, hepatocellular carcinoma, and bladder cancer. In addition, DEK appears to participate in multiple cellular processes, including transcriptional repression, mRNA processing, and chromatin remodeling. Sub-nuclear distribution of this protein, with the attendant functional ramifications, has remained a controversial topic. Here we report that DEK undergoes acetylation in vivo at lysine residues within the first 70 N-terminal amino acids. Acetylation of DEK decreases its affinity for DNA elements within the promoter, which is consistent with the involvement of DEK in transcriptional repression. Furthermore, deacetylase inhibition results in accumulation of DEK within interchromatin granule clusters ( IGCs), sub-nuclear structures that contain RNA processing factors. Overexpression of P/CAF acetylase drives DEK into IGCs, and addition of a newly developed, synthetic, cell-permeable P/CAF inhibitor blocks this movement. To our knowledge, this is the first reported example of acetylation playing a direct role in relocation of a protein to IGCs, and this may explain how DEK can function in multiple pathways that take place in distinct sub-nuclear compartments. These findings also suggest that DEK-associated malignancies and autoimmune diseases might be amenable to treatment with agents that alter acetylation.
C1 Univ Michigan, Dept Internal Med, Div Infect Dis, Ann Arbor, MI 48109 USA.
Johns Hopkins Univ, Cell & Mol Biol Program, Baltimore, MD 21205 USA.
Johns Hopkins Univ, Program Immunol, Baltimore, MD 21205 USA.
Johns Hopkins Univ, Dept Obstet & Gynecol, Baltimore, MD 21205 USA.
Johns Hopkins Univ, Dept Biol Chem, Baltimore, MD 21205 USA.
Johns Hopkins Univ, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA.
Univ Wroclaw, Fac Chem, PL-50383 Wroclaw, Poland.
C3 University of Michigan System; University of Michigan; Johns Hopkins
University; Johns Hopkins University; Johns Hopkins University; Johns
Hopkins University; Johns Hopkins University; University of Wroclaw
RP Univ Michigan, Dept Internal Med, Div Infect Dis, 5220 MSRB 3,1150 W Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM dmarkov@umich.edu
RI Khodadoust, Michael/AAU-3936-2020; Cebrat, Marek/G-9754-2011
OI Cebrat, Marek/0000-0003-4975-4025; Khodadoust,
Michael/0000-0001-9061-7351
FU NCI NIH HHS [T32 CA88784-03, T32 CA07863] Funding Source: Medline; NIDDK
NIH HHS [5P-60-DK20572] Funding Source: Medline; NIGMS NIH HHS [GM62437]
Funding Source: Medline
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NR 71
TC 52
Z9 60
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 9
PY 2005
VL 280
IS 36
BP 31760
EP 31767
DI 10.1074/jbc.M500884200
PG 8
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 961LZ
UT WOS:000231665200054
PM 15987677
OA hybrid
DA 2025-01-07
ER
PT J
AU Ohara, H
Okazaki, K
Tsubouchi, H
Inui, K
Kawa, S
Kamisawa, T
Tazuma, S
Uchida, K
Hirano, K
Yoshida, H
Nishino, T
Ko, SBH
Mizuno, N
Hamano, H
Kanno, A
Notohara, K
Hasebe, O
Nakazawa, T
Nakanuma, Y
Takikawa, H
AF Ohara, Hirotaka
Okazaki, Kazuichi
Tsubouchi, Hirohito
Inui, Kazuo
Kawa, Shigeyuki
Kamisawa, Terumi
Tazuma, Susumu
Uchida, Kazushige
Hirano, Kenji
Yoshida, Hitoshi
Nishino, Takayoshi
Ko, Shigeru B. H.
Mizuno, Nobumasa
Hamano, Hideaki
Kanno, Atsushi
Notohara, Kenji
Hasebe, Osamu
Nakazawa, Takahiro
Nakanuma, Yasuni
Takikawa, Hajime
TI Clinical diagnostic criteria of IgG4-related sclerosing cholangitis 2012
SO JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
LA English
DT Article
DE IgG4; Sclerosing cholangitis; Primary sclerosing cholangitis; Autoimmune
pancreatitis; Cholangiocarcinoma
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; AUTOIMMUNE PANCREATITIS;
EXTRAPANCREATIC LESIONS; BILE-DUCT; IGG4-ASSOCIATED CHOLANGITIS;
LIVER-BIOPSY; CHOLANGIOGRAPHY; CHOLANGIOCARCINOMA; INVOLVEMENT; SPECTRUM
AB Background IgG4-sclerosing cholangitis (IgG4-SC) patients have an increased level of serum IgG4, dense infiltration of IgG4-positive plasma cells with extensive fibrosis in the bile duct wall, and a good response to steroid therapy. However, it is not easy to distinguish IgG4-SC from primary sclerosing cholangitis, pancreatic cancer, and cholangiocarcinoma on the basis of cholangiographic findings alone because various cholangiographic features of IgG4-SC are similar to those of the above progressive or malignant diseases.
Methods The Research Committee of IgG4-related Diseases and the Research Committee of Intractable Diseases of Liver and Biliary Tract in association with the Ministry of Health, Labor and Welfare, Japan and the Japan Biliary Association have set up a working group consisting of researchers specializing in IgG4-SC, and established the new clinical diagnostic criteria of IgG4-SC 2012.
Results The diagnosis of IgG4-SC is based on the combination of the following 4 criteria: (1) characteristic biliary imaging findings, (2) elevation of serum IgG4 concentrations, (3) the coexistence of IgG4-related diseases except those of the biliary tract, and (4) characteristic histopathological features. Furthermore, the effectiveness of steroid therapy is an optional extra diagnostic criterion to confirm accurate diagnosis of IgG4-SC.
Conclusion These diagnostic criteria for IgG4-SC are useful in practice for general physicians and other nonspecialists.
C1 [Ohara, Hirotaka] Nagoya City Univ, Dept Community Based Med Educ, Grad Sch Med Sci, Mizuho Ku, Nagoya, Aichi 4678601, Japan.
[Okazaki, Kazuichi; Uchida, Kazushige] Kansai Med Univ, Dept Internal Med 3, Hirakata, Osaka, Japan.
[Tsubouchi, Hirohito] Kagoshima Univ, Grad Sch Med & Dent Sci, Kagoshima 890, Japan.
[Inui, Kazuo] Fujita Hlth Univ, Dept Internal Med, Teaching Hosp 2, Nagoya, Aichi, Japan.
[Kawa, Shigeyuki] Shinshu Univ, Ctr Hlth Safety & Environm Management, Matsumoto, Nagano 390, Japan.
[Kamisawa, Terumi] Tokyo Metropolitan Komagome Hosp, Tokyo, Japan.
[Tazuma, Susumu] Hiroshima Univ, Dept Gen Med, Grad Sch Med Sci, Programs Appl Med, Hiroshima, Japan.
[Hirano, Kenji] Univ Tokyo, Dept Gastroenterol, Grad Sch Med, Tokyo, Japan.
[Yoshida, Hitoshi] Showa Univ, Sch Med, Div Gastroenterol, Dept Med, Tokyo 142, Japan.
[Nishino, Takayoshi] Tokyo Womens Med Univ, Dept Gastroenterol, Yachiyo Med Ctr, Tokyo, Japan.
[Ko, Shigeru B. H.] Nagoya Univ, Dept Gastroenterol, Grad Sch Med, Nagoya, Aichi 4648601, Japan.
[Mizuno, Nobumasa] Aichi Canc Ctr Hosp, Dept Gastroenterol, Nagoya, Aichi 464, Japan.
[Hamano, Hideaki] Shinshu Univ Hosp, Div Med Informat, Dept Internal Med, Matsumoto, Nagano, Japan.
[Kanno, Atsushi] Tohoku Univ, Div Gastroenterol, Grad Sch Med, Sendai, Miyagi 980, Japan.
[Notohara, Kenji] Kurashiki Cent Hosp, Dept Pathol, Kurashiki, Okayama, Japan.
[Hasebe, Osamu] Nagano Municipal Hosp, Dept Gastroenterol, Nagano, Japan.
[Nakazawa, Takahiro] Nagoya City Univ, Dept Gastroenterol & Metab, Grad Sch Med Sci, Nagoya, Aichi 4678601, Japan.
[Nakanuma, Yasuni] Kanazawa Univ, Dept Human Pathol, Grad Sch Med, Kanazawa, Ishikawa, Japan.
[Takikawa, Hajime] Teikyo Univ, Sch Med, Dept Med, Tokyo 173, Japan.
C3 Nagoya City University; Kansai Medical University; Kagoshima University;
Fujita Health University; Shinshu University; Tokyo Metropolitan Cancer
& Infectious Diseases Center Komagome Hospital; Hiroshima University;
University of Tokyo; Showa University; Tokyo Women's Medical University;
Nagoya University; Aichi Cancer Center; Shinshu University; Tohoku
University; Kurashiki Central Hospital; Nagoya City University; Kanazawa
University; Teikyo University
RP Ohara, H (corresponding author), Nagoya City Univ, Dept Community Based Med Educ, Grad Sch Med Sci, Mizuho Ku, 1 Kawasumi,Mizuho Cho, Nagoya, Aichi 4678601, Japan.
EM hohara@med.nagoya-cu.ac.jp
RI Ko, Shigeru/H-3450-2012; Kanno, Atsushi/J-2685-2019; Uchida,
Kazushige/AAD-4966-2020
OI Uchida, Kazushige/0000-0002-3160-3184
FU Ministry of Health, Labor, and Welfare of Japan; Grants-in-Aid for
Scientific Research [23591012, 24500977, 24591020] Funding Source: KAKEN
FX This work was supported partially by the Research Program of Intractable
Disease provided by the Ministry of Health, Labor, and Welfare of Japan.
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NR 33
TC 244
Z9 287
U1 0
U2 19
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 1868-6974
J9 J HEPATO-BIL-PAN SCI
JI J. Hepato-Biliary-Pancreat. Sci.
PD SEP
PY 2012
VL 19
IS 5
BP 536
EP 542
DI 10.1007/s00534-012-0521-y
PG 7
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 051UN
UT WOS:000312153300006
PM 22717980
DA 2025-01-07
ER
PT J
AU Cutolo, M
Pizzorni, C
Sulli, A
AF Cutolo, Maurizio
Pizzorni, Carmen
Sulli, Alberto
TI Vitamin D endocrine system involvement in autoimmune rheumatic diseases
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE Vitamin D; D hormone; Innate and adaptive immunity; Rheumatoid
arthritis; Systemic lupus erythematosus
ID 1,25-DIHYDROXYVITAMIN D-3; D DEFICIENCY; IMMUNE-SYSTEM; ARTHRITIS;
AROMATASE; DIFFERENTIATION; EXPRESSION; THERAPY; CANCER; COHORT
AB Vitamin D is synthesized from cholesterol in the skin (80-90%) under the sunlight and then metabolized into an active D hormone in liver, kidney and peripheral immune/inflammatory cells. These endocrine-immune effects include also the coordinated activities of the vitamin D-activating enzyme, 1 alpha-hydroxylase (CYP27B1), and the vitamin D receptor (VDR) on cells of the immune system in mediating intracrine and paracrine actions. Vitamin D is implicated in prevention and protection from chronic infections (i.e. tubercolosis), cancer (i.e. breast cancer) and autoimmune rheumatic diseases since regulates both innate and adaptive immunity potentiating the innate response (monocytes/macrophages with antimicrobial activity and antigen presentation), but suppressing the adaptive immunity (land B lymphocyte functions). Vitamin D has modulatory effects on B lymphocytes and Ig production and recent reports have demonstrated that 1,25 (OH)2D3 does indeed exert direct effects on B cell homeostasis. A circannual rhythm of trough vitamin D levels in winter and peaks in summer time showed negative correlation with clinical status at least in rheumatoid arthritis and systemic lupus erythematosus.
Recently, the onset of symptoms of early arthritis during winter or spring have been associated with greater radiographic evidence of disease progression at 12 months possibly are also related to seasonal lower vitamin D serum levels. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Cutolo, Maurizio] Univ Genoa, Dept Internal Med, Res Labs, I-16136 Gnova 6, Italy.
Univ Genoa, Dept Internal Med, Acad Unit Clin Rheumatol, I-16136 Gnova 6, Italy.
C3 University of Genoa; University of Genoa
RP Cutolo, M (corresponding author), Univ Genoa, Dept Internal Med, Res Labs, Viale Benedetto XV 6, I-16136 Gnova, Italy.
EM mcutolo@unige.it
RI Sulli, Alberto/AAD-1257-2022
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NR 42
TC 130
Z9 138
U1 0
U2 13
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD DEC
PY 2011
VL 11
IS 2
BP 84
EP 87
DI 10.1016/j.autrev.2011.08.003
PG 4
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 875WJ
UT WOS:000299065600002
PM 21864722
DA 2025-01-07
ER
PT J
AU Mei, Y
Liu, HY
AF Mei, Yu
Liu, Haiyan
TI IL-37: An anti-inflammatory cytokine with antitumor functions
SO CANCER REPORTS
LA English
DT Review
DE angiogenesis; antitumor immune response; IL-37; inflammation
ID IL-18 BINDING-PROTEIN; INTERLEUKIN 37; HEPATOCELLULAR-CARCINOMA; TUMOR
MICROENVIRONMENT; INNATE INFLAMMATION; NEGATIVE REGULATOR;
GENE-EXPRESSION; COLON-CANCER; IN-VIVO; IMMUNITY
AB BackgroundIL-37 is a newly identified IL-1 family cytokine. Unlike other members in IL-1 family, IL-37 has been demonstrated to be an anti-inflammatory cytokine in many inflammatory and autoimmune diseases. IL-37 is regarded as a dual-function cytokine as both the extracellular and intracellular IL-37 are biologically functional. Extracellular IL-37 can bind to IL-18R alpha and IL-1R8 to form a triple complex, regulating the downstream STAT3 and PTEN signaling. Intracellular IL-37 can interact with Smad3, translocate into nucleus, and regulate downstream target gene expressions. Recently, the role of IL-37 in tumor development has been extensively studied.
Recent findingsIL-37 has been found to play an antitumor role in various types of tumors, such as non-small cell lung cancer, hepatocellular carcinoma, and renal cell carcinoma. Many mechanism studies have been carried out to elaborate the possible effects of IL-37 on tumor growth, immune responses, and tumor angiogenesis. More importantly, the function of IL-37 may be dependent on its concentration and receptor expression. It can form dimers at high concentrations to be inactivated, thus inhibiting its anti-inflammatory function. We focused on the role of IL-37 in various tumor types and provided the hypothesis regarding the underlying mechanisms.
ConclusionIL-37 may affect tumor development through multiple mechanisms: (1) IL-37 directly influences tumor cell viability; (2) IL-37 regulates the immune response to promote the antitumor immunity; and (3) IL-37 suppresses tumor angiogenesis in the tumor microenvironment. Future studies are warranted to further investigate the mechanisms of these multifaceted functions of IL-37 in animal models and cancer patients.
C1 [Liu, Haiyan] Natl Univ Singapore, Immunol Programme, Inst Life Sci, Singapore 117456, Singapore.
[Liu, Haiyan] Natl Univ Singapore, Dept Microbiol & Immunol, Singapore 117456, Singapore.
C3 National University of Singapore; National University of Singapore
RP Liu, HY (corresponding author), Natl Univ Singapore, Immunol Programme, Inst Life Sci, Singapore 117456, Singapore.; Liu, HY (corresponding author), Natl Univ Singapore, Dept Microbiol & Immunol, Singapore 117456, Singapore.
EM micliuh@nus.edu.sg
RI Liu, Haiyan/ABD-8689-2021
OI Liu, Haiyan/0000-0002-4652-469X
FU National University of Singapore; Singapore Ministry of Education
[MOE2018-T2-1-072]
FX National University of Singapore; Singapore Ministry of Education,
Grant/Award Number: MOE2018-T2-1-072
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NR 93
TC 19
Z9 20
U1 1
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2573-8348
J9 CANCER REP-US
JI Cancer Rep.-US
PD APR
PY 2019
VL 2
IS 2
AR e1151
DI 10.1002/cnr2.1151
PG 9
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA OP5WD
UT WOS:000588155900007
PM 32935478
OA Green Published
DA 2025-01-07
ER
PT J
AU Littera, R
Perra, A
Miglianti, M
Piras, IS
Mocci, S
Lai, SR
Melis, M
Zolfino, T
Balestrieri, C
Conti, M
Serra, G
Figorilli, F
Firinu, D
Onali, S
Matta, L
Porcu, C
Pes, F
Fanni, D
Manieli, C
Vacca, M
Cusano, R
Trucas, M
Cipri, S
Tranquilli, S
Rassu, S
Cannas, F
Carta, MG
Kowalik, MA
Giuressi, E
Faa, G
Chessa, L
Giglio, S
AF Littera, Roberto
Perra, Andrea
Miglianti, Michela
Piras, Ignazio S.
Mocci, Stefano
Lai, Sara
Melis, Maurizio
Zolfino, Teresa
Balestrieri, Cinzia
Conti, Maria
Serra, Giancarlo
Figorilli, Francesco
Firinu, Davide
Onali, Simona
Matta, Laura
Porcu, Carmen
Pes, Francesco
Fanni, Daniela
Manieli, Cristina
Vacca, Monica
Cusano, Roberto
Trucas, Marcello
Cipri, Selene
Tranquilli, Stefania
Rassu, Stefania
Cannas, Federica
Carta, Mauro Giovanni
Kowalik, Marta Anna
Giuressi, Erika
Faa, Gavino
Chessa, Luchino
Giglio, Sabrina
TI The double-sided of human leukocyte antigen-G molecules in type 1
autoimmune hepatitis
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE type 1 autoimmune hepatitis; Sardinian population; human leukocyte
antigen; HLA-G alleles; soluble HLA-G; plasma cell; anti-HLA-G
monoclonal antibodies; HLA-G 3'UTR haplotypes
ID HLA-G EXPRESSION; 3' UNTRANSLATED REGION; CLASS-I GENE; T-CELLS;
POLYMORPHISM; ASSOCIATION; POPULATION; COMPLEX; PREVALENCE; HAPLOTYPE
AB The immunomodulatory effects of HLA-G expression and its role in cancers, human liver infections and liver transplantation are well documented, but so far, there are only a few reports addressing autoimmune liver diseases, particularly autoimmune hepatitis (AIH). Method and materialsWe analyzed the genetic and phenotypic characteristics of HLA-G in 205 type 1 AIH patients (AIH-1) and a population of 210 healthy controls from Sardinia (Italy). ResultsAnalysis of the HLA-G locus showed no substantial differences in allele frequencies between patients and the healthy control population. The HLA-G UTR-1 haplotype was the most prevalent in both AIH-1 patients and controls (40.24% and 34.29%). Strong linkage was found between the HLA-G UTR-1 haplotype and HLA-DRB1*03:01 in AIH-1 patients but not controls (D' = 0.92 vs D' = 0.50 respectively; P = 1.3x10(-8)). Soluble HLA-G (sHLA-G) levels were significantly lower in AIH-1 patients compared to controls [13.9 (11.6 - 17.4) U/mL vs 21.3 (16.5 - 27.8) U/mL; P = 0.011]. Twenty-four patients with mild or moderate inflammatory involvement, as assessed from liver biopsy, showed much higher sHLA-G levels compared to the 28 patients with severe liver inflammation [33.5 (23.6 - 44.8) U/mL vs 8.8 (6.1 - 14.5) U/mL; P = 0.003]. Finally, immunohistochemistry analysis of 52 liver biopsies from AIH-1 patients did not show expression of HLA-G molecules in the liver parenchyma. However, a percentage of 69.2% (36/52) revealed widespread expression of HLA-G both in the cytoplasm and the membrane of plasma cells labeled with anti-HLA-G monoclonal antibodies. ConclusionThis study highlights the positive immunomodulatory effect of HLA-G molecules on the clinical course of AIH-1 and how this improvement closely correlates with plasma levels of sHLA-G. However, our results open the debate on the ambiguous role of HLA-G molecules expressed by plasma cells, which are pathognomonic features of AIH-1.
C1 [Littera, Roberto; Lai, Sara; Rassu, Stefania; Giuressi, Erika; Giglio, Sabrina] R Binaghi Hosp, Med Genet, Cagliari, Sardegna, Italy.
[Littera, Roberto; Perra, Andrea; Melis, Maurizio; Cipri, Selene; Chessa, Luchino; Giglio, Sabrina] AART ODV Assoc Advancement Res Transplantat, Cagliari, Italy.
[Perra, Andrea; Trucas, Marcello; Kowalik, Marta Anna] Univ Cagliari, Dept Biomed Sci, Oncol & Mol Pathol Unit, Sect Pathol, Cagliari, Italy.
[Miglianti, Michela; Firinu, Davide; Onali, Simona; Matta, Laura; Porcu, Carmen; Pes, Francesco; Carta, Mauro Giovanni; Chessa, Luchino] Univ Cagliari, Dept Med Sci & Publ Hlth, Cagliari, Italy.
[Piras, Ignazio S.] Translat Genom Res Inst TGen, Neurogenom Div, Phoenix, AZ USA.
[Mocci, Stefano; Vacca, Monica; Tranquilli, Stefania; Cannas, Federica; Giglio, Sabrina] Univ Cagliari, Dept Med Sci & Publ Hlth, Med Genet, Cagliari, Italy.
[Zolfino, Teresa; Figorilli, Francesco] S Michele Hosp, Div Gastroenterol, Azienda Rilievo Nazl & Alta Specializzaz ARNAS, Cagliari, Italy.
[Balestrieri, Cinzia; Conti, Maria; Serra, Giancarlo; Chessa, Luchino] Univ Hosp, Liver Unit, Cagliari, Italy.
[Fanni, Daniela; Faa, Gavino] Univ Hosp San Giovanni Di Dio, Dept Med Sci & Publ Hlth, Div Pathol, Cagliari, Italy.
[Manieli, Cristina] S Michele Hosp, Dept Pathol Anat, Azienda Rilievo Nazl & Alta Specializzaz ARNAS, Cagliari, Italy.
[Cusano, Roberto] Ctr Adv Studies Res & Dev CRS4, Biomed Sect, Cagliari, Italy.
[Giglio, Sabrina] Univ Cagliari, Ctr Res Univ Serv, CeSAR Ctr Serv Ateneo Ric, Monserrato, Italy.
C3 University of Cagliari; University of Cagliari; Translational Genomics
Research Institute; University of Cagliari; University of Cagliari;
Azienda Ospedaliero-Universitaria di Cagliari; Presidio Ospedaliero San
Giovanni di Dio; University of Cagliari
RP Littera, R (corresponding author), R Binaghi Hosp, Med Genet, Cagliari, Sardegna, Italy.; Littera, R; Perra, A; Chessa, L (corresponding author), AART ODV Assoc Advancement Res Transplantat, Cagliari, Italy.; Perra, A (corresponding author), Univ Cagliari, Dept Biomed Sci, Oncol & Mol Pathol Unit, Sect Pathol, Cagliari, Italy.; Chessa, L (corresponding author), Univ Cagliari, Dept Med Sci & Publ Hlth, Cagliari, Italy.; Mocci, S (corresponding author), Univ Cagliari, Dept Med Sci & Publ Hlth, Med Genet, Cagliari, Italy.; Chessa, L (corresponding author), Univ Hosp, Liver Unit, Cagliari, Italy.
EM roby.litter@gmail.com; andrea.perra@unica.it; stefano.mocci.9@gmail.com;
luchino.chessa@unica.it
RI Fanni, Daniela/N-5669-2016; Littera, Roberto/N-9759-2016; Chessa,
Luchino/K-4255-2019; Tranquilli, Stefania/HNI-2218-2023; Carta,
MauroGiovanni/D-9624-2012; Cannas, Federica/AHB-0677-2022; Giglio,
Sabrina Rita/ABB-1093-2020; firinu, davide/AAF-4366-2020; Chessa,
Luchino/H-7561-2012; .Trucas, Marcello/HLX-3148-2023
OI Pes, Francesco/0000-0001-7645-1594; Melis, Maurizio/0000-0002-5857-781X;
Chessa, Luchino/0000-0002-9474-0995; Cipri, Selene/0000-0002-8730-0094;
Cannas, Federica/0000-0001-9827-2730; .Trucas,
Marcello/0000-0003-4725-0413
FU Fondazione di Sardegna [2021-290]
FX The research performed in this report falls within the institutional
responsibilities of the investigators of the participating centers, all
of which pertain to the Italian National Public Health Service. The
authors received no specific funding for this work. Grant funding
(2021-290) was received from the "Fondazione di Sardegna". The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
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NR 78
TC 3
Z9 3
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD OCT 12
PY 2022
VL 13
AR 1007647
DI 10.3389/fimmu.2022.1007647
PG 19
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 5V0FW
UT WOS:000876915100001
PM 36311782
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Moar, P
Tandon, R
AF Moar, Preeti
Tandon, Ravi
TI Galectin-9 as a biomarker of disease severity
SO CELLULAR IMMUNOLOGY
LA English
DT Review
DE Galectin-9; Immunomodulation; Disease severity; Biomarkers
ID GALACTOSIDE-BINDING LECTINS; T-CELL; SERUM GALECTIN-9;
PROGNOSTIC-FACTOR; PLASMA-LEVELS; NASOPHARYNGEAL CARCINOMA;
COLORECTAL-CANCER; CRYSTAL-STRUCTURE; VIRUS-INFECTION; DENDRITIC CELLS
AB Galectin-9 (Gal-9) is a beta-galactoside binding lectin known for its immunomodulatory role in various microbial infections. Gal-9 is expressed in all organ systems and localized in the nucleus, cell surface, cytoplasm and the extracellular matrix. It mediates host-pathogen interactions and regulates cell signalling via binding to its receptors. Gal-9 is involved in many physiological functions such as cell growth, differentiation, adhesion, communication and death. However, recent studies have emphasized on the elevated levels of Gal-9 in autoimmune disorders, viral infections, parasitic invasion, cancer, acute liver failure, atopic dermatitis, chronic kidney disease, type-2 diabetes, coronary artery disease, atherosclerosis and benign infertility-related gynecological disorders. In this paper we have reviewed the potential of Gal-9 as a reliable, sensitive and non-invasive biomarker of disease severity. Tracking changes in Gal-9 levels and its implementation as a biomarker in clinical practice will be an important tool to monitor disease activity and facilitate personalized treatment decisions.
C1 [Moar, Preeti; Tandon, Ravi] Jawaharlal Nehru Univ, Sch Biotechnol, Lab AIDS Res & Immunol, New Delhi, India.
C3 Jawaharlal Nehru University, New Delhi
RP Moar, P; Tandon, R (corresponding author), Jawaharlal Nehru Univ, Sch Biotechnol, Lab AIDS Res & Immunol, New Delhi, India.
EM preeti50_sbt@jnu.ac.in; ravitandon@jnu.ac.in
RI Tandon, Ravi/HIR-8057-2022; Moar, Preeti/HDO-0657-2022
OI Moar, Preeti/0000-0002-7773-3240; Tandon, Ravi/0000-0003-3267-896X
FU Department of Biotechnology (DBT), Government of India
[BT/PR23862/MED/29/1234/2017]; University Grants Commission (UGC),
Government of India
FX We would like to acknowledge Department of Biotechnology (DBT),
Government of India (BT/PR23862/MED/29/1234/2017) for funding. Preeti
Moar would like to thank University Grants Commission (UGC), Government
of India for her Senior Research Fellowship (SRF) and Ravi Tandon is
thankful to UGC-Faculty Recharge Programme (FRP).
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AIDS RES HUM RETROV
RETROVIROLOGY
GLYCOBIOLOGY
NR 218
TC 73
Z9 79
U1 3
U2 28
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0008-8749
EI 1090-2163
J9 CELL IMMUNOL
JI Cell. Immunol.
PD MAR
PY 2021
VL 361
AR 104287
DI 10.1016/j.cellimm.2021.104287
EA JAN 2021
PG 15
WC Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Immunology
GA QH5LN
UT WOS:000618316700010
PM 33494007
DA 2025-01-07
ER
PT J
AU Baues, M
Dasgupta, A
Ehling, J
Prakash, J
Boor, P
Tacke, F
Kiessling, F
Lammers, T
AF Baues, Maike
Dasgupta, Anshuman
Ehling, Josef
Prakash, Jai
Boor, Peter
Tacke, Frank
Kiessling, Fabian
Lammers, Twan
TI Fibrosis imaging: Current concepts and future directions
SO ADVANCED DRUG DELIVERY REVIEWS
LA English
DT Review
ID FATTY LIVER-DISEASE; MAGNETIC-RESONANCE ELASTOGRAPHY;
CARCINOMA-ASSOCIATED-FIBROBLASTS; CLINICAL-PRACTICE GUIDELINES; GLOBAL
LONGITUDINAL STRAIN; MYOCARDIAL FIBROSIS; TRANSIENT ELASTOGRAPHY;
TUMOR-STROMA; HYPERTROPHIC CARDIOMYOPATHY; EXTRACELLULAR-MATRIX
AB Fibrosis plays an important role in many different pathologies. It results from tissue injury, chronic inflammation, autoimmune reactions and genetic alterations, and it is characterized by the excessive deposition of extracellular matrix components. Biopsies are routinely employed for fibrosis diagnosis, but they suffer from several drawbacks, including their invasive nature, sampling variability and limited spatial information. To overcome these limitations, multiple different imaging tools and technologies have been evaluated over the years, including Xray imaging, computed tomography (CT), ultrasound (US), magnetic resonance imaging (MRI), positron emission tomography (PET) and single-photon emission computed tomography (SPECT). These modalities can provide anatomical, functional and molecular imaging information which is useful for fibrosis diagnosis and staging, and they may also hold potential for the longitudinal assessment of therapy responses. Here, we summarize the use of non-invasive imaging techniques for monitoring fibrosis in systemic autoimmune diseases, in parenchymal organs (such as liver, kidney, lung and heart), and in desmoplastic cancers. We also discuss how imaging biomarkers can be integrated in (pre-) clinical research to individualize and improve anti-fibrotic therapies. (C) 2017 Elsevier B.V. All rights reserved.
C1 [Baues, Maike; Dasgupta, Anshuman; Ehling, Josef; Kiessling, Fabian; Lammers, Twan] Uniklin RWTH Aachen, Inst Expt Mol Imaging, Dept Nanomed & Theranost, D-52074 Aachen, Germany.
[Baues, Maike; Dasgupta, Anshuman; Ehling, Josef; Kiessling, Fabian; Lammers, Twan] Rhein Westfal TH Aachen, Helmholtz Inst Biomed Engn, D-52074 Aachen, Germany.
[Prakash, Jai; Lammers, Twan] Univ Twente, MIRA Inst Biomed Technol & Tech Med, Dept Targeted Therapeut, NL-7500 AE Enschede, Netherlands.
[Boor, Peter] Rhein Westfal TH Aachen, Dept Nephrol, D-52074 Aachen, Germany.
[Boor, Peter] Rhein Westfal TH Aachen, Inst Pathol, Uniklin RWTH Aachen, D-52074 Aachen, Germany.
[Tacke, Frank] Rhein Westfal TH Aachen, Uniklin RWTH Aachen, Dept Med 3, D-52074 Aachen, Germany.
[Lammers, Twan] Univ Utrecht, Utrecht Inst Pharmaceut Sci, Dept Pharmaceut, NL-3584 CG Utrecht, Netherlands.
C3 RWTH Aachen University; RWTH Aachen University Hospital; RWTH Aachen
University; Helmholtz Association; University of Twente; RWTH Aachen
University; RWTH Aachen University; RWTH Aachen University Hospital;
RWTH Aachen University; RWTH Aachen University Hospital; Utrecht
University
RP Lammers, T (corresponding author), Uniklin RWTH Aachen, Inst Expt Mol Imaging, Dept Nanomed & Theranost, D-52074 Aachen, Germany.; Lammers, T (corresponding author), Rhein Westfal TH Aachen, Helmholtz Inst Biomed Engn, D-52074 Aachen, Germany.
EM tlammers@ukaachen.de
RI Tacke, Frank/ABF-2212-2020; Boor, Peter/C-7707-2011; Kiessling,
Fabian/ITT-1316-2023; Lammers, Twan/U-2794-2018
OI Boor, Peter/0000-0001-9921-4284; Kiessling, Fabian/0000-0002-7341-0399;
Prakash, Jai/0000-0003-1050-650X; Lammers, Twan/0000-0002-1090-6805
FU German Research Foundation (DFG SFB/TRR57: Organ fibrosis - From
Mechanisms of injury to modulation of disease) [BO3755/3-1, BO3755/6-1];
German Ministry of Education and Research (BMBF Consortium STOP-FSGS)
[01GM1518A]; European Research Council [ERC StG 309495:NeoNallo]
FX The authors gratefully acknowledge financial support by the German
Research Foundation (DFG SFB/TRR57: Organ fibrosis - From Mechanisms of
injury to modulation of disease, BO3755/3-1 and BO3755/6-1), by the
German Ministry of Education and Research (BMBF Consortium STOP-FSGS
number 01GM1518A) and by the European Research Council (ERC StG
309495:NeoNallo). Image templates made freely available by Servier
Medical Art (http://smart.servier.com) were used for the preparation of
the graphical abstract and of several figure panels.
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NR 276
TC 100
Z9 109
U1 0
U2 49
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0169-409X
EI 1872-8294
J9 ADV DRUG DELIVER REV
JI Adv. Drug Deliv. Rev.
PD NOV 1
PY 2017
VL 121
BP 9
EP 26
DI 10.1016/j.addr.2017.10.013
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FQ8QC
UT WOS:000418627000003
PM 29108860
OA Green Accepted, Green Published
DA 2025-01-07
ER
PT J
AU Furman, D
Campisi, J
Verdin, E
Carrera-Bastos, P
Targ, S
Franceschi, C
Ferrucci, L
Gilroy, DW
Fasano, A
Miller, GW
Miller, AH
Mantovani, A
Weyand, CM
Barzilai, N
Goronzy, JJ
Rando, TA
Effros, RB
Lucia, A
Kleinstreuer, N
Slavich, GM
AF Furman, David
Campisi, Judith
Verdin, Eric
Carrera-Bastos, Pedro
Targ, Sasha
Franceschi, Claudio
Ferrucci, Luigi
Gilroy, Derek W.
Fasano, Alessio
Miller, Gary W.
Miller, Andrew H.
Mantovani, Alberto
Weyand, Cornelia M.
Barzilai, Nir
Goronzy, Jorg J.
Rando, Thomas A.
Effros, Rita B.
Lucia, Alejandro
Kleinstreuer, Nicole
Slavich, George M.
TI Chronic inflammation in the etiology of disease across the life span
SO NATURE MEDICINE
LA English
DT Article
ID C-REACTIVE PROTEIN; CORONARY-HEART-DISEASE; SUPPLEMENTATION LOWERS
INFLAMMATION; ADIPOSE-TISSUE; IMMUNE-SYSTEM; SECRETORY PHENOTYPE;
DIABETES-MELLITUS; PHYSICAL-ACTIVITY; HEALTH CONSEQUENCES; CELLULAR
SENESCENCE
AB Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI.
C1 [Furman, David; Campisi, Judith; Verdin, Eric] Buck Inst Res Aging, Novato, CA 94945 USA.
[Furman, David] Stanford Univ, Sch Med, Inst Immun Transplantat & Infect, Stanford 1000 Immunomes Project, Stanford, CA 94305 USA.
[Furman, David] Univ Austral, CONICET, Inst Res Translat Med, Buenos Aires, DF, Argentina.
[Furman, David; Targ, Sasha] Iuve Inc, San Mateo, CA 94401 USA.
[Campisi, Judith] Lawrence Berkeley Natl Lab, Berkeley, CA USA.
[Carrera-Bastos, Pedro] Lund Univ, Skane Univ Hosp, Reg Skane, Ctr Primary Hlth Care Res, Malmo, Sweden.
[Targ, Sasha] Univ Calif San Francisco, Med Scientist Training Program, San Francisco, CA 94143 USA.
[Franceschi, Claudio] IRCCS Inst Neurol Sci Bologna, Bologna, Italy.
[Franceschi, Claudio] Lobachevsky Univ, Dept Appl Math, Nizhnii Novgorod, Russia.
[Franceschi, Claudio] Lobachevsky Univ, Lab Syst Biol Aging, Nizhnii Novgorod, Russia.
[Ferrucci, Luigi] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Gilroy, Derek W.] UCL, Div Med, Ctr Clin Pharmacol & Therapeut, London, England.
[Fasano, Alessio] Harvard Med Sch, MassGen Hosp Children, Boston, MA 02115 USA.
[Miller, Gary W.] Columbia Univ, Sch Publ Hlth, Dept Environm Hlth Sci, Med Ctr, New York, NY USA.
[Miller, Andrew H.] Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA USA.
[Mantovani, Alberto] Humanitas Clin & Res Ctr, Milan, Italy.
[Mantovani, Alberto] Humanitas Univ, Dept Biomed Sci, Milan, Italy.
[Mantovani, Alberto] Queen Mary Univ, Barts & London Sch Med, William Harvey Res Inst, London, England.
[Weyand, Cornelia M.] Stanford Univ, Dept Med, Div Immunol & Rheumatol, Stanford, CA 94305 USA.
[Barzilai, Nir] Albert Einstein Coll Med, Dept Med, New York, NY USA.
[Barzilai, Nir] Albert Einstein Coll Med, Dept Genet, New York, NY USA.
[Goronzy, Jorg J.; Rando, Thomas A.] Stanford Univ, Sch Med, Paul F Glenn Ctr Biol Aging, Stanford, CA 94305 USA.
[Rando, Thomas A.] Vet Affairs Palo Alto Hlth Care Syst, Ctr Tissue Regenerat Repair & Restorat, Palo Alto, CA USA.
[Rando, Thomas A.] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA.
[Effros, Rita B.] Univ Calif Los Angeles, Dept Pathol, Los Angeles, CA 90024 USA.
[Lucia, Alejandro] Univ Europea Madrid, Fac Sport Sci, Madrid, Spain.
[Lucia, Alejandro] Hosp 12 Octubre I 12, Res Inst, Madrid, Spain.
[Kleinstreuer, Nicole] NIEHS, Biostat & Computat Biol Branch, Div Intramural Res, NIH,Dept Hlth & Human Serv, POB 12233, Res Triangle Pk, NC 27709 USA.
[Kleinstreuer, Nicole] NIEHS, NTP Interagency Ctr Evaluat Alternat Toxicol Meth, NIH, Dept Hlth & Human Serv, POB 12233, Res Triangle Pk, NC 27709 USA.
[Slavich, George M.] Univ Calif Los Angeles, Cousins Ctr Psychoneuroimmunol, Los Angeles, CA USA.
[Slavich, George M.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
C3 Buck Institute for Research on Aging; Stanford University; Austral
University; Consejo Nacional de Investigaciones Cientificas y Tecnicas
(CONICET); United States Department of Energy (DOE); Lawrence Berkeley
National Laboratory; Lund University; Skane University Hospital;
University of California System; University of California San Francisco;
IRCCS Istituto delle Scienze Neurologiche di Bologna (ISNB); Lobachevsky
State University of Nizhni Novgorod; Lobachevsky State University of
Nizhni Novgorod; National Institutes of Health (NIH) - USA; NIH National
Institute on Aging (NIA); University of London; University College
London; Harvard University; Massachusetts General Hospital; Harvard
Medical School; Columbia University; Emory University; Humanitas
University; University of London; Queen Mary University London; Stanford
University; Yeshiva University; Yeshiva University; Stanford University;
US Department of Veterans Affairs; Veterans Health Administration (VHA);
VA Palo Alto Health Care System; Stanford University; University of
California System; University of California Los Angeles; European
University of Madrid; Hospital Universitario 12 de Octubre; National
Institutes of Health (NIH) - USA; NIH National Institute of
Environmental Health Sciences (NIEHS); National Institutes of Health
(NIH) - USA; NIH National Institute of Environmental Health Sciences
(NIEHS); University of California System; University of California Los
Angeles; University of California System; University of California Los
Angeles
RP Furman, D (corresponding author), Buck Inst Res Aging, Novato, CA 94945 USA.; Furman, D (corresponding author), Stanford Univ, Sch Med, Inst Immun Transplantat & Infect, Stanford 1000 Immunomes Project, Stanford, CA 94305 USA.; Furman, D (corresponding author), Univ Austral, CONICET, Inst Res Translat Med, Buenos Aires, DF, Argentina.; Furman, D (corresponding author), Iuve Inc, San Mateo, CA 94401 USA.
EM furmand@stanford.edu
RI Fasano, Alessio/K-5486-2016; Weyand, Cornelia/AAH-3343-2021; Goronzy,
Jorg/AFK-1229-2022; Ferrucci, Luigi/AED-9724-2022; Verdin,
Eric/AAB-7999-2019; Mantovani, Alberto/HCI-7449-2022; Slavich,
George/C-6208-2008; Carrera-Bastos, Pedro/ABG-3591-2021; Gilroy,
Derek/AAP-7227-2020; Miller, Andrew/AFL-5625-2022; Kleinstreuer,
Nicole/F-7203-2019
OI Verdin, Eric/0000-0003-3703-3183; Ferrucci, Luigi/0000-0002-6273-1613;
Carrera-Bastos, Pedro/0000-0002-4218-1300; Goronzy,
Jorg/0000-0001-7670-1856; Lucia, Alejandro/0000-0002-5565-0997; Targ,
Sasha/0009-0006-1510-2589; Fasano, Alessio/0000-0002-2134-0261;
Kleinstreuer, Nicole/0000-0002-7914-3682; Furman,
David/0000-0002-3654-9519; Rando, Thomas/0000-0001-5843-8564; Gilroy,
Derek/0000-0003-3476-0844
FU National Institutes of Health (NIH); Buck Institute for Research on
Aging; National Institute on Aging; Glenn Foundation; SENS Foundation;
Ministry of Education and Science of the Russian Federation
[074-02-2018-330]; Horizon 2020 Framework Programme [634821]; JPco-fuND
(ADAGE); National Institute of Aging, NIH; MRC (UK); Wellcome Trust; NIH
[R01 DK104344, P01 AG036695, K08 MH103443]; European Research Commission
[PHII-669415]; Associazione Italiana Ricerca sul Cancro [IG 19014,
5x1000 9962, 21147]; Fondazione Cariplo; Italian Ministry of Health;
UCLA AIDS Institute; Spanish Ministry of Economy and Competitiveness;
Fondos FEDER [PI15/00558, PI18/00139]; Society in Science-Branco Weiss
Fellowship; Brain & Behavior Research Foundation [23958]
FX This work was made possible by support from the National Institutes of
Health (NIH) and the Buck Institute for Research on Aging to D.F., the
National Institute on Aging, Glenn and SENS Foundations, and the Buck
Institute for Research on Aging to J.C.; the Ministry of Education and
Science of the Russian Federation Agreement (074-02-2018-330) and
Horizon 2020 Framework Programme (634821, PROPAG-AGING) and JPco-fuND
(ADAGE) to C.F.; the Intramural Research Program of the National
Institute of Aging, NIH to L.F.; the MRC (UK) and Wellcome Trust to
D.W.G.; NIH grant (R01 DK104344) to A.F.; the European Research
Commission (PHII-669415), Associazione Italiana Ricerca sul Cancro
(Projects IG 19014, 5x1000 9962 and 21147), Fondazione Cariplo, and
Italian Ministry of Health to A.M.; NIH grant (P01 AG036695) to T.A.R.;
the National Institute on Aging and UCLA AIDS Institute to R.B.E.; the
Spanish Ministry of Economy and Competitiveness and Fondos FEDER
(PI15/00558 and PI18/00139) to A.L.; and a Society in Science-Branco
Weiss Fellowship, NARSAD Young Investigator Grant 23958 from the Brain &
Behavior Research Foundation and NIH grant (K08 MH103443) to G.M.S. This
work represents the opinion of the authors and does not reflect official
NIH policy.
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NR 179
TC 2484
Z9 2674
U1 63
U2 513
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2019
VL 25
IS 12
BP 1822
EP 1832
DI 10.1038/s41591-019-0675-0
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA JT2KO
UT WOS:000500824900023
PM 31806905
OA Green Accepted, Bronze
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Maddalo, G
Spolverato, Y
Rugge, M
Farinati, F
AF Maddalo, Gemma
Spolverato, Ylenia
Rugge, Massimo
Farinati, Fabio
TI Gastrin: from pathophysiology to cancer prevention and treatment
SO EUROPEAN JOURNAL OF CANCER PREVENTION
LA English
DT Review
DE autoimmune gastritis; G17DT; gastric atrophy; gastric carcinoids;
hypochlorhydria; neuroendocrine tumors; vaccine
ID HELICOBACTER-PYLORI; ATROPHIC GASTRITIS; CARCINOID-TUMORS; EXPRESSION;
RECEPTOR; HYPERGASTRINEMIA; MANAGEMENT; G17DT; CELLS; RISK
AB Gastrin has been identified as the principal effector of gastric secretion, but several studies have demonstrated its role as a biomarker of cancer risk and as a growth factor for colorectal, stomach, liver, and pancreatic cancer. Hypergastrinemia characterizes autoimmune gastritis, with body and fundic gland atrophy and increased risk for both gastric adenocarcinoma and neuroendocrine tumors. Gastric type I carcinoids develop in the context of autoimmune gastritis because of the stimulus exerted by gastrin on enterochromaffin-like cells and remain gastrin-sensitive for long durations because the removal of hypergastrinemia leads to tumor regression. The treatment of gastric carcinoid is still open to debate, but when the disease frequently relapses, or is multicentric or infiltrating, surgery is advocated or, in the alternative, a costly and long-lasting treatment with long-acting somatostatin analogues is prescribed. A technology allowing the preparation of an immunogen eliciting an immune system response with generation of antibodies against G17 has been developed. This vaccine has been tested in patients with colorectal, pancreatic or advanced gastric cancer. The vaccine has also been used in the treatment of gastric type I carcinoids, and the administration of G17DT in patients harboring these lesions leads to carcinoid regression. Antigastrin vaccination in the treatment of gastrointestinal cancer obviously needs validation, but this immunotherapy may well represent a simple, inexpensive, and active `adjuvant' treatment. (C) 2014 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Maddalo, Gemma; Spolverato, Ylenia; Farinati, Fabio] Padua Univ Hosp, Dept Surg Oncol & Gastroenterol, I-35128 Padua, Italy.
[Rugge, Massimo] Univ Padua, Dept Med, Padua, Italy.
C3 University of Padua; Azienda Ospedaliera - Universita di Padova;
University of Padua
RP Farinati, F (corresponding author), Padua Univ Hosp, Dept Surg Oncol & Gastroenterol, Via Giustiniani 2, I-35128 Padua, Italy.
EM fabio.farinati@unipd.it
RI Farinati, Fabio/A-8267-2012; Rugge, Massimo/K-7525-2016
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NR 62
TC 24
Z9 27
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0959-8278
EI 1473-5709
J9 EUR J CANCER PREV
JI Eur. J. Cancer Prev.
PD JUL
PY 2014
VL 23
IS 4
BP 258
EP 263
DI 10.1097/CEJ.0000000000000008
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AI9XP
UT WOS:000337300400004
PM 24469263
DA 2025-01-07
ER
PT J
AU Beier, JI
Arteel, GE
AF Beier, Juliane I.
Arteel, Gavin E.
TI Environmental exposure as a risk-modifying factor in liver diseases:
Knowns and unknowns
SO ACTA PHARMACEUTICA SINICA B
LA English
DT Review
DE Hepatic injury; Exposomics; Liver disease; Drug-induced liver injury;
Alcoholic liver disease; Non-alcoholic liver disease; Inherited liver
disease; Autoimmune liver disease
ID PRIMARY BILIARY-CIRRHOSIS; PRIMARY SCLEROSING CHOLANGITIS;
TOXICANT-ASSOCIATED STEATOHEPATITIS; VINYL-CHLORIDE;
HEPATOCELLULAR-CARCINOMA; HEPATITIS-C; INTESTINAL MICROBIOME;
MOLECULAR-MECHANISMS; INCREASED PREVALENCE; MONOZYGOTIC TWINS
AB Liver diseases are considered to predominantly possess an inherited or xenobiotic etiology. However, inheritance drives the ability to appropriately adapt to environmental stressors, and disease is the culmination of a maladaptive response. Thus "pure" genetic and "pure" xenobiotic liver diseases are modified by each other and other factors, identified or unknown. The purpose of this review is to highlight the knowledgebase of environmental exposure as a potential risk modifying agent for the development of liver disease by other causes. This exercise is not to argue that all liver diseases have an environmental component, but to challenge the assumption that the current state of our knowledge is sufficient in all cases to conclusively dismiss this as a possibility. This review also discusses key new tools and approaches that will likely be critical to address this question in the future. Taken together, identifying the key gaps in our understanding is critical for the field to move forward, or at the very least to "know what we don't know." (C) 2021 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.
C1 [Beier, Juliane I.; Arteel, Gavin E.] Univ Pittsburgh, Div Gastroenterol Hepatol & Nutr, Dept Med, Pittsburgh, PA 15213 USA.
[Beier, Juliane I.; Arteel, Gavin E.] Pittsburgh Liver Res Ctr, Pittsburgh, PA 15213 USA.
[Beier, Juliane I.; Arteel, Gavin E.] Univ Pittsburgh, Pittsburgh, PA 15213 USA.
[Beier, Juliane I.] Univ Pittsburgh, Dept Environm & Occupat Hlth, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh; Pennsylvania Commonwealth System of
Higher Education (PCSHE); University of Pittsburgh
RP Beier, JI; Arteel, GE (corresponding author), Univ Pittsburgh, Div Gastroenterol Hepatol & Nutr, Dept Med, Pittsburgh, PA 15213 USA.; Beier, JI; Arteel, GE (corresponding author), Pittsburgh Liver Res Ctr, Pittsburgh, PA 15213 USA.; Beier, JI; Arteel, GE (corresponding author), Univ Pittsburgh, Pittsburgh, PA 15213 USA.; Beier, JI (corresponding author), Univ Pittsburgh, Dept Environm & Occupat Hlth, Pittsburgh, PA 15213 USA.
EM jibeier@pitt.edu; gearteel@pitt.edu
RI Arteel, Gavin/AAE-2440-2022
OI Arteel, Gavin/0000-0002-2253-5984; Beier, Juliane/0000-0002-5395-5682
FU NIH [R01 AA021978, P30 DK120531, R21 ES031531]
FX Supported, in part, by grants from NIH (R01 AA021978, P30 DK120531, and
R21 ES031531, USA).
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NR 177
TC 9
Z9 10
U1 0
U2 7
PU INST MATERIA MEDICA, CHINESE ACAD MEDICAL SCIENCES
PI BEIJING
PA C/O EDITORIAL BOARD OF ACTA PHARMACEUTICA SINICA, 1 XIANNONGTAN ST,
BEIJING, 100050, PEOPLES R CHINA
SN 2211-3835
EI 2211-3843
J9 ACTA PHARM SIN B
JI Acta Pharm. Sin. B
PD DEC
PY 2021
VL 11
IS 12
BP 3768
EP 3778
DI 10.1016/j.apsb.2021.09.005
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA YC6BC
UT WOS:000739773600006
PM 35024305
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Bottoni, P
Giardina, B
Scatena, R
AF Bottoni, Patrizia
Giardina, Bruno
Scatena, Roberto
TI Proteomic profiling of heat shock proteins: An emerging molecular
approach with direct pathophysiological and clinical implications
SO PROTEOMICS CLINICAL APPLICATIONS
LA English
DT Review
DE Biomarkers; Cellular stress response; Diagnostics; Neurodegeneration;
Oncoproteomics
ID 2-DIMENSIONAL GEL-ELECTROPHORESIS; SQUAMOUS-CELL CARCINOMA;
DIFFERENTIALLY EXPRESSED PROTEINS; CU/ZN-SUPEROXIDE-DISMUTASE;
BETA-AMYLOID PEPTIDE; STRESS-PROTEINS; CANCER-CELLS; BREAST-CANCER;
HEPATOCELLULAR-CARCINOMA; OXIDATIVE STRESS
AB The HSP family is one of the most ancient and evolutionarily conserved protective protein families found in nature. Originally discovered as inducible molecules capable of maintaining cellular homeostasis against abrupt temperature changes, HSPs were later determined to represent an adaptive physiological response that copes with a variety of different cellular proteotoxic stresses. These physiological molecular chaperones facilitate the synthesis, folding, assembly, trafficking and secretion of specific proteins in various cellular compartments. Most importantly, these proteins guard the whole cell proteome against misfolding and inappropriate aggregation. A series of diversified proteotoxic stresses, including heat, hypoxia/ischemia, free radicals, acidosis, ATP depletion and toxins are capable of inducing a typical cellular stress response characterised by rapid inhibition of overall protein synthesis, with a concomitant dramatic increase in H S P expression. From a pathophsiological point of view, HSP induction has been observed in a wide spectrum of inflammatory and degenerative diseases (from cancer to prion disease by passing to infective and autoimmune diseases) and, intriguingly, overexpression monitoring seems to have potential implications in terms of diagnosis, prognosis and, above all, therapy. Proteomics studies, identifying a series of modification of HSP expression patterns in different diseases, are confirming these promising clinical applications.
C1 [Bottoni, Patrizia; Giardina, Bruno; Scatena, Roberto] Catholic Univ, Dept Lab Med, I-00168 Rome, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli
RP Bottoni, P (corresponding author), Catholic Univ, Dept Lab Med, Largo A Gemelli 8, I-00168 Rome, Italy.
EM patrizia.bottoni@icrm.cnr.it
RI Scatena, Roberto/AES-1637-2022
OI Bottoni, Patrizia/0000-0001-5427-8903
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NR 176
TC 11
Z9 11
U1 0
U2 0
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1862-8346
EI 1862-8354
J9 PROTEOM CLIN APPL
JI Proteom. Clin. Appl.
PD JUN
PY 2009
VL 3
IS 6
BP 636
EP 653
DI 10.1002/prca.200800195
PG 18
WC Biochemical Research Methods; Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 469QQ
UT WOS:000267915300001
PM 21136976
DA 2025-01-07
ER
PT J
AU Elfström, P
Granath, F
Ye, WM
Ludvigsson, JF
AF Elfstrom, Peter
Granath, Fredrik
Ye, Weimin
Ludvigsson, Jonas F.
TI Low Risk of Gastrointestinal Cancer Among Patients With Celiac Disease,
Inflammation, or Latent Celiac Disease
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Autoimmune Disorder; Malignancy; Cancer Incidence; Epidemiology
ID POPULATION-BASED COHORT; GLUTEN-FREE DIET; LIVER-DISEASE;
DERMATITIS-HERPETIFORMIS; MALIGNANCY; MORTALITY; INDIVIDUALS; SMOKING;
PEOPLE; SENSITIVITY
AB BACKGROUND & AIMS: Celiac disease has been associated with gastrointestinal (GI) cancers in small studies; risks have not been estimated from large populations or based on histopathology analyses. METHODS: We examined the risk of GI cancers by using data from cohorts of patients with celiac disease (villous atrophy, Marsh score of 3; n = 28,882) or inflammation (Marsh score of 1-2; n = 12,860); biopsy samples were evaluated at 28 pathology centers. A third cohort included 3705 individuals with latent celiac disease (normal mucosa, but positive serology results). Data were compared with those from an age-and sex-matched population. RESULTS: Of patients with celiac disease, 372 developed incident GI cancers; 347 patients with inflammation and 38 with latent celiac disease developed GI cancers. In the first year after diagnosis and initial biopsy, celiac disease was associated with 5.95-fold increase in risk of incident GI cancer (95% confidence interval [ CI], 4.64-7.64); the hazard ratio [HR] for inflammation was 9.13 (95% CI, 7.19-11.6) and for latent celiac disease was 8.10 (95% CI, 4.69-14.0). After the first year, patients were at no significant increase in risk for GI cancers; the HR for celiac disease was 1.07 (95% CI, 0.93-1.23), for inflammation it was 1.16 (95% CI, 0.98-1.37), and for latent celiac disease it was 0.96 (95% CI, 0.56-1.66). The absolute risk for any GI cancer in patients with celiac disease was 101/100,000 person-years, with an excess risk of 2/100,000 person-years. CONCLUSIONS: Although celiac disease, inflammation, and latent disease all increase risk for GI cancers in the first year after diagnosis, there is no increase in risk thereafter.
C1 [Ludvigsson, Jonas F.] Orebro Univ Hosp, Dept Pediat, S-70185 Orebro, Sweden.
[Elfstrom, Peter] Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp Danderyd, Dept Neonatol, Stockholm, Sweden.
Karolinska Inst, Karolinska Univ Hosp, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden.
[Ye, Weimin] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
C3 Orebro University; Karolinska Institutet; Karolinska University
Hospital; Karolinska Institutet; Karolinska University Hospital;
Karolinska Institutet
RP Ludvigsson, JF (corresponding author), Orebro Univ Hosp, Dept Pediat, S-70185 Orebro, Sweden.
EM jonasludvigsson@yahoo.com
RI Ye, Weimin/A-5939-2008; Ludvigsson, Jonas/A-8560-2012
OI Ludvigsson, Jonas/0000-0003-1024-5602; ye, weimin/0000-0002-6859-4648
FU Orebro University Hospital Research Foundation; Orebro University;
Swedish Society of Medicine; Swedish Research Council; Sven Jerring
Foundation; Orebro Society of Medicine; Karolinska Institutet; Clas
Groschinsky Foundation; Juhlin Foundation; Majblomman Foundation;
Uppsala-Orebro Regional Research Council; Swedish Celiac Society
FX This project was supported by grants from the Orebro University Hospital
Research Foundation, Orebro University, Swedish Society of Medicine, the
Swedish Research Council, the Sven Jerring Foundation, the Orebro
Society of Medicine, the Karolinska Institutet, the Clas Groschinsky
Foundation, the Juhlin Foundation, the Majblomman Foundation, the
Uppsala-Orebro Regional Research Council, and the Swedish Celiac
Society.
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NR 44
TC 70
Z9 73
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD JAN
PY 2012
VL 10
IS 1
BP 30
EP 36
DI 10.1016/j.cgh.2011.06.029
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 872LZ
UT WOS:000298812400014
PM 21723236
DA 2025-01-07
ER
PT J
AU Chen, RH
Du, JM
Zhu, H
Ling, Q
AF Chen, Ruihan
Du, Jiamin
Zhu, Hong
Ling, Qi
TI The role of cGAS-STING signalling in liver diseases
SO JHEP REPORTS
LA English
DT Review
DE cGAS-STING signalling; innate immune response; viral hepatitis;
nonalcoholic fatty liver disease; liver injury; hepatocellular carcinoma
ID GMP-AMP SYNTHASE; C VIRUS NS4B; PATTERN-RECOGNITION RECEPTORS;
ENDOPLASMIC-RETICULUM STRESS; ISCHEMIA-REPERFUSION INJURY; INNATE
IMMUNE-RESPONSE; KUPFFER CELLS; DNA SENSOR; CYCLIC DINUCLEOTIDE;
MITOCHONDRIAL-DNA
AB The recently identified novel cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS) activates the downstream adaptor protein stimulator of interferon genes (STING) by catalysing the synthesis of cyclic GMP-AMP. This in turn initiates an innate immune response through the release of various cytokines, including type I interferon. Foreign DNA (microbial infection) or endogenous DNA (nuclear or mitochondrial leakage) can serve as cGAS ligands and lead to the activation of cGAS-STING signalling. Therefore, the cGAS-STING pathway plays essential roles in infectious diseases, sterile inflammation, tumours, and autoimmune diseases. In addition, cGAS-STING signalling affects the progression of liver inflammation through other mechanisms, such as autophagy and metabolism. In this review, we summarise recent advances in our understanding of the role of cGAS-STING signalling in the innate immune modulation of different liver diseases. Furthermore, we discuss the therapeutic potential of targeting the cGAS-STING pathway in the treatment of liver diseases. (C) 2021 The Authors. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver (EASL).
C1 [Chen, Ruihan; Ling, Qi] Zhejiang Univ, Affiliated Hosp 1, Dept Surg, Sch Med, Hangzhou, Peoples R China.
[Du, Jiamin; Zhu, Hong; Ling, Qi] Zhejiang Univ, Coll Pharmaceut Sci, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Ling, Q (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Dept Surg, Sch Med, Hangzhou, Peoples R China.; Zhu, H; Ling, Q (corresponding author), Zhejiang Univ, Coll Pharmaceut Sci, Hangzhou, Peoples R China.
EM hongzhu@zju.edu.cn; lingqi@zju.edu.cn
RI Du, Jiamin/GVU-9084-2022
OI LING, QI/0000-0002-7377-2381
FU National Natural Science Foundation of China [81771713, 82011530442];
Zhejiang Provincial Natural Science Foundation of China [LR18H030001]
FX This work was supported by the National Natural Science Foundation of
China (81771713 and 82011530442); the Zhejiang Provincial Natural
Science Foundation of China (LR18H030001).
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NR 124
TC 56
Z9 60
U1 8
U2 56
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2589-5559
J9 JHEP REP
JI JHEP Rep.
PD OCT
PY 2021
VL 3
IS 5
AR 100324
DI 10.1016/j.jhepr.2021.100324
EA JUL 2021
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WG4FI
UT WOS:000706949300004
PM 34381984
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Hetz, C
Chevet, E
Harding, HP
AF Hetz, Claudio
Chevet, Eric
Harding, Heather P.
TI Targeting the unfolded protein response in disease
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Review
ID ENDOPLASMIC-RETICULUM-STRESS; SODIUM 4-PHENYLBUTYRATE PROTECTS;
MOLECULAR CHAPERONE-INDUCER; TRANSCRIPTION FACTOR XBP-1; NEURONAL
CELL-DEATH; ER STRESS; MESSENGER-RNA; EIF2-ALPHA DEPHOSPHORYLATION;
TRANSMEMBRANE PROTEIN; DISULFIDE ISOMERASES
AB Stress induced by the accumulation of unfolded proteins in the endoplasmic reticulum (ER) is a feature of specialized secretory cells and is also observed in many diseases, including cancer, diabetes, autoimmune conditions, liver disorders, obesity and neurodegenerative disorders. Cellular adaptation to ER stress is achieved by the activation of the unfolded protein response, which is an integrated signal transduction pathway that modulates many aspects of ER physiology. When these mechanisms of adaptation are insufficient to handle the unfolded protein load, cells undergo apoptosis. Here, we discuss recent advances in the design of novel compounds and therapeutic strategies to manipulate levels of ER stress in disease.
C1 [Hetz, Claudio] Univ Chile, Fac Med, ICBM, Biomed Neurosci Inst,Program Cellular & Mol Biol, Santiago 7, Chile.
[Hetz, Claudio] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Chevet, Eric] Univ Bordeaux Segalen, INSERM, U1053, French Natl Inst Hlth & Med Res, F-33000 Bordeaux, France.
[Harding, Heather P.] Univ Cambridge, Metab Res Labs, Cambridge CB2 0QQ, England.
[Harding, Heather P.] Univ Cambridge, Natl Inst Hlth Res, Cambridge Biomed Res Ctr, Cambridge CB2 0QQ, England.
C3 Universidad de Chile; Harvard University; Harvard T.H. Chan School of
Public Health; Universite de Bordeaux; Institut National de la Sante et
de la Recherche Medicale (Inserm); University of Cambridge; University
of Cambridge
RP Hetz, C (corresponding author), Univ Chile, Fac Med, ICBM, Biomed Neurosci Inst,Program Cellular & Mol Biol, 1027 Independencia,POB 70086, Santiago 7, Chile.
EM chetz@med.uchile.cl; eric.chevet@inserm.fr; hph23@medschl.cam.ac.uk
RI Hetz, Claudio/ABD-7514-2021; Chevet, Eric/E-4992-2016
OI Hetz, Claudio/0000-0003-1120-7966; Harding, Heather
P/0000-0002-7359-7974; Chevet, Eric/0000-0001-5855-4522
FU FONDECYT [1100176]; Millennium Institute [P09-015-F]; Ring Initiative
[ACT 1109]; FONDEF [D11I1007]; ALS Therapy Alliance; Muscular Dystrophy
Association; Michael J. Fox Foundation; Alzheimer's Disease Association;
Institut National de la Sante et la Recherche Medicale (INSERM);
Institut National du Cancer, France; Ligue contre le cancer, France;
Wellcome Trust [084812/Z/08/Z]; Wellcome Trust [084812/Z/08/Z] Funding
Source: Wellcome Trust
FX The authors apologize to all their colleagues whose work could not be
cited owing to space limitations. The authors thank J. Patterson for
helpful discussions about IRE1 inhibitors, and U. Woehlbier and H. Urra
for initial designs of the figures. This work was funded by the
following grants and associations: FONDECYT 1100176; Millennium
Institute No. P09-015-F; Ring Initiative ACT 1109; FONDEF D11I1007; the
ALS Therapy Alliance; the Muscular Dystrophy Association; the Michael J.
Fox Foundation; the Alzheimer's Disease Association (to C. H.); the
Institut National de la Sante et la Recherche Medicale (INSERM); the
Institut National du Cancer, France; the Ligue contre le cancer, France;
and Wellcome Trust Grant 084812/Z/08/Z (to H.P.H.).
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NR 185
TC 720
Z9 844
U1 1
U2 217
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
EI 1474-1784
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD SEP
PY 2013
VL 12
IS 9
BP 703
EP 719
DI 10.1038/nrd3976
PG 17
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA 211EF
UT WOS:000323887000020
PM 23989796
DA 2025-01-07
ER
PT J
AU Kesaraju, P
Jaini, R
Johnson, JM
Altuntas, CZ
Gruden, JJ
Sakalar, C
Tuohy, VK
AF Kesaraju, Pavani
Jaini, Ritika
Johnson, Justin M.
Altuntas, Cengiz Z.
Gruden, Jessica J.
Sakalar, Cagri
Tuohy, Vincent K.
TI Experimental Autoimmune Breast Failure A Model for Lactation
Insufficiency, Postnatal Nutritional Deprivation, and
Prophylactic Breast Cancer Vaccination
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID MOUSE ALPHA-LACTALBUMIN; GRANULOMATOUS MASTITIS; SERUM-CHOLESTEROL;
FEEDING WOMEN; INFANT; DISEASE; MANAGEMENT; RISK
AB Mastitis is a substantial clinical problem in lactating women that may result in severe pain and abrupt termination of breastfeeding, thereby predisposing infants to long-term health risks. Many cases of mastitis involve no known infectious agent and may fundamentally be due to autoimmune-mediated inflammation of the breast. Herein, we develop a murine model of autoimmune mastitis and provide a detailed characterization of its resulting phenotype of breast failure and lactation insufficiency. To generate breast-specific autoimmunity, we immunized SWXJ mice with recombinant mouse a-lactalbumin, a lactation-dependent, breast-specific differentiation protein critical for production of lactose. Mice immunized with a-lactalbumin showed extensive T-cell mediated inflammation in lactating normal breast parenchyma but none in nonlactating normal breast parenchyma. This targeted autoimmune attack resulted in breast failure characterized by lactation insufficiency and decreased ability to nurture offspring. Although immunization with alpha-lactalbumin had no effect on fertility and birth numbers, pups nursed by a-lactalbumin immunized mice showed significantly disrupted growth often accompanied by kwashiorkor-like nutritional abnormalities, including alopecia, liver toxicity, and runting. This experimental model of autoimmune breast failure has useful applications for prophylactic breast cancer vaccination and for addressing inflammatory complications during breastfeeding. In addition, this model is suited for investigating nutritionally based "failure-to-thrive" issues, particularly regarding the long-term implications of postnatal nutritional deprivation. (Am J Pathol 2012, 181:775-784; https://dx-doi-org.a8.sjuku.top/10.1016/j.ajpath.2012.05.025)
C1 [Kesaraju, Pavani; Jaini, Ritika; Johnson, Justin M.; Altuntas, Cengiz Z.; Gruden, Jessica J.; Sakalar, Cagri; Tuohy, Vincent K.] Cleveland Clin, Lerner Res Inst, Dept Immunol, Cleveland, OH 44195 USA.
[Kesaraju, Pavani; Tuohy, Vincent K.] Cleveland State Univ, Dept Biol, Cleveland, OH 44115 USA.
[Tuohy, Vincent K.] Case Western Reserve Univ, Cleveland Clin, Lerner Coll Med, Dept Mol Med, Cleveland, OH 44106 USA.
C3 Cleveland Clinic Foundation; University System of Ohio; Cleveland State
University; University System of Ohio; Case Western Reserve University;
Cleveland Clinic Foundation
RP Tuohy, VK (corresponding author), Cleveland Clin, Lerner Res Inst, Dept Immunol, NB30,9500 Euclid Ave, Cleveland, OH 44195 USA.
EM tuohyv@ccf.org
OI Jaini, Ritika/0000-0002-4580-8789
FU NIH [R01CA-140350]
FX Supported by NIH grant R01CA-140350 (V.K.T.).
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NR 50
TC 9
Z9 10
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0002-9440
EI 1525-2191
J9 AM J PATHOL
JI Am. J. Pathol.
PD SEP
PY 2012
VL 181
IS 3
BP 775
EP 784
DI 10.1016/j.ajpath.2012.05.025
PG 10
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 012QH
UT WOS:000309251100007
PM 22901749
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Ye, JY
Liu, XH
AF Ye, Jingyao
Liu, Xuehong
TI Interactions between endoplasmic reticulum stress and extracellular
vesicles in multiple diseases
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE endoplasmic reticulum stress; extracellular vesicles; interactions;
multiple diseases; UPR signaling pathways
ID UNFOLDED PROTEIN RESPONSE; CANCER CELLS; ER STRESS; EXOSOMES; RELEASE;
APOPTOSIS; CERAMIDE; ATF6-ALPHA; EXPRESSION; SECRETION
AB Immune responses can severely perturb endoplasmic reticulum (ER) function. As a protein-folding factory and dynamic calcium storage compartment, the ER plays a pivotal role in resisting pathogens and in the development of autoimmune diseases and various other diseases, including cancer, cardiovascular, neurological, orthopedic, and liver-related diseases, metabolic disorders, etc. In recent years, an increasing number of studies have shown that extracellular vesicles (EVs) play important roles in these conditions, suggesting that cells carry out some physiological functions through EVs. The formation of EVs is dependent on the ER. ER stress, as a state of protein imbalance, is both a cause and consequence of disease. ER stress promotes the transmission of pathological messages to EVs, which are delivered to target cells and lead to disease development. Moreover, EVs can transmit pathological messages to healthy cells, causing ER stress. This paper reviews the biological functions of EVs in disease, as well as the mechanisms underlying interactions between ER stress and EVs in multiple diseases. In addition, the prospects of these interactions for disease treatment are described.
C1 [Ye, Jingyao] Shandong Univ Tradit Chinese Med, Jinan, Peoples R China.
[Liu, Xuehong] Guangzhou Univ Chinese Med, Sch Clin Med 3, Guangzhou, Peoples R China.
C3 Shandong University of Traditional Chinese Medicine; Guangzhou
University of Chinese Medicine
RP Liu, XH (corresponding author), Guangzhou Univ Chinese Med, Sch Clin Med 3, Guangzhou, Peoples R China.
EM 895147598@qq.com
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NR 78
TC 15
Z9 16
U1 0
U2 21
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD AUG 11
PY 2022
VL 13
AR 955419
DI 10.3389/fimmu.2022.955419
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 3Y9YG
UT WOS:000844077900001
PM 36032078
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Murray, PE
Coffman, JA
Garcia-Godoy, F
AF Murray, Peter E.
Coffman, Jonathan A.
Garcia-Godoy, Franklin
TI Oral Pathogens' Substantial Burden on Cancer, Cardiovascular Diseases,
Alzheimer's, Diabetes, and Other Systemic Diseases: A Public Health
Crisis-A Comprehensive Review
SO PATHOGENS
LA English
DT Review
DE microorganisms; dental; antibiotics; teeth; caries; periodontitis;
P. gingivalis; cardiovascular; antibiotic resistance
ID ATHEROSCLEROTIC VASCULAR-DISEASE; CORONARY-HEART-DISEASE;
PERIODONTAL-DISEASE; FUSOBACTERIUM-NUCLEATUM; RHEUMATOID-ARTHRITIS;
STREPTOCOCCUS-MUTANS; PORPHYROMONAS-GINGIVALIS; TREPONEMA-DENTICOLA;
PREGNANCY OUTCOMES; ACUTE EXACERBATION
AB This review synthesizes the findings from 252 studies to explore the relationship between the oral pathogens associated with periodontitis, dental caries, and systemic diseases. Individuals with oral diseases, such as periodontitis, are between 1.7 and 7.5 times (average 3.3 times) more likely to develop systemic diseases or suffer adverse pregnancy outcomes, underscoring the critical connection between dental and overall health. Oral conditions such as periodontitis and dental caries represent a significant health burden, affecting 26-47% of Americans. The most important oral pathogens, ranked by publication frequency, include the herpes virus, C. albicans, S. mutans, P. gingivalis, F. nucleatum, A. actinomycetemcomitans, P. intermedia, T. denticola, and T. forsythia. The systemic diseases and disorders linked to oral infections, ranked similarly, include cancer, respiratory, liver, bowel, fever, kidney, complications in pregnancy, cardiovascular bacteremia, diabetes, arthritis, autoimmune, bladder, dementia, lupus, and Alzheimer's diseases. Evidence supports the efficacy of dental and periodontal treatments in eliminating oral infections and reducing the severity of systemic diseases. The substantial burden that oral pathogens have on cancer, cardiovascular diseases, Alzheimer's, diabetes, and other systemic diseases poses a significant public health crisis.
C1 [Coffman, Jonathan A.] Amer Univ Hlth Sci, Coll Pharm, Signal Hill, CA 90755 USA.
[Garcia-Godoy, Franklin] Univ Tennessee, Coll Dent, Hlth Sci Ctr, Memphis, TN 38163 USA.
RP Coffman, JA (corresponding author), Amer Univ Hlth Sci, Coll Pharm, Signal Hill, CA 90755 USA.
EM p_e_murray@outlook.com; jcoffman@auhs.edu; godoy@uthsc.edu
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NR 252
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-0817
J9 PATHOGENS
JI Pathogens
PD DEC
PY 2024
VL 13
IS 12
AR 1084
DI 10.3390/pathogens13121084
PG 32
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA Q3T8J
UT WOS:001383957100001
OA gold
DA 2025-01-07
ER
PT J
AU Silva, J
Brito, BS
Silva, IND
Nóbrega, VG
da Silva, MCSM
Gomes, HD
Fortes, FM
Pimentel, AM
Mota, J
Almeida, N
Surlo, VC
Lyra, A
Rocha, R
Santana, GO
AF Silva, Juliana
Brito, Beatriz S.
Silva, Isaac Neri de N.
Nobrega, Viviane G.
da Silva, Maria Carolina S. M.
Gomes, Hemerson Dyego de N.
Fortes, Flora Maria
Pimentel, Andrea M.
Mota, Jaciane
Almeida, Neogelia
Surlo, Valdiana C.
Lyra, Andre
Rocha, Raquel
Santana, Genoile O.
TI Frequency of Hepatobiliary Manifestations and Concomitant Liver Disease
in Inflammatory Bowel Disease Patients
SO BIOMED RESEARCH INTERNATIONAL
LA English
DT Article
ID PRIMARY SCLEROSING CHOLANGITIS; EXTRAINTESTINAL MANIFESTATIONS;
COLORECTAL-CANCER; EPIDEMIOLOGY; PHENOTYPE; HEPATITIS
AB Background. In inflammatory bowel disease (IBD) patients there are reports of the occurrence of hepatobiliary manifestations, so the aim of this study was to evaluate the hepatobiliary manifestations in patients with Crohn's disease (CD) and ulcerative colitis (UC) from an IBD reference center. Methods. Cross-sectional study in an IBD reference center, with interviews and review of medical charts, between July 2015 and August 2016. A questionnaire addressing epidemiological and clinical characteristics was used. Results. We interviewed 306 patients, and the majority had UC (53.9%) and were female (61.8%). Hepatobiliary manifestations were observed in 60 (19.6%) patients with IBD. In the greater part of the patients (56.7%) hepatobiliary disorders were detected after the diagnosis of IBD. In UC (18.2%) patients, the hepatobiliary disorders identified were 11 (6.7%) non-alcoholic fatty liver disease, 9 (5.5%) cholelithiasis, 6 (3.6%) primary sclerosing cholangitis (PSC), 3 (1.8%) hepatotoxicity associated with azathioprine, 1 (0.6%) hepatitis B, and 1 (0.6%) hepatic fibrosis. In CD (21.3%) patients, 11 (7.8%) had cholelithiasis, 11 (7.8%) non-alcoholic fatty liver disease, 4 (2.8%) PSC, 3 (2.1%) hepatotoxicity, 1 (0.7%) hepatitis B, (0.7%) hepatitis C, 1 (0.7%) alcoholic liver disease, and 1 (0.7%) autoimmune hepatitis (AIH). There was one case of PSC/AIH overlap syndrome. Conclusion. The frequency of hepatobiliary disorders was similar in both forms of IBD in patients evaluated. The most common nonspecific hepatobiliary manifestations in IBD patients were non-alcoholic liver disease and cholelithiasis. The most common specific hepatobiliary disorder was PSC in patients with extensive UC or ileocolonic CD involvement; this was seen more frequently in male patients.
C1 [Silva, Juliana; Brito, Beatriz S.; Silva, Isaac Neri de N.; Nobrega, Viviane G.; da Silva, Maria Carolina S. M.; Gomes, Hemerson Dyego de N.; Santana, Genoile O.] Univ Estado Bahia, Dept Life Sci, Rua Silveira Martins 2555, BR-41150000 Salvador, BA, Brazil.
[Fortes, Flora Maria; Pimentel, Andrea M.; Mota, Jaciane; Almeida, Neogelia; Surlo, Valdiana C.] HGRS, Rua Direta Saboeiro S-N, BR-41180780 Salvador, BA, Brazil.
[Lyra, Andre; Santana, Genoile O.] Univ Fed Bahia, Univ Hosp Prof Edgard Santos, Gastroenterol Unit, Rua Augusto Viana Sn 28 Andar, BR-40110060 Salvador, BA, Brazil.
[Rocha, Raquel] Univ Fed Bahia, Escola Nutr, Dept Ciencia Nutr, Ave Araujo Pinho,32, BR-40110150 Salvador, BA, Brazil.
C3 Universidade do Estado Bahia; Universidade Federal da Bahia;
Universidade Federal da Bahia
RP Santana, GO (corresponding author), Univ Estado Bahia, Dept Life Sci, Rua Silveira Martins 2555, BR-41150000 Salvador, BA, Brazil.; Santana, GO (corresponding author), Univ Fed Bahia, Univ Hosp Prof Edgard Santos, Gastroenterol Unit, Rua Augusto Viana Sn 28 Andar, BR-40110060 Salvador, BA, Brazil.
EM genoile@uol.com.br
RI Santana, Genoile/AEW-8038-2022; Surlo, Valdiana/KJL-4105-2024; Silva,
Isaac/HCH-8608-2022; Lyra, Andre/O-8656-2016; Rocha, Raquel/G-3924-2012
OI Rocha, Raquel/0000-0002-2687-2080; SANTANA, GENOILE
OLIVEIRA/0000-0001-5936-9791
CR Bambha K, 2003, GASTROENTEROLOGY, V125, P1364, DOI 10.1016/j.gastro.2003.07.011
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Zippi M, 2014, WORLD J GASTROENTERO, V20, P17463, DOI 10.3748/wjg.v20.i46.17463
NR 21
TC 27
Z9 28
U1 0
U2 8
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-6133
EI 2314-6141
J9 BIOMED RES INT
JI Biomed Res. Int.
PY 2019
VL 2019
AR 7604939
DI 10.1155/2019/7604939
PG 7
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA HL0MV
UT WOS:000458389500001
PM 30834274
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Gronkjær, LL
Lauridsen, MM
AF Gronkjaer, Lea Ladegaard
Lauridsen, Mette Munk
TI Quality of life and unmet needs in patients with chronic liver disease:
A mixed-method systematic review
SO JHEP REPORTS
LA English
DT Review
DE Liver disease; Mixed method; Patient experience; Patient reported
out-comes; Quality of life; Systematic review; Unmet needs
ID CHRONIC HEPATITIS-B; NONALCOHOLIC STEATOHEPATITIS NASH;
HEPATOCELLULAR-CARCINOMA; ILLNESS EXPERIENCE; CIRRHOSIS PATIENTS;
PERCEIVED STIGMA; CHILDREN; FATIGUE; BURDEN; QUESTIONNAIRES
AB Background & Aims: In an attempt to uncover unmet patient needs, this review aims to synthesise quantitative and qualitative studies on patients' quality of life and their experience of having liver disease.
Methods: Three databases (CINAHL, Embase, and PubMed) were searched from January 2000 to October 2020. The methodological quality and data extraction of both quantitative and qualitative studies were screened and appraised using Joanna Briggs Institute instruments for mixed-method systematic reviews and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A convergent, integrated approach to synthesis and integration was used. Studies including patients with autoimmune and cholestatic liver disease, chronic hepatitis B and C, non-alcoholic fatty liver disease and nonalcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma were considered.
Results: The searches produced 5,601 articles, of which 95 (79 quantitative and 16 qualitative) were included in the review. These represented studies from 26 countries and a sample of 37,283 patients. The studies showed that patients' quality of life was reduced. Unmet needs for information and support and perceived stigmatisation severely affected patients' quality of life.
Conclusions: Our study suggests changes to improve quality of life. According to patients, this could be achieved by providing better education and information, being aware of patients' need for support, and raising awareness of liver disease among the general population to reduce misconceptions and stigmatisation.
Registration number: PROSPERO CRD42020173501.
Lay summary: Regardless of aetiology, patients with liver diseases have impaired quality of life. This is associated with disease progression, the presence of symptoms, treatment response, and mental, physical, and social factors such as anxiety, confusion, comorbidities, and fatigue, as well as limitations in daily living, including loneliness, low income, stigmatisation, and treatment costs. Patients highlighted the need for information to understand and manage liver disease, and awareness and support from healthcare professionals to better cope with the disease. In addition, there is a need to raise awareness of liver diseases in the general population to reduce negative preconceptions and stigmatisation. (C) 2021 The Authors. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver (EASL).
C1 [Gronkjaer, Lea Ladegaard; Lauridsen, Mette Munk] Univ Hosp Southern Denmark, Dept Gastroenterol, Finsensgade 35, DK-6700 Esbjerg, Denmark.
C3 University of Southern Denmark; Odense University Hospital
RP Gronkjær, LL (corresponding author), Univ Hosp Southern Denmark, Dept Gastroenterol, Finsensgade 35, DK-6700 Esbjerg, Denmark.
EM lea.ladegaard.gronicjaer@rsyd.dk
RI Lauridsen, Mette/AAX-6491-2020
OI Munk Lauridsen, Mette/0000-0003-0586-8549; Ladegaard Gronkjaer,
Lea/0000-0001-5754-8235
FU Region of Southern Denmark's Foundation for Health Research
FX L.L.G. received a grant from the Region of Southern Denmark's Foundation
for Health Research. The funder played no role in the design,
collection, analysis, or writing of the manuscript.
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NR 113
TC 32
Z9 33
U1 3
U2 31
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2589-5559
J9 JHEP REP
JI JHEP Rep.
PD DEC
PY 2021
VL 3
IS 6
AR 100370
DI 10.1016/j.jhepr.2021.100370
EA NOV 2021
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA XD9RU
UT WOS:000723037800006
PM 34805816
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Goobie, GC
Bernatsky, S
Ramsey-Goldman, R
Clarke, AE
AF Goobie, Gillian C.
Bernatsky, Sasha
Ramsey-Goldman, Rosalind
Clarke, Ann E.
TI Malignancies in systemic lupus erythematosus: a 2015 update
SO CURRENT OPINION IN RHEUMATOLOGY
LA English
DT Review
DE breast cancer; lymphoma; malignancy; systemic lupus erythematosus
ID SHOCK-PROTEIN 27; RESISTANT PROSTATE-CANCER; MANTLE CELL LYMPHOMA;
EPSTEIN-BARR-VIRUS; AUTOIMMUNE-DISEASES; THYROID-CANCER; INCREASED RISK;
LUNG-CANCER; METAANALYSIS; COHORT
AB Purpose of review
Patients with systemic lupus erythematosus (SLE) have altered incidences of certain malignancies as compared with the general population. This review summarizes the recent literature on risk of malignancy in SLE and proposed mechanisms for these altered susceptibilities.
Recent findings
Recent studies have confirmed previous data showing an increased risk of non-Hodgkin's lymphoma, lung, liver, vulvar/vaginal, and thyroid malignancies, whereas demonstrating a decreased risk of breast and prostate cancer. Lymphomagenesis in SLE has been linked to increased activity of multiple inflammatory cytokines as well as possible viral diseases. The decreased rates of hormone-sensitive cancers, such as breast and prostate, are speculated to be related to the presence of lupus autoantibodies and downregulation of certain proteins in SLE. This knowledge has been utilized to investigate new therapeutic modalities for these malignancies. Summary
Recent data confirm previously reported altered malignancy rates in SLE. Most striking in recent years are publications further elucidating mechanisms underlying cancer development in SLE, and subsequent investigations of potential therapeutics modulating these pathways.
C1 [Goobie, Gillian C.] Univ Calgary, Dept Med, Cumming Sch Med, Hlth Sci Ctr, Foothills Campus, Calgary, AB, Canada.
[Bernatsky, Sasha] McGill Univ, Dept Med & Epidemiol & Biostat, Montreal, PQ, Canada.
[Ramsey-Goldman, Rosalind] Northwestern Univ, Feinberg Sch Med, Div Rheumatol, Dept Med, Chicago, IL 60611 USA.
[Clarke, Ann E.] Univ Calgary, Dept Rheumatol, Dept Med, Cumming Sch Med, Calgary, AB, Canada.
C3 University of Calgary; McGill University; Northwestern University;
Feinberg School of Medicine; University of Calgary
RP Bernatsky, S (corresponding author), Univ Calgary, Dept Med, Cumming Sch Med, Hlth Sci Ctr, Foothills Campus,3330 Hosp Dr NW, Calgary, AB T2N 4N1, Canada.
EM gcgoobie@ucalgary.ca
RI Goobie, Gillian/AAT-5587-2021
OI Goobie, Gillian/0000-0001-7982-5635
FU Arthritis Society Chair in Rheumatic Diseases at University of Calgary
FX AEC is the Arthritis Society Chair in Rheumatic Diseases at the
University of Calgary.
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NR 58
TC 67
Z9 68
U1 0
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-8711
EI 1531-6963
J9 CURR OPIN RHEUMATOL
JI Curr. Opin. Rheumatol.
PD SEP
PY 2015
VL 27
IS 5
BP 454
EP 460
DI 10.1097/BOR.0000000000000202
PG 7
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA DD0PS
UT WOS:000369622500005
PM 26125105
OA Bronze, Green Accepted
DA 2025-01-07
ER
PT J
AU Sookoian, S
Pirola, CJ
AF Sookoian, Silvia
Pirola, Carlos J.
TI Review article: shared disease mechanisms between non-alcoholic fatty
liver disease and metabolic syndrome - translating knowledge from
systems biology to the bedside
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
ID GENE; ATHEROSCLEROSIS; LOSARTAN; EXPRESSION; PATHWAYS; OBESITY
AB Background Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease worldwide. Characterised by abnormal fat accumulation in the liver, NAFLD presents high degree of comorbidity with disorders of the metabolic syndrome, including type 2 diabetes, obesity and cardiovascular disease. These comorbidities have strong negative impact on the natural course of NAFLD and vice versa, whereby the presence of NAFLD substantially modifies the course and prognosis of metabolic syndrome-associated diseases. Aim To use systems biology strategies to interrogate disease mechanisms that are common to NAFLD and metabolic syndrome. Methods We mapped shared gene/protein-disease interaction networks, we performed gene-disease enrichment analysis to assess pleiotropy, and we created a gene-drug connectivity network. Results We found that a shared network of genes/proteins is overrepresented by immune response-related pathways, post-translational modifications of nuclear receptors, and platelet-related processes, including activation and platelet signalling. Likewise, gene-based disease-enrichment analysis suggested underlying molecular effectors that are shared with major systemic disorders, including diverse autoimmune diseases, kidney, respiratory and nervous system disorders, cancer and infectious diseases. The shared list of genes/proteins was enriched in drug targets for anti-inflammatory therapy, drugs used to treat cardiovascular diseases, antimicrobial agents and phytochemicals, among many other approved pharmaceutical compounds. By leveraging on publicly available OMICs data, we were able to show that shared loci are not necessarily affected by reverse causality. Conclusion We provide evidence indicating that NAFLD treatment, including severe histological traits, cannot be limited to the use of a single drug, as it rather requires a multi-target therapeutic approach.
C1 [Sookoian, Silvia; Pirola, Carlos J.] Univ Buenos Aires, Inst Med Res A Lanari, Sch Med, Buenos Aires, DF, Argentina.
[Sookoian, Silvia] Univ Buenos Aires, Inst Med Res IDIM, Natl Sci & Tech Res Council CONICET, Dept Clin & Mol Hepatol, Buenos Aires, DF, Argentina.
[Pirola, Carlos J.] Univ Buenos Aires, Natl Sci & Tech Res Council CONICET, Dept Mol Genet & Biol Complex Dis, Inst Med Res IDIM, Buenos Aires, DF, Argentina.
C3 University of Buenos Aires; Centro Nacional Patagonico (CENPAT); Consejo
Nacional de Investigaciones Cientificas y Tecnicas (CONICET); University
of Buenos Aires; Centro Nacional Patagonico (CENPAT); Consejo Nacional
de Investigaciones Cientificas y Tecnicas (CONICET); University of
Buenos Aires
RP Sookoian, S; Pirola, CJ (corresponding author), Inst Invest Med UBA CONICET, Buenos Aires, DF, Argentina.
EM ssookoian@intramed.net; pirola.carlos@conicet.gov.ar
RI Pirola, Carlos/H-2720-2019
OI Sookoian, Silvia/0000-0001-5929-5470
FU Agencia Nacional de Promocion Cientifica y Tecnologica, Fondo para la
Investigacion Cientifica y Tecnologica (FonCyT) [PICT 2014-0432, PICT
2015-0551, PICT 2014-1816, 2016-0135]
FX Agencia Nacional de Promocion Cientifica y Tecnologica, Fondo para la
Investigacion Cientifica y Tecnologica (FonCyT) (PICT 2014-0432 and PICT
2015-0551 to SS, and PICT 2014-1816 and 2016-0135 to CJP).
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NR 34
TC 49
Z9 51
U1 3
U2 23
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD MAR
PY 2019
VL 49
IS 5
BP 516
EP 527
DI 10.1111/apt.15163
PG 12
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA HK9RN
UT WOS:000458329600004
PM 30714632
OA Bronze
DA 2025-01-07
ER
PT J
AU Muramatsu, T
AF Muramatsu, Takashi
TI Midkine: A Promising Molecule for Drug Development to Treat Diseases of
the Central Nervous System
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE Alzheimer's disease; Cerebral infarction; Drug discovery; Glioblastoma;
Ischemia; Midkine; Multiple sclerosis; Neurodegenerative diseases
ID BINDING GROWTH-FACTOR; ACID-RESPONSIVE GENE; CONDITIONALLY REPLICATIVE
ADENOVIRUS; SQUAMOUS-CELL CARCINOMA; EPITHELIAL-MESENCHYMAL
INTERACTIONS; HUMAN HEPATOCELLULAR-CARCINOMA; TRANSIENT FOREBRAIN
ISCHEMIA; ANAPLASTIC LYMPHOMA KINASE; ANGIOGENIC FACTOR MIDKINE;
ACTIVATED PROTEIN-KINASE
AB Midkine (MK) is a heparin-binding cytokine, and promotes growth, survival, migration and other activities of target cells. After describing the general properties of MK, this review focuses on MK and MK inhibitors as therapeutics for diseases in the central nervous system. MK is strongly expressed during embryogenesis especially at the midgestation period, but is expressed only at restricted sites in adults. MK expression is induced upon tissue injury such as ischemic brain damage. Since exogenously administered MK or the gene transfer of MK suppresses neuronal cell death in experimental systems, MK has the potential to treat cerebral infarction. MK might become important also in the treatment of neurodegenerative diseases such as Alzheimer's disease. MK is involved in inflammatory diseases by enhancing migration of leukocytes, inducing chemokine production and suppressing regulatory T cells. Since an aptamer to MK suppresses experimental autoimmune encephalitis, MK inhibitors are promising for the treatment of multiple sclerosis. MK is over-expressed in most malignant tumors including glioblastoma, and is involved in tumor invasion. MK inhibitors may be of value in the treatment of glioblastoma. Furthermore, an oncolytic adenovirus, whose replication is under the control of the MK promoter, inhibits the growth of glioblastoma xenografts. MK inhibitors under development include antibodies, aptamers, glycosaminoglycans, peptides and low molecular weight compounds. siRNA and antisense oligoDNA have proved effective against malignant tumors and inflammatory diseases in experimental systems. Practical information concerning the development of MK and MK inhibitors as therapeutics is described in the final part of the review.
C1 Aichi Gakuin Univ, Dept Hlth Sci, Fac Psychol & Phys Sci, Aichi 4700195, Japan.
C3 Aichi Gakuin University
RP Muramatsu, T (corresponding author), Aichi Gakuin Univ, Dept Hlth Sci, Fac Psychol & Phys Sci, 12 Araike,Iwasaki Cho, Aichi 4700195, Japan.
EM tmurama@dpc.agu.ac.jp
FU Ministry of Education, Culture, Sports, Science and Technology, Japan
FX The author's work mentioned in this review was supported by grants from
the Ministry of Education, Culture, Sports, Science and Technology,
Japan.
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NR 202
TC 82
Z9 91
U1 0
U2 26
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD FEB
PY 2011
VL 17
IS 5
BP 410
EP 423
DI 10.2174/138161211795164167
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 768PE
UT WOS:000290946600002
PM 21375488
OA Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Kocak, M
Erdi, SE
Jorba, G
Maestro, I
Farres, J
Kirkin, V
Martinez, A
Pless, O
AF Kocak, Muhammed
Ezazi Erdi, Saba
Jorba, Guillem
Maestro, Ines
Farres, Judith
Kirkin, Vladimir
Martinez, Ana
Pless, Ole
TI Targeting autophagy in disease: established and new strategies
SO AUTOPHAGY
LA English
DT Review
DE Autophagy activators; autophagy inhibitors; autophagy modulators;
clinical trials; drug discovery
ID IN-VITRO; SELECTIVE AUTOPHAGY; CANCER-CELLS; HEPATOCELLULAR-CARCINOMA;
POLYGLUTAMINE EXPANSIONS; MTORC2 INHIBITOR; ATG4B INHIBITORS; MAMMALIAN
TARGET; KINASE INHIBITOR; BLOCKS AUTOPHAGY
AB Macroautophagy/autophagy is an evolutionarily conserved pathway responsible for clearing cytosolic aggregated proteins, damaged organelles or invading microorganisms. Dysfunctional autophagy leads to pathological accumulation of the cargo, which has been linked to a range of human diseases, including neurodegenerative diseases, infectious and autoimmune diseases and various forms of cancer. Cumulative work in animal models, application of genetic tools and pharmacologically active compounds, has suggested the potential therapeutic value of autophagy modulation in disease, as diverse as Huntington, Salmonella infection, or pancreatic cancer. Autophagy activation versus inhibition strategies are being explored, while the role of autophagy in pathophysiology is being studied in parallel. However, the progress of preclinical and clinical development of autophagy modulators has been greatly hampered by the paucity of selective pharmacological agents and biomarkers to dissect their precise impact on various forms of autophagy and cellular responses. Here, we summarize established and new strategies in autophagy-related drug discovery and indicate a path toward establishing a more efficient discovery of autophagy-selective pharmacological agents. With this knowledge at hand, modern concepts for therapeutic exploitation of autophagy might become more plausible.
C1 [Kocak, Muhammed; Kirkin, Vladimir] Inst Canc Res London, Canc Therapeut Unit, Canc Res UK, Sutton, Surrey, England.
[Ezazi Erdi, Saba; Pless, Ole] Fraunhofer ITMP ScreeningPort, D-22525 Hamburg, Germany.
[Jorba, Guillem; Farres, Judith] Anax Biotech SL, Barcelona, Spain.
[Maestro, Ines; Martinez, Ana] CSIC, Ctr Invest Biol Margarita Salas, Madrid, Spain.
[Martinez, Ana] Inst Salud Carlos III, Ctr Invest Biomed Red Enfermedades Neurodegenerat, Madrid, Spain.
C3 Cancer Research UK; Consejo Superior de Investigaciones Cientificas
(CSIC); CSIC - Centro de Investigaciones Biologicas (CIB); CIBERNED;
Instituto de Salud Carlos III
RP Pless, O (corresponding author), Fraunhofer ITMP ScreeningPort, D-22525 Hamburg, Germany.
EM ole.pless@itmp.fraunhofer.de
RI Pless, Ole/E-8348-2016; Farrés, Jaume/F-8648-2016; Martinez,
Ana/L-6414-2014
OI Farres, Judith/0000-0002-0958-0510; Pless, Ole/0000-0002-1468-316X;
KOCAK, Muhammed/0000-0002-7889-680X; Ezazi Erdi,
Saba/0000-0001-5628-7520; Jorba, Guillem/0000-0001-5209-5353; Martinez,
Ana/0000-0002-2707-8110
FU H2020 MarieSklodowska-Curie Actions [765912 - DRIVE]
FX This research was funded by H2020 MarieSklodowska-Curie Actions (765912
-DRIVE).
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NR 273
TC 113
Z9 122
U1 26
U2 211
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD MAR 4
PY 2022
VL 18
IS 3
BP 473
EP 495
DI 10.1080/15548627.2021.1936359
EA JUL 2021
PG 23
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 0S8FM
UT WOS:000671468500001
PM 34241570
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Arendt, JFB
Nexo, E
AF Arendt, Johan F. B.
Nexo, Ebba
TI Cobalamin Related Parameters and Disease Patterns in Patients with
Increased Serum Cobalamin Levels
SO PLOS ONE
LA English
DT Article
ID TRANSCOBALAMIN LEVELS; HOLO-TRANSCOBALAMIN; TRANSPORT PROTEINS;
VITAMIN-B12; PLASMA; HAPTOCORRIN; FOLATE; QUANTIFICATION; ASSOCIATION;
CELLS
AB Background: Measurement of serum cobalamin levels is routinely used to diagnose cobalamin deficiency. Surprisingly, approximately 15% of patients have high cobalamin levels and no consensus exists regarding the clinical implications.
Methods: Hospital-treated patients above 18 years of age referred for serum cobalamin measurement were included in groups of patients [percentage cobalamin supplemented] with low (<200 pmol/L, n = 200 [6%]), normal (200-600, n = 202 [6%]) high (601-1000, n = 217 [27%]) and very high (>1000, n = 199 [53%]) cobalamin levels. Total and cobalamin-saturated (holo) transcobalamin, total haptocorrin, soluble TC receptor, sCD320, and methylmalonic acid were analyzed. Data on diagnoses and medical prescriptions was obtained through medical files and the Aarhus University Prescription Database.
Results: Among patients not cobalamin supplemented median total haptocorrin and holo transcobalamin levels were markedly higher in the groups with high/very high cobalamin levels compared to groups with low/normal cobalamin levels. Median total transcobalamin and sCD320 levels were similar across the groups. A number of diagnoses were significantly associated to very high Cbl levels (odds ratio (95% confidence interval)): alcoholism (5.74 (2.76-11.96)), liver disease (8.53 (3.59-20.23)), and cancer (5.48 (2.85-10.55)). Elevated haptocorrin levels were seen in patients with alcoholism, cancer, liver-, renal-, autoimmune-, and bronchopulmonary disease. No clinical associations to sCD320 and total and holo transcobalamin levels were found.
Conclusion: In non-supplemented patients, high cobalamin levels were associated to high haptocorrin levels, and several diagnoses, including alcoholism, liver disease and cancer. Our study emphasizes that clinicians should take high serum cobalamin levels into consideration in the diagnostic process.
C1 [Arendt, Johan F. B.; Nexo, Ebba] Aarhus Univ Hosp, Dept Clin Biochem, DK-8000 Aarhus, Denmark.
C3 Aarhus University
RP Arendt, JFB (corresponding author), Aarhus Univ Hosp, Dept Clin Biochem, DK-8000 Aarhus, Denmark.
EM johan.frederik.berg.arendt@sun.au.dk
OI Arendt, Johan Frederik Hakonsen/0000-0003-4423-4813; Nexo,
Ebba/0000-0001-9406-9081
FU Faculty of Health, Aarhus University; Danish Medical Research Council;
Lundbeck Foundation
FX This work was supported by: the Faculty of Health, Aarhus University
(www.health.au.dk); Danish Medical Research Council
(www.fi.dk/raad-og-udvalg/det-frie-forskningsraad/om-dff/faglige-raad/su
ndhed-og-sygdom) and the Lundbeck Foundation (www.lundbeckfonden.dk).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 35
TC 69
Z9 74
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 21
PY 2012
VL 7
IS 9
AR e45979
DI 10.1371/journal.pone.0045979
PG 8
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 014RG
UT WOS:000309392800128
PM 23029349
OA gold, Green Submitted, Green Published
DA 2025-01-07
ER
PT J
AU Ise, H
AF Ise, Hirohiko
TI Vimentin's N-Acetylglucosamine-Binding Activity: Its
Physiological Function
SO TRENDS IN GLYCOSCIENCE AND GLYCOTECHNOLOGY
LA English
DT Review
DE glycopolymers; vimentin; N-acetylglucosamine; lectin; O-GlcNAc proteins
ID CELL-SURFACE VIMENTIN; ASIALOGLYCOPROTEIN RECEPTOR EXPRESSION;
FIBRILLARY ACIDIC PROTEIN; CIRCULATING TUMOR-CELLS;
CENTRAL-NERVOUS-SYSTEM; O-LINKED GLCNAC; INTERMEDIATE-FILAMENTS;
ALZHEIMERS-DISEASE; RAT HEPATOCYTES; LIVER-CELLS
AB Vimentin is known as a cytoskeletal protein that is expressed in mesenchymal and skeletal muscle tissues and plays an important role in the maintenance of the cytoplasmic architecture and cellular integrity. Moreover, vimentin is implicated in various cellular signal transduction pathways involved in cell proliferation and cell migration. Vimentin is highly expressed in lesion sites of various chronic diseases such as fibrosis, cancer, and autoimmune diseases. Vimentin's high expression in various chronic diseases led to investigate its involvement in pathological mechanisms in chronic diseases. We recently reported that vimentin possesses N-acetyl-D-glucosamine (GlcNAc)-binding activity on cell surfaces. In this review, we describe vimentin's GlcNAc-binding activity and discuss our hypothesis regarding its physiological relevance.
C1 [Ise, Hirohiko] Kyushu Univ, Inst Mat Chem & Engn, Nishi Ku, CE41-206,744 Motooka, Fukuoka 8190395, Japan.
C3 Kyushu University
RP Ise, H (corresponding author), Kyushu Univ, Inst Mat Chem & Engn, Nishi Ku, CE41-206,744 Motooka, Fukuoka 8190395, Japan.
EM ise@ms.ifoc.kyushu-u.ac.jp
FU Ministry of Education, Culture, Sports, Science and Technology (MEXT) of
Japan; SOMAR Corp.; Grants-in-Aid for Scientific Research [15K01313]
Funding Source: KAKEN
FX The author is deeply indebted to Professor Toshihiro Akaike and Mitsuaki
Goto (Tokyo Institute of Technology) for his kind encouragement and
discussions. The author is grateful to the Ministry of Education,
Culture, Sports, Science and Technology (MEXT) of Japan and SOMAR Corp.
for funding.
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NR 66
TC 1
Z9 1
U1 0
U2 5
PU GAKUSHIN PUBL CO
PI TOKYO
PA YUSHOKAIN7F, 1-38-12 NIHONBASHIKAKIGARACHO, CHUO-KU, TOKYO, 103-0014,
JAPAN
SN 0915-7352
J9 TRENDS GLYCOSCI GLYC
JI Trends Glycosci. Glycotechnol.
PD SEP
PY 2017
VL 29
IS 169
BP E71
EP E79
DI 10.4052/tigg.1611.1E
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA FX7OV
UT WOS:000426280900001
OA Bronze
DA 2025-01-07
ER
PT J
AU Huang, JK
Lee, HC
AF Jih-Kai Huang
Hsiang-Chun Lee
TI Emerging Evidence of Pathological Roles of Very-Low-Density Lipoprotein
(VLDL)
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE very-low-density lipoprotein (VLDL); VLDL receptor (VLDLR); metabolic
syndrome (MetS); insulin resistance; metabolic associated fatty liver
disease (MAFLD); endocrinological disorders; cardiovascular disorders;
cognitive dysfunction; cancer; atrial myopathy
ID FATTY LIVER-DISEASE; HEPATITIS-C VIRUS; TRIGLYCERIDE-RICH LIPOPROTEINS;
ATHEROSCLEROTIC CARDIOVASCULAR-DISEASE; APOLIPOPROTEIN-E RECEPTOR; LIPID
PROFILE; INSULIN-RESISTANCE; OXIDATIVE STRESS; APOC-III; SUBCLINICAL
HYPOTHYROIDISM
AB Embraced with apolipoproteins (Apo) B and Apo E, triglyceride-enriched very-low-density lipoprotein (VLDL) is secreted by the liver into circulation, mainly during post-meal hours. Here, we present a brief review of the physiological role of VLDL and a systemic review of the emerging evidence supporting its pathological roles. VLDL promotes atherosclerosis in metabolic syndrome (MetS). VLDL isolated from subjects with MetS exhibits cytotoxicity to atrial myocytes, induces atrial myopathy, and promotes vulnerability to atrial fibrillation. VLDL levels are affected by a number of endocrinological disorders and can be increased by therapeutic supplementation with cortisol, growth hormone, progesterone, and estrogen. VLDL promotes aldosterone secretion, which contributes to hypertension. VLDL induces neuroinflammation, leading to cognitive dysfunction. VLDL levels are also correlated with chronic kidney disease, autoimmune disorders, and some dermatological diseases. The extra-hepatic secretion of VLDL derived from intestinal dysbiosis is suggested to be harmful. Emerging evidence suggests disturbed VLDL metabolism in sleep disorders and in cancer development and progression. In addition to VLDL, the VLDL receptor (VLDLR) may affect both VLDL metabolism and carcinogenesis. Overall, emerging evidence supports the pathological roles of VLDL in multi-organ diseases. To better understand the fundamental mechanisms of how VLDL promotes disease development, elucidation of the quality control of VLDL and of the regulation and signaling of VLDLR should be indispensable. With this, successful VLDL-targeted therapies can be discovered in the future.
C1 [Jih-Kai Huang] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Gen Med, Kaohsiung 80708, Taiwan.
[Hsiang-Chun Lee] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Internal Med, Div Cardiol, Kaohsiung 80708, Taiwan.
[Hsiang-Chun Lee] Kaohsiung Med Univ, Coll Med, Sch Med, Dept Internal Med, Kaohsiung 80708, Taiwan.
[Hsiang-Chun Lee] Kaohsiung Med Univ, Coll Med, Lipid Sci & Aging Res Ctr, Kaohsiung 80708, Taiwan.
[Hsiang-Chun Lee] Natl Sun Yat Sen Univ, Inst Med Sci & Technol, Kaohsiung 80708, Taiwan.
[Hsiang-Chun Lee] Natl Pingtung Univ Sci & Technol, Grad Inst Anim Vaccine Technol, Pingtung 91201, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
Kaohsiung Medical University; Kaohsiung Medical University Hospital;
Kaohsiung Medical University; Kaohsiung Medical University; National Sun
Yat Sen University; National Pingtung University Science & Technology
RP Lee, HC (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Internal Med, Div Cardiol, Kaohsiung 80708, Taiwan.; Lee, HC (corresponding author), Kaohsiung Med Univ, Coll Med, Sch Med, Dept Internal Med, Kaohsiung 80708, Taiwan.; Lee, HC (corresponding author), Kaohsiung Med Univ, Coll Med, Lipid Sci & Aging Res Ctr, Kaohsiung 80708, Taiwan.; Lee, HC (corresponding author), Natl Sun Yat Sen Univ, Inst Med Sci & Technol, Kaohsiung 80708, Taiwan.; Lee, HC (corresponding author), Natl Pingtung Univ Sci & Technol, Grad Inst Anim Vaccine Technol, Pingtung 91201, Taiwan.
EM eric86425@gmail.com; hclee@kmu.edu.tw
OI Huang, Jih-Kai/0000-0002-8837-0377; Lee, Hsiang-Chun/0000-0002-5877-9059
FU Kaohsiung Medical University Hospital [KMUH97-7G31, KMUH103-3T03,
KMUH104-4T04, KMUH107-7R11, KMUH108-8R10]; Kaohsiung Medical University
[KMU-TP104D04]; Taiwan Ministry of Science and Technology [MOST
10314-B-037080-MY3]; NSYSU-KMU Joint Research Project [NSYSUKMU
104-P027]; KMU Global Networking Talent Plan [110KMUOR01]
FX This research was funded by Kaohsiung Medical University Hospital
(KMUH97-7G31, KMUH103-3T03, KMUH104-4T04, KMUH107-7R11, and
KMUH108-8R10), Kaohsiung Medical University (KMU-TP104D04), Taiwan
Ministry of Science and Technology grants (MOST 10314-B-037080-MY3), the
NSYSU-KMU Joint Research Project (#NSYSUKMU 104-P027), and the KMU
Global Networking Talent Plan (110KMUOR01).
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NR 240
TC 34
Z9 40
U1 0
U2 27
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD APR
PY 2022
VL 23
IS 8
AR 4300
DI 10.3390/ijms23084300
PG 21
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 0R2LL
UT WOS:000785433300001
PM 35457118
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Qian, X
Chen, HK
Wu, XF
Hu, L
Huang, Q
Jin, Y
AF Qian, Xin
Chen, Hankui
Wu, Xiaofeng
Hu, Ling
Huang, Qi
Jin, Yang
TI Interleukin-17 acts as double-edged sword in anti-tumor immunity and
tumorigenesis
SO CYTOKINE
LA English
DT Review
DE Interleukin (IL)-17; Tumorigenesis; Tumor immunity; Angiogenesis;
Cytokine
ID CELL LUNG-CANCER; CD8(+) T-CELLS; TUMOR MICROENVIRONMENT; TH17 CELLS;
COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA; IN-VIVO; PROMOTES
INVASIVENESS; CLINICAL-RELEVANCE; PROGNOSTIC MARKER
AB Interleukin-17 (IL-17), a proinflammatory cytokine, mainly produced by Th17 cells, participates in both innate and adaptive immune responses and is involved in various diseases, including infectious diseases, autoimmune disorders and cancer. Emerging evidence indicates that IL-17 not only has an oncogenic role in tumorigenesis by regulating tumor angiogenesis and enhancing tumor immune evasion but also exerts anti-tumor functions by enhancing natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) activation and through the recruitment of neutrophils, NK cells and CD4(+) and CD8(+) T cells to tumor tissue. In this review, we provide an overview on the basic biology of IL-17 and recent findings regarding its enigmatic double-edged features in tumorigenesis, with special attention to the roles of IL-17 produced by tumor cells interacting with other factors in the tumor microenvironment. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Qian, Xin; Wu, Xiaofeng] Hubei Univ Med, Taihe Hosp, Dept Resp Med, 32 South Renmin Rd, Shiyan 44200, Hubei Province, Peoples R China.
[Chen, Hankui] Rush Univ, Ctr Canc, Chicago, IL 60612 USA.
[Hu, Ling] Wuhan Univ Sci & Technol, Tianyou Hosp, Wuhan 430064, Peoples R China.
[Huang, Qi; Jin, Yang] Huazhong Univ Sci & Technol, Union Hosp, Dept Resp Med, Tongji Med Coll, 1277 Jiefang Ave, Wuhan 430022, Peoples R China.
C3 Hubei University of Medicine; Rush University; Wuhan University of
Science & Technology; Huazhong University of Science & Technology
RP Jin, Y (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Dept Resp Med, Tongji Med Coll, 1277 Jiefang Ave, Wuhan 430022, Peoples R China.
EM xingiantj@163.com; HANKUI_CHEN@rush.edu; Wu-8921324@qq.com;
232836909@qq.com; huangqi66@126.com; whuhjy@126.com
RI Qian, Xin/HME-0793-2023; Jin, Yang/AAX-2586-2021
OI Qian, Xin/0000-0002-4870-3819
FU National Natural Science Foundation of China [81072400]
FX This work was supported by the National Natural Science Foundation of
China (81072400).
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Zhuang Y, 2012, GASTROENTEROLOGY, V143, P951, DOI 10.1053/j.gastro.2012.06.010
NR 113
TC 98
Z9 118
U1 1
U2 36
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD JAN
PY 2017
VL 89
SI SI
BP 34
EP 44
DI 10.1016/j.cyto.2015.09.011
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA EH4YO
UT WOS:000391780000006
PM 26883678
DA 2025-01-07
ER
PT J
AU Udompap, P
Kim, D
Kim, WR
AF Udompap, Prowpanga
Kim, Donghee
Kim, W. Ray
TI Current and Future Burden of Chronic Nonmalignant Liver Disease
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE Burden; Chronic Liver Disease; Health Economics
ID NONALCOHOLIC FATTY LIVER; PRIMARY BILIARY-CIRRHOSIS; HEPATITIS-C VIRUS;
PRIMARY SCLEROSING CHOLANGITIS; LONG-TERM OUTCOMES; UNITED-STATES;
NATURAL-HISTORY; ALPHA-1-ANTITRYPSIN DEFICIENCY; AUTOIMMUNE HEPATITIS;
FOLLOW-UP
AB Disease burden is an important indicator of the state of health of a population. It can be measured as the frequency (eg, incidence and prevalence) of a condition or its effects including fatal and non-fatal health loss from disease (eg, disability-adjusted life years) as well as the financial costs (eg, direct healthcare costs and indirect healthcare expenditures related to lost income because of premature death). Accurate disease burden information is essential for policy-making such as prioritization of health interventions and allocation of resources. Chronic liver disease (CLD) causes substantial health and economic burden in the United States, where nearly 2 million deaths annually are attributable to CLD. In the recent past, overall mortality rate of CLD has been increasing. Viral hepatitis and alcoholic liver disease are thought to be the most common etiologies of chronic liver diseases. More recently, the prevalence of nonalcoholic fatty liver disease is rapidly increasing, and nonalcoholic steatohepatitis has become a leading indication for liver transplantation. In this article, we assemble available data on the burden of CLD in the United States, focusing on nonmalignant complications, whereas the impact on mortality and healthcare expenses of hepatocellular carcinoma, an important consequence of CLD, is discussed elsewhere.
C1 [Udompap, Prowpanga; Kim, Donghee; Kim, W. Ray] Stanford Univ, Sch Med, Div Gastroenterol & Hepatol, Stanford, CA 94305 USA.
C3 Stanford University
RP Kim, WR (corresponding author), Stanford Univ, Sch Med, Div Gastroenterol & Hepatol, 300 Pasteur Dr,Alway Bldg,Room M211, Stanford, CA 94305 USA.
EM wrkim@stanford.edu
RI Udompap, Prowpanga/JCE-8797-2023; Kim, Woo/AAG-1822-2019; Kim,
Donghee/C-4288-2013
OI Kim, W. Ray/0000-0002-3030-860X; Kim, Donghee/0000-0003-1919-6800
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NR 97
TC 103
Z9 110
U1 2
U2 23
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD NOV
PY 2015
VL 13
IS 12
BP 2031
EP 2041
DI 10.1016/j.cgh.2015.08.015
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CT9WB
UT WOS:000363166200002
PM 26291665
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Sanchez, S
Fang, DA
Xiao, SM
Rezavi, LA
Howard, BM
Caturegli, P
Cihakova, D
AF Sanchez, Sandra
Fang, Diana
Xiao, Shaoming
Rezavi, Lu Ann
Howard, Brittney M.
Caturegli, Patrizio
Cihakova, Daniela
TI Liver kidney microsome antibodies. Analysis of a laboratory series
SO PRACTICAL LABORATORY MEDICINE
LA English
DT Article
DE Immunology; Autoimmune hepatitis; LKM1 antibody; Liver kidney microsomal
antibody; Immunofluorescence
ID AUTOANTIBODIES; PREVALENCE; HEPATITIS; CHILDREN; DISEASE; TYPE-1
AB Objectives: The objectives were to characterize the liver kidney microsome (LKM) antibody profile of a 14-month-old girl with autoimmune hepatitis and analyze the laboratory prevalence of LKM positivity. Design and methods: This is retrospective analysis of the LKM antibody immunofluorescence tests performed by the Immunology Laboratory of Johns Hopkins Hospital from September 8, 2020 to July 31, 2022. LKM positive sera were also tested by an ELISA for LKM1 antibodies, which recognize the cytochrome P450 2D6 antigen. In silico analysis of 2D6 mRNA expression across anatomical sites was performed using Bgee and GTEx Portal databases. Results: Of the total of 1598 patients (893 F, 705 M, ages 0.8-94 years) tested for LKM antibodies, 3 were positive, yielding a 0.2% period prevalence. The clinical diagnosis was autoimmune hepatitis in the index case, acute viral hepatitis in a 3-yo male, and hepatocellular carcinoma in a 54-yo male. LKM antibodies yielded the classical homogenous staining pattern in the liver cytosol and proximal kidney tubular cells. The first two patients were also positive for LKM1 antibodies, whereas the third was negative. 2D6 mRNA was expressed highly in the liver, moderately in the duodenum, and minimally in other tissues. Conclusions: Overall, LKM antibodies are rare. They contribute to establish a diagnosis of auto -immune hepatitis, although they are also found in other liver diseases. The cytochrome P450 2D6 is one of the antigens recognized by LKM antibodies, but other antigens are likely targeted considering that 2D6 is minimally expressed in the kidney and yet LKM antibodies bind to kidney tubuli.
C1 [Sanchez, Sandra; Rezavi, Lu Ann; Howard, Brittney M.; Caturegli, Patrizio; Cihakova, Daniela] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD USA.
[Xiao, Shaoming] Johns Hopkins Univ, Sch Publ Hlth, Dept Biostat, Baltimore, MD USA.
[Caturegli, Patrizio] Johns Hopkins Pathol, Dept Immunol, Ross Bldg, Room 656 720, Rutland Ave, Baltimore, MD 21205 USA.
C3 Johns Hopkins University; Johns Hopkins University; Johns Hopkins
University
RP Caturegli, P (corresponding author), Johns Hopkins Pathol, Dept Immunol, Ross Bldg, Room 656 720, Rutland Ave, Baltimore, MD 21205 USA.
EM pcat@jhmi.edu
RI Cihakova, Daniela/A-9821-2017; Xiao, Shaoming/LRB-5163-2024
OI Caturegli, Patrizio/0000-0001-6768-6308; Sanchez,
Sandra/0000-0003-1866-1619
FU Clinical Immunology Laboratory at Johns Hopkins Hospital
FX Clinical Immunology Laboratory at Johns Hopkins Hospital
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NR 17
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2352-5517
J9 PRACT LAB MED
JI Pract. Lab. Med.
PD JAN
PY 2023
VL 33
AR e00307
DI 10.1016/j.plabm.2023.e00307
EA NOV 2023
PG 7
WC Medical Laboratory Technology
WE Emerging Sources Citation Index (ESCI)
SC Medical Laboratory Technology
GA E5AA5
UT WOS:000975653400001
PM 36660178
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Younossi, ZM
Bernstein, D
Shiffman, ML
Kwo, P
Kim, WR
Kowdley, KV
Jacobson, IM
AF Younossi, Zobair M.
Bernstein, David
Shiffman, Mitchell L.
Kwo, Paul
Kim, W. Ray
Kowdley, Kris V.
Jacobson, Ira M.
TI Diagnosis and Management of Primary Biliary Cholangitis
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
ID PYRUVATE-DEHYDROGENASE COMPLEX; SOLUBLE VITAMIN LEVELS; URSODEOXYCHOLIC
ACID; RISK-FACTORS; BIOCHEMICAL RESPONSE; ANTIMITOCHONDRIAL ANTIBODIES;
HEPATOCELLULAR-CARCINOMA; LIVER-TRANSPLANTATION; CLINICAL-FEATURES;
CONTROLLED-TRIAL
AB Primary biliary cholangitis (PBC) is a chronic, cholestatic, autoimmune disease with a variable progressive course. PBC can cause debilitating symptoms including fatigue and pruritus and, if left untreated, is associated with a high risk of cirrhosis and related complications, liver failure, and death. Recent changes to the PBC landscape include a name change, updated guidelines for diagnosis and treatment as well as new treatment options that have recently become available. Practicing clinicians face many unanswered questions when managing PBC. To assist these healthcare providers in managing patients with PBC, the American College of Gastroenterology (ACG) Institute for Clinical Research & Education, in collaboration with the Chronic Liver Disease Foundation (CLDF), organized a panel of experts to evaluate and summarize the most current and relevant peer-reviewed literature regarding PBC. This, combined with the extensive experience and clinical expertise of this expert panel, led to the formation of this clinical guidance on the diagnosis and management of PBC.
C1 [Younossi, Zobair M.] Inova Fairfax Hosp, Dept Med, 3300 Gallows Rd, Falls Church, VA 22042 USA.
[Bernstein, David] Zucker Sch Med Hofstra Northwell, Dept Hepatol, Hempstead, NY 11549 USA.
[Bernstein, David] Zucker Sch Med Hofstra Northwell, Sandra Atlas Bass Ctr Liver Dis, Hempstead, NY 11549 USA.
[Shiffman, Mitchell L.] Bon Secours Liver Inst Virginia, Bon Secours Med Grp, Richmond, VA 23226 USA.
[Kwo, Paul] Stanford Univ, Med Ctr, Palo Alto, CA 94304 USA.
[Kim, W. Ray] Stanford Univ, Sch Med, Div Gastroenterol & Hepatol, Palo Alto, CA 94304 USA.
[Kowdley, Kris V.] Swedish Med Ctr, Liver Care Network & Organ Care Res, Seattle, WA 98107 USA.
[Jacobson, Ira M.] NYU Langone Hlth, New York, NY 10016 USA.
C3 Inova Fairfax Hospital; Northwell Health; Northwell Health; Stanford
University; Stanford University; Swedish Medical Center; NYU Langone
Medical Center
RP Younossi, ZM (corresponding author), Inova Fairfax Hosp, Dept Med, 3300 Gallows Rd, Falls Church, VA 22042 USA.
EM Zobair.Younossi@inova.org
RI Younossi, Zobair M./JRY-9916-2023; Kowdley, Kris/AAF-5202-2019; Kim,
Woo/AAG-1822-2019
OI Kim, W. Ray/0000-0002-3030-860X
FU Intercept Pharmaceuticals, Inc.
FX This guidance was supported by an unrestricted educational grant from
Intercept Pharmaceuticals, Inc. The selection of the authors and
creation of this guidance was done independently; Intercept
Pharmaceuticals did not play a role.
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NR 142
TC 109
Z9 112
U1 0
U2 17
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD JAN
PY 2019
VL 114
IS 1
BP 48
EP 63
DI 10.1038/s41395-018-0390-3
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HR4ZO
UT WOS:000463156500011
PM 30429590
DA 2025-01-07
ER
PT J
AU Zachou, K
Muratori, P
Koukoulis, GK
Granito, A
Gatselis, N
Fabbri, A
Dalekos, GN
Muratori, L
AF Zachou, K.
Muratori, P.
Koukoulis, G. K.
Granito, A.
Gatselis, N.
Fabbri, A.
Dalekos, G. N.
Muratori, L.
TI Review article: autoimmune hepatitis - current management and challenges
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
ID REGULATORY T-CELLS; SOLUBLE LIVER ANTIGEN; MICROSOMAL ANTIBODY TYPE-1;
PRIMARY BILIARY-CIRRHOSIS; CYCLIC CITRULLINATED PEPTIDE; ALPHA-ACTININ
ANTIBODIES; EPSTEIN-BARR-VIRUS; TERM-FOLLOW-UP; MYCOPHENOLATE-MOFETIL;
HEPATOCELLULAR-CARCINOMA
AB BackgroundAutoimmune hepatitis (AIH) is a disease of unknown aetiology characterised by interface hepatitis, hypergammaglobulinaemia, circulating autoantibodies and a favourable response to immunosuppression.
AimTo review recent advancements in understanding aetiopathogenesis, clinical, serological and histological features, diagnostic criteria and treatment strategies of AIH.
MethodsPublished studies on AIH extracted mainly from PubMed during the last 15years.
ResultsAutoimmune hepatitis has a global distribution affecting any age, both sexes and all ethnic groups. Clinical manifestations are variable ranging from no symptoms to severe acute hepatitis and only seldom to fulminant hepatic failure. Autoimmune attack is perpetuated, possibly via molecular mimicry mechanisms, and favoured by the impaired control of regulatory T-cells. A typical laboratory finding is hypergammaglobulinaemia with selective elevation of IgG, although in 15-25% of patients - particularly children, elderly and acute cases - IgG levels are normal. Liver histology and autoantibodies, although not pathognomonic, still remain the hallmark for diagnosis. Immunosuppressive treatment is mandatory and life-saving; however, to meet strict response criteria, the conventional therapy with prednisolone with or without azathioprine is far from ideal.
ConclusionsAutoimmune hepatitis remains a major diagnostic and therapeutic challenge. The clinician, the hepato-pathologist and the laboratory personnel need to become more familiar with different expressions of the disease, interpretation of liver histology and autoimmune serology. According to the strict definition of treatment response issued by the 2010 AASLD guidelines, many patients are nonresponders to conventional treatment. Newer immunosuppressive agents targeting pathogenetic mechanisms can improve patient management, which needs to be tailored on a case-by-case basis.
C1 [Zachou, K.; Gatselis, N.; Dalekos, G. N.] Univ Thessaly, Sch Med, Dept Med, Biopolis 41110, Larissa, Greece.
[Zachou, K.; Gatselis, N.; Dalekos, G. N.] Univ Thessaly, Sch Med, Res Lab Internal Med, Biopolis 41110, Larissa, Greece.
[Muratori, P.; Granito, A.; Fabbri, A.; Muratori, L.] Alma Mater Studiorum Univ Bologna, Dept Med & Surg Sci, Bologna, Italy.
[Koukoulis, G. K.] Thessally Univ, Sch Med, Dept Pathol, Larisa, Greece.
C3 University of Thessaly; University of Thessaly; University of Bologna
RP Dalekos, GN (corresponding author), Univ Thessaly, Sch Med, Dept Med, Biopolis 41110, Larissa, Greece.
EM dalekos@med.uth.gr
RI Granito, Alessandro/G-9563-2013
OI Granito, Alessandro/0000-0002-0637-739X
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NR 291
TC 121
Z9 131
U1 1
U2 31
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD OCT
PY 2013
VL 38
IS 8
BP 887
EP 913
DI 10.1111/apt.12470
PG 27
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 227RG
UT WOS:000325130700004
PM 24010812
OA Bronze
DA 2025-01-07
ER
PT J
AU Fehér, E
Pongor, E
Altdorfer, K
Kóbori, L
Lengyel, G
AF Feher, Erzsebet
Pongor, Eva
Altdorfer, Karoly
Kobori, Laszlo
Lengyel, Gabriella
TI Neuroimmunomodulation in human autoimmune liver disease
SO CELL AND TISSUE RESEARCH
LA English
DT Article
DE Hepatitis; NPY; SP; TNF-alpha; NF-kappa B
ID NECROSIS-FACTOR-ALPHA; NEUROPEPTIDE-Y NPY; SUBSTANCE-P; NERVE-FIBERS;
HEPATOCELLULAR-CARCINOMA; MESSENGER-RNA; PROTECT MICE; IMMUNE CELLS;
BLOOD; EXPRESSION
AB Bidirectional interaction between immune and nervous systems is considered an important biological process in health and disease. However, little is known about the mechanisms involved in their interaction in the human liver. This study examines the distribution of intrahepatic NPY, SP immunoreactive (IR) nerve fibers and their antomical relationship with immunocells containing tumor necrosis factor-alpha (TNF-alpha) and nuclear factor kappa B (NF-kappa B) in patients with autoimmune hepatitis. Liver specimens were obtained from control liver and autoimmune hepatitis patients. The immunoreactivity was determined by immunohisto- and immunocytochemistry and confocal laser microscopy. In hepatitis, the number of NPY-IR and SP-IR nerve fibers increased significantly. These IR nerve fibers were in very close contact with the lymphocytes. In healthy controls, no NPY-IR, SP-IR or NF-kappa B IR lymphocytes and only a few TNF-alpha positive cells, were observed. In hepatitis, some of the lymphocytes showed immunoreactivity for SP and NPY in the portal area. Fluorescent double-labeled immunostaining revealed that in these cells NPY did not colocalize with TNF-alpha or NF-kappa B. However, some of the SP fluorescence-positive immune cells exhibited immunostaining for p65 of NF-kappa B, where their labeling was detected in the nuclei. Under the electronmicroscope, these cells could be identified (lymphocytes, plasmacells and mast cells). The gap between the IR nerve fibers and immunocells was 1 mu m or even less. Overexpression of SP in lymphocytes may amplify local inflammation, while NPY may contribute to liver homeostasis in hepatitis. Neural immunomodulation (SP antagonists and NPY) might be a novel therapeutic concept in the management of liver inflammation.
C1 [Feher, Erzsebet; Pongor, Eva; Altdorfer, Karoly] Semmelweis Univ, Dept Anat Histol & Embryol, H-1085 Budapest, Hungary.
[Kobori, Laszlo] Semmelweis Univ, Dept Transplantat & Surg, H-1085 Budapest, Hungary.
[Lengyel, Gabriella] Semmelweis Univ, Dept Internal Med 2, H-1085 Budapest, Hungary.
[Feher, Erzsebet] Semmelweis Univ, Dept Anat Histol & Embryol, H-1450 Budapest, Hungary.
C3 Semmelweis University; Semmelweis University; Semmelweis University;
Semmelweis University
RP Fehér, E (corresponding author), Semmelweis Univ, Dept Anat Histol & Embryol, Tuzolto U 58,POB 95, H-1450 Budapest, Hungary.
EM feher@ana.sote.hu
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NR 62
TC 8
Z9 8
U1 0
U2 12
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0302-766X
EI 1432-0878
J9 CELL TISSUE RES
JI Cell Tissue Res.
PD NOV
PY 2013
VL 354
IS 2
BP 543
EP 550
DI 10.1007/s00441-013-1683-x
PG 8
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 240RZ
UT WOS:000326116000018
PM 23881405
DA 2025-01-07
ER
PT J
AU Nicoletti, A
Ponziani, FR
Nardella, E
Ianiro, G
Gasbarrini, A
Dal Verme, LZ
AF Nicoletti, A.
Ponziani, F. R.
Nardella, E.
Ianiro, G.
Gasbarrini, A.
Dal Verme, L. Zileri
TI Biliary tract microbiota: a new kid on the block of liver diseases?
SO EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
LA English
DT Article
DE Biliary microbiota; Gallstones; Cholelithiasis; Primary sclerosing
cholangitis; Primary biliary cholangitis; Biliary tract cancer;
Cholangiocarcinoma; Gallbladder carcinoma; Personalized medicine
ID PRIMARY SCLEROSING CHOLANGITIS; BILE-SALT HYDROLASE; MUCOSA-ASSOCIATED
MICROBIOTA; BROWN PIGMENT GALLSTONES; HEAT-SHOCK-PROTEIN; RIBOSOMAL-RNA
GENE; URSODEOXYCHOLIC ACID; GALLBLADDER CANCER; INTESTINAL MICROBIOTA;
GUT MICROBIOTA
AB The microbiome plays a crucial role in maintaining the homeostasis of the organism. Recent evidence has provided novel insights for understanding the interaction between the microbiota and the host. However, the vast majority of such studies have analyzed the interactions taking place in the intestinal tract.
The biliary tree has traditionally been considered sterile under normal conditions. However, the advent of metagenomic techniques has revealed an unexpectedly rich bacterial community in the biliary tract.
Associations between specific microbiological patterns and inflammatory biliary diseases and cancer have been recently described. Hence, biliary dysbiosis may be a primary trigger in the pathogenesis of biliary diseases. In particular. recent studies have suggested that microorganisms could play a significant role in the development of gallstones, pathogenesis of autoimmune cholangiopathies and biliary carcinogenesis.
Moreover, the intimate connection between the biliary tract, liver and pancreas, could reveal hidden influences on the development of diseases of these organs.
Further studies are needed to deepen the comprehension of the influence of the biliary microbiota in human pathology. This knowledge could lead to the formulation of strategies for modulating the biliary microbiota in order to treat and prevent these pathological conditions.
C1 [Nicoletti, A.; Nardella, E.; Gasbarrini, A.] Univ Cattolica Sacro Cuore, Fdn Policlin Univ Agostino Gemelli IRCCS, Internal Med Gastroenterol & Hepatol, Rome, Italy.
[Ponziani, F. R.; Ianiro, G.; Dal Verme, L. Zileri] Fdn Policlin Univ Agostino Gemelli IRCCS, Internal Med Gastroenterol & Hepatol, Rome, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli
RP Nicoletti, A (corresponding author), Univ Cattolica Sacro Cuore, Fdn Policlin Univ Agostino Gemelli IRCCS, Internal Med Gastroenterol & Hepatol, Rome, Italy.
EM nicoletti.alb@gmail.com
RI Gasbarrini, Antonio/AAB-8487-2019; Nicoletti, Alberto/KXQ-6237-2024;
Ponziani, Francesca Romana/E-4136-2016; Ianiro, Gianluca/K-5578-2016
OI Nicoletti, Alberto/0000-0003-0658-4310; Ianiro,
Gianluca/0000-0002-8318-0515; Nardella, Elisabetta/0000-0001-7119-0364;
Gasbarrini, Antonio/0000-0003-4863-6924; Gasbarrini,
Antonio/0000-0002-6230-1779
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NR 250
TC 14
Z9 15
U1 1
U2 6
PU VERDUCI PUBLISHER
PI ROME
PA VIA GREGORIO VII, ROME, 186-00165, ITALY
SN 1128-3602
J9 EUR REV MED PHARMACO
JI Eur. Rev. Med. Pharmacol. Sci.
PY 2020
VL 24
IS 5
BP 2750
EP 2775
DI 10.26355/eurrev_202003_20548
PG 26
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA KY2JG
UT WOS:000522397800061
PM 32196626
DA 2025-01-07
ER
PT J
AU Passeron, T
King, B
Seneschal, J
Steinhoff, M
Jabbari, A
Ohyama, M
Tobin, DJ
Randhawa, S
Winkler, A
Telliez, JB
Martin, D
Lejeune, A
AF Passeron, Thierry
King, Brett
Seneschal, Julien
Steinhoff, Martin
Jabbari, Ali
Ohyama, Manabu
Tobin, Desmond J.
Randhawa, Simran
Winkler, Aaron
Telliez, Jean-Baptiste
Martin, David
Lejeune, Alexandre
TI Inhibition of T-cell activity in alopecia areata: recent developments
and new directions
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE Alopecia areata; autoimmune disease; T cells; T-cell receptor; JAK
inhibitor
ID INTERNATIONAL EXPERT OPINION; JANUS KINASE INHIBITORS; QUALITY-OF-LIFE;
LOW-DOSE IL-2; HAIR FOLLICLE; PD-1 PATHWAY; C3H/HEJ MICE; SERUM-LEVEL;
RECEPTOR; IMMUNE
AB Alopecia areata (AA) is an autoimmune disease that has a complex underlying immunopathogenesis characterized by nonscarring hair loss ranging from small bald patches to complete loss of scalp, face, and/or body hair. Although the etiopathogenesis of AA has not yet been fully characterized, immune privilege collapse at the hair follicle (HF) followed by T-cell receptor recognition of exposed HF autoantigens by autoreactive cytotoxic CD8+ T cells is now understood to play a central role. Few treatment options are available, with the Janus kinase (JAK) 1/2 inhibitor baricitinib (2022) and the selective JAK3/tyrosine kinase expressed in hepatocellular carcinoma (TEC) inhibitor ritlecitinib (2023) being the only US Food and Drug Administration-approved systemic medications thus far for severe AA. Several other treatments are used off-label with limited efficacy and/or suboptimal safety and tolerability. With an increased understanding of the T-cell-mediated autoimmune and inflammatory pathogenesis of AA, additional therapeutic pathways beyond JAK inhibition are currently under investigation for the development of AA therapies. This narrative review presents a detailed overview about the role of T cells and T-cell-signaling pathways in the pathogenesis of AA, with a focus on those pathways targeted by drugs in clinical development for the treatment of AA. A detailed summary of new drugs targeting these pathways with expert commentary on future directions for AA drug development and the importance of targeting multiple T-cell-signaling pathways is also provided in this review.
C1 [Passeron, Thierry] Univ Cote Azur, Ctr Hosp Univ Nice, Dept Dermatol, Nice, France.
[Passeron, Thierry] Univ Cote Azur, INSERM, U1065, C3M, Nice, France.
[King, Brett] Yale Univ, Sch Med, Dept Dermatol, New Haven, CT USA.
[Seneschal, Julien] Univ Bordeaux, St Andre Hosp, Natl Reference Ctr Rare Skin Dis, Dept Dermatol & Paediat Dermatol, Bordeaux, France.
[Seneschal, Julien] Bordeaux Univ, Ctr Natl Rech Sci CNRS, ImmunoConcept, UMR5164, Bordeaux, France.
[Steinhoff, Martin] Hamad Med Corp, Dept Dermatol & Venereol, Doha, Qatar.
[Steinhoff, Martin] Hamad Med Corp, Translat Res Inst, Acad Hlth Syst, Doha, Qatar.
[Steinhoff, Martin] Hamad Med Corp, Dermatol Inst, Acad Hlth Syst, Doha, Qatar.
[Steinhoff, Martin] Weill Cornell Med Qatar, Dept Dermatol & Venereol, Doha, Qatar.
[Steinhoff, Martin] Qatar Univ, Coll Med, Doha, Qatar.
[Steinhoff, Martin] Weill Cornell Med, Dept Dermatol, New York, NY USA.
[Steinhoff, Martin] Hamad Bin Khalifa Univ, Coll Hlth & Life Sci, Doha, Qatar.
[Jabbari, Ali] Univ Iowa, Dept Dermatol, Iowa City, IA USA.
[Jabbari, Ali] Iowa City VA Med Ctr, Iowa City, IA USA.
[Ohyama, Manabu] Kyorin Univ, Fac Med, Dept Dermatol, Tokyo, Japan.
[Tobin, Desmond J.] Univ Coll Dublin, UCD Charles Inst Dermatol, Sch Med, Dublin, Ireland.
[Randhawa, Simran] Pfizer Inc, New York, NY USA.
[Winkler, Aaron; Telliez, Jean-Baptiste; Martin, David] Pfizer Inc, Cambridge, MA USA.
[Lejeune, Alexandre] Pfizer Inc, Paris, France.
C3 CHU Nice; Universite Cote d'Azur; Universite Cote d'Azur; Institut
National de la Sante et de la Recherche Medicale (Inserm); Yale
University; CHU Bordeaux; Universite de Bordeaux; Centre National de la
Recherche Scientifique (CNRS); CNRS - National Institute for Biology
(INSB); Universite de Bordeaux; Hamad Medical Corporation; Hamad Medical
Corporation; Hamad Medical Corporation; Qatar Foundation (QF); Weill
Cornell Medical College Qatar; Qatar University; Cornell University;
Weill Cornell Medicine; Qatar Foundation (QF); Hamad Bin Khalifa
University-Qatar; University of Iowa; US Department of Veterans Affairs;
Veterans Health Administration (VHA); Iowa City VA Health Care System;
Kyorin University; University College Dublin; Pfizer; Pfizer; Pfizer
RP Lejeune, A (corresponding author), Pfizer Inc, Paris, France.
EM alexandre.lejeune@pfizer.com
RI Ohyama, Manabu/J-5524-2014
OI Jabbari, Ali/0000-0002-8559-7314
FU Pfizer10.13039/100004319; Pfizer, Inc.
FX Medical writing support was provided by Rich Karpowicz, PhD, CMPP, of
Health Interactions, Inc, Hamilton, NJ, USA, and was funded by Pfizer,
Inc. This manuscript was developed in accordance with Good Publication
Practice guidelines. Authors had full control of the content and made
the final decision on all aspects of this publication.
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NR 215
TC 14
Z9 14
U1 1
U2 7
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD NOV 6
PY 2023
VL 14
AR 1243556
DI 10.3389/fimmu.2023.1243556
PG 16
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA Y6MH0
UT WOS:001106376000001
PM 38022501
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wang, JY
Zhang, W
Roehrl, MW
Roehrl, VB
Roehrl, MH
AF Wang, Julia Y.
Zhang, Wei
Roehrl, Michael W.
Roehrl, Victor B.
Roehrl, Michael H.
TI An autoantigen profile of human A549 lung cells reveals viral and host
etiologic molecular attributes of autoimmunity in COVID-19
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE COVID-19; Autoimmunity; Autoantigens; Lung; Atlas; Resource
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; HEPATOCELLULAR-CARCINOMA; PROTEOMIC
IDENTIFICATION; RHEUMATOID-ARTHRITIS; SERUM AUTOANTIBODIES;
MULTIPLE-SCLEROSIS; DERMATAN SULFATE; DISEASE-ACTIVITY; TARGET ANTIGENS;
HIGH PREVALENCE
AB We aim to establish a comprehensive COVID-19 autoantigen atlas in order to understand autoimmune diseases caused by SARS-CoV-2 infection. Based on the unique affinity between dermatan sulfate and autoantigens, we identified 348 proteins from human lung A549 cells, of which 198 are known targets of autoantibodies. Comparison with current COVID data identified 291 proteins that are altered at protein or transcript level in SARSCoV-2 infection, with 191 being known autoantigens. These known and putative autoantigens are significantly associated with viral replication and trafficking processes, including gene expression, ribonucleoprotein biogenesis, mRNA metabolism, translation, vesicle and vesicle-mediated transport, and apoptosis. They are also associated with cytoskeleton, platelet degranulation, IL-12 signaling, and smooth muscle contraction. Host proteins that interact with and that are perturbed by viral proteins are a major source of autoantigens. Orf3 induces the largest number of protein alterations, Orf9 affects the mitochondrial ribosome, and they and E, M, N, and Nsp proteins affect protein localization to membrane, immune responses, and apoptosis. Phosphorylation and ubiquitination alterations by viral infection define major molecular changes in autoantigen origination. This study provides a large list of autoantigens as well as new targets for future investigation, e.g., UBA1, UCHL1, USP7, CDK11A, PRKDC, PLD3, PSAT1, RAB1A, SLC2A1, platelet activating factor acetylhydrolase, and mitochondrial ribosomal proteins. This study illustrates how viral infection can modify host cellular proteins extensively, yield diverse autoantigens, and trigger a myriad of autoimmune sequelae. Our work provides a rich resource for studies into "long COVID" and related autoimmune sequelae.
C1 [Wang, Julia Y.; Roehrl, Michael W.; Roehrl, Victor B.] Curandis, Scarsdale, NY 10583 USA.
[Zhang, Wei] Guizhou Med Univ, Affiliated Hosp, Dept Gastroenterol, Guiyang, Guizhou, Peoples R China.
[Roehrl, Michael H.] Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.
[Roehrl, Michael H.] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, 1275 York Ave, New York, NY 10021 USA.
C3 Guizhou Medical University; Memorial Sloan Kettering Cancer Center;
Memorial Sloan Kettering Cancer Center
RP Wang, JY (corresponding author), Curandis, Scarsdale, NY 10583 USA.; Roehrl, MH (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.; Roehrl, MH (corresponding author), Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, 1275 York Ave, New York, NY 10021 USA.
EM julia@curandis.com; roehrlm@mskcc.org
RI Zhang, Wei/ABD-4849-2021; Roehrl, Michael/AAU-8506-2020
OI Roehrl, Michael/0000-0003-4892-1098
FU US NIH; Cycle for Survival Innovation Grant; NIH/NCI [R21 CA251992];
MSKCC Cancer Center Support Grant [P30 CA008748]; Curandis
FX This work was partially supported by Curandis, the US NIH, and a Cycle
for Survival Innovation Grant (to MHR) . MHR acknowledges the NIH/NCI
R21 CA251992 and MSKCC Cancer Center Support Grant P30 CA008748. The
funding bodies were not involved in the design of the study and the
collection, analysis, and interpretation of data.
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NR 224
TC 26
Z9 26
U1 0
U2 5
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD JUN
PY 2021
VL 120
AR 102644
DI 10.1016/j.jaut.2021.102644
EA MAY 2021
PG 19
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA SF4TO
UT WOS:000652750400005
PM 33971585
OA Green Published, hybrid, Green Submitted
DA 2025-01-07
ER
PT J
AU Morao, B
Ramos, LR
Oliveira, MH
Glória, L
AF Morao, Barbara
Ramos, Lidia Roque
Oliveira, Maria Helena
Gloria, Luisa
TI Malignancy and mass-forming phenotypes of IgG4-related disease: a
challenging diagnosis
SO BMJ CASE REPORTS
LA English
DT Article
DE Pancreas and biliary tract; Pancreatic cancer; Rheumatology
ID AUTOIMMUNE PANCREATITIS; SERUM IGG4; CHOLANGITIS; STRATEGY
AB Mass-forming phenotypes of IgG4-related disease (IgG4-RD) mimic malignancy and histological confirmation can be challenging. A woman in her 70s with HIV infection presented with painless obstructive jaundice and weight loss. Magnetic resonance imaging was suggestive of unresectable cholangiocarcinoma. Tumour markers and serum IgG4 were normal. Percutaneous liver biopsy was consistent with IgG4-RD inflammatory pseudotumour, with complete response to glucocorticoid therapy. Two years later, a new episode of obstructive jaundice occurred, with CT showing a solid lesion in the head of the pancreas with double duct sign and encasement of the portal vein. Re-induction therapy was tried without response. Fine-needle biopsy was consistent with pancreatic cancer. Supportive care was offered and the patient died 8 months later, with no signs of disease progression on subsequent imaging. We discuss the challenges of IgG4-RD diagnosis and treatment and the differential diagnosis between mass-forming phenotypes and malignancy, highlighting the difficulties in managing such patients.
C1 [Morao, Barbara; Ramos, Lidia Roque; Gloria, Luisa] Hosp Beatriz Angelo, Gastroenterol, Lisbon, Portugal.
[Oliveira, Maria Helena] Hosp Cascais, Pathol, Lisbon, Portugal.
RP Glória, L (corresponding author), Hosp Beatriz Angelo, Gastroenterol, Lisbon, Portugal.
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[Лёр Й-М. Lohr J.-M.], 2021, [Российский журнал гастроэнтерологии, гепатологии, колопроктологии, Russian Journal of Gastroenterology, Hepatology, Coloproctology, Rossiiskii zhurnal gastroenterologii, gepatologii, koloproktologii], V31, P80
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NR 25
TC 0
Z9 0
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 1757-790X
J9 BMJ CASE REP
JI BMJ Case Rep.
PD JUL
PY 2024
VL 17
IS 7
AR e257372
DI 10.1136/bcr-2023-257372
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA XX9D6
UT WOS:001265086700004
PM 38960429
DA 2025-01-07
ER
PT J
AU Seki, E
Brenner, DA
AF Seki, Ekihiro
Brenner, David A.
TI Recent advancement of molecular mechanisms of liver fibrosis
SO JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
LA English
DT Article
DE Alcoholic liver disease; Angiogenesis; Autophagy; Hepatic stellate
cells; IL-17; IL-22; IL-33; Liver cirrhosis; Reversal; Senescence
ID HEPATIC STELLATE CELLS; ENDOTHELIAL GROWTH-FACTOR; B-VIRUS INFECTION;
HEPATOCELLULAR-CARCINOMA; MESENCHYMAL TRANSITION; INTESTINAL MICROBIOME;
MICE; INTERLEUKIN-22; INJURY; MYOFIBROBLASTS
AB Liver fibrosis occurs in response to any etiology of chronic liver injury including hepatitis B and C, alcohol consumption, fatty liver disease, cholestasis, and autoimmune hepatitis. Hepatic stellate cells (HSCs) are the primary source of activated myofibroblasts that produce extracellular matrix (ECM) in the liver. Various inflammatory and fibrogenic pathways contribute to the activation of HSCs. Recent studies also discovered that liver fibrosis is reversible and activated HSCs can revert to quiescent HSCs when causative agents are removed. Although the basic research for liver fibrosis has progressed remarkably, sensitive and specific biomarkers as non-invasive diagnostic tools, and effective anti-fibrotic agents have not been developed yet. This review highlights the recent advances in cellular and molecular mechanisms of liver fibrosis, especially focusing on origin of myofibroblasts, inflammatory signaling, autophagy, cellular senescence, HSC inactivation, angiogenesis, and reversibility of liver fibrosis.
C1 [Seki, Ekihiro] Cedars Sinai Med Ctr, Dept Med, Div Gastroenterol, Los Angeles, CA 90048 USA.
[Brenner, David A.] Univ Calif San Diego, Sch Med, La Jolla, CA 92093 USA.
C3 Cedars Sinai Medical Center; University of California System; University
of California San Diego
RP Seki, E (corresponding author), Cedars Sinai Med Ctr, Dept Med, Div Gastroenterol, 8700 Beverly Blvd,Suite D2099, Los Angeles, CA 90048 USA.
EM Ekihiro.Seki@cshs.org
RI Brenner, David/AFC-9624-2022; Seki, Ekihiro/K-2481-2016
OI Brenner, David/0000-0003-2573-525X
FU NIH [R01AA02017204, R01DK085252, P42ES010337]
FX This manuscript was supported by NIH grants R01AA02017204, R01DK085252
and P42ES010337.
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NR 62
TC 245
Z9 281
U1 14
U2 100
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 1868-6974
EI 1868-6982
J9 J HEPATO-BIL-PAN SCI
JI J. Hepato-Biliary-Pancreat. Sci.
PD JUL
PY 2015
VL 22
IS 7
BP 512
EP 518
DI 10.1002/jhbp.245
PG 7
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA CL2XP
UT WOS:000356811400003
PM 25869468
OA Green Accepted, Bronze, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Wu, SS
Yang, ZR
Zhou, JL
Zeng, N
He, ZY
Zhan, SY
Jia, JD
You, H
AF Wu, Shanshan
Yang, Zhirong
Zhou, Jialing
Zeng, Na
He, Zhiying
Zhan, Siyan
Jia, Jidong
You, Hong
TI Systematic review: diagnostic accuracy of non-invasive tests for staging
liver fibrosis in autoimmune hepatitis
SO HEPATOLOGY INTERNATIONAL
LA English
DT Review
DE Autoimmune hepatitis; Liver fibrosis; Non-invasive methods; Transient
elastography
ID MAGNETIC-RESONANCE ELASTOGRAPHY; TRANSIENT ELASTOGRAPHY;
HEPATOCELLULAR-CARCINOMA; CIRRHOSIS; PREDICT; DISEASE; INDEX; BIOPSY;
APRI
AB Background and aimsNon-invasive fibrosis assessment has been highly recommended in many liver diseases. However, comparative diagnostic accuracy of laboratory markers, ultrasound and magnetic resonance elastography (MRE) for fibrosis in autoimmune hepatitis (AIH) patients has not been established.MethodsMedline, Embase and Cochrane Library were searched. Primary outcome was significant fibrosis (SF), advanced fibrosis (AF) and cirrhosis, defined as Metavir stage F2, F3 and F=4 according to liver biopsy. Hierarchical summary receiver operating characteristic curve (ROC) model was used to evaluate diagnostic accuracy of non-invasive methods. Summary area under ROC (AUROC) and diagnostic odds ratio (DOR) with 95% confidence interval (CI) were calculated. The Grading of Recommendations Assessment, Development and Evaluation system was used to assess quality of evidence.ResultsOverall, 16 studies with 861 patients were included, comparing aspartate aminotransferase to platelet ratio index (APRI), fibrosis-4 index (FIB-4), aspartate aminotransferase/alanine aminotransferase ratio, transient elastography (TE), acoustic radiation force impulse, shear wave elastography and MRE versus liver biopsy. Among all non-invasive markers, TE had good performance for fibrosis staging. Summary AUROCs and DORs of TE were 0.90 (95% CI 0.87, 0.92) and 23.7, 0.91 (95% CI 0.89, 0.93) and 31.6, 0.89 (95% CI 0.86, 0.92) and 80.5 for staging SF, AF and cirrhosis, whereas APRI and FIB-4 showed poor performance for detecting AF (DOR, 4.6 and 4.7) and cirrhosis (DOR, 5.5 and 12.9).ConclusionsTE performs well to stage liver fibrosis in patients with AIH, compared with other laboratory non-invasive indexes. Nevertheless, diagnostic accuracy of APRI and FIB-4 is poor.
C1 [Wu, Shanshan; Zhou, Jialing; Zeng, Na; He, Zhiying; Jia, Jidong; You, Hong] Capital Med Univ, Beijing Friendship Hosp, Natl Clin Res Ctr Digest Dis, Beijing 100050, Peoples R China.
[Yang, Zhirong] Univ Cambridge, Sch Clin Med, Dept Publ Hlth & Primary Care, Primary Care Unit, Cambridge CB18RN, England.
[Yang, Zhirong] Harvard Med Sch, Harvard Pilgrim Hlth Care Inst, Dept Populat Med, Boston, MA 02215 USA.
[Zhan, Siyan] Peking Univ, Hlth Sci Ctr, Sch Publ Hlth, Dept Epidemiol & Biostat, Beijing 100191, Peoples R China.
[Jia, Jidong; You, Hong] Capital Med Univ, Beijing Friendship Hosp, Liver Res Ctr, 95 Yong An Rd, Beijing 100050, Peoples R China.
C3 Capital Medical University; University of Cambridge; Harvard University;
Harvard Medical School; Harvard Pilgrim Health Care; Peking University;
Capital Medical University
RP You, H (corresponding author), Capital Med Univ, Beijing Friendship Hosp, Natl Clin Res Ctr Digest Dis, Beijing 100050, Peoples R China.; You, H (corresponding author), Capital Med Univ, Beijing Friendship Hosp, Liver Res Ctr, 95 Yong An Rd, Beijing 100050, Peoples R China.
EM youhong30@sina.com
RI You, Hong/G-6686-2011; liu, junyan/HGV-1505-2022
FU Beijing Municipal Administration of Hospitals' Youth Program
[QML20170107]; Beijing Talents Fund [2016000021469G226]
FX This study is funded by Beijing Municipal Administration of Hospitals'
Youth Program (QML20170107) and Beijing Talents Fund
(2016000021469G226). The sponsor had no role in study design, data
collection, data analysis, data interpretation, or writing of the
report.
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PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1936-0533
EI 1936-0541
J9 HEPATOL INT
JI Hepatol. Int.
PD JAN
PY 2019
VL 13
IS 1
BP 91
EP 101
DI 10.1007/s12072-018-9907-5
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HJ8WT
UT WOS:000457481500011
PM 30443702
DA 2025-01-07
ER
PT J
AU Diskin, CJ
Stokes, TJ
Dansby, LM
Radcliff, L
Carter, TB
AF Diskin, Charles J.
Stokes, Thomas J.
Dansby, Linda M.
Radcliff, Lautrec
Carter, Thomas B.
TI The prevalence and meaning of eosinophilia in renal diseases on a
nephrology consultation service
SO NEPHROLOGY DIALYSIS TRANSPLANTATION
LA English
DT Article
DE diagnosis; eosinophil; renal failure; vascular disease; vascular
physiology
AB Background. In recent years, we have come to understand that the eosinophil is more than the end point in clearance of parasitic infection or a maladaptive response to asthma and allergic reactions. Since eosinophilia has been reported to be common in renal diseases, we thought that an evaluation of the associations of eosinophilia on a renal consultation service would add some value to the understanding of their role in renal disease.
Methods. This was a prospective cross-sectional study of 1339 consecutive patients referred to the nephrology service after hospitalization who were evaluated for the relationship of the amount of serum eosinophils to their diagnosis, gender, age and the presence of autoimmune disease, cancer, infection, liver disease, pleural effusions, allergies and use of prednisone, beta-blockers or beta agonists, in addition to the total white blood count, urine protein, serum concentration creatinine and phosphorus levels and estimated glomerular filtration rate.
Results. The presence of vascular disease correlated the most strongly with increased eosinophil count (partial correlation coefficient, r = 0.18, P = 0.006), followed by pleural effusions (r = 0.17, P = 0.001), while total white cell count (r = -0.18, P = 0.008) and administration of beta-blockers (r = -0.13, P = 0.047) demonstrated significant inverse correlations and the presence of autoimmune disease, cancer, allergies, proteinuria and serum phosphorus concentration demonstrated no significant correlation.
Conclusion. There are multiple associations with increased eosinophil counts in patients seen on a nephrology consultant service; however, their presence appears less often in association with allergies or uremia and more often with vascular disease.
C1 [Diskin, Charles J.; Stokes, Thomas J.; Dansby, Linda M.; Radcliff, Lautrec; Carter, Thomas B.] Auburn Univ, Dept Hypertens Nephrol Dialysis & Transplantat, Opelika, AL 36801 USA.
C3 Auburn University System; Auburn University
RP Diskin, CJ (corresponding author), Auburn Univ, Dept Hypertens Nephrol Dialysis & Transplantat, Opelika, AL 36801 USA.
EM HNDT512@bellsouth.net
RI Diskin, Charles/JLL-4802-2023
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NR 88
TC 14
Z9 14
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0931-0509
EI 1460-2385
J9 NEPHROL DIAL TRANSPL
JI Nephrol. Dial. Transplant.
PD AUG
PY 2011
VL 26
IS 8
BP 2549
EP U1510
DI 10.1093/ndt/gfq745
PG 10
WC Transplantation; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Transplantation; Urology & Nephrology
GA 800CM
UT WOS:000293336500022
PM 21239387
OA Bronze
DA 2025-01-07
ER
PT J
AU Ali, F
Rahul
Naz, F
Jyoti, S
Siddique, YH
AF Ali, Fahad
Rahul
Naz, Falaq
Jyoti, Smita
Siddique, Yasir Hasan
TI Health functionality of apigenin: A review
SO INTERNATIONAL JOURNAL OF FOOD PROPERTIES
LA English
DT Review
DE Apigenin; anti-inflammatory; anti-toxicant; anti-cancer; natural plant
product
ID CELL-CYCLE ARREST; NF-KAPPA-B; HUMAN PROSTATE-CANCER; CHEMOPREVENTIVE
BIOFLAVONOID APIGENIN; TETRACHLORIDE-INDUCED HEPATOTOXICITY;
CASPASE-DEPENDENT APOPTOSIS; OVALBUMIN-INDUCED ASTHMA; INDUCED GENOTOXIC
DAMAGE; NITRIC-OXIDE PRODUCTION; CYTOCHROME-C RELEASE
AB Apigenin is being used by humans in the form of plant extract for the treatment of a number of disorders and inflammatory conditions, until its discovery as a core compound. Apigenin, chemically known as 4, 5, 7,-trihydroxyflavone is a yellow crystalline powder belonging to the flavone class, that is the aglycone of several naturally occurring glycosides. It is insoluble in water but soluble in organic solvents. Numerous pharmacological activities, including anti-inflammatory, anti-toxicant, anti-cancer, etc., are attributed to apigenin. Research has shown that apigenin has numerous molecular targets involved in inflammation. Based on the in vivo, in vitro, and clinical trial studies suggested that apigenin is a potent therapeutic agent to overcome diseases such as rheumatoid arthritis, autoimmune disorders, Parkinson's disease, Alzheimer's disease, and various type of cancers. Delayed plasma clearance and slow decomposition in liver increases its systemic bioavailability, and makes it a strong therapeutic agent in pharmaceutical studies. In the present review, detailed accounts of the properties of apigenin have been discussed.
C1 [Ali, Fahad; Rahul; Naz, Falaq; Jyoti, Smita; Siddique, Yasir Hasan] Aligarh Muslim Univ, Genet Sect, Dept Zool, Fac Life Sci, Aligarh 202002, Uttar Pradesh, India.
C3 Aligarh Muslim University
RP Siddique, YH (corresponding author), Aligarh Muslim Univ, Genet Sect, Dept Zool, Fac Life Sci, Aligarh 202002, Uttar Pradesh, India.
EM yasir_hasansiddique@rediffmail.com
RI JYOTI, SMITA/ABG-2645-2021; siddique, yasir/B-7580-2011; NAZ, Dr.
FALAQ/E-7598-2013
OI NAZ, Dr. FALAQ/0000-0002-3007-0021
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NR 317
TC 194
Z9 201
U1 17
U2 112
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1094-2912
EI 1532-2386
J9 INT J FOOD PROP
JI Int. J. Food Prop.
PY 2017
VL 20
IS 6
BP 1197
EP 1238
DI 10.1080/10942912.2016.1207188
PG 42
WC Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology
GA ES7QL
UT WOS:000399745300001
OA Bronze
HC Y
HP N
DA 2025-01-07
ER
PT J
AU König, R
Cai, P
Guo, X
Ansari, GAS
AF Koenig, Rolf
Cai, Ping
Guo, Xin
Ansari, G. A. S.
TI Transcriptomic analysis reveals early signs of liver toxicity in female
MRL +/+ mice exposed to the acylating chemicals dichloroacetyl chloride
and dichloroacetic anhydride
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID IFN REGULATORY FACTOR-2; VIRUS CORE PROTEIN; T-CELL-ACTIVATION; MALE
B6C3F1 MOUSE; GENE-EXPRESSION; AUTOIMMUNE-RESPONSE; OXIDATIVE STRESS;
HEPATIC METALLOTHIONEIN; RISK-ASSESSMENT; IN-VITRO
AB Dichloroacetyl chloride (DCAC) is a reactive metabolite of trichloroethene (TCE). TCE and its metabolites have been implicated in the induction of organ-specific and systemic autoimmunity, in the acceleration of autoimmune responses, and in the development of liver toxicity and hepatocellular carcinoma. In humans, effects of environmental toxicants are often multifactorial and detected only after. long-term exposure. Therefore, we developed a mouse model to determine mechanisms by which DCAC and related acylating agents affect the liver. Autoimmune-prone female MRL +/+ mice were injected intraperitoneally with 0.2 mmol/kg of DCAC or dichloroacetic anhydride (DCAA) in corn oil twice weekly for six weeks. No overt liver pathology was detectable. Using microarray gene expression analysis, we detected changes in the liver transcriptome consistent with inflammatory processes. Both acylating toxicants up-regulated the expression of acute phase response and inflammatory genes. Furthermore, metallothionein genes were strongly up-regulated, indicating effects of the toxicants on zinc ion homeostasis and stress responses. In addition, DCAC and DCAA induced the up-regulation of several genes indicative of tumorigenesis. Our data provide novel insight into early mechanisms for the induction of liver disease by acylating agents. The data also demonstrate the power of microarray analysis in detecting early changes in liver function following exposure to environmental toxicants.
C1 [Koenig, Rolf; Guo, Xin] Univ Texas Galveston, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA.
[Cai, Ping; Ansari, G. A. S.] Univ Texas Galveston, Med Branch, Dept Pathol, Galveston, TX 77555 USA.
C3 University of Texas System; University of Texas Medical Branch
Galveston; University of Texas System; University of Texas Medical
Branch Galveston
RP König, R (corresponding author), Univ Texas Galveston, Med Branch, Dept Microbiol & Immunol, 301 Univ Blvd, Galveston, TX 77555 USA.
EM rokonig@utmb.edu
RI Konig, Rolf/B-3128-2008
FU NIEHS NIH HHS [P30ES06676, ES11584] Funding Source: Medline
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Ye B, 2001, P NATL ACAD SCI USA, V98, P2317, DOI 10.1073/pnas.041619198
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NR 82
TC 6
Z9 6
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0893-228X
EI 1520-5010
J9 CHEM RES TOXICOL
JI Chem. Res. Toxicol.
PD MAR
PY 2008
VL 21
IS 3
BP 572
EP 582
DI 10.1021/tx7002728
PG 11
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA 275PY
UT WOS:000254085300006
PM 18293905
DA 2025-01-07
ER
PT J
AU Hsu, SJ
Chao, YC
Lin, XH
Liu, HH
Zhang, Y
Hong, WF
Chen, MP
Xu, X
Zhang, L
Ren, ZG
Du, SS
Chen, RX
AF Hsu, Shu-Jung
Chao, Yen-Cheng
Lin, Xia-Hui
Liu, Hua-Hua
Zhang, Yang
Hong, Wei-Feng
Chen, Mao-Pei
Xu, Xin
Zhang, Lan
Ren, Zheng-Gang
Du, Shi-Suo
Chen, Rong-Xin
TI Antinuclear antibody (ANA) status predicts immune-related adverse events
in liver cancer patients undergoing anti-PD-1 therapy
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Article
DE antinuclear antibody; PD-1; immune-related adverse event; primary liver
cancer; common terminology criteria for adverse events
ID CHECKPOINT INHIBITORS; AUTOANTIBODIES; ASSOCIATION; TOXICITIES;
MANAGEMENT; RESISTANCE; HEPATITIS; NIVOLUMAB; BLOCKADE; SAFETY
AB Immune-related adverse events (irAEs) clinically resemble autoimmune diseases, indicating autoantibodies could be potential biomarkers for the prediction of irAEs. This study aimed to assess the predictive value of peripheral blood antinuclear antibody (ANA) status for irAEs, considering the time and severity of irAEs, as well as treatment outcome in liver cancer patients administered anti-PD-1 therapy. Ninety-three patients with advanced primary liver cancer administered anti-PD-1 treatment were analyzed retrospectively. They were divided into the ANA positive (ANA+, titer = 1:100) and negative (ANA-, titer < 1:100) groups. Development of irAEs, progression-free survival (PFS), and overall survival (OS) were assessed. Compared with ANA- patients, ANA+ cases were more prone to develop irAEs (43.3% vs. 19.2%, P = 0.031). With the increase of ANA titers, the frequency of irAEs increased. The time interval between anti-PD-1 therapy and the onset of irAEs was significantly shorter in ANA+ patients compared with the ANA- group (median, 1.7 months vs. 5.0 months, P = 0.022). Moreover, the time between anti-PD-1 therapy and irAE occurrence decreased with increasing ANA titer. In addition, PFS and OS were decreased in ANA+ patients compared with the ANA- group (median PFS, 2.8 months vs. 4.2 months, P = 0.043; median OS, 21.1 months vs. not reached, P = 0.041). IrAEs occur at higher frequency in ANA+ liver cancer patients undergoing anti-PD-1 therapy. ANA titer could help predict irAE development and treatment outcome in these patients.
C1 [Hsu, Shu-Jung; Liu, Hua-Hua; Chen, Mao-Pei; Xu, Xin; Zhang, Lan; Ren, Zheng-Gang; Chen, Rong-Xin] Fudan Univ, Zhongshan Hosp, Liver Canc Inst, Shanghai, Peoples R China.
[Hsu, Shu-Jung; Zhang, Yang; Hong, Wei-Feng; Du, Shi-Suo] Fudan Univ, Zhongshan Hosp, Dept Radiat Oncol, Shanghai, Peoples R China.
[Chao, Yen-Cheng] Fudan Univ, Zhongshan Hosp, Dept Pulm Med, Shanghai, Peoples R China.
[Lin, Xia-Hui] Fudan Univ, Zhongshan Hosp, Dept Gastroenterol & Hepatol, Shanghai, Peoples R China.
[Chen, Rong-Xin] Fudan Univ, Zhongshan Hosp, Liver Canc Inst, 136 Yi Xue Yuan Rd, Shanghai, Peoples R China.
[Du, Shi-Suo] Fudan Univ, Zhongshan Hosp, Dept Radiat Oncol, 136 Yi Xue Yuan Rd, Shanghai, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Fudan University;
Fudan University; Fudan University
RP Chen, RX (corresponding author), Fudan Univ, Zhongshan Hosp, Liver Canc Inst, 136 Yi Xue Yuan Rd, Shanghai, Peoples R China.; Du, SS (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Radiat Oncol, 136 Yi Xue Yuan Rd, Shanghai, Peoples R China.
EM du.shisuo@zs-hospital.sh.cn; chen.rongxin@zs-hospital.sh.cn
RI xu, xin/HNQ-6671-2023; Liu, Huahua/JJF-3455-2023; Wen,
Jing/KCL-6614-2024
OI Hsu, Shu-Jung/0000-0003-4043-7779
FU National Natural Science Foundation of China [82073479]
FX Acknowledgements This study was supported by the National Natural
Science Foundation of China (grant no. 82073479).
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NR 35
TC 3
Z9 3
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0009-9104
EI 1365-2249
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD JUN 5
PY 2023
VL 212
IS 3
BP 239
EP 248
DI 10.1093/cei/uxad036
EA APR 2023
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA I4UT9
UT WOS:000968656300001
PM 36966354
OA Green Published
DA 2025-01-07
ER
PT J
AU Esmaeil, N
Anaraki, SB
Gharagozloo, M
Moayedi, B
AF Esmaeil, Nafiseh
Anaraki, Sima Balouchi
Gharagozloo, Marjan
Moayedi, Behjat
TI Silymarin impacts on immune system as an immunomodulator: One key for
many locks
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE Silymarin; Immunomodulator; Antioxidant; Anti-inflammatory
ID NF-KAPPA-B; ANTIOXIDANT FLAVONOID MIXTURE; PANCREATIC BETA-CELLS;
THALASSEMIA MAJOR PATIENTS; UVB-INDUCED APOPTOSIS; BALB/C MICE;
PHYSIOLOGICAL-RESPONSES; CYTOKINE PRODUCTION; MILK THISTLE; CONSTITUTIVE
ACTIVATION
AB Silymarin is a flavonoid complex extracted from the Silybum marianum plant. It acts as a strong antioxidant and free radical scavenger by different mechanisms. But in addition to antioxidant effects, silymarin/silybin reveals immunomodulatory affects with both immunostimulatory and immunosuppression activities. Different studies have shown that silymarin has the anti-inflammatory effect through the suppression of NF-kappa B signaling pathway and TNF-alpha activation. It also has different immunomodulatory activities in a dose and time-dependent manner. As an immunomodulator agent, silymarin inhibits T-lymphocyte function at low doses while stimulates inflammatory processes at high doses. Studies have shown that silymarin has attenuated autoimmune, allergic, preeclampsia, cancer, and immune-mediated liver diseases and also has suppressed oxidative and nitrosative immunotoxicity. Silymarin also has indicated dual effects on proliferation and apoptosis of different cells. In conclusion, based on the current review, silymarin has a broad spectrum of immunomodulatory functions under different conditions. Recognizing the exact mechanisms of silymarin on cellular and molecular pathways would be very valuable for treatment of immune-mediated diseases. Also further studies are needed to assess the utility of silymarin in protection against autoimmune, cancer, allergic and other diseases in human subjects.
C1 [Esmaeil, Nafiseh; Moayedi, Behjat] Isfahan Univ Med Sci, Sch Med, Dept Immunol, Esfahan 81744176, Iran.
[Anaraki, Sima Balouchi] Shiraz Univ Med Sci, Shiraz Inst Canc Res, Sch Med, Dept Immunol,Sch Med, Shiraz, Iran.
[Gharagozloo, Marjan] Univ Sherbrooke, Dept Pediat, Program Immunol & Allergol, Med Sch, Sherbrooke, PQ, Canada.
C3 Isfahan University of Medical Sciences; Shiraz University of Medical
Science; University of Sherbrooke
RP Esmaeil, N (corresponding author), Isfahan Univ Med Sci, Sch Med, Dept Immunol, Esfahan 81744176, Iran.
EM n_esmaeil@med.mui.ac.ir
RI Gharagozloo, Marjan/ABH-6604-2020; Esmaeil, Nafiseh/AAA-3012-2020
OI Gharagozloo, Marjan/0000-0002-2166-4012; Esmaeil,
Nafiseh/0000-0001-7237-1984
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NR 87
TC 89
Z9 97
U1 3
U2 33
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD SEP
PY 2017
VL 50
BP 194
EP 201
DI 10.1016/j.intimp.2017.06.030
PG 8
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA FE2UT
UT WOS:000408073200024
PM 28672215
DA 2025-01-07
ER
PT J
AU Meng, HW
Niu, RW
You, HM
Wang, L
Feng, R
Huang, C
Li, J
AF Meng, Hongwu
Niu, Ruowen
You, Hongmei
Wang, Ling
Feng, Rui
Huang, Cheng
Li, Jun
TI Interleukin-9 attenuates inflammatory response and hepatocyte apoptosis
in alcoholic liver injury
SO LIFE SCIENCES
LA English
DT Article
DE IL-9; Alcoholic liver injury; Inflammation; Apoptosis; STAT3
ID HEPATIC MACROPHAGES; PROLIFERATION; CELLS; STAT3; RECEPTOR; CANCER;
IL-9; INDUCTION; DISEASE; MODEL
AB Alcoholic liver injury is a liver cell dysfunction disease caused by long-term or excessive alcohol consumption. Inhibiting the production of inflammatory factors is an important way to alleviate liver injury. Interleukin-9 (IL9) is one of the members of IL-2R gamma c family. It has multiple biological functions. Previous studies have shown that IL-9 is a cytokine that is closely related to inflammatory disease, allergic diseases, autoimmune diseases, and parasitic infections. However, no systematic studies have been performed to address the role of IL-9 in ALI. This project aims to investigate the effects of IL-9 on macrophage-related inflammatory response and hepatocyte apoptosis in alcohol-induced liver injury by injecting adeno-associated virus (AAV9) into tail vein. In the ALI model group, western blot and ELISA assays demonstrated that the expression of IL-9 was reduced. Overexpression of IL-9 relieved the injury and reduced the serum levels of IL-6, TNF-alpha in EtOH-induced ALI mouse model. Moreover, by using western blot, it was indicated that IL-9 can inhibit the expression of pro-apoptotic protein, such as cleaved caspase 3 and Bax. In vitro, mouse recombinant protein IL-9 inhibited the expression of IL-6, TNF-alpha in EtOH-induced RAW264.7 cells. Moreover, flow cytometry and western blot results displayed that macrophage-derived IL-9 inhibited hepatocyte apoptosis. After silencing STAT3 in AML-12 cells, the antiapoptotic effect of macrophage-derived IL-9 was further enhanced. These results indicate that IL-9 reduces the production of pro-inflammatory factors in ALI. Furthermore, macrophage-derived IL-9 can reduce hepatocyte apoptosis by inhibiting the activation of the STAT3 pathway.
C1 [Meng, Hongwu; You, Hongmei; Wang, Ling; Feng, Rui; Huang, Cheng; Li, Jun] Anhui Med Univ, Sch Pharm, Anhui Inst Innovat Drugs, Inflammat & Immune Mediated Dis Lab Anhui Prov, Hefei 230032, Peoples R China.
[Niu, Ruowen] Anhui Med Univ, Dept Pharm, Affiliated Hosp 1, Hefei 230022, Peoples R China.
[Meng, Hongwu; You, Hongmei; Wang, Ling; Feng, Rui; Huang, Cheng; Li, Jun] Minist Educ, Key Lab Antiinflammatory Immune Med, Hefei 230032, Peoples R China.
[Meng, Hongwu; You, Hongmei; Wang, Ling; Feng, Rui; Huang, Cheng; Li, Jun] Anhui Med Univ, Inst Liver Dis, Hefei 230032, Peoples R China.
C3 Anhui Medical University; Anhui Medical University; Anhui Medical
University
RP Huang, C; Li, J (corresponding author), Anhui Med Univ, Sch Pharm, Meishan Rd 81, Hefei 230032, Anhui, Peoples R China.
EM huangcheng@ahmu.edu.cn; lj@ahmu.edu.cn
FU National Natural Science Founda-tion of China [U19A2001]
FX This study was supported by the National Natural Science Founda-tion of
China (no. U19A2001) .
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NR 41
TC 12
Z9 12
U1 1
U2 30
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD JAN 1
PY 2022
VL 288
AR 120180
DI 10.1016/j.lfs.2021.120180
EA NOV 2021
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA XS6UW
UT WOS:000733042300010
PM 34843736
DA 2025-01-07
ER
PT J
AU Islam, MM
Takeyama, N
AF Islam, Md. Monirul
Takeyama, Naoshi
TI Role of Neutrophil Extracellular Traps in Health and Disease
Pathophysiology: Recent Insights and Advances
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE neutrophil extracellular traps (NETs); innate immunity; sepsis; lung
disease; cardiovascular disease; liver disease; kidney disease;
diabetes; COVID-19; coagulopathy and thrombotic microangiopathy; cancer;
autoimmunity; preeclampsia; kawasaki disease
ID RESPIRATORY-DISTRESS-SYNDROME; CIRCULATING TUMOR-CELLS; INTENSIVE-CARE
UNITS; DEEP-VEIN THROMBOSIS; NET FORMATION; ELEVATED LEVELS;
CATHEPSIN-G; DNA TRAPS; NETOSIS; HISTONES
AB Neutrophils are the principal trouper of the innate immune system. Activated neutrophils undergo a noble cell death termed NETosis and release a mesh-like structure called neutrophil extracellular traps (NETs) as a part of their defensive strategy against microbial pathogen attack. This web-like architecture includes a DNA backbone embedded with antimicrobial proteins like myeloperoxidase (MPO), neutrophil elastase (NE), histones and deploys in the entrapment and clearance of encountered pathogens. Thus NETs play an inevitable beneficial role in the host's protection. However, recent accumulated evidence shows that dysregulated and enhanced NET formation has various pathological aspects including the promotion of sepsis, pulmonary, cardiovascular, hepatic, nephrological, thrombotic, autoimmune, pregnancy, and cancer diseases, and the list is increasing gradually. In this review, we summarize the NET-mediated pathophysiology of different diseases and focus on some updated potential therapeutic approaches against NETs.
C1 [Islam, Md. Monirul; Takeyama, Naoshi] Aichi Med Univ, Dept Emergency & Crit Care Med, Nagakute, Aichi 4801195, Japan.
[Islam, Md. Monirul] Univ Sci & Technol Chittagong USTC, Dept Biochem & Biotechnol, Chattogram 4202, Bangladesh.
C3 Aichi Medical University; University of Science & Technology Chittagong
(USTC)
RP Takeyama, N (corresponding author), Aichi Med Univ, Dept Emergency & Crit Care Med, Nagakute, Aichi 4801195, Japan.
EM shafinbiochemistry@gmail.com; takeyama@aichi-med-u.ac.jp
RI Islam, Md./HKN-5239-2023
OI Islam, Md. Monirul/0000-0002-3922-9190
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NR 242
TC 24
Z9 27
U1 10
U2 18
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD NOV
PY 2023
VL 24
IS 21
AR 15805
DI 10.3390/ijms242115805
PG 21
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA X7MK3
UT WOS:001100245100001
PM 37958788
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Hickey, SL
McKim, A
Mancuso, CA
Krishnan, A
AF Hickey, Stephanie L.
McKim, Alexander
Mancuso, Christopher A.
Krishnan, Arjun
TI A network-based approach for isolating the chronic inflammation gene
signatures underlying complex diseases towards finding new treatment
opportunities
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE complex disease; inflammation; endophenotype; drug repurposing; network
analysis; functional modules; disease modules
ID DIABETES-MELLITUS; RHEUMATOID-ARTHRITIS; RISK; DISORDERS; DATABASE;
CANCER
AB Complex diseases are associated with a wide range of cellular, physiological, and clinical phenotypes. To advance our understanding of disease mechanisms and our ability to treat these diseases, it is critical to delineate the molecular basis and therapeutic avenues of specific disease phenotypes, especially those that are associated with multiple diseases. Inflammatory processes constitute one such prominent phenotype, being involved in a wide range of health problems including ischemic heart disease, stroke, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease, and autoimmune and neurodegenerative conditions. While hundreds of genes might play a role in the etiology of each of these diseases, isolating the genes involved in the specific phenotype (e.g., inflammation "component ") could help us understand the genes and pathways underlying this phenotype across diseases and predict potential drugs to target the phenotype. Here, we present a computational approach that integrates gene interaction networks, disease-/trait-gene associations, and drug-target information to accomplish this goal. We apply this approach to isolate gene signatures of complex diseases that correspond to chronic inflammation and use SAveRUNNER to prioritize drugs to reveal new therapeutic opportunities.
C1 [Hickey, Stephanie L.; Krishnan, Arjun] Michigan State Univ, Dept Biochem & Mol Biol, E Lansing, MI 48824 USA.
[McKim, Alexander; Mancuso, Christopher A.; Krishnan, Arjun] Michigan State Univ, Dept Computat Math Sci & Engn, E Lansing, MI 48824 USA.
[McKim, Alexander] Michigan State Univ, Genet & Genome Sci Program, E Lansing, MI USA.
[Mancuso, Christopher A.] Univ Colorado, Colorado Sch Publ Hlth, Dept Biostat & Informat, Denver Anschutz Med Campus, Aurora, CO USA.
[Krishnan, Arjun] Univ Colorado, Dept Biomed Informat, Anschutz Med Campus, Aurora, CO 80045 USA.
C3 Michigan State University; Michigan State University; Michigan State
University; Colorado School of Public Health; University of Colorado
System; University of Colorado Anschutz Medical Campus; University of
Colorado System; University of Colorado Anschutz Medical Campus
RP Krishnan, A (corresponding author), Michigan State Univ, Dept Biochem & Mol Biol, E Lansing, MI 48824 USA.; Krishnan, A (corresponding author), Michigan State Univ, Dept Computat Math Sci & Engn, E Lansing, MI 48824 USA.; Krishnan, A (corresponding author), Univ Colorado, Dept Biomed Informat, Anschutz Med Campus, Aurora, CO 80045 USA.
EM arjun.krishnan@cuanschutz.edu
OI Mancuso, Christopher/0000-0003-3081-2758; Hickey,
Stephanie/0000-0002-9768-786X
FU US National Institutes of Health (NIH); NIH Fellowship [R35 GM128765];
Brain and Behavior Research Foundation [F32 GM134595]; [29956]
FX This work was supported by the US National Institutes of Health (NIH)
grant R35 GM128765 to AK and NIH Fellowship F32 GM134595 to CM and a
2021 NARSAD Young Investigator Grant from the Brain and Behavior
Research Foundation (29956) to SH.
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NR 54
TC 2
Z9 2
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD OCT 12
PY 2022
VL 13
AR 995459
DI 10.3389/fphar.2022.995459
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 5V0UO
UT WOS:000876953700001
PM 36313344
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zara, V
Assalve, G
Ferramosca, A
AF Zara, Vincenzo
Assalve, Graziana
Ferramosca, Alessandra
TI Insights into the malfunctioning of the mitochondrial citrate carrier:
Implications for cell pathology
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
LA English
DT Review
DE Mitochondrial carrier family; Metabolic alterations; Congenital
diseases; Inflammation; Autoimmune diseases; Cancer
ID TRICARBOXYLATE TRANSPORT PROTEIN; L-2-HYDROXYGLUTARIC ACIDURIA;
D-2-HYDROXYGLUTARIC ACID; OXIDATIVE STRESS; ONCOMETABOLITE
2-HYDROXYGLUTARATE; CEREBRAL-CORTEX; KEY ROLE; SLC25A1; LIVER;
METABOLISM
AB The mitochondrial citrate carrier (CIC) is a member of the mitochondrial carrier family and is responsible for the transit of tricarboxylates and dicarboxylates across the inner membrane. By modulating the flux of these molecules, it represents the molecular link between catabolic and anabolic reactions that take place in distinct cellular sub-compartments. Therefore, this transport protein represents an important element of investigation both in physiology and in pathology.In this review we critically analyze the involvement of the mitochondrial CIC in several human pathologies, which can be divided into two subgroups, one characterized by a decrease and the other by an increase in the flux of citrate across the inner mitochondrial membrane.In particular, a decrease in the activity of the mitochondrial CIC is responsible for several congenital diseases of different severity, which are also characterized by the increase in urinary levels of L-2-and D-2-hydroxyglutaric acids. On the other hand, an increase in the activity of the mitochondrial CIC is involved, in various ways, in the onset of inflammation, autoimmune diseases, and cancer. Then, understanding the role of CIC and the mechanisms driving the flux of metabolic intermediates between mitochondria and cytosol would potentially allow for manipulation and control of metabolism in pathological conditions.
C1 [Zara, Vincenzo; Assalve, Graziana; Ferramosca, Alessandra] Univ Salento, Dept Biol & Environm Sci & Technol, I-73100 Lecce, Italy.
C3 University of Salento
RP Ferramosca, A (corresponding author), Univ Salento, Dept Biol & Environm Sci & Technol, I-73100 Lecce, Italy.
EM alessandra.ferramosca@unisalento.it
RI Zara, Vincenzo/AAC-2900-2019; Ferramosca, Alessandra/B-8801-2015
OI Ferramosca, Alessandra/0000-0002-8251-9652; Assalve,
Graziana/0009-0002-0165-7920
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NR 102
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0925-4439
EI 1879-260X
J9 BBA-MOL BASIS DIS
JI Biochim. Biophys. Acta-Mol. Basis Dis.
PD AUG
PY 2023
VL 1869
IS 6
AR 166758
DI 10.1016/j.bbadis.2023.166758
EA MAY 2023
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA P8VH9
UT WOS:001053390600001
PM 37209873
OA Bronze
DA 2025-01-07
ER
PT J
AU Zehntner, SP
Bourbonniere, L
Moore, CS
Morris, SJ
Methot, D
Jean, M
Lacasse, E
Hebb, ALO
Robertson, GS
Durkin, J
Gillard, JW
Owens, T
AF Zehntner, Simone P.
Bourbonniere, Lyne
Moore, Craig S.
Morris, Stephen J.
Methot, Danielle
St. Jean, Martine
Lacasse, Eric
Hebb, Andrea L. O.
Robertson, George S.
Durkin, Jon
Gillard, John W.
Owens, Trevor
TI X-linked inhibitor of apoptosis regulates T cell effector function
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
MULTIPLE-SCLEROSIS; CANCER-CELLS; ANTISENSE OLIGONUCLEOTIDES;
DISEASE-ACTIVITY; DOWN-REGULATION; IN-VIVO; XIAP; EXPRESSION
AB To understand how the balance between pro- and anti-apoptotic signals influences effector function in the immune system, we studied the X-linked inhibitor of apoptosis (XIAP), an endogenous regulator of cellular apoptosis. Real-time PCR showed increased XIAP expression in blood of mice with experimental autoimmune encephalomyelitis, correlating with disease severity. Daily administration (10 mg/kg/day i.p.) of a 19-mer antisense oligonucleotide specific for XIAP (ASO-XIAP) abolished disease-associated XIAP mRNA and protein expression, and given from day of onset, alleviated experimental autoimmune encephalomyelitis and prevented relapses. Prophylactic treatment also reduced XIAP expression and prevented disease. Random or 5-base mismatched ASO was not inhibitory, and ASO-XIAP did not affect T cell priming. In ASOXIAP-treated animals, infiltrating cells and inflammatory foci were dramatically reduced within the CNS. Flow cytometry showed an 88-93% reduction in T cells. The proportion of TUNEL+ apoptotic CD4(+) T cells in the CNS was increased from <1.6 to 26% in ASO-XIAP-treated mice, and the proportion of Annexin V-positive CD4(+) T cells in the CNS increased. Neurons and oligodendrocytes were not affected; neither did apoptosis increase in liver, where XIAP knockdown also occurred. ASO-XIAP increased susceptibility of T cells to activation-induced apoptosis in vitro. Our results identify XIAP as a critical controller of apoptotic susceptibility of effector T cell function.
C1 McGill Univ, Montreal Neurol Inst, Neuroimmunol Unit, Montreal, PQ H3A 2T5, Canada.
Aegera Therapeut, Montreal, PQ, Canada.
Univ So Denmark, Med Biotechnol Ctr, Odense, Denmark.
Dalhousie Univ, Fac Med, Dept Pharmacol, Halifax, NS, Canada.
Dalhousie Univ, Fac Med, Dept Psychiat, Halifax, NS, Canada.
C3 McGill University; University of Southern Denmark; Dalhousie University;
Dalhousie University
RP Zehntner, SP (corresponding author), McGill Univ, Montreal Neurol Inst, 3801 Univ St, Montreal, PQ, Canada.
EM simone.zehntner@mcgill.ca
RI Moore, Craig/AGF-9555-2022; Owens, Trevor/B-1196-2010; Moore,
Craig/I-9205-2014
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Trevor/0000-0001-9315-6036; Moore, Craig/0000-0003-3333-435X
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NR 39
TC 22
Z9 26
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD DEC 1
PY 2007
VL 179
IS 11
BP 7553
EP 7560
DI 10.4049/jimmunol.179.11.7553
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 237MK
UT WOS:000251378300043
PM 18025200
OA Bronze
DA 2025-01-07
ER
PT J
AU Fujimori, N
Tanaka, N
Kimura, T
Sano, K
Horiuchi, A
Kato, N
Takahashi, Y
Kuribayashi, N
Sugiura, A
Yamazaki, T
Joshita, S
Umemura, T
Matsumoto, A
Tanaka, E
AF Fujimori, Naoyuki
Tanaka, Naoki
Kimura, Takefumi
Sano, Kenji
Horiuchi, Akira
Kato, Naoyuki
Takahashi, Yoshiyuki
Kuribayashi, Naoya
Sugiura, Ayumi
Yamazaki, Tomoo
Joshita, Satoru
Umemura, Takeji
Matsumoto, Akihiro
Tanaka, Eiji
TI Long-term luseogliflozin therapy improves histological activity of
non-alcoholic steatohepatitis accompanied by type 2 diabetes mellitus
SO CLINICAL JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Luseogliflozin; Sodium-glucose cotransporter 2 inhibitor; Non-alcoholic
steatohepatitis; Non-alcoholic fatty liver disease; Fibrosis
ID FATTY LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA; FIBROSIS; RISK;
PIOGLITAZONE; METAANALYSIS; MORTALITY; METFORMIN; OUTCOMES
AB A 60-year-old Japanese woman was referred to our hospital for further examination of persistent liver dysfunction. She had been suffering from type 2 diabetes mellitus since the age of 50 years. Her hemoglobin A1c (HbA1c) value was as high as 7.8% despite treatment with dipeptidyl peptidase-4 inhibitor, metformin, and sulfonylurea. After excluding viral hepatitis, alcohol or drug-induced liver injury, and autoimmune liver diseases, liver histology evidence of macrovesicular steatosis, hepatocyte ballooning, and pericellular fibrosis confirmed a diagnosis of non-alcoholic steatohepatitis (NASH). Luseogliflozin (2.5 mg/day), a sodium-glucose cotransporter 2 inhibitor (SGLT2I), was co-administered to strengthen glycemic control. Liver enzymes and HbA1c gradually improved without any adverse events. A second liver biopsy at 15 months after luseogliflozin commencement revealed improvements in steatosis, fibrosis, and overall histological activity score. This case demonstrates that long-term luseogliflozin may be a good therapeutic option for diabetic NAFLD/NASH patients. The merits of persistent SGLT2I administration for NAFLD/NASH patients warrant validation in future studies.
C1 [Fujimori, Naoyuki; Kimura, Takefumi; Takahashi, Yoshiyuki; Kuribayashi, Naoya; Sugiura, Ayumi; Yamazaki, Tomoo; Joshita, Satoru; Umemura, Takeji; Matsumoto, Akihiro; Tanaka, Eiji] Shinshu Univ, Dept Internal Med, Div Gastroenterol, Sch Med, Matsumoto, Nagano, Japan.
[Tanaka, Naoki] Shinshu Univ, Dept Metab Regulat, Sch Med, Asahi 3-1-1, Matsumoto, Nagano 3908621, Japan.
[Tanaka, Naoki] Shinshu Univ, Res Ctr Social Syst, Matsumoto, Nagano, Japan.
[Sano, Kenji] Iida Municipal Hosp, Dept Pathol, Iida, Japan.
[Horiuchi, Akira] Showa Inan Gen Hosp, Digest Dis Ctr, Komagane, Japan.
[Kato, Naoyuki] Minakata Clin, Nakagawa, Japan.
C3 Shinshu University; Shinshu University; Shinshu University
RP Tanaka, N (corresponding author), Shinshu Univ, Dept Metab Regulat, Sch Med, Asahi 3-1-1, Matsumoto, Nagano 3908621, Japan.; Tanaka, N (corresponding author), Shinshu Univ, Res Ctr Social Syst, Matsumoto, Nagano, Japan.
EM naopi@shinshu-u.ac.jp
RI Joshita, Satoru/K-5679-2019; Kimura, Takefumi/D-3412-2011
OI Kimura, Takefumi/0000-0002-1481-1029; Tanaka, Naoki/0000-0002-3212-3836
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NR 42
TC 6
Z9 6
U1 0
U2 8
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 1865-7257
EI 1865-7265
J9 CLIN J GASTROENTEROL
JI Clin. J. Gastroenterol.
PD FEB
PY 2020
VL 13
IS 1
BP 83
EP 89
DI 10.1007/s12328-019-01018-1
PG 7
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA KJ5IR
UT WOS:000512094100016
PM 31292843
DA 2025-01-07
ER
PT J
AU Hu, SQ
Cho, EH
Lee, JY
AF Hu, Siqi
Cho, Eun-Hee
Lee, Ji-Young
TI Histone Deacetylase 9: Its Role in the Pathogenesis of Diabetes and
Other Chronic Diseases
SO DIABETES & METABOLISM JOURNAL
LA English
DT Review
DE Autoimmune diseases; Cardiovascular diseases; Chronic disease;
Epigenomics; Histone deacetylases; Neoplasms; Obesity
ID REGULATORY CELL-FUNCTION; HDAC9; TRANSCRIPTION; ACETYLATION;
ATHEROSCLEROSIS; OSTEOCLASTOGENESIS; DIFFERENTIATION; IDENTIFICATION;
CONTRIBUTES; SUPPRESSION
AB As a member of the class Ila histone deacetylascs (HDACs), HDAC9 catalyzes the deacetylation of histones and transcription factors, commonly leading to the suppression of gene transcription. The activity of HDAC9 is regulated transcriptionally and post-translationally. HDAC9 is known to play an essential role in regulating myocyte and adipocyte differentiation and cardiac muscle development. Also, recent studies have suggested that HDAC9 is involved in the pathogenesis of chronic diseases, including cardiovascular diseases, osteoporosis, autoimmunc disease, cancer, obesity, insulin resistance, and liver fibrosis. HDAC9 modulates the expression of genes related to the pathogenesis of chronic diseases by altering chromatin structure in their promotor region or reducing the transcriptional activity of their respective transcription factors. This review summarizes the current knowledge of the regulation of HDAC9 expression and activity. Also, the roles of HDAC9 in the pathogenesis of chronic diseases are discussed, along with potential underlying mechanisms.
C1 [Hu, Siqi; Lee, Ji-Young] Univ Connecticut, Dept Nutr Sci, 27 Manter Rd, Storrs, CT 06269 USA.
[Cho, Eun-Hee] Kangwon Natl Univ, Dept Internal Med, Sch Med, Chunchon, South Korea.
C3 University of Connecticut; Kangwon National University
RP Lee, JY (corresponding author), Univ Connecticut, Dept Nutr Sci, 27 Manter Rd, Storrs, CT 06269 USA.
EM ji-young.lee@uconn.edu
RI Hu, Siqi/AAO-5305-2020
OI Lee, Ji-Young/0000-0002-7945-793X; Hu, Siqi/0000-0002-6171-4635
FU NIH [1R01DK108254-01]; USDA Multistate Hatch [CONS00992]
FX This study was supported by NIH 1R01DK108254-01 and USDA Multistate
Hatch CONS00992 to Ji-Young Lee.
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NR 70
TC 22
Z9 23
U1 0
U2 9
PU KOREAN DIABETES ASSOC
PI SEOUL
PA 101-2104, LOTTE CASTLE PRES, 109 MAPO-DAERO, MAPO-GU, SEOUL, 04146,
SOUTH KOREA
SN 2233-6079
EI 2233-6087
J9 DIABETES METAB J
JI Diabetes Metab. J.
PD APR
PY 2020
VL 44
IS 2
BP 234
EP 244
DI 10.4093/dmj.2019.0243
PG 11
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA LJ3CG
UT WOS:000530045200004
PM 32347025
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Burra, P
Zanetto, A
Schnabl, B
Reiberger, T
Montano-Loza, AJ
Asselta, R
Karlsen, TH
Tacke, F
AF Burra, Patrizia
Zanetto, Alberto
Schnabl, Bernd
Reiberger, Thomas
Montano-Loza, Aldo J.
Asselta, Rosanna
Karlsen, Tom Hemming
Tacke, Frank
TI Hepatic immune regulation and sex disparities
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
ID PRIMARY SCLEROSING CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE; FATTY
LIVER-DISEASE; PRIMARY BILIARY-CIRRHOSIS; GENDER-DIFFERENCES;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; PORTAL-HYPERTENSION;
BODY-COMPOSITION; NITRIC-OXIDE
AB Chronic liver disease is a major cause of morbidity and mortality worldwide. Epidemiology, clinical phenotype and response to therapies for gastrointestinal and liver diseases are commonly different between women and men due to sex-specific hormonal, genetic and immune-related factors. The hepatic immune system has unique regulatory functions that promote the induction of intrahepatic tolerance, which is key for maintaining liver health and homeostasis. In liver diseases, hepatic immune alterations are increasingly recognized as a main cofactor responsible for the development and progression of chronic liver injury and fibrosis. In this Review, we discuss the basic mechanisms of sex disparity in hepatic immune regulation and how these mechanisms influence and modify the development of autoimmune liver diseases, genetic liver diseases, portal hypertension and inflammation in chronic liver disease. Alterations in gut microbiota and their crosstalk with the hepatic immune system might affect the progression of liver disease in a sex-specific manner, creating potential opportunities for novel diagnostic and therapeutic approaches to be evaluated in clinical trials. Finally, we identify and propose areas for future basic, translational and clinical research that will advance our understanding of sex disparities in hepatic immunity and liver disease.
Immune dysregulation is a main feature of chronic liver disease, whose burden increases worldwide. This Review discusses the influence of biological sex in hepatic immune mechanisms in the context of liver disease and identifies sex disparities in research and therapeutics.
Increasing evidence indicates that biological sex modifies hepatic immune regulation, thereby contributing to hepatic immune outcomes in health and disease.Changes in gut microbiota might substantially affect liver diseases in a sex-specific manner through the regulation of sex hormones, bile acid, lipid and hepatic xenobiotic metabolism.Genetics have revealed few clues to sex disparities in liver disease, but dedicated studies are scarce; only for primary biliary cholangitis has a dedicated chromosome X-wide association study been performed.Incidence, phenotype and disease progression in autoimmune liver diseases vary according to sex: men have an increased risk of disease progression, suboptimal treatment response and hepatobiliary malignancies.Sex influences haemodynamics and portal hypertension in animal models; however, whether this translates into sex-specific responses to treatments lowering portal pressure in individuals with chronic liver disease is unclear.Marked differences in body mass composition exist between sexes, both in health and chronic liver disease, potentially affecting the risk of hepatic decompensation and survival.
C1 [Burra, Patrizia; Zanetto, Alberto] Padua Univ Hosp, Dept Surg Oncol & Gastroenterol, Gastroenterol & Multivisceral Transplant Unit, Padua, Italy.
[Schnabl, Bernd] Univ Calif San Diego, Dept Med, La Jolla, CA USA.
[Schnabl, Bernd] VA San Diego Healthcare Syst, Dept Med, San Diego, CA USA.
[Reiberger, Thomas] Med Univ Vienna, Dept Med 3, Div Gastroenterol & Hepatol, Vienna, Austria.
[Montano-Loza, Aldo J.] Univ Alberta Hosp, Div Gastroenterol & Liver Unit, Edmonton, AB, Canada.
[Montano-Loza, Aldo J.] Univ Alberta Hosp, Dept Med, Liver Unit, Edmonton, AB, Canada.
[Asselta, Rosanna] Humanitas Univ, Dept Biomed Sci, Milan, Italy.
[Asselta, Rosanna] IRCCS Humanitas Res Hosp, Milan, Italy.
[Karlsen, Tom Hemming] Oslo Univ Hosp, Dept Transplantat Med, Clin Surg Inflammatory Dis & Transplantat, Oslo, Norway.
[Karlsen, Tom Hemming] Univ Oslo, Oslo, Norway.
[Karlsen, Tom Hemming] Oslo Univ Hosp, Res Inst Internal Med, Clin Surg Inflammatory Dis & Transplantat, Oslo, Norway.
[Tacke, Frank] Charite Univ Med Berlin, Dept Hepatol & Gastroenterol, Campus Virchow Klinikum CVK, Berlin, Germany.
[Tacke, Frank] Campus Charite Mitte CCM, Berlin, Germany.
C3 University of Padua; Azienda Ospedaliera - Universita di Padova;
University of California System; University of California San Diego; US
Department of Veterans Affairs; Veterans Health Administration (VHA); VA
San Diego Healthcare System; Medical University of Vienna; University of
Alberta; University of Alberta; Humanitas University; University of
Oslo; University of Oslo; University of Oslo; Berlin Institute of
Health; Free University of Berlin; Humboldt University of Berlin;
Charite Universitatsmedizin Berlin
RP Burra, P (corresponding author), Padua Univ Hosp, Dept Surg Oncol & Gastroenterol, Gastroenterol & Multivisceral Transplant Unit, Padua, Italy.
EM burra@unipd.it
RI Asselta, Rosanna/AAC-2367-2019; Montano-Loza, Aldo/B-3092-2013; Tacke,
Frank/ABF-2212-2020; Reiberger, Thomas/H-7613-2019; Schnabl,
Bernd/HCH-3471-2022; Burra, Patrizia/AAB-2448-2019
OI Montano-Loza, Aldo J./0000-0002-2511-7980; Burra,
Patrizia/0000-0002-8791-191X; Reiberger, Thomas/0000-0002-4590-3583;
Tacke, Frank/0000-0001-6206-0226
FU NIH center [P30 DK120515]; German Research Foundation [DFG Ta434/8-1,
SFB/TRR 296, CRC1382, 403224013]
FX The authors thank NIH center P30 DK120515 for support to B.S. and the
German Research Foundation (DFG Ta434/8-1, SFB/TRR 296 and CRC1382,
project ID 403224013) for support to F.T.
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NR 250
TC 1
Z9 1
U1 11
U2 11
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1759-5045
EI 1759-5053
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD DEC
PY 2024
VL 21
IS 12
BP 869
EP 884
DI 10.1038/s41575-024-00974-5
EA SEP 2024
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA N2U8V
UT WOS:001306177500001
PM 39237606
DA 2025-01-07
ER
PT J
AU Goubran, M
Wang, WW
Indik, S
Faschinger, A
Wasilenko, ST
Bintner, J
Carpenter, EJ
Zhang, GZ
Nuin, P
Macintyre, G
Wong, GKS
Mason, AL
AF Goubran, Mariam
Wang, Weiwei
Indik, Stanislav
Faschinger, Alexander
Wasilenko, Shawn T.
Bintner, Jasper
Carpenter, Eric J.
Zhang, Guangzhi
Nuin, Paulo
Macintyre, Georgina
Wong, Gane K-S
Mason, Andrew L.
TI Isolation of a Human Betaretrovirus from Patients with Primary Biliary
Cholangitis
SO VIRUSES-BASEL
LA English
DT Article
DE biliary epithelial cells (BEC); common insertion sites (CIS); human
betaretrovirus (HBRV); mouse mammary tumor virus (MMTV); primary biliary
cholangitis (PBC)
ID MAMMARY-TUMOR VIRUS; HUMAN BREAST-CANCER; ENV GENE-SEQUENCES;
EPITHELIAL-CELLS; MOUSE; INTEGRATION; CIRRHOSIS; DNA; IDENTIFICATION;
AUTOIMMUNE
AB A human betaretrovirus (HBRV) has been linked with the autoimmune liver disease, primary biliary cholangitis (PBC), and various cancers, including breast cancer and lymphoma. HBRV is closely related to the mouse mammary tumor virus, and represents the only exogenous betaretrovirus characterized in humans to date. Evidence of infection in patients with PBC has been demonstrated through the identification of proviral integration sites in lymphoid tissue, the major reservoir of infection, as well as biliary epithelium, which is the site of the disease process. Accordingly, we tested the hypothesis that patients with PBC harbor a transmissible betaretrovirus by co-cultivation of PBC patients' lymph node homogenates with the HS578T breast cancer line. Because of the low level of HBRV replication, betaretrovirus producing cells were subcloned to optimize viral isolation and production. Evidence of infection was provided by electron microscopy, RT-PCR, in situ hybridization, cloning of the HBRV proviral genome and demonstration of more than 3400 integration sites. Further evidence of viral transmissibility was demonstrated by infection of biliary epithelial cells. While HBRV did not show a preference for integration proximal to specific genomic features, analyses of common insertion sites revealed evidence of integration proximal to cancer associated genes. These studies demonstrate the isolation of HBRV with features similar to mouse mammary tumor virus and confirm that patients with PBC display evidence of a transmissible viral infection.
C1 [Goubran, Mariam; Wang, Weiwei; Wasilenko, Shawn T.; Bintner, Jasper; Zhang, Guangzhi; Macintyre, Georgina; Wong, Gane K-S; Mason, Andrew L.] Univ Alberta, Ctr Excellence Gastrointestinal Inflammat & Immun, Edmonton, AB T6G 2E1, Canada.
[Indik, Stanislav; Faschinger, Alexander] Univ Vet Med, Dept Virol, A-1210 Vienna, Austria.
[Carpenter, Eric J.; Wong, Gane K-S] Univ Alberta, Dept Biol Sci, Edmonton, AB T6G 2E9, Canada.
[Nuin, Paulo] Univ Alberta, Dept Med Genet, Edmonton, AB T6G 2E1, Canada.
[Wong, Gane K-S; Mason, Andrew L.] Univ Alberta, Li Ka Shing Inst Virol, Edmonton, AB T6G 2E1, Canada.
C3 University of Alberta; University of Veterinary Medicine Vienna;
University of Alberta; University of Alberta; University of Alberta
RP Mason, AL (corresponding author), Univ Alberta, Ctr Excellence Gastrointestinal Inflammat & Immun, Edmonton, AB T6G 2E1, Canada.; Mason, AL (corresponding author), Univ Alberta, Li Ka Shing Inst Virol, Edmonton, AB T6G 2E1, Canada.
EM mgoubran@ualberta.ca; wangweiwei301@gmail.com;
stanislay.indik@vetmeduni.ac.at; alexander.faschinger@gmx.at;
shawn.wasilenko@ualberta.ca; j.bintner@gmail.com; ejc@ualberta.ca;
guzzhca@yahoo.com; nuinsuan@ualberta.ca; georgina.macintyre@ualberta.ca;
gane@ualberta.ca; andrew.mason@ualberta.ca
RI Zhang, Guangzhi/HMF-5722-2023; WONG, Gane/G-5784-2013; Wang,
Weiwei/JNS-1774-2023; Mason, Andrew/D-2938-2013
OI Mason, Andrew/0000-0002-0470-9522; Goubran, Mariam/0000-0002-9181-379X
FU Canadian Institutes for Health Research [MOP115154, MOP 114998];
Canadian Liver Foundation
FX We gratefully acknowledge awards from the Canadian Institutes for Health
Research (MOP115154 and MOP 114998) and the Canadian Liver Foundation,
funds were used to complete the genetic analysis for this study.
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NR 97
TC 7
Z9 7
U1 4
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD MAY
PY 2022
VL 14
IS 5
AR 886
DI 10.3390/v14050886
PG 17
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA 1R3JF
UT WOS:000803268600001
PM 35632628
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Whalley, S
Puvanachandra, P
Desai, A
Kennedy, H
AF Whalley, Simon
Puvanachandra, Prasanthi
Desai, Atman
Kennedy, Hugh
TI Hepatology outpatient service provision in secondary care: a study of
liver disease incidence and resource costs
SO CLINICAL MEDICINE
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; POPULATION
AB This paper discusses the annual incidence of liver disease and resource costs in providing a hepatology service for all new outpatient referrals to a secondary care setting. In a retrospective study, we found that 200 patients (1 in 1,000 of the West Suffolk population) with a mean age of 52 years were referred per year. One-third of patients had cirrhosis (almost half due to alcohol). Annual incidence (per 100,000 population) were as follows: non-alcoholic fatty liver disease (29: of which 23.5 non-cirrhotic and 5.5 cirrhotic), hepatitis C (25), hepatitis B (3), alcohol-related cirrhosis (12.5), primary biliary cirrhosis (3.5), autoimmune hepatitis (3), primary sclerosing cholangitis (2), haemochromatosis (2), hepatocellular carcinoma (1.5) and oesophageal variceal haemorrhage (6.5). Using national indicative tariffs, the total annual hepatology budget was 130K pound (58K pound for resources and 72K pound for clinic attendances). The greatest resource expenditure was on endoscopy (almost half for oesophageal varices) and radiological imaging (one-third of the total budget). These findings will help inform commissioners in hepatology service funding.
C1 W Suffolk Hosp, Dept Gastrohepatol, Bury St Edmunds IP33 2QZ, Suffolk, England.
Norfolk & Norwich Hosp, Norwich, Norfolk, England.
C3 Norfolk & Norwich University Hospitals NHS Foundation Trust; Norfolk &
Norwich University Hospital
RP Whalley, S (corresponding author), W Suffolk Hosp, Dept Gastrohepatol, Hardwick Lane, Bury St Edmunds IP33 2QZ, Suffolk, England.
EM simon.whalley@wsh.nhs.uk
OI Attwood, Prasanthi/0000-0003-3606-704X
CR [Anonymous], 2003, INT STAT CLASS DIS R
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Department of Health, 2005, COMM PAT LED NHS
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NR 13
TC 89
Z9 102
U1 1
U2 6
PU ROY COLL PHYS LONDON EDITORIAL OFFICE
PI LONDON
PA 11 ST ANDREWS PLACE REGENTS PARK, LONDON NW1 4LE, ENGLAND
SN 1470-2118
J9 CLIN MED
JI Clin. Med.
PD APR
PY 2007
VL 7
IS 2
BP 119
EP 124
DI 10.7861/clinmedicine.7-2-119
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 162AU
UT WOS:000246059500011
PM 17491498
OA Green Published, Green Accepted, hybrid
DA 2025-01-07
ER
PT J
AU Endreffy, I
Bjorklund, G
Szerafin, L
Chirumbolo, S
Urbina, MA
Endreffy, E
AF Endreffy, Ildiko
Bjorklund, Geir
Szerafin, Laszlo
Chirumbolo, Salvatore
Urbina, Mauricio A.
Endreffy, Emoke
TI Plasma alpha-L-fucosidase activity in chronic inflammation and
autoimmune disorders in a pediatric cohort of hospitalized patients
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Alpha l-fucosidase; Chronic inflammation; Autoimmune disorders;
Children; Fucosidosis
ID LYSOSOMAL STORAGE DISORDERS; HEPATOCELLULAR-CARCINOMA; DIAGNOSTIC-VALUE;
EXPRESSION; SPECTRUM
AB Human alpha-fucosidase (EC 3.2.1.51) is an enzyme (hydrolase) of particular biological and medical interest, as the inherited deficiency in its activity leads to fucosidosis, a pathology belonging to severe glycoprotein lysosomal storage disorders. Although its importance has increased in latest years, data about its plasma level in children with inflammatory disorders are still lacking. In the present study, plasma activity of alpha-L-fucosidase-1 (FUCA-1) and its potential association with chronic inflammatory pathologies was evaluated in hospitalized individuals, both pediatric and adult ones. A number of 201 Hungarian hospitalized patients, 144 children (1-13 years) and 57 adults (31-88 years), were enrolled in the study and underwent plasma assay of FUCA-1 activity, following the normal routine analytical run in the hospital service. Regression and Pearson tests were evaluated to investigate the relationship between FUCA-1 plasma levels and inflammatory disorders diagnosed with subjects recruited in the study. No correlation of FUCA-1 activity was observed in the pediatric patients with immune (p = 0.9677) or metabolic (p = 0.6974) disorders, but a correlation was reported when comparing clusters of chronic inflammatory and autoimmune disease vs. controls (p < 0.05). Furthermore, a relationship was found between FUCA-1 activity in plasma and inflammatory disorders and autoimmunity both in adults and in the pediatric cohort of patients (Pearson test, p = 0.000148). Alterations in plasma levels of FUCA-1 were significantly associated with chronic inflammatory and autoimmune disorders, both in children and adults. The result of the present study should encourage further research on FUCA-1 as a marker of chronic inflammation and autoimmunity.
C1 [Endreffy, Ildiko] Josa Andras Cty Hosp, Dept Pediat, Nyiregyhaza, Hungary.
[Bjorklund, Geir] Council Nutr & Environm Med, Toften 24, N-8610 Mo I Rana, Norway.
[Szerafin, Laszlo] Josa Andras Cty Hosp, Dept Haematol, Nyiregyhaza, Hungary.
[Chirumbolo, Salvatore] Univ Verona, Dept Neurol & Movement Sci, Verona, Italy.
[Urbina, Mauricio A.] Univ Concepcion, Dept Zool, Concepcion, Chile.
[Endreffy, Emoke] Univ Szeged, Fac Med, Dept Pediat, Szeged, Hungary.
[Endreffy, Emoke] Univ Szeged, Fac Med, Pediat Hlth Care Ctr, Szeged, Hungary.
C3 University of Verona; Universidad de Concepcion; Szeged University;
Szeged University
RP Bjorklund, G (corresponding author), Council Nutr & Environm Med, Toften 24, N-8610 Mo I Rana, Norway.
EM bjorklund@conem.org
RI Chirumbolo, Salvatore/AGF-1981-2022; Bjorklund, Geir/B-7319-2014;
Chirumbolo, Salvatore/L-6865-2016
OI Bjorklund, Geir/0000-0003-2632-3935; Chirumbolo,
Salvatore/0000-0003-1789-8307
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NR 21
TC 9
Z9 10
U1 0
U2 7
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD OCT
PY 2017
VL 65
IS 5
BP 1025
EP 1030
DI 10.1007/s12026-017-8943-x
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA FI3OD
UT WOS:000411873000007
PM 28808940
DA 2025-01-07
ER
PT J
AU Kirstein, MM
Metzler, F
Geiger, E
Heinrich, E
Hallensleben, M
Manns, MP
Vogel, A
AF Kirstein, Martha M.
Metzler, Frauke
Geiger, Elena
Heinrich, Eyk
Hallensleben, Michael
Manns, Michael P.
Vogel, Arndt
TI Prediction of short- and long-term outcome in patients with autoimmune
hepatitis
SO HEPATOLOGY
LA English
DT Article
ID CHRONIC ACTIVE HEPATITIS; SOLUBLE LIVER ANTIGEN;
HEPATOCELLULAR-CARCINOMA; MYCOPHENOLATE-MOFETIL; RISK-FACTORS; CLINICAL
CHARACTERISTICS; FOLLOW-UP; TYPE-1; ANTIBODIES; AZATHIOPRINE
AB Autoimmune hepatitis (AIH) is a chronic inflammatory disease characterized by a loss of tolerance toward the hepatocellular epithelium. Liver transplantation (LT) represents the ultimate therapeutic option for a fulminant course or end-stage liver disease. The aim of this study was to elucidate the clinical, serological, and genetic features of remission, relapse, and overall and LT-free survival. Between 2000 and 2014, 354 AIH patients from Hannover Medical School were included. Clinical, laboratory, and histological reports were analyzed. DRB1 allele analyses were performed in 264 AIH and 399 non-AIH patients. Cox's regression analysis was performed to identify factors significantly associated with survival. Patients diagnosed in childhood were at higher risk for relapses (P=0.003), requirement for LTs (P=0.014, log rank), and had a reduced life expectancy (P<0.001, log rank). Detection of soluble liver antigen/liver pancreas antigen (SLA/LP) antibodies was significantly associated with reduced overall and LT-free survival (P=0.037; P=0.021). Cirrhosis, which was evident in 25% at first diagnosis, was found to be a predictor of poor survival and requirement for LT (P=0.003; P=0.009). DRB1*04:01-positive phenotype was associated with a higher rate of complete remissions and with a lower frequency of cirrhosis and LTs. There were no significant differences for subsequent relapses or survival in patients achieving either partial or complete remission. Conclusion: Diagnosis <18 years, histological cirrhosis at first diagnosis and SLA/LP antibodies are major risk factors for a poor short- and long-term outcome. These patients are in need of high surveillance. Separating patients with positive SLA/LP antibodies into a third group may be reconsidered. DRB1*04:01 positivity has been identified in association with a favorable clinical outcome. (Hepatology 2015;62:1524-1535)
C1 [Kirstein, Martha M.; Metzler, Frauke; Geiger, Elena; Heinrich, Eyk; Manns, Michael P.; Vogel, Arndt] Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, D-30625 Hannover, Germany.
[Hallensleben, Michael] Hannover Med Sch, Inst Transfus Med, D-30625 Hannover, Germany.
C3 Hannover Medical School; Hannover Medical School
RP Vogel, A (corresponding author), Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Carl Neuberg Str 1, D-30625 Hannover, Germany.
EM vogel.arndt@mh-hannover.de
RI Vogel, Arndt/A-8437-2012; Manns, Michael/AFG-3063-2022
OI Vogel, Arndt/0000-0003-0560-5538
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NR 65
TC 105
Z9 108
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD NOV
PY 2015
VL 62
IS 5
BP 1524
EP 1535
DI 10.1002/hep.27983
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CU1EZ
UT WOS:000363264100021
PM 26178791
DA 2025-01-07
ER
PT J
AU Chakkera, HA
Kudva, Y
Kaplan, B
AF Chakkera, H. A.
Kudva, Y.
Kaplan, B.
TI Calcineurin Inhibitors: Pharmacologic Mechanisms Impacting Both Insulin
Resistance and Insulin Secretion Leading to Glucose Dysregulation and
Diabetes Mellitus
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
ID ENDOTHELIAL GROWTH-FACTOR; TYROSINE KINASE INHIBITORS; SINGLE NUCLEOTIDE
POLYMORPHISMS; BREAST-CANCER; CARDIOVASCULAR-DISEASE; GENETIC
POLYMORPHISMS; CARDIO-ONCOLOGY; POTENTIAL ROLE; SUNITINIB;
CARDIOTOXICITY
AB Calcineurin inhibitors (CNIs), including tacrolimus and cyclosporine, are immune-modulating agents used in autoimmune disorders, glomerulonephritides, and after transplantation. CNIs are implicated as diabetogenic drugs but the mechanism is not clearly elucidated. Calcineurin is a cytosolic-phosphatase critical for T-lymphocyte activation. Calcineurin is widely distributed in different tissues responsible for glucose-regulation including pancreas, liver, skeletal muscle, adipocytes, brain, and gut. We describe the pharmacologic effects of CNIs in different tissues and impact on glucose regulation.
C1 [Chakkera, H. A.; Kaplan, B.] Mayo Clin, Div Transplantat, Phoenix, AZ USA.
[Kudva, Y.] Mayo Clin, Div Endocrinol, Rochester, MN USA.
C3 Mayo Clinic; Mayo Clinic Phoenix; Mayo Clinic
RP Chakkera, HA (corresponding author), Mayo Clin, Div Transplantat, Phoenix, AZ USA.
EM chakkera.harini@mayo.edu
OI Chakkera, Harini/0000-0002-9456-0863
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NR 73
TC 76
Z9 86
U1 0
U2 19
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9236
EI 1532-6535
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD JAN
PY 2017
VL 101
IS 1
BP 114
EP 120
DI 10.1002/cpt.546
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EH7BI
UT WOS:000391927400023
PM 27804122
DA 2025-01-07
ER
PT J
AU Lasagna, A
Sacchi, P
AF Lasagna, Angioletta
Sacchi, Paolo
TI The ABC of Immune-Mediated Hepatitis during Immunotherapy in Patients
with Cancer: From Pathogenesis to Multidisciplinary Management
SO CANCERS
LA English
DT Review
DE hepatitis; immune checkpoint inhibitors; immune-related adverse events
(irAEs); CD8+T cells; NAFLD; drug-induced liver injury (DILI);
anti-CTLA4 antibodies; anti-PD-1; anti-PD-L1; viral hepatitis
ID CD8(+) T-CELLS; ADVERSE EVENTS; CHECKPOINT INHIBITORS; AUTOIMMUNE
HEPATITIS; CLINICAL-TRIAL; ACTIVATION; ANTI-CTLA-4; TOXICITIES;
NIVOLUMAB; ANTI-PD-1
AB Simple Summary Immune-mediated hepatotoxicity (IMH) is a not-so-rare complication of immune checkpoint inhibitors (ICIs) and it is extremely heterogeneous in its clinical presentation and severity. This narrative review aims to report the current knowledge on hepatic immune-related adverse events (irAEs) during immunotherapy from pathogenesis to multidisciplinary management.Abstract Immune-mediated hepatotoxicity (IMH) is not-so-rare complication during treatment with immune checkpoint inhibitors (ICIs). This narrative review aims to report the current knowledge on hepatic immune-related adverse events (irAEs) during immunotherapy from pathogenesis to multidisciplinary management. The majority of cases of IMH are asymptomatic and only a few patients may have clinical conditions. The severity of IMH is usually stratified according to Common Terminology for Clinical Adverse Events (CTCAE) criteria, but these scores may overestimate the clinical severity of IMH compared to the Drug-Induced Liver Injury Network (DILIN) scale. The differential diagnosis of IMH is challenging because the elevated liver enzymes can be due to a number of etiologies such as viral infection, autoimmune and metabolic diseases, liver metastases, biliary diseases, and other drugs. The cornerstones of IMH management are represented by withholding or delaying ICI administration and starting immunosuppressive therapy. A multidisciplinary team, including oncologists, hepatologists, internists, and emergency medicine physicians, is essential for the management of IMH.
C1 [Lasagna, Angioletta] Fdn IRCCS Policlin San Matteo, Med Oncol Unit, I-27100 Pavia, Italy.
[Sacchi, Paolo] Fdn IRCCS Policlin San Matteo, Div Infect Dis 1, I-27100 Pavia, Italy.
C3 IRCCS Fondazione San Matteo; IRCCS Fondazione San Matteo
RP Lasagna, A (corresponding author), Fdn IRCCS Policlin San Matteo, Med Oncol Unit, I-27100 Pavia, Italy.
EM a.lasagna@smatteo.pv.it; p.sacchi@smatteo.pv.it
RI Lasagna, Angioletta/AAO-2405-2021
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NR 82
TC 1
Z9 2
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2024
VL 16
IS 4
AR 795
DI 10.3390/cancers16040795
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IZ0L5
UT WOS:001170043900001
PM 38398187
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Zewde, M
Kiyotani, K
Park, JH
Fang, H
Yap, KL
Yew, PY
Alachkar, H
Kato, T
Mai, TH
Ikeda, Y
Matsuda, T
Liu, X
Ren, LL
Deng, B
Harada, M
Nakamura, Y
AF Zewde, Makda
Kiyotani, Kazuma
Park, Jae-Hyun
Fang, Hua
Yap, Kai Lee
Yew, Poh Yin
Alachkar, Houda
Kato, Taigo
Mai, Tu H.
Ikeda, Yuji
Matsuda, Tatsuo
Liu, Xiao
Ren, Lili
Deng, Boya
Harada, Makiko
Nakamura, Yusuke
TI The era of immunogenomics/immunopharmacogenomics
SO JOURNAL OF HUMAN GENETICS
LA English
DT Review
ID CELL-RECEPTOR REPERTOIRE; REGULATORY T-CELLS; GRAFT FAILURE; PD-1
BLOCKADE; FOOD ALLERGY; SOLID TUMORS; BETA-CHAIN; TCR-ALPHA; SURVIVAL;
THERAPY
AB Although germline alterations and somatic mutations in disease cells have been extensively analyzed, molecular changes in immune cells associated with disease conditions have not been characterized in depth. It is clear that our immune system has a critical role in various biological and pathological conditions, such as infectious diseases, autoimmune diseases, drug-induced skin and liver toxicity, food allergy, and rejection of transplanted organs. The recent development of cancer immunotherapies, particularly drugs modulating the immune checkpoint molecules, has clearly demonstrated the importance of host immune cells in cancer treatments. However, the molecular mechanisms by which these new therapies kill tumor cells are still not fully understood. In this regard, we have begun to explore the role of newly developed tools such as next-generation sequencing in the genetic characterization of both cancer cells and host immune cells, a field that is called immunogenomics/immunopharmacogenomics. This new field has enormous potential to help us better understand changes in our immune system during the course of various disease conditions. Here we report the potential of deep sequencing of T-cell and B-cell receptors in capturing the molecular contribution of the immune system, which we believe plays critical roles in the pathogenesis of various human diseases.
C1 [Zewde, Makda; Kiyotani, Kazuma; Park, Jae-Hyun; Fang, Hua; Yap, Kai Lee; Yew, Poh Yin; Alachkar, Houda; Kato, Taigo; Mai, Tu H.; Ikeda, Yuji; Matsuda, Tatsuo; Liu, Xiao; Ren, Lili; Deng, Boya; Harada, Makiko; Nakamura, Yusuke] Univ Chicago, Dept Med, Sect Hematol Oncol, Chicago, IL 60637 USA.
[Kiyotani, Kazuma] Japanese Fdn Canc Res, Canc Precis Med Ctr, Tokyo 1358550, Japan.
C3 University of Chicago; Japanese Foundation for Cancer Research
RP Nakamura, Y (corresponding author), Univ Chicago, Dept Med, Sect Hematol Oncol, Chicago, IL 60637 USA.
EM ynakamura@bsd.uchicago.edu
RI Yap, Kai Lee/JZD-4170-2024; ikeda, yuji/AAH-1095-2020; Kiyotani,
Kazuma/E-3206-2010; Alachkar, Houda/A-6017-2019
OI Yap, Kai Lee/0000-0003-4496-5464; Zewde, Makda
Getachew/0000-0001-6710-630X; Alachkar, Houda/0000-0001-5567-5521
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NR 90
TC 9
Z9 9
U1 0
U2 6
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1434-5161
EI 1435-232X
J9 J HUM GENET
JI J. Hum. Genet.
PD JUL
PY 2018
VL 63
IS 8
BP 865
EP 875
DI 10.1038/s10038-018-0468-1
PG 11
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA GO1QN
UT WOS:000439729100003
PM 29785006
OA Bronze
DA 2025-01-07
ER
PT J
AU Calado, RT
Regal, JA
Kleiner, DE
Schrump, DS
Peterson, NR
Pons, V
Chanock, SJ
Lansdorp, PM
Young, NS
AF Calado, Rodrigo T.
Regal, Joshua A.
Kleiner, David E.
Schrump, David S.
Peterson, Nathan R.
Pons, Veronica
Chanock, Stephen J.
Lansdorp, Peter M.
Young, Neal S.
TI A Spectrum of Severe Familial Liver Disorders Associate with Telomerase
Mutations
SO PLOS ONE
LA English
DT Article
ID IDIOPATHIC PULMONARY-FIBROSIS; NODULAR REGENERATIVE HYPERPLASIA;
DOMINANT DYSKERATOSIS-CONGENITA; APLASTIC-ANEMIA; REVERSE-TRANSCRIPTASE;
CANCER; GENE; RNA; VARIANTS; 5P15.33
AB Background: Telomerase is an enzyme specialized in maintaining telomere lengths in highly proliferative cells. Loss-of-function mutations cause critical telomere shortening and are associated with the bone marrow failure syndromes dyskeratosis congenita and aplastic anemia and with idiopathic pulmonary fibrosis. Here, we sought to determine the spectrum of clinical manifestations associated with telomerase loss-of-function mutations.
Methodology/Principal Findings: Sixty-nine individuals from five unrelated families with a variety of hematologic, hepatic, and autoimmune disorders were screened for telomerase complex gene mutations; leukocyte telomere length was measured by flow fluorescence in situ hybridization in mutation carriers and some non-carriers; the effects of the identified mutations on telomerase activity were determined; and genetic and clinical data were correlated. In six generations of a large family, a loss-of-function mutation in the telomerase enzyme gene TERT associated with severe telomere shortening and a range of hematologic manifestations, from macrocytosis to acute myeloid leukemia, with severe liver diseases marked by fibrosis and inflammation, and one case of idiopathic pulmonary fibrosis but not with autoimmune disorders. Additionally, we identified four unrelated families in which loss-of-function TERC or TERT gene mutations tracked with marrow failure, pulmonary fibrosis, and a spectrum of liver disorders.
Conclusions/Significance: These results indicate that heterozygous telomerase loss-of-function mutations associate with but are not determinant of a large spectrum of hematologic and liver abnormalities, with the latter sometimes occurring in the absence of marrow failure. Our findings, along with the link between pulmonary fibrosis and telomerase mutations, also suggest a common pathogenic mechanism for fibrotic diseases in which defective telomere repair plays important role.
RP Calado, RT (corresponding author), NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
EM calador@nhlbi.nih.gov
RI Chanock, Stephen/AGL-9345-2022; Kleiner, David/N-2770-2013; Calado,
Rodrigo/G-2619-2011
OI Kleiner, David/0000-0003-3442-4453; Calado, Rodrigo/0000-0002-7966-6029
FU Canadian Institutes of Health Research [MOP38075, GMH79042] Funding
Source: Medline; Intramural NIH HHS Funding Source: Medline
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NR 36
TC 185
Z9 195
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 20
PY 2009
VL 4
IS 11
AR e7926
DI 10.1371/journal.pone.0007926
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 522NL
UT WOS:000272004800008
PM 19936245
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Liu, T
Liu, X
Li, WH
AF Liu, Ting
Liu, Xin
Li, Wenhua
TI Tetrandrine, a Chinese plant-derived alkaloid, is a potential candidate
for cancer chemotherapy
SO ONCOTARGET
LA English
DT Review
DE tetrandrine; natural product; cancer; chemotherapy
ID CELL-CYCLE ARREST; JUN NH2-TERMINAL KINASE; SUPPRESSES TUMOR-GROWTH;
ARSENIC TRIOXIDE AS2O3; MULTIDRUG-RESISTANCE; P-GLYCOPROTEIN; IN-VITRO;
BISBENZYLISOQUINOLINE ALKALOIDS; CARCINOMA-CELLS;
HEPATOCELLULAR-CARCINOMA
AB Cancer is a disease caused by the abnormal proliferation and differentiation of cells governed by tumorigenic factors. Chemotherapy is one of the major cancer treatment strategies, and it functions by targeting the physiological capabilities of cancer cells, including sustained proliferation and angiogenesis, the evasion of programmed cell death, tissue invasion and metastasis. Remarkably, natural products have garnered increased attention in the chemotherapy drug discovery field because they are biologically friendly and have high therapeutic effects. Tetrandrine, isolated from the root of Stephania tetrandra S Moore, is a traditional Chinese clinical agent for silicosis, autoimmune disorders, inflammatory pulmonary diseases, cardiovascular diseases and hypertension. Recently, the novel anti-tumor effects of tetrandrine have been widely investigated. More impressive is that tetrandrine affects multiple biological activities of cancer cells, including the inhibition of proliferation, angiogenesis, migration, and invasion; the induction of apoptosis and autophagy; the reversal of multidrug resistance (MDR); and the enhancement of radiation sensitization. This review focuses on introducing the latest information about the anti-tumor effects of tetrandrine on various cancers and its underlying mechanism. Moreover, we discuss the nanoparticle delivery system being developed for tetrandrine and the anti-tumor effects of other bisbenzylisoquinoline alkaloid derivatives on cancer cells. All current evidence demonstrates that tetrandrine is a promising candidate as a cancer chemotherapeutic.
C1 [Liu, Ting; Li, Wenhua] Wuhan Univ, Coll Life Sci, Wuhan 430072, Peoples R China.
[Liu, Xin] Wuhan Univ, Minist Educ, Coll Pharm, Lab Combinatorial Biosynth & Drug Discovery, Wuhan 430072, Peoples R China.
C3 Wuhan University; Wuhan University
RP Li, WH (corresponding author), Wuhan Univ, Coll Life Sci, Wuhan 430072, Peoples R China.
EM whli@whu.edu.cn
FU National Basic Research Program of China [2014CB910600]; National
Natural Science Foundation of China [81273540, 81472684, 31400155];
Program for New Century Excellent Talents in University of Ministry of
Education of China [NCET-13-0436]; Fundamental Research Funds for the
Central Universities [2042014kf0236]
FX This study was supported by the National Basic Research Program of China
(2014CB910600), the National Natural Science Foundation of China
(81273540, 81472684 and 31400155), the Program for New Century Excellent
Talents in University of Ministry of Education of China (NCET-13-0436),
and Fundamental Research Funds for the Central Universities
(2042014kf0236).
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NR 134
TC 133
Z9 139
U1 1
U2 66
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JUN 28
PY 2016
VL 7
IS 26
BP 40800
EP 40815
DI 10.18632/oncotarget.8315
PG 16
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DP6NV
UT WOS:000378614700140
PM 27027348
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Bei, R
Masuelli, L
Trono, P
Orvietani, PL
Losito, S
Marzocchella, L
Vitolo, D
Albonici, L
Mrozek, MA
Di Gennaro, E
Lista, F
Faggioni, G
Ionna, F
Binaglia, L
Manzari, V
Budillon, A
Modesti, A
AF Bei, Roberto
Masuelli, Laura
Trono, Paola
Orvietani, Pier Luigi
Losito, Simona
Marzocchella, Laura
Vitolo, Domenico
Albonici, Loredana
Mrozek, Marie-Agnes
Di Gennaro, Elena
Lista, Florigio
Faggioni, Giovanni
Ionna, Franco
Binaglia, Luciano
Manzari, Vittorio
Budillon, Alfredo
Modesti, Andrea
TI The ribosomal PO protein induces a spontaneous immune response in
patients with head and neck advanced stage carcinoma that is not
dependent on its overexpression in carcinomas
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE immune response; cancer patients; tumor associated; antigens; ribosomal
P0 protein; head and neck
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; MULTIPLE ERBB RECEPTORS; SQUAMOUS-CELL
CARCINOMA; ORAL-CANCER; HEPATOCELLULAR-CARCINOMA; STRATIFIED EPITHELIUM;
EXTRACELLULAR-MATRIX; AUTOIMMUNE-RESPONSE; INDUCED APOPTOSIS;
COLON-CARCINOMA
AB A typical feature in systemic lupus erythemathosus patients is the presence of autoantibodies to the carboxyl-terminal homologous P proteins (P0, P1, P2) domain (C-22 PO epitope). In this report we provide evidence for the in vivo immunogenicity of the PO protein in head and neck cancer patients as well as overexpression by immunohistochemistry of the C-22 PO epitope in invasive carcinomas (55/57). Overexpression of this epitope was also significantly associated with a number of pathological lesions arising in the head and neck stratified epithelium including acanthosis (8/8), benign tumors (11/11), dysplasia (23/25) and in situ carcinomas (9/9). Intermediate cell layer restricted epitope overexpression was observed in well differentiated carcinomas, while undifferentiated tumors showed overexpression throughout the cell layers. Employing recombinant P proteins, sera from 40 of the 57 carcinoma patients and 39 normal donors, were subjected to immunoblot analysis. Immunity to PO protein (7/40) was associated with malignancy and with advanced disease stage, but it was not dependent on the C-22 PO epitope overexpression, although it was the preferential autoantibody target in 4 patients. Increased expression of the C-22 PO epitope on the surface of pharynx cancer cells following cellular stress in vitro, may imply PO protein presentation as an in vivo autoantibody target in cancer patients. Evidence for immunity to the PO protein, as well as overexpression in patients with head and neck carcinoma may be relevant for monitoring cancer progression, in planning immunotherapeutic strategies, and contribute to the understanding of immuno-biological behaviour of head and neck carcinomas.
C1 Univ Roma Tor Vergata, Dept Expt Med & Biochem Sci, I-00133 Rome, Italy.
Univ Roma La Sapienza, Dept Expt Med, Rome, Italy.
Univ Perugia, Dept Internal Med, I-06100 Perugia, Italy.
Ist Nazl Tumori, Expt & Med Oncol, Naples, Italy.
Ctr Studi Ricerche Sanita Veterinaria Esercito, Rome, Italy.
C3 University of Rome Tor Vergata; Sapienza University Rome; University of
Perugia
RP Bei, R (corresponding author), Univ Roma Tor Vergata, Dept Expt Med & Biochem Sci, Via Montpellier 1, I-00133 Rome, Italy.
EM bei@med.uniroma2.it
RI Budillon, Alfredo/K-4763-2016; Masuelli, Laura/AGW-4259-2022;
Di+Gennaro, Elena/ABG-1579-2021; lista, florigio/IQU-3776-2023; Trono,
Paola/ABB-5921-2021; Bei, Roberto/W-8023-2019; ionna,
Franco/K-4564-2016; Losito, Nunzia/Y-6339-2018
OI ionna, Franco/0000-0002-0512-274X; Di Gennaro,
Elena/0000-0001-6223-7845; lista, florigio/0000-0001-5700-4772; Trono,
Paola/0000-0002-2053-6334; Budillon, Alfredo/0000-0002-6330-6053;
Losito, Nunzia/0000-0001-9045-0328; MASUELLI, Laura/0000-0001-8174-8034
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NR 48
TC 16
Z9 18
U1 0
U2 2
PU PROFESSOR D A SPANDIDOS
PI ATHENS
PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE
SN 1019-6439
J9 INT J ONCOL
JI Int. J. Oncol.
PD DEC
PY 2007
VL 31
IS 6
BP 1301
EP 1308
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 236ZG
UT WOS:000251341700004
PM 17982655
DA 2025-01-07
ER
PT J
AU Wang, LN
Sun, P
Wu, YZ
Wang, L
AF Wang, Lina
Sun, Ping
Wu, Yuzhang
Wang, Li
TI Metabolic tissue-resident CD8+T cells: A key player in
obesity-related diseases
SO OBESITY REVIEWS
LA English
DT Article
DE CD8(+)T cell; low-grade chronic inflammation; obesity; obesity-related
diseases
ID INDUCED INSULIN-RESISTANCE; BLOOD LYMPHOCYTE SUBSETS; DIET-INDUCED
OBESITY; ADIPOSE-TISSUE; T-CELL; SUPPRESSOR-CELLS; MACROPHAGE
INFILTRATION; NONALCOHOLIC STEATOHEPATITIS; BARIATRIC SURGERY;
WEIGHT-LOSS
AB Obesity-induced low-grade chronic inflammation in the metabolic tissues, such as adipose tissue (AT) and liver tissue, in individuals with obesity is a major etiological factor for several diseases, such as insulin resistance, type 2 diabetes, fatty liver disease, atherosclerosis and cardiovascular problems, as well as cancer and autoimmune diseases. Previous studies have revealed that tissue-resident macrophages play a crucial role in this process. However, the mechanisms responsible for recruiting and activating macrophages and initiating chronic inflammation in the metabolic tissues have not yet been clearly elucidated. In the most recent decade, there has been a growing emphasis on the critical role of the adaptive CD8(+)T cells in obesity-induced chronic inflammation and related metabolic diseases. In this review, we will summarize the relevant studies in both mice and human regarding the role of metabolic tissue-resident CD8(+)T cells in obesity-related inflammation and diseases, as well as the possible mechanisms underlying the regulation of CD8(+)T cell recruitment, activation and function in the metabolic tissues, and discuss their potential as therapeutic targets for obesity-related diseases.
C1 [Wang, Lina; Wu, Yuzhang; Wang, Li] Third Mil Med Univ, Army Med Univ, Inst Immunol PLA, Chongqing 400038, Peoples R China.
[Wang, Lina; Sun, Ping] Weifang Med Univ, Dept Immunol, Weifang, Peoples R China.
C3 Army Medical University; Shandong Second Medical University
RP Wu, YZ; Wang, L (corresponding author), Third Mil Med Univ, Army Med Univ, Inst Immunol PLA, Chongqing 400038, Peoples R China.
EM wuyuzhang@tmmu.edu.cn; liwang118@tmmu.edu.cn
RI yang, zhiqi/GZL-3610-2022
OI Wu, Yuzhang/0000-0002-4049-0214
FU National Natural Science Foundation of China [31570931, 81871301];
National Key Project for Research AMP; Development of China
[2016YFA0502204]
FX National Natural Science Foundation of China, Grant/Award Numbers:
31570931, 81871301; National Key Project for Research & Development of
China, Grant/Award Number: 2016YFA0502204
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NR 98
TC 19
Z9 20
U1 4
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1467-7881
EI 1467-789X
J9 OBES REV
JI Obes. Rev.
PD MAR
PY 2021
VL 22
IS 3
DI 10.1111/obr.13133
EA SEP 2020
PG 10
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA QG6GI
UT WOS:000569268500001
PM 32935464
DA 2025-01-07
ER
PT J
AU Baig, S
Alamgir, M
AF Baig, Saeeda
Alamgir, Mohiuddin
TI The extrahepatic manifestations of hepatitis B virus
SO JCPSP-JOURNAL OF THE COLLEGE OF PHYSICIANS AND SURGEONS PAKISTAN
LA English
DT Review
DE hepatitis B virus; acute; chronic; autoimmunity; immunization;
extrahepatic
ID CHRONIC LIVER-DISEASE; ANTI-HBE STATUS; SURFACE-ANTIGEN; MEMBRANOUS
NEPHROPATHY; VIRAL-HEPATITIS; POLYARTERITIS-NODOSA; IMMUNE-COMPLEXES;
HBSAG SUBTYPES; POSITIVE HEPATITIS; TRANSGENIC MICE
AB Hepatitis B Virus (HBV) leads to a number of hepatic complications, from acute to chronic hepatitis, cirrhosis and hepatocellular carcinoma, is a well-established fact. Upcoming clinical research, over the years, associates numerous extrahepatic manifestations during the acute and chronic episodes of hepatitis B with significant morbidity and mortality. A causal relationship between HBV and serious autoimmune disorders has also been observed among certain susceptible vaccine recipients in a defined temporal period following immunization. The cause of these extrahepatic manifestations is generally believed to be immune mediated. The most commonly described include skin rash, arthritis, arthralgia, glomerulonephritis, polyarteritis nodosa, and papular acrodermatitis etc. The serum-sickness like "arthritis-dermatitis" prodrome has also been observed in approximately one-third of patients acquiring HBV infections. Skin manifestations of HBV infection typically present as palpable purpura reported to be caused by chronic HBV, although this association remains controversial. To consider the relationship between HBV and other clinically significant disorders as well as serious autoimmune disorders among certain vaccine recipients is the topic of this review. Variable factors that influence extrahepatic manifestation are discussed, including possible synergy between hepatitis B virus and the immune system.
C1 [Baig, Saeeda] Ziauddin Univ Hosp, Dept Biochem, DHA, Karachi, Pakistan.
[Alamgir, Mohiuddin] Ziauddin Univ Hosp, Dept Pathol, Karachi, Pakistan.
C3 Ziauddin University
RP Baig, S (corresponding author), Ziauddin Univ Hosp, Dept Biochem, DHA, 27A-4 3rd Golf Course Rd,Phase 4, Karachi, Pakistan.
EM baigsaeeda@yahoo.com
RI Baig, Saeeda/KFA-8981-2024
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NR 65
TC 29
Z9 31
U1 0
U2 0
PU COLL PHYSICIANS & SURGEONS PAKISTAN
PI KARACHI
PA SEVENTH CENTRAL ST, DEFENCE HOUSING AUTHORITY, KARACHI, 75500, PAKISTAN
SN 1022-386X
EI 1681-7168
J9 JCPSP-J COLL PHYSICI
JI JCPSP-J. Coll. Physicians Surg.
PD JUL
PY 2008
VL 18
IS 7
BP 451
EP 457
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 342CP
UT WOS:000258762500016
PM 18760074
DA 2025-01-07
ER
PT J
AU Yoshizawa, K
Matsumoto, A
Ichijo, T
Umemura, T
Joshita, S
Komatsu, M
Tanaka, N
Tanaka, E
Ota, M
Katsuyama, Y
Kiyosawa, K
Abe, M
Onji, M
AF Yoshizawa, Kaname
Matsumoto, Akihiro
Ichijo, Tetsuya
Umemura, Takeji
Joshita, Satoru
Komatsu, Michiharu
Tanaka, Naoki
Tanaka, Eiji
Ota, Masao
Katsuyama, Yoshihiko
Kiyosawa, Kendo
Abe, Masanori
Onji, Morikazu
TI Long-term outcome of Japanese patients with type 1 autoimmune hepatitis
SO HEPATOLOGY
LA English
DT Article
ID CHRONIC ACTIVE HEPATITIS; HEPATOCELLULAR-CARCINOMA; TREATMENT
WITHDRAWAL; LIVER-DISEASE; RISK-FACTORS; PROGNOSIS; REMISSION;
SUSCEPTIBILITY; ASSOCIATION; EXPERIENCE
AB The long-term outcome of patients with autoimmune hepatitis (AIH) in Japan has not been well-defined. The aim of this study was to clarify the outcome of this disease over a long follow-up period compared with that of the general Japanese population as well as that among patients. A total of 203 AIH patients were enrolled for a mean follow-up period of 131 months. All patients were treated with corticosteroids with or without azathioprine. The overall survival of AIH patients was similar to that of the general population in Japan. The prognosis of AIH subgroups divided according to disease severity, sex, incidence of relapse, liver histology, presence of cirrhosis, probable or definite AIH score, antibody to hepatitis B core antigen antibody positivity, or human leukocyte antigen DR4positivity did not differ greatly among patients. However, the prognosis of patients experiencing two or more relapses was significantly poorer than that of patients with remission or a single relapse both in univariate (P < 0.001) and multivariate (P = 0.020) analyses. The development of liver malignancy was also a possibility among AIH patients with multiple relapses. Severe adverse effects of corticosteroids were rare, even in patients who underwent long-term treatment. Conclusion: Repeated relapses of AIH are significantly associated with a poorer long-term prognosis in Japan. AIH patients can expect a similar prognosis to that of the general population, provided they are adequately managed with continuous low doses of immunosuppressive therapy, especially after the first relapse. (HEPATOLOGY 2012)
C1 [Yoshizawa, Kaname; Matsumoto, Akihiro; Ichijo, Tetsuya; Umemura, Takeji; Joshita, Satoru; Komatsu, Michiharu; Tanaka, Naoki; Tanaka, Eiji] Shinshu Univ, Dept Med, Sch Med, Matsumoto, Nagano 3908621, Japan.
[Ota, Masao] Shinshu Univ, Dept Legal Med, Sch Med, Matsumoto, Nagano 3908621, Japan.
[Katsuyama, Yoshihiko] Shinshu Univ, Dept Pharm, Sch Med, Matsumoto, Nagano 3908621, Japan.
[Yoshizawa, Kaname] Shinshu Ueda Med Ctr, Dept Gastroenterol, Natl Hosp Org, Ueda, Nagano, Japan.
[Kiyosawa, Kendo] Nagano Red Cross Hosp, Nagano, Japan.
[Abe, Masanori; Onji, Morikazu] Ehime Univ, Dept Gastroenterol & Metabol, Grad Sch Med, Matsuyama, Ehime 790, Japan.
C3 Shinshu University; Shinshu University; Shinshu University; Nagano Red
Cross Hospital; Ehime University
RP Yoshizawa, K (corresponding author), Shinshu Univ, Dept Med, Sch Med, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan.
EM kanamey@shinshu-u.ac.jp
RI Joshita, Satoru/K-5679-2019
OI Tanaka, Naoki/0000-0002-3212-3836; Ota, Masao/0000-0002-6400-5658
FU Japanese Ministry of Health, Labor, and Welfare; Japanese Ministry of
Education, Culture, and Technology [22590725]; Grants-in-Aid for
Scientific Research [22133002, 22590725] Funding Source: KAKEN
FX Supported in part by research grants from the Japanese Ministry of
Health, Labor, and Welfare and the Japanese Ministry of Education,
Culture, and Technology (grant no. 22590725).
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NR 36
TC 85
Z9 88
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD AUG
PY 2012
VL 56
IS 2
BP 668
EP 676
DI 10.1002/hep.25658
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 979GF
UT WOS:000306804500030
PM 22334246
DA 2025-01-07
ER
PT J
AU Shang, J
Zha, HR
Sun, YF
AF Shang, Jin
Zha, Haoran
Sun, Yufa
TI Phenotypes, Functions, and Clinical Relevance of Regulatory B Cells in
Cancer
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE regulatory B cell; tumor immunology; tumor microenvironment; cancer
progression; immunotherapy
ID CD4(+) T-CELLS; IMMUNE-RESPONSE INVIVO; HEPATOCELLULAR-CARCINOMA;
SUPPRESSOR-CELLS; DELAYED-HYPERSENSITIVITY; FEEDBACK SUPPRESSION;
AUTOIMMUNE; EXPRESSION; IL-10; BETA
AB In immune system, B cells are classically positive modulators that regulate inflammation and immune responses. Regulatory B cells (Bregs) are a subset of B cells which play crucial roles in various conditions, including infection, allergies, autoimmune diseases, transplantation, and tumors. Until now, unequivocal surface markers for Bregs still lack consensus, although numerous Breg subsets have been identified. Generally, Bregs exert their immunoregulatory functions mainly through cytokine secretion and intercellular contact. In the tumor microenvironment, Bregs suppress effector T cells, induce regulatory T cells and target other tumor-infiltrating immune cells, such as myeloid-derived suppressor cells, natural killer cells and macrophages, to hamper anti-tumor immunity. Meanwhile, the cross-regulations between Bregs and tumor cells often result in tumor escape from immunosurveillance. In addition, accumulating evidence suggests that Bregs are closely associated with many clinicopathological factors of cancer patients and might be potential biomarkers for accessing patient survival. Thus, Bregs are potential therapeutic targets for future immunotherapy in cancer patients. In this review, we will discuss the phenotypes, functions, and clinical relevance of Bregs in cancer.
C1 [Shang, Jin; Sun, Yufa] Cent Mil Commiss PLA, Joint Staff Dept, Guard Bur, Dept Hlth Serv, Beijing, Peoples R China.
[Zha, Haoran] PLA Rocket Force Characterist Med Ctr, Dept Oncol, Beijing, Peoples R China.
RP Sun, YF (corresponding author), Cent Mil Commiss PLA, Joint Staff Dept, Guard Bur, Dept Hlth Serv, Beijing, Peoples R China.
EM dafa20136725@163.com
OI Zha, Haoran/0000-0002-1362-2496
FU National Natural Science Foundation of China [31900627]
FX This work was supported by the National Natural Science Foundation of
China under Grant [number 31900627].
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NR 100
TC 52
Z9 57
U1 2
U2 19
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD OCT 22
PY 2020
VL 11
AR 582657
DI 10.3389/fimmu.2020.582657
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA OL2RD
UT WOS:000585188500001
PM 33193391
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Sandoval-Castellanos, AM
Bhargava, A
Zhao, M
Xu, J
Ning, K
AF Sandoval-Castellanos, Ana M.
Bhargava, Anushka
Zhao, Min
Xu, Jun
Ning, Ke
TI Serine and arginine rich splicing factor 1: a potential target for
neuroprotection and other diseases
SO NEURAL REGENERATION RESEARCH
LA English
DT Review
DE alternative splicing; autoimmune disorders; cancer; hypertension; mRNA;
neuroprotection;; plicing factors;; RSF1
ID HEPATOCELLULAR-CARCINOMA; FACTOR SRSF1; RNA; PROLIFERATION; MECHANISM;
EXPRESSION; PROMOTES; INVASION; CANCER
AB Alternative splicing is the process of producing variably spliced mRNAs by choosing distinct combinations of splice sites within a messenger RNA precursor. This splicing enables mRNA from a single gene to synthesize different proteins, which have different cellular properties and functions and yet arise from the same single gene. A family of splicing factors, Serine-arginine rich proteins, are needed to initiate the assembly and activation of the spliceosome. Serine and arginine rich splicing factor 1, part of the arginine/serine-rich splicing factor protein family, can either activate or inhibit the splicing of mRNAs, depending on the phosphorylation status of the protein and its interaction partners. Considering that serine and arginine rich splicing factor 1 is either an activator or an inhibitor, this protein has been studied widely to identify its various roles in different diseases. Research has found that serine and arginine rich splicing factor 1 is a key target for neuroprotection, showing its promising potential use in therapeutics for neurodegenerative disorders. Furthermore, serine and arginine rich splicing factor 1 might be used to regulate cancer development and autoimmune diseases. In this review, we highlight how serine and arginine rich splicing factor 1 has been studied concerning neuroprotection. In addition, we draw attention to how serine and arginine rich splicing factor 1 is being studied in cancer and immunological disorders, as well as how serine and arginine rich splicing factor 1 acts outside the central or peripheral nervous system.
C1 [Sandoval-Castellanos, Ana M.; Bhargava, Anushka; Ning, Ke] Univ Sheffield, Sheffield Inst Translat Neurosci, SITraN, Sheffield, England.
[Sandoval-Castellanos, Ana M.; Zhao, Min] Univ Calif Davis, Inst Regenerat Cures, Sch Med, Dept Ophthalmol & Vis Sci, Sacramento, CA USA.
[Sandoval-Castellanos, Ana M.; Zhao, Min] Univ Calif Davis, Inst Regenerat Cures, Sch Med, Dept Dermatol, Sacramento, CA USA.
[Xu, Jun; Ning, Ke] Tongji Univ, Sch Med, East Hosp, Shanghai, Peoples R China.
C3 University of Sheffield; University of California System; University of
California Davis; University of California System; University of
California Davis; Tongji University
RP Ning, K (corresponding author), Univ Sheffield, Sheffield Inst Translat Neurosci, SITraN, Sheffield, England.; Ning, K (corresponding author), Tongji Univ, Sch Med, East Hosp, Shanghai, Peoples R China.
EM k.ning@sheffield.ac.uk
RI Zhao, Min/JGM-3156-2023; Ning, Ke/E-7837-2010
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NR 66
TC 5
Z9 6
U1 3
U2 20
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S NO 1498A-2
VILLAGE MAROL, ANDHERI EAST, MUMBAI, Maharashtra, INDIA
SN 1673-5374
EI 1876-7958
J9 NEURAL REGEN RES
JI Neural Regen. Res.
PD JUL
PY 2023
VL 18
IS 7
BP 1411
EP 1416
DI 10.4103/1673-5374.360243
PG 6
WC Cell Biology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Neurosciences & Neurology
GA 9C8CU
UT WOS:000935639600003
PM 36571335
OA gold, Green Submitted, Green Published, Green Accepted
DA 2025-01-07
ER
PT J
AU Yang, SH
Li, L
Xie, YQ
Yao, Y
Gao, CY
Liao, LH
Ma, HD
Gershwin, ME
Lian, ZX
AF Yang, Shu-Han
Li, Liang
Xie, Yu-Qing
Yao, Yuan
Gao, Cai-Yue
Liao, Liang-Huan
Ma, Hong-Di
Gershwin, M. Eric
Lian, Zhe-Xiong
TI IFN-γ-STAT1-iNOS Induces Myeloid Progenitors to Acquire
Immunosuppressive Activity
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE immunosuppression; autoimmune disease; myeloid progenitors; T cells;
bone marrow; IFN-gamma; STAT1; inducible nitride oxide synthase
ID STEM-CELL NICHE; NITRIC-OXIDE PRODUCTION; HEMATOPOIETIC STEM;
BONE-MARROW; IFN-GAMMA; T-CELLS; SUPPRESSOR-CELLS; CANCER;
DIFFERENTIATION; INFLAMMATION
AB Autoimmune diseases often induce dysregulated hematopoiesis with altered number and function of hematopoietic stem and progenitor cells (HSPCs). However, there are limited studies on the direct regulation of HSPCs on T cells, which are often detrimental to autoimmunity. Here, we found that in a murine model of Concanavalin A-induced autoimmune hepatitis, LSK (Lineage(-)Sca-1(+c)-Kit(+))-like cells accumulated in liver, spleen, and bone marrow (BM), which were myeloid progenitors (Lineage(-)Sca-1(+)c-Kit(+)) that upregulated Sca-1 expression upon T cell-derived IFN-gamma stimulation. Strikingly, BM LS-Klike cells from mice induced by Con A to develop autoimmune hepatitis or alternatively myeloid progenitors from wild-type mice possessed strong in vitro suppressive ability. Their suppressive function depended on T cell-derived IFN-gamma in a paracrine fashion, which induced STAT1 phosphorylation, inducible nitric oxide synthase expression, and nitric oxide production. Blocking IFN-gamma/IFN-gamma. receptor interaction, knockout of STAT1, or iNOS inhibition abrogated their suppressive function. In addition, the suppressive function was independent of differentiation; mitomycin C-treated myeloid progenitors maintained T cell suppressive ability in vitro. Our data demonstrate a mechanism of inflammation induced suppressive function of myeloid progenitors, which may participate directly in suppressing T cell-mediated immunopathology.
C1 [Yang, Shu-Han; Li, Liang; Xie, Yu-Qing; Yao, Yuan; Gao, Cai-Yue; Liao, Liang-Huan; Ma, Hong-Di; Lian, Zhe-Xiong] Univ Sci & Technol China, Inst Immunol, Sch Life Sci, Liver Immunol Lab, Hefei, Anhui, Peoples R China.
[Yang, Shu-Han; Li, Liang; Yao, Yuan; Gao, Cai-Yue; Liao, Liang-Huan; Lian, Zhe-Xiong] South China Univ Technol, Inst Life Sci, Sch Med, Chron Dis Lab, Guangzhou, Guangdong, Peoples R China.
[Gershwin, M. Eric] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Lian, Zhe-Xiong] Hefei Natl Lab Phys Sci Microscale, Innovat Ctr Cell Signaling Network, Hefei, Anhui, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
China, CAS; South China University of Technology; University of
California System; University of California Davis
RP Lian, ZX (corresponding author), Univ Sci & Technol China, Inst Immunol, Sch Life Sci, Liver Immunol Lab, Hefei, Anhui, Peoples R China.; Lian, ZX (corresponding author), South China Univ Technol, Inst Life Sci, Sch Med, Chron Dis Lab, Guangzhou, Guangdong, Peoples R China.; Lian, ZX (corresponding author), Hefei Natl Lab Phys Sci Microscale, Innovat Ctr Cell Signaling Network, Hefei, Anhui, Peoples R China.
EM zxlian1@ustc.edu.cn
RI xie, yuqing/KBB-5708-2024; Yao, Yuan/IST-0028-2023; yang,
shuhan/HOC-9267-2023; Li, Liang/L-7803-2018
OI Xie, Yu-Qing/0000-0003-3996-2234; Yang, Shuhan/0009-0004-1715-0416; Li,
Liang/0000-0003-0745-2571
FU National Natural Science Foundation of China [81430034, 91542123];
National Basic Research Program of China (973 Program) [2013CB944900];
Doctoral Program of Higher Education of China [RFDP 20133402110015]
FX This work was supported by the National Natural Science Foundation of
China (81430034 and 91542123), the National Basic Research Program of
China (973 Program-2013CB944900), and the Doctoral Program of Higher
Education of China (RFDP 20133402110015).
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NR 40
TC 7
Z9 7
U1 0
U2 31
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015,
SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 22
PY 2017
VL 8
AR 1192
DI 10.3389/fimmu.2017.01192
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA FH8EV
UT WOS:000411425500001
PM 29018448
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Gutiérrez-Cuevas, J
Santos, A
Armendariz-Borunda, J
AF Gutierrez-Cuevas, Jorge
Santos, Arturo
Armendariz-Borunda, Juan
TI Pathophysiological Molecular Mechanisms of Obesity: A Link between MAFLD
and NASH with Cardiovascular Diseases
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE obesity; comorbidities of obesity; metabolic dysfunction-associated
fatty liver disease; nonalcoholic steatohepatitis; cardiovascular
diseases; insulin resistance; pharmacological strategies
ID FATTY LIVER-DISEASE; PROLIFERATOR-ACTIVATED RECEPTORS; 4 SOUTHERN
STATES; INSULIN-RESISTANCE; NONALCOHOLIC STEATOHEPATITIS;
ATRIAL-FIBRILLATION; HEPATIC STEATOSIS; RISK-FACTOR; METABOLIC SYNDROME;
ASSOCIATION
AB Obesity is now a worldwide epidemic ensuing an increase in comorbidities' prevalence, such as insulin resistance, type 2 diabetes (T2D), metabolic dysfunction-associated fatty liver disease (MAFLD), nonalcoholic steatohepatitis (NASH), hypertension, cardiovascular disease (CVD), autoimmune diseases, and some cancers, CVD being one of the main causes of death in the world. Several studies provide evidence for an association between MAFLD and atherosclerosis and cardio-metabolic disorders, including CVDs such as coronary heart disease and stroke. Therefore, the combination of MAFLD/NASH is associated with vascular risk and CVD progression, but the underlying mechanisms linking MAFLD/NASH and CVD are still under investigation. Several underlying mechanisms may probably be involved, including hepatic/systemic insulin resistance, atherogenic dyslipidemia, hypertension, as well as pro-atherogenic, pro-coagulant, and pro-inflammatory mediators released from the steatotic/inflamed liver. MAFLD is strongly associated with insulin resistance, which is involved in its pathogenesis and progression to NASH. Insulin resistance is a major cardiovascular risk factor in subjects without diabetes. However, T2D has been considered the most common link between MAFLD/NASH and CVD. This review summarizes the evidence linking obesity with MAFLD, NASH, and CVD, considering the pathophysiological molecular mechanisms involved in these diseases. We also discuss the association of MAFLD and NASH with the development and progression of CVD, including structural and functional cardiac alterations, and pharmacological strategies to treat MAFLD/NASH and cardiovascular prevention.
C1 [Gutierrez-Cuevas, Jorge; Armendariz-Borunda, Juan] Univ Guadalajara, Inst Mol Biol Med & Gene Therapy, Dept Mol Biol & Genom, CUCS, Guadalajara 44340, Jalisco, Mexico.
[Santos, Arturo; Armendariz-Borunda, Juan] Tecnol Monterrey, Sch Med & Hlth Sci, Campus Guadalajara, Zapopan 45201, Jalisco, Mexico.
C3 Universidad de Guadalajara; Tecnologico de Monterrey
RP Gutiérrez-Cuevas, J; Armendariz-Borunda, J (corresponding author), Univ Guadalajara, Inst Mol Biol Med & Gene Therapy, Dept Mol Biol & Genom, CUCS, Guadalajara 44340, Jalisco, Mexico.; Armendariz-Borunda, J (corresponding author), Tecnol Monterrey, Sch Med & Hlth Sci, Campus Guadalajara, Zapopan 45201, Jalisco, Mexico.
EM gutierrezcj05@gmail.com; arturo.santos@itesm.mx; armdbo@gmail.com
RI Santos, Arturo/GQQ-1431-2022; Armendáriz-Borunda, Juan/AAU-1471-2021
OI Gutierrez-Cuevas, Jorge/0000-0003-0276-0428; Armendariz-Borunda,
Juan/0000-0002-7101-9943
FU Fondo de Desarrollo Cientifico de Jalisco (FODECIJAL) [8149-2019,
7941-2019]
FX This work has received funding from the Fondo de Desarrollo Cientifico
de Jalisco (FODECIJAL) project 8149-2019 to J.G.-C., and project
7941-2019 to J.A.-B.
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NR 160
TC 110
Z9 112
U1 8
U2 39
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD NOV
PY 2021
VL 22
IS 21
AR 11629
DI 10.3390/ijms222111629
PG 29
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA XE1BM
UT WOS:000723130800001
PM 34769060
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Liu, GL
Chen, XL
Wang, QQ
Yuan, LW
AF Liu, Ganglei
Chen, Xueliang
Wang, Qianqian
Yuan, Lianwen
TI NEK7: a potential therapy target for NLRP3-related diseases
SO BIOSCIENCE TRENDS
LA English
DT Review
DE inhibitors; NF-kappa B signaling; NLRP3-related diseases; NEK7; NLRP3
inflammasome
ID NLRP3 INFLAMMASOME ACTIVATION; GASDERMIN D; HEPATOCELLULAR-CARCINOMA;
DIABETIC-RETINOPATHY; KINASE; MITOCHONDRIA; PYROPTOSIS; PATHWAY; CANCER;
PROLIFERATION
AB NLRP3 inflammasome plays an essential role in innate immunity, yet the activation mechanism of NLRP3 inflammasome is not clear. In human or animal models, inappropriate NLRP3 inflammasome activation is implicated in many NLRP3-related diseases, such as tumors, inflammatory diseases and autoimmune diseases. Until now, a great number of inhibitors have been used to disturb the related signaling pathways, such as IL-1 beta blockade, IL-18 blockade and caspase-1 inhibitors. Unfortunately, most of these inhibitors just disturb the signaling pathways after the activation of NLRP3 inflammasome. Inhibitors that directly regulate NLRP3 to abolish the inflammation response may be more effective. NEK7 is a multifunctional kinase affecting centrosome duplication, mitochondrial regulation, intracellular protein transport, DNA repair and mitotic spindle assembly. Researchers have made significant observations on the regulation of gene transcription or protein expression of the NLRP3 inflammasome signaling pathway by NEK7. Those signaling pathways include ROS signaling, potassium efflux, lysosomal destabilization, and NF-kappa B signaling. Furthermore, NEK7 has been proved to be involved in many NLRP3-related diseases in humans or in animal models. Inhibitors focused on NEK7 may regulate NLRP3 to abolish the inflammation response and NEK7 may be a potential therapeutic target for NLRP3-related diseases.
C1 [Liu, Ganglei; Chen, Xueliang; Yuan, Lianwen] Cent South Univ, Xiangya Hosp 2, Dept Geriatr Surg, 139 Renmin Rd, Changsha 410011, Hunan, Peoples R China.
[Wang, Qianqian] Cent South Univ, Xiangya Med Coll, Affiliated Zhuzhou Hosp, Dept Oncol, Zhuzhou, Hunan, Peoples R China.
C3 Central South University; Central South University
RP Yuan, LW (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Geriatr Surg, 139 Renmin Rd, Changsha 410011, Hunan, Peoples R China.
EM yuanlianwen@csu.edu.cn
RI Wang, Qianqian/AHC-6753-2022
FU National Natural Science Foundation of China [81970493]
FX This study was supported by the National Natural Science Foundation of
China (81970493).
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NR 95
TC 35
Z9 40
U1 15
U2 59
PU IRCA-BSSA
PI TOKYO
PA PEARL CITY KOISHIKAWA 603, 2-4-5 KASUGA, BUNKYO-KU, TOKYO, 112-0003,
JAPAN
SN 1881-7815
EI 1881-7823
J9 BIOSCI TRENDS
JI BioSci. Trends
PD APR
PY 2020
VL 14
IS 2
BP 74
EP 82
DI 10.5582/bst.2020.01029
PG 9
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA LZ9JD
UT WOS:000541534200001
PM 32295992
OA gold
DA 2025-01-07
ER
PT J
AU Angelico, F
AF Angelico, Francesco
TI Chronic liver disease and management with silymarin: an introductory
review of a clinical case collection
SO DRUGS IN CONTEXT
LA English
DT Review
DE chronic liver disease; clinical cases silymarin; drug-induced liver
injury; herbal-induced liver injury; metabolic-associated fatty liver
disease; non-alcoholic fatty liver disease
ID PRACTICE GUIDANCE; FIBROSIS; INJURY; RISK
AB Chronic liver disease (CLD) is a significant global health concern and generally leads to fibrosis, cirrhosis and hepatocellular carcinoma. Various factors, such as metabolic abnormalities, viral infections, alcoholism, genetics and autoimmune responses, contribute to liver damage. CLD is characterized by different phenotypes, including non-alcoholic fatty liver disease, metabolic-associated fatty liver disease, drug-induced liver injury and alcoholic liver disease. These conditions have seen an increase in comorbidities and hospitalizations over the past decade, imposing a substantial burden on patients and healthcare systems. Understanding the underlying mechanisms of liver injury is crucial for effective management and reducing the clinical and economic burden of CLD. Although several attempts have been evaluated to find a drug therapy option for the management of nonalcoholic fatty liver disease and metabolic-associated fatty liver disease, there is no effective drug approved to date. However, different studies have demonstrated that silymarin, the milk thistle extract, could exert hepatoprotective, antioxidant, anti-inflammatory and antifibrotic properties and should therefore be considered an efficacious, tolerable and promising herbal product for the management of liver activity in CLDs. This review discusses the clinical features, diagnosis and available treatments for major liver diseases, acting as an introduction to a clinical case collection based on the management and treatment of major liver diseases with silymarin.
C1 [Angelico, Francesco] Sapienza Univ, Internal Med, Via Antonio Nibby 8, I-00161 Rome, Italy.
C3 Sapienza University Rome
RP Angelico, F (corresponding author), Sapienza Univ, Internal Med, Via Antonio Nibby 8, I-00161 Rome, Italy.
EM francesco.angelico@gmail.com
FU Viatris Inc
FX Editorial assistance was provided by Francesca Cappellini, PhD, Mattia
Zamboni and Aashni Shah (Polistudium SRL Milan, Italy). This assistance
was supported by Viatris Inc.
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NR 35
TC 1
Z9 1
U1 1
U2 4
PU BIOEXCEL PUBL LTD
PI HAYWARDS HEATH
PA 32, QUARRY HILL, HAYWARDS HEATH, WEST SUSSEX, ENGLAND
EI 1740-4398
J9 DRUGS CONTEXT
JI Drugs Context
PD JAN 31
PY 2024
VL 13
AR 202374
DI 10.7573/dic.2023-7-4
PG 9
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA A1N0D
UT WOS:001280257300001
PM 38332944
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Grosjean, I
Roméo, B
Domdom, MA
Belaid, A
D'Andréa, G
Guillot, N
Gherardi, RK
Gal, J
Milano, G
Marquette, CH
Hung, RYJ
Landi, MT
Han, Y
Brest, P
Von Bergen, M
Klionsky, DJ
Amos, CI
Hofman, P
Mograbi, B
AF Grosjean, Iris
Romeo, Barnabe
Domdom, Marie-Angela
Belaid, Amine
D'Andrea, Gregoire
Guillot, Nicolas
Gherardi, Romain K.
Gal, Jocelyn
Milano, Gerard
Marquette, Charles Hugo
Hung, Rayjean J.
Landi, Maria Teresa
Han, Younghun
Brest, Patrick
Von Bergen, Martin
Klionsky, Daniel J.
Amos, Christopher I.
Hofman, Paul
Mograbi, Baharia
TI Autophagopathies: from autophagy gene polymorphisms to precision
medicine for human diseases
SO AUTOPHAGY
LA English
DT Article
DE Autophagy; cancers; diseases; eQTL; pollutants; exposomics;
polymorphism; prognosis; risk; susceptibility; theragnosis
ID GENOME-WIDE ASSOCIATION; TOLL-INTERACTING PROTEIN; SUSCEPTIBILITY LOCI;
LUNG-CANCER; COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA; THR300ALA
VARIANT; CANDIDATE GENES; CROHN-DISEASE; PATHWAY GENES
AB At a time when complex diseases affect globally 280 million people and claim 14 million lives every year, there is an urgent need to rapidly increase our knowledge into their underlying etiologies. Though critical in identifying the people at risk, the causal environmental factors (microbiome and/or pollutants) and the affected pathophysiological mechanisms are not well understood. Herein, we consider the variations of autophagy-related (ATG) genes at the heart of mechanisms of increased susceptibility to environmental stress. A comprehensive autophagy genomic resource is presented with 263 single nucleotide polymorphisms (SNPs) for 69 autophagy-related genes associated with 117 autoimmune, inflammatory, infectious, cardiovascular, neurological, respiratory, and endocrine diseases. We thus propose the term 'autophagopathies' to group together a class of complex human diseases the etiology of which lies in a genetic defect of the autophagy machinery, whether directly related or not to an abnormal flux in autophagy, LC3-associated phagocytosis, or any associated trafficking. The future of precision medicine for common diseases will lie in our ability to exploit these ATG SNP x environment relationships to develop new polygenetic risk scores, new management guidelines, and optimal therapies for afflicted patients.
C1 [Grosjean, Iris; Romeo, Barnabe; Domdom, Marie-Angela; D'Andrea, Gregoire; Guillot, Nicolas; Marquette, Charles Hugo; Brest, Patrick; Hofman, Paul; Mograbi, Baharia] Univ Cote Azur, CNRS, INSERM, IRCAN,FHU OncoAge,Ctr Antoine Lacassagne, Nice, France.
[Belaid, Amine] Univ Cote Azur UCA, INSERM, U1065, C3M,Team 5, F-06204 Nice, France.
[D'Andrea, Gregoire] Cote Azur Univ, Univ Hosp, CHU Nice, Inst Univ Face & Cou,ENT & Head & Neck Surg Dept, Nice, France.
[Gherardi, Romain K.] Paris Est Univ, INSERM, U955, Fac Hlth,Team Relais, Paris, France.
[Gal, Jocelyn] Univ Cote Azur, Ctr Antoine Lacassagne, Epidemiol & Biostat Dept, Nice, France.
[Milano, Gerard] Univ Cote Azur, Ctr Antoine Lacassagne, UPR7497, Nice, France.
[Marquette, Charles Hugo] Univ Cote Azur, CHU Nice, FHU OncoAge, Dept Pulm Med & Oncol, Nice, France.
[Hung, Rayjean J.] Lunenfeld Tanenbaum Res Inst, Sinai Hlth Syst, Toronto, ON, Canada.
[Hung, Rayjean J.] Univ Toronto, Dalla Lana Sch Publ Hlth, Div Epidemiol, Toronto, ON, Canada.
[Landi, Maria Teresa] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Han, Younghun; Amos, Christopher I.] Baylor Coll Med, Inst Clin & Translat Res, Houston, TX 77030 USA.
[Von Bergen, Martin] Helmholtz Ctr Environm Res GmbH UFZ, Dept Mol Syst Biol, Leipzig, Germany.
[Von Bergen, Martin] Univ Leipzig, Inst Biochem, Fac Life Sci, Leipzig, Germany.
[Klionsky, Daniel J.] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
[Hofman, Paul] Univ Cote Azur, CHU Nice, FHU OncoAge, Lab Clin & Expt Pathol LPCE Biobank BB 0033 00025, Nice, France.
C3 Universite Cote d'Azur; Centre National de la Recherche Scientifique
(CNRS); Institut National de la Sante et de la Recherche Medicale
(Inserm); UNICANCER; Centre Antoine Lacassagne; CHU Nice; Universite
Cote d'Azur; Institut National de la Sante et de la Recherche Medicale
(Inserm); Universite Cote d'Azur; CHU Nice; Institut National de la
Sante et de la Recherche Medicale (Inserm); Universite
Paris-Est-Creteil-Val-de-Marne (UPEC); UNICANCER; Centre Antoine
Lacassagne; Universite Cote d'Azur; UNICANCER; Centre Antoine
Lacassagne; Universite Cote d'Azur; Universite Cote d'Azur; CHU Nice;
University of Toronto; Sinai Health System Toronto; Lunenfeld Tanenbaum
Research Institute; University of Toronto; National Institutes of Health
(NIH) - USA; NIH National Cancer Institute (NCI); Baylor College of
Medicine; Helmholtz Association; Helmholtz Center for Environmental
Research (UFZ); Leipzig University; University of Michigan System;
University of Michigan; CHU Nice; Universite Cote d'Azur
RP Mograbi, B (corresponding author), Univ Cote Azur, CNRS, UMR 7284, INSERM,U1081,Inst Res Canc,Nice IRCAN,Ctr Antoine, 33 Ave Valombrose, F-06189 Nice, France.
EM mograbi@unice.fr
RI D Andréa, Grégoire/IAO-1840-2023; Hung, Rayjean/A-7439-2013; Marquette,
Charles/O-4084-2016; Mograbi, Baharia/N-5531-2018; von Bergen,
Martin/D-7960-2011; brest, patrick/B-7311-2012
OI Grosjean, Iris/0000-0002-1017-8270; Romeo, Barnabe/0000-0001-6011-4868;
Gal, Jocelyn/0000-0002-1802-118X; von Bergen,
Martin/0000-0003-2732-2977; Hung, Rayjean/0000-0002-4486-7496; brest,
patrick/0000-0002-1252-4747; Mograbi, Baharia/0000-0002-1025-3429;
D'Andrea, Gregoire/0000-0003-3838-513X; Guillot,
Nicolas/0000-0002-2989-2511; Domdom, Marie Angela/0000-0002-9896-6270
FU Association pour la Recherche contre le Cancer [GENEXPOSOMICS Canc'air];
Canceropole PACA [Immunoquest]; French national research agency
[ANR-11-LABX -0028-01]; NIH [NIGMS GM131919]; Region SUD
[GENEXPOSOMICS]; DREAL PACA; ARS PACA; PRSE PACA [GENEXPOSOMICS]; INCA
Plan Cancer [Plan Cancer]; Children's Medical Safety Research Institute
[R17033DJA]; National Institute of General Medical Sciences
[R35GM131919] Funding Source: NIH RePORTER
FX This work was supported by the Association pour la Recherche contre le
Cancer [GENEXPOSOMICS Canc'air]; Canceropole PACA [Immunoquest]; French
national research agency [ANR-11-LABX -0028-01]; NIH [NIGMS GM131919];
Region SUD [GENEXPOSOMICS]; DREAL PACA, ARS PACA, PRSE PACA
[GENEXPOSOMICS]; INCA Plan Cancer [Plan Cancer]; Children's Medical
Safety Research Institute [Vaccinophagy R17033DJA].
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NR 185
TC 21
Z9 22
U1 0
U2 23
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD NOV 2
PY 2022
VL 18
IS 11
BP 2519
EP 2536
DI 10.1080/15548627.2022.2039994
EA APR 2022
PG 18
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 5V0SO
UT WOS:000778846100001
PM 35383530
OA Green Submitted, Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Markova, AA
Deterding, K
Port, K
Bantel, H
Manns, MP
Cornberg, M
Wedemeyer, H
AF Markova, Antoaneta A.
Deterding, Katja
Port, Kerstin
Bantel, Heike
Manns, Michael P.
Cornberg, Markus
Wedemeyer, Heiner
TI Liver stiffness across different chronic liver disease under therapy
with statin in a real life cohort
SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Article
DE decompensation; fibrosis; follow-up; liver disease; statin
ID ATTENUATES HEPATIC-FIBROSIS; HEPATOCELLULAR-CARCINOMA; NATURAL-HISTORY;
B PATIENTS; CIRRHOSIS; SIMVASTATIN; RISK; ATORVASTATIN; DECOMPENSATION;
HEPATOTOXICITY
AB Introduction Statins have been associated with improved clinical outcomes in patients with viral hepatitis and after variceal bleeding. Still, the clinical benefit of statins is not well defined for different liver diseases. Moreover, associations between statin use and liver stiffness as well as event free survival have not been established.
Methods Liver stiffness was evaluated in 6490 patients with liver disease (January 2012 till December 2016). Two hundred thirty-four of those received statin therapy, 468 controls without statins were selected by a 1:2 case by case matching using age, sex, underlying liver disease and BMI.
Results Statins were given to 234 patients with chronic virus hepatitis (n = 104), nonalcoholic fatty liver disease (n = 52), autoimmune liver disease including autoimmune hepatitis, primary biliary cholangitis and primary sclerosing cholangitis (n = 31) and hepatitis of unknown origin (n = 47). Follow-up data were available for 96 and 119 pairs (mean follow-up 2 years). Statin users showed reduced inflammatory activity. Elevated liver enzymes were reported in 57% of statin-treated compared with 70% of controls (mean alanine aminotransferase level 53 vs. 74 U/l; P < 0.001). Statin use was well tolerated in this cohort. Mean liver stiffness values were 10.7 kPa (SEM 0.7) and 15.5 kPa (SEM 0.7) accordingly (P < 0.0001). Decompensation was less likely to occur in the statin group, both groups do not defer in the incidence of liver tumor occurrence, transplantation or death (odds ratio = 1, P = nonsignificant).
Conclusions Use of statins was well tolerated irrespective of liver disease. Statin users showed reduced hepatic inflammatory activity, less severe markers of liver stiffness and portal hypertension. There might be a beneficial effect of statin on the risk to experience hepatic decompensation. Copyright (C) 2020 Wolters Kluwer Health, Inc. All rights reserved.
C1 [Markova, Antoaneta A.; Deterding, Katja; Port, Kerstin; Bantel, Heike; Manns, Michael P.; Cornberg, Markus; Wedemeyer, Heiner] Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Hannover, Germany.
[Markova, Antoaneta A.; Deterding, Katja; Wedemeyer, Heiner] Essen Univ Hosp, Dept Gastroenterol & Hepatol, Essen, Germany.
C3 Hannover Medical School; University of Duisburg Essen
RP Markova, AA (corresponding author), Essen Univ Hosp, Dept Gastroenterol & Hepatol, Essen, Germany.
EM Antoaneta.markova@uk-essen.de
RI Cornberg, Markus/AAN-6939-2021; Manns, Michael/AFG-3063-2022
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NR 40
TC 1
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0954-691X
EI 1473-5687
J9 EUR J GASTROEN HEPAT
JI Eur. J. Gastroenterol. Hepatol.
PD FEB
PY 2021
VL 33
IS 2
BP 223
EP 229
DI 10.1097/MEG.0000000000001719
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ZB6TD
UT WOS:000756971300014
PM 32282399
DA 2025-01-07
ER
PT J
AU Speckmann, B
Grune, T
AF Speckmann, Bodo
Grune, Tilman
TI Epigenetic effects of selenium and their implications for health
SO EPIGENETICS
LA English
DT Review
DE CBS (Cystathionine beta-lyase); histone modifications; homocysteine;
microRNA; selenite; selenocysteine; selenomethionine
ID DNA METHYLATION; PLASMA HOMOCYSTEINE; PROSTATE-CANCER; DIETARY SELENIUM;
RAT-LIVER; HISTONE DEACETYLASE; FISHER-344 RATS; SELENOPROTEIN P; SERUM
SELENIUM; IN-VIVO
AB Alterations of epigenetic marks are linked to normal development and cellular differentiation as well as to the progression of common chronic diseases. The plasticity of these marks provides potential for disease therapies and prevention strategies. Macro-and micro-nutrients have been shown to modulate disease risk in part via effects on the epigenome. The essential micronutrient selenium affects human health outcomes, e.g., cancers, cardiovascular and autoimmune diseases, via selenoproteins and through a range of biologically active dietary selenocompounds and metabolism products thereof. This review provides an assessment of the current literature regarding epigenetic effects of dietary and synthetic selenocompounds, which include the modulation of marks and editors of epigenetic information and interference with one-carbon metabolism, which provides the methyl donor for DNA methylation. The relevance of a selenium-epigenome interaction for human health is discussed, and we also indicate where future studies will be helpful to gain a deeper understanding of epigenetic effects elicited by selenium.
C1 [Speckmann, Bodo; Grune, Tilman] German Inst Human Nutr Potsdam Rehbrucke, Dept Mol Toxicol, Nuthetal, Germany.
C3 Leibniz Association; Deutsches Institut fur Ernahrungsforschung
Potsdam-Rehbrucke (DIfE)
RP Speckmann, B (corresponding author), German Inst Human Nutr Potsdam Rehbrucke, Dept Mol Toxicol, Nuthetal, Germany.
EM bodo.speckmann@dife.de
OI Grune, Tilman/0000-0003-4775-9973
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NR 86
TC 100
Z9 109
U1 3
U2 37
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1559-2294
EI 1559-2308
J9 EPIGENETICS-US
JI Epigenetics
PD MAR
PY 2015
VL 10
IS 3
BP 179
EP 190
DI 10.1080/15592294.2015.1013792
PG 12
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA CE1YE
UT WOS:000351608000001
PM 25647085
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Ferreira, PAT
Monteiro, LS
Coban, T
Suzen, S
AF Ferreira, Paula A. T.
Monteiro, Luis S.
Coban, T.
Suzen, S.
TI Comparative effect of N-substituted dehydroamino acids and
α-tocopherol on rat liver lipid peroxidation activities
SO JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY
LA English
DT Article
DE Dehydroamino acid; alpha-tocopherol; lipid peroxidation; radical
scavenging; antioxidant
ID CDDO INDUCES APOPTOSIS; ACYL DEHYDROALANINES; MICHAEL ADDITION;
ANTIOXIDANT; DERIVATIVES; DIFFERENTIATION; IDENTIFICATION; NUCLEOPHILES
AB Free radical damage has been associated with a growing number of diseases and conditions, such as autoimmune diseases, neurodegenerative disorders and multiple types of cancer. Some dehydroamino acids and corresponding peptides can function as radical scavengers. In this study the in vitro effects on rat liver lipid peroxidation levels of fourteen N-substituted dehydroamino acid derivatives and alpha-tocopherol were investigated. alpha-Tocopherol is a powerful antioxidant that is beneficial in the treatment of many free radical related diseases. The results indicated that all the compounds showed very good inhibitory effect on the lipid peroxidation compound with alpha-tocopherol at 1 mM concentrations and the inhibition rate was in the range of 70-79 % with the exception of compound 5. At 0.1 mM concentrations compounds 1, 2 and 9 were found more active than alpha-tocopherol. The results confirmed that molecules such as dehydroamino acids which have reactive double bonds can act as a guard in vitro against oxidants.
C1 [Suzen, S.] Ankara Univ, Fac Pharm, Dept Pharmaceut Chem, TR-06100 Ankara, Turkey.
[Coban, T.] Ankara Univ, Fac Pharm, Dept Pharmaceut Toxicol, TR-06100 Ankara, Turkey.
[Ferreira, Paula A. T.; Monteiro, Luis S.] Univ Minho, Dept Chem, P-4710057 Braga, Portugal.
C3 Ankara University; Ankara University; Universidade do Minho
RP Suzen, S (corresponding author), Ankara Univ, Fac Pharm, Dept Pharmaceut Chem, TR-06100 Ankara, Turkey.
EM sibel@pharmacy.ankara.edu.tr
RI Suzen, Sibel/AAF-8030-2020; Ferreira, Paula/A-5274-2013
OI Monteiro, Luis/0000-0001-7779-9250; Ferreira, Paula/0000-0002-3279-6731
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NR 37
TC 13
Z9 16
U1 0
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1475-6366
EI 1475-6374
J9 J ENZYM INHIB MED CH
JI J. Enzym. Inhib. Med. Chem.
PD AUG
PY 2009
VL 24
IS 4
BP 967
EP 971
DI 10.1080/14756360802561162
PG 5
WC Biochemistry & Molecular Biology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 491AH
UT WOS:000269548700008
PM 19555173
OA Bronze, Green Published
DA 2025-01-07
ER
PT J
AU Burra, P
Martin, E
Gitto, S
Villa, E
AF Burra, Patrizia
De Martin, Eleonora
Gitto, Stefano
Villa, Erica
TI Influence of Age and Gender Before and After Liver Transplantation
SO LIVER TRANSPLANTATION
LA English
DT Review
ID CHRONIC HEPATITIS-C; QUALITY-OF-LIFE; PRIMARY BILIARY-CIRRHOSIS;
REDUCED-SIZE LIVER; TERM-FOLLOW-UP; UNITED-STATES; AUTOIMMUNE HEPATITIS;
METABOLIC SYNDROME; HEPATOCELLULAR-CARCINOMA; FIBROSIS PROGRESSION
AB Women constitute a particular group among patients with chronic liver disease and in the postliver transplantation (LT) setting: they are set apart not only by traditional differences with respect to men (ie, body mass index, different etiologies of liver disease, and accessibility to transplantation) but also in increasingly evident ways related to hormonal changes that characterize first the fertile age and subsequently the postmenopausal period (eg, disease course variability and responses to therapy). The aim of this review is, therefore, to evaluate the role of the interplay of factors such as age, gender, and hormones in influencing the natural history of chronic liver disease before and after LT and their importance in determining outcomes after LT. As the population requiring LT ages and the mean age at transplantation increases, older females are being considered for transplantation. Older patients are at greater risk for nonalcoholic steatohepatitis, osteoporosis, and a worse response to antiviral therapy. Female gender per se is associated with a greater risk for osteoporosis because of metabolic changes after menopause, the bodily structure of females, and, in the population of patients with chronic liver disease, the greater prevalence of cholestatic and autoimmune liver diseases. With menopause, the fall of protective estrogen levels can lead to increased fibrosis progression, and this represents a negative turning point for women with chronic liver disease and especially for patients with hepatitis C. Therefore, the notion of gender as a binary female/male factor is now giving way to the awareness of more complex disease processes within the female gender that follow hormonal, social, and age patterns and need to be addressed directly and specifically. Liver Transpl 19:122134, 2013. (c) 2012 AASLD.
C1 [Burra, Patrizia; De Martin, Eleonora] Padua Univ Hosp, Multivisceral Transplant Unit, Dept Surg Oncol & Gastroenterol, Padua, Italy.
[Gitto, Stefano; Villa, Erica] Univ Modena & Reggio Emilia, Dept Gastroenterol, Univ Teaching Hosp, I-41124 Modena, Italy.
C3 University of Padua; Azienda Ospedaliera - Universita di Padova;
Universita di Modena e Reggio Emilia
RP Burra, P (corresponding author), Padua Univ Hosp, Multivisceral Transplant Unit, Dept Surg Oncol & Gastroenterol, Via Giustiniani 2,25128 PD, Padua, Italy.
EM burra@unipd.it; erica.villa@unimore.it
RI Burra, Patrizia/AAB-2448-2019; De Martin, Eleonora/T-6835-2018; Villa,
Erica/A-7576-2012; Gitto, Stefano/J-9922-2018
OI Burra, Patrizia/0000-0002-8791-191X; Villa, Erica/0000-0001-6388-7022;
Gitto, Stefano/0000-0002-8042-6508
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NR 134
TC 52
Z9 53
U1 0
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6465
EI 1527-6473
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD FEB
PY 2013
VL 19
IS 2
BP 122
EP 134
DI 10.1002/lt.23574
PG 13
WC Gastroenterology & Hepatology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA 090MH
UT WOS:000314982700003
PM 23172830
DA 2025-01-07
ER
PT J
AU Pauly, MP
Tucker, LY
Szpakowski, JL
Ready, JB
Baer, D
Hwang, J
Lok, ASF
AF Pauly, Mary Patricia
Tucker, Lue-Yen
Szpakowski, Jean-Luc
Ready, Joanna B.
Baer, David
Hwang, Jessica
Lok, Anna S. -F.
TI Incidence of Hepatitis B Virus Reactivation and Hepatotoxicity in
Patients Receiving Long-term Treatment With Tumor Necrosis Factor
Antagonists
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Hepatitis Flare; Immunosuppression; Serology; Prognostic Factor
ID RHEUMATOID-ARTHRITIS PATIENTS; FACTOR-ALPHA INHIBITORS; ANTI-TNF
THERAPY; HBV REACTIVATION; CROHNS-DISEASE; LIVER; INFLIXIMAB; INFECTION;
AGENTS; RISK
AB BACKGROUND & AIMS: Tumor necrosis factor (TNF) antagonists are the first-line treatment for many autoimmune diseases. However, they have been associated with reactivation of hepatitis B virus (HBV). We determined the rate of HBV reactivation and hepatotoxicity grade 3 or 4 (HT >= 3) in patients treated with an anti-TNF agent for an autoimmune disease.
METHODS: We collected data from 8887 adult patients in the Kaiser Permanente Northern California database who began treatment with TNF antagonists for autoimmune diseases (dermatologic, rheumatologic, or gastrointestinal) from 2001 through 2010, followed through December 2012. We obtained data on HBV infection (52% of patients were screened for HBV before treatment), demographic features, comorbidities, and use of immunosuppressive agents. HBV reactivation was defined as 1 of the following: >1 log increase in HBV DNA, HBV DNA-positive when previously negative, HBV DNA >2000 IU/mL if no baseline level was available, or reverse seroconversion. HT >= 3 was defined according to the National Cancer Institute Common Toxicity Criteria. We performed multivariable logistic regression to identify factors associated with HT >= 3.
RESULTS: Twenty-three patients tested positive for HB surface antigen (HBsAg) at baseline and 9 of these had HBV reactivation; of the 4267 patients with unknown HBV status at baseline, 2 had HBV reactivation. None of the 178 patients who were HBsAg negative and positive for the hepatitis B core antibody (anti-HBc+) had HBV reactivation. HBV reactivation occurred in 1/5 HBsAg+ patients who received prophylactic antiviral therapy and 8/18 who did not (P = .61). No one with HBV reactivation had liver failure. HT >= 3 occurred in 273 patients (2.7%), but only 3 cases were attributed to HBV. Cirrhosis was significantly associated with HT >= 3 (P < .001).
CONCLUSION: In a retrospective analysis of patients treated with TNF antagonists for autoimmune diseases, we found HBV reactivation in 39% of patients who were HBsAg+ before therapy, but not in any patients who were HBsAg-negative and anti-HBc+ before therapy. Patients should be screened for HBV infection before anti-TNF therapy; HBsAg+ patients should receive prophylactic antiviral therapy, but not HBsAg-negative, anti-HBc+ patients.
C1 [Pauly, Mary Patricia; Szpakowski, Jean-Luc; Ready, Joanna B.] Kaiser Permanente Northern Calif, Dept Gastroenterol, Sacramento, CA USA.
[Tucker, Lue-Yen] Kaiser Permanente Northern Calif, Div Res, Sacramento, CA USA.
[Baer, David] Kaiser Permanente Northern Calif, Dept Hematol & Oncol, Sacramento, CA USA.
[Hwang, Jessica] Univ Texas MD Anderson Canc Ctr, Div Internal Med, Dept Gen Internal Med, Houston, TX 77030 USA.
[Lok, Anna S. -F.] Univ Michigan, Dept Internal Med & Gastroenterol, Ann Arbor, MI 48109 USA.
C3 Kaiser Permanente; Kaiser Permanente; Kaiser Permanente; University of
Texas System; UTMD Anderson Cancer Center; University of Michigan
System; University of Michigan
RP Pauly, MP (corresponding author), Univ Calif Davis, Dept Gastroenterol & Hepatol, PSSB 3500 4150 V St, Sacramento, CA 95817 USA.
EM mppauly@ucdavis.edu
OI Hwang, Jessica/0000-0002-5896-4182; Tucker, Lue-Yen/0000-0001-7980-9272
FU Kaiser Permanente Northern California
FX This study was funded by a community benefit grant in 2014 from Kaiser
Permanente Northern California. There was no other funding for this
project. The funds were used to pay for the research associates time and
for statistical analysis.
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NR 33
TC 46
Z9 47
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD DEC
PY 2018
VL 16
IS 12
BP 1964
EP +
DI 10.1016/j.cgh.2018.04.033
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HA5QN
UT WOS:000450331100024
PM 29702293
DA 2025-01-07
ER
PT J
AU Kumar, V
Ahmad, A
AF Kumar, Vijay
Ahmad, Ali
TI Role of MAIT cells in the immunopathogenesis of inflammatory diseases:
New players in old game
SO INTERNATIONAL REVIEWS OF IMMUNOLOGY
LA English
DT Review
DE Autoimmunity; auto-inflammation; chronic infection; inflammation; MAIT
cells; MR-1
ID INVARIANT T-CELLS; INNATE LYMPHOID-CELLS; RECEPTOR HETEROGENEITY;
PERIPHERAL-BLOOD; IMMUNE-RESPONSE; ACTIVATION; MR1; MUCOSA; EXPRESSION;
PATHWAY
AB Current advances in immunology have led to the identification of a population of novel innate immune T cells, called mucosa-associated invariant T (MAIT) cells. The cells in humans express an invariant TCR chain (V7.2-J33) paired with a limited subset of TCR chains (V2, 13 and 22), are restricted by the MHC class I (MH1)-related (MR)-1, and recognize molecules that are produced in the bacterial riboflavin (vitamin B2) biosynthetic pathway. They are present in the circulation, liver and at various mucosal sites (i.e. intestine, lungs and female reproductive tract, etc.). They kill host cells infected with bacteria and yeast, and secrete soluble mediators such as TNF-, IFN-, IL-17, etc. The cells regulate immune responses and inflammation associated with a wide spectrum of acute and chronic diseases in humans. Since their discovery in 1993, significant advances have been made in understanding biology of MAIT cells and the potential role of these cells in the pathogenesis of autoimmune, inflammatory and infectious diseases as well as cancer in humans. The purpose of this review is to provide a current state of our knowledge about MAIT cell biology and delineate their role in autoimmune and inflammatory diseases (sterile or caused by infectious agents) and cancer in humans. A better understanding of the role of MAIT cells in human diseases may lead to novel ways of immunotherapies.
C1 [Kumar, Vijay] Univ Queensland, Fac Med & Biomed Sci, Dept Paediat & Child Care,Mater Res, Childrens Hlth Queensland Clin Unit,Sch Med, Brisbane, Qld, Australia.
[Ahmad, Ali] Univ Montreal, Dept Microbiol Infect Dis & Immunol, CHU Ste Justine, Lab Innate Immun, Montreal, PQ H3T 1C5, Canada.
C3 Mater Research; University of Queensland; Universite de Montreal
RP Ahmad, A (corresponding author), Univ Montreal, Dept Microbiol Infect Dis & Immunol, CHU Ste Justine, Lab Innate Immun, Montreal, PQ H3T 1C5, Canada.; Kumar, V (corresponding author), Univ Queensland, Fac Med & Biomed Sci, Mater Res, Dept Paediat & Child Care,Sch Med, Brisbane, Qld 4078, Australia.
EM v.kumar3@uq.edu.au; ali.ahmad@recherche-ste-justine.qc.ca
RI Kumar, Vijay/O-6315-2014
OI Kumar, Vijay/0000-0001-9741-3597; Ahmad, Ali/0000-0001-7689-7115
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NR 185
TC 21
Z9 21
U1 0
U2 8
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0883-0185
EI 1563-5244
J9 INT REV IMMUNOL
JI Int. Rev. Immunol.
PY 2018
VL 37
IS 2
BP 90
EP 110
DI 10.1080/08830185.2017.1380199
PG 21
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA GA2LR
UT WOS:000428154700003
PM 29106304
DA 2025-01-07
ER
PT J
AU Kuraji, R
Sekino, S
Kapila, Y
Numabe, Y
AF Kuraji, Ryutaro
Sekino, Satoshi
Kapila, Yvonne
Numabe, Yukihiro
TI Periodontal disease-related nonalcoholic fatty liver disease and
nonalcoholic steatohepatitis: An emerging concept of oral-liver axis
SO PERIODONTOLOGY 2000
LA English
DT Review
DE gut microbial dysbiosis; metabolic syndrome; NAFLD; NASH; obesity;
periodontal disease; periodontopathic bacteria; systemic inflammation
ID NECROSIS-FACTOR-ALPHA; GINGIVAL CREVICULAR FLUID; TYPE-2
DIABETES-MELLITUS; TERM-FOLLOW-UP; PORPHYROMONAS-GINGIVALIS;
INSULIN-RESISTANCE; HEPATIC STEATOSIS; ADIPOSE-TISSUE; METABOLIC
SYNDROME; HEPATOCELLULAR-CARCINOMA
AB Periodontal disease, a chronic inflammatory disease of the periodontal tissues, is not only a major cause of tooth loss, but it is also known to exacerbate/be associated with various metabolic disorders, such as obesity, diabetes, dyslipidemia, and cardiovascular disease. Recently, growing evidence has suggested that periodontal disease has adverse effects on the pathophysiology of liver disease. In particular, nonalcoholic fatty liver disease, a hepatic manifestation of metabolic syndrome, has been associated with periodontal disease. Nonalcoholic fatty liver disease is characterized by hepatic fat deposition in the absence of a habitual drinking history, viral infections, or autoimmune diseases. A subset of nonalcoholic fatty liver diseases can develop into more severe and progressive forms, namely nonalcoholic steatohepatitis. The latter can lead to cirrhosis and hepatocellular carcinoma, which are end-stage liver diseases. Extensive research has provided plausible mechanisms to explain how periodontal disease can negatively affect nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, namely via hematogenous or enteral routes. During periodontitis, the liver is under constant exposure to various pathogenic factors that diffuse systemically from the oral cavity, such as bacteria and their by-products, inflammatory cytokines, and reactive oxygen species, and these can be involved in disease promotion of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Also, gut microbiome dysbiosis induced by enteral translocation of periodontopathic bacteria may impair gut wall barrier function and promote the transfer of hepatotoxins and enterobacteria to the liver through the enterohepatic circulation. Moreover, in a population with metabolic syndrome, the interaction between periodontitis and systemic conditions related to insulin resistance further strengthens the association with nonalcoholic fatty liver disease. However, most of the pathologic links between periodontitis and nonalcoholic fatty liver disease in humans are provided by epidemiologic observational studies, with the causal relationship not yet being established. Several systematic and meta-analysis studies also show conflicting results. In addition, the effect of periodontal treatment on nonalcoholic fatty liver disease has hardly been studied. Despite these limitations, the global burden of periodontal disease combined with the recent nonalcoholic fatty liver disease epidemic has important clinical and public health implications. Emerging evidence suggests an association between periodontal disease and liver diseases, and thus we propose the term periodontal disease-related nonalcoholic fatty liver disease or periodontal disease-related nonalcoholic steatohepatitis. Continued efforts in this area will pave the way for new diagnostic and therapeutic approaches based on a periodontologic viewpoint to address this life-threatening liver disease.
C1 [Kuraji, Ryutaro] Nippon Dent Univ Tokyo, Dept Life Sci Dent, Tokyo, Japan.
[Kuraji, Ryutaro; Sekino, Satoshi; Numabe, Yukihiro] Nippon Dent Univ Tokyo, Sch Life Dent Tokyo, Dept Periodontol, Tokyo, Japan.
[Kuraji, Ryutaro; Kapila, Yvonne] Univ Calif San Francisco, Sch Dent, Dept Orofacial Sci, San Francisco, CA USA.
C3 Nippon Dental University; Nippon Dental University; University of
California System; University of California San Francisco
RP Kuraji, R (corresponding author), Nippon Dent Univ Tokyo, Dept Life Sci Dent, Tokyo, Japan.
EM r-kuraji@tky.ndu.ac.jp
RI Sekino, Satoshi/AAV-4370-2020; Kapila, Yvonne/AAG-5418-2021
OI Kapila, Yvonne/0000-0003-1330-0654
FU NIH [R01 DE025225]; Berkelhammer Basic Science Funds; Larry Berkelhammer
funds; Department of Life Science Dentistry and Periodontology; Nippon
Dental University (NDU) School of Life Dentistry at Tokyo; University of
California SanFrancisco (UCSF) Division of Periodontology; AAP Sunstar
Innovation Grant; National Institute of Dental and Craniofacial Research
[R01DE025225] Funding Source: NIH RePORTER
FX Department of Life Science Dentistry and Periodontology; Nippon Dental
University (NDU) School of Life Dentistry at Tokyo; University of
California SanFrancisco (UCSF) Division of Periodontology; AAP Sunstar
Innovation Grant; NIH, Grant/Award Number: R01 DE025225. This work was
supported by funding from NIH R01 DE025225 grant and Berkelhammer Basic
Science Funds to YLK. Larry Berkelhammer funds to Yvonne L. Kapila
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NR 268
TC 50
Z9 51
U1 5
U2 36
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0906-6713
EI 1600-0757
J9 PERIODONTOL 2000
JI Periodontol. 2000
PD OCT
PY 2021
VL 87
IS 1
BP 204
EP 240
DI 10.1111/prd.12387
PG 37
WC Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dentistry, Oral Surgery & Medicine
GA UK2BO
UT WOS:000691780100016
PM 34463983
OA Green Accepted, Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Pei, JH
Dong, R
Yang, YF
Zheng, C
Liu, J
Zheng, S
AF Pei, Jiahao
Dong, Rui
Yang, Yifan
Zheng, Chao
Liu, Jia
Zheng, Shan
TI Association of STAT4 genetic polymorphisms with biliary atresia in
Chinese patients
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE Biliary atresia; gene polymorphism; Han Chinese patients; STAT4; SNP
rs7574865
ID HEPATOCELLULAR-CARCINOMA; SUSCEPTIBILITY; PATHOGENESIS; REPLICATION;
POPULATION; BIOLOGY; DISEASE; ADD3; RISK
AB Biliary atresia (BA) is a devastating disease of the liver characterized by progressive fibro-inflammatory obliteration in neonates. Without effective treatment, end stage of liver, will ultimately lead to die about 2 years old. STAT4 is a now known as a susceptibility gene for autoimmune diseases and a STAT4 minor allele may be associated with several liver diseases. A case-control study was done between 113 patients with BA and 133 healthy controls. The rs7574865 and rs8179673 single nucleotide polymorphisms (SNPs) and rs10168266 SNPs in the STAT4 gene were selected for genotyping. There was no significant difference in allele distribution between BA and controls (rs7574865, P = 0.6213, odds ratio [OR] = 1.098, 95% confidence interval [CI] = 0.758-1.589; rs8179673, P = 0.5702, OR = 0.898, 95% CI = 0.620-1.301; rs10168266, P = 0.9351, OR = 1.016, 95% CI = 0.699-1.477), and similar results were found for the genotype and haplotype frequencies of these STAT4 gene polymorphisms. Our results indicated that these STAT4 gene polymorphisms do not have a major role in the development of BA in Chinese children.
C1 [Zheng, Shan] Fudan Univ, Childrens Hosp, Dept Pediat Surg, 399 Wan Yuan Rd, Shanghai 201102, Peoples R China.
[Zheng, Shan] Minist Hlth, Key Lab Neonatal Dis, 399 Wan Yuan Rd, Shanghai 201102, Peoples R China.
C3 Fudan University
RP Zheng, S (corresponding author), Fudan Univ, Childrens Hosp, Dept Pediat Surg, 399 Wan Yuan Rd, Shanghai 201102, Peoples R China.; Zheng, S (corresponding author), Minist Hlth, Key Lab Neonatal Dis, 399 Wan Yuan Rd, Shanghai 201102, Peoples R China.
EM szheng@shmu.edu.cn
RI Rui, Dong/LDG-0179-2024
FU National Key Clinical Specialty Construction Programs of China;
Municipal Hospitals' Project for Emerging and Frontier Technology of
Shanghai [SHDC12014106]; National Natural Science Foundation of China
[81370472, 81300517, 81100248, 81500394]; Shanghai City Health Bureau
for Youth Scientific Fund Project [20134y100]; Shanghai Rising-Star
Program [15QA1400800]; Science Foundation of Shanghai [13ZR1451800,
14ZR1404000, 14411969860]
FX This study was supported by National Key Clinical Specialty Construction
Programs of China (2014-2016), Municipal Hospitals' Project for Emerging
and Frontier Technology of Shanghai (SHDC12014106), National Natural
Science Foundation of China (no. 81370472, no. 81300517, no. 81100248
and no. 81500394), Shanghai City Health Bureau for Youth Scientific Fund
Project (no. 20134y100), Shanghai Rising-Star Program (A type) (no.
15QA1400800) and The Science Foundation of Shanghai (no. 13ZR1451800,
no. 14ZR1404000 and no. 14411969860).
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NR 26
TC 1
Z9 2
U1 0
U2 9
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2017
VL 10
IS 3
BP 3451
EP 3455
PG 5
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA ER8PR
UT WOS:000399083300110
DA 2025-01-07
ER
PT J
AU Whitington, PF
Malladi, P
Melin-Aldana, H
Azzam, R
Mack, CL
Sahai, A
AF Whitington, PF
Malladi, P
Melin-Aldana, H
Azzam, R
Mack, CL
Sahai, A
TI Expression of osteopontin correlates with portal biliary proliferation
and fibrosis in biliary atresia
SO PEDIATRIC RESEARCH
LA English
DT Article
ID DEFICIENT MICE; HEPATOCELLULAR-CARCINOMA; INTERSTITIAL FIBROSIS;
ENDOTHELIAL-CELLS; EPITHELIAL-CELLS; TRANSGENIC MICE; STELLATE CELLS;
KUPFFER CELLS; MURINE MODEL; HIGH GLUCOSE
AB The acquired or perinatal form of biliary atresia is a Th1 fibro-inflammatory disease affecting both the extrahepatic and intrahepatic bile ducts. Osteopontin (OPN) is a Th1 cytokine implicated in several fibro-inflammatory and autoimmune diseases. We examined the expression of OPN in acquired biliary atresia in comparison to normal liver and several pediatric cholestatic liver diseases. We also assessed OPN expression by cultured human bile duct epithelial cells. We found that liver OPN mRNA and protein expression were significantly increased in biliary atresia versus normal and other cholestatic diseases. OPN expression in biliary atresia was localized to epithelium of proliferating biliary structures (ductules and/or ducts) and bile plugs contained therein. No portal biliary OPN expression could be demonstrated in normal liver, syndromic biliary atresia, biliary obstruction not due to biliary atresia, and idiopathic neonatal hepatitis. OPN expression by human bile duct epithelial cells in culture was responsive to IL-2 and TNF-alpha. Our results demonstrate an up-regulation of OPN expression by interlobular biliary epithelium in biliary atresia, which correlates with biliary proliferation and portal fibrosis. These findings suggest a role for OPN in the pathogenesis of biliary atresia.
C1 Northwestern Univ, Childrens Mem Hosp, Feinberg Sch Med, Dept Pediat, Chicago, IL 60614 USA.
Univ Colorado, Hlth Sci Ctr, Childrens Hosp, Dept Pediat, Denver, CO 80218 USA.
Northwestern Univ, Childrens Mem Hosp, Feinberg Sch Med, Dept Pathol,,Childrens Mem Res Ctr, Chicago, IL 60614 USA.
C3 Northwestern University; Feinberg School of Medicine; Ann & Robert H.
Lurie Children's Hospital of Chicago; University of Colorado System;
University of Colorado Denver; Children's Hospital Colorado; University
of Colorado Anschutz Medical Campus; Ann & Robert H. Lurie Children's
Hospital of Chicago; Northwestern University; Feinberg School of
Medicine
RP Whitington, PF (corresponding author), Northwestern Univ, Childrens Mem Hosp, Feinberg Sch Med, Dept Pediat, 2300 Childrens Plaza,Box 212, Chicago, IL 60614 USA.
EM p-whitington@northwestern.edu
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NR 65
TC 54
Z9 57
U1 0
U2 5
PU INT PEDIATRIC RESEARCH FOUNDATION, INC
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA
SN 0031-3998
J9 PEDIATR RES
JI Pediatr. Res.
PD JUN
PY 2005
VL 57
IS 6
BP 837
EP 844
DI 10.1203/01.PDR.0000161414.99181.61
PG 8
WC Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics
GA 928TC
UT WOS:000229293600016
PM 15845635
OA Bronze
DA 2025-01-07
ER
PT J
AU Alizadeh, D
Katsanis, E
Larmonier, N
AF Alizadeh, Darya
Katsanis, Emmanuel
Larmonier, Nicolas
TI The Multifaceted Role of Th17 Lymphocytes and Their Associated Cytokines
in Cancer
SO CLINICAL & DEVELOPMENTAL IMMUNOLOGY
LA English
DT Review
ID REGULATORY T-CELLS; GROWTH-FACTOR-BETA; TGF-BETA; T(H)17 CELLS;
IFN-GAMMA; HEPATOCELLULAR-CARCINOMA; TRANSCRIPTION FACTOR; TUMOR-GROWTH;
GM-CSF; DEVELOPMENTAL PLASTICITY
AB While the role of T helper 17 lymphocytes (Th17) in the pathogenesis of autoimmune diseases and in infectious immunity has been relatively well defined, the impact of these cells and their associated cytokines on cancer development is still under debate. Although multiple reports have indicated that Th17 can promote anticancer immunity, others have argued that these cells may exhibit tumor-promoting properties. This dichotomy in the function of Th17 lymphocytes in cancer may be related to the versatile nature of these cells, being capable of differentiating into either proinflammatory Th1 or suppressive FoxP3-expressing Treg cells or hybrid T cell subsets depending on the underlying environmental conditions. In the current review, we examine the role of Th17 lymphocytes and Th17-associated cytokines in cancer and discuss how factors that control their final lineage commitment decision may influence the balance between their tumor-promoting versus tumor-suppressing properties.
C1 [Alizadeh, Darya; Katsanis, Emmanuel; Larmonier, Nicolas] Univ Arizona, Canc Biol Grad Interdisciplinary Program, Tucson, AZ 85724 USA.
[Alizadeh, Darya; Katsanis, Emmanuel; Larmonier, Nicolas] Univ Arizona, Dept Pediat, Steele Childrens Res Ctr, Tucson, AZ 85724 USA.
[Katsanis, Emmanuel; Larmonier, Nicolas] Univ Arizona, Dept Immunobiol, Inst BIO5, Tucson, AZ 85724 USA.
[Katsanis, Emmanuel; Larmonier, Nicolas] Univ Arizona, Arizona Canc Ctr, Tucson, AZ 85724 USA.
C3 University of Arizona; University of Arizona; University of Arizona;
University of Arizona; Arizona Center Cancer Care
RP Larmonier, N (corresponding author), Univ Arizona, Canc Biol Grad Interdisciplinary Program, 1501 N Campbell Ave,POB 245073, Tucson, AZ 85724 USA.
EM nrlarmon@email.arizona.edu
RI Katsanis, Emmanuel/D-9600-2011
FU Cancer Biology Training Grant [T32CA009213]; NIH [R01 CA104926]; AZ
Cancer Center [CA023074]; Tee Up for Tots; PANDA Funds
FX This work was supported by Cancer Biology Training Grant T32CA009213
(Darya Alizadeh), NIH grant R01 CA104926, AZ Cancer Center Support Grant
CA023074, Tee Up for Tots, and PANDA Funds.
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NR 126
TC 32
Z9 35
U1 0
U2 7
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1740-2522
EI 1740-2530
J9 CLIN DEV IMMUNOL
JI Clin. Dev. Immunol.
PY 2013
AR 957878
DI 10.1155/2013/957878
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 286DL
UT WOS:000329445300001
OA gold, Green Published, Green Submitted, Green Accepted
DA 2025-01-07
ER
PT J
AU Basit, S
AF Basit, S.
TI Vitamin D in health and disease: a literature review
SO BRITISH JOURNAL OF BIOMEDICAL SCIENCE
LA English
DT Review
DE Diabetes mellitus; Genetics; Neoplasms; Polymorphisms; Vitamin D
ID D-RECEPTOR GENE; SERUM 25-HYDROXYVITAMIN D; SETTING RECOMMENDATION
LEVELS; D-DEFICIENCY; BINDING-PROTEIN; D 1-ALPHA-HYDROXYLASE;
DIABETES-MELLITUS; COLORECTAL-CANCER; D REQUIREMENT; D ASSAYS
AB Vitamin D, a fat-soluble prohormone, is synthesised in response to sunlight. Vitamin D requires two metabolic conversions, 25-hydroxylation in the liver and 1 alpha-hydroxylation in the kidney, to become active hormone. The active form, 1 alpha,25-(OH)(2)D, binds to the vitamin D receptor (VDR) to modulate gene transcription and regulate mineral ion homeostasis. Vitamin D plays several roles in the body, influencing bone health as well as serum calcium and phosphate levels. Furthermore, vitamin D may modify immune function, cell proliferation, differentiation and apoptosis. Vitamin D deficiency has been associated with numerous health outcomes, including risk of rickets in children or osteomalacia in adults, increased risk of fractures, falls, cancer, autoimmune disease, infectious disease, type 1 and type 2 diabetes, hypertension and heart disease, and other diseases such as multiple sclerosis. Here, vitamin D physiology and metabolism, its genomic action and association of polymorphisms in vitamin D pathway genes with different diseases are reviewed by focusing on new findings published in the literature.
C1 Taibah Univ, Ctr Genet & Inherited Dis, Madinah Al Munawara, Saudi Arabia.
C3 Taibah University
RP Basit, S (corresponding author), Taibah Univ, Ctr Genet & Inherited Dis, Madinah Al Munawara, Saudi Arabia.
EM sbasit.phd@gmail.com
RI Basit, Sulman/Q-7939-2018
OI Basit, Sulman/0000-0003-4294-6825
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NR 169
TC 110
Z9 125
U1 2
U2 45
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0967-4845
J9 BRIT J BIOMED SCI
JI Br. J. Biomed. Sci.
PY 2013
VL 70
IS 4
BP 161
EP 172
DI 10.1080/09674845.2013.11669951
PG 12
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA AN8JC
UT WOS:000340849400008
PM 24400428
DA 2025-01-07
ER
PT J
AU Okahata, S
Sakamoto, K
Mitsumatsu, T
Kondo, Y
Noso, S
Ikegami, H
Shiba, T
AF Okahata, Sumie
Sakamoto, Kentaro
Mitsumatsu, Takako
Kondo, Yuko
Noso, Shinsuke
Ikegami, Hiroshi
Shiba, Teruo
TI Fulminant type 1 diabetes associated with Isolated ACTH deficiency
induced by anti-programmed cell death antibody insight into the
pathogenesis of autoimmune endocrinopathy-
SO ENDOCRINE JOURNAL
LA English
DT Article
DE Fulminant type 1 diabetes; Isolated ACTH deficiency; Cytotoxic
T-lymphocyte-associated protein 4; HLA; Nivolumab
ID ISOLATED ADRENOCORTICOTROPIN DEFICIENCY; HYPOPHYSITIS; IMMUNOTHERAPY;
BLOCKADE; THERAPY; ONSET; GENE
AB Therapeutic blocking antibodies against programmed death 1 (PD1) and cytotoxic T-lymphocyte antigen 4 (CTLA4) are applied for advanced cancer therapy, but induce a wide range of immune-related adverse events. In our recent case of a 52-year-old female doctor suffering from breast cancer having metastasized to the lung and liver. it was decided to use nivolumab to prevent the disease progressing after excisional surgeries and multiple chemotherapies. One month after completing the nivolumab course, fatigue, hypoglycemia and hypotension developed and isolated ACTH deficiency (IAD) was diagnosed. A further month later, under steroid supplementation, hyperglycemia emerged alongside thirst and polydipsia, prompting a diagnosis of fulminant type 1 diabetes (ET1D). Her susceptibility to type 1 diabetes was examined by HLA haplotype and CTLA4 gene polymorphism analyses. Polymorphisms CT60G>A and +49G>A in CTLA4 both generated a GG genotype. Our patient manifested one of the rarest combinations of autoimmune disease induced by nivolumab. Whereas the FILA haplotype was unsusceptible to autoimmune type I diabetes, polymorphisms of CTLA4, the antibody of which frequently causes hypophysitis, were susceptible to FT ID. Peripheral modulation of activated T cells, mainly by PD-1 antibodies, induced FT1D associated with IAD in patients with CTLA4 polymorphism. This case reveals hints of the T-cell etiology in T1D and evidence of CTLA4 involvement in IAD.
C1 [Okahata, Sumie; Sakamoto, Kentaro; Mitsumatsu, Takako; Kondo, Yuko; Shiba, Teruo] Toho Univ, Div Diabet & Metab, Ohashi Med Ctr, Tokyo 1538515, Japan.
[Noso, Shinsuke; Ikegami, Hiroshi] Kindai Univ, Dept Endocrinol Metab & Diabet, Fac Med, Osaka 5898511, Japan.
C3 Toho University; Kindai University (Kinki University)
RP Shiba, T (corresponding author), Toho Univ, Div Diabet & Metab, Ohashi Med Ctr, Meguro Ward, 2-22-36 Ohashi, Tokyo 1538515, Japan.
EM teruo.shiba@med.toho-u.ac.jp
RI Ikegami, Hiroshi/AGP-9878-2022; Noso, Shinsuke/CAA-6248-2022
OI Noso, Shinsuke/0000-0002-0943-8450
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NR 27
TC 19
Z9 25
U1 0
U2 6
PU JAPAN ENDOCRINE SOC
PI KYOTO
PA 75 YANAGINOBANBA NISHIIRU-MASUYA-CHO, SANJOU-DORI, NAKAGYOU-KU, KYOTO,
604-8111, JAPAN
SN 0918-8959
EI 1348-4540
J9 ENDOCR J
JI Endocr. J.
PY 2019
VL 66
IS 4
BP 295
EP 300
DI 10.1507/endocrj.EJ18-0328
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA HW5DQ
UT WOS:000466709700002
PM 30814440
OA gold
DA 2025-01-07
ER
PT J
AU Orzáez, M
Gortat, A
Mondragón, L
Perez-Payá, E
AF Orzaez, Mar
Gortat, Anna
Mondragon, Laura
Perez-Paya, Enrique
TI Peptides and Peptide Mimics as Modulators of Apoptotic Pathways
SO CHEMMEDCHEM
LA English
DT Review
DE apoptosis; caspases; inhibitors; peptides; peptidomimetics
ID BCL-2 FAMILY-MEMBERS; TNF RECEPTOR SUPERFAMILY; STRUCTURE-BASED DESIGN;
PROGRAMMED CELL-DEATH; NF-KAPPA-B; INTERLEUKIN-1-BETA CONVERTING-ENZYME;
FLUORESCENCE POLARIZATION ASSAY; REVERSIBLE CASPASE INHIBITORS;
PROTEIN-PROTEIN INTERACTIONS; MEMBRANE-PERMEABLE PEPTIDES
AB Programmed cell death or apoptosis is a noninvasive and strictly regulated cellular process required for organism development and tissue homeostasis. Deficiencies in apoptotic pathways are the source of many diseases such as cancer, neurodegenerative and autoimmune diseases, and disorders related to an inappropriate loss of cells such as heart failure, stroke, and liver injury. Validation of the various points of intervention as targets for drug development has been the subject of a vast number of studies. Peptides are essential tools for drug discovery, as well as preclinical and pharmaceutical drug development.
C1 [Orzaez, Mar; Gortat, Anna; Mondragon, Laura; Perez-Paya, Enrique] Ctr Invest Principe Felipe, Dept Med Chem, Valencia 46012, Spain.
[Perez-Paya, Enrique] CSIC, Inst Biomed Valencia, Valencia 46010, Spain.
C3 Prince Felipe Research Center; Consejo Superior de Investigaciones
Cientificas (CSIC); CSIC - Instituto de Biomedicina de Valencia (IBV)
RP Perez-Payá, E (corresponding author), Ctr Invest Principe Felipe, Dept Med Chem, Avda Autopista Saler 16, Valencia 46012, Spain.
EM eperez@cipf.es
RI Mondragon Martinez, Laura/P-1670-2018; Orzaez, Mar/B-4992-2014
OI Mondragon Martinez, Laura/0000-0002-3257-045X; Orzaez,
Mar/0000-0003-3231-5835
FU Spanish Ministry of Science and Innovation [B102004-998, B102007-60666]
FX This work was partially supported by the Spanish Ministry of Science and
Innovation (grants B102004-998 and B102007-60666), and the Centro de
Investigacion Principe Felipe. L.M. is supported by an FPJ fellowship
from MEC.
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NR 202
TC 4
Z9 8
U1 0
U2 14
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1860-7179
EI 1860-7187
J9 CHEMMEDCHEM
JI ChemMedChem
PD FEB
PY 2009
VL 4
IS 2
BP 146
EP 160
DI 10.1002/cmdc.200800246
PG 15
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 413OU
UT WOS:000263803200001
PM 19021159
DA 2025-01-07
ER
PT J
AU Ivanova, EA
Orekhov, AN
AF Ivanova, Ekaterina A.
Orekhov, Alexander N.
TI T Helper Lymphocyte Subsets and Plasticity in Autoimmunity and Cancer:
An Overview
SO BIOMED RESEARCH INTERNATIONAL
LA English
DT Review
ID GROWTH-FACTOR-BETA; TGF-BETA; TH17 CELLS; TUMOR-IMMUNITY;
HEPATOCELLULAR-CARCINOMA; CYTOKINE PRODUCTION; EFFECTOR FUNCTIONS;
MONONUCLEAR-CELLS; IL-9 PRODUCTION; INTERLEUKIN 22
AB In response to cytokine signalling and other factors, CD4-positive T lymphocytes differentiate into distinct populations that are characterized by the production of certain cytokines and are controlled by different master transcription factors. The spectrum of such populations, which was initially limited to Th1 and Th2 subsets, is currently broadened to include Th17 and Treg subsets, as well as a number of less studied subtypes, such as Tfh, Th9, andTh22. Although these subsets appear to be relatively stable, certain plasticity exists that allows for transition between the subsets and formation of hybrid transition forms. This provides the immune system flexibility needed for adequate response to pathogens but, at the same time, can play a role in the pathogenic processes in cases of deregulation. In this review, we will discuss the properties of T lymphocyte subsets and their plasticity, as well as its implications for cancer and autoimmune diseases.
C1 [Ivanova, Ekaterina A.] Katholieke Univ Leuven, Dept Pediat Nephrol & Growth & Regenerat, B-3000 Louvain, Belgium.
[Ivanova, Ekaterina A.] Katholieke Univ Leuven Hosp, B-3000 Louvain, Belgium.
[Orekhov, Alexander N.] Inst Gen Pathol & Pathophysiol, Lab Angiopathol, Moscow 125315, Russia.
[Orekhov, Alexander N.] Skolkovo Innovat Ctr, Inst Atherosclerosis Res, Moscow 121609, Russia.
[Orekhov, Alexander N.] Moscow MV Lomonosov State Univ, Dept Biophys, Fac Biol, Moscow 119991, Russia.
C3 KU Leuven; Flanders Institute for Biotechnology (VIB); KU Leuven;
University Hospital Leuven; Russian Academy of Medical Sciences;
Institute of General Pathology & Pathophysiology, RAMS; Lomonosov Moscow
State University
RP Ivanova, EA (corresponding author), Katholieke Univ Leuven, Dept Pediat Nephrol & Growth & Regenerat, B-3000 Louvain, Belgium.
EM kate.ivanov@gmail.com
FU Russian Scientific Foundation [14-15-00112]; Russian Science Foundation
[14-15-00112] Funding Source: Russian Science Foundation
FX This work was supported by Russian Scientific Foundation (Grant no.
14-15-00112).
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NR 125
TC 91
Z9 107
U1 0
U2 9
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-6133
EI 2314-6141
J9 BIOMED RES INT
JI Biomed Res. Int.
PY 2015
VL 2015
AR 327470
DI 10.1155/2015/327470
PG 9
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA CW0IQ
UT WOS:000364673200001
PM 26583100
OA Green Published, Green Submitted, hybrid
DA 2025-01-07
ER
PT J
AU Cui, DX
Xu, DQ
Yue, SJ
Yan, CQ
Liu, WJ
Fu, RJ
Ma, WF
Tang, YP
AF Cui, Dongxiao
Xu, Dingqiao
Yue, Shijun
Yan, Chaoqun
Liu, Wenjuan
Fu, Ruijia
Ma, Wenfu
Tang, Yuping
TI Recent advances in the pharmacological applications and liver toxicity
of triptolide
SO CHEMICO-BIOLOGICAL INTERACTIONS
LA English
DT Review
DE Triptolide; Pharmacological applications; Hepatotoxicity; Oxidative
stress; Inflammation; CYP450 enzymes
ID PREGNANE X RECEPTOR; INDUCED HEPATOTOXICITY; OXIDATIVE STRESS; GUT
MICROBIOTA; PPAR-ALPHA; INFLAMMATION; HEPATOCYTES; ACTIVATION;
APOPTOSIS; EFFICACY
AB Triptolide is a predominant active component of Triptergium wilfordii Hook. F, which has been used for the treatment of cancers and autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and diabetic nephropathy. Therefore, triptolide and its derivates are considered to have promising prospects for development into drugs. However, the clinical application of triptolide is limited due to various organ toxicities, especially liver toxicity. The potential mechanism of triptolide-induced hepatotoxicity has attracted increasing attention. Over the past five years, studies have revealed that triptolide-induced liver toxicity is involved in metabolic imbalance, oxidative stress, inflammations, autophagy, apoptosis, and the regulation of cytochrome P450 (CYP450) enzymes, gut microbiota and immune cells. In this review, we summarize the pharmacological applications and hepatotoxicity mechanism of triptolide, which will provide solid theoretical evidence for further research of triptolide.
C1 [Cui, Dongxiao; Xu, Dingqiao; Yue, Shijun; Liu, Wenjuan; Fu, Ruijia; Tang, Yuping] Shaanxi Univ Chinese Med, Key Lab Shaanxi Adm Tradit Chinese Med TCM Compati, State Key Lab Res & Dev Characterist Qin Med Resou, Shaanxi Key Lab Chinese Med Fundamentals & New Dru, Xian, Peoples R China.
[Yan, Chaoqun] Shanxi Med Univ, Sch Pharmaceut Sci, Taiyuan 030001, Peoples R China.
[Ma, Wenfu] Beijing Univ Chinese Med, Sch Life Sci, Beijing 102488, Peoples R China.
C3 Shaanxi University of Chinese Medicine; Shanxi Medical University;
Beijing University of Chinese Medicine
RP Tang, YP (corresponding author), Shaanxi Univ Chinese Med, Key Lab Shaanxi Adm Tradit Chinese Med TCM Compati, State Key Lab Res & Dev Characterist Qin Med Resou, Shaanxi Key Lab Chinese Med Fundamentals & New Dru, Xian, Peoples R China.
EM yupingtang@sntcm.edu.cn
RI Yue, Shi-Jun/ABH-6263-2020; liu, wenjuan/JDX-0971-2023
FU National Natural Science Foundation of China [82274084]; Shaanxi
Administration of Traditional Chinese Medicine Traditional Chinese
Medicine Inheritance and Innovation [2021-02-22-007]; Subject Innovation
Team of Shaanxi University of Chinese Medicine [2019-YL10]
FX National Natural Science Foundation of China (82274084) , Shaanxi
Administration of Traditional Chinese Medicine Traditional Chinese
Medicine Inheritance and Innovation and Key Scientific Research Proj-ect
of "Qin Medicine" Development (2021-02-22-007) , and Subject Innovation
Team of Shaanxi University of Chinese Medicine (2019-YL10) .
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NR 111
TC 12
Z9 12
U1 10
U2 51
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0009-2797
EI 1872-7786
J9 CHEM-BIOL INTERACT
JI Chem.-Biol. Interact.
PD SEP 1
PY 2023
VL 382
AR 110651
DI 10.1016/j.cbi.2023.110651
EA JUL 2023
PG 8
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA P4WG6
UT WOS:001050675200001
PM 37516378
DA 2025-01-07
ER
PT J
AU Afshar, ZM
Babazadeh, A
Janbakhsh, A
Mansouri, F
Sio, TT
Sullman, MJM
Carson-Chahhoud, K
Hosseinzadeh, R
Barary, M
Ebrahimpour, S
AF Mohseni Afshar, Zeinab
Babazadeh, Arefeh
Janbakhsh, Alireza
Mansouri, Feizollah
Sio, Terence T.
Sullman, Mark J. M.
Carson-Chahhoud, Kristin
Hosseinzadeh, Rezvan
Barary, Mohammad
Ebrahimpour, Soheil
TI Coronavirus disease 2019 (Covid-19) vaccination recommendations in
special populations and patients with existing comorbidities
SO REVIEWS IN MEDICAL VIROLOGY
LA English
DT Review
DE Covid-19; efficacy; immunocompromise; safety; SARS-CoV-2; vaccination
ID IMMUNE-RESPONSE; RISK-FACTORS; RHEUMATOID-ARTHRITIS; SARS-COV-2
VACCINES; INFLUENZA VACCINE; UNITED-STATES; IMPACT; OBESITY;
IMMUNOGENICITY; PREGNANCY
AB Vaccination against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a crucial step in ending the current worldwide pandemic. However, several particularly vulnerable groups in the population were not included in sufficient numbers in coronavirus disease 2019 (Covid-19) vaccine trials. Therefore, as science advances, the advice for vaccinating these special populations against Covid-19 will continue to evolve. This focused review provides the latest recommendations and considerations for these special populations (i.e., patients with rheumatologic and autoimmune disorders, cancer, transplant recipients, chronic liver diseases, end-stage renal disease, neurologic disorders, psychiatric disorders, diabetes mellitus, obesity, cardiovascular diseases, chronic obstructive pulmonary disease, human immunodeficiency virus, current smokers, pregnant and breastfeeding women, the elderly, children, and patients with allergic reactions) using the currently available research evidence.
C1 [Mohseni Afshar, Zeinab; Janbakhsh, Alireza; Mansouri, Feizollah] Kermanshah Univ Med Sci, Imam Reza Hosp, Clin Res Dev Ctr, Kermanshah, Iran.
[Babazadeh, Arefeh; Ebrahimpour, Soheil] Babol Univ Med Sci, Hlth Res Inst, Infect Dis & Trop Med Res Ctr, Ganjafrooz Blvd, Babol 4717647745, Iran.
[Sio, Terence T.] Mayo Clin, Dept Radiat Oncol, Phoenix, AZ USA.
[Sullman, Mark J. M.] Univ Nicosia, Dept Social Sci, Nicosia, Cyprus.
[Sullman, Mark J. M.] Univ Nicosia, Dept Life & Hlth Sci, Nicosia, Cyprus.
[Carson-Chahhoud, Kristin] Univ South Australia, Australian Ctr Precis Hlth, Adelaide, SA, Australia.
[Hosseinzadeh, Rezvan; Barary, Mohammad] Babol Univ Med Sci, Student Res Comm, Babol, Iran.
C3 Kermanshah University of Medical Sciences; Babol University of Medical
Sciences; Mayo Clinic; Mayo Clinic Phoenix; University of Nicosia;
University of Nicosia; University of South Australia; Babol University
of Medical Sciences
RP Ebrahimpour, S (corresponding author), Babol Univ Med Sci, Hlth Res Inst, Infect Dis & Trop Med Res Ctr, Ganjafrooz Blvd, Babol 4717647745, Iran.
EM drsoheil1503@yahoo.com
RI Ebrahimpour, Soheil/C-5060-2017; Hosseinzadeh, Rezvan/AAO-1583-2021;
Carson-Chahhoud, Kristin/I-1916-2018; Barary, Mohammad/AAW-3952-2020
OI Sio, Terence/0000-0003-4210-5479; Carson-Chahhoud,
Kristin/0000-0001-9966-9289; Sullman, Mark/0000-0001-7920-6818; Barary,
Mohammad/0000-0001-8733-9370
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NR 178
TC 24
Z9 24
U1 1
U2 23
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1052-9276
EI 1099-1654
J9 REV MED VIROL
JI Rev. Med. Virol.
PD MAY
PY 2022
VL 32
IS 3
AR e2309
DI 10.1002/rmv.2309
EA OCT 2021
PG 17
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Virology
GA 1H5KD
UT WOS:000709877200001
PM 34677889
OA Green Published
DA 2025-01-07
ER
PT J
AU Szajnik, M
Nowak-Markwitz, E
Szczepanski, M
Spaczynski, M
Linke, K
Zeromski, J
AF Szajnik, Marta
Nowak-Markwitz, Ewa
Szczepanski, Miroslaw
Spaczynski, Marek
Linke, Krzysztof
Zeromski, Jan
TI The diagnostic problems in patient with ascites, elevated Ca 125 level
and autoantibodies against nuclear antigens and smooth muscle antigens
mimicking advanced ovarian carcinoma - case study
SO GINEKOLOGIA POLSKA
LA English
DT Article
DE ovarian neoplasms; ascites; CA-125 antigen; autoantibodies
ID DISEASES; BENIGN; SERUM
AB The paper describes a case of 26-year-old patient primarily suspected to suffer from the ovarian or peritoneum cancer due to high level of Ca 125 antigen and ascites. During exploratory laparotomy, neoplastic process was excluded, which was confirmed by histopathological examination. Further diagnostic tests were performed.
The patient was not infected with hepatitic B or C virus, and there was no biochemical evidence of liver disease. Detailed, wide biochemical and immunological investigations detected antinuclear and anti smooth muscle autoantibodies in the blood serum. Afterwards, the patient was admitted to the Department of Gastroenterology and autoimmune chronic hepatitis was confirmed.
C1 [Szajnik, Marta; Nowak-Markwitz, Ewa; Spaczynski, Marek] Univ Med Sci, Dept Gynecol Oncol, Poznan, Poland.
[Szczepanski, Miroslaw; Zeromski, Jan] Univ Med Sci, Dept Clin Immunol, Poznan, Poland.
[Linke, Krzysztof] Univ Med Sci, Dept Gastroenterol & Human Nutr, Poznan, Poland.
RP Nowak-Markwitz, E (corresponding author), Uniwersytet Med, Klin Onkol Ginekol, Ul Polna 33, PL-60535 Poznan, Poland.
EM ewamarkwitz@poczta.fm
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NR 6
TC 1
Z9 2
U1 0
U2 1
PU STUDIO K
PI POZNAN
PA KRZYSZTOF MOLENDA, UL PODGORNA 19-17, POZNAN, 60-828, POLAND
SN 0017-0011
J9 GINEKOL POL
JI Ginekol. Pol.
PD MAY
PY 2008
VL 79
IS 5
BP 375
EP 377
PG 3
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA 333DL
UT WOS:000258132400010
PM 18624115
DA 2025-01-07
ER
PT J
AU Jo, JO
Kang, YJ
Ock, MS
Song, KS
Jeong, MJ
Jeong, SJ
Choi, YH
Ko, EJ
Leem, SH
Kim, S
Kim, HS
Cha, HJ
AF Jo, Jin-Ok
Kang, Yun-Jeong
Ock, Mee Sun
Song, Kyoung Seob
Jeong, Moon-Jin
Jeong, Soon-Jeong
Choi, Yung Hyun
Ko, Eun-Ji
Leem, Sun-Hee
Kim, Suhkmann
Kim, Heui-Soo
Cha, Hee-Jae
TI Expression profiles of HERV-K Env protein in normal and cancerous
tissues
SO GENES & GENOMICS
LA English
DT Article
DE HERV-K; Env; Tissue microarray; Pathology; Expression; Cancer; Normal
ID ENDOGENOUS-RETROVIRUS-K; HUMAN GENOME; CELL; HML-2; ELEMENTS;
MECHANISMS; SEQUENCES; PLACENTA; RNA
AB Human endogenous retroviruses (HERVs) have been proposed as etiological cofactors in chronic diseases such as cancer, autoimmunity and neurological disease. HERV RNA expression is also increased in several autoimmune diseases and cancers. However, only a few studies have analyzed the expression levels of HERV-derived proteins in normal and diseased tissues. Here, we investigated the expression profiles of HERV-K Env protein, which is the most well-known pathogen, from normal and cancer tissue microarray. Normal and cancer tissue microarray slides containing 59 normal or 60 tumor surgical specimens, respectively were immunostained with mouse monoclonal antibody to HERV-K and staining intensity was scored. The expression of HERV-K Env protein is generally low in normal tissues but high in specific tissues including bronchus submucosal gland, salivary gland acini, pancreas acini, testis seminiferous tubule, uterine cervix epithelium, ovary stroma, skin epidermis, and heart. The expression of HERV-K Env protein in tumors was usually higher than normal tissues and specifically high in breast, liver, stomach, prostate, and ovarian cancer. This study provides protein expression profiles of HERV-K Env protein in human normal and cancer tissues and provides a good reference for further studies on the expression patterns and roles of HERV-K Env protein in normal organs and various cancers. Further studies with specific organs or cancers and a statistically significant numbers of samples are necessary.
C1 [Jo, Jin-Ok; Kang, Yun-Jeong; Ock, Mee Sun; Cha, Hee-Jae] Kosin Univ, Coll Med, Dept Parasitol, Busan 602702, South Korea.
[Jo, Jin-Ok; Kang, Yun-Jeong; Ock, Mee Sun; Cha, Hee-Jae] Kosin Univ, Coll Med, Dept Genet, Busan 602702, South Korea.
[Song, Kyoung Seob] Kosin Univ, Coll Med, Dept Physiol, Busan 602702, South Korea.
[Jeong, Moon-Jin] Chosun Univ, Sch Dent, Dept Oral Histol & Dev Biol, Gwangju, South Korea.
[Jeong, Soon-Jeong] Youngsan Univ, Coll Hlth Sci, Dept Dent Hyg, Yangsan, South Korea.
[Choi, Yung Hyun] Dong Eui Univ, Coll Oriental Med, Dept Biochem, Busan, South Korea.
[Ko, Eun-Ji; Leem, Sun-Hee] Dong A Univ, Dept Biol Sci, Busan, South Korea.
[Kim, Suhkmann] Pusan Natl Univ, Coll Nat Sci, Dept Chem, Busan, South Korea.
[Kim, Heui-Soo] Pusan Natl Univ, Coll Nat Sci, Dept Biol Sci, Busan 609735, South Korea.
[Cha, Hee-Jae] Kosin Univ, Coll Med, Inst Med Sci, Busan 602702, South Korea.
C3 Chosun University; Dong-Eui University; Dong A University; Pusan
National University; Pusan National University
RP Cha, HJ (corresponding author), Kosin Univ, Coll Med, Dept Parasitol, Busan 602702, South Korea.; Cha, HJ (corresponding author), Kosin Univ, Coll Med, Dept Genet, Busan 602702, South Korea.; Kim, HS (corresponding author), Pusan Natl Univ, Coll Nat Sci, Dept Biol Sci, Busan 609735, South Korea.; Cha, HJ (corresponding author), Kosin Univ, Coll Med, Inst Med Sci, Busan 602702, South Korea.
EM khs307@pusan.ac.kr; hcha@kosin.ac.kr
RI Kim, Sun-Jae/A-1790-2009; Kim, Heui-Soo/ABF-3773-2021; Kim,
Young-Il/ISS-7678-2023; Ko, Eun-Ji/AAW-4888-2021; 정, 순정/GVU-3261-2022;
Cha, Hee-Jae/AFO-8772-2022
OI Jeong, Soon-Jeong/0000-0002-8959-4663; Ko, Eun-Ji/0000-0002-3758-1019;
Kim, Heui-Soo/0000-0002-5226-6594
FU High-Tech Convergence Technology Development Program through National
Research Foundation of Korea (NRF) - Ministry of Science, ICT& Future
Planning [2014M3C1A3051981]; Kosin University College of Medicine
FX This research was supported by High-Tech Convergence Technology
Development Program through the National Research Foundation of Korea
(NRF) funded by the Ministry of Science, ICT& Future Planning
(2014M3C1A3051981) and a grant from the Kosin University College of
Medicine (2014).
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NR 31
TC 8
Z9 8
U1 1
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1976-9571
EI 2092-9293
J9 GENES GENOM
JI Genes Genom.
PD JAN
PY 2016
VL 38
IS 1
BP 91
EP 107
DI 10.1007/s13258-015-0343-9
PG 17
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA DF3LR
UT WOS:000371246200010
DA 2025-01-07
ER
PT J
AU DuBrock, HM
Krowka, MJ
Forde, KA
Krok, K
Patel, M
Sharkoski, T
Sprys, M
Lin, G
Oh, JK
Mottram, CD
Scanlon, PD
Fallon, MB
Kawut, SM
AF DuBrock, Hilary M.
Krowka, Michael J.
Forde, Kimberly A.
Krok, Karen
Patel, Mamta
Sharkoski, Tiffany
Sprys, Michael
Lin, Grace
Oh, Jae K.
Mottram, Carl D.
Scanlon, Paul D.
Fallon, Michael B.
Kawut, Steven M.
TI Clinical Impact of Intrapulmonary Vascular Dilatation in Candidates for
Liver Transplant
SO CHEST
LA English
DT Article
DE hepatopulmonary syndrome; intrapulmonary vascular dilatation; liver
transplant
ID HEPATOPULMONARY SYNDROME; PORTOPULMONARY HYPERTENSION; REFERENCE VALUES;
GAS-EXCHANGE; CIRRHOSIS; DISEASE; ECHOCARDIOGRAPHY; PROGESTERONE;
POPULATION; GUIDELINES
AB BACKGROUND: Intrapulmonary vascular dilatations (IPVD) frequently are detected in patients with liver disease by the delayed appearance of microbubbles at contrast-enhanced echocardiography. IPVD with an elevated alveolar-arterial (A-a) gradient define hepatopulmonary syndrome (HPS); however, the importance of IPVD in the absence of abnormal gas exchange is unknown. We aimed to determine the clinical impact of IPVD in patients with liver disease.
METHODS: We performed a cross-sectional study within the Pulmonary Vascular Complications of Liver Disease 2 Study, a multicenter, prospective cohort study of patients being evaluated for liver transplant. We excluded patients with obstructive or restrictive lung disease, HPS, or intracardiac shunting. We compared patients with and those without IPVD.
RESULTS: Forty-six patients with IPVD and 81 patients without IPVD were included. Patients with IPVD were more likely to have autoimmune hepatitis and less likely to have cryptogenic cirrhosis and hepatocellular carcinoma. Patients with IPVD had higher Child-Pugh scores (6 [interquartile range (IQR), 5-7] vs 5 [IQR, 4-7]; P = .04), possibly higher Model for End-Stage Liver Disease scores (14.5 [IQR, 11.6-15.8] vs 12.2 [IQR, 9.4-15.5]; P = .06), higher PaO2 levels (97.9 [IQR, 92.0-103.0] vs 89.0 [IQR, 82.0-96.9] mm Hg; P < .001), and lower A-a gradients (9.9 [IQR, 6.2-13.5] vs 14.9 [IQR, 9.0-21.8] mm Hg; P < .001). Symptoms and quality of life were similar between the groups.
CONCLUSIONS: Autoimmune hepatitis and increased liver disease severity were associated with the presence of IPVD, which was characterized by higher PaO2 levels. Future studies to better characterize IPVD pathogenesis and the relationship of IPVD to HPS are warranted.
C1 [DuBrock, Hilary M.; Krowka, Michael J.; Mottram, Carl D.; Scanlon, Paul D.] Mayo Clin, Div Pulm & Crit Care Med, Rochester, MN USA.
[Lin, Grace; Oh, Jae K.] Mayo Clin, Dept Med, Rochester, MN USA.
[Lin, Grace; Oh, Jae K.] Mayo Clin, Dept Cardiovasc Dis, Rochester, MN USA.
[Forde, Kimberly A.; Patel, Mamta; Sharkoski, Tiffany; Sprys, Michael; Kawut, Steven M.] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Forde, Kimberly A.; Patel, Mamta; Sharkoski, Tiffany; Sprys, Michael; Kawut, Steven M.] Univ Penn, Dept Med, Philadelphia, PA 19104 USA.
[Krok, Karen] Penn State Milton S Hershey Med Ctr, Div Gastroenterol, Hershey, PA USA.
[Krok, Karen] Penn State Milton S Hershey Med Ctr, Dept Med, Hershey, PA USA.
[Fallon, Michael B.] Univ Arizona, Dept Med, Phoenix, AZ USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic; University of Pennsylvania;
University of Pennsylvania; Pennsylvania Commonwealth System of Higher
Education (PCSHE); Pennsylvania State University; Penn State Health;
Pennsylvania Commonwealth System of Higher Education (PCSHE);
Pennsylvania State University; Penn State Health; University of Arizona
RP DuBrock, HM (corresponding author), Mayo Clin Minnesota, 200 First St SW, Rochester, MN 55905 USA.
EM dubrock.hilary@mayo.edu
RI DuBrock, Hilary/X-9427-2019
OI Krok, Karen/0000-0001-5849-5251
FU National Heart, Lung, and Blood Institute of the National Institutes of
Health [R01HL113988, K24 HL103844]
FX This study was funded by the National Heart, Lung, and Blood Institute
of the National Institutes of Health [Grants R01HL113988 and K24
HL103844].
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NR 27
TC 15
Z9 15
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0012-3692
J9 CHEST
JI Chest
PD FEB
PY 2018
VL 153
IS 2
BP 414
EP 426
DI 10.1016/j.chest.2017.09.035
PG 13
WC Critical Care Medicine; Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Respiratory System
GA FV1AE
UT WOS:000424292600025
PM 28987478
OA Green Published
DA 2025-01-07
ER
PT J
AU Nipu, MAI
Kundu, S
Alam, SS
Dina, AN
Hasan, MA
Khan, M
Khalil, MI
Hossan, T
Islam, MA
AF Nipu, Md. Ashraful Islam
Kundu, Shoumik
Alam, Sayeda Sadia
Dina, Ashrafun Naher
Hasan, Md. Ashraful
Khan, Mohammad
Khalil, Md. Ibrahim
Hossan, Tareq
Islam, Md Asiful
TI Anticardiolipin Antibodies in Patients with Cancer: A Case-Control Study
SO CANCERS
LA English
DT Article
DE cancer; neoplasms; anticardiolipin antibody; antiphospholipid
antibodies; autoimmunity
ID ANTIPHOSPHOLIPID ANTIBODIES; RISK-FACTORS; PREVALENCE; MECHANISMS;
THROMBOSIS; CRITERIA
AB Antiphospholipid antibodies are highly prevalent in autoimmune diseases and mainly associated with thromboembolic events, which is one of the major reasons for cancer-related mortality. Confirmed adult cancer patients were included (n = 40) with an equal number of age- and sex-matched healthy controls. The presence and concentration of anticardiolipin antibodies were investigated by the enzyme-linked immunosorbent assay using the venous blood samples. aCL antibodies were detected in 60.0% (n = 24) of the cancer patients compared to none in the healthy controls (p < 0.001). The serum concentration of aCL antibodies was significantly higher in cancer patients than controls (p < 0.001) and ranged from 89.0 U/mL to 133.0 U/mL among the aCL-positive patients. All the lung cancer patients (n = 6) were diagnosed with positive aCL, and a borderline significant association of aCL antibody positivity was observed in colon cancer patients (p = 0.051). About 72.7% of the advanced-stage cancer individuals and 81.8% of the cancer patients who underwent surgery were diagnosed with positive aCL antibodies. A significant association of aCL antibody positivity was observed with cancer patients comorbid with heart diseases (p = 0.005). The prevalence and serum levels of aCL antibodies were significantly higher in cancer patients compared to healthy controls. Cancer patients (i.e., lung, liver, and colon), at advanced-stage, comorbid with heart diseases, who underwent surgery, were more likely to be diagnosed with aCL antibodies.
C1 [Nipu, Md. Ashraful Islam; Kundu, Shoumik; Alam, Sayeda Sadia; Hasan, Md. Ashraful; Khalil, Md. Ibrahim; Hossan, Tareq] Jahangirnagar Univ, Fac Biol Sci, Dept Biochem & Mol Biol, Dhaka 1342, Bangladesh.
[Dina, Ashrafun Naher] Enam Med Coll, Dept Pharmacol & Therapeut, Dhaka 1340, Bangladesh.
[Khan, Mohammad] New Age Hlth Sci Res Ctr, Chattogram 4331, Bangladesh.
[Hossan, Tareq] Washington Univ, Dept Bone Marrow Transplant, Sch Med, St Louis, MO 63110 USA.
[Islam, Md Asiful] Univ Birmingham, Inst Metab & Syst Res, Coll Med & Dent Sci, WHO Collaborating Ctr Global Womens Hlth, Birmingham B15 2TT, England.
C3 Jahangirnagar University; Washington University (WUSTL); University of
Birmingham
RP Hossan, T (corresponding author), Jahangirnagar Univ, Fac Biol Sci, Dept Biochem & Mol Biol, Dhaka 1342, Bangladesh.; Hossan, T (corresponding author), Washington Univ, Dept Bone Marrow Transplant, Sch Med, St Louis, MO 63110 USA.; Islam, MA (corresponding author), Univ Birmingham, Inst Metab & Syst Res, Coll Med & Dent Sci, WHO Collaborating Ctr Global Womens Hlth, Birmingham B15 2TT, England.
EM thossan@juniv.edu; m.a.islam@bham.ac.uk
RI Kundu, Shoumik/HSD-8886-2023; Hossan, Tareq/JDV-7366-2023; Khan,
Mohammad/AAA-9567-2019; Hasan, Md. Ashraful/HLQ-5832-2023; Islam, Md
Asiful/C-4655-2013
OI Khan, Mohammad/0000-0003-4711-9976; Khalil, Md.
Ibrahim/0000-0002-8358-0252; Hasan, Md. Ashraful/0000-0003-4008-5494;
Islam, Md Asiful/0000-0001-5937-6473; Hossan, Tareq/0000-0003-4625-2900;
/0000-0002-6795-1391
FU National Science and Technology Fellowship 2019-2020, Bangladesh;
University of Birmingham
FX This research was funded by National Science and Technology Fellowship
2019-2020, Bangladesh. The open-access publication was supported by the
University of Birmingham, Birmingham B15 2TT, UK.
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NR 31
TC 1
Z9 1
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD APR
PY 2023
VL 15
IS 7
AR 2087
DI 10.3390/cancers15072087
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D6JF5
UT WOS:000969766500001
PM 37046748
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Glintborg, D
Andersen, M
AF Glintborg, Dorte
Andersen, Marianne
TI Medical comorbidity in polycystic ovary syndrome with special focus on
cardiometabolic, autoimmune, hepatic and cancer diseases: an updated
review
SO CURRENT OPINION IN OBSTETRICS & GYNECOLOGY
LA English
DT Review
DE BMI; diagnosis codes; morbidity; polycystic ovary syndrome
ID OBESITY; ADIPOSITY; RISK
AB Purpose of reviewPolycystic ovary syndrome (PCOS) is defined by hyperandrogenism, irregular menses and polycystic ovaries when other causes are excluded. The possible implication of increased morbidity in PCOS for screening and follow-up is uncertain and is reviewed in this article.Recent findingsThe increased risk of type 2 diabetes and cardiovascular disease in PCOS is closely associated with BMI. Women with PCOS should be screened for the elements of the metabolic syndrome upon diagnosis. Measurement of HbA1c and the lipid accumulation product could be important tools to differentiate women with high metabolic risk. The immune function in PCOS is impaired with increased secretion of autoantibodies and increased risk of type 1 diabetes, asthma and thyroid disease. The occurrence of thyroid disease could be modified by BMI and D-vitamin status. Screening for diabetes and thyroid disease is part of routine evaluation for endocrine diseases at baseline in PCOS, whereas the necessity of prospective screening for thyroid disease awaits future studies. Especially obese women with PCOS are at an increased risk of nonalcoholic fatty liver disease, gall bladder disease and endometrial cancer.SummaryRecent data support that screening and follow-up in patients with PCOS should be stratified according to BMI.
C1 [Glintborg, Dorte; Andersen, Marianne] Odense Univ Hosp, Dept Endocrinol, Odense C, Denmark.
C3 University of Southern Denmark; Odense University Hospital
RP Glintborg, D (corresponding author), Klovervaenget 6,3rd Floor, DK-5000 Odense C, Denmark.
EM dorte.glintborg@rsyd.dk
RI Andersen, Marianne/AAE-1751-2019; Glintborg, Dorte/AAE-3676-2019
OI Glintborg, Dorte/0000-0002-8338-8025; Andersen,
Marianne/0000-0002-4603-9504
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NR 66
TC 17
Z9 19
U1 0
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-872X
EI 1473-656X
J9 CURR OPIN OBSTET GYN
JI Curr. Opin. Obstet. Gynecol.
PD DEC
PY 2017
VL 29
IS 6
BP 390
EP 396
DI 10.1097/GCO.0000000000000410
PG 7
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA FM5QG
UT WOS:000415091000005
PM 28901968
DA 2025-01-07
ER
PT J
AU Wu, YT
Che, YG
Zhang, Y
Xiong, YL
Shu, C
Jiang, J
Li, GZ
Guo, L
Qiao, TY
Li, SW
Li, O
Chang, N
Zhang, XX
Zhang, MZ
Qiu, D
Xi, HT
Li, JG
Chen, XX
Ye, MX
Zhang, J
AF Wu, Yingtong
Che, Yinggang
Zhang, Yong
Xiong, Yanlu
Shu, Chen
Jiang, Jun
Li, Gaozhi
Guo, Lin
Qiao, Tianyun
Li, Shuwen
Li, Ou
Chang, Ning
Zhang, Xinxin
Zhang, Minzhe
Qiu, Dan
Xi, Hangtian
Li, Jinggeng
Chen, Xiangxiang
Ye, Mingxiang
Zhang, Jian
TI Association between genetically proxied glucosamine and risk of cancer
and non-neoplastic disease: A Mendelian randomization study
SO FRONTIERS IN GENETICS
LA English
DT Article
DE glucosamine; cancer risk; Mendelian randomization; single-nucleotide
polymorphisms; causality
ID PAIN-RELATED DISABILITY; CHONDROITIN SULFATE; CELLS; INHIBITION;
EXPRESSION; PROTEIN; AUTOPHAGY; OSTEOARTHRITIS; SUSCEPTIBILITY;
HYDROCHLORIDE
AB Introduction Observational investigations have examined the impact of glucosamine use on the risk of cancer and non-neoplastic diseases. However, the findings from these studies face limitations arising from confounding variables, reverse causation, and conflicting reports. Consequently, the establishment of a causal relationship between habitual glucosamine consumption and the risk of cancer and non-neoplastic diseases necessitates further investigation.Methods For Mendelian randomization (MR) investigation, we opted to employ single-nucleotide polymorphisms (SNPs) as instruments that exhibit robust associations with habitual glucosamine consumption. We obtained the corresponding effect estimates of these SNPs on the risk of cancer and non-neoplastic diseases by extracting summary data for genetic instruments linked to 49 varied cancer types amounting to 378,284 cases and 533,969 controls, as well as 20 non-neoplastic diseases encompassing 292,270 cases and 842,829 controls. Apart from the primary analysis utilizing inverse-variance weighted MR, we conducted two supplementary approaches to account for potential pleiotropy (MR-Egger and weighted median) and assessed their respective MR estimates. Furthermore, the results of the leave-one-out analysis revealed that there were no outlying instruments.Results Our results suggest divergence from accepted biological understanding, suggesting that genetically predicted glucosamine utilization may be linked to an increased vulnerability to specific illnesses, as evidenced by increased odds ratios and confidence intervals (95% CI) for diseases, such as malignant neoplasm of the eye and adnexa (2.47 [1.34-4.55]), benign neoplasm of the liver/bile ducts (2.12 [1.32-3.43]), benign neoplasm of the larynx (2.01 [1.36-2.96]), melanoma (1.74 [1.17-2.59]), follicular lymphoma (1.50 [1.06-2.11]), autoimmune thyroiditis (2.47 [1.49-4.08]), and autoimmune hyperthyroidism (1.93 [1.17-3.18]). In contrast to prior observational research, our genetic investigations demonstrate a positive correlation between habitual glucosamine consumption and an elevated risk of sigmoid colon cancer, lung adenocarcinoma, and benign neoplasm of the thyroid gland.Conclusion Casting doubt on the purported purely beneficial association between glucosamine ingestion and prevention of neoplastic and non-neoplastic diseases, habitual glucosamine ingestion exhibits dichotomous effects on disease outcomes. Endorsing the habitual consumption of glucosamine as a preventative measure against neoplastic and non-neoplastic diseases cannot be supported.
C1 [Wu, Yingtong; Che, Yinggang; Zhang, Yong; Chang, Ning; Zhang, Minzhe; Qiu, Dan; Xi, Hangtian; Li, Jinggeng; Chen, Xiangxiang; Zhang, Jian] Air Force Med Univ, Xijing Hosp, Dept Pulm & Crit Care Med, Xian, Peoples R China.
[Wu, Yingtong; Li, Shuwen; Li, Ou] Air Force Healthcare Ctr Special Serv, Sanat 1, Hangzhou, Peoples R China.
[Xiong, Yanlu; Shu, Chen; Qiao, Tianyun] Air Force Med Univ, Tangdu Hosp, Dept Thorac Surg, Xian, Peoples R China.
[Jiang, Jun] Air Force Med Univ, Dept Hlth Serv, Xian, Peoples R China.
[Li, Gaozhi] Peoples Liberat Army, Unit 94498, Nanyang, Peoples R China.
[Guo, Lin] Air Force Med Univ, Tangdu Hosp, Dept Obstet & Gynecol, Xian, Peoples R China.
[Zhang, Xinxin] Chinese Peoples Liberat Army Gen Hosp, Coll Pulm & Crit Care Med, Med Ctr 8, Beijing, Peoples R China.
[Ye, Mingxiang] Nanjing Univ, Jinling Hosp, Sch Med, Dept Resp Med, Nanjing, Peoples R China.
C3 Air Force Military Medical University; Air Force Military Medical
University; Air Force Military Medical University; Air Force Military
Medical University; Chinese People's Liberation Army General Hospital;
Nanjing University
RP Zhang, J (corresponding author), Air Force Med Univ, Xijing Hosp, Dept Pulm & Crit Care Med, Xian, Peoples R China.; Ye, MX (corresponding author), Nanjing Univ, Jinling Hosp, Sch Med, Dept Resp Med, Nanjing, Peoples R China.
EM mingxiangye88@163.com; Zhangjfmmu@163.com
RI Zhang, Jianjun/AAH-1943-2020; Zhang, Minzhe/AAC-8284-2019
FU National Natural Science Foundation of China [81773153]; Air-Force
Medical University [2021LC2115]
FX The author(s) declare financial support was received for the research,
authorship, and/or publication of this article. This study was funded by
grants from the National Natural Science Foundation of China (81773153)
and the Air-Force Medical University (2021LC2115).
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NR 81
TC 0
Z9 0
U1 0
U2 0
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD JUN 27
PY 2024
VL 15
AR 1293668
DI 10.3389/fgene.2024.1293668
PG 13
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA XZ6U9
UT WOS:001265549000001
PM 38993479
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Bhat, M
Mara, K
Dierkhising, R
Watt, KD
AF Bhat, Mamatha
Mara, Kristin
Dierkhising, Ross
Watt, Kymberly D.
TI Gender, Race and Disease Etiology Predict De Novo Malignancy Risk After
Liver Transplantation: Insights for Future Individualized Cancer
Screening Guidance
SO TRANSPLANTATION
LA English
DT Article
ID LATE MORTALITY; SKIN-CANCER; RECIPIENTS; SIROLIMUS; IMMUNOSUPPRESSION;
COHORT
AB Background. Malignancy after liver transplant (LT) is a leading cause of mortality, but data is limited. The aim of this study was to identify patients at higher risk for de novo malignancies after LT in a large multicenter database. Methods. The Scientific Registry of Transplant Recipients database comprising all 108 412 LT recipients across the United States between 1987 and March 2015 was analyzed with a median follow-up of 6.95 years. Potential risk factors for malignancies after LT were assessed using Cox regression analysis for the outcome of time to first malignancy. Results. Mean age 51.9 +/- 10.8 years, 64.6% male, 74.5% white, and 15.8% with previous malignancy. Malignancies during follow-up were 4,483 (41.3%) skin, 1519 (14.0%) hematologic, and 4842 (44.7%) solid organ. The 1 0-year probability of de novo malignancy was 11.5% (11.3-11.8%). On multivariable analysis, age by decade (hazard ratio [HR], 1.52; P < 0.001), male sex (HR, 1.28; P < 0.001), white race (compared with other races: HR, 1.45-2.04; P < 0.001), mutiorgan transplant (HR, 1.35; P < 0.001), previous malignancy (HR, 1.34; P < 0.001), and alcoholic liver disease, autoimmune, nonalcoholic steatohepatitis (HR, 1.35; P < 0.001), and primary sclerosing cholangitis pre-LT (compared with hepatitis C virus, P < 0.0as not (P = NS). Conclusions. This large data set demonstrates the effects of ethnicity/race and etiologie01) were associated with higher risk of post-LT malignancy, but type of immunosuppression ws of liver disease, particularly nonalcoholic steatohepatitis as additional risk factors for cancer after LT. Patients with these high-risk characteristics should be more regularly and diligently screened.
C1 [Bhat, Mamatha] Univ Hlth Network, Multiorgan Transplant Program, Toronto, ON, Canada.
[Bhat, Mamatha] Univ Toronto, Dept Med, Toronto, ON, Canada.
[Mara, Kristin] Mayo Clin, Div Biomed Stat & Informat, Rochester, MN USA.
[Dierkhising, Ross; Watt, Kymberly D.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA.
C3 University of Toronto; University Health Network Toronto; University of
Toronto; Mayo Clinic; Mayo Clinic
RP Watt, KD (corresponding author), Mayo Clin & Mayo Fdn, Div Gastroenterol & Hepatol, CH-10200,First St SW, Rochester, MN 55905 USA.
EM watt.kymberly@mayo.edu
RI Bhat, Mamatha/AAC-4333-2020
OI Bhat, Mamatha/0000-0003-1960-8449; Cole, Kristin/0000-0002-8783-0191
CR Alberu J, 2011, TRANSPLANTATION, V92, P303, DOI 10.1097/TP.0b013e3182247ae2
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Xiol X, 2001, LIVER TRANSPLANT, V7, P971, DOI 10.1053/jlts.2001.28744
NR 31
TC 26
Z9 30
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD JAN
PY 2019
VL 103
IS 1
BP 91
EP 100
DI 10.1097/TP.0000000000002113
PG 10
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA HG5UH
UT WOS:000455044100025
PM 29377876
OA Bronze
DA 2025-01-07
ER
PT J
AU Zenouzi, R
Weismüller, TJ
Jorgensen, KK
Bubenheim, M
Lenzen, H
Hübener, P
Schulze, K
Weiler-Normann, C
Sebode, M
Ehlken, H
Pannicke, N
Hartl, J
Peiseler, M
Hübener, S
Karlsen, TH
Boberg, KM
Manns, MP
Lohse, AW
Schramm, C
AF Zenouzi, Roman
Weismueller, Tobias J.
Jorgensen, Kristin K.
Bubenheim, Michael
Lenzen, Henrike
Huebener, Peter
Schulze, Kornelius
Weiler-Normann, Christina
Sebode, Marcial
Ehlken, Hanno
Pannicke, Nadine
Hartl, Johannes
Peiseler, Moritz
Huebener, Sina
Karlsen, Tom H.
Boberg, Kirsten M.
Manns, Michael P.
Lohse, Ansgar W.
Schramm, Christoph
TI No Evidence That Azathioprine Increases Risk of Cholangiocarcinoma in
Patients With Primary Sclerosing Cholangitis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Dysplasia; Surveillance; Thiopurines; Bile Duct Tumor; Immunosuppressant
ID HEPATOCELLULAR-CARCINOMA; LIVER-TRANSPLANTATION; BILIARY DYSPLASIA;
DIAGNOSIS; LYMPHOMA; THERAPY; CANCER
AB BACKGROUND & AIMS: Patients with primary sclerosing cholangitis (PSC) are at increased risk for developing cholangiocarcinoma (CCA). Patients with PSC also can have inflammatory bowel diseases (IBDs) or features of autoimmune hepatitis (AM), and therefore are treated with azathioprine. Azathioprine has been associated with an increased risk for malignancy, therefore we investigated whether azathioprine use affects the risk of CCA in persons with PSC.
METHODS: We performed a retrospective study of well-defined patients with PSC using data collected from 3 large-volume, tertiary care centers in Germany and Norway. We analyzed data from 638 patients (70% men; 5900 patient-years of follow-up evaluation); 91 patients had received azathioprine therapy (considered to be effective at 90 days after first intake). Risk analysis was performed using the Cox proportional hazard model when risks competing with study end points were present.
RESULTS: Of patients who received azathioprine treatment, 3.3% developed CCA, compared with 6.8% of patients without azathioprine treatment. However, azathioprine did not significantly affect the risk for CCA (hazard ratio, 0.96; 95% confidence interval, 0.29-3.13; P = .94). The only factor associated with an increased risk of CCA was age 35 years or older at PSC diagnosis (hazard ratio, 3.87; 95% confidence interval, 1.96-7.67; P < .01). Patient sex, concomitant IBD, or AIH did not affect the risk of CCA. Overall, the cumulative 10-year incidence of CCA was 4.6% and the cumulative 15-year incidence was 7.7%.
CONCLUSIONS: A retrospective analysis of patients with PSC treated at tertiary centers in Europe found no evidence that azathioprine significantly affects the risk of CCA. Azathioprine therefore should not be withheld from patients with PSC and concomitant IBD and/or AIH.
C1 [Zenouzi, Roman; Huebener, Peter; Schulze, Kornelius; Weiler-Normann, Christina; Sebode, Marcial; Ehlken, Hanno; Pannicke, Nadine; Hartl, Johannes; Peiseler, Moritz; Huebener, Sina; Lohse, Ansgar W.; Schramm, Christoph] Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Martinistr 52, D-20246 Hamburg, Germany.
[Weismueller, Tobias J.] Univ Bonn, Dept Internal Med 1, Bonn, Germany.
[Jorgensen, Kristin K.; Karlsen, Tom H.; Boberg, Kirsten M.] Norwegian Primary Sclerosing Cholangitis Res Ctr, Oslo, Norway.
[Boberg, Kirsten M.] Natl Hosp Norway, Oslo Univ Hosp, Div Canc Med Surg & Transplantat, Sect Gastroenterol,Dept Transplantat Med, Oslo, Norway.
[Jorgensen, Kristin K.] Akershus Univ Hosp, Dept Gastroenterol, Lorenskog, Norway.
[Bubenheim, Michael] Univ Rouen, Dept Biostat, Hosp Charles Nicolle, Rouen, France.
[Lenzen, Henrike; Manns, Michael P.] Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Hannover, Germany.
[Boberg, Kirsten M.] Univ Oslo, Inst Clin Med, Oslo, Norway.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Bonn; University of Oslo; National Hospital Norway;
University of Oslo; Universite de Rouen Normandie; CHU de Rouen;
Hannover Medical School; University of Oslo
RP Zenouzi, R; Schramm, C (corresponding author), Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Martinistr 52, D-20246 Hamburg, Germany.
EM rzenouzi@uke.de; cschramm@uke.de
RI Huebener, Peter/AAF-2593-2020; Weismüller, Tobias/I-1879-2019; Schramm,
Christoph/X-6915-2019; Lenzen, Henrike/ACV-9744-2022; Manns,
Michael/AFG-3063-2022; Jørgnensen, Kristin Kaasen/JCP-1730-2023
OI Weismuller, Tobias J./0000-0001-9736-1483; Huebener,
Peter/0000-0001-7558-7625; Hartl, Johannes/0000-0002-4037-9938;
Peiseler, Moritz/0000-0001-6195-3866
FU Deutsche Forschungsgemeinschaft [Sonderforschungsbereich 841, KFO306];
YAEL; Helmut and Hannelore Greve foundation
FX This study was supported by the Deutsche Forschungsgemeinschaft
(Sonderforschungsbereich 841 and KFO306) and by the YAEL and the Helmut
and Hannelore Greve foundation.
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NR 35
TC 14
Z9 15
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD DEC
PY 2016
VL 14
IS 12
BP 1806
EP 1812
DI 10.1016/j.cgh.2016.07.032
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EE0QD
UT WOS:000389283100021
PM 27521513
DA 2025-01-07
ER
PT J
AU Andrade, RJ
Chalasani, N
Björnsson, ES
Suzuki, A
Kullak-Ublick, GA
Watkins, PB
Devarbhavi, H
Merz, M
Lucena, MI
Kaplowitz, N
Aithal, GP
AF Andrade, Raul J.
Chalasani, Naga
Bjornsson, Einar S.
Suzuki, Ayako
Kullak-Ublick, Gerd A.
Watkins, Paul B.
Devarbhavi, Harshad
Merz, Michael
Isabel Lucena, M.
Kaplowitz, Neil
Aithal, Guruprasad P.
TI Drug-induced liver injury
SO NATURE REVIEWS DISEASE PRIMERS
LA English
DT Article
ID SALT EXPORT PUMP; STEVENS-JOHNSON SYNDROME; SINGLE-CENTER EXPERIENCE;
CAUSALITY ASSESSMENT; IN-VITRO; RISK-FACTORS; ACETAMINOPHEN
HEPATOTOXICITY; GLUTAMATE-DEHYDROGENASE; IDIOPATHIC AUTOIMMUNE;
EPIDERMAL NECROLYSIS
AB Drug-induced liver injury (DILI) is an adverse reaction to drugs or other xenobiotics that occurs either as a predictable event when an individual is exposed to toxic doses of some compounds or as an unpredictable event with many drugs in common use. Drugs can be harmful to the liver in susceptible individuals owing to genetic and environmental risk factors. These risk factors modify hepatic metabolism and excretion of the DILI-causative agent leading to cellular stress, cell death, activation of an adaptive immune response and a failure to adapt, with progression to overt liver injury. Idiosyncratic DILI is a relative rare hepatic disorder but can be severe and, in some cases, fatal, presenting with a variety of phenotypes, which mimic other hepatic diseases. The diagnosis of DILI relies on the exclusion of other aetiologies of liver disease as specific biomarkers are still lacking. Clinical scales such as CIOMS/RUCAM can support the diagnostic process but need refinement. A number of clinical variables, validated in prospective cohorts, can be used to predict a more severe DILI outcome. Although no pharmacological therapy has been adequately tested in randomized clinical trials, corticosteroids can be useful, particularly in the emergent form of DILI related to immune-checkpoint inhibitors in patients with cancer.
C1 [Andrade, Raul J.] Univ Malaga, Hosp Univ Virgen de la Victoria, Inst Invest Biomed Malaga IBIMA, Unidad Gest Clin Enfermedades Digest, Malaga, Spain.
[Andrade, Raul J.; Isabel Lucena, M.] Ctr Invest Biomed Red Enfermedades Hepat & Digest, Madrid, Spain.
[Chalasani, Naga] Indiana Univ Sch Med, Div Gastroenterol, Indianapolis, IN 46202 USA.
[Bjornsson, Einar S.] Univ Iceland, Landspitali Univ Hosp Reykjav, Dept Gastroenterol, Reykjavik, Iceland.
[Bjornsson, Einar S.] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Suzuki, Ayako] Duke Univ, Gastroenterol, Durham, NC USA.
[Suzuki, Ayako] Durham VA Med Ctr, Gastroenterol, Durham, NC USA.
[Kullak-Ublick, Gerd A.; Merz, Michael] Univ Zurich, Univ Hosp Zurich, Dept Clin Pharmacol & Toxicol, Zurich, Switzerland.
[Kullak-Ublick, Gerd A.] Novartis Pharmaceut, Mechanist Safety CMO & Patient Safety, Global Drug Dev, Basel, Switzerland.
[Watkins, Paul B.] Univ N Carolina, UNC Eshelman Sch Pharm, Chapel Hill, NC 27515 USA.
[Watkins, Paul B.] Univ N Carolina, Inst Drug Safety Sci, Chapel Hill, NC 27515 USA.
[Devarbhavi, Harshad] St Johns Med Coll Hosp, Dept Gastroenterol & Hepatol, Bangalore, Karnataka, India.
[Merz, Michael] AstraZeneca, Patient Safety, Gaithersburg, MD USA.
[Isabel Lucena, M.] Univ Malaga, Serv Farmacol Clin, Inst Invest Biomed Malaga IBIMA, Hosp Univ Virgen de la Victoria, Malaga, Spain.
[Kaplowitz, Neil] Keck Sch Med, Div Gastroenterol & Liver Dis, Dept Med, Los Angeles, CA USA.
[Aithal, Guruprasad P.] Nottingham Univ Hosp NHS Trust, Natl Inst Hlth Res, Nottingham Digest Dis Biomed Res Ctr, Nottingham, England.
[Aithal, Guruprasad P.] Univ Nottingham, Nottingham, England.
C3 Instituto de Investigacion Biomedica de Malaga y Plataforma en
Nanomedicina (IBIMA); Universidad de Malaga; CIBER - Centro de
Investigacion Biomedica en Red; CIBEREHD; Indiana University System;
Indiana University Bloomington; University of Iceland; University of
Iceland; Duke University; US Department of Veterans Affairs; Veterans
Health Administration (VHA); Durham VA Medical Center; University of
Zurich; University Zurich Hospital; Novartis; University of North
Carolina; University of North Carolina Chapel Hill; The Hamner
Institutes for Health Sciences; University of North Carolina; University
of North Carolina Chapel Hill; St. John's National Academy of Health
Sciences; St. John's Medical College; AstraZeneca; Universidad de
Malaga; Instituto de Investigacion Biomedica de Malaga y Plataforma en
Nanomedicina (IBIMA); University of Nottingham; Nottingham University
Hospital NHS Trust; University of Nottingham
RP Andrade, RJ (corresponding author), Univ Malaga, Hosp Univ Virgen de la Victoria, Inst Invest Biomed Malaga IBIMA, Unidad Gest Clin Enfermedades Digest, Malaga, Spain.; Andrade, RJ; Lucena, MI (corresponding author), Ctr Invest Biomed Red Enfermedades Hepat & Digest, Madrid, Spain.; Lucena, MI (corresponding author), Univ Malaga, Serv Farmacol Clin, Inst Invest Biomed Malaga IBIMA, Hosp Univ Virgen de la Victoria, Malaga, Spain.
EM andrade@uma.es; lucena@uma.es
RI Suzuki, Ayako/A-7656-2009; Devarbhavi, Harshad/AAM-2468-2021
OI Kullak-Ublick, Gerd A./0000-0002-0757-4408; Suzuki,
Ayako/0000-0003-1824-1067; Merz, Michael/0000-0002-2758-5948;
Devarbhavi, Harshad/0000-0002-3593-3746; Aithal,
Guruprasad/0000-0003-3924-4830
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NR 200
TC 445
Z9 472
U1 24
U2 166
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2056-676X
J9 NAT REV DIS PRIMERS
JI Nat. Rev. Dis. Primers
PD AUG 22
PY 2019
VL 5
AR 58
DI 10.1038/s41572-019-0105-0
PG 22
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA IT1PE
UT WOS:000482617400001
PM 31439850
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Itoh, A
Adams, D
Huang, WT
Wu, YH
Kachapati, K
Bednar, KJ
Leung, PSC
Zhang, WC
Flavell, RA
Gershwin, ME
Ridgway, WM
AF Itoh, Arata
Adams, David
Huang, Wenting
Wu, Yuehong
Kachapati, Kritika
Bednar, Kyle J.
Leung, Patrick S. C.
Zhang, Weici
Flavell, Richard A.
Gershwin, M. Eric
Ridgway, William M.
TI Enoxacin Up-Regulates MicroRNA Biogenesis and Down-Regulates Cytotoxic
CD8 T-Cell Function in Autoimmune Cholangitis
SO HEPATOLOGY
LA English
DT Article
ID PRIMARY BILIARY CHOLANGITIS; IRON CHAPERONES PCBP1; TGF-BETA; RNA
INTERFERENCE; TOPOISOMERASE-II; CANCER CELLS; ARGONAUTE; GROWTH;
TRANSCRIPTION; ACTIVATION
AB BACKGROUND AND AIMS: Primary biliary cholangitis (PBC) is a prototypical organ-specific autoimmune disease that is mediated by autoreactive T-cell attack and destruction of cholangiocytes. Despite the clear role of autoimmunity in PBC, immune-directed therapies have failed to halt PBC, including biologic therapies effective in other autoimmune diseases. MicroRNA (miRNA) dysregulation is implicated in the pathogenesis (PBC). In the dominant-negative TGF-beta receptor type II (dnTGF beta RII) mouse model of PBC, autoreactive CD8 T cells play a major pathogenic role and demonstrate a striking pattern of miRNA down-regulation. Enoxacin is a small molecule fluoroquinolone that enhances miRNA biogenesis, partly by stabilizing the interaction of transactivation response RNA-binding protein with Argonaute (Ago) 2.
APPROACH AND RESULTS: We hypothesized that correcting aberrant T-cell miRNA expression with enoxacin in dnTGF beta RII mice could modulate autoreactive T-cell function and prevent PBC. Here, we show that liver-infiltrating dnTGF beta RII CD8 T cells have significantly decreased levels of the miRNA biogenesis molecules prolyl 4-hydroxylase subunit alpha 1 (P4HA1) and Ago2 along with significantly increased levels of granzyme B and perforin. Enoxacin treatment significantly up-regulated miRNAs in dnTGF beta RII CD8 T cells and effectively treated autoimmune cholangitis in dnTGF beta RII mice. Enoxacin treatment directly altered T cells both ex vivo and in vitro, resulting in altered memory subset numbers, decreased proliferation, and decreased interferon-gamma production. Enoxacin significantly decreased CD8 T-cell expression of the transcription factor, Runx3, and significantly decreased perforin expression at both the mRNA and protein levels.
CONCLUSIONS: Enoxacin increases miRNA expression in dnTGF beta RII CD8 T cells, reduces CD8 T-cell pathogenicity, and effectively halted progression of autoimmune biliary disease. Targeting the miRNA pathway is a therapeutic approach to autoimmunity that corrects pathological miRNA abnormalities in autoreactive T cells.
C1 [Itoh, Arata; Adams, David; Huang, Wenting; Wu, Yuehong; Kachapati, Kritika; Bednar, Kyle J.; Ridgway, William M.] Univ Cincinnati, Coll Med, Div Immunol Allergy & Rheumatol, Cincinnati, OH USA.
[Leung, Patrick S. C.; Zhang, Weici; Gershwin, M. Eric; Ridgway, William M.] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Flavell, Richard A.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA.
C3 University System of Ohio; University of Cincinnati; University of
California System; University of California Davis; Yale University
RP Ridgway, WM (corresponding author), Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, 451 Hlth Sci Dr,Suite 6515, Davis, CA 95616 USA.
EM wmridgway@ucdavis.edu
RI Flavell, Richard/ACH-3245-2022
OI Itoh, Arata/0000-0003-0024-5115; Zhang, Weici/0000-0002-3193-6851
FU NIH [2R01DK090019--05]; VA Merit [1I01BX003821--01A1]
FX Supported by NIH 2R01DK090019--05 (to M. E. G. and W. M. R.) and VA
Merit 1I01BX003821--01A1 (to W. M. R.).
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NR 54
TC 11
Z9 12
U1 1
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD AUG
PY 2021
VL 74
IS 2
BP 835
EP 846
DI 10.1002/hep.31724
EA AUG 2021
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA UF3RR
UT WOS:000683244100001
PM 33462854
OA hybrid
DA 2025-01-07
ER
PT J
AU Jeon, YG
Kim, YY
Lee, G
Kim, JB
AF Jeon, Yong Geun
Kim, Ye Young
Lee, Gung
Kim, Jae Bum
TI Physiological and pathological roles of lipogenesis
SO NATURE METABOLISM
LA English
DT Review
ID STEROL-REGULATORY-ELEMENT; FATTY-ACID SYNTHASE; DE-NOVO LIPOGENESIS;
BROWN ADIPOSE-TISSUE; ACETYL-COA CARBOXYLASE; LIVER-X-RECEPTOR;
ATP-CITRATE LYASE; REDUCES HEPATIC STEATOSIS; LEUCINE ZIPPER PROTEIN;
ENZYME GENE-EXPRESSION
AB Lipids are essential metabolites, which function as energy sources, structural components and signalling mediators. Most cells are able to convert carbohydrates into fatty acids, which are often converted into neutral lipids for storage in the form of lipid droplets. Accumulating evidence suggests that lipogenesis plays a crucial role not only in metabolic tissues for systemic energy homoeostasis but also in immune and nervous systems for their proliferation, differentiation and even pathophysiological roles. Thus, excessive or insufficient lipogenesis is closely associated with aberrations in lipid homoeostasis, potentially leading to pathological consequences, such as dyslipidaemia, diabetes, fatty liver, autoimmune diseases, neurodegenerative diseases and cancers. For systemic energy homoeostasis, multiple enzymes involved in lipogenesis are tightly controlled by transcriptional and post-translational modifications. In this Review, we discuss recent findings regarding the regulatory mechanisms, physiological roles and pathological importance of lipogenesis in multiple tissues such as adipose tissue and the liver, as well as the immune and nervous systems. Furthermore, we briefly introduce the therapeutic implications of lipogenesis modulation.
C1 [Jeon, Yong Geun; Kim, Ye Young; Lee, Gung; Kim, Jae Bum] Seoul Natl Univ, Inst Mol Biol & Genet, Ctr Adipocyte Struct & Funct, Sch Biol Sci, Seoul, South Korea.
C3 Seoul National University (SNU)
RP Kim, JB (corresponding author), Seoul Natl Univ, Inst Mol Biol & Genet, Ctr Adipocyte Struct & Funct, Sch Biol Sci, Seoul, South Korea.
EM jaebkim@snu.ac.kr
RI KIM, BYOUNG HYUCK/IRZ-5874-2023; JEON, YONGGEUN/ABE-4093-2021; Kim,
Dong-Young/J-2737-2012
OI KIM, YE YOUNG/0000-0002-3598-5757; Jeon, Yong Geun/0000-0002-1422-9151;
lee, gung/0000-0002-0223-7955; KIM, Jae Bum/0000-0003-2337-6935
FU National Research Foundation - Korean government [NRF-2020R1A3B2078617]
FX AcknowledgementsWe thank all the laboratory members for helping with
reading and commenting on the manuscript. This work was supported by the
National Research Foundation, funded by the Korean government
(NRF-2020R1A3B2078617 to J.B.K.).
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NR 382
TC 60
Z9 66
U1 42
U2 177
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
EI 2522-5812
J9 NAT METAB
JI Nat. Metab.
PD MAY
PY 2023
VL 5
IS 5
BP 735
EP 759
DI 10.1038/s42255-023-00786-y
EA MAY 2023
PG 25
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA H9EC3
UT WOS:000982079100002
PM 37142787
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Mammadova, J
Redden, A
Cruz, R
Ellison, M
Gatewood, T
Duff, C
Canella, A
Somboonwit, C
Sriaroon, C
Dasso, JF
Harville, T
Ismail-Khan, R
Walter, JE
AF Mammadova, Jamila
Redden, Anna
Cruz, Rachel
Ellison, Maryssa
Gatewood, Tyra
Duff, Carla
Canella, Anthony
Somboonwit, Charurut
Sriaroon, Chakrapol
Dasso, Joseph F.
Harville, Terry
Ismail-Khan, Roohi
Walter, Jolan E.
TI Case Report: Initial Treatment Adjustments and Complications in Ovarian
Cancer Patient With Inborn Error of Immunity
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE antibody deficiency; primary immunodeficiency; ovarian cancer; case
report; inborn error of immunity
ID AIDS-DEFINING CANCERS; IMMUNODEFICIENCY
AB BackgroundPatients with inborn errors of immunity (IEI) have increased risk of developing cancers secondary to impaired anti-tumor immunity. Treatment of patients with IEI and cancer is challenging as chemotherapy can exacerbate infectious susceptibility. However, the literature on optimal cancer treatment in the setting of IEI is sparse. ObjectivesWe present a patient with specific antibody deficiency with normal immunoglobins (SADNI), immune dysregulation (ID), and stage III ovarian carcinoma as an example of the need to modify conventional treatment in the context of malignancy, IEI, and ongoing infections. MethodsThis is a retrospective chart review of the patient's clinical manifestations, laboratory evaluation and treatment course. ResultsOur patient is a female with SADNI and ID diagnosed with stage III ovarian carcinoma at 60 years of age. Her ID accounted for antinuclear antibody positive (ANA+) mixed connective tissue diseases, polyarthralgia, autoimmune neutropenia, asthma, autoimmune thyroiditis, and Celiac disease. Due to the lack of precedent in the literature, her treatment was modified with continuous input from infectious disease, allergy/immunology and oncology specialist using a multidisciplinary approach.The patient completed debulking surgery and 6 cycles of chemotherapy. The dosing for immunoglobulin replacement therapy was increased for prophylaxis. Chemotherapy doses were lowered for all cycles preemptively for IEI. The therapy included carboplatin, paclitaxel, bevacizumab, and pegfilgrastim. The patient completed six-months of maintenance medication involving bevacizumab.Her treatment course was complicated by Mycobacterium avium-complex (MAC) infection, elevated bilirubin and liver enzymes attributed to excessive immunoglobulin replacement therapy, and urinary tract infection (UTI) and incontinence.Cancer genetic analysis revealed no targetable markers and primary immunodeficiency gene panel of 407 genes by Invitae was unrevealing. Lab tests revealed no evidence of Epstein-Barr Virus (EBV) infection. Post-chemotherapy imaging revealed no evidence of cancer for 1 year and 4 months, but the disease relapsed subsequently. The patient's lung scarring requires vigilance. ConclusionsOur patient with ovarian cancer and IEI required modified treatment and prevention of complications. In cases of IEI, optimal chemotherapy should be titrated to minimize immunosuppression yet treat cancer aggressively while decreasing the risk of infection with prophylactic antibiotics and prolonged post-treatment surveillance, including pulmonary evaluation.
C1 [Mammadova, Jamila; Cruz, Rachel] Univ S Florida, Morsani Coll Med, Tampa, FL 33612 USA.
[Redden, Anna] Florida Atlantic Univ, Charles E Schmidt Coll Med, Boca Raton, FL USA.
[Ellison, Maryssa; Duff, Carla; Dasso, Joseph F.; Walter, Jolan E.] Univ S Florida, Morsani Coll Med, Dept Pediat, Div Allergy & Immunol, Tampa, FL USA.
[Gatewood, Tyra] H Lee Moffitt Canc Ctr & Res Inst, Dept Pharm, Gynecol & Neuro Oncol Clin, Tampa, FL USA.
[Canella, Anthony; Somboonwit, Charurut; Sriaroon, Chakrapol] Univ S Florida, Morsani Coll Med, Dept Internal Med, Div Infect Dis & Int Med, Tampa, FL USA.
[Harville, Terry] Univ Arkansas Med Sci, Dept Pathol & Lab Serv, Div Hematol, Little Rock, AR USA.
[Harville, Terry] Univ Arkansas Med Sci, Dept Internal Med, Little Rock, AR USA.
[Ismail-Khan, Roohi] H Lee Moffitt Canc Ctr & Res Inst, Dept Cardiooncol, Tampa, FL USA.
C3 State University System of Florida; University of South Florida; State
University System of Florida; Florida Atlantic University; State
University System of Florida; University of South Florida; H Lee Moffitt
Cancer Center & Research Institute; State University System of Florida;
University of South Florida; University of Arkansas System; University
of Arkansas Medical Sciences; University of Arkansas System; University
of Arkansas Medical Sciences; H Lee Moffitt Cancer Center & Research
Institute
RP Mammadova, J (corresponding author), Univ S Florida, Morsani Coll Med, Tampa, FL 33612 USA.
EM jmammadova@usf.edu
RI Walter, Joan/ABD-6225-2021
CR Akram SM., 2022, Mycobacterium Avium Intracellulare
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NR 24
TC 4
Z9 4
U1 0
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JUN 29
PY 2022
VL 12
AR 843741
DI 10.3389/fonc.2022.843741
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2Z9SC
UT WOS:000826907200001
PM 35847860
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Gamblin, TC
Krasinskas, AM
Slivka, AS
Tublin, ME
Demetris, J
Shue, E
Caro, S
Marsh, JW
Moser, AJ
AF Gamblin, T. Clark
Krasinskas, A. M.
Slivka, A. S.
Tublin, M. E.
Demetris, Jake
Shue, Eveline
Caro, Susan
Marsh, J. Wallis
Moser, A. James
TI Fibroinflammatory Biliary Stricture: A Rare Bile Duct Lesion
Masquerading as Cholangiocarcinoma
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Article; Proceedings Paper
CT Digestive Disease Week/107th Annual Meeting of the
American-Gastroenterological-Association
CY MAY 19-24, 2006
CL Los Angeles, CA
SP Amer Gastroenterol Assoc
DE Biliary stricture; Bile duct tumor; Benign; Autoimmune cholangitis
ID EPSTEIN-BARR-VIRUS; CHOLANGITIS GLANDULARIS PROLIFERANS; PRIMARY
SCLEROSING CHOLANGITIS; INFLAMMATORY PSEUDOTUMOR; HILAR
CHOLANGIOCARCINOMA; AUTOIMMUNE PANCREATITIS; DIFFERENTIAL-DIAGNOSIS;
PATHOLOGICAL FEATURES; KLATSKIN TUMORS; LIVER
AB Fibroinflammatory biliary stricture (FIBS) is a rare benign tumor-like process of the extrahepatic bile duct that masquerades as cholangiocarcinoma.
In order to distinguish this unusual entity from cancer, we performed a systematic analysis of 11 patients with FIBS. All patients presented with jaundice; six patients had coexisting autoimmune disease. Preoperative evaluation included computed tomography scan and endoscopic retrograde cholangiopancreatography with benign brush cytology. Surgical treatment included nine bile duct resections with five concurrent liver resections and two incisional biopsies. Light microscopy demonstrated fibrous lesions admixed with chronic inflammation.
Immunohistochemistry demonstrated smooth muscle actin expression in all lesions except one; five tumors exhibited IgG4 positive plasma cells. The lesions were negative for cytokeratin, ALK1, CD21, S100, Ki67, and p53. Six patients received postoperative immunosuppression. At 41 month median follow-up (range 15-58 months), there was no evidence of recurrent FIBS in ten patients, while one was lost to follow-up.
FIBS is a rare myofibroblastic lesion with an immunohistochemical profile distinct from other epithelial and stromal neoplasms of the extrahepatic bile duct. A subset of these cases appear to represent IgG4-related sclerosing cholangitis. Because preoperative cytology is not diagnostic of FIBS, surgical resection remains the mainstay of diagnosis and treatment, while immunosuppression may reduce the risk of recurrence.
C1 [Moser, A. James] Univ Pittsburgh, Sch Med, Div Surg Oncol, Pittsburgh, PA 15261 USA.
[Gamblin, T. Clark; Shue, Eveline; Caro, Susan; Marsh, J. Wallis; Moser, A. James] Univ Pittsburgh, Sch Med, Dept Surg, Pittsburgh, PA 15261 USA.
[Krasinskas, A. M.; Demetris, Jake] Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA 15261 USA.
[Slivka, A. S.] Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15261 USA.
[Tublin, M. E.] Univ Pittsburgh, Sch Med, Dept Radiol, Pittsburgh, PA 15261 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh; Pennsylvania Commonwealth System of
Higher Education (PCSHE); University of Pittsburgh; Pennsylvania
Commonwealth System of Higher Education (PCSHE); University of
Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh
RP Moser, AJ (corresponding author), Univ Pittsburgh, Sch Med, Div Surg Oncol, 497 Scaife Hall,3550 Terrace St, Pittsburgh, PA 15261 USA.
EM moseraj@upmc.edu
RI Moser, A/AAI-2114-2019; Marsh, Wallis/C-6796-2013
FU NICHD NIH HHS [K12 HD 049109] Funding Source: Medline; NIDDK NIH HHS
[DK-51485] Funding Source: Medline
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PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1091-255X
EI 1873-4626
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PD APR
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VL 13
IS 4
BP 713
EP 721
DI 10.1007/s11605-008-0750-1
PG 9
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology; Surgery
GA 440OM
UT WOS:000265709600017
PM 19057967
DA 2025-01-07
ER
PT J
AU D'Amelio, M
Tino, E
Cecconi, F
AF D'Amelio, Marcello
Tino, Elisa
Cecconi, Francesco
TI The apoptosome: Emerging insights and new potential targets for drug
design
SO PHARMACEUTICAL RESEARCH
LA English
DT Review
DE apoptosis and disease; apoptosis induction; apoptosis inhibition;
apoptosome regulation
ID X-LINKED INHIBITOR; MITOCHONDRIAL-MEMBRANE PERMEABILIZATION;
SMALL-MOLECULE INHIBITORS; INDUCED PROXIMITY MODEL; CYTOCHROME-C;
CELL-DEATH; CASPASE ACTIVATION; 3-DIMENSIONAL STRUCTURE; NUCLEOTIDE
EXCHANGE; BCL-2 INHIBITORS
AB Apoptosis plays a crucial role in tissue homeostasis, development and many diseases. The relevance of Apaf1, the molecular core of apoptosome, has been underlined in mitochondria-dependent apoptosis, which according to a growing body of evidence, is involved in various pathologies where the equilibrium of life-and-death is dysregulated, such as heart attack, stroke, liver failure, cancer and autoimmune diseases. Consequently, great interest has emerged in devising therapeutic strategies for regulating the key molecules involved in the life-and-death decision. Here we review recent progress in apoptosis-based pharmacological therapies and, in particular, we point out a possible role of the apoptosome as an emerging and promising pharmacological target.
C1 [D'Amelio, Marcello; Tino, Elisa; Cecconi, Francesco] IRCCS, Fdn Santa Lucia, Lab Mol Neuroembryol, I-00143 Rome, Italy.
[D'Amelio, Marcello; Tino, Elisa; Cecconi, Francesco] Univ Roma Tor Vergata, Dept Biol, Dulbecco Telethon Inst, I-00133 Rome, Italy.
C3 IRCCS Santa Lucia; University of Rome Tor Vergata; Fondazione Telethon;
Dulbecco Telethon Institute (DTI)
RP Cecconi, F (corresponding author), IRCCS, Fdn Santa Lucia, Lab Mol Neuroembryol, I-00143 Rome, Italy.
EM francesco.cecconi@uniroma2.it
RI Cecconi, Francesco/K-3969-2016
OI Cecconi, Francesco/0000-0002-5614-4359; D'Amelio,
Marcello/0000-0001-6526-1832
FU Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom;
Telethon [TCR04004] Funding Source: Medline
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NR 114
TC 43
Z9 48
U1 0
U2 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0724-8741
EI 1573-904X
J9 PHARM RES-DORDR
JI Pharm. Res.
PD APR
PY 2008
VL 25
IS 4
BP 740
EP 751
DI 10.1007/s11095-007-9396-z
PG 12
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA 285AE
UT WOS:000254748900003
PM 17674158
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Sokol, EV
Vasilyev, VI
Kovrigina, AM
Safonova, TN
Nasonov, EL
AF Sokol, E. V.
Vasilyev, V. I.
Kovrigina, A. M.
Safonova, T. N.
Nasonov, E. L.
TI IgG4-related disease and clonal B-cell lymphoid proliferation:
Description of two clinical cases and a review of literature
SO TERAPEVTICHESKII ARKHIV
LA English
DT Article
DE IgG4-related disease; lymphoproliferative diseases; MALT lymphoma;
lacrimal gland; clonality; bone foci
ID NON-HODGKIN-LYMPHOMA; AUTOIMMUNE PANCREATITIS; DISORDERS; RISK; GLAND
AB IgG4-related disease (IgG4-RD) is a systemic immune-related disease that may involve the pancreas, liver, retroperitoneal space, biliary tract, salivary and lacrimal glands, eye socket, lung, and kidney. In term of pathomorphogenesis, it is a fibroinflammatory disease manifesting as a tumor-like lesion of organs, elevated serum IgG4 levels, and a morphofunctional substrate - the development of marked fibrosis and lymphoplasmacytic infiltration in the tissues with the high content of IgG4-positive plasma cells. The detection of a tumor-like nodule frequently leads to that the patients with IgG4-RD undergo major traumatic surgery for presumed cancer. At the same time, a number of investigations show the association of IgG4-RD with the development of cancer and lymphoproliferative diseases. The paper describes two clinical cases: Russia's first diagnosis of MALT lymphoma of the lacrimal gland, IgG4-positive and IgG4-RD with a rare onset with a destruction focus in the cervical vertebrae, multiple organ dysfunction, B-cell clonality in salivary gland tissue and PIgMK secretion. It also reviews world literature on the development of lymphoproliferative diseases in the presence of IgG4-RD.
C1 [Sokol, E. V.; Vasilyev, V. I.; Nasonov, E. L.] VA Nasonova Res Inst Rheumatol, Moscow, Russia.
[Kovrigina, A. M.] Minist Hlth Russia, Hematol Res Ctr, Moscow, Russia.
[Safonova, T. N.] Minist Hlth Russia, Helmholtz Res Inst Eye Dis, Moscow, Russia.
C3 Ministry of Health of the Russian Federation; Russian Academy of Medical
Sciences; National Medical Research Center for Hematology; Helmholtz
National Medical Research Center of Eye Diseases; Ministry of Health of
the Russian Federation
RP Sokol, EV (corresponding author), VA Nasonova Res Inst Rheumatol, Moscow, Russia.
EM name.sokol@gmail.com
RI Palshina, Svetlana/AAA-6828-2019; Safonova, Tatiana/HIA-0595-2022;
Kovrigina, Alla/H-1618-2016
OI Kovrigina, Alla/0000-0002-1082-8659
CR [Anonymous], 2013, Diagn Histopathol, DOI [10.1016/j.mpdhp.2013.01.005, DOI 10.1016/J.MPDHP.2013.01.005]
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NR 31
TC 3
Z9 3
U1 0
U2 4
PU IZDATELSTVO MEDITSINA
PI MOSCOW
PA PETROVERIGSKII PER 6-8, K-142 MOSCOW, RUSSIA
SN 0040-3660
J9 TERAPEVT ARKH
JI Ter. Arkhiv
PY 2015
VL 87
IS 12
BP 77
EP 84
DI 10.17116/terarkh2015871277-84
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DD9AZ
UT WOS:000370219300013
PM 26978423
DA 2025-01-07
ER
PT J
AU Carbone, M
Kodra, Y
Rocchetti, A
Manno, V
Minelli, G
Gerussi, A
Ronca, V
Malinverno, F
Cristoferi, L
Floreani, A
Invernizzi, P
Conti, S
Taruscio, D
AF Carbone, Marco
Kodra, Yllka
Rocchetti, Adele
Manno, Valerio
Minelli, Giada
Gerussi, Alessio
Ronca, Vincenzo
Malinverno, Federica
Cristoferi, Laura
Floreani, Annarosa
Invernizzi, Pietro
Conti, Susanna
Taruscio, Domenica
TI Primary Sclerosing Cholangitis: Burden of Disease and Mortality Using
Data from the National Rare Diseases Registry in Italy
SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
LA English
DT Article
DE rare diseases; primary sclerosing cholangitis; epidemiology; registry;
autoimmune liver disease; cholestatic liver disease
ID EPIDEMIOLOGY; POPULATION
AB Introduction: Studies on the epidemiology of primary sclerosing cholangitis (PSC) are mainly based on tertiary referral centers; and are retrospective case series susceptible to selection bias. The aim of this study was to estimate incidence; survival and cause of mortality of PSC in Italy; using population-based data. Methods: Data collected from the National Rare Diseases Registry (RNMR) and the National Mortality Database (NMD) were integrated and analyzed. Results: We identified 502 PSC incident cases. The crude incidence rate between 2012 and 2014 was 0.10 per 100,000 individuals. Sixty percent were male; mean age at disease onset and at diagnosis were 33 and 37 years; respectively; highlighting a mean diagnostic delay of 4 years. The rate of interregional mobility was 12%. Ten-year survival was 92%. In 32% of cases the cause of death was biliary-related; 12% died of biliary or gallbladder cancer. Conclusions: For rare diseases such as PSC; population-based cohort's studies are of paramount importance. Incidence rates of PSC in Italy are markedly lower and survival much longer than the ones reported from tertiary; single-centre series. Moreover; the diagnostic delay and the patient interregional mobility highlights the need for increasing awareness on the disease and for resource reallocation among Italian regions within the National Health Service
C1 [Carbone, Marco; Gerussi, Alessio; Ronca, Vincenzo; Malinverno, Federica; Cristoferi, Laura; Invernizzi, Pietro] Univ Milano Bicocca, Ctr Autoimmune Liver Dis, Dept Med & Surg, Div Gastroenterol,European Reference Network Hepa, I-20126 Milan, Italy.
[Kodra, Yllka; Rocchetti, Adele; Taruscio, Domenica] Ist Super Sanita, Natl Ctr Rare Dis, I-00161 Rome, Italy.
[Manno, Valerio; Minelli, Giada; Conti, Susanna] Ist Super Sanita, Serv Stat, I-00161 Rome, Italy.
[Floreani, Annarosa] Univ Padua, Dept Surg Oncol & Gastroenterol, I-35100 Padua, Italy.
C3 University of Milano-Bicocca; Istituto Superiore di Sanita (ISS);
Istituto Superiore di Sanita (ISS); University of Padua
RP Carbone, M (corresponding author), Univ Milano Bicocca, Ctr Autoimmune Liver Dis, Dept Med & Surg, Div Gastroenterol,European Reference Network Hepa, I-20126 Milan, Italy.
EM marco.carbone@unimib.it; yllka.kodra@iss.it; adele.rocchetti@iss.it;
valerio.manno@iss.it; giada.minelli@iss.it; a.gerussi@campus.unimib.it;
vincenzo.ronca@unimi.it; federica.malinverno@unimib.it;
laura.cristoferi@unimi.it; annarosa.floreani@unipd.it;
pietro.invernizzi@unimib.it; susanna.conti@iss.it;
domenica.taruscio@iss.it
RI Manno, Valerio/GSI-4281-2022; Gerussi, Alessio/AAM-5199-2020; Minelli,
Giada/AAC-2787-2021; Invernizzi, Pietro/AAB-8367-2022; TARUSCIO,
DOMENICA/A-6646-2015; Cristoferi, Laura/ABA-7458-2022; Ronca,
Vincenzo/AAD-9386-2021
OI CRISTOFERI, LAURA/0000-0001-9846-7474; Manno,
Valerio/0000-0003-0382-5940; Kodra, Yllka/0000-0002-6904-7451; Floreani,
Annarosa/0000-0003-2630-7054; Ronca, Vincenzo/0000-0003-0761-1333;
Minelli, giada/0000-0002-2752-9989; Gerussi, Alessio/0000-0002-5086-0514
FU Fondazione Italiana per la Ricerca in Epatologia (FIRE); Associazione
Italiana Ricerca Colangite Sclerosante (AIRCS); Italian Ministry of
Health [PE-2016-02363915, GR-2018-12367794]
FX This research was funded by Fondazione Italiana per la Ricerca in
Epatologia (FIRE); the Associazione Italiana Ricerca Colangite
Sclerosante (AIRCS); the Italian Ministry of Health for the grants
PE-2016-02363915 and GR-2018-12367794.
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NR 14
TC 17
Z9 17
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1660-4601
J9 INT J ENV RES PUB HE
JI Int. J. Environ. Res. Public Health
PD MAY
PY 2020
VL 17
IS 9
AR 3095
DI 10.3390/ijerph17093095
PG 10
WC Environmental Sciences; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health
GA LR5OY
UT WOS:000535745400119
PM 32365682
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kanwar, JR
Kanwar, RK
Burrow, H
Baratchi, S
AF Kanwar, Jagat R.
Kanwar, Rupinder K.
Burrow, Hannah
Baratchi, Sara
TI Recent Advances on the Roles of NO in Cancer and Chronic Inflammatory
Disorders
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
ID NITRIC-OXIDE SYNTHASE; ENDOTHELIAL GROWTH-FACTOR; NECROSIS-FACTOR-ALPHA;
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; WOODCHUCKS MARMOTA-MONAX;
CHRONIC VIRAL-HEPATITIS; CENTRAL-NERVOUS-SYSTEM; C VIRUS-INFECTION;
NF-KAPPA-B; MULTIPLE-SCLEROSIS
AB Nitric oxide (NO) is a short-life molecule produced by the enzyme known as the nitric oxide synthase (NOS), in a reaction that converts arginine and oxygen into citrulline and NO. There are three isoforms of the enzyme: neuronal NOS (nNOS, also called NOS1), inducible NOS (iNOS or NOS2), and endothelial NOS (eNOS or NOS3). It is now known that each of these isoforms may be expressed in a variety of tissues and cell types. This paper is a review of the current knowledge of various functions of NO in diseases. We discuss in more detail its role in Cancer, the role of NO in myocardial pathophysiology, in central nervous system (CNS) pathologies. Other diseases such as inflammation, asthma, in chronic liver diseases, inflammatory bowel disease (IBD), arthritis, are also discussed. This review also covers the role of NO in cardiovascular, central nervous, pancreas, lung, gut, kidney, myoskeletal and chronic liver diseases (CLD). The ubiquitous role that the simple gas nitric oxide plays in the body, from maintaining vascular homeostasis and fighting infections to acting as a neurotransmitter and its role in cancer, has spurred a lot of interest among researchers all over the world. Nitric oxide plays an important role in the physiologic modulation of coronary artery tone and myocardial function. Nitric oxide from iNOS appears to be a key mediator of such glial-induced neuronal death. The high sensitivity of neurons to NO is partly due to NO causing inhibition of respiration, rapid glutamate release from both astrocytes and neurons, and subsequent excitotoxic death of the neurons.
C1 [Kanwar, Jagat R.; Kanwar, Rupinder K.; Burrow, Hannah; Baratchi, Sara] Deakin Univ, Ctr Biotechnol & Interdisciplinary Biosci BioDeak, ITRI, LIMBR, Geelong, Vic 3217, Australia.
C3 Deakin University
RP Kanwar, JR (corresponding author), Deakin Univ, Ctr Biotechnol & Interdisciplinary Biosci BioDeak, ITRI, LIMBR, Pigdons Rd,Waurn Ponds, Geelong, Vic 3217, Australia.
EM jagat.kanwar@deakin.edu.au
RI Kanwar, Jagat/JDO-1829-2023; Baratchi, Sara/V-2683-2019; Kanwar, Dr
Rupinder Kaur/JBS-5937-2023
OI Baratchi, Sara/0000-0003-3588-7951
FU Centre for Biotechnology and Interdisciplinary Biosciences (BioDeakin);
Institute for Technology & Research Innovation (ITRI); Deakin University
FX The authors would like to thank the Centre for Biotechnology and
Interdisciplinary Biosciences (BioDeakin), Institute for Technology &
Research Innovation (ITRI), Deakin University for financial support.
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NR 245
TC 201
Z9 215
U1 1
U2 28
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PD JUL
PY 2009
VL 16
IS 19
BP 2373
EP 2394
DI 10.2174/092986709788682155
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 474BV
UT WOS:000268258200003
PM 19601787
DA 2025-01-07
ER
PT J
AU Migita, K
Horai, Y
Kozuru, H
Koga, T
Abiru, S
Yamasaki, K
Komori, A
Fujita, Y
Asano, T
Sato, S
Suzuki, E
Matsuoka, N
Kobayashi, H
Watanabe, H
Naganuma, A
Naeshiro, N
Yoshizawa, K
Ohta, H
Sakai, H
Shimada, M
Nishimura, H
Tomizawa, M
Ario, K
Yamashita, H
Kamitsukasa, H
Kohno, H
Nakamura, M
Furukawa, H
Takahashi, A
Kawakami, A
Ohira, H
Yastuhashi, H
AF Migita, Kiyoshi
Horai, Yoshiro
Kozuru, Hideko
Koga, Tomohiro
Abiru, Seigo
Yamasaki, Kazumi
Komori, Atsumasa
Fujita, Yuya
Asano, Tomoyuki
Sato, Shuzo
Suzuki, Eiji
Matsuoka, Naoki
Kobayashi, Hiroko
Watanabe, Hiroshi
Naganuma, Atsushi
Naeshiro, Noriaki
Yoshizawa, Kaname
Ohta, Hajime
Sakai, Hironori
Shimada, Masaaki
Nishimura, Hideo
Tomizawa, Minoru
Ario, Keisuke
Yamashita, Haruhiro
Kamitsukasa, Hiroshi
Kohno, Hiroshi
Nakamura, Minoru
Furukawa, Hiroshi
Takahashi, Atsushi
Kawakami, Atsushi
Ohira, Hiromasa
Yastuhashi, Hiroshi
TI Serum cytokine profiles and Mac-2 binding protein glycosylation isomer
(M2BPGi) level in patients with autoimmune hepatitis
SO MEDICINE
LA English
DT Article
DE autoimmune hepatitis; cytokine; interferon-gamma-inducible protein 10;
soluble intercellular adhesion molecule-1; Wisteria floribunda
agglutinin positive Mac-2-binding protein
ID INTERCELLULAR-ADHESION MOLECULE-1; HEPATOCELLULAR-CARCINOMA; LIVER
FIBROSIS; AGGLUTININ; PATHOGENESIS; WFA(+)-M2BP; PROGNOSIS
AB Autoimmune hepatitis (AIH) is an autoimmune liver disease that is characterized by a progressive destruction of the liver parenchyma and the development of liver fibrosis. We aimed to examine the relationship between circulating cytokines/chemokines and the Mac-2 binding protein glycosylation isomer (M2BPGi) levels in Japanese patients with autoimmune hepatitis (AIH).
We investigated the relationship between circulating cytokines/chemokines and M2BPGi levels in Japanese patients with AIH. Seventy-seven patients with well-documented AIH were enrolled in the National Hospital Organization (NHO)-AIH-liver-network database. We measured the serum levels of 20 cytokines in 31 selected AIH patients before and after steroid treatment using multisuspension cytokine array.
Eleven cytokines and soluble adhesion molecules were increased in untreated AIH patients compared with treated AIH patients. Among these cytokines and soluble adhesion molecules, soluble intercellular adhesion molecule-1 (sICAM-1) and interferon-gamma-inducible protein 10 (IP-10) were most downregulated by steroid therapy in AIH patients. We measured serum sICAM-1 and IP-10 by ELISA and found the levels were significantly higher in AIH patients (n=77) compared with chronic viral hepatitis C patients (n=32). Furthermore, there was a positive correlation between sICAM-1 or IP-10 and alanine aminotransferase, total bilirubin, and circulating M2BPGi levels. M2BPGi levels were increased in AIH patients with high stages of liver fibrosis. Additionally, M2BPGi levels were correlated with the histological grade of inflammation in AIH. Circulating M2BPGi levels were significantly reduced by steroid treatment in AIH patients.
sICAM-1 and IP-10 are useful markers to assess immune-mediated hepatitis activity in AIH and they correlate with circulating M2BPGi. Serum M2BPGi levels increased in untreated AIH patients with active hepatitis and were decreased by steroid therapy. M2BPGi reflects autoimmune-mediated hepatic inflammation as well as liver fibrosis.
C1 [Migita, Kiyoshi; Fujita, Yuya; Asano, Tomoyuki; Sato, Shuzo; Suzuki, Eiji; Matsuoka, Naoki; Kobayashi, Hiroko; Watanabe, Hiroshi] Fukushima Med Univ, Dept Rheumatol, Fukushima, Japan.
[Migita, Kiyoshi; Horai, Yoshiro; Kozuru, Hideko; Abiru, Seigo; Yamasaki, Kazumi; Komori, Atsumasa; Yastuhashi, Hiroshi] Nagasaki Med Ctr, Clin Res Ctr, Nagasaki, Japan.
[Koga, Tomohiro; Kawakami, Atsushi] Nagasaki Univ, Dept Immunol & Rheumatol, Unit Translat Med, Grad Sch Biomed Sci, Nagasaki, Japan.
[Naganuma, Atsushi] Natl Hosp Org, Takasaki Med Ctr, Takasaki, Gunma, Japan.
[Naeshiro, Noriaki] Natl Hosp Org, Higashihiroshima Med Ctr, Hiroshima, Japan.
[Yoshizawa, Kaname] Natl Hosp Org, Shinsyu Ueda Med Ctr, Ueda, Nagano, Japan.
[Ohta, Hajime] Natl Hosp Org, Kanazawa Med Ctr, Kanazawa, Ishikawa, Japan.
[Sakai, Hironori] Natl Hosp Org, Beppu Med Ctr, Beppu, Oita, Japan.
[Shimada, Masaaki] Natl Hosp Org, Nagoya Med Ctr, Naka Ku, Nagoya, Aichi, Japan.
[Nishimura, Hideo] Natl Hosp Org, Asahikawa Med Ctr, Asahikawa, Hokkaido, Japan.
[Tomizawa, Minoru] Natl Hosp Org, Shimoshizu Hosp, Chiba, Japan.
[Ario, Keisuke] Natl Hosp Org, Ureshino Med Ctr, Saga, Japan.
[Yamashita, Haruhiro] Natl Hosp Org, Okayama Med Ctr, Okayama, Okayama, Japan.
[Kamitsukasa, Hiroshi] Natl Hosp Org, Tokyo Natl Hosp, Tokyo, Japan.
[Kohno, Hiroshi] Natl Hosp Org, Kure Med Ctr, Kure, Hiroshima, Japan.
[Nakamura, Minoru] Nagasaki Univ, Dept Hepatol, Grad Sch Biomed Sci, Nagasaki, Japan.
[Furukawa, Hiroshi] Univ Tsukuba, Mol & Genet Epidemiol Lab, Fac Med, Tsukuba, Ibaraki, Japan.
[Takahashi, Atsushi; Ohira, Hiromasa] Fukushima Med Univ, Dept Gastroenterol, Fukushima, Japan.
C3 Fukushima Medical University; Nagasaki University; Nagoya Medical
Center; Nagasaki University; University of Tsukuba; Fukushima Medical
University
RP Migita, K (corresponding author), Fukushima Med Univ, Dept Rheumatol, Sch Med, 1 Hikarigaoka, Fukushima, Fukushima 9601295, Japan.
EM migita@fmu.ac.jp
RI Kawakami, Atsushi/D-3785-2019; Koga, Tomohiro/V-9397-2019; Sato,
Shuzo/AAC-7025-2019; Furukawa, Hiroshi/G-2039-2012
OI Asano, Tomoyuki/0009-0005-6538-1881; Naganuma,
Atsushi/0000-0003-0663-0102; Sato, Shuzo/0000-0002-8110-8261; Koga,
Tomohiro/0000-0003-2077-4428
FU National Hospital Organization
FX This work was supported by a grant from the National Hospital
Organization.
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Z9 18
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD DEC
PY 2018
VL 97
IS 50
AR e13450
DI 10.1097/MD.0000000000013450
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HI3DH
UT WOS:000456326400039
PM 30557999
OA gold, Green Published
DA 2025-01-07
ER
EF
FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Sato, K
Naganuma, A
Nagashima, T
Arai, Y
Mikami, Y
Nakajima, Y
Kanayama, Y
Murakami, T
Uehara, S
Uehara, D
Yamazaki, Y
Murase, T
Nakamura, T
Uraoka, T
AF Sato, Ken
Naganuma, Atsushi
Nagashima, Tamon
Arai, Yosuke
Mikami, Yuka
Nakajima, Yuka
Kanayama, Yuki
Murakami, Tatsuma
Uehara, Sanae
Uehara, Daisuke
Yamazaki, Yuichi
Murase, Takayo
Nakamura, Takashi
Uraoka, Toshio
TI A Newly Developed Method-Based Xanthine Oxidoreductase Activities in
Various Human Liver Diseases
SO BIOMEDICINES
LA English
DT Article
DE xanthine oxidoreductase; liver disease; etiology; alanine
aminotransferase; xanthine; oxidative stress; inflammation
ID HIGHLY SENSITIVE ASSAY; RAT-LIVER; ALKALINE-PHOSPHATASE; OXIDASE;
DEHYDROGENASE; CONVERSION; PLASMA; HYPOXANTHINE; HYPOXIA; FORM
AB Studies evaluating xanthine oxidoreductase (XOR) activities in comprehensive liver diseases are scarce, and different etiologies have previously been combined in groups for comparison. To accurately evaluate XOR activities in liver diseases, the plasma XOR activities in etiology-based comprehensive liver diseases were measured using a novel, sensitive, and accurate assay that is a combination of liquid chromatography and triple quadrupole mass spectrometry to detect [C-13(2), N-15(2)]uric acid using [C-13(2), N-15(2)]xanthine as a substrate. We also mainly evaluated the association between the plasma XOR activities and parameters of liver tests, purine metabolism-associated markers, oxidative stress markers, and an inflammation marker. In total, 329 patients and 32 controls were enrolled in our study. Plasma XOR activities were generally increased in liver diseases, especially in the active phase, such as in patients with hepatitis C virus RNA positivity, those with abnormal alanine transaminase (ALT) levels in autoimmune liver diseases, and uncured hepatocellular carcinoma patients. Plasma XOR activities were numerically highest in patients with acute hepatitis B. Plasma XOR activities were closely correlated with parameters of liver tests, especially serum ALT levels, regardless of etiology and plasma xanthine levels. Our results indicated that plasma XOR activity might reflect the active phase in various liver diseases.
C1 [Sato, Ken; Mikami, Yuka; Nakajima, Yuka; Kanayama, Yuki; Murakami, Tatsuma; Uehara, Daisuke; Yamazaki, Yuichi; Uraoka, Toshio] Gunma Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Maebashi 3718511, Japan.
[Sato, Ken] Heisei Hidaka Clin, Dept Hepatol, Takasaki 3710001, Japan.
[Sato, Ken] Takasaki Univ Hlth & Welf, Dept Healthcare Informat, Takasaki 3700033, Japan.
[Naganuma, Atsushi; Murakami, Tatsuma; Uehara, Sanae] Natl Hosp Org Takasaki Gen Med Ctr, Dept Gastroenterol, Takasaki 3700829, Japan.
[Nagashima, Tamon; Arai, Yosuke] Natl Hosp Org Shibukawa Med Ctr, Dept Gastroenterol, Shibukawa 3770204, Japan.
[Murase, Takayo; Nakamura, Takashi] Sanwa Kagaku Kenkyusho, Mie Res Pk, Inabe 5110406, Japan.
C3 Gunma University; Sanwa Kagaku Kenkyusho Co., Ltd.
RP Sato, K (corresponding author), Gunma Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Maebashi 3718511, Japan.; Sato, K (corresponding author), Heisei Hidaka Clin, Dept Hepatol, Takasaki 3710001, Japan.; Sato, K (corresponding author), Takasaki Univ Hlth & Welf, Dept Healthcare Informat, Takasaki 3700033, Japan.
EM satoken@gunma-u.ac.jp
RI 浦岡, 俊夫/GPX-5394-2022
OI Uraoka, Toshio/0000-0002-4425-4331; nakamura,
takashi/0000-0003-2324-3569; Naganuma, Atsushi/0000-0003-0663-0102
FU Abbvie Inc [523]
FX The research was partly funded by Abbvie Inc (No. 523).
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DI 10.3390/biomedicines11051445
PG 16
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA J7JI8
UT WOS:001011343000001
PM 37239117
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Moscol, MD
AF Davalos Moscol, Milagros
TI Indications for treatment in chronic HCV infection
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Hepatitis C infection; Treatment; Crioglobulinemia; Glomerulonephritis
ID CHRONIC HEPATITIS-C; INTERFERON-ALPHA-2B PLUS RIBAVIRIN; NORMAL
AMINOTRANSFERASE LEVELS; LIVER FIBROSIS PROGRESSION; VIRUS-INFECTION;
PEGINTERFERON ALPHA-2A; NATURAL-HISTORY; CRYOGLOBULINEMIC
GLOMERULONEPHRITIS; RANDOMIZED-TRIAL; UNITED-STATES
AB HCV Infection is a global burden disease and it is related to the development of progressive liver fibrosis, cirrhosis and hepatocellular carcinoma. At least 80% of the persons that have an acute infection evolve to chronicity. This event affects the patient and their contacts for the risk of acquiring the infection. Once chronic HCV is present some factors accelerate progression: older age, obesity, alcohol consumption, etc. Severity of fibrosis is one of the most important factors to be analyzed before deciding to treat a patient. Pegylated interferon and ribavirin is the "standard of care" for this disease, however, it has many side effects, some of them life threatening. That is the reason why this treatment must be indicated in the right moment in the right patient. A complete medical evaluation must be done previously to initiate treatment. Other concurrent problems must be ruled out or treated. Decompensated cirrhosis, autoimmune diseases or other uncontrolled disease are contraindication to HCV treatment. Previous failure to treatment for HCV must be analyzed to identify the reasons for that event and consider retreatment. Cryoglobulinemia and membranoproliferative glomerulonephritis are indications for treatment independent from the severity of liver disease.
EM milagros_davalos@hotmail.com
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NR 44
TC 1
Z9 1
U1 0
U2 3
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PY 2010
VL 9
SU 1
BP S49
EP S53
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 638HZ
UT WOS:000280885700008
DA 2025-01-07
ER
PT J
AU Isernhagen, A
Malzahn, D
Bickeböller, H
Dressel, R
AF Isernhagen, Antje
Malzahn, Doerthe
Bickeboeller, Heike
Dressel, Ralf
TI Impact of the MICA-129Met/Val Dimorphism on NKG2D-Mediated Biological
Functions and Disease Risks
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE NK cells; T cells; activating NK receptor; costimulation;
single-nucleotide polymorphism; autoimmune diseases; cancer;
hematopoietic stem cell transplantation
ID BONE-MARROW-TRANSPLANTATION; GENOME-WIDE ASSOCIATION; NKG2D LIGAND
EXPRESSION; NK CELL ACTIVATION; CHAIN-RELATED GENE; I-RELATED CHAIN;
HEPATOCELLULAR-CARCINOMA; MICA POLYMORPHISM; SOLUBLE MICA; CANCER-RISK
AB The major histocompatibility complex (MHC) class I chain-related A (MICA) is the most polymorphic non-classical MHC class I gene in humans. It encodes a ligand for NKG2D (NK group 2, member D), an activating natural killer (NK) receptor that is expressed mainly on NK cells and CD8(+) T cells. The single-nucleotide polymorphism (SNP) rs1051792 causing a valine (Val) to methionine (Met) exchange at position 129 of the MICA protein is of specific interest. It separates MICA into isoforms that bind NKG2D with high (Met) and low affinities (Val). Therefore, this SNP has been investigated for associations with infections, autoimmune diseases, and cancer. Here, we systematically review these studies and analyze them in view of new data on the functional consequences of this polymorphism. It has been shown recently that the MICA-129Met variant elicits a stronger NKG2D signaling, resulting in more degranulation and IFN-gamma production in NK cells and in a faster costimulation of CD8(+) T cells than the MICA-129Val variant. However, the MICA-129Met isoform also downregulates NKG2D more efficiently than the MICA-129Val isoform. This downregulation impairs NKG2D-mediated functions at high expression intensities of the MICA-Met variant. These features of the MICA-129Met/Val dimorphism need to be considered when interpreting disease association studies. Particularly, in the field of hematopoietic stem cell transplantation, they help to explain the associations of the SNP with outcome including graft-versus-host disease and relapse of malignancy. Implications for future disease association studies of the MICA-129Met/Val dimorphism are discussed.
C1 [Isernhagen, Antje; Dressel, Ralf] Univ Med Ctr Gottingen, Inst Cellular & Mol Immunol, Gottingen, Germany.
[Malzahn, Doerthe; Bickeboeller, Heike] Univ Med Ctr Gottingen, Inst Epidemiol, Gottingen, Germany.
[Dressel, Ralf] DZHK German Ctr Cardiovasc Res, Partner Site Gottingen, Gottingen, Germany.
C3 University of Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of
Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; German Centre for
Cardiovascular Research
RP Dressel, R (corresponding author), Univ Med Ctr Gottingen, Inst Cellular & Mol Immunol, Gottingen, Germany.; Dressel, R (corresponding author), DZHK German Ctr Cardiovasc Res, Partner Site Gottingen, Gottingen, Germany.
EM rdresse@gwdg.de
RI Bickeboller, Heike/V-2318-2018; Dressel, Ralf/R-7065-2016
OI Bickeboller, Heike/0000-0002-3361-5488; Dressel,
Ralf/0000-0002-1651-1214
FU Deutsche Forschungsgemeinschaft [GRK 1034, SFB 1002, TP C05]; European
Union [FP7-PEOPLE-2012-ITN-315963]; Open Access Publication Funds of the
Gottingen University
FX The authors' work was supported by the Deutsche Forschungsgemeinschaft
(GRK 1034 and SFB 1002, TP C05) and the European Union Grant
FP7-PEOPLE-2012-ITN-315963 (CELLEUROPE). They acknowledge support by the
Open Access Publication Funds of the Gottingen University.
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NR 75
TC 42
Z9 44
U1 1
U2 9
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD DEC 12
PY 2016
VL 7
AR 588
DI 10.3389/fimmu.2016.00588
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA EE8DT
UT WOS:000389856000003
PM 28018354
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Filippou, PS
Ren, AH
Korbakis, D
Dimitrakopoulos, L
Soosaipillai, A
Barak, V
Frenkel, S
Pe'er, J
Lotem, M
Merims, S
Molina, R
Blasutig, I
Bogdanos, DP
Diamandis, EP
AF Filippou, Panagiota S.
Ren, Annie H.
Korbakis, Dimitrios
Dimitrakopoulos, Lampros
Soosaipillai, Antoninus
Barak, Vivian
Frenkel, Shahar
Pe'er, Jacob
Lotem, Michal
Merims, Sharon
Molina, Rafael
Blasutig, Ivan
Bogdanos, Dimitrios P.
Diamandis, Eleftherios P.
TI Exploring the potential of mucin 13 (MUC13) as a biomarker for
carcinomas and other diseases
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Article
DE autoimmune diseases; cancer cell lines; immunoassays; malignancies;
MUC13; renal failure
ID CELL-SURFACE MUCIN; OVARIAN-CANCER; MONOCLONAL-ANTIBODY; GASTRIC-CANCER;
EXPRESSION; OVEREXPRESSION; INFLAMMATION; ONCOPROTEIN; PROGRESSION;
PROGNOSIS
AB Background: Mucin 13 (MUC13) is a cell surface glycoprotein aberrantly expressed in a variety of epithelial carcinomas. Thus far, the role of MUC13 in various diseases remains elusive. To the best of our knowledge, this is the first study to examine the potential of MUC13 as a serum biomarker in a variety of carcinomas and other conditions.
Methods: We developed a recombinant MUC13 protein, mouse monoclonal antibodies and enzyme immunoassay (ELISA) for MUC13. We used this assay to measure MUC13 levels in the supernatants of cancer cell lines and a large cohort of serum samples from healthy and diseased individuals.
Results: MUC13 is secreted from cancer cell lines, with highest levels found in ovarian cancer cell lines. MUC13 levels in human sera were significantly increased in patients with renal failure and 20%-30% of patients with ovarian, liver, lung and other cancers. MUC13 was also elevated in 70% of patients with active cutaneous melanoma, but not uveal melanoma. Furthermore, we identified significant MUC13 elevations in the serum of patients with vasculitis (ANCA-positive) autoantibodies, but not in those with inflammatory bowel disease.
Conclusions: Serum MUC13 is frequently elevated not only in a variety of malignant cases but also in some benign pathologies, thus appearing to be a non-specific disease biomarker. Nonetheless, serum MUC13 is clearly highly elevated in some carcinoma patients, and its relationship with tumor progression in this context warrant further research. Future studies that examine the correlation between serum MUC13 levels to stage of cancer could elucidate prognostic potential.
C1 [Diamandis, Eleftherios P.] Mt Sinai Hosp, Joseph & Wolf Lebov Ctr, 60 Murray St Box 32,Flr 6 Rm L6-201, Toronto, ON M5T 3L9, Canada.
[Filippou, Panagiota S.; Ren, Annie H.; Korbakis, Dimitrios; Dimitrakopoulos, Lampros; Diamandis, Eleftherios P.] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada.
[Filippou, Panagiota S.; Blasutig, Ivan; Diamandis, Eleftherios P.] Univ Hlth Network, Dept Clin Biochem, Toronto, ON, Canada.
[Ren, Annie H.; Dimitrakopoulos, Lampros; Soosaipillai, Antoninus; Diamandis, Eleftherios P.] Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON, Canada.
[Korbakis, Dimitrios; Diamandis, Eleftherios P.] Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON, Canada.
[Barak, Vivian] Hadassah Hebrew Univ, Dept Oncol, Med Ctr, Jerusalem, Israel.
[Frenkel, Shahar; Pe'er, Jacob] Hadassah Hebrew Univ, Dept Ophthalmol, Med Ctr, Jerusalem, Israel.
[Lotem, Michal; Merims, Sharon] Hadassah Hebrew Univ Hosp, Sharett Inst Oncol, Jerusalem, Israel.
[Molina, Rafael] Univ Barcelona, Hosp Clin, Barcelona, Spain.
[Bogdanos, Dimitrios P.] Univ Thessaly, Dept Rheumatol & Clin Immunol, Larisa, Greece.
C3 University of Toronto; Sinai Health System Toronto; University of
Toronto; University of Toronto; University Health Network Toronto;
University of Toronto; Sinai Health System Toronto; Lunenfeld Tanenbaum
Research Institute; University of Toronto; Sinai Health System Toronto;
Lunenfeld Tanenbaum Research Institute; Hebrew University of Jerusalem;
Hadassah University Medical Center; Hebrew University of Jerusalem;
Hadassah University Medical Center; Hebrew University of Jerusalem;
Hadassah University Medical Center; University of Barcelona; Hospital
Clinic de Barcelona; University of Thessaly
RP Diamandis, EP (corresponding author), Mt Sinai Hosp, Joseph & Wolf Lebov Ctr, 60 Murray St Box 32,Flr 6 Rm L6-201, Toronto, ON M5T 3L9, Canada.; Diamandis, EP (corresponding author), Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada.; Diamandis, EP (corresponding author), Univ Hlth Network, Dept Clin Biochem, Toronto, ON, Canada.; Diamandis, EP (corresponding author), Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON, Canada.; Diamandis, EP (corresponding author), Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON, Canada.
EM Eleftherios.Diamandis@sinaihealthsystem.ca
RI Bogdanos, Dimitrios/AAF-8620-2020; Peer, Jacob/HSE-3187-2023; Filippou,
Panagiota/ABF-1969-2021
OI Diamandis, Eleftherios/0000-0002-1589-820X; Bogdanos,
Dimitrios/0000-0002-9697-7902; Filippou, Panagiota/0000-0003-3974-988X
FU Mount Sinai Hospital
FX This study was funded by the principal investigator's research fund from
Mount Sinai Hospital.
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NR 37
TC 13
Z9 17
U1 0
U2 14
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
EI 1437-4331
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD NOV
PY 2018
VL 56
IS 11
BP 1945
EP 1953
DI 10.1515/cclm-2018-0139
PG 9
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA GV8UV
UT WOS:000446425900026
PM 29768245
DA 2025-01-07
ER
PT J
AU Horiguchi, S
Ikeda, F
Shiraha, H
Yamamoto, N
Sakakihara, I
Noma, Y
Tsutsumi, K
Kato, H
Hagihara, H
Yasunaka, T
Nakamura, S
Kobashi, H
Kawamoto, H
Yamamoto, K
AF Horiguchi, Shigeru
Ikeda, Fusao
Shiraha, Hidenori
Yamamoto, Naoki
Sakakihara, Ichiro
Noma, Yasuhiro
Tsutsumi, Koichiro
Kato, Hironari
Hagihara, Hiroaki
Yasunaka, Tetsuya
Nakamura, Shinichiro
Kobashi, Haruhiko
Kawamoto, Hirofumi
Yamamoto, Kazuhide
TI Diagnostic usefulness of precise examinations with intraductal
ultrasonography, peroral cholangioscopy and laparoscopy of
immunoglobulin G4-related sclerosing cholangitis
SO DIGESTIVE ENDOSCOPY
LA English
DT Article
DE immunoglobulin G4 (IgG4)-related sclerosing cholangitis; intraductal
ultrasonography; laparoscopy; peroral chlangioscopy
ID AUTOIMMUNE PANCREATITIS; LIVER
AB Herein, a case of immunoglobulin G4 (IgG4)-related sclerosing cholangitis is reported. IgG4 was diagnosed based on observations from peroral cholangioscopy and laparoscopy, and these methods are proposed for definitive and precise diagnosis of this disease. A 76-year-old male patient with inguinal Paget's disease had intrahepatic bile duct dilatations detected with computed tomography at his periodic check-up. Magnetic resonance cholangiography showed stenosis of the upper common bile duct and poststenotic dilatation of left intrahepatic bile ducts. The portal tract and bilateral intrahepatic bile ducts were surrounded by a low-density area, facing a tumor-like lesion at segment 2. Cytological examinations of the stenotic and dilated lesions revealed no cellular atypia. Histological examination of the tumor showed normal liver tissue with infiltration of lymphocytes, indicating an inflammatory pseudotumor. Peroral cholangioscopy excluded the possibility of biliary cancer and indicated that the stenotic legion was of submucosal, not mucosal, origin. Laparoscopic observations showed discoloration with wide yellowish-white lobular markings and wide depressed lesions at segments 2 and 7. Liver histology showed mild cholangitis with infiltration of IgG4-positive plasma cells around the bile ducts. Serum IgG4 levels were elevated. From these findings, the patient was diagnosed with IgG4-related sclerosing cholangitis. After treatment with prednisolone, blood liver enzymes and IgG4 rapidly normalized, bile duct dilatations improved, and the hepatic pseudotumor disappeared. The cholangitis did not recur. In this case, biliary cancer was ruled out by observation with peroral cholangioscopy, and the spread of cholangitis in the liver periphery was verified with laparoscopy; this information could not be obtained with other modalities.
C1 [Horiguchi, Shigeru; Ikeda, Fusao; Shiraha, Hidenori; Yamamoto, Naoki; Sakakihara, Ichiro; Noma, Yasuhiro; Tsutsumi, Koichiro; Kato, Hironari; Hagihara, Hiroaki; Yasunaka, Tetsuya; Nakamura, Shinichiro; Yamamoto, Kazuhide] Okyama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Gastroenterol & Hepatol, Okayama 700858, Japan.
[Kobashi, Haruhiko] Okayama Red Cross Hosp, Dept Hepatol, Okayama, Japan.
[Kawamoto, Hirofumi] Kawasaki Med Sch, Dept Gen Med 2, Okayama, Japan.
C3 Kawasaki Medical School
RP Ikeda, F (corresponding author), Okyama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Gastroenterolgy & Hepatol, Kita Ku, 2-5-1 Shikata Cho, Okayama 700858, Japan.
EM fikeda@md.okayama-u.ac.jp
RI Nakamura, Shinichiro/B-2363-2011; Yamamoto, Naoki/L-2603-2019
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NR 13
TC 9
Z9 10
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0915-5635
EI 1443-1661
J9 DIGEST ENDOSC
JI Dig. Endosc.
PD SEP
PY 2012
VL 24
IS 5
BP 370
EP 373
DI 10.1111/j.1443-1661.2012.01300.x
PG 4
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 994RB
UT WOS:000307947900013
PM 22925292
DA 2025-01-07
ER
PT J
AU Miceli, C
Leri, M
Stefani, M
Bucciantini, M
AF Miceli, Caterina
Leri, Manuela
Stefani, Massimo
Bucciantini, Monica
TI Autophagy-related proteins: Potential diagnostic and prognostic
biomarkers of aging-related diseases
SO AGEING RESEARCH REVIEWS
LA English
DT Review
DE Aging; Autophagy; Biomarkers; Aging-diseases; Clinical practice
ID CHAPERONE-MEDIATED AUTOPHAGY; AMYOTROPHIC-LATERAL-SCLEROSIS; MOUSE
MODEL; CELL-DEATH; ALPHA-SYNUCLEIN; THERAPEUTIC TARGET; METABOLIC
SYNDROME; OXIDATIVE STRESS; LIFE-SPAN; MITOCHONDRIAL DYSFUNCTION
AB Autophagy plays a key role in cellular, tissue and organismal homeostasis and in the production of the energy load needed at critical times during development and in response to nutrient shortage. Autophagy is generally considered as a pro-survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy efficiency declines with age, thus contributing to many different pathophysiological conditions, such as cancer, cardiomyopathy, diabetes, liver disease, autoimmune diseases, infections, and neurodegeneration. Accordingly, it has been proposed that the maintenance of a proper autophagic activity contributes to the extension of the lifespan in different organisms. A better understanding of the interplay between autophagy and risk of age-related pathologies is important to propose nutritional and life-style habits favouring disease pre-vention as well as possible clinical applications aimed at promoting long-term health.
C1 [Miceli, Caterina] Telethon Inst Genet & Med TIGEM, Naples, Italy.
[Leri, Manuela; Stefani, Massimo; Bucciantini, Monica] Univ Florence, Dept Expt Clin & Biomed Sci, Florence, Italy.
C3 Fondazione Telethon; Telethon Institute of Genetics & Medicine (TIGEM);
University of Florence
RP Bucciantini, M (corresponding author), Univ Florence, Dept Expt Clin & Biomed Sci, Florence, Italy.
EM monica.bucciantini@unifi.it
RI Leri, Manuela/M-8431-2019; MICELI, CATERINA/LBH-5335-2024
FU Fondazione Umberto Veronesi
FX Acknowledgements ML was supported by Fondazione Umberto Veronesi.
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NR 264
TC 9
Z9 9
U1 10
U2 24
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 1568-1637
EI 1872-9649
J9 AGEING RES REV
JI Ageing Res. Rev.
PD AUG
PY 2023
VL 89
AR 101967
DI 10.1016/j.arr.2023.101967
EA JUN 2023
PG 18
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA P8QV2
UT WOS:001053270300001
PM 37270146
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Que, WC
Lin, HL
Li, XY
Zhang, BQ
Liu, MB
Hu, X
Fu, JS
Cheng, Y
Qiu, HQ
AF Que, Wancai
Lin, Hailing
Li, Xueyong
Zhang, Bingqing
Liu, Maobai
Hu, Xin
Fu, Junsheng
Cheng, Yu
Qiu, Hongqiang
TI Koumine ameliorates concanavalin A-induced autoimmune hepatitis in mice:
involvement of the Nrf2, NF-KB pathways, and gut microbiota
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Koumine; Autoimmune hepatitis; Concanavalin A; Nrf2; NF -KB; Gut
microbiota
ID GELSEMIUM-ELEGANS BENTH.; IMMUNE-RESPONSES; LIVER-INJURY; EXPRESSION;
ALKALOIDS
AB Gelsemium elegans (Gardner. & Chapm.) Benth. has long been considered a traditional Chinese medicine effective against rheumatoid pain, cancer, cirrhosis, and skin diseases. Koumine (KM), the most abundant alkaloid in G. elegans Benth., demonstrates a variety of biological effects, including antitumor, analgesic, anxiolytic, antiinflammatory, antidepressant, antioxidant, immunoregulatory, and hepatoprotective effects. Furthermore, the relatively low toxicity of KM makes it a promising drug candidate. This study aimed to investigate the protective effects of KM and its possible mechanisms using a concanavalin A (Con A)-induced autoimmune hepatitis (AIH) model in mice. Mice were orally administered different doses of KM for 14 d before Con A tail vein injections. The effects of KM on serum biochemical markers and liver histopathology were then evaluated 12 h after Con A exposure. The Nrf2 and NF-KB signaling pathways and alterations in gut microbiota were determined using western blotting, immunohistochemistry, and 16S rRNA sequencing to explore the underlying mechanisms of KM exposure. KM pretreatment dose-dependently decreased serum liver injury markers (Alanine aminotransferase, and aspartate aminotransferase) and cytokine levels (Tumor necrosis factor-alpha and interleukin-6), as well as the liver pathological damage triggered by Con A. Furthermore, the results of the multi-technique analysis indicated that KM activated the Nrf2 pathway, upregulated the expression of anti-oxidation factors HO-1 and Nrf2, and downregulated the expression of Keap1. Moreover, the NF-KB signaling pathway was inhibited. Interestingly, pre-treatment with KM also significantly improved the composition of the gut microbiota probably because it increases the richness of probiotics. Our findings suggest that KM pretreatment could attenuate Con A-induced AIH, the Nrf2 and NF-KB signaling pathways, and that gut microbiota are involved in the process of the hepatoprotective effect. This study provides a theoretical basis for the development of KM as an effective agent against AIH.
C1 [Que, Wancai; Lin, Hailing; Liu, Maobai; Cheng, Yu; Qiu, Hongqiang] Fujian Med Univ, Dept Pharm, Union Hosp, Fuzhou 350001, Fujian, Peoples R China.
[Li, Xueyong; Zhang, Bingqing; Qiu, Hongqiang] Fujian Med Univ, Coll Pharm, Fuzhou 350004, Fujian, Peoples R China.
[Hu, Xin; Fu, Junsheng] Fujian Agr & Forestry Univ, Coll Life Sci, Fujian 350002, Peoples R China.
[Cheng, Yu; Qiu, Hongqiang] Fujian Med Univ, Dept Pharm, Union Hosp, 29 Xin Quan Rd, Fuzhou 350001, Fujian, Peoples R China.
C3 Fujian Medical University; Fujian Medical University; Fujian Agriculture
& Forestry University; Fujian Medical University
RP Cheng, Y; Qiu, HQ (corresponding author), Fujian Med Univ, Dept Pharm, Union Hosp, 29 Xin Quan Rd, Fuzhou 350001, Fujian, Peoples R China.
EM chengyu@fjmu.edu.cn; hongqiangqiu@fjmu.edu.cn
OI Li, Xueyong/0000-0002-4064-3735
FU Natural Science Foundation of Fujian Province [2021J01761]; Youth
Project of the Health Department of Fujian Province [2020GGB024];
Guiding Project of Natural Science Foundation of Fujian Province
[2021Y0019, 2022Y0019]; Innovation Joint Project of Fujian Science and
Technology [2019Y9051, 2020Y9066]
FX This work was supported by grants from the Natural Science Foundation of
Fujian Province [grant number 2021J01761] , the Youth Project of the
Health Department of Fujian Province [grant number 2020GGB024] , the
Guiding Project of Natural Science Foundation of Fujian Province [grant
number 2021Y0019, 2022Y0019] , and the Innovation Joint Project of
Fujian Science and Technology [grant numbers 2019Y9051, 2020Y9066] .
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NR 63
TC 8
Z9 8
U1 0
U2 16
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD JAN
PY 2023
VL 114
AR 109573
DI 10.1016/j.intimp.2022.109573
EA DEC 2022
PG 14
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA 7L9YC
UT WOS:000906313400001
PM 36527886
OA hybrid
DA 2025-01-07
ER
PT J
AU Brizawasi, A
Ahirwar, AK
Prabhat
Kaim, K
Ahirwar, P
Kumawat, R
Prasad, J
AF Brizawasi, Abhijeet
Ahirwar, Ashok Kumar
Prabhat
Kaim, Kirti
Ahirwar, Pradeep
Kumawat, Rajani
Prasad, Jitender
TI COVID-19: a viewpoint from hepatic perspective
SO HORMONE MOLECULAR BIOLOGY AND CLINICAL INVESTIGATION
LA English
DT Review
DE ACE; complications; COVID-19; hepatic; SARS-CoV-2
ID MANAGEMENT; INDIA
AB Coronaviruses as such are known since last century. The name is derived from their shape which has crown (corona) like radiating spikes. The recent one however is a different one from the Coronavirus involved in SARS (2002-2004) and MERS (2012) in being highly infectious. Initially COVID 19 had a high case fatality rate which has now decreased to a significant extent. Many cases of COVID 19 are asymptomatic with a significant number of positive cases developing a triad of fever, breathlessness and GI symptoms. Recent travel increases the probability of infection. The pathogenesis involves ACE 2 receptors. So, it has been found that there are more cases and mortality among hypertensive individuals. Even higher among the people who use ACE inhibitor in comparison to those who use other anti-hypertensive drugs. Treatment is usually symptomatic. Antiviral drugs and vaccines against COVID-19 are being used. Deranged liver enzymes are common in COVID-19, however, serious liver injury is not much documented. Liver injury is either due to disease itself or due to antiviral drugs. Extra care like strict social distancing, avoiding unnecessary contact is needed for those with autoimmune hepatitis, liver cancer and those who are in immunosuppression because of a scheduled or already liver transplant. Further research is definitely needed in this field. The upcoming researches should also focus on liver injuries associated with disease course and derangements arising as side effects of treatment of COVID-19.
C1 [Ahirwar, Ashok Kumar] Univ Coll Med Sci, Dept Biochem, New Delhi, India.
[Brizawasi, Abhijeet] All India Inst Med Sci, Nagpur, Maharashtra, India.
[Prabhat] All India Inst Med Sci, Dept Biochem, Gorakhpur, Uttar Pradesh, India.
[Kaim, Kirti] ESI Hosp, New Delhi, India.
[Ahirwar, Pradeep] Index Med Coll Hosp & Res Ctr, Dept Radiodiag, Indore, Madhya Pradesh, India.
[Kumawat, Rajani] All India Inst Med Sci, Dept Biochem, Bathinda, Punjab, India.
[Prasad, Jitender] All India Inst Med Sci, Dept Biochem, Deoghar, Jharkhand, India.
C3 University of Delhi; University College of Medical Sciences; All India
Institute of Medical Sciences (AIIMS) Nagpur
RP Ahirwar, AK (corresponding author), Univ Coll Med Sci, Dept Biochem, New Delhi, India.
EM brizawasiabhijeet@gmail.com; drashoklhmc@gmail.com;
drprabhat12811281@yahoo.in; kirti.kaim@gmail.com;
pradeepahirwar21@gmail.com; dr.rajanikumawat@gmail.com;
jeetu.pgs.portblair@gmail.com
OI PRASAD, JITENDER/0000-0002-5594-0214
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NR 37
TC 1
Z9 1
U1 0
U2 0
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1868-1883
EI 1868-1891
J9 HORM MOL BIOL CLIN I
JI Horm. Mol. Biol. Clin. Investig.
PD MAR 30
PY 2023
VL 44
IS 1
BP 97
EP 103
DI 10.1515/hmbci-2022-0026
EA OCT 2022
PG 7
WC Biochemistry & Molecular Biology
WE Emerging Sources Citation Index (ESCI)
SC Biochemistry & Molecular Biology
GA C3FA4
UT WOS:000863419800001
PM 36190156
OA Bronze
DA 2025-01-07
ER
PT J
AU Yousaf, A
Raiker, R
Davis, SM
Gayam, S
Zinn, Z
AF Yousaf, Ahmed
Raiker, Rahul
Davis, Stephen M.
Gayam, Swapna
Zinn, Zachary
TI Association between psoriasis, psoriatic arthritis and gastrointestinal
disease An exploratory nationwide inpatient sample analysis
SO WIENER KLINISCHE WOCHENSCHRIFT
LA English
DT Article
DE Crohn's disease; Ulcerative colitis; Liver disease; Celiac disease;
Cirrhosis
ID INFLAMMATORY-BOWEL-DISEASE; POPULATION-BASED COHORT; ULCERATIVE-COLITIS;
CROHNS-DISEASE; OLMSTED COUNTY; PREVALENCE; RISK; CANCER;
HOSPITALIZATION; MINNESOTA
AB Background Psoriasis is associated with cardiovascular disease, inflammatory bowel disease (IBD), metabolic syndrome, and psychiatric disease. Furthermore, psoriasis is associated with immune dysregulation and systemic inflammation. Objective To determine the association of psoriasis and psoriatic arthritis with IBD and the association of the combination of psoriasis or psoriatic arthritis with IBD and other gastrointestinal illnesses. Methods Discharge data from the 2000-2014 Nationwide Inpatient Sample, Healthcare Cost and Utilization Project (HCUP), which approximates a 20% stratified sample of all US hospitalizations, were analyzed. Multivariable logistic regression was used to examine the association between psoriasis and psoriatic arthritis with IBD and 23 gastrointestinal illnesses adjusting for sociodemographic characteristics. Results Psoriasis was associated with IBD (Crohn's disease adjusted odds ratio (aOR) = 2.13, 95% confidence interval (CI) [2.0-2.3],p < 0.001). When adjusting for sociodemographics and IBD, psoriasis was associated with 21 of 23 gastrointestinal diseases examined, most notably celiac disease, autoimmune hepatitis, and non-alcoholic fatty liver disease. Psoriatic arthritis was also associated with IBD (Crohn's disease, aOR = 1.95, 95% CI [1.7-2.2], and ulcerative colitis, aOR = 2.66, 95% CI [2.4-2.9]). Conclusion Psoriasis and psoriatic arthritis inpatients have an associated increase in IBD and numerous other gastrointestinal illnesses.
C1 [Yousaf, Ahmed; Raiker, Rahul; Zinn, Zachary] West Virginia Univ, Dept Dermatol, 64 Med Ctr Dr, Morgantown, WV 26506 USA.
[Davis, Stephen M.] West Virginia Univ, Dept Hlth Policy Management & Leadership, Morgantown, WV 26506 USA.
[Davis, Stephen M.] West Virginia Univ, Dept Emergency Med, Morgantown, WV USA.
[Gayam, Swapna] West Virginia Univ, Dept Med, Sect Gastroenterol & Hepatol, Morgantown, WV 26506 USA.
C3 West Virginia University; West Virginia University; West Virginia
University; West Virginia University
RP Zinn, Z (corresponding author), West Virginia Univ, Dept Dermatol, 64 Med Ctr Dr, Morgantown, WV 26506 USA.
EM zzinn@hsc.wvu.edu
OI Zinn, Zachary/0000-0001-8763-0328
FU NIGMS NIH HHS [U54 GM104942] Funding Source: Medline
CR Agency for Healthcare Research and Quality, 2019, HCUP DAT HEALTHC COS
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NR 43
TC 8
Z9 9
U1 0
U2 4
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0043-5325
EI 1613-7671
J9 WIEN KLIN WOCHENSCHR
JI Wien. Klin. Wochen.
PD JUN
PY 2021
VL 133
IS 11-12
BP 586
EP 593
DI 10.1007/s00508-020-01740-8
EA SEP 2020
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA SQ7WJ
UT WOS:000572306100001
PM 32965553
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Jankun, J
Wyganowska-Swiatkowska, M
Dettlaff, K
Jelinska, A
Surdacka, A
Watrobska-Swietlikowska, D
Skrzypczak-Jankun, E
AF Jankun, Jerzy
Wyganowska-Swiatkowska, Marzena
Dettlaff, Katarzyna
Jelinska, Anna
Surdacka, Anna
Watrobska-Swietlikowska, Dorota
Skrzypczak-Jankun, Ewa
TI Determining whether curcumin degradation/condensation is actually
bioactivation (Review)
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Review
DE curcumin; turmeric; diseases; bioavailability; degradation
ID NF-KAPPA-B; PHOTOCHEMICAL STABILITY; DEGRADATION-PRODUCTS; OXIDATIVE
DAMAGE; COMPLEX; DRUG; PHARMACOKINETICS; LIPOXYGENASE; METABOLITES;
TETRAHYDROCURCUMIN
AB Curcumin has been shown to exert therapeutic or protective effects against a variety of diseases, such as cancer, pulmonary diseases, neurological, liver, metabolic, autoimmune, cardiovascular diseases and numerous other chronic ailments. Over 116 clinical studies on curcumin in humans were registered with the US National Institutes of Health in 2015. However, it is mystifying how curcumin can be so effective in the treatment of many diseases since it has very low water solubility and bioavailability. Furthermore, curcumin is not stable under various conditions; its degradation or condensation into different bioactive compounds may be responsible for its biological activities rather than curcumin itself. In this review, we provide evidence of curcumin degradation and condensation into different compounds which have or may have health benefits themselves. Literature reviews strongly suggest that these molecules contribute to the observed health benefits, rather than curcumin itself.
C1 [Jankun, Jerzy; Skrzypczak-Jankun, Ewa] Univ Toledo, Dept Urol, Coll Med, Urol Res Ctr, Toledo, OH 43614 USA.
[Wyganowska-Swiatkowska, Marzena; Surdacka, Anna] Pozna Univ Med Sci, Dept Conservat Dent & Periodontol, PL-60812 Poznan, Poland.
[Dettlaff, Katarzyna; Jelinska, Anna] Poznan Univ Med Sci, Dept Pharmaceut Chem, Grunwaldzka 6, PL-60780 Poznan, Poland.
[Watrobska-Swietlikowska, Dorota] Med Univ Gdansk, Dept Pharmaceut Technol, PL-80416 Gdansk, Poland.
C3 University System of Ohio; University of Toledo; Poznan University of
Medical Sciences; Fahrenheit Universities; Medical University Gdansk
RP Jankun, J (corresponding author), Univ Toledo, Dept Urol, Coll Med, Urol Res Ctr, Toledo, OH 43614 USA.
EM jerzy.jankun@utoledo.edu
RI Surdacka, Anna/AAR-5655-2021
OI Dettlaff, Katarzyna/0000-0002-5986-7544; Jankun,
Jerzy/0000-0003-2354-4046; Jelinska, Anna/0000-0002-3019-5844; ,
Anna/0000-0001-9952-0230
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NR 92
TC 90
Z9 93
U1 2
U2 47
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD MAY
PY 2016
VL 37
IS 5
BP 1151
EP 1158
DI 10.3892/ijmm.2016.2524
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA DK7FR
UT WOS:000375091000001
PM 26985652
OA Bronze
DA 2025-01-07
ER
PT J
AU Zhang, T
Rao, QR
Dai, MY
Zhao, Q
Li, F
AF Zhang, Ting
Rao, Qianru
Dai, Manyun
Zhao, Qi
Li, Fei
TI Tripterygium wilfordii protects against an animal model of
autoimmune hepatitis
SO JOURNAL OF ETHNOPHARMACOLOGY
LA English
DT Article
DE Tripterygium wilfordii tablets; Celastrol; Concanavalin A; Autophagy;
TFEB; PXR
ID PREGNANE-X-RECEPTOR; CHOLESTATIC LIVER-INJURY; CELASTROL PROTECTS;
AUTOPHAGY; OBESITY; DYSFUNCTION; DOMAIN
AB Ethnopharmacological relevance: Tripterygium wilfordii tablets (TWT) is widely used to treat autoimmune diseases such as rheumatoid arthritis. Celastrol, one main active ingredient in TWT, has been shown to produce a variety of beneficial effects, including anti-inflammatory, anti-obesity, anti-cancer, and immunomodulatory. However, whether TWT could protect against Concanavalin A (Con A)-induced hepatitis remains unclear.The aim of the study: This study aims to investigate the protective effect of TWT against Con A-induced hepatitis and elucidate the underlying mechanism.Materials and methods: Metabolomic analysis, pathological analysis, biochemical analysis, qPCR and Western blot analysis and the Pxr-null mice were used in this study.Results: The results indicated that TWT and its active ingredient celastrol could protect against Con A-induced acute hepatitis. Plasma metabolomics analysis revealed that metabolic perturbations related to bile acid and fatty acid metabolism induced by Con A were reversed by celastrol. The level of itaconate in the liver was increased by celastrol and speculated as an active endogenous compound mediating the protective effect of celastrol. Administration of 4-octanyl itaconate (4-OI) as a cell-permeable itaconate mimicker was found to attenuate Con A-induced liver injury through activation of the pregnane X receptor (PXR) and enhancement of the transcription factor EB (TFEB)-mediated autophagy.Conclusions: Celastrol increased itaconate and 4-OI promoted activation of TFEB-mediated lysosomal autophagy to protect against Con A-induced liver injury in a PXR-dependent manner. Our study reported a protective effect of celastrol against Con A-induced AIH via an increased production of itaconate and upregulation of TFEB. The results highlighted that PXR and TFEB-mediated lysosomal autophagic pathway may offer promising therapeutic target for the treatment of autoimmune hepatitis.
C1 [Zhang, Ting; Dai, Manyun; Li, Fei] Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resources West Chi, Kunming 650201, Peoples R China.
[Zhang, Ting; Dai, Manyun] Univ Chinese Acad Sci, Beijing 100049, Peoples R China.
[Zhang, Ting; Rao, Qianru; Dai, Manyun; Zhao, Qi; Li, Fei] Sichuan Univ, Sichuan Univ Oxford Univ Huaxi Gastrointestinal Ca, West China Hosp, Frontiers Sci Ctr Dis Related Mol Network,Lab Meta, Chengdu 610041, Peoples R China.
[Li, Fei] Sichuan Univ, West China Hosp, Dept Pharm, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
[Li, Fei] Sichuan Univ, West China Hosp, Frontiers Sci Ctr Dis Related Mol Network, Chengdu 610041, Peoples R China.
C3 Chinese Academy of Sciences; Kunming Institute of Botany, CAS; Chinese
Academy of Sciences; University of Chinese Academy of Sciences, CAS;
Sichuan University; Sichuan University; Sichuan University
RP Li, F (corresponding author), Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resources West Chi, Kunming 650201, Peoples R China.; Li, F (corresponding author), Sichuan Univ, West China Hosp, Frontiers Sci Ctr Dis Related Mol Network, Chengdu 610041, Peoples R China.
EM feili@wchscu.cn
RI Zhang, Ting/P-8913-2017; Dai, Manyun/GZB-0789-2022; zhao,
qi/KGK-3760-2024
FU National Key Research and Development Program of China, China
[2021YFF0702003]; 1.3.5 Project for Disciplines of Excellence from West
China Hospital; Fundamental Research Funds for the Central Universities,
China [2022SCU12054]; "Post-Doctor Research Project, West China
Hospital, Sichuan University, China [2021HXBH041]
FX This work was supported by the National Key Research and Development
Program of China, China (2021YFF0702003) , 1.3.5 Project for Disciplines
of Excellence from West China Hospital, the Fundamental Research Funds
for the Central Universities, China (2022SCU12054) ", "Post-Doctor
Research Project, West China Hospital, Sichuan University, China
(2021HXBH041) ".
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PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0378-8741
EI 1872-7573
J9 J ETHNOPHARMACOL
JI J. Ethnopharmacol.
PD JUN 12
PY 2023
VL 309
AR 116365
DI 10.1016/j.jep.2023.116365
EA MAR 2023
PG 14
WC Plant Sciences; Chemistry, Medicinal; Integrative & Complementary
Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary
Medicine
GA A6ZR1
UT WOS:000956588000001
PM 36907478
DA 2025-01-07
ER
PT J
AU Mazza, S
Soro, S
Verga, MC
Elvo, B
Ferretti, F
Cereatti, F
Drago, A
Grassia, R
AF Mazza, Stefano
Soro, Sara
Verga, Maria Chiara
Elvo, Biagio
Ferretti, Francesca
Cereatti, Fabrizio
Drago, Andrea
Grassia, Roberto
TI Liver-side of inflammatory bowel diseases: Hepatobiliary and
drug-induced disorders
SO WORLD JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Inflammatory bowel diseases; Hepatobiliary disorders; Primary sclerosing
cholangitis; Drug-induced liver injury; Biological drugs; Viral
hepatitis
ID PRIMARY SCLEROSING CHOLANGITIS; ACTIVE RHEUMATOID-ARTHRITIS; CHRONIC
ULCERATIVE-COLITIS; EVIDENCE-BASED CONSENSUS; MAINTENANCE THERAPY;
CROHNS-DISEASE; RISK-FACTORS; HEPATITIS-B; TOFACITINIB CP-690,550;
URSODEOXYCHOLIC ACID
AB Hepatobiliary disorders are among the most common extraintestinal manifestations in inflammatory bowel diseases (IBD), both in Crohn's disease and ulcerative colitis (UC), and therefore represent a diagnostic challenge. Immune-mediated conditions include primary sclerosing cholangitis (PSC) as the main form, variant forms of PSC (namely small-duct PSC, PSC-autoimmune hepatitis overlap syndrome and IgG4-related sclerosing cholangitis) and granulomatous hepatitis. PSC is by far the most common, presenting in up to 8% of IBD patients, more frequently in UC. Several genetic foci have been identified, but environmental factors are preponderant on disease pathogenesis. The course of the two diseases is typically independent. PSC diagnosis is based mostly on typical radiological findings and exclusion of secondary cholangiopathies. Risk of cholangiocarcinoma is significantly increased in PSC, as well as the risk of colorectal cancer in patients with PSC and IBD-related colitis. No disease-modifying drugs are approved to date. Thus, PSC management is directed against symptoms and complications and includes medical therapies for pruritus, endoscopic treatment of biliary stenosis and liver transplant for end-stage liver disease. Other non-immune-mediated hepatobiliary disorders are gallstone disease, whose incidence is higher in IBD and reported in up to one third of IBD patients, non-alcoholic fatty liver disease, pyogenic liver abscess and portal vein thrombosis. Drug-induced liver injury (DILI) is an important issue in IBD, since most IBD therapies may cause liver toxicity; however, the incidence of serious adverse events is low. Thiopurines and methotrexate are the most associated with DILI, while the risk related to anti-tumor necrosis factor-alpha and anti-integrins is low. Data on hepatotoxicity of newer drugs approved for IBD, like anti-interleukin 12/23 and tofacitinib, are still scarce, but the evidence from other rheumatic diseases is reassuring. Hepatitis B reactivation during immunosuppressive therapy is a major concern in IBD, and adequate screening and vaccination is warranted. On the other hand, hepatitis C reactivation does not seem to be a real risk, and hepatitis C antiviral treatment does not influence IBD natural history. The approach to an IBD patient with abnormal liver function tests is complex due to the wide range of differential diagnosis, but it is of paramount importance to make a quick and accurate diagnosis, as it may influence the therapeutic management.
C1 [Mazza, Stefano; Soro, Sara; Verga, Maria Chiara; Elvo, Biagio; Cereatti, Fabrizio; Drago, Andrea; Grassia, Roberto] ASST Cremona, Gastroenterol & Digest Endoscopy Unit, Viale Concordia 1, I-26100 Cremona, Italy.
[Ferretti, Francesca] Univ Milan, Dept Biomed & Clin Sci DIBIC, Gastroenterol Unit, ASST Fatebenefratelli Sacco, I-20157 Milan, Italy.
C3 University of Milan
RP Mazza, S (corresponding author), ASST Cremona, Gastroenterol & Digest Endoscopy Unit, Viale Concordia 1, I-26100 Cremona, Italy.
EM stem311089@gmail.com
RI cereatti, fabrizio/ABD-2661-2020
OI Mazza, Stefano/0000-0002-9068-3209
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NR 173
TC 6
Z9 7
U1 0
U2 4
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5182
J9 WORLD J HEPATOL
JI World J. Hepatol.
PD DEC 27
PY 2021
VL 13
IS 12
DI 10.4254/wjh.v13.i12.1828
PG 23
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA YZ0ZD
UT WOS:000755210800002
PM 35069993
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Vesterhus, M
Karlsen, TH
AF Vesterhus, Mette
Karlsen, Tom Hemming
TI Emerging therapies in primary sclerosing cholangitis: pathophysiological
basis and clinical opportunities
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Primary sclerosing cholangitis; Therapy; Study design; Alkaline
phosphatase
ID DOSE URSODEOXYCHOLIC ACID; GENOME-WIDE ASSOCIATION;
INFLAMMATORY-BOWEL-DISEASE; FECAL MICROBIOTA TRANSPLANTATION; HISTOLOGIC
SCORING SYSTEMS; PRIMARY BILIARY-CIRRHOSIS; PLACEBO-CONTROLLED TRIAL;
ALKALINE-PHOSPHATASE; CHOLESTATIC LIVER; ULCERATIVE-COLITIS
AB Primary sclerosing cholangitis (PSC) is a progressive liver disease, histologically characterized by inflammation and fibrosis of the bile ducts, and clinically leading to multi-focal biliary strictures and with time cirrhosis and liver failure. Patients bear a significant risk of cholangiocarcinoma and colorectal cancer, and frequently have concomitant inflammatory bowel disease and autoimmune disease manifestations. To date, no medical therapy has proven significant impact on clinical outcomes and most patients ultimately need liver transplantation. Several treatment strategies have failed in the past and whilst prescription of ursodeoxycholic acid (UDCA) prevails, controversy regarding benefits remains. Lack of statistical power, slow and variable disease progression, lack of surrogate biomarkers for disease severity and other challenges in trial design serve as critical obstacles in the development of effective therapy. Advances in our understanding of PSC pathogenesis and biliary physiology over recent years has however led to a surge of clinical trials targeting various mechanistic compartments and currently raising hopes for imminent changes in patient management. Here, in light of pathophysiology, we outline and critically evaluate emerging treatment strategies in PSC, as tested in recent or ongoing phase II and III trials, stratified per a triad of targets of nuclear and membrane receptors regulating bile acid metabolism, immune modulators, and effects on the gut microbiome. Furthermore, we revisit the UDCA trials of the past and critically discuss relevant aspects of clinical trial design, including how the choice of endpoints, alkaline phosphatase in particular, may affect the future path to novel, effective PSC therapeutics.
C1 [Vesterhus, Mette; Karlsen, Tom Hemming] Natl Hosp Norway, Oslo Univ Hosp, Div Surg Inflammatory Med & Transplantat, Norwegian PSC Res Ctr,Dept Transplantat Med, N-0424 Oslo, Norway.
[Vesterhus, Mette] Haraldsplass Deaconess Hosp, Dept Med, Bergen, Norway.
[Karlsen, Tom Hemming] Univ Oslo, Inst Clin Med, Oslo, Norway.
[Karlsen, Tom Hemming] Oslo Univ Hosp, Dept Transplantat Med, Sect Gastroenterol, Oslo, Norway.
C3 University of Oslo; National Hospital Norway; University of Oslo;
University of Oslo
RP Karlsen, TH (corresponding author), Natl Hosp Norway, Oslo Univ Hosp, Div Surg Inflammatory Med & Transplantat, Norwegian PSC Res Ctr,Dept Transplantat Med, N-0424 Oslo, Norway.; Karlsen, TH (corresponding author), Univ Oslo, Inst Clin Med, Oslo, Norway.; Karlsen, TH (corresponding author), Oslo Univ Hosp, Dept Transplantat Med, Sect Gastroenterol, Oslo, Norway.
EM t.h.karlsen@medisin.uio.no
RI Vesterhus, Mette/AAX-8767-2020
OI Vesterhus, Mette/0000-0003-1493-2303
FU University of Oslo (Oslo University Hospital)
FX Open Access funding provided by University of Oslo (incl Oslo University
Hospital). We thank Kari C. Toverud for assistance in developing Fig. 1.
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NR 207
TC 55
Z9 59
U1 1
U2 8
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JUN
PY 2020
VL 55
IS 6
BP 588
EP 614
DI 10.1007/s00535-020-01681-z
EA MAR 2020
PG 27
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA LQ1UT
UT WOS:000522015500001
PM 32222826
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Tenca, A
Jaakkola, T
Färkkilä, M
Arola, J
Kolho, KL
AF Tenca, Andrea
Jaakkola, Tytti
Farkkila, Martti
Arola, Johanna
Kolho, Kaija-Leena
TI Impact of paediatric onset primary sclerosing cholangitis on clinical
course and outcome of inflammatory bowel disease: a case-control
population-based study in Finland
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Primary sclerosing cholangitis; autoimmune liver disease; dysplasia;
colorectal cancer; pouchitis; ulcerative colitis
ID WIDE ASSOCIATION ANALYSIS; URSODEOXYCHOLIC ACID; ULCERATIVE-COLITIS;
AUTOIMMUNE HEPATITIS; NATURAL-HISTORY; PSC-IBD; CHILDREN; RISK;
EPIDEMIOLOGY; PHENOTYPE
AB Introduction and aim: The aim of this study was to investigate the outcome of a paediatric onset of inflammatory bowel disease (IBD) in a cohort of subjects with primary sclerosing cholangitis (PSC) and in a matched-age population-based control group without PSC. Methods: We identified 28 IBD-PSC cases (median age at IBD diagnosis 12.5 years, 25-75th: 10-16 years) and selected three IBD controls for each case matched for age and year of IBD diagnosis. All data regarding the gastrointestinal tract and liver were collected at diagnosis and at last follow-up (median 15 years). Results: At diagnosis the prevalence of pancolitis was similar between the groups (78% and 79%, respectively p = -.30), but histologic inflammation was milder in IBD-PSC (61% vs 30%, p = .06). At last follow-up (median age 29 years) pancolitis was less frequent (6% and 33%, respectively p = .04) and the remission higher (76% and 47%, respectively p = .08) in IBD-PSC patients than in IBD patients. Panproctolectomy (32% in IBD-PSC and 34% in IBD, p = 1.0) and the rate of pouchitis (62% and 70%, respectively p = .8) were similar. Conclusions: The outcome of paediatric onset IBD in patients with PSC in adulthood seems to be comparable to those with IBD only.
C1 [Tenca, Andrea; Farkkila, Martti] Univ Helsinki, Dept Med, Clin Gastroenterol, Helsinki, Finland.
[Tenca, Andrea; Farkkila, Martti; Arola, Johanna] Helsinki Univ Hosp, Helsinki, Finland.
[Jaakkola, Tytti; Kolho, Kaija-Leena] Univ Helsinki, Dept Pediat Gastroenterol, Helsinki, Finland.
[Jaakkola, Tytti; Kolho, Kaija-Leena] Childrens Hosp, Helsinki, Finland.
[Arola, Johanna] Univ Helsinki, Dept Pathol, Helsinki, Finland.
C3 University of Helsinki; University of Helsinki; Helsinki University
Central Hospital; University of Helsinki; University of Helsinki
RP Tenca, A (corresponding author), Helsinki Univ Hosp, Dept Med, Clin Gastroenterol, POB 340, Helsinki 00029, Finland.; Tenca, A (corresponding author), Univ Helsinki, POB 340, Helsinki 00029, Finland.
EM ante14@hotmail.it
RI Färkkilä, Martti/AAG-6970-2021
OI Farkkila, Martti/0000-0002-0250-8559; , Andrea/0000-0002-9064-0612
FU Sigrid Juselius Foundation; Paediatric Research Foundation; Helsinki
University Hospital Research Fund
FX The study was supported by the Sigrid Juselius Foundation, the
Paediatric Research Foundation and the Helsinki University Hospital
Research Fund.
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NR 34
TC 4
Z9 4
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD AUG 3
PY 2019
VL 54
IS 8
BP 984
EP 990
DI 10.1080/00365521.2019.1648547
EA AUG 2019
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA JA5NL
UT WOS:000481179000001
PM 31402720
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Snook, AE
Baybutt, TR
Hyslop, T
Waldman, SA
AF Snook, Adam E.
Baybutt, Trevor R.
Hyslop, Terry
Waldman, Scott A.
TI Preclinical Evaluation of a Replication-Deficient Recombinant Adenovirus
Serotype 5 Vaccine Expressing Guanylate Cyclase C and the PADRE T-helper
Epitope
SO HUMAN GENE THERAPY METHODS
LA English
DT Article
DE colorectal cancer; GUCY2C; vaccine
ID COLORECTAL-CANCER; IN-VIVO; AUTOIMMUNE-DISEASE; SYRIAN-HAMSTERS; CELL
RESPONSES; B-CELL; BIODISTRIBUTION; ANTIGEN; VECTOR; SAFETY
AB There is an unmet need for improved therapeutics for colorectal cancer, the second leading cause of cancer mortality worldwide. Adjuvant chemotherapy only marginally improves survival in some patients and has no benefit in others, underscoring the clinical opportunity for novel immunotherapeutic approaches to improve survival in colorectal cancer. In that context, guanylate cyclase C (GUCY2C) is an established biomarker and therapeutic target for metastatic colorectal cancer with immunological characteristics that promote durable antitumor efficacy without autoimmunity. Preliminary studies established non-replicating human type 5 adenovirus (Ad5) expressing GUCY2C as safe and effective to induce GUCY2C-specific immune responses and antitumor immunity in mice. This study characterized the biodistribution, immunogenicity, and safety of a vector expressing GUCY2C fused with the human CD4(+) T helper cell epitope PADRE (Ad5-GUCY2C-PADRE) to advance this vaccine into clinical trials in colorectal cancer patients. Ad5-GUCY2C-PADRE levels were highest in the injection site and distributed in vivo primarily to draining lymph nodes, the liver, spleen and, unexpectedly, to the bone marrow. Immune responses following Ad5-GUCY2C-PADRE administration were characterized by PADRE-specific CD4(+) T-cell and GUCY2C-specific B-cell and CD8(+) T-cell responses, producing antitumor immunity targeting GUCY2C-expressing colorectal cancer metastases in the lungs, without acute or chronic autoimmune or other toxicities. Collectively, these data support Ad5-GUCY2C-PADRE as a safe and effective vaccination strategy in preclinical models and position Ad5-GUCY2C-PADRE for Phase I clinical testing in colorectal cancer patients.
C1 [Snook, Adam E.; Baybutt, Trevor R.; Waldman, Scott A.] Thomas Jefferson Univ, Dept Pharmacol & Expt Therapeut, Philadelphia, PA 19107 USA.
[Hyslop, Terry] Duke Univ, Dept Biostat & Bioinformat, Duke Canc Inst, Durham, NC USA.
C3 Jefferson University; Duke University
RP Snook, AE (corresponding author), 1020 Locust St,JAH 368, Philadelphia, PA 19107 USA.
EM adam.snook@jefferson.edu
RI Snook, Adam/P-2585-2015
OI Snook, Adam/0000-0001-9216-4560; Hyslop, Terry/0000-0002-3930-8876;
Waldman, Scott/0000-0001-6619-175X
FU NIH [P30 CA56036, R01 CA170533]; Targeted Diagnostic and Therapeutics,
Inc.; PhRMA Foundation; Margaret Q. Landenberger Research Foundation;
Pennsylvania Department of Health (SAP) [4100051723]
FX Financial support was provided by: NIH (P30 CA56036, R01 CA170533 to
S.A.W.); Targeted Diagnostic and Therapeutics, Inc. (to S.A.W.); PhRMA
Foundation (to A.E.S.); and Margaret Q. Landenberger Research Foundation
(to A.E.S.). S.A.W. is the Samuel M.V. Hamilton Professor of Thomas
Jefferson University. This project was funded, in part, by a grant from
the Pennsylvania Department of Health (SAP #4100051723). The Department
specifically disclaims responsibility for any analyses, interpretations,
or conclusions. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
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Snook AE, 2012, CANCER IMMUNOL IMMUN, V61, P713, DOI 10.1007/s00262-011-1133-0
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Ying B, 2009, CANCER GENE THER, V16, P625, DOI 10.1038/cgt.2009.6
NR 30
TC 21
Z9 23
U1 0
U2 2
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1946-6536
EI 1946-6544
J9 HUM GENE THER METHOD
JI Hum. Gene Ther. Methods
PD DEC
PY 2016
VL 27
IS 6
BP 238
EP 250
DI 10.1089/hgtb.2016.114
PG 13
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA EG5VF
UT WOS:000391112100004
PM 27903079
OA Green Published
DA 2025-01-07
ER
PT J
AU Cooper, J
Markovinovic, A
Coward, S
Herauf, M
Shaheen, AA
Swain, M
Panaccione, R
Ma, CSP
Lu, CTY
Novak, K
Kroeker, K
Ng, SC
Kaplan, GG
AF Cooper, Jared
Markovinovic, Ante
Coward, Stephanie
Herauf, Michelle
Shaheen, Abdel-Aziz
Swain, Mark
Panaccione, Remo
Ma, Christopher
Lu, Cathy
Novak, Kerri
Kroeker, Karen, I
Ng, Siew C.
Kaplan, Gilaad G.
TI Incidence and Prevalence of Primary Sclerosing Cholangitis: A
Meta-analysis of Population-based Studies
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE primary sclerosing cholangitis; prevalence; incidence; systematic review
ID INFLAMMATORY-BOWEL-DISEASE; AUTOIMMUNE LIVER-DISEASES; OUTCOMES;
EPIDEMIOLOGY; CANCER; DEATH
AB Background Primary sclerosing cholangitis is a chronic liver disease associated with significant morbidity, mortality, and healthcare utilization. We conducted a systematic review and meta-analysis of population-based studies of the incidence and prevalence of primary sclerosing cholangitis.Methods Medline and Embase were systematically searched to identify population-based studies of a defined geographic area and reported the incidence or prevalence of primary sclerosing cholangitis in the general population. Meta-analyses, using random-effects, were performed to calculate overall and country-specific incidence (per 100 000 persons/year) and prevalence rates (per 100 000 persons) with 95% confidence intervals.Results The 14 studies on incidence and the 12 for prevalence originated from North America, Asia, Europe, and Oceania. Incidence and prevalence rates of primary sclerosing cholangitis were 0.87 (95% confidence interval, 0.59-1.29) and 13.53 (95% confidence interval, 10.20-17.94) per 100 000 persons, respectively.Conclusions Both the prevalence and incidence of primary sclerosing cholangitis is low in the general population. Future studies on the incidence and prevalence of primary sclerosing cholangitis in the general population should be directed at Asia, Africa, and Latin America to allow for a more robust assessment of the global epidemiology of primary sclerosing cholangitis.
Primary sclerosing cholangitis is a chronic liver disease with complications such as cirrhosis, cancer, and death. This study summarizes the incidence (0.87 per 100 000) and prevalence (13.53 per 100 000) of PSC and highlight needs in research to study the epidemiology of PSC.
C1 [Cooper, Jared; Markovinovic, Ante; Coward, Stephanie; Herauf, Michelle; Shaheen, Abdel-Aziz; Swain, Mark; Panaccione, Remo; Ma, Christopher; Lu, Cathy; Novak, Kerri; Kaplan, Gilaad G.] Univ Calgary, Dept Med, Div Gastroenterol & Hepatol, Calgary, AB, Canada.
[Cooper, Jared; Kroeker, Karen, I] Univ Alberta, Dept Med, Div Gastroenterol, Edmonton, AB, Canada.
[Ng, Siew C.] Chinese Univ Hong Kong, LKS Inst Digest Dis, Dept Med & Therapeut, State Key Lab Digest Dis, Hong Kong, Peoples R China.
[Kaplan, Gilaad G.] 3280 Hosp Dr NW Calgary,Room 3D03-18, Calgary, AB T2N 4Z6, Canada.
C3 University of Calgary; University of Alberta; Chinese University of Hong
Kong
RP Kaplan, GG (corresponding author), 3280 Hosp Dr NW Calgary,Room 3D03-18, Calgary, AB T2N 4Z6, Canada.
EM ggkaplan@ucalgary.ca
RI Ma, Christopher/AAH-4886-2021; Panaccione, Remo/ABC-1140-2021; Shaheen,
Abdel/AAX-3773-2021
OI Panaccione, Remo/0000-0002-5247-940X; Lu, Cathy/0000-0003-3004-7048;
Coward, Stephanie/0000-0003-0675-7226; Kroeker,
Karen/0000-0002-3886-4213; Ma, Christopher/0000-0002-4698-9948
FU Leona M. and Harry B. Helmsley Charitable Trust [G-2106-04697];
International Organization for the Study of Inflammatory Bowel Disease
(IOIBD); Canadian Institutes of Health Research, Project Scheme
Operating Grant [PJT-162393]
FX The Leona M. and Harry B. Helmsley Charitable Trust (Grant number
G-2106-04697). International Organization for the Study of Inflammatory
Bowel Disease (IOIBD). Canadian Institutes of Health Research, Project
Scheme Operating Grant (Reference number PJT-162393)
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NR 35
TC 0
Z9 0
U1 4
U2 10
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1078-0998
EI 1536-4844
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD DEC 5
PY 2023
VL 30
IS 11
BP 2019
EP 2026
DI 10.1093/ibd/izad276
EA DEC 2023
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA L0N4B
UT WOS:001113055700001
PM 38052097
DA 2025-01-07
ER
PT J
AU Chan, YC
Chen, CL
Lin, CC
Yong, CC
Wu, YJ
Chi, SY
Chou, FF
AF Chan, Yi-Chia
Chen, Chao-Long
Lin, Chih-Che
Yong, Chee-Chien
Wu, Yi-Ju
Chi, Shun-Yu
Chou, Fong-Fu
TI Impact of Thyroid Incidentaloma on Liver Transplant: A Study of 1010
Recipients at a Single Center
SO ANNALS OF TRANSPLANTATION
LA English
DT Article
DE Incidental Findings; Liver Transplantation; Thyroid Diseases
ID DE-NOVO MALIGNANCY; AUTOIMMUNE HEPATITIS; CANCER; FDG; PET;
HYPOTHYROIDISM; ASSOCIATION; PREVALENCE; MANAGEMENT; DIAGNOSIS
AB Background: Thyroid incidentalomas are typically nonpalpable thyroid nodules discovered during radiographic evaluation for a non-thyroid issue. Thyroid incidentalomas visualized by computed tomography (CT) and 18F-flurodeoxyglucose (FDG) positron emission tomography (PET) before living donor liver transplantation (LDLT) are rare. The aim of the study was to analyze the clinical impact of thyroid incidentalomas discovered prior to transplantation.
Material/Methods: This retrospective study recruited 1010 patients undergoing LDLT between 2010 and 2019. CT was performed on each patient, whereas PET was performed on randomized patients (n=498).
Results: The prevalence and malignant risk of thyroid incidentaloma on CT was 2.3% (23/1010) and 13.0% (3/23), respectively. The prevalence of thyroid incidentaloma on PET was 3.0% (15/498). Approximately half of the FDG uptake on PET was diffuse uptake (n=7), whereas the other half was focal uptake (n=8). The malignant risk of PET incidentaloma with focal FDG uptake was 37.5% (3/8). Four asymptomatic thyroid cancers were identified incidentally. After total thyroidectomy followed by LDLT, these patients maintained cancer-free status.
Conclusions: Thyroid incidentalomas occurred at a rate of 2-3% in LDLT candidates. The malignant risk was 13.0% on CT incidentaloma, and 37.5% on PET incidentaloma with focal FDG uptake. Curative treatment of incidental thyroid cancer followed by LDLT without delay can achieve a favorable prognosis.
C1 [Chan, Yi-Chia; Chen, Chao-Long; Lin, Chih-Che; Yong, Chee-Chien; Wu, Yi-Ju] Kaohsiung Chang Gung Mem Hosp, Liver Transplantat Ctr, Kaohsiung, Taiwan.
[Chan, Yi-Chia; Chen, Chao-Long; Lin, Chih-Che; Yong, Chee-Chien; Wu, Yi-Ju; Chi, Shun-Yu; Chou, Fong-Fu] Kaohsiung Chang Gung Mem Hosp, Dept Gen Surg, Kaohsiung, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung Memorial Hospital
RP Chi, SY (corresponding author), Kaohsiung Chang Gung Mem Hosp, Dept Gen Surg, Kaohsiung, Taiwan.
EM abraban@cgmh.org.tw
RI Hsu, Chien-Ning/GLS-4014-2022; Lin, Ying-Chu/C-8679-2009; Chen,
Chao-Long/LMN-0626-2024; chen, yuling/JMQ-4121-2023
OI Chan, YiChia/0000-0003-1779-7338
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NR 35
TC 4
Z9 4
U1 0
U2 1
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
SN 1425-9524
J9 ANN TRANSPL
JI Ann. Transpl.
PD FEB 8
PY 2022
VL 27
AR e934988
DI 10.12659/AOT.934988
PG 8
WC Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery; Transplantation
GA YX6KA
UT WOS:000754208300001
PM 35132052
OA Green Published
DA 2025-01-07
ER
PT J
AU Tadokoro, T
Morishita, A
Sakamoto, T
Fujihara, S
Fujita, K
Mimura, S
Oura, K
Nomura, T
Tani, J
Yoneyama, H
Iwama, H
Himoto, T
Niki, T
Hirashima, M
Masaki, T
AF Tadokoro, Tomoko
Morishita, Asahiro
Sakamoto, Teppei
Fujihara, Shintaro
Fujita, Koji
Mimura, Shima
Oura, Kyoko
Nomura, Takako
Tani, Joji
Yoneyama, Hirohito
Iwama, Hisakazu
Himoto, Takashi
Niki, Toshiro
Hirashima, Mitsuomi
Masaki, Tsutomu
TI Galectin-9 ameliorates fulminant liver injury
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE galectin-9; fulminant hepatitis; microRNA
ID HEPATOCELLULAR-CARCINOMA; HEPATITIS-C; IN-VITRO; APOPTOSIS; SUPPRESSES;
FAILURE; MICRORNAS; LIGAND; PROLIFERATION; INFLAMMATION
AB Fulminant hepatitis is a severe liver disease resulting in hepatocyte necrosis. Galectin-9 (Gal-9) is a tandem-repeat-type galectin that has been evaluated as a potential therapeutic agent for various diseases that regulate the host immune system. Concanavalin A (ConA) injection into mice results in serious, immune-mediated liver injury similar to human viral, autoimmune and fulminant hepatitis. The present study investigated the effects of Gal-9 treatment on fulminant hepatitis in vivo and the effect on the expression of microRNAs (miRNAs), in order to identify specific miRNAs associated with the immune effects of Gal-9. A ConA-induced mouse hepatitis model was used to investigate the effects of Gal-9 treatment on overall survival rates, liver enzymes, histopathology and miRNA expression levels. Histological analyses, TUNEL assay, immunohistochemistry and miRNA expression characterization, were used to investigate the degree of necrosis, fibrosis, apoptosis and infiltration of neutrophils and macrophages. Overall survival rates following ConA administration were significantly higher in Gal-9-treated mice compared with control mice treated with ConA + PBS. Histological examination revealed that Gal-9 attenuated hepatocellular damage, reduced local neutrophil infiltration and prevented the local accumulation of macrophages and liver cell apoptosis in ConA-treated mice. In addition, various miRNAs induced by Gal-9 may contribute to its anti-apoptotic, anti-inflammatory and pro-proliferative effects on hepatocytes. The results of the present study demonstrate that Gal-9 may be a candidate therapeutic target for the treatment of fulminant hepatitis.
C1 [Tadokoro, Tomoko; Morishita, Asahiro; Sakamoto, Teppei; Fujihara, Shintaro; Fujita, Koji; Mimura, Shima; Oura, Kyoko; Nomura, Takako; Tani, Joji; Yoneyama, Hirohito; Masaki, Tsutomu] Kagawa Univ, Dept Gastroenterol & Neurol, Takamatsu, Kagawa 7610793, Japan.
[Iwama, Hisakazu] Kagawa Univ, Life Sci Res Ctr, Fac Med, Takamatsu, Kagawa 7610793, Japan.
[Himoto, Takashi] Kagawa Prefectural Univ Hlth Sci, Dept Med Technol, Takamatsu, Kagawa 7610123, Japan.
[Niki, Toshiro; Hirashima, Mitsuomi] Kagawa Univ, Dept Immunol & Immunopathol, Fac Med, Takamatsu, Kagawa 7610793, Japan.
C3 Kagawa University; Kagawa University; Kagawa University
RP Morishita, A (corresponding author), Kagawa Univ, Dept Gastroenterol & Neurol, Fac Med, 1750-1 Ikenobe,Miki Cho, Takamatsu, Kagawa 7610793, Japan.
EM asahiro@med.kagawa-u.ac.jp
RI Fujita, Koji/X-4478-2019; Fujihara, Shintaro/AAW-6092-2021; Nomura,
Takako/LFT-3521-2024
OI Tadokoro, Tomoko/0000-0001-9975-386X; Fujihara,
Shintaro/0000-0002-1250-6012
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NR 36
TC 11
Z9 13
U1 0
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD JUL
PY 2017
VL 16
IS 1
BP 36
EP 42
DI 10.3892/mmr.2017.6606
PG 7
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA EZ9TZ
UT WOS:000405074100004
PM 28534962
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Agbim, U
Asrani, SK
AF Agbim, Uchenna
Asrani, Sumeet K.
TI Non-invasive assessment of liver fibrosis and prognosis: an update on
serum and elastography markers
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE Elastography; hepatitis C; hepatitis B; liver fibrosis; liver stiffness;
magnetic resonance elastography; nonalcoholic fatty liver disease; shear
wave elastography; vibration-controlled transient elastography
ID MAGNETIC-RESONANCE ELASTOGRAPHY; RADIATION FORCE IMPULSE; TRANSIENT
ELASTOGRAPHY; FATTY LIVER; DIAGNOSTIC-ACCURACY; HEPATIC-FIBROSIS;
HEPATOCELLULAR-CARCINOMA; STIFFNESS MEASUREMENT; PORTAL-HYPERTENSION;
LABORATORY TESTS
AB Introduction: Non-invasive assessment of fibrosis is increasingly utilized in clinical practice to diagnose hepatic fibrosis. Non-invasive assessment of liver fibrosis relies on biologic and/or physical properties to assess tissue fibrosis. Serum markers estimate fibrosis by incorporating markers reflecting hepatic function (indirect markers) and/or markers measuring extracellular matrix degradation/fibrogenesis (direct markers). Radiology based techniques relay the mechanical properties and stiffness of a tissue, with increased stiffness associated with more advanced fibrosis. Areas covered: In this comprehensive review, the recent literature discussing serum markers and elastography-based techniques will be covered. These modalities are also explored in the setting of various liver diseases. Expert opinion: The etiology of liver disease and clinical context should be taken into consideration when non-invasive markers are incorporated in clinical practice. Non-invasive assessment of fibrosis has been most extensively utilized in hepatitis C, followed by hepatitis B and nonalcoholic fatty liver disease, but its role remains less developed in other etiologies of liver disease such as alcohol-associated liver disease and autoimmune liver disease. The role of non-invasive markers in predicting progression or regression of fibrosis, development of liver-related events and survival needs to be further explored.
C1 [Agbim, Uchenna] Univ Tennessee, Ctr Hlth Sci, Dept Surg, Div Transplant Surg, Memphis, TN 38163 USA.
[Asrani, Sumeet K.] Baylor Univ, Med Ctr, Dallas, TX 75246 USA.
C3 University of Tennessee System; University of Tennessee Health Science
Center; Baylor University; Baylor University Medical Center
RP Asrani, SK (corresponding author), Baylor Univ, Med Ctr, Dallas, TX 75246 USA.
EM Sumeet.Asrani@baylorhealth.edu
RI Asrani, Sumeet/Y-6096-2019
FU Baylor Foundation Grant
FX This paper was funded by a Baylor Foundation Grant.
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NR 103
TC 93
Z9 98
U1 2
U2 32
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD APR 3
PY 2019
VL 13
IS 4
BP 361
EP 374
DI 10.1080/17474124.2019.1579641
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HO0WT
UT WOS:000460627100007
PM 30791772
DA 2025-01-07
ER
PT J
AU Hudacko, R
Theise, N
AF Hudacko, Rachel
Theise, Neil
TI Liver Biopsies in Chronic Viral Hepatitis Beyond Grading and Staging
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; CHRONIC ACTIVE HEPATITIS; C VIRUS;
HEPATOCELLULAR-CARCINOMA; CELL DYSPLASIA; HISTOLOGICAL FEATURES;
FIBROSIS PROGRESSION; AUTOIMMUNE HEPATITIS; NATURAL-HISTORY;
CORTICOSTEROID-THERAPY
AB Context.-Knowledge of the etiology and pathogenesis of chronic viral hepatitis has grown immensely during the past 50 years. The terminology used to assess liver biopsies with chronic viral hepatitis and the role of the liver biopsy itself have also evolved during this time. Although the focus of much discussion regarding diagnostic assessment of liver biopsies in patients with viral hepatitis has been on grading of activity and staging of fibrosis, each biopsy is also an opportunity to assess many other important features.
Objectives.-To discuss opportunities provided by biopsies to assess features such as the presence of virus-associated premalignant or malignancy-related changes, and the presence of other concomitant diseases, including fatty liver disease of diverse causes, and hemochromatosis, hereditary or otherwise.
Data Sources.-The data were obtained from published literature and professional experience.
Conclusions.-The evaluation of liver biopsies with chronic viral hepatitis has evolved beyond grading and staging. Pathologists need to be aware of the other features that may have important clinical implications. (Arch Pathol Lab Med. 2011;135:1320-1328; doi: 10.5858/arpa.2011-0021-RA)
C1 [Hudacko, Rachel] NYU, Dept Pathol, Langone Med Ctr, New York, NY 10016 USA.
[Theise, Neil] Albert Einstein Coll Med, Beth Israel Med Ctr, Dept Pathol, Div Digest Dis, New York, NY USA.
[Theise, Neil] Albert Einstein Coll Med, Beth Israel Med Ctr, Dept Med, Div Digest Dis, New York, NY USA.
C3 NYU Langone Medical Center; New York University; Yeshiva University;
Harvard University; Beth Israel Deaconess Medical Center; Harvard
University; Beth Israel Deaconess Medical Center; Yeshiva University
RP Hudacko, R (corresponding author), NYU, Dept Pathol, Langone Med Ctr, 522 1st Ave,SRB 301, New York, NY 10016 USA.
EM rhudacko@gmail.com
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NR 83
TC 18
Z9 22
U1 0
U2 4
PU COLL AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
EI 1543-2165
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD OCT
PY 2011
VL 135
IS 10
BP 1320
EP 1328
DI 10.5858/arpa.2011-0021-RA
PG 9
WC Medical Laboratory Technology; Medicine, Research & Experimental;
Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Research & Experimental Medicine;
Pathology
GA 833HX
UT WOS:000295875600013
PM 21970487
DA 2025-01-07
ER
PT J
AU Bai, P
Ye, HF
Xie, MQ
Saxena, P
Zulewski, H
Charpin-El Hamri, G
Djonov, V
Fussenegger, M
AF Bai, Peng
Ye, Haifeng
Xie, Mingqi
Saxena, Pratik
Zulewski, Henryk
Charpin-El Hamri, Ghislaine
Djonov, Valentin
Fussenegger, Martin
TI A synthetic biology-based device prevents liver injury in mice
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Genetically engineered cells; Gene- and cell-based therapy; Liver
disease; Regeneration; Synthetic biology; Synthetic gene circuits
ID HEPATOCYTE-GROWTH-FACTOR; SERUM BILE-ACIDS; FACTOR GENE-TRANSFER;
DOUBLE-BLIND; GLUCOSE-HOMEOSTASIS; COLORECTAL-CANCER; DIAGNOSTIC-VALUE;
FACTOR PLASMID; REGENERATION; THERAPY
AB Background & Aims: The liver performs a panoply of complex activities coordinating metabolic, immunologic and detoxification processes. Despite the liver's robustness and unique self-regeneration capacity, viral infection, autoimmune disorders, fatty liver disease, alcohol abuse and drug-induced hepatotoxicity contribute to the increasing prevalence of liver failure. Liver injuries impair the clearance of bile acids from the hepatic portal vein which leads to their spill over into the peripheral circulation where they activate the G-protein-coupled bile acid receptor TGR5 to initiate a variety of hepatoprotective processes.
Methods: By functionally linking activation of ectopically expressed TGR5 to an artificial promoter controlling transcription of the hepatocyte growth factor (HGF), we created a closed-loop synthetic signalling network that coordinated liver injury-associated serum bile acid levels to expression of HGF in a self-sufficient, reversible and dose-dependent manner.
Results: After implantation of genetically engineered human cells inside auto-vascularizing, immunoprotective and clinically validated alginate-poly-(L-lysine)-alginate beads into mice, the liver-protection device detected pathologic serum bile acid levels and produced therapeutic HGF levels that protected the animals from acute drug-induced liver failure.
Conclusions: Genetically engineered cells containing theranostic gene circuits that dynamically interface with host metabolism may provide novel opportunities for preventive, acute and chronic healthcare.
Lay summary: Liver diseases leading to organ failure may go unnoticed as they do not trigger any symptoms or significant discomfort. We have designed a synthetic gene circuit that senses excessive bile acid levels associated with liver injuries and automatically produces a therapeutic protein in response. When integrated into mammalian cells and implanted into mice, the circuit detects the onset of liver injuries and coordinates the production of a protein pharmaceutical which prevents liver damage. (C) 2016 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Bai, Peng; Ye, Haifeng; Xie, Mingqi; Saxena, Pratik; Zulewski, Henryk; Fussenegger, Martin] Swiss Fed Inst Technol, Dept Biosyst Sci & Engn, Mattenstr 26, CH-4058 Basel, Switzerland.
[Ye, Haifeng] E China Normal Univ, Shanghai Key Lab Regulatory Biol, Inst Biomed Sci, Dongchuan Rd 500, Shanghai 200241, Peoples R China.
[Ye, Haifeng] E China Normal Univ, Sch Life Sci, Dongchuan Rd 500, Shanghai 200241, Peoples R China.
[Zulewski, Henryk] Univ Basel, Fac Med, Petersgraben 4, CH-4031 Basel, Switzerland.
[Zulewski, Henryk] Stadtspital Triemli, Div Endocrinol & Diabet, Birmensdorferstr 497, CH-8063 Zurich, Switzerland.
[Charpin-El Hamri, Ghislaine] Univ Lyon 1, Dept Genie Biol, 43 Blvd 11 Novembre 1918, F-69100 Villeurbanne, France.
[Djonov, Valentin] Univ Bern, Inst Anat, Baltzerstr 2, CH-3000 Bern, Switzerland.
[Fussenegger, Martin] Univ Basel, Fac Sci, Mattenstr 26, CH-4058 Basel, Switzerland.
C3 Swiss Federal Institutes of Technology Domain; ETH Zurich; East China
Normal University; East China Normal University; University of Geneva;
University of Basel; Triemli Hospital; Universite Claude Bernard Lyon 1;
University of Bern; University of Basel
RP Fussenegger, M (corresponding author), Swiss Fed Inst Technol, Dept Biosyst Sci & Engn, Mattenstr 26, CH-4058 Basel, Switzerland.
EM fussenegger@bsse.ethz.ch
RI Bai, Peng/AAU-8175-2021
OI Djonov, Valentin/0000-0002-5062-1169; Ye, Haifeng/0000-0002-5482-8116
FU European Research Council [321381]; Chinese Scholarship Council;
National Centre of Competence in Research Molecular Systems Engineering
FX This work was supported by a European Research Council advanced grant
(ProNet, no. 321381), a personal fellowship by the Chinese Scholarship
Council to Peng Bai and in part by the National Centre of Competence in
Research Molecular Systems Engineering.
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NR 63
TC 44
Z9 52
U1 2
U2 44
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD JUL
PY 2016
VL 65
IS 1
BP 84
EP 94
DI 10.1016/j.jhep.2016.03.020
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DO8SE
UT WOS:000378053100014
PM 27067456
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Tanakai, A
Mai, X
Takahashi, A
Vierling, JM
AF Tanakai, Atsushi
Mai, Xiong
Takahashi, Atsushi
Vierling, John M.
TI Primary biliary cholangitis
SO LANCET
LA English
DT Review
ID QUALITY-OF-LIFE; PLACEBO-CONTROLLED TRIAL; RISK-FACTORS;
HEPATOCELLULAR-CARCINOMA; ANTIMITOCHONDRIAL ANTIBODIES; CIRRHOSIS;
OSTEOPOROSIS; BEZAFIBRATE; MANAGEMENT; CELLS
AB Primary biliary cholangitis is a chronic, autoimmune, cholestatic disease that mainly affects women aged 40-70 years. Recent epidemiological studies have shown an increasing incidence worldwide despite geographical heterogeneity and a decrease in the female-to-male ratio of those the disease affects. Similar to other autoimmune diseases, primary biliary cholangitis occurs in genetically predisposed individuals upon exposure to environmental triggers, specifically xenobiotics, smoking, and the gut microbiome. Notably, the diversity of the intestinal microbiome is diminished in individuals with primary biliary cholangitis. The intricate interplay among immune cells, cytokines, chemokines, and biliary epithelial cells is postulated as the underlying pathogenic mechanism involved in the development and progression of primary biliary cholangitis, and extensive research has been dedicated to comprehending these complex interactions. Following the official approval of obeticholic acid as second-line treatment for patients with an incomplete response or intolerance to ursodeoxycholic acid, clinical trials have indicated that peroxisome proliferator activator receptor agonists are promising additional second-line drugs. Future dual or triple drug regimens might reach a new treatment goal of normalisation of alkaline phosphatase levels, rather than a decrease to less than 167 times the upper limit of normal levels, and potentially improve long-term outcomes. Improvement of health-related quality of life with better recognition and care of subjective symptoms, such as pruritus and fatigue, is also an important treatment goal. Promising clinical investigations are underway to alleviate these symptoms. Efforts to facilitate better access to medical care and dissemination of current knowledge should enable diagnosis at an earlier stage of primary biliary cholangitis and ensure access to treatments based on risk stratification for all patients.
C1 [Tanakai, Atsushi] Teikyo Univ, Dept Med, Sch Med, Tokyo 1738605, Japan.
[Mai, Xiong] Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Inst Digest Dis, Sch Med,Div Gastroenterol & Hepatol,Key Lab Gastro, Shanghai, Peoples R China.
[Takahashi, Atsushi] Fukushima Med Univ, Dept Gastroenterol, Sch Med, Fukushima, Japan.
[Vierling, John M.] Baylor Coll Med, Dept Med & Surg, Sect Gastroenterol & Hepatol, Houston, TX USA.
[Vierling, John M.] Baylor Coll Med, Div Abdominal Transplantat, Houston, TX USA.
C3 Teikyo University; Shanghai Jiao Tong University; Fukushima Medical
University; Baylor College of Medicine; Baylor College of Medicine
RP Tanakai, A (corresponding author), Teikyo Univ, Dept Med, Sch Med, Tokyo 1738605, Japan.
EM a-tanaka@med.teikyo-u.ac.jp
FX We sincerely thank Kenichi Harada (Department of Human Pathology,
Kanazawa University Graduate School of Medicine, Kanazawa, Japan) who
kindly provided the typical hepatic histopathology in primary
cholangitis for figure 1.
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NR 131
TC 6
Z9 6
U1 12
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD SEP 14
PY 2024
VL 404
IS 10457
BP 1053
EP 1066
DI 10.1016/S0140-6736(24)01303-5
EA SEP 2024
PG 14
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA G3E3P
UT WOS:001315501400001
PM 39216494
OA hybrid
DA 2025-01-07
ER
PT J
AU Jaillon, S
Berthenet, K
Garlanda, C
AF Jaillon, Sebastien
Berthenet, Kevin
Garlanda, Cecilia
TI Sexual Dimorphism in Innate Immunity
SO CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
LA English
DT Review
DE Innate immunity; Sexual dimorphisms; Sex hormones; X-linked
immunodeficiency
ID PLASMACYTOID DENDRITIC CELLS; IFN-ALPHA PRODUCTION;
ESTROGEN-RECEPTOR-ALPHA; GENDER-DIFFERENCES; IN-VIVO;
HEPATOCELLULAR-CARCINOMA; MACROPHAGE PLASTICITY; CHROMOSOME COMPLEMENT;
MURINE MACROPHAGES; POSSIBLE MECHANISM
AB Sexual dimorphisms account for differences in clinical manifestations or incidence of infectious or autoimmune diseases and malignancy between females and males. Females develop enhanced innate and adaptive immune responses than males and are less susceptible to many infections of bacterial, viral, parasitic, and fungal origin and malignancies but in contrast, they are more prone to develop autoimmune diseases. The higher susceptibility to infections in males is observed from birth to adulthood, suggesting that sex chromosomes and not sex hormones have a major role in sexual dimorphism in innate immunity. Sex-based regulation of immune responses ultimately contributes to age-related disease development and life expectancy. Differences between males and females have been described in the expression of pattern recognition receptors of the innate immune response and in the functional responses of phagocytes and antigen presenting cells. Different factors have been shown to account for the sex-based disparity in immune responses, including genetic factors and hormonal mediators, which contribute independently to dimorphism in the innate immune response. For instance, several genes encoding for innate immune molecules are located on the X chromosome. In addition, estrogen and/or testosterone have been reported to modulate the differentiation, maturation, lifespan, and effector functions of innate immune cells, including neutrophils, macrophages, natural killer cells, and dendritic cells. In this review, we will focus on differences between males and females in innate immunity, which represents the first line of defense against pathogens and plays a fundamental role in the activation, regulation, and orientation of the adaptive immune response.
C1 [Jaillon, Sebastien; Garlanda, Cecilia] Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini, I-20090 Milan, Italy.
[Jaillon, Sebastien; Berthenet, Kevin; Garlanda, Cecilia] Humanitas Clin & Res Ctr, Via Manzoni 56, I-20089 Milan, Italy.
C3 Humanitas University
RP Jaillon, S; Garlanda, C (corresponding author), Humanitas Univ, Dept Biomed Sci, Via Rita Levi Montalcini, I-20090 Milan, Italy.; Jaillon, S; Garlanda, C (corresponding author), Humanitas Clin & Res Ctr, Via Manzoni 56, I-20089 Milan, Italy.
EM sebastien.jaillon@humanitasresearch.it;
cecilia.garlanda@humanitasresearch.it
RI ; Jaillon, Sebastien/A-7537-2015; Garlanda, Cecilia/K-4601-2016
OI Berthenet, Kevin/0000-0001-7345-4837; Jaillon,
Sebastien/0000-0002-5600-855X; Garlanda, Cecilia/0000-0002-1510-7703
FU Ministero della Salute [RF-2013-02355470]; Ministry of Education,
University and Research [PRIN 2015YYKPNN]; Associazione Italiana Ricerca
sul Cancro (MFAG 2016) [18475]
FX The contribution of Ministero della Salute (RF-2013-02355470), Ministry
of Education, University and Research (PRIN 2015YYKPNN), and the
Associazione Italiana Ricerca sul Cancro (MFAG 2016 ID 18475) is
gratefully acknowledged.
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NR 118
TC 390
Z9 419
U1 4
U2 93
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1080-0549
EI 1559-0267
J9 CLIN REV ALLERG IMMU
JI Clin. Rev. Allergy Immunol.
PD JUN
PY 2019
VL 56
IS 3
BP 308
EP 321
DI 10.1007/s12016-017-8648-x
PG 14
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA ID7ZY
UT WOS:000471902800004
PM 28963611
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Alazmi, W
Bustamante, M
O'Loughlin, C
Gonzalez, J
Raskin, JB
AF Alazmi, W
Bustamante, M
O'Loughlin, C
Gonzalez, J
Raskin, JB
TI The association of Streptococcus bovis bacteremia and
gastrointestinal diseases:: A retrospective analysis
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Streptococcus bovis; colonic neoplasms; gastrointestinal neoplasms
ID COLONIC LESIONS; ENDOCARDITIS; CARCINOMA; SEPTICEMIA; COLITIS; BOWEL
AB There is a well-established association between Streptococcus bovis bacteremia (SBB) and colorectal cancer. However, SBB is also frequently associated with chronic liver disease and has been described with other gastrointestinal disorders. The aim of the study was to evaluate the prevalence of gastrointestinal disease in patients with SBB. Retrospective analysis of the microbiology database at Jackson Memorial Medical Center, Miami, Florida, between 1992 and 2002, was performed. Patients' clinical records were reviewed, with special focus on underlying gastrointestinal disease or other major comorbidities. Thirty-eight patients (83%) were adults and eight (17%) were pediatric patients. Nineteen patients presented with gastrointestinal disorders associated with SBB (41%). Nine adult patients (19%) had end-stage liver disease (five female). Six patients had alcohol-induced liver disease (one with concomitant chronic hepatitis C), with the remaining three cases related to autoimmune hepatitis, primary biliary cirrhosis, and nonalcoholic steatohepatitis. Colonic neoplasms (adenocarcinoma in 3 and adenomatous polyps in 3) were found in 6 of 10 adult patients in whom colonoscopic evaluation was performed. Seven adult patients had acquired immunodeficiency syndrome (AIDS) (18%). Mortality in the patients with AIDS and SBB was high (71%). No significant association with gastrointestinal diseases was found in the pediatric population. Bacteremia due to S. bovis in adults is frequently associated with hepatic dysfunction (1:4), colonic neoplasms (1:6), and AIDS (1:6). This association was valid for our adult population only. SBB is an early clue to the likely presence of these serious underlying conditions and warrants rigorous investigation when recognized.
C1 Univ Miami, Jackson Mem Med Ctr, Div Gastroenterol, Miami, FL USA.
C3 University of Miami
RP Univ Miami Hosp, Div Gastroenterol, POB 016960 D-49, Miami, FL 33101 USA.
EM jraskin@med.miami.edu
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NR 24
TC 39
Z9 40
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD APR
PY 2006
VL 51
IS 4
BP 732
EP 736
DI 10.1007/s10620-006-3199-7
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 033KD
UT WOS:000236845000016
PM 16614996
DA 2025-01-07
ER
PT J
AU Bhatti, AA
Khan, MF
Bhatti, HUR
Punshi, A
AF Bhatti, Atiq Ahmad
Khan, Muhammad Farooq
Bhatti, Hammad-Ur-Rehman
Punshi, Avinash
TI Frequency of Portal Vein Thrombosis in Patients with Liver Cirrhosis
SO PAKISTAN JOURNAL OF MEDICAL & HEALTH SCIENCES
LA English
DT Article
DE Liver cirrhosis; Portal vein; Thrombosis
ID HEPATOCELLULAR-CARCINOMA; ORG-10172
AB Aim: To determine the frequency of portal vein thrombosis in patients with liver cirrhosis.
Study design: Retrospective/Case-control
Place and duration of study: Department of Medicine, M. Islam Medical & Dental College Gujranwala from 1st April 2019 to 30th September 2020.
Methodology: One hundred patients of both genders were presented in this study. Patients detailed demographics age, sex and body mass index were recorded after taking written consent, Patients were aged between 20-75 years. Patients who had liver cirrhosis were included in this study. Complete patients were undergone for Doppler ultrasonography for observation of portal vein thrombosis.
Results: Out of 100 patients, 60 (60%) were males and 40(40%) patients were females. Mean age of the patients were 47.08 +/- 7.42 years with mean BMI 28.22 +/- 9.61kg/m(2). We found that 60(60%) patients had hepatitis C, 29 (29%) patients had hepatitis B, 7(7%) had chronic liver disease, 3 (3%) patients had autoimmune hepatitis and 1 (1%) patient had other disease (Wilson's).
Conclusion: The frequency of portal vein thrombosis was high among patients of liver cirrhosis and mostly patients of hepatitis C were affected.
C1 [Bhatti, Atiq Ahmad] M Islam Med & Dent Coll, Dept Med, Gujranwala, Pakistan.
[Khan, Muhammad Farooq] Bolan Med Complex Hosp, Dept Gastroenterol, Quetta, Pakistan.
[Bhatti, Hammad-Ur-Rehman] Islam Med Coll, Dept Med, Sialkot, Pakistan.
[Punshi, Avinash] MICU South City Hosp, Karachi, Pakistan.
RP Bhatti, AA (corresponding author), M Islam Med & Dent Coll, Dept Med, Gujranwala, Pakistan.
EM aabhatti72@gmail.com
RI Khan, Muhammad/G-9838-2013
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NR 20
TC 1
Z9 1
U1 0
U2 0
PU LAHORE MEDICAL RESEARCH CENTER LLP
PI LAHORE
PA 590, Karim Block, Allama Iqbal Town, LAHORE, 00000, PAKISTAN
SN 1996-7195
J9 PAK J MED HEALTH SCI
JI Pak. J. Med. Health Sci.
PD APR
PY 2021
VL 15
IS 4
BP 887
EP 888
PG 2
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA SF8XA
UT WOS:000653030300066
DA 2025-01-07
ER
PT J
AU Thuluvath, PJ
Hanish, S
Savva, Y
AF Thuluvath, Paul Joseph
Hanish, Steven
Savva, Yulia
TI Liver Transplantation in Cryptogenic Cirrhosis: Outcome Comparisons
Between NASH, Alcoholic, and AIH Cirrhosis
SO TRANSPLANTATION
LA English
DT Article
ID PORTAL-VEIN THROMBOSIS; NONALCOHOLIC STEATOHEPATITIS;
HEPATIC-ENCEPHALOPATHY; HEPATOCELLULAR-CARCINOMA; INCREASED MORTALITY;
PERFORMANCE STATUS; DIABETES-MELLITUS; TERM OUTCOMES; RISK-FACTORS;
SURVIVAL
AB Background The outcomes of liver transplantation (LT) in patients with cryptogenic cirrhosis (CC) have not been adequately examined except for small case series. We believe that patients currently listed as CC have truly cryptogenic liver disease and may have different post-LT outcomes compared with nonalcoholic steatohepatitis (NASH).
Methods We compared the post-LT outcomes of adults with CC (n = 3241) and compared them with cirrhosis from NASH (n = 4089), alcoholic cirrhosis (AC) (n = 7837), and autoimmune hepatitis (AIH) (n = 1435) using the United Network for Organ Sharing database from 2002 to 2016. We excluded those who had multiorgan transplantation and hepatocellular carcinoma. In addition to the well-known predictors of liver transplant outcomes, we analyzed the impact of Karnofsky Performance Status score at LT on immediate and late outcomes.
Results There were significant differences in clinical characteristics between the groups. Despite these differences in clinical characteristics and risk factors, CC had similar graft and patient survival to NASH, AC, and AIH when assessed by Kaplan-Meier survival. Multivariate Cox regression analysis showed that graft and patient survival was similar in all 4 groups after adjusting for other confounders. Hispanics had a 24% lower risk of death (hazard ratio, 0.76) compared with whites in these combined cohorts after adjusting for all risk factors. In addition to other known risk factors, Karnofsky Performance Status score of 30% or less was associated with a 33% increase in risk of death (hazard ratio, 1.33) on multivariate analysis.
Conclusion Patients with CC had similar graft and patient survival when compared with NASH, AC, and AIH cirrhosis.
C1 [Thuluvath, Paul Joseph; Savva, Yulia] Mercy Med Ctr, Inst Digest Hlth & Liver Dis, Baltimore, MD 21202 USA.
[Thuluvath, Paul Joseph; Hanish, Steven] Univ Maryland, Sch Med, Dept Surg, Baltimore, MD 21201 USA.
[Thuluvath, Paul Joseph; Hanish, Steven] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
C3 Mercy Medical Center - Maryland; University System of Maryland;
University of Maryland Baltimore; University System of Maryland;
University of Maryland Baltimore
RP Thuluvath, PJ (corresponding author), Mercy Med Ctr, Inst Digest Hlth & Liver Dis, Baltimore, MD 21202 USA.
EM thuluvath@gmail.com
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NR 42
TC 18
Z9 19
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD APR
PY 2018
VL 102
IS 4
BP 656
EP 663
DI 10.1097/TP.0000000000002030
PG 8
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA GB3FT
UT WOS:000428942200035
PM 29215462
DA 2025-01-07
ER
PT J
AU Xu, XH
Pan, W
Kang, LH
Feng, H
Song, YQ
AF Xu, Xiao-Heng
Pan, Wei
Kang, Li-Hua
Feng, Hui
Song, Yan-Qiu
TI Association of annexin A2 with cancer development (Review)
SO ONCOLOGY REPORTS
LA English
DT Article
DE cancer; annexin A2; adhesion; proliferation; neovascularization;
invasion and metastasis
ID PRIMER RECOGNITION PROTEINS; METASTASIS-ASSOCIATED PROTEINS;
TISSUE-PLASMINOGEN ACTIVATOR; ENDOTHELIAL PRECURSOR CELLS; II TETRAMER;
BREAST-CANCER; KINASE-C; HEPATOCELLULAR-CARCINOMA; DNA-REPLICATION;
IN-VITRO
AB Annexin A2 (ANXA2) is a well-known calcium-dependent phospholipid binding protein widely distributed in the nucleus, cytoplasm and extracellular surface of various eukaryotic cells. It has been recognized as a pleiotropic protein affecting a wide range of molecular and cellular processes. Dysregulation and abnormal expression of ANXA2 are linked to a large number of prevalent diseases, including autoimmune and neurodegenerative disease, antiphospholipid syndrome, inflammation, diabetes mellitus and a series of cancers. Accumulating data suggest that ANXA2 is aberrantly expressed in a wide spectrum of cancers, and exerts profound effects on tumor cell adhesion, proliferation, apoptosis, invasion and metastasis as well as tumor neovascularization via different modes of action. However, despite significant research, our knowledge of the mechanism by which ANXA2 participates in cancer development remains fragmented. The present review systematically summarizes the effects of ANXA2 on tumor progression, in an attempt to gain an improved understanding of the underlying mechanisms and to provide a potential effective target for cancer therapy.
C1 [Xu, Xiao-Heng; Kang, Li-Hua; Feng, Hui; Song, Yan-Qiu] Jilin Univ, Ctr Canc, Hosp 1, Changchun 130021, Jilin, Peoples R China.
[Pan, Wei] Jilin Univ, Hosp 2, Dept Pediat, Changchun 130021, Jilin, Peoples R China.
C3 Jilin University; Jilin University
RP Song, YQ (corresponding author), Jilin Univ, Ctr Canc, Hosp 1, 71 Xinmin St, Changchun 130021, Jilin, Peoples R China.
EM songyanqiu1957@hotmail.com
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NR 148
TC 68
Z9 71
U1 1
U2 25
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD MAY
PY 2015
VL 33
IS 5
BP 2121
EP 2128
DI 10.3892/or.2015.3837
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CG3LE
UT WOS:000353180900004
PM 25760910
OA Bronze
DA 2025-01-07
ER
PT J
AU Ikuta, Y
Hayashida, Y
Hirata, S
Irie, A
Senju, S
Kubo, T
Nakatsura, T
Monji, M
Sasaki, Y
Baba, H
Nishimura, Y
AF Ikuta, Yoshiaki
Hayashida, Yuki
Hirata, Shinya
Irie, Atsushi
Senju, Satoru
Kubo, Tatsuko
Nakatsura, Tetsuya
Monji, Mikio
Sasaki, Yutaka
Baba, Hideo
Nishimura, Yasuharu
TI Identification of the H2-Kd-restricted cytotoxic T lymphocyte
epitopes of a tumor-associated antigen, SPARC, which can stimulate
antitumor immunity without causing autoimmune disease in mice
SO CANCER SCIENCE
LA English
DT Article
ID HUMAN BREAST-CANCER; DENDRITIC CELLS; HEPATOCELLULAR-CARCINOMA;
NEOPLASTIC PROGRESSION; PEPTIDE VACCINE; HUMAN-MELANOMA; PROTEIN;
EXPRESSION; OSTEONECTIN; GLYPICAN-3
AB We previously reported that the secreted protein acidic and rich in cystein (SPARC) was overexpressed in melanoma in humans, and the serum SPARC level was useful as a novel tumor marker for melanoma. SPARC was also reported to be overexpressed in various human cancers. In this study, we asked whether SPARC-specific cytotoxic T lymphocytes (CTL) could induce antitumor immunity to SPARC-expressing tumor in mice or not as a preclinical study of SPARC-directed anticancer immunotherapy. Because of similarities in the structural motifs of major histocompatibility complex-binding peptides between H2-K-d and HLA-A24 (A*2402), the most common human leukocyte antigen class I allele in the Japanese population, we attempted to identify the H2-K-d-restricted SPARC epitope for CTL in BALB/c mice and we found that the mouse SPARC(143-151) (DYIGPCKYI) and SPARC(225-234) (MYIFPVHWQF) peptides could induce peptide-reactive CTL in BALB/c mice without causing autoimmune diseases. The immunization of mice with SPARC(225-234) peptide-pulsed bone marrow-derived dendritic cells (BMDC) inhibited the growth of s.c. inoculated mouse mammary cancer cell line, N2C, expressing SPARC and these mice lived longer than the mice immunized with peptide-unpulsed BMDC. In conclusion, our study indicated that SPARC peptide-based cancer immunotherapy was effective and safe at least in a mouse tumor prevention model. (Cancer Sci 2009; 100: 132-137)
C1 [Ikuta, Yoshiaki; Hayashida, Yuki; Hirata, Shinya; Irie, Atsushi; Senju, Satoru; Nakatsura, Tetsuya; Monji, Mikio; Nishimura, Yasuharu] Kumamoto Univ, Grad Sch Med Sci, Dept Immunogenet, Kumamoto 8608556, Japan.
[Ikuta, Yoshiaki; Baba, Hideo] Kumamoto Univ, Grad Sch Med Sci, Dept Surg Gastroenterol, Kumamoto 8608556, Japan.
[Hayashida, Yuki; Sasaki, Yutaka] Kumamoto Univ, Grad Sch Med Sci, Dept Gastroenterol & Hepatol, Kumamoto 8608556, Japan.
[Kubo, Tatsuko] Kumamoto Univ, Grad Sch Med Sci, Dept Mol Pathol, Kumamoto 8608556, Japan.
[Nakatsura, Tetsuya] Natl Canc Ctr E, Ctr Innovat Med, Invest Treatment Div, Immunotherapy Sect, Chiba 2778577, Japan.
C3 Kumamoto University; Kumamoto University; Kumamoto University; Kumamoto
University; National Cancer Center - Japan
RP Nishimura, Y (corresponding author), Kumamoto Univ, Grad Sch Med Sci, Dept Immunogenet, 1-1-1 Honjo, Kumamoto 8608556, Japan.
EM mxnishim@gpo.kumamoto-u.ac.jp
FU Ministry of Education, Culture, Sports, Science and Technology, Japan
[17015035, 18014023]; Ministry of Health, Labor and Welfare, Japan; Onco
Therapy Science; Sagawa Foundation for the Promotion of Cancer Research;
Foundation for the Promotion of Cancer Research in Japan; Grants-in-Aid
for Scientific Research [18014023, 17015035] Funding Source: KAKEN
FX This work was supported in part by Grants-in-Aid (nos. 17015035 and
18014023) from the Ministry of Education, Culture, Sports, Science and
Technology, Japan; a Research Grant for Health Sciences from the
Ministry of Health, Labor and Welfare, Japan; funding from: Onco Therapy
Science; the Sagawa Foundation for the Promotion of Cancer Research; and
the Foundation for the Promotion of Cancer Research in Japan.
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U1 0
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PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
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J9 CANCER SCI
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PY 2009
VL 100
IS 1
BP 132
EP 137
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PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 390FN
UT WOS:000262149800019
PM 19068096
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Zhao, JZ
Wang, Q
Tan, AF
Loh, CJL
Toh, HC
AF Zhao, Junzhe
Wang, Qian
Tan, Alexandra F.
Loh, Celestine Jia Ling
Toh, Han Chong
TI Sex differences in cancer and immunotherapy outcomes: the role of
androgen receptor
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE sex; immunotherapy; androgen receptor; tumour microenvironment; gender
oncology
ID SALIVARY DUCT CARCINOMA; ENDOTHELIAL GROWTH-FACTOR; CELL LUNG-CANCER;
HEPATOCELLULAR-CARCINOMA; PROSTATE-CANCER; ESTROGEN-RECEPTOR;
BREAST-CANCER; COLORECTAL-CANCER; POSTMENOPAUSAL WOMEN;
PROGNOSTIC-FACTORS
AB Across the wide range of clinical conditions, there exists a sex imbalance where biological females are more prone to autoimmune diseases and males to some cancers. These discrepancies are the combinatory consequence of lifestyle and environmental factors such as smoking, alcohol consumption, obesity, and oncogenic viruses, as well as other intrinsic biological traits including sex chromosomes and sex hormones. While the emergence of immuno-oncology (I/O) has revolutionised cancer care, the efficacy across multiple cancers may be limited because of a complex, dynamic interplay between the tumour and its microenvironment (TME). Indeed, sex and gender can also influence the varying effectiveness of I/O. Androgen receptor (AR) plays an important role in tumorigenesis and in shaping the TME. Here, we lay out the epidemiological context of sex disparity in cancer and then review the current literature on how AR signalling contributes to such observation via altered tumour development and immunology. We offer insights into AR-mediated immunosuppressive mechanisms, with the hope of translating preclinical and clinical evidence in gender oncology into improved outcomes in personalised, I/O-based cancer care.
C1 [Zhao, Junzhe; Loh, Celestine Jia Ling] Duke NUS Med Sch, Singapore, Singapore.
[Zhao, Junzhe; Wang, Qian; Toh, Han Chong] Natl Canc Ctr, Div Med Oncol, Singapore, Singapore.
[Wang, Qian] China Med Univ, Dept Med Oncol, Canc Hosp, Liaoning Canc Hosp & Inst, Shenyang, Liaoning, Peoples R China.
[Tan, Alexandra F.] Imperial Coll, Sch Med, London, England.
[Loh, Celestine Jia Ling] Sengkang Gen Hosp, Sengkang, Singapore.
C3 National University of Singapore; National Cancer Centre Singapore
(NCCS); China Medical University; Imperial College London
RP Zhao, JZ (corresponding author), Duke NUS Med Sch, Singapore, Singapore.; Zhao, JZ; Wang, Q; Toh, HC (corresponding author), Natl Canc Ctr, Div Med Oncol, Singapore, Singapore.; Wang, Q (corresponding author), China Med Univ, Dept Med Oncol, Canc Hosp, Liaoning Canc Hosp & Inst, Shenyang, Liaoning, Peoples R China.
EM j.zhao@u.duke.nus.edu; wangqian_16@163.com;
toh.han.chong@singhealth.com.sg
RI Zhao, Junzhe/ABC-3146-2020
OI Tan, Alexandra/0009-0009-1100-879X; Zhao, Junzhe/0000-0002-3224-9105
FU National Medical Research Council10.13039/501100001349
FX JZ would like to thank Caroline Lee and Hanry Yu for their mentorship.
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NR 200
TC 2
Z9 2
U1 4
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAY 28
PY 2024
VL 15
AR 1416941
DI 10.3389/fimmu.2024.1416941
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA TP1O3
UT WOS:001242374400001
PM 38863718
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Xu, WC
Chen, SR
Huang, JX
Zheng, ZC
Chen, LX
Lin, JJ
Li, YG
AF Xu, W. C.
Chen, S. R.
Huang, J. X.
Zheng, Z. C.
Chen, L. X.
Lin, J. J.
Li, Y. G.
TI Expression and distribution of S-100 protein, CD83 and apoptosis-related
proteins (Fas, FasL and Bcl-2) in thyroid tissues of autoimmune thyroid
diseases
SO EUROPEAN JOURNAL OF HISTOCHEMISTRY
LA English
DT Article
DE Hashimoto's thyroiditis (HT); Graves' disease (GD); S-100; CD83;
apoptosis-related proteins; immunohistochemistry
ID DENDRITIC CELLS; HASHIMOTOS-THYROIDITIS; GRAVES-DISEASE; T-CELLS;
HEPATOCELLULAR-CARCINOMA; MEDIATED APOPTOSIS; DOWN-REGULATION; IN-VIVO;
LIGAND; THYROCYTES
AB Previous studies have shown that dendritic cells (DCs) and apoptosis-related proteins play a critical role in the pathogenesis of autoimmune thyroid diseases (ATD).This study was designed to investigate the expression and distribution of S-100 protein, CD83 and apoptosis-related proteins (Fas, FasL and Bcl-2) in the thyroid tissues of ATD and their role in ATD pathogenesis as determined by immunochemical staing techniques and other methods. Pathological tissues of 30 patients with Hashimoto's thyroiditis (HT), 30 patients with Graves' disease (GD) and 30 cases of thyroid follicular adenoma (TFA, as control) were used for this study. A higher expression of S-100 in HT (4.2 +/- 3.1%) and GD (3.9 +/- 2.8%) vs TFA (0.95 +/- 0.64%) (p<0.001). was observed as well as a higher expression of CD83 in HT (22.58 +/- 13.96%) and GD (29.92 +/- 14.43%) vs TFA (5.19 +/- 8.08%) (p<0.001). HT thyrocytes adjacent to thyroid infiltrating lymphocytes (TILs) showed greater increases in the levels of Fas and FasL than did the GD thyrocytes while HT TlLs exhibited lower expression of Fas and FasL than did the GD TlLs. GD thyrocytes expressed increased levels of the antiapoptotic protein Bcl-2 as compared to the low levels detected in HT thyrocytes. An opposite pattern was observed in the TILs in GD (low expression of Bcl-2) and HT (high expression of Bcl-2). The findings suggest that the high expression of DC markers is related to the pathogenesis of HT and GD. Up-regulation of both the number and matured functions of DCs may lead to the presentation of more antigens to lymphocytes which are related to the development of autoimmune thyroid diseases. The regulation of Fas/FasL/Bcl-2 in GD favors apoptosis of infiltrating lymphocytes and thyrocyte survival.The regulation of Fas/FasL/Bcl-2 in HT may promote thyrocyte apoptosis leading to hypothyroidism.
C1 [Chen, S. R.; Chen, L. X.] Shantou Univ, Sch Med, Second Hosp, Shantou, Guangdong, Peoples R China.
[Xu, W. C.; Huang, J. X.; Lin, J. J.; Li, Y. G.] Shantou Univ, Sch Med, First Hosp, Shantou, Guangdong, Peoples R China.
C3 Shantou University; Shantou University
RP Chen, SR (corresponding author), Shantou Univ, Sch Med, Second Hosp, Shantou, Guangdong, Peoples R China.
EM xuwcan@163.com
RI zheng, zaichao/IXN-9273-2023
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NR 48
TC 11
Z9 19
U1 0
U2 0
PU PAGEPRESS PUBL
PI PAVIA
PA MEDITGROUP, VIA G BELLI, 4, PAVIA, 27100, ITALY
SN 1121-760X
EI 2038-8306
J9 EUR J HISTOCHEM
JI Eur. J. Histochem.
PD OCT-DEC
PY 2007
VL 51
IS 4
BP 291
EP 300
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 246WE
UT WOS:000252037700008
PM 18162459
DA 2025-01-07
ER
PT J
AU Tadokoro, T
Morishita, A
Masaki, T
AF Tadokoro, Tomoko
Morishita, Asahiro
Masaki, Tsutomu
TI Diagnosis and Therapeutic Management of Liver Fibrosis by MicroRNA
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE liver fibrosis; liver cirrhosis; microRNA; exosomal miRNA
ID HEPATIC STELLATE CELLS; B-VIRUS REPLICATION; HEPATOCELLULAR-CARCINOMA;
CIRCULATING MICRORNAS; EXPRESSION PROFILES; MESSENGER-RNAS; KUPFFER
CELLS; UP-REGULATION; EARLY-STAGE; DISEASE
AB Remarkable progress has been made in the treatment and control of hepatitis B and C viral infections. However, fundamental treatments for diseases in which liver fibrosis is a key factor, such as cirrhosis, alcoholic/nonalcoholic steatohepatitis, autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis, are still under development and remain an unmet medical need. To solve this problem, it is essential to elucidate the pathogenesis of liver fibrosis in detail from a molecular and cellular perspective and to develop targeted therapeutic agents based on this information. Recently, microRNAs (miRNAs), functional RNAs of 22 nucleotides, have been shown to be involved in the pathogenesis of liver fibrosis. In addition, extracellular vesicles called "exosomes" have been attracting attention, and research is being conducted to establish noninvasive and extremely sensitive biomarkers using miRNAs in exosomes. In this review, we summarize miRNAs directly involved in liver fibrosis, miRNAs associated with diseases leading to liver fibrosis, and miRNAs related to complications of cirrhosis. We will also discuss the efficacy of each miRNA as a biomarker of liver fibrosis and pathology, and its potential application as a therapeutic agent.
C1 [Tadokoro, Tomoko; Morishita, Asahiro; Masaki, Tsutomu] Kagawa Univ, Fac Med, Dept Gastroenterol & Neurol, Miki, Kagawa 7610793, Japan.
C3 Kagawa University
RP Morishita, A (corresponding author), Kagawa Univ, Fac Med, Dept Gastroenterol & Neurol, Miki, Kagawa 7610793, Japan.
EM tadokoro.tomoko@kagawa-u.ac.jp; morishita.asahiro@kagawa-u.ac.jp;
tmasaki@med.kagawa-u.ac.jp
OI Tadokoro, Tomoko/0000-0001-9975-386X
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NR 159
TC 42
Z9 43
U1 0
U2 21
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2021
VL 22
IS 15
AR 8139
DI 10.3390/ijms22158139
PG 21
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA TV8DT
UT WOS:000681947800001
PM 34360904
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Hemminki, K
Försti, A
Fallah, M
Sundquist, J
Sundquist, K
Ji, J
AF Hemminki, Kari
Foersti, Asta
Fallah, Mahdi
Sundquist, Jan
Sundquist, Kristina
Ji, Jianguang
TI Risk of cancer in patients with medically diagnosed hay fever or
allergic rhinitis
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE hay fever; allergic rhinitis; cancer risk; immune disturbance;
standardized incidence ratio
ID RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASES; METAANALYSIS; PREVALENCE;
ASTHMA; MALIGNANCY; HISTOLOGY; SURVIVAL; SYMPTOMS; SWEDEN
AB Data on allergic conditions as risk or protective factors for cancer are controversial probably because most studies have used self-reported data on mixed groups of allergies in a case-control setting. We define cancer risks in medically diagnosed hay fever/allergic rhinitis patients in a nationwide cohort study. A total of 138,723 hay fever/allergic rhinitis patients were identified from three Swedish health care databases and standardized incidence ratios (SIRs) were calculated for subsequent cancers identified from the Swedish Cancer Registry. Overall cancer risk was not changed (SIR 1.03). For individual cancers, the highest SIR was observed for nasal cancer (SIR 2.63), followed by testicular (1.46) and endocrine tumors (1.42), and kidney (1.31), prostate (1.18) and breast (1.11) cancers. The results were consistent in the three sources of data and all SIRs were above unity, albeit mainly not statistically significant. The SIRs for nervous system tumors were above unity and of borderline significance. SIRs were decreased for esophageal (0.50), liver (0.62) and lung (0.78) cancers, and the three sources of data agreed in the direction of the effect. The increased risks for testicular, renal, prostate and endocrine cancers may be explained by immunological mechanisms. Excess risk for these cancer accounts for a significant population attributable fraction. Nervous system cancers showed a borderline increase and none of the histological types were significantly decreased, providing strong evidence against the published case-control studies, which have reported protective effects. The reasons for the reduced risks for esophageal, liver and lung cancer remain to be explained.
C1 [Hemminki, Kari; Foersti, Asta; Fallah, Mahdi] German Canc Res Ctr, Div Mol Genet Epidemiol, D-69120 Heidelberg, Germany.
[Hemminki, Kari; Foersti, Asta; Sundquist, Jan; Sundquist, Kristina; Ji, Jianguang] Lund Univ, Ctr Primary Hlth Care Res, Malmo, Sweden.
[Sundquist, Jan; Sundquist, Kristina] Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, CA 94305 USA.
C3 Helmholtz Association; German Cancer Research Center (DKFZ); Lund
University; Stanford University
RP Hemminki, K (corresponding author), German Canc Res Ctr, Div Mol Genet Epidemiol, D-69120 Heidelberg, Germany.
EM k.hemminki@dkfz.de
RI Ji, Jianguang/E-9579-2011; Fallah, Mahdi/A-8745-2008
OI Ji, Jianguang/0000-0003-0324-9496; Fallah, Mahdi/0000-0002-6639-065X
FU ALF funding of Region Skane; Deutsche Krebshilfe
FX Grant sponsors: ALF funding of Region Skane and Deutsche Krebshilfe
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NR 25
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Z9 31
U1 0
U2 21
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2014
VL 135
IS 10
BP 2397
EP 2403
DI 10.1002/ijc.28873
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AP3OB
UT WOS:000341984500019
PM 24692097
OA Bronze
DA 2025-01-07
ER
PT J
AU Niederberger, E
Geisslinger, G
AF Niederberger, Ellen
Geisslinger, Gerd
TI Analysis of NF-κB signaling pathways by proteomic approaches
SO EXPERT REVIEW OF PROTEOMICS
LA English
DT Review
DE cancer; inflammation; NF-kappa B; proteomics
ID MANTLE CELL LYMPHOMA; BREAST-CANCER; RHEUMATOID-ARTHRITIS; LIVER
DEGENERATION; IKK-EPSILON; MOLECULAR PATHOGENESIS; EMBRYONIC LETHALITY;
ESOPHAGEAL CANCER; MICE LACKING; PROTEIN
AB NF-kappa B is a transcription factor that plays important roles in the regulation of apoptosis and inflammation as well as innate and adaptive immunity. Consequently, dysregulations in the NF-kappa B activation cascade have been associated with the pathogenesis of several diseases such as cancer, atherosclerosis and rheumatoid arthritis. Although NF-kappa B signaling pathways have been extensively investigated in this context, its varying components and targets are far from being completely elucidated. There is still an urgent need for the detection of novel NF-kappa B target proteins, novel interaction partners and novel regulators in the activation cascade, in particular with regard to its role in the aforementioned diseases. Therefore, several groups have performed different proteomic approaches to further investigate NF-kappa B signal transduction pathways. Most of these studies have been carried out in the area of cancer research; however, there are also several analyses in the field of inflammatory or autoimmune diseases. Furthermore, there have been a number of basic investigations that principally examined binding partners or so far unknown target proteins of NF-kappa B-related proteins. With these approaches, a number of novel and interesting proteins have been found that interfere with NF-kappa B signal transduction and might have an impact on NF-kappa B-related diseases. The results of these studies are summarized and discussed in this review.
C1 [Niederberger, Ellen; Geisslinger, Gerd] Klinikum Goethe Univ Frankfurt, Pharmazentrum Frankfurt ZAFES, Inst Klin Pharmakol, D-60590 Frankfurt, Germany.
C3 Goethe University Frankfurt; Goethe University Frankfurt Hospital
RP Niederberger, E (corresponding author), Klinikum Goethe Univ Frankfurt, Pharmazentrum Frankfurt ZAFES, Inst Klin Pharmakol, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
EM e.niederberger@em.uni-frankfurt.de
FU German Research Association (Deutsche Forschungsgemeinschaft [DFG]
[NI705/2-1]
FX Support was provided from the German Research Association (Deutsche
Forschungsgemeinschaft [DFG] NI705/2-1), Kennedyallee 40, 53175 Bonn.
The authors have no other relevant affiliations or financial involvement
with any organization or entity with a financial interest in or
financial conflict with the subject matter or materials discussed in the
manuscript apart from those disclosed.
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NR 104
TC 12
Z9 14
U1 0
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1478-9450
EI 1744-8387
J9 EXPERT REV PROTEOMIC
JI Expert Rev. Proteomics
PD APR
PY 2010
VL 7
IS 2
BP 189
EP 203
DI 10.1586/EPR.10.1
PG 15
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 590FV
UT WOS:000277211100012
PM 20377387
DA 2025-01-07
ER
PT J
AU Mason, AL
Wasilenko, ST
AF Mason, Andrew L.
Wasilenko, Shawn T.
TI Other Potential Medical Therapies: The Use of Antiviral Agents to
Investigate and Treat Primary Biliary Cirrhosis
SO CLINICS IN LIVER DISEASE
LA English
DT Article
ID MAMMARY-TUMOR VIRUS; HUMAN BREAST-CANCER; URSODEOXYCHOLIC ACID
TREATMENT; ENV GENE-SEQUENCES; COMBINATION ANTIRETROVIRAL THERAPY;
RANDOMIZED CONTROLLED-TRIAL; LIVER-TRANSPLANTATION; DOUBLE-BLIND; HUMAN
BETARETROVIRUS; VIRAL-INFECTION
AB A human betaretrovirus has been characterized in patients with primary biliary cirrhosis (PBC) and the related mouse mammary tumor virus linked with autoimmune biliary disease in the NOD.c3c4 mouse model. Translational Studies have been performed in patients who have PBC to investigate the role of viral infection in disease. Patients treated with Combivir experienced significant improvements in hepatic biochemistry, clinical symptoms, and histology with evidence of reversal of ductopenia. Preliminary Studies suggest that the NOD.c3c4 mouse model of PBC provides a good model to test safer and more potent drug regimens for future use in trials for patients who have PBC.
C1 [Mason, Andrew L.; Wasilenko, Shawn T.] Univ Alberta, Zeidler Ledcor Ctr, Div Gastroenterol, Edmonton, AB T6G 2X8, Canada.
C3 University of Alberta
RP Mason, AL (corresponding author), Univ Alberta, Zeidler Ledcor Ctr, Div Gastroenterol, 130 Univ Campus, Edmonton, AB T6G 2X8, Canada.
EM andrew.mason@ualberta.ca
RI Mason, Andrew/D-2938-2013
OI Mason, Andrew/0000-0002-0470-9522
FU GlaxoSmithKline; Axcan Pharma; Canaidan Institutes for Health Research;
Alberta Heritage Foundation for Medical Research; Canadian Liver
Foundation
FX The Clinical trials were supported by GlaxoSmithKline and Axcan Pharma
and the research by Canaidan Institutes for Health Research. Alberta
Heritage Foundation for Medical Research, and the Canadian Liver
Foundation.
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NR 78
TC 14
Z9 14
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD MAY
PY 2008
VL 12
IS 2
BP 445
EP +
DI 10.1016/j.cld.2008.02.006
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 437LB
UT WOS:000265487900014
PM 18456190
DA 2025-01-07
ER
PT J
AU Damasceno, JX
Guedes, MIF
Leite, CAC
Monteiro, AJ
Fonteles, MC
Jimenez, MEZ
de Lima, V
Ribeiro, TR
Fonteles, CSR
AF Damasceno, Juliana Ximenes
Florindo Guedes, Maria Izabel
Chaves Leite, Christiane Araujo
Monteiro, Andre Jalles
Fonteles, Manasses Claudino
Zurita Jimenez, Maria Esther
de Lima, Vilma
Ribeiro, Thyciana Rodrigues
Roriz Fonteles, Cristiane Sa
TI Salivary immunoglobulin levels in juvenile autoimmune hepatitis
SO ARCHIVES OF ORAL BIOLOGY
LA English
DT Article
DE Autoimmune hepatitis; Saliva; Immunoglobulin
ID LIVER-DISEASE; DIAGNOSTIC UTILITY; BIOMARKERS; ANTIBODIES; CRITERIA;
MARKERS; CANCER; VIRUS; FLUID; IGG
AB Aims: The aim of the present study was to investigate the presence of immunoglobulins (Ig) in whole saliva from patients affected by autoimmune hepatitis (AIH).
Design: Twelve individuals with AIH and 12 healthy individuals without (CON) autoimmune hepatitis, aged 8-18 years, participated in this study. Non-stimulated whole saliva was collected and centrifuged. Supernatants were separated and lyophilized. Salivary pH was measured and immunoglobulins were analyzed through ELISA technique.
Results: Salivary pH (CON, 7.17 +/- 0.45; AIH, 6.92 +/- 0.43) did not differ between groups (p = 0.183). Measurable levels of IgG, IgA, IgM and IgE were detected on all patients. IgG levels were higher in AIH individuals (CON, 1.058 +/- 0.386; AIH, 1.635 +/- 0.373; p = 0.001), whereas IgA (CON, 0.915 +/- 0.187; AIH, 0.995 +/- 0.235; p = 0.362), IgM (CON, 0.683 +/- 0.147, AIH, 0.646 +/- 0.161; p = 0.561) and IgE levels (CON, 1.241 +/- 0.378; AIH, 1.312 +/- 0.412; p = 0.664) did not present differences between groups.
Conclusions: The results of the present study suggest differences in salivary IgG levels between individuals with and without AIH. Thus, saliva has the potential of becoming an important diagnostic tool for the assessment of AIH.
C1 [Damasceno, Juliana Ximenes] Christus Univ Ctr, Fortaleza, Ceara, Brazil.
[Chaves Leite, Christiane Araujo; Monteiro, Andre Jalles; Zurita Jimenez, Maria Esther; de Lima, Vilma; Ribeiro, Thyciana Rodrigues; Roriz Fonteles, Cristiane Sa] Univ Fed Ceara, Fortaleza, Ceara, Brazil.
[Florindo Guedes, Maria Izabel; Fonteles, Manasses Claudino] Univ Estadual Ceara, Fortaleza, Ceara, Brazil.
C3 Universidade Federal do Ceara; Universidade Estadual do Ceara
RP Damasceno, JX (corresponding author), Ctr Univ Christus, Curso Odontol, Rua Joao Adolfo Gurgel 133, BR-60190060 Fortaleza, Ceara, Brazil.
EM coordodontologia03@unichristus.edu.br
RI Guedes, Maria/AFU-7412-2022; Fonteles, Cristiane/F-8391-2012; Ribeiro,
Thyciana/ABC-1677-2020; Lima, Vilma/ABE-8964-2020; Lima,
Vilma/H-2348-2016
OI Florindo Guedes, Maria Izabel/0000-0002-4569-8663; Ribeiro,
Thyciana/0000-0002-6614-6809; Lima, Vilma/0000-0002-8652-4133
FU Coordination for the Improvement of Higher Education Personnel (CAPES),
Brazil
FX This work was supported by the Coordination for the Improvement of
Higher Education Personnel (CAPES), Brazil.
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Zilberman Y, 2015, BIOSENS BIOELECTRON, V67, P465, DOI 10.1016/j.bios.2014.09.006
NR 38
TC 4
Z9 4
U1 0
U2 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0003-9969
EI 1879-1506
J9 ARCH ORAL BIOL
JI Arch. Oral Biol.
PD AUG
PY 2018
VL 92
BP 51
EP 56
DI 10.1016/j.archoralbio.2018.04.014
PG 6
WC Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dentistry, Oral Surgery & Medicine
GA GL2AM
UT WOS:000436915400007
PM 29751148
DA 2025-01-07
ER
PT J
AU Dooley, J
Pasciuto, E
Lagou, V
Lampi, Y
Dresselaers, T
Himmelreich, U
Liston, A
AF Dooley, James
Pasciuto, Emanuela
Lagou, Vasiliki
Lampi, Yulia
Dresselaers, Tom
Himmelreich, Uwe
Liston, Adrian
TI NOD mice, susceptible to pancreatic autoimmunity, demonstrate delayed
growth of pancreatic cancer
SO ONCOTARGET
LA English
DT Article
DE pancreatic cancer; MRI; immune; NOD
ID NONOBESE DIABETIC MOUSE; HEPATOCELLULAR-CARCINOMA; SURVIVAL; CELLS;
ADENOCARCINOMA; EXPRESSION; BLOCKADE; MELANOMA; MODEL
AB Pancreatic cancer is a high mortality form of cancer, with a median survival only six months. There are multiple associated risk factors associated, most importantly type 2 diabetes, obesity, pancreatitis and smoking. The relative rarity of the disease, however, has made it difficult to dissect causative risk factors, especially with related risk factors. A major unanswered question with important therapeutic implications is the effect of immunological responses on pancreatic cancer formation, with data from other cancers suggesting the potential for local immunological responses to either increase cancer development or increase cancer elimination. Due to the rarity and late diagnosis of pancreatic cancer direct epidemiological evidence is lacking, thus necessitating a reliance on animal models. Here we investigated the relationship between pancreatic autoimmunity and cancer by backcrossing the well characterised Ela1-Tag transgenic model of pancreatic cancer onto the pancreatic autoimmune susceptible NOD mouse strain. Through longitudinal magnetic resonance imaging we found that the NOD genetic background delayed the onset of pancreatic tumours and substantially slowed the growth rate of tumours after development. These results suggest that elevated autoimmune surveillance of the pancreas limits tumour formation and growth, identifying pancreatic cancer as a promising target for immune checkpoint blockade therapies that unleash latent autoimmunity.
C1 [Dooley, James; Pasciuto, Emanuela; Lagou, Vasiliki; Lampi, Yulia; Liston, Adrian] VIB, Translat Immunol Lab, Leuven, Belgium.
[Dooley, James; Pasciuto, Emanuela; Lagou, Vasiliki; Lampi, Yulia; Liston, Adrian] KU Leuven Univ Leuven, Dept Microbiol & Immunol, Leuven, Belgium.
[Dresselaers, Tom; Himmelreich, Uwe] KU Leuven Univ Leuven, Dept Imaging & Pathol, Biomed MRI MoSAIC, Leuven, Belgium.
C3 Flanders Institute for Biotechnology (VIB); KU Leuven; KU Leuven
RP Liston, A (corresponding author), VIB, Translat Immunol Lab, Leuven, Belgium.; Liston, A (corresponding author), KU Leuven Univ Leuven, Dept Microbiol & Immunol, Leuven, Belgium.
EM adrian.liston@vib.be
RI Pasciuto, Emanuela/AAP-2982-2020; Lagou, Vasiliki/N-8451-2013; Liston,
Adrian/G-8606-2013
OI Lagou, Vasiliki/0000-0003-3165-8940; Pasciuto,
Emanuela/0000-0002-5391-9585; Himmelreich, Uwe/0000-0002-2060-8895;
Dresselaers, Tom/0000-0002-0884-5142; Dooley, James/0000-0003-3154-4708
FU IUAP (T-TIME); VIB
FX This work was supported by the IUAP (T-TIME) and VIB.
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NR 28
TC 1
Z9 1
U1 0
U2 5
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD OCT 6
PY 2017
VL 8
IS 46
BP 80167
EP 80174
DI 10.18632/oncotarget.21261
PG 8
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FJ1HN
UT WOS:000412465700008
PM 29113292
OA Green Published, gold, Green Submitted, Green Accepted
DA 2025-01-07
ER
PT J
AU Fiorucci, S
Marchianò, S
Urbani, G
Di Giorgio, C
Distrutti, E
Zampella, A
Biagioli, M
AF Fiorucci, Stefano
Marchiano, Silvia
Urbani, Ginevra
Di Giorgio, Cristina
Distrutti, Eleonora
Zampella, Angela
Biagioli, Michele
TI Immunology of bile acids regulated receptors
SO PROGRESS IN LIPID RESEARCH
LA English
DT Review
DE Bile acids; Bile acids regulated receptors; Intestinal microbiota;
Metagenomic and metabolomic; Intestinal dysbiosis; Immune mediated
diseases; Autoimmune cholangiopathies; Metabolic dysfunction associated
liver steatosis; liver disease (MASLD); Immune check point inhibitors
ID FARNESOID-X-RECEPTOR; PRIMARY SCLEROSING CHOLANGITIS;
VITAMIN-D-RECEPTOR; ROR-GAMMA-T; PRIMARY BILIARY-CIRRHOSIS; NF-KAPPA-B;
INFLAMMATORY-BOWEL-DISEASE; INHIBITORY FACTOR-RECEPTOR; DEPENDENT
GENE-EXPRESSION; NUCLEAR HORMONE-RECEPTOR
AB Bile acids are steroids formed at the interface of host metabolism and intestinal microbiota. While primary bile acids are generated in the liver from cholesterol metabolism, secondary bile acids represent the products of microbial enzymes. Close to 100 different enzymatic modifications of bile acids structures occur in the human intestine and clinically guided metagenomic and metabolomic analyses have led to the identification of an extraordinary number of novel metabolites. These chemical mediators make an essential contribution to the composition and function of the postbiota, participating to the bidirectional communications of the intestinal microbiota with the host and contributing to the architecture of intestinal-liver and -brain and -endocrine axes. Bile acids exert their function by binding to a group of cell membrane and nuclear receptors collectively known as bile acid-regulated receptors (BARRs), expressed in monocytes, tissue-resident macrophages, CD4+ T effector cells, including Th17, T regulatory cells, dendritic cells and type 3 of intestinal lymphoid cells and NKT cells, highlighting their role in immune regulation. In this review we report on how bile acids and their metabolitesmodulate the immune system in inflammations and cancers and could be exploiting for developing novel therapeutic approaches in these disorders.
C1 [Fiorucci, Stefano; Marchiano, Silvia; Urbani, Ginevra; Di Giorgio, Cristina; Biagioli, Michele] Univ Perugia, Dipartimento Med & Chirurg, Piazza L Severi 1, I-06100 Perugia, Italy.
[Distrutti, Eleonora] Azienda Osped Perugia, SC Gastroenterol Epatol, Perugia, Italy.
[Zampella, Angela] Univ Napoli Federico II, Dept Pharm, Naples, Italy.
C3 University of Perugia; University of Perugia; Azienda Ospedaliera di
Perugia; University of Naples Federico II
RP Fiorucci, S (corresponding author), Univ Perugia, Dipartimento Med & Chirurg, Piazza L Severi 1, I-06100 Perugia, Italy.
EM Stefano.fiorucci@unipg.it
RI Stefano, Fiorucci/IUM-9317-2023; Biagioli, Michele/AAF-6419-2019
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NR 420
TC 6
Z9 6
U1 10
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7827
EI 1873-2194
J9 PROG LIPID RES
JI Prog. Lipid Res.
PD JUL
PY 2024
VL 95
AR 101291
DI 10.1016/j.plipres.2024.101291
EA AUG 2024
PG 29
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA D2D4F
UT WOS:001294339800001
PM 39122016
DA 2025-01-07
ER
PT J
AU Liu, Y
Dai, LP
Liu, WH
Shi, GX
Zhang, JY
AF Liu, Yuan
Dai, Liping
Liu, Weihong
Shi, Guixiu
Zhang, Jianying
TI Autoantibody to MDM2: A Potential Serological Marker of Systemic Lupus
Erythematosus
SO JOURNAL OF IMMUNOLOGY RESEARCH
LA English
DT Article
ID TUMOR-ASSOCIATED ANTIGEN; HEPATOCELLULAR-CARCINOMA; SUPPRESSOR P53;
CANCER-THERAPY; IMMUNODIAGNOSIS; INFLAMMATION; ANTIBODIES; PROMOTES;
LINE
AB Introduction. Systemic lupus erythematosus (SLE) is one of the systemic autoimmune diseases characterized by the polyclonal autoantibody production. The human homologue of the mouse double minute 2 (MDM2) is well known as the negative regulator of p53. MDM2 has been reported to be overexpressed in SLE animal model and to promote SLE. Since abnormally expressed proteins can induce autoimmune response, anti-MDM2 autoantibody was examined in SLE patients. Methods. Anti-MDM2 antibody in sera from 43 SLE patients and 69 healthy persons was investigated by ELISA. Positive samples were further confirmed by western blotting. The immunological feathers of anti-MDM2 positive sera were analyzed by indirect immunofluorescence assay. Anti-p53 was also investigated in SLE patients by ELISA, and the correlation of anti-MDM2 and anti-p53 was analyzed. Results. The presence of anti-MDM2 in SLE patients was 23.30%, much higher than normal healthy persons (4.30%). These anti-MDM2 positive sera present a nuclear staining pattern. The presence of anti-p53 in SLE patients was 39.50%, and the titer of anti-MDM2 was positively correlated with anti-p53 in SLE patients. Conclusions. Anti-MDM2 autoantibody was detected at high prevalence in SLE patients. The detection of anti-MDM2 in SLE patients should be clinically useful.
C1 [Liu, Yuan; Shi, Guixiu] Xiamen Univ, Affiliated Hosp 1, Dept Rheumatol & Clin Immunol, Xiamen 361003, Peoples R China.
[Liu, Yuan; Dai, Liping; Liu, Weihong; Zhang, Jianying] Univ Texas El Paso, Dept Biol Sci, El Paso, TX 79968 USA.
C3 Xiamen University; University of Texas System; University of Texas El
Paso
RP Shi, GX (corresponding author), Xiamen Univ, Affiliated Hosp 1, Dept Rheumatol & Clin Immunol, 55 Zhenhai Rd, Xiamen 361003, Peoples R China.
EM guixiu.shi@gmail.com; jzhang@utep.edu
RI liu, yuan/AFR-1867-2022; Zhang, Jianying/F-3798-2010; Dai,
Liping/E-6089-2013
OI shi, guixiu/0000-0003-4044-3394; Liu, Yuan/0000-0003-2668-0350
FU The Scripps Research Institute; National Institutes of Health (NIH)
[SC1CA166016]; NIH [5G12MD007592]; Border Biological Research Center
(BBRC) Core Facilities at The University of Texas at El Paso (UTEP)
FX The authors thank Dr. Eng M. Tan (The Scripps Research Institute) for
his support. This work was supported by a grant (SC1CA166016) from the
National Institutes of Health (NIH). They also thank the Border
Biological Research Center (BBRC) Core Facilities at The University of
Texas at El Paso (UTEP) for their support, which were funded by NIH
grant (5G12MD007592).
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NR 28
TC 9
Z9 10
U1 0
U2 6
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-8861
EI 2314-7156
J9 J IMMUNOL RES
JI J Immunol. Res.
PY 2015
VL 2015
AR 963568
DI 10.1155/2015/963568
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CJ5SU
UT WOS:000355550100001
PM 26090506
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Unsal, V
Cicek, M
Sabancilar, I
AF Unsal, Velid
Cicek, Mustafa
Sabancilar, Ilhan
TI Toxicity of carbon tetrachloride, free radicals and role of antioxidants
SO REVIEWS ON ENVIRONMENTAL HEALTH
LA English
DT Review
DE antioxidants; carbon tetrachloride; hepatotoxicity; nephrotoxicity;
neurotoxicity; oxidative stress
ID INDUCED OXIDATIVE STRESS; POLYUNSATURATED FATTY-ACIDS; INDUCED
TESTICULAR TOXICITY; DRUG-INDUCED NEPHROTOXICITY; INDUCED LIVER-INJURY;
CCL4-INDUCED NEPHROTOXICITY; INDUCED HEPATOTOXICITY; NATURAL
ANTIOXIDANTS; AQUEOUS EXTRACT; PROTECTIVE ROLE
AB Several chemicals, including environmental toxicants and clinically useful drugs, cause severe cellular damage to different organs of our body through metabolic activation to highly reactive substances such as free radicals. Carbon tetrachloride is an organic compound of which chemical formula is CCl4. CCl4 is strong toxic in the kidney, testicle, brain, heart, lung, other tissues, and particularly in the liver. CCl4 is a powerful hepatoxic, nephrotoxic and prooxidant agent which is widely used to induce hepatotoxicity in experimental animals and to create hepatocellular carcinoma, hepatic fibrosis/cirrhosis and liver injury, chemical hepatitis model, renal failure model, and nephrotoxicity model in recent years. The damage-causing mechanism of CCl4 in tissues can be explained as oxidative damage caused by lipid peroxidation which starts after the conversion of CCl4 to free radicals of highly toxic trichloromethyl radicals (center dot CCl3) and trichloromethyl peroxyl radical (center dot CCl3O2) via cytochrome P450 enzyme. Complete disruption of lipids (i.e., peroxidation) is the hallmark of oxidative damage. Free radicals are structures that contain one or more unpaired electrons in atomic or molecular orbitals. These toxic free radicals induce a chain reaction and lipid peroxidation in membrane-like structures rich in phospholipids, such as mitochondria and endoplasmic reticulum. CCl4-induced lipid peroxidation is the cause of oxidative stress, mitochondrial stress, endoplasmic reticulum stress. Free radicals trigger many biological processes, such as apoptosis, necrosis, ferroptosis and autophagy. Recent researches state that the way to reduce or eliminate these CCl4-induced negative effects is the antioxidants originated from natural sources. For normal physiological function, there must be a balance between free radicals and antioxidants. If this balance is in favor of free radicals, various pathological conditions occur. Free radicals play a role in various pathological conditions including Pulmonary disease, ischemia / reperfusion rheumatological diseases, autoimmune disorders, cardiovascular diseases, cancer, kidney diseases, hypertension, eye diseases, neurological disorders, diabetes and aging. Free radicals are antagonized by antioxidants and quenched. Antioxidants do not only remove free radicals, but they also have anti-inflammatory, anti-allergic, antithrombotic, antiviral, and anti-carcinogenic activities. Antioxidants contain high phenol compounds and antioxidants have relatively low side effects compared to synthetic drugs. The antioxidants investigated in CCI4 toxicity are usually antioxidants from plants and are promising because of their rich resources and low side effects. Data were investigated using PubMed, EBSCO, Embase, Web of Science, DOAJ, Scopus and Google Scholar, Carbon tetrachloride, carbon tetrachloride-induced toxicity, oxidative stress, and free radical keywords. This study aims to enlighten the damage-causing mechanism created by free radicals which are produced by CCl4 on tissues/cells and to discuss the role of antioxidants in the prevention of tissue/cell damage. In the future, Antioxidants can be used as a therapeutic strategy to strengthen effective treatment against substances with high toxicity such as CCl4 and increase the antioxidant capacity of cells.
C1 [Unsal, Velid] Mardin Artuklu Univ, Fac Hlth Sci, Dept Nutr & Dietet, Mardin, Turkey.
[Cicek, Mustafa] Kahramanmaras Sutcu Imam Univ, Fac Med, Dept Anat, Kahramanmaras, Turkey.
[Sabancilar, Ilhan] Dicle Univ, Hlth Sci Inst, Dept Biochem, Diyarbakir, Turkey.
C3 Mardin Artuklu University; Kahramanmaras Sutcu Imam University; Dicle
University
RP Unsal, V (corresponding author), Mardin Artuklu Univ, Fac Hlth Sci, Dept Nutr & Dietet, Mardin, Turkey.
EM velidunsal@gmail.com; mustafacicek_GOP@hotmail.com;
ilhan.sabancilar@dicle.edu.tr
RI ÇİÇEK, Mustafa/ABT-6574-2022; Sabancılar, İlhan/GOV-7189-2022; UNSAL,
VELID/A-6189-2019
OI UNSAL, VELID/0000-0003-1415-0563; Cicek, Mustafa/0000-0001-8925-0230;
Sabancilar, Ilhan/0000-0002-0773-2752
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NR 148
TC 150
Z9 155
U1 28
U2 159
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 0048-7554
EI 2191-0308
J9 REV ENVIRON HEALTH
JI Rev. Environ. Health
PY 2021
VL 36
IS 2
BP 279
EP 295
DI 10.1515/reveh-2020-0048
PG 17
WC Environmental Sciences; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health
GA SK6UV
UT WOS:000656354100012
PM 32970608
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Elbadry, M
Moussa, AM
Eltabbakh, M
Al Balakosy, A
Abdalgaber, M
Abdeen, N
El Sheemy, RY
Afify, S
El-Kassas, M
AF Elbadry, Mohamed
Moussa, Abdelmajeed M.
Eltabbakh, Mohamed
Al Balakosy, Amira
Abdalgaber, Mohammad
Abdeen, Nermeen
El Sheemy, Reem Y.
Afify, Shimaa
El-Kassas, Mohamed
TI The art of managing hepatitis C virus in special population groups: a
paradigm shift
SO EGYPTIAN LIVER JOURNAL
LA English
DT Review
DE Hepatitis C virus; Hepatitis C comorbidities; Extrahepatic
manifestation; Special population; Direct-acting antiviral
ID ACTING ANTIVIRAL REGIMENS; TREATMENT-EXPERIENCED PATIENTS; SYSTEMIC
AUTOIMMUNE-DISEASES; ALPHA-2A PLUS RIBAVIRIN; GENOTYPE 1 INFECTION;
HEPATOCELLULAR-CARCINOMA; MIXED CRYOGLOBULINEMIA; PEGYLATED-INTERFERON;
SINGLE-ARM; OPEN-LABEL
AB The first direct-acting antiviral (DAA) medications were approved for the treatment of chronic hepatitis C virus (HCV) in 2011. Later, the appearance of novel DAAs had revolutionized the landscape of HCV treatment whose early treatment options were limited to interferon (IFN) either alone or in combinations. This review discusses the paradigm shift in legibility for treating different groups of patients with HCV after the introduction of DAAs, along with the consequent changes in treatment guidelines. IFN-based therapy was the firstly used for treating chronic HCV. Unfortunately, it exhibited many pitfalls, such as low efficacy in some patients and unsuitability for usage in lots of patients with some specific conditions, which could be comorbidities such as autoimmune thyroiditis, or liver related as in decompensated cirrhosis. Furthermore, IFN failed to treat all the extrahepatic manifestations of HCV. Nowadays, the breakthroughs brought by DAAs have benefited the patients and enabled the treatment of those who could not be treated or did not usually respond well to IFN. DAAs achieve a high success rate of HCV eradication in addition to avoiding unfavorable harms and, sometimes, adverse effects related to the previously used PEGylated IFN regimens.
C1 [Elbadry, Mohamed; El-Kassas, Mohamed] Helwan Univ, Fac Med, Endem Med Dept, Cairo, Egypt.
[Moussa, Abdelmajeed M.] Aswan Univ, Fac Med, Trop Med & Gastroenterol Dept, Aswan, Egypt.
[Eltabbakh, Mohamed; Al Balakosy, Amira] Ain Shams Univ, Fac Med, Trop Med, Cairo, Egypt.
[Abdalgaber, Mohammad] Police Author Hosp, Gastroenterol Dept, Giza, Egypt.
[Abdeen, Nermeen] Alexandria Univ, Trop Med Dept, Alexandria, Egypt.
[El Sheemy, Reem Y.] Minia Univ, Trop Med Dept, Al Minya, Egypt.
[Afify, Shimaa] Natl Hepatol & Trop Med Res Inst Cairo, Gastroenterol Dept, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); Helwan University; Egyptian Knowledge
Bank (EKB); Aswan University; Egyptian Knowledge Bank (EKB); Ain Shams
University; Egyptian Knowledge Bank (EKB); Alexandria University;
Egyptian Knowledge Bank (EKB); Minia University; Egyptian Knowledge Bank
(EKB); National Hepatology & Tropical Medicine Research Institute
(NHTMRI)
RP El-Kassas, M (corresponding author), Helwan Univ, Fac Med, Endem Med Dept, Cairo, Egypt.
EM m_elkassas@hq.helwan.edu.eg
RI Elbadry, Mohamed/ABD-3435-2020; El-Kassas, Mohamed/F-8306-2019
OI El Sheemy, Reem/0000-0001-8158-8878; Elbadry,
Mohamed/0000-0002-9020-8870; El-Kassas, Mohamed/0000-0002-3396-6894
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NR 87
TC 1
Z9 1
U1 0
U2 13
PU SPRINGEROPEN
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, GWENT N1 9XW, ENGLAND
SN 2090-6218
EI 2090-6226
J9 EGYPT LIVER J
JI Egypt. Liver J.
PD NOV 15
PY 2022
VL 12
IS 1
AR 61
DI 10.1186/s43066-022-00226-8
PG 11
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA 6F7WX
UT WOS:000884270600001
OA gold
DA 2025-01-07
ER
PT J
AU Liberal, R
Grant, CR
Longhi, MS
Mieli-Vergani, G
Vergani, D
AF Liberal, Rodrigo
Grant, Charlotte R.
Longhi, Maria Serena
Mieli-Vergani, Giorgina
Vergani, Diego
TI Diagnostic criteria of autoimmune hepatitis
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
ID HEPATOCELLULAR-CARCINOMA; OVERLAP SYNDROME; AUTOANTIBODIES; DISEASE;
MANAGEMENT; CHILDHOOD; SEROLOGY; ANTIGEN
AB Autoimmune hepatitis (AIH) is a chronic immune-mediated liver disorder characterised by female preponderance, elevated transaminase and immunoglobulin G levels, seropositivity for autoantibodies and interface hepatitis. Presentation is highly variable, therefore AIH should be considered during the diagnostic workup of any increase in liver enzyme levels. A set of inclusion and exclusion criteria for the diagnosis of AIH have been established by the International Autoimmune Hepatitis Group (IAIHG). There are two main types of AIH: type 1, positive for anti-nuclear (ANA) and/or anti-smooth muscle antibodies (SMAs) and type 2, defined by the presence of anti-liver kidney microsomal antibody type 1 (LKM-1) and/or anti-liver cytosol type 1 (LC-1) autoantibodies. The central role of autoantibodies in the diagnosis of AIH has led the IAIHG to produce a consensus statement detailing appropriate and effective methods for their detection. Autoantibodies should be tested by indirect immunofluorescence at an initial dilution of 1/40 in adults and 1/10 in children on a freshly prepared rodent substrate that includes kidney, liver and stomach sections to allow for the simultaneous detection of all reactivities relevant to AIH. Anti-LKM-1 is often confused with anti-mitochondrial antibody (AMA) if rodent kidney is used as the sole immunofluorescence substrate. The identification of the molecular targets of anti-LKM-1 and AMA has led to the establishment of immuno-assays based on the use of the recombinant or purified autoantigens. Perinuclear anti-nuclear neutrophil antibody (p-ANNA) is an additional marker of AIH-1; anti soluble liver antigen (SLA) antibodies are specific for autoimmune liver disease, can be present in AIH-1 and AIH-2 and are associated with a more severe clinical course. Anti-SLA are detectable by ELISA or radio-immuno-assays, but not by immunofluorescence. AIH is exquisitely responsive to immunosuppressive treatment, which should be instituted promptly to prevent rapid deterioration and promote remission and long-term survival. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Liberal, Rodrigo; Grant, Charlotte R.; Longhi, Maria Serena; Mieli-Vergani, Giorgina; Vergani, Diego] Kings Coll Hosp London, Kings Coll London, Sch Med, Paediat Liver GI & Nutr Ctr, London SE5 9RS, England.
[Liberal, Rodrigo; Grant, Charlotte R.; Longhi, Maria Serena; Mieli-Vergani, Giorgina; Vergani, Diego] Kings Coll Hosp London, Kings Coll London, Sch Med, Inst Liver Studies, London SE5 9RS, England.
[Liberal, Rodrigo] Univ Porto, Fac Med, P-4100 Oporto, Portugal.
C3 King's College Hospital NHS Foundation Trust; King's College Hospital;
University of London; King's College London; University of London;
King's College London; King's College Hospital NHS Foundation Trust;
King's College Hospital; Universidade do Porto
RP Vergani, D (corresponding author), Kings Coll Hosp London, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
EM diego.vergani@kcl.ac.uk
RI Vergani, Diego/H-7610-2019; Mieli-Vergani, Giorgina/G-5616-2011
OI Mieli-Vergani, Giorgina/0000-0002-8215-4489
FU Medical Research Council [G0902288, MR/J006742/1] Funding Source:
Medline; MRC [G0902288] Funding Source: UKRI
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NR 40
TC 64
Z9 73
U1 0
U2 27
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD APR-MAY
PY 2014
VL 13
IS 4-5
SI SI
BP 435
EP 440
DI 10.1016/j.autrev.2013.11.009
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AE2AM
UT WOS:000333775700022
PM 24418295
DA 2025-01-07
ER
PT J
AU Huang, WY
He, WJ
Shi, XM
He, XS
Dou, L
Gao, YF
AF Huang, Wenyong
He, Wenjing
Shi, Xiaomin
He, Xiaoshun
Dou, Lang
Gao, Yifang
TI The Role of CD1d and MR1 Restricted T Cells in the Liver
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE iNKT cells; MAIT cells; liver diseases; innate T cells; CD1d restriction
ID INVARIANT NKT CELLS; NATURAL-KILLER-CELLS; IMPAIRED CYTOTOXIC FUNCTIONS;
INNATE IMMUNE-SYSTEM; CHRONIC HEPATITIS-B; MAIT CELLS; INKT CELLS;
HEPATOCELLULAR-CARCINOMA; VIRUS-REPLICATION; ANTIGEN RECEPTOR
AB The liver is one of the most important immunological organs that remains tolerogenic in homeostasis yet promotes rapid responses to pathogens in the presence of a systemic infection. The composition of leucocytes in the liver is highly distinct from that of the blood and other lymphoid organs, particularly with respect to enrichment of innate T cells, i.e., invariant NKT cells (iNKT cells) and Mucosal-Associated Invariant T cells (MAIT cells). In recent years, studies have revealed insights into their biology and potential roles in maintaining the immune-environment in the liver. As the primary liver-resident immune cells, they are emerging as significant players in the human immune system and are associated with an increasing number of clinical diseases. As such, innate T cells are promising targets for modifying host defense and inflammation of various liver diseases, including viral, autoimmune, and those of tumor origin. In this review, we emphasize and discuss some of the recent discoveries and advances in the biology of innate T cells, their recruitment and diversity in the liver, and their role in various liver diseases, postulating on their potential application in immunotherapy.
C1 [Huang, Wenyong; He, Wenjing; Shi, Xiaomin; He, Xiaoshun; Dou, Lang; Gao, Yifang] Sun Yat Sen Univ, Affiliated Hosp 1, Organ Transplantat Unit, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University
RP Gao, YF (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 1, Organ Transplantat Unit, Guangzhou, Guangdong, Peoples R China.
EM gaoyf26@sysu.edu.cn
OI Gao, Yifang/0000-0003-2817-9391
FU Natural Science Foundation of Guangdong Province [2018A030313019]
FX YG is supported by Natural Science Foundation of Guangdong Province
(Grant number: 2018A030313019).
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NR 129
TC 17
Z9 20
U1 0
U2 23
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD OCT 30
PY 2018
VL 9
AR 2424
DI 10.3389/fimmu.2018.02424
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA GY5XX
UT WOS:000448658500001
PM 30425710
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhao, XY
Xu, C
Ding, Y
Yan, NL
AF Zhao, Xuye
Xu, Chang
Ding, Yi
Yan, Nianlong
TI The multifaceted functions of NFE2L1 in metabolism and associated
disorders
SO LIFE SCIENCES
LA English
DT Article
DE Metabolism; Diabetes; Lipids; Proteostasis
ID TRANSCRIPTION FACTOR NRF1; GENE-EXPRESSION; PROTEASOME; INHIBITION;
CLONING; LIPODYSTROPHY; DEFICIENCY; MEMBRANE; FACTOR-1; PATHWAY
AB Nuclear factor erythroid 2-related factor 1 (NFE2L1, also known as Nrf1) is a crucial member of the CNC-bZIP subfamily of transcription factors expressed ubiquitously throughout our body. Recent findings have revealed its association with various metabolic processes, encompassing glucose, lipid, and protein metabolism. In the realm of glucose metabolism, NFE2L1 exerts regulatory control by modulating pancreatic beta cells and insulin production. It also influences glucose metabolism in liver and the insulin sensitivity of adipose tissue. Regarding lipid metabolism, NFE2L1 governs this process by influencing the expression of specific adipogenic and lipolysis genes in both liver and adipose tissue. Additionally, NFE2L1 regulates specific lipids, such as cholesterol. These involvements underlie various manifestations of NFE2L1 deficiency such as adipocyte hypertrophy, inflammation, and steatohepatitis. In the realm of protein metabolism, NFE2L1 serves as a major transcription factor regulating the 26S proteasome genes expression, which dysfunction has been related with multiple diseases including neurodegenerative diseases, cancers, autoimmune conditions, etc. In this comprehensive review, we summarize the diverse roles that NFE2L1 plays in glucose, lipid, and protein metabolism, as well as its impact on diseases related to these metabolic processes.
C1 [Zhao, Xuye; Xu, Chang; Yan, Nianlong] Nanchang Univ, Jiangxi Med Coll, Sch Basic Med Sci, Dept Biochem & Mol Biol, Nanchang 330006, Jiangxi, Peoples R China.
[Zhao, Xuye; Xu, Chang] Nanchang Univ, Queen Mary Coll, Jiangxi Med Coll, Nanchang 330031, Jiangxi, Peoples R China.
[Zhao, Xuye; Xu, Chang] Queen Mary Univ London, Sch Biol & Biomed Sci, London, England.
[Ding, Yi] Nanchang Univ, Ganzhou Peoples Hosp, Dept Spine Surg, Affiliated Ganzhou Hosp, Ganzhou 341000, Jiangxi, Peoples R China.
C3 Nanchang University; Nanchang University; University of London; Queen
Mary University London; Nanchang University
RP Yan, NL (corresponding author), Nanchang Univ, Jiangxi Med Coll, Sch Basic Med Sci, Dept Biochem & Mol Biol, Nanchang 330006, Jiangxi, Peoples R China.
EM yannianlong@ncu.edu.cn
FU National Natural Science Foundation of China [32060213]; Jiangxi
Provincial Department of Science and Technology [20232ACB206004,
20224BAB206012]
FX We acknowledge the support from grants by the National Natural Science
Foundation of China (No. 32060213) and the Jiangxi Provincial Department
of Science and Technology (No. 20232ACB206004 and 20224BAB206012) .
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NR 77
TC 0
Z9 0
U1 2
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD SEP 1
PY 2024
VL 352
AR 122906
DI 10.1016/j.lfs.2024.122906
EA JUL 2024
PG 7
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA YU0D7
UT WOS:001270873000001
PM 38992575
DA 2025-01-07
ER
PT J
AU Glick, D
Barth, S
Macleod, KF
AF Glick, Danielle
Barth, Sandra
Macleod, Kay F.
TI Autophagy: cellular and molecular mechanisms
SO JOURNAL OF PATHOLOGY
LA English
DT Review
DE autophagy; apoptosis; stress; mechanisms; energy; disease; cancer;
neurodegeneration; infection
ID GENOME-WIDE ASSOCIATION; MITOCHONDRIAL AUTOPHAGY; CROHN-DISEASE;
PROTEIN; DEGRADATION; STARVATION; CLEARANCE; NIX; PATHOGENESIS;
INHIBITION
AB Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy can be either non-selective or selective in the removal of specific organelles, ribosomes and protein aggregates, although the mechanisms regulating aspects of selective autophagy are not fully worked out. In addition to elimination of intracellular aggregates and damaged organelles, autophagy promotes cellular senescence and cell surface antigen presentation, protects against genome instability and prevents necrosis, giving it a key role in preventing diseases such as cancer, neurodegeneration, cardiomyopathy, diabetes, liver disease, autoimmune diseases and infections. This review summarizes the most up-to-date findings on how autophagy is executed and regulated at the molecular level and how its disruption can lead to disease. Copyright (C) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
C1 [Glick, Danielle; Barth, Sandra; Macleod, Kay F.] Univ Chicago, Gordon Ctr Integrat Sci, Ben May Dept Canc Res, Chicago, IL 60637 USA.
[Glick, Danielle; Macleod, Kay F.] Univ Chicago, Gordon Ctr Integrat Sci, Comm Canc Biol, Chicago, IL 60637 USA.
C3 University of Chicago; University of Chicago
RP Macleod, KF (corresponding author), Univ Chicago, Gordon Ctr Integrat Sci, Ben May Dept Canc Res, Chicago, IL 60637 USA.
EM kmacleod@uchicago.edu
FU National Cancer Institute [RO1 CA131188]; Swiss National Foundation
[PBZHP3-123296]; Swiss National Science Foundation (SNF) [PBZHP3-123296]
Funding Source: Swiss National Science Foundation (SNF)
FX The authors acknowledge financial support from the National Cancer
Institute (Grant No. RO1 CA131188; to KFM) and the Swiss National
Foundation (Award No. PBZHP3-123296; to SB).
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NR 86
TC 2739
Z9 3206
U1 7
U2 430
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3417
EI 1096-9896
J9 J PATHOL
JI J. Pathol.
PD MAY
PY 2010
VL 221
IS 1
BP 3
EP 12
DI 10.1002/path.2697
PG 10
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA 595RD
UT WOS:000277629100002
PM 20225336
OA Green Accepted, Green Submitted
DA 2025-01-07
ER
PT J
AU Sarici, KB
Akbulut, S
Uremis, MM
Garzali, IU
Kucukakcali, Z
Koc, C
Turkoz, Y
Usta, S
Baskiran, A
Aloun, A
Yilmaz, S
AF Sarici, Kemal Baris
Akbulut, Sami
Uremis, Muhammed Mehdi
Garzali, Ibrahim Umar
Kucukakcali, Zeynep
Koc, Cemalettin
Turkoz, Yusuf
Usta, Sertac
Baskiran, Adil
Aloun, Ali
Yilmaz, Sezai
TI Evaluation of Bone Mineral Metabolism After Liver Transplantation by
Bone Mineral Densitometry and Biochemical Markers
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article
ID OSTEOPOROSIS; TURNOVER; FRACTURE; DISEASE
AB Aim. This study aimed to evaluate the course of bone and mineral metabolism after liver trans-plantation (LT) in patients with chronic liver disease.Methods. One hundred four patients who had undergone LT and had a minimum of 6 months of follow-up after LT were included in this prospective cohort study. The following parameters were evaluated for each patient: preoperative and postoperative (postoperative day [POD]30, POD90, POD180) osteocalcin, bone-specific alkaline phosphatase (BALP), type 1 collagen, beta-C-terminal end telopeptide (b-CTx), vitamin D, parathyroid hormone (PTH), ALP, calcium, phosphate, sedimentation, and bone mineral densitometer scores (L2, L4, L total, and F total). The parameters were compared in terms of sex, presence of liver tumor (hepatocellular carci-noma [HCC; n = 19] vs non-HCC [n = 85]), and presence of autoimmune liver disease (autoim-mune liver disease [ALD; n = 8] vs non-ALD [n = 96]). Results. The median age of the patients (n = 81 men and n = 23 women) was 52 years (95% CI, 50-56). There was a significant change in the defined time intervals in parameters such as osteocalcin (P < .001), BALP (P < .001), b-CTx (P < .001), vitamin D (P < .001), PTH (P < .001), ALP (P = .001), calcium (P < .001), phosphate (P = .001), L2 (P = .038), L total (P = .026), and F total (P < .001) scores. There was a significant difference in POD90 ALP (P = .033), POD180 calcium (P = .011), POD180 phosphate (P = .011), preoperative sedimentation (P = .032), and POD180 F total (P = .013) scores between both sexes. There was a significant difference in POD180 osteocalcin (P = .023), POD180 b-CTx (P = .017), and preOP calcium (P = .003) among the HCC and non-HCC groups. Furthermore, we found significant differences in preoperative ALP (P = .008), preop-erative sedimentation (P = .019), POD90 (P = .037) and POD180 L2 (P = .005) scores, preoperative (P = .049) and POD180 L4 (P = .017), and POD180 L total (P = .010) and F total (P = .022) scores between the patients with and without ALD. Conclusion. This study shows that the bone and mineral metabolism of the LT recipients was negatively affected after LT. In addition, we showed that bone and mineral metabolism was more prominent in patients with HCC, and bone mineral density scores were higher in patients with ALD.
C1 [Sarici, Kemal Baris; Akbulut, Sami; Koc, Cemalettin; Usta, Sertac; Baskiran, Adil; Yilmaz, Sezai] Inonu Univ, Liver Transplant Inst, Fac Med, Malatya, Turkiye.
[Akbulut, Sami; Kucukakcali, Zeynep] Inonu Univ, Fac Med, Dept Biostat & Med Informat, Malatya, Turkiye.
[Uremis, Muhammed Mehdi; Turkoz, Yusuf] Inonu Univ, Fac Med, Dept Med Biochem, Malatya, Turkiye.
[Garzali, Ibrahim Umar] Aminu Kano Teaching Hosp, Dept Surg, Kano, Nigeria.
[Aloun, Ali] Royal Med Serv, King Hussein Med Ctr, Amman, Jordan.
[Akbulut, Sami] Inonu Univ, Fac Med, Dept Surg & Liver Transplantat, Dept Biostat & Med Informat, Elazig Yolu 10 Km, TR-44280 Malatya, Turkiye.
C3 Inonu University; Inonu University; Inonu University; Inonu University
RP Akbulut, S (corresponding author), Inonu Univ, Fac Med, Dept Surg & Liver Transplantat, Dept Biostat & Med Informat, Elazig Yolu 10 Km, TR-44280 Malatya, Turkiye.
EM akbulutsami@gmail.com
RI Türköz, Yusuf/ABG-7931-2020; SARICI, KEMAL BARIŞ/ABI-4356-2020;
BASKIRAN, ADIL/ABI-2356-2020; GARZALI, IBRAHIM UMAR/ITU-1475-2023;
Uremis, Muhammed Mehdi/V-5830-2019; Akbulut, Sami/L-9568-2014
OI Akbulut, Sami/0000-0002-6864-7711; Baskiran, Adil/0000-0002-7536-1631;
Garzali, Ibrahim Umar/0000-0002-9797-851X; Uremis, Muhammed
Mehdi/0000-0003-2296-2422
FU Inonu University Scientific Research Projects Coordination Unit
[TSA-2018-1312]
FX ACKNOWLEDGMENTS This study was supported by Inonu University Scientific
Research Projects Coordination Unit (Project TSA-2018-1312) .
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NR 22
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0041-1345
EI 1873-2623
J9 TRANSPL P
JI Transplant. Proc.
PD JUN
PY 2023
VL 55
IS 5
BP 1239
EP 1244
DI 10.1016/j.transproceed.2023.03.034
EA JUN 2023
PG 6
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA M9OR1
UT WOS:001033439000001
PM 37127514
DA 2025-01-07
ER
PT J
AU Fargo, MV
Grogan, SP
Saguil, A
AF Fargo, Matthew V.
Grogan, Scott P.
Saguil, Aaron
TI Evaluation of Jaundice in Adults
SO AMERICAN FAMILY PHYSICIAN
LA English
DT Article
ID INDUCED LIVER-INJURY; HEMOLYTIC-ANEMIA; DISEASE; CHOLESTASIS;
MECHANISMS; DISORDERS; DIAGNOSIS; PATIENT
AB Jaundice in adults can be an indicator of significant underlying disease. It is caused by elevated serum bilirubin levels in the unconjugated or conjugated form. The evaluation of jaundice relies on the history and physical examination. The initial laboratory evaluation should include fractionated bilirubin, a complete blood count, alanine transaminase, aspartate transaminase, alkaline phosphatase, gamma-glutamyltransferase, prothrombin time and/or international normalized ratio, albumin, and protein. Imaging with ultrasonography or computed tomography can differentiate between extrahepatic obstructive and intrahepatic parenchymal disorders. Ultrasonography is the least invasive and least expensive imaging method. A more extensive evaluation may include additional cancer screening, biliary imaging, autoimmune antibody assays, and liver biopsy. Unconjugated hyperbilirubinemia occurs with increased bilirubin production caused by red blood cell destruction, such as hemolytic disorders, and disorders of impaired bilirubin conjugation, such as Gilbert syndrome. Conjugated hyperbilirubinemia occurs in disorders of hepatocellular damage, such as viral and alcoholic hepatitis, and cholestatic disorders, such as choledocholithiasis and neo- plastic obstruction of the biliary tree. Copyright (C) 2017 American Academy of Family Physicians.
C1 [Fargo, Matthew V.] Bavaria Med Act, Clin Serv, Vilseck, Germany.
[Grogan, Scott P.] Eisenhower Army Med Ctr, Ft Gordon, GA USA.
[Saguil, Aaron] Uniformed Serv Univ Hlth Sci, Recruitment & Adm, F Edward Hebert Sch Med, Bethesda, MD 20814 USA.
C3 United States Department of Defense; United States Army; Uniformed
Services University of the Health Sciences - USA
RP Fargo, MV (corresponding author), US Army Med Dept, CMR 411,Box 4384, APO, AE 09112 USA.
EM matthew.v.fargo.mil@mail.mil
CR [Anonymous], 2012, ACR APPR CRIT
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NR 29
TC 58
Z9 62
U1 0
U2 19
PU AMER ACAD FAMILY PHYSICIANS
PI KANSAS CITY
PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 USA
SN 0002-838X
EI 1532-0650
J9 AM FAM PHYSICIAN
JI Am. Fam. Physician
PD FEB 1
PY 2017
VL 95
IS 3
BP 164
EP 168
PG 5
WC Primary Health Care; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA EJ6XD
UT WOS:000393363100008
PM 28145671
DA 2025-01-07
ER
PT J
AU Wang, JJ
Ni, R
Jiang, TT
Peng, D
Ming, Y
Cui, HJ
Liu, Y
AF Wang, Jingjing
Ni, Rui
Jiang, Tingting
Peng, Dan
Ming, Yue
Cui, Hongjuan
Liu, Yao
TI The applications of functional materials-based nano-formulations in the
prevention, diagnosis and treatment of chronic inflammation-related
diseases
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE nanotechnology; chronic inflammation; prevention; diagnosis; treatment
ID NF-KAPPA-B; MACROPHAGE POLARIZATION; VITAMIN-E; NANOPARTICLES; MODEL;
ACID; NANOSTRUCTURES; AMELIORATION; ANTIOXIDANT; MECHANISMS
AB Chronic inflammation, in general, refers to systemic immune abnormalities most often caused by the environment or lifestyle, which is the basis for various skin diseases, autoimmune diseases, cardiovascular diseases, liver diseases, digestive diseases, cancer, and so on. Therapeutic strategies have focused on immunosuppression and anti-inflammation, but conventional approaches have been poor in enhancing the substantive therapeutic effect of drugs. Nanomaterials continue to attract attention for their high flexibility, durability and simplicity of preparation, as well as high profitability. Nanotechnology is used in various areas of clinical medicine, such as medical diagnosis, monitoring and treatment. However, some related problems cannot be ignored, including various cytotoxic and worsening inflammation caused by the nanomaterials themselves. This paper provides an overview of functional nanomaterial formulations for the prevention, diagnosis and treatment of chronic inflammation-related diseases, with the intention of providing some reference for the enhancement and optimization of existing therapeutic approaches.
C1 [Wang, Jingjing; Ni, Rui; Jiang, Tingting; Peng, Dan; Ming, Yue; Liu, Yao] Army Med Univ, Daping Hosp, Dept Pharm, Chongqing, Peoples R China.
[Wang, Jingjing; Cui, Hongjuan; Liu, Yao] Southwest Univ, Med Res Inst, Chongqing, Peoples R China.
C3 Army Medical University; Southwest University - China
RP Liu, Y (corresponding author), Army Med Univ, Daping Hosp, Dept Pharm, Chongqing, Peoples R China.; Cui, HJ; Liu, Y (corresponding author), Southwest Univ, Med Res Inst, Chongqing, Peoples R China.
EM hcui@swu.edu.cn; swhliuyao@163.com
RI Jiang, Tingting/GLS-5518-2022; Yao, Liu/LJM-3304-2024
FU Chongqing Clinical Pharmacy Key Specialties Construction Project
[425Z41]; Chongqing Special Project for Technological Innovation and
Application Development [CSTC2021jscx-gksb-N0013]; Chongqing Traditional
Chinese Medicine Research Project [2023ZDXM032]
FX This work was financially supported by The Chongqing Clinical Pharmacy
Key Specialties Construction Project (No. 425Z41), The Chongqing Special
Project for Technological Innovation and Application Development (NO.
CSTC2021jscx-gksb-N0013) and The Chongqing Traditional Chinese Medicine
Research Project (NO. 2023ZDXM032).
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NR 225
TC 0
Z9 0
U1 9
U2 29
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD AUG 1
PY 2023
VL 14
AR 1222642
DI 10.3389/fphar.2023.1222642
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA P3XD0
UT WOS:001049996300001
PM 37593176
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Petrick, JL
Yang, BY
Altekruse, SF
Van Dyke, AL
Koshiol, J
Graubard, BI
McGlynn, KA
AF Petrick, Jessica L.
Yang, Baiyu
Altekruse, Sean F.
Van Dyke, Alison L.
Koshiol, Jill
Graubard, Barry I.
McGlynn, Katherine A.
TI Risk factors for intrahepatic and extrahepatic cholangiocarcinoma in the
United States: A population-based study in SEER-Medicare
SO PLOS ONE
LA English
DT Article
ID PRIMARY LIVER-CANCER; CHRONIC HEPATITIS-C; VIRUS-INFECTION; INDUCED
HYPERTHYROIDISM; METAANALYSIS; DISEASE; OBESITY; CHOLECYSTECTOMY;
INFLAMMATION; GALLSTONES
AB Objectives
Intrahepatic (ICC) and extrahepatic (ECC) cholangiocarcinomas are rare tumors that arise from the epithelial cells of the bile ducts, and the etiology of both cancer types is poorly understood. Thus, we utilized the Surveillance, Epidemiology, and End Results (SEER)Medicare resource to examine risk factors and novel preexisting medical conditions that may be associated with these cancer types.
Methods
Between 2000 and 2011, 2,092 ICC and 2,981 ECC cases and 323,615 controls were identified using the SEER-Medicare database. Logistic regression was used to calculate adjusted odds ratios (OR) and 95% confidence intervals (CI). &&Results Non-alcoholic fatty liver disease was associated with approximately 3-fold increased risks of ICC (OR = 3.52, 95% CI: 2.87-4.32) and ECC (OR = 2.93, 95% CI: 2.42-3.55). Other metabolic conditions, including obesity and type 2 diabetes, were also associated with increased risks of both cancer types. Smoking was associated with a 46% and 77% increased ICC and ECC risk, respectively. Several autoimmune/inflammatory conditions, including type 1 diabetes and gout, were associated with increased risks of ICC/ECC. As anticipated, viral hepatitis, alcohol-related disorders, and bile duct conditions were associated with both cancer types. However, thyrotoxicosis and hemochromatosis were associated with an increased risk of ICC but not ECC, but did not remain significantly associated after Bonferroni correction.
Conclusions
In this study, risk factors for ICC and ECC were similar, with the exceptions of thyrotoxicosis and hemochromatosis. Notably, metabolic conditions were associated with both cancer types. As metabolic conditions are increasing in prevalence, these could be increasingly important risk factors for both types of cholangiocarcinoma.
C1 [Petrick, Jessica L.; Yang, Baiyu; Van Dyke, Alison L.; Koshiol, Jill; Graubard, Barry I.; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Yang, Baiyu] Stanford Univ, Stanford Canc Inst, Palo Alto, CA 94304 USA.
[Altekruse, Sean F.] NHLBI, Bldg 10, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI); Stanford Cancer Institute; Stanford University; National
Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood
Institute (NHLBI)
RP Petrick, JL (corresponding author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM jessica.petrick@nih.gov
RI Petrick, Jessica/AAA-9079-2020; Koshiol, Jill/L-8686-2014; Petrick,
Jessica/P-1678-2017
OI Koshiol, Jill/0000-0002-3832-6204; Petrick, Jessica/0000-0001-6580-450X
FU National Cancer Institute; National Cancer Institute [ZIACP010158]
Funding Source: NIH RePORTER
FX This work was supported by the Intramural Research Program of the
National Cancer Institute to KAM. The funder had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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TC 138
Z9 145
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 19
PY 2017
VL 12
IS 10
AR e0186643
DI 10.1371/journal.pone.0186643
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA FK0UN
UT WOS:000413195900091
PM 29049401
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Bhat, R
Tonutti, A
Timilsina, S
Selmi, C
Gershwin, ME
AF Bhat, Rithika
Tonutti, Antonio
Timilsina, Suraj
Selmi, Carlo
Gershwin, M. Eric
TI Perspectives on Mycophenolate Mofetil in the Management of Autoimmunity
SO CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
LA English
DT Review
DE Mycophenolate mofetil; Systemic sclerosis; Mycophenolic acid
ID INTERSTITIAL LUNG-DISEASE; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
METHYLPREDNISOLONE PLUS AZATHIOPRINE; EULAR/ERA-EDTA RECOMMENDATIONS;
RANDOMIZED CONTROLLED-TRIAL; INTRAVENOUS CYCLOPHOSPHAMIDE; OPEN-LABEL;
LONG-TERM; NONRENAL MANIFESTATIONS; LIVER-TRANSPLANTATION
AB Before becoming a cornerstone in the treatment of numerous immune-mediated diseases, mycophenolate mofetil (MMF) was first introduced as an immunosuppressive agent in transplant immunology and later received the attention of rheumatologists and clinicians involved in the management of autoimmune diseases. MMF is now a widespread immunosuppressive drug for the treatment of several conditions, including lupus nephritis, interstitial lung disease associated with systemic sclerosis, and anti-neutrophil cytoplasm antibody (ANCA)-associated vasculitis while being efficacious also as rescue therapy in various orphan diseases, including dermatomyositis and IgA-associated nephropathy. Similarly, case reports or series support a possible use of MMF in other rare autoimmune diseases. Beyond modulating lymphocyte activation, MMF acts on other immune and non-immune cells and these effects may explain the therapeutic profile of this medication. The effects of MMF are broadly characterized by the impact on the immune system and the antiproliferative and antifibrotic changes induced. In this latter case, mechanistic data on fibroblasts may in the future allow to reevaluate the use of MMF in selected patients with inflammatory arthritis or systemic sclerosis. Attention must be paid towards the possible occurrence of adverse events, such as gastrointestinal complaints and teratogenicity, while the risk of infections and cancer related to MMF needs to be further investigated.
C1 [Bhat, Rithika; Timilsina, Suraj; Gershwin, M. Eric] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Tonutti, Antonio; Selmi, Carlo] Humanitas Univ, Dept Biomed Sci, Milan, Italy.
[Tonutti, Antonio; Selmi, Carlo] IRCCS Humanitas Res Hosp, Rheumatol & Clin Immunol, Milan, Italy.
C3 University of California System; University of California Davis;
Humanitas University
RP Gershwin, ME (corresponding author), Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.; Selmi, C (corresponding author), Humanitas Univ, Dept Biomed Sci, Milan, Italy.; Selmi, C (corresponding author), IRCCS Humanitas Res Hosp, Rheumatol & Clin Immunol, Milan, Italy.
EM carlo.selmi@hunimed.eu; megershwin@ucdavis.edu
RI Selmi, Carlo/ABG-4899-2021; Tonutti, Antonio/LSJ-1920-2024
OI Timilsina, Suraj/0000-0003-2483-3878; Tonutti,
Antonio/0009-0000-9534-6853
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NR 179
TC 10
Z9 10
U1 1
U2 5
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1080-0549
EI 1559-0267
J9 CLIN REV ALLERG IMMU
JI Clin. Rev. Allergy Immunol.
PD AUG
PY 2023
VL 65
IS 1
SI SI
BP 86
EP 100
DI 10.1007/s12016-023-08963-3
EA JUN 2023
PG 15
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA L7KV3
UT WOS:001011507700001
PM 37338709
DA 2025-01-07
ER
PT J
AU Huang, QT
Cao, W
Mielke, LA
Seillet, C
Belz, GT
Jacquelot, N
AF Huang, Qiutong
Cao, Wang
Mielke, Lisa Anna
Seillet, Cyril
Belz, Gabrielle T.
Jacquelot, Nicolas
TI Innate Lymphoid Cells in Colorectal Cancers: A Double-Edged Sword
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE tumor immunology; adaptive immunity; innate immunity; tumor
immunosurveillance; immunotherapy
ID INFLAMMATORY-BOWEL-DISEASE; NK CELLS; TUMOR MICROENVIRONMENT; LIVER
METASTASIS; IMMUNE CELLS; COLON-CANCER; ADENOMA; IL-17A; INTERLEUKIN-22;
RECEPTOR
AB The immune system plays a fundamental role at mucosal barriers in maintaining tissue homeostasis. This is particularly true for the gut where cells are flooded with microbial-derived signals and antigens, which constantly challenge the integrity of the intestinal barrier. Multiple immune cell populations equipped with both pro- and anti-inflammatory functions reside in the gut tissue and these cells tightly regulate intestinal health and functions. Dysregulation of this finely tuned system can progressively lead to autoimmune disease and inflammation-driven carcinogenesis. Over the last decade, the contribution of the adaptive immune system in controlling colorectal cancer has been studied in detail, but the role of the innate system, particularly innate lymphoid cells (ILCs), have been largely overlooked. By sensing their microenvironment, ILCs are essential in supporting gut epithelium repair and controling bacterial- and helminth-mediated intestinal infections, highlighting their important role in maintaining tissue integrity. Accumulating evidence also suggests that they may play an important role in carcinogenesis including intestinal cancers. In this review, we will explore the current knowledge about the pro- and anti-tumor functions of ILCs in colorectal cancer.
C1 [Huang, Qiutong; Cao, Wang; Seillet, Cyril; Belz, Gabrielle T.; Jacquelot, Nicolas] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia.
[Huang, Qiutong; Cao, Wang; Seillet, Cyril; Belz, Gabrielle T.; Jacquelot, Nicolas] Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia.
[Mielke, Lisa Anna] Olivia Newton John Canc Res Inst, Heidelberg, Vic, Australia.
[Mielke, Lisa Anna] La Trobe Univ, Sch Canc Med, Heidelberg, Vic, Australia.
[Belz, Gabrielle T.] Univ Queensland, Diamantina Inst, Brisbane, Qld, Australia.
C3 Walter & Eliza Hall Institute; University of Melbourne; La Trobe
University; Olivia Newton-John Cancer Research Institute; La Trobe
University; University of Queensland
RP Belz, GT; Jacquelot, N (corresponding author), Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia.; Belz, GT; Jacquelot, N (corresponding author), Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia.; Belz, GT (corresponding author), Univ Queensland, Diamantina Inst, Brisbane, Qld, Australia.
EM belz@wehi.edu.au; jacquelot.n@wehi.edu.au
RI Jacquelot, Nicolas/AAY-6937-2020; Seillet, Cyril/AAF-1888-2019; Belz,
Gabrielle/C-9350-2013
OI Huang, Qiutong/0000-0002-4556-0605; Belz, Gabrielle/0000-0002-9660-9587;
Mielke, Lisa/0000-0002-9522-9320; Cao, Wang/0000-0001-8023-6096;
Jacquelot, Nicolas/0000-0003-0282-1892
FU National Health and Medical Research Council (NHMRC) of Australia
[APP1165443, 1122277, 1054925]; NHMRC [APP1135898, APP1123000];
Victorian Cancer Agency; Cure Cancer Australia through the Cancer
Australia Priority-driven Cancer Research Scheme [APP1163990]; Cancer
Australia through the Cancer Australia Priority-driven Cancer Research
Scheme [APP1163990]; Rebecca L. Cooper Foundation Medical Research
Foundation; Australian Government Research Training Program Scholarship;
National Health and Medical Research Council of Australia [1122277]
Funding Source: NHMRC
FX This work was supported by grants and fellowships from the National
Health and Medical Research Council (NHMRC) of Australia (APP1165443,
1122277, and 1054925 GB and CS), fellowships from the NHMRC (APP1135898
GB, APP1123000 CS), Victorian Cancer Agency (LM), Cure Cancer Australia
and Cancer Australia through the Cancer Australia Priority-driven Cancer
Research Scheme (APP1163990 NJ), The Rebecca L. Cooper Foundation
Medical Research Foundation (GB), and an Australian Government Research
Training Program Scholarship (QH). This work was made possible through
Victorian State Government Operational Infrastructure Support and
Australian Government NHMRC Independent Research Institute
Infrastructure Support scheme.
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NR 116
TC 16
Z9 16
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 15
PY 2020
VL 10
AR 3080
DI 10.3389/fimmu.2019.03080
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA KG5CD
UT WOS:000509964200001
PM 32010138
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Gruba, N
Wysocka, M
Brzezinska, M
Dezbowski, D
Sienczyk, M
Gorodkiewicz, E
Guszcz, T
Czaplewski, C
Rolka, K
Lesner, A
AF Gruba, Natalia
Wysocka, Magdalena
Brzezinska, Magdalena
Dezbowski, Dawid
Sienczyk, Marcin
Gorodkiewicz, Ewa
Guszcz, Tomasz
Czaplewski, Cezary
Rolka, Krzysztof
Lesner, Adam
TI Bladder cancer detection using a peptide substrate of the 20S proteasome
SO FEBS JOURNAL
LA English
DT Article
DE bladder cancer biomarker; combinatorial chemistry; fluorescence assay;
human 20S proteasome; intramolecularly quenched peptides
ID PROTEIN-DEGRADATION; MAMMALIAN-CELLS; RAT-LIVER; INHIBITORS; PLASMA;
SYSTEM; OPTIMIZATION; CARFILZOMIB; COMPLEXES; DISEASES
AB The 20S catalytic core of the human 26S proteasome can be secreted from cells, and high levels of extracellular 20S proteasome have been linked to many types of cancers and autoimmune diseases. Several diagnostic approaches have been developed that detect 20S proteasome activity in plasma, but these suffer from problems with efficiency and sensitivity. In this report, we describe the optimization and synthesis of an internally quenched fluorescent substrate of the 20S proteasome, and investigate its use as a potential diagnostic test in bladder cancer. This peptide, 2-aminobenzoic acid (ABZ)-Val-Val-Ser-Tyr-Ala-Met-Gly-Tyr(3-NO2)-NH2, is cleaved by the chymotrypsin 20S proteasome subunit and displays an excellent specificity constant value (9.7 x 10(5) M-1.s(-1)) and a high k(cat) (8 s(-1)). Using this peptide, we identified chymotrypsin-like proteasome activity in the majority of urine samples obtained from patients with bladder cancer, whereas the proteasome activity in urine samples from healthy volunteers was below the detection limit (0.5 pM). These findings were confirmed by an inhibitory study and immunochemistry methods.
C1 [Gruba, Natalia; Wysocka, Magdalena; Brzezinska, Magdalena; Dezbowski, Dawid; Czaplewski, Cezary; Rolka, Krzysztof; Lesner, Adam] Univ Gdansk, Fac Chem, Wita Stwosza 63, PL-80308 Gdansk, Poland.
[Sienczyk, Marcin] Wroclaw Univ Technol, Fac Chem, Wroclaw, Poland.
[Gorodkiewicz, Ewa] Univ Bialystok, Inst Chem, Dept Electrochem, Bialystok, Poland.
[Guszcz, Tomasz] J Sniadecki Prov Hosp Bialystok, Dept Urol, Bialystok, Poland.
C3 Fahrenheit Universities; University of Gdansk; Wroclaw University of
Science & Technology; University of Bialystok
RP Lesner, A (corresponding author), Univ Gdansk, Fac Chem, Wita Stwosza 63, PL-80308 Gdansk, Poland.
EM adam.lesner@ug.edu.pl
RI Czaplewski, Cezary/E-1503-2016; guszcz, tomasz/Z-1249-2018; Lesner,
Adam/M-2732-2019; Sienczyk, Marcin/I-3869-2012
OI Lesner, Adam/0000-0001-8335-3431; Debowski, Dawid/0000-0002-5868-3276;
Rolka, Krzysztof/0000-0002-4537-700X; Gruba,
Natalia/0000-0003-3281-9945; Wysocka, Magdalena/0000-0003-2216-5597;
Czaplewski, Cezary/0000-0002-0294-3403
FU Polish Ministry of Science and Higher Education Iuventus PLUS
[0624/IP32011/7]; Polish National Science Center [UMO-2011/01/D/
ST5/02778]; Wroclaw University of Technology [S40630/ Z0313]
FX This project was funded by Polish Ministry of Science and Higher
Education Iuventus PLUS 0624/IP32011/7 and Polish National Science
Center UMO-2011/01/D/ ST5/02778. MS is grateful for support to Wroclaw
University of Technology (Statute Funds S40630/ Z0313). The authors
would like to thank Dr Keri Csencsits-Smith (University of Texas Health
Science Center at Houston, TX, USA) for critical reading of the
manuscript, Professor Krzysztof Szajowski (Department of Mathematics,
Faculty of Fundamental Problems of Technology, Wroclaw University of
Technology) and Mateusz Psurski (Faculty of Chemistry, Wroclaw
University of Technology) for helpful discussion on statistical
analysis.
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NR 47
TC 14
Z9 15
U1 0
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1742-464X
EI 1742-4658
J9 FEBS J
JI FEBS J.
PD AUG
PY 2016
VL 283
IS 15
BP 2929
EP 2948
DI 10.1111/febs.13786
PG 20
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA DW4HH
UT WOS:000383603300013
PM 27326540
OA Bronze
DA 2025-01-07
ER
PT J
AU Nevzorova, YA
Cubero, FJ
AF Nevzorova, Yulia A.
Cubero, Francisco Javier
TI Obesity under the moonlight of c-MYC
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE c-Myc; obesity; MASLD; gut-liver axis; T2DM
ID BETA-CELL MASS; ADIPOSE-TISSUE; ADIPOCYTE DIFFERENTIATION; HIGH GLUCOSE;
SIRT1; EXPRESSION; ACTIVATION; PROLIFERATION; ADIPOGENESIS; INFLAMMATION
AB The moonlighting protein c-Myc is a master regulator of multiple biological processes including cell proliferation, differentiation, angiogenesis, apoptosis and metabolism. It is constitutively and aberrantly expressed in more than 70% of human cancers. Overwhelming evidence suggests that c-Myc dysregulation is involved in several inflammatory, autoimmune, metabolic and other non-cancerous diseases. In this review, we addressed the role of c-Myc in obesity. Obesity is a systemic disease, accompanied by multi-organ dysfunction apart from white adipose tissue (WAT), such as the liver, the pancreas, and the intestine. c-Myc plays a big diversity of functions regulating cellular proliferation, the maturation of progenitor cells, fatty acids (FAs) metabolism, and extracellular matrix (ECM) remodeling. Moreover, c-Myc drives the expression of a wide range of metabolic genes, modulates the inflammatory response, induces insulin resistance (IR), and contributes to the regulation of intestinal dysbiosis. Altogether, c-Myc is an interesting diagnostic tool and/or therapeutic target in order to mitigate obesity and its consequences.
C1 [Nevzorova, Yulia A.; Cubero, Francisco Javier] Univ Complutense Madrid, Sch Med, Dept Immunol Ophthalmol & ENT, Madrid, Spain.
[Nevzorova, Yulia A.; Cubero, Francisco Javier] Ctr Invest Biomed Red Enfermedades Hepat & Digest, Madrid, Spain.
[Nevzorova, Yulia A.; Cubero, Francisco Javier] Inst Invest Sanitaria Gregorio Maranon IiSGM, Madrid, Spain.
C3 Complutense University of Madrid; CIBER - Centro de Investigacion
Biomedica en Red; CIBEREHD
RP Nevzorova, YA (corresponding author), Univ Complutense Madrid, Sch Med, Dept Immunol Ophthalmol & ENT, Madrid, Spain.; Nevzorova, YA (corresponding author), Ctr Invest Biomed Red Enfermedades Hepat & Digest, Madrid, Spain.; Nevzorova, YA (corresponding author), Inst Invest Sanitaria Gregorio Maranon IiSGM, Madrid, Spain.
EM yulianev@ucm.es
RI chen, chenbo/AEA-9700-2022
FU MICINN [PID2020-117827RB-IOO/AEI/10.13039/501100011033,
PID2020-117941RB-IOO//AEI/10.13039/501100011033, S2022/BMD-7409];
Comunidad de Madrid; European Horizon's research and innovation program
[HORIZON-HLTH-2022-STAYHLTH-02, 101095679, 970935]; Horizon Europe -
Pillar II [101095679] Funding Source: Horizon Europe - Pillar II
FX This work was supported by MICINN
PID2020-117827RB-IOO/AEI/10.13039/501100011033,
PID2020-117941RB-IOO//AEI/10.13039/501100011033 and EXOHEP2
(S2022/BMD-7409) from Comunidad de Madrid. This project has received
funding from the European Horizon's research and innovation program
HORIZON-HLTH-2022-STAYHLTH-02 under agreement No 101095679. The research
group belongs to the validated Research Groups Ref. 970935 "Liver
Pathophysiology".
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NR 157
TC 5
Z9 5
U1 2
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD DEC 5
PY 2023
VL 11
AR 1293218
DI 10.3389/fcell.2023.1293218
PG 14
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA CP1R0
UT WOS:001126362800001
PM 38116204
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Gardner, CS
Bashir, MR
Marin, D
Nelson, RC
Choudhury, KR
Ho, LM
AF Gardner, Carly S.
Bashir, Mustafa R.
Marin, Daniele
Nelson, Rendon C.
Choudhury, Kingshuk Roy
Ho, Lisa M.
TI Diagnostic performance of imaging criteria for distinguishing autoimmune
cholangiopathy from primary sclerosing cholangitis and bile duct
malignancy
SO ABDOMINAL IMAGING
LA English
DT Article
DE Autoimmune cholangiopathy; IgG4; Primary sclerosing cholangitis;
Cholangiocarcinoma
ID DIFFERENTIAL-DIAGNOSIS; PANCREATITIS; CHOLANGIOCARCINOMA;
CHOLANGIOGRAPHY; INVOLVEMENT; FEATURES; CARCINOMA; SPECTRUM; THERAPY;
DISEASE
AB To determine the diagnostic performance of imaging criteria for distinguishing Ig-G4-associated autoimmune cholangiopathy (IAC) from primary sclerosing cholangitis (PSC) and bile duct malignancy.
A medical records search between January 2008 and October 2013 identified 10 patients (8 M, 2 F, mean age 61 years, range 34-82) with a clinical diagnosis of IAC. Fifteen cases of PSC (6 M, 9 F, mean age 50, range 22-65) and 15 cases of biliary malignancy (7 M, 8 F, mean age 65, range 48-84) were randomly selected for comparative analysis. Three abdominal radiologists independently reviewed MRI with MRCP (n = 32) or CT (n = 8) and ERCP (n = 8) for the following IAC imaging predictors: single-wall bile duct thickness > 2.5 mm, continuous biliary involvement, gallbladder involvement, liver disease, peribiliary mass, or pancreatic and renal abnormalities. Each radiologist provided an imaging-based diagnosis (IAC, PSC, or cancer). Imaging predictor sensitivity, specificity, accuracy, and association with IAC using Fisher's exact test. Inter-reader agreement determined using Fleiss' kappa statistics.
For diagnosis of IAC, sensitivities and specificities were high (70-93%). Pancreatic abnormality was strongest predictor for distinguishing IAC from PSC and cancer, with high diagnostic performance (70-80% sensitivity, 87-97% specificity), significant association (p < 0.01), and moderate inter-reader agreement (kappa = 0.59). Continuous biliary involvement was moderately predictive (50-100% sensitivity, 53-83% specificity) and trended toward significant association in distinguishing from PSC (p = 0.01-0.19), but less from cancer (p = 0.06-0.62).
It remains difficult to distinguish IAC from PSC or bile duct malignancy based on imaging features alone. The presence of pancreatic abnormalities, including peripancreatic rind, atrophy, abnormal enhancement, or T2 signal intensity, strongly favors a diagnosis of IAC.
C1 [Gardner, Carly S.] Baylor Coll Med, Dept Radiol, Houston, TX 77030 USA.
[Bashir, Mustafa R.; Marin, Daniele; Nelson, Rendon C.; Choudhury, Kingshuk Roy; Ho, Lisa M.] Duke Univ, Med Ctr, Dept Radiol, Durham, NC 27710 USA.
[Bashir, Mustafa R.] Duke Univ, Med Ctr, Ctr Adv Magnet Resonance Dev, Durham, NC 27710 USA.
C3 Baylor College of Medicine; Duke University; Duke University
RP Ho, LM (corresponding author), Duke Univ, Med Ctr, Dept Radiol, Box 3808, Durham, NC 27710 USA.
EM lisa.ho@duke.edu
RI Bashir, Mustafa/P-3428-2015; Marin, Daniele/Q-7701-2016
OI Ho, Lisa/0000-0002-2885-1531
CR Ahn KS, 2012, J HEPATO-BIL-PAN SCI, V19, P405, DOI 10.1007/s00534-011-0436-z
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NR 29
TC 19
Z9 23
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-8925
EI 1432-0509
J9 ABDOM IMAGING
JI Abdom. Imaging
PD OCT
PY 2015
VL 40
IS 8
BP 3052
EP 3061
DI 10.1007/s00261-015-0543-4
PG 10
WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
GA CV0PD
UT WOS:000363952000012
PM 26350286
DA 2025-01-07
ER
PT J
AU Lajarín-Cuesta, R
Arribas, RL
De Los Ríos, C
AF Lajarin-Cuesta, Rocio
Arribas, Raquel L.
De Los Rios, Cristobal
TI Ligands for Ser/Thr phosphoprotein phosphatases: a patent review
(2005-2015)
SO EXPERT OPINION ON THERAPEUTIC PATENTS
LA English
DT Review
DE PP5; PP2A; cancer; Ser/Thr phosphatases; PP2B; neurodegeneration;
phosphoprotein phosphatases; PP1; calcineurin; PP3
ID 2A SUBUNIT INTERACTION; PROTEIN PHOSPHATASE; TETRATRICOPEPTIDE REPEAT;
NORCANTHARIDIN ANALOGS; SELECTIVE-INHIBITION; ANTICANCER ACTIVITY;
CANCER-CELLS; SERINE/THREONINE PHOSPHATASES; HEPATOCELLULAR-CARCINOMA;
ALZHEIMERS-DISEASE
AB Introduction: The role played by phosphoprotein phosphatases (PPP) enzymes makes them of interest as therapeutic targets to treat pathologies including neurodegenerative diseases, cancer and autoimmune diseases, but also liable to cause severe side effects. This fact has hindered the study of PPP ligands as potential drugs. Fortunately, recent advances in the comprehension of PPP biochemistry have given rise to the development of refined pharmacological strategies to selectively target phosphatases and limit the possible generation of adverse reactions.
Areas covered: This review summarizes the most relevant patents claiming the use of PPP ligands to treat human diseases in the last decade (2005-2015). It also includes some pharmacological strategies aiming to indirectly modulate PPP functionality by interacting with PPP-regulating enzymes.
Expert opinion: There is still much work to be done to validate PPP enzymes as eligible targets for the development of new drugs. The most significant barrier is likely to be persuading the majority of the scientific community that PPP enzymes are not too unspecific. Few patents disclosed the rational design of direct PPP ligands, while many inventions relied on long chain peptides-based approaches. Overall, the future of ligands for PPP enzymes as therapeutics seems both challenging and exciting.
C1 [Lajarin-Cuesta, Rocio; Arribas, Raquel L.; De Los Rios, Cristobal] Univ Autonoma Madrid, Fac Med, Inst Teofilo Hernando, Dept Farmacol & Terapeut, C Arzobispo Morcillo 4, E-28029 Madrid, Spain.
[De Los Rios, Cristobal] Hosp Univ Princesa, Inst Invest Sanitaria, Serv Farmacol Clin, Madrid, Spain.
C3 Autonomous University of Madrid; Hospital de La Princesa
RP De Los Ríos, C (corresponding author), Univ Autonoma Madrid, Fac Med, Inst Teofilo Hernando, Dept Farmacol & Terapeut, C Arzobispo Morcillo 4, E-28029 Madrid, Spain.; De Los Ríos, C (corresponding author), Hosp Univ Princesa, Inst Invest Sanitaria, Serv Farmacol Clin, Madrid, Spain.
EM cristobal.delosrios@uam.es
RI de los Ríos, Cristóbal/KLZ-8150-2024; Lopez Arribas,
Raquel/KYP-5345-2024
OI Lopez Arribas, Raquel/0000-0002-2507-1521; de los Rios,
Cristobal/0000-0002-6456-7589
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NR 129
TC 10
Z9 10
U1 0
U2 21
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1354-3776
EI 1744-7674
J9 EXPERT OPIN THER PAT
JI Expert Opin. Ther. Patents
PD MAR 3
PY 2016
VL 26
IS 3
BP 389
EP 407
DI 10.1517/13543776.2016.1135903
PG 19
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DF4LX
UT WOS:000371320900004
PM 26853448
DA 2025-01-07
ER
PT J
AU Burra, P
AF Burra, Patrizia
TI Liver abnormalities and endocrine diseases
SO BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE Addison's disease; Adrenocortical dysfunction; Alcoholic liver disease;
Amenorrhoea; Amiodarone; Androgens; Autoimmune diseases; Cirrhosis;
Coagulation; Cushing's syndrome; Diabetes; Oestrogens; Gonadal
dysfunction; Gonadotropin; Growth hormone; Hepatitis; Hyperlipidaemia;
Hyperthyroidism; Hypogonadism; Hypothyroidism; Insulin resistance;
Infertility; Liver transplantation; Non-alcoholic steatohepatitis;
Metabolic syndrome; Obesity; progesterone; Propylthiouracil; Sexual
dysfunction; Steatosis; Thyrotoxicosis
ID NONALCOHOLIC FATTY LIVER; GROWTH-FACTOR-I; THYROID-DYSFUNCTION;
GLUCOSE-METABOLISM; RISK-FACTOR; HORMONE; HYPOTHYROIDISM; PREVALENCE;
STEATOHEPATITIS; HEPATOTOXICITY
AB The liver and its pleotropic functions play a fundamental role in regulating metabolism, and is also an inevitable target of multiple metabolic disorders. The numerous and constant relationships and feedback mechanisms between the liver and all endocrine organs is reflected by the fact that an alteration of one oftentimes results in the malfunction of the other.
Hypo- and hyperthyroidism are frequently associated with hepatic alterations, and thyroid diseases must be excluded in transaminase elevation of unknown cause. Drugs such as propylthiouracil, used in the treatment of hyperthyroidism, may induce liver damage, and other drugs such as amiodarone, carbamazepine, and several chemotherapeutic agents can lead to both thyroid and liver abnormalities. Liver diseases such as hepatitis, hepatocellular carcinoma, and cirrhosis may cause altered levels of thyroid hormones, and alcoholic liver disease, both due to the noxious substance ethanol as well as to the hepatic damage it causes, may be responsible for altered thyroid function.
Both excess and insufficiency of adrenal function may result in altered liver function, and adrenocortical dysfunction may be present in patients with cirrhosis, especially during episodes of decompensation. Again an important player which affects both the endocrine system and the liver, alcohol may be associated with pseudo-Cushing syndrome.
Sex hormones, both intrinsic as well as extrinsically administered, have an important impact on liver function. While oestrogens are related to cholestatic liver damage, androgens are the culprit of adenomas and hepatocellular carcinoma, among others. Chronic liver disease, on the other hand, has profound repercussions on sex hormone metabolism, inducing feminization in men and infertility and amenorrhoea in women.
Lastly, metabolic syndrome, the pandemia of the present and future centuries, links the spectrum of liver damage ranging from steatosis to cirrhosis, to the array of endocrine alterations that are features of the syndrome, including insulin resistance, central obesity, and hyperlipidaemia.
Clinical practice must integrally evaluate the effects of the intricate and tight relationship between the liver and the endocrine system, in order to better address all manifestations, complications, and prevent deterioration of one or the other organ-system. (C) 2013 Elsevier Ltd. All rights reserved.
C1 Padua Univ Hosp, Multivisceral Transplant Unit, Dept Surgely Oncol & Gastroenterol, I-35128 Padua, PD, Italy.
C3 University of Padua; Azienda Ospedaliera - Universita di Padova
RP Burra, P (corresponding author), Padua Univ Hosp, Multivisceral Transplant Unit, Dept Surgely Oncol & Gastroenterol, Via Giustiniani 2, I-35128 Padua, PD, Italy.
EM burra@unipd.it
RI Burra, Patrizia/AAB-2448-2019
OI Burra, Patrizia/0000-0002-8791-191X
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NR 64
TC 60
Z9 70
U1 0
U2 36
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1521-6918
EI 1532-1916
J9 BEST PRACT RES CL GA
JI Best Pract. Res. Clin. Gastroenterol.
PD AUG
PY 2013
VL 27
IS 4
BP 553
EP 563
DI 10.1016/j.bpg.2013.06.014
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 244AK
UT WOS:000326359300008
PM 24090942
DA 2025-01-07
ER
PT J
AU Vítek, L
Tiribelli, C
AF Vitek, Libor
Tiribelli, Claudio
TI Bilirubin: The yellow hormone?
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Bilirubin; benign hyperbilirubinemia; Gilbert syndrome; hormone
ID SERUM BILIRUBIN; MOLECULAR-BASIS; BILIVERDIN; EXPRESSION; BIOMARKERS;
TESTS
AB Bilirubin is a tetrapyrrolic compound originating from heme catabolism. Although originally considered only a potentially dangerous waste product, it has become increasingly evident that this molecule represents an important modulator of various biological functions in the human body. Bilirubin appears to have versatile functions, from cell signaling (behaving almost like a "real" hormonal substance), modulation of metabolism, to immune regulation, affecting biological activities with apparent clinical and even therapeutic consequences. These activities may be the reason for the lower incidence of diseases of civilisation (cardiovascular diseases, arterial hypertension, diabetes, obesity, metabolic syndrome, certain cancers, autoimmune, and neurodegenerative diseases) observed in individuals with a chronic mild unconjugated hyperbilirubinemia, a typical sign of Gilbert's syndrome. While higher serum concentrations of unconjugated bilirubin may serve as an important protective factor against these diseases, low levels of bilirubin are associated with the opposite effect. (C) 2021 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Vitek, Libor] Charles Univ Prague, Fac Gen Hosp, Prague, Czech Republic.
[Vitek, Libor] Charles Univ Prague, Fac Med 1, Prague, Czech Republic.
[Tiribelli, Claudio] Fdn Italiana Fegato, Bldg Q,AREA Sci Pk,Basovizza Campus, I-34149 Trieste, Italy.
C3 Charles University Prague; General University Hospital Prague; Charles
University Prague
RP Tiribelli, C (corresponding author), Fdn Italiana Fegato, Bldg Q,AREA Sci Pk,Basovizza Campus, I-34149 Trieste, Italy.; Vítek, L (corresponding author), Charles Univ Prague, Fac Med 1, Dept Internal Med 4, Katerinska 32, Prague 12000 2, Czech Republic.; Vítek, L (corresponding author), Charles Univ Prague, Fac Med 1, Inst Med Biochem, Katerinska 32, Prague 12000 2, Czech Republic.; Vítek, L (corresponding author), Charles Univ Prague, Fac Med 1, Lab Diagnost, Katerinska 32, Prague 12000 2, Czech Republic.
EM vitek@cesnet.cz; ctliver@fegato.it
RI Tiribelli, Claudio/A-4716-2014; Vitek, Libor/A-2645-2008
OI Tiribelli, Claudio/0000-0001-6596-7595; Vitek, Libor/0000-0002-5318-0151
FU Czech Ministry of Health [RVO-VFN64165/2021]; Czech Health Research
Council [NV18-07-00342]; Czech Science Foundation [21-01799S];
Fondazione Italiana Fegato
FX This work was supported by grants RVOVFN64165/2021 from the Czech
Ministry of Health, NV18-07-00342 from the Czech Health Research Council
and 21-01799S from the Czech Science Foundation (LV), and by an
intramural grant from Fondazione Italiana Fegato (CT). The funding
bodies had no role in the collection, management, analysis, and
interpretation of the data; preparation, review, or approval of the
manuscript; and decision to submit the manuscript for publication.
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NR 46
TC 65
Z9 69
U1 2
U2 31
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD DEC
PY 2021
VL 75
IS 6
BP 1485
EP 1490
DI 10.1016/j.jhep.2021.06.010
EA NOV 2021
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WZ6JB
UT WOS:000720070100004
PM 34153399
DA 2025-01-07
ER
PT J
AU Yamamoto, Y
Gaynor, RB
AF Yamamoto, Y
Gaynor, RB
TI IκB kinases:: key regulators of the NF-κB pathway
SO TRENDS IN BIOCHEMICAL SCIENCES
LA English
DT Review
ID LYMPHOTOXIN-BETA-RECEPTOR; SEVERE LIVER DEGENERATION; IKK-ALPHA;
DEFICIENT MICE; GENE-EXPRESSION; HISTONE H3; TRANSCRIPTIONAL ACTIVITY;
SIGNALING PATHWAYS; NF-KAPPA-B2 P100; MAJOR CULPRIT
AB The nuclear factor (NF)-kappaB pathway is important for the expression of a wide variety of genes that are involved in the control of the host immune and inflammatory response, and in the regulation of cellular proliferation and survival. The constitutive activation of this pathway is associated with inflammatory and autoimmune diseases, such as asthma, rheumatoid arthritis and inflammatory bowel disease, in addition to atherosclerosis, Alzheimer's disease, cancer and diabetes. One of the key steps in activating the NF-kappaB pathway is the stimulation of the IkappaB (inhibitor of kappaB) kinases. Recent data indicate that these kinases activate the NF-kappaB pathway through distinct steps that are operative in both the cytoplasm and the nucleus. A better understanding of the mechanisms that activate this pathway provides the potential for defining new therapeutic targets that might prevent the aberrant activation of NF-kappaB in a variety of human diseases.
C1 Univ Texas, SW Med Ctr, Dept Med, Div Hematol Oncol, Dallas, TX 75390 USA.
C3 University of Texas System; University of Texas Southwestern Medical
Center Dallas; University of Texas Dallas
RP Univ Texas, SW Med Ctr, Dept Med, Div Hematol Oncol, Dallas, TX 75390 USA.
EM gaynor_richard@lilly.com
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NR 71
TC 553
Z9 631
U1 1
U2 25
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0968-0004
EI 1362-4326
J9 TRENDS BIOCHEM SCI
JI Trends Biochem.Sci.
PD FEB
PY 2004
VL 29
IS 2
BP 72
EP 79
DI 10.1016/j.tibs.2003.12.003
PG 8
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 780BH
UT WOS:000189350900004
PM 15102433
DA 2025-01-07
ER
PT J
AU Hoofnagle, JH
AF Hoofnagle, Jay H.
TI Reactivation of Hepatitis B
SO HEPATOLOGY
LA English
DT Article; Proceedings Paper
CT NIH Consensus Development Conference on Management of Hepatitis B Virus
CY OCT 20-22, 2008
CL Bethesda, MD
SP Natl Inst Hlth
ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION;
ANTIBODY-POSITIVE DONORS; LOW-DOSE METHOTREXATE; NON-HODGKINS-LYMPHOMA;
ORTHOTOPIC LIVER-TRANSPLANTATION; PREEMPTIVE LAMIVUDINE THERAPY; VIRUS
HBV REACTIVATION; SURFACE-ANTIGEN; CORE ANTIBODY
AB Reactivation of hepatitis B refers to the abrupt increase in hepatitis B virus (HBV) replication in a patient with inactive or resolved hepatitis B. Reactivation can occur spontaneously, but more typically is triggered by immunosuppressive therapy of cancer, autoimmune disease, or organ transplantation. Reactivation can be transient and clinically silent, but often causes a flare of disease that can be severe resulting in acute hepatic failure. Most instances of reactivation resolve spontaneously, but if immune suppression is continued, re-establishment of chronic hepatitis occurs which can lead to progressive liver injury and cirrhosis. The best-described instances of reactivation occur in hepatitis B surface antigen (HBsAg) carriers with inactive or minimally active disease who are given cancer chemotherapy for lymphoma or leukemia. Typically, serum HBV DNA rises during chemotherapy, followed by a disease flare and HBV DNA clearance with immune reconstitution after chemotherapy is stopped. Special forms of reactivation occur after solid organ and bone marrow transplantation in which chronic infection often results. Several randomized, placebo-controlled trials have shown that reactivation can be prevented by antiviral prophylaxis. Routine prophylaxis is therefore recommended for persons with HBsAg undergoing cancer chemotherapy or transplantation, but major questions remain. Which patients should be screened for HBsAg and should all be treated? Which antiviral should be used and for how long? Should persons with resolved hepatitis B without HBsAg receive prophylaxis? Future research should address the underlying molecular mechanisms of reactivation as well as its optimal means of diagnosis, treatment, and prevention in different patient populations. (HEPATOLOGY 2009; 49:S156-S165.)
C1 NIDDKD, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Institute of
Diabetes & Digestive & Kidney Diseases (NIDDK)
RP Hoofnagle, JH (corresponding author), NIDDKD, Div Digest Dis & Nutr, NIH, Bldg 31,Room 9A27,31 Ctr Dr, Bethesda, MD 20892 USA.
EM HoofnagleJ@extra.niddk.nih.gov
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NR 91
TC 447
Z9 477
U1 0
U2 15
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD MAY
PY 2009
VL 49
IS 5
SU S
BP S156
EP S165
DI 10.1002/hep.22945
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology
GA 439ZZ
UT WOS:000265668700019
PM 19399803
OA Bronze
DA 2025-01-07
ER
PT J
AU Salehi, AM
Hasanzarrini, M
Salehi, H
Jenabi, E
AF Salehi, Amir Mohammad
Hasanzarrini, Maryam
Salehi, Hossain
Jenabi, Ensiyeh
TI Liraglutide and Liver Injury: Rare Case Report with Literature Review
SO ENDOCRINE METABOLIC & IMMUNE DISORDERS-DRUG TARGETS
LA English
DT Article
DE Liraglutide; Drug-induced liver injury; Type 2 diabetes mellitus; GLP-1;
LFT; diarrhea; hypoglycemia
AB Background: Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist used for the treatment of type 2 diabetes mellitus (T2DM). So far, few severe side effects have been reported for it.Case Presentation: A 41-year-old woman was admitted to the Emergency Room with diffuse abdominal pain. The patient had a known case of T2DM, fatty liver disease, and hypertension and was treated with Metformin, Liraglutide, and Losartan. Her liver functional test (LFT) was consistent with hepatocellular injury; however, laboratory tests and abdominal ultrasound were used to rule out autoimmune hepatitis. Due to concerns for drug-induced liver injury (DILL), liraglutide was discontinued and N-acetyl cysteine was prescribed. On the fifth day of hospitalization, the patient's symptoms resolved and his LFT started to decrease on the sixth day after 2 months, the patient's liver enzyme levels returned to normal.Conclusion: Liraglutide is one of the most important drugs in the treatment of T2DM.The most common side effects of this drug are constipation, nausea, vomiting, diarrhea, indigestion, and loss of appetite. In rare cases, symptoms of thyroid cancer, pancreatitis, and hypoglycemia have been reported, however, DILL is one of the extremely rare side effect of Liraglutide. It is important to increase the awareness of physicians about the liver injury of Liraglutide.
C1 [Salehi, Amir Mohammad] Hamadan Univ Med Sci, Student Res Comm, Hamadan, Iran.
[Hasanzarrini, Maryam] Hamadan Univ Med Sci, Shahid Beheshti Hosp, Clin Res Dev Unit, Hamadan, Iran.
[Salehi, Hossain] Islamic Azad Univ Med Sci, Farheekhtegan Hosp, Gastroenterol Ward, Tehran, Iran.
[Jenabi, Ensiyeh] Hamadan Univ Med Sci, Autism Spectrum Disorders Res Ctr, Hamadan, Iran.
C3 Hamadan University of Medical Sciences; Hamadan University of Medical
Sciences; Islamic Azad University; Hamadan University of Medical
Sciences
RP Hasanzarrini, M (corresponding author), Hamadan Univ Med Sci, Shahid Beheshti Hosp, Clin Res Dev Unit, Hamadan, Iran.
EM M.hasanzarrini@umsha.ac.ir
RI Salehi, Amir Mohammad/GOE-4189-2022; Hasanzarrini, Maryam/AAL-6496-2021;
Jenabi, Ensiyeh/S-6919-2017
OI Jenabi, Ensiyeh/0000-0002-4536-0814; Salehi, Amir
Mohammad/0000-0002-1724-6432
CR Abboud G, 2007, DRUG SAFETY, V30, P277, DOI 10.2165/00002018-200730040-00001
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Teschke R., 2015, J. Liver Clin. Res, V2, P1008
NR 16
TC 0
Z9 0
U1 2
U2 2
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1871-5303
EI 2212-3873
J9 ENDOCR METAB IMMUNE
JI Endocr. Metab. Immune Disord.-Drug Targets
PY 2024
VL 24
IS 6
BP 725
EP 729
DI 10.2174/0118715303180615231011053011
PG 5
WC Endocrinology & Metabolism; Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Immunology; Pharmacology & Pharmacy
GA PN6Q8
UT WOS:001214801100001
PM 37885115
DA 2025-01-07
ER
PT J
AU Chiao, EY
Engels, EA
Kramer, JR
Pietz, K
Henderson, L
Giordano, TP
Landgren, O
AF Chiao, Elizabeth Y.
Engels, Eric A.
Kramer, Jennifer R.
Pietz, Kenneth
Henderson, Louise
Giordano, Thomas P.
Landgren, Ola
TI Risk of Immune Thrombocytopenic Purpura and Autoimmune Hemolytic Anemia
Among 120 908 US Veterans With Hepatitis C Virus Infection
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID HCV-ASSOCIATED THROMBOCYTOPENIA; ALPHA-INTERFERON TREATMENT; CHRONIC
LIVER-DISEASE; UNITED-STATES; HEPATOCELLULAR-CARCINOMA; PREVALENCE;
ERADICATION; EXPERIENCE; PATIENT; BINDING
AB Background: There is emerging evidence that hepatitis C virus (HCV) infection play a role in the etiology of immune thrombocytopenia purpura (ITP) and autoimmune hemolytic anemia (AIHA), both of which are severe autoimmune cytopenias.
Methods: To determine if HCV infection increases the risk for ITP and AIHA, we calculated the incidence rates of ITP and AIHA among 120 691 HCV-infected and 454 905 matched HCV-uninfected US veterans who received diagnoses during the period 1997 to 2004. After excluding individuals with a prior diagnosis of a lymphoproliferative disease, human immunodeficiency virus, or cirrhosis, we fitted Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) as measures of risks.
Results: We found 296 ITP and 90 AIHA cases. Among HCV-infected vs HCV-uninfected persons, the overall incidence rates of ITP were 30.2 and 18.5 per 100 000 person-years, and for AIHA they were 11.4 and 5.0 per 100 000 person-years, respectively. Hepatitis C virus was associated with elevated risks for ITP (HR, 1.8; 95% CI, 1.4-2.3) and AIHA (HR, 2.8; 95% CI, 1.8-4.2). The ITP incidence was increased among both untreated and treated HCV-infected persons (HR, 1.7; 95%, CI, 1.3-2.2 and HR, 2.4; 95% CI, 1.5-3.7, respectively), whereas AIHA incidence was elevated only among treated HCV-infected persons (HR, 11.6; 95% CI, 7.0-19.3).
Conclusions: Individuals infected with HCV are at an increased risk for ITP, whereas the development of AIHA seems to be associated with HCV treatment. It may be beneficial to test individuals newly diagnosed as having ITP for HCV infection.
C1 [Chiao, Elizabeth Y.; Kramer, Jennifer R.; Pietz, Kenneth; Henderson, Louise; Giordano, Thomas P.] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Chiao, Elizabeth Y.; Kramer, Jennifer R.; Pietz, Kenneth; Henderson, Louise; Giordano, Thomas P.] Michael E DeBakey VA Med Ctr, Houston Ctr Qual Care & Utilizat Studies, Hlth Serv Res & Dev Serv, Houston, TX 77030 USA.
[Engels, Eric A.; Landgren, Ola] NCI, Natl Inst Hlth, Bethesda, MD 20892 USA.
C3 Baylor College of Medicine; Baylor College of Medicine; Baylor College
Medical Hospital; National Institutes of Health (NIH) - USA; NIH
National Cancer Institute (NCI)
RP Chiao, EY (corresponding author), Baylor Coll Med, Dept Med, 2002 Holcombe Rd, Houston, TX 77030 USA.
EM echiao@bcm.edu
OI Chiao, Elizabeth/0000-0001-5752-2916; Giordano,
Thomas/0000-0002-9346-5530
FU Intramural Program of the National Cancer Institute; National Institutes
of Health; Houston VA Health Services Research and Development Center of
Excellence (HFP 90-020); National Cancer Institute; National Institutes
of Health [K23CA124318]; Health Services Research and Development
Service; National Cancer Institute [ZIACP010150] Funding Source: NIH
RePORTER
FX This material is based on work supported by the Intramural Program of
the National Cancer Institute, National Institutes of Health, and in
part by the Houston VA Health Services Research and Development Center
of Excellence (HFP 90-020). Dr Chiao received support from the National
Cancer Institute, National Institutes of Health, grant K23CA124318. Dr
Kramer received support from the Health Services Research and
Development Service, , grant MRP05315. Dr Giordano received support from
the NatioOffice of Research and Development, Department of Veterans
Affairsnal Institute of Mental Health, National Institutes of Health,
grant K23MH67505.
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NR 44
TC 60
Z9 62
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0003-9926
EI 1538-3679
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD FEB 23
PY 2009
VL 169
IS 4
BP 357
EP 363
DI 10.1001/archinternmed.2008.576
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 410SW
UT WOS:000263599600005
PM 19237719
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Takahashi, N
Ghazale, AH
Smyrk, TC
Mandrekar, JN
Chari, ST
AF Takahashi, Naoki
Ghazale, Amaar H.
Smyrk, Thomas C.
Mandrekar, Jayawant N.
Chari, Suresh T.
TI Possible Association Between IgG4-Associated Systemic Disease With or
Without Autoimmune Pancreatitis and non-Hodgkin Lymphoma
SO PANCREAS
LA English
DT Article
DE autoimmune pancreatitis; IgG4-associated systemic disease; non-Hodgkin
lymphoma; pancreas; IgG4
ID PRIMARY SJOGRENS-SYNDROME; PRIMARY SCLEROSING CHOLANGITIS; MR-IMAGING
FINDINGS; RHEUMATOID-ARTHRITIS; RISK; CANCER; INVOLVEMENT; CT;
METHOTREXATE; THERAPY
AB Objectives: IgG4-associated systemic disease (ISD) is a multiorgan fibroinflammatory disorder whose pancreatic manifestation is called autoimmune pancreatitis (AIP). We describe 3 patients who developed non-Hodgkin lymphoma during the follow-up of ISD.
Methods: At our institution's pancreas clinic, we have prospectively and retrospectively examined patients with ISD with (n = 101) or without (n = 10) AIP (mean age, 59 years; 90 males and 21 females). We reviewed the medical records of all 111 patients to identify patients who developed non-Hodgkin lymphoma during the follow-up since their first presentation of ISD. Standardized incidence rate was calculated.
Results: The 111 patients with ISD with or without AIP had 331 patient-years of observation during which 3 patients had a diagnosis of non-Hodgkin lymphoma 3 to 5 years after the diagnosis of ISD. In these patients who later developed lymphoma, ISD involved the pancreas (AIP) in 2 and salivary gland in 1. non-Hodgkin lymphoma had extranodal involvement in all patients (liver [n = 2], adrenal glands [n = 1], kidney [n = 1], and lung [n = 1]). Standardized incidence rate was 16.0 (95% confidence interval, 3.3-45.5).
Conclusions: We report 3 cases of non-Hodgkin lymphoma that developed during the follow-up of ISD suggesting that patients with ISD may be at an increased risk of developing non-Hodgkin lymphoma.
C1 [Takahashi, Naoki] Mayo Clin, Dept Radiol, Rochester, MN 55905 USA.
[Ghazale, Amaar H.; Chari, Suresh T.] Mayo Clin, Div Gastroenterol & Hepatol, Dept Internal Med, Rochester, MN 55905 USA.
[Smyrk, Thomas C.] Mayo Clin, Div Anat Pathol, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
[Mandrekar, Jayawant N.] Mayo Clin, Div Biostat, Dept Hlth Sci Res, Rochester, MN 55905 USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic; Mayo Clinic
RP Takahashi, N (corresponding author), Mayo Clin, Dept Radiol, 200 1st St SW, Rochester, MN 55905 USA.
EM takahashi.naoki@mayo.edu
RI Chari, Suresh/K-9297-2015
OI Takahashi, Naoki/0000-0002-7946-6078; Chari, Suresh/0000-0002-3924-0971
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NR 38
TC 100
Z9 117
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
J9 PANCREAS
JI Pancreas
PD JUL
PY 2009
VL 38
IS 5
BP 523
EP 526
DI 10.1097/MPA.0b013e31819d73ca
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 469PB
UT WOS:000267910900006
PM 19258916
DA 2025-01-07
ER
PT J
AU Cross, T
Antoniades, C
Harrison, P
AF Cross, Timothy
Antoniades, Charalambos
Harrison, Phillip
TI Non-invasive markers for the prediction of fibrosis in chronic hepatitis
C infection
SO HEPATOLOGY RESEARCH
LA English
DT Review
DE fibrogenesis; fibroscan; fibrosis; hepatitis C; non-invasive markers
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ALANINE AMINOTRANSFERASE RATIO; LIVER
STIFFNESS MEASUREMENT; BIOCHEMICAL MARKERS; TRANSIENT ELASTOGRAPHY;
ASPARTATE-AMINOTRANSFERASE; PEGINTERFERON ALPHA-2A; SAMPLING
VARIABILITY; DISEASE PROGRESSION; PLUS RIBAVIRIN
AB Liver fibrosis occurs as a result of chronic liver injury and is the hallmark of chronic liver disease. The final stage of progressive liver fibrosis is cirrhosis, which is implicated in portal hypertension, end-stage liver disease and hepatocellular carcinoma. Liver biopsy has historically been the gold standard test for the assessment of liver fibrosis for liver diseases such as viral hepatitis, autoimmune hepatitis and primary biliary cirrhosis. Improved serological tests have enhanced the diagnosis of these conditions and reduced the need for liver biopsy. Liver biopsy is unpopular among patients and clinicians. It is associated with morbidity and mortality, and in addition is subject to sampling error, inter- and intra-observer variability. There is therefore a need for non-invasive markers of liver fibrosis that are accurate, reliable, cheap and easy to use. The aim of this review is to examine the different non-invasive methods that can be used to estimate the severity of fibrosis. The methods evaluated include clinical examination, routine laboratory investigations, imaging tests, specialized tests of liver function and finally serum extra-cellular matrix markers of fibrosis. The review mainly focuses on fibrogenesis in the context of chronic hepatitis C infection.
C1 [Harrison, Phillip] Kings Coll London, Div Gene & Cell Based Therapy, Dept Liver Studies & Transplantat, London SE5 9PJ, England.
[Cross, Timothy; Antoniades, Charalambos] Kings Coll Hosp London, Inst Liver Studies, London SE5 8RX, England.
C3 University of London; King's College London; King's College Hospital NHS
Foundation Trust; King's College Hospital; University of London; King's
College London
RP Harrison, P (corresponding author), Kings Coll London, Div Gene & Cell Based Therapy, Dept Liver Studies & Transplantat, Denmark Hill Campus,Bessemer Rd, London SE5 9PJ, England.
EM phillip.harrison@kcl.ac.uk
RI Harrison, Phillip/D-5374-2009
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NR 62
TC 9
Z9 9
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD AUG
PY 2008
VL 38
IS 8
BP 762
EP 769
DI 10.1111/j.1872-034X.2008.00364.x
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 323YD
UT WOS:000257483500002
PM 18462378
DA 2025-01-07
ER
PT J
AU Huang, Z
Xu, YS
Wan, MP
Zeng, XX
Wu, JM
AF Huang, Zheng
Xu, Yesha
Wan, Maoping
Zeng, Xixi
Wu, Jianmin
TI miR-340: A multifunctional role in human malignant diseases
SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Review
DE microRNAs; miR-340; malignant diseases; cancers; drug resistance
ID MICRORNA-340 INDUCES APOPTOSIS; CANCER CELL-PROLIFERATION; HUMAN
GASTRIC-CANCER; COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA;
DOWN-REGULATION; TUMOR-GROWTH; CISPLATIN RESISTANCE; OSTEOSARCOMA CELLS;
BONE-MARROW
AB MicroRNAs (miRNAs) are a class of short non-coding RNAs of approximately 22 nucleotides in length, which function by binding to the 3' UTR sequences of their target mRNAs. It has been reported that dysregulated miRNAs play pivotal roles in numerous diseases, including cancers, such as gastric, breast, colorectal, ovarian, and other cancers. Recent research efforts have been devoted to translating these basic discoveries into clinical applications that could improve the therapeutic outcome in patients with cancer. Early studies have shown that miR-340 may act either as an oncogene or a tumor suppressor by targeting genes related to proliferation, apoptosis, and metastasis, as well as those associated with diagnosis, treatment, chemoresistance, and prognosis. miR-340 has been shown to have a role in other diseases, such as autoimmune diseases, acute stroke, and alcoholic steatohepatitis. Nevertheless, the roles of miR-340 in human malignancies are still unclear, and the associated mechanisms are complex, involving a variety of signaling pathways, such as Wnt/beta-catenin and the JAK-STAT pathways. Herein, we review the crucial roles of miR-340 in human cancers through the analysis of the latest research studies, with the aim of clarifying miR-340 function in malignant disease diagnosis, treatment, and prognosis, and to propose further investigations.
C1 [Huang, Zheng; Xu, Yesha; Wan, Maoping; Zeng, Xixi; Wu, Jianmin] Wenzhou Med Univ, Inst Genom Med, 1 Cent North Rd, Wenzhou 325035, Zhejiang, Peoples R China.
[Huang, Zheng] Chinese Univ Hong Kong, Dept Anesthesia & Intens Care, Hong Kong, Peoples R China.
C3 Wenzhou Medical University; Chinese University of Hong Kong
RP Wu, JM (corresponding author), Wenzhou Med Univ, Inst Genom Med, 1 Cent North Rd, Wenzhou 325035, Zhejiang, Peoples R China.
EM jianminwu81@hotmail.com
RI Zeng, Xixi/LZE-4162-2025
FU National Natural Sciences Foundation of China [NSFC-81472651]; Zhejiang
Provincial Natural Sciences Foundation [LY20H160016]
FX This work was supported by the National Natural Sciences Foundation of
China (grant NSFC-81472651) and Zhejiang Provincial Natural Sciences
Foundation (LY20H160016). We would like to thank Editage
(www.editage.cn) for English language editing.
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NR 118
TC 27
Z9 28
U1 0
U2 11
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-2288
J9 INT J BIOL SCI
JI Int. J. Biol. Sci.
PY 2021
VL 17
IS 1
BP 236
EP 246
DI 10.7150/ijbs.51123
PG 11
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA QL5MG
UT WOS:000621120800010
PM 33390846
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Subleski, JJ
Wiltrout, RH
Weiss, JM
AF Subleski, Jeff J.
Wiltrout, Robert H.
Weiss, Jonathan M.
TI Application of tissue-specific NK and NKT cell activity for tumor
immunotherapy
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE NK cells; NKT cells; Liver microenvironment; Immunotherapy; Cancer
ID NATURAL-KILLER-CELLS; APOPTOSIS-INDUCING LIGAND; IFN-GAMMA;
IMMUNE-RESPONSE; T-CELLS; IN-VIVO; ALPHA-GALACTOSYLCERAMIDE;
IMMUNOREGULATORY AXIS; RECEPTOR EXPRESSION; CRITICAL-APPRAISAL
AB Natural killer (NK) and NKT cells are a first line of defense against pathogens and transformed cells. However, dysregulation of their function can lead to autoimmune disease. A better understanding of the mechanisms controlling NK and NKT effector function should lead to the development of improved strategies for the treatment of many diseases. The site in which NK and NKT cells reside should be taken into account, because accumulating evidence suggests that the tissue microenvironment strongly influences their function. In this regard, the liver represents a unique immunologic organ in which the balance between the need for tolerance and the ability to respond rapidly to pathogens and tissue injury is tightly regulated. NK cells in the liver have augmented cytolytic activity as compared to other organs, which is consistent with a role for liver-associated NK cells in being critical effector cells for inhibiting tumor metastasis in the liver. Several studies also suggest that hepatic NKT cells have different functions than those in other organs. Whereas splenic and thymic NKT cells have been shown to suppress diabetes development, facilitate the induction of systemic tolerance and are regulated by IL-4 and other Th2 cytokines, certain subsets of NKT cells in the liver are important sources of Th1 cytokines such as Interferon gamma, and are the primary mediators of anti-tumor responses. The unique properties and roles as critical effector cells make NK and NKT cells within the liver microenvironment attractive targets of immunotherapeutic approaches that have the goal of controlling tumor metastasis in the liver. Published by Elsevier Ltd.
C1 [Subleski, Jeff J.; Wiltrout, Robert H.; Weiss, Jonathan M.] Natl Canc Inst, Canc & Inflammat Program, Ft Detrick, MD 21702 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI)
RP Weiss, JM (corresponding author), Natl Canc Inst, Canc & Inflammat Program, 1050 Boyles St, Ft Detrick, MD 21702 USA.
EM jsubleski@mail.ncifcrf.gov; wiltrour@mail.nih.gov; weissj@ncifcrf.gov
OI Subleski, Jeff/0000-0002-7442-1807
FU Intramural NIH HHS [Z99 CA999999] Funding Source: Medline
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NR 75
TC 44
Z9 51
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD NOV-DEC
PY 2009
VL 33
IS 3-4
SI SI
BP 275
EP 281
DI 10.1016/j.jaut.2009.07.010
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 534KZ
UT WOS:000272896800016
PM 19682859
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Moghadam, AR
Tutunchi, S
Namvaran-Abbas-Abad, A
Yazdi, M
Bonyadi, F
Mohajeri, D
Mazani, M
Marzban, H
Los, MJ
Ghavami, S
AF Moghadam, Adel Rezaei
Tutunchi, Soheil
Namvaran-Abbas-Abad, Ali
Yazdi, Mina
Bonyadi, Fatemeh
Mohajeri, Daryoush
Mazani, Mohammad
Marzban, Hassan
Los, Marek J.
Ghavami, Saeid
TI Pre-administration of turmeric prevents methotrexate-induced liver
toxicity and oxidative stress
SO BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
DE Lipid peroxides; Total antioxidant status; Antioxidant enzymes; Serum
liver biomarkers; Hepatocellular injury; Cell death
ID LIPID-PEROXIDATION; CURCUMA-LONGA; RHEUMATOID-ARTHRITIS; ANTIOXIDANT
ENZYMES; PROTECTIVE ROLE; INJURY; MECHANISMS; ACID; DISEASE;
TETRAHYDROCURCUMIN
AB Background: Methotrexate (MTX) is an antimetabolite broadly used in treatment of cancer and autoimmune diseases. MTX-induced hepatotoxicity limits its application. We investigated hepatoprotective effects of turmeric in MTX-induced liver toxicity.
Methods: All experiments were performed on male Wistar albino rats that were randomly divided into six groups. Group one received saline orally for 30 days (control group), groups two and three received turmeric extract (100, 200 mg/kg respectively) orally for 30 days, group four received single dose, of MTX IP at day 30, groups five and six received turmeric extract 100 and 200 mg/kg orally respectively for 30 days and single dose of methoterxate IP (20 mg/kg) at day 30. Four days after MTX injection animals were sacrificed and evaluated. Blood ALT and AST (indicators of hepatocyte injury), ALP and bilirubin (markers of biliary function), albumin (reflect liver synthetic function) as well as the plasma TAS concentration (antioxidant defenses) were determined. The cellular antioxidant defense activities were examined in liver tissue samples using SOD, CAT, and GSH-Px for the oxidative stress, and MDA for lipid peroxidation. In addition, liver damage was evaluated histopathologically.
Results: MTX significantly induced liver damage (P < 0.05) and decreased its antioxidant capacity, while turmeric was hepatoprotective. Liver tissue microscopic evaluation showed that MTX treatment induced severe centrilobular and periportal degeneration, hyperemia of portal vein, increased artery inflammatory cells infiltration and necrosis, while all of histopathological changes were attenuated by turmeric (200 mg/kg).
Conclusion: Turmeric extract can successfully attenuate MTX-hepatotoxicity. The effect is partly mediated through extract's antinflammatory activity.
C1 [Moghadam, Adel Rezaei; Tutunchi, Soheil] Islamic Azad Univ, Fac Vet Med, Tabriz Branch, Tabriz, Iran.
[Namvaran-Abbas-Abad, Ali] Islamic Azad Univ, Tabriz Branch, Young Researchers & Elite club, Tabriz, Iran.
[Namvaran-Abbas-Abad, Ali] Islamic Azad Univ, Tabriz Branch, Young Researchers & Elite club, Shiraz, Iran.
[Yazdi, Mina] Univ Tehran, Fac Vet Med, Tehran, Iran.
[Bonyadi, Fatemeh] Islamic Azad Univ, Fac Med, Tehran Branch, Tehran, Iran.
[Mohajeri, Daryoush] Islamic Azad Univ, Dept Pathobiol, Tabriz Branch, Tabriz, Iran.
[Mazani, Mohammad] Ardabil Univ Med Sci, Dept Biochem, Ardebil, Iran.
[Marzban, Hassan; Ghavami, Saeid] Univ Manitoba, Fac Hlth Sci, Coll Med, Dept Human Anat & Cell Sci, Winnipeg, MB, Canada.
[Ghavami, Saeid] Univ Manitoba, Fac Hlth Sci, Coll Med, Children Hosp Res Inst Manitoba, Winnipeg, MB, Canada.
[Los, Marek J.] Linkoping Univ, Dept Clin & Expt Med IKE, Div Cell Biol, Linkoping, Sweden.
[Los, Marek J.] Linkoping Univ, Integrat Regenerat Med Ctr IGEN, Linkoping, Sweden.
[Los, Marek J.] Pomeranian Med Univ, Dept Pathol, Szczecin, Poland.
[Los, Marek J.] Med Univ Silesia, Sch Med, ENT Dept, Katowice, Poland.
[Ghavami, Saeid] Shiraz Med Univ, Ctr Hlth Policy Res, Shiraz, Iran.
C3 Islamic Azad University; Islamic Azad University; Islamic Azad
University; University of Tehran; Islamic Azad University; Islamic Azad
University; Ardabil University of Medical Sciences; University of
Manitoba; University of Manitoba; Children's Hospital Research Institute
of Manitoba; Linkoping University; Linkoping University; Pomeranian
Medical University; Medical University Silesia; Shiraz University of
Medical Science
RP Los, MJ (corresponding author), Linkoping Univ, Dept Clin & Expt Med IKE, Div Cell Biol, Linkoping, Sweden.
EM marek.los@liu.se; saeid.Ghavami@gmail.com
RI mazani, mohammad/J-5080-2017; Łos, Marek/C-4038-2013; Mohajeri,
Daryoush/Z-4581-2019; Ghavami, Saeid/Q-8918-2016; Abad, Ali/O-9915-2014
OI Ghavami, Saeid/0000-0001-5948-508X; Mohajeri,
Daryoush/0000-0002-1635-081X; mazani, mohammad/0000-0001-9537-8572; Los,
Marek/0000-0001-9518-1411
FU University of Manitoba start-up fund; Linkoping University; IGEN;
Cancerfonden [2013/391]; VR-NanoVision [K2012-99X-22325-01-5]
FX SG was supported by University of Manitoba start-up fund. MJ Los kindly
acknowledges the core/startup support from Linkoping University, from
IGEN, from Cancerfonden (2013/391), and from VR-NanoVision
(K2012-99X-22325-01-5).
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NR 88
TC 79
Z9 82
U1 0
U2 21
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1472-6882
J9 BMC COMPLEM ALTERN M
JI BMC Complement. Altern. Med.
PD JUL 22
PY 2015
VL 15
AR 246
DI 10.1186/s12906-015-0773-6
PG 13
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA CN1SX
UT WOS:000358201500004
PM 26199067
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Guo, XH
Zheng, BW
Wang, JH
Zhao, TJ
Zheng, Y
AF Guo, Xinhua
Zheng, Bowen
Wang, Jiahui
Zhao, Tiejian
Zheng, Yang
TI Exploring the mechanism of action of Chinese medicine in regulating
liver fibrosis based on the alteration of glucose metabolic pathways
SO PHYTOTHERAPY RESEARCH
LA English
DT Review
DE Chinese medicine; glucose metabolism reprogramming; liver fibrosis
ID HEPATIC STELLATE CELLS; PYRUVATE-KINASE M2; HYPOXIA-INDUCED INJURY;
GROWTH-FACTOR; POSITIVE REGULATION; CANCER; ACTIVATION; EXPRESSION;
GLYCOLYSIS; HEDGEHOG
AB In recent years, metabolic reprogramming in liver fibrosis has become a research hotspot in the field of liver fibrosis at home and abroad. Liver fibrosis is a pathological change caused by chronic liver injury from a variety of causes. Liver fibrosis is a common pathological feature of many chronic liver diseases such as chronic hepatitis B, non-alcoholic steatohepatitis, and autoimmune hepatitis, as well as the pathogenesis of the disease. The development of chronic liver disease into cirrhosis must go through the pathological process of liver fibrosis, in which hepatic stellate cells (HSC) play an important role. Following liver injury, HSC are activated and transdifferentiated into scar-forming myofibroblasts, which drive the trauma healing response and which rely on the deposition of collagen-rich extracellular matrix to maintain tissue integrity. This reaction will continue without strict control, which will lead to excessive accumulation of matrix and liver fibrosis. The mechanisms and clinical studies of liver fibrosis have been the focus of research in liver diseases. In recent years, several studies have revealed the mechanism of HSC metabolic reprogramming and the impact of this process on liver fibrosis, in which glucose metabolic reprogramming plays an important role in the activation of HSC, and it mainly meets the energy demand of HSC activation by upregulating glycolysis. Glycolysis is the process by which one molecule of glucose is broken down into two molecules of pyruvate and produces energy and lactate under anaerobic conditions. Various factors have been found to be involved in regulating the glycolytic process of HSC, including glucose transport, intracellular processing of glucose, exosome secretion, and lactate production, etc. Inhibition of the glycolytic process of HSC can be an effective strategy against liver fibrosis. Currently, the combined action of multiple targets and links of Chinese medicine such as turmeric, comfrey, rhubarb and scutellaria baicalensis against the mechanism of liver fibrosis can effectively improve or even reverse liver fibrosis. This paper summarizes that turmeric extract curcumin, comfrey extract comfreyin, rhubarb, Subtle yang yu yin granules, Scutellaria baicalensis extract oroxylin A and cardamom extract cardamomin affect liver fibrosis by regulating gluconeogenic reprogramming. Therefore, studying the mechanism of action of TCM in regulating liver fibrosis through reprogramming of glucose metabolism is promising to explore new methods and approaches for Chinese Medicine modernization research.
C1 [Guo, Xinhua; Zheng, Bowen; Zhao, Tiejian] Guangxi Univ Chinese Med, Coll Basic Med, Dept Physiol, Nanning, Peoples R China.
[Wang, Jiahui; Zheng, Yang] Guangxi Univ Chinese Med, Fac Chinese Med Sci, Dept Med, Nanning 530021, Peoples R China.
C3 Guangxi University of Chinese Medicine; Guangxi University of Chinese
Medicine
RP Zheng, Y (corresponding author), Guangxi Univ Chinese Med, Fac Chinese Med Sci, Dept Med, Nanning 530021, Peoples R China.
EM zhengy@gxtcmu.edu.cn
RI Zheng, Bowen/GRS-9430-2022; guo, xin/KRP-4196-2024
OI zheng, yang/0000-0001-7646-511X; Xinhua, Guo/0000-0002-5585-3188
FU National Natural Science Foundation of China [81660705, 81960761,
81960751, 82204755]; Guangxi Young and Middle-aged Teachers & Research
Ability Improvement Project [2022KY1667]; Guangxi
ZhuangyaoPharmaceutical Key Laboratory [GXZYZZ2020-07, GXZYZZ2019-1];
Guangxi Natural Science Foundation Youth Project [2020GXNSFBA297094];
Guangxi University of Traditional Chinese Medicine School-levelProject
Youth Fund [2020QN006]; Faculty of Chinese Medicine Science Guangxi
University of Chinese Medicine Research Project [2022QJ001, 2022MS008]
FX National Natural Science Foundation of China,Grant/Award Numbers:
81660705, 81960761, 81960751, 82204755; Guangxi Young and Middle-aged
Teachers & Research Ability Improvement Project, Grant/Award
Number:2022KY1667; Guangxi ZhuangyaoPharmaceutical Key Laboratory,
Grant/AwardNumbers: GXZYZZ2020-07, GXZYZZ2019-1;Guangxi Natural Science
Foundation Youth Project, Grant/Award Number:2020GXNSFBA297094; Guangxi
University of Traditional Chinese Medicine School-levelProject Youth
Fund, Grant/Award Number:2020QN006; Faculty of Chinese Medicine Science
Guangxi University of Chinese Medicine Research Project,
Grant/AwardNumbers: 2022QJ001, 2022MS008
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NR 105
TC 5
Z9 6
U1 5
U2 38
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0951-418X
EI 1099-1573
J9 PHYTOTHER RES
JI Phytother. Res.
PD OCT
PY 2024
VL 38
IS 10
SI SI
BP 4865
EP 4876
DI 10.1002/ptr.7667
EA NOV 2022
PG 12
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA K4F8O
UT WOS:000890229800001
PM 36433866
DA 2025-01-07
ER
PT J
AU Díaz, LA
Villota-Rivas, M
Barrera, F
Lazarus, JV
Arrese, M
AF Diaz, Luis Antonio
Villota-Rivas, Marcela
Barrera, Francisco
V. Lazarus, Jeffrey
Arrese, Marco
TI The burden of liver disease in Latin America
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Public policy; Cirrhosis; Alcohol; Alcohol-related liver disease; ARLD;
Alcohol use disorder; Steatosis; Steatotic liver disease; NAFLD; MASLD;
MASH
ID PRIMARY BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE
HEPATITIS; HISPANIC PATIENTS; NAFLD PREVALENCE; RISK-FACTORS; PNPLA3;
TRANSPLANTATION; ASSOCIATION; COUNTRIES
AB Liver disease poses a substantial burden in Latin America. This burden is primarily attributed to a high level of alcohol consumption and the increasing prevalence of risk factors associated with metabolic dysfunctionassociated steatotic liver disease (MASLD), such as sedentary lifestyles, easy access to ultra-processed foods, obesity, and type 2 diabetes mellitus. These epidemiological trends are cause for concern, especially considering that there are significant challenges in addressing them due to disparities in access to liver disease screening and care. In this article, we aim to provide an overview of the current situation regarding liver disease in Latin America. We also discuss recent multinational proposals designed to address the growing MASLD burden via its integration into existing non-communicable diseases policies, at both local and global levels. Additionally, we emphasize the urgent need to establish effective public health policies that target both MASLD risk factors and excessive alcohol consumption. Furthermore, we discuss the development of liver transplantation programs, areas for improvement in medical education and research capabilities, and how the fostering of extensive collaboration among all stakeholders is crucial for addressing liver disease in the region. (c) 2023 Fundaci & oacute;n Cl & iacute;nica M & eacute;dica Sur, A.C. Published by Elsevier Espa & ntilde;a, S.L.U. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)
C1 [Diaz, Luis Antonio; Barrera, Francisco; Arrese, Marco] Pontificia Univ Catolica Chile, Escuela Med, Dept Gastroenterol, Santiago, Chile.
[Diaz, Luis Antonio; Barrera, Francisco; Arrese, Marco] Observ Multicentr Enfermedades Gastrointestinales, Santiago, Chile.
[Villota-Rivas, Marcela; V. Lazarus, Jeffrey] Univ Barcelona, Hosp Clin, Barcelona Inst Global Hlth ISGlobal, Barcelona, Spain.
[V. Lazarus, Jeffrey] CUNY, Grad Sch Publ Hlth & Hlth Policy CUNY SPH, New York, NY USA.
[V. Lazarus, Jeffrey; Arrese, Marco] Global NASH Council, Washington, DC 20037 USA.
C3 Pontificia Universidad Catolica de Chile; ISGlobal; University of
Barcelona; Hospital Clinic de Barcelona; City University of New York
(CUNY) System
RP Arrese, M (corresponding author), Pontificia Univ Catolica Chile, Escuela Med, Dept Gastroenterol, Santiago, Chile.; Arrese, M (corresponding author), Observ Multicentr Enfermedades Gastrointestinales, Santiago, Chile.; Arrese, M (corresponding author), Global NASH Council, Washington, DC 20037 USA.
EM marrese@uc.cl
RI ARRESE, MARCO/ABB-9061-2021; Villota-Rivas, Marcela/CAJ-5665-2022;
Lazarus, Jeffrey V./R-6248-2018
OI Lazarus, Jeffrey V./0000-0001-9618-2299; Villota-Rivas,
Marcela/0000-0002-7332-735X
FU European Union [825510]; MCIN/AEI [CEX2018-000806-S]; Generalitat de
Catalunya through the CERCA Program
FX This project has received partial funding from the European Union's
Horizon 2020 Research and Innovation Programme under grant agreement no.
825510. M.V.-R. and J.V.L. acknowledge support to ISGlobal from the
grant CEX2018-000806-S, funded by MCIN/AEI/10.13039/501100011033, and
the 'Generalitat de Catalunya', through the CERCA Program, outside of
the submitted work.
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WHO, Implementation roadmap 2023-2030 for the global action plan for the prevention and control of noncommunicable diseases 2013-2030
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worldbank, World Bank Open Data
Younossi Z, 2019, HEPATOLOGY, V69, P2672, DOI 10.1002/hep.30251
NR 146
TC 4
Z9 5
U1 2
U2 2
PU ELSEVIER ESPANA
PI MADRID
PA CALLE DE ZURBANO, 76-4TH FLR LEFT, MADRID, 28010, SPAIN
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD MAY-JUN
PY 2024
VL 29
IS 3
AR 101175
DI 10.1016/j.aohep.2023.101175
EA APR 2024
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA SN4X8
UT WOS:001235129200001
PM 37922988
OA gold
DA 2025-01-07
ER
PT J
AU Biewenga, M
Verhelst, X
Baven-Pronk, M
Putter, H
van den Berg, A
Colle, I
Schouten, J
Sermon, F
Van Steenkiste, C
van Vlierberghe, H
van der Meer, A
van Hoek, B
AF Biewenga, Maaike
Verhelst, Xavier
Baven-Pronk, Martine
Putter, Hein
van den Berg, Aad
Colle, Isabelle
Schouten, Jeoffrey
Sermon, Filip
Van Steenkiste, Christophe
van Vlierberghe, Hans
van der Meer, Adriaan
van Hoek, Bart
CA Dutch Autoimmune Hepatitis Study G
TI Aminotransferases During Treatment Predict Long-Term Survival in
Patients With Autoimmune Hepatitis Type 1: A Landmark Analysis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Long Term Survival; Biochemical Remission; Treatment Response;
Immunoglobulin G
ID HEPATOCELLULAR-CARCINOMA; BIOCHEMICAL REMISSION; DISEASE COURSE;
WITHDRAWAL; CIRRHOSIS; THERAPY; RELAPSE
AB BACKGROUND & AIMS: Biochemical remission, important treatment goal in autoimmune hepatitis (AIH), has been associated with better long-term survival. The aim of this study was to determine the independent prognostic value of aminotransferases and immunoglobulin G (IgG) during treatment on long-term transplant-free survival in AIH.
METHODS: In a multicenter cohort alanine aminotransferase, aspartate aminotransferase (AST), and IgG were collected at diagnosis and 6, 12, 24, and 36 months after start of therapy and related to long-term outcome using Kaplan-Meier survival and Cox regression analysis with landmark analysis at these time points, excluding patients with follow-up ending before each landmark.
RESULTS: A total of 301 AIH patients with a median follow-up of 99 (range, 7-438) months were included. During follow-up, 15 patients required liver transplantation and 33 patients died. Higher AST at 12 months was associated with worse survival (hazard ratio [HR], 1.86; P <.001), while IgG was not associated with survival (HR, 1.30; P =.53). In multivariate analysis AST at 12 months (HR, 2.13; P <.001) was predictive for survival independent of age, AST at diagnosis and cirrhosis. Multivariate analysis for AST yielded similar results at 6 months (HR, 2.61; P =.001), 24 months (HR, 2.93; P =.003), and 36 months (HR, 3.03; P =.010). There was a trend toward a worse survival in patients with mildly elevated aminotransferases (1-1.53 upper limit of normal) compared with patients with normal aminotransferases (P =.097).
CONCLUSIONS: Low aminotransferases during treatment are associated with a better long-term survival in autoimmune hepatitis. IgG was not associated with survival in first 12 months of treatment. Normalization of aminotransferases should be the treatment goal for autoimmune hepatitis to improve long-term survival.
C1 [Biewenga, Maaike; Schouten, Jeoffrey; van Hoek, Bart] Leiden Univ, Med Ctr, Dept Gastroenterol & Hepatol, C4-P,POB 9600, NL-2300 RC Leiden, Netherlands.
[Verhelst, Xavier; van Vlierberghe, Hans] UZ Ghent, Dept Gastroenterol & Hepatol, Ghent, Belgium.
[Verhelst, Xavier; van Vlierberghe, Hans] European Reference Network RARE LIVER, Ghent, Belgium.
[Baven-Pronk, Martine] Green Heart Hosp, Dept Gastroenterol & Hepatol, Gouda, Netherlands.
[Putter, Hein] Leiden Univ, Med Ctr, Dept Biomed Data Sci, Leiden, Netherlands.
[van den Berg, Aad] Univ Med Ctr Groningen, Dept Gastroenterol & Hepatol, Groningen, Netherlands.
[van den Berg, Aad] European Reference Network RARE LIVER, Groningen, Netherlands.
[Colle, Isabelle] ASZ Aalst, Dept Gastroenterol & Hepatol, Aalst, Belgium.
AZ Nikolaas, Dept Gastroenterol & Hepatol, St Niklaas, Belgium.
[Sermon, Filip] OLV Aalst, Dept Gastroenterol & Hepatol, Aalst, Belgium.
[Van Steenkiste, Christophe] AZ Maria Middelares Ghent, Dept Gastroenterol & Hepatol, Ghent, Belgium.
[Van Steenkiste, Christophe] Univ Hosp Antwerp, Dept Gastroenterol & Hepatol, Antwerp, Belgium.
[van der Meer, Adriaan] Erasmus MC, Dept Gastroenterol & Hepatol, Rotterdam, Netherlands.
C3 Leiden University - Excl LUMC; Leiden University; Leiden University
Medical Center (LUMC); Ghent University; Ghent University Hospital;
Leiden University - Excl LUMC; Leiden University; Leiden University
Medical Center (LUMC); University of Groningen; University of Antwerp;
Erasmus University Rotterdam; Erasmus MC
RP van Hoek, B (corresponding author), Leiden Univ, Med Ctr, Dept Gastroenterol & Hepatol, C4-P,POB 9600, NL-2300 RC Leiden, Netherlands.
EM b.van_hoek@lumc.nl
RI van der Meer, Adriaan/HTO-1167-2023; Verhelst, Xavier/ABF-6965-2021; van
Hoek, Bart/AAU-8953-2020; de Boer, Ynto/D-9242-2013; Putter,
Hein/C-2244-2018
OI van Hoek, Bart/0000-0001-6527-764X; Van Vlierberghe,
Hans/0000-0003-0647-9238; de Boer, Ynto/0000-0002-4066-7593; Putter,
Hein/0000-0001-5395-1422; Drenth, Joost PH/0000-0001-8027-3073;
Verhelst, Xavier/0000-0002-2798-5415; Van Steenkiste,
Christophe/0000-0001-5167-744X
FU Zambon Pharma
FX Maaike Biewenga was supported by an unrestricted grant from Zambon
Pharma.
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NR 29
TC 11
Z9 11
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD AUG
PY 2022
VL 20
IS 8
BP 1776
EP +
DI 10.1016/j.cgh.2021.05.024
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 8R8WW
UT WOS:000928169700015
PM 34022454
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Holick, MF
AF Holick, Michael F.
TI Vitamin D: Evolutionary, Physiological and Health Perspectives
SO CURRENT DRUG TARGETS
LA English
DT Review
DE Vitamin D; sunlight; 25-hydroxyvitamin D; 1,25-dihydroxyvitamin D;
skeleton; cancer; diabetes; vitamin D deficiency; autoimmune disease
ID ULTRAVIOLET-B IRRADIANCE; 3RD NATIONAL-HEALTH; D DEFICIENCY;
HYPOVITAMINOSIS-D; 1,25-DIHYDROXYVITAMIN D-3; CANCER INCIDENCE; SUN
EXPOSURE; SERUM 25-HYDROXYVITAMIN-D; D SUPPLEMENTATION; BREAST-CANCER
AB Vitamin D, the sunshine vitamin, has been important not only for the evolution of a healthy calcified vertebrate skeleton but it also evolved into a hormone that has a wide diversity of biologic effects. During exposure to sunlight the ultraviolet B radiation converts 7-dehydrocholesterol to previtamin D-3 which in turn rapidly isomerizes to vitamin D-3. Once formed, vitamin D-3 is metabolized in the liver to 25-hydroxyvitamin D3 and in the kidneys to its active form 1,25-dihydroxyvitamin D-3. 1,25-dihydroxyvitamin D-3 interacts with its vitamin D receptor in calcium regulating tissues to regulate calcium metabolism and bone health. It is now recognized that most cells in the body have a vitamin D receptor and they also have the capability of producing 1,25-dihydroxyvitamin D-3 which in turn is capable of regulating a wide variety of genes that have important functions in regulating cell growth, modulating immune function and cardiovascular health. Epidemiologic evidence and prospective studies have linked vitamin D deficiency with increased risk of many chronic diseases including autoimmune diseases, cardiovascular disease, deadly cancers, type II diabetes and infectious diseases. Vitamin D deficiency and insufficiency have been defined as a 25-hydroxyvitamin D <20 ng/ml and 21-29 ng/ml respectively. For every 100 IU of vitamin D ingested the blood level of 25-hydroxyvitamin D, the measure vitamin D status, increases by similar to 1 ng/ml. It is estimated that children need at least 400-1000 IU of vitamin D a day while teenagers and adults need at least 2000 IU of vitamin D a day to satisfy their body's vitamin D requirement. It is estimated that 1 billion people worldwide are vitamin D deficient or insufficient. Correcting and preventing this deficiency could have an enormous impact on reducing health costs worldwide.
C1 Boston Univ, Sch Med, Med Ctr,Vitamin Skin & Bone Res Lab D, Dept Med,Sect Endocrinol Nutr & Diabet, Boston, MA 02118 USA.
C3 Boston University
RP Holick, MF (corresponding author), Boston Univ, Sch Med, Med Ctr,Vitamin Skin & Bone Res Lab D, Dept Med,Sect Endocrinol Nutr & Diabet, 85 E Newton St,M-1013, Boston, MA 02118 USA.
EM mfholick@bu.edu
RI Holick, Michael/AFG-9586-2022
OI Holick, Michael/0000-0001-6023-9062
FU NIH grants 1UL1RR025771 and the UV Foundation. [1UL1RR025771]; UV
Foundation
FX This work was supported in part by NIH grants 1UL1RR025771 and the UV
Foundation.
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NR 104
TC 241
Z9 282
U1 2
U2 65
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-4501
EI 1873-5592
J9 CURR DRUG TARGETS
JI Curr. Drug Targets
PD JAN
PY 2011
VL 12
IS 1
BP 4
EP 18
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 692WJ
UT WOS:000285186300002
PM 20795941
DA 2025-01-07
ER
PT J
AU Xia, XF
Liang, C
Liu, H
Xue, F
Hu, QD
Chen, W
Ma, T
Zhang, Y
Bai, XL
Liang, TB
AF Xia, Xuefeng
Liang, Chao
Liu, Hao
Xue, Fei
Hu, Qida
Chen, Wei
Ma, Tao
Zhang, Yun
Bai, Xueli
Liang, Tingbo
TI Effects of Trichostatin A in a Rat Model of Acute Graft-Versus-Host
Disease After Liver Transplantation
SO TRANSPLANTATION
LA English
DT Article
DE Liver transplantation (LTx); Acute graft-versus-host disease (aGVHD);
CD4(+)CD25(+) regulatory T cell (Treg); Foxp3; Trichostatin A (TSA)
ID REGULATORY T-CELLS; HISTONE-DEACETYLASE INHIBITORS; MATCHING RATS;
TOLERANCE; CANCER; EXPRESSION; RAPAMYCIN; DRUGS
AB Background. Acute graft-versus-host disease (aGVHD) is a rare but serious and life-threatening complication of liver transplantation (LTx). Previously, we have demonstrated that the development of aGVHD after LTx (LTx-aGVHD) is associated with a decreased percentage of regulatory T cells (Tregs) in the peripheral blood of recipients. Histone deacetylase inhibitors promote the production of Tregs and some, such as suberoylanilide hydroxamic acid and trichostatin A (TSA), are used to treat autoimmune diseases, including GVHD after bone marrow transplantation.
Methods. In this study, LTx-aGVHD rats were treated with TSA continuously for 7 days from day 8 to 14 after LTx. Subsequently, splenic T cells were used for in vitro investigations of the mechanism of action of transplantation.
Results. All LTx-aGVHD rats developed typical LTx-aGVHD symptoms after TSA treatment and died from LTx-aGVHD. The percentage frequency of Tregs in peripheral blood mononuclear cells was slightly up-regulated after TSA treatment, whereas TSA dramatically down-regulated Foxp3 protein and mRNA levels both in vivo and in vitro. Furthermore, TSA impaired T-cell proliferation and production of proinflammatory and anti-inflammatory cytokines in vitro.
Conclusion. TSA does not abrogate LTx-aGVHD in rats due to down-regulation of Tregs.
C1 [Xia, Xuefeng; Liang, Chao; Liu, Hao; Hu, Qida; Chen, Wei; Ma, Tao; Zhang, Yun; Bai, Xueli; Liang, Tingbo] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Surg, Hangzhou 310009, Zhejiang, Peoples R China.
[Xue, Fei] Henan Prov Peoples Hosp, Organ Transplantat Ctr, Dept Hepatobiliary & Pancreat Surg, Zhengzhou, Henan Province, Peoples R China.
C3 Zhejiang University; Zhengzhou University
RP Liang, TB (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Surg, Hangzhou 310009, Zhejiang, Peoples R China.
EM liangtingbo@zju.edu.cn
RI Liang, Tingbo/IVV-7969-2023; Li, xiaotong/GYV-4890-2022; Chen,
Wei/X-6211-2019; Hu, Qida/B-4558-2009
OI Hu, Qida/0000-0002-9092-7808
FU National Science Fund for Distinguished Young Scholars [30925033];
National Natural Science Foundation of China [81273260]; Zhejiang
Provincial Program for the Cultivation of High-Level Innovative Health
Talents
FX This work was supported by the National Science Fund for Distinguished
Young Scholars (No. 30925033), the National Natural Science Foundation
of China (No. 81273260), and the Zhejiang Provincial Program for the
Cultivation of High-Level Innovative Health Talents.
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NR 38
TC 5
Z9 7
U1 0
U2 20
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD JUL 15
PY 2013
VL 96
IS 1
BP 25
EP 33
DI 10.1097/TP.0b013e318295c04d
PG 9
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA 299EJ
UT WOS:000330378000006
PM 23694951
OA Bronze
DA 2025-01-07
ER
PT J
AU Chen, ZX
Shao, JG
Shen, Y
Zhang, J
Hua, Y
Wang, LJ
Qin, G
AF Chen, Zhi-Xian
Shao, Jian-Guo
Shen, Yi
Zhang, Jian
Hua, Yu
Wang, Lu-Jun
Qin, Gang
TI Prognostic Implications of Antibodies to Soluble Liver Antigen in
Autoimmune Hepatitis A PRISMA-Compliant Meta-Analysis
SO MEDICINE
LA English
DT Review
ID TERM-FOLLOW-UP; HEPATOCELLULAR-CARCINOMA; AUTOANTIBODIES; SLA/LP;
SPECIFICITY; PANCREAS; MARKERS; DISEASE
AB Prognostic evaluation is important for the management of patients with autoimmune hepatitis (AIH). Although some autoantibodies have been associated with disease activity and outcomes, the implication of antibodies to soluble liver antigen (anti-SLA) remains controversial.To conduct a meta-analysis of observational studies which addressed differences in clinical characteristics by anti-SLA status in patients with AIH.Three databases PUBMED, EMBASE, and OVID were systemically searched up to January 2015 using the terms soluble liver antigen or liver-pancreas antigen and autoimmune hepatitis with restriction to English-language.Studies were included if at least 50 patients with objective diagnosis of AIH were enrolled, anti-SLA detection was performed for the patients, and prognostic outcomes and/or disease severity were reported.Two investigators independently reviewed retrieved literature and evaluated eligibility. Discrepancy was resolved by discussion and a third investigator. Quality of included studies was evaluated using Newcastle-Ottawa Quality Assessment Scale (NOS). Data were pooled using fixed-effect or random-effect models.Prognostic outcomes included death from hepatic failure or requirement for liver transplantation, and responses to immunosuppressive therapy regarding remission or relapse. Results were combined on the odds ratio (OR) or standardized mean difference (SMD) scales.Eight studies were enrolled in this study, involving a total of 1297 AIH patients among whom 195 with anti-SLA. Pooled serum AST levels tended to be lower in anti-SLA seropositive patients. The presence of anti-SLA conferred 3.1-fold increased risk of hepatic death in AIH patients. The remission rates were comparable between anti-SLA seropositive and seronegative AIH patients, while anti-SLA positivity was associated with nearly 2-fold increased risk of relapse after drug withdrawal. Human leukocyte antigen (HLA) allotype DR3 was positively associated with anti-SLA.Antibodies to SLA may be an indicator of increased risks of hepatic death and treatment relapse for AIH patients. Our findings suggest that the anti-SLA seropositive patients should be maintained indefinitely on individually adjusted medication to improve their prognosis.
C1 [Chen, Zhi-Xian] Nantong Hlth Coll Jiangsu Prov, Dept Clin Pharm, Nantong, Peoples R China.
[Shao, Jian-Guo; Hua, Yu; Wang, Lu-Jun; Qin, Gang] Nantong Univ, Nantong Peoples Hosp 3, Ctr Liver Dis, Nantong 226006, Jiangsu, Peoples R China.
[Shen, Yi; Zhang, Jian] Nantong Univ, Dept Epidemiol & Med Stat, Nantong 226006, Jiangsu, Peoples R China.
C3 Nantong University; Nantong University
RP Qin, G (corresponding author), Nantong Univ, Nantong Peoples Hosp 3, Ctr Liver Dis, 99 Mid Youth Rd, Nantong 226006, Jiangsu, Peoples R China.
EM ljwang@ntu.edu.cn; tonygqin@ntu.edu.cn
RI Qin, Gang/AFV-1685-2022
OI Qin, Gang/0000-0002-4363-2572
FU Natural Science Foundation of Jiangsu Province, China [BK2012653];
National Natural Science Foundation of China (NSFC) [81370520];
Department of Health, Jiangsu Province, China [Q201208]
FX This study was supported in part by grant number BK2012653 from the
Natural Science Foundation of Jiangsu Province, China, by grant number
81370520 from National Natural Science Foundation of China (NSFC), and
by the Young Investigator Grant number Q201208 from the Department of
Health, Jiangsu Province, China.
CR [Anonymous], HEPATOL RES
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NR 30
TC 10
Z9 13
U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD JUN
PY 2015
VL 94
IS 23
AR e953
DI 10.1097/MD.0000000000000953
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA CQ6MU
UT WOS:000360719300001
PM 26061326
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Moriya, K
Sato, S
Nishimura, N
Kawaratani, H
Takaya, H
Kaji, K
Namisaki, T
Uejima, M
Nagamatsu, S
Matsuo, H
Yoshiji, H
AF Moriya, Kei
Sato, Shinya
Nishimura, Norihisa
Kawaratani, Hideto
Takaya, Hiroaki
Kaji, Kosuke
Namisaki, Tadashi
Uejima, Masakazu
Nagamatsu, Shinsaku
Matsuo, Hideki
Yoshiji, Hitoshi
TI Efficacy of Serum Ferritin-Zinc Ratio for Predicting Advanced Liver
Fibrosis in Patients with Autoimmune Hepatitis
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE autoimmune hepatitis; zinc; ferritin; liver fibrosis; biomarker
ID SIMPLE NONINVASIVE INDEX; C PATIENTS; ACCURACY; OUTCOMES; DISEASE
AB Background/Aims: The search for noninvasive biomarkers that can efficiently estimate the extent of liver fibrosis progression is ongoing. Although Fibrosis-4 (FIB-4), the aspartate transaminase-to-platelet ratio index (APRI), and the Forns index have been reported as useful biomarkers, their investigation in autoimmune hepatitis (AIH) is limited. This study aimed to examine the usefulness of these serological indices and a newly developed index in predicting liver fibrosis progression in AIH. Methods: The study analyzed data from 190 patients diagnosed with AIH at our institution between 1990 and 2015. Their histological liver fibrosis progression and clinical long-term prognosis were evaluated retrospectively (cohort 1). In 90 patients, receiver operating characteristic (ROC) curves were compared to choose severe fibrosis cases with respect to existing indices (FIB-4, APRI, and Forns index) and the ferritin-zinc ratio (cohort 2). Results: In cohort 1, liver-related death and hepatocellular carcinoma rates were significantly higher in the severe (n = 27) than in the mild (n = 63) fibrosis group (p = 0.0001 and 0.0191, respectively). In cohort 2, liver-related death in the severe fibrosis group was significantly frequent (p = 0.0071), and their ferritin-zinc ratio was higher (median 2.41 vs. 0.62, p = 0.0011). ROC analyses were performed to compare the ability of the ferritin-zinc ratio, FIB-4, APRI, and the Forns index to predict severe and mild fibrosis. Accordingly, areas under the ROC were 0.732, 0.740, 0.721, and 0.729, respectively. Conclusions: The serum ferritin-zinc ratio can noninvasively predict liver fibrosis progression in AIH and be applied to predict long-term prognosis.
C1 [Moriya, Kei; Sato, Shinya; Nishimura, Norihisa; Kawaratani, Hideto; Takaya, Hiroaki; Kaji, Kosuke; Namisaki, Tadashi; Uejima, Masakazu; Nagamatsu, Shinsaku; Matsuo, Hideki; Yoshiji, Hitoshi] Nara Med Univ, Dept Gastroenterol, Kashihara 6348521, Japan.
[Moriya, Kei; Uejima, Masakazu; Nagamatsu, Shinsaku; Matsuo, Hideki] Nara Prefecture Gen Med Ctr, Dept Gastroenterol, 897-5, 2-Chome, Shichijo Nishimachi, Nara 6308581, Japan.
C3 Nara Medical University
RP Moriya, K (corresponding author), Nara Med Univ, Dept Gastroenterol, Kashihara 6348521, Japan.
EM moriyak@naramed-u.ac.jp; shinyasato@naramed-u.ac.jp;
nishimuran@naramed-u.ac.jp; kawara@naramed-u.ac.jp;
htky@naramed-u.ac.jp; kajik@naramed-u.ac.jp; tadashin@naramed-u.ac.jp;
m3m16d333@yahoo.co.jp; joe.montana.no16@gmail.com; h.matsuo@nara-hp.jp;
yoshijih@naramed-u.ac.jp
RI Nishimura, Norihisa/AAC-1300-2021
OI Yoshiji, Hitoshi/0000-0002-5243-8544; Namisaki,
Tadashi/0000-0002-3158-5318; Kawaratani, Hideto/0000-0002-4361-0592;
Nishimura, Norihisa/0000-0002-6295-3283
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NR 41
TC 0
Z9 0
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD JUL
PY 2023
VL 12
IS 13
AR 4463
DI 10.3390/jcm12134463
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA M2NY2
UT WOS:001028611700001
PM 37445498
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Chen, XJ
Wang, ZY
Han, S
Wang, Z
Zhang, Y
Li, XD
Xia, N
Yu, WJ
Jia, CY
Ni, Y
Pu, LY
AF Chen, Xuejiao
Wang, Ziyi
Han, Sheng
Wang, Zeng
Zhang, Yu
Li, Xiangdong
Xia, Nan
Yu, Wenjie
Jia, Chenyang
Ni, Yong
Pu, Liyong
TI Targeting SYK of monocyte-derived macrophages regulates liver fibrosis
via crosstalking with Erk/Hif1α and remodeling liver inflammatory
environment
SO CELL DEATH & DISEASE
LA English
DT Article
ID TYROSINE KINASE SYK; ACTIVATION; HYPOXIA; INHIBITION; INJURY
AB Liver fibrosis is a danger signal indicating a huge risk of liver cancer occurrence, but there is still no effective clinical means to regulate the progress of liver fibrosis. Although a variety of drugs targeting SYK have been developed for tumors and autoimmune diseases, the mechanism and specific efficacy of SYK's role in liver fibrosis are not yet clear. Our studies based on chronic CCL4, bile duct ligation, and subacute TAA mouse models show that SYK in monocyte-derived macrophages (MoMFs) is fully dependent on phosphorylation of Erk to up-regulate the expression of Hif1 alpha, thereby forming the crosstalk with SYK to drive liver fibrosis progress. We have evaluated the ability of the small molecule SYK inhibitor GS9973 in a variety of models. Contrary to previous impressions, high-frequency administration of GS9973 will aggravate CCL4-induced liver fibrosis, which is especially unsuitable for patients with cholestasis whose clinical features are bile duct obstruction. In addition, we found that inhibition of MoMFs SYK impairs the expression of CXCL1, on one hand, it reduces the recruitment of CD11bhiLy6Chi inflammatory cells, and on the other hand, it promotes the phenotype cross-dress process of pro-resolution MoMFs, thereby remodeling the chronic inflammatory environment of the fibrotic liver. Our further findings indicate that on the basis of the administration of CCR2/CCR5 dual inhibitor Cenicriviroc, further inhibiting MoMFs SYK may give patients with fibrosis additional benefits.
C1 [Chen, Xuejiao; Wang, Ziyi; Han, Sheng; Wang, Zeng; Zhang, Yu; Li, Xiangdong; Xia, Nan; Yu, Wenjie; Pu, Liyong] Nanjing Med Univ, Affiliated Hosp 1, Hepatobiliary Ctr, Nanjing, Peoples R China.
[Chen, Xuejiao; Wang, Ziyi; Han, Sheng; Wang, Zeng; Zhang, Yu; Li, Xiangdong; Xia, Nan; Yu, Wenjie; Pu, Liyong] Chinese Acad Med Sci, Key Lab Liver Transplantat, Nanjing, Peoples R China.
[Chen, Xuejiao; Wang, Ziyi; Han, Sheng; Wang, Zeng; Zhang, Yu; Li, Xiangdong; Xia, Nan; Yu, Wenjie; Pu, Liyong] Nanjing Med Univ, NHC Key Lab Living Donor Liver Transplantat, Nanjing, Jiangsu, Peoples R China.
[Jia, Chenyang; Ni, Yong] Shenzhen Univ, Shenzhen Peoples Hosp 2, Dept Hepatopancreatobiliary Surg, Affiliated Hosp 1, Shenzhen, Guangdong, Peoples R China.
C3 Nanjing Medical University; Chinese Academy of Medical Sciences - Peking
Union Medical College; Nanjing Medical University; Shenzhen University
RP Pu, LY (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Hepatobiliary Ctr, Nanjing, Peoples R China.; Pu, LY (corresponding author), Chinese Acad Med Sci, Key Lab Liver Transplantat, Nanjing, Peoples R China.; Pu, LY (corresponding author), Nanjing Med Univ, NHC Key Lab Living Donor Liver Transplantat, Nanjing, Jiangsu, Peoples R China.; Ni, Y (corresponding author), Shenzhen Univ, Shenzhen Peoples Hosp 2, Dept Hepatopancreatobiliary Surg, Affiliated Hosp 1, Shenzhen, Guangdong, Peoples R China.
EM niyong123456@163.com; puliyong@njmu.edu.cn
RI Xia, Nan/ABG-4600-2021; 张, 语/GYA-5347-2022; TANG, JINGYU/HNQ-5979-2023
OI ziyi, wang/0000-0002-8619-711X
FU National Natural Science Foundation of China [81870443, 81273261];
Shenzhen Foundation of Science and Technology [JCYJ20170817172116272];
Sanming Project of Medicine in Shenzhen [SZSM201812079]
FX This study was supported by the National Natural Science Foundation of
China (81870443, 81273261) and the Shenzhen Foundation of Science and
Technology (grant number JCYJ20170817172116272), Sanming Project of
Medicine in Shenzhen (SZSM201812079).
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NR 51
TC 19
Z9 20
U1 2
U2 14
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD DEC 1
PY 2021
VL 12
IS 12
AR 1123
DI 10.1038/s41419-021-04403-2
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA XG5IY
UT WOS:000724787500002
PM 34853322
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Yang, Q
Wang, JW
Liu, R
Wang, ZQ
Li, YF
Zhang, YF
Hao, XH
Huang, YB
Xie, W
Wei, HS
AF Yang, Qi
Wang, Jianwei
Liu, Ran
Wang, Zhiqiang
Li, Yufeng
Zhang, Yifan
Hao, Xiaohua
Huang, Yubo
Xie, Wen
Wei, Hongshan
TI Amelioration of concanavalin A-induced autoimmune hepatitis by magnesium
isoglycyrrhizinate through inhibition of
CD4+CD25-CD69+ subset proliferation
SO DRUG DESIGN DEVELOPMENT AND THERAPY
LA English
DT Article
DE autoimmune hepatitis; drug therapy; concanavalin A; mouse; adaptive
immunity; regulatory T-cell
ID REGULATORY T-CELLS; HEPATOCELLULAR-CARCINOMA; LIVER-DISEASE;
TRANSPLANTATION; ACID; INFLAMMATION; PROGRESSION; THERAPIES
AB Magnesium isoglycyrrhizinate (MGL) is a new stereoisomer of glycyrrhizic acid, which is clinically used as a hepatoprotective medicine with more potent effects and less side effects than glycyrrhizic acid. This study was designed to evaluate the protective effects and possible mechanism of MGL against concanavalin A (Con A)-induced autoimmune hepatitis. Hepatitis was induced by Con A in C57/6J mice with or without MGL administration; injury score and serum ALT were evaluated. The CD4(+) T-cells were isolated from splenocytes and challenged with Con A after coculturing with MGL. The injury score was significantly improved in MGL-treated mice after Con A challenging for 12 and 24 hours compared with those merely challenged with Con A. Similar trends were observed in the serum levels of ALT and AST. The most interesting result was that MGL administration significantly decreased the frequency of CD4(+)CD25(-)CD69(+) T-cells rather than CD4(+)CD25(+)CD69(+) T-cells in peripheral blood mononuclear cells, after Con A challenging 12 and 24 hours. Moreover, the serum ALT levels were markedly correlated with the frequency of CD4(+)CD25(-)CD69(+) cells, but only weakly correlated with CD4(+)CD25(+)CD69(+) cells in peripheral blood mononuclear cells. More importantly, MGL (5 mg/mL) almost completely eliminated the proliferation of the CD25-CD69(+) subset in primary CD4(+) T-cells after Con A challenge. Compared with merely Con A-challenged mice, those with MGL administration significantly demonstrated decreased NALP3, NLRP6, and caspase-3 expression, in which the NALP3 and caspase-3 downregulated in a dose-dependent manner. Our results indicate that MGL may have potential as a therapeutic agent in autoimmune hepatitis by ameliorating liver injury. Its molecular mechanism may be involved in inhibiting CD4(+)CD25(-)CD69(+) subset proliferation and downregulating inflammasome expression in liver tissue.
C1 [Yang, Qi; Wang, Zhiqiang; Zhang, Yifan; Wei, Hongshan] Peking Univ, Hlth Sci Ctr, Beijing Ditan Teaching Hosp, Beijing 100871, Peoples R China.
[Wang, Jianwei; Liu, Ran; Li, Yufeng; Hao, Xiaohua; Huang, Yubo; Xie, Wen; Wei, Hongshan] Capital Med Univ, Beijing Ditan Hosp, Inst Infect Dis, 8 Jingshun East St, Beijing 100015, Peoples R China.
C3 Capital Medical University; Peking University; Capital Medical
University
RP Wei, HS (corresponding author), Capital Med Univ, Beijing Ditan Hosp, Inst Infect Dis, 8 Jingshun East St, Beijing 100015, Peoples R China.
EM drwei@ccmu.edu.cn
RI Wang, Zhiqiang/AAO-7592-2021; Zhang, Yifan/T-3312-2019; Wang,
Jianwei/AAV-2918-2021
FU National Natural Science Foundation of China [81271901]; Beijing Natural
Science Foundation [7152073]; Science Foundation of Capital Medicine
Development [2014-2-2171]; Capital Foundation for Clinical
Characteristic Applied Research Projects [Z141107002514132];
Collaborative Innovation Center of Infectious Diseases [PXM
2015_014226_000058]
FX This work was supported by the National Natural Science Foundation of
China (Number 81271901); Beijing Natural Science Foundation (Number
7152073); Science Foundation of Capital Medicine Development (Number
2014-2-2171); and Capital Foundation for Clinical Characteristic Applied
Research Projects (Number Z141107002514132) to Professor Wei and partly
supported by Collaborative Innovation Center of Infectious Diseases (PXM
2015_014226_000058). The authors would like to acknowledge Yu Hao for
assistance with flow cytometry procedures, and Drs Junyan Han, Youluan
Zhu, and Qi Wang for helpful comments and discussion.
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NR 33
TC 34
Z9 37
U1 0
U2 12
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1177-8881
J9 DRUG DES DEV THER
JI Drug Des. Dev. Ther.
PY 2016
VL 10
BP 443
EP 453
DI 10.2147/DDDT.S92440
PG 11
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DB5YE
UT WOS:000368589000001
PM 26869766
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Ren, X
Wang, R
Yu, XT
Cai, B
Guo, F
AF Ren, Xin
Wang, Rong
Yu, Xiao-ting
Cai, Bo
Guo, Fei
TI Regulation of histone H3 lysine 9 methylation in inflammation
SO ALL LIFE
LA English
DT Review
DE methylation; demethylation; inflammation
ID NONALCOHOLIC FATTY LIVER; T-CELL DIFFERENTIATION; SMOOTH-MUSCLE-CELLS;
EPIGENETIC REGULATION; METABOLIC MEMORY; DNA METHYLATION; DYNAMIC
CHANGES; DEMETHYLASE 1; TNF-ALPHA; DISEASE
AB Inflammation is a defense mechanism that the immune system uses in response to harmful stimuli such as pathogens, damaged cells, toxic compounds, or irradiation. These stimuli may induce inflammatory response and potentially tissue damage in respiratory, cardiovascular, digestive, nervous, endocrine, urinary, or reproductive systems. Inflammatory diseases include a broad array of disorders and conditions that are characterized by inflammation, ranging from autoimmune disease, atopic dermatitis, asthma, chronic obstructive pulmonary disease, inflammatory bowel disease, glomerulonephritis, hepatitis, reperfusion injury, transplant rejection, diabetes, cancer, Parkinson's disease, multiple sclerosis, to depression. Epigenetic mechanisms play crucial roles in many biological processes by regulating transcriptional activation or repression. Histone post-translational modifications have emerged as prospective therapeutic targets. Methylation of histone 3 at lysine 9 is one of the most highly conserved epigenetic marks that correlate well with gene silencing. The methylation status of H3K9 modulates immune cell differentiation and immune responses and therefore influences the outcome of cancer, infection, and other inflammatory diseases. Here, we review the high impact and innovate discoveries in this field, highlight the critical role of the H3K9 methylation/de-methylation in human inflammatory diseases, discuss potential new therapeutic strategies based on a better understanding of the biology of H3K9 methylation modifications.
C1 [Ren, Xin; Wang, Rong; Yu, Xiao-ting; Guo, Fei] Nanchang Univ, Dept Burn, Affiliated Hosp 1, Nanchang 330006, Jiangxi, Peoples R China.
[Cai, Bo] Nanchang Univ, Dept Gynecol & Obstet, Affiliated Hosp 1, Nanchang, Jiangxi, Peoples R China.
C3 Nanchang University; Nanchang University
RP Guo, F (corresponding author), Nanchang Univ, Dept Burn, Affiliated Hosp 1, Nanchang 330006, Jiangxi, Peoples R China.
EM guoki2005@126.com
RI zhang, yuanming/A-9839-2014; Rong, Wang/KCZ-0377-2024
FU National Natural Science Foundation of China [81972445, 81860342,
81772083]
FX This research was supported by grant funding from the National Natural
Science Foundation of China [grant number 81972445, 81860342 and
81772083 FG]. We sincerely thank Alec Griffith of Brigham and Women's
Hospital and Harvard Medical School for English language revision.
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NR 130
TC 1
Z9 1
U1 1
U2 23
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 2689-5293
EI 2689-5307
J9 ALL LIFE
JI All Life
PD JAN 1
PY 2021
VL 14
IS 1
BP 492
EP 508
DI 10.1080/26895293.2021.1931477
PG 17
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA SM3JP
UT WOS:000657506300001
OA gold
DA 2025-01-07
ER
PT J
AU Resheq, YJ
Quaas, A
von Renteln, D
Schramm, C
Lohse, AW
Lüth, S
AF Resheq, Yazid J.
Quaas, Alexander
von Renteln, Daniel
Schramm, Christoph
Lohse, Ansgar W.
Lueth, Stefan
TI Infiltration of peritumoural but tumour-free parenchyma with
IgG4-positive plasma cells in hilar cholangiocarcinoma and pancreatic
adenocarcinoma
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article
DE Autoimmune pancreatitis; IgG4; IgG4-associated cholangitis; Malignancy
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; PRIMARY SCLEROSING
CHOLANGITIS; MALIGNANT BILIARY OBSTRUCTION; AUTOIMMUNE PANCREATITIS;
IGG4-RELATED DISEASE; IGG4-ASSOCIATED CHOLANGITIS; DIAGNOSTIC-CRITERIA;
STEROID-THERAPY; SERUM IGG4; FEATURES
AB Background: Recently, new guidelines for diagnosing IgG4-associated cholangitis have been published devaluing the diagnostic significance of IgG4-positive plasma cells and steroid trials. We sought to evaluate the utility of IgG4-positive plasma cells in discriminating IgG4-associated cholangitis from hilar cholangiocarcinoma and autoimmune pancreatitis from pancreatic adenocarcinoma under conditions when malignancy is likely to be missed.
Methods: Resection specimens obtained from patients with hilar cholangiocarcinoma, pancreatic adenocarcinoma or hepatocellular carcinoma were re-evaluated for IgG4-positivity. Histological analysis focussed on peritumoural but tumour-free sections. Perioperative biochemical and clinical data were reviewed.
Results: Nineteen patients with hilar cholangiocarcinoma and 29 patients with pancreatic adenocarcinoma were eligible for histological re-evaluation. Six of 19 (32%) patients with hilar cholangiocarcinoma and 5 of 29 (17%) patients with pancreatic adenocarcinoma were IgG4-positive (>= 20 IgG4-positive plasma cells per high power field). Patients with IgG4-positive hilar cholangiocarcinoma showed significantly higher levels of serum total bilirubin (3.6 mg/dl vs. 1.8 mg/dl; P < 0.05) and serum alanine-aminotransferase (median 343 U/l vs. 63 U/l, P < 0.05) compared to IgG4-negative patients with hilar cholangiocarcinoma.
Conclusions: IgG4-positive plasma cells are of limited utility especially in distinguishing hilar cholangiocarcinoma from IgG4-associated cholangitis even when combined with clinical parameters and may be misleading under conditions when malignancy is missed. (C) 2013 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Resheq, Yazid J.; Schramm, Christoph; Lohse, Ansgar W.; Lueth, Stefan] Univ Med Ctr Hamburg Eppendorf, Dept Med 1, D-20246 Hamburg, Germany.
[Quaas, Alexander] Univ Med Ctr Hamburg Eppendorf, Inst Pathol, D-20246 Hamburg, Germany.
[von Renteln, Daniel] Univ Med Ctr Hamburg Eppendorf, Dept Interdisciplinary Endoscopy, D-20246 Hamburg, Germany.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Hamburg; University Medical Center Hamburg-Eppendorf
RP Resheq, YJ (corresponding author), Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Martinistr 52, D-20246 Hamburg, Germany.
EM yazidresheq@gmx.de
RI Schramm, Christoph/X-6915-2019
OI Schramm, Christoph/0000-0002-4264-1928; Luth, Stefan/0000-0001-9946-0960
FU medical research trust of the university medical centre of
Hamburg-Eppendorf, Germany; Deutsche Forschungsgemeinschaft [LU B62/2-1
581069]
FX The authors are grateful for funding by the medical research trust of
the university medical centre of Hamburg-Eppendorf, Germany, and the
Deutsche Forschungsgemeinschaft (Grant: LU B62/2-1 581069).
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NR 38
TC 12
Z9 15
U1 0
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1590-8658
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD OCT
PY 2013
VL 45
IS 10
BP 859
EP 865
DI 10.1016/j.dld.2013.03.007
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 219AI
UT WOS:000324475200012
PM 23602806
DA 2025-01-07
ER
PT J
AU Holick, MF
AF Holick, Michael F.
TI Vitamin D: A D-Lightful Solution for Health
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Article
DE vitamin D; osteoporosis; cancer; diabetes; influenza; 25-hydroxyvitamin
D; autoimmune diseases
ID SERUM 25-HYDROXYVITAMIN-D LEVELS; RANDOMIZED CONTROLLED-TRIALS; D
DEFICIENCY; D SUPPLEMENTATION; SOLAR ULTRAVIOLET; BREAST-CANCER; RISK;
PREVENTION; SUNLIGHT; RICKETS
AB Throughout evolution, sunlight-produced vitamin D in the skin has been critically important for health. Vitamin D, known as the sunshine vitamin, is actually a hormone. Once it is produced in the skin or ingested from the diet, it is converted sequentially in the liver and kidneys to its biologically active form 1,25-dihydroxyvitamin D. This hormone interacts with its receptor in the small intestine to increase the efficiency of intestinal calcium and phosphate absorption for the maintenance of the skeleton throughout life. Vitamin D deficiency during the first few years of life results in a flattened pelvis, making it difficult for childbirth. Vitamin D deficiency causes osteopenia and osteoporosis, increasing risk of fracture. Essentially, every tissue and cell in the body has a vitamin D receptor. Therefore, vitamin D deficiency has been linked to increased risk for preeclampsia, requiring a cesarean section for birthing, multiple sclerosis, rheumatoid arthritis, types I and II diabetes, heart disease, dementia, deadly cancers, and infectious diseases. Therefore, sensible sun exposure along with vitamin D supplementation of at least 2000 IU/d for adults and 1000 IU/d for children is essential to maximize their health.
C1 Boston Univ, Sch Med, Dept Med,Med Ctr, Sect Endocrinol Nutr & Diabet,Vitamin Skin & Bone, Boston, MA 02118 USA.
C3 Boston University
RP Holick, MF (corresponding author), Boston Univ, Sch Med, Dept Med,Med Ctr, Sect Endocrinol Nutr & Diabet,Vitamin Skin & Bone, 85 E Newton St,M-1013, Boston, MA 02118 USA.
EM mfholick@bu.edu
RI Holick, Michael/AFG-9586-2022
OI Holick, Michael/0000-0001-6023-9062
FU National Center for Research Resources [R13 RR023236]; UV Foundation
FX Supported in part by a grant from the National Center for Research
Resources (R13 RR023236).This work was supported in part by the UV
Foundation.
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NR 53
TC 162
Z9 174
U1 1
U2 37
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1081-5589
EI 1708-8267
J9 J INVEST MED
JI J. Invest. Med.
PD AUG
PY 2011
VL 59
IS 6
BP 872
EP 880
PG 9
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA 796PA
UT WOS:000293062800014
PM 21415774
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Gurung, A
Assis, DN
McCarty, TR
Mitchell, KA
Boyer, JL
Jain, D
AF Gurung, Ananta
Assis, David N.
McCarty, Thomas R.
Mitchell, Kisha A.
Boyer, James L.
Jain, Dhanpat
TI Histologic features of autoimmune hepatitis: a critical appraisal
SO HUMAN PATHOLOGY
LA English
DT Article
DE Autoimmune hepatitis; Histologic features; Kupffer cell hyaline globules
(KcHG); Plasma-lymphocytic inflammation; Plasma cell clusters
ID HEPATOCELLULAR-CARCINOMA; SIMPLIFIED CRITERIA; DIAGNOSIS; CELLS
AB We speculate that the "typical" histologic features (lymphoplasmacytic interface hepatitis, emperipolesis, and hepatocyte rosettes) of autoimmune hepatitis (AIH) are related to severity of hepatitis rather than etiology. We critically appraised various histologic features of AIH and compared them with cases of chronic hepatitis with similar inflammatory grade and fibrosis stage. Fifty-one patients with clinically confirmed AIH were identified at our institution, of which 43 biopsies (from 42 patients) were taken before initiation of therapy and formed the study group. Hepatitis C biopsies with similar grade and stage served as controls. Kupffer cell hyaline globules (KcHGs; P =.03), prominence of plasma cells in portal tracts (P =.003), "plasma-lymphocytic" inflammation (defined as plasma cells > lymphocytes), or as clusters (defined as >= 5) within portal tracts (P =.002) or lobules (P =.001) were significantly associated with AIH. Rosettes and emperipolesis lacked significance when controlled for inflammatory grade (rosettes, P = 1; emperipolesis, P =.4), supporting our hypothesis. Based on our findings, we developed a modified scoring system in which typical features require the presence of both (1) prominent plasma cells (plasma cells comprise >= 20% of inflammatory cells or presence of plasma cell clusters) and (2) KcHG. "Compatible" features include prominent plasma cells but lack KcHG, and "atypical" features include the presence of another disease process. Although application of this scoring system in our patients decreased the sensitivity to 77% (from 100%), it increased the specificity to 67% (from 0%). Further studies with different control groups are needed to validate these findings. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Gurung, Ananta; Mitchell, Kisha A.; Jain, Dhanpat] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA.
[Gurung, Ananta] Royal Columbian Hosp, Dept Pathol, 330 E Columbia St, New Westminster, BC V3L 3W7, Canada.
[Assis, David N.; McCarty, Thomas R.; Boyer, James L.] Yale Univ, Sch Med, Internal Med, New Haven, CT 06520 USA.
C3 Yale University; Yale University
RP Gurung, A (corresponding author), Royal Columbian Hosp, Dept Pathol, 330 E Columbia St, New Westminster, BC V3L 3W7, Canada.
EM ananta.gurung@fraserhealth.ca
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NR 18
TC 40
Z9 43
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD DEC
PY 2018
VL 82
BP 51
EP 60
DI 10.1016/j.humpath.2018.07.014
PG 10
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA HG4TV
UT WOS:000454968800007
PM 30041025
DA 2025-01-07
ER
PT J
AU Sioka, C
Assimakopoulos, A
Fotopoulos, A
AF Sioka, Chrissa
Assimakopoulos, Assimakis
Fotopoulos, Andreas
TI The diagnostic role of 18F fluorodeoxyglucose positron
emission tomography in patients with fever of unknown origin
SO EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Review
DE F-18 fluorodeoxyglucose positron emission tomography; autoimmune
disease; cancer; fever of unknown origin; infection
ID IN-111-LABELED LEUKOCYTE SCINTIGRAPHY; GIANT-CELL ARTERITIS; FDG-PET;
CLINICAL-VALUE; F-18-FDG-PET/CT; SPECTRUM; BIOPSY; MANAGEMENT; DISEASES;
UTILITY
AB BackgroundIdentification of aetiology for fever of unknown origin (FUO) is challenging, due to the high rates of undiagnosed cases. The current diagnostic approach includes initially first-line procedures such as general examination and various laboratory tests and basic imaging techniques followed by second-line tests such as more advanced imaging techniques including F-18 fluorodeoxyglucose positron emission tomography (FDG PET) and tissue biopsies. If no diagnosis is obtained, more invasive measures may be in order such as liver biopsy and exploratory laparotomy.
Materials and methodsThis review article is based on the relative published material found on MEDLINE and PubMed up to August 2014. We looked for the terms fever of unknown origin, FDG PET' in combination with cancer, infection and autoimmune disease'.
ResultsSeveral clinical studies have investigated the utility of the FDG PET during the diagnostic approach of FUO. Recent evidence suggests that FDG PET has the advantage of total body imaging and may depict all common causes of FUO such as infections, noninfectious inflammatory causes and tumours because they all exhibit glucose hypermetabolism. Depiction of an abnormal lesion on FDG PET could guide clinicians to the next diagnostic procedure (another imaging method, culture, biopsy or surgery) to establish the diagnosis.
ConclusionsEmerging evidence suggests that FDG PET, when available, may provide critical diagnostic information early during evaluation of FUO.
C1 [Sioka, Chrissa; Assimakopoulos, Assimakis] Univ Ioannina, Neurosurg Res Inst, Ioannina 45500, Greece.
[Sioka, Chrissa; Fotopoulos, Andreas] Univ Ioannina, Dept Nucl Med, Ioannina 45500, Greece.
C3 University of Ioannina; University of Ioannina
RP Sioka, C (corresponding author), Univ Ioannina, Neurosurg Res Inst, Ioannina 45500, Greece.
EM csioka@yahoo.com
RI Sioka, Chrissa/J-3381-2019
OI Sioka, Chrissa/0000-0002-2184-4945
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NR 73
TC 24
Z9 26
U1 1
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2972
EI 1365-2362
J9 EUR J CLIN INVEST
JI Eur. J. Clin. Invest.
PD JUN
PY 2015
VL 45
IS 6
BP 601
EP 608
DI 10.1111/eci.12439
PG 8
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA CI3JY
UT WOS:000354645200009
PM 25823953
DA 2025-01-07
ER
PT J
AU Mitrovic, N
Sabanovic, M
Vujovic, A
Jovanovic, J
Nikolic, N
Jug, M
Todorovic, N
Filipovic, A
Milosevic, I
AF Mitrovic, Nikola
Sabanovic, Milos
Vujovic, Ankica
Jovanovic, Jaroslava
Nikolic, Natasa
Jug, Martina
Todorovic, Nevena
Filipovic, Ana
Milosevic, Ivana
TI Influence of chronic liver diseases on the course and outcome of
COVID-19
SO PLOS ONE
LA English
DT Article
AB IntroductionCoronavirus disease of 2019 (COVID-19) is a global health problem. The impact of chronic liver diseases on the course and outcome of COVID-19 is still the subject of research. The aim of this study was to show the characteristics of COVID-19 patients with chronic liver diseases, and to establish the risk factors for unfavourable outcome. MethodsA retrospective observational study was conducted at the Infectious Disease Clinic in Belgrade, Serbia, and included 80 patients with chronic liver diseases and COVID-19 within a time frame of two years (between 15 March 2020 and 15 March 2022). Characteristics of the affected persons, as well as the risk factors for a fatal outcome, were analyzed. ResultsOf the 80 subjects in the study, 23.8% had chronic viral hepatitis, 12.5% autoimmune liver diseases and alcoholic liver disease respectively, 30% had non-alcoholic fatty liver disease, while 11.2% had chronic liver diseases of unknown aetiology. A total of 33.7% had cirrhosis, 6.3% hepatocellular carcinoma and 5% had liver transplants. A total of 92.5% of respondents had pneumonia (21.2% were critically ill). A deterioration of chronic liver disease was registered among 33.7% of patients, and decompensation in 3.8%; 76.3% patients recovered, while 23.7% had a lethal outcome. Risk factors for lethal outcome by univariate analysis were: alcoholic liver disease, cirrhosis, increased transaminases values prior to COVID-19, malignancy, severe pneumonia and dyspnea. In a multivariate analysis, the presence of liver cirrhosis (OR = 69.1, p = 0.001) and severe pneumonia (OR = 22.3, p = 0.006) remained independently predictive for lethal outcome. ConclusionThese findings will help with the evaluation of COVID-19 patients who have chronic liver diseases and will improve their risk stratification.
C1 [Mitrovic, Nikola; Vujovic, Ankica; Nikolic, Natasa; Milosevic, Ivana] Univ Belgrade, Fac Med, Belgrade, Serbia.
[Mitrovic, Nikola; Sabanovic, Milos; Vujovic, Ankica; Jovanovic, Jaroslava; Nikolic, Natasa; Jug, Martina; Todorovic, Nevena; Filipovic, Ana; Milosevic, Ivana] Univ Clin Ctr Serbia, Dept Hepatol, Clin Infect & Trop Dis, Belgrade, Serbia.
C3 University of Belgrade; Clinical Centre of Serbia
RP Milosevic, I (corresponding author), Univ Belgrade, Fac Med, Belgrade, Serbia.; Milosevic, I (corresponding author), Univ Clin Ctr Serbia, Dept Hepatol, Clin Infect & Trop Dis, Belgrade, Serbia.
EM ivana.milosevic@med.bg.ac.rs
RI Mitrovic, Nikola/ABA-3801-2020
OI Vujovic, Ankica/0000-0001-9570-215X
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U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD JUL 14
PY 2023
VL 18
IS 7
AR e0288350
DI 10.1371/journal.pone.0288350
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA M6UO7
UT WOS:001031549800031
PM 37450541
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Solinas, C
Pusole, G
Demurtas, L
Puzzoni, M
Mascia, R
Morgan, G
Giampieri, R
Scartozzi, M
AF Solinas, Cinzia
Pusole, Grazia
Demurtas, Laura
Puzzoni, Marco
Mascia, Roberta
Morgan, Gilberto
Giampieri, Riccardo
Scartozzi, Mario
TI Tumor infiltrating lymphocytes in gastrointestinal tumors: Controversies
and future clinical implications
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Tumor infiltrating lymphocytes; Gastrointestinal tumors; Microsatellite
instability; Prognosis; Immunotherapy
ID REGULATORY T-CELLS; HEPATOCELLULAR-CARCINOMA; GASTRIC-CANCER; FAVORABLE
PROGNOSIS; COLORECTAL-CANCER; SUPPRESSOR-CELLS; PD-1 BLOCKADE; B-CELLS;
MOLECULAR SUBTYPES; CTLA-4 BLOCKADE
AB Chronic inflammation following infections, autoimmune diseases or exposure to environmental irritants plays a crucial role in tumor development and influences the host immune response to neoplastic cells. The presence of an anti-tumor immune infiltrate is often associated with better outcomes in gastro-intestinal primary cancers, particularly in those with high microsatellite instability (MSI-H). Immunotherapeutic drugs inhibiting the PD-1 and PD-L1 pathway showed promising results in the treatment of these patients in the metastatic setting. The aim of this review is to resume the role tumor infiltrating lymphocytes (TILs) play in gastrointestinal tumors, underlining their potential value as a prognostic and predictive biomarker. TILs assessment could identify subsets of patients with high extent of TILs and better prognosis, that could be spared from adjuvant systemic treatments. Immune infiltration parameters might be additional predictors of a greater benefit from the immunotherapy with the immune checkpoint blockade. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Solinas, Cinzia] Inst Jules Bordet, Mol Immunol Unit, Blvd Waterloo 127, B-1000 Brussels, Belgium.
[Solinas, Cinzia] Univ Libre Bruxelles, Blvd Waterloo 127, B-1000 Brussels, Belgium.
[Pusole, Grazia; Demurtas, Laura; Puzzoni, Marco; Mascia, Roberta; Scartozzi, Mario] Univ Cagliari, Med Oncol, Policlin Univ Ss 554 Bivio Sestu Km 4-5, Monserrato, CA, Italy.
[Morgan, Gilberto] Skane Univ Hosp, Med Oncol, Lund, Sweden.
[Giampieri, Riccardo] UNIVPM, Med Oncol, Ancona, Italy.
C3 Institut Jules Bordet; Universite Libre de Bruxelles; University of
Cagliari; Lund University; Skane University Hospital; Marche Polytechnic
University
RP Scartozzi, M (corresponding author), Policlin Univ Monserrato, AOU Cagliari, Oncol Med, Ss 554 Bivio Sestu Km 4500, I-09042 Cagliari, Italy.
EM czsolinas@gmail.com; grazia.pusole@gmail.com; lau.demi@tiscali.it;
marcopuzzoni@gmail.com; roboa@hotmail.it; Gilberto.Morgan@Skane.se;
riccardo.giampieri81@gmail.com; marioscartozzi@gmail.com
RI PUZZONI, MARCO/T-5453-2019; Mascia, Roberta/ABD-8709-2020; Solinas,
Cinzia/AAC-2103-2020; Pusole, Grazia/G-4945-2018
OI mascia, roberta/0000-0002-7174-0220; SCARTOZZI,
MARIO/0000-0001-5977-5546; Pusole, Grazia/0000-0002-1866-1371; puzzoni,
marco/0000-0001-5880-4309; DEMURTAS, LAURA/0000-0002-9749-7628
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NR 100
TC 34
Z9 35
U1 0
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD FEB
PY 2017
VL 110
BP 106
EP 116
DI 10.1016/j.critrevonc.2016.11.016
PG 11
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA EJ9GB
UT WOS:000393533500011
PM 28109400
DA 2025-01-07
ER
PT J
AU Chen, K
Li, XY
Shang, YQ
Chen, DX
Qu, SY
Shu, JX
Zhang, M
Wang, ZY
Huang, JM
Wu, MH
Ming, SQ
Wu, YJ
AF Chen, Kang
Li, Xingyu
Shang, Yuqi
Chen, Daxiang
Qu, Siying
Shu, Jinxian
Zhang, Mei
Wang, Zhiying
Huang, Jinmei
Wu, Minhao
Ming, Siqi
Wu, Yongjian
TI FGL1-LAG3 axis impairs IL-10-Producing regulatory T cells associated
with Systemic lupus erythematosus disease activity
SO HELIYON
LA English
DT Article
DE Systemic lupus erythematosus; Regulatory T cell; Lymphocyte-activation
protein 3; Fibrinogen-like protein 1
ID LIVER INVOLVEMENT; STAT3 ACTIVATION; LAG-3; TH17; CANCER; INFLAMMATION;
IMBALANCE; RESPONSES; IMMUNITY; BALANCE
AB Background: Systemic Lupus Erythematosus (SLE) is a prototypic autoimmune disease, which is accompanied by liver damage. However, it remains unknown whether liver damage is associated with SLE progression. Method: ology: HepG2 and L-02 cells were stimulated with cytokines, and FGL1 mRNA and protein expression levels were determined using Real-time PCR and ELISA, respectively. Regulatory T cells (Treg) isolated from healthy individuals as well as patients with SLE and SLE and liver damage (SLE-LD) were cultured with autologous effector CD4+T cells in the presence of a func-tional antibody or isotype control. The expression levels of LAG3, CD25, PD-1, CXCR5, ICOS and OX40 were evaluated by flow cytometry. FGL1, IL-10, IL-17a and IL-21 levels in serum or culture supernatants were quantified by ELISA. Results: Patients with SLE-LD exhibits higher disease activity indices and anti-dsDNA antibody levels. Importantly, fibrinogen-like protein 1 (FGL1), a key factor released from the injured liver, is up-regulated in patients with SLE-LD and is associated with disease activity. FGL1 expression is induced by the inflammatory cytokine IL-6 signaling in hepatocytes. Higher expression of the FGL1 receptor lymphocyte activation gene 3 (LAG3) is detected in Treg cells from patients with SLE-LD. The FGL1-LAG3 signaling axis inhibits Treg cell proliferation and impairs the suppressive activity of Treg cells by limiting IL-10 secretion. Furthermore, FGL1-LAG3 signaling promotes the production of pathogenic IL-17a and IL-21 by CD4+T cells by reducing IL-10 level produced by Treg in patients with SLE. Conclusions: The FGL1-LAG3 signal axis is a key mechanism that subverts the suppressive function of Treg cells. This may provide a new therapeutic target for SLE and SLE-induced liver damage.
C1 [Chen, Kang; Wang, Zhiying] Zhongshan City Peoples Hosp, Dept Lab Med, Zhongshan 528403, Guangdong, Peoples R China.
[Li, Xingyu; Wu, Minhao; Wu, Yongjian] Sun Yat sen Univ, Affiliated Hosp 5, Ctr Infect & Immun, Zhuhai 519000, Guangdong, Peoples R China.
[Li, Xingyu; Wu, Minhao; Wu, Yongjian] Sun Yat sen Univ, Affiliated Hosp 5, Guangdong Prov Engn Res Ctr Mol Imaging, Zhuhai 519000, Guangdong, Peoples R China.
[Li, Xingyu; Ming, Siqi] Guangdong Prov Hosp Chinese Med, Dept Lab Med, Zhuhai 519015, Guangdong, Peoples R China.
[Shang, Yuqi] Guangzhou Med Univ, Affiliated Hosp 1, Dept Nephrol, Guangzhou, Guangdong, Peoples R China.
[Chen, Daxiang; Huang, Jinmei] Southern Med Univ, Dermatol Hosp, Dept Lab Med, Guangzhou 510091, Guangdong, Peoples R China.
[Qu, Siying] Zhuhai Hosp Integrated Tradit Chinese & Western Me, Peoples Hosp Zhuhai 2, Dept Clin Lab, Zhuhai 519020, Guangdong, Peoples R China.
[Shu, Jinxian] Sun Yat sen Univ, Affiliated Hosp 5, Dept Pharm, Zhuhai 519000, Guangdong, Peoples R China.
[Zhang, Mei] Guangzhou Med Univ, Affiliated Hosp 6, Qingyuan Peoples Hosp, Qingyuan 511518, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
Guangzhou University of Chinese Medicine; Guangzhou Medical University;
Southern Medical University - China; Sun Yat Sen University; Guangzhou
Medical University
RP Wu, MH; Wu, YJ (corresponding author), Sun Yat sen Univ, Affiliated Hosp 5, Ctr Infect & Immun, Zhuhai 519000, Guangdong, Peoples R China.; Wu, MH; Wu, YJ (corresponding author), Sun Yat sen Univ, Affiliated Hosp 5, Guangdong Prov Engn Res Ctr Mol Imaging, Zhuhai 519000, Guangdong, Peoples R China.; Ming, SQ (corresponding author), Guangdong Prov Hosp Chinese Med, Dept Lab Med, Zhuhai 519015, Guangdong, Peoples R China.; Huang, JM (corresponding author), Southern Med Univ, Dermatol Hosp, Dept Lab Med, Guangzhou 510091, Guangdong, Peoples R China.
EM jinmeih2013@163.com; wuminhao@mail.sysu.edu.cn; msq615117@163.com;
wuyj228@mail.sysu.edu.cn
RI zhang, mm/IWV-4201-2023; Li, Xingyu/AHE-0001-2022; Shang,
Yuqi/JAC-1348-2023
FU National Natural Science Foundation of China [82270016, 82102249];
Natural Science Foundation of Guangdong Province [2023A1515030065];
Sixth Affiliated Hospital of Guangzhou Medical University; Qingyuan
People's Hospital [202301-102, 202301-405]
FX This work was supported by grants from National Natural Science
Foundation of China (82270016, 82102249) , the Natural Science
Foundation of Guangdong Province (2023A1515030065) , the open research
funds from the Sixth Affiliated Hospital of Guangzhou Medical
University, Qingyuan People's Hospital (202301-102, 202301-405) . The
authors thank all members of Department of Immunology, Zhongshan School
of Medicine, Sun Yat-sen University for technical support.
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NR 75
TC 1
Z9 1
U1 1
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD OCT
PY 2023
VL 9
IS 10
AR e20806
DI 10.1016/j.heliyon.2023.e20806
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA FY6Y8
UT WOS:001149465900001
PM 37916085
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Yoshihara, E
Masaki, S
Matsu, Y
Chen, Z
Tian, H
Yodoi, J
AF Yoshihara, Eiji
Masaki, So
Matsu, Yoshiyuki
Chen, Zhe
Tian, Hai
Yodoi, Junji
TI Thioredoxin/Txnip: redoxisome, as a redox switch for the pathogenesis of
diseases
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE thioredoxin; Txnip; redoxisome; inflammation; diabetes mellitus; redox
regulation
ID INTERACTING PROTEIN TXNIP; UP-REGULATED PROTEIN-1; BETA-CELL; BINDING
PROTEIN-2; OXIDATIVE STRESS; ACTIVE-SITE; HEPATOCELLULAR-CARCINOMA;
NLRP3 INFLAMMASOME; LUNG INFLAMMATION; CRYSTAL-STRUCTURE
AB During the past few decades, it has been widely recognized that Reduction-Oxidation (redox) responses occurring at the intra- and extra-cellular levels are one of most important biological phenomena and dysregulated redox responses are involved in the initiation and progression of multiple diseases.Thioredoxin1 (Trx1) andThioredoxin2 (Trx2), mainly located in the cytoplasm and mitochondria, respectively, are ubiquitously expressed in variety of cells and control cellular reactive oxygen species by reducing the disulfides into thiol groups. Thioredoxin interacting protein (Txnip/thioredoxin binding protein-2/vitamin D3 upregulated protein) directly binds to Trx1 and Trx2 (Trx) and inhibit the reducing activity of Trx through their disulfide exchange. Recent studies have revealed that Trx1 and Txnip are involved in some critical redox-dependent signal pathways including NLRP-3 inflammasome activation in a redox-dependent manner. Therefore, Trx/Txnip, a redox-sensitive signaling complex is a regulator of cellular redox status and has emerged as a key component in the link between redox regulation and the pathogenesis of diseases. Here, we review the novel functional concept of the redox-related protein complex, named "Redoxisome," consisting of Trx/Txnip, as a critical regulator for intra- and extra-cellular redox signaling, involved in the pathogenesis of various diseases such as cancer, autoimmune disease, and diabetes.
C1 [Yoshihara, Eiji; Masaki, So; Matsu, Yoshiyuki; Chen, Zhe; Yodoi, Junji] Kyoto Univ, Inst Virus Res, Kyoto 6068397, Japan.
[Tian, Hai; Yodoi, Junji] JBPA Res Inst, Adv Chem Technol Ctr Kyoto ACT Kyoto, Kyoto, Japan.
[Tian, Hai; Yodoi, Junji] Redox Bio Sci Inc, Kyoto, Japan.
C3 Kyoto University
RP Yodoi, J (corresponding author), Kyoto Univ, Inst Virus Res, Kyoto 6068397, Japan.
EM yodoi@virus.kyoto-u.ac.jp
RI Yodoi, Junji/F-6189-2011; Chen, Zhe/F-6273-2010
OI Matsuo, Yoshiyuki/0000-0002-3183-4871; Yoshihara,
Eiji/0000-0001-6324-6495
FU Scientific Research from the Ministry of Education, Culture, Sports,
Science and Technology of Japan; Program for Promotion of Fundamental
Studies in Health Sciences of National Institute of Biomedical
Innovation (NIBIO); World Class University through Ewha Womans
University [R31-10010]; Uehara memorial research foundation; Japan
Society for the Promotion of Science (JSPS)
FX We thank Dr. Maryam Ahmadian for kind English editing. This study was
supported by a Grant-in-Aid for Scientific Research from the Ministry of
Education, Culture, Sports, Science and Technology of Japan, and by the
Program for Promotion of Fundamental Studies in Health Sciences of
National Institute of Biomedical Innovation (NIBIO). This work was
supported in part by the World Class University Grant R31-10010 through
the Ewha Womans University. Eiji Yoshihara is supported by the Uehara
memorial research foundation and the Japan Society for the Promotion of
Science (JSPS) as a research fellow in abroad. We apologize for those
references we could not include due to space limitations.
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NR 108
TC 268
Z9 307
U1 2
U2 54
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 9
PY 2014
VL 4
AR 514
DI 10.3389/fimmu.2013.00514
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CH4VR
UT WOS:000354031900002
PM 24409188
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Hawes, MC
Wen, FS
Elquza, E
AF Hawes, Martha C.
Wen, Fushi
Elquza, Emad
TI Extracellular DNA: A Bridge to Cancer
SO CANCER RESEARCH
LA English
DT Review
ID CIRCULATING NUCLEIC-ACIDS; DEOXYRIBONUCLEASE ACTIVITY;
PANCREATIC-CANCER; LIVER METASTASIS; ROOT-TIP; TRAPS; SERUM;
NEUTROPHILS; PLASMA; RESISTANCE
AB DNase I is a secreted enzyme whose function has been presumed to control "waste management" in the human system, by degrading DNA that leaks from dead and dying cells. Emerging studies have instead yielded evidence that DNase I plays a central role in newly defined dynamics of immune and autoimmune diseases, as well as cancer and vascular disorders, including thrombosis. Cancer cells have been reported to be associated with distinctive extracellular structures that facilitate aggregation and implantation. The fact that DNA is a component of such structures and that it plays a role in cancer development is illustrated by direct evidence: DNase I added to tumor cells eliminates the structures and inhibits tumorigenicity of some cancer cell lines. DNase I injected into experimental animals, moreover, results in significant inhibition of metastasis. Despite independent observations of such phenomena in diverse cancers for over 50 years, the potential for using DNase I as a clinical tool to prevent or treat cancer remains unexplored. The discovery of neutrophil extracellular traps has yielded a conceptual framework for interpreting how extracellular DNA may function in cancer development and why it may prove to be an important clinical target in stopping cancer outside the cell. (C) 2015 AACR.
C1 [Hawes, Martha C.] Univ Arizona, Inst Life Sci Bio5, Dept Soil Water & Environm Sci, Tucson, AZ 85721 USA.
[Wen, Fushi] Ventana Med Syst Inc, Roche Tissue Diag, Oro Valley, AZ USA.
[Elquza, Emad] Univ Arizona, Arizona Canc Ctr, Div Hematol Oncol, Tucson, AZ 85721 USA.
C3 University of Arizona; Roche Holding; Ventana Medical Systems, Inc.;
University of Arizona; Arizona Center Cancer Care
RP Hawes, MC (corresponding author), Univ Arizona, 1177 E Fourth St, Tucson, AZ 85721 USA.
EM mhawes@email.arizona.edu
FU National Science Foundation; Direct For Biological Sciences; Division Of
Integrative Organismal Systems [1032339] Funding Source: National
Science Foundation
FX M.C. Hawes was supported by the National Science Foundation for research
on exDNA in plant defense.
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NR 58
TC 54
Z9 70
U1 0
U2 26
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT 15
PY 2015
VL 75
IS 20
BP 4260
EP 4264
DI 10.1158/0008-5472.CAN-15-1546
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CX3MA
UT WOS:000365601900003
PM 26392072
OA Bronze
DA 2025-01-07
ER
PT J
AU Sekai, I
Hagiwara, S
Watanabe, T
Kudo, M
AF Sekai, Ikue
Hagiwara, Satoru
Watanabe, Tomohiro
Kudo, Masatoshi
TI A case with hepatic immune-related adverse events caused by nivolumab
exhibiting impaired accumulation of regulatory T cells
SO CLINICAL JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Nivolumab; Hepatic immune-related adverse effects; Regulatory T cells
AB Systemic administration of anti-programmed cell death 1 (PD-1) antibody (Ab) has achieved remarkable success in metastatic cancers. The blockade of PD-1-mediated signaling pathways sometimes cause immune-related adverse events (irAEs) due to restored anti-cancer as well as anti-self immunity. Although the liver is a preferential organ for irAEs, the immuno-pathogenesis underlying hepatic irAEs has been poorly understood. We describe a 57-year-old man with Stage IV lung cancer who underwent the first-line regimen composed of carboplatin and paclitaxel. Nivolumab treatment (3.2 mg/kg, every 3 weeks) was initiated when the disease progressed after the first chemotherapy. Sequential occurrence of irAEs involving the multiorgan systems was observed. He developed hepatic irAEs (Grade 3) after endocrine, lung, and cutaneous irAEs. Lobular hepatitis characterized by predominant infiltration of CD8(+) T cells was seen in the liver biopsy specimens. Interestingly, defective accumulation of regulatory T cells (Tregs) expressing forkhead box protein P3 (FOXP3) was evident in this case with hepatic irAEs as compared with typical cases with autoimmune hepatitis. This case suggests that hepatic irAEs are characterized not only by lobular infiltration of CD8(+) T cells but also by defective accumulation of FOXP3(+) Tregs.
C1 [Sekai, Ikue; Hagiwara, Satoru; Watanabe, Tomohiro; Kudo, Masatoshi] Kindai Univ, Dept Gastroenterol & Hepatol, Fac Med, 377-2 Ohno Higashi, Osaka 5898511, Japan.
C3 Kindai University (Kinki University)
RP Hagiwara, S (corresponding author), Kindai Univ, Dept Gastroenterol & Hepatol, Fac Med, 377-2 Ohno Higashi, Osaka 5898511, Japan.
EM ikuie@gmail.com; hagi-318@hotmail.co.jp; tomohiro@med.kindai.ac.jp;
m-kudo@med.kindai.ac.jp
RI Kudo, Masatoshi/AAA-9744-2019; Watanabe, Tomohiro/ABA-4712-2021
OI Hagiwara, Satoru/0000-0002-3412-4701; Watanabe,
Tomohiro/0000-0002-6175-8064
CR Aoki N, 2011, GASTROENTEROLOGY, V140, P1322, DOI 10.1053/j.gastro.2011.01.002
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NR 25
TC 5
Z9 5
U1 0
U2 2
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 1865-7257
EI 1865-7265
J9 CLIN J GASTROENTEROL
JI Clin. J. Gastroenterol.
PD AUG
PY 2021
VL 14
IS 4
BP 1191
EP 1196
DI 10.1007/s12328-020-01317-y
EA MAR 2021
PG 6
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA TR1DP
UT WOS:000627018200001
PM 33665689
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Alboraie, MA
Afifi, ME
Elghamry, FG
Shalaby, HA
Elshennawy, GE
Abdelaziz, AA
Shaheen, MU
El-Seoud, ARA
AF Alboraie, Mohamed A.
Afifi, Mahmoud E.
Elghamry, Fathy G.
Shalaby, Helmy A.
Elshennawy, Gamal E.
Abdelaziz, Ahmed A.
Shaheen, Mohamed U.
El-Seoud, Amany R. Abo
TI Egy-Score Predicts Severe Hepatic Fibrosis and Cirrhosis in Egyptians
With Chronic Liver Diseases: A Pilot Study
SO HEPATITIS MONTHLY
LA English
DT Article
DE Alpha-Macroglobulins; CA-19-9 Antigen; Biological Markers; Fibrosis;
Liver Cirrhosis
ID TRANSIENT ELASTOGRAPHY; MARKERS; SERUM; DIAGNOSIS; CA-19-9; TESTS
AB Background: Non-invasive methods for assessment of hepatic fibrosis are increasingly needed. Recent studies showed that combined elevation of tumor markers CA 19-9 and CA 125 is predictive of severe hepatic fibrosis or cirrhosis with high specificity.
Objectives: We aimed at developing a new panel of surrogate biomarkers for prediction of the stage of hepatic fibrosis by combining tumor markers with other known biomarkers of hepatic fibrosis.
Patients and Methods: A total of 92 patients with different types of chronic liver diseases (chronic hepatitis B, chronic hepatitis C and autoimmune hepatitis), were prospectively enrolled in our cohort. They were subjected to: ALT, AST, GGT, ALP, total bilirubin, INR, total cholesterol, albumin, platelet count, cancer antigen 19-9 (CA 19-9), cancer antigen 125 (CA 125), cancer antigen 15-3 (CA 15-3), haptoglobin, alpha-2-macroglobulin, apolipoprotein A1, abdominal ultrasound, liver biopsy and histological staging of hepatic fibrosis using the METAVIR system.
Results: Combined elevation of CA 19-9 and CA 125 with a summated value >37 U/mL is predictive of severe hepatic fibrosis or cirrhosis (stage F3-F4 METAVIR) with a probability of 77.6%. Multivariate analysis showed that the most relevant collection of biomarkers for prediction of stage of hepatic fibrosis is: CA 19-9, age, alpha-2-macroglobulin, total bilirubin, platelet count & albumin. We developed a new score, named the "Egy-Score", using a regression equation composed of this panel of biomarkers. Egy-Score could differentiate no or early fibrosis (stage F0-F2 METAVIR) from severe fibrosis or cirrhosis (stage F3-F4 METAVIR) with 83.7% accuracy.
Conclusions: Non-invasive assessment of hepatic fibrosis could be done using the Egy-Score. Egy-Score could differentiate no or early fibrosis (stage F0-F2 METAVIR) from severe fibrosis or cirrhosis (stage F3-F4 METAVIR) with 83.7% accuracy.
C1 [Alboraie, Mohamed A.; Afifi, Mahmoud E.; Elghamry, Fathy G.; Shalaby, Helmy A.; Elshennawy, Gamal E.; Abdelaziz, Ahmed A.] Al Azhar Univ, Dept Internal Med, Cairo 11651, Egypt.
[Shaheen, Mohamed U.] Al Azhar Univ, Dept Clin Pathol, Cairo 11651, Egypt.
[El-Seoud, Amany R. Abo] Zagazig Univ, Dept Community Med & Publ Hlth, Zagazig, Egypt.
C3 Egyptian Knowledge Bank (EKB); Al Azhar University; Egyptian Knowledge
Bank (EKB); Al Azhar University; Egyptian Knowledge Bank (EKB); Zagazig
University
RP Alboraie, MA (corresponding author), Al Azhar Univ, Dept Internal Med, Cairo 11651, Egypt.
EM m.alboraie@gmail.com
RI Shaheen, Usama/ABB-6806-2021; Alboraie, Mohamed/F-5688-2011
OI Shaheen, Usama/0000-0002-2970-8964; Alboraie,
Mohamed/0000-0002-8490-9822
CR Abraldes JG, 2012, GASTROENT HEPAT-BARC, V35, P488, DOI 10.1016/j.gastrohep.2012.02.010
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Berzigotti A, 2013, J HEPATOL
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NR 37
TC 7
Z9 7
U1 0
U2 2
PU KOWSAR PUBL
PI HOENSBROEK
PA PATERSWEG 22,, HOENSBROEK, LIMBURG 6431 GC, NETHERLANDS
SN 1735-143X
EI 1735-3408
J9 HEPAT MON
JI Hepat. Mon.
PD JUN
PY 2013
VL 13
IS 6
AR e10810
DI 10.5812/hepatmon.10810
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 187NT
UT WOS:000322126500012
PM 24046790
OA Green Submitted, Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Friedrich, M
Pracht, K
Mashreghi, MF
Jäck, HM
Radbruch, A
Seliger, B
AF Friedrich, Michael
Pracht, Katharina
Mashreghi, Mir-Farzin
Jaeck, Hans-Martin
Radbruch, Andreas
Seliger, Barbara
TI The role of the miR-148/-152 family in physiology and disease
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Review
DE Cancer; Diseases; Epigenetic; Lymphocytes; MicroRNA-148/-152 family;
miRNA regulation; Post-transcriptional regulation
ID HLA-G EXPRESSION; INHIBITS CELL-PROLIFERATION; GLIOBLASTOMA STEM-CELLS;
GASTRIC-CANCER; TUMOR-SUPPRESSOR; MICRORNA-148A SUPPRESSES; DNA
METHYLATION; POSTTRANSCRIPTIONAL REGULATION; HEPATOCELLULAR-CARCINOMA;
MESENCHYMAL TRANSITION
AB MicroRNAs (miRNAs) are endogenously encoded similar to 22 nt small non-coding RNAs. They function as key players of many cellular processes by base pairing with target mRNAs and thereby impairing gene expression at the post-transcriptional level. Recent findings demonstrate a critical role of many miRNAs in immune cell differentiation and immune responses, which is also associated with the development and progression of many tumor and non-tumor diseases. Here we review the multifaceted miRNA-148/-152 family members consisting of miR-148a, miR-148b and miR-152. Next to regulation mechanisms that control the expression of this miRNA family, we will focus on (i) the role of miR-148a in regulating B and T lymphocyte function and its role in associated diseases and (ii) the importance of miR-148/-152 family members for cancer initiation, tumor growth and metastasis formation. In addition, this review aims to highlight some selected targets of the miRNA-148/-152 family members, which are involved in the biology of cancer and maintenance of epigenetic patterns. In conclusion, members of the miR-148/-152 family might represent prognostic markers and/or potential therapeutic targets for treatment of autoimmune disorders, chronic inflammatory diseases and multiple types of cancer.
C1 [Friedrich, Michael; Seliger, Barbara] Martin Luther Univ Halle Wittenberg, Inst Med Immunol, Halle, Germany.
[Pracht, Katharina; Jaeck, Hans-Martin] Univ Erlangen Nurnberg, Dept Internal Med 3, Nikolaus Fiebiger Ctr, Div Mol Immunol, Erlangen, Germany.
[Mashreghi, Mir-Farzin; Radbruch, Andreas] Deutsch Rheuma Forsch Zentrum DRFZ, Berlin, Germany.
C3 Martin Luther University Halle Wittenberg; University of Erlangen
Nuremberg
RP Seliger, B (corresponding author), Martin Luther Univ Halle Wittenberg, Inst Med Immunol, Halle, Germany.
EM Barbara.Seliger@uk-halle.de
RI Pracht, Katharina/KCX-8352-2024; Mashreghi, Mir-Farzin/AFL-8690-2022;
Radbruch, Andreas/ADI-4973-2022
OI Mashreghi, Mir-Farzin/0000-0002-8015-6907; Seliger,
Barbara/0000-0002-5544-4958; Jack, Hans-Martin/0000-0002-6332-8463;
Pracht, Katharina/0000-0002-8943-4897; Radbruch,
Andreas/0000-0001-5753-0000
FU Deutsche Forschungsgemeinschaft [Se581-23, GRK1591/BS, TRR130, GRK1660];
European Research Council Advanced Grant IMMEMO [ERC-2010-AdG.20100317,
268987]; state of Berlin; European Regional Development Fund (ERDF)
[EFRE 1.8/11]
FX Part of this work was funded by the Deutsche Forschungsgemeinschaft to
B.S. (Se581-23) GRK1591/BS, H.-M.J (TRR130 and GRK1660). This work was
supported by a European Research Council Advanced Grant IMMEMO
(ERC-2010-AdG.20100317 Grant 268987 awarded to A.R.). M.F.M is supported
by the state of Berlin and the "European Regional Development Fund"
(ERDF 2014-2020, EFRE 1.8/11, Deutsches Rheuma-Forschungszentrum).
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NR 136
TC 90
Z9 102
U1 2
U2 24
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD DEC
PY 2017
VL 47
IS 12
BP 2026
EP 2038
DI 10.1002/eji.201747132
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA FP0FC
UT WOS:000417273800003
PM 28880997
OA Bronze
DA 2025-01-07
ER
PT J
AU Aliyu, M
Zohora, FT
Anka, AU
Ali, K
Maleknia, S
Saffarioun, M
Azizi, G
AF Aliyu, Mansur
Zohora, Fatema Tuz
Anka, Abubakar Umar
Ali, Kashif
Maleknia, Shayan
Saffarioun, Mohammad
Azizi, Gholamreza
TI Interleukin-6 cytokine: An overview of the immune regulation, immune
dysregulation, and therapeutic approach
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE Interleukin 6; Inflammation; Autoimmunity; Immunotherapy; Immune
regulation; Immune dysregulation
ID ANTI-INTERLEUKIN-6 MONOCLONAL-ANTIBODY; NECROSIS-FACTOR-ALPHA;
NF-KAPPA-B; T-CELLS; CELIAC-DISEASE; RHEUMATOID-ARTHRITIS;
ULCERATIVE-COLITIS; GENE POLYMORPHISM; SIGNALING PATHWAY;
PROSTATE-CANCER
AB Several studies have shown that interleukin 6 (IL-6) is a multifunctional cytokine with both pro-inflammatory and anti-inflammatory activity, depending on the immune response context. Macrophages are among several cells that secrete IL-6, which they express upon activation by antigens, subsequently inducing fever and production of acute-phase proteins from the liver. Moreover, IL-6 induces the final maturation of B cells into memory B cells and plasma cells as well as an adaptive role for short-term energy allocation. Activation of IL-6 receptors results in the intracellular activation of the JAK/STAT pathway with resultant production of inflammatory cytokines. Several mechanisms-controlled IL-6 expression, but aberrant production was shown to be crucial in the pathogenesis of many diseases, which include autoimmune and chronic inflammatory diseases. IL-6 in combination with transforming growth factor beta (TGF-beta) induced differentiation of naive T cells to Th17 cells, which is the cornerstone in autoimmune diseases. Recently, IL-6 secretion was shown to form the backbone of hypercytokinemia seen in the Coronavirus disease 2019 (COVID-19)-associated hyperinflammation and multiorgan failure. There are two classes of approved IL-6 inhibitors: anti-IL-6 receptor monoclonal antibodies (e.g., tocilizumab) and anti-IL-6 monoclonal antibodies (i.e., siltuximab). These drugs have been evaluated in patients with rheumatoid arthritis, juvenile idiopathic arthritis, cytokine release syndrome, and COVID-19 who have systemic inflammation. JAK/STAT pathway blockers were also successfully used in dampening IL-6 signal transduction. A better understanding of different mechanisms that modulate IL-6 expression will provide the much-needed solution with excellent safety and efficacy profiles for the treatment of autoimmune and inflammatory diseases in which IL-6 derives their pathogenesis.
C1 [Aliyu, Mansur] Tehran Univ Med Sci Int Campus TUMS IC, Sch Publ Hlth, Dept Immunol, Tehran, Iran.
[Aliyu, Mansur] Bayero Univ, Coll Hlth Sci, Fac Clin Sci, Dept Med Microbiol, Kano, Nigeria.
[Zohora, Fatema Tuz] Monash Univ Malaysia, Jeffrey Cheah Sch Med & Hlth Sci, Subang Jaya, Malaysia.
[Anka, Abubakar Umar] Ahmadu Bello Univ, Coll Med Sci, Dept Med Lab Sci, Zaria, Nigeria.
[Ali, Kashif] Khan Univ Mardan, Dept Pharm Abdul Wali, Mardan, Pakistan.
[Maleknia, Shayan; Saffarioun, Mohammad] Alborz Univ Med Sci, Biopharmaceut Res Ctr, AryoGen Pharmed Inc, Karaj, Iran.
[Azizi, Gholamreza] Alborz Univ Med Sci, Non Communicable Dis Res Ctr, Karaj, Iran.
[Azizi, Gholamreza] Alborz Univ Med Sci, Non Communicable Dis Res Ctr, Res, Karaj, Iran.
C3 Bayero University; Monash University; Monash University Malaysia; Ahmadu
Bello University
RP Azizi, G (corresponding author), Alborz Univ Med Sci, Non Communicable Dis Res Ctr, Karaj, Iran.; Azizi, G (corresponding author), Alborz Univ Med Sci, Non Communicable Dis Res Ctr, Res, Karaj, Iran.
EM azizi@abzums.ac.ir
RI ZOHORA, FATEMA TUZ/HDO-0264-2022; Azizi, Gholamreza/B-9477-2018; Aliyu,
Mansur/GRR-7550-2022
OI Aliyu, Mansur/0000-0002-4223-2788; Zohora, Fatema
Tuz/0000-0001-6609-3324
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Zdravkovic N., 2017, PHYSL PATHOLOGY CYTO
NR 201
TC 94
Z9 100
U1 18
U2 85
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD OCT
PY 2022
VL 111
AR 109130
DI 10.1016/j.intimp.2022.109130
EA AUG 2022
PG 14
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA 4Y1CY
UT WOS:000861271500004
PM 35969896
OA Bronze
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Viswanatha, DS
Dogan, A
AF Viswanatha, D. S.
Dogan, A.
TI Hepatitis C virus and lymphoma
SO JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
ID NON-HODGKINS-LYMPHOMA; MIXED CRYOGLOBULINEMIA; BCL-2 REARRANGEMENT;
SOMATIC HYPERMUTATION; IMMUNOGLOBULIN GENE; VILLOUS LYMPHOCYTES; SPLENIC
LYMPHOMA; ANTIGEN RECEPTOR; HCV INFECTION; B-CELLS
AB Hepatitis C virus (HCV) is well known for its aetiological role in chronic non-A, non-B viral hepatitis, liver cirrhosis and hepatocellular carcinoma; in addition, the virus has also been implicated in a number of extra-hepatic "autoimmune'' disease manifestations. A causative association between HCV and non-Hodgkin lymphoma (NHL) was postulated relatively recently and has been the subject of intense investigation, as well as some debate. On the strength of epidemiological data, emerging biological investigations and clinical observations, HCV appears to be involved in the pathogenesis of at least a proportion of patients with NHL. Morphologically, HCV-associated lymphomas represent a variety of histological subtypes including marginal zone lymphoma (splenic, nodal and extranodal), small lymphocytic lymphoma/chronic lymphocytic leukaemia, lymphoplasmacytic lymphoma and diffuse large B-cell lymphoma. Remarkably, some HCV-associated NHL appears to be highly responsive to antiviral therapy, providing some clinical evidence for this relationship, as well as the prospect for novel therapeutic intervention.
C1 Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Dogan, A (corresponding author), Mayo Clin, Dept Lab Med & Pathol, 200 1st St SW, Rochester, MN 55905 USA.
EM ahmet@mayo.edu
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NR 47
TC 53
Z9 55
U1 0
U2 5
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0021-9746
EI 1472-4146
J9 J CLIN PATHOL
JI J. Clin. Pathol.
PD DEC
PY 2007
VL 60
IS 12
BP 1378
EP 1383
DI 10.1136/jcp.2007.051870
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 235MR
UT WOS:000251238900013
PM 18042694
OA Green Published
DA 2025-01-07
ER
PT J
AU Zhao, M
Liu, MY
AF Zhao, Michael
Liu, Mingyao
TI New Avenues for Nanoparticle-Related Therapies
SO NANOSCALE RESEARCH LETTERS
LA English
DT Article
DE Nanodrug delivery; Systemic diseases; Local delivery; Ex vivo lung
perfusion; Translational research
ID EX-VIVO PERFUSION; ISOLATED HEPATIC PERFUSION; DRUG-DELIVERY; LIVER
METASTASES; LUNG PERFUSION; DONOR LUNGS; AMINO-ACID; NANOMEDICINE;
TRANSPLANTATION; PEPTIDE
AB Development of nanoparticle-based drug delivery systems has been attempted for the treatment of cancer over the past decade. The enhanced permeability and retention (EPR) effect is the major mechanism to passively deliver nanodrugs to tumor tissue. However, a recent systematic review demonstrated limited success of these studies, with the clearance of nanoparticles by the mononuclear phagocytic system (MPS) being a major hurdle. Herein, we propose that nanotechnologists should reconsider their research focuses, aiming for therapeutic targets other than cancer. Treatments for diseases that do not (or less) rely on EPR should be considered, such as active targeting or MPS evasion systems. For example, systemic delivery of drugs through intravenous injection can be used to treat sepsis, multi-organ failure, metabolic disorders, blood diseases, immune and autoimmune diseases, etc. Local delivery of nanodrugs to organs such as the lung, rectum, or bladder may enhance the local drug concentration with less clearance via MPS. In transplant settings, ex vivo organ perfusion provides a new route to repair injury of isolated organs in the absence of MPS. Based on a similar concept, chemotherapy with in vivo lung perfusion techniques and other isolated organ perfusion provides opportunities for cancer therapy.
C1 [Zhao, Michael; Liu, Mingyao] Univ Hlth Network, Toronto Gen Hosp, Latner Thorac Surg Res Labs, Res Inst, 101 Coll St,Room TMDT2-814, Toronto, ON M5G 1L7, Canada.
[Zhao, Michael; Liu, Mingyao] Univ Toronto, Inst Med Sci, Toronto, ON, Canada.
[Liu, Mingyao] Univ Toronto, Dept Surg, Toronto, ON, Canada.
[Liu, Mingyao] Univ Toronto, Dept Med, Toronto, ON, Canada.
[Liu, Mingyao] Univ Toronto, Dept Physiol, Toronto, ON, Canada.
C3 University of Toronto; University Health Network Toronto; Toronto
General Hospital; University of Toronto; University of Toronto;
University of Toronto; University of Toronto
RP Liu, MY (corresponding author), Univ Hlth Network, Toronto Gen Hosp, Latner Thorac Surg Res Labs, Res Inst, 101 Coll St,Room TMDT2-814, Toronto, ON M5G 1L7, Canada.; Liu, MY (corresponding author), Univ Toronto, Inst Med Sci, Toronto, ON, Canada.; Liu, MY (corresponding author), Univ Toronto, Dept Surg, Toronto, ON, Canada.; Liu, MY (corresponding author), Univ Toronto, Dept Med, Toronto, ON, Canada.; Liu, MY (corresponding author), Univ Toronto, Dept Physiol, Toronto, ON, Canada.
EM mingyao.liu@utoronto.ca
RI Zhao, Michael/JXL-9119-2024; Liu, Mingyao/JFK-7090-2023
OI Liu, Mingyao/0000-0002-9188-8417
FU Canadian Institutes of Health Research [MOP-42546, MOP-119514,
PJT-148847]; Ontario Research Fund-Research Excellence award
FX This work is supported by the Canadian Institutes of Health Research
(operating grants MOP-42546, MOP-119514, and PJT-148847) and an Ontario
Research Fund-Research Excellence award.
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NR 44
TC 15
Z9 23
U1 1
U2 21
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1556-276X
J9 NANOSCALE RES LETT
JI Nanoscale Res. Lett.
PD MAY 8
PY 2018
VL 13
AR 136
DI 10.1186/s11671-018-2548-8
PG 5
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary;
Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science; Physics
GA GG3LS
UT WOS:000432593900001
PM 29740711
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Bush, H
Golabi, P
Otgonsuren, M
Rafiq, N
Venkatesan, C
Younossi, ZM
AF Bush, Haley
Golabi, Pegah
Otgonsuren, Munkhzul
Rafiq, Nila
Venkatesan, Chapy
Younossi, Zobair M.
TI Nonalcoholic Fatty Liver is Contributing to the Increase in Cases of
Liver Disease in US Emergency Departments
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE prevalence; mortality; length of stay; cost
ID HEPATITIS-C VIRUS; UNITED-STATES; RESOURCE UTILIZATION; MEDICARE
BENEFICIARIES; INPATIENT; MORTALITY; TRENDS; BURDEN; CARE;
STEATOHEPATITIS
AB Goals/Background: We aimed to assess temporal changes in the different types of liver disease (LD) cases and outcomes from emergency departments (EDs) across the United States.
Study: We used data from the National Inpatient Survey database from 2005 to 2011. The International Classification of Diseases, Ninth Revision (ICD-9) clinical modification codes identified hepatitis C virus (HCV), hepatitis B virus (HBV), alcoholic liver disease (ALD), nonalcoholic fatty liver disease (NAFLD), and other LDs including autoimmune hepatitis. We excluded cases without LD, nonhepatocellular carcinoma-related cancers, human immunodeficiency virus infection, or those with missing information. Logistic regression was used to estimate odds ratios with 95% confidence intervals. Controls were matched to cases without LD.
Results: During the study period, 20,641,839 cases were seen in EDs. Of these, 1,080,008 cases were related to LD and were matched to controls without LD (N=19,557,585). The number of cases with LD increased from 123,873 (2005) to 188,501 (2011) (P<0.0001). Among cases with LD, diagnosis of HCV, HBV, and ALD remained stable during the study years (41.60% vs. 38.20%, 3.70% vs. 2.80%, and 41.4% vs. 38.5%, respectively), whereas NAFLD doubled [6.00% of all LD (2005) to 11.90% of all LD (2011) (P<0.0001)]. Diagnosis of LD in the ED independently predicted increased patient mortality [odds ratio, 1.20 (1.17 to 1.22)].
Conclusions: The number of LD cases presenting to EDs is increasing, and a diagnosis of LD is associated with a higher patient mortality for those admitted through the ED. There is a dramatic increase of NAFLD diagnoses in the ED.
C1 [Bush, Haley; Golabi, Pegah; Otgonsuren, Munkhzul; Rafiq, Nila; Younossi, Zobair M.] Inova Fairfax Hosp, Inova Hlth Syst, Betty & Guy Beatty Ctr Integrated Res, Falls Church, VA USA.
[Rafiq, Nila; Venkatesan, Chapy; Younossi, Zobair M.] Inova Fairfax Hosp, Ctr Liver Dis, Dept Med, Falls Church, VA USA.
C3 Inova Fairfax Hospital; Inova Health System; Inova Fairfax Hospital
RP Younossi, ZM (corresponding author), Guy Beatty Ctr Integrated Res, Claude Moore Hlth Educ & Res Bldg,3300 Gallows Rd, Falls Church, VA 22042 USA.
EM zobair.younossi@inova.org
RI Younossi, Zobair M./JRY-9916-2023
OI Golabi, Pegah/0000-0001-9818-0983
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NR 23
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD JAN
PY 2019
VL 53
IS 1
BP 58
EP 64
DI 10.1097/MCG.0000000000001026
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HE6XH
UT WOS:000453562800016
PM 29608451
DA 2025-01-07
ER
PT J
AU Morita, SY
Tsuji, T
Terada, T
AF Morita, Shin-ya
Tsuji, Tokuji
Terada, Tomohiro
TI Protocols for Enzymatic Fluorometric Assays to Quantify Phospholipid
Classes
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE enzymatic fluorometric measurement; phosphatidylcholine;
phosphatidylethanolamine; phosphatidylserine; phosphatidic acid;
phosphatidylinositol; phosphatidylglycerol; cardiolipin; sphingomyelin
ID CHARACTERIZING OBSTRUCTIVE-JAUNDICE; HYDROGEN-PEROXIDE; PULMONARY
SURFACTANT; PLASMA SPHINGOMYELIN; LIPOPROTEIN-X; LIPIDS; OXIDASE;
PHOSPHATIDYLETHANOLAMINE; PHOSPHATIDYLSERINE; ACID
AB Phospholipids, consisting of a hydrophilic head group and two hydrophobic acyl chains, are essential for the structures of cell membranes, plasma lipoproteins, biliary mixed micelles, pulmonary surfactants, and extracellular vesicles. Beyond their structural roles, phospholipids have important roles in numerous biological processes. Thus, abnormalities in the metabolism and transport of phospholipids are involved in many diseases, including dyslipidemia, atherosclerosis, cholestasis, drug-induced liver injury, neurological diseases, autoimmune diseases, respiratory diseases, myopathies, and cancers. To further clarify the physiological, pathological, and molecular mechanisms and to identify disease biomarkers, we have recently developed enzymatic fluorometric assays for quantifying all major phospholipid classes, phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, phosphatidic acid, phosphatidylinositol, phosphatidylglycerol + cardiolipin, and sphingomyelin. These assays are specific, sensitive, simple, and high-throughput, and will be applicable to cells, intracellular organelles, tissues, fluids, lipoproteins, and extracellular vesicles. In this review, we present the detailed protocols for the enzymatic fluorometric measurements of phospholipid classes in cultured cells.
C1 [Morita, Shin-ya; Tsuji, Tokuji; Terada, Tomohiro] Shiga Univ, Dept Pharm, Med Sci Hosp, Otsu, Shiga 5202192, Japan.
C3 Shiga University
RP Morita, SY (corresponding author), Shiga Univ, Dept Pharm, Med Sci Hosp, Otsu, Shiga 5202192, Japan.
EM smorita@belle.shiga-med.ac.jp
RI TSUJI, Tokuji/KLY-3379-2024; Morita, Shin-ya/U-2793-2019
OI Morita, Shin-ya/0000-0003-4079-707X
FU PRIME from Japan Agency for Medical Research and Development (AMED);
JSPS KAKENHI grant [JP19K23799]; Research Foundation for Pharmaceutical
Sciences
FX This work was supported in part by the PRIME from Japan Agency for
Medical Research and Development (AMED), by JSPS KAKENHI grant number
JP19K23799, and by a grant from the Research Foundation for
Pharmaceutical Sciences.
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NR 79
TC 15
Z9 15
U1 4
U2 16
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2020
VL 21
IS 3
AR 1032
DI 10.3390/ijms21031032
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA KY4PQ
UT WOS:000522551606018
PM 32033167
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhang, RW
Tian, AY
Wang, J
Shen, XL
Qi, GX
Tang, YQ
AF Zhang, Rongwei
Tian, Ayong
Wang, Jun
Shen, Xueli
Qi, Guoxian
Tang, Yanqing
TI miR26a Modulates Th17/Treg Balance in the EAE
Model of Multiple Sclerosis by Targeting IL6
SO NEUROMOLECULAR MEDICINE
LA English
DT Article
DE Multiple sclerosis; Experimental autoimmune encephalomyelitis; miR26a;
T(h)17; T-reg; IL6
ID REGULATORY T-CELLS; MICRORNA EXPRESSION; AUTOIMMUNE ENCEPHALOMYELITIS;
IMMUNE-SYSTEM; LIVER-CANCER; DIFFERENTIATION; MIR-26A; LESIONS;
INFLAMMATION; LYMPHOCYTES
AB A number of different microRNAs (miRNAs) have been implicated in various autoimmune diseases, including multiple sclerosis (MS). T helper (T-h)17 and regulatory T cells (T-regs) have likewise been implicated as key players in MS, and a functional imbalance of these cell types is increasingly recognized as a key etiological factor in the disease. Although specific panels of transcription factors and cytokines are known to regulate the T(h)17/T-reg balance, the role of noncoding RNAs remains poorly understood. The inflammatory cytokine, interleukin (IL)6, appears to play a critical role in both the development of the T(h)17 response and the inhibition of T-reg functions. In this research, an IL6-associated miRNA, miR26a, was identified, and its normally downregulated expression was shown to be highly correlated with disease severity in patients suffering from MS as well as in C57BL/6 mice with experimental autoimmune encephalomyelitis (EAE; a well-established animal model of human MS). Using the EAE model system, in vivo silencing of miR26a was found to result in increased expression of T(h)17-related cytokines and increased severity of EAE, while overexpression of miR26a was found to result in reduced expression of T(h)17-related cytokines and a milder form of EAE. By contrast, T-reg cell-specific transcription factor, Foxp3, was found to be positively correlated with miR26a expression. Finally, miR26a was found to downregulate T(h)17 and to upregulate T-reg cell function through its targeting of IL6. Taken together, our data indicate an important role for miR26a in maintaining the T(h)17 and T-reg cell balance in MS that involves repression of IL6 expression.
C1 [Zhang, Rongwei; Shen, Xueli; Qi, Guoxian; Tang, Yanqing] China Med Univ, Affiliated Hosp 1, Dept Gerontol & Geriatr, Shenyang 110001, Liaoning, Peoples R China.
[Tian, Ayong] China Med Univ, Affiliated Hosp 1, Dept Anesthesiol, Shenyang 110001, Liaoning, Peoples R China.
[Wang, Jun] China Med Univ, Affiliated Hosp 1, Dept Neurol, Shenyang 110001, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; China Medical
University
RP Zhang, RW (corresponding author), China Med Univ, Affiliated Hosp 1, Dept Gerontol & Geriatr, 155 Nanjing North St, Shenyang 110001, Liaoning, Peoples R China.
EM rongweizhang@126.com
RI Zhang, Qing xia/JFH-8246-2023
FU National Natural Science Foundation of China [81100889]; Liaoning
Province Scientific Research Foundation for Doctors, China [20111106];
Liaoning Province Nature Science Foundation, China [2012225021-73]
FX The work was supported by grants from the National Natural Science
Foundation of China (No. 81100889), the Liaoning Province Scientific
Research Foundation for Doctors, China (No. 20111106), and the Liaoning
Province Nature Science Foundation, China (No. 2012225021-73).
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NR 46
TC 71
Z9 78
U1 0
U2 26
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1535-1084
EI 1559-1174
J9 NEUROMOL MED
JI Neuromol. Med.
PD MAR
PY 2015
VL 17
IS 1
BP 24
EP 34
DI 10.1007/s12017-014-8335-5
PG 11
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA CB8VW
UT WOS:000349910700003
PM 25362566
DA 2025-01-07
ER
PT J
AU Bernardes, D
Oliveira-Lima, OC
da Silva, TV
Juliano, MA
dos Santos, DM
Carvalho-Tavares, J
AF Bernardes, D.
Oliveira-Lima, O. C.
Vitarelli da Silva, T.
Juliano, M. A.
Moreira dos Santos, D.
Carvalho-Tavares, J.
TI Metabolic Alterations in Experimental Autoimmune Encephalomyelitis in
Mice: Effects of Prior Physical Exercise
SO NEUROPHYSIOLOGY
LA English
DT Article
DE experimental autoimmune encephalomyelitis (EAE); physical exercise;
cachexia; body mass; metabolic shifts
ID RAT SKELETAL-MUSCLE; MULTIPLE-SCLEROSIS; CANCER CACHEXIA; DISEASES;
BRAIN
AB Experimental autoimmune encephalomyelitis (EAE) induces significant reduction of the body mass concomitant to sickness behavior and anorexia. We investigated whether regular physical exercise prevents metabolic alterations associated with body mass loss occurring during EAE inflammatory peak. Female C57BL/6 mice were assigned to the unexercised and exercised (trained) groups. In four weeks, EAE was induced in half of the animals in each group, and the exercise protocol was maintained until 10 days post-induction (dpi 10) completing 6 weeks of regular exercise (forced swimming). At dpi 14, the relative mass of metabolic tissues, serum levels of triglycerides, cholesterol, and glucose, glycogen contents in the muscle and liver, and muscle levels of cytokines were measured. A significantly decreased clinical score associated with attenuation of the body mass loss in exercised EAE animals, as compared to the non-exercised ones, was observed. The associated metabolic parameters were not modified by this approach, although negative correlations between some parameters and clinical score at dpi 14 were observed. Although the prior program of aerobic exercise is capable of decreasing clinical score and body mass loss, it is not sufficient to modify metabolic outcomes associated with inflammation at the EAE peak.
C1 [Bernardes, D.; Oliveira-Lima, O. C.; Vitarelli da Silva, T.; Carvalho-Tavares, J.] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Fisiol & Biofis, Belo Horizonte, MG, Brazil.
[Juliano, M. A.] Univ Fed Sao Paulo, Dept Biofis, Sao Paulo, Brazil.
[Moreira dos Santos, D.] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Bioquim & Imunol, Belo Horizonte, MG, Brazil.
C3 Universidade Federal de Minas Gerais; Universidade Federal de Sao Paulo
(UNIFESP); Universidade Federal de Minas Gerais
RP Carvalho-Tavares, J (corresponding author), Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Fisiol & Biofis, Belo Horizonte, MG, Brazil.
EM julianat@icb.ufmg.br
RI Bernardes, Danielle/J-7767-2012
OI Bernardes, Danielle/0000-0002-0936-4236
FU Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq,
Brazil); Fundacao do Amparo a Pesquisa do Estado de Minas Gerais
(FAPEMIG, Minas Gerais, Brazil); Coordenacao de Aperfeicoamento de
Pessoal de Nivel Superior (CAPES, Brazil)
FX This work is a part of the DB PhD thesis. It received financial support
from the Conselho Nacional de Desenvolvimento Cientifico e Tecnologico
(CNPq, Brazil), the Fundacao do Amparo a Pesquisa do Estado de Minas
Gerais (FAPEMIG, Minas Gerais, Brazil), and the Coordenacao de
Aperfeicoamento de Pessoal de Nivel Superior (CAPES, Brazil).
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NR 17
TC 9
Z9 9
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0090-2977
EI 1573-9007
J9 NEUROPHYSIOLOGY+
JI Neurophysiology
PD APR
PY 2016
VL 48
IS 2
BP 117
EP 121
DI 10.1007/s11062-016-9577-7
PG 5
WC Neurosciences; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Physiology
GA DV4BX
UT WOS:000382870900008
DA 2025-01-07
ER
PT J
AU Udalova, IA
Ruhmann, M
Thomson, SJP
Midwood, KS
AF Udalova, Irina A.
Ruhmann, Michaela
Thomson, Scott J. P.
Midwood, Kim S.
TI Expression and Immune Function of Tenascin-C
SO CRITICAL REVIEWS IN IMMUNOLOGY
LA English
DT Article
DE tissue injury; pathogen infection; inflammation; fibrosis; gene
regulation; DAMP
ID EXTRACELLULAR-MATRIX PROTEIN; GROWTH-FACTOR-BETA; MARROW STROMAL CELLS;
GENE-EXPRESSION; TGF-BETA; SPLICE VARIANTS; HUMAN-SKIN; INFLAMMATORY
CYTOKINES; LIVER FIBROSIS; SUBEPITHELIAL FIBROSIS
AB Our immune system is designed to protect us from danger. Upon pathogen invasion and tissue injury, activation of both innate and adaptive immunity enables us to combat infection and to repair tissue damage. Tenascin-C is a large, extracellular matrix glycoprotein that has a very tightly controlled pattern of expression. Little or no tenascin-C is expressed in most healthy adult tissues; however, it is rapidly and transiently induced at sites of tissue injury and infection. Persistent tenascin-C expression is associated with pathologies such as chronic, non-healing wounds, autoimmune diseases, cancer, and fibrotic diseases. We discuss the myriad roles that this multifunctional molecule plays during the immune response, with a focus on how tissue levels of tenascin-C are regulated and the consequences of misregulated tenascin-C expression in immune regulated disease pathogenesis.
C1 [Udalova, Irina A.; Ruhmann, Michaela; Thomson, Scott J. P.; Midwood, Kim S.] Univ London Imperial Coll Sci Technol & Med, Fac Med, Div Rheumatol, Kennedy Inst, London W6 8LH, England.
C3 Imperial College London; University of Oxford
RP Midwood, KS (corresponding author), Univ London Imperial Coll Sci Technol & Med, Fac Med, Div Rheumatol, Kennedy Inst, 65 Aspenlea Rd, London W6 8LH, England.
EM k.midwood@imperial.ac.uk
RI Udalova, Irina/KYP-5574-2024
OI Udalova, Irina/0000-0002-6716-2528
FU Kennedy Institute Trustees; Arthritis Research UK; Medical Research
Council [81726, 82189]; European Community [Model-In 222008]; MRC
[G0700108] Funding Source: UKRI
FX The work was supported by the Kennedy Institute Trustees, Arthritis
Research UK, the Medical Research Council (81726 to K.S.M. and 82189 to
I.A.U.), and by European Community Seventh Framework Programme
FP7/2007-2013 (Model-In 222008).
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NR 260
TC 100
Z9 111
U1 2
U2 20
PU BEGELL HOUSE INC
PI DANBURY
PA 50 NORTH ST, DANBURY, CT 06810 USA
SN 1040-8401
EI 2162-6472
J9 CRIT REV IMMUNOL
JI Crit. Rev. Immunol.
PY 2011
VL 31
IS 2
BP 115
EP 145
DI 10.1615/CritRevImmunol.v31.i2.30
PG 31
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 764OW
UT WOS:000290642400003
PM 21542790
DA 2025-01-07
ER
PT J
AU Sun, LM
Muo, CH
Liang, JA
Chang, SN
Sung, FC
Kao, CH
AF Sun, L-M
Muo, C-H
Liang, J-A
Chang, S-N
Sung, F-C
Kao, C-H
TI Increased risk of cancer for patients with ankylosing spondylitis: a
nationwide population-based retrospective cohort study
SO SCANDINAVIAN JOURNAL OF RHEUMATOLOGY
LA English
DT Article
ID RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASE; RA-224; MALIGNANCIES;
MORTALITY; LYMPHOMA
AB Objectives: Few studies have investigated the relationship between ankylosing spondylitis (AS) and other inflammatory spondyloarthritis and subsequent cancer. The aim of this study was to determine whether AS is associated with cancer risk.
Method: We used data from the National Health Insurance (NHI) system of Taiwan to investigate this association. The AS cohort included 4133 patients, and each patient was randomly frequency matched with four persons without AS based on sex, age, and entry year (control cohort). We conducted a Cox proportional hazards regression analysis to estimate the influence of AS on cancer risk.
Results: Among patients with AS, the overall risk of developing cancer was 38% higher than that of people without AS, and the difference was significant [adjusted hazard ratio (HR) 1.38, 95% confidence interval (CI) 1.18-1.60]. This phenomenon held true even when we analysed males and females separately. The risk of developing lung or head and neck cancer among patients with AS was significantly higher; and risks for liver, bladder, and uterus cancers were marginally significantly higher.
Conclusions: This nationwide population-based cohort study shows that Taiwanese patients with AS have a higher risk of developing cancer, particularly lung or head and neck cancer.
C1 [Sun, L-M] Kaohsiung Armed Forces Gen Hosp, Zuoying Branch, Dept Radiat Oncol, Kaohsiung, Taiwan.
[Muo, C-H; Sung, F-C] China Med Univ Hosp, Management Off Hlth Data, Taichung, Taiwan.
[Liang, J-A] China Med Univ Hosp, Dept Radiat Oncol, Taichung, Taiwan.
[Liang, J-A; Sung, F-C; Kao, C-H] China Med Univ, Coll Med, Grad Inst Clin Med Sci, Taichung 404, Taiwan.
[Liang, J-A; Kao, C-H] China Med Univ, Coll Med, Sch Med, Taichung 404, Taiwan.
[Chang, S-N] Taichung Vet Gen Hosp, Dept Med Res, Taichung, Taiwan.
[Kao, C-H] China Med Univ Hosp, Dept Nucl Med, PET Ctr, Taichung, Taiwan.
C3 China Medical University Taiwan; China Medical University Hospital -
Taiwan; China Medical University Taiwan; China Medical University
Hospital - Taiwan; China Medical University Taiwan; China Medical
University Taiwan; Taichung Veterans General Hospital; China Medical
University Taiwan; China Medical University Hospital - Taiwan
RP Kao, CH (corresponding author), China Med Univ, Coll Med, Grad Inst Clin Med Sci, 2 Yuh Der Rd, Taichung 404, Taiwan.
EM d10040@mail.cmuh.org.tw
FU Taiwan Department of Health Clinical Trial and Research Centre and for
Excellence [DOH102-TD-B-111-004]; Taiwan Department of Health Cancer
Research Centre for Excellence [DOH102-TD-C-111-005]; [DMR-101-061];
[DMR-100-076]
FX This study was supported in part by study projects (DMR-101-061 and
DMR-100-076) in our hospital and the Taiwan Department of Health
Clinical Trial and Research Centre and for Excellence
(DOH102-TD-B-111-004), and the Taiwan Department of Health Cancer
Research Centre for Excellence (DOH102-TD-C-111-005).
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NR 28
TC 32
Z9 33
U1 0
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0300-9742
EI 1502-7732
J9 SCAND J RHEUMATOL
JI Scand. J. Rheumatol.
PY 2014
VL 43
IS 4
BP 301
EP 306
DI 10.3109/03009742.2013.863969
PG 6
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA AN3CF
UT WOS:000340461800008
PM 24559186
DA 2025-01-07
ER
PT J
AU Ding, DH
Li, JF
Xu, LZ
Wang, JY
Tan, D
Lin, WY
AF Ding, Donghao
Li, Jiangfeng
Xu, Lizhen
Wang, Jiangyan
Tan, Dan
Lin, Weiying
TI Development of an activatable hydrogen sulfide-specific two-photon
fluorescent probe for bioimaging in an air pouch inflammation model
SO JOURNAL OF MATERIALS CHEMISTRY B
LA English
DT Article
ID CANCER; H2S
AB Inflammation caused by traumatic, ischemic, infectious, autoimmune or toxic injury may further trigger cancer and even death. Overexpression of hydrogen sulfide (H2S) in vivo has been identified as a biomarker for various types of inflammation. Identification-responsive fluorescence imaging probes have broad application prospects for in vivo diagnosis of inflammation. However, it is a challenge to design an imaging probe that concurrently responds to the target molecules to improve the sensitivity and specificity of inflammation detection. Herein, we designed and synthesized an activatable two-photon fluorescent probe to detect H2S. Fl-H2S had high selectivity, excellent photostabLe signals and Low detection Limit for recognizing H2S. In addition, Fl-H2S showed excellent two-photon fluorescence properties in cell and Liver tissue visualization experiments, with a penetration depth of up to 126 mu m in Liver tissue. Most importantly, the unique probe Fl-H2S was the first probe to monitor H2S levels in a mouse air pouch inflammation model by fluorescence imaging technology. We expect Fl-H2S to become an effective tool for longitudinal monitoring of inflammation, diagnosis of inflammation and prediction of underlying pathogenesis of related diseases by detecting H2S.
C1 [Ding, Donghao; Li, Jiangfeng; Xu, Lizhen; Wang, Jiangyan; Tan, Dan; Lin, Weiying] Guangxi Univ, Sch Chem & Chem Engn, Inst Opt Mat & Chem Biol, Guangxi Key Lab Electrochem Energy Mat, Nanning 530004, Guangxi, Peoples R China.
C3 Guangxi University
RP Lin, WY (corresponding author), Guangxi Univ, Sch Chem & Chem Engn, Inst Opt Mat & Chem Biol, Guangxi Key Lab Electrochem Energy Mat, Nanning 530004, Guangxi, Peoples R China.
EM weiyinglin2013@163.cam
RI Wang, Jiangyan/L-8968-2016
OI li, jiangfeng/0000-0001-6366-4021
FU National Natural Science Foundation of China [21672083, 21877048,
22077048]; Guangxi Natural Science Foundation [2021GXNSFDA075003,
AD21220061]; Guangxi University [A3040051003]
FX This work was financially supported by the National Natural Science
Foundation of China (21672083, 21877048, and 22077048), Guangxi Natural
Science Foundation (2021GXNSFDA075003, AD21220061), and the startup fund
of Guangxi University (A3040051003).
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NR 29
TC 8
Z9 8
U1 11
U2 65
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 2050-750X
EI 2050-7518
J9 J MATER CHEM B
JI J. Mat. Chem. B
PD JUN 22
PY 2022
VL 10
IS 24
BP 4568
EP 4574
DI 10.1039/d2tb00681b
EA MAY 2022
PG 7
WC Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science
GA 2H5FF
UT WOS:000803189800001
PM 35639477
DA 2025-01-07
ER
PT J
AU Zhao, L
Qiu, DK
Ma, X
AF Zhao, Li
Qiu, De Kai
Ma, Xiong
TI Th17 cells: The emerging reciprocal partner of regulatory T cells in the
liver
SO JOURNAL OF DIGESTIVE DISEASES
LA English
DT Review
DE cytokine; homeostasis; inflammation; regulatory T cell; Th17 cell
ID PRIMARY BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; MESSENGER-RNA;
PERIPHERAL-BLOOD; CYTOKINE PROFILE; GENE-EXPRESSION; INNATE IMMUNITY;
ACUTE REJECTION; TGF-BETA; INTERLEUKIN-17
AB T helper cells that produce interleukin-17 (IL-17) (Th17 cells) have recently been identified as the third distinct subset of effector T cells, the differentiation of which depends on specific transcription nuclear factor retinoic acid-related orphan nuclear receptor-gamma t. Emerging data have suggested that Th17 cells play an important role in innate immunity, adaptive immunity and autoimmunity. Interestingly, there is a reciprocal relationship between Th17 cells and regulatory T cells (Treg), not only in development, but also in their effector function. Transforming growth factor (TGF)-beta induces Treg-specific transcription factor Forkhead box P3(FOXP3), while the addition of IL-6 to TGF-beta inhibits the generation of Treg cells and induces Th17 cells. It is proposed that the fine balance between Th17 and Treg cells is crucial for maintenance of immune homeostasis. In addition to IL-6, other factors such as retinoic acid, rapamycin, or cytokines (e.g., IL-2 and IL-27) could dictate the balance between Th17 and Treg cells. Since Treg cells play an important role in hepatic immunity with overregulation in chronic viral hepatitis and hepatic carcinoma, and inadequate inhibition in autoimmune liver diseases, graft rejection and acute liver failure, it is reasonable to assume that Th17 cells may play a reciprocal role in these diseases. Thus, future research on the Treg/Th17 balance may provide an opportunity to illustrate the pathogenesis of hepatic inflammation and to explore new therapeutic targets for immune-related liver diseases.
C1 [Zhao, Li; Qiu, De Kai; Ma, Xiong] Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Inst Digest Dis, Dept Gastroenterol,Sch Med, Shanghai 200001, Peoples R China.
C3 Shanghai Jiao Tong University
RP Ma, X (corresponding author), Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Inst Digest Dis, Dept Gastroenterol,Sch Med, Shanghai 200001, Peoples R China.
EM maxiongmd@163.com
OI Ma, Xiong/0000-0001-9616-4672
FU Shanghai Leading Academic Discipline Project [Y0205]; National Natural
Science Foundation of China [30571730, 30972751]
FX Grant support: This work was partially supported by Shanghai Leading
Academic Discipline Project Grant (Y0205, XM) and awards from the
National Natural Science Foundation of China (nos 30571730 and 30972751
XM).
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NR 75
TC 55
Z9 62
U1 0
U2 15
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-2972
EI 1751-2980
J9 J DIGEST DIS
JI J. Dig. Dis.
PD JUN
PY 2010
VL 11
IS 3
BP 126
EP 133
DI 10.1111/j.1751-2980.2010.00428.x
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 601PV
UT WOS:000278075900002
PM 20579216
DA 2025-01-07
ER
PT J
AU Wakil, A
Muzahim, Y
Awadallah, M
Kumar, V
Mazzaferro, N
Greenberg, P
Pyrsopoulos, N
AF Wakil, Ali
Muzahim, Yasameen
Awadallah, Mina
Kumar, Vikash
Mazzaferro, Natale
Greenberg, Patricia
Pyrsopoulos, Nikolaos
TI Trends of autoimmune liver disease inpatient hospitalization and
mortality from 2011 to 2017: A United States nationwide analysis
SO WORLD JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Autoimmune hepatitis; Autoimmune liver disease; Epidemiology;
Cost-Effective care; Admissions trend; Mortality rate
ID MEDICAL PROGRESS; TRANSPLANTATION; DIAGNOSIS; HEPATITIS
AB BACKGROUND Autoimmune liver diseases (AiLD) encompass a variety of disorders that target either the liver cells (autoimmune hepatitis, AIH) or the bile ducts [(primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC)]. These conditions can progress to chronic liver disease (CLD), which is characterized by fibrosis, cirrhosis, and hepatocellular carcinoma. Recent studies have indicated a rise in hospitalizations and associated costs for CLD in the US, but information regarding inpatient admissions specifically for AiLD remains limited. AIM To examine the trends and mortality of inpatient hospitalization of AiLD from 2011 to 2017. METHODS This study is a retrospective analysis utilizing the National Inpatient Sample (NIS) databases. All subjects admitted between 2011 and 2017 with a diagnosis of AiLD (AIH, PBC, PSC) were identified using the International Classification of Diseases (ICD-9) and ICD-10 codes. primary AiLD admission was defined if the first admission code was one of the AiLD codes. secondary AiLD admission was defined as having the AiLD diagnosis anywhere in the admission diagnosis (25 diagnoses). Subjects aged 21 years and older were included. The national estimates of hospitalization were derived using sample weights provided by NIS. chi(2) tests for categorical data were used. The primary trend characteristics were in-hospital mortality, hospital charges, and length of stay. RESULTS From 2011 to 2017, hospitalization rates witnessed a significant decline, dropping from 83263 admissions to 74850 admissions (P < 0.05). The patients hospitalized were predominantly elderly (median 53% for age > 65), mostly female (median 59%) (P < 0.05), and primarily Caucasians (median 68%) (P < 0.05). Medicare was the major insurance (median 56%), followed by private payer (median 27%) (P < 0.05). The South was the top geographical distribution for these admissions (median 33%) (P < 0.05), with most admissions taking place in big teaching institutions (median 63%) (P < 0.05). Total charges for admissions rose from 66031 in 2011 to 78987 in 2017 (P < 0.05), while the inpatient mortality rate had a median of 4.9% (P < 0.05), rising from 4.67% in 2011 to 5.43% in 2017. The median length of stay remained relatively stable, changing from 6.94 days (SD = 0.07) in 2011 to 6.51 days (SD = 0.06) in 2017 (P < 0.05). Acute renal failure emerged as the most common risk factor associated with an increased death rate, affecting nearly 68% of patients (P < 0.05). CONCLUSION AiLD-inpatient hospitalization showed a decrease in overall trends over the studied years, however there is a significant increase in financial burden on healthcare with increasing in-hospital costs along with increase in mortality of hospitalized patient with AiLD.
C1 [Wakil, Ali; Kumar, Vikash] Brooklyn Hosp Ctr, Dept Gastroenterol & Hepatol, Brooklyn, NY 11201 USA.
[Muzahim, Yasameen] Univ Iowa Hosp & Clin, Dept Gastroenterol & Hepatol, Iowa City, IA 52242 USA.
[Awadallah, Mina; Pyrsopoulos, Nikolaos] Rutgers New Jersey Med Sch, Dept Gastroenterol & Hepatol, Newark, NJ 07103 USA.
[Mazzaferro, Natale; Greenberg, Patricia] Rutgers Sch Publ Hlth, Dept Biostat & Epidemiol, Piscataway, NJ 08854 USA.
C3 Brooklyn Hospital Center; University of Iowa; Rutgers University System;
Rutgers University New Brunswick; Rutgers University Biomedical & Health
Sciences; Rutgers University System
RP Pyrsopoulos, N (corresponding author), Rutgers New Jersey Med Sch, Dept Gastroenterol & Hepatol, Newark, NJ 07103 USA.
EM pyrsopni@njms.rutgers.edu
RI Kumar, Vikash/KAM-2125-2024
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Tanaka T, 2015, INTRACTABLE RARE DIS, V4, P33, DOI 10.5582/irdr.2014.01034
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NR 32
TC 0
Z9 0
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5182
J9 WORLD J HEPATOL
JI World J. Hepatol.
PD JUL 27
PY 2024
VL 16
IS 7
DI 10.4254/wjh.v16.i7.1029
PG 11
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA A2T7Q
UT WOS:001281112300005
PM 39086532
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Wang, HM
Chen, ZJ
McCluskey, J
Corbett, AJ
AF Wang, Huimeng
Chen, Zhenjun
McCluskey, James
Corbett, Alexandra J.
TI Mouse models illuminate MAIT cell biology
SO MOLECULAR IMMUNOLOGY
LA English
DT Article
DE Mucosal-associated invariant T (MAIT) cells; Mouse models; Infection;
Disease; Immune protection; Immunopathology
ID INVARIANT T-CELLS; TISSUE-REPAIR; LIVER-DISEASE; TCR; ACTIVATION;
EXPRESSION; HETEROGENEITY; DERIVATIVES; METASTASES; INFILTRATE
AB The field of mucosal-associated invariant T cell (MAIT) biology has grown rapidly since the identification of the vitamin-B-based antigens recognised by these specialised T cells. Over the past few years, our understanding of the complexities of MAIT cell function has developed, as they find their place among the other better known cells of the immune system. Key questions relate to understanding when MAIT cells help, when they hinder or cause harm, and when they do not matter. Exploiting mouse strains that differ in MAIT cell numbers, leveraged by specific detection of MAIT cells using MR1-tetramers, it has now been shown that MAIT cells play important immune roles in settings that include bacterial and viral infections, autoimmune diseases and cancer. We have also learnt much about their development, modes of activation and response to commensal microbiota, and begun to try ways to manipulate MAIT cells to improve disease outcomes. Here we review recent studies that have assessed MAIT cells in models of disease.
C1 [Wang, Huimeng; Chen, Zhenjun; McCluskey, James; Corbett, Alexandra J.] Univ Melbourne, Dept Microbiol & Immunol, Peter Doherty Inst Infect & Immun, Melbourne, Vic 3000, Australia.
[Wang, Huimeng] Guangzhou Med Univ, Affiliated Hosp 1, Guangzhou Inst Resp Dis, State Key Lab Resp Dis, Guangzhou 510182, Guangdong, Peoples R China.
C3 University of Melbourne; Peter Doherty Institute; Guangzhou Medical
University; State Key Laboratory of Respiratory Disease
RP Corbett, AJ (corresponding author), Univ Melbourne, Dept Microbiol & Immunol, Peter Doherty Inst Infect & Immun, Melbourne, Vic 3000, Australia.
EM corbetta@unimelb.edu.au
RI Wang, Huimeng/AAE-6554-2022; Corbett, Alexandra/A-1225-2019; McCluskey,
James/A-1291-2007
OI McCluskey, James/0000-0002-8597-815X
FU Australian Research Council (ARC) [FT160100083]; National Health and
Medical Research Council of Australia (NHMRC) [1113293, 1125493];
National Institute Of Allergy And Infectious Diseases of the National
Institutes of Health (NIH) [R01AI148407]; National Health and Medical
Research Council of Australia [1125493] Funding Source: NHMRC;
Australian Research Council [FT160100083] Funding Source: Australian
Research Council
FX AJC is supported by a Future Fellowship (FT160100083) from the
Australian Research Council (ARC). The authors are supported by research
grants from the National Health and Medical Research Council of
Australia (NHMRC) (1113293, 1125493) and the National Institute Of
Allergy And Infectious Diseases of the National Institutes of Health
(NIH) (R01AI148407). The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
NIH, NHMRC or ARC.
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NR 107
TC 9
Z9 10
U1 2
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
EI 1872-9142
J9 MOL IMMUNOL
JI Mol. Immunol.
PD FEB
PY 2021
VL 130
BP 55
EP 63
DI 10.1016/j.molimm.2020.12.007
PG 9
WC Biochemistry & Molecular Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Immunology
GA PS6BL
UT WOS:000608007700008
PM 33360377
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Oikonomou, KG
Zachou, K
Dalekos, GN
AF Oikonomou, Katerina G.
Zachou, Kalliopi
Dalekos, George N.
TI Alpha-actinin: A multidisciplinary protein with important role in B-cell
driven autoimmunity
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE alpha-Actinin; Filamentous actin; Smooth muscle autoantibodies; Systemic
lupus etythematosus; Autoimmune hepatitis; Lupus nephritis; Liver
autoimmunity
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; ANTI-DNA ANTIBODIES; SOLUBLE LIVER
ANTIGEN; CHRONIC ACTIVE HEPATITIS; SEGMENTAL GLOMERULOSCLEROSIS;
CRYOELECTRON MICROSCOPY; MUTANT ALPHA-ACTININ-4; GENE AMPLIFICATION;
STRUCTURAL PROTEIN; NEPHROTIC SYNDROME
AB Alpha-actinin (alpha-actinin) is a ubiquitous cytoskeletal protein, which belongs to the superfamily of filamentous actin (F-actin) crosslinking proteins. It is present in multiple subcellular regions of both muscle and non-muscle cells, including cell-cell and cell-matrix contact sites, cellular protrusions and stress fiber dense regions and thus, it seems to bear multiple important roles in the cell by linking the cytoskeleton to many different transmembrane proteins in a variety of junctions. Four isoforms of human alpha-actinin have already been identified namely, the "muscles" alpha-actinin-2 and alpha-actinin-3 and the "non-muscles" alpha-actinin-1 and alpha-actinin-4. The precise functions of alpha-actinin isoforms as well as the precise role and significance of their binding to F-actin particularly in-vivo, have been elusive. They are generally believed to represent key structural components of large-scale F-actin cohesion in cells required for cell shape and motility. alpha-Actinin-2 has been implicated in myopathies such as nemalin body myopathy, hypertrophic and dilated cardiomyopathy and it may have at least an indirect pathogenetic role in diseases of the central nervous system (CNS) like schizophrenia, epilepsy, ischemic brain damage, CNS lupus and neurodegenerative disorders. The role of "non-muscle" alpha-actinins in the kidney seems to be crucial as an essential component of the glomerular filtration barrier. Therefore, they have been implicated in the pathogenesis of familial focal segmental glomerulosclerosis, nephrotic syndrome, IgA nephropathy, focal segmental glomerulosclerosis and minimal change disease. alpha-Actinin is also expressed on the membrane and cytosol of parenchymal and ductal cells of the liver and it seems that it interacts with hepatitis C virus in an essential way for the replication of the virus. Finally alpha-actinin, especially alpha-actinin-4, has been implicated in cancer cell progression and metastasis, as well as the migration of several cell types participating in the immune response. Based on these functions, the accumulating reported evidence of the importance of alpha-actinin as a target autoantigen in the pathogenesis of autoimmune diseases, particularly systemic lupus erythematosus and autoimmune hepatitis, is also discussed along with the possible perspectives that are potentially emerging from the study of this peculiar molecule in health and disease. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Zachou, Kalliopi; Dalekos, George N.] Univ Thessaly, Sch Med, Dept Med, Biopolis 41110, Larissa, Greece.
[Zachou, Kalliopi; Dalekos, George N.] Univ Thessaly, Sch Med, Res Lab Internal Med, Biopolis 41110, Larissa, Greece.
[Oikonomou, Katerina G.; Zachou, Kalliopi; Dalekos, George N.] Ctr Res & Technol Thessaly, Inst Biomed Res & Technol, Larisa, Greece.
C3 University of Thessaly; University of Thessaly
RP Dalekos, GN (corresponding author), Univ Thessaly, Sch Med, Dept Med, Biopolis 41110, Larissa, Greece.
EM dalekos@med.uth.gr
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NR 115
TC 73
Z9 82
U1 0
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD MAY
PY 2011
VL 10
IS 7
BP 389
EP 396
DI 10.1016/j.autrev.2010.12.009
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 770XT
UT WOS:000291122500004
PM 21241830
DA 2025-01-07
ER
PT J
AU Nam, D
Chapiro, J
Paradis, V
Seraphin, TP
Kather, JN
AF Nam, David
Chapiro, Julius
Paradis, Valerie
Seraphin, Tobias Paul
Kather, Jakob Nikolas
TI Artificial intelligence in liver diseases: Improving diagnostics,
prognostics and response prediction
SO JHEP REPORTS
LA English
DT Review
DE Artificial intelli-gence; deep learning; machine learning; diagnostic
support system; imaging; multimodal data integration
ID CONVOLUTIONAL NEURAL-NETWORK; HEPATOCELLULAR-CARCINOMA; RADIOMICS;
MACHINE; CLASSIFICATION; QUANTIFICATION; VARIABILITY; MODEL; RISK; BIAS
AB Clinical routine in hepatology involves the diagnosis and treatment of a wide spectrum of meta-bolic, infectious, autoimmune and neoplastic diseases. Clinicians integrate qualitative and quanti-tative information from multiple data sources to make a diagnosis, prognosticate the disease course, and recommend a treatment. In the last 5 years, advances in artificial intelligence (AI), particularly in deep learning, have made it possible to extract clinically relevant information from complex and diverse clinical datasets. In particular, histopathology and radiology image data contain diagnostic, prognostic and predictive information which AI can extract. Ultimately, such AI systems could be implemented in clinical routine as decision support tools. However, in the context of hepatology, this requires further large-scale clinical validation and regulatory approval. Herein, we summarise the state of the art in AI in hepatology with a particular focus on histopathology and radiology data. We present a roadmap for the further development of novel biomarkers in hep-atology and outline critical obstacles which need to be overcome.(c) 2022 The Authors. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver (EASL). This is an open access article under the CC BY license (http://creativecommons.org/licenses/ by/4.0/).
C1 [Nam, David; Chapiro, Julius] Yale Sch Med, Dept Radiol & Biomed Imaging, Sect Intervent Radiol, New Haven, CT USA.
[Paradis, Valerie] Univ Paris, Ctr Rech inflammat, CRI, INSERM U1149, Paris, France.
[Paradis, Valerie] Univ Paris, Hop Beaujon, AP HP, Dept Pathol, Clichy, France.
[Seraphin, Tobias Paul] Heinrich Heine Univ Dusseldorf, Univ Hosp Dusseldorf, Med Fac, Dept Gastroenterol Hepatol & Infect Dis, Dusseldorf, Germany.
[Seraphin, Tobias Paul; Kather, Jakob Nikolas] Univ Hosp RWTH Aachen, Dept Med 3, Aachen, Germany.
[Kather, Jakob Nikolas] Univ Leeds, Leeds Inst Med Res St Jamess, Pathol & Data Analyt, Leeds, England.
[Kather, Jakob Nikolas] Univ Hosp Heidelberg, Natl Ctr Tumor Dis NCT, Med Oncol, Heidelberg, Germany.
[Kather, Jakob Nikolas] RWTH Univ Hosp, Dept Med 3, D-52074 Aachen, Germany.
C3 Yale University; Institut National de la Sante et de la Recherche
Medicale (Inserm); Universite Paris Cite; Assistance Publique Hopitaux
Paris (APHP); Universite Paris Cite; Hopital Universitaire Beaujon -
APHP; Heinrich Heine University Dusseldorf; Heinrich Heine University
Dusseldorf Hospital; RWTH Aachen University; RWTH Aachen University
Hospital; University of Leeds; Helmholtz Association; German Cancer
Research Center (DKFZ); Ruprecht Karls University Heidelberg; RWTH
Aachen University; RWTH Aachen University Hospital
RP Kather, JN (corresponding author), RWTH Univ Hosp, Dept Med 3, D-52074 Aachen, Germany.
EM jakob.kather@gmail.com
RI Seraphin, Tobias/AAY-1710-2021; Paradis, Valerie/X-9097-2019; Kather,
Jakob Nikolas/D-4279-2015
OI Seraphin, Tobias/0000-0001-9884-8752; Kather, Jakob
Nikolas/0000-0002-3730-5348; Paradis, Valerie/0000-0003-3142-3762
FU German Federal Ministry of Health [ZMVI1-2520DAT111]; Max-Eder-Programme
of the German Cancer Aid [70113864]; National Institutes of Health
[R01CA206180]; Society of Interventional Oncology; Radiological Society
of North America; Philips; Yale Center for Clinical Investigation;
Guerbet
FX JNK is supported by the German Federal Ministry of Health (DEEP LIVER,
ZMVI1-2520DAT111) and the Max-Eder-Programme of the German Cancer Aid
(grant #70113864) . TPS is supported by the German Federal Ministry of
Health (DEEP LIVER, ZMVI1-2520DAT111) . JC reports grants from the
National Institutes of Health (R01CA206180) , Society of Interventional
Oncology, Radiological Society of North America, Philips, Guerbet,
Boston Scientific and the Yale Center for Clinical Investigation.
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NR 111
TC 84
Z9 87
U1 35
U2 142
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2589-5559
J9 JHEP REP
JI JHEP Rep.
PD APR
PY 2022
VL 4
IS 4
AR 100443
DI 10.1016/j.jhepr.2022.100443
EA FEB 2022
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 0Y2UX
UT WOS:000790250200004
PM 35243281
OA gold, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Xiang, S
Liu, JP
Dong, NG
Shi, JW
Xiao, YQ
Wang, Y
Hu, XJ
Gong, L
Wang, WS
AF Xiang, Shui
Liu, Jinping
Dong, Nianguo
Shi, Jiawei
Xiao, Yaqiong
Wang, Yu
Hu, Xingjian
Gong, Li
Wang, Wenshuo
TI Suppressor of Cytokine Signaling 3 Is a Negative Regulator for
Neointimal Hyperplasia of Vein Graft Stenosis
SO JOURNAL OF VASCULAR RESEARCH
LA English
DT Article
DE Coronary artery bypass graft; Vascular smooth muscle cell proliferation;
Vein graft stenosis
ID HEPATOCELLULAR-CARCINOMA; SH2 DOMAIN; SOCS3; INFLAMMATION; MECHANISMS;
JAK/STAT; THERAPY; PROTEIN; GROWTH; GENE
AB Coronary artery bypass graft (CABG) surgery is one of the most effective treatments for coronary artery disease. However, neointimal hyperplasia and ultimate luminal occlusion that is caused by vascular smooth muscle cell (VSMC) migration, proliferation and inflammatory response impede the long-term prognosis. The SOCS3 protein is involved in modulating various autoimmune and inflammatory diseases. However, the role of SOCS3 in vein graft disease is still unclear. We found that the mRNA and protein expression levels of IL-1 beta, IL-6, MCP-1, ICAM-1, TNF-alpha, STAT3, P-STAT3 and SOCS3 were significantly higher in the graft samples compared to normal veins. After transfecting the recombinant adenovirus carrying the rat SOCS3 gene into cultured rat VSMCs or grafting veins in rat, SOCS3 overexpression was found to significantly inhibit VSMC migration and proliferation in vitro and neointimal hyperplasia in vivo, respectively. Furthermore, SOCS3 overexpression inhibited VSMC migration and growth in vitro and alleviated VSMC inflammation in vitro by inhibiting STAT3 activation and phosphorylation. In conclusion, SOCS3 is a crucial physiological negative regulator for vein graft failure and provides a novel target for vein graft stenosis therapy after CABG. (C) 2014 S. Karger AG, Basel
C1 [Xiang, Shui; Liu, Jinping; Dong, Nianguo; Shi, Jiawei; Xiao, Yaqiong; Hu, Xingjian; Gong, Li; Wang, Wenshuo] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Cardiovasc Surg, Wuhan 30022, Peoples R China.
[Wang, Yu] Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Biochem & Mol Biol, Wuhan 30022, Peoples R China.
[Xiang, Shui] Cent Hosp Enshi Autonomous Prefecture, Dept Cardiothorac Surg, Enshi, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
Science & Technology
RP Dong, NG (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Cardiovasc Surg, Wuhan 30022, Peoples R China.
EM dongnianguo@hotmail.com
RI Wang, wenshuo/AAO-1848-2020; Xiao, Yaqiong/KVY-4590-2024; Shi,
Jiawei/KDU-6911-2024
FU National Nature Science Fund of China [30872540, 81270322, 81270297]
FX This work was supported by the National Nature Science Fund of China
(30872540, 81270322 and 81270297).
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Z9 18
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J9 J VASC RES
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PY 2014
VL 51
IS 2
BP 132
EP 143
DI 10.1159/000355193
PG 12
WC Physiology; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology; Cardiovascular System & Cardiology
GA AJ4RM
UT WOS:000337663500006
PM 24685947
DA 2025-01-07
ER
PT J
AU Acharya, SK
AF Acharya, Subrat Kumar
TI Overview of acute liver failure in India
SO INDIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Acute liver failure; Hepatitis viruses; Severe acute liver injury
ID NATIONAL ASSOCIATION; FULMINANT-HEPATITIS; CONSENSUS STATEMENT; EARLY
INDICATORS; DISEASE; MODEL; TRANSPLANTATION; PROGNOSIS
AB Acute liver failure (ALF) is an infrequent, but serious complication subsequent to severe acute liver injury (sALI) due to various hepatotoxic agents such as hepatotropic virus(es) and drugs such as anti-tubercular medications, paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics and anti-cancer and anti-epileptic therapy and due to metabolic and autoimmune disease flares. ALF after sALI presents with encephalopathy associated with prolonged international normalized ratio (INR). Mortality in ALF is high and ranges between 50% and 80%. Due to severe liver damage, multiple sequels consequent to hepatic dysfunction result in complications such as hyperammonemia that culminates in encephalopathy associated with cerebral edema; innate immune paralysis resulting in increased frequency of infections and endotoxemia causing decrease in systemic vascular resistance (SVR) and tissue hypoperfusion and damage-associated molecular patterns (DAMPs) released from damaged hepatic parenchyma inducing pro-inflammatory cytokine storm, which may cause other organ dysfunctions. Certain etiologies such as hepatitis E virus and hepatitis A virus-related ALF or paracetamol-ALF (hyper-acute presentation) have better survival than remaining causes. In addition, if etiology-specific treatment (antivirals for ALF related to hepatitis B virus (HBV) or Herpes simplex virus (HSV) or N-acetylcysteine for paracetamol) is available, then the outcome with treatment is better. About half of the patients can be salvaged with medical therapy. All patients need intensive care and organ support to provide time for the liver to regenerate. Various prognostic models to predict high probability of mortality have been described, which should be used to select patient early during the disease for liver transplantation, which is associated with high long-term survival in these sick patients. The Indian National Association for Study of the Liver (INASL) recommends the ALF-Early Dynamic (ALFED) model as a preferred prognostic model in the Indian scenario, where hepatitis viruses are a dominant etiology of ALF and occur on a na & iuml;ve liver with good regenerative capacity.
C1 [Acharya, Subrat Kumar] KIIT Univ, Kalinga Inst Med Sci, Bhubaneswar 751024, India.
[Acharya, Subrat Kumar] Fortis Escorts Digest & Liver Inst, New Delhi 110025, India.
C3 Kalinga Institute of Industrial Technology (KIIT)
RP Acharya, SK (corresponding author), KIIT Univ, Kalinga Inst Med Sci, Bhubaneswar 751024, India.; Acharya, SK (corresponding author), Fortis Escorts Digest & Liver Inst, New Delhi 110025, India.
EM subratacharya@gmail.com
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U2 1
PU SPRINGER INDIA
PI NEW DELHI
PA 7TH FLOOR, VIJAYA BUILDING, 17, BARAKHAMBA ROAD, NEW DELHI, 110 001,
INDIA
SN 0254-8860
EI 0975-0711
J9 INDIAN J GASTROENTER
JI Indian J. Gastroenterol.
PD APR
PY 2024
VL 43
IS 2
BP 296
EP 311
DI 10.1007/s12664-024-01589-z
EA MAY 2024
PG 16
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA SD4A1
UT WOS:001221281600003
PM 38722512
DA 2025-01-07
ER
PT J
AU Kreiniz, N
Katz, OB
Polliack, A
Tadmor, T
AF Kreiniz, Natalia
Katz, Ofrat Beyar
Polliack, Aaron
Tadmor, Tamar
TI The Clinical Spectrum of Hepatic Manifestations in Chronic Lymphocytic
Leukemia
SO CLINICAL LYMPHOMA MYELOMA & LEUKEMIA
LA English
DT Review
DE CLL; Drug toxicity; Hepatitis; Hepatomegaly; Liver
ID B-VIRUS REACTIVATION; GIANT-CELL HEPATITIS; ACUTE LIVER-FAILURE; RICHTER
SYNDROME; HEMATOLOGICAL MALIGNANCIES; HEPATOCELLULAR-CARCINOMA; DISEASE;
IDELALISIB; PATIENT; CRYOGLOBULINEMIA
AB Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western world, characterized by the presence of long-lived circulating leukemic cells in the peripheral blood that may infiltrate all organs, particularly those of the reticulo-endothelial system. Liver enlargement and elevation of liver enzymes related to specific involvement by the underlying disease are well-recognized features in these patients. In CLL, the differential diagnosis of liver disorders is broad and includes liver infiltration by leukemic cells, immunologic manifestations associated with CLL, primary and secondary hepatic malignancies, drug-induced hepatotoxicity, infections, and Richter transformation. The above conditions can cause serious and even fatal complications such as acute liver failure. The aim of this study was to summarize all available published literature on hepatic manifestations encountered in CLL. This review contains sections on liver enlargement because of leukemic infiltration, autoimmune-induced hepatic dysfunction, acute liver failure, drug-induced liver toxicity, and associated malignancies. A high index of clinical suspicion and appropriate diagnostic evaluation, including liver biopsy in special circumstances, are important for both accurate diagnosis and deciding on the most appropriate treatment to prevent the development of fatal complications of acute liver failure.
C1 [Kreiniz, Natalia; Tadmor, Tamar] Bnai Zion Med Ctr, Hematol Unit, 47 Golomb St, IL-31048 Haifa, Israel.
[Katz, Ofrat Beyar] Rambam Hlth Care Campus, Haifa, Israel.
[Polliack, Aaron] Hebrew Univ Jerusalem, Hadassah Univ Hosp, Hematol Dept, Med Sch, Jerusalem, Israel.
C3 Bnai Zion Medical Center; Hebrew University of Jerusalem
RP Tadmor, T (corresponding author), Bnai Zion Med Ctr, Hematol Unit, 47 Golomb St, IL-31048 Haifa, Israel.
EM tamar.tadmor@b-zion.org.il
RI Kreiniz, Natalia/HGB-0195-2022; Katz, Ofrat/AAO-1790-2020
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NR 77
TC 10
Z9 11
U1 0
U2 4
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 2152-2650
EI 2152-2669
J9 CL LYMPH MYELOM LEUK
JI Clin. Lymphoma Myeloma Leuk.
PD DEC
PY 2017
VL 17
IS 12
BP 863
EP 869
DI 10.1016/j.clml.2017.07.008
PG 7
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA FN6EK
UT WOS:000416105700024
PM 28803824
DA 2025-01-07
ER
PT J
AU Gan, LL
Zhu, X
Gao, Y
Zhong, MY
Liao, SB
Huang, G
Yan, YM
AF Gan, Lulu
Zhu, Xuan
Gao, Yue
Zhong, Mingyao
Liao, Shibo
Huang, Gao
Yan, Yimin
TI A review on nondiabetic hypoglycemia from various causes: Case series
report
SO MEDICINE
LA English
DT Review
DE insulin autoimmune syndrome; insulinoma; nondiabetic hypoglycemia;
non-islet cell tumor-induced hypoglycemia
ID DISEASE
AB Rationale:Hypoglycemia is common in patients with glucose regulation disorders and related diabetic treatments but is rare in nondiabetic patients. Severe hypoglycemia can cause harm to patients' cognition, consciousness, central nervous system, cardiovascular and cerebrovascular system, and even death. However, the most fundamental way to control hypoglycemia is to identify the cause and deal with the primary disease. This article introduces 3 cases of nondiabetic hypoglycemia with different causes, aiming to improve our understanding of nondiabetic hypoglycemia and improve the ability of early diagnosis and differential diagnosis.Patient concerns:Case 1 is a 19-year-old female with a history of recurrent coma, and magnetic resonance imaging and endoscopic ultrasound of the pancreas suggest insulinoma. Case 2 is a 74-year-old male with a history of viral hepatitis, and computerized tomography shows multiple nodules in the liver, which is diagnosed as liver cancer. Case 3 is a 39-year-old female with a history of taking methimazole, who tested positive for insulin antibodies, and was diagnosed with insulin autoimmune syndrome.Diagnosis:All 3 patients were diagnosed with nondiabetic hypoglycemia, but the causes varied, and included insulinoma, non-islet cell tumor-induced hypoglycemia, and insulin autoimmune syndrome.Interventions:Case 1 underwent pancreatic tail resection; case 2 refused anti-tumor treatment and received glucose injections for palliative treatment only; and case 3 stopped taking methimazole.Outcomes:After surgery, the blood sugar in case 1 returned to normal, and the blood sugar in case 2 was maintained at about 6.0 mmol/L. The symptoms of hypoglycemia gradually improved in case 3 after stopping the medication.Lessons:Non-diabetic hypoglycemia requires further examination to clarify the cause, and the correct differential diagnosis can provide timely and effective treatment, improving the patient's prognosis.
C1 [Gan, Lulu; Liao, Shibo; Huang, Gao; Yan, Yimin] Wuhan Univ Sci & Technol, Xiaogan Hosp, Cent Hosp Xiaogan, Dept Endocrinol, Xiaogan 432000, Hubei, Peoples R China.
[Gan, Lulu; Zhu, Xuan; Gao, Yue; Zhong, Mingyao; Yan, Yimin] Wuhan Univ Sci & Technol, Med Coll, Wuhan, Peoples R China.
C3 Wuhan University of Science & Technology; Wuhan University of Science &
Technology
RP Yan, YM (corresponding author), Wuhan Univ Sci & Technol, Xiaogan Hosp, Cent Hosp Xiaogan, Dept Endocrinol, Xiaogan 432000, Hubei, Peoples R China.
EM ganlulu2021@163.com; 840938189@163.com; gy863696@163.com;
pjbxylh@163.com; liaoshibo@163.com; 251070713@qq.com;
yanyimin180@163.com
RI Gao, Yue/KWT-8530-2024
OI Yan, Yimin/0000-0002-3351-4732
FU Youth Talents Project of Joint Fund of Hubei Health Commission
[WJ2019H170]; Xiaogan Natural Science Project [XGKJ2020010033]
FX This study was supported by Youth Talents Project of Joint Fund of Hubei
Health Commission (WJ2019H170) and Xiaogan Natural Science Project
(XGKJ2020010033).
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NR 18
TC 1
Z9 1
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD NOV 24
PY 2023
VL 102
IS 47
AR e36273
DI 10.1097/MD.0000000000036273
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA AD3Z5
UT WOS:001116496400110
PM 38013348
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Stanford, SM
Bottini, N
AF Stanford, Stephanie M. M.
Bottini, Nunzio
TI Targeting protein phosphatases in cancer immunotherapy and autoimmune
disorders
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Review
ID ENRICHED TYROSINE PHOSPHATASE; INTESTINAL EPITHELIAL-CELLS; EFFECTOR
T-CELLS; HEPATOCELLULAR-CARCINOMA; RHEUMATOID-ARTHRITIS; NONRECEPTOR
TYPE-2; CUTTING EDGE; INHIBITION; PTPN22; SHP-1
AB Dysregulated protein phosphorylation is implicated in numerous human diseases, but targeting protein phosphates has traditionally proved challenging. Here, Stanford and Bottini provide an overview of protein phosphatase families, focusing on their roles in autoimmunity and tumour immunity. Emerging strategies to tackle these targets and agents in development are assessed.
Protein phosphatases act as key regulators of multiple important cellular processes and are attractive therapeutic targets for various diseases. Although extensive effort has been dedicated to phosphatase-targeted drug discovery, early expeditions for competitive phosphatase inhibitors were plagued by druggability issues, leading to the stigmatization of phosphatases as difficult targets. Despite challenges, persistent efforts have led to the identification of several drug-like, non-competitive modulators of some of these enzymes - including SH2 domain-containing protein tyrosine phosphatase 2, protein tyrosine phosphatase 1B, vascular endothelial protein tyrosine phosphatase and protein phosphatase 1 - reigniting interest in therapeutic targeting of phosphatases. Here, we discuss recent progress in phosphatase drug discovery, with emphasis on the development of selective modulators that exhibit biological activity. The roles and regulation of protein phosphatases in immune cells and their potential as powerful targets for immuno-oncology and autoimmunity indications are assessed.
C1 [Stanford, Stephanie M. M.; Bottini, Nunzio] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
C3 University of California System; University of California San Diego
RP Stanford, SM; Bottini, N (corresponding author), Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
EM ststanford@health.ucsd.edu; nbottini@health.ucsd.edu
FU NIH [R01AI148073, R01HL151306, R01AR066053, R01DK106233, R01HL152717,
R01AI070544, R21CA245621]; American Diabetes Association [1-15-INI-13]
FX The authors were supported by grants R01AI148073, R01HL151306,
R01AR066053, R01DK106233, R01HL152717 and R01AI070544 to N.B. and
R21CA245621 to S.M.S. from the NIH, and Pathway to Stop Diabetes Grant
1-15-INI-13 to S.M.S. from the American Diabetes Association.
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NR 273
TC 46
Z9 50
U1 17
U2 74
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1474-1776
EI 1474-1784
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD APR
PY 2023
VL 22
IS 4
BP 273
EP 294
DI 10.1038/s41573-022-00618-w
EA JAN 2023
PG 22
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA D3WA2
UT WOS:000919924800001
PM 36693907
OA Bronze, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Rubín, A
Aguilera, V
Berenguer, M
AF Rubin, A.
Aguilera, V.
Berenguer, M.
TI Liver transplantation and hepatitis C
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Review
ID VIRUS-INFECTED RECIPIENTS; ANTIVIRAL THERAPY; FIBROSIS PROGRESSION;
TRANSIENT ELASTOGRAPHY; NATURAL-HISTORY; PEGYLATED-INTERFERON; DONOR
AGE; RECURRENCE; RIBAVIRIN; IMPACT
AB Hepatitis C virus (HCV)-related end-stage cirrhosis with/without hepatocellular carcinoma is the primary indication for liver transplantation in many countries. Unfortunately, HCV is not eliminated by transplantation and graft re-infection is the rule, resulting in HCV-related graft disease. The natural history of recurrent hepatitis is variable; overall, progression to cirrhosis occurs in 20-30% and allograft failure in 10% after 5-10 years from transplantation. The use of poor quality organs, particularly from old donors, has a significant negative impact on disease severity and transplant outcome. In contrast, antiviral therapy, particularly if it results in permanent eradication of the virus, is associated with improved histology, reduced rate of graft decompensation and enhanced outcome. Disease monitoring, through protocol liver biopsies and new non-invasive tools, is essential to select patients at need of antiviral therapy. Peginterferon with ribavirin, used similarly to what is done in the non-transplant setting, is currently the treatment of choice; sustained viral response is achieved in about 35% of cases. Side effects, particularly anemia, are extremely frequent and sometimes severe (rejection, de novo autoimmune hepatitis). Retransplantation (RT) is the last option for the small subset of patients with allograft failure due to HCV recurrence who fulfil minimum criteria based on RT survival models. (C) 2011 Elsevier Masson SAS. All rights reserved.
C1 [Berenguer, M.] Hosp Univ & Politecn La Fe, Inst Salud Carlos III, Hepatol Liver Transplantat unit, Digest Med Serv, Valencia 46026, Spain.
Hosp Univ & Politecn La Fe, Inst Salud Carlos III, Natl Network Ctr Hepatol & Gastroenterol Res, Valencia 46026, Spain.
C3 Hospital Universitari i Politecnic La Fe; Instituto de Salud Carlos III;
Instituto de Salud Carlos III; Hospital Universitari i Politecnic La Fe
RP Berenguer, M (corresponding author), Hosp Univ & Politecn La Fe, Inst Salud Carlos III, Hepatol Liver Transplantat unit, Digest Med Serv, Bulevar S-N, Valencia 46026, Spain.
EM MBHAYM@TELELINE.ES
RI Berenguer, Marina/ABG-8602-2020; AGUILERA SANCHO-TELLO, MARIA
VICTORIA/ABH-8070-2020
OI Berenguer, Marina/0000-0001-9246-4264; AGUILERA SANCHO-TELLO, MARIA
VICTORIA/0000-0001-6492-0357
CR Bacchetti P, 2010, INT J BIOSTAT, V6, DOI 10.2202/1557-4679.1213
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Selzner N, 2009, TRANSPLANTATION, V88, P1214, DOI 10.1097/TP.0b013e3181bd783c
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NR 55
TC 49
Z9 50
U1 0
U2 8
PU ELSEVIER MASSON
PI MILANO
PA VIA PALEOCAPA 7, 20121 MILANO, ITALY
SN 2210-7401
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD DEC
PY 2011
VL 35
IS 12
BP 805
EP 812
DI 10.1016/j.clinre.2011.04.009
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 883EA
UT WOS:000299615600006
PM 21963086
DA 2025-01-07
ER
PT J
AU Ludewig, B
Krebs, P
Metters, H
Tatzel, J
Türeci, Ö
Sahin, U
AF Ludewig, B
Krebs, P
Metters, H
Tatzel, J
Türeci, Ö
Sahin, U
TI Molecular characterization of virus-induced autoantibody responses
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
DE autoantibodies; tumor immunity; virus-induced immunopathology; SEREX
ID HUMAN TUMOR-ANTIGENS; B-CELL REPERTOIRE; IMMUNE-RESPONSES;
CANCER-PATIENTS; AUTOIMMUNE-DISEASE; MEMBRANE PROTEIN; HUMAN NEOPLASMS;
DEFICIENT MICE; IDENTIFICATION; ANTIBODIES
AB Here we present a comprehensive molecular mapping of virus-induced autoimmune B cell responses obtained by serological identification of antigens by recombinant expression cloning analysis. Immunoscreening of cDNA expression libraries of various organs (lung, liver, and spleen) using sera from mice infected with cytopathic (vaccinia virus [VV]) or noncytopathic (lymphocytic choriomeningitis virus [LCMV]) viruses revealed a broad specificity of the elicited autoantibody response. Interestingly, the majority of the identified autoantigens have been previously described as autoantigens in humans. We found that induction of virus-induced autoanti-bodies of the immunoglobulin G class largely depends on the CD40-CD40L-mediated interaction between T and B cells. Furthermore, antibody titers against a number of autoantigens were comparable to the concomitantly induced antiviral antibody response. Comparison of serum reactivity against a selected panel of autoantigens after infection with VV, LCMV, or vesicular stomatitis virus showed that the different virus infections triggered distinct autoantibody responses, suggesting that virus infections may leave specific "autoantibody fingerprints" in the infected host.
C1 Kantonsspital St Gallen, Res Dept, CH-9007 St Gallen, Switzerland.
Univ Zurich Hosp, Inst Expt Immunol, Dept Pathol, CH-8091 Zurich, Switzerland.
Univ Mainz, Dept Internal Med, D-55131 Mainz, Germany.
C3 Kantonsspital St. Gallen; University of Zurich; University Zurich
Hospital; Johannes Gutenberg University of Mainz
RP Ludewig, B (corresponding author), Kantonsspital St Gallen, Res Dept, Rotschacherstr 95, CH-9007 St Gallen, Switzerland.
EM burkhard.ludewig@kssg.ch
RI Sahin, Ugur/L-4818-2017; Krebs, Philippe/A-3449-2012
OI Sahin, Ugur/0000-0003-0363-1564; Krebs, Philippe/0000-0003-4918-6654
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NR 45
TC 33
Z9 36
U1 0
U2 2
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD SEP 6
PY 2004
VL 200
IS 5
BP 637
EP 646
DI 10.1084/jem.20040358
PG 10
WC Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Research & Experimental Medicine
GA 854IC
UT WOS:000223895300010
PM 15353556
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Montalvao, F
Garcia, Z
Celli, S
Breart, B
Deguine, J
Van Rooijen, N
Bousso, P
AF Montalvao, Fabricio
Garcia, Zacarias
Celli, Susanna
Breart, Beatrice
Deguine, Jacques
Van Rooijen, Nico
Bousso, Philippe
TI The mechanism of anti-CD20-mediated B cell depletion revealed by
intravital imaging
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID MONOCLONAL-ANTIBODY; MACROPHAGES; LYMPHOCYTE; THERAPY; CANCER
AB Anti-CD20 Ab therapy has proven successful for treating B cell malignancies and a number of autoimmune diseases. However, how anti-CD20 Abs operate in vivo to mediate B cell depletion is not fully understood. In particular, the anatomical location, the type of effector cells, and the mechanism underlying anti-CD20 therapy remain uncertain. Here, we found that the liver is a major site for B cell depletion and that recirculation accounts for the decrease in B cell numbers observed in secondary lymphoid organs. Using intravital imaging, we established that, upon anti-CD20 treatment, Kupffer cells (KCs) mediate the abrupt arrest and subsequent engulfment of B cells circulating in the liver sinusoids. KCs were also effective in depleting malignant B cells in a model of spontaneous lymphoma. Our results identify Ab-dependent cellular phagocytosis by KCs as a primary mechanism of anti-CD20 therapy and provide an experimental framework for optimizing the efficacy of therapeutic Abs.
C1 [Montalvao, Fabricio; Garcia, Zacarias; Celli, Susanna; Breart, Beatrice; Deguine, Jacques; Bousso, Philippe] Inst Pasteur, Dynam Immune Responses Unit, F-75015 Paris, France.
[Montalvao, Fabricio; Garcia, Zacarias; Celli, Susanna; Breart, Beatrice; Deguine, Jacques; Bousso, Philippe] INSERM, U668, Paris, France.
[Van Rooijen, Nico] Vrije Univ Amsterdam Med Ctr, Dept Mol Cell Biol, Amsterdam, Netherlands.
C3 Pasteur Network; Universite Paris Cite; Institut Pasteur Paris; Institut
National de la Sante et de la Recherche Medicale (Inserm); Vrije
Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER
RP Bousso, P (corresponding author), Inst Pasteur, Dynam Immune Responses Unit, 25 Rue Dr Roux, F-75015 Paris, France.
EM philippe.bousso@pasteur.fr
RI Van Rooijen, Nico/Z-1578-2019; Breart, Beatrice/M-7123-2014; Celli,
Susanna/M-7138-2014; BOUSSO, Philippe/M-6547-2014
OI Montalvao Ferreira, Fabricio/0000-0002-3872-929X; Garcia,
Zacarias/0000-0003-0774-809X; Deguine, Jacques/0000-0001-9218-3040;
BOUSSO, Philippe/0000-0002-6362-561X
FU Institut Pasteur, INSERM; Fondation pour la Recherche Medicale; European
Research Council
FX We thank F. Lemaitre for help in the generating cell lines. This work
was supported by Institut Pasteur, INSERM, the Fondation pour la
Recherche Medicale, and an European Research Council starting grant
(LymphocyteContacts).
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NR 25
TC 149
Z9 166
U1 0
U2 13
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2013
VL 123
IS 12
BP 5098
EP 5103
DI 10.1172/JCI70972
PG 6
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 263RQ
UT WOS:000327826100017
PM 24177426
OA Green Submitted, Bronze, Green Published
DA 2025-01-07
ER
PT J
AU Daimary, UD
Girisa, S
Parama, D
Verma, E
Kumar, A
Kunnumakkara, AB
AF Daimary, Uzini Devi
Girisa, Sosmitha
Parama, Dey
Verma, Elika
Kumar, Aviral
Kunnumakkara, Ajaikumar B.
TI Embelin: A novel XIAP inhibitor for the prevention and treatment of
chronic diseases
SO JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
LA English
DT Review
DE anti-cancer; antioxidant; embelin; STAT3; XIAP
ID NF-KAPPA-B; TRAIL-INDUCED APOPTOSIS; X-LINKED INHIBITOR; CELL
LUNG-CANCER; HIGH-FAT DIET; HEPATOCELLULAR-CARCINOMA CELLS; INDUCED
OXIDATIVE STRESS; STAT3 SIGNALING CASCADE; NEGATIVE BREAST-CANCER;
XENOGRAFT MOUSE MODEL
AB Chronic diseases are a serious health concern worldwide, especially in the elderly population. Most chronic diseases like cancer, cardiovascular ailments, neurodegenerative disorders, and autoimmune diseases are caused due to the abnormal functioning of multiple signaling pathways that give rise to critical anomalies in the body. Although a lot of advanced therapies are available, these have failed to entirely cure the disease due to their less efficacy. Apart from this, they have been shown to manifest disturbing side effects which hamper the patient's quality of life to the extreme. Since the last few decades, extensive studies have been done on natural herbs due to their excellent medicinal benefits. Components present in natural herbs target multiple signaling pathways involved in diseases and therefore hold high potential in the prevention and treatment of various chronic diseases. Embelin, a benzoquinone, is one such agent isolated from Embelia ribes, which has shown excellent biological activities toward several chronic ailments by upregulating a number of antioxidant enzymes (e.g., SOD, CAT, GSH, etc.), inhibiting anti-apoptotic genes (e.g., TRAIL, XIAP, survivin, etc.), modulating transcription factors (e.g., NF-kappa B, STAT3, etc.) blocking inflammatory biomarkers (e.g., NO, IL-1 beta, IL-6, TNF-alpha, etc.), monitoring cell cycle synchronizing genes (e.g., p53, cyclins, CDKs, etc.), and so forth. Several preclinical studies have confirmed its excellent therapeutic activities against malicious diseases like cancer, obesity, heart diseases, Alzheimer's, and so forth. This review presents an overview of embelin, its therapeutic prospective, and the molecular targets in different chronic diseases.
C1 [Daimary, Uzini Devi; Girisa, Sosmitha; Parama, Dey; Verma, Elika; Kumar, Aviral; Kunnumakkara, Ajaikumar B.] Indian Inst Technol IIT Guwahati, DBT AIST Int Ctr Translat & Environm Res DAICTR, Dept Biosci & Bioengn, Canc Biol Lab, Gauhati 781039, Assam, India.
C3 Indian Institute of Technology System (IIT System); Indian Institute of
Technology (IIT) - Guwahati
RP Kunnumakkara, AB (corresponding author), Indian Inst Technol IIT Guwahati, DBT AIST Int Ctr Translat & Environm Res DAICTR, Dept Biosci & Bioengn, Canc Biol Lab, Gauhati 781039, Assam, India.
EM kunnumakkara@iitg.ac.in
RI Kumar, Aviral/HJH-1434-2023; Kunnumakkara, Ajaikumar/AAH-5214-2019;
Girisa, Sosmitha/JGD-3270-2023; Kunnumakkara, Ajaikumar/H-8566-2012
OI VERMA, ELIKA/0000-0002-6642-7280; Kumar, Aviral/0000-0002-9893-1430;
Kunnumakkara, Ajaikumar/0000-0001-9121-6816
FU Indian Council of Medical Research (ICMR), Government of India
[NCD/NER/4/2018-19]
FX Indian Council of Medical Research (ICMR), Government of India,
Grant/Award Number: NCD/NER/4/2018-19 (dt. 22.06.2018)
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NR 266
TC 14
Z9 14
U1 2
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1095-6670
EI 1099-0461
J9 J BIOCHEM MOL TOXIC
JI J. Biochem. Mol. Toxicol.
PD FEB
PY 2022
VL 36
IS 2
AR e22950
DI 10.1002/jbt.22950
EA NOV 2021
PG 27
WC Biochemistry & Molecular Biology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Toxicology
GA YY8NX
UT WOS:000723208300001
PM 34842329
DA 2025-01-07
ER
PT J
AU Anjiki, N
Hoshino, R
Ohnishi, Y
Hioki, K
Irie, Y
Ishige, A
Watanabe, K
AF Anjiki, N
Hoshino, R
Ohnishi, Y
Hioki, K
Irie, Y
Ishige, A
Watanabe, K
TI A Kampo formula Juzen-taiho-to induces expression of metallothioneins in
mice
SO PHYTOTHERAPY RESEARCH
LA English
DT Article
DE Juzen-taiho-to; JTX; metallothionein; Kampo; herbal medicine; mouse
ID MEDICINE; CELLS
AB Juzen-taiho-to (JTX), one of the commonly prescribed traditional Japanese herbal medicines (Kampo), is indicated for adjunctive treatment of cancers and autoimmune diseases. To understand the mechanisms underlying the clinical effects of JTX, the effects of orally administered JTX on the expression of metallothioneins (MTs) were examined in the liver, spleen, small and large intestines of mice. In addition, the expression of MTs in specific pathogen free (SPF) mice was examined to understand the participation of intestinal bacteria in the expression of MTs. JTX enhanced expression of MT-I and -II significantly in the liver of SPF mice. Induction of MT-II expression was observed also in the small intestine. Intestinal bacteria appeared to have no effect on MTs expression. Neither expression of MT-III nor its induction was observed in any tissue. These findings strongly suggest that MTs should mediate at least some effects of JTX in mice. Copyright (c) 2005 John Wiley & Sons, Ltd.
C1 Keio Univ, Sch Med, Dept Oriental Med, Shinjuku Ku, Tokyo 1608582, Japan.
Cent Inst Expt Anim, Kawasaki, Kanagawa 2160001, Japan.
C3 Keio University
RP Keio Univ, Sch Med, Dept Oriental Med, Shinjuku Ku, 35 Shinano Machi, Tokyo 1608582, Japan.
EM iymkdks@yahoo.co.jp
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SN 0951-418X
EI 1099-1573
J9 PHYTOTHER RES
JI Phytother. Res.
PD OCT
PY 2005
VL 19
IS 10
BP 915
EP 917
DI 10.1002/ptr.1747
PG 3
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 984XR
UT WOS:000233341200016
PM 16261526
DA 2025-01-07
ER
PT J
AU Fu, JX
Guo, Q
Feng, Y
Cheng, P
Wu, AH
AF Fu, Jinxing
Guo, Qing
Feng, Yuan
Cheng, Peng
Wu, Anhua
TI Dual role of fucosidase in cancers and its clinical potential
SO JOURNAL OF CANCER
LA English
DT Review
DE Fucosidase; defucosylation; cancer; microenvironment; signaling pathway
ID ALPHA-L-FUCOSIDASE; ORAL PRECANCEROUS CONDITIONS; FUCOSYL-TRANSFERASE;
HEPATOCELLULAR-CARCINOMA; CORE FUCOSYLATION; DOWN-REGULATION; GENE
FUCA1; EXPRESSION; SERUM; GLYCOSYLATION
AB Glycosidases and glycosyltransferases greatly impact malignant phenotype of tumors though genetics and epigenetics mechanisms. As the member of glycoside hydrolase (GH) families 29A, alpha-L-fucosidases (AFUs) are involved in the hydrolysis of terminal L-fucose residues linked via alpha-1,2, alpha-1,3, alpha-1,4 or alpha-1,6 to the reducing end of N-acetyl glucosamine (GlcNAc) of oligosaccharide chains. The defucosylation process mediated by AFUs contributes to the development of various diseases, such as chronic inflammatory diseases, immune disorders, and autoimmune diseases by reducing the interaction between fucosylated adhesion molecules supporting leukocyte extravasation. AFUs also impair crucial cell-extracellular matrix (ECM) interactions and presumably subsequent cell signaling pathways, which lead to changes in tumor function and behavior. There are two isoforms of AFUs in human, namely alpha-L-fucosidase 1 (FUCA1) and alpha-L-fucosidase 2 (FUCA2), respectively. FUCA1 is a p53 target gene and can hydrolyze different fucosylation sites on epidermal growth factor receptor (EGFR), thereby determining the activation of EGFR. FUCA2 mediates the adhesion between Helicobacter pylori and gastric mucosa and is upregulated in 24 tumor types. Besides, based on the participation of AFU in signaling pathways and tumor progression, we discuss the prospect of AFU as a therapeutic target.
C1 [Fu, Jinxing; Guo, Qing; Feng, Yuan; Cheng, Peng; Wu, Anhua] China Med Univ, Dept Neurosurg, First Hosp, Shenyang, Peoples R China.
[Cheng, Peng; Wu, Anhua] China Med Univ, First Hosp, 155 Nanjingbei St, Shenyang 110001, Liaoning, Peoples R China.
C3 China Medical University; China Medical University
RP Cheng, P; Wu, AH (corresponding author), China Med Univ, First Hosp, 155 Nanjingbei St, Shenyang 110001, Liaoning, Peoples R China.
EM chengpengcmu@sina.com; ahwu@cmu.edu.cn
RI Cheng, Peng/R-6211-2016
FU National Natural Science Foundation of China [81872057, 81872054];
Natural Science Foundation of Liaoning Province [20180550063,
20170541020, 2020BS117]
FX Funding This work was supported by the National Natural Science
Foundation of China (no. 81872057 to P. Cheng; 81872054 to A. Wu) , and
the Natural Science Foundation of Liaoning Province (no. 20180550063, to
P. Cheng. no. 20170541020, no. 2020BS117, to Q. Guo.) .
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PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2022
VL 13
IS 10
BP 3121
EP 3132
DI 10.7150/jca.75840
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4U9ZP
UT WOS:000859144200003
PM 36046653
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Li, DY
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AF Li, Dianyang
Yu, Wenying
Lai, Maode
TI Towards understandings of serine/arginine-rich splicing factors
SO ACTA PHARMACEUTICA SINICA B
LA English
DT Review
DE Alternative splicing; RNA metabolism; Cancer therapy; Tauopathy;
Autoimmune diseases; Small molecule inhibitor
ID RNA-RECOGNITION MOTIFS; TAU EXON 10; CANCER-ASSOCIATED GENES;
MESSENGER-RNA; SR PROTEIN; FACTOR ASF/SF2; FACTOR SF2/ASF;
HEPATOCELLULAR-CARCINOMA; UP-REGULATION; PROCESSIVE PHOSPHORYLATION
AB Serine/arginine-rich splicing factors (SRSFs) refer to twelve RNA-binding proteins which regulate splice site recognition and spliceosome assembly during precursor messenger RNA splicing. SRSFs also participate in other RNA metabolic events, such as transcription, translation and nonsense -mediated decay, during their shuttling between nucleus and cytoplasm, making them indispensable for genome diversity and cellular activity. Of note, aberrant SRSF expression and/or mutations elicit fallacies in gene splicing, leading to the generation of pathogenic gene and protein isoforms, which highlights the therapeutic potential of targeting SRSF to treat diseases. In this review, we updated current understanding of SRSF structures and functions in RNA metabolism. Next, we analyzed SRSF-induced aberrant gene expression and their pathogenic outcomes in cancers and non-tumor diseases. The development of some well-characterized SRSF inhibitors was discussed in detail. We hope this review will contribute to future studies of SRSF functions and drug development targeting SRSFs.& COPY; 2023 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Li, Dianyang; Lai, Maode] China Pharmaceut Univ, Sch Basic Med & Clin Pharm, Nanjing 210009, Peoples R China.
[Yu, Wenying] China Pharmaceut Univ, State Key Lab Nat Med, Nanjing 210009, Peoples R China.
[Lai, Maode] Zhejiang Univ, Chinese Acad Med Sci 2019RU042, Res Unit Intelligence Classificat Tumor Pathol & P, Key Lab Dis Prote Zhejiang Prov,Dept Pathol,Sch Me, Hangzhou 310058, Peoples R China.
C3 China Pharmaceutical University; China Pharmaceutical University;
Zhejiang University
RP Lai, MD (corresponding author), China Pharmaceut Univ, Sch Basic Med & Clin Pharm, Nanjing 210009, Peoples R China.; Yu, WY (corresponding author), China Pharmaceut Univ, State Key Lab Nat Med, Nanjing 210009, Peoples R China.; Lai, MD (corresponding author), Zhejiang Univ, Chinese Acad Med Sci 2019RU042, Res Unit Intelligence Classificat Tumor Pathol & P, Key Lab Dis Prote Zhejiang Prov,Dept Pathol,Sch Me, Hangzhou 310058, Peoples R China.
EM ywy@cpu.edu.cn; lmd@zju.edu.cn
RI 余, 文颖/HIR-4518-2022
FU National Natural Science Foundation of China [82150203]
FX This work was supported by grants from the National Natural Science
Foundation of China (Grant No. 82150203) .
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NR 257
TC 20
Z9 22
U1 3
U2 26
PU INST MATERIA MEDICA, CHINESE ACAD MEDICAL SCIENCES
PI BEIJING
PA C/O EDITORIAL BOARD OF ACTA PHARMACEUTICA SINICA, 1 XIANNONGTAN ST,
BEIJING, 100050, PEOPLES R CHINA
SN 2211-3835
EI 2211-3843
J9 ACTA PHARM SIN B
JI Acta Pharm. Sin. B
PD AUG
PY 2023
VL 13
IS 8
BP 3181
EP 3207
DI 10.1016/j.apsb.2023.05.022
EA AUG 2023
PG 27
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA Q8ZM4
UT WOS:001060346300001
PM 37655328
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Tian, ZG
Gershwin, ME
Zhang, C
AF Tian, Zhigang
Gershwin, M. Eric
Zhang, Cai
TI Regulatory NK cells in autoimmune disease
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Review
DE Natural killer cells; Autoimmunity; Regulatory NK cells; Immune
tolerance
ID NATURAL-KILLER-CELLS; NONOBESE DIABETIC MICE; CENTRAL-NERVOUS-SYSTEM;
SLAM FAMILY RECEPTORS; INDUCED LIVER-INJURY; HLA-C ALLELES;
MULTIPLE-SCLEROSIS; ANKYLOSING-SPONDYLITIS; ADAPTIVE IMMUNITY; DENDRITIC
CELLS
AB As major components of innate immunity, NK cells not only exert cell-mediated cytotoxicity against tumor cells or infected cells, but also act to regulate the function of other immune cells by secretion of cytokines and chemokines, thus providing surveillance in early defense against viruses, intracellular bacteria and cancer cells. However, the effector function of NK cells must be exquisitely controlled in order to prevent inadvertent attack against self normal cells. The activity of NK cells is defined by integration of signals coming from inhibitory and activation receptors. Inhibitory receptors not only distinguish healthy from diseased cells by recognize self-MHC class I molecules on cell surfaces with "missing-self' model, but also provide an educational signal that generates functional NK cells. NK cells enrich in immunotolerance organ and recent findings of different regulatory NK cell subsets have indicated the unique role of NK cells in maintenance of homeostasis. Once the self-tolerance is broken, autoimmune response may occur. Although data has demonstrated that NK cells play important role in autoimmune disorders, NK cells seemed to act as a two edged weapon and play opposite roles with both regulatory and inducer activity even in the same disease. The precise role and regulatory mechanisms need to be further determined. In this review, we focus on recent research on the association of NK cells and antoimmune diseases, particularly the genetic correlation, the immune tolerance and misrecognition of NK cells, the regulatory function of NK cells, and their potential role in autoimmunity. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Tian, Zhigang] Univ Sci & Technol China, Sch Life Sci, Hefei 230027, Peoples R China.
[Gershwin, M. Eric] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Zhang, Cai] Shandong Univ, Sch Pharm, Jinan 250012, Shandong, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
China, CAS; University of California System; University of California
Davis; Shandong University
RP Tian, ZG (corresponding author), Univ Sci & Technol China, Sch Life Sci, Hefei 230027, Peoples R China.
EM tzg@ustc.edu.cn; caizhangsd@163.com
RI Zhang, Chenyang/AAJ-1371-2020; Tian, Zhigang/J-3512-2013
FU Ministry of Science & Technology of China [2012CB519004, 2009CB522403];
Natural Science Foundation of China [91029303, 30730084, 30911120480,
31021061, 90713033, 30901307]; National Science & Technology Major
Projects [2012ZX10002-014]; National Institutes of Health [DK39588]
FX This work was supported by the Ministry of Science & Technology of China
(973 Basic Science Project 2012CB519004, 2009CB522403), Natural Science
Foundation of China (#91029303, #30730084, #30911120480, #31021061,
#90713033, #30901307), National Science & Technology Major Projects
(2012ZX10002-014) and National Institutes of Health Grant DK39588.
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NR 123
TC 89
Z9 103
U1 1
U2 52
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD SEP
PY 2012
VL 39
IS 3
SI SI
BP 206
EP 215
DI 10.1016/j.jaut.2012.05.006
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 007OU
UT WOS:000308898800012
PM 22704425
DA 2025-01-07
ER
PT J
AU Ali, AH
Tabibian, JH
Carey, EJ
Lindor, KD
AF Ali, Ahmad H.
Tabibian, James H.
Carey, Elizabeth J.
Lindor, Keith D.
TI Emerging drugs for the treatment of Primary Biliary Cholangitis
SO EXPERT OPINION ON EMERGING DRUGS
LA English
DT Review
DE bile duct disorders; outcomes; transplantation; cholestasis; Primary
biliary cholangitis; ursodeoxycholic acid; pharmacotherapy
ID MESENCHYMAL STEM-CELLS; URSODEOXYCHOLIC-ACID THERAPY; HEPATIC STELLATE
CELLS; FARNESOID-X-RECEPTOR; JUVENILE IDIOPATHIC ARTHRITIS; COMBINATION
ANTIRETROVIRAL THERAPY; PRIMARY SCLEROSING CHOLANGITIS; MURINE
AUTOIMMUNE CHOLANGITIS; ELASTOGRAPHY-BASED ASSESSMENT; RANDOMIZED
CONTROLLED-TRIALS
AB Introduction: Primary biliary cholangitis (PBC) is an autoimmune chronic disease of the liver that can progress to cirrhosis and hepatocellular carcinoma. It affects approximately 1 in 4,000 with a 10:1 female to male ratio. The diagnosis of PBC can be made based on serum antimitochondrial antibodies (AMA) in a patient with abnormally high serum alkaline phosphatase after ruling out other causes of cholestasis and biliary obstruction. Genome-wide association studies have revealed several human leukocyte antigen (HLA) and non-HLA risk loci in PBC, and complex environmental-host immunogenetic interactions are believed to underlie the etiopathogenesis of the disease. Fatigue and pruritus are the most common and often problematic symptoms; although often mild, these can be severe and life-alternating in a subset of patients. Ursodeoxycholic acid (UDCA) is the only drug approved by the United States Food and Drug Administration for the treatment of PBC. Clinical trials have shown that UDCA significantly improves transplant-free survival. However, nearly 40% of PBC patients do not respond adequately to PBC and are at higher risk for serious complications when compared to PBC patients with complete response to UDCA.
Areas Covered: Here we provide a detailed discussion regarding novel therapeutic agents and potential areas for further investigation in PBC-related research.
Expert Opinion: Results of ongoing clinical trials and emerging treatment paradigms for PBC will likely further improve medical management of this disorder in the near future.
C1 [Ali, Ahmad H.; Carey, Elizabeth J.; Lindor, Keith D.] Mayo Clin, Div Gastroenterol & Hepatol, Phoenix, AZ USA.
[Tabibian, James H.] Hosp Univ Penn, Wilmott Barna Ctr Endoscop Innovat Res & Training, Div Gastroenterol, 3400 Spruce St, Philadelphia, PA 19104 USA.
[Lindor, Keith D.] Arizona State Univ, Coll Hlth Solut, Phoenix, AZ USA.
C3 Mayo Clinic; Mayo Clinic Phoenix; University of Pennsylvania; Arizona
State University; Arizona State University-Downtown Phoenix
RP Ali, AH (corresponding author), Mayo Clin, Div Gastroenterol & Hepatol, Phoenix, AZ USA.
EM ali.ahmad@mayo.edu
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NR 239
TC 13
Z9 15
U1 0
U2 14
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1472-8214
EI 1744-7623
J9 EXPERT OPIN EMERG DR
JI Expert Opin Emerg. Drugs
PD JAN 2
PY 2016
VL 21
IS 1
BP 39
EP 56
DI 10.1517/14728214.2016.1150999
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DE6GV
UT WOS:000370732900001
PM 26901615
DA 2025-01-07
ER
PT J
AU Bilaj, F
Hyslop, WB
Rivero, H
Firat, Z
Vaidean, G
Shrestha, R
Woosley, JT
Semelka, RC
AF Bilaj, F
Hyslop, WB
Rivero, H
Firat, Z
Vaidean, G
Shrestha, R
Woosley, JT
Semelka, RC
TI MR imaging findings in autoimmune hepatitis. Correlation with clinical
staging
SO RADIOLOGY
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; ABNORMALITIES; SPECTRUM; PATTERNS; LIVER
AB PURPOSE: To retrospectively evaluate the morphologic and enhancement features of the liver on magnetic resonance (MR) images obtained in patients with autoimmune hepatitis (AIH) and to determine if there is a correlation between MR imaging findings and severity of clinical disease as measured with the Mayo end-stage liver disease (MELD) score.
MATERIALS AND METHODS: This study was compliant with the Health Insurance Portability and Accountability Act and approved by the institutional review board. The need for informed consent was waived. Thirty-two patients (29 female and three male patients; mean age, 44 years; age range, 14-69 years) undergoing treatment for AIH underwent unenhanced and gadolinium-enhanced MR imaging. Two radiologists reviewed all cases independently to determine the presence of patchy or heterogeneous liver enhancement, biliary duct changes, lymphadenopathy, and findings of portal hypertension. Fibrosis was graded as mild, moderate, or severe reticular (corresponding to a grading scale of 1-3) or as confluent. Agreement between radiologists was assessed by using K coefficients. Mean MELD scores were compared across fibrosis categories by using the Kruskal-Wallis analysis of variance.
RESULTS: Of the 32 patients, two (6%) had no imaging findings of cirrhosis. Thirty patients (94%) had reticular fibrosis with a mean grade of 1.8. Six patients had confluent fibrosis, and all six had associated reticular fibrosis. Mild intrahepatic biliary duct dilatation involving the right and left lobes was observed in four patients (12%). Lymphadenopathy was observed in 12% of patients. None of the patients had hepatocellular carcinoma. There was no significant overall association between fibrosis grade and MELD score (P =.36).
CONCLUSION: Although fibrosis is a common feature in AIH and is often moderate to severe, no significant correlation between fibrosis grade and MELD score was found.(c) RSNA, 2005.
C1 Univ N Carolina, Dept Radiol, Chapel Hill, NC 27599 USA.
Univ N Carolina, Dept Med, Chapel Hill, NC 27599 USA.
Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA.
Univ N Carolina, Sch Publ Hlth, Cardiovasc Dis Program, Chapel Hill, NC 27599 USA.
C3 University of North Carolina; University of North Carolina Chapel Hill;
University of North Carolina; University of North Carolina Chapel Hill;
University of North Carolina; University of North Carolina Chapel Hill;
University of North Carolina; University of North Carolina Chapel Hill
RP Univ N Carolina, Dept Radiol, CB 7510,101 Manning Dr, Chapel Hill, NC 27599 USA.
EM richsem@med.unc.edu
RI Vaidean, G/L-5747-2019
OI Georgeta, Vaidean/0000-0003-1612-9864
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NR 16
TC 23
Z9 30
U1 0
U2 1
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD SEP
PY 2005
VL 236
IS 3
BP 896
EP 902
DI 10.1148/radiol.2363041262
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 957ZR
UT WOS:000231412600021
PM 16118168
DA 2025-01-07
ER
PT J
AU Lee, SE
Kim, SC
AF Lee, Sang Eun
Kim, Soo-Chan
TI Paraneoplastic pemphigus
SO DERMATOLOGICA SINICA
LA English
DT Review
DE Autoantibodies to plakin and desmoglein; Cellular immunity; Humoral
immunity; Paraneoplastic pemphigus
ID DENDRITIC CELL-SARCOMA; CHRONIC LYMPHOCYTIC-LEUKEMIA; INFLAMMATORY
MYOFIBROBLASTIC TUMOR; AUTOIMMUNE MULTIORGAN SYNDROME;
LICHEN-PLANUS-PEMPHIGOIDES; CASTLEMANS-DISEASE; INDIRECT
IMMUNOFLUORESCENCE; BRONCHIOLITIS OBLITERANS; HEPATOCELLULAR-CARCINOMA;
IMMUNOLOGICAL FEATURES
AB Paraneoplastic pemphigus (PNP) is a life-threatening autoimmune mucocutaneous blistering disease associated with malignancy, particularly lymphoproliferative neoplasms. Clinically, it is characterized by severe and intractable mucositis and polymorphous cutaneous eruptions, ranging from blisters to lichenoid lesions. The histologic features are also diverse according to the morphology of the clinical lesions, ranging from suprabasal acantholysis to interface changes with necrotic keratinocytes. PNP is characterized by the production of autoantibodies against the plakin family proteins as well as the desmoglein 1 and 3, which are target antigens of ordinary pemphigus. Thus, indirect immunofluorescence on substrates other than skin is useful in the diagnosis of PNP. The presence of anti-desmoglein antibodies have been demonstrated by enzyme-linked immunosorbent assay. The gold standard for the diagnosis of PNP however, is the detection of the characteristic circulating autoantibodies against 210-kDa envoplakin and 190-kDa periplakin by immunoblotting or immunoprecipitation. It is now accepted that both humoral and cellular immunities are involved in the pathogenesis of PNP. Anti-desmoglein 3 antibodies are known to play a pathogenic role in the initiation of acantholytic blister formation. Autoreactive CD8+cytotoxic T cells induced by antitumor immune response are also involved in the development of mucocutaneous manifestations and bronchiolotis obliterans. The prognosis of PNP depends on the nature of the underlying neoplasm, with high mortality rate due to sepsis or multi-organ failure, particularly bronchiolitis obliterans. Although the combined use of immunosuppressive agents and rituximab has been administered in treating PNP, to date, there are no consistently effective treatments for PNP. Copyright (C) 2010, Taiwanese Dermatological Association. Published by Elsevier Taiwan LLC. All rights reserved.
C1 Yonsei Univ, Coll Med, Dept Dermatol, Seoul 135720, South Korea.
Yonsei Univ, Coll Med, Cutaneous Biol Res Inst, Seoul 135720, South Korea.
C3 Yonsei University; Yonsei University Health System; Yonsei University;
Yonsei University Health System
RP Kim, SC (corresponding author), Yonsei Univ, Coll Med, Dept Dermatol, Gangnam Severance Hosp, 712 Eonjuro, Seoul 135720, South Korea.
EM kimsc@yuhs.ac
RI Lee, SangHun/GPW-6306-2022; Kim, Sunghoon/AAE-8314-2020
OI Lee, Sang Eun/0000-0003-4720-9955
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NR 122
TC 54
Z9 56
U1 0
U2 9
PU ELSEVIER TAIWAN
PI TAIPEI
PA RM N-412, 4F, CHIA HSIN BUILDING 11, NO 96, ZHONG SHAN N ROAD SEC 2,
TAIPEI, 10449, TAIWAN
SN 1027-8117
EI 2223-330X
J9 DERMATOL SIN
JI Dermatol. Sin.
PD MAR
PY 2010
VL 28
IS 1
BP 1
EP 14
PG 14
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA 575ZW
UT WOS:000276114100001
DA 2025-01-07
ER
PT J
AU Pischke, S
Karsten, W
Hadem, J
Schmidt, S
Heinz, KH
Helfritz, F
Strassburg, CP
Lobers, J
Zender, L
Tutarel, O
Wedemeyer, J
Manns, MP
Wedemeyer, H
Rifai, K
Gebel, M
AF Pischke, Sven
Karsten, Wursthorn
Hadem, Johannes
Schmidt, Sebastian
Heinz, Karl Heiringhoff
Helfritz, Fabian
Strassburg, Christian P.
Lobers, Joachim
Zender, Lars
Tutarel, Oktay
Wedemeyer, Jochen
Manns, Michael P.
Wedemeyer, Heiner
Rifai, Kinan
Gebel, Michael
TI Liver transplantation: A new risk factor for intestinal intussusceptions
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Ultrasound; Intussusception; Liver transplantation; Risk factor;
Hepaticojejunostomy
ID SMALL-BOWEL INTUSSUSCEPTION; ADULTS; DIAGNOSIS; INFECTION; CHILDHOOD
AB Background. Intestinal intussusception in adults is associated with chronic inflammatory bowel disease, coeliac disease, abdominal tumors or previous abdominal surgery but most often of unknown origin. Aim. The aim of our study was to evaluate circumstances and identify risk factors for intussusceptions. Methods. All 65,928 abdominal ultrasound examinations performed at our tertiary medical center between January 2001 and June 2008 were analyzed retrospectively for the diagnosis "intussusception". After identifying individuals with sonographically proven intussusception we analyzed various patients' characteristics including age, gender and underlying disease as well as sonographic findings such as localization of the intussusception, absence or presence of ascites and lymph nodes. Results. We identified 32 cases of intussusceptions [mean age 45 years (range 18 to 88); 18 patients were male]. Twelve patients (38%) had a history of abdominal surgery including 8 patients who had undergone liver transplantation (2 patients with primary sclerosing cholangitis, 1 patient with cystic fibrosis, 1 patient with sarcoidosis, 1 patient with hepatocellular carcinoma and HCV infection, 1 patient with autoimmune hepatitis, 1 patient with Crigler-Najar-syndrome and one patient with echinococcus). A hepaticojejunostomy had been performed in 4 of the patients after liver transplantation. Liver transplanted patients were significantly overrepresented in the intussusception group compared with the overall cohort of patients undergoing abdominal ultrasound examination (25% vs. 8%, Chi-Square-test, p = 0.0023).
C1 [Pischke, Sven; Karsten, Wursthorn; Hadem, Johannes; Schmidt, Sebastian; Heinz, Karl Heiringhoff; Helfritz, Fabian; Strassburg, Christian P.; Lobers, Joachim; Zender, Lars; Tutarel, Oktay; Wedemeyer, Jochen; Manns, Michael P.; Wedemeyer, Heiner; Rifai, Kinan; Gebel, Michael] Hannover Med Sch, D-30625 Hannover, Germany.
C3 Hannover Medical School
RP Pischke, S (corresponding author), Hannover Med Sch, Carl Neuberg Str 1, D-30625 Hannover, Germany.
EM pischke.sven@mh-hannover.de
RI Manns, Michael/AFG-3063-2022
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NR 28
TC 2
Z9 3
U1 0
U2 0
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD JAN-MAR
PY 2011
VL 10
IS 1
BP 38
EP 42
DI 10.1016/S1665-2681(19)31585-6
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 752RE
UT WOS:000289709400007
PM 21301008
OA hybrid
DA 2025-01-07
ER
PT J
AU Hijioka, M
Ito, T
Igarashi, H
Fujimori, N
Lee, L
Nakamura, T
Jensen, RT
Takayanagi, R
AF Hijioka, Masayuki
Ito, Tetsuhide
Igarashi, Hisato
Fujimori, Nao
Lee, Lingaku
Nakamura, Taichi
Jensen, Robert T.
Takayanagi, Ryoichi
TI Serum chromogranin A is a useful marker for Japanese patients with
pancreatic neuroendocrine tumors
SO CANCER SCIENCE
LA English
DT Article
DE Chromogranin A; Japan; pancreatic cancer; pancreatic neuroendocrine
tumors; proton pump inhibitors
ID NEURON-SPECIFIC ENOLASE; ENDOCRINE NEOPLASIA TYPE-1; ETHNIC-DIFFERENCES;
PLASMA; CARCINOMA; DIAGNOSIS; DISEASE; UTILITY; CANCER; DISCONTINUATION
AB Although chromogranin A (CGA) is a useful marker for pancreatic neuroendocrine tumors (pNET) in the West, its usefulness in Japanese populations is unclear. To assess this, we evaluated the serum CGA levels in 189 patients with various pancreatic diseases, including proven pNET (n=69), pancreatic cancer (PC) (n=50), chronic pancreatitis (CP) (n=50) and autoimmune pancreatitis (AIP) (n=20), and 112 normal controls (controls) using an ELISA kit. The mean CGA level of patients with pNET was significantly higher than any of the other groups (407.8 +/- 984.6ng/mL [pNET] vs 91.8 +/- 101.8ng/mL [PC], 93.6 +/- 57.5ng/mL [CP], 69.9 +/- 52.4ng/mL [AIP] and 62.5 +/- 48.3ng/mL [controls]). Limiting the analysis to patients not using proton pump inhibitors (PPI), the CGA level of patients with PC or CP was not significantly different compared with the controls. Discriminant analysis revealed that the best cut-off value of CGA to distinguish patients with pNET from the controls was 78.7ng/mL, with a sensitivity and specificity of 53.6% and 78.6%, respectively. In patients with pNET, significant factors associating with elevated CGA levels were tumor classification, tumor size, and the presence of liver metastases in univariate analysis as well as PPI use and the presence of liver metastases in multivariate analysis. We show that CGA is a useful marker for diagnosing pNET in Japanese populations and for distinguishing patients with pNET from patients with other pancreatic diseases. The increased use of CGA in Japan will likely be a helpful tool in managing these patients, as found in the West.
C1 [Hijioka, Masayuki; Ito, Tetsuhide; Igarashi, Hisato; Fujimori, Nao; Lee, Lingaku; Nakamura, Taichi; Takayanagi, Ryoichi] Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioreguratory Sci, Fukuoka 8128582, Japan.
[Nakamura, Taichi; Jensen, Robert T.] NIDDK, Digest Dis Branch, NIH, Bethesda, MD USA.
C3 Kyushu University; National Institutes of Health (NIH) - USA; NIH
National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK)
RP Ito, T (corresponding author), Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioreguratory Sci, 3-1-1 Maidashi, Fukuoka 8128582, Japan.
EM itopapa@intmed3.med.kyushu-u.ac.jp
RI Jensen, Robert/AFL-2290-2022
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NR 52
TC 27
Z9 29
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1347-9032
EI 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD NOV
PY 2014
VL 105
IS 11
BP 1464
EP 1471
DI 10.1111/cas.12533
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AU1HL
UT WOS:000345371600012
PM 25220535
OA Green Published
DA 2025-01-07
ER
PT J
AU Ren, H
Jin, YZ
Huang, HH
Wu, W
Dai, XM
Fang, WJ
Qin, J
Li, HJ
Zhao, P
AF Ren, Hui
Jin, Yuzhi
Huang, Huanhuan
Wu, Wei
Dai, Xiaomeng
Fang, Weijia
Qin, Jing
Li, Hongjun
Zhao, Peng
TI In vivo engineering chimeric antigen receptor immune cells
with emerging nanotechnologies
SO NANO TODAY
LA English
DT Review
DE Cell therapy; In vivo engineering CAR-cell; Chimeric antigen receptor;
CAR delivery; Targeted vectors
ID CAR-T-CELLS; NATURAL-KILLER-CELLS; VIRAL VECTORS; MESSENGER-RNA; GENE
DELIVERY; HEPATOCELLULAR-CARCINOMA; POLYETHYLENIMINE PEI; LIPID
NANOPARTICLES; B-CELL; THERAPY
AB Adoptive cell therapy with chimeric antigen receptor (CAR) has revolutionized cancer treatment in the past decade. Now several adoptive cell therapies are approved, and researchers are extending the application of adoptive cell therapy beyond oncology, such as autoimmune diseases, inherited blood disorders, infectious diseases and fibrosis. Evidence from clinical studies underscores the potential of cell therapy in cancer and noncancerous conditions. However, conventional manufacture of adoptive CAR-cell ex vivo is time-consuming and expensive in which immune cells are extracted from the patients, engineered to target cancer cells and reinjected to the body. The ways to produce CAR-cell in the body, as a promising alternative, may make the awfully expensive and personalized cell therapy more accessible. Here, we thoroughly summarize the current state of clinical trials on adoptive cell therapy, representing by CAR-T, CAR-nature killer cell (CAR-NK) and CARMacrophage (CAR-M), and highlight the latest advances in off-the-shelf nanocarrier- and virus-based in vivo CAR cargo delivery strategies, and corresponding precision targeting strategies, to provide a future perspective regarding in vivo engineering CAR-cell.
C1 [Ren, Hui; Jin, Yuzhi; Dai, Xiaomeng; Fang, Weijia; Zhao, Peng] Zhejiang Univ, Affiliated Hosp 1, Sch Med, Dept Med Oncol, Hangzhou 310009, Peoples R China.
[Ren, Hui; Jin, Yuzhi; Huang, Huanhuan; Dai, Xiaomeng; Fang, Weijia; Li, Hongjun; Zhao, Peng] Zhejiang Univ, Natl Key Lab Adv Drug Delivery & Release Syst, Hangzhou 310058, Peoples R China.
[Huang, Huanhuan; Qin, Jing] Chinese Acad Sci, Zhejiang Canc Hosp, Hangzhou Inst Med HIM, Dept Thorac Med Oncol, Hangzhou 310022, Peoples R China.
[Wu, Wei] Zhejiang Canc Hosp, Dept Hepatopancreatobiliary & Gastr Med Oncol, Hangzhou 310022, Peoples R China.
[Li, Hongjun] Zhejiang Univ, Liangzhu Lab, Hangzhou 311121, Peoples R China.
[Li, Hongjun] Zhejiang Univ, Jinhua Inst, Jinhua 321299, Peoples R China.
[Li, Hongjun] Zhejiang Univ, Coll Pharmaceut Sci, Key Lab Adv Drug Delivery Syst Zhejiang Prov, Hangzhou 310058, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang Cancer Hospital;
Chinese Academy of Sciences; Hangzhou Institute of Medicine, CAS;
Zhejiang Cancer Hospital; Zhejiang University; Liangzhu Laboratory;
Zhejiang University; Zhejiang University
RP Zhao, P (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Sch Med, Dept Med Oncol, Hangzhou 310009, Peoples R China.; Li, HJ; Zhao, P (corresponding author), Zhejiang Univ, Natl Key Lab Adv Drug Delivery & Release Syst, Hangzhou 310058, Peoples R China.; Qin, J (corresponding author), Chinese Acad Sci, Zhejiang Canc Hosp, Hangzhou Inst Med HIM, Dept Thorac Med Oncol, Hangzhou 310022, Peoples R China.
EM qinjing@zjcc.org.cn; hongjun@zju.edu.cn; zhaop@zju.edu.cn
RI Li, Hongjun/U-5093-2017
FU National Natural Science Foundation of China [52173142]
FX This work was supported by the National Natural Science Foundation of
China (82473336 and 82074208) to P.Z., and the National Natural Science
Foundation of China (52173142) to H.L.
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NR 167
TC 0
Z9 0
U1 13
U2 13
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1748-0132
EI 1878-044X
J9 NANO TODAY
JI Nano Today
PD DEC
PY 2024
VL 59
AR 102517
DI 10.1016/j.nantod.2024.102517
EA OCT 2024
PG 17
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA J1C1G
UT WOS:001334508000001
DA 2025-01-07
ER
PT J
AU Goyal, S
Sakhuja, P
AF Goyal, Surbhi
Sakhuja, Puja
TI Autoimmune pancreatitis: Current perspectives
SO INDIAN JOURNAL OF PATHOLOGY AND MICROBIOLOGY
LA English
DT Review
DE Autoimmune pancreatitis; histology; idiopathic duct-centric
pancreatitis; IgG4-related disease; IgG4-related sclerosing cholangitis;
IgG4-related inflammatory pseudotumor; lymphoplasmacytic pancreatitis
ID IGG4-RELATED SCLEROSING CHOLANGITIS; HEPATIC INFLAMMATORY PSEUDOTUMOR;
EUS-GUIDED FNA; SERUM IGG4; CLINICOPATHOLOGICAL FEATURES;
STEROID-THERAPY; LIVER-BIOPSY; BILE-DUCT; DIAGNOSIS; DISEASE
AB Over the last two decades, our knowledge and understanding regarding the pathogenesis and biology of autoimmune pancreatitis (AIP) have improved tremendously. Type 1 AIP or IgG4-related pancreatitis (IgG4-RP) is now believed to be the prototype of the multisystemic IgG4-related disease. In view of clinical features like obstructive jaundice and mass-forming lesions in the pancreas in elderly men, type 1 AIP often mimics pancreatic cancer. IgG4-related sclerosing cholangitis concomitantly involving the extrahepatic and intrahepatic biliary tree is the most common extrapancreatic involvement seen in up to 80% of these patients, which needs to distinguish from cholangiocarcinoma. Histology is characterised by lymphoplasmacytic inflammation, abundant IgG4 positive plasma cell infiltration, storiform fibrosis and obliterative phlebitis. Apart from histology, high serum IgG4 levels, pancreatic parenchymal and duct imaging findings and other organ involvement aid in diagnosis especially in cases where definitive histology is not evident. Also, these parameters lay the foundation of various diagnostic criteria proposed over last few years. On the contrary, histology alone is the mainstay for establishing diagnosis of idiopathic duct-centric pancreatitis (IDCP) as it lacks any specific serological marker or imaging. Since both types of AIP respond dramatically to corticosteroid treatment, a biopsy is crucial to establish the preoperative diagnosis and to exclude malignancy so as to avoid unnecessary surgery. This review discusses the morphologic spectrum, treatment and prognosis of IgG4-RP and IDCP with an emphasis on approach to diagnosis with relevant histologic features, differential diagnoses and the challenges faced during biopsy interpretation.
C1 [Goyal, Surbhi; Sakhuja, Puja] GIPMER, Dept Pathol, New Delhi 110002, India.
C3 Govind Ballabh Pant Institute of Postgraduate Medical Education &
Research
RP Sakhuja, P (corresponding author), GIPMER, Dept Pathol, New Delhi 110002, India.
EM pujasak@gmail.com
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NR 76
TC 4
Z9 4
U1 0
U2 3
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S NO 1498A-2
VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 0377-4929
EI 0974-5130
J9 INDIAN J PATHOL MICR
JI Indian J. Pathol. Microbiol.
PD JUN
PY 2021
VL 64
IS 5
SI SI
BP 149
EP 159
DI 10.4103/ijpm.ijpm_59_21
PG 11
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA SU1ZC
UT WOS:000662939600029
PM 34135159
OA gold
DA 2025-01-07
ER
PT J
AU Vyas, HS
Upadhyay, KK
Devkar, RV
AF Vyas, Hitarthi S.
Upadhyay, Kapil K.
Devkar, Ranjitsinh, V
TI miRNAs Signatures in Patients with Acute Liver Injury: Clinical Concerns
and Correlations
SO CURRENT MOLECULAR MEDICINE
LA English
DT Review
DE microRNAs; acute liver injury; patients; biomarker; cirrhosis; murine
models
ID HEPATITIS-B-VIRUS; INDUCED UP-REGULATION; HEPATOCELLULAR-CARCINOMA;
ALANINE AMINOTRANSFERASE; CIRCULATING MICRORNAS; AUTOIMMUNE HEPATITIS;
SERUM MICRORNA-122; EXPRESSION; BIOMARKERS; PROFILES
AB Non-coding RNAs can be highly exploited for their biological significance in living systems. miRNAs are in the upstream position of cellular regulation cascade and hold merit in its state. A plethora of information is available on a wide variety of miRNAs that undergo alterations in experimentally induced models of liver injuries. The underlying mechanisms governed by these miRNAs have been inferred through cell-based experiments but the scientific knowledge on miRNA signatures in patients with liver injury are primordial and lack scientific clarity. Hence, it is crucial to get insight into the status and synergy of miRNAs in patients, with varying degrees of acute toxic manifestations in the liver. Though some miRNAs are being investigated in clinical trials, a major research lacuna exists with regard to the functional role of other miRNAs in liver diseases. This review article is a meticulous compilation of disease based or drug/alcohol based acute liver injuries in patients and resultant alteration in their miRNA profile. Investigative reports on underlying miRNA-liver crosstalk in cell-based or murine models are also discussed herein to draw a correlation with clinical findings.
C1 [Vyas, Hitarthi S.; Upadhyay, Kapil K.; Devkar, Ranjitsinh, V] Maharaja Sayajirao Univ Baroda, Fac Sci, Dept Zool, Div Metab Endocrinol, Vadodara 390002, Gujarat, India.
C3 Maharaja Sayajirao University Baroda
RP Devkar, RV (corresponding author), Maharaja Sayajirao Univ Baroda, Fac Sci, Dept Zool, Div Metab Endocrinol, Vadodara 390002, Gujarat, India.
EM rv.devkar-zoo@msubaroda.ac.in
RI Vyas, Hitarthi/ITT-1786-2023; Upadhyay, Kapil/AAU-2192-2020
OI Upadhyay, Kapil/0000-0002-0000-5085; Vyas, Hitarthi/0000-0001-8706-2594
FU Lady Tata Memorial Trust
FX This study was supported by The Lady Tata Memorial Trust.
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NR 67
TC 3
Z9 3
U1 0
U2 9
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1566-5240
EI 1875-5666
J9 CURR MOL MED
JI Curr. Mol. Med.
PY 2020
VL 20
IS 5
BP 325
EP 335
DI 10.2174/1566524020666191211153546
PG 11
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA LJ3TL
UT WOS:000530090500001
PM 31823701
DA 2025-01-07
ER
PT J
AU Portenkirchner, C
Kienle, P
Horisberger, K
AF Portenkirchner, Carmen
Kienle, Peter
Horisberger, Karoline
TI Checkpoint Inhibitor-Induced Colitis-A Clinical Overview of Incidence,
Prognostic Implications and Extension of Current Treatment Options
SO PHARMACEUTICALS
LA English
DT Review
DE immune checkpoint inhibitor; immune checkpoint inhibitor-induced
colitis; colitis; irAE; IBD; resumption; fecal transplantation;
ileostomy
ID ADVERSE EVENTS; HEPATOCELLULAR-CARCINOMA; CANCER-PATIENTS; DOUBLE-BLIND;
OPEN-LABEL; IPILIMUMAB; NIVOLUMAB; MELANOMA; BLOCKADE; PD-1
AB In recent years, anti-tumor immunotherapies have witnessed a major breakthrough with the emergence of immune checkpoint inhibitors (ICIs). However, the use of ICIs has also brought an era of a certain class of adverse events that differ from those of classical chemotherapies and are more reminiscent of autoimmune diseases. This article focuses exclusively on colitis as an irAE with emphasis on vulnerable patient groups, the prognostic significance of colitis, treatment, and new therapeutic approaches that may be applicable. Colitis itself is associated with a favorable oncological outcome of the underlying disease but is as well the most common irAE leading to discontinuation of therapy. Especially in vulnerable patient groups such as IBD patients and elderly patients, colitis occurs more frequently as a side effect. It is precisely in these two patient groups that side effects more often lead to discontinuation of therapy. Therefore, in addition to the current therapy of colitis through immunosuppression, the focus should also be on new forms of therapy of severe colitis, such as fecal transplantation or ileostomy creation.
C1 [Portenkirchner, Carmen] Cantonal Hosp Baden, Dept Surg, CH-5404 Baden, Switzerland.
[Portenkirchner, Carmen; Horisberger, Karoline] Univ Hosp Zurich, Dept Abdominal & Transplantat Surg, Ramistr 100, CH-8091 Zurich, Switzerland.
[Kienle, Peter] Theresienkrankenhaus, Dept Gen & Visceral Surg, D-68165 Mannheim, Germany.
[Kienle, Peter] St Hedwig Klin GmbH, D-68165 Mannheim, Germany.
C3 University of Zurich; University Zurich Hospital
RP Horisberger, K (corresponding author), Univ Hosp Zurich, Dept Abdominal & Transplantat Surg, Ramistr 100, CH-8091 Zurich, Switzerland.
EM Carmen.Portenkirchner@ksb.ch; p.kienle@theresienkrankenhaus.de;
karoline.horisberger@usz.ch
RI Horisberger, Karoline/ISV-4201-2023
OI Horisberger, Karoline/0000-0001-6143-6607; Portenkirchner,
Carmen/0000-0002-0667-8336
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NR 109
TC 19
Z9 19
U1 0
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1424-8247
J9 PHARMACEUTICALS-BASE
JI Pharmaceuticals
PD APR
PY 2021
VL 14
IS 4
AR 367
DI 10.3390/ph14040367
PG 15
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA RR8RV
UT WOS:000643359400001
PM 33923423
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Bataller, R
Sancho-Bru, P
Ginès, P
Brenner, DA
AF Bataller, R
Sancho-Bru, P
Ginès, P
Brenner, DA
TI Liver fibrogenesis:: A new role for the renin-angiotensin system
SO ANTIOXIDANTS & REDOX SIGNALING
LA English
DT Review
ID HEPATIC STELLATE CELLS; DUCT-LIGATED RATS; FIBROSIS DEVELOPMENT;
AUTOIMMUNE HEPATITIS; MOLECULAR-MECHANISMS; RECEPTOR ANTAGONIST;
COLLAGEN-SYNTHESIS; MESSENGER-RNA; INJURY; ACTIVATION
AB Liver fibrosis is the consequence of chronic liver injury of any etiology. When advanced, fibrosis causes portal hypertension and liver insufficiency, and is a risk factor for developing hepatocellular carcinoma. In the last decade, there have been major advances in the knowledge of the pathogenesis of hepatic fibrosis. Hepatic stellate cells (HSCs) are recognized as the main collagen-producing cells in the injured liver, and key fibrogenic factors have been identified. Among these factors, the renin-angiotensin system (RAS) appears to play a major role. Angiotensin II (Ang II) mediates key biological actions involved in hepatic tissue repair, including myofibroblast proliferation, infiltration of inflammatory cells, and collagen synthesis. Activated HSCs secrete Ang 11, which induces fibrogenic actions through the activation of NADPH oxidase. Importantly, the blockade of the RAS attenuates fibrosis development in different experimental models of chronic liver injury. Based on these studies, it has been proposed that the blockade of the RAS could be effective in preventing fibrosis progression in chronic liver diseases. Although no prospective studies have evaluated the antifibrotic effect of RAS inhibitors in patients with chronic liver diseases, controlled clinical trials are under way.
C1 Hosp Clin Barcelona, Liver Unit, Inst Malalties Digest & Metab, IDIBAPS, E-08036 Barcelona, Catalonia, Spain.
Columbia Univ, New York, NY USA.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; Columbia
University
RP Hosp Clin Barcelona, Liver Unit, Inst Malalties Digest & Metab, IDIBAPS, Villarroel 170, E-08036 Barcelona, Catalonia, Spain.
EM bataller@clinic.ub.es
RI Brenner, David/AFC-9624-2022; Ginès, Pere/X-2892-2019; Sancho-Bru,
Pau/D-4900-2014; Gines, Pere/B-6646-2009
OI Sancho-Bru, Pau/0000-0001-5569-9259; Gines, Pere/0000-0003-4657-4504;
Brenner, David/0000-0003-2573-525X; Bataller, Ramon/0000-0002-1119-7799
FU NIAAA NIH HHS [5 R01 AA015955] Funding Source: Medline
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TC 127
Z9 145
U1 0
U2 19
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1523-0864
EI 1557-7716
J9 ANTIOXID REDOX SIGN
JI Antioxid. Redox Signal.
PD SEP-OCT
PY 2005
VL 7
IS 9-10
BP 1346
EP 1355
DI 10.1089/ars.2005.7.1346
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 958VR
UT WOS:000231476800029
PM 16115040
DA 2025-01-07
ER
PT J
AU García, JI
Noia, JL
Muñoz, JED
AF Iglesias Garcia, J.
Larino Noia, J.
Dominguez Munoz, J. E.
TI Endoscopic ultrasound in the diagnosis and staging of pancreatic cancer
SO REVISTA ESPANOLA DE ENFERMEDADES DIGESTIVAS
LA English
DT Article
DE Endoscopic ultrasound; Pancreatic cancer; Diagnosis; Stanging
ID FINE-NEEDLE-ASPIRATION; EUS-GUIDED FNA; HELICAL COMPUTED-TOMOGRAPHY;
VASCULAR INVASION; DIFFERENTIAL-DIAGNOSIS; AMPULLARY CARCINOMA;
LIVER-LESIONS; LINEAR-ARRAY; ULTRASONOGRAPHY; BIOPSY
AB Pancreatic cancer is the 5(th) leading cause of cancer-related death in Western countries. The 5-year survival rate is approximately 4%, without significant changes over the last 50 years. This poor survival rate and bad prognosis are associated with the diagnosis of advanced-stage disease, which precludes the only potential curative treatment - surgical resection. In this setting, the main objective in the management of pancreatic cancer is to perform an early diagnosis and a correct staging of the disease. Endoscopic ultrasonography (EUS) appears to be an essential tool for the diagnosis and staging of pancreatic cancer. EUS diagnostic accuracy for detecting pancreatic tumors ranges from 85 to 100%, clearly superior to other imaging techniques. EUS accuracy for the local staging of pancreatic cancer ranges from 70 to 90%, superior or equivalent to other imaging modalities. EUS-guided fine-needle aspiration allows a cyto-histological diagnosis in nearly 90% of cases, with a very low complication rate. At present, the formal indications for EUS-guided fine-needle aspiration are the necessity of palliative treatment or whenever the possibility of neoadjuvant treatment is present. It could be also indicated to differentiate pancreatic adenocarcinoma from other pancreatic conditions, like lymphoma, metastasis, autoimmune pancreatitis or chronic pancreatitis. We can conclude that EUS is an essential tool in the management of patients with pancreatic tumors.
C1 [Iglesias Garcia, J.; Larino Noia, J.; Dominguez Munoz, J. E.] Univ Hosp Santiago de Compostela, Dept Gastroenterol, Fdn Res Digest Dis, La Coruna, Spain.
C3 Complexo Hospitalario Universitario de Santiago de Compostela
RP García, JI (corresponding author), Univ Hosp Santiago de Compostela, Dept Gastroenterol, Fdn Res Digest Dis, C Choupana S-N, Santiago De Compostela 15706, Spain.
EM julioiglesiasgarcia@hotmail.es
RI Dominguez-Munoz, J. Enrique/Q-8922-2017
OI Dominguez-Munoz, J. Enrique/0000-0001-8283-3185
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NR 88
TC 41
Z9 45
U1 0
U2 8
PU ARAN EDICIONES, S A
PI MADRID
PA CASTELLO, 128, 28006 MADRID, SPAIN
SN 1130-0108
EI 2340-4167
J9 REV ESP ENFERM DIG
JI Rev. Esp. Enferm. Dig.
PD SEP
PY 2009
VL 101
IS 9
BP 631
EP 638
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 519JJ
UT WOS:000271762100006
PM 19803666
DA 2025-01-07
ER
PT J
AU Komura, Y
Kimura, S
Takaura, A
Hirasawa, Y
Segawa, K
Muranishi, H
Imataki, O
Kumayama, Y
Homma, K
AF Komura, Yasuo
Kimura, Shintarou
Takaura, Ayana
Hirasawa, Yumi
Segawa, Katsunori
Muranishi, Hiromi
Imataki, Osamu
Kumayama, Yoshihisa
Homma, Koichiro
TI Therapeutic Apheresis Using a β2-Microglobulin Removal Column Reduces
Circulating Tumor Cell Count
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Article
DE beta 2-microglobulin; circulating tumor cell; metastasis; recurrence;
therapeutic apheresis
ID PODOPLANIN; EXPRESSION; PROGNOSIS
AB An elevated serum beta 2-microglobulin (beta 2M) level is indicative of impaired glomerular filtration and prerenal diseases, such as malignant tumors, autoimmune disorders, and liver diseases. An elevated serum beta 2M level has been shown to promote metastasis via the induction of epithelial-mesenchymal transition (EMT) in cancer cells. However, the therapeutic potential of targeting beta 2M remains unclear. Here, we aimed to investigate the efficacy of Filtor, a small polymethyl methacrylate fiber-based beta 2M removal column, in reducing the beta 2M level and suppressing cancer cell-induced EMT and metastasis. We assessed the effects of Filtor on the changes in metastasis based on the number of circulating tumor cells (CTCs), which reflects the post-EMT cancer cell population. We performed therapeutic apheresis using Filtor on a male patient with sinonasal neuroendocrine carcinoma, a female patient with a history of colorectal cancer, and another female patient with a history of pancreatic ductal adenocarcinoma. Significantly low serum beta 2M levels and CTC counts were observed immediately and 4 weeks after treatment compared with those in the pretreatment phase. Moreover, the CTC count immediately after therapeutic intervention was markedly reduced, likely because Filtor had trapped CTCs directly. These findings suggest that therapeutic apheresis with Filtor can prevent cancer metastasis and recurrence by directly removing CTCs.
C1 [Komura, Yasuo; Takaura, Ayana; Segawa, Katsunori; Muranishi, Hiromi] Rinku Med Clin, 2F Med Rinku Port,3-41 Rinku Ouraiminami, Osaka 5980047, Japan.
[Kimura, Shintarou; Hirasawa, Yumi] StateArt Inc, 2-9-12 Horidome Cho,Chuo Ku, Tokyo 1030012, Japan.
[Imataki, Osamu] Kagawa Univ, Fac Med, 1750-1 Ikenobe, Miki, Kagawa 7610793, Japan.
[Kumayama, Yoshihisa] Osaka ISEN Coll Med Care & Welf, Osaka 5310076, Japan.
[Homma, Koichiro] Keio Univ, Sch Med, Dept Emergency & Crit Care Med, 35 Shinanomachi,Shinjuku Ku, Tokyo 1608582, Japan.
C3 Kagawa University; Keio University
RP Homma, K (corresponding author), Keio Univ, Sch Med, Dept Emergency & Crit Care Med, 35 Shinanomachi,Shinjuku Ku, Tokyo 1608582, Japan.
EM ykomura@rinku-medical-clinic.com; s.kimura@stateart.co.jp;
takaura@rinku-medical-clinic.com; y.hirasawa@stateart.co.jp;
segawa@create-consulting.jp; muranishi@kyoto.krg.or.jp;
imataki.osamu@kagawa-u.ac.jp; homma888@keio.jp; homma@keio.jp
OI Komura, Yasuo/0009-0002-4498-4059
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NR 26
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4426
J9 J PERS MED
JI J. Pers. Med.
PD JUN
PY 2024
VL 14
IS 6
AR 640
DI 10.3390/jpm14060640
PG 8
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA WO9T4
UT WOS:001255941800001
PM 38929860
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Licata, A
Giammanco, A
Minissale, MG
Pagano, S
Petta, S
Averna, M
AF Licata, Anna
Giammanco, Antonina
Minissale, Maria Giovanna
Pagano, Salvatore
Petta, Salvatore
Averna, Maurizio
TI Liver and Statins: A Critical Appraisal of the Evidence
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Statins; liver damage; genetic susceptibility; single nucleotide
polymorphisms (SNPs); MetS; HCV
ID HEPATITIS-C VIRUS; NONALCOHOLIC FATTY LIVER; CORONARY-HEART-DISEASE;
CAUSE-SPECIFIC MORTALITY; HEPATOCELLULAR-CARCINOMA;
MYOCARDIAL-INFARCTION; AUTOIMMUNE HEPATITIS; COMBINATION THERAPY;
LOWERING TREATMENT; METABOLIC SYNDROME
AB Adverse drug reactions (ADRs) represent an important cause of morbidity and mortality worldwide. Statins are a class of drugs whose main adverse effects are drug-induced liver injury (DILI) and myopathy. Some of these may be predictable, due to their pharmacokinetic and pharmacodynamic properties, while others, unfortunately, are idiosyncratic. Genetic factors may also influence patient susceptibility to DILI and myopathy in the case of statins. This review will first discuss the role of statins in cardiovascular disease treatment and prevention and the underlying mechanisms of action. Furthermore, to explore the susceptibility of statin-induced adverse events such as myopathy and hepatotoxicity, it will then focus on the recent Genome-Wide Association Studies (GWAS) concerning the transporter genes, Cytochrome P450 (CYP), organic anion-transporting polypeptide (OATP) and ABCB1 and ABCC1, which seem to play a role in the development of clinically relevant adverse events. Finally, we appraise the evidence for and against the use of statins in metabolic syndrome and in HCV-infected patients, in terms of their safety and efficacy in cardiovascular events.
C1 [Licata, Anna; Minissale, Maria Giovanna; Petta, Salvatore] Univ Palermo, Dipartimento Med Interna & Specialist, DIBIMIS, Sez Gastroenterol & Epatol, Palermo, Italy.
[Giammanco, Antonina; Pagano, Salvatore; Averna, Maurizio] Univ Palermo, Dipartimento Med Interna & Specialist, DIBIMIS, Sez Med Interna & Malattie Metab, Palermo, Italy.
C3 University of Palermo; University of Palermo
RP Licata, A (corresponding author), Dipartimento Biomed Med Interna & Specialist DIBI, Sez Gastroenterol & Epatol, Piazza Clin 2, I-90127 Palermo, Italy.
EM anna.licata@unipa.it
RI Averna, Maurizio/U-9527-2017; Giammanco, Antonina/AAA-8904-2019; Licata,
Anna/ADF-0000-2022
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NR 97
TC 14
Z9 16
U1 0
U2 9
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2018
VL 25
IS 42
BP 5835
EP 5846
DI 10.2174/0929867325666180327095441
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA HK3VM
UT WOS:000457846900005
PM 29589533
DA 2025-01-07
ER
PT J
AU Kawamura, H
Govindarajan, S
Aswad, F
Machida, K
Lai, MMC
Sung, VMH
Dennert, G
AF Kawamura, Hiroki
Govindarajan, Sugantha
Aswad, Fred
Machida, Keigo
Lai, Michael M. C.
Sung, Vicky M. -H.
Dennert, Gunther
TI HCV core expression in hepatocytes protects against autoimmune liver
injury and promotes liver regeneration in mice
SO HEPATOLOGY
LA English
DT Article
ID C VIRUS CORE; KILLER T-CELLS; HEPATITIS-C; INHIBITS INTERFERON;
GENE-EXPRESSION; STAT3; ACTIVATION; IMMUNITY; FAS; MECHANISMS
AB Hepatitis C virus (HCV) infection causes acute and chronic liver disease often leading to liver cirrhosis and hepatocellular carcinoma. Numerous studies have shown that despite induction of virus specific immunity, a curative response is often not attained; this has led to the hypothesis that HCV genes modulate immunity, thereby enabling chronic infections. This study examined the effects on immune-mediated liver injury in transgenic mice expressing core protein throughout the body and bone marrow chimeras expressing core protein in either the lymphoid compartment or liver parenchyma. Presence of core protein in the liver parenchyma but not in lymphoid cells protects from autoimmune hepatitis induced by mitogen concanavalin A (ConA). Consistent with this observation, core transgenic hepatocytes are relatively resistant to death induced by anti-Fas antibody and tumor necrosis factor alpha (TNF alpha). This protective effect is associated with preferential activation of signal transducer and activation of transcription factor 3 (STAT3) versus STAT1 in livers of ConA-injected animals. In agreement with this effect of core protein on the Janus kinase (JAK)-STAT signaling pathway, transgenic mice accelerate liver regeneration after partial hepatectomy but are not protected from hepatocyte death. In conclusion, HCV core inhibits STAT I and stimulates STAT3 activation, which protects infected hepatocytes from attack by the cell-mediated immune system and promotes their proliferation.
C1 Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Mol Microbiol, Los Angeles, CA 90089 USA.
Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Immunol, Los Angeles, CA 90089 USA.
C3 University of Southern California; University of Southern California
RP Dennert, G (corresponding author), Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Mol Microbiol, 1441 Eastlake Ave, Los Angeles, CA 90089 USA.
EM dennert@usc.edu
RI Lai, Michael/I-7001-2012
OI Machida, Keigo/0000-0002-9721-8553
FU NIAID NIH HHS [U10 AI 40038, AI 43954] Funding Source: Medline
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NR 29
TC 28
Z9 31
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2006
VL 44
IS 4
BP 936
EP 944
DI 10.1002/hep.21360
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 095WE
UT WOS:000241338200020
PM 17006910
DA 2025-01-07
ER
PT J
AU Cacoub, P
Comarmond, C
AF Cacoub, Patrice
Comarmond, Cloe
TI New insights into HCV-related rheumatologic disorders: A review
SO JOURNAL OF ADVANCED RESEARCH
LA English
DT Review
DE HCV; Cryoglobulinemia; Vasculitis; Lymphoma; Arthritis; Treatment
ID HEPATITIS-C-VIRUS; NON-HODGKINS-LYMPHOMA; MIXED CRYOGLOBULINEMIA
VASCULITIS; MONOCLONAL-ANTIBODY TREATMENT; RANDOMIZED CONTROLLED-TRIAL;
INTERFERON PLUS RIBAVIRIN; B-CELL; EXTRAHEPATIC MANIFESTATIONS;
ANTIVIRAL TREATMENT; INSULIN-RESISTANCE
AB Hepatitis C virus ( HCV) infected patients are known to be exposed to major liver complications i.e. cirrhosis and hepatocellular carcinoma. In addition, many extrahepatic manifestations including rheumatologic disorders have been reported in up to two-third of HCV infected patients. These manifestations include frank auto-immune and rheumatic diseases ( such as arthralgia, myalgia, arthritis, sicca syndrome and vasculitis) which may dominate the course of infection. Until recently, the standard of care of HCV has been the use of interferon-alpha based regimens, which not only had limited effectiveness in HCV cure but were poorly tolerated. In patients with rheumatic diseases interferon-based regimens may be problematic given their association with a wide variety of autoimmune toxicities. Recent therapeutic advances with new direct anti-HCV therapies ( interferon-free) which are more effective and better tolerated, make screening for this comorbidity in patients with rheumatic disorders more important than ever. This review aimed to outline main HCV extrahepatic with a special focus on rheumatologic manifestations. (C) 2016 Production and hosting by Elsevier B.V. on behalf of Cairo University.
C1 [Cacoub, Patrice; Comarmond, Cloe] UPMC Univ Paris 06, Sorbonne Univ, UMR 7211, F-75005 Paris, France.
[Cacoub, Patrice; Comarmond, Cloe] DHU i2B, Inflammat Immunopathol Biotherapy Dept, F-75005 Paris, France.
[Cacoub, Patrice; Comarmond, Cloe] INSERM, UMR S 959, F-75013 Paris, France.
[Cacoub, Patrice; Comarmond, Cloe] CNRS, FRE3632, F-75005 Paris, France.
[Cacoub, Patrice; Comarmond, Cloe] Grp Hosp Pitie Salpetriere, AP HP, Dept Internal Med & Clin Immunol, F-75013 Paris, France.
C3 Sorbonne Universite; Institut National de la Sante et de la Recherche
Medicale (Inserm); Centre National de la Recherche Scientifique (CNRS);
Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
Pitie-Salpetriere - APHP; Sorbonne Universite
RP Cacoub, P (corresponding author), UPMC Univ Paris 06, Sorbonne Univ, UMR 7211, F-75005 Paris, France.; Cacoub, P (corresponding author), DHU i2B, Inflammat Immunopathol Biotherapy Dept, F-75005 Paris, France.; Cacoub, P (corresponding author), INSERM, UMR S 959, F-75013 Paris, France.; Cacoub, P (corresponding author), CNRS, FRE3632, F-75005 Paris, France.; Cacoub, P (corresponding author), Grp Hosp Pitie Salpetriere, AP HP, Dept Internal Med & Clin Immunol, F-75013 Paris, France.
EM patrice.cacoub@aphp.fr
RI COMARMOND, Chloé/AAN-1192-2021
OI Cacoub, Patrice/0000-0002-6727-4992
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NR 137
TC 19
Z9 22
U1 0
U2 8
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2090-1232
EI 2090-1224
J9 J ADV RES
JI J. Adv. Res.
PD MAR
PY 2017
VL 8
IS 2
BP 89
EP 97
DI 10.1016/j.jare.2016.07.005
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA EM7RD
UT WOS:000395509100002
PM 28149645
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Gupta, Y
Möller, S
Witte, M
Belheouane, M
Sezin, T
Hirose, M
Vorobyev, A
Niesar, F
Bischof, J
Ludwig, RJ
Zillikens, D
Sadik, CD
Restle, T
Häsler, R
Baines, JF
Ibrahim, SM
AF Gupta, Yask
Moeller, Steffen
Witte, Mareike
Belheouane, Meriem
Sezin, Tanya
Hirose, Misa
Vorobyev, Artem
Niesar, Felix
Bischof, Julia
Ludwig, Ralf J.
Zillikens, Detlef
Sadik, Christian D.
Restle, Tobias
Haesler, Robert
Baines, John F.
Ibrahim, Saleh M.
TI Dissecting genetics of cutaneous miRNA in a mouse model of an autoimmune
blistering disease
SO BMC GENOMICS
LA English
DT Article
DE MicroRNA; Expression QTL; Epistasis; Autoimmune skin blistering disease;
Co-expression analysis
ID QUANTITATIVE TRAIT LOCI; MICRORNA BIOGENESIS; SMALL RNAS; EXPRESSION;
IDENTIFICATION; DIFFERENTIATION; TRANSCRIPTION; GENES
AB Background: MicroRNAs (miRNAs) are small endogenous non-coding RNAs that control genes at post-transcriptional level. They are essential for development and tissue differentiation, and such altered miRNA expression patterns are linked to the pathogenesis of inflammation and cancer. There is evidence that miRNA expression is genetically controlled similar to the transcription of protein-coding genes and previous studies identified quantitative trait loci (QTL) for miRNA expression in the liver. So far, little attention has been paid to miRNA expression in the skin. Moreover, epistatic control of miRNA expression remains unknown. In this study, we characterize genetic regulation of cutaneous miRNA and their correlation with skin inflammation using a previously established murine autoimmune-prone advanced intercross line.
Results: We identified in silico 42 eQTL controlling the expression of 38 cutaneous miRNAs and furthermore found two chromosomal hot-spots on chromosomes 2 and 8 that control the expression of multiple miRNAs. Moreover, for 8 miRNAs an interacting effect from pairs of SNPs was observed. Combining the constraints on genes from the statistical interaction of their loci and further using curated protein interaction networks, the number of candidate genes for association of miRNAs was reduced to a set of several genes. A cluster analysis identified miR-379 and miR-223 to be associated with EBA severity/onset, where miR-379 was observed to be associated to loci on chromosome 6.
Conclusion: The murine advanced intercross line allowed us to identify the genetic loci regulating multiple miRNA in skin. The recurrence of trans-eQTL and epistasis suggest that cutaneous miRNAs are regulated by yet an unexplored complex gene networks. Further, using co-expression analysis of miRNA expression levels we showed that multiple miRNA contribute to multiple pathways that might be involved in pathogenesis of autoimmune skin blistering disease. Specifically, we provide evidence that miRNA such as miR-223 and miR-379 may play critical role in disease progression and severity.
C1 [Gupta, Yask; Moeller, Steffen; Witte, Mareike; Hirose, Misa; Vorobyev, Artem; Bischof, Julia; Ludwig, Ralf J.; Zillikens, Detlef; Ibrahim, Saleh M.] Med Univ Lubeck, Lubeck Inst Expt Dermatol, D-23538 Lubeck, Germany.
[Sezin, Tanya; Zillikens, Detlef; Sadik, Christian D.] Med Univ Lubeck, Dept Dermatol, D-23538 Lubeck, Germany.
[Belheouane, Meriem; Baines, John F.] Max Planck Inst Evolutionary Biol, Plon, Germany.
[Belheouane, Meriem; Baines, John F.] Univ Kiel, Inst Expt Med, Kiel, Germany.
[Niesar, Felix; Restle, Tobias] Med Univ Lubeck, Inst Mol Med, D-23538 Lubeck, Germany.
[Haesler, Robert] IKMB, Mol Cell Biol, Kiel, Germany.
C3 University of Lubeck; University of Lubeck; Max Planck Society;
University of Kiel; University of Lubeck
RP Ibrahim, SM (corresponding author), Med Univ Lubeck, Lubeck Inst Expt Dermatol, D-23538 Lubeck, Germany.
EM saleh.ibrahim@uksh.de
RI Häsler, Robert/A-4908-2009; Baines, John/B-3580-2010; Hirose,
Misa/A-2858-2014; Vorobyev, Artem/AAH-9400-2021; Ludwig,
Ralf/F-3996-2018; Ibrahim, Saleh/AAO-9541-2020; Zillikens,
Detlef/C-8572-2011; Ludwig, Ralf/A-2629-2008; Sadik,
Christian/G-9593-2014; Moller, Steffen/B-5368-2013
OI Ludwig, Ralf/0000-0002-1394-1737; Hirose, Misa/0000-0002-8909-4693;
Sadik, Christian/0000-0001-6701-048X; Bischof,
Julia/0000-0002-6672-6571; Hasler, Robert/0000-0003-4174-8229; Vorobyev,
Artem/0000-0002-1542-0732; Ibrahim, Saleh/0000-0001-7827-2290; Moller,
Steffen/0000-0002-7187-4683
FU Deutsche Forschungsgemeinschaft: the research training programs
Modulation of Autoimmunity [GRK1727/1]; Genes, Environment and
Inflammation [GRK 1743/1]; Excellence Cluster Inflammation at Interfaces
[EXC 306/2]
FX The project has been funded by Deutsche Forschungsgemeinschaft: the
research training programs Modulation of Autoimmunity [GRK1727/1],
Genes, Environment and Inflammation [GRK 1743/1] and Excellence Cluster
Inflammation at Interfaces [EXC 306/2]. We thank Miriam Freitag, Illona
Klamfuss, Susen Moller and Andreia de Castro Marques for help with the
AIL line.
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NR 50
TC 10
Z9 10
U1 0
U2 5
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD FEB 16
PY 2016
VL 17
AR 112
DI 10.1186/s12864-016-2455-2
PG 14
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA DD9DC
UT WOS:000370224900001
PM 26879236
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Hagiwara, S
Watanabe, T
Kudo, M
Minaga, K
Komeda, Y
Kamata, K
Kimura, M
Hayashi, H
Nakagawa, K
Ueshima, K
Minami, Y
Aoki, T
Takita, M
Morita, M
Cishina, H
Ida, H
Park, AM
Nishida, N
AF Hagiwara, Satoru
Watanabe, Tomohiro
Kudo, Masatoshi
Minaga, Kosuke
Komeda, Yoriaki
Kamata, Ken
Kimura, Masatomo
Hayashi, Hidetoshi
Nakagawa, Kazuhiko
Ueshima, Kazuomi
Minami, Yasunori
Aoki, Tomoko
Takita, Masahiro
Morita, Masahiro
Cishina, Hirokazu
Ida, Hiroshi
Park, Ah-Mee
Nishida, Naoshi
TI Clinicopathological analysis of hepatic immune-related adverse events in
comparison with autoimmune hepatitis and graft-versus host disease
SO SCIENTIFIC REPORTS
LA English
DT Article
ID REGULATORY T-CELLS; PERSISTENCE
AB Immune checkpoint inhibitors (ICIs) targeting programmed cell death 1 (PD-1) and cytotoxic T-lymphocyte antigen-4 (CTLA-4) are widely used to treat advanced metastatic cancers. Neutralisation of PD-1 or CTLA-4 by ICIs results in immune-related adverse events (irAEs). The clinicopathological features of twelve patients with hepatic irAEs were evaluated and compared to those of ten patients with autoimmune hepatitis (AIH) or graft-versus-host disease (GVHD). No significant difference was seen in serum levels of transaminases, whereas serum levels of IgG and anti-nuclear antibody were higher in patients with AIH than in those with GVHD or hepatic irAEs. Inflammation was limited to the liver lobes in patients with GVHD or hepatic irAEs, whereas patients with AIH exhibited both portal and lobular inflammation. Immunohistochemical analyses revealed a predominant infiltration of CD8(+) T cells and defective accumulation of regulatory T cells (Tregs) expressing forkhead box p3 (FOXP3) in the lobular areas of patients with hepatic irAEs and GVHD. In contrast, periportal lesions of patients with AIH were characterised by an infiltration of CD4(+) T cells, CD8(+) T cells, CD20(+) B cells, and FOXP3(+) Tregs. Overall, the activation of CD8(+) T cells in the absence of activation of Tregs potentially underlies the immunopathogenesis of hepatic irAEs.
C1 [Hagiwara, Satoru; Watanabe, Tomohiro; Kudo, Masatoshi; Minaga, Kosuke; Komeda, Yoriaki; Kamata, Ken; Ueshima, Kazuomi; Minami, Yasunori; Aoki, Tomoko; Takita, Masahiro; Morita, Masahiro; Cishina, Hirokazu; Ida, Hiroshi; Nishida, Naoshi] Kindai Univ, Fac Med, Dept Gastroenterol & Hepatol, 377-2 Ohno Higashi, Osaka 5898511, Japan.
[Kimura, Masatomo] Kindai Univ, Fac Med, Dept Pathol, Osaka, Japan.
[Hayashi, Hidetoshi; Nakagawa, Kazuhiko] Kindai Univ, Fac Med, Dept Med Oncol, Osaka, Japan.
[Park, Ah-Mee] Kindai Univ, Fac Med, Dept Microbiol, Osaka, Japan.
C3 Kindai University (Kinki University); Kindai University (Kinki
University); Kindai University (Kinki University); Kindai University
(Kinki University)
RP Hagiwara, S; Nishida, N (corresponding author), Kindai Univ, Fac Med, Dept Gastroenterol & Hepatol, 377-2 Ohno Higashi, Osaka 5898511, Japan.
EM hagi-318@hotmail.co.jp; naoshi@med.kindai.ac.jp
RI Minaga, Kosuke/AAD-2107-2020; Park, Ah-Mee/AAS-2545-2020; Kudo,
Masatoshi/AAA-9744-2019; Watanabe, Tomohiro/ABA-4712-2021; NAKAGAWA,
KAZUHIKO/ADM-9196-2022; Komeda, Yoriaki/AAF-6652-2020
OI Komeda, Yoriaki/0000-0002-0068-8461; Watanabe,
Tomohiro/0000-0002-6175-8064
FU Japan Society for the Promotion of Science (KAKENHI) [18H03554,
18K07922, 19K08455]; Smoking Research Foundation; Yakult BioScience
Foundation; Takeda Science Foundation; SENSHIN Medical Research
Foundation; Grants-in-Aid for Scientific Research [21K07950, 20K11546,
18H03554, 18K07922, 21K07287, 21K07184] Funding Source: KAKEN
FX This work was supported in part by a Grant-in-Aid for Scientific
Research from the Japan Society for the Promotion of Science (KAKENHI:
18H03554, N. Nishida, 18K07922, M. Kudo, 19K08455) and a grant from
Smoking Research Foundation (N. Nishida), from Yakult BioScience
Foundation (T. Watanabe), Takeda Science Foundation (T. Watanabe), and
SENSHIN Medical Research Foundation (T. Watanabe).
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TC 14
Z9 14
U1 0
U2 3
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD APR 29
PY 2021
VL 11
IS 1
AR 9242
DI 10.1038/s41598-021-88824-1
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA SK4QK
UT WOS:000656201900007
PM 33927311
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Jia, YC
Ding, YX
Mei, WT
Wang, YT
Zheng, Z
Qu, YX
Liang, K
Li, J
Cao, F
Li, F
AF Jia, Yu-Chen
Ding, Yi-Xuan
Mei, Wen-Tong
Wang, Yu-Ting
Zheng, Zhi
Qu, Yuan-Xu
Liang, Kuo
Li, Jia
Cao, Feng
Li, Fei
TI Extracellular vesicles and pancreatitis: mechanisms, status and
perspectives
SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Review
DE pancreatitis; extracellular vesicles; exosomes; biomarkers
ID ACUTE LUNG INJURY; CELLS-DERIVED EXOSOMES; STEM-CELLS; CIRCULATING
EXOSOMES; AUTOIMMUNE PANCREATITIS; EXOCRINE PANCREAS; TREATMENT OPTIONS;
LIVER FIBROSIS; IN-VITRO; CANCER
AB Comprehensive reviews and large population-based cohort studies have played an important role in the diagnosis and treatment of pancreatitis and its sequelae. The incidence and mortality of pancreatitis have been reduced significantly due to substantial advancements in the pathophysiological mechanisms and clinically effective treatments. The study of extracellular vesicles (EVs) has the potential to identify cell-to-cell communication in diseases such as pancreatitis. Exosomes are a subset of EVs with an average diameter of 50 similar to 150 nm. Their diverse and unique constituents include nucleic acids, proteins, and lipids, which can be transferred to trigger phenotypic changes of recipient cells. In recent years, many reports have indicated the role of EVs in pancreatitis, including acute pancreatitis, chronic pancreatitis and autoimmune pancreatitis, suggesting their potential influence on the development and progression of pancreatitis. Plasma exosomes of acute pancreatitis can effectively reach the alveolar cavity and activate alveolar macrophages to cause acute lung injury. Furthermore, upregulated exosomal miRNAs can be used as biomarkers for acute pancreatitis. Here, we summarized the current understanding of EVs in pancreatitis with an emphasis on their biological roles and their potential use as diagnostic biomarkers and therapeutic agents for this disease.
C1 [Jia, Yu-Chen; Ding, Yi-Xuan; Mei, Wen-Tong; Zheng, Zhi; Qu, Yuan-Xu; Liang, Kuo; Li, Jia; Cao, Feng; Li, Fei] Capital Med Univ, Xuanwu Hosp, Dept Gen Surg, Beijing, Peoples R China.
[Jia, Yu-Chen; Ding, Yi-Xuan; Mei, Wen-Tong; Zheng, Zhi; Qu, Yuan-Xu; Liang, Kuo; Li, Jia; Cao, Feng; Li, Fei] Capital Med Univ, Clin Ctr Acute Pancreatitis, Beijing, Peoples R China.
[Wang, Yu-Ting] Capital Med Univ, Beijing, Peoples R China.
C3 Capital Medical University; Capital Medical University; Capital Medical
University
RP Cao, F; Li, F (corresponding author), Capital Med Univ, Xuanwu Hosp, Dept Gen Surg, Beijing, Peoples R China.; Cao, F; Li, F (corresponding author), Capital Med Univ, Clin Ctr Acute Pancreatitis, Beijing, Peoples R China.
EM caofeng1221@163.com; feili36@ccmu.edu.cn
RI Jia, Yuchen/AAI-2613-2020
OI Jia, Yuchen/0009-0009-7113-3736
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NR 133
TC 13
Z9 13
U1 2
U2 19
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-2288
J9 INT J BIOL SCI
JI Int. J. Biol. Sci.
PY 2021
VL 17
IS 2
BP 549
EP 561
DI 10.7150/ijbs.54858
PG 13
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA QG2YQ
UT WOS:000617456600013
PM 33613112
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Rojas-Feria, M
Castro, M
Suárez, E
Ampuero, J
Romero-Gómez, M
AF Rojas-Feria, Maria
Castro, Manuel
Suarez, Emilio
Ampuero, Javier
Romero-Gomez, Manuel
TI Hepatobiliary manifestations in inflammatory bowel disease: The gut, the
drugs and the liver
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Inflammatory bowel disease; Hepatobiliary disorders; Extraintestinal
manifestations; Primary sclerosing cholangitis; Drug-induced liver
injury; Hepatotoxicity; Hepatitis B; Hepatitis C
ID PRIMARY SCLEROSING CHOLANGITIS; CHRONIC HEPATITIS-C; PRIMARY
BILIARY-CIRRHOSIS; FACTOR-ALPHA ANTAGONISTS; TERM-FOLLOW-UP;
ULCERATIVE-COLITIS; CROHNS-DISEASE; NATURAL-HISTORY; URSODEOXYCHOLIC
ACID; OVERLAP SYNDROME
AB Abnormal liver biochemical tests are present in up to 30% of patients with inflammatory bowel disease (IBD), and therefore become a diagnostic challenge. Liver and biliary tract diseases are common extraintestinal manifestations for both Crohn's disease and ulcerative colitis (UC), and typically do not correlate with intestinal activity. Primary sclerosing cholangitis (PSC) is the most common hepatobiliary manifestation of IBD, and is more prevalent in UC. Approximately 5% of patients with UC develop PSC, with the prevalence reaching up to 90%. Cholangiocarcinoma and colon cancer risks are increased in these patients. Less common disorders include autoimmune hepatitis/PSC overlap syndrome, IgG4-associated cholangiopathy, primary biliary cirrhosis, hepatic amyloidosis, granulomatous hepatitis, cholelithiasis, portal vein thrombosis, liver abscess, and non-alcoholic fatty liver disease. Hepatitis B reactivation during immunosuppressive therapy is a major concern, with screening and vaccination being recommended in serologically negative cases for patients with IBD. Reactivation prophylaxis with entecavir or tenofovir for 6 to 12 mo after the end of immunosuppressive therapy is mandatory in patients showing as hepatitis B surface antigen (HBsAg) positive, independently from viral load. HBsAg negative and anti-HBc positive patients, with or without anti-HBs, should be closely monitored, measuring alanine aminotransferase and hepatitis B virus DNA within 12 mo after the end of therapy, and should be treated if the viral load increases. On the other hand, immunosuppressive therapy does not seem to promote reactivation of hepatitis C, and hepatitis C antiviral treatment does not influence IBD natural history either. Most of the drugs used for IBD treatment may induce hepatotoxicity, although the incidence of serious adverse events is low. Abnormalities in liver biochemical tests associated with aminosalicylates are uncommon and are usually not clinically relevant. Methotrexate-related hepatotoxicity has been described in 14% of patients with IBD, in a dose-dependent manner. Liver biopsy is not routinely recommended. Biologics-related hepatotoxicity is rare, but has been shown most frequently in patients treated with infliximab. Thiopurines have been associated with veno-occlusive disease, regenerative nodular hyperplasia, and liver peliosis. Routine liver biochemical tests are recommended, especially during the first month of treatment. All these conditions should be considered in IBD patients with clinical or biochemical features suggestive of hepatobiliary involvement. Diagnosis and management of these disorders usually involve hepatologists and gastroenterologists due to its complexity. (C) 2013 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Rojas-Feria, Maria; Castro, Manuel; Suarez, Emilio; Ampuero, Javier; Romero-Gomez, Manuel] Univ Seville, Valme Univ Hosp, Unit Med & Surg Management Digest Dis, E-41014 Seville, Spain.
[Rojas-Feria, Maria; Castro, Manuel; Suarez, Emilio; Ampuero, Javier; Romero-Gomez, Manuel] Univ Seville, Valme Univ Hosp, CIBERehd, E-41014 Seville, Spain.
C3 Hospital Valme; University of Sevilla; Hospital Valme; CIBER - Centro de
Investigacion Biomedica en Red; CIBEREHD; University of Sevilla
RP Romero-Gómez, M (corresponding author), Univ Seville, Valme Univ Hosp, Unit Med & Surg Management Digest Dis, Avda Bellavista S-N, E-41014 Seville, Spain.
EM mromerogomez@us.es
RI de Moura, Manuel/L-4259-2017; Ampuero, Javier/AAI-2582-2019;
Romero-Gomez, Manuel/L-8030-2014
OI Romero-Gomez, Manuel/0000-0001-8494-8947; Ampuero,
Javier/0000-0002-8332-2122
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NR 142
TC 87
Z9 96
U1 0
U2 15
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 14
PY 2013
VL 19
IS 42
BP 7327
EP 7340
DI 10.3748/wjg.v19.i42.7327
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 253FM
UT WOS:000327068600014
PM 24259964
OA Green Published, Green Submitted, hybrid
DA 2025-01-07
ER
PT J
AU Miao, K
Zhang, L
AF Miao, Kang
Zhang, Li
TI Application of Immune Checkpoint Inhibitors in Solid Organ
Transplantation Recipients: A Systematic Review
SO INTERDISCIPLINARY SCIENCES-COMPUTATIONAL LIFE SCIENCES
LA English
DT Review
DE Solid organ transplantation; Immune checkpoint inhibitors; Host versus
graft response; Immunosuppressant drugs
ID RENAL-ALLOGRAFT RECIPIENT; METASTATIC MELANOMA;
HEPATOCELLULAR-CARCINOMA; GRAFT-REJECTION; LIVER-TRANSPLANTATION;
TUMOR-REGRESSION; PD-1 INHIBITION; NIVOLUMAB; CANCER; IPILIMUMAB
AB Background Solid organ transplantation (SOT) is a treatment method for end-stage organ diseases and improve their life quality, while using long-term immunosuppressant drugs (ISD) is needed to suppress the function of the immune system. Immune checkpoint inhibitors (ICIs) are a class of anti-tumor drugs that kill tumors by activating the autoimmune system. The primary objective of our systematic review is to investigate the risk factors for organ rejection and the efficacy of ICIs in solid organ transplantation recipients (SOTRs). Methods We searched four databases to find relevant articles up to January 2021. A total of 61 articles involving 106 SOTRs met the screening criteria and were included in our systematic review. The collected data were statistical described, and the risk factors were analyzed by logistic regression. Results Forty-four patients (41.5%) developed host-versus-graft response (HVGR) after ICIs. mTOR inhibitors (pre-ICIs) (p = 0.069, OR = 0.377, 95% CI 0.132-1.078) and calcineurin inhibitors (post-ICIs) (p = 0.056, OR = 0.375, 95%CI 0.137-1.025) may help reduce the incidence of HVGR. Hormones (pre-ICIs) (p = 0.026, OR = 3.150, 95%CI 1.150-8.628) and anti-metabolites (pre-ICIs) (p = 0.022, OR = 3.214, 95%CI 1.185-8.720) may adversely affect the efficacy of ICIs. Only 35.6% of patients both responded well to ICIs treatment and did not develop HVGR. Conclusions Our systematic review summarizes the use of ICIs in SOTRs and evaluates the efficacy of ICIs and the risk factors that induce HVGR. Through risk factor analysis, we found that mTOR inhibitors and calcineurin inhibitors may help to reduce the occurrence of HVGR; hormones and anti-metabolic drugs may have adverse effects on the efficacy of ICIs. In addition, there is a contradictory relationship between the occurrence of HVGR and the efficacy of ICIs.
C1 [Miao, Kang; Zhang, Li] Chinese Acad Med Sci & Peking Union Med Coll, Peking Union Med Hosp, Dept Pulm & Crit Care Med, 53 Dongdan North Ave, Beijing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Peking Union Medical College
RP Zhang, L (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Peking Union Med Hosp, Dept Pulm & Crit Care Med, 53 Dongdan North Ave, Beijing, Peoples R China.
EM zhanglipumch1026@sina.com
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NR 85
TC 6
Z9 6
U1 0
U2 13
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1913-2751
EI 1867-1462
J9 INTERDISCIP SCI
JI Interdiscip. Sci.
PD DEC
PY 2021
VL 13
IS 4
BP 801
EP 814
DI 10.1007/s12539-021-00437-4
EA JUN 2021
PG 14
WC Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Mathematical & Computational Biology
GA WH4GP
UT WOS:000663992800001
PM 34152556
DA 2025-01-07
ER
PT J
AU Beyaert, R
Beaugerie, L
Van Assche, G
Brochez, L
Renauld, JC
Viguier, M
Cocquyt, V
Jerusalem, G
Machiels, JP
Prenen, H
Masson, P
Louis, E
De Keyser, F
AF Beyaert, Rudi
Beaugerie, Laurent
Van Assche, Gert
Brochez, Lieve
Renauld, Jean-Christophe
Viguier, Manuelle
Cocquyt, Veronique
Jerusalem, Guy
Machiels, Jean-Pascal
Prenen, Hans
Masson, Pierre
Louis, Edouard
De Keyser, Filip
TI Cancer risk in immune-mediated inflammatory diseases (IMID)
SO MOLECULAR CANCER
LA English
DT Review
DE Antirheumatic agents; Autoimmune diseases; Biological products; Cancer;
Inflammation; Tumor necrosis factor
ID TUMOR-NECROSIS-FACTOR; LONG-TERM SAFETY; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
POPULATION-BASED COHORT; NF-KAPPA-B; NONMELANOMA SKIN-CANCER;
RHEUMATOID-ARTHRITIS; BOWEL-DISEASE; HEPATOCELLULAR-CARCINOMA;
ULCERATIVE-COLITIS
AB Inflammation and cancer have a profound yet ambiguous relationship. Inflammation - especially chronic inflammation - has protumorigenic effects, but inflammatory cells also mediate an immune response against the tumor and immunosuppression is known to increase the risk for certain tumors.
This article reviews current literature on the role of inflammation in cancer and the cancer risk in immune-mediated inflammatory diseases (IMIDs). We discuss the effect on cancer risk of different drug classes used in the treatment of IMIDs treatment, including biologicals such as tumor necrosis factor (TNF) inhibitors.
Overall cancer incidence and mortality risk are similar to the general population in inflammatory bowel disease (IBD), and slightly increased for rheumatoid arthritis and psoriasis, with risk profiles differing for different tumor types. Increased risk for non-melanoma skin cancer is associated with thiopurine treatment in IBD, with the combination of anti-TNF and methotrexate in rheumatoid arthritis and with PUVA, cyclosporine and anti-TNF treatment in psoriasis. Data on the safety of using biologic or immunosuppressant therapy in IMID patients with a history of cancer are scarce.
This review provides clinicians with a solid background to help them in making decisions about treatment of immune-mediated diseases in patients with a tumor history.
This article is related to another review article in Molecular Cancer: http://www.molecular-cancer.com/content/12/1/86.
C1 [Beyaert, Rudi] Univ Ghent VIB, Dept Biomed Mol Biol, Ghent, Belgium.
[Beyaert, Rudi] Univ Ghent VIB, Dept Mol Biomed Res, Ghent, Belgium.
[Beaugerie, Laurent] Hop St Antoine, AP HP, Dept Gastroenterol, F-75012 Paris, France.
[Beaugerie, Laurent] Univ Paris 06, UPMC, F-75005 Paris, France.
[Van Assche, Gert] Univ Hosp Leuven, Dept Gastroenterol, Louvain, Belgium.
[Brochez, Lieve] Ghent Univ Hosp, Dept Dermatol, Ghent, Belgium.
[Renauld, Jean-Christophe] Catholic Univ Louvain, Ludwig Inst Canc Res, B-1200 Brussels, Belgium.
[Renauld, Jean-Christophe] Catholic Univ Louvain, Expt Med Unit, B-1200 Brussels, Belgium.
[Viguier, Manuelle] AP HP, Paris, France.
[Viguier, Manuelle] Univ Paris 07, Hop St Louis, Dept Dermatol, Paris, France.
[Cocquyt, Veronique] Ghent Univ Hosp, Dept Med Oncol, Ghent, Belgium.
[Jerusalem, Guy] Univ Liege, Dept Med Oncol, Liege, Belgium.
[Machiels, Jean-Pascal] Catholic Univ Louvain, Dept Med Oncol Unit, B-1200 Brussels, Belgium.
[Machiels, Jean-Pascal] Clin Univ St Luc, B-1200 Brussels, Belgium.
[Prenen, Hans] Univ Hosp Gasthuisberg, Dept Digest Oncol, B-3000 Louvain, Belgium.
[Masson, Pierre] Catholic Univ Louvain, de Duve Inst, B-1200 Brussels, Belgium.
[Louis, Edouard] CHU, Liege, Belgium.
[Louis, Edouard] Univ Liege, Liege, Belgium.
[De Keyser, Filip] Univ Ghent, Dept Rheumatol, B-9000 Ghent, Belgium.
C3 Flanders Institute for Biotechnology (VIB); Ghent University; Flanders
Institute for Biotechnology (VIB); Ghent University; Assistance Publique
Hopitaux Paris (APHP); Sorbonne Universite; Hopital Universitaire
Saint-Antoine - APHP; Sorbonne Universite; KU Leuven; University
Hospital Leuven; Ghent University; Ghent University Hospital; Ludwig
Institute for Cancer Research; Universite Catholique Louvain; Universite
Catholique Louvain; Assistance Publique Hopitaux Paris (APHP);
Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
Hopital Universitaire Saint-Louis - APHP; Ghent University; Ghent
University Hospital; University of Liege; Universite Catholique Louvain;
Universite Catholique Louvain; Cliniques Universitaires Saint-Luc; KU
Leuven; University Hospital Leuven; Universite Catholique Louvain;
University of Liege; University of Liege; Ghent University
RP De Keyser, F (corresponding author), Univ Ghent, Dept Rheumatol, 0K12,Pintelaan 185, B-9000 Ghent, Belgium.
EM filip.dekeyser@ugent.be
RI ; Beyaert, Rudi/B-2589-2009; Renauld, Jean-Christophe/B-7268-2012
OI Prenen, Hans/0000-0001-8802-7352; Beyaert, Rudi/0000-0002-5704-582X;
Beaugerie, Laurent/0000-0002-5012-4146; Renauld,
Jean-Christophe/0000-0003-1736-2131
FU Abbott; Belgian Foundation against Cancer; IAP; FWO; IWT; Hercules
Foundation; GOA; Ghent University
FX This work was written following the Spring Lecture Sessions on cancer
and immune mediated inflammatory disorders of the Academy of Immunology
for Clinicians - Belgium and supported by an unrestricted educational
grant from Abbott. Rudi Beyaert is supported by grants from the "Belgian
Foundation against Cancer", "IAP", "FWO", "IWT", and the "Hercules
Foundation", "GOA"and "Group-ID MRP"initiatives of the Ghent University.
The authors acknowledge the medical writing contributions of Veerle
Persy, MD, PhD (Hugin Mugin Research) and Phil Leventhal, PhD
(4Clinics).
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NR 147
TC 105
Z9 111
U1 0
U2 25
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD AUG 29
PY 2013
VL 12
AR 98
DI 10.1186/1476-4598-12-98
PG 12
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA 209TV
UT WOS:000323783900001
PM 23987103
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Ueno, Y
AF Ueno, Yoshiyuki
TI The Current Endeavors to Understand the Pathogenesis of Intractable
Liver Diseases
SO TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Review
DE fulminant hepatitis; hepatitis B virus; intractable liver diseases;
liver failure; primary biliary cirrhosis
ID PRIMARY BILIARY-CIRRHOSIS; HEPATITIS-B-VIRUS; FISCAL YEAR 2008;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE CHOLANGITIS; FULMINANT-HEPATITIS;
CHOLANGIOCYTES; JAPAN; MICE; INFECTION
AB The death due to liver diseases accounts for more the 35,000 cases every year in Japan for decades. Among these liver diseases, the Ministry of Health, Labor, and Welfare of Japan has named both fulminant hepatitis and primary biliary cirrhosis (PBC) as intractable liver diseases, since the precise mechanism of these diseases are unclear. Accordingly, there are no effective medical treatments other than liver transplantation toward these diseases. However, still the number of the liver transplantation performed in Japan is small. Thus, we have focused on the pathogenesis of these two intractable conditions. The fulminant hepatitis is a distinct form of acute hepatitis, and hepatitis B virus infection accounts for 20 similar to 30% of this lethal condition. Only tiny proportions of patients with acute HBV infection develop fulminant hepatitis (less than 10%). It has been widely believed both viral and host factors contribute for fulminant hepatitis, although still unknown factors are expected to be involved. On the other hand, PBC is a chronic progressive cholestatic liver disease. Clinical features of PBC include female predominance (80 to 90%), the presence of antimitochondrial antibody (up to 95%), and elevated serum levels of immunoglobulin M. Eventually, patients with PBC will develop liver failure due to biliary cirrhosis in spite of medical interventions. Immune-mediated processes are believed to be responsible for the pathogenesis, although the precise mechanism is yet to be determined. In this review article, our endeavors to understand the mechanism of these intractable liver diseases are discussed. (C) 2012 Tohoku University Medical Press
C1 Yamagata Univ, Fac Med, Dept Gastroenterol, Yamagata 9909585, Japan.
C3 Yamagata University
RP Ueno, Y (corresponding author), Yamagata Univ, Fac Med, Dept Gastroenterol, 2-2-2 Iidanishi, Yamagata 9909585, Japan.
EM y-ueno@med.id.yamagata-u.ac.jp
RI Ueno, Yoshiyuki/R-9242-2019
FU Tohoku University Graduate School of Medicin
FX The receipt of the 2010 Gold Prize from Tohoku University School of
Medicine was possible only with the outstanding mentorship from
Professor Tooru Shimosewaga, and outstanding colleagues in hepatologists
group at Tohoku University Graduate School of Medicine. Also, we are
grateful for numbers of paramedics and technicians for supporting our
experiments, especially staffs in experimental animal facility and cell
culture laboratory.
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NR 36
TC 3
Z9 3
U1 0
U2 1
PU TOHOKU UNIV MEDICAL PRESS
PI SENDAI
PA 2-1, SEIRYO-MACHI, AOBA-KU, SENDAI, MIYAGI 980-8575, JAPAN
SN 0040-8727
EI 1349-3329
J9 TOHOKU J EXP MED
JI Tohoku J. Exp. Med.
PD MAR
PY 2012
VL 226
IS 3
BP 171
EP 175
DI 10.1620/tjem.226.171
PG 5
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA 910KI
UT WOS:000301635200001
PM 22333558
OA Bronze
DA 2025-01-07
ER
PT J
AU Tao, YN
Zhang, Q
Wang, HY
Yang, XY
Mu, HR
AF Tao, Yining
Zhang, Qi
Wang, Haoyu
Yang, Xiyu
Mu, Haoran
TI Alternative splicing and related RNA binding proteins in human health
and disease
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID HEPATOCELLULAR-CARCINOMA; PANCREATIC-CANCER; BREAST-CANCER;
TRANSLATIONAL CONTROL; EMERGING ROLES; GEMCITABINE RESISTANCE;
CELL-DIFFERENTIATION; CISPLATIN RESISTANCE; CRITICAL REGULATOR;
GENE-EXPRESSION
AB Alternative splicing (AS) serves as a pivotal mechanism in transcriptional regulation, engendering transcript diversity, and modifications in protein structure and functionality. Across varying tissues, developmental stages, or under specific conditions, AS gives rise to distinct splice isoforms. This implies that these isoforms possess unique temporal and spatial roles, thereby associating AS with standard biological activities and diseases. Among these, AS-related RNA-binding proteins (RBPs) play an instrumental role in regulating alternative splicing events. Under physiological conditions, the diversity of proteins mediated by AS influences the structure, function, interaction, and localization of proteins, thereby participating in the differentiation and development of an array of tissues and organs. Under pathological conditions, alterations in AS are linked with various diseases, particularly cancer. These changes can lead to modifications in gene splicing patterns, culminating in changes or loss of protein functionality. For instance, in cancer, abnormalities in AS and RBPs may result in aberrant expression of cancer-associated genes, thereby promoting the onset and progression of tumors. AS and RBPs are also associated with numerous neurodegenerative diseases and autoimmune diseases. Consequently, the study of AS across different tissues holds significant value. This review provides a detailed account of the recent advancements in the study of alternative splicing and AS-related RNA-binding proteins in tissue development and diseases, which aids in deepening the understanding of gene expression complexity and offers new insights and methodologies for precision medicine.
C1 [Tao, Yining; Wang, Haoyu; Yang, Xiyu; Mu, Haoran] Shanghai Jiao Tong Univ, Shanghai Gen Hosp, Sch Med, Dept Orthoped, Shanghai 200000, Peoples R China.
[Tao, Yining; Wang, Haoyu; Yang, Xiyu; Mu, Haoran] Shanghai Bone Tumor Inst, Shanghai 200000, Peoples R China.
[Zhang, Qi] Shanghai Jiao Tong Univ, Sch Med, Dept Biochem & Mol Cell Biol, Shanghai Key Lab Tumor Microenvironm & Inflammat, Shanghai 200000, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University
RP Mu, HR (corresponding author), Shanghai Jiao Tong Univ, Shanghai Gen Hosp, Sch Med, Dept Orthoped, Shanghai 200000, Peoples R China.; Mu, HR (corresponding author), Shanghai Bone Tumor Inst, Shanghai 200000, Peoples R China.
EM dr_muhaoran@163.com
RI Yang, Xiyu/KBC-4381-2024; Yang, Yu/GYJ-1931-2022; Mu,
Haoran/AFM-0882-2022; Haoyu, Wang/ABA-7508-2021
OI MU, HAORAN/0000-0003-4763-1363
FU National Natural Science Foundation of China (National Science
Foundation of China) [82272773, 82373177, 82203043]; Shanghai Key
Laboratory for Tumor Microenvironment and Inflammation - National
Natural Science Foundation of China
FX We would be deeply grateful to Professor Bing Li [Department of
Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for
Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University
School of Medicine] for his valuable suggestions and feedback that
greatly improved this work. We would also like to express the
appreciation to Dr. Zhengdong Cai, Dr. Wei Sun, and Dr. Yingqi Hua
[Department of Orthopedics, Shanghai General Hospital, School of
Medicine, Shanghai Jiao Tong University] for their support and
encouragement throughout our work. We wish to thank Professor YunPeng
Zhang [College of Bioinformatics Science and Technology, Harbin Medical
University] for his kind assistance in figures in this work. This study
was funded by the National Natural Science Foundation of China
(82272773, 82373177, and 82203043).
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NR 509
TC 30
Z9 32
U1 24
U2 49
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD FEB 2
PY 2024
VL 9
IS 1
AR 26
DI 10.1038/s41392-024-01734-2
PG 33
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA GT9C4
UT WOS:001155031200001
PM 38302461
OA gold, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Gu, JJ
Su, CY
Huang, F
Zhao, YW
Li, J
AF Gu, Junjie
Su, Chongying
Huang, Fei
Zhao, Yuwei
Li, Jing
TI Past, Present and Future: The Relationship Between Circular RNA and
Immunity
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE circRNAs; immunity; immune-related diseases; autoimmune diseases; tumor;
infectious diseases
ID MICROARRAY EXPRESSION PROFILE; BLOOD MONONUCLEAR-CELLS; MACROPHAGE
ACTIVATION; HEPATOCELLULAR-CARCINOMA; ENHANCES RESISTANCE; DENDRITIC
CELLS; GASTRIC-CANCER; PROLIFERATION; SUPPRESSION; PROGRESSION
AB The immune system has evolved since the birth of humans. However, immune-related diseases have not yet been overcome due to the lack of expected indicators and targeting specificity of current medical technology, subjecting patients to very uncomfortable physical and mental experiences and high medical costs. Therefore, the requirements for treatments with higher specificity and indicative ability are raised. Fortunately, the discovery of and continuous research investigating circular RNAs (circRNAs) represent a promising method among numerous methods. Although circRNAs wear regarded as metabolic wastes when discovered, as a type of noncoding RNA (ncRNA) with a ring structure and wide distribution range in the human body, circRNAs shine brilliantly in medical research by virtue of their special nature and structure-determined functions, such as high stability, wide distribution, high detection sensitivity, acceptable reproducibility and individual differences. Based on research investigating the role of circRNAs in immunity, we systematically discuss the hotspots of the roles of circRNAs in immune-related diseases, including expression profile analyses, potential biomarker research, ncRNA axis/network construction, impacts on phenotypes, therapeutic target seeking, maintenance of nucleic acid stability and protein binding research. In addition, we summarize the current situation of and problems associated with circRNAs in immune research, highlight the applications and prospects of circRNAs in the treatment of immune-related diseases, and provide new insight into future directions and new strategies for laboratory research and clinical applications.
C1 [Gu, Junjie; Su, Chongying; Huang, Fei; Li, Jing] Sichuan Univ, West China Hosp Stomatol, Chinese Acad Med Sci, Natl Clin Res Ctr Oral Dis,Res Unit Oral Carcinoge, Chengdu, Peoples R China.
[Zhao, Yuwei] Chengdu Blood Ctr, Blood Res Lab, Chengdu, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Sichuan University
RP Li, J (corresponding author), Sichuan Univ, West China Hosp Stomatol, Chinese Acad Med Sci, Natl Clin Res Ctr Oral Dis,Res Unit Oral Carcinoge, Chengdu, Peoples R China.; Zhao, YW (corresponding author), Chengdu Blood Ctr, Blood Res Lab, Chengdu, Peoples R China.
EM cdbczyw@163.com; lijing1984@scu.edu.cn
RI LI, Jing/HNB-5575-2023
FU National Natural Science Foundation of China [81872211, 82072999];
Sichuan Science and Technology Program [2020YJ0102]; Innovation Research
Project of Sichuan University [2022SCUH0029]; CAMS Innovation Fund for
Medical Sciences [2020-I2M-CT-A-023]
FX This work was supported by grants from the National Natural Science
Foundation of China (81872211 and 82072999), the Sichuan Science and
Technology Program (2020YJ0102), the Innovation Research Project of
Sichuan University (2022SCUH0029), and the CAMS Innovation Fund for
Medical Sciences (2020-I2M-C&T-A-023).
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NR 167
TC 8
Z9 9
U1 0
U2 18
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAY 25
PY 2022
VL 13
AR 894707
DI 10.3389/fimmu.2022.894707
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 1Y1DN
UT WOS:000807884900001
PM 35693804
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Malik, SM
deVera, ME
Fontes, P
Shaikh, O
Sasatomi, E
Ahmad, J
AF Malik, Shahid M.
deVera, Michael E.
Fontes, Paulo
Shaikh, Obaid
Sasatomi, Eizaburo
Ahmad, Jawad
TI Recurrent Disease Following Liver Transplantation for Nonalcoholic
Steatohepatitis Cirrhosis
SO LIVER TRANSPLANTATION
LA English
DT Article
ID PLACEBO-CONTROLLED TRIAL; HEPATOCELLULAR-CARCINOMA; CRYPTOGENIC
CIRRHOSIS; RISK-FACTORS; AUTOIMMUNE HEPATITIS; ALLOGRAFT-REJECTION;
SURVIVAL; IMPACT; PIOGLITAZONE; PREVALENCE
AB Recurrence of the original disease following liver transplantation is not uncommon and can lead to graft failure. There are limited data on recurrent fatty liver disease following liver transplantation. The aim of this study was to determine the incidence of recurrent fatty liver disease in patients with biopsy-proven nonalcoholic steatohepatitis, its effect on survival, and whether there are any predictive factors for recurrence. We analyzed patients undergoing liver transplantation for nonalcoholic steatohepatitis cirrhosis from 1997 to 2008 at a single center. Patients undergoing transplantation for cholestatic disease, alcohol, hepatitis C, or cryptogenic cirrhosis were controls. Ninety-eight patients underwent transplantation for nonalcoholic steatohepatitis cirrhosis. Recurrent fatty liver disease was seen in 70%, 25% had recurrent nonalcoholic steatohepatitis, and 18% had stage II/IV or greater fibrosis at a mean of 18 months. No patients with recurrent nonalcoholic steatohepatitis developed graft failure or required retransplantation at a follow-up of 3 years. No recipient or donor factors were associated with disease recurrence, although patients with recurrent nonalcoholic steatohepatitis had a higher incidence of diabetes, weight gain, and dyslipidemia at the time of diagnosis of recurrence. One-third of patients with recurrent nonalcoholic steatohepatitis had normal liver enzymes at the time of diagnosis post-transplantation. In conclusion, recurrent fatty liver disease is common following liver transplantation for nonalcoholic steatohepatitis cirrhosis but does not lead to early allograft failure. Recurrent nonalcoholic steatohepatitis can occur despite normal liver enzymes, and features of metabolic syndrome are associated with disease recurrence. Liver Transpl 15:1843-1851, 2009. (C) 2009 AASLD.
C1 [Malik, Shahid M.; Shaikh, Obaid; Ahmad, Jawad] Univ Pittsburgh, Div Gastroenterol Hepatol & Nutr, Sch Med, Pittsburgh, PA 15213 USA.
[deVera, Michael E.; Fontes, Paulo] Univ Pittsburgh, Thomas E Starzl Transplantat Inst, Sch Med, Pittsburgh, PA 15213 USA.
[Sasatomi, Eizaburo] Univ Pittsburgh, Dept Pathol, Sch Med, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh; Pennsylvania Commonwealth System of
Higher Education (PCSHE); University of Pittsburgh
RP Ahmad, J (corresponding author), Univ Pittsburgh, Div Gastroenterol Hepatol & Nutr, Sch Med, Pittsburgh, PA 15213 USA.
EM javbob@hotmail.com
RI Shaikh, Obaid/AAL-5339-2021
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NR 43
TC 88
Z9 91
U1 0
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6465
EI 1527-6473
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD DEC
PY 2009
VL 15
IS 12
BP 1843
EP 1851
DI 10.1002/lt.21943
PG 9
WC Gastroenterology & Hepatology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA 527MH
UT WOS:000272370700024
PM 19938117
OA Bronze
DA 2025-01-07
ER
PT J
AU Chrostek, L
Cylwik, B
Gruszewska, E
Panasiuk, A
Szmitkowski, M
AF Chrostek, Lech
Cylwik, Bogdan
Gruszewska, Ewa
Panasiuk, Anatol
Szmitkowski, Maciej
TI N-Latex CDT Results in Liver Diseases
SO ALCOHOL AND ALCOHOLISM
LA English
DT Article
ID CARBOHYDRATE-DEFICIENT TRANSFERRIN; GAMMA-GLUTAMYL-TRANSFERASE; PRIMARY
BILIARY-CIRRHOSIS; ALCOHOL-CONSUMPTION; HEPATITIS; MARKER; ABUSE; HPLC;
DIAGNOSIS; DRINKING
AB Aims: The aim of this study was to test whether liver diseases of alcoholic and non-alcoholic origin cause false-positive carbohydrate-deficient transferrin (CDT) results when the particle-enhanced immunonephelometry for CDT assays is used and to assess the effect of liver disease severity on N-Latex CDT results. Methods: Blood was sampled from 245 newly admitted patients suffering from liver diseases: alcoholic and non-alcoholic cirrhosis (AC), chronic viral (B and C) and non-viral hepatitis, toxic and autoimmune hepatitis (AIH), hepatocellular carcinoma and primary biliary cirrhosis (PBC). CDT was determined by particle-enhanced imunononephelometry using the N-Latex CDT test. Results: There were significant differences in %CDT levels between liver diseases of various etiologies. The %CDT level in AC was higher than that in chronic hepatitis (non-viral and viral C). In turn, the %CDT level in chronic hepatitis C was lower than that in toxic hepatitis. The frequency of false-positive %CDT results in liver diseases of non-alcoholic origin was 13/146, and was highest in AIH (4/14). There were no CDT-positive results in PBC and chronic hepatitis B. The frequency of CDT-positive results in alcoholic liver diseases was 24/59 in cirrhosis and 10/34 in hepatitis. Serum levels of %CDT in cirrhotic patients are correlated with the severity of the disease assessed by the Child-Pugh score. Conclusion: We concluded that the liver diseases affect the relative but not absolute values of CDT when using the assay with the monoclonal antibodies directed against CDT. The CDT results from N-Latex CDT test reflect the severity of liver dysfunction.
C1 [Chrostek, Lech; Cylwik, Bogdan; Gruszewska, Ewa; Szmitkowski, Maciej] Med Univ, Dept Biochem Diagnost, PL-15269 Bialystok, Poland.
[Panasiuk, Anatol] Med Univ, Dept Infect Dis, PL-15540 Bialystok, Poland.
C3 Medical University of Bialystok; Medical University of Bialystok
RP Chrostek, L (corresponding author), Med Univ, Dept Biochem Diagnost, Waszyngtona 15A, PL-15269 Bialystok, Poland.
EM chrostek@umwb.edu.pl
RI Gruszewska, Ewa/T-1062-2018; Chrostek, Lech/T-2219-2018; Cylwik,
Bogdan/S-5063-2018
OI Gruszewska, Ewa/0000-0002-7702-5148; Chrostek, Lech/0000-0001-6701-1861;
Cylwik, Bogdan/0000-0002-9890-7334
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NR 18
TC 10
Z9 10
U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0735-0414
J9 ALCOHOL ALCOHOLISM
JI Alcohol Alcohol.
PD JUL-AUG
PY 2012
VL 47
IS 4
BP 428
EP 432
DI 10.1093/alcalc/ags053
PG 5
WC Substance Abuse
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Substance Abuse
GA 963NX
UT WOS:000305629400011
PM 22582186
DA 2025-01-07
ER
PT J
AU Scheid, JF
Rosenbaum, MW
Przybyszewski, EM
Krishnan, K
Forcione, DG
Iafrate, AJ
Staller, KD
Misdraji, J
Lennerz, JK
Pitman, MB
Pratt, DS
AF Scheid, Johannes F.
Rosenbaum, Matthew W.
Przybyszewski, Eric M.
Krishnan, Kumar
Forcione, David G.
Iafrate, Anthony J.
Staller, Kyle D.
Misdraji, Joseph
Lennerz, Jochen K.
Pitman, Martha Bishop
Pratt, Daniel S.
TI Next-generation sequencing in the evaluation of biliary strictures in
patients with primary sclerosing cholangitis
SO CANCER CYTOPATHOLOGY
LA English
DT Article
DE autoimmune liver disease; biliary brushings; biliary dysplasia;
cholangiocarcinoma; cholestatic liver disease
ID IN-SITU HYBRIDIZATION; LIVER-TRANSPLANTATION; CANCER;
CHOLANGIOCARCINOMA; MUTATIONS; CYTOLOGY
AB BACKGROUND Primary sclerosing cholangitis (PSC) is a well-described risk factor for the development of cholangiocarcinoma (CCA). Early detection of CCA in these patients is of great importance because it expands options for therapeutic interventions, including liver transplantation. Current diagnostic tests for the evaluation of biliary strictures are limited to biliary brushing (BB) cytology and fluorescence in situ hybridization (FISH). Next-generation sequencing (NGS) has become an important diagnostic tool in oncology and may be a useful tool for diagnosing CCA on BBs. It is not clear how NGS performs when it is added to BB cytology and FISH in patients with PSC. METHODS This study reports the authors' experience with NGS performed as a prospective cotest with cytology and FISH on BBs obtained from 60 patients with PSC followed at Massachusetts General Hospital. A duct with malignancy was defined as a high-risk (HR) stricture with either high-grade dysplasia or CCA. RESULTS NGS was better than FISH and cytology in detecting HR strictures, which showed multiple genetic mutations in all cases. NGS provided specific mutational information, and NGS results were reproducible in longitudinal samples. CONCLUSIONS Adding NGS to BB cytology and FISH in the evaluation of biliary strictures for patients with PSC may provide additional information that could help to inform clinical management.
C1 [Scheid, Johannes F.; Przybyszewski, Eric M.; Krishnan, Kumar; Staller, Kyle D.; Pratt, Daniel S.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Rosenbaum, Matthew W.] Beth Israel Deaconess Med Ctr, Dept Pathol, 330 Brookline Ave, Boston, MA 02215 USA.
[Forcione, David G.] Boca Raton Reg Hosp, Boca Raton, FL USA.
[Iafrate, Anthony J.; Misdraji, Joseph; Lennerz, Jochen K.; Pitman, Martha Bishop] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Pratt, Daniel S.] Massachusetts Gen Hosp, Autoimmune & Cholestat Liver Ctr, Boston, MA 02114 USA.
C3 Harvard University; Massachusetts General Hospital; Harvard University;
Beth Israel Deaconess Medical Center; Harvard University; Massachusetts
General Hospital; Harvard University; Massachusetts General Hospital
RP Pratt, DS (corresponding author), Massachusetts Gen Hosp, 55 Fruit St, Boston, MA 02114 USA.
EM dspratt@mgh.harvard.edu
RI Misdraji, Joseph/AGX-4779-2022; Staller, Kyle/W-5582-2019
FU National Institutes of Health [5T32DK007191-45]; National Institute of
Diabetes and Digestive and Kidney Diseases [T32DK007191] Funding Source:
NIH RePORTER
FX Johannes F. Scheid was supported by a T-32 grant from the National
Institutes of Health (5T32DK007191-45).
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Zou SS, 2014, NAT COMMUN, V5, DOI 10.1038/ncomms6696
NR 30
TC 10
Z9 10
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1934-662X
EI 1934-6638
J9 CANCER CYTOPATHOL
JI Cancer Cytopathol.
PD MAR
PY 2022
VL 130
IS 3
BP 215
EP 230
DI 10.1002/cncy.22528
EA NOV 2021
PG 16
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA ZM1EJ
UT WOS:000713740900001
PM 34726838
OA Bronze
DA 2025-01-07
ER
PT J
AU Li, HB
Li, GS
Zhao, XY
Wu, YK
Ma, W
Liu, YL
Gong, FM
Liang, SF
AF Li, Hongbin
Li, Guoshun
Zhao, Xinyu
Wu, Yongkang
Ma, Wen
Liu, Yuling
Gong, Fengming
Liang, Shufang
TI Complementary serum proteomic analysis of autoimmune hepatitis in mice
and patients
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Autoimmune hepatitis; Serum proteomics; Isobaric tags for relative and
absolute quantification (iTRAQ)
ID PROTEIN EXPRESSION; ALPHA-FETOPROTEIN; IDENTIFICATION; BIOMARKER;
CANCER; C3; AUTOANTIGENS; MODEL
AB Background: Autoimmune hepatitis (AIH) is a chronic liver disease caused by inflammation of the liver. The etiology of AIH remains elusive, and there are no reliable serum biomarkers.
Methods: In order to identify candidate biomarkers, 2-DE analysis of serum proteins was performed using a mouse model of AIH induced by treatment with concanavalin A (ConA). To enrich samples for low abundance molecules a commercial albumin removal reagent was used. In an independent analysis, candidate biomarkers were identified in AIH patient's serum by a targeted iTRAQ (isobaric tags for relative and absolute quantification) identification. Candidates were validated in independent cohorts of ConA treated mice and AIH patients by ELISA (enzyme-linked immuno sorbent assay).
Results: Nine proteins were differentially expressed in AIH mice treated with con-A. Two of these, the third component of complement (C3) and alpha-2-macroglobulin (A2M) were also up-regulated in AIH patient's sera by a targeted iTRAQ identification. In separate validation studies, serum C3 and A2M levels were increased in mice with ConA treatment after 20-40 h and in 34 AIH patients in a subgroup analysis, females with AIH aged 20-50 years old displayed the largest increases in serum A2M level. Biological network analysis implements the complement cascade and protease inhibitors in the pathogenesis of AIH.
Conclusion: The serum proteins C3 and A2M are increased both in a mouse model and in patients with AIH by both 2-DE and iTRAQ methods. This integrated serum proteomics investigation should be applicable for translational researchers to study other medical conditions.
C1 [Li, Hongbin; Li, Guoshun; Zhao, Xinyu; Ma, Wen; Liu, Yuling; Gong, Fengming; Liang, Shufang] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
[Li, Hongbin; Li, Guoshun; Zhao, Xinyu; Ma, Wen; Liu, Yuling; Gong, Fengming; Liang, Shufang] Sichuan Univ, West China Hosp, Ctr Canc, Chengdu 610041, Peoples R China.
[Wu, Yongkang] Sichuan Univ, West China Hosp, West China Med Sch, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Liang, SF (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
EM zizi2006@scu.edu.cn
RI Li, Hongbin/LGY-0603-2024; Liang, Shufang/AAW-8143-2021
OI Li, Hongbin/0000-0003-2709-3633
FU National Key Basic Research Program of China [2011CB910703,
2013CB911303]; National Natural Sciences Foundation of China [31071235,
30970654, 30801374]; New Century Excellent Talents in University
[NCET-10-0595]; Doctoral Program of Higher Education [20120181110025];
Sichuan Province Program [2010JQ0016, 2012SZ0002]; Chengdu City Science
& Technology Bureau Project [11DXYB356JH-027]
FX This work was financially supported by the grants from National Key
Basic Research Program of China (2011CB910703, 2013CB911303), National
Natural Sciences Foundation of China (31071235,30970654, 30801374), and
grants for New Century Excellent Talents in University (NCET-10-0595),
specialized research fund for the Doctoral Program of Higher Education
(20120181110025). This research was also funded by Sichuan Province
Program (2010JQ0016, 2012SZ0002) and Chengdu City Science & Technology
Bureau Project (11DXYB356JH-027).
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NR 42
TC 13
Z9 13
U1 0
U2 11
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD JUN 13
PY 2013
VL 11
AR 146
DI 10.1186/1479-5876-11-146
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 178KI
UT WOS:000321446300001
PM 23763817
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Miura, H
Kitamura, S
Yamada, H
AF Miura, Hideaki
Kitamura, Shigehiro
Yamada, Haruki
TI A variant form of autoimmune pancreatitis successfully treated by
steroid therapy, accompanied by von Meyenburg complex
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune pancreatitis; Diagnostic criteria; IgG4; Biliary hamartoma;
von Meyenburg complex
ID DIAGNOSTIC-CRITERIA; RETROPERITONEAL FIBROSIS; SCLEROSING PANCREATITIS;
MASS; CHOLANGITIS; FEATURES; ENTITY
AB Diagnostic criteria for autoimmune pancreatitis (AIP) have been proposed and used clinically because, despite its unique clinicopathological features, AIP does not have disease-specific serological tests for confirmation. However, diagnosis of a patient with pancreatic lesions mimicking cancer who deviates from these diagnostic criteria is still difficult. We present herein a patient with a variant form of AIP successfully diagnosed by fine-needle biopsy, whose response to steroid therapy was excellent. A 55-year-old Japanese man was admitted to hospital because of jaundice and pancreatic head mass. AIP was considered as one of the differential diagnoses; however, as the patient showed neither pancreatic duct narrowing nor immunological abnormalities, he did not meet the Japanese diagnostic criteria for AIR Histopathology of the pancreatic mass demonstrated abundant infiltration by lymphocytes and interstitial fibrosis, which suggested AIR Immunoreaction to IgG4, which is supposed to be specific to Alp, was not observed; however, response to subsequent prednisolone therapy was good, with dramatic pancreatic head mass regression. Aside from the pancreatic head mass, diffusely spreading small lesions were observed throughout the liver. The likelihood of a potential association with extrapancreatic lesions of AIP was considered and led us to carry out a liver biopsy, which revealed biliary hamartoma, also called von Meyenburg complex (VMC). As IgG4-positive plasma cell infiltration was not demonstrated in the hamartomatous regions, the hepatic condition was thought to have occurred incidentally; however, to the best of our knowledge, this is the first report in which the association between AIP and VMC was investigated and discussed. (c) 2009 The WIG Press and Baishideng. All rights reserved.
C1 [Miura, Hideaki; Yamada, Haruki] Social Insurance Cent Gen Hosp, Dept Internal Med, Shinjuku Ku, Tokyo 1690073, Japan.
[Kitamura, Shigehiro] Social Insurance Cent Gen Hosp, Dept Pathol, Shinjuku Ku, Tokyo 1690073, Japan.
RP Miura, H (corresponding author), Social Insurance Cent Gen Hosp, Dept Internal Med, Shinjuku Ku, 3-22-1 Hyakunin Cho, Tokyo 1690073, Japan.
EM h.miura@shahochu.jp
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NR 27
TC 1
Z9 1
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD FEB 7
PY 2009
VL 15
IS 5
BP 622
EP 627
DI 10.3748/wjg.15.622
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 408AU
UT WOS:000263406200017
PM 19195067
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Wu, B
Zhang, JP
Chen, Y
Chen, SY
Liu, HL
AF Wu, Bing
Zhang, Junpei
Chen, Ying
Chen, Shiyao
Liu, Hailing
TI Association between non-alcoholic fatty liver disease and the risk of
pulmonary nodules in patients with intestinal polyps
SO JOURNAL OF THORACIC DISEASE
LA English
DT Article
DE Non-alcoholic fatty liver disease (NAFLD); pulmonary nodules; obesity;
lung cancer; intestinal polyps
AB Background: Associations between metabolic risk factors and lung cancer remain elusive, and evidence on the linkage between non-alcoholic fatty liver disease (NAFLD) and pulmonary nodules is limited. This study sought to examine the independent association between NAFLD and the risk of pulmonary nodules. Methods: Cross-sectional analyses of 1,119 patients with intestinal polyps hospitalized at the Department of Gastroenterology, Minhang District Central Hospital of Shanghai, China, were conducted. NAFLD was diagnosed based on hepatic ultrasonography or computed tomography (CT) findings of hepatic steatosis, with exclusion criteria ensuring patients had no history of significant alcohol consumption, viral infections, or hepatic autoimmune diseases. The currently accepted definition of a pulmonary nodule is a solid or sub- solid shadow <= 3 cm in diameter that appears as a solid or semi-solid pattern on a chest CT scan (our specific treatment is pulmonary nodule size: 5 mm to 3 cm). Adjusted 95% confidence intervals (CIs) and odds ratios (ORs) for NAFLD and the clinical features connected with pulmonary nodule risk were determined using a multivariable logistic regression analysis. Results: Among the 979 intestinal polyp patients, the prevalence rates of NAFLD and pulmonary nodules were 25.9% and 32.8%, respectively. Patients with pulmonary nodules exhibited higher rates of NAFLD (31.5% vs. 23.3%, P=0.006) and obesity (41.4% vs. 32.5%, P=0.006) compared to those without pulmonary nodules. After removing all the possible confounding variables, the adjusted ORs for NAFLD, an older age, smoking, and obesity were 1.370 (95% CI: 1.006-1.867, P=0.04), 1.022 (95% CI: 1.010-1.033), 1.599 (95% CI: 1.033-2.475), and 1.410 (95% CI: 1.057-1.880), respectively (all P values <0.05). NAFLD showed a significant association with an increased risk of pulmonary nodules. Conclusions: NAFLD was independently linked to an increased incidence of pulmonary nodules in intestinal polyp patients, which emphasizes the importance of screening and managing these conditions in lung cancer prevention.
C1 [Wu, Bing; Zhang, Junpei; Chen, Ying; Chen, Shiyao; Liu, Hailing] Fudan Univ, Minhang Dist Cent Hosp Shanghai, Dept Gastroenterol, 170 Xinsong Rd, Shanghai 201100, Peoples R China.
C3 Fudan University
RP Liu, HL (corresponding author), Fudan Univ, Minhang Dist Cent Hosp Shanghai, Dept Gastroenterol, 170 Xinsong Rd, Shanghai 201100, Peoples R China.
EM 18918169307@163.com
FU METTL14 study of the molecular mechanism of promoting liver fibrosis
through m6A modification District Science and Technology Commission
[2022MHZ090]; Liver cirrhosis esophageal and gastric varices screening
and endoscopic treatment technology popularization and application
Shanghai Municipal Health Commission [2019SY028]
FX This study was supported by METTL14 study of the molecular mechanism of
promoting liver fibrosis through m6A modification District Science and
Technology Commission (No. 2022MHZ090), and Liver cirrhosis esophageal
and gastric varices screening and endoscopic treatment technology
popularization and application Shanghai Municipal Health Commission (No.
2019SY028).
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NR 48
TC 0
Z9 0
U1 1
U2 1
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2072-1439
EI 2077-6624
J9 J THORAC DIS
JI J. Thorac. Dis.
PD JUN
PY 2024
VL 16
IS 6
BP 3990
EP 3999
DI 10.21037/jtd-24-754
PG 10
WC Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Respiratory System
GA A8U6G
UT WOS:001285237100019
PM 38983169
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Naeem, M
Bano, N
Manzoor, S
Ahmad, A
Munawar, N
Razak, SIA
Lee, TY
Devaraj, S
Hazafa, A
AF Naeem, Muhammad
Bano, Naheed
Manzoor, Saba
Ahmad, Aftab
Munawar, Nayla
Razak, Saiful Izwan Abd
Lee, Tze Yan
Devaraj, Sutha
Hazafa, Abu
TI Pathogenetic Mechanisms of Liver-Associated Injuries, Management, and
Current Challenges in COVID-19 Patients
SO BIOMOLECULES
LA English
DT Review
DE liver injury; SARS-CoV-2; liver transplants; chronic liver disease;
COVID-19; NFALD; management; interleukins; liver cirrhosis
ID DISEASE; TRANSPLANTATION; EXPRESSION; HEALTH; ACE2; IL-6
AB The global outbreak of COVID-19 possesses serious challenges and adverse impacts for patients with progression of chronic liver disease and has become a major threat to public health. COVID-19 patients have a high risk of lung injury and multiorgan dysfunction that remains a major challenge to hepatology. COVID-19 patients and those with liver injury exhibit clinical manifestations, including elevation in ALT, AST, GGT, bilirubin, TNF-alpha, and IL-6 and reduction in the levels of CD4 and CD8. Liver injury in COVID-19 patients is induced through multiple factors, including a direct attack of SARS-CoV-2 on liver hepatocytes, hypoxia reperfusion dysfunction, cytokine release syndrome, drug-induced hepatotoxicity caused by lopinavir and ritonavir, immune-mediated inflammation, renin-angiotensin system, and coagulopathy. Cellular and molecular mechanisms underlying liver dysfunction are not fully understood in severe COVID-19 attacks. High mortality and the development of chronic liver diseases such as cirrhosis, alcoholic liver disease, autoimmune hepatitis, nonalcoholic fatty liver disease, and hepatocellular carcinoma are also associated with patients with liver damage. COVID-19 patients with preexisting or developing liver disease should be managed. They often need hospitalization and medication, especially in conjunction with liver transplants. In the present review, we highlight the attack of SARS-CoV-2 on liver hepatocytes by exploring the cellular and molecular events underlying the pathophysiological mechanisms in COVID-19 patients with liver injury. We also discuss the development of chronic liver diseases during the progression of SARS-CoV-2 replication. Lastly, we explore management principles in COVID-19 patients with liver injury and liver transplantation.
C1 [Naeem, Muhammad] Hebei Normal Univ, Coll Life Sci, Shijiazhuang, Peoples R China.
[Bano, Naheed] Muhammad Nawaz Sharif Univ Agr, Dept Fisheries & Aquaculture, Multan 60000, Pakistan.
[Manzoor, Saba] Univ Sialkot, Dept Zool, Sialkot 51310, Pakistan.
[Ahmad, Aftab] Univ Agr Faisalabad, Ctr Adv Studies Agr & Food Secur CAS AFS, Biochem, Faisalabad 38040, Pakistan.
[Munawar, Nayla] United Arab Emirates Univ, Coll Sci, Dept Chem, Al Ain 15551, U Arab Emirates.
[Razak, Saiful Izwan Abd] Univ Teknol Malaysia, Fac Elect Engn, Dept Biomed Engn & Hlth Sci, BioInspired Device & Tissue Engn Res Grp BioInspi, Johor Baharu 81310, Malaysia.
[Razak, Saiful Izwan Abd] Univ Teknol Malaysia, Inst Human Centred Engn, Sports Innovat & Technol Ctr, Johor Baharu 81310, Malaysia.
[Lee, Tze Yan] Perdana Univ, Sch Liberal Arts Sci & Technol PUScLST, Suite 9 2,9th Floor, Kuala Lumpur 50490, Malaysia.
[Devaraj, Sutha] AIMST Univ, Fac Med, Bedong 08100, Malaysia.
[Hazafa, Abu] Univ Salerno, Scuola Med Salernitana, Dept Med Surg & Dent, I-84081 Baronissi, Italy.
[Hazafa, Abu] Univ Agr Faisalabad, Dept Biochem, Faisalabad 38040, Pakistan.
C3 Hebei Normal University; University of Agriculture Faisalabad; United
Arab Emirates University; Universiti Teknologi Malaysia; Universiti
Teknologi Malaysia; Perdana University; AIMST University; University of
Salerno; University of Agriculture Faisalabad
RP Munawar, N (corresponding author), United Arab Emirates Univ, Coll Sci, Dept Chem, Al Ain 15551, U Arab Emirates.; Hazafa, A (corresponding author), Univ Salerno, Scuola Med Salernitana, Dept Med Surg & Dent, I-84081 Baronissi, Italy.; Hazafa, A (corresponding author), Univ Agr Faisalabad, Dept Biochem, Faisalabad 38040, Pakistan.
EM nmunawar@uaeu.ac.ae; ahazafa@unisa.it
RI Tze Yan, Lee/AGZ-7530-2022; Razak, Saiful/AAM-6136-2020; Devaraj,
Sutha/AAK-5539-2020; Bano, Naheed/ABG-5766-2021; Hazafa,
Abu/AAO-1858-2020; Ahmad, Aftab/L-9718-2015; Naeem,
Muhammad/ABC-7331-2021
OI Hazafa, Abu/0000-0002-5118-9419; Devaraj, Sutha/0000-0003-0092-840X;
Munawar, Nayla/0000-0001-9448-2845; Ahmad, Aftab/0000-0002-2792-9771;
Abd Razak, Saiful Izwan/0000-0001-7477-0284; Naeem,
Muhammad/0000-0002-5078-5470; Tze Yan, Lee/0000-0002-9780-5248
FU United Arab Emirates University (UAEU) [31S414]; UPAR; [12S094]
FX The research is funded by United Arab Emirates University (UAEU)
research grant number 31S414 and UPAR grant 2022, 12S094.
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NR 92
TC 5
Z9 6
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD JAN
PY 2023
VL 13
IS 1
AR 99
DI 10.3390/biom13010099
PG 16
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 8B6YR
UT WOS:000917070000001
PM 36671484
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Haider, MB
Al Sbihi, A
Reddy, SN
Green, P
AF Haider, Maryam Bilal
Al Sbihi, Ali
Reddy, Sushmitha Nanja
Green, Peter
TI Prevalence of malignant neoplasms in celiac disease patients - a
nationwide United States population-based study
SO WORLD JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE Celiac disease; Malignant neoplasm; Autoimmune disorder; Hospitalized
patients; Healthcare utilization; Gastrointestinal malignancies;
Lymphomas; Epidemiology
ID T-CELL LYMPHOMA; SMALL-BOWEL ADENOCARCINOMA; NON-HODGKIN-LYMPHOMA;
DERMATITIS-HERPETIFORMIS; THYROID-CANCER; RISK; MORTALITY; COHORT;
DEATH; INDIVIDUALS
AB BACKGROUND Celiac disease (CeD) is an autoimmune disorder triggered by the immune response to gluten in genetically predisposed individuals. Recent research has unveiled a heightened risk of developing specific malignant neoplasms (MN) and various malignancies, including gastrointestinal, lymphomas, skin, and others, in individuals with CeD. AIM To investigate the prevalence of MN in hospitalized CeD patients in the United States. METHODS Using data from the National Inpatient Sample spanning two decades, from January 2000 to December 2019, we identified 529842 CeD patients, of which 78128 (14.75%) had MN. Propensity score matching, based on age, sex, race, and calendar year, was employed to compare CeD patients with the general non-CeD population at a 1:1 ratio. RESULTS Positive associations were observed for several malignancies, including small intestine, lymphoma, nonmelanoma skin, liver, melanoma skin, pancreas myelodysplastic syndrome, biliary, stomach, and other neuroendocrine tumors (excluding small and large intestine malignant carcinoid), leukemia, uterus, and testis. Conversely, CeD patients exhibited a reduced risk of respiratory and secondary malignancies. Moreover, certain malignancies showed null associations with CeD, including head and neck, nervous system, esophagus, colorectal, anus, breast, malignant carcinoids, bone and connective tissues, myeloma, cervix, and ovary cancers. CONCLUSION Our study is unique in highlighting the detailed results of positive, negative, or null associations between different hematologic and solid malignancies and CeD. Furthermore, it offers insights into evolving trends in CeD hospital outcomes, shedding light on advancements in its management over the past two decades. These findings contribute valuable information to the understanding of CeD's impact on health and healthcare utilization.
C1 [Haider, Maryam Bilal] Northshore Univ Hlth Syst, Dept Gastroenterol, 2650 Ridge Ave, Evanston, IL 60201 USA.
[Al Sbihi, Ali] Univ Miami, Miller Sch Med, Dept Hematol Oncol, Miami, FL 33101 USA.
[Reddy, Sushmitha Nanja] Wayne State Univ, Karmanos Canc Inst, Dept Hematol Oncol, Detroit, MI 48235 USA.
[Green, Peter] Columbia Univ, Celiac Dis Ctr, New York, NY 10032 USA.
C3 NorthShore University Health System; University of Miami; Wayne State
University; Barbara Ann Karmanos Cancer Institute; Columbia University
RP Haider, MB (corresponding author), Northshore Univ Hlth Syst, Dept Gastroenterol, 2650 Ridge Ave, Evanston, IL 60201 USA.
EM mhaider@northshore.org
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West J, 2004, BRIT MED J, V329, P716, DOI 10.1136/bmj.38169.486701.7C
NR 80
TC 1
Z9 1
U1 1
U2 1
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2218-4333
J9 WORLD J CLIN ONCOL
JI World J. Clin. Oncol.
PD AUG 24
PY 2024
VL 15
IS 8
DI 10.5306/wjco.v15.i8.1048
PG 14
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA E5C0E
UT WOS:001303167200004
PM 39193153
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Ravi, PK
Balakrishna, JP
Dhawale, L
AF Ravi, Padma Kanchi
Balakrishna, Janardhana Papayya
Dhawale, Lavina
TI Role of Mesenchymal Stem Cells Derived Exosomes and Its Regenerative
Potential
SO ENTOMOLOGY AND APPLIED SCIENCE LETTERS
LA English
DT Article
DE MSCs; multi-lineage differentiation; exosomes; regenerative medicine;
therapeutic application
ID BONE-MARROW; EXTRACELLULAR VESICLES
AB Background: Mesenchymal stem cells (MSCs) are a striking basis for intractable patients since they possess immunomodulatory/anti-inflammatory potential and multi-lineage differentiation capability. Several positive mediated effects have been indicated in MSCs based transplantation on preclinical and clinical application entailed for the treatment of many kinds of diseases. Main text: MSCs used in the treatment of various diseases comprise autoimmune disease, cancer, liver cirrhosis, cardiovascular diseases, and ischemic stroke. The paracrine factors of the exosomes involved in signal transduction by regulation and differentiation of new tissue during tissue injury repair. Robust progress in the isolation of multipotent progenitor cells, commonly defined as mesenchymal stromal/stem cells (MSCs), which have revealed an urge in cell therapy and regenerative medicine. Conclusion: Therefore the application of these MSCs derived exosomes obtained from several tissues has revealed to be beneficial for therapeutic application and publicized to be reliable for a cure in regenerative medicine. This review recapitulates the contemporary strategies implicated in the substantial role of MSC-derived exosomes as a remedy agent.
C1 [Ravi, Padma Kanchi] Sri Padmavati Mahila Visvavidyalayam, Dept Biotechnol, Tirupati, Andhra Pradesh, India.
[Balakrishna, Janardhana Papayya; Dhawale, Lavina] Stellixir Biotech Private Ltd, Dept Biotechnol, Peenya 2nd Stage Ind Area, Bangalore, Karnataka, India.
C3 Sri Padmavati Mahila Vishwavidyalayam
RP Ravi, PK (corresponding author), Sri Padmavati Mahila Visvavidyalayam, Dept Biotechnol, Tirupati, Andhra Pradesh, India.
EM thulasipadi@gmail.com
RI Padma, Kanchi ravi/ABE-8270-2021
CR Chen LW, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0001886
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Jung J, 2013, STEM CELLS, V31, P1584, DOI 10.1002/stem.1396
Kern S, 2006, STEM CELLS, V24, P1294, DOI 10.1634/stemcells.2005-0342
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NR 24
TC 0
Z9 0
U1 0
U2 2
PU ENTOMOLOGY & APPLIED SCIENCE RESEARCH LETTERS-EASLETTERS
PI HARAYANA
PA CYBER CITY, DLF PHASE 2, GURGAON-122002, HARAYANA, 00000, INDIA
SN 2349-2864
J9 ENTOMOL APPL SCI LET
JI Entomol. Appl. Sci. Lett.
PY 2020
VL 7
IS 2
BP 11
EP 19
PG 9
WC Entomology
WE Emerging Sources Citation Index (ESCI)
SC Entomology
GA OK4PI
UT WOS:000584634100002
DA 2025-01-07
ER
PT J
AU Ciesielka, J
Jakimow, K
Tekiela, N
Peisert, L
Kwasniewska, A
Kata, D
Chudek, J
AF Ciesielka, Jakub
Jakimow, Krzysztof
Tekiela, Natalia
Peisert, Laura
Kwasniewska, Anna
Kata, Dariusz
Chudek, Jerzy
TI Significantly Elevated CA 19-9 after COVID-19 Vaccination and Literature
Review of Non-Cancerous Cases with CA 19-9 > 1000 U/mL
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE antigen; CA 19-9; sialyl lewis A antigen; gastrointestinal cancer
antigen; COVID-19 virus vaccines
ID SERUM CA 19.9; AUTOIMMUNE PANCREATITIS; CARBOHYDRATE ANTIGEN-19-9;
INFLAMMATORY PSEUDOTUMOR; DIAGNOSTIC-CRITERIA; CA19-9 LEVELS; LIVER;
CANCER; LEVEL; CYST
AB Background: CA 19-9 is a commonly assessed tumor marker, considered characteristic of pancreatic ductal adenocarcinoma (PDAC) and biliary tract cancers; however, the positive predictive value of CA 19.9 is too low, and the usage of CA 19.9 as a screening tool in the healthy population remains controversial. Methods: The presented case illustrates a reversed diagnosis of highly elevated serum CA 19-9 levels in a 54-year-old female complaining of pain in the epigastric region, shortly after COVID-19 vaccination. Laboratory tests showed a significantly elevated level of the CA 19-9 marker (>12,000 U/mL, reference value: <37 U/mL) with normal pancreatic enzyme activity. The patient underwent imaging examination, which showed no abnormalities, except for increased pancreatic dimension and areas of fluid signal in the pancreas in magnetic resonance imaging (MRI), which may correspond to autoimmune pancreatitis (AIP). The patient remains asymptomatic with a recommendation for a follow-up MRI in 12 months. Results: A literature review conducted revealed multi-causal CA 19-9 increases above 1000 U/mL, including non-cancerous diseases of the lung, pancreas, liver, ovary, kidney, and others. The median concentration of CA 19-9 regardless of the cause of disease was 2810 U/mL (IQR +/- 6895). The median CA 19-9 values in men and women were 3500 (IQR +/- 10,050) and 2455 (IQR +/- 3927), respectively, and differ significantly between the compared groups (p < 0.05). There was no difference between CA 19-9 values and the categorized cause of the increase. Conclusions: Conducting differential diagnosis, it should not be forgotten that most international guidelines recommend the use of CA 19-9 only in conjunction with pathology of pancreas in radiological imaging; however, even such a combination can point the diagnostic pathway in the wrong direction. A highly elevated CA 19-9 level, typically associated with PDAC, may be the result of benign disease including AIP related to COVID-19 vaccination.
C1 [Ciesielka, Jakub; Jakimow, Krzysztof; Tekiela, Natalia; Peisert, Laura] Med Univ Silesia, Dept Internal Med & Oncol Chemotherapy, Students Res Grp, PL-40055 Katowice, Poland.
[Kwasniewska, Anna] Med Univ Silesia, Mielecki Hosp, Dept Radiol, PL-40055 Katowice, Poland.
[Kata, Dariusz] Med Univ Silesia, Dept Hematol & Bone Marrow Transplantat, PL-40055 Katowice, Poland.
[Chudek, Jerzy] Med Univ Silesia, Dept Internal Med & Oncol Chemotherapy, PL-40055 Katowice, Poland.
C3 Medical University Silesia; Medical University Silesia; Medical
University Silesia; Medical University Silesia
RP Ciesielka, J (corresponding author), Med Univ Silesia, Dept Internal Med & Oncol Chemotherapy, Students Res Grp, PL-40055 Katowice, Poland.; Chudek, J (corresponding author), Med Univ Silesia, Dept Internal Med & Oncol Chemotherapy, PL-40055 Katowice, Poland.
EM jakubciesielka@gmail.com; krzysztof.jakimow@gmail.com;
s76501@365.sum.edu.pl; s76008@365.sum.edu.pl; dkata@wp.pl; chj@poczta.fm
RI Chudek, Jerzy/I-2826-2019
OI Tekiela, Natalia/0009-0000-5208-251X; Ciesielka,
Jakub/0000-0002-8174-9982; Chudek, Jerzy/0000-0002-6367-7794; Jakimow,
Krzysztof/0000-0001-9563-4855
FU Medical University of Silesia
FX No Statement Available
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NR 76
TC 0
Z9 0
U1 1
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD MAR
PY 2024
VL 13
IS 5
AR 1263
DI 10.3390/jcm13051263
PG 13
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA KX6D3
UT WOS:001183295100001
PM 38592088
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Lin, CH
Lin, CP
Huang, ST
AF Lin, Chia-Hui
Lin, Chun-Pang
Huang, Sheng-Teng
TI Successful intervention with Chinese herbal medicine for
hyperthyroidism: Two case reports and a literature review
SO EXPLORE-THE JOURNAL OF SCIENCE AND HEALING
LA English
DT Article
DE Autoimmune thyroid disease; Chinese herbal medicine; Graves' disease
ID GRAVES-DISEASE; PRUNELLA-VULGARIS; GOITER; AUTOIMMUNITY; EFFICACY;
ANXIETY; CANCER; LIVER; SAN
AB Background: Hyperthyroidism, the excessive production of thyroid hormones, is most commonly attributed to autoimmune dysfunction such as Graves' disease. Western medical treatment of hyperthyroidism includes antithyroid medications, radioiodine, and thyroidectomy, all of which are associated with side effects. We describe the successful treatment of two patients with Graves' disease who used Chinese herbal medicine (CHM) with or without Western medicine. Case presentation: Both cases (a 50-year-old female [case 1] and a 56-year-old male [case 2]) received the Chinese herbal formula Jia Wei Xiao Yao San (JWXYS) as well as Prunella vulgaris, Fritillaria thunbergii, and Crassostrea gigas. Elevated thyroid hormone levels were restored to normal after 10 months of treatment in case 1 and 8 months in case 2. Neither patient experienced any complications or side effects during CHM treatment. Notably, symptoms and thyroid hormone levels have remained well controlled in both patients over 1 year of follow-up until the time of this report. To explore the possible mechanisms involved in CHM treatment of hyperthyroidism, we searched biomedical literature databases and reviewed the literature up to June 2020. Conclusions: As for the hyperthyroidism almost was controlled by Western medicine instead of CHM, we report that JWXYS as well as Prunella vulgaris, Fritillaria thunbergii, and Crassostrea gigas was a safe and effective formula and we propose that CHM may be considered as either a first choice or combination therapy to control hyperthyroidism. (c) 2020 Elsevier Inc. All rights reserved.
C1 [Lin, Chia-Hui; Huang, Sheng-Teng] China Med Univ Hosp, Dept Chinese Med, 2 Yude Rd, Taichung 404332, Taiwan.
[Lin, Chun-Pang; Huang, Sheng-Teng] China Med Univ, An Nan Hosp, 66,Sect 2,Zhanghe Rd, Tainan 709, Taiwan.
[Huang, Sheng-Teng] China Med Univ, Sch Chinese Med, 91 Xueshi Rd, Taichung 40402, Taiwan.
[Huang, Sheng-Teng] China Med Univ Hosp, Dept Med Res, Canc Res Ctr Tradit Chinese Med, 2 Yude Rd, Taichung 404332, Taiwan.
C3 China Medical University Taiwan; China Medical University Hospital -
Taiwan; China Medical University Taiwan; China Medical University
Taiwan; China Medical University Taiwan; China Medical University
Hospital - Taiwan
RP Huang, ST (corresponding author), China Med Univ Hosp, Dept Chinese Med, 2 Yude Rd, Taichung 404332, Taiwan.
EM sheng.teng@yahoo.com
OI Huang, Sheng-Teng/0000-0002-7495-6115
FU Ministry of Science and Technology of Taiwan [MOST 108-2320-B-039-022];
China Medical University Hospital [DMR-108-007, DMR-108-009,
DMR-108-044, DMR-109-199, CRS-108-001]; An-Nan Hospital, China Medical
University [ANHRF-108-06, ANHRF-108-08]; Chinese Medicine Research
Center, China Medical University, under the Higher Education Sprout
Project, Ministry of Education in Taiwan [CMRC-CHM-1]
FX This work was supported and funded by the Ministry of Science and
Technology of Taiwan (MOST 1082320B039022) , China Medical University
Hospital (DMR108007, DMR108009, DMR108044, DMR-109-199 and CRS108001) ,
AnNan Hospital, China Medical University (ANHRF-108-06 and ANHRF-108-08)
and the Chinese Medicine Research Center, China Medical University,
under the Higher Education Sprout Project, Ministry of Education
(CMRC-CHM-1) in Taiwan.
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NR 45
TC 7
Z9 9
U1 6
U2 27
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1550-8307
EI 1878-7541
J9 EXPLORE-NY
JI Explore-J Sci. Heal.
PD JUL-AUG
PY 2021
VL 17
IS 4
BP 344
EP 350
DI 10.1016/j.explore.2020.10.007
EA JUN 2021
PG 7
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA TB9FY
UT WOS:000668251200013
PM 33109498
DA 2025-01-07
ER
PT J
AU Piotrowska, M
Spodzieja, M
Kuncewicz, K
Rodziewicz-Motowidlo, S
Orlikowska, M
AF Piotrowska, Marta
Spodzieja, Marta
Kuncewicz, Katarzyna
Rodziewicz-Motowidlo, Sylwia
Orlikowska, Marta
TI CD160 protein as a new therapeutic target in a battle against
autoimmune, infectious and lifestyle diseases. Analysis of the
structure, interactions and functions
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Protein CD160; Therapeutic target; Immune checkpoint; Signaling
receptor; Immune system
ID T-LYMPHOCYTE SUBSET; NK CELL APOPTOSIS; CLASS-I MOLECULES; INTRAVITREAL
BEVACIZUMAB; INHIBITORY RECEPTOR; TRANSMEMBRANE ISOFORM; NEOVASCULAR
GLAUCOMA; DIABETIC-RETINOPATHY; CUTTING EDGE; HLA-C
AB The glycosylphosphatidylinositol-anchored transmembrane glycoprotein CD160 (cluster of differentiation 160) is a member of the immunoglobulin superfamily. Four isoforms, which differ by the presence or absence of an immunoglobulin-like domain and the mode of anchoring in the cell membrane, have been identified. CD160 has a significant impact on the proper functioning of the immune system by activating natural killer cells and inhibiting T cells. CD160 is a natural ligand for herpes virus entry mediator (HVEM), a member of the tumor necrosis factor superfamily. The CD160-HVEM complex is a rare example of direct interaction between the two different superfamilies. The interaction of these two proteins leads to the inhibition of CD4+ T cells which, in consequence, leads to the inhibition of the correct response of the immune system. Available research articles indicate that CD160 plays a role in various types of cancer, chronic viral diseases, malaria, paroxysmal nocturnal hemoglobinuria, atherosclerosis, autoimmune diseases, skin inflammation, acute liver damage and retinal vascular disease.
We present here an overview of the CD160 protein, the general characteristics of the receptor and its isoforms, details of structural studies of CD160 and the CD160-HVEM complex, as well as a description of the role of this protein in selected human diseases. (C) 2021 Elsevier Masson SAS. All rights reserved.
C1 [Piotrowska, Marta; Spodzieja, Marta; Kuncewicz, Katarzyna; Rodziewicz-Motowidlo, Sylwia; Orlikowska, Marta] Univ Gdansk, Fac Chem, Dept Biomed Chem, Wita Stwosza 63, PL-80308 Gdansk, Poland.
C3 Fahrenheit Universities; University of Gdansk
RP Orlikowska, M (corresponding author), Univ Gdansk, Fac Chem, Dept Biomed Chem, Wita Stwosza 63, PL-80308 Gdansk, Poland.
EM marta.orlikowska@ug.edu.pl
RI Spodzieja, Marta/HSB-7719-2023
OI Kuncewicz, Katarzyna/0000-0003-4730-3343; Orlikowska,
Marta/0000-0002-5814-8767
FU National Science Center [2016/21/D/NZ1/02777]
FX The work was created as a result of the research project no.
2016/21/D/NZ1/02777 financed by the National Science Center.
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NR 85
TC 8
Z9 10
U1 1
U2 6
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD NOV 15
PY 2021
VL 224
AR 113694
DI 10.1016/j.ejmech.2021.113694
EA JUL 2021
PG 12
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA WA8BY
UT WOS:000703110000023
PM 34273660
DA 2025-01-07
ER
PT J
AU Chu, WM
Chao, WC
Chen, DY
Ho, WL
Chen, HH
AF Chu, Wei-Min
Chao, Wen-Cheng
Chen, Der-Yuan
Ho, Wei-Li
Chen, Hsin-Hua
TI Incidence and risk factors of mental illnesses among patients with
systemic autoimmune rheumatic diseases: an 18-year population-based
study
SO RHEUMATOLOGY
LA English
DT Article; Early Access
DE rheumatic disease; mental illness; incidence; population-based study
ID QUALITY-OF-LIFE; INSURANCE RESEARCH DATABASE; PRIMARY SJOGRENS-SYNDROME;
LUPUS-ERYTHEMATOSUS; HEPATOCELLULAR-CARCINOMA; DEPRESSION; ANXIETY; SLE;
SCHIZOPHRENIA; PATHOGENESIS
AB Objective This study aimed to assess the incidence and risk factors surrounding mental illnesses in patients diagnosed with systemic autoimmune rheumatic diseases (SARDs).Methods This retrospective cohort study used nationwide, population-based claim data taken from Taiwan's National Health Insurance Research Database (NHIRD) to identify patients certified as having a catastrophic illness for systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis (SSc), dermatomyositis (DM), polymyositis (PM) or Sj & ouml;gren's syndrome (SS) from the years 2002-2020. We furthermore calculated the incidence of mental illness in patients diagnosed with SARDs while exploring factors associated with the development of mental illness using multivariable Cox regression analysis shown as adjusted hazard ratios (HRs) with 95% confidence intervals (CIs).Results Among the 28 588 participants, the average age was 47.4 (SD 14.9) years, with most participants being female (76.4%). When compared with patients with rheumatoid arthritis, patients with SLE (HR: 1.20, 95% CI: 1.10-1.32), SS (HR: 1.29, 95% CI: 1.19-1.39), and DM (HR: 1.28, 95% CI: 1.04-1.32) showed a significantly increased risk of developing mental illness. Additionally, when compared with patients with rheumatoid arthritis, patients with SLE (HR: 1.32, 95% CI: 1.21-1.44), SSc (HR: 1.20, 95% CI: 1.02-1.41), SS (HR: 1.17, 95% CI: 1.08-1.26), DM (HR: 1.73, 95% CI: 1.44-2.07), and PM (HR: 1.64, 95% CI: 1.32-2.03) showed a significantly increased risk of antidepressant use.Conclusion This population-based cohort study revealed that patients diagnosed with SLE, SS, and DM had significantly higher risks of developing mental illness when compared with patients with RA.
C1 [Chu, Wei-Min] Taichung Vet Gen Hosp, Dept Family Med, Taichung, Taiwan.
[Chu, Wei-Min] Natl Yang Ming Chiao Tung Univ, Sch Med, Taipei, Taiwan.
[Chu, Wei-Min; Chao, Wen-Cheng; Chen, Hsin-Hua] Natl Chung Hsing Univ, Coll Med, Dept Postbaccalaureate Med, Taichung, Taiwan.
[Chu, Wei-Min] Natl Chung Hsing Univ, Coll Med, Geriatr & Gerontol Res Ctr, Taichung, Taiwan.
[Chu, Wei-Min] Natl Ctr Geriatr & Gerontol, Dept Epidemiol Aging, Aichi, Japan.
[Chao, Wen-Cheng] Taichung Vet Gen Hosp, Dept Crit Care Med, Taichung, Taiwan.
[Chao, Wen-Cheng] Natl Chung Hsing Univ, Big Data Ctr, Taichung, Taiwan.
[Chao, Wen-Cheng] Feng Chia Univ, Dept Automat Control Engn, Taichung, Taiwan.
[Chen, Der-Yuan] China Med Univ Hosp, Deparment Rheumatol & Immunol, Taichung, Taiwan.
[Chen, Der-Yuan] China Med Univ, Coll Med, Taichung, Taiwan.
[Ho, Wei-Li] Taichung Vet Gen Hosp, Div Allergy Immunol & Rheumatol, Chiayi Branch, Chiayi, Taiwan.
[Chen, Hsin-Hua] Taichung Vet Gen Hosp, Dept Internal Med, Div Gen Med, Div Allergy Immunol & Rheumatol, Taichung, Taiwan.
[Chen, Hsin-Hua] Chung Hsing Univ, Inst Biomed Sci, Rong Hsing Res Ctr Translat Med, Taichung, Taiwan.
[Chen, Hsin-Hua] Rong Hsing Res Ctr Translat Med, Taichung, Taiwan.
[Chen, Hsin-Hua] Big Data Ctr, Taichung, Taiwan.
[Chen, Hsin-Hua] Taichung Vet Gen Hosp, Dept Internal Med, 1650 Taiwan Blvd,Sect 4, Taichung, Taiwan.
C3 Taichung Veterans General Hospital; National Yang Ming Chiao Tung
University; National Chung Hsing University; National Chung Hsing
University; National Center for Geriatrics & Gerontology; Taichung
Veterans General Hospital; National Chung Hsing University; Feng Chia
University; China Medical University Taiwan; China Medical University
Hospital - Taiwan; China Medical University Taiwan; Taichung Veterans
General Hospital; Taichung Veterans General Hospital; National Chung
Hsing University; Taichung Veterans General Hospital
RP Chen, HH (corresponding author), Taichung Vet Gen Hosp, Dept Internal Med, 1650 Taiwan Blvd,Sect 4, Taichung, Taiwan.
EM shc5555@hotmail.com
FU Taichung Veterans General Hospital, Taiwan [TCVGH-IRB, CE22166A]
FX The authors thank our colleagues from Taichung Veterans General Hospital
for their great work in the handling of statistical analysis. We also
wish to thank Mr Sung-Hsi Wei (epediat@gmail.com), who helped review our
manuscript from a patient's perspective while providing valuable
feedback. Patient Wei applauded our efforts and suggested that we use
social media to disseminate the results of our study. The study received
approval from the Institutional Review Board of Taichung Veterans
General Hospital (TCVGH-IRB, CE22166A), while consent from the patients
was waived by the IRB due to its retrospective design.
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NR 49
TC 3
Z9 3
U1 2
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1462-0324
EI 1462-0332
J9 RHEUMATOLOGY
JI RHEUMATOLOGY
PD 2024 APR 5
PY 2024
DI 10.1093/rheumatology/keae203
EA APR 2024
PG 9
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA OL5F1
UT WOS:001207434400001
PM 38579187
DA 2025-01-07
ER
PT J
AU Zheng, B
Fuji, RN
Elkins, K
Yu, SF
Fuh, FK
Chuh, J
Tan, C
Hongo, JA
Raab, H
Kozak, KR
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Polson, AG
AF Zheng, Bing
Fuji, Reina N.
Elkins, Kristi
Yu, Shang-Fan
Fuh, Franklin K.
Chuh, Josefa
Tan, Christine
Hongo, Jo-Anne
Raab, Helga
Kozak, Katherine R.
Williams, Marna
McDorman, Elena
Eaton, Dan
Ebens, Allen
Polson, Andrew G.
TI In vivo effects of targeting CD79b with antibodies and
antibody-drug conjugates
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID HUMAN B-CELLS; LYMPHOPROLIFERATIVE DISORDERS; AUTOIMMUNE-DISEASE;
FLOW-CYTOMETRY; CANCER-THERAPY; ANTIGEN; EPRATUZUMAB; EXPRESSION
AB Antibodies directed against B cells are in use for the treatment of non-Hodgkin's lymphoma and autoimmune disorders. The B-cell-restricted surface antigen CD79b, a signaling component of the B-cell receptor, has been shown as a promising antibody target in mouse efficacy models of systemic lupus erythematosus. Anti-CD79b antibody-drug conjugates (ADC), cytotoxic drugs linked through specialized chemical linkers to antibodies, are effective in mouse xenograft models of non-Hodgkin's lymphoma. We were interested in evaluating the systemic effects of anti-CD79b antibodies and ADCs in normal animals as a step toward the development of these molecules as therapeutics. As we were unable to identify any cell surface binding anti-human CD79b antibodies that were cross-reactive to other species, we developed an antibody to cynomolgus monkey (Macaca fascicularis) CD79b (anti-cyCD79b). The anti-cynomolgus antibody, anti-cyCD79b (10D10), and the maytansine (tubulin inhibitor)-conjugated ADC, anti-cyCD79b (10D10)-MCC-DM1, were administered to cynomolgus monkeys at similar to 30 mg/kg (6,000 mu g DM1/m(2)) for two doses 3 weeks apart. Anti-cyCD79b and anti-cyCD79b-MCC-DM1 resulted in peripheral blood B-cell depletion of similar to 65% and similar to 94%, respectively. In addition, anti-cyCD79b-MCC-DM1 resulted in near-complete absence of splenic germinal centers, an observation supporting an effect on dividing B cells. Both molecules were well tolerated, with minimal findings for the antibody and findings for the ADC limited to the lymphoid and hematopoietic systems, liver, and peripheral nerves. These preclinical data suggest that targeting CD79b with antibodies or ADCs may provide safe and effective therapies for B-cell malignancies and autoimmune diseases. [Mol Cancer Ther 2009;8(10):2937-46]
C1 [Zheng, Bing; Fuji, Reina N.; Elkins, Kristi; Yu, Shang-Fan; Fuh, Franklin K.; Chuh, Josefa; Tan, Christine; Hongo, Jo-Anne; Raab, Helga; Kozak, Katherine R.; Williams, Marna; McDorman, Elena; Eaton, Dan; Ebens, Allen; Polson, Andrew G.] Genentech Inc, San Francisco, CA 94080 USA.
C3 Roche Holding; Genentech
RP Polson, AG (corresponding author), Genentech Inc, 1 DNA Way, San Francisco, CA 94080 USA.
EM polson@gene.com
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NR 24
TC 37
Z9 47
U1 0
U2 14
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD OCT
PY 2009
VL 8
IS 10
BP 2937
EP 2946
DI 10.1158/1535-7163.MCT-09-0369
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 507IJ
UT WOS:000270845500017
PM 19808977
OA Bronze
DA 2025-01-07
ER
PT J
AU Verstuyf, A
Carmeliet, G
Bouillon, R
Mathieu, C
AF Verstuyf, Annemieke
Carmeliet, Geert
Bouillon, Roger
Mathieu, Chantal
TI Vitamin D: a pleiotropic hormone
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE activated vitamin D; bone; calcium; cancer; immunology
ID RECEPTOR NULL MICE; 1,25-DIHYDROXYVITAMIN D-3; COLORECTAL-CANCER;
BLOOD-PRESSURE; MULTIPLE-SCLEROSIS; D SUPPLEMENTATION; RANDOMIZED-TRIAL;
BREAST-CANCER; CALCIUM; RISK
AB The secosteroid hormone 1 alpha,25-dihydroxyvitamin D-3 (1,25(OH)(2)D-3) is the natural ligand for the vitamin D receptor, a member of the nuclear receptor superfamily. Upon binding of the ligand, the vitamin D receptor heterodimerizes with the retinoid X receptor and binds to vitamin D response elements in the promoter region of target genes to induce/repress their expression. The target genes that have been identified so far are heterogeneous in nature and reflect the great spectrum of biological activities of 1,25(OH)(2)D-3. Within the last two decades, the receptor has been shown to be present not only in classical target tissues such as bone, kidney, and intestine, but also in many other nonclassical tissues, for example, in the immune system (T and B cells, macrophages, and monocytes), in the reproductive system (uterus, testis, ovary, prostate, placenta, and mammary glands), in the endocrine system (pancreas, pituitary, thyroid, and adrenal cortex), in muscles (skeletal, smooth, and heart muscles), and in brain, skin, and liver. Besides the almost universal presence of vitamin D receptors, different cell types (for example, keratinocytes, monocytes, bone, placenta) are capable of metabolizing 25-hydroxyvitamin D-3 to 1,25(OH)(2)D-3 by the enzyme 25(OH) D-3-1 alpha-hydroxylase, encoded by CYP27B1. The combined presence of CYP27B1 and the specific receptor in several tissues introduced the idea of a paracrine/autocrine role for 1,25(OH)(2)D-3. Moreover, it has been demonstrated that 1,25(OH)(2)D-3 can induce differentiation and inhibit proliferation of normal and malignant cells. Moreover, vitamin D deficiency is associated with an increased risk for nearly all major human diseases such as cancer, autoimmune diseases, cardiovascular, and metabolic diseases. In addition to the treatment of bone disorders with 1,25(OH)(2)D-3, these newly discovered functions open perspectives for the use of 1,25(OH)(2)D-3 as an immune modulator (for example, for the treatment of autoimmune diseases or prevention of graft rejection), inhibitor of cell proliferation, and inducer of cell differentiation (cancer). Kidney International (2010) 78, 140-145; doi:10.1038/ki.2010.17; published online 24 February 2010
C1 [Verstuyf, Annemieke; Carmeliet, Geert; Bouillon, Roger; Mathieu, Chantal] Katholieke Univ Leuven, Lab Expt Med & Endocrinol, B-3000 Louvain, Belgium.
C3 KU Leuven
RP Bouillon, R (corresponding author), Katholieke Univ Leuven, Lab Expt Med & Endocrinol, Herestr 49 O&N1 Bus 902, B-3000 Louvain, Belgium.
EM roger.bouillon@med.kuleuven.be
RI mathieu, chantal/ABD-5505-2021
OI Verstuyf, Annemieke/0000-0003-3193-2698; Mathieu,
Chantal/0000-0002-4055-5233
FU FWO Vlaanderen (FWO) [G.0587.09, G.0553.06, G.0552.06]; University of
Leuven [GOA/04/10, EF/05/007]; Belgium Program on Interuniversity Poles
of Attraction [P6/34]
FX We thank Femke Baeke and Lieve Verlinden for the creation of the figures
and Evelyne van Etten for editorial assitance. CM is a clinical
researcher for the Fund for Scientific Research (FWO-Vlaanderen). The
work in the author's laboratories was supported by FWO Vlaanderen (FWO
G.0587.09, G.0553.06, G.0552.06), the University of Leuven (GOA/04/10,
EF/05/007), and Belgium Program on Interuniversity Poles of Attraction
(P6/34).
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NR 42
TC 256
Z9 279
U1 0
U2 18
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0085-2538
EI 1523-1755
J9 KIDNEY INT
JI Kidney Int.
PD JUL
PY 2010
VL 78
IS 2
BP 140
EP 145
DI 10.1038/ki.2010.17
PG 6
WC Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Urology & Nephrology
GA 618SE
UT WOS:000279375200005
PM 20182414
OA Bronze
DA 2025-01-07
ER
PT J
AU Wu, JH
Song, LW
Lu, MJ
Gao, Q
Xu, SF
Zhou, PK
Ma, T
AF Wu, Jinghong
Song, Liwei
Lu, Mingjun
Gao, Qing
Xu, Shaofa
Zhou, Ping-Kun
Ma, Teng
TI The multifaceted functions of DNA-PKcs: implications for the therapy of
human diseases
SO MEDCOMM
LA English
DT Review
DE class switch recombination; DNA damage; DNA-PKcs; innate immunity; V(D)J
recombination
ID DEPENDENT-PROTEIN-KINASE; CLASS-SWITCH RECOMBINATION; STRAND BREAK
REPAIR; NATURAL-KILLER-CELLS; IL-7 RECEPTOR-ALPHA; CRYO-EM STRUCTURE;
CATALYTIC-SUBUNIT; DAMAGE RESPONSE; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE
REGULATOR
AB The DNA-dependent protein kinase (DNA-PK), catalytic subunit, also known as DNA-PKcs, is complexed with the heterodimer Ku70/Ku80 to form DNA-PK holoenzyme, which is well recognized as initiator in the nonhomologous end joining (NHEJ) repair after double strand break (DSB). During NHEJ, DNA-PKcs is essential for both DNA end processing and end joining. Besides its classical function in DSB repair, DNA-PKcs also shows multifaceted functions in various biological activities such as class switch recombination (CSR) and variable (V) diversity (D) joining (J) recombination in B/T lymphocytes development, innate immunity through cGAS-STING pathway, transcription, alternative splicing, and so on, which are dependent on its function in NHEJ or not. Moreover, DNA-PKcs deficiency has been proven to be related with human diseases such as neurological pathogenesis, cancer, immunological disorder, and so on through different mechanisms. Therefore, it is imperative to summarize the latest findings about DNA-PKcs and diseases for better targeting DNA-PKcs, which have shown efficacy in cancer treatment in preclinical models. Here, we discuss the multifaceted roles of DNA-PKcs in human diseases, meanwhile, we discuss the progresses of DNA-PKcs inhibitors and their potential in clinical trials. The most updated review about DNA-PKcs will hopefully provide insights and ideas to understand DNA-PKcs associated diseases.
DNA-PKcs is involved in nervous system diseases, senescence, asthma, cardiovascular disease, cancers, chronic kidney diseases, and rheumatoid arthritis. image
C1 [Wu, Jinghong; Lu, Mingjun; Gao, Qing; Ma, Teng] Capital Med Univ, Beijing Chest Hosp, Beijing TB & Thorac Tumor Res Inst, Canc Res Ctr, Beijing 101149, Peoples R China.
[Song, Liwei; Xu, Shaofa] Capital Med Univ, Beijing Chest Hosp, Beijing TB & Thorac Tumor Res Inst, Dept Thorac Surg, Beijing, Peoples R China.
[Zhou, Ping-Kun] Beijing Inst Radiat Med, Beijing Key Lab Radiobiol, Beijing 100850, Peoples R China.
C3 Capital Medical University; Capital Medical University; Academy of
Military Medical Sciences - China
RP Ma, T (corresponding author), Capital Med Univ, Beijing Chest Hosp, Beijing TB & Thorac Tumor Res Inst, Canc Res Ctr, Beijing 101149, Peoples R China.; Zhou, PK (corresponding author), Beijing Inst Radiat Med, Beijing Key Lab Radiobiol, Beijing 100850, Peoples R China.
EM zhoupk@nic.bmi.ac.cn; mateng82913@163.com
RI song, li/GXF-9343-2022; Zhou, Ping-Kun/GSJ-3972-2022
FU National Natural Science Foundation of China; Beijing Municipal Public
Welfare Development and Reform Pilot Project for Medical Research
Institutes [JYY2023-14]; [82273130]
FX We sincerely thank the editors and reviewers for their efforts in
improving this paper. This study was supported by National Natural
Science Foundation of China (82273130) and Beijing Municipal Public
Welfare Development and Reform Pilot Project for Medical Research
Institutes (PWD&RPP-MRI) (JYY2023-14).
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NR 253
TC 0
Z9 0
U1 13
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2688-2663
J9 MEDCOMM
JI MedComm
PD JUL
PY 2024
VL 5
IS 7
AR e613
DI 10.1002/mco2.613
PG 24
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA UQ5Q1
UT WOS:001249540600001
PM 38898995
OA gold
DA 2025-01-07
ER
PT J
AU Wang, JY
Zhang, W
Roehrl, VB
Roehrl, MW
Roehrl, MH
AF Wang, Julia Y.
Zhang, Wei
Roehrl, Victor B.
Roehrl, Michael W.
Roehrl, Michael H.
TI An autoantigen-ome from HS-Sultan B-Lymphoblasts offers a molecular map
for investigating autoimmune sequelae of COVID-19
SO AUSTRALIAN JOURNAL OF CHEMISTRY
LA English
DT Article
DE autoantibodies; autoantigens; autoimmunity; COVID; dermatan sulfate;
Epstein-Barr virus; long COVID; SARS-CoV-2
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; SMALL NUCLEAR RIBONUCLEOPROTEIN;
TUMOR-ASSOCIATED ANTIGENS; HEPATOCELLULAR-CARCINOMA; SERUM
AUTOANTIBODIES; TARGET ANTIGENS; PROTEOMIC IDENTIFICATION; ANTITUBULIN
ANTIBODIES; CLINICAL-SIGNIFICANCE; GEL-ELECTROPHORESIS
AB To understand how COVID-19 may induce autoimmune diseases, we have been compiling an atlas of COVID autoantigens (autoAgs). Using dermatan sulfate (DS) affinity enrichment of autoantigenic proteins extracted from HS-Sultan lymphoblasts, we identified 362 DS-affinity proteins, of which at least 201 (56%) are confirmed autoAgs. Comparison with available multi-omic COVID data shows that 315 (87%) of the 362 proteins are affected in SARS-CoV-2 infection via altered expression, interaction with viral components, or modification by phosphorylation or ubiquitination, at least 186 (59%) of which are known autoAgs. These proteins are associated with gene expression, mRNA processing, mRNA splicing, translation, protein folding, vesicles, and chromosome organization. Numerous nuclear autoAgs were identified, including both classical antinuclear antibodies (ANAs) and extractable nuclear antigens (ENAs) of systemic autoimmune diseases and unique autoAgs involved in the DNA replication fork, mitotic cell cycle, or telomerase maintenance. We also identified many uncommon autoAgs involved in nucleic acid and peptide biosynthesis and nucleocyto-plasmic transport, such as aminoacyl-tRNA synthetases. In addition, this study found autoAgs that potentially interact with multiple SARS-CoV-2 Nsp and Orf components, including CCT/TriC chaperonin, insulin degrading enzyme, platelet-activating factor acetylhydrolase, and the ezrin-moesin-radixin family. Furthermore, B-cell-specific IgM-associated endoplasmic reticulum (ER) complex (including MBZ1, BiP, heat shock proteins, and protein disulfide-isomerases) is enriched by DS-affinity and up-regulated in B-cells of COVID-19 patients, and a similar IgH-associated ER complex was also identified in autoreactive pre-B1 cells in our previous study, which suggests a role of autoreactive B1 cells in COVID-19 that merits further investigation. In summary, this study demonstrates that virally infected cells are characterized by alterations of proteins with propensity to become autoAgs, thereby providing a possible explanation for infection-induced autoimmunity. The COVID autoantigen-ome provides a valuable molecular resource and map for investigation of COVID-related autoimmune sequelae and considerations for vaccine design.
C1 [Wang, Julia Y.; Roehrl, Victor B.; Roehrl, Michael W.] Curandis, Boston, MA 02124 USA.
[Zhang, Wei] Affiliated Hosp Guizhou Med Univ, Dept Gastroenterol, Guiyang, Guizhou, Peoples R China.
[Roehrl, Michael H.] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA.
[Roehrl, Michael H.] Harvard Med Sch, Boston, MA USA.
C3 Guizhou Medical University; Harvard University; Beth Israel Deaconess
Medical Center; Harvard University; Harvard Medical School
RP Wang, JY (corresponding author), Curandis, Boston, MA 02124 USA.; Roehrl, MH (corresponding author), Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA.
EM julia@curandis.com; michael_roehrl@bidmc.harvard.edu
RI Zhang, Wei/D-3447-2017; Roehrl, Michael/AAU-8506-2020
OI Wang, Julia Y./0000-0002-9458-5825; Roehrl, Michael/0000-0003-4892-1098
FU NIH/NCI [R21 CA251992, R21 CA263262, U01 CA263986]; Cycle for Survival
Equinox Innovation Grant; Neuroendocrine Tumor Research Foundation
(NETRF); MSKCC Cancer Center Support Grant [P30 CA008748]; Curandis
FX This work was partially supported by Curandis. MHR acknowledges grants
from the NIH/NCI (R21 CA251992, R21 CA263262, and U01 CA263986), a Cycle
for Survival Equinox Innovation Grant, an Investigator Grant from the
Neuroendocrine Tumor Research Foundation (NETRF), and MSKCC Cancer
Center Support Grant P30 CA008748. The funding bodies were not involved
in the design of the study and the collection, analysis, and
interpretation of data.
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NR 217
TC 1
Z9 1
U1 7
U2 10
PU CSIRO PUBLISHING
PI CLAYTON SOUTH
PA Private Bag 10, CLAYTON SOUTH, VIC 3169, AUSTRALIA
SN 0004-9425
EI 1445-0038
J9 AUST J CHEM
JI Aust. J. Chem.
PY 2023
VL 76
IS 8
SI SI
BP 525
EP 557
DI 10.1071/CH22267
EA JUL 2023
PG 33
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA NE5J1
UT WOS:001032416200001
OA Green Submitted, hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Venereau, E
De Leo, F
Mezzapelle, R
Careccia, G
Musco, G
Bianchi, ME
AF Venereau, Emilie
De Leo, Federica
Mezzapelle, Rosanna
Careccia, Giorgia
Musco, Giovanna
Bianchi, Marco E.
TI HMGB1 as biomarker and drug target
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Sepsis; Autoimmunity; Cancer; Trauma; Inflammation; Redox
ID MOBILITY GROUP BOX-1; CELL-SURFACE RECEPTOR; CHROMOSOMAL-PROTEIN 1;
ACUTE LUNG INJURY; END-PRODUCTS; ETHYL PYRUVATE; LIVER-INJURY;
ISCHEMIA-REPERFUSION; BARRIER DYSFUNCTION; GLYCYRRHIZIC ACID
AB High Mobility Group Box 1 protein was discovered as a nuclear protein, but it has a "second life" outside the cell where it acts as a damage-associated molecular pattern. HMGB1 is passively released or actively secreted in a number of diseases, including trauma, chronic inflammatory disorders, autoimmune diseases and cancer. Extracellular HMGB1 triggers and sustains the inflammatory response by inducing cytokine release and by recruiting leucocytes. These characteristics make extracellular HMGB1 a key molecular target in multiple diseases. A number of strategies have been used to prevent HMGB1 release or to inhibit its activities. Current pharmacological strategies include antibodies, peptides, decoy receptors and small molecules. Noteworthy, salicylic acid, a metabolite of aspirin, has been recently found to inhibit HMGB1. HMGB1 undergoes extensive post-translational modifications, in particular acetylation and oxidation, which modulate its functions. Notably, high levels of serum HMGB1, in particular of the hyper-acetylated and disulfide isoforms, are sensitive disease biomarkers and are associated with different disease stages. In the future, the development of isoform-specific HMGB1 inhibitors may potentiate and fine-tune the pharmacological control of inflammation. We review here the current therapeutic strategies targeting HMGB1, in particular the emerging and relatively unexplored small molecules-based approach. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Venereau, Emilie; Mezzapelle, Rosanna; Careccia, Giorgia; Bianchi, Marco E.] IRCCS San Raffaele Sci Inst, Chromatin Dynam Unit, Milan, Italy.
[Venereau, Emilie] HMGBiotech Srl, Milan, Italy.
[De Leo, Federica; Musco, Giovanna] IRCCS San Raffaele Sci Inst, Biomol NMR Unit, Milan, Italy.
[Careccia, Giorgia] Univ Milano Bicocca, Milan, Italy.
[Bianchi, Marco E.] San Raffaele Univ, Milan, Italy.
C3 Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
University of Milano-Bicocca; Vita-Salute San Raffaele University
RP Bianchi, ME (corresponding author), San Raffaele Univ, Milan, Italy.; Bianchi, ME (corresponding author), Inst Sci, Milan, Italy.
EM bianchi.marco@hsr.it
RI Mezzapelle, Rosanna/AAA-8407-2019; Bianchi, Marco/K-3417-2018; Careccia,
Giorgia/AAN-1914-2020; Venereau, Emilie/AAN-4856-2020; musco,
giovanna/I-7122-2012; De Leo, Federica/K-7107-2016
OI Mezzapelle, Rosanna/0000-0002-1271-8998; Careccia,
Giorgia/0000-0003-4049-5186; Bianchi, Marco Emilio/0000-0002-5329-6445;
musco, giovanna/0000-0002-0469-2994; Venereau,
Emilie/0000-0002-6590-7434; De Leo, Federica/0000-0001-8554-8507
FU Associazione Italiana Ricerca sul Cancro [IG-14233]; Ministero della
Salute [GR-2011-02351814]; AIRC and Marie Curie Actions, FP7
People-COFUND (iCARE Reintegration fellowship) [16258]
FX This work was supported by a grant from Associazione Italiana Ricerca
sul Cancro to M.E. Bianchi (IG-14233) and Ministero della Salute to E.
Venereau (GR-2011-02351814). G.M. and F.D.L. thank support by AIRC and
Marie Curie Actions, FP7 People-COFUND (iCARE 2014 Reintegration
fellowship, project number 16258).
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NR 134
TC 190
Z9 208
U1 2
U2 83
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
J9 PHARMACOL RES
JI Pharmacol. Res.
PD SEP
PY 2016
VL 111
BP 534
EP 544
DI 10.1016/j.phrs.2016.06.031
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DY0JV
UT WOS:000384784000051
PM 27378565
DA 2025-01-07
ER
PT J
AU Zhang, J
Jia, GR
Zuo, CJ
Jia, NY
Wang, H
AF Zhang, Jian
Jia, Guorong
Zuo, Changjing
Jia, Ningyang
Wang, Hui
TI 18F-FDG PET/CT helps differentiate autoimmune pancreatitis
from pancreatic cancer
SO BMC CANCER
LA English
DT Article
DE Autoimmune pancreatitis; Pancreatic cancer; Positron-emission tomography
ID POSITRON-EMISSION-TOMOGRAPHY; IMAGING FINDINGS; FDG PET/CT; DISEASE;
ACCUMULATION; UTILITY; LESIONS
AB Background: F-18-FDG PET/CT could satisfactorily show pancreatic and extra-pancreatic lesions in AIP, which can be mistaken for pancreatic cancer (PC). This study aimed to identify F-18-FDG PET/CT findings that might differentiate AIP from PC.
Methods: FDG-PET/CT findings of 26 AIP and 40 PC patients were reviewed. Pancreatic and extra-pancreatic lesions related findings, including maximum standardized uptake values (SUVmax) and patterns of FDG uptake, were identified and compared.
Results: All 26 patients with AIP had increased pancreatic FDG uptake. Focal abnormal pancreatic FDG activities were found in 38/40 (95.00%) PC patients, while longitudinal were found in 18/26 (69.23%) AIP patients. SUVmax was significantly different between AIP and PC, both in early and delayed PET/CT scans (p < 0.05). AUCs were 0.700 (early SUVmax), 0.687 (delayed SUVmax), 0.683 (early lesions/liver SUVmax), and 0.715 (delayed lesion/liver SUVmax). Bile duct related abnormalities were found in 12/26 (46.15%) AIP and 10/40 (25.00%) PC patients, respectively. Incidentally, salivary and prostate gland SUVmax in AIP patients were higher compared with those of PC patients (p < 0.05). In males, an inverted "V" shaped high FDG uptake in the prostate was more frequent in AIP than PC patients (56.00%, 14/25 vs. 5.71%, 2/35). Increased FDG activity in extra-pancreatic bile duct was present in 4/26 of AIP patients, while was observed in none of the PC patients. Only in AIP patients, both diffuse pancreatic FDG accumulation and increased inverted "V" shaped FDG uptake in the prostate could be found simultaneously.
Conclusions: F-18-FDG PET/CT findings might help differentiate AIP from PC.
C1 [Zhang, Jian; Wang, Hui] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Nucl Med, Shanghai 200092, Peoples R China.
[Zhang, Jian; Jia, Guorong; Zuo, Changjing] Second Mil Med Univ, Changhai Hosp, Dept Nucl Med, Shanghai 200433, Peoples R China.
[Jia, Ningyang] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Dept Radiol, Shanghai 200433, Peoples R China.
C3 Shanghai Jiao Tong University; Naval Medical University; Naval Medical
University
RP Wang, H (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Nucl Med, Shanghai 200092, Peoples R China.
EM wanghui@xinhuamed.com.cn
FU Shanghai Science and Technology Committee [10410708800]; National
Natural Science Foundation of China [81170435, 81471714]
FX This study was supported by Shanghai Science and Technology Committee
(grant number 10410708800); National Natural Science Foundation of China
(grant number 81170435, 81471714).
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NR 26
TC 38
Z9 40
U1 2
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD OCT 23
PY 2017
VL 17
AR 695
DI 10.1186/s12885-017-3665-y
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FK4MK
UT WOS:000413468400004
PM 29061130
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Zhou, C
Jia, HM
Liu, YT
Yu, M
Chang, X
Ba, YM
Zou, ZM
AF Zhou, Chao
Jia, Hong-mei
Liu, Yue-tao
Yu, Meng
Chang, Xing
Ba, Yuan-ming
Zou, Zhong-mei
TI Metabolism of glycerophospholipid, bile acid and retinol is correlated
with the early outcomes of autoimmune hepatitis
SO MOLECULAR BIOSYSTEMS
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; SERUM BIOMARKERS;
PLASMA; METABOLOMICS; PROFILES; IDENTIFICATION; METABONOMICS;
BIOCHEMISTRY; VALIDATION
AB Autoimmune hepatitis (AIH) is a complex liver disease with an increasing prevalence in recent years and can develop into the severe or fulminant form if the patients are not diagnosed accurately or treated in time. However, AIH accurate diagnosis, especially at the early stage, is still difficult to perform due to the absence of specific diagnostic markers and the large heterogeneity of its clinical, laboratory and histological features. To evaluate the biochemical process of AIH at the early stage, we investigated serum metabolic alterations in mice with liver injury induced by concanavalin A (Con A), which closely mimics the immune and inflammatory response of AIH in humans. Metabonomic profiling was performed by ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC Q-TOF MS). As a result, fourteen metabolites were detected as potential biomarkers related to the early stage of the liver injury, including two bile acids (taurocholic acid (V1) and taurochenodeoxycholic acid (V2)), three long-chain acylcarnitines (tetradecanoylcarnitine (V4), linoleyl carnitine (V8) and L-palmitoylcarnitine (V9)), seven glycerophospholipids (lysoPE (18 : 0/0 : 0) (V3), lysoPC (16 : 0) (V5), lysoPC (18 : 1) (V7), lysoPC (18 : 0) (V10), lysoPC (20: 1) (V11), lysoPE (22 : 0/0 : 0) (V12) and lysoPC (20: 0) (V13)), a bilirubin (V14), and a retinyl ester (V6). Moreover, partial least square regression analysis (RLS-RA) showed that metabolism of glycerophospholipids (P2), bile acids (P4) and retinol (P5) was highly correlated with the clinical outcomes, suggesting they played key roles in the early stage of the liver injury. Our results also demonstrated that a metabonomic approach coupled with PLS-RA is a powerful tool with which changes can be characterized in the levels of endogenous metabolites associated with disease progression and to assist in further understanding the molecular mechanism of the disease.
C1 [Zhou, Chao; Jia, Hong-mei; Liu, Yue-tao; Yu, Meng; Chang, Xing; Zou, Zhong-mei] Chinese Acad Med Sci, Inst Med Plant Dev, Beijing 100193, Peoples R China.
[Zhou, Chao; Jia, Hong-mei; Liu, Yue-tao; Yu, Meng; Chang, Xing; Zou, Zhong-mei] Peking Union Med Coll, Beijing 100193, Peoples R China.
[Ba, Yuan-ming] Hubei Prov Hosp TCM, Wuhan 430091, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Institute of Medicinal Plant Development - CAMS; Chinese Academy of
Medical Sciences - Peking Union Medical College; Peking Union Medical
College
RP Zou, ZM (corresponding author), Chinese Acad Med Sci, Inst Med Plant Dev, Beijing 100193, Peoples R China.
EM zmzou@implad.ac.cn
RI Zou, Zhong-Mei/KXR-6775-2024
OI Zou, Zhong-mei/0000-0002-2466-3146
FU National S & T Major Special Project of China on Major New Drug
Innovation [2013ZX09508104]; National Traditional Chinese Medicine
Clinical Research Center Professional Work Construction Special Project
[JDZX2012057]
FX This study has been financially supported by National S & T Major
Special Project of China on Major New Drug Innovation (No.
2013ZX09508104) and National Traditional Chinese Medicine Clinical
Research Center Professional Work Construction Special Project (No.
JDZX2012057).
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NR 45
TC 40
Z9 43
U1 1
U2 44
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 1742-206X
EI 1742-2051
J9 MOL BIOSYST
JI Mol. Biosyst.
PY 2016
VL 12
IS 5
BP 1574
EP 1585
DI 10.1039/c6mb00092d
PG 12
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA DK5CG
UT WOS:000374936700016
PM 26961243
DA 2025-01-07
ER
PT J
AU Zegarska, P
Markowska, U
Ploszaj, M
AF Zegarska, Paulina
Markowska, Urszula
Ploszaj, Malgorzata
TI The importance of acute-phase proteins as markers in cancers
SO MEDICAL STUDIES-STUDIA MEDYCZNE
LA English
DT Review
DE acute-phase proteins; biological tumour marker; C-reactive protein;
tumour necrosis factor-alpha; haptoglobins
ID C-REACTIVE PROTEIN; N-GLYCANS; HAPTOGLOBIN; INFLAMMATION; FUCOSYLATION;
PROGNOSIS; COLON
AB YY Acute-phase proteins (APPs) form a group of heterogeneous proteins whose synthesis takes place in the liver. This involves mediators such as cytokines and constitutes a response to acute inflammations, bacterial infections, tumours, and autoimmune diseases. C-reactive protein is among the most important APPs. It participates in cancerous processes, especially in colon and rectal cancer. Another APP is haptoglobin. This glycoprotein prevents iron loss and kidney damage, and is associated with diagnostic neoplastic progression connected with fucosylation. Fucoso-haptoglobin is a highly effective marker for prognosis because an increased concentration of this complex is indicative of the distant metastases amount. Another APP is acidic alpha-glycoprotein (AGP), which increases to a serious level during acute inflammations and tumour-promoting processes. Its protective role involves platelet aggregation inhibition and chemotactic activity. The purpose of this study was to review the role of selected acute phase proteins in cancer promotion and progression.
C1 [Zegarska, Paulina] Cardinal Stefan Wyszynski Univ, Coll Med, Fac Med, Warsaw, Poland.
[Markowska, Urszula] Univ Wroclaw, Inst Psychol, Dept Hist & Educ Sci, Warsaw, Poland.
[Ploszaj, Malgorzata] Pedag Univ, Inst Psychol, Krakow, Poland.
C3 Cardinal Stefan Wyszynski University in Warsaw; University of Wroclaw;
University of the National Education Commission
RP Markowska, U (corresponding author), Univ Wroclaw, Inst Psychol, Dept Hist & Educ Sci, Warsaw, Poland.
EM u.markowska01@gmail.com
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NR 31
TC 0
Z9 0
U1 0
U2 1
PU TERMEDIA PUBLISHING HOUSE LTD
PI POZNAN
PA KLEEBERGA ST 2, POZNAN, 61-615, POLAND
SN 1899-1874
EI 2300-6722
J9 MED STUD
JI MED. STUD.
PY 2021
VL 37
IS 4
BP 344
EP 348
DI 10.5114/ms.2021.112391
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA YD9AG
UT WOS:000740725500011
OA gold
DA 2025-01-07
ER
PT J
AU Jin, ZY
El-Deiry, WS
AF Jin, ZY
El-Deiry, WS
TI Overview of cell death signaling pathways
SO CANCER BIOLOGY & THERAPY
LA English
DT Review
DE apoptosis; death receptor; mitochondria; caspase; cancer
ID TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; APOPTOSIS-INDUCING LIGAND;
TRAIL-INDUCED APOPTOSIS; MYC-INDUCED APOPTOSIS; DENSITY-LIPOPROTEIN
RECEPTOR; ENDOPLASMIC-RETICULUM STRESS; CASPASE-MEDIATED ACTIVATION;
SEVERE LIVER DEGENERATION; DOMAIN-CONTAINING PROTEIN
AB Apoptosis plays an important role in development and maintenance of tissue homeostasis. Intensive efforts have been made to explore the molecular mechanisms of the apoptotic signaling pathways including the initiation, mediation, execution and regulation of apoptosis. Caspases are central effectors of apoptosis. Cells undergo apoptosis through two major pathways, the extrinsic pathway (death receptor pathway) or the intrinsic pathway (the mitochondrial pathway). Finally, the contents of dead cells are packaged into apoptotic bodies, which are recognized by neighboring cells or macrophages and cleared by phagocytosis. Cellular apoptosis is tightly controlled by a complex regulatory networks including balancing pro-survival signals. De-regulation of apoptosis may lead to pathological disorders such as developmental defects, autoimmune diseases, neurodegeneration or cancer. Increasing attention is being focused on alternative signaling pathways leading to cell death including necrosis, autophagy, and mitotic catastrophe. Understanding of cell death signaling pathways is relevant to understanding cancer and to developing more effective therapeutics.
C1 Univ Penn, Sch Med, Dept Med Hematol Oncol, Philadelphia, PA 19104 USA.
Univ Penn, Sch Med, Dept Genet, Philadelphia, PA 19104 USA.
Univ Penn, Sch Med, Dept Pharmacol, Philadelphia, PA 19104 USA.
Univ Penn, Sch Med, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
C3 University of Pennsylvania; University of Pennsylvania; University of
Pennsylvania; University of Pennsylvania
RP Univ Penn, Sch Med, Dept Med Hematol Oncol, 415 Curie Blvd,CRB 437A, Philadelphia, PA 19104 USA.
EM wafik@mail.med.upenn.edu
RI El-Deiry, Wafik/AAJ-6080-2020
OI El-Deiry, Wafik/0000-0002-9577-8266
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NR 344
TC 1027
Z9 1226
U1 10
U2 226
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4047
EI 1555-8576
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD FEB
PY 2005
VL 4
IS 2
BP 139
EP 163
DI 10.4161/cbt.4.2.1508
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 957GX
UT WOS:000231359400003
PM 15725726
OA Bronze
DA 2025-01-07
ER
PT J
AU Koeck, ES
Iordanskaia, T
Sevilla, S
Ferrante, SC
Hubal, MJ
Freishtat, RJ
Nadler, EP
AF Koeck, Emily S.
Iordanskaia, Tatiana
Sevilla, Samantha
Ferrante, Sarah C.
Hubal, Monica J.
Freishtat, Robert J.
Nadler, Evan P.
TI Adipocyte exosomes induce transforming growth factor beta pathway
dysregulation in hepatocytes: a novel paradigm for obesity-related liver
disease
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE Obesity; Nonalcoholic fatty liver disease; Exosomes; Pediatric surgery;
Transforming growth; Factor beta
ID ADIPOSE-TISSUE; MATRIX METALLOPROTEINASES; EXTRACELLULAR VESICLES;
METABOLIC SYNDROME; BILIARY ATRESIA; GENE-EXPRESSION; VISCERAL FAT;
FIBROSIS; INFLAMMATION; CELLS
AB Background: The pathogenesis of nonalcoholic fatty liver disease (NAFLD) has been attributed to increased systemic inflammation and insulin resistance mediated by visceral adipose tissue (VAT), although the exact mechanisms are undefined. Exosomes are membrane-derived vesicles containing messenger RNA, microRNA, and proteins, which have been implicated in cancer, neurodegenerative, and autoimmune diseases, which we postulated may be involved in obesity-related diseases. We isolated exosomes from VAT, characterized their content, and identified their potential targets. Targets included the transforming growth factor beta (TGF-beta) pathway, which has been linked to NAFLD. We hypothesized that adipocyte exosomes would integrate into HepG2 and hepatic stellate cell lines and cause dysregulation of the TGF-beta pathway.
Methods: Exosomes from VAT from obese and lean patients were isolated and fluorescently labeled, then applied to cultured hepatic cell lines. After incubation, culture slides were imaged to detect exosome uptake. In separate experiments, exosomes were applied to cultured cells and incubated 48-h. Gene expression of TGF-beta pathway mediators was analyzed by polymerase chain reaction, and compared with cells, which were not exposed to exosomes.
Results: Fluorescent-labeled exosomes integrated into both cell types and deposited in a perinuclear distribution. Exosome exposure caused increased tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) and integrin alpha v beta-5 expression and decreased matrix metalloproteinase-7 and plasminogen activator inhibitor-1 expression in to HepG2 cells and increased expression of TIMP-1, TIMP-4, Smad-3, integrins alpha v beta-5 and alpha v beta-8, and matrix metalloproteinase-9 in hepatic stellate cells.
Conclusions: Exosomes from VAT integrate into liver cells and induce dysregulation of TGF-beta pathway members in vitro and offers an intriguing possibility for the pathogenesis of NAFLD. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Koeck, Emily S.; Iordanskaia, Tatiana; Sevilla, Samantha; Hubal, Monica J.; Nadler, Evan P.] Childrens Natl Med Ctr, Sheikh Zayed Inst Pediat Surg Innovat, Washington, DC 20010 USA.
[Ferrante, Sarah C.; Hubal, Monica J.; Freishtat, Robert J.; Nadler, Evan P.] George Washington Univ, Sch Med & Hlth Sci, Dept Integrat Syst Biol, Washington, DC 20052 USA.
[Ferrante, Sarah C.; Hubal, Monica J.; Freishtat, Robert J.] Childrens Natl Med Ctr, Med Genet Res Ctr, Washington, DC 20010 USA.
[Freishtat, Robert J.] Childrens Natl Med Ctr, Div Emergency Med, Washington, DC 20010 USA.
C3 Children's National Health System; George Washington University;
Children's National Health System; Children's National Health System
RP Nadler, EP (corresponding author), Childrens Natl Med Ctr, Sheikh Zayed Inst Pediat Surg Innovat, 111 Michigan Ave NW, Washington, DC 20010 USA.
EM enadler@childrensnational.org
OI Freishtat, Robert/0000-0002-7411-2342; Hubal,
Monica/0000-0001-6579-6036; Sevilla, Samantha/0000-0002-8734-9875
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NR 49
TC 152
Z9 169
U1 1
U2 53
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
EI 1095-8673
J9 J SURG RES
JI J. Surg. Res.
PD DEC
PY 2014
VL 192
IS 2
BP 268
EP 275
DI 10.1016/j.jss.2014.06.050
PG 8
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA AU2BA
UT WOS:000345419900007
PM 25086727
DA 2025-01-07
ER
PT S
AU Sims, GP
Rowe, DC
Rietdijk, ST
Herbst, R
Coyle, AJ
AF Sims, Gary P.
Rowe, Daniel C.
Rietdijk, Svend T.
Herbst, Ronald
Coyle, Anthony J.
BE Paul, WE
Littman, DR
Yokoyama, WM
TI HMGB1 and RAGE in Inflammation and Cancer
SO ANNUAL REVIEW OF IMMUNOLOGY, VOL 28
SE Annual Review of Immunology
LA English
DT Review; Book Chapter
DE high mobility group box 1; necrosis; S100 proteins; Toll-like receptors;
tolerance; autoimmune disease
ID GLYCATION END-PRODUCTS; MOBILITY GROUP BOX-1; PLASMACYTOID DENDRITIC
CELLS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; MELANOMA INHIBITORY-ACTIVITY;
MOLECULAR-PATTERN MOLECULES; LIVER ISCHEMIA-REPERFUSION; CHROMATIN
PROTEIN HMGB1; DNA-BINDING PROTEINS; NF-KAPPA-B
AB The immune system has evolved to respond not only to pathogens, but also to signals released from dying cells. Cell death through necrosis induces inflammation, whereas apoptotic cell death provides an important signal for tolerance induction. High mobility group box 1 (HMGB1) is a DNA-binding nuclear protein, released actively following cytokine stimulation as well as passively during cell death; it is the prototypic damage-associated molecular pattern (DAMP) molecule and has been implicated in several inflammatory disorders. HMGB1 can associate with other molecules, including TLR ligands and cytokines, and activates cells through the differential engagement of multiple surface receptors including TLR2, TLR4, and RAGE. RAGE is a multiligand receptor that binds structurally diverse molecules, including not only HMGB1, but also S100 family members and amyloid-beta. RAGE activation has been implicated in sterile inflammation as well as in cancer, diabetes, and Alzheimer's disease. While HMGB1 through interactions with TLRs may also be important, this review focuses on the role of the HMGB1-RAGE axis in inflammation and cancer.
C1 [Sims, Gary P.; Rowe, Daniel C.; Herbst, Ronald; Coyle, Anthony J.] Medimmune Inc, Dept Resp Inflammat & Autoimmune Dis, Gaithersburg, MD 20878 USA.
[Rietdijk, Svend T.] Univ Amsterdam, Acad Med Ctr, Dept Gastroenterol & Hepatol, NL-1105 AZ Amsterdam, Netherlands.
C3 AstraZeneca; Medimmune; University of Amsterdam; Academic Medical Center
Amsterdam
RP Sims, GP (corresponding author), Medimmune Inc, Dept Resp Inflammat & Autoimmune Dis, 1 Medimmune Way, Gaithersburg, MD 20878 USA.
EM CoyleA@Medimmune.com
RI Rietdijk, Svend/AAH-7519-2021; , gary/Q-6552-2019
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Wolf R, 2008, J IMMUNOL, V181, P1499, DOI 10.4049/jimmunol.181.2.1499
Yan SF, 2008, NAT CLIN PRACT ENDOC, V4, P285, DOI 10.1038/ncpendmet0786
Yan SF, 2009, EXPERT REV MOL MED, V11, DOI 10.1017/S146239940900101X
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NR 147
TC 1163
Z9 1341
U1 0
U2 246
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0897 USA
SN 0732-0582
BN 978-0-8243-3028-6
J9 ANNU REV IMMUNOL
JI Annu. Rev. Immunol.
PY 2010
VL 28
BP 367
EP 388
DI 10.1146/annurev.immunol.021908.132603
PG 22
WC Immunology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA BOR04
UT WOS:000277363600015
PM 20192808
DA 2025-01-07
ER
PT J
AU Kumari, N
Kathirvel, S
Arora, A
Jain, V
Sikka, P
AF Kumari, Neha
Kathirvel, Soundappan
Arora, Aashima
Jain, Vanita
Sikka, Pooja
TI Pattern of non-communicable diseases during pregnancy and their effect
on feto-maternal outcome: A prospective observational study
SO INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS
LA English
DT Article
DE autoimmune disorders; cardiovascular diseases; chronic hypertension;
diabetes mellitus; non‐ communicable diseases; pregnancy; seizure
disorders
ID COUNTRIES; BURDEN
AB Objective To assess patterns of non-communicable diseases (NCDs) and pregnancy outcomes of women in a tertiary care hospital.
Methods This was a prospective observational study, conducted over 1 year. All NCDs in women who delivered or aborted were studied. Maternal and neonatal outcomes were noted.
Results In all, 1003 NCDs occurred in 894 women. Chronic hypertension was the commonest, involving 309 (30.8%) women. Others included cardiovascular (159, 15.9%), neurological (142, 14.2%), endocrine (115, 11.5%), autoimmune (76, 7.6%), chronic kidney (48, 4.8%), and chronic respiratory (43, 4.3%) diseases, psychiatric disorders (38, 3.8%), cancers (20, 2.0%), and chronic liver disease (18, 1.8%). Most (599, 67.0%) were diagnosed before pregnancy and 145 (16.2%), 81 (9.1%), and 69 (7.7%) were diagnosed in the first, second, and third trimesters, respectively. Maternal deaths occurred in 6 (0.7%) women and near miss in 19 (2.1%) women. Only 9 (1.5%) women with NCD diagnosed before pregnancy had maternal near miss or death, compared with 16 (5.4%) diagnosed during pregnancy (P < 0.001). Of live births, 281 (35.3%) were low birth weight, 49 (6.1%) were very low birth weight, and 24 (3.0%) were extremely low birth weight.
Conclusion Chronic hypertension was the commonest NCD, which along with cardiovascular and neurological disorders constituted around 60% of all NCDs. One-third of NCDs were initially diagnosed during pregnancy. Maternal morbidity was lower if NCDs were diagnosed before pregnancy.
C1 [Kumari, Neha; Arora, Aashima; Jain, Vanita; Sikka, Pooja] Postgrad Inst Med Educ & Res, Dept Obstet & Gynaecol, Sect 12, Chandigarh 160012, India.
[Kathirvel, Soundappan] Postgrad Inst Med Educ & Res, Dept Community Med, Chandigarh, India.
[Kathirvel, Soundappan] Postgrad Inst Med Educ & Res, Sch Publ Hlth, Chandigarh, India.
C3 Post Graduate Institute of Medical Education & Research (PGIMER),
Chandigarh; Post Graduate Institute of Medical Education & Research
(PGIMER), Chandigarh; Post Graduate Institute of Medical Education &
Research (PGIMER), Chandigarh
RP Sikka, P (corresponding author), Postgrad Inst Med Educ & Res, Dept Obstet & Gynaecol, Sect 12, Chandigarh 160012, India.
EM drpoojasikka@yahoo.com
RI Soundappan, Kathirvel/ACF-3981-2022
OI Kathirvel, Soundappan/0000-0002-4839-0138; , aashima/0000-0001-6776-4249
CR [Anonymous], LANCET
Guleria R, 1990, J Assoc Physicians India, V38, P902
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Hiralal K, 2012, J OBSTET GYN INDIA, V62, P301, DOI 10.1007/s13224-012-0220-2
Kanguru L, 2014, GLOBAL HEALTH ACTION, V7, DOI 10.3402/gha.v7.23987
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WHO, 2018, TIME DELIVER REPOR
Yadav S, 2014, GLOBAL HEALTH ACTION, V7, P84, DOI 10.3402/gha.v7.23248
NR 10
TC 2
Z9 2
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7292
EI 1879-3479
J9 INT J GYNECOL OBSTET
JI Int. J. Gynecol. Obstet.
PD FEB
PY 2022
VL 156
IS 2
BP 331
EP 335
DI 10.1002/ijgo.13678
EA MAR 2021
PG 5
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA YD5GD
UT WOS:000635432000001
PM 33730403
DA 2025-01-07
ER
PT J
AU Fellerhoff-Losch, B
Korol, SV
Ganor, Y
Gu, SH
Cooper, I
Eilam, R
Besser, M
Goldfinger, M
Chowers, Y
Wank, R
Birnir, B
Levite, M
AF Fellerhoff-Losch, Barbara
Korol, Sergiy V.
Ganor, Yonatan
Gu, Songhai
Cooper, Itzik
Eilam, Raya
Besser, Michal
Goldfinger, Meidan
Chowers, Yehuda
Wank, Rudolf
Birnir, Bryndis
Levite, Mia
TI Normal human CD4+ helper T cells express Kv1.1 voltage-gated
K+ channels, and selective Kv1.1 block in T cells induces by
itself robust TNFα production and secretion and activation of the NFκB
non-canonical pathway
SO JOURNAL OF NEURAL TRANSMISSION
LA English
DT Article
DE Autoimmune diseases; Immunotherapy; Inflammation; Kv1.1; NF kappa B;
Non-canonical pathway; Pro-inflammatory cytokines; T cells; TNF alpha;
Voltage-gated potassium channels
ID ISOLATED LIMB PERFUSION; NECROSIS-FACTOR-ALPHA; EXPERIMENTAL AUTOIMMUNE
ENCEPHALOMYELITIS; POTASSIUM CHANNELS; ION CHANNELS; RECEPTOR;
MELPHALAN; MELANOMA; CALCIUM; GENE
AB TNF alpha is a very potent and pleiotropic pro-inflammatory cytokine, essential to the immune system for eradicating cancer and microorganisms, and to the nervous system, for brain development and ongoing function. Yet, excess and/or chronic TNF alpha secretion causes massive tissue damage in autoimmune, inflammatory and neurological diseases and injuries. Therefore, many patients with autoimmune/inflammatory diseases receive anti-TNF alpha medications. TNF alpha is secreted primarily by CD4(+) T cells, macrophages, monocytes, neutrophils and NK cells, mainly after immune stimulation. Yet, the cause for the pathologically high and chronic TNF alpha secretion is unknown. Can blocking of a particular ion channel in T cells induce by itself TNF alpha secretion? Such phenomenon was never revealed or even hypothesized. In this interdisciplinary study we discovered that: (1) normal human T cells express Kv1.1 voltage-gated potassium channel mRNA, and the Kv1.1 membrane-anchored protein channel; (2) Kv1.1 is expressed in most CD4(+) CD3(+) helper T cells (mean CD4(+)CD3(+)Kv1.1(+) ? T cells of 7 healthy subjects: 53.09 +/- 22.17 %), but not in CD8(+)CD3(+) cytotoxic T cells (mean CD8(+)cD3(+)Kv1.1(+) T cells: 4.12 +/- 3.04 %); (3) electrophysiological whole-cell recordings in normal human T cells revealed Kv currents; (4) Dendrotoxin-K (DTX-K), a highly selective Kv1.1 blocker derived from snake toxin, increases the rate of rise and decay of Kv currents in both resting and activated T cells, without affecting the peak current; (5) DTX-K by itself induces robust TNF alpha production and secretion by normal human T cells, without elevating IFNc, IL-4 and IL-10; (6) intact Ca2(+) channels are required for DTX-induced TNF alpha secretion; (7) selective anti-Kv1.1 antibodies also induce by themselves secretion; (8) DTX-K activates NF kappa B in normal human T cells via the unique non-canonical-pathway; (9) injection of Kv1.1-blocked human T cells to SCID mice, causes recruitment of resident mouse cells into the liver, alike reported after TNF alpha injection into the brain. Based on our discoveries we speculate that abnormally blocked Kv1.1 in T cells (and other immune cells?), due to either anti-Kv1.1 autoimmune antibodies, or Kv1.1-blocking toxins alike DTX-K, or Kv1.1-blocking genetic mutations, may be responsible for the chronic/excessive TNF alpha in autoimmune/inflammatory diseases. Independently, we also hypothesize that selective block of Kv1.1 in CD4(+) T cells of patients with cancer or chronic infectious diseases could be therapeutic, since it may: a. augment beneficial secretion and delivery of TNF alpha to the disease-affected sites; b. induce recruitment and extravasation of curative immune cells and factors; c. improve accessibility of drugs to the brain and few peripheral organs thanks to TNF alpha-induced increased permeability of organ's barriers.
C1 [Fellerhoff-Losch, Barbara] Immunis eV & Immunotherapy Res Ctr, Munich, Bavaria, Germany.
[Korol, Sergiy V.; Birnir, Bryndis] Uppsala Univ, Dept Neurosci, Uppsala, Sweden.
[Ganor, Yonatan] Univ Paris 05, Sorbonne Paris Cite, Dept Infect Immun & Inflammat,Cochin Inst, CNRS UMR8104,INSERM,U1016, Paris, France.
[Gu, Songhai; Wank, Rudolf] Immunotherapy Res Ctr, Munich, Bavaria, Germany.
[Cooper, Itzik] Haim Sheba Med Ctr, Joseph Sagol Neurosci Ctr, Tel Hashomer, Israel.
[Eilam, Raya] Weizmann Inst Sci, Vet Resources, IL-76100 Rehovot, Israel.
[Besser, Michal] Ella Inst Treatment & Res Melanoma, Sheba Med Ctr, Tel Hashomer, Israel.
[Goldfinger, Meidan] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Pain Med Inst, IL-69978 Tel Aviv, Israel.
[Chowers, Yehuda] Technion Israel Inst Technol, Dept Gastroenterol, Rambam Hlth Care Campus, Haifa, Israel.
[Chowers, Yehuda] Technion Israel Inst Technol, Bruce Rappaport Sch Med, Haifa, Israel.
[Levite, Mia] Hebrew Univ Jerusalem, Fac Med, Sch Pharm, Jerusalem, Israel.
[Levite, Mia] Hadassah Univ Hosp, Inst Gene Therapy, IL-91120 Jerusalem, Israel.
[Levite, Mia] Acad Coll Tel Aviv Jaffa, Sch Behav Sci, Tel Aviv, Israel.
C3 Uppsala University; Universite Paris Cite; Centre National de la
Recherche Scientifique (CNRS); CNRS - National Institute for Biology
(INSB); Institut National de la Sante et de la Recherche Medicale
(Inserm); Chaim Sheba Medical Center; Weizmann Institute of Science;
Chaim Sheba Medical Center; Tel Aviv University; Tel Aviv Sourasky
Medical Center; Rambam Health Care Campus; Technion Israel Institute of
Technology; Technion Israel Institute of Technology; Rappaport Faculty
of Medicine; Hebrew University of Jerusalem; Hebrew University of
Jerusalem
RP Levite, M (corresponding author), Hebrew Univ Jerusalem, Fac Med, Sch Pharm, Jerusalem, Israel.; Levite, M (corresponding author), Hadassah Univ Hosp, Inst Gene Therapy, IL-91120 Jerusalem, Israel.; Levite, M (corresponding author), Acad Coll Tel Aviv Jaffa, Sch Behav Sci, Tel Aviv, Israel.
EM mial@ekmd.huji.ac.il
RI ; Korol, Sergiy V./S-3442-2016
OI Birnir, Bryndis/0000-0002-1763-0266; Chowers,
Yehuda/0000-0001-5130-845X; Korol, Sergiy V./0000-0001-8279-2790; Ganor,
Yonatan/0000-0003-4430-7744; cooper, itzik/0000-0003-0723-5542; Besser,
Michal/0000-0002-9233-0458
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NR 61
TC 6
Z9 7
U1 0
U2 13
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0300-9564
EI 1435-1463
J9 J NEURAL TRANSM
JI J. Neural Transm.
PD MAR
PY 2016
VL 123
IS 3
BP 137
EP 157
DI 10.1007/s00702-015-1446-9
PG 21
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA DI0CQ
UT WOS:000373162900001
PM 26611796
DA 2025-01-07
ER
PT J
AU Kimura, M
Kimura, H
Ishikawa, H
Matsuo, H
Takada, M
Matsuo, K
AF Kimura, Masamune
Kimura, Hideki
Ishikawa, Hiroki
Matsuo, Hisayasu
Takada, Masahiko
Matsuo, Koushun
TI Hepatic Encephalopathy Mimicking Creutzfeldt-Jakob Disease on
Laboratory, Physiological, and imaging Evaluations
SO AMERICAN JOURNAL OF CASE REPORTS
LA English
DT Article
DE Creutzfeldt-Jakob Disease, Sporadic; Diffusion Magnetic Resonance
Imaging; Hepatic Encephalopathy
AB Objective: Unusual clinical course
Background: Creutzfeldt-Jakob disease (CID) is an irreversible, neurodegenerative, prion disease presenting with cognitive, behavioral, and motor dysfunction. The clinical presentations or laboratory findings of treatable autoimmune and metabolic processes may mimic those of CD Hepatic encephalopathy (HE) is a complication of severe hepatic failure that is characterized by neuropsychiatric manifestations. A case of HE whose laboratory, physiological, and imaging results were similar to that of Creutzfeldt-Jakob disease (CJD) in the process of treatment for HE is presented.
Case Report: An 84-year-old woman with hepatic encephalopathy (HE) was admitted to our hospital because of acute consciousness disturbance. She had chronic hepatitis type C, liver cirrhosis, and hepatocellular carcinoma, and had had an episode of HE once. Her severe consciousness disturbance did not improve after treatment for concurrent hyperammonemia, unlike in her previous episode. Diffusion-weighted brain magnetic resonance imaging (MRI) showed widespread hyperintensity of the whole cortex. Her electroencephalogram showed periodic sharp wave complexes (PSWC5). Both total t-tau and 14-3-3 proteins were detected in her cerebrospinal fluid. According to these clinical data, CJD was highly suspected. However, the consciousness disturbance was alleviated by the tenth day of admission, and her general condition was markedly improved, which supported the initial diagnosis of HE.
Conclusions: The present results suggest that treatable disorders, such as HE, should be considered before making a final diagnosis of a fatal disease such as CJD, since the spectrum of diseases that CJD mimics is vast. We should also aggressively treat patients with severe conditions from which recovery is possible.
C1 [Kimura, Masamune; Matsuo, Koushun] Ohmihachiman Community Med Ctr, Div Neurol, Omihachiman, Shiga, Japan.
[Kimura, Masamune] Kobe City Med Ctr Gen Hosp, Div Neurol, Kobe, Hyogo, Japan.
[Kimura, Hideki] Ohmihachiman Community Med Ctr, Div Cardiol, Omihachiman, Shiga, Japan.
[Ishikawa, Hiroki] Ohmihachiman Community Med Ctr, Div Gastroenterol, Omihachiman, Shiga, Japan.
[Matsuo, Hisayasu; Takada, Masahiko] Ohmihachiman Community Med Ctr, Div Radiol, Omihachiman, Shiga, Japan.
C3 Kobe City Medical Center General Hospital
RP Kimura, M (corresponding author), Ohmihachiman Community Med Ctr, Div Neurol, Omihachiman, Shiga, Japan.; Kimura, M (corresponding author), Kobe City Med Ctr Gen Hosp, Div Neurol, Kobe, Hyogo, Japan.
EM masamune_kimura@kcho.jp
OI Kimura, Masamune/0000-0003-2173-8664
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NR 16
TC 2
Z9 3
U1 0
U2 0
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
EI 1941-5923
J9 AM J CASE REP
JI Am. J. Case Rep.
PD AUG 22
PY 2021
VL 22
AR e932958
DI 10.12659/AJCR.932958
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA UJ1MV
UT WOS:000691059300001
PM 34420027
OA Green Published
DA 2025-01-07
ER
PT J
AU Arinaga-Hino, T
Ide, T
Akiba, J
Suzuki, H
Kuwahara, R
Amano, K
Kawaguchi, T
Sano, T
Inoue, E
Koga, H
Mitsuyama, K
Koga, Y
Torimura, T
AF Arinaga-Hino, Teruko
Ide, Tatsuya
Akiba, Jun
Suzuki, Hiroyuki
Kuwahara, Reiichiro
Amano, Keisuke
Kawaguchi, Toshihiro
Sano, Tomoya
Inoue, Eisuke
Koga, Hironori
Mitsuyama, Keiichi
Koga, Yasutoshi
Torimura, Takuji
TI Growth differentiation factor 15 as a novel diagnostic and therapeutic
marker for autoimmune hepatitis
SO SCIENTIFIC REPORTS
LA English
DT Article
ID MACROPHAGE INHIBITORY CYTOKINE-1; BIOMARKER; CRITERIA; MEMBER
AB Growth differentiation factor 15 (GDF15) has been reported to be associated with fibrosis and cancer in liver disease. Diagnosis of autoimmune hepatitis (AIH) is often difficult because of the lack of specific markers. We investigated whether GDF15 is useful for diagnosing AIH and determined its therapeutic effects. We enrolled 171 Japanese patients as follows: AIH (n = 45), hepatitis B (HB) (n = 17), hepatitis C (HC) (n = 15), primary biliary cholangitis (PBC) (n = 20), and 74 healthy controls. Serum GDF15 levels were measured, and immunohistological analyses of GDF15 were performed using liver tissue of AIH patients. (1) GDF15 levels (pg/ml) were higher in AIH (1994.3 +/- 1258.0) and HC (1568.0 +/- 822.3) than in HB (953.2 +/- 871.4), PBC (643.9 +/- 247.0), and controls (475.3 +/- 145.3) (p < 0.0001), as well as in cirrhosis patients (n = 31) than in non-cirrhosis patients (n = 66) (1926.6 +/- 1026.0 vs. 1249.1 +/- 1124.1, p < 0.0001). In non-cirrhosis patients, GDF15 levels were higher in AIH (1914.0 +/- 1327.2) than in HC (955.7 +/- 502.7), HB (519.3 +/- 197.5), and PBC (643.9 +/- 247.0) (p < 0.0001). (2) GDF15 was positively correlated with M2BPGi (r = 0.7728), total bilirubin (r = 0.6231), and PT-INR (r = 0.6332). (3) GDF15 levels could be used to distinguish AIH from other liver diseases in non-cirrhosis patients, with an area under the curve of 0.9373 (sensitivity 93.6%, specificity 79.3%, cut-off value 931.3). (4) GDF15 in AIH decreased after treatment. (5) Immunohistological analyses in AIH liver tissues revealed that GDF15 was strongly expressed in inflammatory cells, hepatic cytoplasm, and sinusoidal endothelial cells, but decreased after treatment. GDF15 is a novel diagnostic marker for AIH and is also expected to be a therapeutic marker for AIH. Clinical Trials Registration: The study protocol was approved by the institutional review board of Kurume University (Approval No.: 19049).
C1 [Arinaga-Hino, Teruko; Ide, Tatsuya; Suzuki, Hiroyuki; Kuwahara, Reiichiro; Amano, Keisuke; Kawaguchi, Toshihiro; Sano, Tomoya; Koga, Hironori; Mitsuyama, Keiichi; Torimura, Takuji] Kurume Univ, Div Gastroenterol, Sch Med, Dept Med, 67 Asahi Machi, Kurume, Fukuoka 8300011, Japan.
[Akiba, Jun] Kurume Univ Hosp, Dept Diagnost Pathol, Kurume, Fukuoka, Japan.
[Inoue, Eisuke] Showa Univ Res Adm Ctr, Shinagawa Ku, Tokyo, Japan.
[Koga, Yasutoshi] Kurume Univ, Sch Med, Cognit & Mol Res Inst Brain Dis, Kurume, Fukuoka, Japan.
C3 Kurume University; Kurume University; Kurume University
RP Arinaga-Hino, T (corresponding author), Kurume Univ, Div Gastroenterol, Sch Med, Dept Med, 67 Asahi Machi, Kurume, Fukuoka 8300011, Japan.
EM terukoh@med.kurume-u.ac.jp
RI Suzuki, Hiroyuki/HNS-6826-2023
OI Suzuki, Hiroyuki/0000-0003-2383-5038
FU Ministry of Education, Culture, Sports, Science and Technology (MEXT)
[25461571]; Japan Agency for Medical Research and Development (AMED)
[JP17ek0109088, JP19ek0109336]; Grants-in-Aid for Scientific Research
[25461571] Funding Source: KAKEN
FX This research was supported by Grant #25461571 (Y.K.) from the Ministry
of Education, Culture, Sports, Science and Technology (MEXT), by grants
No. JP17ek0109088 and JP19ek0109336 (Y.K.) from the Japan Agency for
Medical Research and Development (AMED).
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PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD MAY 24
PY 2022
VL 12
IS 1
AR 8759
DI 10.1038/s41598-022-12762-9
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 1M4YF
UT WOS:000799975800099
PM 35610317
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Vidalino, L
Doria, A
Quarta, S
Zen, M
Gatta, A
Pontisso, P
AF Vidalino, Laura
Doria, Andrea
Quarta, Santina
Zen, Margherita
Gatta, Angelo
Pontisso, Patrizia
TI SERPINB3, apoptosis and autoimmunity
SO AUTOIMMUNITY REVIEWS
LA English
DT Article
DE SERPINB3; Apoptosis; Autoimmunity
ID SQUAMOUS-CELL CARCINOMA; ANTIGEN; INFECTIONS; INHIBITOR; SUPPRESSION;
PROTEASE; DEATH; SCC; SUPERFAMILY; EXPRESSION
AB SERPINB3 (Squamous Cell Carcinoma Antigen, SCCA1) is a member of the ov-serpins, a serine protease inhibitors family expressed in many cell types including normal epithelium, leukocytes, tumors of epithelial origin and primary liver cancer. Several studies, carried out in vitro and in vivo, have documented an important role of SERPINB3 in the modulation of programmed cell death by different mechanisms, both in inflammatory processes and in cancer. SERPINB3 significantly attenuates apoptosis by contrasting cytochrome c release from the mitochondria and by antichemotactic effect for NK cells. Mechanisms involved in apoptosis induction and regulation play a key role in the balance between cell proliferation and death. Imbalance of this equilibrium may contribute to the development of autoimmune diseases, as defective apoptosis of immune cells leads to deregulated autoreactive cell proliferation. Since defective programmed cell death represents a critical feature of autoimmunity, the involvement of SERPINB3 in this pathological field deserves further studies. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Vidalino, Laura; Quarta, Santina; Gatta, Angelo; Pontisso, Patrizia] Univ Padua, Dept Clin & Expt Med, Clin Med 5, I-35128 Padua, Italy.
[Doria, Andrea; Zen, Margherita] Univ Padua, Dept Clin & Expt Med, Rheumatol Unit, I-35128 Padua, Italy.
C3 University of Padua; University of Padua
RP Pontisso, P (corresponding author), Univ Padua, Dept Clin & Expt Med, Clin Med 5, Via Giustiniani 2, I-35128 Padua, Italy.
EM patrizia@unipd.it
RI Fassina, Giorgio/I-7127-2012; PONTISSO, PATRIZIA/K-3574-2018
OI Quarta, Santina/0000-0002-9348-1485; PONTISSO,
PATRIZIA/0000-0003-2077-9202; Doria, Andrea/0000-0003-0548-4983;
Fassina, Giorgio/0000-0003-1845-2657
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PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
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BP 108
EP 112
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PG 5
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 526HA
UT WOS:000272277100007
PM 19332150
DA 2025-01-07
ER
PT J
AU Dairov, A
Sekenova, A
Alimbek, S
Nurkina, A
Shakhatbayev, M
Kumasheva, V
Kuanysh, S
Adish, Z
Issabekova, A
Ogay, V
AF Dairov, Aidar
Sekenova, Aliya
Alimbek, Symbat
Nurkina, Assiya
Shakhatbayev, Miras
Kumasheva, Venera
Kuanysh, Sandugash
Adish, Zhansaya
Issabekova, Assel
Ogay, Vyacheslav
TI Psoriasis: The Versatility of Mesenchymal Stem Cell and Exosome
Therapies
SO BIOMOLECULES
LA English
DT Review
DE psoriasis; mesenchymal stem cell; mesenchymal-stem-cell-derived exosome;
cell therapy; immunomodulation; preconditioning; in vitro; in vivo;
clinical study
ID IMIQUIMOD-INDUCED PSORIASIS; STROMAL CELLS; EXPRESSION; IL-23; SKIN;
CORTICOSTEROIDS; INFLAMMATION; PATHOGENESIS; DIAGNOSIS; MSCS
AB Mesenchymal stem cells (MSCs) are multilineage differentiating stromal cells with extensive immunomodulatory and anti-inflammatory properties. MSC-based therapy is widely used in the treatment of various pathologies, including bone and cartilage diseases, cardiac ischemia, diabetes, and neurological disorders. Along with MSCs, it is promising to study the therapeutic properties of exosomes derived from MSCs (MSC-Exo). A number of studies report that the therapeutic properties of MSC-Exo are superior to those of MSCs. In particular, MSC-Exo are used for tissue regeneration in various diseases, such as healing of skin wounds, cancer, coronary heart disease, lung injury, liver fibrosis, and neurological, autoimmune, and inflammatory diseases. In this regard, it is not surprising that the scientific community is interested in studying the therapeutic properties of MSCs and MSC-Exo in the treatment of psoriasis. This review summarizes the recent advancements from preclinical and clinical studies of MSCs and MSC-Exo in the treatment of psoriasis, and it also discusses their mechanisms of therapeutic action involved in the treatment of this disease.
C1 [Dairov, Aidar; Sekenova, Aliya; Alimbek, Symbat; Nurkina, Assiya; Shakhatbayev, Miras; Kumasheva, Venera; Issabekova, Assel; Ogay, Vyacheslav] Natl Ctr Biotechnol, Stem Cell Lab, Astana 010000, Kazakhstan.
[Dairov, Aidar; Ogay, Vyacheslav] LN Gumilyov Eurasian Natl Univ, Dept Gen Biol & Genom, Astana 010008, Kazakhstan.
[Kuanysh, Sandugash] Astana Med Univ, Obstet & Gynecol, Astana 010000, Kazakhstan.
[Adish, Zhansaya] Natl Ctr Biotechnol, Lab Immunochem & Immunobiotechnol, Astana 010000, Kazakhstan.
[Adish, Zhansaya] LN Gumilyov Eurasian Natl Univ, Dept Nat Sci, Astana 010008, Kazakhstan.
C3 National Center for Biotechnology (NCB); L.N. Gumilyov Eurasian National
University; Astana Medical University; National Center for Biotechnology
(NCB); L.N. Gumilyov Eurasian National University
RP Issabekova, A (corresponding author), Natl Ctr Biotechnol, Stem Cell Lab, Astana 010000, Kazakhstan.
EM aidardairov@gmail.com; a.sekenova@biocenter.kz; symbatalimbek@gmail.com;
nurkina@biocenter.kz; shakhatbayev@biocenter.kz; kumasheva@biocenter.kz;
zhansaya.adish@mail.ru; issabekova@biocenter.kz; ogay@biocenter.kz
RI Dairov, Aidar/JXL-4174-2024; Adish, Zhansaya/HSB-0288-2023
FU the Ministry of Education and Science of the Republic of Kazakhstan
[AP13068269]; Ministry of Education and Science of the Republic of
Kazakhstan: 102 "Grant funding for scientific research" program
FX This research was financially supported by the Ministry of Education and
Science of the Republic of Kazakhstan: 102 "Grant funding for scientific
research" program, No. AP13068269 "Study of therapeutic effect of
exosomes derived from cytokine-preconditioned mesenchymal stem cells in
mouse model of psoriasis" project.
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National Psoriasis Foundation, About us
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NR 152
TC 0
Z9 0
U1 3
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD NOV
PY 2024
VL 14
IS 11
AR 1351
DI 10.3390/biom14111351
PG 25
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA N8Q3P
UT WOS:001366909300001
PM 39595528
OA gold
DA 2025-01-07
ER
PT J
AU Wang, J
Malik, N
Yin, M
Smyrk, TC
Czaja, AJ
Ehman, RL
Venkatesh, SK
AF Wang, Jin
Malik, Neera
Yin, Meng
Smyrk, Thomas C.
Czaja, Albert J.
Ehman, Richard L.
Venkatesh, Sudhakar K.
TI Magnetic resonance elastography is accurate in detecting advanced
fibrosis in autoimmune hepatitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE autoimmune hepatitis; advanced fibrosis; magnetic resonance
elastography; liver stiffness; cirrhosis
ID RADIATION FORCE IMPULSE; FATTY LIVER-DISEASE; TRANSIENT ELASTOGRAPHY;
STIFFNESS MEASUREMENT; HEPATOCELLULAR-CARCINOMA; CIRRHOSIS; DIAGNOSIS;
CRITERIA; ARFI; PERFORMANCE
AB AIM
To assess the value of magnetic resonance elastography (MRE) in detecting advanced fibrosis/cirrhosis in autoimmune hepatitis (AIH).
METHODS
In this retrospective study, 36 patients (19 treated and 17 untreated) with histologically confirmed AIH and liver biopsy performed within 3 mo of MRE were identified at a tertiary care referral center. Liver stiffness (LS) with MRE was calculated by a radiologist, and inflammation grade and fibrosis stage in liver biopsy was assessed by a pathologist in a blinded fashion. Two radiologists evaluated morphological features of cirrhosis on conventional magnetic resonance imaging (MRI). Accuracy of MRE was compared to laboratory markers and MRI for detection of advanced fibrosis/cirrhosis.
RESULTS
Liver fibrosis stages of 0, 1, 2, 3 and 4 were present in 4, 6, 7, 6 and 13 patients respectively. There were no significant differences in distribution of fibrosis stage and inflammation grade between treated and untreated patient groups. LS with MRE demonstrated stronger correlation with liver fibrosis stage in comparison to laboratory markers for chronic liver disease (r = 0.88 vs -0.48-0.70). A trend of decreased mean LS in treated patients compared to untreated patients was observed (3.7 kPa vs 3.84 kPa) but was not statistically significant. MRE had an accuracy/sensitivity/specificity/positive predictive value/negative predictive value of 0.97/90%/100%/100%/90% and 0.98/92.3%/96%/92.3%/96% for detection of advanced fibrosis and cirrhosis, respectively. The performance of MRE was significantly better than laboratory tests for detection of advanced fibrosis (0.97 vs 0.53-0.80, p < 0.01), and cirrhosis (0.98 vs 0.58-0.80, p < 0.01) and better than conventional MRI for diagnosis of cirrhosis (0.98 vs 0.78, p = 0.002).
CONCLUSION
MRE is a promising modality for detection of advanced fibrosis and cirrhosis in patients with AIH with superior diagnostic accuracy compared to laboratory assessment and MRI.
C1 [Wang, Jin; Malik, Neera; Yin, Meng; Ehman, Richard L.; Venkatesh, Sudhakar K.] Mayo Clin, Coll Med, Dept Radiol, 200 First St SW, Rochester, MN 55905 USA.
[Wang, Jin] Sun Yat Sen Univ, Dept Radiol, Affiliated Hosp 3, Guangzhou 510630, Guangdong, Peoples R China.
[Smyrk, Thomas C.] Mayo Clin, Coll Med, Lab Med & Pathol, 200 First St SW, Rochester, MN 55905 USA.
[Czaja, Albert J.] Mayo Clin, Coll Med, Dept Gastroenterol & Hepatol, 200 First St SW, Rochester, MN 55905 USA.
C3 Mayo Clinic; Sun Yat Sen University; Mayo Clinic; Mayo Clinic
RP Venkatesh, SK (corresponding author), Mayo Clin, Coll Med, Dept Radiol, 200 First St SW, Rochester, MN 55905 USA.
EM venkatesh.sudhakar@mayo.edu
RI Yin, Meng/K-3519-2019; Venkatesh, Sudhakar/T-9385-2019
OI Venkatesh, Sudhakar/0000-0002-7514-1030; Yin, Meng/0000-0001-6778-192X
FU National Institutes of Health [EB001981, EB017197]; National Natural
Science Foundation of China [81271562]
FX Supported by National Institutes of Health, No. EB001981 to Ehman RL and
No. EB017197 to Yin M; and the National Natural Science Foundation of
China, No. 81271562 to Wang J.
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NR 54
TC 46
Z9 47
U1 0
U2 8
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD FEB 7
PY 2017
VL 23
IS 5
BP 859
EP 868
DI 10.3748/wjg.v23.i5.859
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EI6KO
UT WOS:000392604600012
PM 28223730
OA Green Published, hybrid, Green Submitted
DA 2025-01-07
ER
PT J
AU Abu-Yaghi, N
Obiedat, A
Abdaljaleel, M
Ar'ar, T
Al-Abbadi, M
AF Abu-Yaghi, Nakhleh
Obiedat, Abdelrahman
Abdaljaleel, Maram
Ar'ar, Tala
Al-Abbadi, Mousa
TI Diplopia and Vision Loss Associated With Presumed Systemic
Lymphohistiocytic Disease: A Case Report
SO CLINICAL MEDICINE INSIGHTS-CASE REPORTS
LA English
DT Article
DE Lymphohistiocytic pleuritis; diplopia; vision loss; case report
ID INFILTRATION; PATHOGENESIS
AB Systemic lymphohistiocytic infiltration is a rare peculiar condition that can raise the possibility of more specific entities such as autoimmune disease, drug interaction, viral or mycobacterial infection, or malignancy. A hyper-inflammatory state can ensue leading to multi-organ failure. We report the case of a 42-year-old Jordanian male with a past history of moderate Covid-19 infection presenting with binocular diplopia and acute loss of vision in the left eye. Ophthalmic evaluation revealed limitation of extraocular motility in all directions of gaze in the left eye and a visual acuity of 6/30 with a sluggish pupil. Orbital imaging revealed a 10 mm mass at the orbital apex suspicious of malignant metastasis. A positron emission tomography CT scan showed significant pleural thickening and was highly suggestive of metastatic mesothelioma seeding to the orbit, liver, and bone. A CT guided biopsy of the right lung was negative for malignancy but had features of lymphohistiocytic pleuritis. The patient dramatically succumbed to respiratory and renal failure. Systemic lymphohistiocytic infiltration is an aggressive benign inflammatory process that may masquerade as malignancy and raise the possibility of past viral infections, autoimmune diseases, or cancer. A high index of suspicion and a multidisciplinary approach is warranted. In this particular devastating instance, a diagnostic dilemma presented to the eye clinic with diplopia, loss of vision, and an orbital mass, culminating in rapid onset respiratory and renal failure and death.
C1 [Abu-Yaghi, Nakhleh] Univ Jordan, Sch Med, Special Surg Dept, Ophthalmol Div, Amman, Jordan.
[Obiedat, Abdelrahman] Univ Jordan, Sch Med, Amman, Jordan.
[Abdaljaleel, Maram; Ar'ar, Tala; Al-Abbadi, Mousa] Univ Jordan, Sch Med, Dept Pathol Microbiol & Forens Med, Amman, Jordan.
C3 University of Jordan; University of Jordan; University of Jordan
RP Abu-Yaghi, N (corresponding author), Univ Jordan, Ophthalmol Div, POB 5799, Amman 11118, Jordan.
EM n.abuyaghi@ju.edu.jo
RI ABDALJALEEL, MARAM/T-5343-2019; Abu-Yaghi, Nakhleh/N-5922-2015
OI Obiedat, Abdelrahman/0000-0001-5490-1101; Abdaljaleel,
Maram/0000-0002-9257-2596; Abu-Yaghi, Nakhleh/0000-0002-6509-4082
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NR 13
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1179-5476
J9 CLIN MED INSIGHT-CAS
JI Clin. Med. Insights-Case Rep.
PY 2022
VL 15
DI 10.1177/11795476221137262
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 7J6BS
UT WOS:000904667200061
PM 36439702
OA Green Published
DA 2025-01-07
ER
PT J
AU Tsai, HH
Yen, RF
Lin, CL
Kao, CH
AF Tsai, Hsin-Hsi
Yen, Ruoh-Fang
Lin, Cheng-Li
Kao, Chia-Hung
TI Increased risk of dementia in patients hospitalized with acute kidney
injury: A nationwide population-based cohort study
SO PLOS ONE
LA English
DT Article
ID DISEASE; PREVALENCE; EPIDEMIOLOGY; MORTALITY; OUTCOMES
AB Purpose
To determine whether acute kidney injury (AKI) is a risk factor for dementia.
Methods
This nationwide population-based cohort study was based on data from the Taiwan National Health Insurance Research Database for 2000-2011. The incidence and relative risk of dementia were assessed in 207788 patients hospitalized for AKI. The comparison control was selected using the propensity score based on age, sex, index year and comorbidities.
Results
During the 12-year follow-up, patients with AKI had a significantly higher incidence for developing dementia than did the controls (8.84 vs 5.75 per 1000 person -y). A 1.88-fold increased risk of dementia (95% confidence interval, 1.76-2.01) was observed after adjustment for age, sex, and several comorbidities (diabetes, hypertension, hyperlipidemia, head injury, depression, stroke, chronic obstructive pulmonary disease, coronary artery disease, congestive heart failure, atrial fibrillation, cancer, liver disease, chronic infection/inflammation, autoimmune disease, malnutrition).
Conclusions
We found that patients with AKI exhibited a significantly increased risk of developing dementia. This study provides evidence on the association between AKI and long-term adverse outcomes. Additional clinical studies investigating the related pathways are warranted.
C1 [Tsai, Hsin-Hsi] Natl Taiwan Univ Hosp, Dept Neurol, Taipei, Taiwan.
[Yen, Ruoh-Fang] Natl Taiwan Univ Hosp, Dept Nucl Med, Taipei, Taiwan.
[Yen, Ruoh-Fang] Natl Taiwan Univ, Coll Med, Dept Radiol, Taipei, Taiwan.
[Lin, Cheng-Li] China Med Univ Hosp, Management Off Hlth Data, Taichung, Taiwan.
[Lin, Cheng-Li] China Med Univ, Coll Med, Taichung, Taiwan.
[Kao, Chia-Hung] China Med Univ, Grad Inst Clin Med Sci, Taichung, Taiwan.
[Kao, Chia-Hung] China Med Univ, Sch Med, Coll Med, Taichung, Taiwan.
[Kao, Chia-Hung] China Med Univ Hosp, Dept Nucl Med, Taichung, Taiwan.
[Kao, Chia-Hung] China Med Univ Hosp, PET Ctr, Taichung, Taiwan.
[Kao, Chia-Hung] Asia Univ, Dept Bioinformat & Med Engn, Taichung, Taiwan.
C3 National Taiwan University; National Taiwan University Hospital;
National Taiwan University; National Taiwan University Hospital;
National Taiwan University; China Medical University Taiwan; China
Medical University Hospital - Taiwan; China Medical University Taiwan;
China Medical University Taiwan; China Medical University Taiwan; China
Medical University Taiwan; China Medical University Hospital - Taiwan;
China Medical University Taiwan; China Medical University Hospital -
Taiwan; Asia University Taiwan
RP Kao, CH (corresponding author), China Med Univ, Grad Inst Clin Med Sci, Taichung, Taiwan.; Kao, CH (corresponding author), China Med Univ, Sch Med, Coll Med, Taichung, Taiwan.; Kao, CH (corresponding author), China Med Univ Hosp, Dept Nucl Med, Taichung, Taiwan.; Kao, CH (corresponding author), China Med Univ Hosp, PET Ctr, Taichung, Taiwan.; Kao, CH (corresponding author), Asia Univ, Dept Bioinformat & Med Engn, Taichung, Taiwan.
EM d10040@mail.cmuh.org.tw
RI Lin, Cheng-Li/AAU-1138-2021; Tsai, Cynthia/AAT-2420-2021
OI Lin, Cheng-Li/0000-0001-9926-3668; YEN, RUOH-FANG/0000-0003-1648-6482
FU Taiwan Ministry of Health and Welfare Clinical Trial and Research Center
of Excellence [MOHW105-TDU-B-212-133019]; China Medical University
Hospital; Academia Sinica Taiwan Biobank Stroke Biosignature Project
[BM10501010037]; NRPB Stroke Clinical Trial Consortium
[MOST105-2325-B-039-003]; Tseng-Lien Lin Foundation, Taichung, Taiwan;
Taiwan Brain Disease Foundation, Taipei, Taiwan; Katsuzo and Kiyo
Aoshima Memorial Funds, Japan; CMU under the Aim for Top University Plan
of the Ministry of Education, Taiwan
FX This study is supported in part by Taiwan Ministry of Health and Welfare
Clinical Trial and Research Center of Excellence
(MOHW105-TDU-B-212-133019), China Medical University Hospital, Academia
Sinica Taiwan Biobank Stroke Biosignature Project (BM10501010037), NRPB
Stroke Clinical Trial Consortium (MOST105-2325-B-039-003), Tseng-Lien
Lin Foundation, Taichung, Taiwan, Taiwan Brain Disease Foundation,
Taipei, Taiwan, and Katsuzo and Kiyo Aoshima Memorial Funds, Japan; and
CMU under the Aim for Top University Plan of the Ministry of Education,
Taiwan. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript. No
additional external funding received for this study.
CR [Anonymous], CARDIOL RES PRACT
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Wu YT, 2015, LANCET NEUROL
NR 33
TC 32
Z9 34
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD FEB 13
PY 2017
VL 12
IS 2
AR e0171671
DI 10.1371/journal.pone.0171671
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA EL2AZ
UT WOS:000394423800037
PM 28192452
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Zhao, Y
Hasse, S
Bourgoin, SG
AF Zhao, Yang
Hasse, Stephan
Bourgoin, Sylvain G.
TI Phosphatidylserine-specific phospholipase A1: A friend or the devil in
disguise
SO PROGRESS IN LIPID RESEARCH
LA English
DT Review
DE Phosphatidylserine; Lysophosphatidylserine; PLA1A;
Lysophosphatidylserine receptors; Autoimmunity; Cancer
ID LYSOPHOSPHATIDYLSERINE-SPECIFIC LYSOPHOSPHOLIPASE; STIMULATES
CHEMOTACTIC MIGRATION; GENE-EXPRESSION; MECHANISTIC ASSESSMENT;
ACTIVATED PLATELETS; PANCREATIC LIPASE; APOPTOTIC CELLS; RETINOIC ACID;
MAST-CELLS; FATTY-ACID
AB Various human tissues and cells express phospholipase A1 member A (PLA1A), including the liver, lung, prostate gland, and immune cells. The enzyme belongs to the pancreatic lipase family. PLA1A specifically hydrolyzes sn-1 fatty acid of phosphatidylserine (PS) or 1-acyl-lysophosphatidylserine (1-acyl-lysoPS). PS externalized by activated cells or apoptotic cells or extracellular vesicles is a potential source of substrate for the production of unsaturated lysoPS species by PLA1A. Maturation and functions of many immune cells, such as T cells, dendritic cells, macrophages, and mast cells, can be regulated by PLA1A and lysoPS. Several lysoPS receptors, including GPR34, GPR174 and P2Y10, have been identified. High serum levels and high PLA1A expression are associated with autoimmune disorders such as Graves' disease and systemic lupus erythematosus. Increased expression of PLA1A is associated with metastatic melanomas. PLA1A may contribute to cardiometabolic disorders through mediating cholesterol transportation and producing lysoPS. Furthermore, PLA1A is necessary for hepatitis C virus assembly and can play a role in the antivirus innate immune response. This review summarizes recent findings on PLA1A expression, lysoPS and lysoPS receptors in autoimmune disorders, cancers, cardiometabolic disorders, antivirus immune responses, as well as regulations of immune cells.
C1 [Zhao, Yang; Hasse, Stephan; Bourgoin, Sylvain G.] Univ Laval, CHU Quebec, Ctr ARThrite, Dept Microbiol Infectiol & Immunol,Ctr Rech, Quebec City, PQ G1V 4G2, Canada.
C3 Laval University
RP Bourgoin, SG (corresponding author), Div Infect Dis & Immun, 2705 Boul Laurier, Quebec City, PQ G1V 4G2, Canada.
EM sylvain.bourgoin@crchudequebec.ulaval.ca
OI Bourgoin, Sylvain/0000-0001-9779-0368
FU Canadian Institutes for Health Research [MOP-142210]; China Scholarship
Council (CSC)
FX This work was supported by the Canadian Institutes for Health Research
(MOP-142210). YZ was the recipient of a scholarship from the China
Scholarship Council (CSC).
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NR 139
TC 22
Z9 22
U1 0
U2 23
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7827
EI 1873-2194
J9 PROG LIPID RES
JI Prog. Lipid Res.
PD JUL
PY 2021
VL 83
AR 101112
DI 10.1016/j.plipres.2021.101112
EA JUN 2021
PG 10
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA UI6TO
UT WOS:000690737000006
PM 34166709
DA 2025-01-07
ER
PT J
AU Chernyavskaya, Y
Mudbhary, R
Zhang, C
Tokarz, D
Jacob, V
Gopinath, S
Sun, XC
Wang, S
Magnani, E
Madakashira, BP
Yoder, JA
Hoshida, Y
Sadler, KC
AF Chernyavskaya, Yelena
Mudbhary, Raksha
Zhang, Chi
Tokarz, Debra
Jacob, Vinitha
Gopinath, Smita
Sun, Xiaochen
Wang, Shuang
Magnani, Elena
Madakashira, Bhavani P.
Yoder, Jeffrey A.
Hoshida, Yujin
Sadler, Kirsten C.
TI Loss of DNA methylation in zebrafish embryos activates retrotransposons
to trigger antiviral signaling
SO DEVELOPMENT
LA English
DT Article
DE Transposon; DNA methylation; Uhrf1; Interferon; Antiviral
ID HIV-1 REVERSE-TRANSCRIPTASE; STEM-CELLS; SRA DOMAIN;
HEPATOCELLULAR-CARCINOMA; ENDOGENOUS RETROVIRUSES; INTERFERON RESPONSE;
AUTOIMMUNE-DISEASE; TELEOST FISH; HUMAN UHRF1; GENOME
AB Complex cytoplasmic nucleotide-sensing mechanisms can recognize foreign DNA based on a lack of methylation and initiate an immune response to clear the infection. Zebrafish embryos with global DNA hypomethylation caused by mutations in the ubiquitin-like with PHD and ring finger domains 1 (uhrf1) or DNA methyltransferase 1 (dnmt1) genes exhibit a robust interferon induction characteristic of the first line of defense against viral infection. We found that this interferon induction occurred in non-immune cells and examined whether intracellular viral sensing pathways in these cells were the trigger. RNA-seq analysis of uhrf1 and dnmt1 mutants revealed widespread induction of Class I retrotransposons and activation of cytoplasmic DNA viral sensors. Attenuating Sting, phosphorylated Tbk1 and, importantly, blocking reverse transcriptase activity suppressed the expression of interferon genes in uhrf1 mutants. Thus, activation of transposons in cells with global DNA hypomethylation mimics a viral infection by activating cytoplasmic DNA sensors. This suggests that antiviral pathways serve as surveillance of cells that have derepressed intragenomic parasites due to DNA hypomethylation.
C1 [Chernyavskaya, Yelena; Mudbhary, Raksha; Zhang, Chi; Jacob, Vinitha; Gopinath, Smita; Sun, Xiaochen; Wang, Shuang; Magnani, Elena; Hoshida, Yujin; Sadler, Kirsten C.] Icahn Sch Med Mt Sinai, Div Liver Dis, Dept Med, 1 Gustave L Levy Pl,Box 1020, New York, NY 10029 USA.
[Chernyavskaya, Yelena; Mudbhary, Raksha; Zhang, Chi; Jacob, Vinitha; Gopinath, Smita; Wang, Shuang; Magnani, Elena; Sadler, Kirsten C.] Icahn Sch Med Mt Sinai, Dept Dev & Regenerat Biol, 1 Gustave L Levy Pl,Box 1020, New York, NY 10029 USA.
[Chernyavskaya, Yelena; Zhang, Chi; Magnani, Elena; Madakashira, Bhavani P.; Hoshida, Yujin; Sadler, Kirsten C.] New York Univ Abu Dhabi, Program Biol, Abu Dhabi, U Arab Emirates.
[Mudbhary, Raksha; Jacob, Vinitha; Sadler, Kirsten C.] Icahn Sch Med Mt Sinai, Grad Sch Biomed Sci, 1 Gustave L Levy Pl,Box 1020, New York, NY 10029 USA.
[Tokarz, Debra; Yoder, Jeffrey A.] North Carolina State Univ, Dept Mol Biomed Sci, Raleigh, NC 27607 USA.
[Tokarz, Debra; Yoder, Jeffrey A.] North Carolina State Univ, Ctr Comparat Med & Translat Res, Raleigh, NC 27607 USA.
[Sun, Xiaochen; Hoshida, Yujin] Icahn Sch Med Mt Sinai, Liver Canc Program, Tisch Canc Inst, 1 Gustave L Levy Pl,Box 1020, New York, NY 10029 USA.
C3 Icahn School of Medicine at Mount Sinai; Icahn School of Medicine at
Mount Sinai; New York University; New York University Abu Dhabi; Icahn
School of Medicine at Mount Sinai; North Carolina State University;
North Carolina State University; Icahn School of Medicine at Mount Sinai
RP Sadler, KC (corresponding author), Icahn Sch Med Mt Sinai, Div Liver Dis, Dept Med, 1 Gustave L Levy Pl,Box 1020, New York, NY 10029 USA.; Sadler, KC (corresponding author), Icahn Sch Med Mt Sinai, Dept Dev & Regenerat Biol, 1 Gustave L Levy Pl,Box 1020, New York, NY 10029 USA.; Sadler, KC (corresponding author), New York Univ Abu Dhabi, Program Biol, Abu Dhabi, U Arab Emirates.; Sadler, KC (corresponding author), Icahn Sch Med Mt Sinai, Grad Sch Biomed Sci, 1 Gustave L Levy Pl,Box 1020, New York, NY 10029 USA.
EM kirsten.edepli@nyu.edu
RI Yoder, Jeffrey/I-5329-2019; Hoshida, Yujin/R-7513-2019
OI Wang, Shuang/0000-0001-5037-4316; Yoder, Jeff/0000-0002-6083-1311;
Sadler Edepli, Kirsten/0000-0002-1100-4125
FU National Institutes of Health [6R01DK080789, R01DK099558, F30DK094503,
T32CA078207-14]; European Commission Framework Programme 7 [Heptromic]
[259744]
FX This work was supported by grants from the National Institutes of Health
[6R01DK080789 to K.C.S., R01DK099558 to Y.H., F30DK094503 to V.J. and
T32CA078207-14 to support Y.C.] and the European Commission Framework
Programme 7 [Heptromic, proposal number 259744 to Y.H.]. Deposited in
PMC for release after 12 months.
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NR 92
TC 44
Z9 50
U1 1
U2 19
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0950-1991
EI 1477-9129
J9 DEVELOPMENT
JI Development
PD AUG 15
PY 2017
VL 144
IS 16
BP 2925
EP 2939
DI 10.1242/dev.147629
PG 15
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA FD5JR
UT WOS:000407567200008
PM 28698226
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Zachou, K
Azariadis, K
Sofia, M
Lyberopoulou, A
Arvaniti, P
Gatselis, N
Spyrou, V
Billinis, C
Dalekos, GN
AF Zachou, Kalliopi
Azariadis, Kalliopi
Sofia, Marina
Lyberopoulou, Aggeliki
Arvaniti, Pinelopi
Gatselis, Nikolaos
Spyrou, Vassiliki
Billinis, Charalambos
Dalekos, George N.
TI Acute non-A, non-B, non-C hepatitis differences and similarities between
hepatitis E virus infection and autoimmune hepatitis, with phylogenetic
analysis of hepatitis E virus in humans and wild boars
SO ANNALS OF GASTROENTEROLOGY
LA English
DT Article
DE Hepatitis E virus; acute autoimmune hepatitis; genotyping; wild boars
ID HEPATOCELLULAR-CARCINOMA; IGG SEROPREVALENCE; LARGE COHORT; DISEASE;
MYCOPHENOLATE; DIAGNOSIS; EFFICACY; CRITERIA; WORKERS; SWINE
AB Background Hepatitis E virus (HEV) infection incidence is increasing in Europe, accounting for the majority of acute hepatitis cases. We investigated the prevalence and clinical characteristics of acute hepatitis E (AHE) in patients with acute non-A/B/C hepatitis from central Greece, their differences from acute autoimmune hepatitis (AIH) patients and the molecular similarity of human strains to local HEV strains in wild boars.
Methods Sera from 20 patients with non-A/B/C acute hepatitis (2015-2017) were tested prospectively for anti-HEV IgM, IgG antibodies and HEV-RNA. Sera from patients diagnosed with acute AIH (2000-2015; n=56) were tested retrospectively. Liver tissue samples from 40 wild boars were tested for HEV-RNA. Positive wild boar and patients' samples were sequenced and phylogenetically analyzed.
Results Twelve of the 76 (16%) patients were diagnosed with AHE: HEV-RNA 11.5x10(4) (38.7-39.7x10(6)) IU/mL; 11/20 (55%) acute non-A/B/C hepatitis and 1/56 (2%) AIH patients. Patients with AHE were older than those without, predominately men, with higher alanine aminotransferase but lower IgG levels (P=0.005 and P=0.002, respectively), and had high titers of smooth muscle antibodies. Liver biopsies, performed in 6/12 patients with HEV infection, revealed histology compatible with AIH. HEV strains from both patients and wild boars belonged to genotype 3.
Conclusions Approximately one sixth of patients with acute non-A/B/C hepatitis had autochthonous HEV infection with AIH features. Therefore, a careful workup to exclude HEV should be carried out in all acute hepatitis cases before a definite diagnosis of AIH is established. Wild boars seem to be an important reservoir of HEV in Greece.
C1 [Zachou, Kalliopi; Azariadis, Kalliopi; Lyberopoulou, Aggeliki; Arvaniti, Pinelopi; Gatselis, Nikolaos; Dalekos, George N.] Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Dept Med, Larisa, Greece.
[Zachou, Kalliopi; Azariadis, Kalliopi; Lyberopoulou, Aggeliki; Arvaniti, Pinelopi; Gatselis, Nikolaos; Dalekos, George N.] Gen Univ Hosp Larissa, Natl Expertise Ctr Greece Autoimmune Liver Dis, Res Lab Internal Med, Larisa, Greece.
[Zachou, Kalliopi; Azariadis, Kalliopi; Lyberopoulou, Aggeliki; Arvaniti, Pinelopi; Gatselis, Nikolaos; Dalekos, George N.] Gen Univ Hosp Larissa, European Reference Network Hepatol Dis ERN RARE L, Larisa, Greece.
[Sofia, Marina; Billinis, Charalambos] Univ Thessaly, Dept Microbiol & Parasitol, Fac Vet Sci, Kardhitsa, Greece.
[Spyrou, Vassiliki] Univ Thessaly, Fac Anim Sci, Larisa, Greece.
[Billinis, Charalambos] Univ Thessaly, Fac Publ & One Hlth, Kardhitsa, Greece.
C3 General University Hospital of Larissa; General University Hospital of
Larissa; General University Hospital of Larissa; University of Thessaly;
University of Thessaly; University of Thessaly
RP Zachou, K (corresponding author), Gen Univ Hosp Larissa, European Reference Network Hepatol Dis ERN RARE L, Natl Expertise Ctr Greece Autoimmune Liver Dis, Dept Med,Med, Larisa 41110, Greece.; Zachou, K (corresponding author), Gen Univ Hosp Larissa, European Reference Network Hepatol Dis ERN RARE L, Res Lab Internal Med, Natl Expertise Ctr Greece Autoimmune Liver Dis, Larisa 41110, Greece.
EM zachoukalliopi@gmail.com
OI Lyberopoulou, Aggeliki/0000-0003-2839-0031
FU European Union Seventh Framework Programme (2007-2013) [222 633]
FX Part of the outcomes of this research, conducted at the Faculty of
Veterinary Science of the University of Thessaly, received partial
funding from the European Union Seventh Framework Programme (2007-2013)
under grant agreement no. 222 633 (WildTech)
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NR 46
TC 4
Z9 4
U1 0
U2 1
PU HELLENIC SOC GASTROENTEROLOGY
PI ATHENS
PA DEMOKRATIAS AVE 67, ATHENS, 15451, GREECE
SN 1108-7471
EI 1792-7463
J9 ANN GASTROENTEROL
JI Ann. Gastroenterol.
PY 2022
VL 35
IS 5
BP 532
EP +
DI 10.20524/aog.2022.0731
EA JUL 2022
PG 11
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA CP3R3
UT WOS:000826933700001
PM 36061156
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Li, SL
Yi, ZJ
Deng, MH
Scott, MJ
Yang, CX
Li, WB
Lei, Z
Santerre, NM
Loughran, P
Billiar, TR
AF Li, Shilai
Yi, Zhongjie
Deng, Meihong
Scott, Melanie J.
Yang, Chenxuan
Li, Wenbo
Lei, Zhao
Santerre, Nicole M.
Loughran, Patricia
Billiar, Timothy R.
TI TSLP protects against liver I/R injury via activation of the PI3K/Akt
pathway
SO JCI INSIGHT
LA English
DT Article
ID THYMIC STROMAL LYMPHOPOIETIN; REPERFUSION INJURY; HEPATIC ISCHEMIA;
GROWTH-FACTOR; AUTOPHAGY; EXPRESSION; AKT; GENERATION; RESPONSES;
MEDIATE
AB Thymic stromal lymphopoietin (TSLP) is a cytokine mainly released by epithelial cells that plays important roles in inflammation, autoimmune disease, and cancer. While TSLP is expressed in the liver at high levels, the role of TSLP in liver ischemia/reperfusion (I/R) injury remains unknown. Experiments were carried out to determine the role of TSLP in liver I/R injury. Wild-type (WT) and TSLP receptor-knockout (TSLPR-/-) mice were subjected to liver partial warm I/R injury. Liver injury was assessed by measuring serum alanine aminotransferase (ALT) level, necrotic areas by liver histology, hepatocyte death, and local hepatic inflammatory responses. Signal pathways were explored in vivo and in vitro to identify possible mechanisms for TSLP in I/R injury. TSLP and TSLPR protein expression increased during liver I/R in vivo and following hepatocyte hypoxia/ reoxygenation in vitro. Deletion of TSLPR or neutralization of TSLP with anti-TSLP antibody exacerbated liver injury in terms of serum ALT levels as well as necrotic areas in liver histology. Administration of exogenous recombinant mouse TSLP to WT mice significantly reduced liver damage compared with controls, but failed to prevent I/R injury in TSLPR-/- mice. TSLP induced autophagy in hepatocytes during liver I/R injury. Mechanistically, Akt was activated in WT mice during liver I/R injury. The opposite results were observed in TSLPR-/- mice. In addition, TSLP could directly induce Akt activation in hepatocytes independent of nonpa renchyma I cells in vitro. Furthermore, the Akt agonist, insulin-like growth factor-1 (IGF-1), prevented I/R injury in TSLPR-/- mice and an Akt inhibitor, LY294002, blocked the protective effects of TSLP in WT mice subjected to I/R. Our data indicate that TSLP protects against liver I/R injury via activation of the PI3K/Akt pathway. Through this pathway, TSLP induces autophagy in hepatocytes. Thus, TSLP is a potent inhibitor of stress-induced hepatocyte necrosis.
C1 [Li, Shilai; Yi, Zhongjie; Deng, Meihong; Scott, Melanie J.; Yang, Chenxuan; Li, Wenbo; Lei, Zhao; Santerre, Nicole M.; Loughran, Patricia; Billiar, Timothy R.] Univ Pittsburgh, Dept Surg, Pittsburgh, PA 15213 USA.
[Li, Shilai] Guangxi Med Univ, Dept Emergency, Affiliated Hosp 1, Nanning, Peoples R China.
[Yi, Zhongjie; Lei, Zhao] Cent S Univ, Xiangya Hosp 3, Dept Hepatobiliary Surg, Changsha, Hunan, Peoples R China.
[Yang, Chenxuan] Tsinghua Univ, Sch Med, Beijing, Peoples R China.
[Li, Wenbo] Cent S Univ, Xiangya Hosp 2, Dept Plast Surg, Changsha, Hunan, Peoples R China.
[Loughran, Patricia] Univ Pittsburgh, Ctr Biol Imaging, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Guangxi Medical University; Central South University;
Tsinghua University; Central South University; Pennsylvania Commonwealth
System of Higher Education (PCSHE); University of Pittsburgh
RP Billiar, TR (corresponding author), Univ Pittsburgh, Dept Surg, Pittsburgh, PA 15213 USA.
EM billiartr@upmc.edu
RI li, wenbo/AAF-3106-2019; Loughran, Patricia/AAB-1184-2021; huang,
yizhou/KPA-7194-2024
OI Deng, Meihong/0000-0003-1901-347X; Loughran,
Patricia/0000-0001-9375-1724
FU NIH [R35-GM127027]; Medical Excellence Award - Creative Research
Development Grant from the First Affiliated Hospital of Guangxi Medical
University; National Natural Science Foundation of China [81960358]
FX This work was supported by NIH grant R35-GM127027 (to TRB), Medical
Excellence Award funded by the Creative Research Development Grant from
the First Affiliated Hospital of Guangxi Medical University (to SL), and
National Natural Science Foundation of China grant no. 81960358 (to SL).
We thank Lauryn Kohut, Hong Liao, Danielle Reiser, Wentao Gao, and
Richard A. Shapiro for technical assistance with in vivo and in vitro
experiments.
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NR 41
TC 31
Z9 35
U1 0
U2 9
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
EI 2379-3708
J9 JCI INSIGHT
JI JCI Insight
PD NOV 14
PY 2019
VL 4
IS 22
AR e129013
DI 10.1172/jci.insight.129013
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA JN5SY
UT WOS:000496959200008
PM 31723054
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Schupack, DA
Mars, RAT
Voelker, DH
Abeykoon, JP
Kashyap, PC
AF Schupack, Daniel A.
Mars, Ruben A. T.
Voelker, Dayne H.
Abeykoon, Jithma P.
Kashyap, Purna C.
TI The promise of the gut microbiome as part of individualized treatment
strategies
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
ID CLOSTRIDIUM-DIFFICILE INFECTION; FATTY LIVER-DISEASE; INTERNATIONAL
SCIENTIFIC ASSOCIATION; INVASIVE ESCHERICHIA-COLI; FECAL MICROBIOTA;
INTESTINAL MICROBIOTA; NONALCOHOLIC STEATOHEPATITIS;
RHEUMATOID-ARTHRITIS; CONSENSUS STATEMENT; TREATMENT RESPONSE
AB Variability in disease presentation, progression and treatment response has been a central challenge in medicine. Although variability in host factors and genetics are important, it has become evident that the gut microbiome, with its vast genetic and metabolic diversity, must be considered in moving towards individualized treatment. In this Review, we discuss six broad disease groups: infectious disease, cancer, metabolic disease, cardiovascular disease, autoimmune or inflammatory disease, and allergic and atopic diseases. We highlight current knowledge on the gut microbiome in disease pathogenesis and prognosis, efficacy, and treatment-related adverse events and its promise for stratifying existing treatments and as a source of novel therapies. The Review is not meant to be comprehensive for each disease state but rather highlights the potential implications of the microbiome as a tool to individualize treatment strategies in clinical practice. Although early, the outlook is optimistic but challenges need to be overcome before clinical implementation, including improved understanding of underlying mechanisms, longitudinal studies with multiple data layers reflecting gut microbiome and host response, standardized approaches to testing and reporting, and validation in larger cohorts. Given progress in the microbiome field with concurrent basic and clinical studies, the microbiome will likely become an integral part of clinical care within the next decade.
The gut microbiota is increasingly recognized as an important factor in disease development, progression and treatment response. This Review highlights the promise of strategies that target the gut microbiome in the treatment of disease, including cancer and infectious and metabolic diseases.
C1 [Schupack, Daniel A.; Mars, Ruben A. T.; Kashyap, Purna C.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
[Voelker, Dayne H.] Mayo Clin, Div Internal Med, Rochester, MN USA.
[Abeykoon, Jithma P.] Mayo Clin, Div Hematol & Oncol, Rochester, MN USA.
[Kashyap, Purna C.] Mayo Clin, Dept Physiol & Biomed Engn, Rochester, MN 55905 USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic; Mayo Clinic
RP Kashyap, PC (corresponding author), Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.; Kashyap, PC (corresponding author), Mayo Clin, Dept Physiol & Biomed Engn, Rochester, MN 55905 USA.
EM kashyap.purna@mayo.edu
RI Abeykoon, Jithma/S-4730-2019
OI Voelker, Dayne/0000-0003-4896-7678
FU NIH [DK114007]; Center for Individualized Medicine and Department of
Medicine Mayo Clinic, Rochester, MN, USA; National Institute of Diabetes
and Digestive and Kidney Diseases [R01DK114007] Funding Source: NIH
RePORTER
FX The authors thank L. Busby for her secretarial assistance. This work is
supported by funding from NIH DK114007, Center for Individualized
Medicine and Department of Medicine Mayo Clinic, Rochester, MN, USA.
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NR 260
TC 83
Z9 89
U1 5
U2 63
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1759-5045
EI 1759-5053
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD JAN
PY 2022
VL 19
IS 1
BP 7
EP 25
DI 10.1038/s41575-021-00499-1
EA AUG 2021
PG 19
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA XT7CZ
UT WOS:000690338700003
PM 34453142
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Boozari, M
Butler, AE
Sahebkar, A
AF Boozari, Motahare
Butler, Alexandra E.
Sahebkar, Amirhossein
TI Impact of curcumin on toll-like receptors
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Review
DE cancer; curcumin; infection; inflammation; ischemia; TLRs
ID NF-KAPPA-B; PATTERN-RECOGNITION RECEPTORS; URINARY-TRACT-INFECTION;
INDUCED LIVER-INJURY; SIGNALING PATHWAY; IFN-GAMMA; INFLAMMATORY
RESPONSE; PIPERINE COMBINATION; PHYTOSOMAL CURCUMIN; METABOLIC SYNDROME
AB Toll-like receptors (TLRs) have a pivotal role in the activation of innate immune response and inflammation. TLRs can be divided into two subgroups including extracellular TLRs that recognize microbial membrane components (TLR1, 2, 4, 5, 6, and 10), and intracellular TLRs that recognize microbial nucleic acids (TLR3, 7, 8, and 9). Curcumin is a dietary polyphenol from Curcuma longa L. that is reputed to have diverse biological and pharmacological effects. Extensive research has defined the molecular mechanisms through which curcumin mediates its therapeutic effects. One newly defined and important target of curcumin is the TLR, where it exerts an inhibitory effect. In the current study, we focus upon the TLR antagonistic effect of curcumin and curcumin's therapeutic effect as mediated via TLR inhibition. The available evidence indicates that curcumin inhibits the extracellular TLR 2 and 4 and intracellular TLR9 and thereby exerts a therapeutic effect in diseases such as cancer, inflammation, infection, autoimmune, and ischemic disease. Curcumin effectively modulates the TLR response and thereby exerts its potent therapeutic effects.
C1 [Boozari, Motahare] Mashhad Univ Med Sci, Sch Pharm, Dept Pharmacognosy, Mashhad, Razavi Khorasan, Iran.
[Butler, Alexandra E.] Qatar Biomed Res Inst, Diabet Res Ctr, Doha, Qatar.
[Sahebkar, Amirhossein] Mashhad Univ Med Sci, Neurogen Inflammat Res Ctr, Mashhad, Razavi Khorasan, Iran.
[Sahebkar, Amirhossein] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Biotechnol Res Ctr, Mashhad, Razavi Khorasan, Iran.
[Sahebkar, Amirhossein] Mashhad Univ Med Sci, Sch Pharm, Mashhad, Razavi Khorasan, Iran.
C3 Mashhad University of Medical Sciences; Qatar Foundation (QF); Hamad Bin
Khalifa University-Qatar; Qatar Biomedical Research Institute (QBRI);
Mashhad University of Medical Sciences; Mashhad University of Medical
Sciences; Mashhad University of Medical Sciences
RP Sahebkar, A (corresponding author), Mashhad Univ Med Sci, Sch Med, Dept Med Biotechnol, POB 91779-48564, Mashhad, Razavi Khorasan, Iran.
EM sahebkara@mums.ac.ir
RI Sahebkar, Amirhossein/B-5124-2018; Boozari, Motahareh/ABE-8523-2020
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NR 133
TC 50
Z9 54
U1 4
U2 45
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD AUG
PY 2019
VL 234
IS 8
BP 12471
EP 12482
DI 10.1002/jcp.28103
PG 12
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA HX2SA
UT WOS:000467240800030
PM 30623441
DA 2025-01-07
ER
PT J
AU Bonifazi, M
Bravi, F
Gasparini, S
La Vecchia, C
Gabrielli, A
Wells, AU
Renzoni, EA
AF Bonifazi, Martina
Bravi, Francesca
Gasparini, Stefano
La Vecchia, Carlo
Gabrielli, Armando
Wells, Athol U.
Renzoni, Elisabetta A.
TI Sarcoidosis and Cancer Risk Systematic Review and Meta-analysis of
Observational Studies
SO CHEST
LA English
DT Review
ID INFLAMMATORY DISEASES; AUTOIMMUNE-DISEASES; HODGKIN-LYMPHOMA; FOLLOW-UP;
DISORDERS; ASSOCIATION; SUSCEPTIBILITY; METHOTREXATE; PREVALENCE;
MALIGNANCY
AB BACKGROUND: An increased cancer risk in patients with sarcoidosis has been suggested, although results are conflicting in a number of case-control and cohort studies. We conducted a systematic review of all available data and performed a meta-analysis to better define and quantify the association between sarcoidosis and cancer.
METHODS: We searched Medline and Embase for all original articles on cancer and sarcoidosis published up to January 2013. Two independent authors reviewed all titles/abstracts to identify studies according to predefined selection criteria. We derived summary estimates using a random-effects model and reported them as relative risk (RR). Publication bias was evaluated using a funnel plot and was quantified by the Egger test.
RESULTS: Sixteen original studies, involving > 25,000 patients, were included in the present review. The summary RR to develop all invasive cancers was 1.19 (95% CI, 1.07-1.32). The results for selected cancer sites indicated a significantly increased risk of skin (RR, 2.00; 95% CI, 1.69-2.36), hematopoietic (RR, 1.92; 95% CI, 1.41-2.62), upper digestive tract (RR, 1.73; 95% CI, 1.07-2.79), kidney (RR, 1.55; 95% CI, 1.21-1.99), liver (RR, 1.79; 95% CI, 1.03-3.11), and colorectal cancers (RR, 1.33; 95% CI, 1.07-1.67). There was no evidence of publication bias for all cancers (P = .9), nor for any specific cancer site.
CONCLUSIONS: The present meta-analysis suggests a significant, though moderate, association between sarcoidosis and malignancy.
C1 [Bonifazi, Martina] Ist Ric Farmacol Mario Negri, IRCCS, Dept Epidemiol, I-20256 Milan, Italy.
[Bravi, Francesca; La Vecchia, Carlo] Univ Milan, Dept Clin Sci & Community Hlth, Milan, Italy.
[Gasparini, Stefano] Univ Politecn Marche, Dept Biomed Sci & Publ Hlth, Ancona, Italy.
[Gabrielli, Armando] Univ Politecn Marche, Dept Clin & Mol Sci, Ancona, Italy.
[Wells, Athol U.; Renzoni, Elisabetta A.] Royal Brompton & Harefield NHS Fdn Trust, Interstitial Lung Dis Unit, Royal Brompton Hosp, London, England.
C3 Istituto di Ricerche Farmacologiche Mario Negri IRCCS; University of
Milan; Marche Polytechnic University; Marche Polytechnic University;
Royal Brompton & Harefield NHS Foundation Trust; Royal Brompton Hospital
RP Bonifazi, M (corresponding author), Ist Ric Farmacol Mario Negri, IRCCS, Dept Epidemiol, Via Masa 19, I-20256 Milan, Italy.
EM martina.bonifazi@marionegri.it
RI La Vecchia, Carlo/Z-1710-2019; Gabrielli, Armando/AAC-3173-2019
OI La Vecchia, Carlo/0000-0003-1441-897X; Renzoni,
Elisabetta/0000-0002-1118-797X; Bravi, Francesca/0000-0003-0173-5319
FU "Fondazione di Medicina Molecolare e Terapia Cellulare" (Universita
Politecnica delle Marche, Ancona); Italian Association for Cancer
Research [10068]; NIHR Respiratory Disease Biomedical Research Unit at
Royal Brompton & Harefield NHS Foundation Trust; Imperial College London
FX This work has been partly supported by the "Fondazione di Medicina
Molecolare e Terapia Cellulare" (Universita Politecnica delle Marche,
Ancona), the Italian Association for Cancer Research [Grant 10068 to
Istituto di Ricerche Farmacologiche Mario Negri-IRCCS], and by the NIHR
Respiratory Disease Biomedical Research Unit at Royal Brompton &
Harefield NHS Foundation Trust and Imperial College London.
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NR 53
TC 109
Z9 111
U1 0
U2 10
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0012-3692
EI 1931-3543
J9 CHEST
JI Chest
PD MAR
PY 2015
VL 147
IS 3
BP 778
EP 791
DI 10.1378/chest.14-1475
PG 14
WC Critical Care Medicine; Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Respiratory System
GA CC5RC
UT WOS:000350419200057
PM 25340385
DA 2025-01-07
ER
PT J
AU Bieber, S
Halldorson, JB
Finn, E
Ahmad, S
Chamberlain, JS
Odom, GL
AF Bieber, Scott
Halldorson, Jeffrey B.
Finn, Eric
Ahmad, Suhail
Chamberlain, Jeffrey S.
Odom, Guy L.
TI Extracorporeal Delivery of rAAV with Metabolic Exchange and Oxygenation
SO SCIENTIFIC REPORTS
LA English
DT Article
ID RECOMBINANT ADENOASSOCIATED VIRUS; GENE-TRANSFER; FACTOR-IX; EFFICIENT
TRANSDUCTION; PROTEIN ADSORPTION; SKELETAL-MUSCLE; VECTORS; HEMOPHILIA;
EXPRESSION; LIVER
AB Over the past decade much progress has been made towards the treatment of disease with recombinant adeno-associated viral vectors, ranging from cancer to muscular dystrophies, and autoimmune diseases to cystic fibrosis. Given inherent challenges of vector delivery we developed a system incorporating commercially available dialysis equipment. This concept was evaluated in vitro utilizing rAAV expressing the reporter gene human placental alkaline phosphatase. A number of pre-circulating conditions were assessed. Vector recovery was evaluated by quantitative vector genome analysis and cellular transduction assays. A dialysis circulation time course was established, and results were recorded across varied conditions ranging from approximately 2 to 90% retention of viable vector. This approach is unique in that it focuses on efficient localized, isolated and continual delivery of vector to target tissues, provides for the preservation of tissue integrity with dialysis for metabolic exchange and allows for the transfer of oxygen through a secondary membrane post-dialysis.
C1 [Bieber, Scott; Ahmad, Suhail] Univ Washington, Dept Med, Div Nephrol, Seattle, WA 98195 USA.
[Halldorson, Jeffrey B.] Univ Calif San Diego, Dept Surg, Div Transplantat, San Diego, CA 92103 USA.
[Finn, Eric; Chamberlain, Jeffrey S.; Odom, Guy L.] Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
[Chamberlain, Jeffrey S.] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
C3 University of Washington; University of Washington Seattle; University
of California System; University of California San Diego; University of
Washington; University of Washington Seattle; University of Washington;
University of Washington Seattle
RP Odom, GL (corresponding author), Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
EM godom@uw.edu
OI Chamberlain, Jeffrey/0000-0001-5299-0059
FU Advanced Nephrology Dialysis Fellowship at the University of Washington;
Northwest Kidney Centers; National Institutes of Health [AR40864,
AG033610]
FX We thank James Allen for critical reading of the manuscript, and Steve
Hauschka for insightful experimental suggestions. Additionally we thank
Arlene Chen for administrative support. SB was supported by the Advanced
Nephrology Dialysis Fellowship at the University of Washington with
funding from the Northwest Kidney Centers. JSC supported by funding from
the National Institutes of Health (grants AR40864 and AG033610). The
authors have no conflicts of interest to disclose.
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NR 32
TC 2
Z9 3
U1 0
U2 4
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD MAR 26
PY 2013
VL 3
AR 1538
DI 10.1038/srep01538
PG 7
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 112MM
UT WOS:000316596300001
PM 23528884
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Afzali, A
Berry, K
Ioannou, GN
AF Afzali, Anita
Berry, Kristin
Ioannou, George N.
TI Excellent posttransplant survival for patients with nonalcoholic
steatohepatitis in the United States
SO LIVER TRANSPLANTATION
LA English
DT Article
ID FATTY LIVER-DISEASE; CRYPTOGENIC CIRRHOSIS; NATURAL-HISTORY;
TRANSPLANTATION; POPULATION; PREVALENCE
AB Because of the ongoing epidemics of obesity and diabetes, nonalcoholic steatohepatitis (NASH) may become a leading indication for liver transplantation. There are concerns about the posttransplant survival of patients with NASH because of associated cardiovascular and metabolic risk factors. We aimed to determine recent trends in the proportion of patients undergoing transplantation for NASH-related cirrhosis in the United States and to estimate their posttransplant survival. We used data provided by the United Network for Organ Sharing for first-time adult cadaveric liver transplants performed in the United States between January 1, 1997 and October 31, 2010 (n = 53,738). The proportion of liver transplants performed for NASH-related cirrhosis increased dramatically from 1.2% in 1997-2003 to 7.4% in 2010 when NASH was the fourth most common indication for transplantation. The posttransplant survival of patients with NASH (n = 1810) at 1 (87.6%), 3 (82.2%), and 5 years (76.7%) was superior to the survival of patients with hepatocellular carcinoma, hepatitis C virus, alcoholic liver disease, acute hepatic necrosis, hemochromatosis, or cryptogenic liver disease and was inferior to the survival of only 4 groups of patients (those with primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis, or hepatitis B virus). In conclusion, NASH-related cirrhosis is increasing rapidly as an indication for liver transplantation in the United States and is associated with excellent posttransplant survival. Liver Transpl 18:2937, 2012. (C) 2011 AASLD.
C1 [Afzali, Anita; Ioannou, George N.] Univ Washington, Div Gastroenterol, Dept Med, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Berry, Kristin] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Afzali, Anita; Ioannou, George N.] Vet Affairs Puget Sound Hlth Care Syst, Res Enhancement Award Program, Seattle, WA USA.
C3 US Department of Veterans Affairs; Veterans Health Administration (VHA);
Vet Affairs Puget Sound Health Care System; University of Washington;
University of Washington Seattle; University of Washington; University
of Washington Seattle; US Department of Veterans Affairs; Veterans
Health Administration (VHA); Vet Affairs Puget Sound Health Care System
RP Afzali, A (corresponding author), Univ Washington, Div Gastroenterol, Dept Med, Vet Affairs Puget Sound Hlth Care Syst, 1959 NE Pacific St,Suite AA103,Box 356424, Seattle, WA 98195 USA.
EM anitaa@medicine.washington.edu
FU Health Resources and Services Administration [234-2005-370011C]
FX This work was supported in part by the Health Resources and Services
Administration (contract 234-2005-370011C). The content is the
responsibility of the authors alone and does not necessarily reflect the
views or policies of the Department of Health and Human Services, nor
does mention of trade names, commercial products, or organizations imply
endorsement by the US Government.
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NR 21
TC 108
Z9 112
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1527-6465
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD JAN
PY 2012
VL 18
IS 1
BP 29
EP 37
DI 10.1002/lt.22435
PG 9
WC Gastroenterology & Hepatology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA 867VO
UT WOS:000298483100005
PM 21932374
DA 2025-01-07
ER
PT J
AU Duma, D
Collins, JB
Chou, JW
Cidlowski, JA
AF Duma, Danielle
Collins, Jennifer B.
Chou, Jeff W.
Cidlowski, John A.
TI Sexually Dimorphic Actions of Glucocorticoids Provide a Link to
Inflammatory Diseases with Gender Differences in Prevalence
SO SCIENCE SIGNALING
LA English
DT Article
ID LIVER GENE-EXPRESSION; NF-KAPPA-B; GROWTH-HORMONE; RAT-LIVER; SEX;
RECEPTOR; MECHANISMS; CYTOCHROME; INDUCTION; ESTROGEN
AB Males and females show differences in the prevalence of many major diseases that have important inflammatory components to their etiology. These gender-specific diseases, which include autoimmune diseases, hepatocellular carcinoma, diabetes, and osteoporosis, are largely considered to reflect the actions of sex hormones on the susceptibility to inflammatory stimuli. However, inflammation reflects a balance between pro-and anti-inflammatory signals, and investigation of gender-specific responses to the latter has been neglected. Glucocorticoids are the primary physiological anti-inflammatory hormones in mammals, and synthetic derivatives of these hormones are prescribed as anti-inflammatory agents, irrespective of patient gender. We explored the possibility that sexually dimorphic actions of glucocorticoid regulation of gene expression may contribute to the dimorphic basis of inflammatory disease by evaluating the rat liver, a classic glucocorticoid-responsive organ. Surprisingly, glucocorticoid administration expanded the set of hepatic sexually dimorphic genes. Eight distinct patterns of glucocorticoid-regulated gene expression were identified, which included sex-specific genes. Our experiments also defined specific genes with altered expression in response to glucocorticoid treatment in both sexes, but in opposite directions. Pathway analysis identified sex-specific glucocorticoid-regulated gene expression in several canonical pathways involved in susceptibility to and progression of diseases with gender differences in prevalence. Moreover, a comparison of the number of genes involved in inflammatory disorders between sexes revealed 84 additional glucocorticoid-responsive genes in the male, suggesting that the anti-inflammatory actions of glucocorticoids are more effective in males. These gender-specific actions of glucocorticoids in liver were substantiated in vivo with a sepsis model of systemic inflammation.
C1 [Duma, Danielle; Cidlowski, John A.] NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
[Collins, Jennifer B.] NIEHS, Microarray Facil, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Chou, Jeff W.] Wake Forest Univ, Bowman Gray Sch Med, Dept Biostat Sci, Winston Salem, NC 27157 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Institute of
Environmental Health Sciences (NIEHS); National Institutes of Health
(NIH) - USA; NIH National Institute of Environmental Health Sciences
(NIEHS); Wake Forest University; Wake Forest Baptist Medical Center
RP Cidlowski, JA (corresponding author), NIEHS, Lab Signal Transduct, NIH, MD F3-07,POB 12233, Res Triangle Pk, NC 27709 USA.
EM cidlows1@niehs.nih.gov
RI Cidlowski, John/G-2548-2019
OI Cidlowski, John/0000-0003-1420-0516
FU Intramural NIH HHS [Z01 ES090057-13, Z01 ES090057-12] Funding Source:
Medline
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2010, DATABASE NUCL RECEPT
NR 48
TC 138
Z9 150
U1 0
U2 12
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1945-0877
EI 1937-9145
J9 SCI SIGNAL
JI Sci. Signal.
PD OCT 12
PY 2010
VL 3
IS 143
AR ra74
DI 10.1126/scisignal.2001077
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 662LH
UT WOS:000282808300001
PM 20940427
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Garrido, I
Liberal, R
Macedo, G
AF Garrido, Isabel
Liberal, Rodrigo
Macedo, Guilherme
TI Review article: COVID-19 and liver disease-what we know on 1st May 2020
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
ID B-VIRUS REACTIVATION; CLINICAL CHARACTERISTICS; TOCILIZUMAB TREATMENT;
RHEUMATOID-ARTHRITIS; VIRAL-INFECTIONS; CORONAVIRUS; SAFETY;
HYDROXYCHLOROQUINE; PHARMACOKINETICS; PNEUMONIA
AB Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative pathogen of coronavirus disease 2019 (COVID-19), became a global threat to human health. Liver impairment has been frequently reported as a common manifestation, although its clinical significance is still unclear, particularly in patients with underlying chronic liver disease (CLD).
Aims To summarise the changes in liver function tests during SARS-CoV-2 infection and the impact of COVID-19 in patients with underlying CLD.
Methods A literature review using online database PubMed was done using the search terms "SARS-CoV-2", "COVID-19", "liver", "cirrhosis" and "liver transplantation".
Results COVID-19 is frequently associated with different degrees of abnormal liver function tests, most notably transaminases, which are usually transitory and of mild degree. Available evidence suggests that liver injury may result from direct pathogenic effect by the virus, systemic inflammation or toxicity from commonly used drugs in this subset of patients. SARS-CoV-2 infection in children is associated with minimal or no increase in liver enzymes, thus the presence of abnormal liver function tests should trigger evaluation for underlying liver diseases. Although it seems that patients with CLD are not at greater risk for acquiring the infection, those with cirrhosis, hepatocellular carcinoma, non-alcoholic fatty liver disease, autoimmune liver diseases or liver transplant may have a greater risk for severe COVID-19.
Conclusions Abnormal liver function tests during the course of COVID-19 are common, though clinically significant liver injury is rare. Further research is needed focusing on the effect of existing liver-related comorbidities on treatment and outcome of COVID-19.
C1 [Garrido, Isabel; Liberal, Rodrigo; Macedo, Guilherme] Ctr Hosp Sao Joao, Dept Gastroenterol & Hepatol, Alameda Prof Hernani Monteiro, P-4200319 Porto, Portugal.
[Garrido, Isabel; Liberal, Rodrigo; Macedo, Guilherme] World Gastroenterol Org WGO Porto Training Ctr, Porto, Portugal.
C3 Sao Joao Hospital
RP Garrido, I (corresponding author), Ctr Hosp Sao Joao, Dept Gastroenterol & Hepatol, Alameda Prof Hernani Monteiro, P-4200319 Porto, Portugal.
EM isabelmng@hotmail.com
RI Macedo, Manuel/L-8038-2013
OI Garrido, Isabel/0000-0002-7801-466X; Macedo,
Guilherme/0000-0002-9387-9872
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NR 76
TC 117
Z9 127
U1 0
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD JUL
PY 2020
VL 52
IS 2
BP 267
EP 275
DI 10.1111/apt.15813
EA JUN 2020
PG 9
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA MC6HY
UT WOS:000536991400001
PM 32402090
OA Green Published
DA 2025-01-07
ER
PT J
AU Radaeva, S
Sun, R
Pan, HN
Hong, F
Gao, B
AF Radaeva, S
Sun, R
Pan, HN
Hong, F
Gao, B
TI Interleukin 22 (IL-22) plays a protective role in T cell-mediated murine
hepatitis: IL-22 is a survival factor for hepatocytes via STAT3
activation
SO HEPATOLOGY
LA English
DT Article
ID INDUCED LIVER-INJURY; GROWTH-FACTOR; CYCLIN D1; INDUCIBLE FACTOR;
FUNCTIONAL-CHARACTERIZATION; NEOPLASTIC DEVELOPMENT; AUTOIMMUNE
HEPATITIS; IL-TIF; INHIBITION; PROLIFERATION
AB The central role of T cell activation in hepatocellular injury has been well documented. In this article, we provide evidence suggesting that T cells may also play a protective role in liver disease by releasing interleukin-22 (IL-22), a recently identified T cell-derived cytokine whose biological significance is unclear. IL-22 messenger RNA and protein expression are significantly elevated in T cell-mediated hepatitis induced by concanavalin A (ConA) but are less extensively elevated in the carbon tetrachloride-induced liver injury model. Activated CD3(+) T cells are likely responsible for the production of IL-22 in the liver after injection of ConA. The IL-22 receptor is normally expressed at high levels by hepatocytes and further induced after ConA injection. IL-22 blockade with a neutralizing antibody reduces signal transducer and activator of transcription factor 3 (STAT3) activation and worsens liver injury in T cell-mediated hepatitis, whereas injection of recombinant IL-22 attenuates such injury. In vitro treatment with recombinant IL-22 or overexpression of IL-22 promotes cell growth and survival in human hepatocellular carcinoma HepG2 cells. Stable overexpression of IL-22 in HepG2 cells constitutively activates STAT3 and induces expression of a variety of antiapoptotic (e.g., Bcl-2, Bcl-xL, Mcl-1) and mitogenic (e.g., c-myc, cyclin D1, Rb2, CDK4) proteins. Blocking STAT3 activation abolishes the antiapoptotic and mitogenic actions of IL-22 in hepatic cells. In conclusion, the T cell-derived cytokine IL-22 is a survival factor for hepatocytes; this suggests that T cell activation may also prevent and repair liver injury by releasing hepatoprotective cytokine IL-22 in addition to its previously documented central role in hepatocellular injury.
C1 NIAAA, Sect Liver Biol, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Institute on
Alcohol Abuse & Alcoholism (NIAAA)
RP NIAAA, Sect Liver Biol, Lab Physiol Studies, NIH, Pk Bldg,Rm 120,12420 Parklawn Dr,MSC 8115, Bethesda, MD 20892 USA.
EM bgao@mail.nih.gov
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NR 47
TC 496
Z9 581
U1 0
U2 31
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD MAY
PY 2004
VL 39
IS 5
BP 1332
EP 1342
DI 10.1002/hep.20184
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 815NX
UT WOS:000221050100019
PM 15122762
OA Bronze
DA 2025-01-07
ER
PT J
AU Weiskirchen, R
Lonardo, A
AF Weiskirchen, Ralf
Lonardo, Amedeo
TI PNPLA3 as a driver of steatotic liver disease: navigating from
pathobiology to the clinics via epidemiology
SO JOURNAL OF TRANSLATIONAL GENETICS AND GENOMICS
LA English
DT Review
DE MASLD; PNPLA3 gene; cardio-nephro-metabolic syndrome; precision
medicine; sex differences; steatotic liver disease; Cirrhosis;
extrahepatic outcomes; ethnicity; hepatocellular carcinoma; insulin
resistance; liver transplantation
ID THAN-G VARIANT; INSULIN-RESISTANCE; I148M VARIANT; RS738409
POLYMORPHISM; TM6SF2; GENE; FIBROSIS; RISK; EDITORIALPNPLA3GENOTYPE;
METAANALYSIS
AB Steatotic liver disease (SLD), particularly metabolic dysfunction-associated SLD, represents a significant public health concern worldwide. Among the various factors implicated in the development and progression of this condition, the patatin-like phospholipase domain-containing protein 3 ( PNPLA3 ) gene has emerged as a critical player. Variants of PNPLA3 are associated with altered lipid metabolism, leading to increased hepatic fat accumulation and subsequent inflammation and fibrosis. Understanding the role of PNPLA3 not only enhances our comprehension of the pathomechanisms driving SLD but also informs potential therapeutic strategies. The molecular mechanisms through which PNPLA3 variants contribute to lipid dysregulation and hepatocyte injury in SLD are critically discussed in the present review article. We extensively analyze clinical cohorts and population- based studies underpinning the association between PNPLA3 polymorphisms and the risk of developing SLD, and its liver-related and protean extrahepatic outcomes, in concert with other risk modifiers, notably including age, sex, and ethnicity in adults and children. We also discuss the increasingly recognized role played by the PNPLA3 gene in liver transplantation, autoimmune hepatitis, and acquired immunodeficiency syndrome. Finally, we examine the clinical implications of PNPLA3 diagnostics regarding risk stratification and targeted therapies for patients affected by SLD in the context of precision medicine approaches.
C1 [Weiskirchen, Ralf] RWTH Univ Hosp Aachen, Inst Mol Pathobiochem Expt Gene Therapy & Clin Ch, Pauwelsstr 30, D-52074 Aachen, Germany.
[Lonardo, Amedeo] Azienda Osped Univ Modena, Osped Baggiovara, Dept Internal Med, Via Giardini 1135, I-41100 Modena, Italy.
RP Weiskirchen, R (corresponding author), RWTH Univ Hosp Aachen, Inst Mol Pathobiochem Expt Gene Therapy & Clin Ch, Pauwelsstr 30, D-52074 Aachen, Germany.; Lonardo, A (corresponding author), Azienda Osped Univ Modena, Osped Baggiovara, Dept Internal Med, Via Giardini 1135, I-41100 Modena, Italy.
EM rweiskirchen@ukaachen.de; a.lonardo@libero.it
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NR 128
TC 0
Z9 0
U1 0
U2 0
PU OAE PUBLISHING INC
PI ALHAMBRA
PA 245 E MAIN ST, ST122, ALHAMBRA, CA 91801 USA
EI 2578-5281
J9 J TRANSL GENET GENOM
JI J. Transl. Genet. Genom.
PY 2024
VL 8
IS 4
BP 355
EP 377
DI 10.20517/jtgg.2024.70
PG 23
WC Genetics & Heredity
WE Emerging Sources Citation Index (ESCI)
SC Genetics & Heredity
GA O7K4N
UT WOS:001372868800001
OA gold
DA 2025-01-07
ER
PT J
AU Tana, MM
Shums, Z
Milo, J
Norman, GL
Leung, PS
Gershwin, ME
Noureddin, M
Kleiner, DE
Zhao, XC
Heller, T
Hoofnagle, JH
AF Tana, Michele M.
Shums, Zakera
Milo, Jay
Norman, Gary L.
Leung, Patrick S.
Gershwin, M. Eric
Noureddin, Mazen
Kleiner, David E.
Zhao, Xiongce
Heller, Theo
Hoofnagle, Jay H.
TI The Significance of Autoantibody Changes Over Time in Primary Biliary
Cirrhosis
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE Autoantibodies; Primary biliary cirrhosis; Prognosis; Autoimmune liver
disease; Serum markers; Ursodiol
ID SYSTEMIC LUPUS-ERYTHEMATOSUS; ANTINUCLEAR ANTIBODIES; DISEASE
PROGRESSION; MYASTHENIA-GRAVIS; CORRELATE; ANTIGENS
AB Objectives: In primary biliary cirrhosis (PBC), the antimitochondrial antibody is a cornerstone of diagnosis, but there have been conflicting reports about the correlation of autoantibodies with disease stage and prognosis. We studied whether autoantibody levels changed over time and sought correlations with clinical outcomes in a cohort of patients with PBC.
Methods: We tested serial serum samples from patients with PBC at a research institution for several autoantibodies. Long-term clinical follow-up data were used to calculate the slopes (change over time) for autoantibodies, platelet count, Ishak fibrosis score, biopsy copper, and number of portal areas with bile ducts. An adverse clinical outcome was defined as hepatic decompensation, development of hepatocellular carcinoma, liver transplantation, or liver-related death. We performed linear or logistic regression or Fisher exact test as appropriate, adjusting for multiple comparisons.
Results: Twenty-seven patients with PBC with 145 serum samples were studied. Of the cohort, 85% was white, 81% was female, and median follow-up time was 20 years. Of the autoantibodies tested, only sp100 changed significantly over time. The sp100 slope was inversely associated with the Ishak fibrosis slope (parameter estimate, -0.05; P=.0003).
Conclusions: While changes in most autoantibodies over time do not seem to correlate with clinical outcomes in PBC, a change in the sp100 autoantibody level may have prognostic utility with respect to the development of fibrosis on liver biopsy.
C1 [Tana, Michele M.; Noureddin, Mazen; Kleiner, David E.; Zhao, Xiongce; Heller, Theo; Hoofnagle, Jay H.] NIDDK, NIH, Bethesda, MD 20892 USA.
[Shums, Zakera; Milo, Jay; Norman, Gary L.] Inova Diagnost, San Diego, CA USA.
[Leung, Patrick S.; Gershwin, M. Eric] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Institute of
Diabetes & Digestive & Kidney Diseases (NIDDK); Inova Diagnostics, Inc.;
University of California System; University of California Davis
RP Tana, MM (corresponding author), 1001 Potrero Ave,3D9, San Francisco, CA 94110 USA.
EM michele.tana@ucsf.edu
RI ; Kleiner, David/N-2770-2013
OI Heller, Theo/0000-0002-2643-6289; Kleiner, David/0000-0003-3442-4453
FU National Institute of Diabetes and Digestive and Kidney Diseases
[P30DK026743] Funding Source: NIH RePORTER; Intramural NIH HHS [Z99
DK999999] Funding Source: Medline; NIDDK NIH HHS [P30 DK026743, T32
DK007202] Funding Source: Medline
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NR 31
TC 28
Z9 32
U1 0
U2 13
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9173
EI 1943-7722
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD OCT
PY 2015
VL 144
IS 4
BP 601
EP 606
DI 10.1309/AJCPQV4A7QAEEFEV
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA CR7XJ
UT WOS:000361565000009
PM 26386081
OA Bronze, Green Accepted
DA 2025-01-07
ER
PT J
AU Khaliq, S
Khaliq, SA
Zahur, M
Ijaz, B
Jahan, S
Ansar, M
Riazuddin, S
Hassan, S
AF Khaliq, Saba
Khaliq, Sadaf A.
Zahur, Muzna
Ijaz, Bushra
Jahan, Shah
Ansar, Muhammad
Riazuddin, Sheikh
Hassan, Sajida
TI RNAi as a new therapeutic strategy against HCV
SO BIOTECHNOLOGY ADVANCES
LA English
DT Review
DE Hepatitis C Virus; RNAi; siRNA design; siRNA delivery
ID HEPATITIS-C-VIRUS; SMALL-INTERFERING RNA; DOUBLE-STRANDED-RNA;
GENE-EXPRESSION; IN-VIVO; STRUCTURAL FEATURES; PROTEIN EXPRESSION;
MESSENGER-RNA; CELL-CULTURE; PLASMID DNA
AB Hepatitis C virus is a major cause of liver associated diseases all over the world. Irrespective of the significant advances in the current therapy, drugs and vaccines are restricted with many factors such as toxicity, complexity, cost and resistance. New technologies particularly RNA interference (RNAi) mediated by small interfering RNA (siRNA) have become more and more interesting and effective therapeutic entities to silence pathogenic gene products associated with disease, including cancer, viral infections and autoimmune disorders. RNAi works at a posttranscriptional level by targeting mRNA as a mean for inhibiting the synthesis of the encoded protein. Several reports have indicated the efficiency and specificity of synthetic and vector based siRNAs inhibiting HCV replication. In the present review, we focused on the recent development in the potential use and issues regarding siRNA as a therapy for HCV. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Khaliq, Saba; Zahur, Muzna; Ijaz, Bushra; Jahan, Shah; Ansar, Muhammad; Riazuddin, Sheikh; Hassan, Sajida] Univ Punjab, Funct & Appl Genom Lab, Natl Ctr Excellence Mol Biol, Lahore 53700, Pakistan.
[Khaliq, Sadaf A.] Govt Coll Univ, Lahore, Pakistan.
C3 University of Punjab; National Center of Excellence in Molecular Biology
- Pakistan; Government College University Lahore
RP Khaliq, S (corresponding author), Univ Punjab, Funct & Appl Genom Lab, Natl Ctr Excellence Mol Biol, Lahore 53700, Pakistan.
EM sabahat711@yahoo.com; sajihassan2004@yahoo.com
RI jahan, shah/JCE-5141-2023; Ijaz, Bushra/C-3331-2019; Ansar,
Muhammad/R-8017-2019; Khaliq, saba/W-2723-2017; Jahan, Shah/G-3728-2017
OI Khaliq, saba/0000-0002-0345-7394; Ansar, Muhammad/0000-0001-7299-3185;
Jahan, Shah/0000-0002-1730-5025
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NR 105
TC 27
Z9 31
U1 0
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0734-9750
EI 1873-1899
J9 BIOTECHNOL ADV
JI Biotechnol. Adv.
PD JAN-FEB
PY 2010
VL 28
IS 1
BP 27
EP 34
DI 10.1016/j.biotechadv.2009.08.004
PG 8
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA 551RH
UT WOS:000274226200004
PM 19729057
DA 2025-01-07
ER
PT J
AU Liu, KT
Chan, HM
Lin, TJ
AF Liu, Kuan-Ting
Chan, Hon-Man
Lin, Tzeng-Jih
TI An unusual presentation of metastatic gastric adenocarcinoma - Acute
onset of right neck swelling
SO JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION
LA English
DT Article
DE central vein; gastric cancer; malignancy; thrombosis
ID JUGULAR-VEIN-THROMBOSIS
AB Central venous thrombosis is an uncommon problem associated with malignancy. We present here a 53-year-old male who visited the emergency room because of right neck swelling. Fluid accumulation over deep neck space led to the diagnosis of suspected hemorrhage, and central venous thrombosis was found by computed tomography. This patient had no other precipitating cause. Autoimmune disorders, hypercoagulation and malignancy surveys were performed during hospitalization. Elevated serum tissue polypeptide antigen and CA130 were noted, and multiple liver metastases were found by another computed tomography. Subsequently, gastric adenocarcinoma was confirmed after gastroendoscopy. Gastric adenocarcinoma with distal metastases was finally diagnosed. This case reminds us that central venous thrombosis is a sign of many diseases. Malignancy, including gastric adenocarcinoma, is one of the causes that should be considered.
C1 Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Emergency Med, Kaohsiung 807, Taiwan.
Kaohsiung Med Univ, Coll Med, Fac Med, Kaohsiung, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
Kaohsiung Medical University
RP Lin, TJ (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Emergency Med, 100 Shih Chuan 1st Rd, Kaohsiung 807, Taiwan.
EM ttiinngg@ms2.hinet.net
RI Lin, Tzeng-Jih/D-5026-2009; liu, kt/AFU-9413-2022
OI Liu, Kuan-Ting/0000-0002-1355-5019
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NR 9
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER TAIWAN
PI TAIPEI
PA RM N-412, 4F, CHIA HSIN BUILDING 11, NO 96, ZHONG SHAN N ROAD SEC 2,
TAIPEI, 10449, TAIWAN
SN 0929-6646
EI 1876-0821
J9 J FORMOS MED ASSOC
JI J. Formos. Med. Assoc.
PD JUL
PY 2007
VL 106
IS 7
BP 589
EP 591
DI 10.1016/S0929-6646(07)60011-4
PG 3
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 197UT
UT WOS:000248582700011
PM 17660150
DA 2025-01-07
ER
PT J
AU Kumar, MA
Baba, SK
Sadida, HQ
Marzooqi, SA
Jerobin, J
Altemani, FH
Algehainy, N
Alanazi, MA
Abou-Samra, AB
Kumar, R
Akil, ASAS
Macha, MA
Mir, R
Bhat, AA
AF Kumar, Mudasir A.
Baba, Sadaf K.
Sadida, Hana Q.
Marzooqi, Sara Al.
Jerobin, Jayakumar
Altemani, Faisal H.
Algehainy, Naseh
Alanazi, Mohammad A.
Abou-Samra, Abdul-Badi
Kumar, Rakesh
Al-Shabeeb Akil, Ammira S.
Macha, Muzafar A.
Mir, Rashid
Bhat, Ajaz A.
TI Extracellular vesicles as tools and targets in therapy for diseases
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID MESENCHYMAL STEM-CELLS; PLATELET-DERIVED MICROPARTICLES; PRE-METASTATIC
NICHE; HUMAN ATHEROSCLEROTIC PLAQUES; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
IMPAIR ENDOTHELIAL FUNCTION; PROMOTE TUMOR PROGRESSION; FIELD-FLOW
FRACTIONATION; BREAST-CANCER CELLS; MEMBRANE-VESICLES
AB Extracellular vesicles (EVs) are nano-sized, membranous structures secreted into the extracellular space. They exhibit diverse sizes, contents, and surface markers and are ubiquitously released from cells under normal and pathological conditions. Human serum is a rich source of these EVs, though their isolation from serum proteins and non-EV lipid particles poses challenges. These vesicles transport various cellular components such as proteins, mRNAs, miRNAs, DNA, and lipids across distances, influencing numerous physiological and pathological events, including those within the tumor microenvironment (TME). Their pivotal roles in cellular communication make EVs promising candidates for therapeutic agents, drug delivery systems, and disease biomarkers. Especially in cancer diagnostics, EV detection can pave the way for early identification and offers potential as diagnostic biomarkers. Moreover, various EV subtypes are emerging as targeted drug delivery tools, highlighting their potential clinical significance. The need for non-invasive biomarkers to monitor biological processes for diagnostic and therapeutic purposes remains unfulfilled. Tapping into the unique composition of EVs could unlock advanced diagnostic and therapeutic avenues in the future. In this review, we discuss in detail the roles of EVs across various conditions, including cancers (encompassing head and neck, lung, gastric, breast, and hepatocellular carcinoma), neurodegenerative disorders, diabetes, viral infections, autoimmune and renal diseases, emphasizing the potential advancements in molecular diagnostics and drug delivery.
C1 [Kumar, Mudasir A.; Baba, Sadaf K.; Macha, Muzafar A.] Islamic Univ Sci & Technol, Watson Crick Ctr Mol Med, Awantipora 192122, Kashmir, India.
[Sadida, Hana Q.; Marzooqi, Sara Al.; Al-Shabeeb Akil, Ammira S.; Bhat, Ajaz A.] Sidra Med, Dept Human Genet Precis Med Diabet, Obes & Canc Program, Doha, Qatar.
[Jerobin, Jayakumar; Abou-Samra, Abdul-Badi] Hamad Med Corp, Qatar Metab Inst, Acad Hlth Syst, Doha, Qatar.
[Altemani, Faisal H.; Algehainy, Naseh; Alanazi, Mohammad A.; Mir, Rashid] Univ Tabuk, Fac Appl Med Sci, Prince Fahad Bin Sultan Chair Biomed Res, Dept Med Lab Technol, Tabuk, Saudi Arabia.
[Kumar, Rakesh] Shri Mata Vaishno Devi Univ, Sch Biotechnol, Katra, India.
C3 Sidra Medical & Research Center; Hamad Medical Corporation; University
of Tabuk; Shri Mata Vaishno Devi University
RP Bhat, AA (corresponding author), Sidra Med, Dept Human Genet Precis Med Diabet, Obes & Canc Program, Doha, Qatar.; Mir, R (corresponding author), Univ Tabuk, Fac Appl Med Sci, Prince Fahad Bin Sultan Chair Biomed Res, Dept Med Lab Technol, Tabuk, Saudi Arabia.
EM rashidmirtabuk@gmail.com; abhat@sidra.org
RI Bhat, Ajaz/V-3642-2019; Alanazi, Mohammad/HTP-5235-2023; MIR,
RASHID/AAH-1895-2019; Mir, Rashid/GOV-3522-2022; Algehainy, Naseh
A./JNR-2432-2023
OI Sadida, Hana/0009-0003-2932-0323; Jerobin,
Jayakumar/0000-0001-6421-3601; Alanazi, Mohammad/0000-0001-6766-3237;
Algehainy, Naseh/0000-0001-8557-0499
FU Sidra Medicine Research Fund to Ajaz A. Bhat [SDR400105]; Sidra Medicine
Precision Program
FX The authors thank the Sidra Medicine Precision Program for providing the
funding necessary to carry out this study. Figures were created using
BioRender.
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NR 688
TC 119
Z9 122
U1 119
U2 154
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD FEB 5
PY 2024
VL 9
IS 1
AR 27
DI 10.1038/s41392-024-01735-1
PG 41
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA GY6V0
UT WOS:001156284100001
PM 38311623
OA Green Published, gold
HC Y
HP Y
DA 2025-01-07
ER
PT J
AU Paskonis, M
Masalaite, L
Buivydiene, A
Sokolovas, V
Jurgaitis, J
Jurevicius, S
Mikalauskas, S
Gutauskas, M
Spuras, J
Sarkaite, R
Samuilis, A
Rutkauskaite, D
Misionis, N
Dukstaite, A
Serpytis, M
Kekstas, G
Rainiene, T
Barakauskiene, A
Valantinas, J
Strupas, K
AF Paskonis, Marius
Masalaite, Laura
Buivydiene, Arida
Sokolovas, Vitalijus
Jurgaitis, Jonas
Jurevicius, Saulius
Mikalauskas, Saulius
Gutauskas, Marijus
Spuras, Jonas
Sarkaite, Renata
Samuilis, Arturas
Rutkauskaite, Dileta
Misionis, Nerijus
Dukstaite, Asta
Serpytis, Mindaugas
Kekstas, Gintautas
Rainiene, Tatjana
Barakauskiene, Ausrine
Valantinas, Jonas
Strupas, Kestutis
TI Orthotopic liver transplantation: The first experience and results of
the Vilnius University Hospital Santariskiu Klinikos
SO ANNALS OF TRANSPLANTATION
LA English
DT Article
DE orthotopic liver transplantation; results; survival; complications
ID HEPATIC-ARTERY THROMBOSIS; BILIARY COMPLICATIONS; DIABETES-MELLITUS;
RISK-FACTORS; MANAGEMENT; MORTALITY; IMPACT; THROMBOLYSIS; INFECTION;
SURVIVAL
AB Background: Liver transplantation has become the treatment of choice for chronic and acute end-stage liver failure as well as for selected cases of malignancies and metabolic disorders. We report our first experience of the orthotopic liver transplantation.
Material/Methods: Between 2005 and 2008 16 cadaveric orthotopic liver transplantations in 16 adults (12 males, 4 females, mean age 44 years) were performed. Main indications for orthotopic liver transplantation were cholestatic liver disease (31%), viral-induced cirrhosis (25%), alcoholic liver disease (19%), hepatocellular carcinoma associated with hepatitis virus infection (13%), autoimmune cirrhosis (6%), cryptogenic acute liver failure (6%). Mean follow-up was 15 month (range: 4 days - 43 month).
Results: Intraabdominal haemorrhage was observed in 6 patients (37.5%). Vascular complications were observed in 3 patients (18.75%). Biliary complication were observed in 3 patients (18.75%). Overall 1 year patient survival was 87,5%. Four (25%) patients died during follow-up. All patients died because of sepsis and multiorgan system failure.
Conclusions: Our first results showed drat secret of successful liver transplantation is perfect: interdisciplinary team approuch, including selection of the recipient and timing of transplantation, the operative procedure itself, prevention and treatment of complications, the perioperative anaesthesiological and intensive-care management, and carefull follow up after transplantation.
C1 [Paskonis, Marius; Sokolovas, Vitalijus; Jurgaitis, Jonas; Jurevicius, Saulius; Mikalauskas, Saulius; Strupas, Kestutis] Vilnius State Univ, Ctr Abdominal Surg, Hosp Santariskiu Klinikos, LT-08661 Vilnius, Lithuania.
[Masalaite, Laura; Sokolovas, Vitalijus; Mikalauskas, Saulius; Serpytis, Mindaugas; Valantinas, Jonas; Strupas, Kestutis] Vilnius State Univ, Fac Med, LT-08661 Vilnius, Lithuania.
[Masalaite, Laura; Buivydiene, Arida; Dukstaite, Asta; Valantinas, Jonas] Vilnius State Univ, Ctr Hepatol Gastroenterol & Dietet, Hosp Santariskiu Klinikos, LT-08661 Vilnius, Lithuania.
[Gutauskas, Marijus] Vilnius State Univ, Ctr Vasc Surg, Hosp Santariskiu Klinikos, LT-08661 Vilnius, Lithuania.
[Spuras, Jonas; Sarkaite, Renata; Serpytis, Mindaugas; Kekstas, Gintautas] Vilnius State Univ, Ctr Anaesthesiol Intens Care & Pain Management, Hosp Santariskiu Klinikos, LT-08661 Vilnius, Lithuania.
[Samuilis, Arturas; Rutkauskaite, Dileta; Misionis, Nerijus] Vilnius State Univ, Ctr Radiol, Hosp Santariskiu Klinikos, LT-08661 Vilnius, Lithuania.
[Rainiene, Tatjana] Vilnius State Univ, Ctr Lab Diagnost, Hosp Santariskiu Klinikos, Clin Immunol Lab, LT-08661 Vilnius, Lithuania.
[Barakauskiene, Ausrine] Natl Ctr Pathol, Vilnius, Lithuania.
C3 Vilnius University; Vilnius University; Vilnius University; Vilnius
University; Vilnius University; Vilnius University; Vilnius University;
Vilnius University Hospital Santariskiu Klinikos
RP Paskonis, M (corresponding author), Vilnius State Univ, Ctr Abdominal Surg, Hosp Santariskiu Klinikos, Santariskiu Str 2, LT-08661 Vilnius, Lithuania.
EM mpaskonis@yahoo.com
RI Jurgaitis, Jonas/HNS-4552-2023; Masalaite, Laura/HKP-1894-2023;
Mikalauskas, Saulius/U-2748-2017
OI BUIVYDIENE, ARIDA/0000-0002-4417-4198
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NR 52
TC 0
Z9 0
U1 2
U2 8
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
SN 1425-9524
J9 ANN TRANSPL
JI Ann. Transpl.
PD JAN-MAR
PY 2010
VL 15
IS 1
BP 14
EP 24
PG 11
WC Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery; Transplantation
GA 585JQ
UT WOS:000276821900002
PM 20305313
DA 2025-01-07
ER
PT J
AU Onishi, H
Theisen, D
Zachoval, R
Reiser, MF
Zech, CJ
AF Onishi, Hiromitsu
Theisen, Daniel
Zachoval, Reinhart
Reiser, Maximilian F.
Zech, Christoph J.
TI Intrahepatic diffuse periportal enhancement patterns on hepatobiliary
phase gadoxetate disodium-enhanced liver MR images: Do they correspond
to periportal hyperintense patterns on T2-weighted images?
SO MEDICINE
LA English
DT Article
DE Gd-EOB-DTPA; liver; magnetic resonance imaging; primary biliary
cirrhosis; primary sclerosing cholangitis
ID GD-EOB-DTPA; PRIMARY BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA;
IMAGING-CORRELATION; CLINICAL-EVALUATION; SIGNAL INTENSITY;
MULTIDETECTOR CT; DISEASE; TRANSPORTERS; FIBROSIS
AB The purpose of this study was to investigate the findings of diffuse periportal enhancement in the liver on hepatobiliary phase gadoxetate disodium-enhanced magnetic resonance images by comparing with the finding of periportal hyperintensity on T2-weighted images and to reveal their clinical significance.Nineteen consecutive patients with diffuse periportal enhancement on hepatobiliary phase images constituted the study population. The intrahepatic diffuse periportal enhancement finding was assessed on whether it corresponded to periportal hyperintense patterns on T2-weighted images or not in the location, and the cases were classified into 2 groups according to this characteristic. Signal intensities at the periportal areas were also assessed on T1-, T2-, diffusion-weighted and dynamic images. Furthermore, possible associations between these image findings and the final diagnoses were explored.In 7 of the 19 patients, periportal enhancement area corresponded with the periportal hyperintensity area on T2-weighted images. In the remaining 12 patients, the finding of periportal T2-hyperintensity was absent or the periportal enhancement differed from the periportal T2-hyperintensity in the location. Diseases of the former group comprised autoimmune hepatitis, acute exacerbation of chronic hepatitis and acute alcoholic steatohepatitis, and those of the latter group primary sclerosing cholangitis, autoimmune hepatitis-primary biliary cirrhosis overlap syndrome, and liver cirrhosis with miscellaneous etiology.Diffuse periportal enhancement during the hepatobiliary phase did not always correspond to periportal hyperintensity on T2-weighted images. In the classification based on whether enhancement area corresponded or not, each enhancement pattern appeared in different groups of liver diseases. Specifically, the former (corresponding) was associated with active inflammation such as hepatitis and the latter (not corresponding) was predominantly associated with a chronic change such as cirrhosis. Appropriate recognition of these periportal enhancement patterns may contribute to the improved diagnosis of diffuse liver diseases.
C1 [Onishi, Hiromitsu; Theisen, Daniel; Reiser, Maximilian F.; Zech, Christoph J.] Ludwig Maximilians Univ Hosp Munich, Inst Clin Radiol, Munich, Germany.
[Onishi, Hiromitsu] Osaka Univ, Grad Sch Med, Dept Radiol, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan.
[Zachoval, Reinhart] Ludwig Maximilians Univ Hosp Munich, Dept Internal Med 2, Munich, Germany.
[Zech, Christoph J.] Univ Hosp Basel, Clin Radiol & Nucl Med, Basel, Switzerland.
C3 University of Munich; Osaka University; University of Munich; University
of Basel
RP Onishi, H (corresponding author), Osaka Univ, Grad Sch Med, Dept Radiol, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan.
EM h-onishi@radiol.med.osaka-u.ac.jp
FU Japan Society for the Promotion of Science (JSPS KAKENHI) [24591761];
Japanese Society for Magnetic Resonance in Medicine; Grants-in-Aid for
Scientific Research [24591761] Funding Source: KAKEN
FX This work has been supported in part by from Japan Society for the
Promotion of Science (JSPS KAKENHI Grant Number 24591761) and Japanese
Society for Magnetic Resonance in Medicine.
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NR 35
TC 6
Z9 6
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD MAR
PY 2019
VL 98
IS 11
AR e14784
DI 10.1097/MD.0000000000014784
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HQ7AI
UT WOS:000462571200035
PM 30882651
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Nanjundappa, RH
Christen, U
Umeshappa, CS
AF Nanjundappa, Roopa H.
Christen, Urs
Umeshappa, Channakeshava S.
TI Distinct immune surveillance in primary biliary cholangitis and primary
sclerosing cholangitis is linked with discrete cholangiocarcinoma risk
SO HEPATOLOGY COMMUNICATIONS
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; DOWN-REGULATION; SEX-DIFFERENCES; T-CELLS;
CANCER; CIRRHOSIS; TH1; LYMPHOCYTES; SUPPRESSES; ANTIGEN
AB Primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC) are 2 major liver autoimmune diseases. PBC is common in women and primarily affects intrahepatic small bile duct epithelial cells, known as cholangiocytes. In contrast, PSC is dominant in men and primarily affects medium and big intrahepatic and extrahepatic bile duct epithelial cells. Cholangiocarcinoma (CCA) is a malignancy arising from cholangiocytes, and its incidence is increasing worldwide in both men and women. Numerous retrospective and clinical studies have suggested that PBC patients rarely develop CCA compared to PSC patients. CCA is accountable for the higher deaths in PSC patients due to ineffective therapies and our inability to diagnose the disease at an early stage. Therefore, it is paramount to understand the differences in immune surveillance mechanisms that render PBC patients more resistant while PSC patients are susceptible to CCA development. Here, we review several potential mechanisms contributing to differences in the susceptibility to CCA in PBC versus PSC patients.
C1 [Nanjundappa, Roopa H.; Umeshappa, Channakeshava S.] Dalhousie Univ, Dept Microbiol & Immunol, 5850 Univ Ave, Halifax B3K 6R8, NS, Canada.
[Christen, Urs] Goethe Univ Frankfurt, Dept Gen Pharmacol & Toxicol, Pharmazentrum Frankfurt, Frankfurt, Germany.
[Umeshappa, Channakeshava S.] IWK Hlth Ctr, Dept Pediat, Halifax, NS, Canada.
C3 Dalhousie University; Goethe University Frankfurt; Dalhousie University
RP Umeshappa, CS (corresponding author), Dalhousie Univ, Dept Microbiol & Immunol, 5850 Univ Ave, Halifax B3K 6R8, NS, Canada.
EM rp740063@dal.ca; christen@med.uni-frankfurt.de; csumesha@dal.ca
RI Christen, Urs/A-7338-2009
FU Department of Microbiology and Immunology, Faculty of Medicine,
Dalhousie University; Canada Research Chair Tier 2 award by the Canadian
Institutes of Health Research; Dalhousie medical research foundation
accelerated fellowship; Goethe University Frankfurt; LOEWE
(Landes-Offensive zur Entwicklung Wissenschaftlich-ouml;konomischer
Exzellenz) [TMP-IF-01]
FX This work was supported by Start-up funding by the by the Department of
Microbiology and Immunology, Faculty of Medicine, Dalhousie University.
Channake-shava S. Umeshappa is supported by the Canada Research Chair
Tier 2 award by the Canadian Institutes of Health Research. Roopa H.
Nanjundappa is supported by the Dalhousie medical research foundation
accelerated fellowship. Urs Christen is supported by the Goethe
University Frankfurt and the LOEWE (Landes-Offensive zur Entwicklung
Wissenschaftlich-oekonomischer Exzellenz) TMP-IF-01.
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NR 59
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2471-254X
J9 HEPATOL COMMUN
JI Hepatol. Commun.
PD SEP
PY 2023
VL 7
IS 9
AR e0218
DI 10.1097/HC9.0000000000000218
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA O6DH4
UT WOS:001044687100001
PM 37555943
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Riella, LV
Bagley, J
Iacomini, J
Alegre, ML
AF Riella, Leonardo V.
Bagley, Jessamyn
Iacomini, John
Alegre, Maria-Luisa
TI Impact of environmental factors on alloimmunity and transplant fate
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Review
ID REGULATORY T-CELLS; INTESTINAL BARRIER FUNCTION; APOLIPOPROTEIN-E;
LIVER-TRANSPLANTATION; CARBON-MONOXIDE; ACUTE REJECTION; GUT BACTERIA;
KIDNEY-TRANSPLANTATION; MOLECULAR-MECHANISMS; DENDRITIC CELLS
AB Although gene-environment interactions have been investigated for many years to understand people's susceptibility to autoimmune diseases or cancer, a role for environmental factors in modulating alloimmune responses and transplant outcomes is only now beginning to emerge. New data suggest that diet, hyperlipidemia, pollutants, commensal microbes, and pathogenic infections can all affect T cell activation, differentiation, and the kinetics of graft rejection. These observations reveal opportunities for novel therapeutic interventions to improve graft outcomes as well as for noninvasive biomarker discovery to predict or diagnose graft deterioration before it becomes irreversible. In this Review, we will focus on the impact of these environmental factors on immune function and, when known, on alloimmune function, as well as on transplant fate.
C1 [Riella, Leonardo V.] Brigham & Womens Hosp, Renal Div, Schuster Family Transplantat Res Ctr, 75 Francis St, Boston, MA 02115 USA.
[Bagley, Jessamyn; Iacomini, John] Tufts Univ, Sch Med, Dept Dev Mol & Chem Biol, Sackler Sch Biomed Sci,Program Immunol, Boston, MA 02111 USA.
[Bagley, Jessamyn; Iacomini, John] Tufts Univ, Sch Med, Dept Dev Mol & Chem Biol, Sackler Sch Biomed Sci,Program Genet, Boston, MA 02111 USA.
[Alegre, Maria-Luisa] Univ Chicago, Dept Med, 924 E 57th St,JFK R312, Chicago, IL 60637 USA.
C3 Harvard University; Brigham & Women's Hospital; Tufts University; Tufts
University; University of Chicago
RP Alegre, ML (corresponding author), Univ Chicago, Dept Med, 924 E 57th St,JFK R312, Chicago, IL 60637 USA.
EM malegre@midway.uchicago.edu
RI Riella, Leonardo/AAC-8182-2019
OI Alegre, Maria-Luisa/0000-0001-5707-6194
FU American Heart Association [12FTF120070328]; NIH [R01-AI116714,
7-04-RA-45]; [R01-AI115716]
FX This work was supported in part by American Heart Association grant
12FTF120070328 to LVR, NIH grant R01-AI116714 and Grant-in-Aid
7-04-RA-45 from the American Heart Association to JI, and R01-AI115716
to MLA.
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NR 170
TC 7
Z9 7
U1 0
U2 10
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD JUN 30
PY 2017
VL 127
IS 7
BP 2482
EP 2491
DI 10.1172/JCI90596
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA EZ2RM
UT WOS:000404557400006
PM 28481225
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Sawadpanich, K
Promasen, P
Mairiang, P
Sukeepaisarnjareon, W
Sangchan, A
Suttichaimongkol, T
Tangvoraphonkchai, K
Foocharoen, C
AF Sawadpanich, Kookwan
Promasen, Palinee
Mairiang, Pisaln
Sukeepaisarnjareon, Wattana
Sangchan, Apichat
Suttichaimongkol, Tanita
Tangvoraphonkchai, Kawin
Foocharoen, Chingching
TI Incidence and Predictors of an Abnormal Liver Function Test Among 674
Systemic Sclerosis Patients: A Cohort Study
SO OPEN ACCESS RHEUMATOLOGY-RESEARCH AND REVIEWS
LA English
DT Article
DE systemic sclerosis; scleroderma; scleroderma and related disorders;
hepatitis; cholestasis; cholestatic hepatitis; abnormal liver function
test; liver; cohort study
ID NONALCOHOLIC FATTY LIVER; AUTOIMMUNE HEPATITIS; CLINICAL-FEATURES; SKIN
INVOLVEMENT; DISEASE; SCLERODERMA; SEVERITY; OVERLAP; CLASSIFICATION;
PREVALENCE
AB Background: Abnormal liver function tests (LFTs) can indicate cirrhosis or liver cancer leading to mortality among systemic sclerosis (SSc) patients. No recent studies have investigated the clinical predictors of an abnormal LFT in SSc. We aimed to determine the incidence of abnormal LFT (including from hepatitis and cholestasis) and to identify its clinical predictors in SSc patients.Methods: An historical cohort was conducted on 674 adult SSc patients who attended the Scleroderma Clinic, Khon Kaen University, between January 2012 and November 2019 and who underwent routine screening for LFT. A Cox regression was used to analyze the clinical predictors of abnormal LFT.Results: Four hundred and thirty cases, representing 4190 person-years, had abnormal LFTs (viz, from hepatitis, cholestasis, and cholestatic hepatitis) for an incidence rate of 10.2 per 100 person-years. The respective incidence of hepatitis, cholestasis, and cholestatic hepatitis was 20.5, 12.9, and 20.4 per 100 person-years. The respective median first-time detection of hepatitis, cholestasis, and cholestatic hepatitis was 3.0, 5.9, and 2.8 years, and none had signs or symptoms suggestive of liver disease. According to the Cox regression analysis, the predictors of an abnormal LFT in SSc were elderly onset of SSc (hazard ratio (HR) 1.02), alcoholic drinking (HR 1.74), high modified Rodnan Skin Score (mRSS) (HR 1.03), edematous skin (HR 2.94), Raynaud's phenomenon (HR 1.39), hyperCKaemia (HR 1.88), and methotrexate use (HR 1.55). In contrast, current sildenafil treatment (HR 0.63) and high serum albumin (HR 0.70) were protective factors.Conclusion: Occult hepatitis, cholestasis, and cholestatic hepatitis can be detected in SSc patients using LFT screening, especially in cases of early disease onset. The long-term outcome is uncertain, and more longitudinal research is required.
C1 [Sawadpanich, Kookwan; Promasen, Palinee; Mairiang, Pisaln; Sukeepaisarnjareon, Wattana; Sangchan, Apichat; Suttichaimongkol, Tanita; Tangvoraphonkchai, Kawin] Khon Kaen Univ, Fac Med, Dept Med, Div Gastroenterol & Hepatol, Khon Kaen 40002, Thailand.
[Foocharoen, Chingching] Khon Kaen Univ, Fac Med, Dept Med, Div Rheumatol, Khon Kaen 40002, Thailand.
C3 Khon Kaen University; Khon Kaen University
RP Foocharoen, C (corresponding author), Khon Kaen Univ, Fac Med, Dept Med, Div Rheumatol, Khon Kaen 40002, Thailand.
EM fching@kku.ac.th
RI Suttichaimongkol, Tanita/JDW-6886-2023
OI Foocharoen, Chingching/0000-0002-1964-4389
FU Research and Graduate Studies, Khon Kaen University, Thailand;
Scleroderma Research Group, Khon Kaen University; Faculty of Medicine,
Khon Kaen University
FX The authors thank (a) the Research and Graduate Studies, Khon Kaen
University, Thailand, the Scleroderma Research Group and Faculty of
Medicine, Khon Kaen University, for the support, and (b) Mr. Bryan
Roderick Hamman-under the aegis of the Publication Clinic Khon Kaen
University, Thailand-for assistance with the English-language
presentation.
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NR 55
TC 0
Z9 0
U1 0
U2 0
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-156X
J9 OPEN ACCESS RHEUMATO
JI Open Access Rehumatol.
PY 2023
VL 15
BP 81
EP 92
DI 10.2147/OARRR.S410165
PG 12
WC Rheumatology
WE Emerging Sources Citation Index (ESCI)
SC Rheumatology
GA H3ZN7
UT WOS:000995383000001
PM 37214354
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Lahner, E
Capasso, M
Carabotti, M
Annibale, B
AF Lahner, Edith
Capasso, Marina
Carabotti, Marilia
Annibale, Bruno
TI Incidence of cancer (other than gastric cancer) in pernicious anaemia: A
systematic review with meta-analysis
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Review
DE Autoimmune gastritis; Biliary tract cancer; Cancer risk; Leukaemia;
Lymphoma; Meta-analysis; Pernicious anaemia; Systematic review
ID UPPER GASTROINTESTINAL-TRACT; FOLLOW-UP; PROMOTER METHYLATION; POSSIBLE
ASSOCIATION; AUTOIMMUNE-DISEASES; ATROPHIC GASTRITIS; COLORECTAL-CANCER;
SERUM PEPSINOGENS; MULTIPLE-MYELOMA; FOLATE-DEFICIENT
AB Background: Pernicious anaemia (PA) is associated with increased gastric cancer risk, but the evidence is conflicting regarding the associated risk of other cancers.
Aim: To systematically determine the incidence rates of gastro-intestinal cancers other than gastric cancers (GI-other-than-GC) and non-gastrointestinal cancers (non-GIC) in PA adults, globally and per tumour site, and the risk associated with PA for GI-other than GC and non-GIC. Methods: Studies of PA patients reporting the incidence of GI-other-than-GCs and non-GICs were identified with MEDLINE (PubMed)-EMBASE (from first date available to April 2017). A meta-analysis of annual cancer incidence rates was performed. The outcome was the cumulative incidence of GI-other-than-GCs and non-GICs (ratio between the numbers of new cancer cases identified during the follow-up period and the number of PA patients) and the incidence rate expressed as the rate of events-per-time-unit (person-years).
Results: Of 82,257 PA patients, the pooled incidence rates/100 person-years for non-GCs and non-GICs of 0.27 (95% CI: 0.16-0.42) and 0.23 (95% CI: 0.22-0.25) were calculated by meta-analysis. Compared to the GLOBOCAN data for the general population from the countries of the included studies, the meta-analysis showed an overall relative risk (RR) of cancer in PA of 0.68 (95% CI: 0.48-0.95). PA patients had a lower RR of colorectal, breast, liver, oesophageal, lung, thyroid, ovary, non-melanoma skin and kidney cancers but had a higher RR of biliary tract cancer (1.81: 1.21-2.70), multiple myeloma (2.83: 1.76-4.55), Hodgkin's lymphoma (3.0: 1.35-6.68), non-Hodgkin's lymphoma (2.08: 1.58-2.75), and leukaemia (1.56: 1.16-2.12).
Conclusion: An overall lower RR of cancers-other-than-gastric-cancer in PA patients but an increased RR of biliary tract cancers and haematological malignancies was observed. (c) 2018 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Lahner, Edith; Capasso, Marina; Carabotti, Marilia; Annibale, Bruno] Sapienza Univ Rome, Med Surg Dept Clin Sci & Translat Med, Rome, Italy.
C3 Sapienza University Rome
RP Lahner, E (corresponding author), Sapienza Univ Rome, Dept Med Surg Sci & Translat Med, Via Grottarossa 1035, I-00189 Rome, Italy.
EM edith.lahner@uniroma1.it
RI Annibale, Bruno/A-5372-2008; Lahner, Edith/AAM-1039-2021
FU Sapienza University
FX This paper was funded in part by a grant from Sapienza University, funds
of Oncology Doctorate 2016.
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NR 62
TC 16
Z9 19
U1 1
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD AUG
PY 2018
VL 50
IS 8
BP 780
EP 786
DI 10.1016/j.dld.2018.05.012
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GN8GK
UT WOS:000439397500006
PM 29887343
DA 2025-01-07
ER
PT J
AU Ranhotra, HS
AF Ranhotra, Harmit S.
TI The interplay between retinoic acid receptor-related orphan receptors
and human diseases
SO JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION
LA English
DT Review
DE Orphan nuclear receptors; metabolic syndrome; autoimmunity; inflammation
ID ROR-GAMMA-T; LYMPHOID ORGAN DEVELOPMENT; NUCLEAR HORMONE-RECEPTORS;
LIVER-X-RECEPTOR; GENE-EXPRESSION; DRUG-METABOLISM; TRANSCRIPTIONAL
REGULATION; XENOBIOTIC RESPONSE; IMMUNE-RESPONSE; STRESS-RESPONSE
AB The retinoic acid receptor-related orphan receptors (RORs) are an important subfamily of transcriptional regulators of the nuclear receptors superfamily. Their discovery over a decade ago by gene cloning strategy have revealed three major isoforms of these orphan receptors in animals. Generation and analyses of isoform-specific ROR null mice have provided revealed-vital roles for the RORs in animals. The RORs undoubtedly participate in a host of biological functions such a metabolism, immunity, development and differentiation, angiogenesis, circadian clock, xenobiotic/drug metabolism and other tissue physiologies for optimal animal survival. Moreover, intense work in the last one decade also revealed a host of human diseases being modulated by the RORs. A number of diseases, such as cancer, autoimmune diseases, inflammation, osteoporosis, metabolic syndrome etc., strongly support the involvement of RORs in their onset and progression. By involving in such diseases, the RORs are indeed a critical factor for optimal cell function and are being intensely investigated as novel targets for drug interventions in the treatment of various diseases. This review focuses on the current knowledge and status about RORs in a number of human disease conditions.
C1 St Edmunds Coll, Dept Biochem, Orphan Nucl Receptors Lab, Shillong 793003, Meghalaya, India.
RP Ranhotra, HS (corresponding author), St Edmunds Coll, Dept Biochem, Orphan Nucl Receptors Lab, Shillong 793003, Meghalaya, India.
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NR 90
TC 10
Z9 12
U1 0
U2 12
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1079-9893
J9 J RECEPT SIG TRANSD
JI J. Recept. Signal Transduct.
PD AUG
PY 2012
VL 32
IS 4
BP 181
EP 189
DI 10.3109/10799893.2012.692120
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 975QM
UT WOS:000306526000002
PM 22686165
DA 2025-01-07
ER
PT J
AU Milovanovic, M
Volarevic, V
Radosavljevic, G
Jovanovic, I
Pejnovic, N
Arsenijevic, N
Lukic, ML
AF Milovanovic, Marija
Volarevic, Vladislav
Radosavljevic, Gordana
Jovanovic, Ivan
Pejnovic, Nada
Arsenijevic, Nebojsa
Lukic, Miodrag L.
TI IL-33/ST2 axis in inflammation and immunopathology
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE IL-33/ST2 axis; Con A hepatitis; EAE; MLD-STZ diabetes; Mouse breast
cancer
ID SOLUBLE ST2 PROTEIN; TUMOR-ASSOCIATED MACROPHAGES; REGULATORY T-CELLS;
LIVER-INJURY; IFN-GAMMA; DENDRITIC CELLS; ACQUIRED-IMMUNITY; INDUCED
HEPATITIS; PROTECTIVE ROLE; DUAL FUNCTION
AB Interleukin-33 (IL-33), a member of the IL-1 family of cytokines, binds to its plasma membrane receptor, heterodimeric complex consisted of membrane-bound ST2L and IL-1R accessory protein, inducing NFkB and MAPK activation. IL-33 exists as a nuclear precursor and may act as an alarmin, when it is released after cell damage or as negative regulator of NF kappa B gene transcription, when acts in an intracrine manner. ST2L is expressed on several immune cells: Th2 lymphocytes, NK, NKT and mast cells and on cells of myeloid lineage: monocytes, dendritic cells and granulocytes. IL-33/ST2 axis can promote both Th1 and Th2 immune responses depending on the type of activated cell and microenvironment and cytokine network in damaged tissue. We previously described and discuss here the important role of IL-33/ST2 axis in experimental models of type 1 diabetes, experimental autoimmune encephalomyelitis, fulminant hepatitis and breast cancer. We found that ST2 deletion enhance the development of T cell-mediated autoimmune disorders, EAE and diabetes mellitus type I. Disease development was accompanied by dominantly Th1/Th17 immune response but also higher IL-33 production, which suggest that IL-33 in receptor independent manner could promote the development of inflammatory autoreactive T cells. IL-33/ST2 axis has protective role in Con A hepatitis. ST2-deficient mice had more severe hepatitis with higher influx of inflammatory cells in liver and dominant Th1/Th17 systemic response. Pretreatment of mice with IL-33 prevented Con A-induced liver damage through prevention of apoptosis of hepatocytes and Th2 amplification. Deletion of IL-33/ST2 axis enhances cytotoxicity of NK cells, production of IFN-gamma in these cells and systemic production of IFN-gamma, IL-17 and TNF-alpha, which leads to attenuated tumor growth. IL-33 treatment of tumor-bearing mice suppresses activity of NK cells, dendritic cell maturation and enhances alternative activation of macrophages. In conclusion, we observed that IL-33 has attenuated anti-inflammatory effects in T cell-mediated responses and that both IL-33 and ST2 could be further explored as potential therapeutic targets in treatment of immune-mediated diseases.
C1 [Milovanovic, Marija; Volarevic, Vladislav; Radosavljevic, Gordana; Jovanovic, Ivan; Pejnovic, Nada; Arsenijevic, Nebojsa; Lukic, Miodrag L.] Univ Kragujevac, Ctr Mol Med & Stem Cell Res, Fac Med, Kragujevac 34000, Serbia.
C3 University of Kragujevac
RP Lukic, ML (corresponding author), Univ Kragujevac, Ctr Mol Med & Stem Cell Res, Fac Med, Svetozara Markovica 69, Kragujevac 34000, Serbia.
EM miodrag.lukic@medf.kg.ac.rs
RI Volarevic, Vladislav/ABH-8934-2020; Lukic, Miodrag/U-8848-2019;
Milovanovic, Marija/HPB-6090-2023
OI Volarevic, Vladislav/0000-0001-5948-9902; Arsenijevic,
Nebojsa/0000-0002-2107-3490; Lukic, Miodrag/0000-0002-3563-632X;
Jovanovic, Ivan/0000-0002-1169-2378; Radosavljevic,
Gordana/0000-0001-6016-0725; Volarevic, Vladislav/0000-0002-9057-9460;
Milovanovic, Marija/0000-0002-6894-1275; Pejnovic,
Nada/0000-0002-2279-9197
FU Ministry of Education and Science, Republic of Serbia [ON175069,
ON175071, ON175103]
FX This study is supported by grants ON175069, ON175071 and ON175103 from
Ministry of Education and Science, Republic of Serbia. We thank Dr.
Andrew McKenzie for providing us ST2 knockout mice and also thank Milan
Milojevic for excellent technical assistance.
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NR 97
TC 218
Z9 257
U1 3
U2 61
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD APR
PY 2012
VL 52
IS 1-2
SI SI
BP 89
EP 99
DI 10.1007/s12026-012-8283-9
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 929JN
UT WOS:000303057600010
PM 22392053
DA 2025-01-07
ER
PT J
AU Puustinen, L
Boyd, S
Mustonen, H
Arkkila, P
Arola, J
Färkkilä, M
AF Puustinen, Lauri
Boyd, Sonja
Mustonen, Harri
Arkkila, Perttu
Arola, Johanna
Farkkila, Martti
TI Prognostic value of clinical variables and liver histology for
development of fibrosis and cirrhosis in autoimmune hepatitis
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune hepatitis; liver histology; liver fibrosis; liver cirrhosis;
biopsy; prognosis
ID HEPATOCELLULAR-CARCINOMA; MANAGEMENT; DIAGNOSIS; MALIGNANCIES; AIH
AB Objective: In autoimmune hepatitis, data on the prognostic value of baseline liver biopsy and the sequential histology is controversial. Our aim was to evaluate the prognostic value of clinical variables and biopsy at the time of diagnosis and during the disease course.Materials and methods: All 98 patients in our hospital during 1995-2012 were included. Sequential biopsies were available in 66 patients. Analyses based on clinical and histological variables were performed to find parameters predicting the progression of fibrosis, and development of cirrhosis.Results: At the time of diagnosis, 7% were cirrhotic. Fibrosis progressed in 28 (42%) patients, remained stable in 26 (39%) and resolved in 12 (18%) patients. Findings which predicted fibrosis progression, were baseline total inflammation (odds ratio 1.7, 95% CI 1.01-2.8), cumulative total inflammation (1.8, 95% CI 1.01-3.2, rosette formation (2.8, 95% CI 1.1-7.1), absence of pericholangitis (0.4, 95% CI 0.1-1.0) and necrosis (1.4, 95% CI 1.0-2.0). Risk factors for the development of cirrhosis were cholestasis (4.6, 95% CI 1.2-16.9), interphase inflammation (3.4, 95% CI 1.1-10.4), and necrosis (3.3, 95% CI 1.2-9.7). In a cumulative model, cumulative total inflammation (4.5, 95% CI 1.4-15.0), necrosis (6.7, 95% CI 1.3-34.6), or cumulative immunoglobulin G load (61.8, 95% CI 2.0-1954.3) were risk factors. None of the patients with histological pericholangitis or granulomas developed cirrhosis.Conclusions: The histology provides prognostic information regarding progression of fibrosis or the development of cirrhosis. The total cumulative inflammatory activity predicts the progression of fibrosis, whereas baseline fibrosis, interphase inflammation, cholestasis, necrosis, as well as the cumulative total inflammation and cumulative immunoglobulin G, are risk factors for cirrhosis.
C1 [Puustinen, Lauri; Arkkila, Perttu; Farkkila, Martti] Helsinki Univ Hosp, Dept Med, Gastroenterol Clin, Helsinki, Finland.
[Boyd, Sonja; Arola, Johanna] Helsinki Univ Hosp, Haartman Inst & Huslab, Dept Pathol, Helsinki, Finland.
[Mustonen, Harri] Univ Helsinki, Helsinki Univ Hosp, Dept Surg, Helsinki, Finland.
[Farkkila, Martti] Univ Helsinki, Dept Gastroenterol, Helsinki, Finland.
C3 University of Helsinki; Helsinki University Central Hospital; University
of Helsinki; Helsinki University Central Hospital; University of
Helsinki; Helsinki University Central Hospital; University of Helsinki
RP Puustinen, L (corresponding author), Helsinki Univ Hosp, Haartmaninkatu 4,POB 340, Helsinki 00029, Finland.
EM lauri.puustinen@helsinki.fi
RI Färkkilä, Martti/AAG-6970-2021; Boyd, Sonja/H-9981-2016
OI Farkkila, Martti/0000-0002-0250-8559; Mustonen, Harri
Kalevi/0000-0001-5632-6796
FU Instrumentarium Research Foundation; Mary Och Georg C. Ehrnrooth
foundation; Orion-Farmos Research Foundation
FX Financial support has been received from Instrumentarium Research
Foundation, Mary Och Georg C. Ehrnrooth foundation and Orion-Farmos
Research Foundation for primary author's study leave.
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PU TAYLOR & FRANCIS LTD
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PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
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PG 7
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WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EI4UL
UT WOS:000392488800011
PM 27846740
DA 2025-01-07
ER
PT J
AU Cousin, E
Cousin, I
Aziz, K
Chailloux, P
Breton, E
AF Cousin, Elie
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Aziz, Karim
Chailloux, Pascal
Breton, Estelle
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SO PEDIATRICS
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; DIAGNOSTIC-CRITERIA; CHOLANGITIS; CHILDREN
AB Autoimmune pancreatitis (AIP) is rare in teenagers and difficult to diagnose. There are no clear and established diagnostic criteria in the pediatric population to distinguish subtype 1 and subtype 2. Here, we report the case of a 16-year-old white French teenager admitted to the pediatric emergency service with more than 1 year's history of pain originating from the epigastric and the right hypochondriac regions, with bloody diarrhea. After exclusion of pancreatic cancer and other common causes of acute pancreatitis, the diagnosis of AIP was suspected. Biological analyses revealed acute pancreatitis with severe cholestasis and an elevated level of serum immunoglobulin G4. Magnetic resonance cholangiography revealed a voluminous pancreas presenting a typical "sausage-like" aspect. Anatomopathological analyses of the liver biopsy specimen revealed a biliary obstruction due to pancreatic involvement without the typical aspect of chronic destructive cholangitis. Corticotherapy and immunosuppressive treatment proved effective after 1 week of treatment. Without a pancreatic biopsy specimen, the distinction between AIP type 1 and 2 could not be made clearly in this case. The succession of clinical observations could allow clinicians to recognize, treat, and manage AIP in children.
C1 [Cousin, Elie; Breton, Estelle] St Brieuc Hosp, Dept Pediat, 10 Rue Marcel Proust, F-22000 St Brieuc, France.
[Aziz, Karim; Chailloux, Pascal] St Brieuc Hosp, Dept Gastroenterol, St Brieuc, France.
[Cousin, Ianis] Brest Univ Hosp, Dept Pediat Surg, Brest, France.
C3 CHU Brest
RP Cousin, E (corresponding author), St Brieuc Hosp, Dept Pediat, 10 Rue Marcel Proust, F-22000 St Brieuc, France.
EM cousin.elie@live.fr
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NR 26
TC 6
Z9 7
U1 0
U2 1
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD APR
PY 2018
VL 141
SU 5
BP S456
EP S461
AR e20160765
DI 10.1542/peds.2016-0765
PG 6
WC Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics
GA HG1TH
UT WOS:000454743300016
PM 29610171
OA Bronze
DA 2025-01-07
ER
PT J
AU Zhu, QQ
Li, N
Han, QY
Li, Z
Zhang, GY
Li, F
Zhang, PP
Chen, JH
Lv, Y
Liu, ZW
AF Zhu, Qianqian
Li, Na
Han, Qunying
Li, Zhu
Zhang, Guoyu
Li, Fang
Zhang, Pingping
Chen, Jinghong
Lv, Yi
Liu, Zhengwen
TI Single-Nucleotide Polymorphism at CYP27B1-1260, but Not VDR Taq
I, Is Possibly Associated with Persistent Hepatitis B Virus Infection
SO GENETIC TESTING AND MOLECULAR BIOMARKERS
LA English
DT Article
ID VITAMIN-D-RECEPTOR; FATTY LIVER-DISEASE; T-CELLS; C VIRUS;
1,25-DIHYDROXYVITAMIN D-3; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE-DISEASE;
GENE POLYMORPHISMS; ADDISONS-DISEASE; MESSENGER-RNA
AB Background: Vitamin D, beyond its role in calcium and bone metabolism, exhibits immunomodulatory effects on innate and adaptive immune pathways and is suggestively related to liver diseases. Objective: This study investigated the association of single-nucleotide polymorphisms in genes involved in vitamin D functions with hepatitis B virus (HBV) infection. Methods: Five hundred Chinese Han subjects, including 274 chronic HBV patients, 68 HBV infection resolvers, and 158 healthy controls without HBV infection, were studied. The CYP27B1-1260 promoter and the VDR Taq I polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism. Results: Although there was no difference between HBV patients and healthy controls, HBV patients and healthy controls had a higher frequency of the CYP27B1-1260 genotype CC (15.0% vs. 2.9%, p = 0.004 and 13.3% vs. 2.9%, p = 0.006, respectively) and allele C (38.3% vs. 25.7%, p = 0.006 and 39.2% vs. 25.7%, p = 0.006, respectively) compared with resolvers. The genotype and allele frequencies of the VDR Taq I polymorphism had no difference between patients, resolvers, and healthy controls. Conclusion: These results suggest that the CYP27B1-1260 promoter polymorphism is possibly associated with the persistence, but not susceptibility to HBV infection in Chinese HBV patients, and that the VDR Taq I polymorphism is not suggested to be related to chronic HBV infection.
C1 [Zhu, Qianqian; Li, Na; Han, Qunying; Li, Zhu; Zhang, Guoyu; Li, Fang; Zhang, Pingping; Liu, Zhengwen] Xi An Jiao Tong Univ, Sch Med, Affiliated Hosp 1, Dept Infect Dis, Xian 710061, Shaanxi, Peoples R China.
[Chen, Jinghong] Xi An Jiao Tong Univ, Sch Med, Inst Endem Dis, Key Lab Environm & Genes Related Dis,Minist Educ, Xian 710061, Shaanxi, Peoples R China.
[Lv, Yi] Xi An Jiao Tong Univ, Sch Med, Affiliated Hosp 1, Dept Hepatobiliary Surg, Xian 710061, Shaanxi, Peoples R China.
[Lv, Yi; Liu, Zhengwen] Xi An Jiao Tong Univ, Inst Adv Surg Technol & Engn, Xian 710061, Shaanxi, Peoples R China.
C3 Xi'an Jiaotong University; Xi'an Jiaotong University; Xi'an Jiaotong
University; Xi'an Jiaotong University
RP Liu, ZW (corresponding author), Xi An Jiao Tong Univ, Sch Med, Affiliated Hosp 1, Dept Infect Dis, 277 Yanta W Rd, Xian 710061, Shaanxi, Peoples R China.
EM liuzhengwen@medmail.com.cn
RI Zhang, Yuanyuan/GRX-6061-2022; Li, Zhiqiang/AAI-4003-2021; yang,
zhiqi/GZL-3610-2022
FU National Natural Science Foundation of China [30972758]
FX This work was supported in part by funding from the National Natural
Science Foundation of China (Grant no. 30972758). We thank Dr. Hamad
Haider for his careful editing of the English language.
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NR 48
TC 12
Z9 14
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1945-0265
EI 1945-0257
J9 GENET TEST MOL BIOMA
JI Genet. Test. Mol. Biomark.
PD SEP
PY 2012
VL 16
IS 9
BP 1115
EP 1121
DI 10.1089/gtmb.2012.0148
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 005KO
UT WOS:000308749500022
PM 22963605
OA Green Published
DA 2025-01-07
ER
PT J
AU Arai, S
Miyazaki, T
AF Arai, Satoko
Miyazaki, Toru
TI A scavenging system against internal pathogens promoted by the
circulating protein apoptosis inhibitor of macrophage (AIM)
SO SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Review
DE Apoptosis inhibitor of macrophage; Non-professional phagocyte; Acute
kidney injury; Scavenger receptor; Macrophage; Phagocytosis
ID HEPATOCELLULAR-CARCINOMA; SPERMATOGENIC CELLS; EPITHELIAL-CELLS;
SERTOLI-CELLS; KIDNEY INJURY; RECEPTOR; PHAGOCYTOSIS;
PHOSPHATIDYLSERINE; RECOGNITION; CLEARANCE
AB An internal system designed to ward off and remove unnecessary or hazardous materials is intrinsic to animals. In addition to exogenous pathogens, a number of self-molecules, such as apoptotic or necrotic dead cells, their debris, and the oxides or peroxides of their cellular components, are recognized as extraneous substances. It is essential to eliminate these internal pathogens as quickly as possible because their accumulation can cause chronic inflammation as well as autoimmune responses, possibly leading to onset or progression of certain diseases. Apoptosis inhibitor of macrophage (AIM, also called CD5L) is a circulating protein that is a member of the scavenger receptor cysteine-rich superfamily, and we recently found that during acute kidney injury, AIM associates with intraluminal dead cell debris accumulated in renal proximal tubules and enhances clearance of luminal obstructions, thereby facilitating repair. Thus, AIM acts as a marker for phagocytes so that they can efficiently recognize and engulf the debris as their targets. In this chapter, we give an overview of the professional and non-professional phagocytes, and how soluble scavenging molecules such as AIM contribute to improvement of diseases by stimulating phagocytic activity.
C1 [Arai, Satoko; Miyazaki, Toru] Univ Tokyo, Fac Med, Ctr Dis Biol & Integrat Med, Lab Mol Biomed Pathogenesis,Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.
[Miyazaki, Toru] Japan Agcy Med Res & Dev, AMED CREST, Tokyo, Japan.
[Miyazaki, Toru] Max Planck Univ Tokyo Ctr Integrat Inflammol, Tokyo, Japan.
C3 University of Tokyo
RP Arai, S (corresponding author), Univ Tokyo, Fac Med, Ctr Dis Biol & Integrat Med, Lab Mol Biomed Pathogenesis,Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.
EM sarai@m.u-tokyo.ac.jp
OI Arai, Satoko/0000-0002-6145-8686; Miyazaki, Toru/0000-0003-3842-4362
FU AMED-CREST, Japan Agency for Medical Research Development
[JP17gm0610009, JP18gm0610009]; JSPS [16H06389, 16H05313]; Grants-in-Aid
for Scientific Research [16H06389, 16H05313] Funding Source: KAKEN
FX This work was supported by the AMED-CREST, Japan Agency for Medical
Research Development (grant numbers JP17gm0610009 and JP18gm0610009 to
T.M.) and JSPS Grants-inAid for Scientific Research ([S], grant number
16H06389 to T.M., and [B], grant number 16H05313 to S.A.).
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NR 45
TC 27
Z9 29
U1 0
U2 5
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1863-2297
EI 1863-2300
J9 SEMIN IMMUNOPATHOL
JI Semin. Immunopathol.
PD NOV
PY 2018
VL 40
IS 6
SI SI
BP 567
EP 575
DI 10.1007/s00281-018-0717-6
PG 9
WC Immunology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pathology
GA GY9WZ
UT WOS:000449004600006
PM 30310974
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Nishikawa, H
Enomoto, H
Iwata, Y
Hasegawa, K
Nakano, C
Takata, R
Nishimura, T
Yoh, K
Aizawa, N
Sakai, Y
Ikeda, N
Takashima, T
Iijima, H
Nishiguchi, S
AF Nishikawa, Hiroki
Enomoto, Hirayuki
Iwata, Yoshinori
Hasegawa, Kunihiro
Nakano, Chikage
Takata, Ryo
Nishimura, Takashi
Yoh, Kazunori
Aizawa, Nobuhiro
Sakai, Yoshiyuki
Ikeda, Naoto
Takashima, Tomoyuki
Iijima, Hiroko
Nishiguchi, Shuhei
TI Clinical significance of serum Wisteria floribunda agglutinin
positive Mac-2-binding protein level and high-sensitivity C-reactive
protein concentration in autoimmune hepatitis
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE autoimmune hepatitis; high-sensitivity C-reactive protein; inflammation
activity; liver fibrosis; Wisteria floribunda agglutinin positive
Mac-2-binding protein
ID SIMPLE NONINVASIVE INDEX; LIVER FIBROSIS; HEPATOCELLULAR-CARCINOMA;
CIRRHOSIS; PREDICT; PROGNOSIS; SEVERITY; DISEASES; ARTICLE; JAPAN
AB Aim: We aimed to examine the relationship between the Wisteria floribunda agglutinin positive Mac-2-binding protein (WFA(+)-M2BP) level and high-sensitivity C-reactive protein (hCRP) concentration and liver histological findings for patients with autoimmune hepatitis (AIH).
Methods: A total of 84 AIH patients (median age, 64 years) were analyzed. We examined the effect of pretreatment WFA(+)-M2BP level and hCRP concentration on histological findings of liver fibrosis and liver inflammation activity comparing with other laboratory markers. Receiver-operator curve (ROC) analysis was performed for calculating the area under the ROC (AUROC).
Results: The median WFA(+)-M2BP values in each fibrosis stage were: 1.5 cut-off index (COI) in F1, 2.1 in F2, 3.3 in F3 and 9.8 in F4 (P < 0.001). The median WFA(+)-M2BP values in each liver inflammation stage were: 1.6 COI in A1, 2.5 in A2 and 5.4 in A3 (P < 0.001). For predicting liver cirrhosis (F4), WFA(+)-M2BP yielded the highest AUROC (0.853). For predicting advanced liver fibrosis (F3 or F4), WFA(+)-M2BP, FIB-4 index and hyaluronic acid yielded the highest AUROC (0.747). For predicting severe liver inflammation activity (A3), WFA(+)-M2BP yielded the highest AUROC (0.739). The hCRP concentration in patients with A3 (median, 2230 ng/mL) was significantly higher than that in patients with A1 or A2 (median, 854.5 ng/mL) (P < 0.01). WFA(+)-M2BP level significantly correlated with hCRP concentration (r(s) = 0.461, P < 0.001).
Conclusion: WFA(+)-M2BP can be a useful marker for assessing liver histological findings in AIH patients and it correlated well with hCRP concentration.
C1 [Nishikawa, Hiroki; Enomoto, Hirayuki; Iwata, Yoshinori; Hasegawa, Kunihiro; Nakano, Chikage; Takata, Ryo; Nishimura, Takashi; Yoh, Kazunori; Aizawa, Nobuhiro; Sakai, Yoshiyuki; Ikeda, Naoto; Takashima, Tomoyuki; Iijima, Hiroko; Nishiguchi, Shuhei] Hyogo Coll Med, Dept Hepatobiliary & Pancreat Dis, Dept Internal Med, 1-1 Mukogawacho, Nishinomiyashi, Hyogo 6638501, Japan.
C3 Hyogo Medical University
RP Enomoto, H (corresponding author), Hyogo Coll Med, Dept Hepatobiliary & Pancreat Dis, Dept Internal Med, 1-1 Mukogawacho, Nishinomiyashi, Hyogo 6638501, Japan.
EM enomoto@hyo-med.ac.jp
FU Chugai Pharmaceutical; MSD; Dainippon Sumitomo Pharma; Ajinomoto Pharma;
Otsuka Pharmaceutical; Grants-in-Aid for Scientific Research [15K09029]
Funding Source: KAKEN
FX In the past year, Shuhei Nishiguchi received financial support from
Chugai Pharmaceutical, MSD, Dainippon Sumitomo Pharma, Ajinomoto Pharma
and Otsuka Pharmaceutical. The remaining authors declare that they have
no conflicts of interest.
CR Abe M, 2014, J GASTROENTEROL
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NR 36
TC 68
Z9 70
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD JUN
PY 2016
VL 46
IS 7
BP 613
EP 621
DI 10.1111/hepr.12596
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DS6UL
UT WOS:000380918200001
PM 26406984
DA 2025-01-07
ER
PT J
AU Lundbo, LF
Harboe, ZB
Sandholdt, H
Smith-Hansen, L
Valentiner-Branth, P
Hoffmann, S
Benfield, T
AF Lundbo, Lene Fogt
Harboe, Zitta Barrella
Sandholdt, Hakon
Smith-Hansen, Lars
Valentiner-Branth, Palle
Hoffmann, Steen
Benfield, Thomas
TI Comorbidity Increases the Risk of Invasive Meningococcal Disease in
Adults
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
DE Neisseria meningitidis; sepsis; meningitis; comorbidity
ID IMMUNIZATION PRACTICES; ADVISORY-COMMITTEE; ASPLENIC PATIENTS;
INFECTIONS; PREVENTION; RECOMMENDATIONS; IMMUNOGENICITY; VACCINES
AB In this Danish case-control-study that included >1200 cases over 4 decades, certain comorbidities increased risk of invasive meningococcal disease, ranging from a 2- to 40-fold increased risk. Vaccination and increased focus on appropriate medical care may be warranted in these populations.
Background Risk of invasive meningococcal disease (IMD) is increased in patients with complement deficiency and human immunodeficiency virus (HIV) infection. Risk associated with comorbidity is not well described. Methods This was a nationwide adult case-control study. Cases for the period 1977-2018 were identified by the national meningococcus reference laboratory. Matched controls were identified by registry linkage. Comorbidities diagnosed prior to IMD were based on the International Classification of Diseases, Eighth or Tenth Revision. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated by logistic regression after adjustment for sex, age, and other comorbidities. Results We identified 1221 cases (45% male), with a median age of 45 years (interquartile range, 22-64 years). The dominant meningococcal serogroups were B (n = 738) and C (n = 337). Increased risk of IMD was associated with solid organ transplantation (SOT) (OR 40.47 [95% CI: 4.84-337.23]), hemolytic anemia (OR 7.56 [95% CI: 2.63-21.79]), renal disease (OR 2.95 [95% CI: 1.77-4.92]), liver disease (OR 2.54 [95% CI: 1.58-4.08]), cancer (OR 2.31 [95% CI: 1.85-2.89]), diabetes (OR 1.74 [95% CI: 1.27-2.39]), neurological disease (OR 1.72 [95% CI: 1.20-2.46]), and autoimmune disease (OR 1.70 [95% CI: 1.63-2.11]). Having 1, 2, and >= 3 comorbidities was associated with increased risk of IMD (ORs 1.6-3.5). Increased risk was not associated with specific serogroups. Conclusions This study of adults with IMD over 4 decades showed increased risk of IMD associated with renal disease, immunological disorders, liver disease, cancer, and SOT ranging from a 2- to 40-fold increased risk. Vaccination may be warranted in these populations.
C1 [Lundbo, Lene Fogt; Sandholdt, Hakon; Benfield, Thomas] Copenhagen Univ Hosp Amager & Hvidovre, Ctr Res & Disrupt Infect Dis, Dept Infect Dis, Hvidovre, Denmark.
[Harboe, Zitta Barrella] Copenhagen Univ Hosp North Zealand, Dept Pulm & Infect Dis, Copenhagen, Denmark.
[Harboe, Zitta Barrella] Statens Serum Inst, Dept Microbiol Surveillance & Res, Copenhagen, Denmark.
[Harboe, Zitta Barrella; Benfield, Thomas] Univ Copenhagen, Fac Hlth Sci, Dept Clin Med, Copenhagen, Denmark.
[Smith-Hansen, Lars] Copenhagen Univ Hosp Amager & Hvidovre, Dept Clin Res, Hvidovre, Denmark.
[Valentiner-Branth, Palle] Statens Serum Inst, Dept Infect Dis Epidemiol & Prevent, Infect Dis Preparedness, Copenhagen, Denmark.
[Hoffmann, Steen] Statens Serum Inst, Dept Bacteria Parasites & Fungi, Infect Dis Preparedness, Copenhagen, Denmark.
C3 Statens Serum Institut; University of Copenhagen; Statens Serum
Institut; Statens Serum Institut
RP Lundbo, LF (corresponding author), Univ Copenhagen, Hvidovre Hosp, Dept Infect Dis 144, Kettegaard Alle 30, D-2650 Hvidovre, Denmark.
EM lene.fogt.lundbo@regionh.dk
RI Harboe, Zitta Barrella/AAZ-2569-2020
OI Benfield, Thomas/0000-0003-0698-9385; Harboe, Zitta
Barrella/0000-0001-5552-0095; valentiner-branth,
palle/0000-0002-6229-5268; Fogt Lundbo, Lene/0000-0001-8595-859X
CR [Anonymous], PCR DET CHAR BACT ME
Benamu E, 2016, CURR OPIN INFECT DIS, V29, P319, DOI 10.1097/QCO.0000000000000279
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NR 30
TC 5
Z9 6
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
EI 1537-6591
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD AUG 24
PY 2022
VL 75
IS 1
BP 125
EP 130
DI 10.1093/cid/ciab856
EA FEB 2022
PG 6
WC Immunology; Infectious Diseases; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Infectious Diseases; Microbiology
GA 3Z6FV
UT WOS:000764175600001
PM 34569601
DA 2025-01-07
ER
PT J
AU Frank, AK
Chung, BK
De Novales, MLL
Engesaeter, LK
Hoyle, HW
Ogaard, J
Heslop, J
Karlsen, TH
Tysoe, O
Brevini, T
Tchorz, JS
Vallier, L
Mohorianu, I
Sampaziotis, F
Melum, E
AF Frank, Anna Katharina
Chung, Brian K.
De Novales, Miguel Larraz Lopez
Engesaeter, Lise Katrine
Hoyle, Henry William
Ogaard, Jonas
Heslop, James
Karlsen, Tom H.
Tysoe, Olivia
Brevini, Teresa
Tchorz, Jan S.
Vallier, Ludovic
Mohorianu, Irina
Sampaziotis, Fotios
Melum, Espen
TI Single-Cell Transcriptomic Profiling of Cholangiocyte Organoids Derived
from Bile Ducts of Primary Sclerosing Cholangitis Patients
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Cholangiopathies; In vitro modeling; Single-cell sequencing;
Cholangiocarcinoma; Autoimmune liver disorders; Biliary epithelial cells
ID PLURIPOTENT STEM-CELLS; SENESCENCE; ACTIVATION; MODEL
AB Background and AimsPrimary sclerosing cholangitis (PSC) is a chronic inflammatory liver disorder without effective medical treatment which is characterized by inflammation and fibrotic structures around the bile ducts. Biliary epithelial cells (cholangiocytes) are the target and potential disease drivers in PSC, yet little is known if cholangiocytes from PSC patients differ from non-PSC controls. To characterize cholangiocytes at early rather than end-stage disease, cholangiocyte organoids (COs) were derived from diseased bile ducts of PSC patients and compared to organoids generated from disease controls.MethodsCholangiocytes were obtained during endoscopic retrograde cholangiopancreatography (ERCP) brushing of diseased bile duct areas and expanded as organoids using previously established culture methods. Stable CO lines were analyzed for cell type identity, basic cholangiocyte function, and transcriptomic signature.ResultsWe demonstrate that cholangiocytes, derived from the damaged area within the bile ducts of PSC patients, can be expanded in culture without displaying functional or genetic disease-related features. We further show that COs from patients who later were diagnosed with dysplasia exhibit higher expression of the cancer-associated genes PGC, FXYD2, MIR4435-2HG, and HES1.ConclusionsOur results demonstrate that PSC organoids are largely similar to control organoids after culture and highlight the significance of COs as a tool for regenerative medicine approaches as well as their potential for discovering new potential biomarkers for diagnosing cholangiocarcinoma.
C1 [Frank, Anna Katharina; Chung, Brian K.; Engesaeter, Lise Katrine; Hoyle, Henry William; Ogaard, Jonas; Karlsen, Tom H.; Melum, Espen] Oslo Univ Hosp Rikshosp, Norwegian PSC Res Ctr, Dept Transplantat Med, Div Surg & Specialized Med, Oslo, Norway.
[Frank, Anna Katharina; Chung, Brian K.; Engesaeter, Lise Katrine; Hoyle, Henry William; Ogaard, Jonas; Karlsen, Tom H.; Melum, Espen] Oslo Univ Hosp Rikshosp, Res Inst Internal Med, Div Surg & Specialized Med, Oslo, Norway.
[Frank, Anna Katharina; Chung, Brian K.; Hoyle, Henry William; Karlsen, Tom H.; Melum, Espen] Univ Oslo, Inst Clin Med, Fac Med, Oslo, Norway.
[Frank, Anna Katharina; Hoyle, Henry William; Melum, Espen] Univ Oslo, Inst Basic Med Sci, Hybrid Technol Hub, Oslo, Norway.
[De Novales, Miguel Larraz Lopez; Heslop, James; Tysoe, Olivia; Brevini, Teresa; Mohorianu, Irina; Sampaziotis, Fotios] Univ Cambridge, Cambridge Stem Cell Inst, Jeffrey Cheah Biomed Ctr, Wellcome Trust Med Res Council, Cambridge CB2 0AW, England.
[Engesaeter, Lise Katrine; Karlsen, Tom H.; Melum, Espen] Oslo Univ Hosp Rikshosp, Dept Transplantat Med, Div Surg & Specialized Med, Sect Gastroenterol, Oslo, Norway.
[Tysoe, Olivia; Sampaziotis, Fotios] Univ Cambridge, Dept Surg, Cambridge, England.
[Tchorz, Jan S.] Novartis Pharm AG, Novartis Inst Biomed Res, Basel, Switzerland.
[Vallier, Ludovic] Charite Univ Med Berlin, Berlin Inst Hlth, Ctr Regenerat Therapies, Berlin, Germany.
[Vallier, Ludovic] Max Plank Inst Mol Genet, Berlin, Germany.
[Sampaziotis, Fotios] Univ Cambridge, Dept Med, Cambridge, England.
[Sampaziotis, Fotios] Cambridge Univ Hosp NHS Fdn Trust, Cambridge Liver Unit, Cambridge, England.
C3 University of Oslo; National Hospital Norway; University of Oslo;
National Hospital Norway; University of Oslo; University of Oslo;
University of Cambridge; University of Oslo; National Hospital Norway;
University of Cambridge; Novartis; Berlin Institute of Health; Free
University of Berlin; Humboldt University of Berlin; Charite
Universitatsmedizin Berlin; Max Planck Society; University of Cambridge;
University of Cambridge
RP Melum, E (corresponding author), Oslo Univ Hosp Rikshosp, Norwegian PSC Res Ctr, Dept Transplantat Med, Div Surg & Specialized Med, Oslo, Norway.; Melum, E (corresponding author), Oslo Univ Hosp Rikshosp, Res Inst Internal Med, Div Surg & Specialized Med, Oslo, Norway.; Melum, E (corresponding author), Univ Oslo, Inst Clin Med, Fac Med, Oslo, Norway.; Melum, E (corresponding author), Univ Oslo, Inst Basic Med Sci, Hybrid Technol Hub, Oslo, Norway.; Melum, E (corresponding author), Oslo Univ Hosp Rikshosp, Dept Transplantat Med, Div Surg & Specialized Med, Sect Gastroenterol, Oslo, Norway.
EM espen.melum@medisin.uio.no
RI vallier, ludovic/C-6368-2011
OI Tchorz, Jan/0000-0003-1745-6621; Vallier, Ludovic/0000-0002-3848-2602
FU Scientia Fellowship European Union`s Horizon 2020 research and
innovation program
FX No Statement Available
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NR 39
TC 1
Z9 1
U1 3
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD OCT
PY 2024
VL 69
IS 10
BP 3810
EP 3823
DI 10.1007/s10620-024-08570-y
EA AUG 2024
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA J2T3X
UT WOS:001293456500001
PM 39160386
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Gül-Klein, S
Hegermann, H
Röhle, R
Schmelzle, M
Tacke, F
Schöning, W
Öllinger, R
Dziodzio, T
Maier, P
Plewe, JM
Horst, D
Sauer, IM
Pratschke, J
Lachmann, N
Eurich, D
AF Guel-Klein, Safak
Hegermann, Henriette
Roehle, Robert
Schmelzle, Moritz
Tacke, Frank
Schoening, Wenzel
Oellinger, Robert
Dziodzio, Tomasz
Maier, Patrick
Plewe, Julius M.
Horst, David
Sauer, Igor Maximilian
Pratschke, Johann
Lachmann, Nils
Eurich, Dennis
TI Donor-Specific Antibodies Against Donor Human Leukocyte Antigen are
Associated with Graft Inflammation but Not with Fibrosis Long-Term After
Liver Transplantation: An Analysis of Protocol Biopsies
SO JOURNAL OF INFLAMMATION RESEARCH
LA English
DT Article
DE human leukocyte antigen antibodies; donor-specific antibodies; liver
biopsy; liver transplantation
ID MEDIATED REJECTION; HLA ANTIBODIES; AUTOIMMUNE HEPATITIS;
IMMUNOSUPPRESSION; ALLOANTIBODIES; DYSFUNCTION; RECIPIENTS; SUBCLASS;
IMMUNITY; IMPACT
AB Background: Donor-specific antibodies (DSA) against donor human leukocyte antigen after liver transplantation, which are associated with histological changes, have been widely studied with respect to their sustained impact on transplant function. However, their long-term impact after liver transplantation remains unclear.
Methods: We performed a cross-sectional analysis from June 2016 to July 2017 that included all patients who presented themselves for scheduled follow-up after receiving a liver transplantation between September 1989 and December 2016. In addition to a liver protocol biopsy, patients were screened for human leukocyte antigen antibodies (HLAab) and donor-specific antibodies. Subsequently, the association between human leukocyte antigen antibodies, donor-specific antibodies, histologic and clinical features, and immunosuppression was analyzed.
Results: Analysis for human leukocyte antigen antibodies and donor-specific antibodies against donor human leukocyte antigen was performed for 291 and 271 patients. A significant association between higher inflammation grades and the presence of human leukocyte antigen antibodies and donor-specific antibodies was detected, while fibrosis stages remained unaffected. These results were confirmed by multivariate logistic regression for inflammation showing a significant increase for presence of human leukocyte antigen antibodies and donor-specific antibodies (OR: 4.43; 95% CI: 1.67-12.6; p=0.0035). Furthermore, the use of everolimus in combination with tacrolimus was significantly associated with the status of negative human leukocyte antigen antibodies and donor-specific antibodies. Viral etiology for liver disease, hepatocellular carcinoma (HCC) and higher steatosis grades of the graft were significantly associated with a lower rate of human leukocyte antigen antibodies. The impact of human leukocyte antigen antibodies and donor-specific antibodies against donor human leukocyte antigen was associated with higher levels of laboratory parameters, such as transaminases and bilirubin.
Conclusion: Donor-specific antibodies against donor human leukocyte antigen are associated with histological and biochemical graft inflammation after liver transplantation, while fibrosis seems to be unaffected. Future studies should validate these findings for longer observation periods and specific subgroups.
C1 [Guel-Klein, Safak; Hegermann, Henriette; Roehle, Robert; Schmelzle, Moritz; Tacke, Frank; Schoening, Wenzel; Oellinger, Robert; Dziodzio, Tomasz; Maier, Patrick; Plewe, Julius M.; Horst, David; Sauer, Igor Maximilian; Pratschke, Johann; Lachmann, Nils; Eurich, Dennis] Charite Univ Med Berlin, Berlin, Germany.
[Guel-Klein, Safak; Hegermann, Henriette; Roehle, Robert; Schmelzle, Moritz; Tacke, Frank; Schoening, Wenzel; Oellinger, Robert; Dziodzio, Tomasz; Maier, Patrick; Plewe, Julius M.; Horst, David; Sauer, Igor Maximilian; Pratschke, Johann; Lachmann, Nils; Eurich, Dennis] Free Univ Berlin, Berlin, Germany.
[Guel-Klein, Safak; Hegermann, Henriette; Roehle, Robert; Schmelzle, Moritz; Tacke, Frank; Schoening, Wenzel; Oellinger, Robert; Dziodzio, Tomasz; Maier, Patrick; Plewe, Julius M.; Horst, David; Sauer, Igor Maximilian; Pratschke, Johann; Lachmann, Nils; Eurich, Dennis] Humboldt Univ, Berlin, Germany.
[Guel-Klein, Safak; Hegermann, Henriette; Schmelzle, Moritz; Schoening, Wenzel; Oellinger, Robert; Dziodzio, Tomasz; Maier, Patrick; Plewe, Julius M.; Pratschke, Johann; Eurich, Dennis] Berlin Inst Hlth, Dept Surg, Campus Charite Mitte, Campus Virchow Klinikum, Berlin, Germany.
[Roehle, Robert; Sauer, Igor Maximilian] Berlin Inst Hlth, Inst Biometry & Clin Epidemiol, Berlin, Germany.
[Roehle, Robert] Berlin Inst Hlth, Coordinating Ctr Clin Studies, Berlin, Germany.
[Roehle, Robert] Berlin Inst Hlth BIH, Berlin, Germany.
[Tacke, Frank] Berlin Inst Hlth, Dept Hepatol & Gastroenterol, Campus Charite Mitte, Campus Virchow Klinikum, Berlin, Germany.
[Horst, David] Charite Univ Med Berlin, Berlin Inst Hlth, Inst Pathol, Berlin, Germany.
[Lachmann, Nils] Charite Univ Med Berlin, Berlin Inst Hlth, HLA Lab, Inst Transfus Med Histocompatibil & Immunogenet, Berlin, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
University of Berlin; Charite Universitatsmedizin Berlin; Free
University of Berlin; Humboldt University of Berlin; Berlin Institute of
Health; Free University of Berlin; Humboldt University of Berlin;
Charite Universitatsmedizin Berlin; Berlin Institute of Health; Berlin
Institute of Health; Berlin Institute of Health; Berlin Institute of
Health; Free University of Berlin; Humboldt University of Berlin;
Charite Universitatsmedizin Berlin; Berlin Institute of Health; Free
University of Berlin; Humboldt University of Berlin; Charite
Universitatsmedizin Berlin; Berlin Institute of Health; Free University
of Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
Berlin; University of Hamburg; University Medical Center
Hamburg-Eppendorf
RP Gül-Klein, S (corresponding author), Charite Univ Med Berlin, Dept Surg, Campus Charite Mitte, Augustenburger Pl 1, D-13353 Berlin, Germany.; Gül-Klein, S (corresponding author), Charite Univ Med Berlin, Campus Virchow Klinikum, Augustenburger Pl 1, D-13353 Berlin, Germany.
EM safak.guel@charite.de
RI Sauer, Igor/AAM-4217-2021; Öllinger, Robert/D-1538-2009; Eurich,
Dennis/AAX-8022-2021; Tacke, Frank/ABF-2212-2020
OI Schoning, Wenzel/0000-0002-0446-5126; Tacke, Frank/0000-0001-6206-0226;
Plewe, Julius Maximilian/0000-0001-6084-8837; Ollinger,
Robert/0000-0002-4499-1673; Hegermann, Henriette/0000-0002-6514-5169;
Dziodzio, Tomasz/0000-0002-3337-4573
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NR 51
TC 4
Z9 4
U1 0
U2 1
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-7031
J9 J INFLAMM RES
JI J. Inflamm. Res.
PY 2021
VL 14
BP 2697
EP 2712
DI 10.2147/JIR.S307778
PG 16
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA TA3DP
UT WOS:000667131000001
PM 34188517
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Mosolits, S
Ullenhag, G
Mellstedt, H
AF Mosolits, S
Ullenhag, G
Mellstedt, H
TI Therapeutic vaccination in patients with gastrointestinal malignancies.
A review of immunological and clinical results
SO ANNALS OF ONCOLOGY
LA English
DT Review
DE clinical effects; gastrointestinal tumours; immune response; therapy;
vaccination
ID ACTIVE SPECIFIC IMMUNOTHERAPY; COLORECTAL-CANCER PATIENTS;
COLONY-STIMULATING FACTOR; TUMOR-CELL VACCINE; HUMAN CARCINOEMBRYONIC
ANTIGEN; PHASE-I TRIAL; CD8(+) T-CELL; MONOCLONAL-ANTIBODY VACCINE;
IMMUNE-RESPONSES; DENDRITIC CELLS
AB Gastrointestinal (GI) malignancies are the most common types of human cancers. Despite the introduction of new cytotoxic drugs, a large proportion remains incurable. There is a great need to develop new complementary therapeutic modalities. Strategies exploiting targeted therapies are expanding. The focus of the present article is to review active specific immunotherapy (vaccination) in patients with GI malignancies. The review comprises a description of the immunogenicity of GI malignancies, various types of tumour antigens and mechanisms of action of cancer vaccines. Tumour escape from immune surveillance, vaccine strategies and adjuvants are also described. Clinical and immunological endpoints of cancer immunotherapy are outlined. Results of therapeutic vaccine trials published mainly during the last 5 years in PubMed enrolling a minimum of six patients with GI malignancies are included. Studies presented at the two last annual meetings of the American Society of Clinical Oncology are also covered. More than 2000 patients have been vaccinated with tumour antigens (self antigens). The procedure is safe and no autoimmune disorders have been observed after > 4 years follow-up in a substantial number of patients. Humoral and cellular tumour antigen-specific immune responses were induced. A correlation between immune responses and prolonged overall survival was seen in several studies. The most encouraging results were noted in randomised controlled phase II/III trials including over 1300 colorectal carcinoma patients with minimal residual disease. A statistically significantly improved disease-free or overall survival was shown either in all vaccinated or in sub-groups of patients. Promising results were also reported in pancreatic and hepatocellular carcinoma. If the results of the randomised controlled trials hold true, active specific immunotherapy may provide a new promising targeted therapeutic approach in GI malignancies With minimal toxicity. Further enlarged randomised controlled studies are warranted to confirm the results, particularly in colon carcinoma with minimal residual disease.
C1 Karolinska Univ Hosp, Dept Oncol, Canc Ctr Karolinska, Immune & Gene Therapy Lab, S-17176 Stockholm, Sweden.
Univ Uppsala Hosp, Dept Oncol, S-75185 Uppsala, Sweden.
C3 Karolinska Institutet; Karolinska University Hospital; Uppsala
University; Uppsala University Hospital
RP Karolinska Univ Hosp, Dept Oncol, Canc Ctr Karolinska, Immune & Gene Therapy Lab, S-17176 Stockholm, Sweden.
EM hakan.mellstedt@karolinska.se
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NR 126
TC 57
Z9 70
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD JUN
PY 2005
VL 16
IS 6
BP 847
EP 862
DI 10.1093/annonc/mdi192
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 936PM
UT WOS:000229867900002
PM 15829493
OA Bronze
DA 2025-01-07
ER
PT J
AU Shin, M
Moon, HH
Kim, JM
Park, JB
Kwon, CHD
Kim, SJ
Lee, SK
Joh, JW
AF Shin, Milljae
Moon, Hyung Hwan
Kim, Jong Man
Park, Jae Berm
Kwon, Choon Hyuck David
Kim, Sung-Joo
Lee, Suk-Koo
Joh, Jae-Won
TI Significance of True-Positive and False-Positive Pretransplantation
Lymphocytotoxic Crossmatch in Primary Liver Allograft Outcomes
SO TRANSPLANTATION
LA English
DT Article
DE Autoantibody; Graft outcome; Liver transplantation; Lymphocytotoxic
crossmatch
ID FLOW-CYTOMETRY; AUTOIMMUNE CONDITIONS; GRAFT-REJECTION; IMMUNE-SYSTEM;
TRANSPLANTATION; SURVIVAL; ANTIBODIES; RISK; RECIPIENTS; CANCER
AB Background. At the time of transplantation, a recipient's serum is tested against the prospective donor's lymphocytes to identify specific reactivity and to look for a donor-specific crossmatch (CXM). Here, we investigated the relationship between the pretransplantation lymphocytotoxic CXM results and the long-term outcome of liver transplantation at a single center.
Methods. From October 1998 to April 2011, medical records, laboratory data, and pretransplantation lymphocytotoxic CXM results were collected from 1133 consecutive liver transplant recipients.
Results. We performed liver transplantations on 80 (7.1%) patients after a true-positive CXM (t+CXM). The t+CXM group exhibited higher initial aminotransferase levels immediately after transplantation compared with a negative CXM group. However, no significant differences in rejection, biliary or vascular complications, viral disease recurrence, or de novo malignancies were found. Although overall graft and patient survival did not differ between the groups, liver-specific graft survival was inferior in the t+CXM group. It was also found that, in 42 (3.7%) recipients, initially positive results converted to final negative results after the elimination of immunoglobulin Mautoantibodies. We defined this subpopulation as a false-positive CXM. Significantly decreased posttransplantation aminotransferase levels with a higher incidence of de novo malignancies were observed in this group compared with negative controls.
Conclusion. Our findings demonstrate that t+CXM transplants show increased aspartate aminotransferase and alanine aminotransferase peak immediately after transplantation, which influences liver-specific graft outcomes. Additionally, the presence of circulating immunoglobulin M autoantibodies against recipients' own antigens may be protective in liver grafts. However, this may be a predisposing factor for de novo malignancies.
C1 [Shin, Milljae; Moon, Hyung Hwan; Kim, Jong Man; Park, Jae Berm; Kwon, Choon Hyuck David; Kim, Sung-Joo; Lee, Suk-Koo; Joh, Jae-Won] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Surg, Seoul 135710, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center
RP Joh, JW (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Surg, 50 Irwon Dong, Seoul 135710, South Korea.
EM jw.joh@samsung.com
RI Kim, Jong/AAH-5295-2020; Kwon, Choon/H-7263-2019; Kim, Sung/C-9604-2011;
park, hy/O-5934-2014
OI Kim, Jongman/0000-0002-1903-8354; Joh, Jae-Won/0000-0003-1732-6210;
Kwon, ChoonHyuck David/0000-0002-1082-3321
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NR 46
TC 10
Z9 10
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD JUN 15
PY 2013
VL 95
IS 11
BP 1410
EP 1417
DI 10.1097/TP.0b013e31828d155a
PG 8
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA 299EE
UT WOS:000330377400019
PM 23542470
OA Bronze
DA 2025-01-07
ER
PT J
AU Ezhilarasan, D
AF Ezhilarasan, Devaraj
TI Hepatotoxic potentials of methotrexate: Understanding the possible
toxicological molecular mechanisms
SO TOXICOLOGY
LA English
DT Review
DE Methotrexate; Drug induced liver injury; Psoriasis; Rheumatoid arthritis
ID INDUCED LIVER-INJURY; INDUCED OXIDATIVE STRESS; RHEUMATOID-ARTHRITIS;
TREATED PATIENTS; ASIAN PATIENTS; RISK-FACTORS; PSORIASIS; HEPATITIS;
APOPTOSIS; FIBROSIS
AB Methotrexate (MTX) is one of the most effective and widely used drugs in the management of autoimmune and dermatological diseases. Rheumatoid arthritis and psoriasis patients who are under long term MTX-therapy are at high risk of developing a liver injury. Accumulation of intracellular MTX-polyglutamate (MTX-PG), a metabolite of MTX triggers oxidative stress, inflammation, steatosis, fibrosis, and apoptosis in hepatocytes. MTX-PG causes oxidative stress in the liver by inducing lipid peroxidation thereby releasing reactive oxygen species and suppressing antioxidant response elements. MTX-PG induces several pro-inflammatory signaling pathways and cytokines such as tumor necrosis factor-alpha, nuclear factor kappa B and interleukin 6 (IL-6), IL-beta 1, IL-12. MTX-PG depletes hepatic folate level and decreases RNA and DNA synthesis leading to hepatocyte death. MTX-PG inhibits 5-aminoimidazole-4-carboxamide ribonucleotide transformylase enzyme and thereby causes accumulation of intracellular adenosine, which causes activation of hepatic stellate cells, extracellular matrix accumulation and hepatic fibrosis. MTX-PG induces hepatocytes apoptosis by activation of caspase 3 via the intrinsic pathway. Clinically, aggravation of underlying fatty liver to non-alcoholic steatohepatitis with fibrosis seems to be an important mechanism of liver injury in MTX-treated RA patients. Therefore, there is a need for monitoring liver injury in RA, psoriatic and cancer patients with NAFLD and fibrosis risk factors during MTX treatment. This review summarizes the possible molecular mechanism of MTX-induced hepatotoxicity. It may pave the way for early detection of liver injury and develop novel strategies for treating MTX mediated hepatotoxicity.
C1 [Ezhilarasan, Devaraj] Saveetha Dent Coll, Saveetha Inst Med & Tech Sci, Dept Pharmacol, Mol Med & Toxicol Div,Blue Lab, Chennai 600077, Tamil Nadu, India.
C3 Saveetha Institute of Medical & Technical Science; Saveetha Dental
College & Hospital
RP Ezhilarasan, D (corresponding author), Saveetha Dent Coll, Saveetha Inst Med & Tech Sci, Dept Pharmacol, Biomed Res Unit, 162 PH Rd, Chennai 600077, Tamil Nadu, India.; Ezhilarasan, D (corresponding author), Saveetha Dent Coll, Saveetha Inst Med & Tech Sci, Lab Anim Ctr, 162 PH Rd, Chennai 600077, Tamil Nadu, India.
EM ezhild@gmail.com
RI Devaraj, Ezhilarasan/L-1347-2015
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NR 97
TC 91
Z9 96
U1 5
U2 15
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0300-483X
J9 TOXICOLOGY
JI Toxicology
PD JUN 30
PY 2021
VL 458
AR 152840
DI 10.1016/j.tox.2021.152840
EA JUN 2021
PG 8
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA TL2FK
UT WOS:000674669100012
PM 34175381
DA 2025-01-07
ER
PT J
AU Mao, LM
Dong, HT
Yang, PZ
Zhou, HY
Huang, XK
Lin, XM
Kijlstra, A
AF Mao, Liming
Dong, Hongtao
Yang, Peizeng
Zhou, Hongyan
Huang, Xiangkun
Lin, Xiaomin
Kijlstra, Aize
TI MALDI-TOF/TOF-MS reveals elevated serum haptoglobin and amyloid A in
Behcet's disease
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE Behcet's disease; serum; Hp; SAA; VKH syndrome
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; HIGH-ABUNDANT PROTEINS;
PROTEOME ANALYSIS; MATRIX METALLOPROTEINASES; HEPATOCELLULAR-CARCINOMA;
RHEUMATOID-ARTHRITIS; CEREBROSPINAL-FLUID; MASS-SPECTROMETRY; T-CELLS;
BIOMARKERS
AB Behcet's disease (BD) is a multisystemic autoimmune disease with unclear etiology and pathogenesis. To screen aberrant serum proteins in BD, serum samples were obtained from eight male BD patients with active uveitis and eight male healthy volunteers with informed consent. The serum samples from active BD patients and normal controls were pooled. Highly abundant serum proteins (albumin and IgG) were depleted from these two samples using an affinity capture based kit. The obtained samples were subjected to two-dimensional gel electrophoresis (2-DE). Protein spots were visualized with the "blue silver" staining. Differently expressed proteins were subsequently identified by matrix-assisted laser desorption /ionization tandem time-of-flight mass spectrometry (MALDI-TOF/TOF-MS). Western blot and enzyme-linked immunosorbent assay (ELISA) were performed using the serum samples from 18 patients with active BD, 6 patients with inactive BD, 22 patients with Vogt-Koyanagi-Harada (VKH) syndrome, and 20 healthy volunteers to validate the results of 2-DE and MS. Proteomic profiles of the pooled samples were compared, and approximately 800 protein spots were observed in each of the gels. Expression levels of four of the protein spots in active BD were significantly higher than those in the normal controls. Mass spectrometric protein identification revealed that the four protein spots corresponded to two proteins: haptoglobin (Hp) and serum amyloid A (SAA). Western blot and ELISA showed that Hp was only overexpressed in active BD but not in inactive BD, VKH syndrome, or healthy controls. An obvious band of SAA was detected in 72.2% of the serum samples from BD patients, whereas a vague band of this protein was found in 10.0% of the tested normal samples and 9.1% of VKH samples. Our results revealed a significantly increased expression of Hp and SAA in serum of active BD patients. These two proteins may be involved in the development of BD.
C1 [Mao, Liming; Dong, Hongtao; Zhou, Hongyan; Huang, Xiangkun; Lin, Xiaomin] Sun Yat Sen Univ, State Key Lab Ophthalmol, Zhongshan Ophthalm Ctr, Guangzhou 510275, Guangdong, Peoples R China.
[Yang, Peizeng] Chongqing Med Univ, Affiliated Hosp 1, Chongqing, Peoples R China.
[Kijlstra, Aize] Wageningen Univ, Div Anim Prod, Anim Sci Grp, Wageningen, Netherlands.
[Kijlstra, Aize] Wageningen Univ, Div Anim Prod, Res Ctr, Wageningen, Netherlands.
[Kijlstra, Aize] Univ Maastricht, Dept Ophthalmol, Maastricht, Netherlands.
C3 Sun Yat Sen University; Chongqing Medical University; Animal Sciences
Group of Wageningen UR; Wageningen University & Research; Wageningen
University & Research; Maastricht University
RP Yang, PZ (corresponding author), Youyi Rd 1, Chongqing 400016, Peoples R China.
EM peizengy@126.com
RI Yang, Peizeng/C-6336-2013
OI Mao, Liming/0000-0002-9740-820X; Yang, Peizeng/0000-0002-2647-6619
FU National Natural Science Foundation [30400487]; Natural Science
Foundation [30630064]; International Cooperation in Science and
Technology, Guangdong province [2006A50107001]; National Supporting
Project of P. R. China [2007BAI18B10]; Ministry of Health, P.R. China
FX We thank all the patients and the controls for participating in this
study. We also thank Dr. Ju-tao Feng from Liver Cancer Institute & Zhong
Shan Hospital of Fudan University for his constructive suggestions, Mr.
Dong-jiang Liao from State Key Laboratory of Ophthalmology of Sun
Yat-sen University for technical assistance, and Mr. Xin-wen Zhou from
Proteome Research Center of Fudan University Biomedical Institute for
help in mass spectrometry analysis. This work was supported by National
Natural Science Foundation (30400487), Key Project of Natural Science
Foundation (30630064), Project of International Cooperation in Science
and Technology, Guangdong province (2006A50107001), National Supporting
Project of P. R. China (2007BAI18B10) and Clinical Key Project of
Ministry of Health, P.R. China.
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NR 52
TC 19
Z9 22
U1 0
U2 10
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
J9 J PROTEOME RES
JI J. Proteome Res.
PD OCT
PY 2008
VL 7
IS 10
BP 4500
EP 4507
DI 10.1021/pr800279m
PG 8
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 356NG
UT WOS:000259784300028
PM 18754684
DA 2025-01-07
ER
PT J
AU Liang, T
Chen, XY
Su, M
Chen, HQ
Lua, GZ
Liang, K
AF Liang, Tao
Chen, Xiaoyu
Su, Min
Chen, Hongqiu
Lua, Guozhe
Liang, Kun
TI Vitamin C exerts beneficial hepatoprotection against Concanavalin
A-induced immunological hepatic injury in mice through inhibition of
NF-κB signal pathway
SO FOOD & FUNCTION
LA English
DT Article
ID NITRIC-OXIDE SYNTHASE; INNATE IMMUNITY; LIVER-DISEASES; AUTOIMMUNE
HEPATITIS; INFLAMMATION; ACTIVATION; CANCER; CYCLOOXYGENASE-2;
TRANSCRIPTION; DYSFUNCTION
AB The present study was designed to investigate the potential benefits of vitamin C (VC) in treating immunological liver injury induced by Concanavalin A (Con A, 20 mg kg(-1)) in mice. Interestingly, VC administration significantly reduced serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total-bilirubin (T-bilirubin) in Con A-lesioned mice, while serum concentrations of albumin and total-protein (T-protein) were increased. Moreover, inflammatory cytokine profiles, such as interferon-gamma (IFN-gamma), interleukin-4 (IL-4), interleukin-6 (IL-6) and interleukin-8 (IL-8), were decreased in liver tissue by VC administration. Morphological examination showed that Con A-induced liver damage was effectively mitigated. As shown in RT-PCR assay, VC administration resulted in down-regulated mRNA expressions of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). In addition, VC contributed towards the reduction of intrahepatic tumor necrosis factor alpha (TNF-alpha) and the receptor (TNF-R) protein levels, as well as decreasing IKK beta, p-I kappa B alpha, p50 and NF-kappa B expressions; furthermore, VC blocked intranuclear DNA-binding NF-kappa B locus. Our findings show that VC effectively attenuates Con A-mediated immunotoxicity in liver tissue, through an underlying mechanism which relates to dampening of the intrahepatic NF-kappa B signal pathway, thereby reducing cytotoxicity within hepatocytes.
C1 [Liang, Tao; Lua, Guozhe] Guangxi Univ Med, Coll Stomatol, Nanning 530021, Peoples R China.
[Chen, Xiaoyu] Peoples Hosp Guangxi Zhuang Autonomous Reg, Dept Clin Pharm, Nanning 530021, Guangxi, Peoples R China.
[Su, Min] Guilin Med Univ, Fac Basic Med, Guilin 541004, Guangxi, Peoples R China.
[Chen, Hongqiu] Guigang City Peoples Hosp, Dept Pathol, Guigang 537100, Guangxi, Peoples R China.
[Liang, Kun] Guangxi Med Univ, Affiliated Hosp 1, Western Hosp, Emergency Dept, Nanning 530007, Guangxi, Peoples R China.
C3 Guangxi Medical University; Guilin Medical University; Guangxi Medical
University
RP Liang, T (corresponding author), Guangxi Univ Med, Coll Stomatol, Nanning 530021, Peoples R China.
EM liang_hospital@163.com
FU National Natural Science Foundation of China [81260343]
FX This research is supported in part by the National Natural Science
Foundation of China (no. 81260343).
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NR 39
TC 16
Z9 17
U1 2
U2 19
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 2042-6496
EI 2042-650X
J9 FOOD FUNCT
JI Food Funct.
PD SEP
PY 2014
VL 5
IS 9
BP 2175
EP 2182
DI 10.1039/c4fo00224e
PG 8
WC Biochemistry & Molecular Biology; Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Food Science & Technology
GA AO0QQ
UT WOS:000341016500021
PM 25030772
DA 2025-01-07
ER
PT J
AU Hussein, AA
Ahmed, MH
Mustafa, NG
AF Hussein, A. A.
Ahmed, Mareb H.
Mustafa, N. G.
TI Biochemical and histological investigation of azathioprine and melatonin
in rats
SO JOURNAL OF THE HELLENIC VETERINARY MEDICAL SOCIETY
LA English
DT Article
DE Azathioprine; Biochemical; Histological; Liver; Melatonin
ID INDUCED LIVER-INJURY; ANTIOXIDANT; DISEASE
AB Azathioprine (AZA) is a purine antagonist, also known as Imuran, Azasan and Azamun, is a commonly prescribed immunosuppressive drug that is used in the management of many conditions (cancer, inflammatory bowel diseases, post -transplant immunosuppression, and various autoimmune diseases). However, their therapeutic role has been under debate because of their hepatotoxicity. Monitoring liver function in patients with hepatic impairment who are taking AZA is recommended. Melatonin (MEL) is a hormone usually produced at night by the pineal gland that acts to regulate the day and night cycle. Melatonin in supplements is usually made in a lab and is frequently used for the treatment of insomnia caused by shift work and jet lag. It is a well-known natural antioxidant, improving the hepatic detoxification system. There are numerous studies investigating the effects of MEL on liver injuries. Melatonin could control proliferation, reducing apoptosis, inflammation, and suppressing autophagic cell death in different pathophysiological conditions. The current study was undertaken to determine whether MEL could improve and ameliorate structural and biochemical changes in the liver that were induced by AZA. The 24 male adult rats were grouped as follows: The first group (G1) was given normal saline orally for 4 weeks and was listed as a control, while the second group (G2) was given AZA orally (20 mg/kg B.Wt.) for 4 weeks. MEL (10 mg/kg, B.Wt.) was given to the third group (G3) for four weeks. The fourth group (G4): given AZA (20 mg/kg B.Wt.) and MEL (10 mg/kg B.Wt.) for 4 weeks. Liver sections of the AZA-treated group showed degeneration and necrosis of hepatocytes with increased numbers of kupffer cells. Group 4 showed the normal architecture of liver tissue with increased numbers of kupffer cells. The serum biochemical profiles showed an increase in serum aspartate (AST) and alanine aminotransferase (ALT) enzymes, and a reduction in albumin and total protein in the group treated with AZA, while the liver function tests in the third and fourth groups showed a nonsignificant difference from the control group. We concluded from the results of this study that AZA induces structural and biochemical changes in the liver, and these effects could be improved by the administration of MEL in the last group.
C1 [Hussein, A. A.; Mustafa, N. G.] Univ Mosul, Coll Vet Med, Dept Physiol Biochem & Pharmacol, Mosul, Iraq.
[Ahmed, Mareb H.] AlNoor Univ Coll, Bartella, Iraq.
C3 University of Mosul; Alnoor University
RP Hussein, AA (corresponding author), Univ Mosul, Coll Vet Med, Dept Physiol Biochem & Pharmacol, Mosul, Iraq.
EM ahmvet@uomosul.edu.iq
RI Mustafa, Nashaat/W-2535-2017
FU University of Mosul
FX ACKNOWLEDGMENT We would like to thank the University of Mosul for
financial support and facilities that provided for the completion this
article.
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NR 25
TC 0
Z9 0
U1 0
U2 0
PU HELLENIC VETERINARY MEDICAL SOC
PI ATHENS
PA 158 PATISSION ST, ATHENS, 112 57, GREECE
SN 1792-2720
J9 J HELL VET MED SOC
JI J. Hell. Vet. Med. Soc.
PD JAN-MAR
PY 2024
VL 75
IS 1
DI 10.12681/jhvms.31190
PG 9
WC Veterinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Veterinary Sciences
GA OR7A7
UT WOS:001209055000017
DA 2025-01-07
ER
PT J
AU Tunali-Akbay, T
Sehirli, O
Ercan, F
Sener, G
AF Tunali-Akbay, Tugba
Sehirli, Ozer
Ercan, Feriha
Sener, Goksel
TI Resveratrol Protects Against Methotrexate-Induced Hepatic Injury in Rats
SO JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES
LA English
DT Article
ID HUMAN-BLOOD; TRANS-RESVERATROL; FOLIC-ACID; TOXICITY; DEHYDROGENASES;
MELATONIN; BIOPSIES; CELLS; LIVER; TIME
AB Purpose. The aim of this study was to investigate the possible protective effect of resveratrol on some liver and blood parameters in methotrexate (MTX) induced toxicity in rats. MTX is used widely to treat various neoplastic diseases such as acute lymphoblastic leukemia, lymphoma, solid cancers, and autoimmune diseases. We hypothesized that resveratrol has a potential to decrease the oxidant damage in MTX-induced hepatic injury. Methods. Following a single dose of methotrexate (20 mg/kg, i.p.), either saline or resveratrol (10 mg/kg, orally) was administered for 5 days. After decapitation of the rats, trunk blood was obtained and the liver was removed to measure malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) and tissue factor (TF) activities and collagen content. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activity were measured in the serum samples, while TNF-alpha and total antioxidant capacity were assayed in plasma samples. Results. Our results showed that MTX administration increased the hepatic MDA levels, MPO and TF activities and collagen contents and decreased GSH, while these alterations were reversed in resveratrol-treated group. Elevated AST and ALT activities ALT and TNF-alpha level observed following MTX treatment was depressed with resveratrol.. Conclusions. The present study showed that resveratrol protects against MTX-induced hepatic injury and may be of therapeutic potential in alleviating the systemic side effects of this chemotherapeutic agent.
C1 [Tunali-Akbay, Tugba] Marmara Univ, Sch Dent, Dept Biochem, TR-34365 Istanbul, Turkey.
[Sehirli, Ozer; Sener, Goksel] Marmara Univ, Sch Pharm, Dept Pharmacol, TR-34365 Istanbul, Turkey.
[Ercan, Feriha] Marmara Univ, Sch Med, Dept Histol & Embryol, TR-34365 Istanbul, Turkey.
C3 Marmara University; Marmara University; Marmara University
RP Tunali-Akbay, T (corresponding author), Marmara Univ, Fac Dent, Dept Basic Sci, TR-34365 Istanbul, Turkey.
EM ttunali@marmara.edu.tr
RI Tunali Akbay, Tugba/AAS-4127-2020; Şehirli, Ahmet/ABA-5455-2020; Şener,
Göksel/AAN-4461-2021
OI Tunali-Akbay, Tugba/0000-0002-2091-9298; Sener,
Goksel/0000-0001-7444-6193
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NR 42
TC 77
Z9 81
U1 0
U2 11
PU CANADIAN SOC PHARMACEUTICAL SCIENCES
PI EDMONTON
PA 3118 DENTISTRY-PHARMACY CENTRE UNIV ALBERTA CAMPUS, EDMONTON, ALBERTA
T6G2N8, CANADA
SN 1482-1826
J9 J PHARM PHARM SCI
JI J. Pharm. Pharm. Sci.
PY 2010
VL 13
IS 2
BP 303
EP 310
DI 10.18433/J30K5Q
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 649QN
UT WOS:000281787800008
PM 20816014
OA gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Miron, RJ
Estrin, NE
Sculean, A
Zhang, YF
AF Miron, Richard J.
Estrin, Nathan E.
Sculean, Anton
Zhang, Yufeng
TI Understanding exosomes: Part 2-Emerging leaders in regenerative medicine
SO PERIODONTOLOGY 2000
LA English
DT Review
DE dermasomes; exosomes; immunosomes; regenerative medicine;
ultra-centrifugation
ID MESENCHYMAL STEM-CELLS; SPINAL-CORD-INJURY; PULMONARY
ARTERIAL-HYPERTENSION; POSTTRAUMATIC-STRESS-DISORDER;
ISCHEMIA-REPERFUSION INJURY; SMALL EXTRACELLULAR VESICLES; TYPE-2
DIABETES-MELLITUS; MARROW STROMAL CELLS; MSC-DERIVED EXOSOMES;
MICROGLIAL-MEDIATED NEUROINFLAMMATION
AB Exosomes are the smallest subset of extracellular signaling vesicles secreted by most cells with the ability to communicate with other tissues and cell types over long distances. Their use in regenerative medicine has gained tremendous momentum recently due to their ability to be utilized as therapeutic options for a wide array of diseases/conditions. Over 5000 publications are currently being published yearly on this topic, and this number is only expected to dramatically increase as novel therapeutic strategies continue to be developed. Today exosomes have been applied in numerous contexts including neurodegenerative disorders (Alzheimer's disease, central nervous system, depression, multiple sclerosis, Parkinson's disease, post-traumatic stress disorders, traumatic brain injury, peripheral nerve injury), damaged organs (heart, kidney, liver, stroke, myocardial infarctions, myocardial infarctions, ovaries), degenerative processes (atherosclerosis, diabetes, hematology disorders, musculoskeletal degeneration, osteoradionecrosis, respiratory disease), infectious diseases (COVID-19, hepatitis), regenerative procedures (antiaging, bone regeneration, cartilage/joint regeneration, osteoarthritis, cutaneous wounds, dental regeneration, dermatology/skin regeneration, erectile dysfunction, hair regrowth, intervertebral disc repair, spinal cord injury, vascular regeneration), and cancer therapy (breast, colorectal, gastric cancer and osteosarcomas), immune function (allergy, autoimmune disorders, immune regulation, inflammatory diseases, lupus, rheumatoid arthritis). This scoping review is a first of its kind aimed at summarizing the extensive regenerative potential of exosomes over a broad range of diseases and disorders.
C1 [Miron, Richard J.; Sculean, Anton] Univ Bern, Dept Periodontol, Bern, Switzerland.
[Estrin, Nathan E.] Adv PRF Educ, Venice, FL USA.
[Estrin, Nathan E.] Lake Erie Coll Osteopath Med, Sch Dent Med, Bradenton, FL USA.
[Zhang, Yufeng] Univ Wuhan, Dept Oral Implantol, Wuhan, Peoples R China.
C3 University of Bern; Wuhan University
RP Miron, RJ (corresponding author), Univ Bern, Dept Periodontol, Bern, Switzerland.
EM rick@themironlab.com
RI ZHANG, YAN/AAB-7383-2022
FU Universitat Bern
FX Open access funding provided by Universitat Bern.
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NR 1280
TC 8
Z9 8
U1 17
U2 30
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0906-6713
EI 1600-0757
J9 PERIODONTOL 2000
JI Periodontol. 2000
PD FEB
PY 2024
VL 94
IS 1
BP 257
EP 414
DI 10.1111/prd.12561
EA APR 2024
PG 158
WC Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dentistry, Oral Surgery & Medicine
GA RL4G8
UT WOS:001198670000001
PM 38591622
OA hybrid
DA 2025-01-07
ER
PT J
AU Grant, WB
Cross, HS
Garland, CF
Gorham, ED
Moan, J
Peterlik, M
Porojnicu, AC
Reichrath, J
Zittermann, A
AF Grant, William B.
Cross, Heide S.
Garland, Cedric F.
Gorham, Edward D.
Moan, Johan
Peterlik, Meinrad
Porojnicu, Alina C.
Reichrath, Joerg
Zittermann, Armin
TI Estimated benefit of increased vitamin D status in reducing the economic
burden of disease in western Europe
SO PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY
LA English
DT Review
DE Cancer; Cardiovascular disease; Cathelicidin; Congestive heart failure;
Diabetes mellitus; Economic burden; Infectious disease; Influenza;
Metabolic disease; Pneumonia; 25-Hydroxyvitamin D; Ultraviolet-B;
Vitamin D
ID ULTRAVIOLET-B IRRADIANCE; NUTRITION EXAMINATION SURVEY; SERUM
25-HYDROXYVITAMIN-D CONCENTRATION; RANDOMIZED CONTROLLED-TRIALS;
CANCER-MORTALITY RATES; LONG-TERM PROGNOSIS; 3RD NATIONAL-HEALTH; D
ENDOCRINE-SYSTEM; COD-LIVER OIL; D DEFICIENCY
AB Vitamin D has important benefits in reducing the risk of many conditions and diseases. Those diseases for which the benefits are well supported and that have large economic effects include many types of cancer, cardiovascular diseases, diabetes mellitus, several bacterial and viral infections, and autoimmune diseases such as multiple sclerosis. Europeans generally have low serum 25-hydroxyvitamin D [25(OH)D] levels owing to the high latitudes, largely indoor living, low natural dietary sources of vitamin D such as cold-water ocean fish, and lack of effective vitamin D fortification of food in most countries. Vitamin D dose-disease response relations were estimated from observational studies and randomized controlled trials. The reduction in direct plus indirect economic burden of disease was based on increasing the mean serum 25(OH)D level to 40 ng/ml, which could be achieved by a daily intake of 2000-3000 IU of vitamin D. For 2007, the reduction is estimated at (sic)187,000 million/year. The estimated cost of 2000-3000 IU of vitamin D3/day along with ancillary costs such as education and testing might be about (sic)10,000 million/year. Sources of vitamin D could include a combination of food fortification, supplements, and natural and artificial UVB irradiation, if properly acquired. Additional randomized controlled trials are warranted to evaluate the benefits and risks of vitamin D supplementation. However, steps to increase serum 25(OH)D levels can be implemented now based on what is already known. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Grant, William B.] Sunlight Nutr & Hlth Res Ctr SUNARC, San Francisco, CA 94164 USA.
[Garland, Cedric F.; Gorham, Edward D.] Univ Calif San Diego, Dept Family & Prevent Med 0631C, La Jolla, CA 92093 USA.
[Cross, Heide S.; Peterlik, Meinrad] Med Univ Vienna, Dept Pathophysiol, A-1090 Vienna, Austria.
[Moan, Johan; Porojnicu, Alina C.] Inst Canc Res, Dept Radiat Biol, N-0310 Oslo, Norway.
[Reichrath, Joerg] Saarland Univ Hosp, Clin Dermatol Venerol & Allergol, D-66421 Homburg, Germany.
[Zittermann, Armin] Ruhr Univ Bochum, Dept Thorac & Cardiovasc Surg, Heart & Diabet Ctr N Rhine Westfalia, D-32545 Bad Oeynhausen, Germany.
C3 University of California System; University of California San Diego;
Medical University of Vienna; Universitatsklinikum des Saarlandes; Ruhr
University Bochum
RP Grant, WB (corresponding author), Sunlight Nutr & Hlth Res Ctr SUNARC, POB 641603, San Francisco, CA 94164 USA.
EM wbgrant@infionline.net; heide.cross@meduniwien.ac.at; cgarland@ucsd.edu;
gorham@nhrc.navy.mil; johan.moan@labmed.uio.no;
meinrad.peterlik@meduniwien.ac.at; a.c.porojnicu@usit.uio.no;
hajrei@uniklinik-saarland.de; guezit@web.de
RI Peterlik, Meinrad/A-6597-2009; Cross, Heide/H-3812-2011; Grant,
William/B-8311-2009
OI Grant, William/0000-0002-1439-3285
FU European Sunlight Association; UV Foundation; Vitamin D Society (Canada)
FX W.B.G. received funding for this study from the European Sunlight
Association. He also receives funding from the UV Foundation (McLean,
VA) and has received funding from the Vitamin D Society (Canada). The
other authors have no conflicts of interest to declare.
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2008, ALTERN MED REV, V13, P153
NR 157
TC 117
Z9 130
U1 0
U2 21
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0079-6107
J9 PROG BIOPHYS MOL BIO
JI Prog. Biophys. Mol. Biol.
PD FEB-MAY
PY 2009
VL 99
IS 2-3
BP 104
EP 113
DI 10.1016/j.pbiomolbio.2009.02.003
PG 10
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Biochemistry & Molecular Biology; Biophysics
GA 502NX
UT WOS:000270468300004
PM 19268496
OA Bronze
DA 2025-01-07
ER
PT J
AU Kostadinova, F
Schwaderer, J
Sebeo, V
Brunner, T
AF Kostadinova, Feodora
Schwaderer, Juliane
Sebeo, Veronica
Brunner, Thomas
TI Why does the gut synthesize glucocorticoids?
SO ANNALS OF MEDICINE
LA English
DT Review
DE Extra-adrenal glucocorticoid synthesis; colorectal cancer; inflammatory
bowel disease; intestinal epithelium; liver receptor homolog-1
ID INTESTINAL EPITHELIAL-CELLS; INFLAMMATORY-BOWEL-DISEASE; NUCLEAR
RECEPTOR LRH-1; CROHNS-DISEASE; CORTICOSTEROID-THERAPY; THYMOCYTE
DEVELOPMENT; GENE-EXPRESSION; LUNG; STEROIDOGENESIS; MAINTENANCE
AB Glucocorticoids (GC) are steroid hormones with important implications in the treatment of various inflammatory and autoimmune diseases. At the same time GC are known to have numerous side-effects. Endogenous GC are predominantly produced by the adrenal glands, and adrenal-derived GC serve important functions in the regulation of development, metabolism, and immune regulation. The last two decades of research have led to the identification of numerous alternative sources of extra-adrenal GC synthesis. Among other tissues the intestine and lung are capable of locally producing considerable amounts of immunoregulatory GC. This local steroidogenesis in these mucosal tissues appears to be regulated by transcription factors and mediators different from those in the adrenals, likely reflecting an adaptation to the local requirements and conditions. Here we summarize the current knowledge about the extra-adrenal GC synthesis in the mucosal tissues, with special emphasis on the intestinal epithelium, and its implication on the regulation of immune homeostasis and inflammatory processes.
C1 [Kostadinova, Feodora; Schwaderer, Juliane; Sebeo, Veronica; Brunner, Thomas] Univ Konstanz, Dept Biol, D-78457 Constance, Germany.
C3 University of Konstanz
RP Brunner, T (corresponding author), Univ Konstanz, Dept Biol, Chair Biochem Pharmacol, Box 660,Univ Str 10, D-78457 Constance, Germany.
EM thomas.brunner@uni-konstanz.de
FU German Science Foundation (DFG); University of Konstanz
FX Work on the regulation of the intestinal glucocorticoid synthesis has
been supported by equipment grants from the German Science Foundation
(DFG), and grants from the University of Konstanz. The authors report no
conflicts of interest.
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NR 48
TC 30
Z9 33
U1 0
U2 14
PU INFORMA HEALTHCARE
PI NEW YORK
PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA
SN 0785-3890
EI 1365-2060
J9 ANN MED
JI Ann. Med.
PD NOV
PY 2014
VL 46
IS 7
BP 490
EP 497
DI 10.3109/07853890.2014.932920
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA AT3XW
UT WOS:000344869500005
PM 25041451
DA 2025-01-07
ER
PT J
AU Giaccone, G
Kim, C
Thompson, J
McGuire, C
Kallakury, B
Chahine, JJ
Manning, M
Mogg, R
Blumenschein, WM
Tan, MT
Subramaniam, DS
Liu, SV
Kaplan, IM
McCutcheon, JN
AF Giaccone, Giuseppe
Kim, Chul
Thompson, Jillian
McGuire, Colleen
Kallakury, Bhaskar
Chahine, Joeffrey J.
Manning, Maria
Mogg, Robin
Blumenschein, Wendy M.
Tan, Ming T.
Subramaniam, Deepa S.
Liu, Stephen V.
Kaplan, Ian M.
McCutcheon, Justine N.
TI Pembrolizumab in patients with thymic carcinoma: a single-arm,
single-centre, phase 2 study
SO LANCET ONCOLOGY
LA English
DT Article
ID CELL LUNG-CANCER; EPITHELIAL TUMORS; PD-1 BLOCKADE; SOLID TUMORS;
OPEN-LABEL; THYMOMA; CHEMOTHERAPY; MALIGNANCIES; EXPRESSION; NEOPLASMS
AB Background Treatment options are limited for patients with thymic carcinoma. These aggressive tumours are not typically associated with paraneoplastic autoimmune disorders, and strong PD-L1 expression has been reported in thymic epithelial tumours. We aimed to assess the activity of pembrolizumab, a monoclonal antibody that targets PD-1, in patients with advanced thymic carcinoma.
Methods We completed a single-arm phase 2 study of pembrolizumab in patients with recurrent thymic carcinoma who had progressed after at least one line of chemotherapy. This was a single-centre study performed at Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA. Key inclusion criteria were an Eastern Cooperative Oncology Group performance status of 0-2, no history of autoimmune disease or other malignancy requiring treatment or laboratory abnormality, and adequate organ function. Patients received 200 mg of pembrolizumab every 3 weeks for up to 2 years. The primary objective of the study was the proportion of patients who had achieved a response assessed with Response Evaluation Criteria in Solid Tumors version 1.1. Analysis was per protocol, in all eligible patients. The study is registered with ClinicalTrials. gov, number NCT02364076, and is closed to accrual; we report the final analysis.
Findings 41 patients were enrolled from March 12, 2015, to Dec 16, 2016, of whom 40 were eligible and evaluable and one was excluded because of elevated liver enzymes at screening. The median follow-up was 20 months (IQR 14-26). The proportion of patients who achieved a response was 22.5% (95% CI 10.8-38.5); one (3%) patient achieved a complete response, eight (20%) patients achieved partial responses, and 21 (53%) patients achieved stable disease. The most common grade 3 or 4 adverse events were increased aspartate aminotransferase and alanine aminotransferase (five [13%] patients each). Six (15%) patients developed severe autoimmune toxicity, including two (5%) patients with myocarditis. There were 17 deaths at the time of analysis, but no deaths due to toxicity.
Interpretation Pembrolizumab is a promising treatment option in patients with thymic carcinoma. Because severe autoimmune disorders are more frequent in thymic carcinoma than in other tumour types, careful monitoring is essential.
C1 [Giaccone, Giuseppe; Kim, Chul; Thompson, Jillian; McGuire, Colleen; Kallakury, Bhaskar; Chahine, Joeffrey J.; Manning, Maria; Tan, Ming T.; Subramaniam, Deepa S.; Liu, Stephen V.; McCutcheon, Justine N.] Georgetown Univ, Dept Oncol, Lombardi Comprehens Canc Ctr, Washington, DC USA.
[Mogg, Robin; Blumenschein, Wendy M.] Merck & Co Inc, Kenilworth, NJ USA.
[Kaplan, Ian M.] Adapt Biotechnol, Seattle, WA USA.
C3 Georgetown University; Merck & Company; Merck & Company USA
RP Giaccone, G (corresponding author), Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
EM gg496@georgetown.edu
RI Liu, Stephen/E-5688-2019
OI Liu, Stephen/0000-0002-4852-3914
FU Merck Co
FX Merck & Co.
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Weissferdt A, 2017, MODERN PATHOL, V30, P826, DOI 10.1038/modpathol.2017.6
NR 31
TC 266
Z9 279
U1 1
U2 22
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD MAR
PY 2018
VL 19
IS 3
BP 347
EP 355
DI 10.1016/S1470-2045(18)30062-7
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FX9YD
UT WOS:000426466100050
PM 29395863
OA Green Accepted
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Ghavami, S
Hashemi, M
Kadkhoda, K
Alavian, SM
Bay, GH
Los, M
AF Ghavami, S
Hashemi, M
Kadkhoda, K
Alavian, SM
Bay, GH
Los, M
TI Apoptosis in liver diseases - detection and therapeutic applications
SO MEDICAL SCIENCE MONITOR
LA English
DT Review
DE apoptosis; cirrhosis; cytochrome c; death receptors; hepatitis;
mitochondrial death pathway
ID TUMOR-NECROSIS-FACTOR; MITOCHONDRIAL PERMEABILITY TRANSITION; PRIMARY
BILIARY-CIRRHOSIS; CHRONIC HEPATITIS-C; VIRUS NS2 PROTEIN; NF-KAPPA-B;
CYTOCHROME-C; CELL-DEATH; MEDIATED APOPTOSIS; CASPASE ACTIVATION
AB The liver is continuously exposed to a large antigenic load that includes pathogens, toxins, tumor cells and dietary antigens. Amongst the hepatitis viruses, only hepatitis B virus (HBV) and hepatitis C virus (HCV) cause chronic hepatitis, which can progress to cirrhosis and hepatocellular carcinoma. Of the different antiviral defense systems employed by the tissue, apoptosis significantly contributes to the prevention of viral replication, dissemination, and persistence. Loss of tolerance to the liver autoantigens may result in autoimmune hepatitis (AIH). This review outlines the recent findings that highlight the role and mechanisms of apoptotic processes in the course of liver diseases. Among factors that contribute to liver pathology, we discuss the role of tumor necrosis factor (TNF)-alpha, HBx, ds-PKR, TRAIL, FasL, and IL-1 alpha. Since TNF and FasL-induced hepatocyte apoptosis is implicated in a wide range of liver diseases, including viral hepatitis, alcoholic hepatitis, ischemia/reperfusion liver injury, and fulminant hepatic failure, these items will be discussed in greater detail in this review. We also highlight some recent discoveries that pave the way for the development of new therapeutic strategies by protecting hepatocytes (for example by employing Bcl-2, Bcl-X-L or A1/Bfl-1, IAPs, or synthetic caspase inhibitors), or by the induction of apoptosis in stellate cells. The assessment of the severity of liver disease, as well as monitoring of patients with chronic liver disease, remains a major challenge in clinical hepatology practice. Therefore, a separate chapter is devoted to a novel cytochrome c - based method useful for the diagnosis and monitoring of fulminant hepatitis.
C1 CancerCare Manitoba, Manitoba Inst Cell Biol, Winnipeg, MB, Canada.
Univ Manitoba, Manitoba Inst Cell Biol, Dept Biochem & Med Genet, Winnipeg, MB R3E 0V9, Canada.
Zahedan Univ Med Sci, Sch Med, Dept Clin Biochem, Zahedan, Iran.
Baghyat Allah Med Univ, Sch Med, Dept Internal Med, Tehran, Iran.
C3 CancerCare Manitoba Foundation; University of Manitoba; Zahedan
University of Medical Sciences
RP Univ Manitoba, Manitoba Inst Cell Biol, Dept Biochem & Med Genet, ON60090675 McDermot Ave, Winnipeg, MB R3E 0V9, Canada.
RI Łos, Marek/C-4038-2013; Ghavami, Saeid/Q-8918-2016; Ghorashi,
Seyed/C-1529-2016; hashemi, Mohammad/H-2446-2016
OI Alavian., Seyed Moayed/0000-0002-4443-6602; Los,
Marek/0000-0001-9518-1411; Ghavami, Saeid/0000-0001-5948-508X; hashemi,
Mohammad/0000-0002-6074-7101
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NR 112
TC 86
Z9 95
U1 0
U2 6
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
SN 1643-3750
J9 MED SCI MONITOR
JI Med. Sci. Monitor
PD NOV
PY 2005
VL 11
IS 11
BP RA337
EP RA345
PG 9
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 986BG
UT WOS:000233423100023
PM 16258409
DA 2025-01-07
ER
PT J
AU Zhang, YA
Shen, XZ
Zhu, JM
Liu, TT
AF Zhang, Yi-An
Shen, Xi-Zhong
Zhu, Ji-Min
Liu, Tao-Tao
TI Extensive Metastatic Cholangiocarcinoma Associated With IgG4-Related
Sclerosing Cholangitis Misdiagnosed as Isolated IgG4-Related Sclerosing
Cholangitis A Case Report and Literature Review
SO MEDICINE
LA English
DT Article
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; ADVANCED PANCREATIC-CANCER;
CARBOHYDRATE ANTIGEN 19-9; SERUM IGG4 CONCENTRATIONS; BILIARY-TRACT
CANCER; REGULATORY T-CELLS; AUTOIMMUNE PANCREATITIS; FDG-PET/CT;
DISEASE; GEMCITABINE
AB As cholangiographic features of IgG4-related sclerosing cholangitis (IgG4-SC) resemble those of cholangiocarcinoma, it is highly confusing between the 2 conditions on the basis of cholangiographic findings. This study presents a case of extensive metastatic cholangiocarcinoma with IgG4-SC misdiagnosed as isolated IgG4-SC, and reviews recent studies of the 2 diseases.A 56-year-old man with no family history of malignant tumors or liver diseases presented with recurrent mild abdominal pain and distention for 3 months. Magnetic resonance cholangiopancreatography showed a 3.7cm nodular lesion with unclear boundary in segment VI of the liver. Serum IgG4 and CA19-9 were slightly elevated. Histopathological examination was consistent with the consensus statement on the pathology of IgG4-SC. IgG4-SC was thus considered. Due to his mild symptoms, glucocorticoid was not given at first. However, 3 months after his first admission, he had more severe abdominal pain and further elevated serum CA19-9. Actually he was found suffering from extensive metastatic cholangiocarcinoma with IgG4-SC by exploratory laparotomy.The present case serves as a reminder that extensive metastatic cholangiocarcinoma with or without IgG4-SC may be misdiagnosed as an isolated IgG4-SC case if one relies solely on elevated serum and tissue IgG4 levels. We emphasize on the importance of repeated core needle biopsy or exploratory laparoscopy/laparotomy before immunosuppressive drugs are given, and on follow-up of imaging findings and serum CA19-9 once immunosuppressive therapy is started.
C1 [Zhang, Yi-An; Shen, Xi-Zhong; Zhu, Ji-Min; Liu, Tao-Tao] Fudan Univ, Zhongshan Hosp, Dept Gastroenterol, 180 Fenglin Rd, Shanghai 200032, Peoples R China.
[Shen, Xi-Zhong] Fudan Univ, Zhongshan Hosp, Shanghai Inst Liver Dis, Shanghai 200032, Peoples R China.
[Shen, Xi-Zhong] Fudan Univ, Key Lab Med Mol Virol, Shanghai Med Coll, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University; Fudan University
RP Zhu, JM (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gastroenterol, 180 Fenglin Rd, Shanghai 200032, Peoples R China.
EM zhu.jimin@zs-hospital.sh.cn; liu.taotao@zs-hospital.sh.cn
RI Zhu, Ji-Min/HDN-1451-2022; liu, taotao/GSI-7460-2022; Shen,
Xizhong/IAQ-4843-2023
OI Zhu, Ji-Min/0000-0002-2150-473X
FU National Nature Science Foundation of China [81272388, 81301820,
81472673, 81402273]; Ministry of Education of China [20120071110058];
National Clinical Key Special Subject of China
FX This work was supported by National Nature Science Foundation of China
(no. 81272388, 81301820, 81472673, and 81402273), Doctoral Fund of
Ministry of Education of China (20120071110058), and the National
Clinical Key Special Subject of China.
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NR 45
TC 8
Z9 8
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD NOV
PY 2015
VL 94
IS 45
AR e2052
DI 10.1097/MD.0000000000002052
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DC9JJ
UT WOS:000369537400068
PM 26559312
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Zhao, LY
Yang, ZX
Zheng, MH
Shi, L
Gu, MY
Liu, G
Miao, F
Chang, Y
Huang, FH
Tang, NP
AF Zhao, Liyuan
Yang, Zixuan
Zheng, Minhui
Shi, Lei
Gu, Mengyun
Liu, Gang
Miao, Feng
Chang, Yan
Huang, Fanghua
Tang, Naping
TI Recombinant adeno-associated virus 8 vector in gene therapy:
Opportunities and challenges
SO GENES & DISEASES
LA English
DT Review
DE AAV8; Adeno-associated virus; Gene therapy; Primates; Recombinant;
Rodents
ID HEMOPHILIA-A MICE; NEUTRALIZING ANTIBODIES; EFFICIENT TRANSDUCTION;
LIVER TRANSDUCTION; PERIPHERAL VEIN; RHESUS-MONKEYS; VIRAL VECTORS;
MOUSE MODEL; AAV VECTOR; SEROTYPE-8
AB In recent years, significant breakthroughs have been made in the field of gene ther-apy. Adeno-associated virus (AAV) is one of the most promising gene therapy vectors and a powerful tool for delivering the gene of interest. Among the AAV vectors, AAV serotype 8 (AAV8) has attracted much attention for its efficient and stable gene transfection into specific tissues. Currently, recombinant AAV8 has been widely used in gene therapy research on a va-riety of diseases, including genetic diseases, cancers, autoimmune diseases, and viral diseases. This paper reviewed the applications and challenges of using AAV8 as a vector for gene ther-apy, with the aim of providing a valuable resource for those pursuing the application of viral vectors in gene therapy. 2023 The Authors. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons. org/licenses/by-nc-nd/4.0/).
C1 [Zhao, Liyuan] Anhui Univ Tradit Chinese Med, Hefei 230000, Anhui, Peoples R China.
[Zhao, Liyuan; Tang, Naping] Yangtze Delta Pharmaceut Coll, Yangtze Delta Drug Adv Res Inst, Nantong 226133, Peoples R China.
[Yang, Zixuan; Zheng, Minhui; Shi, Lei; Gu, Mengyun; Chang, Yan; Tang, Naping] Shanghai Duomirui Biotechnol Ltd, China State Inst Pharmaceut Ind, Shanghai 201203, Peoples R China.
[Zhao, Liyuan; Liu, Gang; Miao, Feng] InnoStar Biotech Nantong Co Ltd, Nantong 226133, Peoples R China.
[Huang, Fanghua] Natl Med Prod Adm, Ctr Drug Evaluat, Beijing 100022, Peoples R China.
[Tang, Naping] Shanghai Innostar Biotech Co Ltd, China State Inst Pharmaceut Ind, 199 Guoshoujing Rd, Shanghai 201203, Peoples R China.
[Huang, Fanghua] Natl Med Prod Adm, Ctr Drug Evaluat, 128 Jianguo Rd, Beijing 100022, Peoples R China.
C3 Anhui University of Chinese Medicine
RP Tang, NP (corresponding author), Shanghai Innostar Biotech Co Ltd, China State Inst Pharmaceut Ind, 199 Guoshoujing Rd, Shanghai 201203, Peoples R China.; Huang, FH (corresponding author), Natl Med Prod Adm, Ctr Drug Evaluat, 128 Jianguo Rd, Beijing 100022, Peoples R China.
EM huangfh@cde.org.cn; napingtang@innostar.cn
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NR 68
TC 11
Z9 11
U1 21
U2 42
PU KEAI PUBLISHING LTD
PI BEIJING
PA 16 DONGHUANGCHENGGEN NORTH ST, Building 5, Room 411, BEIJING, DONGCHENG
DISTRICT 100009, PEOPLES R CHINA
SN 2352-4820
EI 2352-3042
J9 GENES DIS
JI Genes Dis.
PD JAN
PY 2024
VL 11
IS 1
BP 283
EP 293
DI 10.1016/j.gendis.2023.02.010
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA P8JU1
UT WOS:001053086300001
PM 37588223
OA gold, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Roche, DEM
Chandler, KB
AF Roche, Daniel E. Marrero
Chandler, Kevin Brown
TI Clinical glycoprotein mass spectrometry: The future of disease detection
and monitoring
SO JOURNAL OF MASS SPECTROMETRY
LA English
DT Article
DE clinical; early detection; glycomics; glycopeptide; glycoproteomics;
monitoring; N-glycosylation; O-glycosylation
ID N-GLYCOSYLATION; GLYCOPEPTIDES; SERUM; GLYCOFORMS; DIAGNOSIS; MARKERS
AB Protein glycosylation is the co- and/or post-translational modification of proteins with oligosaccharides (glycans). This process is not template based and can introduce a heterogeneous set of glycan modifications onto substrate proteins. Glycan structures preserve biomolecular information from the cell, with glycoproteins from different cell types and tissues displaying distinct patterns of glycosylation. Several decades of research have revealed that glycan structures also differ between normal physiology and disease. This suggests that the information stored in glycoproteins and glycans can be utilized for disease diagnosis and monitoring. Methods that enable sensitive and site-specific measurement of protein glycosylation in clinical settings, such as nano-flow liquid chromatography tandem mass spectrometry, are therefore essential. The purpose of this perspective is to discuss recent advances in mass spectrometry and the potential of these advances to facilitate the detection and monitoring of disease-specific glycoprotein glycoforms. Glycoproteomics, the system-wide characterization of glycoprotein identity inclusive of site-specific characterization of carbohydrate modifications on proteins, and glycomics, the characterization of glycan structures, will be discussed in this context. Quantitative measurement of glycopeptide markers via parallel reaction monitoring is highlighted. The development of promising glycopeptide markers for autoimmune disease, liver disease, and liver cancer is discussed. Synthetic glycopeptide standards, ambient ionization mass spectrometry, and consideration of glyco-biomarkers in two- and three-dimensional space within tissue will be critical to the advancement of this field. The authors envision a future in which glycoprotein mass spectrometry workflows will be integrated into clinical settings, to aid in the rapid diagnosis and monitoring of disease.
C1 [Roche, Daniel E. Marrero; Chandler, Kevin Brown] Florida Int Univ, Translat Glycobiol Inst, Herbert Wertheim Coll Med, Dept Cellular & Mol Med, Miami, FL 33199 USA.
[Chandler, Kevin Brown] Florida Int Univ, Biomol Sci Inst, Miami, FL 33199 USA.
C3 State University System of Florida; Florida International University;
State University System of Florida; Florida International University
RP Chandler, KB (corresponding author), Florida Int Univ, Translat Glycobiol Inst, Herbert Wertheim Coll Med, Dept Cellular & Mol Med, Miami, FL 33199 USA.
EM kchandle@fiu.edu
RI Chandler, Kevin/AAA-4334-2020
OI Marrero Roche, Daniel Ernesto/0000-0002-8038-7748; Chandler,
Kevin/0000-0001-5514-9652
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NR 55
TC 0
Z9 0
U1 12
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1076-5174
EI 1096-9888
J9 J MASS SPECTROM
JI J. Mass Spectrom.
PD SEP
PY 2024
VL 59
IS 9
AR e5083
DI 10.1002/jms.5083
PG 6
WC Biochemical Research Methods; Chemistry, Analytical; Spectroscopy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Spectroscopy
GA D1W7U
UT WOS:001294165400001
PM 39162140
DA 2025-01-07
ER
PT J
AU Das, UN
AF Das, UN
TI Perinatal supplementation of long-chain polyunsaturated fatty acids,
immune response and adult diseases
SO MEDICAL SCIENCE MONITOR
LA English
DT Article
DE long-chain polyunsaturated fatty acids; T cells; cytokines; atopy;
asthma; adult diseases; perinatal programming; low-grade systemic
inflammation; immune response
ID GAMMA-LINOLENIC ACID; INDUCED DIABETES-MELLITUS; FISH-OIL
SUPPLEMENTATION; NECROSIS-FACTOR-ALPHA; C-REACTIVE PROTEIN; COD-LIVER
OIL; RHEUMATOID-ARTHRITIS; INDUCED CYTOTOXICITY; CHILDHOOD LEUKEMIA;
GENE-EXPRESSION
AB Both omega-6 and omega-3 long-chain polyunsaturated fatty acids (LCPUFAs) modulate T(H)1 and T(H)2 cell generation, their cytokine production, and cell proliferation and thus may serve as endogenous anti-inflammatory molecules. LCPUFAs suppress the production of tumor necrosis factor-alpha (TNF-alpha) (and so also of OX40, since it belongs to the family of TNFR) and the expression of Bcl-2, suggesting that these fatty acids have the ability to prevent/suppress autoimmune diseases. Human breast milk contains substantial amounts of both omega-3 and omega-6 fatty acids. This indicates that LCPUFAs present in human breast milk suppress the levels of OX40 and decrease the expression of Bcl-x(L) and Bcl-2 on exposure to self-antigens and thus, protects against the development of autoimmune diseases in later life. In view of this, I propose that supplementation of appropriate amounts of LCPUFAs during perinatal period protects against atopy, asthma, auto-immune diseases, type 1 and type 2 diabetes mellitus, hypertension, coronary heart disease, metabolic syndrome X, lymphomas, leukemias and other cancers, schizophrenia, depression and other adult diseases in which low-grade systemic inflammation plays a significant role. It is also likely that perinatal supplementation of LCPUFAs in adequate amounts modulates the expression of genes concerned with immune response, angiogenesis, central osmo/sodium and glucose sensors etc. This renders various tissues and organs including T cells and macrophages, endothelial cells, hypothalamic neurons, and various cardiovascular tissues to be able to counteract the pathological mechanisms that tend to induce various adult diseases by blunting the inflammatory responses in those who received adequate amounts of LCPUFAs during the perinatal period compared to those who did not.
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RP UND Life Sci, 1083 Main St, Walpole, ME 02081 USA.
EM undurti@hotmail.com
RI Das, Undurti/A-7918-2009
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2003, NATURE NEUROSCIENCE, V6, P323
NR 75
TC 27
Z9 32
U1 0
U2 3
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
SN 1643-3750
J9 MED SCI MONITOR
JI Med. Sci. Monitor
PD MAY
PY 2004
VL 10
IS 5
BP HY19
EP HY25
PG 7
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 867HN
UT WOS:000224833400001
PM 15114276
DA 2025-01-07
ER
PT J
AU Marmur, J
Bergquist, A
Stål, P
AF Marmur, Joel
Bergquist, Annika
Stal, Per
TI Liver transplantation of patients with cryptogenic cirrhosis: Clinical
characteristics and outcome
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Cryptogenic cirrhosis; liver transplantation; non-alcohol fatty liver
disease; survival
ID LONG-TERM OUTCOMES; HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC
STEATOHEPATITIS; NATURAL-HISTORY; DISEASE; OBESITY; PREVALENCE;
DIAGNOSIS; HEPATITIS; SURVIVAL
AB Objectives. Non-alcoholic fatty liver disease (NAFLD), autoimmune hepatitis (AIH) and unapparent alcohol abuse may be underlying causes of cryptogenic cirrhosis, but the frequencies of these underlying factors differ between studies. Also, previous studies have shown various outcomes after orthotopic liver transplantation (OLT) for cryptogenic cirrhosis. The aims of this study were (1) to evaluate the presence of NAFLD in patients with cryptogenic cirrhosis evaluated for OLT and (2) to compare the severity of liver disease and patient survival in OLT candidates with cryptogenic cirrhosis and those with cirrhosis of another known origin. Material and methods. Four-hundred and seventy adult patients with end-stage liver cirrhosis evaluated for OLT between 1990 and 2004 were included, of whom 39 had cryptogenic cirrhosis. Clinical, histological and laboratory data that had been prospectively collected were re-evaluated. Results. Seventeen (44%) of the cryptogenic patients had NAFLD in a previous liver biopsy and/or clinical features of the metabolic syndrome. Two patients had occult alcohol over-consumption and one patient had burnt-out AIH. Cryptogenic patients had significantly higher frequencies of diabetes, ascites, and hyponatraemia and weight loss. Patient survival was similar between cryptogenic patients and cirrhotics with a known aetiology. Conclusions. Re-evaluation of patient data discovered probable underlying aetiologies in 51% of patients with cryptogenic cirrhosis evaluated for OLT, of which NAFLD was the most common (44%). Although cryptogenic patients had a more advanced liver disease when evaluated for OLT, patient survival was similar. Recent weight loss was significantly more common in cryptogenic patients, possibly being a sign of liver decompensation and signalling a need for OLT evaluation.
C1 [Marmur, Joel] Ersta Hosp, Dept Gastroenterol & Hepatol, Karolinska Inst, S-11691 Stockholm, Sweden.
[Bergquist, Annika; Stal, Per] Karolinska Univ Hosp, Stockholm, Sweden.
C3 Karolinska Institutet; Ersta Sjukhus; Karolinska Institutet; Karolinska
University Hospital
RP Marmur, J (corresponding author), Ersta Hosp, Dept Gastroenterol & Hepatol, Karolinska Inst, Box 4619, S-11691 Stockholm, Sweden.
EM joel.marmur@erstadiakoni.se
RI Bergquist, Annika/HOH-4007-2023; Stål, Per/J-2154-2019
OI Bergquist, Annika/0000-0002-3858-6241; Stal, Per/0000-0003-2915-1964
FU Swedish Society of Medicine; Karolinska Institutet
FX This study was supported by grants from the Swedish Society of Medicine
(Bengt Ihre's fund) and from the Karolinska Institutet.
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NR 26
TC 19
Z9 20
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD JAN
PY 2010
VL 45
IS 1
BP 60
EP 69
DI 10.3109/00365520903384742
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 553CY
UT WOS:000274344000009
PM 20030578
DA 2025-01-07
ER
PT J
AU Zhou, X
Wang, F
Zhou, RJ
Song, XM
Xie, ML
AF Zhou, Xiang
Wang, Feng
Zhou, Ruijun
Song, Xiuming
Xie, Meilin
TI Apigenin: A current review on its beneficial biological activities
SO JOURNAL OF FOOD BIOCHEMISTRY
LA English
DT Review
DE apigenin; biological activity; natural products; plant flavonoids
ID BREAST-CANCER CELLS; ACUTE LUNG INJURY; ISCHEMIA/REPERFUSION INJURY;
FLAVONOID APIGENIN; INDUCED EXPRESSION; GROWTH-INHIBITION; OXIDATIVE
STRESS; PROSTATE-CANCER; DENDRITIC CELL; BLOOD-PRESSURE
AB Apigenin, identified as 4,5,7-trihydroxyflavone, is a natural flavonoid compound present in a variety of fruits, vegetables, functional foods, and medicinal plants. Many studies have revealed that apigenin has the cytostatic and cytotoxic effects on the various cancer cells, prevents the atherogenesis, hypertension, cardiac hypertrophy, ischemia/reperfusion-induced heart injury, and autoimmune myocarditis, protects the chemicals- and ischemia/reperfusion-induced liver injury, inhibits the asthma, bleomycin-induced pulmonary fibrosis, abnormal behavior, and oxygen and glucose deprivation/reperfusion-induced neural cell apoptosis, improves the pancreatitis, type 2 diabetes and its complication, osteoporosis, and collagen-induced arthritis. These biological effects suggest that apigenin may be a potential health promoting agent. In the article, we will review these effects and possible biochemical mechanisms.
Practical applicationsApigenin-rich chamomile, propolis, and garlic oil have been used in the prevention ane cure of hypertension and chemicals-induced liver injury as food supplements. However, their bioactive components and mechanisms have not been fully elucidated. Apigenin may be a common effective component and play an important role in the process of therapy. In addition, apigenin itself may also be considered as a potential functional food, but the further development will be needed to apply to the prevention and treatment of some-related diseases in the future.
C1 [Zhou, Xiang; Wang, Feng; Zhou, Ruijun; Xie, Meilin] Soochow Univ, Dept Pharmacol, Coll Pharmaceut Sci, Jiangsu Key Lab Prevent & Translat Med Geriatr Di, 199 Renai Rd,Suzhou Ind Pk, Suzhou 215123, Jiangsu, Peoples R China.
[Song, Xiuming] Lianyungang Runzhong Pharmaceut Co Ltd, Lianyungang 222069, Jiangsu, Peoples R China.
C3 Soochow University - China
RP Xie, ML (corresponding author), Soochow Univ, Dept Pharmacol, Coll Pharmaceut Sci, Jiangsu Key Lab Prevent & Translat Med Geriatr Di, 199 Renai Rd,Suzhou Ind Pk, Suzhou 215123, Jiangsu, Peoples R China.
EM xiemeilin@suda.edu.cn
RI WANG, FENG/AFQ-3739-2022
OI Wang, Feng/0000-0001-7203-0098
FU Science and Technology Funds of Jiangsu Province [BY2015039-09]
FX Science and Technology Funds of Jiangsu Province, Grant/Award Number:
BY2015039-09
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NR 89
TC 87
Z9 94
U1 6
U2 79
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-8884
EI 1745-4514
J9 J FOOD BIOCHEM
JI J. Food Biochem.
PD AUG
PY 2017
VL 41
IS 4
AR e12376
DI 10.1111/jfbc.12376
PG 11
WC Biochemistry & Molecular Biology; Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Food Science & Technology
GA FC8IU
UT WOS:000407085800005
OA gold
DA 2025-01-07
ER
PT J
AU Kim, WJ
Kim, GR
Cho, HJ
Choi, JM
AF Kim, Won-Ju
Kim, Gil-Ran
Cho, Hyun-Jung
Choi, Je-Min
TI The Cysteine-Containing Cell-Penetrating Peptide AP Enables Efficient
Macromolecule Delivery to T Cells and Controls Autoimmune
Encephalomyelitis
SO PHARMACEUTICS
LA English
DT Article
DE T cell; immune regulation; cell-penetrating peptide; AP; CTLA-4;
multiple sclerosis; experimental autoimmune encephalomyelitis EAE; drug
delivery system
ID ATOPIC-DERMATITIS; PROTEIN; LOCALIZATION; ENDOCYTOSIS; CANCER
AB T cells are key immune cells involved in the pathogenesis of several diseases, rendering them important therapeutic targets. Although drug delivery to T cells is the subject of continuous research, it remains challenging to deliver drugs to primary T cells. Here, we used a peptide-based drug delivery system, AP, which was previously developed as a transdermal delivery peptide, to modulate T cell function. We first identified that AP-conjugated enhanced green fluorescent protein (EGFP) was efficiently delivered to non-phagocytic human T cells. We also confirmed that a nine-amino acid sequence with one cysteine residue was the optimal sequence for protein delivery to T cells. Next, we identified the biodistribution of AP-dTomato protein in vivo after systemic administration, and transduced it to various tissues, such as the spleen, liver, intestines, and even to the brain across the blood-brain barrier. Next, to confirm AP-based T cell regulation, we synthesized the AP-conjugated cytoplasmic domain of CTLA-4, AP-ctCTLA-4 peptide. AP-ctCTLA-4 reduced IL-17A expression under Th17 differentiation conditions in vitro and ameliorated experimental autoimmune encephalomyelitis, with decreased numbers of pathogenic IL-17A(+)GM-CSF+ CD4 T cells. These results collectively suggest the AP peptide can be used for the successful intracellular regulation of T cell function, especially in the CNS.
C1 [Kim, Won-Ju; Kim, Gil-Ran; Cho, Hyun-Jung; Choi, Je-Min] Hanyang Univ, Dept Life Sci, Coll Nat Sci, Seoul 04763, South Korea.
[Kim, Won-Ju; Kim, Gil-Ran; Cho, Hyun-Jung; Choi, Je-Min] Hanyang Univ, Res Inst Nat Sci, Seoul 04763, South Korea.
[Choi, Je-Min] Hanyang Univ, Res Inst Convergence Basic Sci, Seoul 04763, South Korea.
C3 Hanyang University; Hanyang University; Hanyang University
RP Choi, JM (corresponding author), Hanyang Univ, Dept Life Sci, Coll Nat Sci, Seoul 04763, South Korea.; Choi, JM (corresponding author), Hanyang Univ, Res Inst Nat Sci, Seoul 04763, South Korea.; Choi, JM (corresponding author), Hanyang Univ, Res Inst Convergence Basic Sci, Seoul 04763, South Korea.
EM kwj8996@gmail.com; godqhr3079@gmail.com; chohj730@hanmail.net;
jeminchoi@hanyang.ac.kr
OI Kim, Wonju/0000-0002-1800-0485
FU Bio and Medical Technology Development Program of the National Research
Foundation - Korean government [NRF-2017M3A9C8027972]; Basic Science
Research Program of the National Research Foundation - Korean government
[NRF-2019R1A2C3006155, NRF-2020R1A4A1018398]; Original Technology
Research Program for Brain Science of the National Research Foundation -
Korean government [NRF-2019M3C7A1032655]
FX This research was supported by grants awarded to J.-M.C. from the Bio
and Medical Technology Development Program (NRF-2017M3A9C8027972), the
Basic Science Research Program (NRF-2019R1A2C3006155,
NRF-2020R1A4A1018398), and the Original Technology Research Program for
Brain Science (NRF-2019M3C7A1032655) of the National Research Foundation
funded by the Korean government.
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NR 41
TC 7
Z9 7
U1 3
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD AUG
PY 2021
VL 13
IS 8
AR 1134
DI 10.3390/pharmaceutics13081134
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA UI0DQ
UT WOS:000690289800001
PM 34452095
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Miyachi, K
Hosaka, H
Nakamura, N
Miyakawa, H
Mimori, T
Shibata, M
Matsushima, S
Chinoh, H
Horigome, T
Hankins, RW
Zhang, M
Fritzler, MJ
AF Miyachi, K
Hosaka, H
Nakamura, N
Miyakawa, H
Mimori, T
Shibata, M
Matsushima, S
Chinoh, H
Horigome, T
Hankins, RW
Zhang, M
Fritzler, MJ
TI Anti-p97/VCP antibodies: An autoantibody marker for a subset of primary
biliary cirrhosis patients with milder disease?
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID VALOSIN-CONTAINING PROTEIN; NUCLEAR-PORE COMPLEX; ENVELOPE; PROGRESSION;
SERA; EXPRESSION; PROGNOSIS; CARCINOMA; RECOGNIZE; EXTRACTS
AB We previously reported that 12.5% of primary biliary cirrhosis (PBC) sera reacted with a 95 kDa cytosol protein (p95c) that was subsequently identified as a p97/valosin-containing protein (VCP). The clinical features and course of the six anti-p97/VCP-positive PBC patients with Scheuer's stage 1 and 2 liver biopsies were monitored for an average of 15 years. This group was compared with 50 PBC patients that did not have detectable anti-VCP. Autoantibodies to a full-length recombinant p97/VCP were assayed by immunoprecipitation. All six PBC patients with anti-VCP had antibodies to the mitochondrial pyruvate dehydrogenase complex-E2 antigen as measured by an addressable laser bead immunoassay. The first was a male with no evidence of liver failure that died of cerebral infarction at the age of 85. The second was a 73-year-old female with Hashimoto's thyroiditis who has remained clinically stable without ursodeoxycolic acid (UDCA) treatment. Although the third had no HCV antibodies, he developed hepatocellular carcinoma at the age of 76 and died of renal failure at 78. The fourth was a 50-year-old female who remained clinically stable during follow-up and the fifth with Hashimoto's thyroiditis and stable liver function following UCDA treatment. The sixth was a male patient presenting a mild clinical course. The clinical course of these patients was in contrast to the 50 comparison group PBC patients who did not have anti-p97/VCP. As the six PBC patients with anti-p97/VCP antibodies had slowly progressive liver disease and no mortality related to autoimmune liver disease, our observations suggest that this autoantibody might be an indicator of a favourable prognosis.
C1 Hlth Sci Res Inst Inc, Diagnost Div 1, Yokohama, Kanagawa, Japan.
Saiseikai Nanbu Hosp, Dept Gastroenterol & Pathol, Yokohama, Kanagawa, Japan.
Teikyo Univ, Sch Med, Dept Internal Med 4, Mizonokuchi Hosp, Kawasaki, Kanagawa, Japan.
Kyoto Univ, Grad Sch Med, Kyoto, Japan.
Kanto Med Ctr NTT EC, Tokyo, Japan.
Natl Yokohama Med Ctr, Yokohama, Kanagawa, Japan.
Niigata Univ, Fac Sci, Niigata 95021, Japan.
Univ Calgary, Fac Med, Calgary, AB, Canada.
C3 Teikyo University; Kyoto University; Kanto Medical Center NTT EC;
Niigata University; University of Calgary
RP Hlth Sci Res Inst Inc, Hodogaya Ku, 106 Godo Cho, Yokohama, Kanagawa 2400005, Japan.
EM mkiyomitsumd_8@hotmail.com
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NR 36
TC 20
Z9 21
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAY
PY 2006
VL 63
IS 5
BP 376
EP 382
DI 10.1111/j.1365-3083.2006.01747.x
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 036SZ
UT WOS:000237097000008
PM 16640662
DA 2025-01-07
ER
PT J
AU Liu, ZY
Bao, ZY
Yu, B
Chen, LH
Yang, GR
AF Liu, Zhaiyi
Bao, Zhiyue
Yu, Bo
Chen, Lihong
Yang, Guangrui
TI Pemetrexed ameliorates Con A-induced hepatic injury by restricting M1
macrophage activation
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Pemetrexed; Concanavalin A; Liver injury; Macrophage; NF-kappa B
ID CELL LUNG-CANCER; LIVER-INJURY; KUPFFER CELLS; MECHANISMS; MODELS;
CHEMOTHERAPY; CARBOPLATIN; PATHWAY
AB Autoimmune hepatitis (AIH), characterized by immune-driven liver destruction and cytokine production, is a progressive inflammatory liver condition that may progress to hepatic cirrhosis or tumors. However, the underlying mechanism is not well understood, and the treatment options for this disease are limited. Pemetrexed (PEM), a clinically used anti-folate drug for treating various tumors, was found to inhibit the nuclear factor (NF)-kappa B signaling pathways that exert an important role in the development of AIH. Here, we investigated the impact of PEM on immune-mediated hepatic injuries using a murine model of Concanavalin A (Con A)-induced hepatitis, a well-established model for AIH.Mice received intraperitoneal PEM injections 3 times at 12-hour intervals, and two hours later, they were challenged with Con A. Liver samples and serum were collected after 10 h. The results indicate that PEM significantly improved mouse survival rates and lowered serum transaminase levels. Moreover, PEM effectively alleviated oxidative stress, reduced histopathological liver damage, and mitigated hepatocyte apoptosis. Notably, it reduced the activation of M1-type macrophages in the liver. The expression of proinflammatory cytokines and genes associated with M1 macrophages, such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-12, IL-1 beta, and inducible nitric oxide synthase (iNOS), was also decreased. Finally, the results indicated that PEM regulates M1 macrophage activation by modulating the NF-kappa B signaling pathways.Overall, these results demonstrate that PEM effectively guards against immune-mediated hepatic injuries induced by Con A by inhibiting M1 macrophage activation through the NF-kappa B signaling pathways and indicate the potential of PEM as a practical treatment option for AIH in clinical settings.
C1 [Liu, Zhaiyi; Yang, Guangrui] Shanghai Univ Med & Hlth Sci, Affiliated Zhoupu Hosp, Shanghai, Peoples R China.
[Liu, Zhaiyi; Bao, Zhiyue; Yang, Guangrui] Dalian Univ Technol, Sch Bioengn, Dalian, Liaoning, Peoples R China.
[Yu, Bo; Yang, Guangrui] Shanghai Univ Med & Hlth Sci, Sch Clin Med, Shanghai, Peoples R China.
[Chen, Lihong] East China Normal Univ, Hlth Sci Ctr, Shanghai, Peoples R China.
C3 Shanghai University of Medicine & Health Sciences; Dalian University of
Technology; Shanghai University of Medicine & Health Sciences; East
China Normal University
RP Yang, GR (corresponding author), Shanghai Univ Med & Hlth Sci, Affiliated Zhoupu Hosp, Shanghai, Peoples R China.
EM guangrui.yang@hotmail.com
RI Yu, Hua/B-8854-2012; YANG, GUANGRUI/JCD-8873-2023; Yang,
Guangrui/F-9693-2013
OI Yang, Guangrui/0000-0002-8310-8257
FU National Natural Science Foundation of China [32171165, 31871190]
FX Funding This work was supported by grants from the National
Natural Science Foundation of China (32171165, 31871190) .
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NR 42
TC 1
Z9 1
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD DEC
PY 2023
VL 125
AR 111158
DI 10.1016/j.intimp.2023.111158
EA NOV 2023
PN A
PG 11
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA Z4QJ2
UT WOS:001111935700001
PM 37925950
DA 2025-01-07
ER
PT J
AU Jiffry, MZM
Pires, FC
Perozo, MA
Rangsipat, N
Tabares, D
AF Jiffry, Mohamed Zakee Mohamed
Pires, Felipe Carmona
Perozo, Maria A.
Rangsipat, Napat
Tabares, Daniel
TI A Rare Case of Pertuzumab-Induced Toxic Epidermal Necrolysis
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE anti-her2 therapy; autoimmune blistering skin disease; toxic epidermal
necrolysis (ten); pertuzumab; her-2 positive breast cancer
ID STEVENS-JOHNSON-SYNDROME; MANAGEMENT
AB Pertuzumab is a targeted therapy drug that is employed in the management of human epidermal growth factor receptor 2 (HER2)-positive breast cancer and works by blocking the ability of cancer cells to receive growth and proliferation signals. Toxic epidermal necrolysis (TEN) is a severe cutaneous manifestation characterized by widespread erythema, necrosis, and bullous detachment of the skin involving more than 10% of the body surface area (BSA) and may be precipitated by an immunologic response to the administration of certain medications. However, TEN development as a consequence of HER2 inhibitor therapy has not been described in the existing literature. A 44-year-old female with a history of metastatic breast cancer to the liver presented with a diffuse blistering rash following a first-time administration of pertuzumab three days prior. Her rash began as painful and pruritic blisters 12 hours after the last infusion of pertuzumab and progressed to involve her arms, chest, groin, and thighs with a positive Nikolsky sign. She was managed supportively with high-dose steroids and antihistamines, and although her hospital course was complicated by hypotension requiring pressor support, she gradually made a full recovery and was released to a rehabilitation facility.
C1 [Jiffry, Mohamed Zakee Mohamed; Pires, Felipe Carmona; Perozo, Maria A.] Danbury Hosp, Internal Med, Danbury, CT 06810 USA.
[Rangsipat, Napat] Amer Univ Caribbean, Sch Med, Cupecoy, Sint Maarten.
RP Jiffry, MZM (corresponding author), Danbury Hosp, Internal Med, Danbury, CT 06810 USA.
EM zakeejiffry@gmail.com
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NR 12
TC 0
Z9 0
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD MAY 31
PY 2023
VL 15
IS 5
AR e39797
DI 10.7759/cureus.39797
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA K8EW9
UT WOS:001018725800003
PM 37398793
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Kekilli, M
Tunc, B
Beyazit, Y
Kurt, M
Onal, IK
Ulker, A
Haznedaroglu, IC
AF Kekilli, Murat
Tunc, Bilge
Beyazit, Yavuz
Kurt, Mevlut
Onal, Ibrahim Koral
Ulker, Aysel
Haznedaroglu, Ibrahim Celalettin
TI Circulating CD4+CD25+ Regulatory T Cells in the Pathobiology of
Ulcerative Colitis and Concurrent Primary Sclerosing Cholangitis
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Ulcerative colitis; Primary sclerosing cholangitis; CD4+CD25+T cells;
Pathophysiology
ID LIVER-TRANSPLANTATION; PATIENT; PROCTOCOLECTOMY; EXPANSION; CANCER
AB Immunopathogenetic features of primary sclerosing cholangitis (PSC) in ulcerative colitis (UC) still remains unclear. Peripheral blood CD4+CD25+ regulatory T cells have a key role in the induction and maintenance of peripheral self-tolerance and inhibit several organ-specific autoimmune diseases. Therefore, CD4+CD25+ T cells are believed to play an essential role in autoimmune diseases. The aim of the present study is to analyze the role of CD4+CD25+ T cells in the pathogenesis of UC-associated PSC.
This study evaluated the levels of CD4+CD25+ T cells in peripheral blood mononuclear cells (PBMC) of 27 UC patients with PSC and 20 UC patients as controls. CD4+CD25+ T cells were isolated from PBMC with a direct immunofluorescence technique, using mice monoclonal antibodies namely FITC-labeled anti-CD4 and PE-labeled anti-CD25. In each patient, CD4+CD25+ T cells percentage in PBMC were studied by flow cytometry, and then the number of CD4+CD25+ T cells were calculated.
Twenty-seven UC patients with PSC and 20 UC patients without PSC as controls were enrolled in the present study. The percentage of CD4+CD25+ regulatory T cells among PBMC were significantly elevated in UC + PSC patients compared with UC patients without PSC (p = 0.04).
CD4+CD25+ T cells were found to be elevated in UC patients with PSC suggesting a partial role of activated T cell response in the disease pathophysiology. Our findings imply that CD4+CD25+ regulatory T cells may play a key role in the immunopathogenesis of UC-associated PSC and may affect the therapeutic management of these diseases.
C1 [Kekilli, Murat; Tunc, Bilge; Beyazit, Yavuz; Kurt, Mevlut; Onal, Ibrahim Koral; Ulker, Aysel] Turkiye Yuksek Ihtisas Training & Res Hosp, Dept Gastroenterol, TR-06100 Ankara, Turkey.
[Haznedaroglu, Ibrahim Celalettin] Hacettepe Univ, Dept Hematol, Ankara, Turkey.
C3 Turkey Specialized Higher Education & Research Hospital; Hacettepe
University
RP Kekilli, M (corresponding author), Turkiye Yuksek Ihtisas Training & Res Hosp, Dept Gastroenterol, Kizilay Sok 2, TR-06100 Ankara, Turkey.
EM drkekilli@gmail.com
RI kekilli, murat/H-2770-2016; Kurt, Mevlut/Q-2093-2015; Beyazit,
Yavuz/AAI-5785-2021; Haznedaroglu, Ibrahim/AAB-2114-2019; Haznedaroglu,
Ibrahim C./B-7408-2009
OI Haznedaroglu, Ibrahim C./0000-0001-8028-9462
CR Berglund D, 2012, TRANSPL IMMUNOL, V26, P27, DOI 10.1016/j.trim.2011.09.003
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NR 28
TC 9
Z9 9
U1 0
U2 9
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD MAY
PY 2013
VL 58
IS 5
BP 1250
EP 1255
DI 10.1007/s10620-012-2511-y
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 149VU
UT WOS:000319350300016
PM 23306841
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Lilford, RJ
Bentham, L
Girling, A
Litchfield, I
Lancashire, R
Armstrong, D
Jones, R
Marteau, T
Neuberger, J
Gill, P
Cramb, R
Olliff, S
Arnold, D
Khan, K
Armstrong, MJ
Houlihan, DD
Newsome, PN
Chilton, PJ
Moons, K
Altman, D
AF Lilford, R. J.
Bentham, L.
Girling, A.
Litchfield, I.
Lancashire, R.
Armstrong, D.
Jones, R.
Marteau, T.
Neuberger, J.
Gill, P.
Cramb, R.
Olliff, S.
Arnold, D.
Khan, K.
Armstrong, M. J.
Houlihan, D. D.
Newsome, P. N.
Chilton, P. J.
Moons, K.
Altman, D.
TI Birmingham and Lambeth Liver Evaluation Testing Strategies (BALETS): a
prospective cohort study
SO HEALTH TECHNOLOGY ASSESSMENT
LA English
DT Article
ID HEPATITIS-C VIRUS; PRIMARY-CARE; ASYMPTOMATIC PATIENTS; ALANINE
AMINOTRANSFERASE; MULTIPLE IMPUTATION; GENERAL-POPULATION;
COST-EFFECTIVENESS; MISSING DATA; ILLNESS PERCEPTIONS;
ALCOHOL-CONSUMPTION
AB Objective: To evaluate mildly abnormal liver function test (LFT) results in general practice among patients who do not have known liver disease.
Design: Prospective cohort study of people with abnormal LFT results identified in primary care. Participants were intensively investigated using a common protocol and followed up for 2 years. Substudies investigated the psychological sequelae of abnormal test results, clinicians' reasons for testing, decision options when LFT results were abnormal and early detection of liver fibrosis.
Setting: Eleven primary-care practices: eight in Birmingham and three in Lambeth.
Participants: Adults with abnormal LFT results who did not have pre-existing or obvious liver disease. Eight analytes were included in the panel of LFTs.
Main outcome measures: Statistical tests were used to identify the interactions between clinical features, the initial pattern of abnormal LFT results and (1) specific viral, genetic and autoimmune diseases, such as viral hepatitis, haemochromatosis and primary biliary cirrhosis; (2) a range of other serious diseases, such as metastatic cancer and hypothyroidism; (3) 'fatty liver' not associated with the above; and (4) the absence of detectable disease.
Results: Fewer than 5% of people with abnormal LFT results had a specific disease of the liver, and many of these were unlikely to need treatment. The diagnostic potential of the LFT panel is largely subsumed into just two analytes: alanine aminotransferase (ALT) and alkaline phosphatase (ALP). Gamma-glutamyltransferase (GGT) offers a small increase in sensitivity at the margin at the cost of a large loss of specificity. Eighty-four per cent of abnormal LFT results remain abnormal on retesting 1 month later. In many cases, carrying out a definitive or specific test will be more efficient than repeating LFTs, with a view to specific testing only if the test remains abnormal. An ultrasound diagnosis of 'fatty liver' was present in nearly 40% of patients with abnormal LFTs and a small amount of weight loss over 2 years was associated with a reduced incidence of liver fat. There was a J-shaped relationship between alcohol intake and fatty liver in men. An abnormal LFT result causes temporary anxiety, which does not appear to promote sustained behaviour change.
Conclusions: Liver disease is rare among people with abnormal LFT results in primary care. Only two analytes (ALT and ALP) are helpful in identifying the majority of liver disease. GGT adds little information in return for a high false-positive rate but it is sensitive to alcohol intake. LFT results seldom revert from abnormal to normal over a 1-month period, and modelling shows that repeating an abnormal LFT panel, as recommended in the current guidelines, is inefficient. LFTs are often undertaken to meet perceived patient need for a blood test, but as they are neither specific nor indicative of any particular disease they are among the least suitable tests for this purpose. Obesity and raised ALT provide strong evidence for a presumptive diagnosis of 'fatty' liver. Abnormal LFTs and 'fatty' liver provoke only short-term anxiety and neither is associated with sustained weight loss. Even a small amount of weight loss reduces liver fat.
Future work recommendations: (1) the cases of 'fatty liver' and controls should be followed up in the long term to identify features that predict development of hepatosteatosis and then cirrhosis; (2) the acceptability of replacing the traditional six- to eight-analyte LFT panel with a drop down menu including the ALT/ALP combination should be evaluated.
C1 [Lilford, R. J.; Bentham, L.; Girling, A.; Litchfield, I.; Lancashire, R.; Neuberger, J.; Gill, P.; Chilton, P. J.] Univ Birmingham, Sch Hlth & Populat Sci, Edgbaston, England.
[Armstrong, D.; Jones, R.] Kings Coll London, Dept Primary Care & Publ Hlth Sci, London WC2R 2LS, England.
[Marteau, T.] Kings Coll London, Hlth Psychol Sect, London WC2R 2LS, England.
[Cramb, R.; Olliff, S.; Khan, K.] Queen Elizabeth Hosp, Birmingham B15 2TH, W Midlands, England.
[Arnold, D.] Cardiff Univ, Sch Med, Cardiff CF10 3AX, S Glam, Wales.
[Armstrong, M. J.; Houlihan, D. D.; Newsome, P. N.] Natl Inst Hlth, Res Biomed Res Unit, Birmingham, W Midlands, England.
[Moons, K.] Univ Med Ctr Utrecht, Utrecht, Netherlands.
[Altman, D.] Univ Oxford, Ctr Stat Med, Oxford, England.
C3 University of Birmingham; University of London; King's College London;
University of London; King's College London; University of Birmingham;
Cardiff University; Utrecht University; Utrecht University Medical
Center; University of Oxford
RP Lilford, RJ (corresponding author), Univ Birmingham, Sch Hlth & Populat Sci, Edgbaston, England.
RI Girling, Alan/A-7843-2012; Litchfield, Ian/AFO-0944-2022; Neuberger,
James/ABG-3010-2020; Armstrong, David/AAI-4476-2021; Newsome,
Philip/D-4495-2018; Khan, Khalid Saeed/AAT-8824-2020
OI Litchfield, Ian/0000-0002-1169-5392; Chilton, Peter/0000-0001-8809-9735;
Marteau, Theresa/0000-0003-3025-1129; Armstrong,
David/0000-0003-3652-9662; Lilford, Richard/0000-0002-0634-984X;
Newsome, Philip/0000-0001-6085-3652; Arnold, David/0000-0003-3158-7740;
Khan, Khalid Saeed/0000-0001-5084-7312; Armstrong,
Matthew/0000-0002-3425-1161; Girling, Alan/0000-0003-2022-045X
FU National Institute for Health Research Health Technology Assessment
programme; MRC [G0800808, G0802350] Funding Source: UKRI
FX The National Institute for Health Research Health Technology Assessment
programme.
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NR 177
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Z9 43
U1 0
U2 11
PU NIHR JOURNALS LIBRARY
PI SOUTHAMPTON
PA UNIV SOUTHAMPTON, EVALUATION, TRIALS & STUDIES COORDINATING CENTRE,
ALPHA HOUSE, ENTERPRISE RD, SOUTHAMPTON, SO16 7NS, ENGLAND
SN 1366-5278
EI 2046-4924
J9 HEALTH TECHNOL ASSES
JI Health Technol. Assess.
PD JUL
PY 2013
VL 17
IS 28
BP 1
EP +
DI 10.3310/hta17280
PG 300
WC Health Care Sciences & Services
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Health Care Sciences & Services
GA 179HT
UT WOS:000321511400001
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Al-Chalabi, T
Boccato, S
Portmann, BC
McFarlane, IG
Heneghan, MA
AF Al-Chalabi, Thawab
Boccato, Sylvia
Portmann, Bernard C.
McFarlane, Ian G.
Heneghan, Michael A.
TI Autoimmune hepatitis (AIH) in the elderly: A systematic retrospective
analysis of a large group of consecutive patients with definite AM
followed at a tertiary referral centre
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE autoimmune hepatitis; old age; immunosenescence; cirrhosis
ID CHRONIC ACTIVE HEPATITIS; IMMUNOSUPPRESSIVE THERAPY;
HEPATOCELLULAR-CARCINOMA; LIVER; TERMINOLOGY; REMISSION; DISEASE
AB Background/Aims: A few reports have suggested that AIH may be less severe in the elderly and may be underdiagnosed, but there is a paucity of data.
Methods:We have undertaken a systematic analysis of 164 consecutive patients (36 males, 128 females) with definite AIH (median score 23, range 18-28) attending our clinics, comparing those presenting at age > 60 years (Group 1, n = 43) with those presenting at < 60 years (Group 2, n = 121).
Results:Median (range) duration of follow-up was 9 years (1-28) in Group 1 and 14 years (1-33) in Group 2. Median ages (ranges) at presentation were: Group 1 = 65 (60-79) and Group 2 = 41 (6-59). Group 1 patients had a significantly increased incidence of ascites at presentation (p < 0.001) and a lower incidence of relapse (42% vs. 70%, p = 0.002), but there were no significant differences between the groups with respect to mode of onset (acute, insidious, asymptomatic), other clinical signs at presentation, biochemical parameters, types or titres of autoantibodies, incidence of histological cirrhosis, response to therapy or related side effects. There were also no significant differences in liver-related deaths or transplantation, or the frequencies of HLA DR3 or DR4 - although there was an increased frequency of the A1-B8-DR3/4 haplotype in Group 2 (40% vs. 22%, p = 0.138).
Conclusions: These findings suggest that AIH often presents in older patients, who frequently have severe disease. Active management in these patients can lead to a normal life expectancy. (c) 2006 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 Kings Coll London, Inst Liver Studies, London WC2R 2LS, England.
C3 University of London; King's College London
RP Heneghan, MA (corresponding author), Kings Coll London, Inst Liver Studies, London WC2R 2LS, England.
EM Michael.Heneghan@kingsch.nhs.uk
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NR 33
TC 145
Z9 153
U1 0
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD OCT
PY 2006
VL 45
IS 4
BP 575
EP 583
DI 10.1016/j.jhep.2006.04.007
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 094YU
UT WOS:000241276100023
PM 16899323
DA 2025-01-07
ER
PT J
AU Hubler, MJ
Kennedy, AJ
AF Hubler, Merla J.
Kennedy, Anion J.
TI Role of lipids in the metabolism and activation of immune cells
SO JOURNAL OF NUTRITIONAL BIOCHEMISTRY
LA English
DT Review
DE Inflammation; Macrophages; T lymphocytes; Oxysterols; Fatty acids
ID ENDOPLASMIC-RETICULUM STRESS; POLYUNSATURATED FATTY-ACIDS; REGULATORY
T-CELLS; LIVER-X RECEPTORS; INSULIN-RESISTANCE; MACROPHAGE POLARIZATION;
INFLAMMATORY RESPONSES; ENDOTHELIAL-CELLS; MYELOID CELLS;
ATHEROSCLEROSIS
AB Immune cell plasticity has extensive implications in the pathogenesis and resolution of metabolic disorders, cancers, autoimmune diseases and chronic inflammatory disorders. Over the past decade, nutritional status has been discovered to influence the immune response. In metabolic disorders such as obesity, immune cells interact with various classes of lipids, which are capable of controlling the plasticity of macrophages and T lymphocytes. The purpose of this review is to discuss lipids and their impact on innate and adaptive immune responses, focusing on two areas: (1) the impact of altering lipid metabolism on immune cell activation, differentiation and function and (2) the mechanism by which lipids such as cholesterol and fatty acids regulate immune cell plasticity. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Hubler, Merla J.; Kennedy, Anion J.] Vanderbilt Univ, Sch Med, Dept Mol Physiol & Biophys, Nashville, TN 37212 USA.
C3 Vanderbilt University
RP Kennedy, AJ (corresponding author), 702 Light Hall, Nashville, TN 37232 USA.
EM arion.kennedy@vanderbilt.edu
OI Kennedy, Arion/0000-0002-8443-3131
FU NHLBI NIH HHS [K01 HL121010] Funding Source: Medline; NIDDK NIH HHS [F30
DK103438] Funding Source: Medline; NIGMS NIH HHS [T32 GM007347] Funding
Source: Medline
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NR 86
TC 165
Z9 181
U1 0
U2 56
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0955-2863
EI 1873-4847
J9 J NUTR BIOCHEM
JI J. Nutr. Biochem.
PD AUG
PY 2016
VL 34
BP 1
EP 7
DI 10.1016/j.jnutbio.2015.11.002
PG 7
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA DS1YS
UT WOS:000380421700001
PM 27424223
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Mizrahi, M
Ilan, Y
AF Mizrahi, Meir
Ilan, Yaron
TI The Gut Mucosa as a Site for Induction of Regulatory T-Cells
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE Oral tolerance; regulatory T-cells
ID MYELIN BASIC-PROTEIN; ORAL IMMUNE REGULATION; GROWTH-FACTOR-BETA;
INFLAMMATORY-BOWEL-DISEASE; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
HISTOCOMPATIBILITY COMPLEX ALLOPEPTIDES; EXPERIMENTAL ALLERGIC
ENCEPHALOMYELITIS; HEPATOCELLULAR-CARCINOMA GROWTH; INTESTINAL
EPITHELIAL-CELLS; LATENCY-ASSOCIATED PEPTIDE
AB Regulatory T lymphocytes (Tregs) are specialized for immune suppression and are important regulators of the immune response in various settings. Tregs actively suppress enteroantigen-reactive cells and contribute to the maintenance of intestinal immune homeostasis. Distinct Treg subsets coexist in the intestinal mucosa and mesenteric lymph nodes. Disturbances in Treg number and function are associated with immune-mediated disorders. Therefore, Tregs are potential targets for immunotherapies.
The gut mucosal immune system is the largest lymphoid organ in the body. This site has continuous antigenic challenges from food antigens, antigens of the abundant normal bacterial flora, and pathogens. Despite this constant antigenic stimulation, controlled inflammatory responses and suppression of inflammation appear to be the rule. The gut immune system differentiates the antigenic signals from the high background noise of food and bacterial antigens. This tight regulation required to maintain homeostasis is achieved through multiple non-immune and immune factors.
Oral tolerance is a mechanism in which the gastrointestinal immune system inhibits or promotes its reaction toward an orally administered antigen. Mucosal tolerance is attractive as an approach to the treatment of autoimmune and inflammatory diseases; the benefits of using an oral tolerance approach are: lack of toxicity, ease of administration over time, and antigen-specific mechanisms of action. Multiple mechanisms of tolerance are induced by oral antigen administration. Recent data suggest that oral antigen administration of antigens may promote activation of different types of regulatory T lymphocytes, enabling treatment of immune mediated disorders.
This review summarizes the recent data on induction of regulatory T-cells by oral antigen administration as a possible mechanism of oral tolerance.
C1 [Mizrahi, Meir; Ilan, Yaron] Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Med, Liver Unit, IL-91120 Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hadassah University Medical Center
RP Ilan, Y (corresponding author), Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Med, Liver Unit, POB 12000, IL-91120 Jerusalem, Israel.
EM ilan@hadassah.org.il
FU The Roaman-Epstein Liver Research Foundation
FX This work was supported in part by the following grant: The
Roaman-Epstein Liver Research Foundation ( to Y. I.).
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NR 201
TC 42
Z9 47
U1 2
U2 15
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1381-6128
EI 1873-4286
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD APR
PY 2009
VL 15
IS 11
BP 1191
EP 1202
DI 10.2174/138161209787846784
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 520KJ
UT WOS:000271842600005
PM 19355960
DA 2025-01-07
ER
PT J
AU Asghar, K
Brain, J
Palmer, JM
Douglass, S
Naemi, FMA
O'Boyle, G
Kirby, J
Ali, S
AF Asghar, Kashif
Brain, John
Palmer, Jeremy M.
Douglass, Stephen
Naemi, Fatmah M. A.
O'Boyle, Graeme
Kirby, John
Ali, Simi
TI Potential role of indoleamine 2,3-dioxygenase in primary biliary
cirrhosis
SO ONCOLOGY LETTERS
LA English
DT Article
DE indoleamine 2,3-dioxygenase; primary biliary cirrhosis; immortalized
biliary epithelial cells; tryptophan metabolites
ID HUMAN DENDRITIC CELLS; REGULATORY T-CELLS; GROWTH-FACTOR-BETA;
TRYPTOPHAN-METABOLISM; IDO ACTIVATION; INHIBITION; EXPRESSION;
MECHANISM; PROLIFERATION; RECEPTOR
AB Indoleamine 2,3-dioxygenase (IDO)-induced immunosuppression can be clinically beneficial for autoimmune diseases. Primary biliary cirrhosis (PBC) is characterized by autoimmune lesions of intrahepatic bile duct epithelial cells that may lead to irreversible cirrhosis or hepatocellular carcinoma. The present study assessed the expression and function of IDO in a cell culture model and in PBC patients. IDO expression was monitored in a human immortalized but non-malignant biliary epithelial cell (iBEC) line. Increased expression of IDO1/2 was observed in the iBECs following stimulation with interferon-gamma (IFN-gamma). The induction of IDO was IFN-gamma-dependent, but was independent of the transforming growth factor-beta (TGF-beta) pathway. IDO enzymatic activity was observed in the supernatant of iBECs following stimulation with IFN-gamma using colorimetric assays. A total of 47 serum samples from PBC patients were used to examine IDO activity by high-performance liquid chromatography, with samples from 24 healthy volunteers used as controls. Patients with PBC exhibited an increased rate of tryptophan to kynurenine conversion (P>0.01). Liver sections from patients with PBC (n=5) and those of healthy controls (n=5) were used for immunohistochemical studies. IDO expression was observed in biliary epithelial cells and in hepatocytes of PBC patients. Finally, the effect of tryptophan metabolites on human cluster of differentiation (CD) 4(+) T cells in inducing polarization towards a regulatory T cell phenotype was examined. 3-Hydroxykynurenine significantly upregulated the fraction of CD4(+) cells expressing forkhead box p3 (Foxp3). The results of the present study suggest a therapeutic opportunity for the management of PBC and indicate that tryptophan catabolism could serve as a potential biomarker to monitor disease progression.
C1 [Asghar, Kashif; Brain, John; Palmer, Jeremy M.; Douglass, Stephen; Naemi, Fatmah M. A.; O'Boyle, Graeme; Kirby, John; Ali, Simi] Univ Newcastle, Med Sch, Inst Cellular Med, Appl Immunobiol & Transplantat Res Grp, 3rd Floor,William Leech Bldg, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
[Asghar, Kashif] Natl Univ Sci & Technol, Atta Ur Rahman Sch Appl Biosci, Healthcare Biotechnol Dept, Islamabad 44000, Pakistan.
[Asghar, Kashif] Shaukat Khanum Mem Canc Hosp & Res Ctr, Dept Basic Sci Res, Lahore 54000, Pakistan.
C3 Newcastle University - UK; National University of Sciences & Technology
- Pakistan; Shaukat Khanum Memorial Cancer Hospital & Research Centre
RP Ali, S (corresponding author), Univ Newcastle, Med Sch, Inst Cellular Med, Appl Immunobiol & Transplantat Res Grp, 3rd Floor,William Leech Bldg, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
EM simi.ali@ncl.ac.uk
RI Douglass, Stephen/ABH-4878-2020
OI O'Boyle, Graeme/0000-0002-0472-8061; Kirby, John/0000-0003-2543-4131
FU Marie Curie Innovative Doctoral Programme [FP7-PEOPLE-2013-ITN]; Medical
Research Council UK Primary Biliary Cirrhosis Programme [MR/L001489/1]
FX The present study was supported by grants from the Marie Curie
Innovative Doctoral Programme (grant no. FP7-PEOPLE-2013-ITN), and
Medical Research Council UK Primary Biliary Cirrhosis Programme (grant
no. MR/L001489/1).
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NR 44
TC 10
Z9 12
U1 0
U2 4
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD NOV
PY 2017
VL 14
IS 5
BP 5497
EP 5504
DI 10.3892/ol.2017.6834
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FM5NQ
UT WOS:000415083000059
PM 29113177
OA gold, Green Published, Green Accepted
DA 2025-01-07
ER
PT J
AU Benson, M
AF Benson, M.
TI Clinical implications of omics and systems medicine: focus on predictive
and individualized treatment
SO JOURNAL OF INTERNAL MEDICINE
LA English
DT Review
DE clinical translation; omics; systems medicine
ID PROTEIN-INTERACTION NETWORKS; DISEASE; CANCER; BIOLOGY; ASTHMA;
EMERGENCE; PROGNOSIS; MODULES
AB Many patients with common diseases do not respond to treatment. This is a key challenge to modern health care, which causes both suffering and enormous costs. One important reason for the lack of treatment response is that common diseases are associated with altered interactions between thousands of genes, in combinations that differ between subgroups of patients who do or do not respond to a given treatment. Such subgroups, or even distinct disease entities, have been described recently in asthma, diabetes, autoimmune diseases and cancer. High-throughput techniques (omics) allow identification and characterization of such subgroups or entities. This may have important clinical implications, such as identification of diagnostic markers for individualized medicine, as well as new therapeutic targets for patients who do not respond to existing drugs. For example, whole-genome sequencing may be applied to more accurately guide treatment of neurodevelopmental diseases, or to identify drugs specifically targeting mutated genes in cancer. A study published in 2015 showed that 28% of hepatocellular carcinomas contained mutated genes that potentially could be targeted by drugs already approved by the US Food and Drug Administration. A translational study, which is described in detail, showed how combined omics, computational, functional and clinical studies could identify and validate a novel diagnostic and therapeutic candidate gene in allergy. Another important clinical implication is the identification of potential diagnostic markers and therapeutic targets for predictive and preventative medicine. By combining computational and experimental methods, early disease regulators may be identified and potentially used to predict and treat disease before it becomes symptomatic. Systems medicine is an emerging discipline, which may contribute to such developments through combining omics with computational, functional and clinical studies. The aims of this review are to provide a brief introduction to systems medicine and discuss how it may contribute to the clinical implementation of individualized treatment, using clinically relevant examples.
C1 [Benson, M.] Linkoping Univ, Fac Hlth Sci, Dept Pediat, Ctr Individualized Med, S-58183 Linkoping, Sweden.
C3 Linkoping University
RP Benson, M (corresponding author), Linkoping Univ, Ctr Individualized Med, Dept Pediat, S-58183 Linkoping, Sweden.
EM mikael.benson@liu.se
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NR 59
TC 46
Z9 48
U1 0
U2 21
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0954-6820
EI 1365-2796
J9 J INTERN MED
JI J. Intern. Med.
PD MAR
PY 2016
VL 279
IS 3
BP 229
EP 240
DI 10.1111/joim.12412
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DF8ON
UT WOS:000371617800002
PM 26891944
OA Green Submitted, Bronze
DA 2025-01-07
ER
PT J
AU Ansari, JA
Malik, JA
Ahmed, S
Manzoor, M
Ahemad, N
Anwar, S
AF Ansari, Jeba Ajgar
Malik, Jonaid Ahmad
Ahmed, Sakeel
Manzoor, Muntaha
Ahemad, Nafees
Anwar, Sirajudheen
TI Recent advances in the therapeutic applications of selenium
nanoparticles
SO MOLECULAR BIOLOGY REPORTS
LA English
DT Review
DE Selenium; Nutrient; Nanoparticles; Therapeutic application; Clinical
translation
ID BARRIER DYSFUNCTION; IN-VITRO; ANTIOXIDANT; CELLS; CYTOTOXICITY;
INHIBITION; EFFICIENCY; DELIVERY; CARRIER; GROWTH
AB Selenium nanoparticles (SeNPs) are an appealing carrier for the targeted delivery. The selenium nanoparticles are gaining global attention because of the potential therapeutic applications in several diseases e.g., rheumatoid arthritis (RA), inflammatory bowel disease (IBD), asthma, liver, and various autoimmune disorders like psoriasis, cancer, diabetes, and a variety of infectious diseases. Despite the fact still there is no recent literature that summarises the therapeutic applications of SeNPs. There are some challenges that need to be addressed like finding targets for SeNPs in various diseases, and the various functionalization techniques utilized to increase SeNP's stability while facilitating wide drug-loaded SeNP distribution to tumor areas and preventing off-target impacts need to focus on understanding more about the therapeutic aspects for better understanding the science behind it. Keeping that in mind we have focused on this gap and try to summarize all recent key targeted therapies for SeNPs in cancer treatment and the numerous functionalization strategies. We have also focused on recent advancements in SeNP functionalization methodologies and mechanisms for biomedical applications, particularly in anticancer, anti-inflammatory, and anti-infection therapeutics. Based on our observation we found that SeNPs could potentially be useful in suppressing viral epidemics, like the ongoing COVID-19 pandemic, in complement to their antibacterial and antiparasitic uses. SeNPs are significant nanoplatforms with numerous desirable properties for clinical translation.
C1 [Ansari, Jeba Ajgar] Dr Babasaheb Ambedkar Marathwada Univ, Govt Coll Pharm, Dept Pharmaceut, BAMU, Aurangabad, India.
[Malik, Jonaid Ahmad] Indian Inst Technol Ropar, Dept Biomed Engn, Rupnagar, India.
[Ahmed, Sakeel] Natl Inst Pharmaceut Educ & Res, Dept Pharmacol & Toxicol, Ahmadabad, Gujarat, India.
[Manzoor, Muntaha] Sherikashmir Inst Med Sci, Dept Clin Pharmacol, Srinagar, India.
[Ahemad, Nafees] Monash Univ Malaysia, Sch Pharm, Jalan Lagoon Selatan, Petaling Jaya 47500, Selangor, Malaysia.
[Anwar, Sirajudheen] Univ Hail, Coll Pharm, Dept Pharmacol & Toxicol, Hail, Saudi Arabia.
C3 Dr. Babasaheb Ambedkar Marathwada University (BAMU); Indian Institute of
Technology System (IIT System); Indian Institute of Technology (IIT) -
Ropar; National Institute of Pharmaceutical Education & Research, S.A.S.
Nagar (Mohali); Sher-i-Kashmir Institute of Medical Sciences; Monash
University; Monash University Malaysia; University Ha'il
RP Ahemad, N (corresponding author), Monash Univ Malaysia, Sch Pharm, Jalan Lagoon Selatan, Petaling Jaya 47500, Selangor, Malaysia.; Anwar, S (corresponding author), Univ Hail, Coll Pharm, Dept Pharmacol & Toxicol, Hail, Saudi Arabia.
EM nafees.ahemad@monash.edu; si.anwar@uoh.edu.sa
FU CAUL
FX No funding was received. Open Access funding enabled and organized by
CAUL and its Member Institutions
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NR 100
TC 5
Z9 5
U1 22
U2 24
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0301-4851
EI 1573-4978
J9 MOL BIOL REP
JI Mol. Biol. Rep.
PD DEC
PY 2024
VL 51
IS 1
AR 688
DI 10.1007/s11033-024-09598-z
PG 20
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA YC6P4
UT WOS:001266330700006
PM 38796570
OA hybrid
DA 2025-01-07
ER
PT J
AU Li, ML
Hu, T
Tie, C
Qu, L
Zheng, H
Zhang, JL
AF Li, Menglin
Hu, Ting
Tie, Cai
Qu, Liang
Zheng, Hao
Zhang, Jinlan
TI Quantitative Proteomics and Targeted Fatty Acids Analysis Reveal the
Damage of Triptolide in Liver and Kidney
SO PROTEOMICS
LA English
DT Article
DE Fatty acids; Kidney; Liver; Toxicity; Triptolide
ID TRIPTERYGIUM-WILFORDII; OXIDATIVE STRESS; TOXICITY; METABOLISM; INJURY;
NEPHROTOXICITY; MECHANISM; DISEASES; PATHWAY; CANCER
AB Triptolide (TP), the major active component in Tripterygium wilfordii Hook. f., is widely used for the treatment of rheumatoid arthritis and autoimmune diseases. However, organ toxicity, especially hepatotoxicity and nephrotoxicity, limits its clinical application. To fully understand the mechanism underlying TP toxicity, iTRAQ-based 2D-LC-MS/MS proteomics is used to detect differentially expressed proteins in the livers and kidneys of mice administered the LD50 dose of TP. Functional annotation revealed that multiple pathways are involved in TP toxicity, including acute-phase response signaling, the antigen presentation pathway, FXR/RXR activation, LPS/IL-1-mediated inhibition of RXR function, and EIF2 signaling.Members of the cytochromeP450 protein family that are involved in fatty acid (FA) metabolism, such as CYP2E1, show significant differences in expression among groups. Additionally, the proteomics data suggested that FAs are involved in TP-induced toxicity. FA analysis is conducted using HPLC-MRM to characterize the differences among various groups exposed to TP for different times. It has been found that 20 FAs in the liver show significant differences in abundance among groups, whereas in the kidneys, six FAs show significant differences in abundance. By integrating the proteomic and targeted FA analyses, it has been found that differently expressed proteins and FAs both participate in pathways including cellular lipolytic activity, peroxisomal fatty acid beta-oxidation, and so on. Our data contribute to understanding the mechanisms underlying TP-induced organ toxicity. The results may help to improve the clinical efficacy and safety of TP in the future.
C1 [Li, Menglin; Hu, Ting; Tie, Cai; Qu, Liang; Zheng, Hao; Zhang, Jinlan] Chinese Acad Med Sci, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Beijing, Peoples R China.
[Li, Menglin; Hu, Ting; Tie, Cai; Qu, Liang; Zheng, Hao; Zhang, Jinlan] Peking Union Med Coll, Beijing, Peoples R China.
[Qu, Liang] Pharmaron Beijing Co Ltd, BDA, Beijing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Institute of Materia Medica - CAMS; Chinese Academy of Medical Sciences
- Peking Union Medical College; Peking Union Medical College
RP Zhang, JL (corresponding author), Chinese Acad Med Sci, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Beijing, Peoples R China.; Zhang, JL (corresponding author), Peking Union Med Coll, Beijing, Peoples R China.
EM zhjl@imm.ac.cn
RI zheng, hao/ITV-1342-2023; HU, TING/KRQ-7397-2024
OI Tie, Cai/0000-0003-1541-6407; li, menglin/0000-0001-8639-5899
FU National Natural Science Foundation of China [81273484]
FX The authors thank Dr. Sun Wei for supporting the proteomics analysis.
This work was supported by a grant from National Natural Science
Foundation of China (Grant No. 81273484).
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NR 34
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Z9 23
U1 5
U2 59
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1615-9853
EI 1615-9861
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AR 1700001
DI 10.1002/pmic.201700001
PG 10
WC Biochemical Research Methods; Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA FN3TK
UT WOS:000415922400008
PM 28895652
DA 2025-01-07
ER
PT J
AU Nakano, M
Nakajima, M
AF Nakano, Masataka
Nakajima, Miki
TI Significance of A-to-I RNA editing of transcripts modulating
pharmacokinetics and pharmacodynamics
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE RNA editing; Post-transcriptional regulation; Pharmacokinetics;
Pharmacodynamics
ID CA2+-PERMEABLE AMPA RECEPTORS; JORO SPIDER TOXIN; ADENOSINE DEAMINASES;
DOWN-REGULATION; MESSENGER-RNA; MDR1/P-GLYCOPROTEIN EXPRESSION;
DIHYDROFOLATE-REDUCTASE; MULTIDRUG-RESISTANCE; UNWINDING ACTIVITY; HUMAN
LIVER
AB RNA editing is a post-transcriptional process that alters the nucleotide sequence of RNA transcripts to generate transcriptome diversity. Among the various types of RNA editing, adenosine-to-inosine (A-to-I) RNA editing is the most frequent type of RNA editing in mammals. Adenosine deaminases acting on RNA (ADAR) enzymes, ADAR1 and ADAR2, convert adenosines in double-stranded RNA structures into inosines by hydrolytic deamination. Inosine forms a base pair with cytidine as if it were guanosine; therefore, the conversion may affect the amino acid sequence, splicing, microRNA targeting, and miRNA maturation. It became apparent that disrupted RNA editing or abnormal ADAR expression is associated with several diseases including cancer, neurological disorders, metabolic diseases, viral infections, and autoimmune disorders. The biological significance of RNA editing in pharmacokinetics/pharmacodynamics (PK/PD)-related genes is starting to be demonstrated. The authors conducted pioneering studies to reveal that RNA editing modulates drug metabolism potencies in the human liver, as well as the response of cancer cells to chemotherapy agents. Awareness of the importance of RNA editing in drug therapy is growing. This review summarizes the current knowledge on the RNA editing that affects the expression and function of drug response-related genes. Continuing studies on the RNA editing that regulates pharmacokinetics/pharmacodynamics would provide new beneficial information for personalized medicine. (C) 2017 Elsevier Inc. All rights reserved.
C1 [Nakano, Masataka; Nakajima, Miki] Kanazawa Univ, Drug Metab & Toxicol, Fac Pharmaceut Sci, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
C3 Kanazawa University
RP Nakajima, M (corresponding author), Kanazawa Univ, Drug Metab & Toxicol, Fac Pharmaceut Sci, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
EM nmiki@p.kanazawa-u.ac.jp
RI Nakajima, Miki/C-3990-2015
OI Nakano, Masataka/0009-0006-9884-2768
FU Japan Society for the Promotion of Science [15H04663]; Grants-in-Aid for
Scientific Research [15H04663, 16J00832] Funding Source: KAKEN
FX The authors' studies were supported by Grant-in-Aid for Scientific
Research (B) from the Japan Society for the Promotion of Science
[15H04663].
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NR 127
TC 26
Z9 27
U1 0
U2 13
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
EI 1879-016X
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD JAN
PY 2018
VL 181
BP 13
EP 21
DI 10.1016/j.pharmthera.2017.07.003
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FU5JT
UT WOS:000423889700002
PM 28716651
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Buell, C
Koo, J
AF Buell, Catherine
Koo, John
TI Long-term safety of mycophenolate mofetil and cyclosporine: A review
SO JOURNAL OF DRUGS IN DERMATOLOGY
LA English
DT Review
ID SEVERE PLAQUE PSORIASIS; PEMPHIGUS-VULGARIS; LIVER-TRANSPLANTATION;
RHEUMATOID-ARTHRITIS; ATOPIC-DERMATITIS; RENAL-FUNCTION; THERAPY;
MULTICENTER; PREGNANCY; EFFICACY
AB The prevailing notion in dermatology is that mycophenolate mofetil (MMF) is safer than cyclosporine (CsA), but that CsA has greater efficacy. This literature review evaluates the available long-term safety data of MMF and CsA. Literature in the fields of dermatology, autoimmune disease, and transplantation were retrieved from PubMed. Data regarding immunosuppressive and non-immunosuppressive side effects of MMF and CsA are presented along with available pregnancy safety data. Surprisingly, there is a paucity of data on long-term MMF monotherapy. Transplant data is presented separately due to the concomitant use of other immunosuppressants along with MMF. Trends that can be identified include a less discernable cancer or end-organ damage risk in MMF compared to CsA. However, MMF appears to have a greater risk in pregnancy and increased reports of herpes simplex and zoster infection compared to CsA.
C1 [Buell, Catherine] Univ Calif Los Angeles, Charles R Drew Univ, Los Angeles, CA 90025 USA.
[Koo, John] Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94143 USA.
C3 Charles R. Drew University of Medicine & Science; University of
California System; University of California Los Angeles; University of
California System; University of California San Francisco
RP Buell, C (corresponding author), Univ Calif Los Angeles, Charles R Drew Univ, 2112 S Beverly Glen Blvd, Los Angeles, CA 90025 USA.
EM catherinebuell@hotmail.com
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NR 54
TC 29
Z9 32
U1 0
U2 1
PU JOURNAL OF DRUGS IN DERMATOLOGY
PI NEW YORK
PA 377 PARK AVE SOUTH, 6TH FLOOR, NEW YORK, NY 10016 USA
SN 1545-9616
J9 J DRUGS DERMATOL
JI J. Drugs Dermatol.
PD AUG
PY 2008
VL 7
IS 8
BP 741
EP 748
PG 8
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA 343KC
UT WOS:000258851100004
PM 18720690
DA 2025-01-07
ER
PT J
AU Hov, JR
Boberg, KM
Taraldsrud, E
Vesterhus, M
Boyadzhieva, M
Solberg, IC
Schrumpf, E
Vatn, MH
Lie, BA
Molberg, O
Karlsen, TH
AF Hov, Johannes R.
Boberg, Kirsten M.
Taraldsrud, Eli
Vesterhus, Mette
Boyadzhieva, Maria
Solberg, Inger Camilla
Schrumpf, Erik
Vatn, Morten H.
Lie, Benedicte A.
Molberg, Oyvind
Karlsen, Tom H.
TI Antineutrophil antibodies define clinical and genetic subgroups in
primary sclerosing cholangitis
SO LIVER INTERNATIONAL
LA English
DT Article
DE antineutrophil cytoplasmic antibodies; HLA; primary sclerosing
cholangitis
ID INFLAMMATORY-BOWEL-DISEASE; INTERNATIONAL CONSENSUS STATEMENT;
GENOME-WIDE ASSOCIATION; ULCERATIVE-COLITIS; CYTOPLASMIC ANTIBODIES;
SUSCEPTIBILITY LOCI; AUTOIMMUNE-DISEASES; RISK LOCI; ANCA; HETEROGENEITY
AB Background & Aims: The strongest genetic risk factors in primary sclerosing cholangitis (PSC) are encoded in the HLA complex. Antineutrophil cytoplasmic antibodies (ANCA) have been reported in up to 94% of PSC patients, but their clinical significance and immunogenetic basis are ill defined. We aimed to characterize clinical and genetic associations of ANCA in PSC.
Methods: Antineutrophil cytoplasmic antibodies were analysed with indirect immunofluorescence in 241 Norwegian PSC patients. HLA-B and HLA-DRB1 genotyping was performed in the patients and in 368 healthy controls. Data on perinuclear ANCA (pANCA) and HLA-DRB1 were available from 274 ulcerative colitis (UC) patients without known liver disease.
Results: Antineutrophil cytoplasmic antibodies were found in 193 (80%) of the PSC patients, with pANCA in 169 (70%). ANCA-positive patients were younger than ANCA negative at diagnosis of PSC and had a lower frequency of biliary cancer (9% vs 19%, P=.047). There were no differences between PSC patients with and without inflammatory bowel disease. Genetically, the strong PSC risk factors HLA-B*08 (frequency in healthy 13%) and DRB1*03 (14%) were more prevalent in ANCA-positive than -negative patients (43% vs 25%, P=.0012 and 43% vs 25%, P=.0015 respectively). The results were similar when restricting the analysis to pANCA-positive patients. In UC patients without liver disease, HLA-DRB1*03 was more prevalent in pANCA-positive compared with -negative patients (P=.03).
Conclusions: Antineutrophil cytoplasmic antibodies identified PSC patients with particular clinical and genetic characteristics, suggesting that ANCA may mark a clinically relevant pathogenetic subgroup in the PSC-UC disease spectrum.
C1 [Hov, Johannes R.; Boberg, Kirsten M.; Vesterhus, Mette; Schrumpf, Erik; Karlsen, Tom H.] Oslo Univ Hosp Rikshospitalet, Norwegian PSC Res Ctr, Dept Transplantat Med Inflammatory Med & Transpla, Oslo, Norway.
[Hov, Johannes R.; Boberg, Kirsten M.; Taraldsrud, Eli; Schrumpf, Erik; Vatn, Morten H.; Lie, Benedicte A.; Molberg, Oyvind; Karlsen, Tom H.] Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway.
[Hov, Johannes R.; Boberg, Kirsten M.; Karlsen, Tom H.] Oslo Univ Hosp Rikshospitalet, Dept Transplantat Med Inflammatory Med & Transpla, Div Surg, Gastroenterol Sect, Oslo, Norway.
[Hov, Johannes R.; Karlsen, Tom H.] Oslo Univ Hosp, Internal Med Res Inst, Div Surg Inflammatory Med & Transplantat, Oslo, Norway.
[Hov, Johannes R.; Taraldsrud, Eli; Lie, Benedicte A.; Karlsen, Tom H.] Univ Oslo, Fac Med, KG Jebsen Inflammat Res Ctr, Inst Clin Med, Oslo, Norway.
[Taraldsrud, Eli; Lie, Benedicte A.] Oslo Univ Hosp Rikshospitalet, Dept Immunol, Oslo, Norway.
[Vesterhus, Mette] Haukeland Hosp, Natl Ctr Ultrasound Gastroenterol, N-5021 Bergen, Norway.
[Boyadzhieva, Maria] Med Univ Sofia, Clin Ctr Endocrinol, Sofia, Bulgaria.
[Solberg, Inger Camilla] Oslo Univ Hosp Ulleval, Dept Gastroenterol, Div Med, Oslo, Norway.
[Vatn, Morten H.] Akershus Univ Hosp, EpiGen Inst, Campus AHUS, Nordbyhagen, Norway.
[Molberg, Oyvind] Oslo Univ Hosp Rikshospitalet, Rheumatol Unit, Oslo, Norway.
C3 University of Oslo; National Hospital Norway; University of Oslo;
University of Oslo; National Hospital Norway; University of Oslo;
University of Oslo; University of Oslo; National Hospital Norway;
University of Bergen; Haukeland University Hospital; Medical University
Sofia; University of Oslo; University of Oslo; University of Oslo;
National Hospital Norway
RP Hov, JR (corresponding author), Oslo Univ Hosp Rikshospitalet, Norwegian PSC Res Ctr, Dept Transplantat Med, Oslo, Norway.
EM j.e.r.hov@medisin.uio.no
RI Boyadzhieva, Maria/HMP-4195-2023; Hov, Johannes/J-1480-2019; Vesterhus,
Mette/AAX-8767-2020
OI Vesterhus, Mette/0000-0003-1493-2303
FU Norwegian PSC Research Centre; Norwegian Research Council [240787/F20]
FX This study was supported by the Norwegian PSC Research Centre. JRH is
funded by the Norwegian Research Council (240787/F20).
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NR 38
TC 26
Z9 29
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD MAR
PY 2017
VL 37
IS 3
BP 458
EP 465
DI 10.1111/liv.13238
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EM0SL
UT WOS:000395027900019
PM 27558072
DA 2025-01-07
ER
PT J
AU Liu, YP
Song, JJ
Yang, J
Zheng, JL
Yang, L
Gao, J
Tian, S
Liu, Z
Meng, XB
Wang, JC
Dai, ZF
Tang, YD
AF Liu, Yupeng
Song, Jingjing
Yang, Juan
Zheng, Jilin
Yang, Ling
Gao, Jun
Tian, Song
Liu, Zhen
Meng, Xiangbin
Wang, Jian-Cheng
Dai, Zhifei
Tang, Yi-Da
TI Tumor Necrosis Factor α-Induced Protein 8-Like 2 Alleviates Nonalcoholic
Fatty Liver Disease Through Suppressing Transforming Growth Factor
Beta-Activated Kinase 1 Activation
SO HEPATOLOGY
LA English
DT Article
ID NEGATIVE REGULATOR; INSULIN-RESISTANCE; CARDIOVASCULAR-DISEASE; TIPE2;
TAK1; INFLAMMATION; STEATOSIS; FIBROSIS; INNATE; PATHOGENESIS
AB Background and Aims NAFLD prevalence has increased rapidly and become a major global health problem. Tumor necrosis factor alpha-induced protein 8-like 2 (TIPE2) plays a protective role in a cluster of liver diseases, such as autoimmune hepatitis, hepatitis B, and hepatocellular carcinoma. However, the function of TIPE2 in NAFLD remains unknown. Here, we investigated the role of TIPE2 in the development of NAFLD. Approach and Results Our study found that in vitro overexpression or knockout of TIPE2 significantly ameliorated or aggravated lipid accumulation and inflammation in hepatocytes exposed to metabolic stimulation, respectively. Consistently, in vivo hepatic steatosis, insulin resistance, inflammation, and fibrosis were alleviated in hepatic Tipe2-transgenic mice but exaggerated in hepatic Tipe2-knockout mice treated by metabolic challenges. RNA sequencing revealed that TIPE2 was significantly associated with the mitogen-activated protein kinase pathway. Mechanistic experiments demonstrated that TIPE2 bound with transforming growth factor beta-activated kinase 1 (TAK1), prevented tumor necrosis factor receptor-associated factor 6-mediated TAK1 ubiquitination and subsequently inhibited the TAK1 phosphorylation and activation of TAK1-c-Jun N-terminal kinase (JNK)/p38 signaling. Further investigation showed that blocking the activity of TAK1 reversed the worsening of hepatic metabolic disorders and inflammation in hepatic-specific Tipe2-knockout hepatocytes and mice treated with metabolic stimulation. Conclusions TIPE2 suppresses NAFLD advancement by blocking TAK1-JNK/p38 pathway and is a promising target molecule for NAFLD therapy.
C1 [Liu, Yupeng; Song, Jingjing; Zheng, Jilin; Gao, Jun; Meng, Xiangbin; Tang, Yi-Da] Chinese Acad Med Sci & Peking Union Med Coll, Dept Cardiol, State Key Lab Cardiovasc Dis, Fuwai Hosp,Natl Ctr Cardiovasc Dis, Beijing, Peoples R China.
[Liu, Yupeng; Song, Jingjing; Zheng, Jilin; Tang, Yi-Da] Chinese Acad Med Sci & Peking Union Med Coll, Grad Sch, Peking Union Med Coll, Beijing, Peoples R China.
[Yang, Juan; Yang, Ling; Tian, Song; Liu, Zhen] Wuhan Univ, Dept Cardiol, Renmin Hosp, Wuhan, Peoples R China.
[Gao, Jun] Hebei Med Univ, Dept Cardiol, First Hosp, Shijiazhuang, Hebei, Peoples R China.
[Meng, Xiangbin] Zhengzhou Univ Peoples Hosp, Dept Cardiol, Cent China Fuwai Hosp, Cent China Branch,Natl Cardiovasc Ctr,Henan Prov, Zhengzhou, Henan, Peoples R China.
[Wang, Jian-Cheng] Peking Univ, Beijing Key Lab Mol Pharmaceut & New Drug Deliver, State Key Lab Nat & Biomimet Drugs, Sch Pharmaceut Sci, Beijing, Peoples R China.
[Dai, Zhifei] Peking Univ, Dept Biomed Engn, Coll Future Technol, Beijing, Peoples R China.
[Tang, Yi-Da] Peking Univ Third Hosp, Dept Cardiol, Key Lab Mol Cardiovasc Sci, Minist Educ, 49 Huayuanbei Rd, Beijing 100191, Peoples R China.
[Tang, Yi-Da] Peking Univ Third Hosp, Inst Vasc Med, Key Lab Mol Cardiovasc Sci, Minist Educ, 49 Huayuanbei Rd, Beijing 100191, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College; Fu
Wai Hospital - CAMS; Peking Union Medical College; Chinese Academy of
Medical Sciences - Peking Union Medical College; Peking Union Medical
College; Wuhan University; Hebei Medical University; Zhengzhou
University; Peking University; Peking University
RP Tang, YD (corresponding author), Peking Univ Third Hosp, Dept Cardiol, Key Lab Mol Cardiovasc Sci, Minist Educ, 49 Huayuanbei Rd, Beijing 100191, Peoples R China.; Tang, YD (corresponding author), Peking Univ Third Hosp, Inst Vasc Med, Key Lab Mol Cardiovasc Sci, Minist Educ, 49 Huayuanbei Rd, Beijing 100191, Peoples R China.
EM tangyida@bjmu.edu.cn
RI Tian, Song/HJI-2076-2023; Song, Jing/HRC-8045-2023; wang,
jian-cheng/AAR-3728-2021
FU National Key R&D Program of China [2020YFC2004700]; National Natural
Science Foundation of China [81825003, 91957123, 81800327, 81900272];
CAMS Innovation Fund for Medical Sciences [CIFMS 2016-I2M-1-009];
Beijing Municipal Science & Technology Commission [Z181100006318005,
Z201100006820002]
FX Supported by grants from National Key R&D Program of China
(2020YFC2004700), National Natural Science Foundation of China
(81825003, 91957123, 81800327, 81900272), CAMS Innovation Fund for
Medical Sciences (CIFMS 2016-I2M-1-009), and Beijing Municipal Science &
Technology Commission (Z181100006318005, Z201100006820002).
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NR 44
TC 14
Z9 15
U1 1
U2 20
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD SEP
PY 2021
VL 74
IS 3
BP 1300
EP 1318
DI 10.1002/hep.31832
EA JUL 2021
PG 19
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA UQ4CI
UT WOS:000678491900001
PM 33768585
DA 2025-01-07
ER
PT J
AU Zeng, YF
Li, YT
Xu, Z
Gan, WQ
Lu, LR
Huang, XH
Lin, CS
AF Zeng, Yingfu
Li, Yiting
Xu, Zhen
Gan, Weiqiang
Lu, Lirong
Huang, Xiaohui
Lin, Chaoshuang
TI Myeloid-derived suppressor cells expansion is closely associated with
disease severity and progression in HBV-related acute-on-chronic liver
failure
SO JOURNAL OF MEDICAL VIROLOGY
LA English
DT Article
DE cell-mediated immunity; hepatitis B virus; immunomodulation
ID DOWN-REGULATION; EXPRESSION; RESPONSES
AB Dysregulation of the host immune responses induced by host hepatitis B virus (HBV) interactions has been observed in acute-on-chronic liver failure (ACLF). Myeloid-derived suppressor cells (MDSCs), well known for their immunomodulatory properties, can suppress T-cell function by regulating the expression of CD3 zeta chain in cancer and autoimmune/infectious diseases while rarely have been studied in ACLF. In this study, MDSCs, CD4(+)/CD8(+) T cells, and CD3 zeta chain were analyzed by flow cytometry in peripheral blood mononuclear cells obtained from HBV-related ACLF patients, chronic hepatitis B (CHB) patients and healthy controls. ACLF patients were followed up for dynamic detection of MDSCs and observation of outcomes after treatment. Interestingly, peripheral CD14(+)CD33(+)CD11b(+)HLA-DR-/low MDSCs from ACLF patients were significantly increased compared to those from CHB patients and healthy controls. CD4(+)/CD8(+) T cell frequency and CD3 zeta chain expression in T cells were decreased in ACLF patients compared to those of healthy controls and were negatively correlated with matched MDSC frequency. Meanwhile, the frequency of MDSCs was closely correlated with biochemical parameters that are relevant for liver injury rather than virological parameters. Moreover, a lower level of MDSCs was correlated with a better short-term prognosis (within 4 weeks but not at 8 weeks), and MDSCs remained high in ACLF patients whose conditions worsened within a 4-week follow-up period after treatment. These results suggest that MDSCs are closely involved in cell-mediated immunity in HBV-related ACLF and that peripheral MDSC expansion is closely associated with disease severity and progression in HBV-related ACLF, which may serve as a predictor of short-term prognosis.
C1 [Zeng, Yingfu; Xu, Zhen; Gan, Weiqiang; Lin, Chaoshuang] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Infect Dis, 600 Tianhe Rd, Guangzhou 510630, Guangdong, Peoples R China.
[Li, Yiting] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Gen Practice, Guangzhou, Guangdong, Peoples R China.
[Lu, Lirong] Kunming Med Univ, Affiliated Hosp 1, Dept Infect Dis, Kunming, Yunnan, Peoples R China.
[Huang, Xiaohui] Sun Yat Sen Univ, Affiliated Hosp 3, Guangdong Key Lab Liver Dis Res, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Kunming Medical
University; Sun Yat Sen University
RP Lin, CS (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 3, Dept Infect Dis, 600 Tianhe Rd, Guangzhou 510630, Guangdong, Peoples R China.
EM lchaosh@mail.sysu.edu.cn
RI huang, xiaohui/KRP-2903-2024
FU National Nature Science Foundation of China [31370907]
FX National Nature Science Foundation of China, Grant/Award Number:
31370907
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NR 33
TC 20
Z9 22
U1 0
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0146-6615
EI 1096-9071
J9 J MED VIROL
JI J. Med. Virol.
PD AUG
PY 2019
VL 91
IS 8
BP 1510
EP 1518
DI 10.1002/jmv.25466
PG 9
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA IF6UI
UT WOS:000473215200017
PM 30905084
DA 2025-01-07
ER
PT J
AU Westermann, R
Zobbe, K
Cordtz, R
Haugaard, JH
Dreyer, L
AF Westermann, Rasmus
Zobbe, Kristian
Cordtz, Rene
Haugaard, Jeanette H.
Dreyer, Lene
TI Increased cancer risk in patients with cutaneous lupus erythematosus and
systemic lupus erythematosus compared with the general population: A
Danish nationwide cohort study
SO LUPUS
LA English
DT Article
DE Cutaneous lupus erythematosus; systemic lupus erythematosus; cancer;
autoimmune diseases; epidemiology
ID BREAST-CANCER; MALIGNANCIES; LYMPHOMA; REGISTRY; QUALITY; SLE
AB Objectives
To investigate if patients with cutaneous lupus erythematosus (CLE) or systemic lupus erythematosus (SLE) have an increased risk of cancer compared with the general population, and furthermore to identify specific cancer types associated with increased risk.
Methods
This is an observational cohort study of 5310 patients with CLE or SLE identified in the Danish National Patient Register from 1 January 1995 to 31 December 2014. The cohort was followed up for cancer by linkage to the Danish Cancer Registry. Based on the age, sex, and calendar specific cancer rates of the general population of Denmark, standardised incidence ratios (SIRs) were calculated.
Results
The patients with CLE or SLE were followed for 40.724 person-years, each group's average duration of follow-up being 6.9 and 8.1 years. The SIR for overall cancer (except non-melanoma skin cancer (NMSC)) was increased in patients with CLE 1.35 (95%CI 1.15 to 1.58) and patients with SLE 1.45 (95%CI 1.30 to 1.62). Both groups had high risks of hematological - including a 3-4-fold increased risk of non-Hodgkin lymphoma -, pancreatic, and lung cancers. Several cancers associated with oncogenic viruses as liver and tongue/mouth/pharynx were increased in the SLE group, while the risk of ovarian cancer was increased 2-4-fold only in the CLE group.
Conclusion
The overall risk of cancer was significantly increased in both patients with CLE and SLE. SIRs for hematological, pancreatic and lung cancers were elevated in both groups. Extra awareness of cancer in patients with SLE and patients with CLE should be considered.
C1 [Westermann, Rasmus; Cordtz, Rene; Dreyer, Lene] Aalborg Univ Hosp, Dept Rheumatol, Reberbansgade 15, DK-9000 Aalborg, Denmark.
[Westermann, Rasmus; Zobbe, Kristian] Rigshosp Gentofte, Ctr Rheumatol & Spine Dis, Copenhagen, Denmark.
[Zobbe, Kristian] Univ Copenhagen, Bispebjerg Frederiksberg Hosp, Parker Inst, Copenhagen, Denmark.
[Haugaard, Jeanette H.] Herlev & Gentofte Univ Hosp, Dept Dermatol Allergy & Venerol, Copenhagen, Denmark.
C3 Aalborg University; Aalborg University Hospital; Rigshospitalet;
University of Copenhagen; Bispebjerg Hospital
RP Westermann, R (corresponding author), Aalborg Univ Hosp, Dept Rheumatol, Reberbansgade 15, DK-9000 Aalborg, Denmark.
EM westermann2@live.dk
RI Westermann, Rasmus/ITU-6866-2023; Cordtz, rene/W-5412-2019
OI Cordtz, Rene/0000-0002-5271-2574; Westermann, Rasmus/0000-0002-8148-9658
FU [THU0288]
FX We hereby confirm that no industry affiliations or financial support
need to be declared. The abstract was presented as a poster presentation
at the EULAR 2020 E-Congress, June 3-6 2020 (Abstract number THU0288).
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NR 46
TC 16
Z9 16
U1 0
U2 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0961-2033
EI 1477-0962
J9 LUPUS
JI Lupus
PD APR
PY 2021
VL 30
IS 5
BP 752
EP 761
DI 10.1177/0961203321990106
EA JAN 2021
PG 10
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA RH6EM
UT WOS:000637122400001
PM 33497306
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Nakazawa, T
Naitoh, I
Hayashi, K
Sano, H
Miyabe, K
Shimizu, S
Joh, T
AF Nakazawa, Takahiro
Naitoh, Itaru
Hayashi, Kazuki
Sano, Hitoshi
Miyabe, Katsuyuki
Shimizu, Shuya
Joh, Takashi
TI Inflammatory bowel disease of primary sclerosing cholangitis: A distinct
entity?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Primary sclerosing cholangitis; Primary sclerosing cholangitis;
Inflammatory bowel disease; inflammatory bowel disease-associated with
primary sclerosing cholangitis; Immunoglobulin G4-related sclerosing
cholangitis
ID DOSE URSODEOXYCHOLIC ACID; ULCERATIVE-COLITIS; AUTOIMMUNE PANCREATITIS;
LIVER-TRANSPLANTATION; COLORECTAL NEOPLASIA; CLINICAL PROFILE; CANCER;
RISK; CHOLANGIOGRAPHY; PATHOGENESIS
AB This is a review of the characteristic findings of inflammatory bowel disease (IBD) associated with primary sclerosing cholangitis (PSC) and their usefulness in the diagnosis of sclerosing cholangitis. PSC is a chronic inflammatory disease characterized by idiopathic fibrous obstruction and is frequently associated with IBD. IBD-associated with PSC (PSC-IBD) shows an increased incidence of pancolitis, mild symptoms, and colorectal malignancy. Although an increased incidence of pancolitis is a characteristic finding, some cases are endoscopically diagnosed as right-sided ulcerative colitis. Pathological studies have revealed that inflammation occurs more frequently in the right colon than the left colon. The frequency of rectal sparing and backwash ileitis should be investigated in a future study based on the same definition. The cholangiographic findings of immunoglobulin G4-related sclerosing cholangitis (IgG4-SC) are similar to those of PSC. The rare association between IBD and IgG4-SC and the unique characteristics of PSC- IBD are useful findings for distinguishing PSC from IgG4-SC. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Nakazawa, Takahiro; Naitoh, Itaru; Hayashi, Kazuki; Miyabe, Katsuyuki; Shimizu, Shuya; Joh, Takashi] Nagoya City Univ, Grad Sch Med Sci, Dept Gastroenterol & Metab, Nagoya, Aichi 4678601, Japan.
[Sano, Hitoshi] Gifu Prefectual Tajimi Hosp, Dept Gastroenterol, Gifu 5070042, Japan.
C3 Nagoya City University
RP Nakazawa, T (corresponding author), Nagoya City Univ, Grad Sch Med Sci, Dept Gastroenterol & Metab, Mizuho Ku, 1 Kawasumi,Mizuho Cho, Nagoya, Aichi 4678601, Japan.
EM tnakazaw@med.nagoya-cu.ac.jp
RI ; Naitoh, Itaru/AAB-7252-2020
OI Miyabe, Katsuyuki/0000-0002-4915-9835; Naitoh, Itaru/0000-0001-8342-886X
FU Grants-in-Aid for Scientific Research [23591015] Funding Source: KAKEN
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NR 47
TC 29
Z9 33
U1 0
U2 2
PU BAISHIDENG PUBL GRP CO LTD
PI WANCHAI
PA ROOM 1701, 17-F, HENAN BUILDING, NO. 90, JAFFE RD, WANCHAI, HONG KONG
100025, PEOPLES R CHINA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 28
PY 2014
VL 20
IS 12
BP 3245
EP 3254
DI 10.3748/wjg.v20.i12.3245
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AE0PH
UT WOS:000333667700019
PM 24696608
OA Green Published, Green Submitted, hybrid
DA 2025-01-07
ER
PT J
AU Tilg, H
Adolph, TE
Tacke, F
AF Tilg, Herbert
Adolph, Timon E.
Tacke, Frank
TI Therapeutic modulation of the liver immune microenvironment
SO HEPATOLOGY
LA English
DT Review
ID NECROSIS-FACTOR-ALPHA; PRIMARY SCLEROSING CHOLANGITIS; HUMAN GUT
MICROBIOME; NLRP3 INFLAMMASOME ACTIVATION; CHIMERIC MONOCLONAL-ANTIBODY;
SEVERE ALCOHOLIC HEPATITIS; IL-1 RECEPTOR ANTAGONIST; AUTOIMMUNE
HEPATITIS; AKKERMANSIA-MUCINIPHILA; TNF-ALPHA
AB Inflammation is a hallmark of progressive liver diseases such as chronic viral or immune-mediated hepatitis, alcohol-associated liver disease, and NAFLD. Preclinical and clinical studies have provided robust evidence that cytokines and related cellular stress sensors in innate and adaptive immunity orchestrate hepatic disease processes. Unresolved inflammation and liver injury result in hepatic scarring, fibrosis, and cirrhosis, which may culminate in HCC. Liver diseases are accompanied by gut dysbiosis and a bloom of pathobionts, fueling hepatic inflammation. Anti-inflammatory strategies are extensively used to treat human immune-mediated conditions beyond the liver, while evidence for immunomodulatory therapies and cell therapy-based strategies in liver diseases is only emerging. The development and establishment of novel immunomodulatory therapies for chronic liver diseases has been dampened by several clinical challenges, such as invasive monitoring of therapeutic efficacy with liver biopsy in clinical trials and risk of DILI in several studies. Such aspects prevented advancements of novel medical therapies for chronic inflammatory liver diseases. New concepts modulating the liver immune environment are studied and eagerly awaited to improve the management of chronic liver diseases in the future.
C1 [Tilg, Herbert; Adolph, Timon E.] Med Univ Innsbruck, Dept Internal Med Gastroenterol Hepatol Endocrinol, Innsbruck, Austria.
[Tacke, Frank] Charite Univ Med Berlin, Dept Hepatol & Gastroenterol, Campus Virchow Klinikum, Berlin, Germany.
[Tacke, Frank] Campus Charite Mitte, Berlin, Germany.
[Tilg, Herbert] Med Univ Innsbruck, Dept Internal Med 1, Anichstr 35, A-6020 Innsbruck, Austria.
C3 Medical University of Innsbruck; Berlin Institute of Health; Free
University of Berlin; Humboldt University of Berlin; Charite
Universitatsmedizin Berlin; Berlin Institute of Health; Free University
of Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
Berlin; Medical University of Innsbruck
RP Tilg, H (corresponding author), Med Univ Innsbruck, Dept Internal Med 1, Anichstr 35, A-6020 Innsbruck, Austria.
EM Herbert.Tilg@i-med.ac.at
RI Tilg, Herbert/AEO-9569-2022; Tacke, Frank/ABF-2212-2020
OI Tacke, Frank/0000-0001-6206-0226
FU VASCage (Centre for Promoting Vascular Health in the Ageing Community);
Austrian Ministry for Transport, Innovation and Technology; Austrian
Ministry for Digital and Economic Affairs; federal states Tyrol,
Salzburg and Vienna; Austrian Science Fund (FWF) [P33070]; European
Research Council [ERC STG: 101039320]; German Research Foundation (DFG)
[403224013]; German Ministry of Education and Research (BMBF); Austrian
Science Fund (FWF) [P33070] Funding Source: Austrian Science Fund (FWF)
FX Herbert Tilg is supported by the excellence initiative VASCage (Centre
for Promoting Vascular Health in the Ageing Community), an R & D
K-Centre (COMET program - Competence Centers for Excellent Technologies)
funded by the Austrian Ministry for Transport, Innovation and
Technology, the Austrian Ministry for Digital and Economic Affairs and
the federal states Tyrol, Salzburg and Vienna. Timon E. Adolph is
supported by the Austrian Science Fund (FWF P33070) and the European
Research Council (ERC - STG: 101039320). Frank Tacke is supported by the
German Research Foundation (DFG SFBfTRR 296 and CRC1382, Project-ID
403224013) and the German Ministry of Education and Research (BMBF
DEEP-HCC consortium, BMBF lmmun Avatar consortium).
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NR 279
TC 10
Z9 9
U1 3
U2 23
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD NOV
PY 2023
VL 78
IS 5
BP 1581
EP 1601
DI 10.1097/HEP.0000000000000386
EA APR 2023
PG 21
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA U8JK2
UT WOS:001058670000001
PM 37057876
DA 2025-01-07
ER
PT J
AU Liang, HF
Manne, S
Shick, J
Lissoos, T
Dolin, P
AF Liang, Huifang
Manne, Sudhakar
Shick, Jesse
Lissoos, Trevor
Dolin, Paul
TI Incidence, prevalence, and natural history of primary sclerosing
cholangitis in the United Kingdom
SO MEDICINE
LA English
DT Article
DE Clinical Practice Research Datalink (CPRD); hazard ratio; incidence;
natural history; prevalence; primary sclerosing cholangitis (PSC)
ID INFLAMMATORY-BOWEL-DISEASE; POPULATION-BASED COHORT; ANEMIA;
ASSOCIATION; COMMUNITY; MORTALITY; SPECTRUM; RISK
AB Primary sclerosing cholangitis (PSC) is a rare obliterative fibrotic condition of the bile ducts. We assessed PSC epidemiology and natural history within the UK Clinical Practice Research Datalink (CPRD).
Incidence and natural history of PSC were evaluated in a retrospective cohort study using linkage of CPRD, Hospital Episode Statistics, and Office for National Statistics data. Data from age, sex, and general practice-matched population controls provided a context for the incident PSC patients. Liver disease other than PSC was defined as autoimmune hepatitis, hepatitis, hepatomegaly, liver failure, cirrhosis, portal hypertension, cholangiocarcinoma, or hepatobiliary cancer.
The age-standardized incidence of PSC was 0.68 (95% confidence interval [CI] 0.45-0.99) per 100,000 person-years and the age-standardized prevalence was 5.58 (95% CI 4.82-7.35) per 100,000 during 1998 to 2014. In all, 250 incident PSC patients met the inclusion criteria and each was matched with 5 controls (mean age 54 +/- 18 years, men 63.2%). A higher percentage of PSC patients had a history of inflammatory bowel disease (54% vs 2%) and liver disease other than PSC (22% vs 1%) than controls (standardized difference(weighted) >0.1). During a median follow-up of 5 years, PSC patients were more likely to develop adverse health outcomes. The mortality rate per 1000 person-years was 3-fold higher in PSC than population controls (49.5 vs 16.1; incidence rate ratio 3.1, 95% CI 2.2-4.2).
The incidence and prevalence of PSC observed in the UK CPRD were either comparable with or higher than previous studies. Compared with the general population, PSC patients had worse health outcomes including PSC disease progression, complications, and higher mortality.
C1 [Liang, Huifang; Manne, Sudhakar; Shick, Jesse] Takeda Dev Ctr Amer Inc, Deerfield, IL USA.
[Lissoos, Trevor] Takeda Pharmaceut USA Inc, Deerfield, IL USA.
[Dolin, Paul] Takeda Dev Ctr Europe Ltd, London, England.
C3 Takeda Pharmaceutical Company Ltd; Takeda Development Center Americas,
Inc.; Takeda Pharmaceutical Company Ltd; Takeda Pharmaceuticals USA Inc.
(TPUSA); Takeda Pharmaceutical Company Ltd; Takeda Development Centre
Europe Ltd.
RP Liang, HF (corresponding author), Takeda Dev Ctr Amer Inc, Pharmacoepidemiol, One Takeda Pkwy, Deerfield, IL 60015 USA.
EM huifang.liang@gmail.com
RI Liang, Huifang/IZQ-4814-2023; Liang, Huifang/A-8224-2010
OI Liang, Huifang/0000-0002-4145-4784
FU Takeda Development Center Americas, Inc.; Takeda Development Centre
Europe Ltd.
FX This study was funded by Takeda Development Center Americas, Inc., and
Takeda Development Centre Europe Ltd.
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
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SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD JUN
PY 2017
VL 96
IS 24
AR e7116
DI 10.1097/MD.0000000000007116
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA EX9QZ
UT WOS:000403594100017
PM 28614231
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Mok, K
Wu, C
Chan, S
Wong, G
Wong, VWS
Ma, B
Lui, R
AF Mok, Kevin
Wu, Claudia
Chan, Stephen
Wong, Grace
Wong, Vincent Wai-Sun
Ma, Brigette
Lui, Rashid
TI Clinical Management of Gastrointestinal and Liver Toxicities of Immune
Checkpoint Inhibitors
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE ICI; Immune checkpoint inhibitors; Immune-related adverse events;
Immunotherapy; irAE; Toxicity
ID DOUBLE-BLIND; ANTI-PD-1; FEATURES; IPILIMUMAB; IMMUNOTHERAPY;
CHOLANGITIS; NIVOLUMAB; DIAGNOSIS; HEPATITIS; PATHWAYS
AB Immune checkpoint inhibitors have transformed the treatment paradigm for various types of cancer. Nonetheless, with the utilization of these groundbreaking treatments, immune-related adverse events (irAEs) are increasingly encountered. Colonic and hepatic involvement are among the most frequently encountered irAEs. Drug-induced side effects, infectious causes, and tumor-related symptoms are the key differentials for irAE complications. Potential risk factors for the development of irAEs include combination use of immune checkpoint inhibitors, past development of irAEs with other immunotherapy treatments, certain concomitant drugs, and a pre-existing personal or family history of autoimmune illness such as inflammatory bowel disease. The importance of early recognition, timely and proper management cannot be understated, as there are profound clinical implications on the overall cancer treatment plan and prognosis once these adverse events occur. Herein, we cover the clinical management of the well-established gastrointestinal irAEs of enterocolitis and hepatitis, and also provide an overview of several other emerging entities.
C1 [Mok, Kevin; Ma, Brigette; Lui, Rashid] Chinese Univ Hong Kong, Dept Clin Oncol, Prince Wales Hosp, Hong Kong, Peoples R China.
[Wu, Claudia; Wong, Grace; Wong, Vincent Wai-Sun; Lui, Rashid] Chinese Univ Hong Kong, Prince Wales Hosp, Dept Med & Therapeut, Div Gastroenterol & Hepatol, Hong Kong, Peoples R China.
[Wu, Claudia; Wong, Grace; Wong, Vincent Wai-Sun; Ma, Brigette; Lui, Rashid] Chinese Univ Hong Kong, Inst Digest Dis, Hong Kong, Peoples R China.
[Chan, Stephen] Chinese Univ Hong Kong, Prince Wales Hosp, Hong Kong Canc Inst,Dept Clin Oncol, YK Pao Ctr Canc,State Key Lab Translat Oncol, Hong Kong, Peoples R China.
[Lui, Rashid] Prince Wales Hosp, Dept Med & Therapeut, Shatin, Lui Che Woo Clin Sci Bldg, 9-F, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong; Prince of Wales Hospital; Chinese
University of Hong Kong; Prince of Wales Hospital; Chinese University of
Hong Kong; Chinese University of Hong Kong; Prince of Wales Hospital;
Chinese University of Hong Kong; Prince of Wales Hospital
RP Lui, R (corresponding author), Prince Wales Hosp, Dept Med & Therapeut, Shatin, Lui Che Woo Clin Sci Bldg, 9-F, Hong Kong, Peoples R China.
EM rashidlui@cuhk.edu.hk
RI Wong, Vincent/K-3864-2014
OI Mok, Kevin/0000-0002-3638-3395
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NR 92
TC 1
Z9 2
U1 2
U2 3
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD MAR
PY 2024
VL 23
IS 1
BP 4
EP 13
DI 10.1016/j.clcc.2023.12.003
EA MAR 2024
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OR8L2
UT WOS:001209092500001
PM 38172003
DA 2025-01-07
ER
PT J
AU Amirullah, NA
Abdullah, E
Abidin, NZ
Abdullah, N
Manickam, S
AF Amirullah, Nur Amalina
Abdullah, Erlina
Abidin, Nurhayati Zainal
Abdullah, Noorlidah
Manickam, Sivakumar
TI Therapeutic potential of mushrooms: A review on NF-κB modulation in
chronic inflammation
SO FOOD BIOSCIENCE
LA English
DT Review
DE Bioactive compounds; Chronic diseases; Fungal metabolites; Inflammation;
Medicinal mushrooms; Neuroinflammation
ID DEEP EUTECTIC SOLVENT; OXIDATIVE STRESS; ANTIINFLAMMATORY PROPERTIES;
MEDICINAL MUSHROOM; METABOLIC SYNDROME; EDIBLE MUSHROOMS; P38 MAPK;
PATHWAY; TARGET; CANCER
AB Numerous mushroom species are valued not just for their flavor but also for their health advantages. Historically, these mushrooms have been utilized for medicinal purposes across different parts of the world. Research has revealed that metabolites derived from these fungi have health benefits. Recently, there has been a growing interest in understanding how these fungal metabolites provide their healing effects and comprehend their mechanisms of action. A primary focus is the nuclear factor NF-kappa B, kappa B, a family of transcription factors essential for regulating inflammation, cell proliferation, and apoptosis. Dysregulation and abnormal activation of NF-kappa B kappa B proteins are associated with a variety of diseases. Various studies have investigated mushroom compounds and their impact on various conditions, including inflammatory bowel disease, gut health, metabolic syndrome, neuroinflammation, liver injury, renal and pulmonary diseases, and autoimmune disorders. This review provides a comprehensive summary of the NF-kappa B kappa B signaling pathway and other related inflammatory pathways. It discusses the bioactive compounds found in mushrooms, their potential to alleviate various diseases, and the specific inflammatory pathways, particularly NF-kappa B, kappa B, that these bioactives target.
C1 [Amirullah, Nur Amalina; Abdullah, Erlina; Abidin, Nurhayati Zainal; Abdullah, Noorlidah] Univ Malaya, Inst Biol Sci, Fac Sci, Kuala Lumpur 50603, Malaysia.
[Amirullah, Nur Amalina] Univ Putra Malaysia, Fac Med & Hlth Sci, Dept Nutr, Serdang 43400, Malaysia.
[Abdullah, Erlina] Lincoln Univ Coll, Fac Appl Sci, Dept Biotechnol, Petaling Jaya 47301, Selangor, Malaysia.
[Manickam, Sivakumar] Univ Teknol Brunei, Fac Engn, Petr & Chem Engn Dept, BE-1410 Bandar Seri Begawan, Brunei.
C3 Universiti Malaya; Universiti Putra Malaysia; Lincoln University
College; University of Technology Brunei
RP Amirullah, NA (corresponding author), Univ Malaya, Inst Biol Sci, Fac Sci, Kuala Lumpur 50603, Malaysia.
EM amalinaamirullah@upm.edu.my
RI ABIDIN, NURHAYATI/B-9429-2010; MANICKAM, SIVAKUMAR/I-2228-2014;
abdullah, erlina/KCJ-9315-2024
OI MANICKAM, SIVAKUMAR/0000-0001-9102-4013
FU Universiti Malaya Special Research Fund Assistance (BKS) [BKS013-2018];
Universiti Malaya Research University Grant (RU Faculty) [GPF008B-2018];
Universiti Malaya
FX The authors received support from the Universiti Malaya Special Research
Fund Assistance (BKS) [BKS013-2018] and the Universiti Malaya Research
University Grant (RU Faculty) [GPF008B-2018] , which made this work
possible. The authors thank Universiti Malaya for this support.
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NR 174
TC 1
Z9 1
U1 7
U2 7
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2212-4292
EI 2212-4306
J9 FOOD BIOSCI
JI Food Biosci.
PD DEC
PY 2024
VL 62
AR 105059
DI 10.1016/j.fbio.2024.105059
EA SEP 2024
PG 25
WC Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology
GA H8E9T
UT WOS:001325729400001
DA 2025-01-07
ER
PT J
AU Roszkowska, P
Klimczak, E
Ostrycharz, E
Raczka, A
Wojciechowska-Koszko, I
Dybus, A
Cheng, YH
Yu, YH
Mazgaj, S
Hukowska-Szematowicz, B
AF Roszkowska, Paulina
Klimczak, Emilia
Ostrycharz, Ewa
Raczka, Aleksandra
Wojciechowska-Koszko, Iwona
Dybus, Andrzej
Cheng, Yeong-Hsiang
Yu, Yu-Hsiang
Mazgaj, Szymon
Hukowska-Szematowicz, Beata
TI Small Intestinal Bacterial Overgrowth (SIBO) and Twelve Groups of
Related Diseases-Current State of Knowledge
SO BIOMEDICINES
LA English
DT Review
DE gut microbiota; small intestinal bacteria overgrowth; SIBO; diet;
dysbiosis; microbial ecology
ID IRRITABLE-BOWEL-SYNDROME; OROCECAL TRANSIT-TIME; CHRONIC HEART-FAILURE;
FATTY LIVER-DISEASE; GASTROINTESTINAL MOTILITY; GUT MICROBIOTA; CLINICAL
EFFECTIVENESS; SYSTEMIC-SCLEROSIS; PERIPHERAL-BLOOD; HIGH PREVALENCE
AB The human gut microbiota creates a complex microbial ecosystem, characterized by its high population density, wide diversity, and complex interactions. Any imbalance of the intestinal microbiome, whether qualitative or quantitative, may have serious consequences for human health, including small intestinal bacterial overgrowth (SIBO). SIBO is defined as an increase in the number of bacteria (103-105 CFU/mL), an alteration in the bacterial composition, or both in the small intestine. The PubMed, Science Direct, Web of Science, EMBASE, and Medline databases were searched for studies on SIBO and related diseases. These diseases were divided into 12 groups: (1) gastrointestinal disorders; (2) autoimmune disease; (3) cardiovascular system disease; (4) metabolic disease; (5) endocrine disorders; (6) nephrological disorders; (7) dermatological diseases; (8) neurological diseases (9); developmental disorders; (10) mental disorders; (11) genetic diseases; and (12) gastrointestinal cancer. The purpose of this comprehensive review is to present the current state of knowledge on the relationships between SIBO and these 12 disease groups, taking into account risk factors and the causal context. This review fills the evidence gap on SIBO and presents a biological-medical approach to the problem, clearly showing the groups and diseases having a proven relationship with SIBO, as well as indicating groups within which research should continue to be expanded.
C1 [Roszkowska, Paulina; Wojciechowska-Koszko, Iwona] Pomeranian Med Univ, Dept Diagnost Immunol, St Powstancow Wielkopolskich 72, PL-70111 Szczecin, Poland.
[Klimczak, Emilia; Ostrycharz, Ewa; Mazgaj, Szymon; Hukowska-Szematowicz, Beata] Univ Szczecin, Inst Biol, St Z Felczaka 3c, PL-71412 Szczecin, Poland.
[Ostrycharz, Ewa] Univ Szczecin, Doctoral Sch, St A Mickiewicza 16, PL-71412 Szczecin, Poland.
[Ostrycharz, Ewa; Hukowska-Szematowicz, Beata] Univ Szczecin, Mol Biol & Biotechnol Ctr, St Waska 13, PL-71412 Szczecin, Poland.
[Raczka, Aleksandra; Dybus, Andrzej] West Pomeranian Univ Technol, Dept Genet, St Aleja Piastow 45, PL-70311 Szczecin, Poland.
[Cheng, Yeong-Hsiang; Yu, Yu-Hsiang] Natl Ilan Univ, Dept Biotechnol & Anim Sci, Yilan 26047, Taiwan.
C3 Pomeranian Medical University; University of Szczecin; University of
Szczecin; University of Szczecin; West Pomeranian University of
Technology; National Ilan University
RP Hukowska-Szematowicz, B (corresponding author), Univ Szczecin, Inst Biol, St Z Felczaka 3c, PL-71412 Szczecin, Poland.; Hukowska-Szematowicz, B (corresponding author), Univ Szczecin, Mol Biol & Biotechnol Ctr, St Waska 13, PL-71412 Szczecin, Poland.
EM paulina.roszkowska@pum.edu.pl; klimczak-emilia@wp.pl;
ewa.ostrycharz@usz.edu.pl; aleksandra.raczka@zut.edu.pl;
iwona.wojciechowska.koszko@pum.edu.pl; andrzej.dybus@zut.edu.pl;
yhcheng@ems.niu.edu.tw; yuyh@niu.edu.tw; szymon.p.mazgaj@gmail.com;
beata.hukowska-szematowicz@usz.edu.pl
RI Yu, Yu-Hsiang/J-4424-2019; Hukowska-Szematowicz, Beata/AAT-9501-2021;
Dybus, Andrzej/I-3274-2016
OI Hukowska-Szematowicz, Beata/0000-0002-2776-2799; Dybus,
Andrzej/0000-0002-1116-6933; Yu, Yu-Hsiang/0000-0001-9629-8478
FU Pomeranian Medical University in Szczecin
FX No Statement Available
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NR 211
TC 2
Z9 2
U1 5
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD MAY
PY 2024
VL 12
IS 5
AR 1030
DI 10.3390/biomedicines12051030
PG 34
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA SD1J1
UT WOS:001232425400001
PM 38790992
OA gold
DA 2025-01-07
ER
PT J
AU Chen, CT
Tseng, YC
Yang, CW
Lin, HH
Chen, PJ
Huang, TY
Shih, YL
Chang, WK
Hsieh, TY
Chu, HC
AF Chen, Chun-Ting
Tseng, Yu-Chen
Yang, Chih-Wei
Lin, Hsuan-Hwai
Chen, Peng-Jen
Huang, Tien-Yu
Shih, Yu-Lueng
Chang, Wei-Kuo
Hsieh, Tsai-Yuan
Chu, Heng-Cheng
TI Increased Risks of Spontaneous Bacterial Peritonitis and Interstitial
Lung Disease in Primary Biliary Cirrhosis Patients With Concomitant
Sjogren Syndrome
SO MEDICINE
LA English
DT Article
ID INFILTRATING MONONUCLEAR-CELLS; ASCITIC FLUID; PULMONARY INVOLVEMENT;
PROTEIN-CONCENTRATION; PREDICTIVE FACTORS; RENAL INVOLVEMENT;
THYROID-DISEASE; MANAGEMENT; DIAGNOSIS; COMORBIDITIES
AB The incidence of Sjogren syndrome (SS) in primary biliary cirrhosis (PBC) patients is high. The influence of SS on the clinical outcomes of PBC patients, however, remains unclear. Our study retrospectively collected data on PBC-only patients and PBC patients with concomitant SS (PBC-SS) to compare the clinical differences of long-term outcomes between them.
A total of 183 patients were diagnosed with PBC from January 1999 to December 2014 at our hospital. Of these, the authors excluded patients with diabetes, hypertension, advanced liver cirrhosis at initial diagnosis of PBC (Child-Turcotte-Pugh classification score of >= 7) and other liver diseases (ie, alcoholic liver disease, alpha-antitrypsin deficiency, viral hepatitis, and primary sclerosing cholangitis), and autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. Of the remaining 125 patients, 77 (61.6%) were PBC-only and 48 (38.4%) were PBC-SS patients.
The mean follow-up duration was 8.76 years. During the observation period, the incidence of interstitial lung disease was higher in the PBC-SS group than in the PBC-only group (P = 0.005). The occurrence of spontaneous bacterial peritonitis was significantly different in PBC-SS patients than in PBC-only patients (P = 0.002). The overall survival was lower in PBC-SS patients than in PBC-only patients (P = 0.033). Although the incidence of hepatocellular carcinoma, end-stage renal disease, variceal bleeding, and hypothyroidism were all higher in the PBC-SS group than in the PBC-only group, the differences were not significant.
Our study suggests that PBC-SS patients have a higher risk of developing interstitial lung disease and spontaneous bacterial peritonitis and have a poor prognosis. Aggressive surveillance of thyroid and pulmonary functions should therefore be performed in these patients.
C1 [Chen, Chun-Ting; Tseng, Yu-Chen; Yang, Chih-Wei; Lin, Hsuan-Hwai; Chen, Peng-Jen; Huang, Tien-Yu; Shih, Yu-Lueng; Chang, Wei-Kuo; Hsieh, Tsai-Yuan] Natl Def Med Ctr, Div Gastroenterol, Dept Internal Med, Triserv Gen Hosp, Taipei, Taiwan.
[Chu, Heng-Cheng] Taipei Med Univ Hosp, Div Gastroenterol, Dept Internal Med, Taipei, Taiwan.
C3 National Defense Medical Center; Tri-Service General Hospital; Taipei
Medical University; Taipei Medical University Hospital
RP Chu, HC (corresponding author), 252 Wu Xing St,Xinyi Dist 110, Taipei, Taiwan.
EM chu5583@ms55.hinet.net
RI Cheng, Ann-Lii/ACM-0936-2022
OI Yang, Chih Wei/0000-0001-9282-811X
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NR 40
TC 21
Z9 25
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD JAN
PY 2016
VL 95
IS 2
AR e2537
DI 10.1097/MD.0000000000002537
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DE4YD
UT WOS:000370635900001
PM 26765478
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Lalazar, G
Preston, S
Zigrnond, E
Ben Yáacov, A
Ilan, Y
AF Lalazar, Gadi
Preston, Sarah
Zigrnond, Ehud
Ben Yaacov, Arni
Ilan, Yaron
TI Glycolipids as immune modulatory tools
SO MINI-REVIEWS IN MEDICINAL CHEMISTRY
LA English
DT Review
ID KILLER T-CELLS; VERSUS-HOST-DISEASE; NKT CELLS;
ALPHA-GALACTOSYLCERAMIDE; MURINE MODEL; ALTERED NKT; T(H)2 BIAS;
RECOGNITION; GLUCOCEREBROSIDE; ANTIGENS
AB NKT cells are a subset of regulatory lymphocytes characterized by co-expression of the NK cell receptor-CD161 and an invariant TCR-alpha chain (V alpha 14-J alpha 28). They are most abundant in the liver, spleen, and bone marrow. NKT lymphocytes have been implicated in the regulation of autoimmune processes in both mice and humans. Activation of NKT lymphocytes leads to rapid amplification of either IFN gamma or IL4, endowing these cells with the capability to mediate both pro-inflammatory and anti-inflammatory immune responses. Activation of this subset of cells is associated with significant liver damage in the Concanavalin A immune mediated hepatitis model. Administration of CD1d ligand has a protective role in collagen-induced arthritis in mice. Disease amelioration was associated with a shift in the immune balance from a pathological Th1 type response towards a protective Th2 type response. In humans, patients with SLE, scleroderma, diabetes, multiple sclerosis, and rheumatoid arthritis have lower numbers of peripheral NKT cells. NKT lymphocytes promote tumor rejection in experimental models of tumor immunotherapy. In contrast, NKT lymphocyte-related anti-tumor activity is associated with pro-inflammatory Th1-type immune responses. NKT cells were shown to have a role in suppression of hepatocellular carcinoma (HCC) via immune regulation towards tumor derived antigens, and adoptive transfer of dendritic cells pulsed ex vivo with the same antigens.
NKT lymphocytes are activated by interaction of their TCR with glycolipids presented by CD1d, a nonpolymorphic, MHC class I-like molecule expressed by antigen presenting cells, and also by hepatocytes. Several possible ligands for NKT cells have recently been suggested including CD1d bound Glucocerebroside. Glucocerebroside (GC, beta-glucosylceramide), a naturally occurring glycolipid, is a metabolic intermediate in the anabolic and catabolic pathways of complex glycosphingolipids. Its synthesis from ceramide is catalyzed by the enzyme glucosylceramide synthase. Inherited deficiency of glucocerebrosidase, a lysosomal hydrolase, results in Gaucher's disease. Patients with Gaucher's disease have altered humoral and cellular immune profiles and increased peripheral blood NKT lymphocytes. CD1d-bound glucocerebroside does not activate NKT cells directly, and may inhibit activation of NKT cells by alpha-GalCer. On the other hand, glucosylceramide-synthase deficiency was shown to lead to defective ligand presentation by CD1d, with secondary inhibition of NKT cell activation. Recent studies have suggested that a number of glycolipids, including GC, have an immune modulatory effect in several immune mediated disorders. The ability to alter NKT lymphocyte function in various settings and the potential application of natural glycolipids for treatment are discussed.
C1 Hebrew Univ Jerusalem, Dept Med, Hadassah Med Ctr, Liver Unit, IL-91120 Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hadassah University Medical Center
RP Ilan, Y (corresponding author), Hebrew Univ Jerusalem, Dept Med, Hadassah Med Ctr, Liver Unit, POB 12000, IL-91120 Jerusalem, Israel.
EM ilan@hadassah.org.il
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NR 53
TC 59
Z9 71
U1 0
U2 16
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-5575
EI 1875-5607
J9 MINI-REV MED CHEM
JI Mini-Rev. Med. Chem.
PD NOV
PY 2006
VL 6
IS 11
BP 1249
EP 1253
DI 10.2174/138955706778742722
PG 5
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 089YO
UT WOS:000240918000007
PM 17100636
DA 2025-01-07
ER
PT J
AU Meng, ZJ
Ma, ZY
Zhang, EJ
Kosinska, AD
Liu, J
Zhang, XY
Zhou, TL
Wu, J
Dahmen, U
Dirsch, O
Yang, DL
Roggendorf, M
Lu, MJ
AF Meng, Zhongji
Ma, Zhiyong
Zhang, Ejuan
Kosinska, Anna D.
Liu, Jia
Zhang, Xiaoyong
Zhou, Tianlun
Wu, Jun
Dahmen, Uta
Dirsch, Olaf
Yang, Dongliang
Roggendorf, Michael
Lu, Mengji
TI Novel Woodchuck Hepatitis Virus (WHV) Transgene Mouse Models Show
Sex-Dependent WHV Replicative Activity and Development of Spontaneous
Immune Responses to WHV Proteins
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID CYTOTOXIC T-LYMPHOCYTES; B-VIRUS; HEPATOCELLULAR-CARCINOMA;
GENE-EXPRESSION; CELL RESPONSE; CORE PROTEIN; IN-VIVO; INFECTION; MICE;
IMMUNIZATION
AB The woodchuck model is an informative model for studies on hepadnaviral infection. In this study, woodchuck hepatitis virus (WHV) transgenic (Tg) mouse models based on C57BL/6 mice were established to study the pathogenesis associated with hepadnaviral infection. Two lineages of WHV Tg mice, harboring the WHV wild-type genome (lineage 1217) and a mutated WHV genome lacking surface antigen (lineage 1281), were generated. WHV replication intermediates were detected by Southern blotting. DNA vaccines against WHV proteins were applied by intramuscular injection. WHV-specific immune responses were analyzed by flow cytometry and enzyme-linked immunosorbent assays (ELISAs). The presence of WHV transgenes resulted in liver-specific but sex-and age-dependent WHV replication in Tg mice. Pathological changes in the liver, including hepatocellular dysplasia, were observed in aged Tg mice, suggesting that the presence of WHV transgenes may lead to liver diseases. Interestingly, Tg mice of lineage 1281 spontaneously developed T-and B-cell responses to WHV core protein (WHcAg). DNA vaccination induced specific immune responses to WHV proteins in WHV Tg mice, indicating a tolerance break. The magnitude of the induced WHcAg-specific immune responses was dependent on the effectiveness of different DNA vaccines and was associated with a decrease in WHV loads in mice. In conclusion, sex-and age-dependent viral replication, development of autoimmune responses to viral antigens, pathological changes in the liver in WHV Tg mice, and the possibility of breaking immune tolerance toWHVtransgenes will allow future studies on pathogenesis related to hepadnaviral infection and therapeutic vaccines.
C1 [Meng, Zhongji; Ma, Zhiyong; Zhang, Ejuan; Kosinska, Anna D.; Liu, Jia; Zhang, Xiaoyong; Roggendorf, Michael; Lu, Mengji] Univ Duisburg Essen, Univ Hosp Essen, Inst Virol, Essen, Germany.
[Meng, Zhongji] Hubei Univ Med, Taihe Hosp, Dept Infect Dis, Shiyan, Peoples R China.
[Zhou, Tianlun] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Wu, Jun; Yang, Dongliang] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Infect Dis, Wuhan 430074, Peoples R China.
[Dahmen, Uta] Univ Jena, Univ Hosp Jena, Dept Gen Visceral & Vasc Surg, Jena, Germany.
[Dirsch, Olaf] Univ Jena, Univ Hosp Jena, Inst Pathol, Jena, Germany.
C3 University of Duisburg Essen; Hubei University of Medicine; Fox Chase
Cancer Center; Huazhong University of Science & Technology; Friedrich
Schiller University of Jena; Friedrich Schiller University of Jena
RP Lu, MJ (corresponding author), Univ Duisburg Essen, Univ Hosp Essen, Inst Virol, Essen, Germany.
EM mengji.lu@uni-due.de; mengji.lu@uni-due.de
RI Lu, Mengji/ABF-9410-2020; ZHOU, Tianlun/LNP-3229-2024
OI Meng, Zhongji/0000-0003-0401-535X; Kosinska, Anna D./0000-0002-6352-1415
FU German Research Foundation [TRR60, GK1045, GK1949]; Chinese Research
Foundation [Z20102101, 2011BCB030, 2013ZX10002-001]
FX This study was supported by grants from the German Research Foundation
(TRR60, GK1045, and GK1949) and the Chinese Research Foundation
(Z20102101, 2011BCB030, and 2013ZX10002-001).
CR [Anonymous], use of laboratory animals
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NR 38
TC 9
Z9 9
U1 0
U2 8
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD FEB
PY 2014
VL 88
IS 3
BP 1573
EP 1581
DI 10.1128/JVI.02086-13
PG 9
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA 291UU
UT WOS:000329857000015
PM 24257601
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Sun, YQ
Zhang, JY
Lv, S
Wang, H
Gong, M
Du, N
Liu, HH
Zhang, N
Jing, J
Zhou, C
Zhang, F
Wang, ZR
AF Sun, Yongqiang
Zhang, Ji-Yuan
Lv, Sa
Wang, Huan
Gong, Man
Du, Ning
Liu, Honghong
Zhang, Ning
Jing, Jing
Zhou, Chao
Zhang, Fan
Wang, Zongren
TI Interleukin-33 Promotes Disease Progression in Patients with Primary
Biliary Cirrhosis
SO TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
DE disease progression; immune pathogenesis; interleukin-33; liver lesion;
primary biliary cirrhosis
ID IL-33/ST2 AXIS; LIVER-DAMAGE; CELLS; INNATE; TARGET
AB Primary biliary cirrhosis (PBC) is a progressive autoimmune liver disease that can cause a series of complications, including cirrhosis, liver failure and hepatocellular carcinoma. Interleukin-33 (IL-33) is expressed in various non-hematopoietic cells and a certain population of immune cells, and exerts its biological effects by binding to the specific receptor, suppression of tumorigenicity 2 (ST2). A soluble form of ST2 (sST2) has been postulated to act as a decoy receptor for IL-33. In this study, we aimed to investigate the role of IL-33 in the pathogenesis of PBC. The study included 20 healthy controls and 68 patients with PBC. We thus found the increased serum IL-33 levels in PBC patients. Its elevated levels were positively correlated with serum alkaline phosphatase levels (a key parameter for the definition of PBC) and with Child-Pugh scores, which were used to determine the prognosis of liver cirrhosis. Moreover, the serum concentrations of sST2 were significantly higher in PBC patients compared with healthy subjects, irrespective of the disease severity. Importantly, the cells that express IL-33 and/or myeloperoxidase (a marker for neutrophils) were accumulated in the livers of PBC patients, and their number increased with the severity of liver lesions. Lastly, in vitro chemotaxis assays revealed that IL-33 enhanced the migration of neutrophils. These data suggest that IL-33 may affect the progress of PBC by recruiting neutrophils to the liver. This expanded knowledge of IL-33 in PBC patients is important for developing therapeutic strategies (e.g., neutralization of IL-33), selecting optimal clinical management, and predicting prognosis.
C1 [Sun, Yongqiang; Wang, Zongren] Fourth Mil Med Univ, Xijing Hosp, Dept Tradit Chinese Med, Xian 710032, Shanxi, Peoples R China.
[Sun, Yongqiang; Gong, Man; Du, Ning; Liu, Honghong; Zhang, Ning; Jing, Jing; Zhou, Chao; Zhang, Fan] Beijing 302 Hosp, Integrat Med Ctr Liver Dis, Beijing, Peoples R China.
[Zhang, Ji-Yuan; Lv, Sa] Beijing 302 Hosp, Res Ctr Biol Therapy, Beijing, Peoples R China.
[Wang, Huan] Fourth Mil Med Univ, Tangdu Hosp, Dept Dermatol, Xian 710032, Shanxi, Peoples R China.
C3 Air Force Military Medical University; Fifth Medical Center of Chinese
PLA General Hospital; Fifth Medical Center of Chinese PLA General
Hospital; Air Force Military Medical University
RP Wang, ZR (corresponding author), Fourth Mil Med Univ, Xijing Hosp, Dept Tradit Chinese Med, Xian 710032, Shanxi, Peoples R China.
EM yanfengyun2011@126.com
FU Beijing Nova Program of China [Z121107002512071]; National Natural
Science Foundation of China [81302593, 81271848]
FX This study is supported by the grant of Beijing Nova Program of China
(Z121107002512071) and the National Natural Science Foundation of China
(No. 81302593 and No. 81271848).
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NR 23
TC 16
Z9 17
U1 0
U2 7
PU TOHOKU UNIV MEDICAL PRESS
PI SENDAI
PA 2-1, SEIRYO-MACHI, AOBA-KU, SENDAI, MIYAGI 980-8575, JAPAN
SN 0040-8727
EI 1349-3329
J9 TOHOKU J EXP MED
JI Tohoku J. Exp. Med.
PD DEC
PY 2014
VL 234
IS 4
BP 255
EP 261
DI 10.1620/tjem.234.255
PG 7
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA AX5EW
UT WOS:000346950600002
PM 25400121
OA Bronze
DA 2025-01-07
ER
PT J
AU Carbone, J
Micheloud, D
Salcedo, M
Rincon, D
Bañares, R
Clemente, G
Jensen, J
Sarmiento, E
Rodriguez-Molina, J
Fernandez-Cruz, E
AF Carbone, J.
Micheloud, D.
Salcedo, M.
Rincon, D.
Banares, R.
Clemente, G.
Jensen, J.
Sarmiento, E.
Rodriguez-Molina, J.
Fernandez-Cruz, E.
TI Humoral and cellular immune monitoring might be useful to identify liver
transplant recipients at risk for development of infection
SO TRANSPLANT INFECTIOUS DISEASE
LA English
DT Article
DE liver transplantation; hypergammaglobulinemia; complement; infection;
risk factors; immune monitoring
ID SERUM IMMUNOGLOBULINS; COMPLEMENT; REJECTION; DISEASE;
HYPOGAMMAGLOBULINEMIA
AB J. Carbone, D. Micheloud, M. Salcedo, D. Rincon, R. Banares, G. Clemente, J. Jensen, E. Sarmiento, J. Rodriguez-Molina, E. Fernandez-Cruz. Humoral and cellular immune monitoring might be useful to identify liver transplant recipients at risk for development of infection.Transpl Infect Dis 2008: 10: 396-402
Orthotopic liver transplantation (OLT) is a successful therapy for patients with end-stage liver disease, and infection remains a significant cause of morbidity and mortality for patients undergoing this procedure. To assess humoral and cellular immunity markers as potential risk factors for development of infection, 46 consecutive liver transplant recipients (hepatitis C virus cirrhosis [n=17], alcoholic liver disease [n=15], hepatocellular carcinoma [n=9], autoimmune hepatitis [n=2], and other [n=3]) performed at a single center were prospectively studied. Maintenance therapy included tacrolimus (n=37) or cyclosporine (n=9) and prednisone. During follow-up, 27 patients had at least 1 episode of infection (58.7%). Pre-OLT immunoglobulin G (IgG) hypergammaglobulinemia (relative risk [RR] 2.78; 95% confidence interval [CI], 1.17-6.60, P=0.02), pre-OLT IgA hypergammaglobulinemia (RR 2.77, CI=1.24-6.19, P=0.012), and pre-OLT C3 hypocomplementemia (RR 3.02, CI=1.21-7.55, P=0.018) were associated with an increased risk for development of infection. Monitoring of Ig and complement levels might help to identify the risk of developing infection in OLT.
C1 [Carbone, J.] Univ Hosp Gregorio Maranon, Dept Immunol, Clin Immunol Unit, Madrid 28007, Spain.
[Salcedo, M.; Rincon, D.; Banares, R.; Clemente, G.] Univ Hosp Gregorio Maranon, Liver Transplant Unit, Madrid 28007, Spain.
C3 General University Gregorio Maranon Hospital; General University
Gregorio Maranon Hospital
RP Carbone, J (corresponding author), Univ Hosp Gregorio Maranon, Dept Immunol, Clin Immunol Unit, Dr Esquerdo 46, Madrid 28007, Spain.
EM carbone@teleline.es
RI Banares, Rafael/J-1460-2012
OI Sarmiento, Elizabeth/0000-0001-8435-8912; Carbone,
Javier/0000-0003-2056-0534; Micheloud, Dariela/0000-0001-9036-8703;
Banares, Rafael/0000-0002-0412-8437; Rincon, Diego/0000-0002-4470-7724
FU Instituto de Salud Carlos III [FIS05/0839]
FX The authors would like to thank Mr Juan Delgado, Mrs Maria Luz Medel,
Mrs Maria Angeles Jodar, and Mrs Dolores de Marcos (Immunochemistry
Section of the Immunology Department) for performing humoral immunity
studies. They also thank Dr Juana Gil for validation of results of
lymphocyte subsets. J.C. was supported by a grant of the Instituto de
Salud Carlos III (FIS05/0839).
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NR 25
TC 28
Z9 29
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-2273
J9 TRANSPL INFECT DIS
JI Transpl. Infect. Dis.
PD DEC
PY 2008
VL 10
IS 6
BP 396
EP 402
DI 10.1111/j.1399-3062.2008.00329.x
PG 7
WC Immunology; Infectious Diseases; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Infectious Diseases; Transplantation
GA 375AU
UT WOS:000261085700004
PM 18657086
DA 2025-01-07
ER
PT J
AU Ali, AH
Hachem, M
Ahmmed, MK
AF Ali, Abdelmoneim H.
Hachem, Mayssa
Ahmmed, Mirja Kaizer
TI Docosahexaenoic acid-loaded nanoparticles: A state-of-the-art of
preparation methods, characterization, functionality, and therapeutic
applications
SO HELIYON
LA English
DT Review
ID LOW-DENSITY-LIPOPROTEIN; POLYUNSATURATED FATTY-ACIDS; ZINC-OXIDE
NANOPARTICLES; COA DESATURASE 1; SILVER NANOPARTICLES; CLINICAL
TRANSLATION; DELIVERY; ZEIN; DHA; CELLS
AB Docosahexaenoic acid (DHA, C22:6 n-3), an omega -3 polyunsaturated fatty acid, offers several beneficial effects. DHA helps in reducing depression, autoimmune diseases, rheumatoid arthritis, attention deficit hyperactivity syndrome, and cardiovascular diseases. It can stimulate the development of brain and nerve, alleviate lipids metabolism -related disorders, and enhance vision development. However, DHA susceptibility to chemical oxidation, poor water solubility, and unpleasant order could restrict its applications for nutritional and therapeutic purposes. To avoid these drawbacks and enhance its bioavailability, DHA can be encapsulated using an effective delivery system. Several encapsulation methods are recognized, and DHA-loaded nanoparticles have demonstrated numerous benefits. In clinical studies, positive influences on the development of several diseases have been reported, but some assumptions are conflicting and need more exploration, since DHA has a systemic and not a targeted release at the required level. This might cause the applications of nanoparticles that could allow DHA release at the required level and improve its efficiency, thus resulting in a better controlling of several diseases. In the current review, we focused on researches investigating the formulation and development of DHA-loaded nanoparticles using different delivery systems, including low -density lipoprotein, zinc oxide, silver, zein, and resveratrol-stearate. Silver-DHA nanoparticles presented a typical particle size of 24 nm with an incorporation level of 97.67 %, while the entrapment efficiency of zinc oxide-DHA nanoparticles represented 87.3 %. By using zein/Poly (lactic - co -glycolic acid) stabilized nanoparticles, DHA 's encapsulation level reached 84.6 %. We have also highlighted the characteristics, functionality and medical implementation of these nanoparticles in the treatment of inflammations, brain disorders, diabetes as well as hepatocellular carcinoma.
C1 [Ali, Abdelmoneim H.] Khalifa Univ Sci & Technol, Dept Chem & Petr Engn, Abu Dhabi 127788, U Arab Emirates.
[Hachem, Mayssa] Khalifa Univ Sci & Technol, Dept Chem, Abu Dhabi 127788, U Arab Emirates.
[Hachem, Mayssa] Khalifa Univ Sci & Technol, Healthcare Engn Innovat Grp, Abu Dhabi 127788, U Arab Emirates.
[Ahmmed, Mirja Kaizer] Chattogram Vet & Anim Sci Univ, Dept Fishing & Postharvest Technol, Chattogram, Bangladesh.
[Ahmmed, Mirja Kaizer] Massey Univ, Riddet Inst, Palmerston North, New Zealand.
C3 Khalifa University of Science & Technology; Khalifa University of
Science & Technology; Khalifa University of Science & Technology; Massey
University
RP Hachem, M (corresponding author), Khalifa Univ Sci & Technol, Dept Chem, Abu Dhabi 127788, U Arab Emirates.; Hachem, M (corresponding author), Khalifa Univ Sci & Technol, Healthcare Engn Innovat Grp, Abu Dhabi 127788, U Arab Emirates.
EM mayssa.hachem@ku.ac.ae
RI Ali, Abdelmoneim/AAD-8583-2019; Ahmmed, Dr. Mirja Kaizer/AAA-5000-2019
OI Ahmmed, Dr. Mirja Kaizer/0000-0003-4467-0615; Hachem,
Mayssa/0000-0003-1986-8304
FU Khalifa University [ESIG 8474000472, RIG 8474000575]
FX This research was funded by Khalifa University, internal funding ESIG
8474000472 and RIG 8474000575. All authors gratefully acknowledge the
support of staff and faculty colleagues at the Department of Chemistry,
Khalifa University, Abu Dhabi, UAE.
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NR 120
TC 1
Z9 1
U1 8
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD MAY 15
PY 2024
VL 10
IS 9
AR e30946
DI 10.1016/j.heliyon.2024.e30946
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA TH1L3
UT WOS:001240282900001
PM 38774069
OA gold
DA 2025-01-07
ER
PT J
AU Kaleta, B
AF Kaleta, Beata
TI Osteopontin and Transplantation: Where Are We Now?
SO ARCHIVUM IMMUNOLOGIAE ET THERAPIAE EXPERIMENTALIS
LA English
DT Review
DE Immunomodulation; Osteopontin; Rejection; Transplantation
ID VERSUS-HOST-DISEASE; STEM-CELL TRANSPLANTATION;
HEPATOCELLULAR-CARCINOMA; LIVER-TRANSPLANTATION; HEART-TRANSPLANTATION;
CYTOKINE PROFILES; VIRAL-HEPATITIS; EXPRESSION; SURVIVAL; REJECTION
AB Organ transplantation represents the optimal therapeutic tool for patients with end-stage organ failure. Hematopoietic stem cell transplantation (HSCT) is likewise an effective therapy for a wide range of malignant and non-malignant diseases. Better understanding of transplantation immunology and the use of multi-modal immunosuppression protocols, can decrease the risk of graft failure and graft-versus-host disease (GVHD) after HSCT. Nevertheless, a major challenge of modern transplantology still seems to be finding non-invasive biomarkers for recipients selection, monitoring of allograft function, and diagnosis of rejection. Since proinflammatory cytokine osteopontin (OPN) is closely involved in regulating both adaptive and innate immune responses, as well as the pathogenesis of inflammatory and autoimmune diseases, it is likely to play an important role in organ and HSC transplantation. This review is to summarize recent advances in our knowledge about OPN function in the kidney, heart, liver, lung, and HSC transplantation. Most studies found that elevated OPN is associated with poorer graft function in kidney, heart, liver and lung recipients. Moreover, some reports suggested that this protein can play role in GVHD pathogenesis. However, due to relatively small number of similar studies, as well as some inconclusive results, future investigation in this field is needed to verify if OPN can serve as a biomarker of organ and HSC transplantation. The knowledge about such markers will promote our understanding of the mechanisms underlying graft dysfunction and posttransplant mortality. In addition, such knowledge may be helpful in the development of new treatment strategies and identification of recipients with increased risk of allograft failure.
C1 [Kaleta, Beata] Med Univ Warsaw, Dept Clin Immunol, Nowogrodzka 59 St, PL-02006 Warsaw, Poland.
C3 Medical University of Warsaw
RP Kaleta, B (corresponding author), Med Univ Warsaw, Dept Clin Immunol, Nowogrodzka 59 St, PL-02006 Warsaw, Poland.
EM beata.kaleta@wum.edu.pl
RI Kaleta, Beata/AAJ-6530-2020
OI Kaleta, Beata/0000-0002-0697-2594
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NR 83
TC 4
Z9 5
U1 0
U2 48
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 0004-069X
EI 1661-4917
J9 ARCH IMMUNOL THER EX
JI Arch. Immunol. Ther. Exp.
PD DEC
PY 2021
VL 69
IS 1
AR 15
DI 10.1007/s00005-021-00617-6
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA SF8YQ
UT WOS:000653034500001
PM 34019147
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Khalil, AA
Kabapy, NF
Deraz, SF
Smith, C
AF Khalil, Ashraf A.
Kabapy, Nihal F.
Deraz, Sahar F.
Smith, Christopher
TI Heat shock proteins in oncology: Diagnostic biomarkers or therapeutic
targets?
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
ID HUMAN HEPATOCELLULAR-CARCINOMA; BREAST-CANCER CELLS; NEGATIVE
REGULATION; TRANSCRIPTIONAL RESPONSE; MOLECULAR CHAPERONES;
RHEUMATOID-ARTHRITIS; MEDIATED APOPTOSIS; DOWN-REGULATION;
OVARIAN-CANCER; LUNG-CANCER
AB Heat shock proteins (HSP) are a family of proteins induced in cells exposed to different insults. This induction of HSPs allows cells to survive stress conditions. Mammalian HSPs have been classified into six families according to their molecular size: HSP100, HSP90, HSP70, HSP60, HSP40 and small HSPs (15 to 30 kDa) including HSP27. These proteins act as molecular chaperones either helping in the refolding of misfolded proteins or assisting in their elimination if they become irreversibly damaged. In recent years, proteomic studies have characterized several different HSPs in various tumor types which may be putative clinical biomarkers or molecular targets for cancer therapy. This has led to the development of a series of molecules capable of inhibiting HSPs. Numerous studies speculated that over-expression of HSP is in part responsible for resistance to many anti-tumor agents and chemotherapeutics. Hence, from a pharmacological point of view, the co-administration of HSP inhibitors together with other anti-tumor agents is of major importance in overcoming therapeutic resistance. In this review, we provide an overview of the current status of HSPs in autoimmune, cardiovascular, and neurodegenerative diseases with special emphasis on cancer. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Khalil, Ashraf A.; Kabapy, Nihal F.; Deraz, Sahar F.] Inst Genet Engn & Biotechnol, Dept Prot Technol, Alexandria, Egypt.
[Smith, Christopher] Manchester Metropolitan Univ, Manchester M14 6HR, Lancs, England.
C3 Manchester Metropolitan University
RP Khalil, AA (corresponding author), Inst Genet Engn & Biotechnol, Dept Prot Technol, Alexandria, Egypt.
EM ashraf_khalil@msn.com
RI deraz, sahar/V-8333-2017
OI deraz, sahar/0000-0002-6830-4065
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NR 211
TC 168
Z9 192
U1 0
U2 45
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0304-419X
EI 1879-2561
J9 BBA-REV CANCER
JI Biochim. Biophys. Acta-Rev. Cancer
PD DEC
PY 2011
VL 1816
IS 2
BP 89
EP 104
DI 10.1016/j.bbcan.2011.05.001
PG 16
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA 859NE
UT WOS:000297882300001
PM 21605630
DA 2025-01-07
ER
PT J
AU Huang, JF
Yu, ML
Dai, CY
Chuang, WL
AF Huang, Jee-Fu
Yu, Ming-Lung
Dai, Chia-Yen
Chuang, Wan-Long
TI Glucose abnormalities in hepatitis C virus infection
SO KAOHSIUNG JOURNAL OF MEDICAL SCIENCES
LA English
DT Review
DE Direct-acting antiviral agents; Hepatitis C virus; Insulin resistance;
Pegylated interferon; Ribavirin
ID TYPE-2 DIABETES-MELLITUS; PEGINTERFERON PLUS RIBAVIRIN; PEGYLATED
INTERFERON-ALPHA; IMPAIRED FASTING GLUCOSE; INSULIN-RESISTANCE; PROTEASE
INHIBITORS; RISK-FACTORS; ASSOCIATION; GENOTYPE; IL28B
AB Hepatitis C virus (HCV) infection is one of the most important causes of cirrhosis and hepatocellular carcinoma and has a tremendous impact on public health worldwide. HCV is both hepatotropic and lymphotropic. Replication of HCV in diseased extrahepatic organs and tissues may either trigger latent autoimmunity or induce autoimmune disorders. In addition to established liver injury, type 2 diabetes mellitus (T2DM) is an important feature of extrahepatic metabolic disorders which is attributed to HCV infection. It also has some impact on the disease activity, disease course, clinical outcomes, and treatment efficacy of antiviral therapy. Previous experimental and clinical findings have highly suggested that HCV per se is diabetogenic. The cause-effect interaction between a common endocrine disorder and an infectious disease is an important issue to elucidate. Although the precise mechanisms whereby HCV infection leads to insulin resistance (IR) and glucose abnormalities are not entirely clear, it differs from the usual pathogenesis of T2DM in those with non-HCV liver diseases. This review initially highlights epidemiological and pathophysiological studies addressing the mutual link between chronic HCV infection (CHC) and T2DM. The characteristics of glucose abnormalities in this special population are depicted from the current evidence. The mutual roles of IR and CHC with respect to the prediction of treatment efficacy, how treatment response affects IR, and the role of pancreatic beta cell function in the entire suite are discussed. With the rapid progression of antiviral therapy for CHC in the past decade, we have also listed some points of future perspective in this issue. Copyright (C) 2012, Kaohsiung Medical University. Published by Elsevier Taiwan LLC. All rights reserved.
C1 [Huang, Jee-Fu] Kaohsiung Med Univ, Kaohsiung Municipal Hsiao Kang Hosp, Dept Internal Med, Kaohsiung, Taiwan.
[Huang, Jee-Fu; Yu, Ming-Lung; Dai, Chia-Yen; Chuang, Wan-Long] Kaohsiung Med Univ, Coll Med, Fac Internal Med, Kaohsiung, Taiwan.
[Yu, Ming-Lung; Dai, Chia-Yen; Chuang, Wan-Long] Kaohsiung Med Univ Hosp, Dept Internal Med, Hepatobiliary Div, Kaohsiung 807, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Municipal Siao-Gang Hospital;
Kaohsiung Medical University; Kaohsiung Medical University; Kaohsiung
Medical University Hospital
RP Chuang, WL (corresponding author), Kaohsiung Med Univ Hosp, Dept Internal Med, Hepatobiliary Div, 100 Tzyou 1st Rd, Kaohsiung 807, Taiwan.
EM jf71218@gmail.com
RI Huang, Jee-Fu/AAX-4622-2020; Yu, Ming-Lung/AAZ-4306-2020; Chuang,
Wan-Long/C-9536-2009
OI Yu, Ming-Lung/0000-0001-8145-1900; Huang, Jee-Fu/0000-0002-2752-7051;
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NR 60
TC 24
Z9 28
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1607-551X
EI 2410-8650
J9 KAOHSIUNG J MED SCI
JI Kaohsiung J. Med. Sci.
PD FEB
PY 2013
VL 29
IS 2
BP 61
EP 68
DI 10.1016/j.kjms.2012.11.001
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 117CS
UT WOS:000316930300001
PM 23347806
OA gold
DA 2025-01-07
ER
PT J
AU Gu, M
Jin, YXZ
Gao, X
Xia, WY
Xu, T
Pan, SY
AF Gu, Min
Jin, Yuexinzi
Gao, Xun
Xia, Wenying
Xu, Ting
Pan, Shiyang
TI Novel insights into IL-37: an anti-inflammatory cytokine with emerging
roles in anti-cancer process
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE IL-37; inflammation inhibition; immunomodulation; anti-tumor;
immunotherapy
ID HEPATOCELLULAR-CARCINOMA; INNATE INFLAMMATION; INTERLEUKIN 37;
MESENCHYMAL TRANSITION; COLORECTAL-CANCER; MULTIPLE-MYELOMA;
MESSENGER-RNA; FAMILY; CELLS; EXPRESSION
AB Interleukin-37 (IL-37) is a newly discovered member of IL-1 family. The cytokine was proved to have extensive protective effects in infectious diseases, allergic diseases, metabolic diseases, autoimmune diseases and tumors since its discovery. IL-37 was mainly produced by immune and some non-immune cells in response to inflammatory stimulus. The IL-37 precursors can convert into the mature forms after caspase-1 cleavage and activation intracellularly, and then bind to Smad-3 and transfer to the nucleus to inhibit the production and functions of proinflammatory cytokines; extracellularly, IL-37 binds to cell surface receptors to form IL-37/IL-18R alpha/IL-1R8 complex to exert immunosuppressive function via inhibiting/activating multiple signal pathways. In addition, IL-37 can attenuate the pro-inflammatory effect of IL-18 through directly or forming an IL-37/IL-18BP/IL-18R beta complex. Therefore, IL-37 has the ability to suppress innate and acquired immunity of the host, and effectively control inflammatory stimulation, which was considered as a new hallmark of cancer. Specifically, it is concluded that IL-37 can inhibit the growth and migration of tumor cells, prohibit angiogenesis and mediate the immunoregulation in tumor microenvironment, so as to exert effective anti-tumor effects. Importantly, latest studies also showed that IL-37 may be a novel therapeutic target for cancer monitoring. In this review, we summarize the immunoregulation roles and mechanisms of IL-37 in anti-tumor process, and discuss its progress so far and potential as tumor immunotherapy.
C1 [Gu, Min; Jin, Yuexinzi; Xia, Wenying; Xu, Ting; Pan, Shiyang] Nanjing Med Univ, Affiliated Hosp 1, Dept Lab Med, Nanjing, Peoples R China.
[Gu, Min; Jin, Yuexinzi; Xia, Wenying; Xu, Ting; Pan, Shiyang] Branch Natl Clin Res Ctr Lab Med, Nanjing, Peoples R China.
[Gao, Xun] Southeast Univ, Zhongda Hosp, Ctr Clin Lab Med, Nanjing, Peoples R China.
C3 Nanjing Medical University; Southeast University - China
RP Pan, SY (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Dept Lab Med, Nanjing, Peoples R China.; Pan, SY (corresponding author), Branch Natl Clin Res Ctr Lab Med, Nanjing, Peoples R China.
EM sypan@njmu.edu.cn
FU The author(s) declare financial support was received for the research,
authorship, and/or publication of this article. This work was supported
by grants from the National Natural Science Foundation of China
(82272401, 82202610), Jiangsu Province Capability [82272401, 82202610];
National Natural Science Foundation of China [ZDXK202239]; Jiangsu
Province Capability Improvement Project through Science and Technology
and Education; Priority Academic Program Development of Jiangsu Higher
Education Institutions
FX The author(s) declare financial support was received for the research,
authorship, and/or publication of this article. This work was supported
by grants from the National Natural Science Foundation of China
(82272401, 82202610), Jiangsu Province Capability Improvement Project
through Science and Technology and Education (ZDXK202239) and the
Priority Academic Program Development of Jiangsu Higher Education
Institutions.
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PD OCT 20
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DI 10.3389/fimmu.2023.1278521
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA W5PQ3
UT WOS:001092148800001
PM 37928545
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Li, GY
Li, QJ
Ping, MM
Jiao, ZY
Wang, XX
Cheng, J
Guo, JZ
Cheng, Y
AF Li, Guangyao
Li, Qijiao
Ping, Miaomiao
Jiao, Ziying
Wang, Xingxing
Cheng, Juan
Guo, Jizheng
Cheng, Ya
TI SLAMF8 can predict prognosis of pan-cancer and the immunotherapy
response effectivity of gastric cancer
SO AGING-US
LA English
DT Article
DE SLAMF8; pan-cancer; biomarker; TME; immunotherapy
ID EXPRESSION; INNATE; FAMILY; TIGIT; LAG-3; CD96; SAP
AB SLAMF8, the eighth member of the Signaling Lymphocytic Activation Molecule Family (SLAMF), functions in the regulation of the development and activity of diverse immune cells as a costimulatory receptor within the SLAMF family. Studies had revealed that SLAMF8 is expressed higher in several autoimmune inflammation diseases and tumors. Nevertheless, the connection between SLAMF8 and pan-cancer remains undisclosed. The research investigated the correlation between SLAMF8 and various factors including the immune microenvironment, microsatellite instability, immune novel antigen, gene mutation, immune regulatory factors, immune blockade TMB, and immune or molecular subtypes of SLAMF8 in verse cancer types. Immunohistochemistry was ultimately employed to validate the presence of the SLAMF8 gene in various tumor types including hepatocellular carcinoma, prostate adenocarcinoma, and kidney renal clear cell carcinoma. Furthermore, the relationship between SLAMF8 expression and the therapeutic efficacy of the PD1 blockade agent, Sintilimab, treatment in gastric cancer was validated. The result of differential analysis suggested that SLAMF8 was over-expressed in pan-cancer compared with paracancerous tissues. The analysis of survival indicated a connection between SLAMF8 and the overall prognosis in different types of cancers, where higher levels of SLAMF8 were found to be significantly linked to unfavorable outcomes in patients but favorable outcome of immunotherapy in gastric cancer. Significant correlations were observed between SLAMF8 levels and pan-cancer tumorigenesis, tumor metabolism, and immunity. As a result, SLAMF8 may become an important prognostic biomarker in the majority of tumors and a hopeful gene target for immunotherapy against gastric cancer.
C1 [Li, Guangyao] Second Peoples Hosp Wuhu, Dept Gastrointestinal Surg, Wuhu 241000, Anhui, Peoples R China.
[Li, Qijiao; Ping, Miaomiao; Jiao, Ziying; Wang, Xingxing; Cheng, Juan; Guo, Jizheng] Anhui Med Univ, Sch Basic Med Sci, Hefei 230032, Anhui, Peoples R China.
[Cheng, Ya] Anhui Med Univ, Affiliated Hosp 1, Dept Emergency Surg, Hefei 230032, Anhui, Peoples R China.
C3 Anhui Medical University; Anhui Medical University
RP Cheng, J; Guo, JZ (corresponding author), Anhui Med Univ, Sch Basic Med Sci, Hefei 230032, Anhui, Peoples R China.; Cheng, Y (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Emergency Surg, Hefei 230032, Anhui, Peoples R China.
EM juancheng@ahmu.edu.cn; guojizheng@ahmu.edu.cn;
2336020145@stu.ahmu.edu.cn
FU Anhui Provincial Health Commission Provincial Financial Support for
Youth Programs [AHWJ2023A30159]
FX This work is funded by the Anhui Provincial Health Commission Provincial
Financial Support for Youth Programs (AHWJ2023A30159) .
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NR 40
TC 0
Z9 0
U1 3
U2 3
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD MAY 30
PY 2024
VL 16
IS 10
BP 8944
EP 8964
PG 21
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA TB6F2
UT WOS:001238829900032
PM 38787377
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Fujino, Y
Tamakoshi, A
Hoshiyama, Y
Mikami, H
Okamoto, N
Ohno, Y
Yoshimura, T
AF Fujino, Y
Tamakoshi, A
Hoshiyama, Y
Mikami, H
Okamoto, N
Ohno, Y
Yoshimura, T
CA Japan Collaboration Study Grp
TI Prospective study of transfusion history and thyroid cancer incidence
among females in Japan
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE thyroid cancer; blood transfusion; hepatitis C virus; immunomodulation;
Japanese population
ID HEPATITIS-C VIRUS; STOMACH-CANCER; EXTRAHEPATIC MANIFESTATIONS; HIGH
PREVALENCE; HCV; AUTOIMMUNE; RISK; INFECTION; DEATH; CONSUMPTION
AB A link between hepatitis C virus (HCV) infection and thyroid cancer was recently reported in a series of case-control studies in southern Italy. A prospective study could reinforce these findings. However, cohort studies that began before 1990 rarely assessed serological HCV infection. In addition, thyroid cancer is rare and generally has a good prognosis. Therefore, incidence outcome data are required, rather than mortality data, to evaluate the risk of thyroid cancer. Blood transfusion history might be a possible substitute measure to evaluate the cancer risks associated with HCV infection because blood transfusions were the major HCV transmission route in Japan until 1992. The purpose of our study was therefore to examine the association between transfusion history and thyroid cancer. A baseline survey of members of the JACC Study was conducted from 1988 until 1990, which involved 110,792 participants from 45 areas throughout Japan. Data were collected from a total of 37,983 women with no history of cancer at the baseline (337,906 person-years) and 79 cases of thyroid cancer were identified among this group. A history of blood transfusion marginally increased the risk of thyroid cancer [risk ratio (RR) = 1.77, 95% confidence interval (Cl) = 0.95-3.30], and a history of transfusion and/or liver disease significantly increased the thyroid cancer risk (RR = 1.84, 95% Cl = 1.07-3.16). These results indirectly support an association between HCV and thyroid cancer. In addition, our data reveal an association between blood transfusion and thyroid cancer, which might be facilitated by transfusion-associated immunomodulation. (C) 2004 Wiley-Liss, Inc.
C1 Univ Occupat & Environm Hlth, IIES, Dept Clin Epidemiol, Yahatanishi Ku, Kitakyushu, Fukuoka 8078555, Japan.
Cardiff Univ, Dept Epidemiol Stat & Publ Hlth, Cardiff CF4 4XN, S Glam, Wales.
Nagoya Univ, Grad Sch Med, Program Hlth Community Med,Field Social Life Sci, Dept Prevent Med Biostat & Med Decis Making, Nagoya, Aichi, Japan.
Showa Univ, Sch Med, Dept Publ Hlth, Tokyo, Japan.
Chiba Canc Ctr, Res Inst, Div Epidemiol, Chiba, Japan.
Kanagawa Canc Ctr, Res Inst, Dept Epidemiol, Yokohama, Kanagawa, Japan.
Asahi Rosai Hosp, Labour Welf Corp, Asahi, Japan.
C3 University of Occupational & Environmental Health - Japan; Cardiff
University; Nagoya University; Showa University; Chiba Cancer Center;
Kanagawa Prefectural Cancer Center
RP Univ Occupat & Environm Hlth, IIES, Dept Clin Epidemiol, Yahatanishi Ku, 1-1,Iseigaoka, Kitakyushu, Fukuoka 8078555, Japan.
EM zenq@med.uoeh-u.ac.jp
RI Fujino, Yoshihisa/F-3054-2010; Tamakoshi, Akiko/D-5105-2012
OI Fujino, Yoshihisa/0000-0002-9126-206X
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NR 26
TC 12
Z9 14
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 20
PY 2004
VL 112
IS 4
BP 722
EP 725
DI 10.1002/ijc.20440
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 865QG
UT WOS:000224717000024
PM 15382057
DA 2025-01-07
ER
PT J
AU Alfwuaires, MA
AF Alfwuaires, Manal A.
TI Galangin mitigates oxidative stress, inflammation, and apoptosis in a
rat model of methotrexate hepatotoxicity
SO ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
LA English
DT Article
DE Galangin; Methotrexate; Hepatotoxicity; Flavonoids; Apoptosis;
Antioxidants
ID PPAR-GAMMA; HEPATOCELLULAR-CARCINOMA; INDUCED NEPHROTOXICITY; NRF2/HO-1
PATHWAY; CELL-DEATH; ACID; LIVER; ANTIOXIDANT; INHIBITION; BERBERINE
AB Methotrexate (MTX) is an efficient chemotherapeutic agent for treating various malignancies and autoimmune diseases. However, the long-term use of MTX can result in hepatotoxicity and this limits its use. Galangin (Gal) is a potent flavonoid with various biological activities; however, its protective effect against MTX hepatotoxicity has not been previously investigated. This study evaluated the hepatoprotective of Gal against MTX-induced liver injury. Rats received Gal for 10 days and a single dose of MTX (20 mg/kg) at day 7. The administration of MTX induced liver damage reflected by increased serum biomarkers of liver function and histopathological manifestations. MTX increased hepatic reactive oxygen species (ROS), nitric oxide (NO), malondialdehyde (MDA), and pro-inflammatory cytokines (TNF-alpha, IL-1 beta, and IL-6), and diminished GSH and antioxidant enzymes. Gal relieved liver injury, ameliorated liver function, oxidative stress, and inflammation markers, and increased antioxidants in MTX-treated rats. In addition, Gal decreased the expression of inflammation and apoptosis markers in MTX-treated rats. In conclusion, Gal possesses a hepatoprotective effect mediated by attenuating oxidative damage, inflammation, and apoptosis in rats.
C1 [Alfwuaires, Manal A.] King Faisal Univ, Dept Biol Sci, Fac Sci, Al Hasa 31982, Saudi Arabia.
C3 King Faisal University
RP Alfwuaires, MA (corresponding author), King Faisal Univ, Dept Biol Sci, Fac Sci, Al Hasa 31982, Saudi Arabia.
EM malfwuaires@kfu.edu.sa
RI al-fwuaires., Manal/H-9123-2016
OI al-fwuaires., Manal/0000-0001-7426-6811
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NR 73
TC 18
Z9 20
U1 2
U2 20
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0944-1344
EI 1614-7499
J9 ENVIRON SCI POLLUT R
JI Environ. Sci. Pollut. Res.
PD MAR
PY 2022
VL 29
IS 14
BP 20279
EP 20288
DI 10.1007/s11356-021-16804-z
EA NOV 2021
PG 10
WC Environmental Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology
GA ZN4QS
UT WOS:000713975100001
PM 34729716
DA 2025-01-07
ER
PT J
AU Pellegrini, L
Parrilli, G
Santonicola, A
Cinquanta, L
Caputo, C
Ciacci, C
Zingone, F
AF Pellegrini, Lucienne
Parrilli, Gianpaolo
Santonicola, Antonella
Cinquanta, Luigi
Caputo, Cesare
Ciacci, Carolina
Zingone, Fabiana
TI Lack of Clinical Relevance of ANA and ASMA Positivity in Patients with
Liver Transplantation without a History of Autoimmune Diseases
SO BIOMED RESEARCH INTERNATIONAL
LA English
DT Article
ID ANTINUCLEAR ANTIBODIES; ANTITISSUE ANTIBODIES; AUTOANTIBODIES;
HEPATITIS; RISK; AGE
AB The relevance of isolated autoimmunity elevation in orthotopic liver transplantation (OLT) patients is unknown. Our aim was to analyse how serum autoantibodies change in time and to evaluate their clinical relevance in OLT patients. Patients were invited to provide samples to evaluate ANA, AMA, ASMA, and LKM at the time of enrolment (T0), after 6 months (T6), and after 12 months (T12). We included 114 patients in the study (76% males, median age 62.5 years), finding isolated elevation of at least one serum antibody in up to 80% of them. We described fluctuating positive autoantibodies in the one year of observation, with only 45.6% of patients positive for ANA and less than 2% positive for ASMA, at all three times. Isolated elevation of tissue antibodies was not related to gender, age, HCC at transplant, early rejection, cause of transplantation, immunotherapy taken, and age at the time of the study. We did not detect a higher prevalence of positive autoimmunity in patients with signs of liver injury. ANA and ASMA evaluation in patients with liver transplantation and no history of autoimmune disease has no clinical relevance, since it varies in time and is not related to any risk factors or liver injury. Routine autoimmunity evaluation should be avoided.
C1 [Pellegrini, Lucienne; Parrilli, Gianpaolo; Santonicola, Antonella; Caputo, Cesare; Ciacci, Carolina; Zingone, Fabiana] Univ Salerno, Dept Med & Surg, Liver Following Transplantat Ctr, AOU San Giovanni Dio & Ruggi dAragona, Salerno, Italy.
[Cinquanta, Luigi] AOU San Giovanni Dio & Ruggi dAragona, UOC Clin Pathol Dept, Salerno, Italy.
C3 University of Salerno
RP Zingone, F (corresponding author), Univ Salerno, Dept Med & Surg, Liver Following Transplantat Ctr, AOU San Giovanni Dio & Ruggi dAragona, Salerno, Italy.
EM fabiana.zingone@outlook.com
RI Zingone, Fabiana/AGP-7008-2022; ciacci, carolina/A-2594-2012;
Santonicola, Antonella/F-2389-2016; Zingone, Fabiana/O-5361-2018
OI ciacci, carolina/0000-0002-7426-1145; Santonicola,
Antonella/0000-0001-9094-765X; Zingone, Fabiana/0000-0003-1133-1502
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NR 18
TC 3
Z9 3
U1 0
U2 1
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-6133
EI 2314-6141
J9 BIOMED RES INT
JI Biomed Res. Int.
PY 2017
VL 2017
AR 2456916
DI 10.1155/2017/2456916
PG 7
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA EQ6UU
UT WOS:000398220000001
PM 28337446
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Liu, Y
Liao, XN
Wang, Y
Chen, SJ
Sun, YC
Lin, QY
Shi, GX
AF Liu, Yuan
Liao, Xining
Wang, Ying
Chen, Shiju
Sun, Yuechi
Lin, Qingyan
Shi, Guixiu
TI Autoantibody to MDM2: A potential serological marker of primary
Sjogren's syndrome
SO ONCOTARGET
LA English
DT Article
DE primary Sjogren's syndrome; anti-MDM2 autoantibody; biomarker;
Immunology and Microbiology Section; Immune response; Immunity
ID TUMOR-ASSOCIATED ANTIGEN; HEPATOCELLULAR-CARCINOMA; CLASSIFICATION
CRITERIA; P53; IMMUNODIAGNOSIS; PROMOTES
AB Introduction: Primary Sjogren's Syndrome (pSS) is one of the autoimmune diseases characterized by polyclonal autoantibody production. The human homologue of the mouse double minute 2 (MDM2) is an important negative regulator of p53. Our previous study indicated that autoantibody to MDM2 can be detected in systemic lupus erythematosus patients. The purpose of this study is to study anti-MDM2 autoantibody in pSS patients.
Methods: Anti-MDM2 autoantibody in sera from 100 pSS patients and 74 normal controls was investigated by ELISA. Positive samples were further confirmed by western blotting. Expression of MDM2 in labial gland tissue from pSS patients and normal controls was checked by immunohistochemistry. The difference in clinical characteristics and laboratory findings between anti-MDM2 positive and anti-MDM2 negative pSS patients was analyzed.
Results: The presence of anti-MDM2 autoantibody in pSS patients was 21.0%, significantly higher than normal controls (5.40%). MDM2 was overexpressed in labial gland from pSS patients. pSS patients with positive anti-MDM2 were characterized by longer disease duration and more lymphocytes focal gathering in labial gland. Prevalence of anemia, thrombocytopenia and anti-SSB was significantly higher in pSS patients with anti-MDM2 autoantibody. Titer of anit-MDM2 was negatively associated with hemoglobin level, platelet count, complement 3 level and complement 4 level, positively associated with European Sjogren's syndrome disease activity index (ESSDAI) and level of IgG.
Conclusions: Anti-MDM2 autoantibody may be used as a potential serological biomarker in pSS disease activity evaluation. Study on the role of anti-MDM2 or MDM2 in pSS may help us know the pathogenesis mechanism of pSS better.
C1 [Liu, Yuan; Chen, Shiju; Sun, Yuechi; Lin, Qingyan; Shi, Guixiu] Xiamen Univ, Affiliated Hosp 1, Dept Rheumatol & Clin Immunol, Xiamen, Peoples R China.
[Liao, Xining] Xiamen Univ, Coll Med, Xiamen, Fujian, Peoples R China.
[Wang, Ying] Xiamen Univ, ChengGong Hosp, Dept Endocrinol, Xiamen, Fujian, Peoples R China.
C3 Xiamen University; Xiamen University; Xiamen University
RP Shi, GX (corresponding author), Xiamen Univ, Affiliated Hosp 1, Dept Rheumatol & Clin Immunol, Xiamen, Peoples R China.
EM guixiu.shi@gmail.com
RI liu, yuan/AFR-1867-2022
OI shi, guixiu/0000-0003-4044-3394; Liu, Yuan/0000-0003-2668-0350
FU NSFC (Natural Science Foundation of China) [U1605223]; NSFC [81501407]
FX The work was supported by NSFC (Natural Science Foundation of China)
Grant U1605223 to Dr Guixiu Shi and NSFC grant 81501407 to Dr Yuan Liu.
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U2 6
PU IMPACT JOURNALS LLC
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PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD FEB 28
PY 2017
VL 8
IS 9
BP 14306
EP 14313
DI 10.18632/oncotarget.14882
PG 8
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EN4YV
UT WOS:000396013700010
PM 28147328
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Chen, LC
Ogbutor, C
Kelley, KJ
Senna, MM
AF Chen, Li-Chi
Ogbutor, Chino
Kelley, Kristen J.
Senna, Maryanne M.
TI Patient Considerations when Using Ritlecitinib for Alopecia Areata in
Adolescents: Guidance for the Clinicians
SO SKIN APPENDAGE DISORDERS
LA English
DT Review; Early Access
DE Janus kinase inhibitor; Ritlecitinib; Alopecia areata; Adolescents;
Patient considerations
ID JANUS KINASE INHIBITOR; QUALITY-OF-LIFE; GROWTH; JAK; CORTICOSTEROIDS;
TOFACITINIB; LYMPHOCYTES; VARIANTS; EFFICACY; CHILDREN
AB Background: Alopecia areata (AA) is an autoimmune disease characterized by non-scarring hair loss that can affect children, adolescents, and adults. Ritlecitinib, an orally administered Janus kinase (JAK) 3/tyrosine kinase expressed in hepatocellular carcinoma (TEC) kinase family inhibitor, is the fi rst and currently the only treatment approved by the US Food and Drug Administration for adolescents (aged 12-17 years) with severe AA. Summary: The ALLEGRO phase 2b-3 trial demonstrated that 25% and 50% of adolescents with a Severity of Alopecia Tool (SALT) score >= 50 at baseline achieved a SALT score <= 20 at week 24 and week 48 after receiving 50 mg ritlecitinib daily, respectively. The most common adverse events were headache, acne, and nasopharyngitis in adolescents. This review summarizes the mechanism of action, clinical trial evidence on efficacy and safety profile, factors associated with treatment response to JAK inhibitors for AA, and vaccination considerations for adolescents. Key Messages: This review aims to facilitate the risk-benefit assessment and shared decision-making between clinicians and patients and provide clinical considerations and management recommendations for ritlecitinib use in adolescents with AA.
C1 [Chen, Li-Chi; Ogbutor, Chino; Kelley, Kristen J.; Senna, Maryanne M.] Lahey Hosp & Med Ctr, Dept Dermatol, Burlington, MA 01805 USA.
[Senna, Maryanne M.] Harvard Med Sch, Dept Dermatol, Boston, MA 02115 USA.
C3 Lahey Hospital & Medical Center; Harvard University; Harvard Medical
School
RP Senna, MM (corresponding author), Lahey Hosp & Med Ctr, Dept Dermatol, Burlington, MA 01805 USA.; Senna, MM (corresponding author), Harvard Med Sch, Dept Dermatol, Boston, MA 02115 USA.
EM maryanne.m.senna@lahey.org
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NR 59
TC 0
Z9 0
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 2296-9195
EI 2296-9160
J9 SKIN APPENDAGE DISOR
JI Skin. Appendage Disord.
PD 2024 NOV 7
PY 2024
DI 10.1159/000541392
EA NOV 2024
PG 8
WC Dermatology
WE Emerging Sources Citation Index (ESCI)
SC Dermatology
GA P6J4N
UT WOS:001378946300001
DA 2025-01-07
ER
PT J
AU Khan, A
Dias, F
Neekhra, S
Singh, B
Srivastava, R
AF Khan, Amreen
Dias, Faith
Neekhra, Suditi
Singh, Barkha
Srivastava, Rohit
TI Designing and Immunomodulating Multiresponsive Nanomaterial for Cancer
Theranostics
SO FRONTIERS IN CHEMISTRY
LA English
DT Review
DE immunomodulation; nanomedicine; cancer; nanomaterials; theranostics;
imaging; clinical trials
ID REGULATORY T-CELLS; TUMOR-ASSOCIATED MACROPHAGES; NATURAL-KILLER-CELLS;
CHECKPOINT BLOCKADE; DRUG-DELIVERY; POLYMERIC NANOPARTICLES;
PHOTOTHERMAL THERAPY; GOLD NANOPARTICLES; DENDRITIC CELLS;
HEPATOCELLULAR-CARCINOMA
AB Cancer has been widely investigated yet limited in its manifestation. Cancer treatment holds innovative and futuristic strategies considering high disease heterogeneity. Chemotherapy, radiotherapy and surgery are the most explored pillars; however optimal therapeutic window and patient compliance recruit constraints. Recently evolved immunotherapy demonstrates a vital role of the host immune system to prevent metastasis recurrence, still undesirable clinical response and autoimmune adverse effects remain unresolved. Overcoming these challenges, tunable biomaterials could effectively control the co-delivery of anticancer drugs and immunomodulators. Current status demands a potentially new approach for minimally invasive, synergistic, and combinatorial nano-biomaterial assisted targeted immune-based treatment including therapeutics, diagnosis and imaging. This review discusses the latest findings of engineering biomaterial with immunomodulating properties and implementing novel developments in designing versatile nanosystems for cancer theranostics. We explore the functionalization of nanoparticle for delivering antitumor therapeutic and diagnostic agents promoting immune response. Through understanding the efficacy of delivery system, we have enlightened the applicability of nanomaterials as immunomodulatory nanomedicine further advancing to preclinical and clinical trials. Future and present ongoing improvements in engineering biomaterial could result in generating better insight to deal with cancer through easily accessible immunological interventions.
C1 [Khan, Amreen; Neekhra, Suditi; Singh, Barkha; Srivastava, Rohit] Indian Inst Technol, Dept Biosci & Bioengn, Mumbai, Maharashtra, India.
[Khan, Amreen; Singh, Barkha] Indian Inst Technol, Ctr Res Nanotechnol & Sci, Mumbai, Maharashtra, India.
[Dias, Faith] Thadomal Shahani Engn Coll, Dept Chem Engn, Mumbai, Maharashtra, India.
C3 Indian Institute of Technology System (IIT System); Indian Institute of
Technology (IIT) - Bombay; Indian Institute of Technology System (IIT
System); Indian Institute of Technology (IIT) - Bombay
RP Srivastava, R (corresponding author), Indian Inst Technol, Dept Biosci & Bioengn, Mumbai, Maharashtra, India.
EM rsrivasta@iitb.ac.in
RI SIngh, Barkha/HJZ-2560-2023
OI Neekhra, Suditi/0000-0002-1267-9108; Khan, Amreen/0000-0001-8792-3702;
SINGH, BARKHA/0000-0003-0060-5109; Dias, Faith/0009-0000-2963-7900
FU Department of Biotechnology, Government of India
FX This work was supported by the Department of Biotechnology, Government
of India.
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NR 223
TC 7
Z9 7
U1 2
U2 31
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-2646
J9 FRONT CHEM
JI Front. Chem.
PD JAN 29
PY 2021
VL 8
AR 631351
DI 10.3389/fchem.2020.631351
PG 20
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA QF7BM
UT WOS:000617047700001
PM 33585406
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Di Donato, V
D'Oria, O
Giannini, A
Bogani, G
Fischetti, M
Santangelo, G
Tomao, F
Palaia, I
Perniola, G
Muzii, L
Panici, PB
AF Di Donato, Violante
D'Oria, Ottavia
Giannini, Andrea
Bogani, Giorgio
Fischetti, Margherita
Santangelo, Giusi
Tomao, Federica
Palaia, Innocenza
Perniola, Giorgia
Muzii, Ludovico
Panici, Pierluigi Benedetti
TI Age-Adjusted Charlson Comorbidity Index Predicts Survival in Endometrial
Cancer Patients
SO GYNECOLOGIC AND OBSTETRIC INVESTIGATION
LA English
DT Article
DE Endometrial cancer; Age-adjusted Charlson comorbidity index; Prognostic
factor; Tailored therapy
ID PROTON PUMP INHIBITORS; CARDIOVASCULAR-DISEASE; IMPACT; OUTCOMES; RISK;
POPULATION; SCORE
AB Objective: Comorbidity scores are increasingly used to reduce potential confounding in oncologic research. This is of paramount importance in endometrial cancer (EC) since it is characterized by quite indolent behavior. Here, we aim to evaluate the impact of various comorbidities and concurrent medications used on survival outcomes, adopting the age-adjusted Charlson comorbidity index (A-CCI). Design: This is an observational study. Charts of 257 EC patients were retrieved. Methods: We retrospectively evaluated data of patients who underwent surgical treatment for EC. A-CCI was calculated by summing the weighted comorbidities and age of each patient. A binomial value was assigned to different comorbidities and different drugs. Oncologic outcomes were evaluated using Cox proportional hazard models adjusted for age. Results: A-CCI >= 3 correlated with more aggressive tumor features (47.6% vs. 26.8%, p = 0.001), higher risk of recurrence (29.7% vs. 11.6%, p = 0.001), death (20.7% vs. 7.1%, p = 0.002), and death due to disease (16.6% vs. 6.3%, p = 0.012). Considering comorbidities and drugs at parsimonious multivariable analysis model: cardiac disease, liver disease, and proton pump inhibitors (PPIs) use were independent predictors of disease-free survival. Cardiac disease, autoimmune disease, and PPIs use were independent predictors of overall survival. Diabetes was the only independent predictor for cause-specific survival. Limitations: The major limitation of the present study is its retrospective nature and the relatively small sample size that limit the possibility to have firm conclusions. Conclusion: Patients with EC are characterized by a high burden of comorbidities. Comorbidities are associated directly with survival outcomes. Further attention is needed to improve the active management of comorbidities soon after EC treatments. Interventional studies are needed to improve patients' outcomes. (C) 2022 S. Karger AG, Basel
C1 [Di Donato, Violante; Fischetti, Margherita; Tomao, Federica; Palaia, Innocenza; Perniola, Giorgia; Muzii, Ludovico; Panici, Pierluigi Benedetti] Sapienza Univ, Umberto I Hosp, Dept Maternal & Child Hlth & Urol Sci, Rome, Italy.
[D'Oria, Ottavia; Giannini, Andrea] Sapienza Univ, St Andrea Univ Hosp, Dept Med & Surg Sci & Translat Med, PhD Course Translat Med & Oncol, Rome, Italy.
[Bogani, Giorgio] Fdn IRCCS Ist Nazl Tumori Milano, Milan, Italy.
[Santangelo, Giusi] Sapienza Univ Rome, Dept Expt Med, Rome, Italy.
C3 Sapienza University Rome; University Hospital Sapienza Rome; Sapienza
University Rome; Azienda Ospedaliera Sant'Andrea; Fondazione IRCCS
Istituto Nazionale Tumori Milan; Sapienza University Rome
RP D'Oria, O (corresponding author), Sapienza Univ, St Andrea Univ Hosp, Dept Med & Surg Sci & Translat Med, PhD Course Translat Med & Oncol, Rome, Italy.
EM ottavia.doria@uniroma1.it
RI Di Donato, Violante/O-1742-2019; Muzii, Ludovico/I-2148-2019; Bogani,
Giorgio/N-1389-2013; Perniola, Giorgia/J-4336-2012; D'Oria,
Ottavia/HJY-0040-2023; Giannini, Andrea/ABN-8431-2022; Di Donato,
Violante/J-1556-2012
OI Giannini, Andrea/0000-0002-4388-0082; SANTANGELO,
GIUSI/0000-0001-7917-035X; Bogani, Giorgio/0000-0001-8373-8569; Di
Donato, Violante/0000-0002-9254-5790; D'Oria,
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NR 34
TC 41
Z9 41
U1 0
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0378-7346
EI 1423-002X
J9 GYNECOL OBSTET INVES
JI Gynecol.Obstet.Invest.
PY 2022
VL 87
IS 3-4
BP 191
EP 199
DI 10.1159/000525405
PG 9
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA 7B1ZB
UT WOS:000898939200003
PM 35793638
DA 2025-01-07
ER
PT J
AU Ginwala, R
Bhavsar, R
Chigbu, DI
Jain, P
Khan, ZK
AF Ginwala, Rashida
Bhavsar, Raina
Chigbu, De Gaulle I.
Jain, Pooja
Khan, Zafar K.
TI Potential Role of Flavonoids in Treating Chronic Inflammatory Diseases
with a Special Focus on the Anti-Inflammatory Activity of Apigenin
SO ANTIOXIDANTS
LA English
DT Review
DE natural products; flavonoids; apigenin; dendritic cells;
neuroinflammation; chronic inflammation
ID NF-KAPPA-B; FATTY LIVER-DISEASE; DENDRITIC CELLS; NATURAL-PRODUCTS; DRUG
DISCOVERY; HUMAN BREAST; IMMUNOSTIMULATORY FUNCTION; EXPERIMENTAL
COLITIS; COGNITIVE DEFICITS; DOWN-REGULATION
AB Inflammation has been reported to be intimately linked to the development or worsening of several non-infectious diseases. A number of chronic conditions such as cancer, diabetes, cardiovascular disorders, autoimmune diseases, and neurodegenerative disorders emerge as a result of tissue injury and genomic changes induced by constant low-grade inflammation in and around the affected tissue or organ. The existing therapies for most of these chronic conditions sometimes leave more debilitating effects than the disease itself, warranting the advent of safer, less toxic, and more cost-effective therapeutic alternatives for the patients. For centuries, flavonoids and their preparations have been used to treat various human illnesses, and their continual use has persevered throughout the ages. This review focuses on the anti-inflammatory actions of flavonoids against chronic illnesses such as cancer, diabetes, cardiovascular diseases, and neuroinflammation with a special focus on apigenin, a relatively less toxic and non-mutagenic flavonoid with remarkable pharmacodynamics. Additionally, inflammation in the central nervous system (CNS) due to diseases such as multiple sclerosis (MS) gives ready access to circulating lymphocytes, monocytes/macrophages, and dendritic cells (DCs), causing edema, further inflammation, and demyelination. As the dearth of safe anti-inflammatory therapies is dire in the case of CNS-related disorders, we reviewed the neuroprotective actions of apigenin and other flavonoids. Existing epidemiological and pre-clinical studies present considerable evidence in favor of developing apigenin as a natural alternative therapy against chronic inflammatory conditions.
C1 [Ginwala, Rashida; Bhavsar, Raina; Chigbu, De Gaulle I.; Jain, Pooja; Khan, Zafar K.] Drexel Univ, Dept Microbiol & Immunol, Coll Med, Ctr Canc Biol,Inst Mol Med & Infect Dis, Philadelphia, PA 19129 USA.
[Ginwala, Rashida; Bhavsar, Raina; Chigbu, De Gaulle I.; Jain, Pooja; Khan, Zafar K.] Drexel Univ, Ctr Mol Virol & Neuroimmunol, Ctr Canc Biol, Inst Mol Med & Infect Dis,Coll Med, Philadelphia, PA 19129 USA.
C3 Drexel University; Drexel University
RP Khan, ZK (corresponding author), Drexel Univ, Dept Microbiol & Immunol, Coll Med, Ctr Canc Biol,Inst Mol Med & Infect Dis, Philadelphia, PA 19129 USA.
EM rag78@drexel.edu; rmb345@drexel.edu; dic26@drexel.edu; pj27@drexel.edu;
zkk22@drexel.edu
RI Chigbu, DeGaulle/AAN-7685-2021
FU NIH/NINDS [R01 NS097147]
FX These studies have been funded in part with NIH/NINDS R01 NS097147 to
PJ.
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NR 186
TC 324
Z9 340
U1 7
U2 113
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-3921
J9 ANTIOXIDANTS-BASEL
JI Antioxidants
PD FEB
PY 2019
VL 8
IS 2
AR 35
DI 10.3390/antiox8020035
PG 28
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Food Science &
Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Food Science
& Technology
GA HO1UD
UT WOS:000460695700007
PM 30764536
OA Green Submitted, Green Published, gold
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Ahmed, ZSO
Hussein, S
Ghandour, RA
Azouz, AA
El-Sakhawy, MA
AF Ahmed, Zainab Sabry Othman
Hussein, Shaymaa
Ghandour, Rehab A.
Azouz, Asmaa A.
El-Sakhawy, Mohamed A.
TI Evaluation of the effect of methotrexate on the hippocampus, cerebellum,
liver, and kidneys of adult male albino rat Histopathological,
immunohistochemical and biochemical studies
SO ACTA HISTOCHEMICA
LA English
DT Article
DE Methotrexate; Neurotoxicity; Nephrotoxicity; Hepatotoxicity; Apoptosis;
Oxidative stress
ID LOW-DOSE METHOTREXATE; INDUCED OXIDATIVE STRESS; RHEUMATOID-ARTHRITIS;
INDUCED HEPATOTOXICITY; CHLOROGENIC ACID; RENAL TOXICITY; CELL-CYCLE;
APOPTOSIS; DAMAGE; EXPRESSION
AB Methotrexate (MTX) has been used for treatment of autoimmune diseases, inflammatory disorders as rheumatic arthritis, and different types of cancers. However, it has shown adverse effects on vital organs. The current study was conducted to investigate the toxic effect of MTX on the hippocampus, cerebellum, liver and kidneys of adult male albino rats. MTX was injected weekly at 5 mg/kg body weight via I/P injection for 6 weeks. At the end of the experiment, histopathological, immunohistochemical and biochemical evaluation were performed on the hippocampus, cerebellum, liver, and kidney tissues of the sacrificed rats. We observed that methotrexate induced neural tissue damage in the hippocampus and cerebellum, degeneration of hepatocytes, congestion of the central vein and blood sinusoids of the liver, distortion in the renal corpuscles and necrosis of the renal tubule. Immunohistochemical findings revealed strong positive expression of Caspase-3, PCNA and GFAP. Biochemical studies revealed significant elevation in the serum levels of AST and ALT, in addition to high serum concentrations of creatinine and urea. Also, MTX injection increased MDA, while it decreased GSH, SOD and AChE levels. We conclude the ability of MTX to induce oxidative stress that results into apoptosis and tissue injury, leading to neurotoxicity, hepatotoxicity, and nephrotoxicity.
C1 [Ahmed, Zainab Sabry Othman; Hussein, Shaymaa; El-Sakhawy, Mohamed A.] Cairo Univ, Fac Vet Med, Dept Cytol & Histol, Giza 12211, Egypt.
[Ghandour, Rehab A.] Cairo Univ, Fac Vet Med, Dept Physiol, Giza 12211, Egypt.
[Azouz, Asmaa A.] Cairo Univ, Fac Vet Med, Dept Pharmacol, Giza 12211, Egypt.
C3 Egyptian Knowledge Bank (EKB); Cairo University; Egyptian Knowledge Bank
(EKB); Cairo University; Egyptian Knowledge Bank (EKB); Cairo University
RP Ahmed, ZSO (corresponding author), Cairo Univ, Fac Vet Med, Dept Cytol & Histol, Giza 12211, Egypt.
EM zainah.sabry@cu.edu.eg; Shaymaahussein77@yahoo.com;
Rehabghandour1@gmail.com; azoz@hotmail.com; Profsakhawy@yahoo.com
RI Sabry, Zainab/KGM-9196-2024
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NR 69
TC 8
Z9 9
U1 0
U2 3
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0065-1281
EI 1618-0372
J9 ACTA HISTOCHEM
JI Acta Histochem.
PD FEB
PY 2021
VL 123
IS 2
AR 151682
DI 10.1016/j.acthis.2021.151682
EA JAN 2021
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA RL8VS
UT WOS:000639244000008
PM 33465564
DA 2025-01-07
ER
PT J
AU Takada, I
Makishima, M
AF Takada, Ichiro
Makishima, Makoto
TI Peroxisome proliferator-activated receptor agonists and antagonists: a
patent review (2014-present)
SO EXPERT OPINION ON THERAPEUTIC PATENTS
LA English
DT Review
DE Adverse effects; metabolic disease; inflammation; skeletal disease;
neurological disease; nuclear receptors; function-selective ligands
ID LIVER-X RECEPTORS; PPAR-GAMMA; ANTIDIABETIC AGENTS; LIPID-METABOLISM;
BETA-OXIDATION; DELTA; LIGANDS; ALPHA; ACID; IDENTIFICATION
AB Introduction: Peroxisome proliferator-activated receptors (PPARs), PPAR alpha, PPAR delta, and PPAR gamma, play an important role in the regulation of various physiological processes, specifically lipid and energy metabolism and immunity. PPAR alpha agonists (fibrates) and PPAR gamma agonists (thiazolidinediones) are used for the treatment of hypertriglyceridemia and type 2 diabetes, respectively. PPAR delta activation enhances mitochondrial and energy metabolism but PPAR delta-acting drugs are not yet available. Many synthetic ligands for PPARs have been developed to expand their therapeutic applications. Areas covered: The authors searched recent patent activity regarding PPAR ligands. Novel PPAR alpha agonists, PPAR delta agonists, PPAR gamma agonists, PPAR alpha/gamma dual agonists, and PPAR gamma antagonists have been claimed for the treatment of metabolic disease and inflammatory disease. Methods for the combination of PPAR ligands with other drugs and expanded application of PPAR agonists for bone and neurological disease have been also claimed. Expert opinion: Novel PPAR ligands and the combination of PPAR ligands with other drugs have been claimed for the treatment of mitochondrial disease, inflammatory/autoimmune disease, neurological disease, and cancer in addition to metabolic diseases including dyslipidemia and type 2 diabetes. Selective therapeutic actions of PPAR ligands should be exploited to avoid adverse effects. More basic studies are needed to elucidate the molecular mechanisms of selective actions.
C1 [Takada, Ichiro; Makishima, Makoto] Nihon Univ, Dept Biomed Sci, Div Biochem, Sch Med, Tokyo, Japan.
C3 Nihon University
RP Makishima, M (corresponding author), Nihon Univ, Dept Biomed Sci, Div Biochem, Sch Med,Itabashi Ku, 30-1 Oyaguchi Kamicho, Tokyo 1738610, Japan.
EM makishima.makoto@nihon-u.ac.jp
FU Nihon University School of Medicine
FX This paper was funded by research budget from Nihon University School of
Medicine.
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NR 114
TC 100
Z9 113
U1 3
U2 84
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3776
EI 1744-7674
J9 EXPERT OPIN THER PAT
JI Expert Opin. Ther. Patents
PD JAN 2
PY 2020
VL 30
IS 1
BP 1
EP 13
DI 10.1080/13543776.2020.1703952
EA DEC 2019
PG 13
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA KA9OA
UT WOS:000503518500001
PM 31825687
DA 2025-01-07
ER
PT J
AU Yin, XD
Jia, PJ
Pang, Y
He, JH
AF Yin, Xiao-Dong
Jia, Pei-Jie
Pang, Yan
He, Jing-Hua
TI Protective Effect of FTY720 on Several Markers of Liver Injury Induced
by Concanavalin A in Mice
SO CURRENT THERAPEUTIC RESEARCH-CLINICAL AND EXPERIMENTAL
LA English
DT Article
DE concanavalin A; FTY720; liver injury; nuclear factor-kappa B; tumor
necrosis factor-alpha
ID FACTOR-KAPPA-B; HEPATIC-INJURY; RECEPTOR; MODEL; DISEASE
AB BACKGROUND: 2-Amino-2-[2-(4-octylphenyl)ethyl] propane-1,3-diol hydrochloride (FTY720) is a novel agent with protective effect on several markers of liver injury. It is a chemical substance derived by modifying myriocin from the ascomycete Isaria sinclairii. It has been reported that FTY720 is able to treat autoimmune encephalomyelitis, renal cancer, asthma, and multiple sclerosis. More potent clinical applications of FTY720 need to be investigated.
OBJECTIVE: The aim of this study was to evaluate the protective effect of FTY720 on several markers of experimental liver injury and to investigate the possible mechanism of action.
METHODS: Concanavalin A (Con A) at a dose of 15 mg/kg was intravenously. injected in mice, and 10 days before the Con A challenge, 1 mg/kg, 3 mg/kg, and 6 mg/kg of FTY720 were administered to mice. The liver injury was monitored biochemically by measuring serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and tumor necrosis factor-alpha (TNF-alpha) levels. TNF-alpha and nuclear factor-kappa B (NF-kappa B) in liver tissue were detected by Western blot analysis.
RESULTS: FTY720, when administered intragastrically for 10 days in mice with Con A induced liver injury, dose-dependently reduced serum ALT and AST and TNF-alpha levels. The differences were statistically significant (P <= 0.05). It was also found that FTY720 decreases TNF-alpha and NF-kappa B protein expression in liver tissue.
CONCLUSIONS: FTY720 is able to improve several markers of Con A induced liver injury in mice, including serum ALT, serum AST, TNF-alpha, and NF-kappa B, which might be at least in part related to its ability to reduce TNF-alpha/NF-kappa B cascade activity. (Curr Ther Res Clin Exp. 2012;73:140-149) (c) 2012 Elsevier HS Journals, Inc. All rights reserved.
C1 [He, Jing-Hua] Tianjin Med Univ, Basic Med Sch, Dept Pharmacol, Tianjin 300070, Peoples R China.
[Yin, Xiao-Dong; Jia, Pei-Jie; Pang, Yan] Tianjin Union Med Ctr, Dept Oncol, Tianjin, Peoples R China.
C3 Tianjin Medical University
RP He, JH (corresponding author), Tianjin Med Univ, Basic Med Sch, Dept Pharmacol, Tianjin 300070, Peoples R China.
EM hejinghuatj@yahoo.com.cn
RI Yin, Xiaodong/A-1516-2017
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NR 29
TC 5
Z9 8
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0011-393X
EI 1879-0313
J9 CURR THER RES CLIN E
JI Curr. Ther. Res.-Clin. Exp.
PD AUG-OCT
PY 2012
VL 73
IS 4-5
BP 140
EP 149
DI 10.1016/j.curtheres.2012.07.001
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 009LI
UT WOS:000309026900003
PM 24653516
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Joo, M
Chang, SH
Kim, H
Gardner, JM
Ro, JY
AF Joo, Mee
Chang, Sun Hee
Kim, Hanseong
Gardner, Jerad M.
Ro, Jae Yun
TI Primary gastrointestinal clear cell sarcoma: report of 2 cases, one case
associated with IgG4-related sclerosing disease, and review of
literature
SO ANNALS OF DIAGNOSTIC PATHOLOGY
LA English
DT Article
DE Clear cell sarcoma; Small intestine; IgG4; Sclerosis
ID AUTOIMMUNE PANCREATITIS; MALIGNANT-MELANOMA; SOFT PARTS; SERUM IGG4;
SIALADENITIS; INFILTRATION; DIAGNOSIS; CANCER; TUMOR
AB Clear cell sarcoma (CCS) is a distinctive soft tissue sarcoma that shows melanocytic differentiation. Primary gastrointestinal (GI) CCSs have been rarely reported, but to our knowledge, no association between GI CCSs and immunoglobulin G4 (IgG4)-related sclerosing disease has been described in the literature. We experienced 2 cases of CCS that arose in the small intestine and metastasized to the liver. Histologic features and immunophenotype were typical of CCS. One of them showed a unique peritumoral sclerosing inflammatory reaction, which was highly reminiscent of IgG4-related sclerosing inflammatory disease. Dense lymphoplasmacytic infiltration with extensive sclerosis and obliterative phlebitis was observed in the immediate vicinity of the primary and metastatic tumors, but not in the distant areas from the tumor. The average number of IgG4-positive plasma cells was more than 50 per high-power field. We report 2 cases of primary GI CCS with one case showing a unique peritumoral IgG4-related lymphoplasmacytic sclerosing inflammation. (c) 2009 Elsevier Inc. All rights reserved.
C1 [Gardner, Jerad M.; Ro, Jae Yun] Cornell Univ, Methodist Hosp, Dept Pathol, Houston, TX 77030 USA.
[Joo, Mee; Chang, Sun Hee; Kim, Hanseong] Inje Univ, Ilsan Paik Hosp, Dept Pathol, Goyang, South Korea.
[Gardner, Jerad M.; Ro, Jae Yun] Cornell Univ, Weill Med Coll, Houston, TX 77030 USA.
C3 Houston Methodist; Cornell University; Inje University; Cornell
University
RP Ro, JY (corresponding author), Cornell Univ, Methodist Hosp, Dept Pathol, Houston, TX 77030 USA.
EM jaero@tmhs.org
RI Gardner, Jerad/G-6028-2011
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NR 15
TC 31
Z9 36
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1092-9134
EI 1532-8198
J9 ANN DIAGN PATHOL
JI Ann. Diagn. Pathol.
PD FEB
PY 2009
VL 13
IS 1
BP 30
EP 35
DI 10.1016/j.anndiagpath.2008.10.003
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 393YY
UT WOS:000262413600005
PM 19118779
DA 2025-01-07
ER
PT J
AU Voumvouraki, A
Koulentaki, M
Tzardi, M
Sfakianaki, O
Manousou, P
Notas, G
Kouroumalis, E
AF Voumvouraki, Argyro
Koulentaki, Mairi
Tzardi, Maria
Sfakianaki, Ourania
Manousou, Penelope
Notas, George
Kouroumalis, Elias
TI Increased TGF-β3 in primary biliary cirrhosis: An abnormality related to
pathogenesis?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Transforming growth factor-beta; Primary biliary cirrhosis; Liver
fibrosis; Cirrhosis
ID GROWTH-FACTOR-BETA; REGULATORY T-CELLS; HUMAN HEPATOCELLULAR-CARCINOMA;
HEPATIC STELLATE CELLS; LATENT TGF-BETA; ANTIMITOCHONDRIAL ANTIBODIES;
RAT-LIVER; AUTOIMMUNE CHOLANGITIS; FOXP3 EXPRESSION; MICE
AB AIM: To investigate the transforming growth factor-beta (TGF-beta) isoforms in the peripheral and hepatic venous blood of primary biliary cirrhosis (PBC) patients.
METHODS: We examined TGF-beta 1, TGF-beta 2 and TGF-beta 3 (enzyme-linked immunosorbent assay), in 27 stage IV PBC patients (27 peripheral and 15 hepatic vein sera), 35 early (I-II) PBC and 60 healthy controls. As disease controls 28 hepatitis C virus (HCV) cirrhosis (28 peripheral and 17 hepatic vein serum), 44 chronic HCV hepatitis and 38 HCV-related hepatocellular carcinomas were included. We also tested liver tissue by immunohistochemistry to identify localization of TGF isoforms.
RESULTS: TGF-beta 1 was significantly decreased in all cirrhotics (PBC III-IV: median 13.4 ng/mL; range, 7.4-26.2, HCV cirrhosis: 11.6 ng/mL; range, 5.0-33.8), compared to controls (30.9 ng/mL; range, 20.9-37.8). TGF-beta 2 was increased in viral cirrhosis but not in PBC and chronic hepatitis. TGF-beta 3 (47.2 pg/mL; range, 27.0-79.7 in healthy controls) was increased in early and late PBC (I - II : 94.3 pg/mL; range, 41.5-358.6; III - IV: 152.8 pg/mL; range, 60.4-361.2; P < 0.001) and decreased in viral cirrhosis (37.4 pg/mL; range, 13.3-84.0; P < 0.05). Hepatic vein TGF-beta levels were analogous to those in peripheral blood. Immunohistochemistry identified all isoforms in portal tract lymphocytes, sinusoidal cells and cholangiocytes. TGF-beta 3 was additionally over-expressed in hepatocytes in PBC patients.
CONCLUSION: The serum profile of TGF-beta isoforms is different in cirrhotics. Increased TGF-beta 3 is characteristic of PBC. These findings may be related to the immunological abnormalities of PBC. (C) 2010 Baishideng. All rights reserved.
C1 [Voumvouraki, Argyro; Koulentaki, Mairi; Kouroumalis, Elias] Univ Crete, Univ Hosp Dept Gastroenterol, Fac Med, GR-71100 Iraklion, Crete, Greece.
[Voumvouraki, Argyro; Sfakianaki, Ourania; Manousou, Penelope; Notas, George; Kouroumalis, Elias] Univ Crete, Liver Res Lab, Fac Med, GR-71100 Iraklion, Crete, Greece.
[Tzardi, Maria] Univ Crete, Univ Hosp Dept Pathol, Fac Med, GR-71100 Iraklion, Crete, Greece.
[Notas, George] Univ Crete, Lab Expt Endocrinol, Fac Med, GR-71100 Iraklion, Crete, Greece.
C3 University of Crete; University of Crete; University of Crete;
University of Crete
RP Kouroumalis, E (corresponding author), Univ Crete, Univ Hosp Dept Gastroenterol, Fac Med, POB 1352, GR-71100 Iraklion, Crete, Greece.
EM kouroum@med.uoc.gr
RI Notas, George/K-3709-2019
OI Notas, George/0000-0002-2506-5252; Manousou,
Pinelopi/0000-0002-5363-1565; Koulentaki, Mairi/0000-0002-5665-6741
FU University of Crete
FX Supported by Research funds of the University of Crete
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NR 49
TC 9
Z9 10
U1 0
U2 1
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD OCT 28
PY 2010
VL 16
IS 40
BP 5057
EP 5064
DI 10.3748/wjg.v16.i40.5057
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 673PL
UT WOS:000283675300008
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Bao, XH
Liang, YJ
Chang, HM
Cai, TJ
Feng, BJ
Gordon, K
Zhu, YK
Shi, HL
He, YD
Xie, LY
AF Bao, Xuhui
Liang, Yongjun
Chang, Hanman
Cai, Tianji
Feng, Baijie
Gordon, Konstantin
Zhu, Yuekun
Shi, Hailian
He, Yundong
Xie, Liyi
TI Targeting proprotein convertase subtilisin/kexin type 9 (PCSK9): from
bench to bedside
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID LOW-DENSITY-LIPOPROTEIN; SMOOTH-MUSCLE-CELLS; HEPATITIS-C VIRUS;
LOSS-OF-FUNCTION; AUTOSOMAL-DOMINANT HYPERCHOLESTEROLEMIA; MONOCYTE
CHEMOATTRACTANT PROTEIN-1; ENDOPLASMIC-RETICULUM STRESS;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; ARTHRITIS RECENT ADVANCES; PLASMA PCSK9
AB Proprotein convertase subtilisin/kexin type 9 (PCSK9) has evolved as a pivotal enzyme in lipid metabolism and a revolutionary therapeutic target for hypercholesterolemia and its related cardiovascular diseases (CVD). This comprehensive review delineates the intricate roles and wide-ranging implications of PCSK9, extending beyond CVD to emphasize its significance in diverse physiological and pathological states, including liver diseases, infectious diseases, autoimmune disorders, and notably, cancer. Our exploration offers insights into the interaction between PCSK9 and low-density lipoprotein receptors (LDLRs), elucidating its substantial impact on cholesterol homeostasis and cardiovascular health. It also details the evolution of PCSK9-targeted therapies, translating foundational bench discoveries into bedside applications for optimized patient care. The advent and clinical approval of innovative PCSK9 inhibitory therapies (PCSK9-iTs), including three monoclonal antibodies (Evolocumab, Alirocumab, and Tafolecimab) and one small interfering RNA (siRNA, Inclisiran), have marked a significant breakthrough in cardiovascular medicine. These therapies have demonstrated unparalleled efficacy in mitigating hypercholesterolemia, reducing cardiovascular risks, and have showcased profound value in clinical applications, offering novel therapeutic avenues and a promising future in personalized medicine for cardiovascular disorders. Furthermore, emerging research, inclusive of our findings, unveils PCSK9's potential role as a pivotal indicator for cancer prognosis and its prospective application as a transformative target for cancer treatment. This review also highlights PCSK9's aberrant expression in various cancer forms, its association with cancer prognosis, and its crucial roles in carcinogenesis and cancer immunity. In conclusion, this synthesized review integrates existing knowledge and novel insights on PCSK9, providing a holistic perspective on its transformative impact in reshaping therapeutic paradigms across various disorders. It emphasizes the clinical value and effect of PCSK9-iT, underscoring its potential in advancing the landscape of biomedical research and its capabilities in heralding new eras in personalized medicine.
C1 [Bao, Xuhui] Fudan Univ, Inst Therapeut Canc Vaccines, Pudong Med Ctr, Shanghai, Peoples R China.
[Bao, Xuhui; He, Yundong] East China Normal Univ, Sch Life Sci, Shanghai Key Lab Regulatory Biol, Shanghai, Peoples R China.
[Bao, Xuhui; Feng, Baijie] Fudan Univ, Dept Oncol, Pudong Med Ctr, Shanghai, Peoples R China.
[Bao, Xuhui] Fudan Univ, Ctr Clin Res, Pudong Med Ctr, Shanghai, Peoples R China.
[Bao, Xuhui] Fudan Univ, Clin Res Ctr Cell Based Immunotherapy, Shanghai, Peoples R China.
[Bao, Xuhui] Duke Univ, Dept Pathol, Med Ctr, Durham, NC 27710 USA.
[Liang, Yongjun] Fudan Univ, Ctr Med Res & Innovat, Pudong Med Ctr, Shanghai, Peoples R China.
[Chang, Hanman] IIT, Inst Food Safety & Hlth, Chicago, IL USA.
[Cai, Tianji] Univ Macau, Dept Sociol, Taipa, Macao, Peoples R China.
[Gordon, Konstantin] Peoples Friendship Univ Russia, Med Inst, Moscow, Russia.
[Gordon, Konstantin] A Tsyb Med Radiol Res Ctr, Obninsk, Russia.
[Zhu, Yuekun] Harbin Med Univ, Affiliated Hosp 1, Dept Colorectal Surg, Harbin, Heilongjiang, Peoples R China.
[Shi, Hailian] Shanghai Univ Tradit Chinese Med, Inst Chinese Mat Med, Shanghai Key Lab Cpd Chinese Med, Zhangjiang Hitech Pk, Shanghai, Peoples R China.
[Xie, Liyi] Fudan Univ, Dept Radiat Oncol, Shanghai Canc Ctr, Shanghai, Peoples R China.
[Xie, Liyi] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
C3 Fudan University; East China Normal University; Fudan University; Fudan
University; Fudan University; Duke University; Fudan University;
Illinois Institute of Technology; University of Macau; Peoples
Friendship University of Russia; Harbin Medical University; Shanghai
University of Traditional Chinese Medicine; Fudan University; Fudan
University
RP Bao, XH (corresponding author), Fudan Univ, Inst Therapeut Canc Vaccines, Pudong Med Ctr, Shanghai, Peoples R China.; Bao, XH; He, YD (corresponding author), East China Normal Univ, Sch Life Sci, Shanghai Key Lab Regulatory Biol, Shanghai, Peoples R China.; Bao, XH (corresponding author), Fudan Univ, Dept Oncol, Pudong Med Ctr, Shanghai, Peoples R China.; Bao, XH (corresponding author), Fudan Univ, Ctr Clin Res, Pudong Med Ctr, Shanghai, Peoples R China.; Bao, XH (corresponding author), Fudan Univ, Clin Res Ctr Cell Based Immunotherapy, Shanghai, Peoples R China.; Bao, XH (corresponding author), Duke Univ, Dept Pathol, Med Ctr, Durham, NC 27710 USA.; Xie, LY (corresponding author), Fudan Univ, Dept Radiat Oncol, Shanghai Canc Ctr, Shanghai, Peoples R China.; Xie, LY (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
EM xuhui_bao@fudan.edu.cn; ydhe@bio.ecnu.edu.cn; xiely0922@gmail.com
RI bao, xuhui/G-3191-2017; Cai, Tianji/R-8697-2019; Gordon,
Konstantin/O-1778-2015
OI Gordon, Konstantin/0000-0002-3146-5615
FU National Natural Science Foundation of China (National Science
Foundation of China) [82272817]; National Natural Science Foundation of
China [22PJ1412400, 22PJ1402700]; Shanghai Pujiang Program
[PKJ2022-Y50]; Science and Technology Development Fund of Shanghai
Pudong New Area
FX This work was supported by the National Natural Science Foundation of
China (No. 82272817, to X.B.), Shanghai Pujiang Program (No.
22PJ1412400, to X.B., and No. 22PJ1402700, to Y.H.), and Science and
Technology Development Fund of Shanghai Pudong New Area (No.
PKJ2022-Y50, to X.B.). We thank Home for Researchers
(www.home-for-researchers.com) for their service to improve our figures.
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NR 501
TC 21
Z9 22
U1 29
U2 44
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD JAN 8
PY 2024
VL 9
IS 1
AR 13
DI 10.1038/s41392-023-01690-3
PG 49
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA EF1N0
UT WOS:001137415600002
PM 38185721
OA gold
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Indriolo, A
Ravelli, P
AF Indriolo, Amedeo
Ravelli, Paolo
TI Clinical management of inflammatory bowel disease in the organ recipient
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Inflammatory bowel disease; Ulcerative colitis; Crohn's disease; Primary
sclerosing cholangitis; Liver transplantation; Heart transplantation;
Renal transplantation; Anti-tumor necrosis factor alpha therapy
ID PRIMARY SCLEROSING CHOLANGITIS; ORTHOTOPIC LIVER-TRANSPLANTATION;
POUCH-ANAL ANASTOMOSIS; ULCERATIVE-COLITIS; COLORECTAL NEOPLASIA;
INCREASED RISK; MYCOPHENOLATE-MOFETIL; CROHNS-DISEASE; CASE SERIES;
IMMUNOSUPPRESSION
AB There was estimated a higher incidence of de novo inflammatory bowel disease (IBD) after solid organ transplantation than in the general population. The onset of IBD in the organ transplant recipient population is an important clinical situation which is associated to higher morbidity and difficulty in the medical therapeutic management because of possible interaction between anti-reject therapy and IBD therapy. IBD course after liver transplantation ( LT) is variable, but about one third of patients may worsen, needing an increase in medical therapy or a colectomy. Active IBD at the time of LT, discontinuation of 5-aminosalicylic acid or azathioprine at the time of LT and use of tacrolimus-based immunosuppression may be associated with an unfavorable outcome of IBD after LT. Anti-tumor necrosis factor alpha (TNF alpha) therapy for refractory IBD may be an effective and safe therapeutic option after LT. The little experience of the use of biological therapy in transplanted patients, with concomitant anti-rejection therapy, suggests there be a higher more careful surveillance regarding the risk of infectious diseases, autoimmune diseases, and neoplasms. An increased risk of colorectal cancer (CRC) is present also after LT in IBD patients with primary sclerosing cholangitis (PSC). An annual program of endoscopic surveillance with serial biopsies for CRC is recommended. A prophylactic colectomy in selected IBD/PSC patients with CRC risk factors could be a good management strategy in the CRC prevention, but it is used infrequently in the majority of LT centers. About 30% of patients develop multiple IBD recurrence and 20% of patients require a colectomy after renal transplantation. Like in the liver transplantation, anti-TNF alpha therapy could be an effective treatment in IBD patients with conventional refractory therapy after renal or heart transplantation. A large number of patients are needed to confirm the preliminary observations. Regarding the higher clinical complexity of this subgroup of IBD patients, a close multidisciplinary approach between an IBD dedicated gastroenterologist and surgeon and an organ transplantation specialist is necessary in order to have the best clinical management of IBD after transplantation.
C1 [Indriolo, Amedeo; Ravelli, Paolo] Papa Giovanni XXIII Hosp, Dept Gastroenterol, Digest Endoscopy Unit, I-24127 Bergamo, Italy.
C3 ASST Papa Giovanni XXIII
RP Indriolo, A (corresponding author), Papa Giovanni XXIII Hosp, Dept Gastroenterol, Digest Endoscopy Unit, Piazza OMS 1, I-24127 Bergamo, Italy.
EM amedeo.indriolo@gmail.com
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NR 63
TC 31
Z9 34
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD APR 7
PY 2014
VL 20
IS 13
BP 3525
EP 3533
DI 10.3748/wjg.v20.i13.3525
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AF0SC
UT WOS:000334423300014
PM 24707135
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Hall, C
McLaren, M
Mosse, C
AF Hall, Catherine
McLaren, Mairi
Mosse, Charles
TI A pancreatic mass and extreme elevation of CA 19-9: a benign masquerade
of cholangiocarcinoma
SO JOURNAL OF SURGICAL CASE REPORTS
LA English
DT Article
ID PREOPERATIVE HISTOLOGICAL DIAGNOSIS; AUTOIMMUNE PANCREATITIS; CANCER;
RISK; TUMOR
AB Carbohydrate antigen 19-9 (CA 19-9) is a specific tumour marker for pancreato-biliary malignancy. Immunoglobulin G4-related disease (IgG4-RD) is an immune-mediated condition in which IgG4 deposits infiltrate various organs, including the biliary tract manifesting IgG4 sclerosing cholangitis and pseudotumours. An 83-year-old woman presented with severe obstructive jaundice, weight loss and an extreme elevation of CA 19-9 level of 3295 kU/L. Magnetic resonance cholangiopancreatography (MRCP) revealed a pancreatic mass amputating the biliary tree. Liver function tests revealed a cholestatic pattern and severe hyperbilirubinaemia (289umol/L). IgG4 level was found to be high at 7.97 g/L. After treatment with high-dose corticosteroids, repeat MRCP 2 months later revealed disappearance of the pancreatic mass. There was also normalization of the bilirubin and a dramatic decrease of CA 19-9. This case reports the highest published benign elevation of Ca19.9 level in the setting of IgG4 disease. Differentiation between cholangiocarcinoma and IgG4-RD is important, as the treatment is vastly different.
C1 [Hall, Catherine; McLaren, Mairi; Mosse, Charles] Canberra Hosp, Div Surg, Garran 2605, Australia.
C3 Australian National University; Canberra Hospital
RP Hall, C (corresponding author), Canberra Hosp, Div Surg, Garran 2605, Australia.
EM cjhall311@gmail.com
OI Hall, Catherine/0000-0002-4188-8072
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NR 15
TC 1
Z9 1
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 2042-8812
J9 J SURG CASE REP
JI J. Surg. Case Rep.
PD FEB 1
PY 2022
VL 2022
IS 2
AR rjac018
DI 10.1093/jscr/rjac018
PG 3
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA ZB5MN
UT WOS:000756886100003
PM 35186252
OA Green Published, gold
DA 2025-01-07
ER
PT S
AU Lahita, RG
Schaefer, RA
Bradlow, HL
Kreek, MJ
AF Lahita, Robert G.
Schaefer, Robert A.
Bradlow, H. Leon
Kreek, Mary Jeanne
BE Bradlow, HL
Carruba, G
TI Clues to Understanding the Oxidation of Estradiol in Humans
SO STEROID ENZYMES AND CANCER
SE Annals of the New York Academy of Sciences
LA English
DT Article; Proceedings Paper
CT 9th Advanced Course on Steroid Enzymes and Cancer
CY MAY 03-08, 2008
CL Erice, ITALY
DE liver disease; alterations in estrogen metabolism; alterations;
cirrhosis
ID SYSTEMIC LUPUS-ERYTHEMATOSUS; CHRONIC ALCOHOL-ABUSE; LIVER-DISEASE;
HEPATOCELLULAR-CARCINOMA; METABOLISM; ESTROGEN; RAT; MEN; HYDROXYLATION;
TESTOSTERONE
AB Determination of 2- and 16 alpha-hydroxylation of estradiol in patients with a variety of liver disorders using a dynamic method of quantitating the extent of hydroxylation revealed specific and characteristic differences in the metabolic response. Patients with acute or silent variants of hepatitis B had estrogen metabolite patterns that were indistinguishable from those found in the control subjects. Female patients with autoimmune hepatitis (formerly known as lupoid hepatitis), however, showed a moderate significant decrease (P < 0.01) in 2-hydroxylation as compared with normal controls (mean 16.3 +/- 1.9 vs. 33.9 +/- 2.5), with no significant change in 16 alpha-hydroxylation. Male and female subjects with chronic alcoholic cirrhosis were almost devoid of 2-hydroxylation (mean 2.9 +/- 0.5, P < 0.01), but did show a significant increase in 16 alpha-hydroxylation (P < 0.01). The results, therefore, show that the alterations in patterns of biological oxidation are highly specific and do not reflect a general inability to metabolize estrogens in the cirrhotic patient. However, the results also suggest the possibility that a substantial fraction of 16 alpha-hydroxylation may occur elsewhere in the body at sites other than in the liver, explaining why this biotransformation pathway is elevated, while the reaction at C-2 is almost absent in the alcoholic cirrhotic subjects.
C1 [Lahita, Robert G.] Beth Israel Deaconess Med Ctr, Newark, NJ USA.
[Kreek, Mary Jeanne] Rockefeller Univ, New York, NY 10021 USA.
[Schaefer, Robert A.] New York Hosp, Cornell Med Ctr, New York, NY 10021 USA.
[Bradlow, H. Leon] Hackensack Univ, Jurist Inst Res, Med Ctr, Hackensack, NJ USA.
C3 Harvard University; Beth Israel Deaconess Medical Center; Rockefeller
University; Cornell University; NewYork-Presbyterian Hospital;
Hackensack University Medical Center
RP Lahita, RG (corresponding author), Newark Beth Israel Med Ctr, Dept Med, 201 Lyons Ave, Newark, NJ 07112 USA.
EM rlahita@au.net
OI Bradlow, H Leon/0000-0002-2397-3679
FU New York State Office of Alcoholism and Substance Abuse Services;;
NIH-DRR [M01-RR-00102]; Tiger Fund; Murray and Isabella Rayburn
Foundation.
FX This work was supported in part by the following grants of Dr. Kreek:
DHHS-NIH-NIDA P60-DAO5130 Research Center; New York State Office of
Alcoholism and Substance Abuse Services; NIH-DRR earlier grant to The
Rockefeller University Hospital General Clinical Research Center
(M01-RR-00102); and by grants from the Tiger Fund and the Murray and
Isabella Rayburn Foundation.
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NR 32
TC 4
Z9 6
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER STREET, HOBOKEN, NJ, UNITED STATES
SN 0077-8923
BN 978-1-57331-745-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2009
VL 1155
BP 242
EP 251
DI 10.1111/j.1749-6632.2009.04359.x
PG 10
WC Oncology; Multidisciplinary Sciences
WE Conference Proceedings Citation Index - Science (CPCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Science & Technology - Other Topics
GA BJC65
UT WOS:000264751500026
PM 19250211
OA Green Accepted, Bronze
DA 2025-01-07
ER
PT J
AU Murphy, G
Dawsey, SM
Engels, EA
Ricker, W
Parsons, R
Etemadi, A
Lin, SW
Abnet, CC
Freedman, ND
AF Murphy, Gwen
Dawsey, Sanford M.
Engels, Eric A.
Ricker, Winnie
Parsons, Ruth
Etemadi, Arash
Lin, Shih-Wen
Abnet, Christian C.
Freedman, Neal D.
TI Cancer Risk After Pernicious Anemia in the US Elderly Population
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Chronic Atrophic Autoimmune Gastritis; Acid Secretion; Parietal Cells;
Stomach Cancer
ID GASTRIC CARCINOID-TUMORS; SERUM PEPSINOGENS; COHORT; CARCINOGENESIS;
ADENOCARCINOMA; PREVENTION; PREVALENCE; HISTOLOGY; STOMACH; DISEASE
AB BACKGROUND & AIMS: Pernicious anemia, a result of autoimmune gastritis, is the most common cause of vitamin B-12 deficiency, affecting 2% to 5% of the elderly population. Treatment with vitamin B-12 cures the anemia, but not the gastritis. Findings from small studies have indicated that patients with pernicious anemia could have an increased risk of cancer.
METHODS: We performed a population-based, case-control study of individuals in the Surveillance, Epidemiology, and End Results-Medicare database, comparing 1,138,390 cancer cases (age, 66-99 y) with 100,000 matched individuals without cancer (controls). Individuals with pernicious anemia were identified based on their medical claims within the year before selection for the study. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression, and models were adjusted for sex, age, and calendar year of diagnosis and selection.
RESULTS: Compared with controls, we found individuals with pernicious anemia to be at increased risk for noncardia gastric adenocarcinoma (OR, 2.18; 95% CI, 1.94-2.45) and gastric carcinoid tumors (OR, 11.43; 95% CI, 8.90-14.69). In addition, people with pernicious anemia have an increased risk of developing tonsilar cancer (OR, 2.00; 95% CI, 1.40-2.85), hypopharyngeal cancer (OR, 1.92; 95% CI, 1.35-2.73), esophageal squamous cell carcinoma (OR, 2.12; 95% CI, 1.76-2.55), small intestinal cancer (OR, 1.63; 95% CI, 1.32-2.02), liver cancer (OR, 1.49; 95% CI, 1.28-1.73), myeloma (OR, 1.55; 95% CI, 1.37-1.75), acute myeloid leukemia (OR, 1.68; 95% CI, 1.46-1.93), and myelodysplastic syndrome (OR, 2.87; 95% CI, 2.53-3.26). People with pernicious anemia have a lower risk of rectal cancer than the general population (OR, 0.82; 95% CI, 0.74-0.92).
CONCLUSIONS: In a population-based, case-control study of individuals in the Surveillance, Epidemiology, and End Results-Medicare database, we found individuals with pernicious anemia to have significantly increased risks of gastric carcinoid tumors, adenocarcinomas, and other cancers located throughout the body.
C1 [Murphy, Gwen; Dawsey, Sanford M.; Engels, Eric A.; Etemadi, Arash; Lin, Shih-Wen; Abnet, Christian C.; Freedman, Neal D.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Ricker, Winnie; Parsons, Ruth] Informat Management Serv Inc, Calverton, MD USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI); Information Management Services, Inc.
RP Murphy, G (corresponding author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,6E314, Bethesda, MD 20892 USA.
EM murphygw@mail.nih.gov
RI Abnet, Christian/JAC-5179-2023; Murphy, Gwen/GQB-3897-2022; Etemadi,
Arash/Y-7082-2018; Etemadi, Arash/C-1386-2016; Freedman,
Neal/B-9741-2015; Abnet, Christian/C-4111-2015; Murphy,
Gwen/AFR-8275-2022
OI Etemadi, Arash/0000-0002-3458-1072; Freedman, Neal/0000-0003-0074-1098;
Abnet, Christian/0000-0002-3008-7843; Murphy, Gwen/0000-0003-0118-5337
FU National Cancer Institute at the US National Institutes of Health;
National Cancer Institute [ZIACP010127] Funding Source: NIH RePORTER
FX This work was supported by the Intramural Research Program of the
National Cancer Institute at the US National Institutes of Health.
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NR 31
TC 100
Z9 103
U1 1
U2 17
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD DEC
PY 2015
VL 13
IS 13
BP 2282
EP +
DI 10.1016/j.cgh.2015.05.040
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CW7PK
UT WOS:000365191300016
PM 26079040
OA Green Accepted, Bronze
DA 2025-01-07
ER
PT J
AU Haeusler, RA
McGraw, TE
Accili, D
AF Haeusler, Rebecca A.
McGraw, Timothy E.
Accili, Domenico
TI Biochemical and cellular properties of insulin receptor signalling
SO NATURE REVIEWS MOLECULAR CELL BIOLOGY
LA English
DT Review
ID FORKHEAD TRANSCRIPTION FACTOR; GENOME-WIDE ASSOCIATION;
TYROSINE-PHOSPHATASE 1B; HEPATIC GLUCOSE-PRODUCTION;
GTPASE-ACTIVATING-PROTEIN; REGULATED MEMBRANE AMINOPEPTIDASE;
ENDOPLASMIC-RETICULUM MEMBRANES; LIVER-SPECIFIC DELETION; FATTY-ACID
SYNTHESIS; FACTOR FOXO1
AB The mechanism of insulin action is a central theme in biology and medicine. In addition to the rather rare condition of insulin deficiency caused by autoimmune destruction of pancreatic beta-cells, genetic and acquired abnormalities of insulin action underlie the far more common conditions of type 2 diabetes, obesity and insulin resistance. The latter predisposes to diseases ranging from hypertension to Alzheimer disease and cancer. Hence, understanding the biochemical and cellular properties of insulin receptor signalling is arguably a priority in biomedical research. In the past decade, major progress has led to the delineation of mechanisms of glucose transport, lipid synthesis, storage and mobilization. In addition to direct effects of insulin on signalling kinases and metabolic enzymes, the discovery of mechanisms of insulin-regulated gene transcription has led to a reassessment of the general principles of insulin action. These advances will accelerate the discovery of new treatment modalities for diabetes.
C1 [Haeusler, Rebecca A.] Columbia Univ Coll Phys & Surg, Dept Pathol & Cell Biol, 630 W 168th St, New York, NY 10032 USA.
[McGraw, Timothy E.] Weill Cornell Med, Dept Biochem, New York, NY 10065 USA.
[McGraw, Timothy E.] Weill Cornell Med, Dept Cardiothorac Surg, New York, NY 10065 USA.
[Accili, Domenico] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
C3 Columbia University; Cornell University; Weill Cornell Medicine; Cornell
University; Weill Cornell Medicine; Columbia University
RP Accili, D (corresponding author), Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
EM da230@cumc.columbia.edu
OI Haeusler, Rebecca/0000-0002-6973-9845
FU NIH [DK57539, DK64819, DK58282, HL81723, DK52852, HL125649]
FX The authors thank U. Pajvani and R. Leibel for stimulating discussions
and helpful comments. Supported by NIH grants DK57539, DK64819, DK58282,
HL81723, DK52852 and HL125649.
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NR 245
TC 466
Z9 551
U1 11
U2 264
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-0072
EI 1471-0080
J9 NAT REV MOL CELL BIO
JI Nat. Rev. Mol. Cell Biol.
PD JAN
PY 2018
VL 19
IS 1
BP 31
EP 44
DI 10.1038/nrm.2017.89
PG 14
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FS5MX
UT WOS:000419843100007
PM 28974775
OA Green Accepted
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Lee, H
Yoo, G
Pak, D
Lee, JH
AF Lee, Hyeongyu
Yoo, Gilsung
Pak, Daewoo
Lee, Jong -Han
TI Evaluation of D-dimer and prothrombin time in alcohol related liver
cirrhosis with comparison of machine learning analyses
SO INTERNATIONAL JOURNAL OF MEDICAL INFORMATICS
LA English
DT Article
DE Liver cirrhosis; Prothrombin time (PT); D-dimer; Machine learning
ID HEPATOCELLULAR-CARCINOMA; FIBROSIS; MORTALITY; ASSOCIATION; SCORE
AB Objectives: Liver cirrhosis (LC) can be caused by obesity, alcohol consumption, viral infection, and autoimmune disease. Early diagnosis and management of LC is important for patient quality of life. Non-invasive diagnostic methods are useful for predicting the current status and mortality risk of LC. The purpose of this study is to identify relevant diagnostic factors measured in routine laboratory test of alcohol-related liver cirrhosis (ALC) patients. Methods: This study analyzed data from 127 patients with ALC, including their laboratory test results and clinical information, including coagulation parameters, hematologic parameters, and biochemical parameters. These data were used to compare the performance of the prediction models from three machine learning algorithms including K-nearest neighbor (KNN), support vector machine (SVM), and random forest (RF). Results: Higher Model for End-stage Liver Disease (MELD) score were associated with prothrombin time (PT) and D-dimer. Logistic and multiple linear regression analyses revealed significant factors predicting mortality in the MELD group. Machine learning approaches were used to predict death in ALC patients using some laboratory parameters associated with mortality. The prediction model based on SVM exhibited better prediction performance than others. Conclusion: PT and D-dimer were the factors that were most strongly associated with 90-day mortality, and machine learning methods can create prediction models with good predictive power.
C1 [Lee, Hyeongyu; Yoo, Gilsung; Lee, Jong -Han] Yonsei Univ, Wonju Coll Med, Dept Lab Med, Wonju, South Korea.
[Pak, Daewoo] Yonsei Univ, Div Data Sci, Wonju, South Korea.
C3 Yonsei University; Yonsei University
RP Lee, JH (corresponding author), Yonsei Univ, Wonju Coll Med, Dept Lab Med, Wonju, South Korea.
EM cello425@yonsei.ac.kr
FU Yonsei University Wonju College of Medicine
FX Funding This study was supported by Yonsei University Wonju
College of Medicine.
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NR 24
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 1386-5056
EI 1872-8243
J9 INT J MED INFORM
JI Int. J. Med. Inform.
PD JUN
PY 2024
VL 186
AR 105407
DI 10.1016/j.ijmedinf.2024.105407
EA MAR 2024
PG 6
WC Computer Science, Information Systems; Health Care Sciences & Services;
Medical Informatics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Computer Science; Health Care Sciences & Services; Medical Informatics
GA QF9J7
UT WOS:001219578900001
PM 38518675
DA 2025-01-07
ER
PT J
AU Su, CW
Hung, HH
Huo, TI
Huang, YH
Li, CP
Lin, HC
Lee, PC
Lee, SD
Wu, JC
AF Su, Chien-Wei
Hung, Hung-Hsu
Huo, Teh-Ia
Huang, Yi-Hsiang
Li, Chung-Pin
Lin, Han-Chieh
Lee, Pui-Ching
Lee, Shou-Dong
Wu, Jaw-Ching
TI Natural history and prognostic factors of primary biliary cirrhosis in
Taiwan: a follow-up study up to 18 years
SO LIVER INTERNATIONAL
LA English
DT Article
DE antimitochondrial antibody; primary biliary cirrhosis; prognosis
ID URSODEOXYCHOLIC-ACID THERAPY; RANDOMIZED CONTROLLED-TRIALS;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE CHOLANGITIS; CLINICAL-FEATURES;
LIVER-DISEASE; SURVIVAL; METAANALYSIS; EPIDEMIOLOGY; PREVALENCE
AB Purpose: The natural history of primary biliary cirrhosis (PBC) has been little studied in Asia. We conducted a Taiwanese cohort study on the natural history of PBC and analysed the prognostic factors. Methods: This study enrolled 96 consecutive PBC patients between 1985 and 2006 to evaluate the baseline characteristics and outcomes. Results: There were 74 females and 22 males. Eighty-five were positive for antimitochondrial antibodies in sera, and 11 were negative. The clinical manifestations and prognosis were similar between these two groups. In a median follow-up of 47.5 +/- 55.8 months, 27 patients died. Multivariate analysis indicated that the independent prognostic factors were serum albumin (P=0.021), creatinine (P=0.033) and ursodeoxycholic acid treatment (P=0.008). Besides, 42 patients developed adverse outcomes. Albumin (P < 0.001), bilirubin (P=0.019) and prothrombin time (PT) (P=0.010) were significant factors. Moreover, a Mayo risk score < 5, a Model for End-Stage Liver Disease (MELD) score < 6, a Child-Pugh stage A and early liver histology were associated with favourable outcomes. Conclusions: Serum albumin, bilirubin and PT were independent prognostic factors of adverse outcomes for Taiwanese PBC patients. Besides, the Mayo risk score, the MELD score, the Child-Pugh stage and liver histology were also validated to predict survival.
C1 [Su, Chien-Wei; Huang, Yi-Hsiang; Wu, Jaw-Ching] Natl Yang Ming Univ, Inst Clin Med, Taipei 112, Taiwan.
[Su, Chien-Wei; Hung, Hung-Hsu; Huo, Teh-Ia; Huang, Yi-Hsiang; Li, Chung-Pin; Lin, Han-Chieh; Lee, Pui-Ching; Lee, Shou-Dong] Taipei Vet Gen Hosp, Dept Med, Div Gastroenterol, Taipei, Taiwan.
[Su, Chien-Wei; Huo, Teh-Ia; Huang, Yi-Hsiang; Li, Chung-Pin; Lin, Han-Chieh; Lee, Shou-Dong] Natl Yang Ming Univ, Fac Med, Taipei 112, Taiwan.
[Huo, Teh-Ia] Natl Yang Ming Univ, Inst Pharmacol, Taipei 112, Taiwan.
[Wu, Jaw-Ching] Taipei Vet Gen Hosp, Dept Med Res & Educ, Taipei, Taiwan.
C3 National Yang Ming Chiao Tung University; Taipei Veterans General
Hospital; National Yang Ming Chiao Tung University; National Yang Ming
Chiao Tung University; Taipei Veterans General Hospital
RP Wu, JC (corresponding author), Natl Yang Ming Univ, Inst Clin Med, Taipei 112, Taiwan.
EM jcwu@vghtpe.gov.tw
RI Huang, Yi-Hsiang/ADX-9119-2022; Lin, Han/GRF-1081-2022; Li,
Chung-Pin/AHE-5783-2022; Su, Chien-Wei/C-1521-2012
OI Huang, Yi-Hsiang/0000-0001-5241-5425; Su, Chien-Wei/0000-0003-3889-7004
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NR 42
TC 24
Z9 24
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD OCT
PY 2008
VL 28
IS 9
BP 1305
EP 1313
DI 10.1111/j.1478-3231.2008.01715.x
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 345CV
UT WOS:000258974500019
PM 18346129
OA Bronze
DA 2025-01-07
ER
PT J
AU Suryadevara, V
Nazeer, SS
Sreedhar, H
Adelaja, O
Kajdacsy-Balla, A
Natarajan, V
Walsh, MJ
AF Suryadevara, Vidyani
Nazeer, Shaiju S.
Sreedhar, Hari
Adelaja, Oluwatobi
Kajdacsy-Balla, Andre
Natarajan, Viswanathan
Walsh, Michael J.
TI Infrared spectral microscopy as a tool to monitor lung fibrosis
development in a model system
SO BIOMEDICAL OPTICS EXPRESS
LA English
DT Article
ID VIBRATIONAL SPECTROSCOPY; PULMONARY-FIBROSIS; RAMAN-SPECTROSCOPY;
CANCER; TISSUE; DIAGNOSIS; MECHANISMS
AB Tissue fibrosis is a progressive and destructive disease process that can occur in many different organs including the liver, kidney, skin, and lungs. Fibrosis is typically initiated by inflammation as a result of chronic insults such as infection, chemicals and autoimmune diseases. Current approaches to examine organ fibrosis are limited to radiological and histological analyses. Infrared spectroscopic imaging offers a potential alternative approach to gain insight into biochemical changes associated with fibrosis progression. In this study, we demonstrate that IR imaging of a mouse model of pulmonary fibrosis can identify biochemical changes observed with fibrosis progression and the beginning of resolution using K-means analysis, spectral ratios and multivariate data analysis. This study demonstrates that IR imaging may be a useful approach to understand the biochemical events associated with fibrosis initiation, progression and resolution for both the clinical setting and for assessing novel anti-fibrotic drugs in a model system. (C) 2020 Optical Society of America under the terms of the OSA Open Access Publishing Agreement
C1 [Suryadevara, Vidyani; Walsh, Michael J.] Univ Illinois, Dept Bioengn, Chicago, IL 60607 USA.
[Nazeer, Shaiju S.; Sreedhar, Hari; Adelaja, Oluwatobi; Kajdacsy-Balla, Andre; Walsh, Michael J.] Univ Illinois, Dept Pathol, Chicago, IL 60612 USA.
[Natarajan, Viswanathan] Univ Illinois, Dept Pharmacol, Chicago, IL 60612 USA.
C3 University of Illinois System; University of Illinois Chicago;
University of Illinois Chicago Hospital; University of Illinois System;
University of Illinois Chicago; University of Illinois Chicago Hospital;
University of Illinois System; University of Illinois Chicago;
University of Illinois Chicago Hospital
RP Walsh, MJ (corresponding author), Univ Illinois, Dept Bioengn, Chicago, IL 60607 USA.; Walsh, MJ (corresponding author), Univ Illinois, Dept Pathol, Chicago, IL 60612 USA.
EM walshm@uic.edu
RI Suryadevara, Vidyani/AAZ-1606-2020; S NAZEER, SHAIJU/GXN-1804-2022
OI Sreedhar, Hari/0000-0002-9725-4984; Suryadevara,
Vidyani/0000-0003-4081-2989; NAZEER, SHAIJU S/0000-0002-8409-1426;
Walsh, Michael/0000-0002-4749-0946
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NR 51
TC 6
Z9 6
U1 0
U2 4
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 2156-7085
J9 BIOMED OPT EXPRESS
JI Biomed. Opt. Express
PD JUL 1
PY 2020
VL 11
IS 7
BP 3996
EP 4007
DI 10.1364/BOE.394730
PG 12
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA MK0DJ
UT WOS:000548457000008
PM 33014581
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Liang, L
Shen, YJ
Hu, Y
Liu, HP
Cao, JP
AF Liang, Le
Shen, Yujuan
Hu, Yuan
Liu, Haipeng
Cao, Jianping
TI cGAS exacerbates Schistosoma japonicum infection in a STING-type
I IFN-dependent and independent manner
SO PLOS PATHOGENS
LA English
DT Article
ID CYCLIC GMP-AMP; CYTOSOLIC DNA SENSOR; PATHWAY; INFLAMMATION; INTERFERON;
SYNTHASE; ACTIVATION; DAMAGE; IMMUNOPATHOLOGY; SENESCENCE
AB Schistosomiasis, which is caused by infection with Schistosoma spp., is characterized by granuloma and fibrosis in response to egg deposition. Pattern recognition receptors are important to sense invading Schistosoma, triggering an innate immune response, and subsequently shaping adaptive immunity. Cyclic GMP-AMP synthase (cGAS) was identified as a major cytosolic DNA sensor, which catalyzes the formation of cyclic GMP-AMP (cGAMP), a critical second messenger for the activation of the adaptor protein stimulator of interferon genes (STING). The engagement of STING by cGAMP leads to the activation of TANK-binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), and the subsequent type I interferon (IFN) response. cGAS is suggested to regulate infectious diseases, autoimmune diseases, and cancer. However, the function of cGAS in helminth infection is unclear. In this study, we found that Cgas deficiency enhanced the survival of mice infected with S. japonicum markedly, without affecting the egg load in the liver. Consistently, Cgas deletion alleviated liver pathological impairment, reduced egg granuloma formation, and decreased fibrosis severity. In contrast, Sting deletion reduced the formation of egg granulomas markedly, but not liver fibrosis. Notably, Cgas or Sting deficiency reduced the production of IFNI3 drastically in mice infected with S. japonicum. Intriguingly, intravenous administration of recombinant IFNI3 exacerbated liver damage and promoted egg granuloma formation, without affecting liver fibrosis. Clodronate liposome-mediated depletion of macrophages indicated that macrophages are the major type of cells contributing to the induction of the type I IFN response during schistosome infection. Moreover, cGAS is important for type I IFN production and phosphorylation of TBK1 and IRF3 in response to stimulation with S. japonicum egg- or adult worm-derived DNA in macrophages. Our results clarified the immunomodulatory effect of cGAS in the regulation of liver granuloma formation during S. japonicum infection, involving sensing schistosome-derived DNA and producing type I IFN. Additionally, we showed that cGAS regulates liver fibrosis in a STING type I - IFN independent manner.
C1 [Liang, Le; Shen, Yujuan; Hu, Yuan; Cao, Jianping] Chinese Ctr Trop Dis Res, Natl Inst Parasit Dis, Chinese Ctr Dis Control & Prevent, Shanghai, Peoples R China.
[Liang, Le; Shen, Yujuan; Hu, Yuan; Cao, Jianping] Natl Hlth Commiss Peoples Republ China, Key Lab Parasite & Vector Biol, Shanghai, Peoples R China.
[Liang, Le; Shen, Yujuan; Hu, Yuan; Cao, Jianping] World Hlth Org Collaborating Ctr Trop Dis, Shanghai, Peoples R China.
[Liang, Le] Shanghai Univ Med & Hlth Sci, Shanghai, Peoples R China.
[Liang, Le; Shen, Yujuan; Hu, Yuan; Cao, Jianping] Shanghai Jiao Tong Univ, Sch Global Hlth, Chinese Ctr Trop Dis Res, Sch Med, Shanghai, Peoples R China.
[Liu, Haipeng] Tongji Univ, Clin & Translat Res Ctr, Shanghai Pulm Hosp, Sch Med, Shanghai, Peoples R China.
[Liu, Haipeng] Tongji Univ, Shanghai Pulm Hosp, Sch Med, Cent Lab, Shanghai, Peoples R China.
C3 Chinese Center for Disease Control & Prevention; National Institute of
Parasitic Diseases, Chinese Center for Disease Control & Prevention;
World Health Organization; Shanghai University of Medicine & Health
Sciences; Shanghai Jiao Tong University; Tongji University; Tongji
University
RP Cao, JP (corresponding author), Chinese Ctr Trop Dis Res, Natl Inst Parasit Dis, Chinese Ctr Dis Control & Prevent, Shanghai, Peoples R China.; Cao, JP (corresponding author), Natl Hlth Commiss Peoples Republ China, Key Lab Parasite & Vector Biol, Shanghai, Peoples R China.; Cao, JP (corresponding author), World Hlth Org Collaborating Ctr Trop Dis, Shanghai, Peoples R China.; Cao, JP (corresponding author), Shanghai Jiao Tong Univ, Sch Global Hlth, Chinese Ctr Trop Dis Res, Sch Med, Shanghai, Peoples R China.
EM caojp@yahoo.com
RI Cao, Jianping/AFL-5468-2022
OI Liu, Haipeng/0000-0002-3338-6291; Cao, Jianping/0000-0002-1974-0047
FU National Nature Science Foundation of China [81772225, 81971969]; Fifth
Round of Three-Year Public Health Action Plan of Shanghai
[GWV-10.1-XK13]
FX This work was supported by the National Nature Science Foundation of
China (Nos. 81772225 and 81971969 to JC) and the Fifth Round of
Three-Year Public Health Action Plan of Shanghai [grant number
GWV-10.1-XK13 to JC]. The funders had no role in the study design, data
collection, and analysis, decision to publish, or preparation of the
manuscript.
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NR 68
TC 12
Z9 13
U1 0
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7366
EI 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD FEB
PY 2022
VL 18
IS 2
AR e1010233
DI 10.1371/journal.ppat.1010233
PG 22
WC Microbiology; Parasitology; Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology; Parasitology; Virology
GA 1C7SG
UT WOS:000793314100001
PM 35108342
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Miri, S
Rasooli, A
Brar, SK
AF Miri, Saba
Rasooli, Azadeh
Brar, Satinder Kaur
TI Data on changes of NF-κB gene expression in liver and lungs as a
biomarker and hepatic injury in CLP-induced septic rats
SO DATA IN BRIEF
LA English
DT Article; Data Paper
DE Sepsis; Inflammation; NF-kappa B; Gene expression; Hepatic cell
evaluation
ID SEPSIS; MODEL
AB Nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) is a ubiquitous transcription factor, which plays a key role in regulating immune response against infection. Increased and/or prolonged activation of NF-kappa B has been linked to cancer, inflammatory, autoimmune diseases and viral infection. The purpose of this set of data was to evaluate NF-kappa B gene expression in cecal ligation and puncture (CLP)- induced septic rats and associated hepatic cell changes. Here, we provide the information about the evaluation of NF-kappa B gene expression using Real-time PCR and histopathological data of liver-related to our study published in the Turkish Journal of Medical Sciences [1]. Also, the information of the primers and more details about gene expression evaluation by real-time PCR of the targeted gene is provided. The data present here introduced another biomarker in liver and lung of CLPinduced septic rats and also confirmed hepatic dysfunction based on the pathological data. The histopathologic assessment showed normal condition in control group, mild infiltration of neutrophils in the liver parenchyma and portal tracts in LAP group (laparotomy) but severe congestion, severe neutrophil infiltration in the liver parenchyma and portal tracts in the CLP group. The data from real-time PCR showed that NF-kappa B expression was significantly increased in the CLP group compared with the control and LAP group, so it can be a biomarker for (CLP)-induced sepsis. This set of data and our previous study underscored the powerful potential of using the real-time PCR method to determine the involvement of genes such as MPO, CD177, and NF-kappa B in infectious diseases like sepsis. (C) 2019 The Authors. Published by Elsevier Inc.
C1 [Miri, Saba; Brar, Satinder Kaur] Univ Quebec, INRS ETE, 490 Rue Couronne, Quebec City, PQ G1K 9A9, Canada.
[Rasooli, Azadeh] Payame e Noor Univ, Fac Sci, Dept Biochem, Tehran, Iran.
[Brar, Satinder Kaur] York Univ, Lassonde Sch Engn, Dept Civil Engn, Toronto, ON M3J1P3, Canada.
C3 University of Quebec; Institut national de la recherche scientifique
(INRS); York University - Canada
RP Brar, SK (corresponding author), Univ Quebec, INRS ETE, 490 Rue Couronne, Quebec City, PQ G1K 9A9, Canada.
EM satinder.brar@ete.inrs.ca
RI Rasooli, Azadeh/AAF-2036-2020
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NR 4
TC 6
Z9 6
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2352-3409
J9 DATA BRIEF
JI Data Brief
PD AUG
PY 2019
VL 25
AR 104117
DI 10.1016/j.dib.2019.104117
PG 6
WC Multidisciplinary Sciences
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics
GA JK8QJ
UT WOS:000495104500144
PM 31428666
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Zaky, S
Alboraie, M
El Badry, M
Metwally, MA
Abdelaziz, A
Fouad, Y
Abd-Elsalam, S
Mahmoud, A
Shiha, G
Baki, AA
El Kassas, M
Esmat, G
AF Zaky, Samy
Alboraie, Mohamed
El Badry, Mohamed
Metwally, Mohamed A.
Abdelaziz, Ahmed
Fouad, Yasser
Abd-Elsalam, Sherief
Mahmoud, Abdelmajeed
Shiha, Gamal
Baki, Amin Abdel
El Kassas, Mohamed
Esmat, Gamal
TI Management of liver disease patients in different clinical situations
during COVID-19 pandemic
SO EGYPTIAN LIVER JOURNAL
LA English
DT Review
DE SARS-CoV-2; COVID-19; Liver diseases; Hepatitis C; Hepatitis B
ID CIRRHOTIC-PATIENTS; TRANSPLANTATION; OUTCOMES; IMPACT; COMORBIDITIES;
CORONAVIRUS; INFECTION; DIAGNOSIS; INJURY; SAFETY
AB Chronic liver diseases are common worldwide, especially in developing countries. The rapid spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)/(COVID-19) leads to the infection of many patients with underlying chronic liver diseases. As a relatively new disease, management of COVID-19, in the context of chronic liver disease, is mainly based on the experience of the treating physician and the available data. In this review, we summarize the available evidence about the management of liver disease patients, in the context of COVID-19 infection, which can increase the severity of viral hepatitis B. Also, its clearance in HBV patients is delayed. A sixfold increased severity of COVID-19 was reported in obese patients with metabolic associated fatty liver disease (MAFDL). In patients with autoimmune liver disease (AILD), it is not recommended to change their immunosuppressive therapy (as long as they are not infected with COVID-19), in order to avoid a flare of liver disease. However, immunosuppressant drugs should be modified, in the case of infection with COVID-19. To date, no data suggest an increased risk or severity in metabolic liver diseases, such as hemochromatosis, Wilson's disease, or alpha-1 antitrypsin deficiency. Patients with liver cirrhosis should be carefully managed with minimum exposure to healthcare facilities. Basic investigations for follow-up can be scheduled at wider intervals; if patients need admission, this should be in COVID-19-clean areas. Patients with hepatocellular carcinomas may have a poor prognosis according to preliminary reports from China. The course of COVID-19 in liver transplant recipients on immunosuppression seems to have a benign course, based on few reports in children and adults. The hepatotoxicity of COVID-19 drugs ranges from mild liver enzyme elevation to a flare of underlying liver diseases. Therefore, the decision should be customized. Telemedicine can minimize the exposure of healthcare workers and patients to infection with COVID-19 and decrease the consumption of personal protective equipment.
C1 [Zaky, Samy] Al Azhar Univ, Hepatogastroenterol & Infect Dis Dept, Cairo, Egypt.
[Alboraie, Mohamed] Al Azhar Univ, Dept Internal Med, Cairo, Egypt.
[El Badry, Mohamed; El Kassas, Mohamed] Helwan Univ, Fac Med, Endem Med Dept, 2 Ahmed Elzomor St, Cairo, Egypt.
[Metwally, Mohamed A.] Benha Univ, Hepatol Gastroenterol & Infect Dis Dept, Banha, Egypt.
[Abdelaziz, Ahmed] Al Azhar Univ, Hepatogastroenterol & Infect Dis, Dumyat, Egypt.
[Fouad, Yasser] Minia Univ, Minia Fac Med, Trop Med Dept, Al Minya, Egypt.
[Abd-Elsalam, Sherief] Tanta Univ, Trop Med Dept, Tanta, Egypt.
[Mahmoud, Abdelmajeed] Aswan Univ, Trop Med & Gastroenterol Dept, Aswan, Egypt.
[Shiha, Gamal] Mansoura Univ, Fac Med, Internal Med Dept, Mansoura, Egypt.
[Baki, Amin Abdel] Natl Hepatol & Trop Med Res Inst, Dept Hepatol, Cairo, Egypt.
[Esmat, Gamal] Cairo Univ, Fac Med, Endem Med & Hepatol Dept, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); Al Azhar University; Egyptian Knowledge
Bank (EKB); Al Azhar University; Egyptian Knowledge Bank (EKB); Helwan
University; Egyptian Knowledge Bank (EKB); Benha University; Egyptian
Knowledge Bank (EKB); Al Azhar University; Egyptian Knowledge Bank
(EKB); Minia University; Egyptian Knowledge Bank (EKB); Tanta
University; Egyptian Knowledge Bank (EKB); Aswan University; Egyptian
Knowledge Bank (EKB); Mansoura University; Egyptian Knowledge Bank
(EKB); National Hepatology & Tropical Medicine Research Institute
(NHTMRI); Egyptian Knowledge Bank (EKB); Cairo University
RP El Badry, M (corresponding author), Helwan Univ, Fac Med, Endem Med Dept, 2 Ahmed Elzomor St, Cairo, Egypt.
EM melbadry2002@yahoo.com
RI Elbadry, Mohamed/ABD-3435-2020; Zaky, Samy/AAB-6469-2021; Alboraie,
Mohamed/F-5688-2011; Abdel Baki, Amin/AAW-1717-2021; Fouad,
Yasser/Y-7180-2018; El-Kassas, Mohamed/F-8306-2019; abd-elsalam,
sherief/L-3274-2018
OI fouad, yasser/0000-0001-7989-5318; Zaky, Samy/0000-0003-4123-9221;
El-Kassas, Mohamed/0000-0002-3396-6894; abd-elsalam,
sherief/0000-0003-4366-2218; Elbadry, Mohamed/0000-0002-9020-8870
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NR 91
TC 3
Z9 3
U1 0
U2 6
PU SPRINGEROPEN
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, GWENT N1 9XW, ENGLAND
SN 2090-6218
EI 2090-6226
J9 EGYPT LIVER J
JI Egypt. Liver J.
PD MAR 26
PY 2021
VL 11
IS 1
AR 21
DI 10.1186/s43066-021-00091-x
PG 12
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA 3N8FV
UT WOS:000836381500001
PM 34777868
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Zhao, JJ
Chu, FY
Xu, HL
Guo, MM
Shan, S
Zheng, W
Tao, YJ
Zhou, Y
Hu, Y
Chen, C
Ren, T
Xu, L
AF Zhao, Juanjuan
Chu, Fengyun
Xu, Hualin
Guo, Mengmeng
Shan, Shan
Zheng, Wen
Tao, Yijing
Zhou, Ya
Hu, Yan
Chen, Chao
Ren, Tao
Xu, Lin
TI C/EBPα/miR-7 Controls CD4+ T-Cell Activation and Function and
Orchestrates Experimental Autoimmune Hepatitis in Mice
SO HEPATOLOGY
LA English
DT Article
AB Background and Aims Increasing evidence in recent years has suggested that microRNA-7 (miR-7) is an important gene implicated in the development of various diseases including HCC. However, the role of miR-7 in autoimmune hepatitis (AIH) is unknown.
Approach and Results Herein, we showed that miR-7 deficiency led to exacerbated pathology in Concanavalin-A-induced murine acute autoimmune liver injury (ALI) model, accompanied by hyperactivation state of CD4(+) T cells. Depletion of CD4(+) T cells reduced the effect of miR-7 deficiency on the pathology of ALI. Interestingly, miR-7 deficiency elevated CD4(+) T-cell activation, proliferation, and cytokine production in vitro. Adoptive cell transfer experiments showed that miR-7(def) CD4(+) T cells could exacerbate the pathology of ALI. Further analysis showed that miR-7 expression was up-regulated in activated CD4(+) T cells. Importantly, the transcription of pre-miR-7b, a major resource of mature miR-7 in CD4(+) T cells, was dominantly dependent on transcription factor CCAAT enhancer binding protein alpha (C/EBP alpha), which binds to the core promoter region of the miR-7b gene. Global gene analysis showed that mitogen-activated protein kinase 4 (MAPK4) is a target of miR-7 in CD4(+) T cells. Finally, the loss of MAPK4 could ameliorate the activation state of CD4(+) T cells with or without miR-7 deficiency. Our studies document the important role of miR-7 in the setting of AIH induced by Concanavalin-A. Specifically, we provide evidence that the C/EBP alpha/miR-7 axis negatively controls CD4(+) T-cell activation and function through MAPK4, thereby orchestrating experimental AIH in mice.
Conclusions This study expands on the important role of miR-7 in liver-related diseases and reveals the value of the C/EBP alpha/miR-7 axis in CD4(+) T-cell biological function for the pathogenesis of immune-mediated liver diseases.
C1 [Zhao, Juanjuan; Chu, Fengyun; Xu, Hualin; Guo, Mengmeng; Zheng, Wen; Tao, Yijing; Hu, Yan; Chen, Chao; Xu, Lin] Zunyi Med Univ, Special Key Lab Gene Detect & Therapy Guizhou Pro, Zunyi, Guizhou, Peoples R China.
[Zhao, Juanjuan; Chu, Fengyun; Xu, Hualin; Guo, Mengmeng; Zheng, Wen; Tao, Yijing; Hu, Yan; Chen, Chao; Xu, Lin] Zunyi Med Univ, Dept Immunol, Zunyi 563003, Guizhou, Peoples R China.
[Shan, Shan; Ren, Tao] Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6, Dept Resp Med, Shanghai 200233, Peoples R China.
[Zhou, Ya] Zunyi Med Univ, Dept Med Phys, Zunyi, Guizhou, Peoples R China.
C3 Zunyi Medical University; Zunyi Medical University; Shanghai Jiao Tong
University; Zunyi Medical University
RP Xu, L (corresponding author), Zunyi Med Univ, Dept Immunol, Zunyi 563003, Guizhou, Peoples R China.; Ren, T (corresponding author), Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6, Dept Resp Med, Shanghai 200233, Peoples R China.
EM Rentaosh@126.com; xulinzhouya@163.com
RI shan, shan/JJE-3718-2023; zhao, juan/KHC-8840-2024
OI Xu, Lin/0000-0002-6889-0279; Zhao, Juanjuan/0000-0001-9253-8083
FU National Natural Science foundation of China [31760258, 81673014];
Program for New Century Excellent Talents in University, Ministry of
Education of China [NCET-12-0661]; Program for High-Level Innovative
Talents in Guizhou Province [QKH-RC-2016-4031]; Program for Excellent
Young Talents of Zunyi Medical University [15ZY-001]; Zunyi Science and
Technology Bureau [ZSKH-SZ-2016-38]; Zunyi Medical University
[ZSKH-SZ-2016-38]; Outstanding Academic Leaders Plan of Shanghai
Municipal Science and Technology Committee [16XD1403100]; National Key
RD Plan [2017YFA0104600]
FX Supported by the National Natural Science foundation of China (31760258
and 81673014), Program for New Century Excellent Talents in University,
Ministry of Education of China (NCET-12-0661), Program for High-Level
Innovative Talents in Guizhou Province (QKH-RC-2016-4031), Program for
Excellent Young Talents of Zunyi Medical University (15ZY-001), Program
for Science and Technology Joint Fund Project in Zunyi Science and
Technology Bureau and Zunyi Medical University (ZSKH-SZ--2016-38),
Outstanding Academic Leaders Plan of Shanghai Municipal Science and
Technology Committee (16XD1403100), and National Key R&D Plan
(2017YFA0104600).
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Z9 25
U1 1
U2 16
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD JUL
PY 2021
VL 74
IS 1
BP 379
EP 396
DI 10.1002/hep.31607
EA APR 2021
PG 18
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA TN1VG
UT WOS:000640973100001
PM 33125780
DA 2025-01-07
ER
PT J
AU Tomasevic, R
Gluvic, Z
Mijac, D
Sokic-Milutinovic, A
Lukic, S
Milosavljevic, T
AF Tomasevic, Ratko
Gluvic, Zoran
Mijac, Dragana
Sokic-Milutinovic, Aleksandra
Lukic, Snezana
Milosavljevic, Tomica
TI Anemia as a Problem: GEH Approach
SO DIGESTIVE DISEASES
LA English
DT Review
DE Iron deficiency; Anemia; Gastroenterologist; Endoscopy
ID IRON-DEFICIENCY ANEMIA; HELICOBACTER-PYLORI; CELIAC-DISEASE;
GASTROINTESTINAL EVALUATION; AUTOIMMUNE GASTRITIS; CLINICAL GUIDELINES;
COLORECTAL-CANCER; OCCULT; DIAGNOSIS; MANAGEMENT
AB Background: Anemia is present in almost 5% of adults worldwide and accompanies clinical findings in many diseases. Diseases of the gastrointestinal (GI) tract and liver are a common cause of anemia, so patients with anemia are often referred to a gastroenterologist. Summary: Anemia could be caused by various factors such as chronic bleeding, malabsorption, or chronic inflammation. In clinical practice, iron deficiency anemia and the combined forms of anemia due to different pathophysiological mechanisms are most common. Esophagogastroduodenoscopy, colonoscopy, and the small intestine examinations in specific situations play a crucial role in diagnosing anemia. In anemic, GI asymptomatic patients, there are recommendations for bidirectional endoscopy. Although GI malignancies are the most common cause of chronic bleeding, all conditions leading to blood loss, malabsorption, and chronic inflammation should be considered. From a gastroenterologist's perspective, the clinical spectrum of anemia is vast because many different digestive tract diseases lead to bleeding. Key Messages: The gastroenterological approach in solving anemia's problem requires an optimal strategy, consideration of the accompanying clinical signs, and the fastest possible diagnosis. Although patients with symptoms of anemia are often referred to gastroenterologists, the diagnostic approach requires further improvement in everyday clinical practice.
C1 [Tomasevic, Ratko; Gluvic, Zoran] Univ Belgrade, Univ Clin Hosp Ctr Zemun Belgrade, Sch Med, Clin Internal Med, Belgrade, Serbia.
[Mijac, Dragana; Sokic-Milutinovic, Aleksandra; Lukic, Snezana] Univ Belgrade, Clin Ctr Serbia, Sch Med, Clin Gastroenterol & Hepatol, Belgrade, Serbia.
[Milosavljevic, Tomica] Gen Hosp Euromed, Belgrade, Serbia.
C3 University of Belgrade; University of Belgrade; Clinical Centre of
Serbia
RP Tomasevic, R (corresponding author), Univ Belgrade, Univ Clin Hosp Ctr Zemun Belgrade, Sch Med, Clin Internal Med, Belgrade, Serbia.
EM tomasevicratko@gmail.com
RI Gluvic, Zoran/Q-5190-2019
OI Milosavljevic, Tomica/0000-0002-4396-7532; Gluvic,
Zoran/0000-0001-6371-6610; Lukic, Snezana/0000-0002-4646-1131; Mijac,
Dragana/0000-0002-9386-4056
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NR 82
TC 0
Z9 0
U1 0
U2 6
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PY 2022
VL 40
IS 2
BP 133
EP 141
DI 10.1159/000516480
EA APR 2021
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 3D9II
UT WOS:000721612200001
PM 33866318
OA Bronze
DA 2025-01-07
ER
PT J
AU Becker, NP
Martitz, J
Renko, K
Stoedter, M
Hybsier, S
Cramer, T
Schomburg, L
AF Becker, Niels-Peter
Martitz, Janine
Renko, Kostja
Stoedter, Mette
Hybsier, Sandra
Cramer, Thorsten
Schomburg, Lutz
TI Hypoxia reduces and redirects selenoprotein biosynthesis
SO METALLOMICS
LA English
DT Article
ID SELENOCYSTEINE INCORPORATION; SELENIUM DEFICIENCY; RESPONSE SYNDROME;
SEPTIC SHOCK; SEPSIS; SERUM; LIVER; ASSAY
AB Selenium deficiency constitutes a risk factor for the incidence and negative course of severe diseases including sepsis, stroke, autoimmune diseases or cancer. In this study, hypoxia is identified as a powerful stimulus to redirect selenoprotein biosynthesis causing reduced selenoprotein P expression and diminished selenium export from hepatocytes in favour of increased biosynthesis of the essential protective intracellular phospholipid hydroperoxide glutathione peroxidase GPX4. Specifically, hypoxia decreases transcript concentrations of central factors controlling selenium and selenocysteine metabolism including selenophosphate synthetase-2, phosphoseryl-tRNA(SerSec) kinase and selenocysteine lyase, which are all proven to be rate-limiting enzymes in selenoprotein biosynthesis. These effects are paralleled by a general decline of selenoprotein expression; however, not all selenoproteins are affected to the same extent by hypoxia, and GPX4 constitutes an exception as its expression becomes slightly increased. Supplemental selenium is able to overcome the hypoxia-dependent down regulation of selenoprotein expression in our cell culture model system, supporting the concept of using selenium as an adjuvant treatment option in severe diseases. Although it remains to be tested whether these effects constitute a hepatocyte-specific response, the selenium-dependent decline of selenoprotein P biosynthesis under hypoxic conditions may explain the progressive selenium deficit developing in severe diseases.
C1 [Becker, Niels-Peter; Martitz, Janine; Renko, Kostja; Stoedter, Mette; Hybsier, Sandra; Schomburg, Lutz] Charite, Inst Expt Endocrinol, CVK, D-13353 Berlin, Germany.
[Cramer, Thorsten] Charite, Med Klin Schwerpunkt Hepatol & Gastroenterol, CVK, D-13353 Berlin, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
University of Berlin; Charite Universitatsmedizin Berlin; Berlin
Institute of Health; Free University of Berlin; Humboldt University of
Berlin; Charite Universitatsmedizin Berlin
RP Schomburg, L (corresponding author), Charite, Inst Expt Endocrinol, CVK, D-13353 Berlin, Germany.
EM lutz.schomburg@charite.de
RI Schomburg, Lutz/D-8096-2013; Cramer, Thorsten/S-2479-2016
OI Schomburg, Lutz/0000-0001-9445-1555; Cramer,
Thorsten/0000-0002-6462-239X
FU Deutsche Forschungsgemeinschaft (DFG) [GraKo 1208, SCHO849/4-1,
RE3038/1-1]; Federal Ministry of Economics and Technology [KF2263202CS2]
FX We thank Katja Schreiber, Carola Geiler and Vartiter Seher for excellent
technical assistance. The study was supported by the Deutsche
Forschungsgemeinschaft (DFG; GraKo 1208, SCHO849/4-1, RE3038/1-1) and
Federal Ministry of Economics and Technology (BMWi; KF2263202CS2).
Finally, the authors would like to express their gratitude to an
anonymous reviewer for his/her constructive remarks on their study.
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NR 34
TC 57
Z9 58
U1 1
U2 15
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 1756-5901
EI 1756-591X
J9 METALLOMICS
JI Metallomics
PY 2014
VL 6
IS 5
BP 1079
EP 1086
DI 10.1039/c4mt00004h
PG 8
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA AG1BF
UT WOS:000335149200012
PM 24700164
OA Green Submitted, hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Ogrin, C
AF Ogrin, Cristina
TI Increased Bone Alkaline Phosphatase and Isolated Subcortical Bone Uptake
of Technetium-99m Hydroxymethylene Diphosphonate in the Lower
Extremities in a Patient with Graves' Disease: A Distinctly Unusual
Variant of Graves' Acropachy
SO THYROID
LA English
DT Article
AB Background: Thyroid acropachy is an extreme manifestation of autoimmune thyroid disease characterized by soft tissue swelling and periosteal bone changes, usually occurring in the fingers, toes, and lower extremities. Here, a patient with a distinctly unusual variant of thyroid acropachy is presented.
Patient findings: The patient was a 48-year-old woman with Graves' disease and mild ophthalmopathy, who was euthyroid after treatment with Methimazole. Because of a persistently elevated serum alkaline phosphatase (ALP) with elevated bone fraction, a bone scan was performed. This showed increased uptake in the subcortical areas of the lower extremity bones. On questioning, she admitted to mild pain in her lower extremities. She had no other features of thyroid acropachy. Secondary causes of increased ALP, such as cancer, liver disease, and vitamin D deficiency, were excluded by appropriate tests. Therefore, and in view of the patient's underlying Graves' disease, a diagnosis of thyroid acropachy was made.
Summary and conclusions: Periosteal reaction in the long bones of the lower extremities is unusual in thyroid acropachy, and when it occurs, it is more likely to be associated with overt pain or prominent extrathyroidal manifestations of Graves' disease. This patient very likely had a variant of thyroid acropachy. This variant may be underreported because of its generally asymptomatic nature.
C1 Berwick Hosp Med, Berwick, PA 18603 USA.
RP Ogrin, C (corresponding author), Berwick Hosp Med, 751 E 16th St, Berwick, PA 18603 USA.
EM crisogrin@aol.com
CR Bisschop PH, 2007, THYROID, V17, P689, DOI 10.1089/thy.2006.0255
Fatourechi V, 2002, J CLIN ENDOCR METAB, V87, P5435, DOI 10.1210/jc.2002-020746
Proust-Lemoine E, 2005, PRESSE MED, V34, P367
NR 3
TC 4
Z9 4
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1050-7256
J9 THYROID
JI Thyroid
PD NOV
PY 2008
VL 18
IS 11
BP 1227
EP 1229
DI 10.1089/thy.2008.0078
PG 3
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 373GG
UT WOS:000260958400013
PM 19014329
DA 2025-01-07
ER
PT J
AU Culver, EL
Bungay, HK
Betts, M
Forde, C
Buchel, O
Manganis, C
Warren, BF
Cummings, FR
Keshav, S
Travis, SPL
Chapman, RW
AF Culver, Emma L.
Bungay, Helen K.
Betts, Margaret
Forde, Colm
Buchel, Otto
Manganis, Charis
Warren, Bryan F.
Cummings, Fraser R.
Keshav, Satish
Travis, Simon P. L.
Chapman, Roger W.
TI Prevalence and long-term outcome of sub-clinical primary sclerosing
cholangitis in patients with ulcerative colitis
SO LIVER INTERNATIONAL
LA English
DT Article
DE colorectal dysplasia; magnetic resonance cholangiogram; normal liver
function; primary sclerosing cholangitis; ulcerative colitis
ID INFLAMMATORY-BOWEL-DISEASE; GENOME-WIDE ASSOCIATION; MAGNETIC-RESONANCE;
URSODEOXYCHOLIC ACID; AUTOIMMUNE HEPATITIS; COLORECTAL-CANCER; RISK;
CHOLANGIOGRAPHY; EPIDEMIOLOGY; SURVEILLANCE
AB Background Primary sclerosing cholangitis (PSC) is closely associated with inflammatory bowel disease, particularly ulcerative colitis (UC), with an increased risk of biliary and colorectal malignancy. We sought to clarify the prevalence, characteristics and long-term outcome of sub-clinical PSC diagnosed by magnetic resonance cholangiogram (MRC) in patients with UC and normal liver biochemistry, with or without colorectal dysplasia (CRD).
Methods In this prospective case-control study, 70 patients with UC and normal liver function (51 extensive UC, 19 CRD), 28 healthy volunteers (negative controls) and 28 patients with PSC and cholestasis (positive controls) underwent MRC and blood evaluation. MRC scans were interpreted blindly by two radiologists who graded individually, the scans as definitive for PSC, possible for PSC or normal. Clinical outcome was assessed by blood monitoring, abdominal imaging and endoscopic surveillance.
Results 7/51 (14%) with extensive UC and 4/19 (21%) with CRD had biliary abnormalities on MRC consistent with PSC. 7/11 (64%) with sub-clinical PSC had isolated intrahepatic duct involvement. Sub-clinical PSC was associated with advanced age (P = .04), non-smoking (P = .03), pANCA (P = .04), quiescent colitis (P = .02), absence of azathioprine (P = .04) and high-grade CRD (P = .03). Inter-observer (kappa = 0.88) and intra-observer (kappa = 0.96) agreement for MRC interpretation was high. No negative controls were assessed as definite PSC, 4/28 were considered on blinding as possible PSC. During follow-up of sub-clinical PSC (median 10.1(3.1-11.9) years), four patients developed abnormal liver biochemistry, two had radiological progression of PSC and seven developed malignancy, including two biliary and one colorectal carcinoma.
Conclusions Prevalence of sub-clinical PSC appears high in patients with extensive UC and normal liver biochemistry, with or without CRD. Disease progression and malignancy were identified on long-term follow-up. MRC should be considered for all patients with extensive UC or CRD to stratify surveillance.
C1 [Culver, Emma L.; Manganis, Charis; Cummings, Fraser R.; Keshav, Satish; Travis, Simon P. L.; Chapman, Roger W.] Univ Oxford, John Radcliffe Hosp, Nuffield Dept Med, Translat Gastroenterol Unit, Oxford, England.
[Bungay, Helen K.; Betts, Margaret; Forde, Colm] John Radcliffe Hosp, Radiol Dept, Oxford, England.
[Bungay, Helen K.; Betts, Margaret; Forde, Colm] Churchill Hosp, Oxford, England.
[Forde, Colm] Queen Elizabeth Hosp, Radiol Dept, Birmingham, W Midlands, England.
[Buchel, Otto] Rondebosch Med Ctr, Cape Town, South Africa.
[Warren, Bryan F.] John Radcliffe Hosp, Histopathol Dept, Oxford, England.
[Cummings, Fraser R.] Southampton Gen Hosp, Gastroenterol Dept, Southampton, Hants, England.
C3 University of Oxford; University of Oxford; University of Oxford;
University of Birmingham; University of Oxford; University of
Southampton
RP Chapman, RW (corresponding author), John Radcliffe Hosp, Translat Gastroenterol Dept, Oxford OX3 9DU, England.
EM roger.chapman@ndm.ox.ac.uk
OI Travis, Simon/0000-0002-2690-4361; Culver, Emma/0000-0001-9644-8392
FU Department of Health Funding Source: Medline
CR Abdalian R, 2008, HEPATOLOGY, V47, P949, DOI 10.1002/hep.22073
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NR 41
TC 14
Z9 15
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD NOV
PY 2020
VL 40
IS 11
BP 2744
EP 2757
DI 10.1111/liv.14645
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA OK4BD
UT WOS:000584597100016
PM 32841490
OA hybrid
DA 2025-01-07
ER
PT J
AU Gao, Y
Li, L
Hu, XX
Zhang, WH
Li, Y
AF Gao, Ying
Li, Lan
Hu, Xingxing
Zhang, Weihua
Li, Yu
TI Interleukin-35 has a Protective Role in Infectious Mononucleosis-Induced
Liver Inflammation Probably by Inhibiting CD8+ T Cell
Function
SO ARCHIVUM IMMUNOLOGIAE ET THERAPIAE EXPERIMENTALIS
LA English
DT Article
DE Interleukin-35; CD8(+) T lymphocytes; Infectious mononucleosis; Liver
inflammation; Immunoregulation
ID EPSTEIN-BARR-VIRUS; HELPER 17 CELLS; HEPATITIS; IL-35; FAILURE
AB Interleukin (IL)-35 plays an immunosuppressive role in infectious diseases, autoimmune disorders, and cancers. However, IL-35 expression and its regulation of CD8(+) T cells in infectious mononucleosis (IM) are not fully understood. In this study, three groups of participants were compared, including twenty-three patients of IM without liver inflammation, twenty-eight patients of IM with liver inflammation, and twenty-one controls. Plasma and peripheral blood mononuclear cells (PBMCs) were isolated. CD8(+) T cells were purified. Plasma IL-35 was measured by ELISA. PBMCs and CD8(+) T cells were stimulated with recombinant human IL-35 in vitro. Perforin and granzyme B secretion was assessed by ELISPOT. Immune checkpoint molecule expression was investigated by flow cytometry. CD8(+) T cells were co-cultured with HepG2 cells in direct contact and indirect contact manner. The cytotoxicity of CD8(+) T cells was calculated by measuring lactate dehydrogenase release and proinflammatory cytokine expression. There was no significant difference in plasma IL-35 levels between patients with IM without liver inflammation and the controls, but the IL-35 level was notably increased in patients with IM who presented with liver inflammation and negatively correlated with aminotransferase. CD8(+) T cells in patients with IM with liver inflammation showed stronger cytotoxicity. IL-35 stimulation inhibited CD8(+) T cell-induced target cell death in patients with IM, mainly through suppression of IFN-gamma/TNF-alpha secretion and elevation of immune checkpoint molecule expression, but did not affect perforin or granzyme B secretion. The current data indicated that IL-35 dampened the cytotoxicity of CD8(+) T cells in patients with IM probably via repression of cytokine secretion. Elevated IL-35 may protect against CD8(+) T cell-induced liver inflammation in patients with IM.
C1 [Gao, Ying; Li, Lan; Hu, Xingxing; Zhang, Weihua] Xian Med Univ, Shaanxi Prov Peoples Hosp, Dept Hematol, Affiliated Hosp, Xian 710068, Shaanxi, Peoples R China.
[Li, Yu] Xian Med Univ, Shaanxi Prov Peoples Hosp, Dept Infect Dis, Affiliated Hosp, 256 West Youyi Rd, Xian 710068, Shaanxi, Peoples R China.
C3 Xi'an Medical University; Xi'an Medical University
RP Li, Y (corresponding author), Xian Med Univ, Shaanxi Prov Peoples Hosp, Dept Infect Dis, Affiliated Hosp, 256 West Youyi Rd, Xian 710068, Shaanxi, Peoples R China.
EM drlee2810@126.com
RI Li, Yuxin/K-9197-2016
OI Li, Yufang/0009-0006-9174-8162; Li, Yu/0000-0002-1949-7737
FU SPPH Incubator Fund for Development of Science and Technology
[2021YJY-19]; SPPH Foundation for Development of Science and Technology
[2021BJ-26]; Xi'an Foundation for Development of Science and Technology
[20YXYJ0009(11)]; International Science and Technology Cooperation
Projects of Shaanxi Province [2022KW-14]; Scientific and Technological
Innovation Team of Shaanxi Province [2021TD-40]
FX This work was supported by a grant from the SPPH Incubator Fund for
Development of Science and Technology (2021YJY-19), SPPH Foundation for
Development of Science and Technology (2021BJ-26), Xi'an Foundation for
Development of Science and Technology [20YXYJ0009(11)], International
Science and Technology Cooperation Projects of Shaanxi Province
(2022KW-14), and Scientific and Technological Innovation Team of Shaanxi
Province (2021TD-40).
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NR 42
TC 2
Z9 2
U1 0
U2 2
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 0004-069X
EI 1661-4917
J9 ARCH IMMUNOL THER EX
JI Arch. Immunol. Ther. Exp.
PD DEC
PY 2022
VL 70
IS 1
AR 25
DI 10.1007/s00005-022-00663-8
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 5F1YW
UT WOS:000866118700001
PM 36219249
DA 2025-01-07
ER
PT J
AU Dias, IRDR
Lo, HH
Zhang, KX
Law, BYK
Nasim, AA
Chung, SK
Wong, VKW
Liu, L
AF Dias, Ivo Ricardo de Seabra Rodrigues
Lo, Hang Hong
Zhang, Kaixi
Law, Betty Yuen Kwan
Nasim, Ali Adnan
Chung, Sookja Kim
Wong, Vincent Kam Wai
Liu, Liang
TI Potential therapeutic compounds from traditional Chinese medicine
targeting endoplasmic reticulum stress to alleviate rheumatoid arthritis
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Rheumatoid arthritis; Endoplasmic reticulum stress; Traditional Chinese
medicine; Therapeutic drug; Stress modulation
ID UNFOLDED PROTEIN RESPONSE; CELL-CYCLE ARREST; TXNIP/NLRP3 INFLAMMASOME
ACTIVATION; FIBROBLAST-LIKE SYNOVIOCYTES; NONALCOHOLIC FATTY LIVER;
LUNG-CANCER CELLS; ER-STRESS; INDUCED APOPTOSIS; MEDIATED APOPTOSIS;
TANSHINONE IIA
AB Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease which affects about 0.5-1% of people with symptoms that significantly impact a sufferer's lifestyle. The cells involved in propagating RA tend to display pro-inflammatory and cancer-like characteristics. Medical drug treatment is currently the main avenue of RA therapy. However, drug options are limited due to severe side effects, high costs, insufficient disease retardation in a majority of patients, and therapeutic effects possibly subsiding over time. Thus there is a need for new drug therapies. Endoplasmic reticulum (ER) stress, a condition due to accumulation of misfolded proteins in the ER, and subsequent cellular responses have been found to be involved in cancer and inflammatory pathologies, including RA. ER stress protein markers and their modulation have therefore been suggested as therapeutic targets, such as GRP78 and CHOP, among others. Some current RA therapeutic drugs have been found to have ER stress-modulating properties. Traditional Chinese Medicines (TCMs) frequently use natural products that affect multiple body and cellular targets, and several medicines and/or their isolated compounds have been found to also have ER stress-modulating capabilities, including TCMs used in RA treatment by Chinese Medicine practitioners. This review encourages, in light of the available information, the study of these RA-treating, ER stressmodulating TCMs as potential new pharmaceutical drugs for use in clinical RA therapy, along with providing a list of other ER stress-modulating TCMs utilized in treatment of cancers, inflammatory diseases and other diseases, that have potential use in RA treatment given similar ER stress-modulating capacity.
C1 [Dias, Ivo Ricardo de Seabra Rodrigues; Zhang, Kaixi; Nasim, Ali Adnan; Chung, Sookja Kim; Wong, Vincent Kam Wai] Macau Univ Sci & Technol, Dr Nehers Biophys Lab Innovat Drug Discovery, Macau, Peoples R China.
[Dias, Ivo Ricardo de Seabra Rodrigues; Lo, Hang Hong; Zhang, Kaixi; Law, Betty Yuen Kwan; Nasim, Ali Adnan; Wong, Vincent Kam Wai; Liu, Liang] Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Macau, Peoples R China.
[Chung, Sookja Kim] Macau Univ Sci & Technol, Fac Med, Macau, Peoples R China.
[Law, Betty Yuen Kwan; Wong, Vincent Kam Wai; Liu, Liang] Guangdong Hong Kong Macau Joint Lab Chinese Med &, Macau, Peoples R China.
C3 Macau University of Science & Technology; Macau University of Science &
Technology; Macau University of Science & Technology
RP Chung, SK; Wong, VKW; Liu, L (corresponding author), Macau Univ Sci & Technol, Dr Nehers Biophys Lab Innovat Drug Discovery, State Key Lab Qual Res Chinese Med, Ave Wai Long, Taipa, Macao, Peoples R China.; Chung, SK; Wong, VKW; Liu, L (corresponding author), Macau Univ Sci & Technol, Fac Med, Ave Wai Long, Taipa, Macao, Peoples R China.
EM skchung@must.edu.mo; kawwong@must.edu.mo; lliu@must.edu.mo
OI Zhang, Kaixi/0000-0003-2073-7264; Nasim, Ali Adnan/0000-0002-9554-0899;
Lo, Hang Hong/0000-0002-9392-0214; Wong, Vincent Kam
Wai/0000-0002-2951-8108
FU Guangdong Basic and Applied Basic Research Foundation, China
[2020B1515130005]; 2020 Guangdong Provincial Science and Technology
Innovation Strategy Special Fund, China (Guangdong-Hong Kong-Macau Joint
Lab) [2020B1212030006]; FDCT, Macao S.A.R., China grants; Dr. Neher's
Biophysics Laboratory for Innovative Drug Discovery from the Macao
Science and Technology Development Fund, Macao S.A.R., China
[0048/2018/A2, 001/2020/ALC]; Foshan Medicine Dengfeng Project of China,
China (2019-2021)
FX This work was supported by Guangdong Basic and Applied Basic Research
Foundation, China (No.: 2020B1515130005), the 2020 Guangdong Provincial
Science and Technology Innovation Strategy Special Fund, China
(Guangdong-Hong Kong-Macau Joint Lab, No: 2020B1212030006), FDCT, Macao
S.A.R., China grants and the granted project of Dr. Neher's Biophysics
Laboratory for Innovative Drug Discovery from the Macao Science and
Technology Development Fund, Macao S.A.R., China (Project codes:
0048/2018/A2; 001/2020/ALC), and Foshan Medicine Dengfeng Project of
China, China (2019-2021). The graphical abstract and Figs. 1-3 were made
utilizing the web-based software BioRender.com.
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NR 226
TC 30
Z9 31
U1 6
U2 86
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD AUG
PY 2021
VL 170
AR 105696
DI 10.1016/j.phrs.2021.105696
EA JUN 2021
PG 20
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA TT0IJ
UT WOS:000680035100021
PM 34052360
DA 2025-01-07
ER
PT J
AU Holick, MF
AF Holick, MF
TI Sunlight and vitamin D for bone health and prevention of autoimmune
diseases, cancers, and cardiovascular disease
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article; Proceedings Paper
CT Conference on Vitamin D and Health in the 21st Century
CY OCT 09-10, 2003
CL Bethesda, MD
SP NCI, NIH, DHHS, US Ctr Dis Control & Prevent, USDA Agr Res Serv, NIAMS, DNRC, NIDDK, ORWH, Coca Cola N Amer, Natl Dairy Council
DE vitamin D; sunlight; cancer; diabetes; bone
ID 1,25-DIHYDROXYVITAMIN D-3; D DEFICIENCY; HYPOVITAMINOSIS-D;
ULTRAVIOLET-B; SECONDARY HYPERPARATHYROIDISM; MULTIPLE-SCLEROSIS;
GENE-EXPRESSION; D INSUFFICIENCY; D INTOXICATION; SKIN PIGMENT
AB Most humans depend on sun exposure to satisfy their requirements for vitamin D. Solar ultraviolet B photons are absorbed by 7-dehydrocholesterol in the skin, leading to its transformation to previtamin D-3, which is rapidly converted to vitamin D-3. Season, latitude, time of day, skin pigmentation, aging, sunscreen use, and glass all influence the cutaneous production of vitamin D-3. Once formed, vitamin D-3 is metabolized in the liver to 25-hydroxyvitamin D-3 and then in the kidney to its biologically active form, 1,25-dihydroxyvitamin D-3. Vitamin D deficiency is an unrecognized epidemic among both children and adults in the United States. Vitamin D deficiency not only causes rickets among children but also precipitates and exacerbates osteoporosis among adults and causes the painful bone disease osteomalacia. Vitamin D deficiency has been associated with increased risks of deadly cancers, cardiovascular disease, multiple sclerosis, rheumatoid arthritis, and type 1 diabetes mellitus. Maintaining blood concentrations of 25-hydroxyvitamin D above 80 nmol/L (similar to30 ng/mL) not only is important for maximizing intestinal calcium absorption but also may be important for providing the extrarenal la-hydroxylase that is present in most tissues to produce 1,25-dihydroxyvitamin D-3. Although chronic excessive exposure to sunlight increases the risk of nonmelanoma skin cancer, the avoidance of all direct sun exposure increases the risk of vitamin D deficiency, which can have serious consequences. Monitoring serum 25-hydroxyvitamin D concentrations yearly should help reveal vitamin D deficiencies. Sensible sun exposure (usually 5-10 min of exposure of the arms and legs or the hands, arms, and face, 2 or 3 times per week) and increased dietary and supplemental vitamin D intakes are reasonable approaches to guarantee vitamin D sufficiency.
C1 Boston Univ, Med Ctr, Dept Med, Sect Endocrinol Nutr & Diabet, Boston, MA USA.
Boston Univ, Med Ctr, Vitamin D Skin & Bone Res Lab, Boston, MA USA.
C3 Boston University; Boston University
RP Boston Univ, Sch Med, 715 Albany St,M-1013, Boston, MA 02118 USA.
EM mfholick@bu.edu
RI Holick, Michael/AFG-9586-2022
OI Holick, Michael/0000-0001-6023-9062
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NR 126
TC 1920
Z9 2218
U1 14
U2 140
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD DEC
PY 2004
VL 80
IS 6
SU S
BP 1678S
EP 1688S
DI 10.1093/ajcn/80.6.1678S
PG 11
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Nutrition & Dietetics
GA 879ID
UT WOS:000225708700002
PM 15585788
OA Bronze
DA 2025-01-07
ER
PT J
AU Ru, Q
Li, YS
Chen, L
Wu, YX
Min, JX
Wang, FD
AF Ru, Qin
Li, Yusheng
Chen, Lin
Wu, Yuxiang
Min, Junxia
Wang, Fudi
TI Iron homeostasis and ferroptosis in human diseases: mechanisms and
therapeutic prospects
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID FATTY LIVER-DISEASE; SPINAL-CORD-INJURY; ISCHEMIA-REPERFUSION INJURY;
GLUTATHIONE-PEROXIDASE 4; TRAUMATIC BRAIN-INJURY; BETA-THALASSEMIA
MAJOR; ACUTE KIDNEY INJURY; OXIDATIVE STRESS; SKELETAL-MUSCLE;
CELL-DEATH
AB Iron, an essential mineral in the body, is involved in numerous physiological processes, making the maintenance of iron homeostasis crucial for overall health. Both iron overload and deficiency can cause various disorders and human diseases. Ferroptosis, a form of cell death dependent on iron, is characterized by the extensive peroxidation of lipids. Unlike other kinds of classical unprogrammed cell death, ferroptosis is primarily linked to disruptions in iron metabolism, lipid peroxidation, and antioxidant system imbalance. Ferroptosis is regulated through transcription, translation, and post-translational modifications, which affect cellular sensitivity to ferroptosis. Over the past decade or so, numerous diseases have been linked to ferroptosis as part of their etiology, including cancers, metabolic disorders, autoimmune diseases, central nervous system diseases, cardiovascular diseases, and musculoskeletal diseases. Ferroptosis-related proteins have become attractive targets for many major human diseases that are currently incurable, and some ferroptosis regulators have shown therapeutic effects in clinical trials although further validation of their clinical potential is needed. Therefore, in-depth analysis of ferroptosis and its potential molecular mechanisms in human diseases may offer additional strategies for clinical prevention and treatment. In this review, we discuss the physiological significance of iron homeostasis in the body, the potential contribution of ferroptosis to the etiology and development of human diseases, along with the evidence supporting targeting ferroptosis as a therapeutic approach. Importantly, we evaluate recent potential therapeutic targets and promising interventions, providing guidance for future targeted treatment therapies against human diseases.
C1 [Ru, Qin; Chen, Lin; Wu, Yuxiang] Jianghan Univ, Inst Intelligent Sport & Proact Hlth, Dept Hlth & Phys Educ, Wuhan, Peoples R China.
[Li, Yusheng] Cent South Univ, Xiangya Hosp, Dept Orthoped, Changsha, Peoples R China.
[Li, Yusheng] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Peoples R China.
[Min, Junxia] Zhejiang Univ, Affiliated Hosp 1, Sch Med, Hangzhou, Peoples R China.
[Wang, Fudi] Zhejiang Univ, Affiliated Hosp 2, Sch Publ Hlth, Sch Med,State Key Lab Expt Hematol, Hangzhou, Peoples R China.
C3 Jianghan University; Central South University; Central South University;
Zhejiang University; Zhejiang University
RP Wu, YX (corresponding author), Jianghan Univ, Inst Intelligent Sport & Proact Hlth, Dept Hlth & Phys Educ, Wuhan, Peoples R China.; Min, JX (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Sch Med, Hangzhou, Peoples R China.; Wang, FD (corresponding author), Zhejiang Univ, Affiliated Hosp 2, Sch Publ Hlth, Sch Med,State Key Lab Expt Hematol, Hangzhou, Peoples R China.
EM yxwu@jhun.edu.cn; junxiamin@zju.edu.cn; fwang@zju.edu.cn
RI Wu, Yuxiang/ABE-7091-2021; Wang, Fudi/L-7888-2018; Min,
Junxia/E-7622-2016
OI Wang, Fudi/0000-0001-8730-0003; Min, Junxia/0000-0001-8099-6327
FU National Natural Science Foundation of China [31970689, 32330047,
31930057, 82071970, 82072506]; Science Fund for Distinguished Young
Scholars of Hubei Province [2023AFA109]; Hubei Provincial Natural
Science Foundation of China [2024AFB971]
FX This work was supported in part by the National Natural Science
Foundation of China (31970689 to J.M.; 32330047 and 31930057 to F.W.;
and 82071970 to Y.W. and 82072506 to Y.L.), the Science Fund for
Distinguished Young Scholars of Hubei Province (2023AFA109 to Y.W.) and
Hubei Provincial Natural Science Foundation of China (2024AFB971 to
Q.R.).
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NR 1001
TC 2
Z9 2
U1 46
U2 46
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD OCT 14
PY 2024
VL 9
IS 1
AR 271
DI 10.1038/s41392-024-01969-z
PG 64
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA J4I7Y
UT WOS:001336724500002
PM 39396974
OA gold
DA 2025-01-07
ER
PT J
AU Holick, MF
AF Holick, Michael F.
TI Vitamin D Status: Measurement, Interpretation, and Clinical Application
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Vitamin D; 25-Hydroxyvitamin D; Sunlight; Parathyroid Hormone; Cancer
ID CIRCULATING CONCENTRATION; CALCIUM; ASSAY; 25-HYDROXYVITAMIN-D;
SUPPLEMENTATION; PREVALENCE; PLASMA
AB Vitamin D, the sunshine vitamin, is now recognized not only for its importance in promoting bone health in children and adults but also for other health benefits, including reducing the risk of chronic diseases such as autoimmune diseases, common cancer, and cardiovascular disease. Vitamin D made in the skin or ingested in the diet is biologically inert and requires 2 successive hydroxylations first in the liver on carbon 25 to form 25-hydroxyvitamin D [25(OH)D], and then in the kidney for a hydroxylation on carbon I to form the biologically active form of vitamin D, 1,25-dihydroxyvitamin D [1,25(OH)(2)D]. With the identification of 25(OH)D and 1,25(OH)(2)D, methods were developed to measure these metabolites in the circulation. Serum 25(OH)D is the barometer for vitamin D status. Serum 1,25(OH)(2)D provides no information about vitamin D status and is often normal or even increased as the result of secondary hyperparathyroidism associated with vitamin D deficiency. Most experts agree that 25(OH)D of <20 ng/mL is considered to be vitamin D deficiency, whereas a 25(OH)D of 21-29 ng/mL is considered to be insufficient. The goal should be to maintain both children and adults at a level >30 ng/mL to take full advantage of all the health benefits that vitamin D provides.
C1 Boston Univ, Sch Med, Dept Med,Med Ctr, Sect Endocrinol Nutr & Diabet,Vitamin D Skin & Bo, Boston, MA 02118 USA.
C3 Boston University
RP Holick, MF (corresponding author), Boston Univ, Sch Med, Dept Med,Med Ctr, Sect Endocrinol Nutr & Diabet,Vitamin D Skin & Bo, 715 Albany St,M-1013, Boston, MA 02118 USA.
EM mfholick@bu.edu
RI Holick, Michael/AFG-9586-2022
OI Holick, Michael/0000-0001-6023-9062
FU NIH [M01RR00533, AR36963]; UV Foundation
FX This work was supported in part by NIH grants M01RR00533 and AR36963 and
the UV Foundation.
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NR 33
TC 1136
Z9 1313
U1 0
U2 84
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1047-2797
EI 1873-2585
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD FEB
PY 2009
VL 19
IS 2
BP 73
EP 78
DI 10.1016/j.annepidem.2007.12.001
PG 6
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Public, Environmental & Occupational Health
GA 407UC
UT WOS:000263388800001
PM 18329892
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Liang, JU
Tian, C
Zeng, YL
Yang, QF
Liu, YY
Liu, YT
Wu, JJ
Hu, Y
Gu, FF
Zhang, K
Wang, Y
Zhang, Y
Liu, L
AF Liang, Jinyan
Tian, Chen
Zeng, Yulan
Yang, Qifan
Liu, Yangyang
Liu, Yuting
Wu, Jingjing
Hu, Yue
Gu, Feifei
Zhang, Kai
Wang, Yan
Zhang, Yong
Liu, Li
TI FOXA1+ regulatory T cells: A novel T cell subset that
suppresses antitumor immunity in lung cancer
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Lung cancer; Regulatory T cells; FOXA1; Treatment response
ID MECHANISMS; INFILTRATION; BLOCKADE; STAGE; FOXP3
AB Introduction: Regulatory T cells (Tregs) are important in the tumor microenvironment. Many subpopulations of Tregs have participated in suppressing antitumor immunity. Recently, FOXA1(+) Tregs were reported as a novel subset of Tregs that control autoimmune diseases. However, their clinical value in lung cancer is unknown.
Methods: We included 92 subjects in this study. Peripheral blood samples were collected from 15 lung cancer patients. Another 45 advanced stage lung cancer patients with malignant pleural effusion were enrolled for the analysis of FOXA1(+) Tregs in pleural effusions. Lung cancer tissues were collected from 3 patients. In vitro experiments were conducted to ascertain the influence of FOXA1(+) Tregs on T cells. Tumor-bearing mice model was utilized to explore the effects of Foxa1(+) Treg on tumor growth and the prognoses.
Results: Our data demonstrated that FOXA1(+) Tregs were increased in lung cancer. Moreover, patients with more FOXA1(+) Tregs showed more liver metastases and poorer treatment responses. In vitro assays revealed that FOXA1(+) Tregs inhibited the proliferation of T cells, the production of IFN-gamma and IL-2 by T cells. FOXA1(+) Tregs promoted tumor growth and indicated poor prognosis in the mice model of lung cancer.
Discussion: Collectively, our study is the first to investigate the suppressive function of FOXA1(+) Tregs against T cells in lung cancer, and the results showed that FOXA1(+) Tregs are markers of poor treatment responses in lung cancer patients. The inhibition of FOXA1(+) Tregs represents a promising new strategy to enhance antitumor immunity. (C) 2019 The Authors. Published by Elsevier Inc.
C1 [Liang, Jinyan; Tian, Chen; Zeng, Yulan; Yang, Qifan; Liu, Yangyang; Liu, Yuting; Wu, Jingjing; Hu, Yue; Gu, Feifei; Zhang, Kai; Liu, Li] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Canc Ctr, Wuhan 430022, Hubei, Peoples R China.
[Zhang, Yong] Huazhong Univ Sci & Technol, Tongji Med Coll, Hubei Canc Hosp, Dept Radiat Oncol, Wuhan 430022, Hubei, Peoples R China.
[Wang, Yan] Chinese Acad Sci, Anal & Testing Ctr, Inst Hydro Biol, Wuhan, Hubei, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
Science & Technology; Chinese Academy of Sciences
RP Liu, L (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Canc Ctr, Wuhan 430022, Hubei, Peoples R China.; Zhang, Y (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Hubei Canc Hosp, Dept Radiat Oncol, Wuhan 430022, Hubei, Peoples R China.
EM yongzhang8587520@sina.com; liulist2013@163.com
RI Yu, Yan/GYV-4514-2022; liu, yuxin/GRY-3592-2022; jingjing,
wu/AGQ-5050-2022
OI Liu, Li/0000-0003-2314-8756
FU National Natural Science Foundation of China [81773056, 81602501];
Natural Science Foundations of Hubei Province [2016CFB217]
FX This work was supported by two grants from the National Natural Science
Foundation of China (No. 81773056, 81602501) and one grant from the
Natural Science Foundations of Hubei Province (No. 2016CFB217).
CR [Anonymous], CANCER
[Anonymous], NAT MED
[Anonymous], CELL CYCLE
[Anonymous], MOL CELL
[Anonymous], J MOL MED
[Anonymous], ENHANCER REPROGR PRO
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NR 33
TC 16
Z9 18
U1 1
U2 19
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD JUN 18
PY 2019
VL 514
IS 1
BP 308
EP 315
DI 10.1016/j.bbrc.2019.04.152
PG 8
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA IA2QS
UT WOS:000469406800045
PM 31036318
OA hybrid
DA 2025-01-07
ER
PT J
AU Osiecki, M
Kierkus, J
Pawlowska, J
Wozniak, M
Jankowska, I
Teisseyre, M
Dadalski, M
Jarzebicka, D
Stefanowicz, M
Czubkowski, P
AF Osiecki, Marcin
Kierkus, Jaroslaw
Pawlowska, Joanna
Wozniak, Malgorzata
Jankowska, Irena
Teisseyre, Mikolaj
Dadalski, Maciej
Jarzebicka, Dorota
Stefanowicz, Marek
Czubkowski, Piotr
TI The Course of Ulcerative Colitis After Pediatric Liver Transplantation
for Sclerosing Cholangitis
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; CLINICAL-COURSE; RISK-FACTORS; RECURRENCE;
IMMUNOSUPPRESSION; MANAGEMENT; CHILDREN; DIAGNOSIS; THERAPY
AB Background. Primary sclerosing cholangitis (PSC) and autoimmune sclerosing cholangitis (ASC) are often associated with ulcerative colitis (UC). The impact on the course of UC remains unclear, and up-to-date evidence in pediatric populations is scarce. The aim of the study was to analyze the course of UC in pediatric patients transplanted owing to PSC or ASC.
Material and Methods. We retrospectively reviewed data from children with PSC/ASC and UC who underwent orthotopic liver transplantation (OLT). In all patients UC diagnosis was based on clinical presentation, endoscopy, and histology.
Results. Seventeen patients (9 female) with PSC or ASC underwent OLT from deceased donors at a median age of 16.8 years (range = 11.5-18.2 years). In 15 patients, UC was diagnosed before OLT (median age of diagnosis = 10.6 years; range = 6.6-18.0 years), and 2 patients developed UC after OLT. Ten patients (59%) presented with pancolitis on initial endoscopy. Disease activity was severe in 9 patients (53%) and most patients improved after initial treatment with steroids. Before OLT only 2 patients (13%) had severe disease activity. After OLT, 4 patients developed flares of the disease. These patients were successfully treated and remained in remission at the end of the posttransplant follow-up period (median = 3.76 years; range = 0.4-15.5 years). None of the patients developed colorectal cancer or underwent colectomy during 3.7 years of post-OLT follow-up.
Conclusion. In our experience, the course of UC was not aggravated by OLT for PSC, and UC did not adversely affect patient or graft survival.
C1 [Osiecki, Marcin; Kierkus, Jaroslaw; Pawlowska, Joanna; Wozniak, Malgorzata; Jankowska, Irena; Teisseyre, Mikolaj; Dadalski, Maciej; Jarzebicka, Dorota; Czubkowski, Piotr] Childrens Mem Hlth Inst, Dept Gastroenterol Hepatol Feeding Disorders & Pa, Al Dzieci Polskich 20, PL-04730 Warsaw, Poland.
[Stefanowicz, Marek] Childrens Mem Hlth Inst, Dept Paediat Surg & Organ Transplantat, Warsaw, Poland.
C3 Children's Memorial Health Institute; Children's Memorial Health
Institute
RP Osiecki, M (corresponding author), Childrens Mem Hlth Inst, Dept Gastroenterol Hepatol Feeding Disorders & Pa, Al Dzieci Polskich 20, PL-04730 Warsaw, Poland.
EM marcin.osiek@wp.pl
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NR 35
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0041-1345
EI 1873-2623
J9 TRANSPL P
JI Transplant. Proc.
PD JAN-FEB
PY 2021
VL 53
IS 1
BP 244
EP 249
DI 10.1016/j.transproceed.2020.09.011
EA JAN 2021
PG 6
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA RZ4IJ
UT WOS:000648560100034
PM 33162100
DA 2025-01-07
ER
PT J
AU Huang, JF
Zhao, Q
Dai, MY
Xiao, XR
Zhang, T
Zhu, WF
Li, F
AF Huang, Jian-Feng
Zhao, Qi
Dai, Man-Yun
Xiao, Xue-Rong
Zhang, Ting
Zhu, Wei-Feng
Li, Fei
TI Gut microbiota protects from triptolide-induced hepatotoxicity: Key role
of propionate and its downstream signalling events
SO PHARMACOLOGICAL RESEARCH
LA English
DT Article
DE Triptolide; Hepatotoxicity; Gut microbiota; Propionate; Metabolomics
ID FATTY-ACIDS; COMBINATION; METABOLITES; ACTIVATION; ARTHRITIS; PROTOCOL;
RECEPTOR; BIOLOGY; HUMANS; INJURY
AB As a potential drug for treating inflammatory, autoimmune diseases and cancers, triptolide (TP) is greatly limited in clinical practice due to its severe toxicity, particularly for liver injury. Recently, metabolic homeostasis was vitally linked to drug-induced liver injury and gut microbiota was established to play an important role. In this study, we aimed to investigate the functions of gut microbiota on TP-induced hepatotoxicity using metabolomics in mice. Here, predepletion of gut microbiota by antibiotic treatment strikingly aggravated liver injury and caused mortality after treated with a relatively safe dosage of TP at 0.5 mg/kg, which could be reversed by gut microbial transplantation. The loss of gut microbiota prior to TP treatment dramatically elevated long chain fatty acids and bile acids in plasma and liver. Further study suggested that gut microbiota-derived propionate contributed to the protective effect of gut microbiota against TP evidenced by ameliorative inflammatory level (Tnfa, Il6 and Cox2), ATP, malondialdehyde and hepatic histology. Supplementing with propionate significantly decreased the mRNA levels of genes involved in fatty acid biosynthesis (Srebp1c, Fasn and Elovl6), resulting in the decreased long chain fatty acids in liver. Moreover, TP restricted the growth of Firmicutes and led to the deficiency of short chain fatty acids in cecum content. In conclusion, our study warns the risk for TP and its preparations when antibiotics are co-administrated. Intervening by foods, prebiotics and probiotics toward gut microbiota or supplementing with propionate may be a clinical strategy to improve toxicity induced by TP.
C1 [Huang, Jian-Feng; Zhao, Qi; Dai, Man-Yun; Xiao, Xue-Rong; Zhang, Ting; Li, Fei] Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resources West Ch, Kunming 650201, Yunnan, Peoples R China.
[Huang, Jian-Feng; Dai, Man-Yun; Zhang, Ting] Univ Chinese Acad Sci, Beijing 100049, Peoples R China.
[Zhu, Wei-Feng] Jiangxi Univ Tradit Chinese Med, Academician Workstn, Nanchang 330004, Jiangxi, Peoples R China.
C3 Chinese Academy of Sciences; Kunming Institute of Botany, CAS; Chinese
Academy of Sciences; University of Chinese Academy of Sciences, CAS;
Jiangxi University of Traditional Chinese Medicine
RP Li, F (corresponding author), Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resources West Ch, Kunming 650201, Yunnan, Peoples R China.
EM lifeib@mail.kib.ac.cn
RI Li, Fei/I-8918-2019; Dai, Manyun/GZB-0789-2022; zhao, qi/KGK-3760-2024;
Huang, Jianfeng/F-8634-2011
FU National Key Research and Development Program of China [2017YFC1700906,
2017YFC1702900]; Double Thousand Program of Jiangxi Province
[jxsq2018102022]; CAS "Light of West China" Program [Y72E8211W1];
Kunming Institute of Botany [Y76E1211K1, Y4662211K1]; State Key
Laboratory of Phytochemistry and Plant Resources in West China
[52Y67A9211Z1]
FX This work was supported by the National Key Research and Development
Program of China (2017YFC1700906, 2017YFC1702900), Double Thousand
Program of Jiangxi Province (jxsq2018102022), CAS "Light of West China"
Program (Y72E8211W1), Kunming Institute of Botany (Y76E1211K1,
Y4662211K1), and State Key Laboratory of Phytochemistry and Plant
Resources in West China (52Y67A9211Z1).
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NR 52
TC 41
Z9 45
U1 5
U2 45
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
J9 PHARMACOL RES
JI Pharmacol. Res.
PD MAY
PY 2020
VL 155
AR 104752
DI 10.1016/j.phrs.2020.104752
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA LF8YV
UT WOS:000527701100019
PM 32169656
DA 2025-01-07
ER
PT J
AU Abdelaziz, AI
Mantawy, EM
Gad, AM
Fawzy, HM
Azab, SS
AF Abdelaziz, Aya, I
Mantawy, Eman M.
Gad, Amany M.
Fawzy, Hala M.
Azab, Samar S.
TI Activation of pCREB/Nrf-2 signaling mediates re-positioning of
liraglutide as hepato-protective for methotrexate -induced liver injury
(MILI)
SO FOOD AND CHEMICAL TOXICOLOGY
LA English
DT Article
DE Methotrexate; Liraglutide; Nrf 2; Nuclear factor erythroid 2-related
factor2; HO-1; Heme oxygenase-1; P-CREB; Phosphorylated cAMP response
element-binding protein
ID PEPTIDE-1 RECEPTOR AGONISTS; INDUCED OXIDATIVE STRESS; INDUCED
HEPATOTOXICITY; ANALOG LIRAGLUTIDE; HEME OXYGENASE-1; PPAR-GAMMA;
INFLAMMATORY RESPONSE; PSORIASIS PATIENTS; DOWN-REGULATION; CROSS-TALK
AB Methotrexate (MTX) is commonly used to treat several types of cancer and autoimmune diseases. However, there is increasing concern over its organs toxicities particularly liver toxicity. Liraglutide, a glucagon like peptide-1 agonist, possesses antioxidant and anti-inflammatory features. This study aimed to explore the potential protective effect of liraglutide pre-treatment in ameliorating MTX-induced hepatotoxicity and to further investigate the underlying mechanisms. Rats received 1.2 mg/kg liraglutide intraperitoneal twice daily for 7 days before MTX. Results revealed that liraglutide significantly decreased activities of liver enzymes and oxidative stress in hepatocytes. Furthermore, NF-kB expression and related inflammatory markers (TNF-alpha, COX-2 and IL-6) were reduced in the pre-treatment group of liraglutide. These data validate the advantageous effects of liraglutide in MTX hepatotoxic animals. In addition, liraglutide increased the expression of the antioxidant transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf-2), along with the transcription of downstream phosphorylated cAMP response element-binding protein (pCREB) which increases the activity of Nrf-2. Additionally, caspase-3 expression/activity and BAX/Bcl-2 ratio were decreased following liraglutide pre-treatment. In conclusion, it was confirmed that liraglutide enhanced the antioxidant activity of liver cells by activating the Nrf-2 and pCREB signaling, thereby, reducing liver cell inflammation and apoptosis induced by MTX.
C1 [Abdelaziz, Aya, I; Gad, Amany M.; Fawzy, Hala M.] Natl Org Drug Control & Res, Dept Pharmacol, Cairo, Egypt.
[Mantawy, Eman M.; Azab, Samar S.] Ain Shams Univ, Dept Pharmacol & Toxicol, Fac Pharm, Cairo 11566, Egypt.
C3 National Organization for Drug Control & Research (NODCAR); Egyptian
Knowledge Bank (EKB); Ain Shams University
RP Azab, SS (corresponding author), Ain Shams Univ, Dept Pharmacol & Toxicol, Fac Pharm, Cairo 11566, Egypt.
EM samar_saad_azab@pharma.asu.edu.eg
RI Ismail, Aya/AAB-6533-2021; Gad, Amany/AAB-5425-2019
OI Azab, Samar/0000-0002-0253-8280; Gad, Amany/0000-0002-6175-184X; Ismail,
Aya/0000-0001-9076-8387
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NR 98
TC 8
Z9 8
U1 1
U2 13
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0278-6915
EI 1873-6351
J9 FOOD CHEM TOXICOL
JI Food Chem. Toxicol.
PD OCT
PY 2019
VL 132
AR 110719
DI 10.1016/j.fct.2019.110719
PG 12
WC Food Science & Technology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Toxicology
GA IW0JB
UT WOS:000484647100031
PM 31362085
DA 2025-01-07
ER
PT J
AU Madir, A
Bozin, T
Mikolasevic, I
Milic, S
Stimac, D
Mijic, M
Kanzaj, TF
Biloglav, Z
Lucijanic, M
Lucijanic, I
Grgurevic, I
AF Madir, Anita
Bozin, Tonci
Mikolasevic, Ivana
Milic, Sandra
Stimac, Davor
Mijic, Maja
Kanzaj, Tajana Filipec
Biloglav, Zrinka
Lucijanic, Marko
Lucijanic, Iva
Grgurevic, Ivica
TI Epidemiological and clinical features of primary biliary cholangitis in
two Croatian regions: a retrospective study
SO CROATIAN MEDICAL JOURNAL
LA English
DT Article
ID URSODEOXYCHOLIC ACID; BIOCHEMICAL RESPONSE; SURVIVAL ANALYSIS;
CIRRHOSIS; CHOLESTASIS; PROGRESSION; PREVALENCE; RECURRENCE; PROGNOSIS;
DISEASE
AB Aim To assess the measures of disease frequency and determine the clinical features of primary biliary cholangitis (PBC) in two Croatian regions.
Methods Databases of two tertiary hospitals, one located in the continental and one in the coastal region of Croatia, were retrospectively searched for PBC patients diagnosed from 2007 to 2018. Epidemiologic data analysis was restricted to patients from each hospital's catchment area. We analyzed factors related to response to therapy and event-free survival (EFS), defined as absence of ascites, variceal bleeding, encephalopathy, hepatocellular carcinoma, liver transplantation (LT), or death. In addition, we determined clinical and demographic data of transplanted PBC patients.
Results Out of 83 PBC patients, 86.7% were female, with a median age at diagnosis of 55 years. Average PBC incidence for the 11-year period was 0.79 and 0.89 per 100 000 population, whereas the point prevalence on December 31, 2017 was 11.5 and 12.5 in the continental and coastal region, respectively. Of 76 patients with complete medical records, 21% had an advanced disease stage, 31.6% had an associated autoimmune condition, and all received ursodeoxycholic acid. EFS rate at 5 years was 95.8%. In an age and sex-adjusted multivariate Cox regression model, the only factor significantly associated with inferior EFS was no response to therapy (HR = 18.4; P=0.018). Of all Croatian patients who underwent LT, 3.8% had PBC, with the survival rate at 5 years after LT of 93.4%.
Conclusion This study gives pioneer insights into the epidemiological and clinical data on PBC in Croatia, thus complementing the PBC map of Southeast Europe.
C1 [Madir, Anita; Bozin, Tonci; Grgurevic, Ivica] Univ Hosp Dubrava, Dept Gastroenterol Hepatol & Clin Nutr, Zagreb, Croatia.
[Madir, Anita; Kanzaj, Tajana Filipec; Biloglav, Zrinka; Grgurevic, Ivica] Univ Zagreb, Sch Med, Zagreb, Croatia.
[Mikolasevic, Ivana; Milic, Sandra; Stimac, Davor] Univ Hosp Ctr Rijeka, Dept Gastroenterol & Hepatol, Rijeka, Croatia.
[Mikolasevic, Ivana; Milic, Sandra; Stimac, Davor] Univ Rijeka, Sch Med, Rijeka, Croatia.
[Mijic, Maja; Kanzaj, Tajana Filipec] Univ Hosp Merkur, Dept Gastroenterol & Hepatol, Zagreb, Croatia.
[Biloglav, Zrinka] Andrija Stampar Sch Publ Hlth, Dept Med Stat Epidemiol & Med Informat, Zagreb, Croatia.
[Lucijanic, Marko] Univ Hosp Dubrava, Dept Hematol, Zagreb, Croatia.
[Lucijanic, Iva] Cty Hosp Karlovac, Dept Dermatol & Venereol, Karlovac, Croatia.
[Grgurevic, Ivica] Univ Zagreb, Fac Pharm & Biochem, Zagreb, Croatia.
C3 University of Zagreb; University of Rijeka; University of Rijeka;
University of Zagreb
RP Grgurevic, I (corresponding author), Univ Hosp Dubrava, Dept Med, Dept Gastroenterol Hepatol & Clin Nutr, Avenija Gojka Suska 6, Zagreb 10000, Croatia.
EM ivica.grgurevic@zg.htnet.hr
RI Kanizaj, Tajana/AAQ-6438-2020; Štimac, Davor/ABF-7086-2020; Milić,
Sandra/S-5858-2018; Lucijanic, Marko/AEJ-3313-2022; Grgurevic,
Ivica/AEN-2615-2022
OI Lucijanic, Marko/0000-0002-1372-2040; Madir, Anita/0000-0001-5789-1869
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NR 34
TC 10
Z9 10
U1 0
U2 6
PU MEDICINSKA NAKLADA
PI ZAGREB
PA VLASKA 69, HR-10000 ZAGREB, CROATIA
SN 0353-9504
EI 1332-8166
J9 CROAT MED J
JI Croat. Med. J.
PD DEC
PY 2019
VL 60
IS 6
BP 494
EP 502
DI 10.3325/cmj.2019.60.494
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA KB2VN
UT WOS:000506358000003
PM 31894914
OA Green Published, Green Accepted, gold
DA 2025-01-07
ER
PT J
AU Shao, X
Uojima, H
Arai, T
Ogawa, Y
Setsu, T
Atsukawa, M
Furuichi, Y
Arase, Y
Horio, K
Hidaka, H
Nakazawa, T
Kako, M
Kagawa, T
Iwakiri, K
Nakajima, A
Terai, S
Tanaka, Y
Koizumi, W
AF Shao, Xue
Uojima, Haruki
Arai, Taeang
Ogawa, Yuji
Setsu, Toru
Atsukawa, Masanori
Furuichi, Yoshihiro
Arase, Yoshitaka
Horio, Kazue
Hidaka, Hisashi
Nakazawa, Takahide
Kako, Makoto
Kagawa, Tatehiro
Iwakiri, Katsuhiko
Nakajima, Atsushi
Terai, Shuji
Tanaka, Yasuhito
Koizumi, Wasaburo
TI The Risk of Cirrhosis and Its Complications Based on PNPLA3 rs738409 G
Allele Frequency
SO DIGESTIVE DISEASES
LA English
DT Article; Early Access
DE Patatin-like phospholipase domain-containing 3 genotype; Liver
cirrhosis; Hepatic encephalopathy; Varix hemorrhage; Hepatic ascites
ID JAPANESE PATIENTS; LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA; ADVANCED
FIBROSIS; POLYMORPHISM; METAANALYSIS; SEVERITY; VARIANT; GENE
AB Background: Data regarding the influence of patatin-like phospholipase domain-containing 3 (PNPLA3) polymorphism for patients with liver cirrhosis (LC) are scarce. Objective: This study assesses the role of the PNPLA3 polymorphism for the development of LC and its complications by the findings of genetic examinations. Methods: Patients with LC caused by virus (n = 157), alcohol (n = 104), nonalcoholic fatty liver disease (NAFLD) (n = 106), or autoimmune disease (n = 33) and without LC (n = 128) were enrolled. LC was composed of the presence and absence of complications, such as variceal bleeding, hepatic ascites, and hepatic encephalopathy. To assess the role of the PNPLA3 polymorphism, odds ratio (OR) for the rs738409 variant was calculated for the patients between (i) with LC and without LC in the entire cohort and (ii) the presence and absence of complications in the patients with LC. Results: There was a significant difference among the patients without LC and those with alcohol, NAFLD-related LC in the frequency of G alleles (p < 0.001, both). According to complications of LC, the OR for NAFLD-related cirrhosis significantly increased in the presence of the two mutated alleles (OR = 3.165; p = 0.046) when the wild type was used as the reference. However, there were no significant risks for the complications in the virus and alcohol-related cirrhosis unless there was a presence of G alleles. Conclusion: The PNPLA3 polymorphism was associated with the risk of NAFLD-related LC and its complications.
C1 [Shao, Xue; Uojima, Haruki; Horio, Kazue; Hidaka, Hisashi; Nakazawa, Takahide; Koizumi, Wasaburo] Kitasato Univ, Sch Med, Dept Gastroenterol, Internal Med, Sagamihara, Japan.
[Shao, Xue] Second Hosp Jilin Univ, Dept Hepatopancreatobiliary Med, Changchun, Peoples R China.
[Uojima, Haruki; Kako, Makoto] Shonan Kamakura Gen Hosp, Dept Gastroenterol, Kamakura, Japan.
[Arai, Taeang] Chiba Hokusoh Hosp, Nippon Med Sch, Dept Internal Med, Div Gastroenterol, Chiba, Japan.
[Ogawa, Yuji] Yokohama City Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Yokohama, Japan.
[Setsu, Toru; Terai, Shuji] Niigata Univ, Grad Sch Med & Dent Sci, Div Gastroenterol & Hepatol, Niigata, Japan.
[Atsukawa, Masanori; Iwakiri, Katsuhiko] Nippon Med Sch, Dept Internal Med, Div Gastroenterol & Hepatol, Bunkyo City, Japan.
[Furuichi, Yoshihiro] Tokyo Med Univ Hosp, Dept Gastroenterol & Hepatol, Shinjuku Ku, Tokyo, Japan.
[Arase, Yoshitaka; Kagawa, Tatehiro] Tokai Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol, Shibuya City, Tokyo, Japan.
[Tanaka, Yasuhito] Nagoya City Univ, Grad Sch Med Sci, Dept Virol, Nagoya, Japan.
[Tanaka, Yasuhito] Nagoya City Univ, Grad Sch Med Sci, Liver Unit, Nagoya, Japan.
C3 Kitasato University; Jilin University; Nippon Medical School; Yokohama
City University; Niigata University; Nippon Medical School; Tokyo
Medical University; Tokai University; Nagoya City University
RP Uojima, H (corresponding author), Kitasato Univ, Sch Med, Dept Gastroenterol, Internal Med, Sagamihara, Japan.; Uojima, H (corresponding author), Shonan Kamakura Gen Hosp, Dept Gastroenterol, Kamakura, Japan.
EM kiruha@kitasato-u.ac.jp
RI Uojima, Haruki/LPP-6195-2024; Furuichi, Yoshihiro/AAS-4980-2020; Kagawa,
Tatehiro/AAF-7300-2020
OI Terai, Shuji/0000-0002-5439-635X; Hidaka, Hisashi/0000-0002-4151-5663;
Tanaka, Yasuhito/0000-0002-2473-6966
FU Research Program on Hepatitis from the Japan AMED (Agency for Medical
Research and Development) [JP19fk0210048, JP20fk0210048]
FX This study was partly supported by the Research Program on Hepatitis
from the Japan AMED (Agency for Medical Research and Development) Grant
No.: JP19fk0210048 and JP20fk0210048.
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NR 31
TC 7
Z9 7
U1 1
U2 7
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PD 2021 NOV 22
PY 2021
DI 10.1159/000521062
EA NOV 2021
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 3R7TP
UT WOS:000839110800001
PM 34808618
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Hann, A
Oo, YH
Perera, MTPR
AF Hann, Angus
Oo, Ye H.
Perera, M. Thamara P. R.
TI Regulatory T-Cell Therapy in Liver Transplantation and Chronic Liver
Disease
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE Treg; liver; transplant; cirrhosis; immunity; rejection; cell therapy
ID SINUSOIDAL ENDOTHELIAL-CELLS; ARTERIAL BUFFER RESPONSE; HEPATIC STELLATE
CELLS; HEPATOCELLULAR-CARCINOMA; EXTRACELLULAR-MATRIX; BLOOD-FLOW;
TOLERANCE; FIBROSIS; DIFFERENTIATION; GENERATION
AB The constant exposure of the liver to gut derived foreign antigens has resulted in this organ attaining unique immunological characteristics, however it remains susceptible to immune mediated injury. Our understanding of this type of injury, in both the native and transplanted liver, has improved significantly in recent decades. This includes a greater awareness of the tolerance inducing CD4(+) CD25(+) CD127(low) T-cell lineage with the transcription factor FoxP3, known as regulatory T-Cells (Tregs). These cells comprise 5-10% of CD4(+) T cells and are known to function as an immunological "braking" mechanism, thereby preventing immune mediated tissue damage. Therapies that aim to increase Treg frequency and function have proved beneficial in the setting of both autoimmune diseases and solid organ transplantations. The safety and efficacy of Treg therapy in liver disease is an area of intense research at present and has huge potential. Due to these cells possessing significant plasticity, and the potential for conversion towards a T-helper 1 (Th1) and 17 (T(h)17) subsets in the hepatic microenvironment, it is pre-requisite to modify the microenvironment to a Treg favourable atmosphere to maintain these cells' function. In addition, implementation of therapies that effectively increase Treg functional activity in the liver may result in the suppression of immune responses and will hinder those that destroy tumour cells. Thus, fine adjustment is crucial to achieve this immunological balance. This review will describe the hepatic microenvironment with relevance to Treg function, and the role these cells have in both native diseased and transplanted livers.
C1 [Hann, Angus; Oo, Ye H.; Perera, M. Thamara P. R.] Queen Elizabeth Hosp Birmingham, Liver Unit, Birmingham, W Midlands, England.
[Hann, Angus; Oo, Ye H.; Perera, M. Thamara P. R.] Univ Birmingham, Ctr Liver & Gastrointestinal Res, Birmingham, W Midlands, England.
[Hann, Angus; Oo, Ye H.; Perera, M. Thamara P. R.] Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham Biomed Res Ctr, Natl Inst Hlth Res NIHR, Birmingham, W Midlands, England.
[Oo, Ye H.] Univ Hosp Birmingham NHS Fdn Trust, Ctr Rare Dis, ERN Rare Liver Ctr, Birmingham, W Midlands, England.
C3 University of Birmingham; University of Birmingham; University of
Birmingham; University of Birmingham
RP Perera, MTPR (corresponding author), Queen Elizabeth Hosp Birmingham, Liver Unit, Birmingham, W Midlands, England.; Perera, MTPR (corresponding author), Univ Birmingham, Ctr Liver & Gastrointestinal Res, Birmingham, W Midlands, England.; Perera, MTPR (corresponding author), Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham Biomed Res Ctr, Natl Inst Hlth Res NIHR, Birmingham, W Midlands, England.
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NR 113
TC 15
Z9 16
U1 2
U2 21
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD OCT 14
PY 2021
VL 12
AR 719954
DI 10.3389/fimmu.2021.719954
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA WQ5BR
UT WOS:000713832100001
PM 34721383
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Du, WJ
Zhen, JH
Zeng, ZQ
Zheng, ZM
Xu, Y
Qin, LY
Chen, SJ
AF Du, Wen-Jun
Zhen, Jun-Hui
Zeng, Zhao-Qing
Zheng, Zhao-Min
Xu, Yan
Qin, Lai-Ying
Chen, Shi-Jun
TI Expression of Interleukin-17 associated with disease progression and
liver fibrosis with hepatitis B virus infection: IL-17 in HBV infection
SO DIAGNOSTIC PATHOLOGY
LA English
DT Article
DE Asymptomatic; Hepatitis B surface antigen Carriers; Interleukin-17;
Hepatitis B virus; Chronic hepatitis B; Liver cirrhosis; Primary
hepatitis carcinoma; Chronic liver failure; Fibrosis
ID NF-KAPPA-B; T-CELLS; GENE-EXPRESSION; TGF-BETA; PROTEIN; GROWTH;
INFLAMMATION; ACTIVATION; HEPATOCYTES; AIRWAYS
AB Background/objectives: As a proinflammatory cytokine, interleukin-17 (IL-17) contributes to the inflammation of many autoimmune diseases. We examined IL-17 levels in serum and tissues from patients with chronic hepatitis B virus infection (HBV), and especially evaluated the role of IL-17 in the pathogenesis and progression of liver fibrosis.
Materials and methods: Whole venous blood was obtained from four patient groups: chronic hepatitis B (CHB, n = 47), liver cirrhosis (LC, n = 49), primary hepatocellular carcinoma (PHC, n = 44), chronic liver failure (CLF, n = 33), and a normal control group (n = 20). HBsAg was positive in all patients. Liver biopsy samples were acquired from asymptomatic HBsAg carriers (ASC, n = 35), CHB (n = 57), and LC (n = 31) patients. We performed ELISA to measure IL-17 levels in serum samples, and used reverse RT-PCR to measure IL-17 mRNA levels in peripheral blood mononuclear cells (PBMC). IL-17 protein expression was detected in liver biopsy tissues by immunohistochemistry.
Results: Compared to normal controls, serum IL-17 protein and mRNA levels were significantly higher in the four infection groups. LC patients exhibited the highest serum IL-17 and PBMC mRNA levels. No significant differences were found between the other three groups. High levels of IL-17 were also observed in tissues from CHB and LC patients, compared to ASC. IL-17 expression was mainly located in the portal area and was positively correlated with inflammation grade and fibrosis stage.
Conclusions: IL-17 expression was found to be increased with increasing degrees of liver fibrosis. This suggests that IL-17 may not only induce the inflammation, but also contribute to disease progression and chronicity.
Virtual Slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/5306959258322482
C1 [Du, Wen-Jun; Zhen, Jun-Hui; Chen, Shi-Jun] Shandong Univ, Sch Med, Jinan 250100, Peoples R China.
[Du, Wen-Jun; Zeng, Zhao-Qing; Zheng, Zhao-Min; Xu, Yan; Qin, Lai-Ying; Chen, Shi-Jun] Shandong Univ, Sch Med, Jinan Infect Dis Hosp, Dept Liver Dis, Jinan 250100, Peoples R China.
[Zhen, Jun-Hui] Shandong Univ, Sch Med, Dept Pathol, Jinan 250100, Peoples R China.
C3 Shandong University; Shandong University; Shandong University
RP Chen, SJ (corresponding author), Shandong Univ, Sch Med, Jinan 250100, Peoples R China.
EM crbdwj@126.com
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NR 25
TC 72
Z9 81
U1 0
U2 21
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1746-1596
J9 DIAGN PATHOL
JI Diagn. Pathol.
PD FEB 28
PY 2013
VL 8
AR 40
DI 10.1186/1746-1596-8-40
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 101OS
UT WOS:000315784900001
PM 23448394
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kleinstreuer, NC
Dix, DJ
Houck, KA
Kavlock, RJ
Knudsen, TB
Martin, MT
Paul, KB
Reif, DM
Crofton, KM
Hamilton, K
Hunter, R
Shah, I
Judson, RS
AF Kleinstreuer, Nicole C.
Dix, David J.
Houck, Keith A.
Kavlock, Robert J.
Knudsen, Thomas B.
Martin, Matthew T.
Paul, Katie B.
Reif, David M.
Crofton, Kevin M.
Hamilton, Kerry
Hunter, Ronald
Shah, Imran
Judson, Richard S.
TI In Vitro Perturbations of Targets in Cancer Hallmark Processes
Predict Rodent Chemical Carcinogenesis
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE cancer hallmarks; carcinogenesis; predictive toxicology; in vitro and
alternatives; bioinformatics
ID REPRODUCTIVE TOXICITY; SULINDAC SULFIDE; HUMAN THYROCYTES; TUMOR-CELLS;
EXPRESSION; MODEL; INHIBITION; MECHANISMS; CHEMOKINES; GROWTH
AB Thousands of untested chemicals in the environment require efficient characterization of carcinogenic potential in humans. A proposed solution is rapid testing of chemicals using in vitro high-throughput screening (HTS) assays for targets in pathways linked to disease processes to build models for priority setting and further testing. We describe a model for predicting rodent carcinogenicity based on HTS data from 292 chemicals tested in 672 assays mapping to 455 genes. All data come from the EPA ToxCast project. The model was trained on a subset of 232 chemicals with in vivo rodent carcinogenicity data in the Toxicity Reference Database (ToxRefDB). Individual HTS assays strongly associated with rodent cancers in ToxRefDB were linked to genes, pathways, and hallmark processes documented to be involved in tumor biology and cancer progression. Rodent liver cancer endpoints were linked to well-documented pathways such as peroxisome proliferatoractivated receptor signaling and TP53 and novel targets such as PDE5A and PLAUR. Cancer hallmark genes associated with rodent thyroid tumors were found to be linked to human thyroid tumors and autoimmune thyroid disease. A model was developed in which these genes/pathways function as hypothetical enhancers or promoters of rat thyroid tumors, acting secondary to the key initiating event of thyroid hormone disruption. A simple scoring function was generated to identify chemicals with significant in vitro evidence that was predictive of in vivo carcinogenicity in different rat tissues and organs. This scoring function was applied to an external test set of 33 compounds with carcinogenicity classifications from the EPA's Office of Pesticide Programs and successfully (p = 0.024) differentiated between chemicals classified as possible/probable/likely carcinogens and those designated as not likely or with evidence of noncarcinogenicity. This model represents a chemical carcinogenicity prioritization tool supporting targeted testing and functional validation of cancer pathways.
C1 [Kleinstreuer, Nicole C.; Dix, David J.; Houck, Keith A.; Kavlock, Robert J.; Knudsen, Thomas B.; Martin, Matthew T.; Reif, David M.; Shah, Imran; Judson, Richard S.] US EPA, Natl Ctr Computat Toxicol, Off Res & Dev, Res Triangle Pk, NC 27711 USA.
[Paul, Katie B.; Crofton, Kevin M.] US EPA, Natl Hlth & Environm Effects Lab, Off Res & Dev, Res Triangle Pk, NC 27711 USA.
[Hamilton, Kerry; Hunter, Ronald] US EPA, Assoc Sch Publ Hlth ASPH Environm Publ Hlth, Washington, DC 20460 USA.
C3 United States Environmental Protection Agency; United States
Environmental Protection Agency; United States Environmental Protection
Agency
RP Judson, RS (corresponding author), US EPA, Natl Ctr Computat Toxicol, Off Res & Dev, 109 TW Alexander Dr B205-01, Res Triangle Pk, NC 27711 USA.
EM judson.richard@epa.gov
RI Friedman, Katie/L-5657-2019; Judson, Richard/AEC-6432-2022; Houck,
Keith/G-8654-2014; Shah, Syed/B-8275-2011; Kleinstreuer,
Nicole/F-7203-2019; Crofton, Kevin/J-4798-2015
OI Reif, David/0000-0001-7815-6767; Shah, Imran/0000-0003-0808-0140;
Friedman, Katie/0000-0002-2710-1691; Kleinstreuer,
Nicole/0000-0002-7914-3682; Houck, Keith/0000-0002-0055-2249; Judson,
Richard/0000-0002-2348-9633; Crofton, Kevin/0000-0003-1749-9971;
Hamilton, Kerry/0000-0003-2991-7325
FU U.S. Environmental Protection Agency (EPA)
FX U.S. Environmental Protection Agency (EPA).
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NR 79
TC 58
Z9 63
U1 1
U2 48
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD JAN
PY 2013
VL 131
IS 1
BP 40
EP 55
DI 10.1093/toxsci/kfs285
PG 16
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA 072EV
UT WOS:000313652900005
PM 23024176
OA Green Submitted, Bronze
DA 2025-01-07
ER
PT J
AU Azadian, R
Mohammadalipour, A
Memarzadeh, MR
Hashemnia, M
Aarabi, MH
AF Azadian, Razieh
Mohammadalipour, Adel
Memarzadeh, Mohammad Reza
Hashemnia, Mohammad
Aarabi, Mohammad Hosein
TI Examining hepatoprotective effects of astaxanthin against
methotrexate-induced hepatotoxicity in rats through modulation of
Nrf2/HO-1 pathway genes
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Article
DE Astaxanthin; Hepatotoxicity; Methotrexate; Oxidative stress; Nrf2; HO-1
ID CISPLATIN-INDUCED NEPHROTOXICITY; OXIDATIVE STRESS; LIVER-INJURY;
EXPRESSION; EXTRACT; NRF2; CANCER; ACID
AB Methotrexate (MTX), as a folic acid antagonist, is an effective drug in treating a wide range of malignancies and autoimmune diseases. However, the clinical use of MTX has been limited due to its side effects, the most common of which is hepatotoxicity. In this study, rats were randomly divided into six groups: three treatment groups received methotrexate and different doses of astaxanthin (AX) for 14 days. At the end of the study, blood samples were collected to determine serum levels of ALT, AST, ALP, and LDH. Also, liver tissues were isolated to evaluate antioxidant enzymes and markers of oxidative stress, histopathological damage, and expression of NF-E2-related transcription factor (Nrf2) and Heme oxygenase-1 (HO-1) genes. The results showed that administration of MTX significantly increased the levels of ALT, AST, ALP, and LDH in the blood, markers of oxidative stress, and histopathological damage in liver tissue and significantly reduced the levels of antioxidant enzymes and the expression of Nrf2 and HO-1 genes. On the other hand, treatment with AX decreased blood levels of ALT, AST, ALP, and LDH and oxidative stress markers and remarkably raises the activity of antioxidant enzymes and expression of Nrf2 and HO-1 genes in liver tissue. In addition, histopathological lesions were improved with AX administration. The findings of this study indicated that AX may be useful for the prevention of MTX-induced hepatotoxicity by improving oxidative and inflammatory changes.
C1 [Azadian, Razieh; Mohammadalipour, Adel; Aarabi, Mohammad Hosein] Isfahan Univ Med Sci, Sch Pharm & Pharmaceut Sci, Dept Clin Biochem, Esfahan, Iran.
[Memarzadeh, Mohammad Reza] Barij Essence Med Plants Res Ctr, Kashan, Iran.
[Hashemnia, Mohammad] Razi Univ, Fac Vet Med, Dept Pathobiol, Kermanshah, Iran.
C3 Isfahan University of Medical Sciences; Razi University
RP Aarabi, MH (corresponding author), Isfahan Univ Med Sci, Sch Pharm & Pharmaceut Sci, Dept Clin Biochem, Esfahan, Iran.
EM azadian0016@yahoo.com; mohammadalipour@pharm.mui.ac.ir;
m.r.memarzadeh63@gmail.com; m.hashemnia@razi.ac.ir;
mh.aarabi@pharm.mui.ac.ir
RI Aarabi, Mohammad/AFA-3968-2022; Mohammadalipour, Adel/M-3886-2018;
Hashemnia, Mohammad/HGC-1644-2022
OI Mohammadalipour, Adel/0000-0002-2598-9439; Hashemnia,
Mohammad/0000-0002-2899-4794; Aarabi, Mohammad
Hosein/0000-0001-6514-4492
FU Isfahan University of Medical Sciences, Iran [298058]
FX AcknowledgementsThis study was supported by a grant (No: 298058) from
Isfahan University of Medical Sciences, Iran. The authors would like to
extend their deep and sincere gratitude to each and every one of those
who helped them.
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NR 39
TC 5
Z9 5
U1 1
U2 7
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0028-1298
EI 1432-1912
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD JAN
PY 2024
VL 397
IS 1
BP 371
EP 380
DI 10.1007/s00210-023-02581-8
EA JUL 2023
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GY3L0
UT WOS:001030519700002
PM 37450013
DA 2025-01-07
ER
PT J
AU Ioannou, K
Samara, P
Livaniou, E
Derhovanessian, E
Tsitsilonis, OE
AF Ioannou, Kyriaki
Samara, Pinelopi
Livaniou, Evangelia
Derhovanessian, Evelyna
Tsitsilonis, Ourania E.
TI Prothymosin alpha: a ubiquitous polypeptide with potential use in cancer
diagnosis and therapy
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Review
DE Thymic peptides; Prothymosin alpha; Thymosin alpha 1; Anticancer
therapy; Tumor markers
ID KILLER-CELL ACTIVITY; PERIPHERAL-BLOOD LYMPHOCYTES; COLORECTAL TUMOR
PATIENTS; DOSE INTERFERON-ALPHA; PRIMARY BREAST-CANCER; LEWIS
LUNG-CARCINOMA; PATIENTS IN-VITRO; THYMOSIN ALPHA-1; ANTITUMOR-ACTIVITY;
HEPATOCELLULAR-CARCINOMA
AB The thymus is a central lymphoid organ with crucial role in generating T cells and maintaining homeostasis of the immune system. More than 30 peptides, initially referred to as "thymic hormones," are produced by this gland. Although the majority of them have not been proven to be thymus-specific, thymic peptides comprise an effective group of regulators, mediating important immune functions. Thymosin fraction five (TFV) was the first thymic extract shown to stimulate lymphocyte proliferation and differentiation. Subsequent fractionation of TFV led to the isolation and characterization of a series of immunoactive peptides/polypeptides, members of the thymosin family. Extensive research on prothymosin alpha (proT alpha) and thymosin alpha 1 (T alpha 1) showed that they are of clinical significance and potential medical use. They may serve as molecular markers for cancer prognosis and/or as therapeutic agents for treating immunodeficiencies, autoimmune diseases and malignancies. Although the molecular mechanisms underlying their effect are yet not fully elucidated, proT alpha and T alpha 1 could be considered as candidates for cancer immunotherapy. In this review, we will focus in principle on the eventual clinical utility of proT alpha, both as a tumor biomarker and in triggering anticancer immune responses. Considering the experience acquired via the use of T alpha 1 to treat cancer patients, we will also discuss potential approaches for the future introduction of proT alpha into the clinical setting.
C1 [Ioannou, Kyriaki; Samara, Pinelopi; Tsitsilonis, Ourania E.] Univ Athens, Dept Anim & Human Physiol, Fac Biol, Athens 15784, Greece.
[Livaniou, Evangelia] Natl Ctr Sci Res Demokritos, Immunopeptide Chem Lab, Inst Radioisotopes & Radiodiagnost Prod, Athens 15310, Greece.
[Derhovanessian, Evelyna] Univ Tubingen, Tubingen Ageing & Tumour Immunol Grp, Med Res Ctr, Sch Med, D-72072 Tubingen, Germany.
C3 National & Kapodistrian University of Athens; National Centre of
Scientific Research "Demokritos"; Eberhard Karls University of Tubingen
RP Tsitsilonis, OE (corresponding author), Univ Athens, Dept Anim & Human Physiol, Fac Biol, Athens 15784, Greece.
EM rtsitsil@biol.uoa.gr
RI Tsitsilonis, Ourania/AAF-3168-2019
OI Samara, Pinelopi/0009-0001-2249-7068; Livaniou,
Evangelia/0000-0003-0165-9029
FU European Union [REGPOT-CT-2011-284460]; National Strategic Reference
Framework (NSRF); Deutscher Akademischer Austauschdienst (DAAD) [IKYDA
61/2003, IKYDA 165/2010]; BMBF [0315890F, 982838]
FX We thank Dr. Margarita Skopeliti for compiling the figure and critically
reading the manuscript. Co-financed by: the European Union (European
Social Fund-ESF) and Greek national funds through the Operational
Program "Education and Lifelong Learning" of the National Strategic
Reference Framework (NSRF)-Research Funding Program: Heracleitus II.
Investing in knowledge society through the European Social Fund (to K.
I.); the Hellenic State Scholarship Foundation (IKY) and the Deutscher
Akademischer Austauschdienst (DAAD), IKYDA 61/2003 and IKYDA 165/2010;
the European Union FP7 Capacities grant REGPOT-CT-2011-284460, INsPiRE;
NATO SfP Project 982838; "GERONTOSHIELD" (BMBF Project 0315890F).
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NR 117
TC 42
Z9 51
U1 2
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
EI 1432-0851
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD MAY
PY 2012
VL 61
IS 5
BP 599
EP 614
DI 10.1007/s00262-012-1222-8
PG 16
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA 935HL
UT WOS:000303509600001
PM 22366887
OA Green Published
DA 2025-01-07
ER
PT J
AU Askenase, PW
Szczepanik, M
Itakura, A
Kiener, C
Campos, RA
AF Askenase, PW
Szczepanik, M
Itakura, A
Kiener, C
Campos, RA
TI Extravascular T-cell recruitment requires initiation begun by
Vα14+ NKT cells and B-1B cells
SO TRENDS IN IMMUNOLOGY
LA English
DT Review
ID DELAYED-TYPE HYPERSENSITIVITY; NONOBESE DIABETIC MICE;
TUMOR-NECROSIS-FACTOR; B-CELLS; CONTACT SENSITIVITY; DEFICIENT MICE;
MAST-CELLS; PROTECTIVE IMMUNITY; AUTOIMMUNE-DISEASE; ACTIVATED RAS
AB Contact sensitivity and delayed hypersensitivity are principal in vivo models for recruitment of effector T cells into tissues. New data suggest that T-cell recruitment depends on an early antigen-specific 'initiation process'. To begin, glycolipids released following skin immunization induce Valpha14(+) invariant natural killer T cells in the liver to produce interleukin-4, which, together with dispersed antigen, coactivates specific peritoneal B-1 B cells to produce circulating antigen-specific IgM antibodies within just one day. At elicitation, these antibodies form complexes with the antigen, thereby activating complement locally, generating C5a; this acts on local mast cells and platelets to release vasoactive serotonin and tumor necrosis factor-alpha, leading to T-cell recruitment. Similar 'initiation processes' probably mediate the recruitment of effector T cells in autoimmunity, asthma, infections and cancers.
C1 Yale Univ, Sch Med, Dept Internal Med, Allergy & Clin Immunol Sect, New Haven, CT 06520 USA.
Jagiellonian Univ, Coll Med, Dept Human Dev Biol, PL-31121 Krakow, Poland.
C3 Yale University; Jagiellonian University; Collegium Medicum Jagiellonian
University
RP Yale Univ, Sch Med, Dept Internal Med, Allergy & Clin Immunol Sect, 333 Cedar St, New Haven, CT 06520 USA.
EM philip.askenase@yale.edu
RI Szczepanik, Marian/ABA-7001-2021
OI Szczepanik, Marian/0000-0002-0388-2382
FU NIAID NIH HHS [AI 07174, AI 059801] Funding Source: Medline
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TC 73
Z9 82
U1 0
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4906
EI 1471-4981
J9 TRENDS IMMUNOL
JI Trends Immunol.
PD AUG
PY 2004
VL 25
IS 8
BP 441
EP 449
DI 10.1016/j.it.2004.06.003
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 846EN
UT WOS:000223298200011
PM 15275644
DA 2025-01-07
ER
PT J
AU Tyler, A
Mahoney, JM
Carter, GW
AF Tyler, Anna
Mahoney, J. Matthew
Carter, Gregory W.
TI Genetic Interactions Affect Lung Function in Patients with Systemic
Sclerosis
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE Epistasis; Systemic Sclerosis; Scleroderma; Wnt Signaling
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; MESENCHYMAL TRANSITION ENDOMT;
ENDOTHELIAL GROWTH-FACTOR; HEPATOCELLULAR-CARCINOMA; SPHINGOSINE
1-PHOSPHATE; LYSOPHOSPHATIDIC ACID; PULMONARY-FIBROSIS; WEB SERVER;
EXPRESSION; PATHOGENESIS
AB Scleroderma, or systemic sclerosis (SSc), is an autoimmune disease characterized by progressive fibrosis of the skin and internal organs. The most common cause of death in people with SSc is lung disease, but the pathogenesis of lung disease in SSc is insufficiently understood to devise specific treatment strategies. Developing targeted treatments requires not only the identification of molecular processes involved in SSc-associated lung disease, but also understanding of how these processes interact to drive pathology. One potentially powerful approach is to identify alleles that interact genetically to influence lung outcomes in patients with SSc. Analysis of interactions, rather than individual allele effects, has the potential to delineate molecular interactions that are important in SSc-related lung pathology. However, detecting genetic interactions, or epistasis, in human cohorts is challenging. Large numbers of variants with low minor allele frequencies, paired with heterogeneous disease presentation, reduce power to detect epistasis. Here we present an analysis that increases power to detect epistasis in human genome-wide association studies (GWAS). We tested for genetic interactions influencing lung function and autoantibody status in a cohort of 416 SSc patients. Using Matrix Epistasis to filter SNPs followed by the Combined Analysis of Pleiotropy and Epistasis (CAPE), we identified a network of interacting alleles influencing lung function in patients with SSc. In particular, we identified a three-gene network comprising WNT5A, RBMS3, and MSI2, which in combination influenced multiple pulmonary pathology measures. The associations of these genes with lung outcomes in SSc are novel and high-confidence. Furthermore, gene coexpression analysis suggested that the interactions we identified are tissue-specific, thus differentiating SSc-related pathogenic processes in lung from those in skin.
C1 [Tyler, Anna; Carter, Gregory W.] Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA.
[Mahoney, J. Matthew] Univ Vermont, Larner Coll Med, Dept Neurol Sci, Burlington, VT USA.
[Mahoney, J. Matthew] Univ Vermont, Dept Comp Sci, Burlington, VT USA.
C3 Jackson Laboratory; University of Vermont; University of Vermont
RP Carter, GW (corresponding author), Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA.
EM gregory.carter@jax.org
FU National Institutes of Health [R01GM115518]
FX This work was supported by the National Institutes of Health grant
R01GM115518. Genotype and phenotype data for the Genome-Wide Association
Study in Systemic Sclerosis Study were provided by Maureen D. Mayes,
University of Texas Health Science Center, Houston, Texas. Funding
support for the original study was provided by the National Institutes
of Health, and by other sources detailed in Nat Genet. 2010
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NR 83
TC 6
Z9 7
U1 0
U2 6
PU GENETICS SOCIETY AMERICA
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 2160-1836
J9 G3-GENES GENOM GENET
JI G3-Genes Genomes Genet.
PD JAN
PY 2020
VL 10
IS 1
BP 151
EP 163
DI 10.1534/g3.119.400775
PG 13
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA KA8DP
UT WOS:000506031000014
PM 31694854
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU John, N
Ibrahim, B
Ebaid, M
Saab, S
AF John, Nimy
Ibrahim, Brittney
Ebaid, Mark
Saab, Sammy
TI Outcomes in Patients with Liver Dysfunction Post SARS-CoV-2 Infection:
What Should We Measure?
SO HEPATIC MEDICINE-EVIDENCE AND RESEARCH
LA English
DT Review
DE COVID-19; liver injury; cirrhosis; thrombosis; cholangiopathy
ID PORTAL-VEIN THROMBOSIS; B-VIRUS REACTIVATION; COVID-19; INJURY;
MANAGEMENT
AB Aim: Since 2019, the COVID-19 pandemic wreaked havoc all over the world. Early in the course of the pandemic, multiple hepatic manifestations of COVID-19 were noted. We aim to categorize hepatic dysfunction and its outcome in COVID-19 infection.Methods: This is a review article based on a literature search in PubMed and Medline databases for articles detailing short-term and long-term outcomes of COVID-19 related liver dysfunction.Results: The most common hepatic manifestation of COVID-19 was aspartate amino transferase (AST) predominant transaminase elevation. Transaminases improve once the COVID-19 infection resolves. In addition, COVID-19 cholangiopathy, autoimmune hepatitis associated COVID-19, and splanchnic venous thrombosis triggered by COVID-19 are other manifestations. Patients with preexisting liver disease, especially those with cirrhosis, have poor prognosis with COVID-19 infections compared to the general population. Elevations in liver tests were associated with severe COVID-19 infections. Patients with chronic liver disease have a higher risk of morbidity and mortality from COVID-19 infection. Among patients with chronic liver disease, decompensated liver cirrhosis, hepatocellular carcinoma and alcohol-associated liver disease were associated with an increased risk of severity and mortality from COVID-19 infection. Interactions between antiviral therapy for COVID-19 and hepatitis B/hepatitis C medications must be considered in patients with chronic viral hepatitis and COVID-19 infection. COVID-19 vaccination-related hepatic dysfunction has been reported.Conclusion: COVID-19 is here to stay. Hepatic dysfunction in COVID-19 signals severe COVID-19 infections. Patients with chronic liver disease have higher mortality from COVID-19 than general population. It is important to remember the lessons learned throughout the covid pandemic to take care of patients with COVID-19 now and in the future. Further studies are needed to document long-term outcomes in patients with COVID-19 who developed hepatic dysfunction.
C1 [John, Nimy; Saab, Sammy] Univ Calif Los Angeles, Dept Med, Los Angeles, CA USA.
[Ibrahim, Brittney; Ebaid, Mark; Saab, Sammy] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA USA.
[Saab, Sammy] Dept Med, 200 Med Plaza,Suite 214, Los Angeles, CA 90095 USA.
[Saab, Sammy] Dept Surg, 200 Med Plaza,Suite 214, Los Angeles, CA 90095 USA.
C3 University of California System; University of California Los Angeles;
University of California System; University of California Los Angeles
RP Saab, S (corresponding author), Univ Calif Los Angeles, Dept Surg, Los Angeles, CA USA.; Saab, S (corresponding author), Dept Med, 200 Med Plaza,Suite 214, Los Angeles, CA 90095 USA.; Saab, S (corresponding author), Dept Surg, 200 Med Plaza,Suite 214, Los Angeles, CA 90095 USA.
EM Ssaab@mednet.ucla.edu
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NR 81
TC 0
Z9 0
U1 3
U2 8
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1535
J9 HEPATIC MED-EVID RES
JI HEPATIC MED.-EVID. RES.
PY 2023
VL 15
BP 185
EP 193
DI 10.2147/HMER.S371507
PG 9
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA U6SA7
UT WOS:001086071000001
PM 37850074
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Hirano, T
AF Hirano, Toshio
TI IL-6 in inflammation, autoimmunity and cancer
SO INTERNATIONAL IMMUNOLOGY
LA English
DT Review
DE cytokine storm of COVID-19; IL-6 amplifier; local initiation model;
NF-kappa B; STAT3
ID NF-KAPPA-B; STIMULATORY FACTOR-II; EPITHELIAL-MESENCHYMAL TRANSITION;
REGULATORY T-CELLS; INSERTION DELETION POLYMORPHISM; HUMAN
HEPATOCELLULAR-CARCINOMA; TUMOR-ASSOCIATED MACROPHAGES; PERSISTENT STAT3
ACTIVATION; SERUM INTERLEUKIN-6 LEVELS; CYTOKINE RECEPTOR GP130
AB IL-6 is involved both in immune responses and in inflammation, hematopoiesis, bone metabolism and embryonic development. IL-6 plays roles in chronic inflammation (closely related to chronic inflammatory diseases, autoimmune diseases and cancer) and even in the cytokine storm of corona virus disease 2019 (COVID-19). Acute inflammation during the immune response and wound healing is a well-controlled response, whereas chronic inflammation and the cytokine storm are uncontrolled inflammatory responses. Non-immune and immune cells, cytokines such as IL-1 beta, IL-6 and tumor necrosis factor alpha (TNF alpha) and transcription factors nuclear factor-kappa B (NF-kappa B) and signal transducer and activator of transcription 3 (STAT3) play central roles in inflammation. Synergistic interactions between NF-kappa B and STAT3 induce the hyper-activation of NF-kappa B followed by the production of various inflammatory cytokines. Because IL-6 is an NF-kappa B target, simultaneous activation of NF-kappa B and STAT3 in non-immune cells triggers a positive feedback loop of NF-kappa B activation by the IL-6-STAT3 axis. This positive feedback loop is called the IL-6 amplifier (IL-6 Amp) and is a key player in the local initiation model, which states that local initiators, such as senescence, obesity, stressors, infection, injury and smoking, trigger diseases by promoting interactions between non-immune cells and immune cells. This model counters dogma that holds that autoimmunity and oncogenesis are triggered by the breakdown of tissue-specific immune tolerance and oncogenic mutations, respectively. The IL-6 Amp is activated by a variety of local initiators, demonstrating that the IL-6-STAT3 axis is a critical target for treating diseases.
C1 [Hirano, Toshio] Natl Inst Quantum & Radiol Sci & Technol, Inage Ku, 4-9-1 Anagawa, Chiba 2638555, Japan.
[Hirano, Toshio] Hokkaido Univ, Inst Genet Med, Div Mol Psychoimmunol, Sapporo, Hokkaido 0600815, Japan.
[Hirano, Toshio] Hokkaido Univ, Grad Sch Med, Sapporo, Hokkaido 0600815, Japan.
C3 National Institutes for Quantum Science & Technology; Hokkaido
University; Hokkaido University
RP Hirano, T (corresponding author), Natl Inst Quantum & Radiol Sci & Technol, Inage Ku, 4-9-1 Anagawa, Chiba 2638555, Japan.; Hirano, T (corresponding author), Hokkaido Univ, Inst Genet Med, Div Mol Psychoimmunol, Sapporo, Hokkaido 0600815, Japan.; Hirano, T (corresponding author), Hokkaido Univ, Grad Sch Med, Sapporo, Hokkaido 0600815, Japan.
EM hirano.toshio@qst.go.jp
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NR 377
TC 658
Z9 707
U1 36
U2 251
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0953-8178
EI 1460-2377
J9 INT IMMUNOL
JI Int. Immunol.
PD MAR
PY 2021
VL 33
IS 3
BP 127
EP 148
DI 10.1093/intimm/dxaa078
PG 22
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA RJ0HK
UT WOS:000637284100001
PM 33337480
OA hybrid, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Barisas, DAG
Choi, K
AF Barisas, Derek A. G.
Choi, Kyunghee
TI Extramedullary hematopoiesis in cancer
SO EXPERIMENTAL AND MOLECULAR MEDICINE
LA English
DT Review
ID COLONY-STIMULATING FACTOR; LEUKEMIA INHIBITORY FACTOR; BONE-MARROW
ADIPOCYTES; STEM-CELL NICHE; RECEPTOR TYROSINE KINASE; REDUCED CLINICAL
BENEFIT; TUMOR-NECROSIS-FACTOR; C-KIT RECEPTOR; SELF-RENEWAL; PROGENITOR
CELLS
AB Hematopoiesis can occur outside of the bone marrow during inflammatory stress to increase the production of primarily myeloid cells at extramedullary sites; this process is known as extramedullary hematopoiesis (EMH). As observed in a broad range of hematologic and nonhematologic diseases, EMH is now recognized for its important contributions to solid tumor pathology and prognosis. To initiate EMH, hematopoietic stem cells (HSCs) are mobilized from the bone marrow into the circulation and to extramedullary sites such as the spleen and liver. At these sites, HSCs primarily produce a pathological subset of myeloid cells that contributes to tumor pathology. The EMH HSC niche, which is distinct from the bone marrow HSC niche, is beginning to be characterized. The important cytokines that likely contribute to initiating and maintaining the EMH niche are KIT ligands, CXCL12, G-CSF, IL-1 family members, LIF, TNF alpha, and CXCR2. Further study of the role of EMH may offer valuable insights into emergency hematopoiesis and therapeutic approaches against cancer. Exciting future directions for the study of EMH include identifying common and distinct EMH mechanisms in cancer, infectious diseases, and chronic autoimmune diseases to control these conditions.
Changes to hematopoiesis, or the creation of blood and immune cells, in cancers are the focus of this review by Barisas et al. They discuss conditions that promote extramedullary hematopoiesis (EMH), which produces blood cells outside the bone marrow. They also discuss the impact of tumor-derived factors, including interleukin-1 alpha and leukemia inhibitory factor, on EMH. The team recently discovered that these specific factors stimulate the development of myeloid cells known for suppressing the immune system and aiding tumor growth. This suggests that targeting the pathways associated with these elements could be a new approach to cancer treatment. Research also indicates that EMH might be a common characteristic in other inflammation-related diseases, providing unique opportunities for further studies.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
C1 [Barisas, Derek A. G.; Choi, Kyunghee] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
C3 Washington University (WUSTL)
RP Choi, K (corresponding author), Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
EM kchoi@wustl.edu
OI Choi, Kyunghee/0000-0002-9634-9375
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NR 235
TC 7
Z9 7
U1 1
U2 2
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1226-3613
EI 2092-6413
J9 EXP MOL MED
JI Exp. Mol. Med.
PD MAR
PY 2024
VL 56
IS 3
BP 549
EP 558
DI 10.1038/s12276-024-01192-4
EA MAR 2024
PG 10
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA MR6O6
UT WOS:001178988200004
PM 38443597
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kim, JH
Byun, JH
Kim, MH
Lee, SK
Kim, SC
Kim, HJ
Lee, SS
Kim, SY
Lee, MG
AF Kim, Jin Hee
Byun, Jae Ho
Kim, Myung-Hwan
Lee, Sung Koo
Kim, Song Cheol
Kim, Hyoung Jung
Lee, Seung Soo
Kim, So Yeon
Lee, Moon-Gyu
TI Pancreatic Duct in Autoimmune Pancreatitis Intraindividual Comparison
of Magnetic Resonance Pancreatography at 1.5 T and 3.0 T
SO PANCREAS
LA English
DT Article
DE pancreatitis; autoimmune disease; magnetic resonance imaging; magnetic
resonance cholangiopancreatography; endoscopic retrograde
cholangiopancreatography
ID MAGNETIC-RESONANCE CHOLANGIOPANCREATOGRAPHY; 3.0 T; DIAGNOSTIC-CRITERIA;
MR CHOLANGIOGRAPHY; CANCER; LIVER; CONSENSUS; STRATEGY; ERCP
AB Objective: The aim of this study was to intraindividually compare magnetic resonance pancreatography (MRP) image quality at 1.5 T and 3.0 T when demonstrating main pancreatic duct (MPD) abnormalities in patients with autoimmune pancreatitis (ATP).
Methods: Thirty prospectively enrolled patients with AIP underwent MRP at both 1.5 T and 3.0 T followed by endoscopic retrograde pancreatography before treatment. Two readers independently analyzed the MRP images and graded the visualization of MPD strictures and full-length MPD, using endoscopic retrograde pancreatography as the reference standard, as well as overall image artifacts on a 4-point scale. The contrast between the MPD and periductal area was calculated using a region-of-interest measurement.
Results: Visualization scores of MPD strictures and full-length MPD, and summed scores of each qualitative analysis, were significantly greater at 3.0-T MRP than at 1.5-T MRP for both readers (P <= 0.02). There were less image artifacts at 3.0 T compared with 1.5 T (P <= 0.052). The contrast between the MPD and periductal area was significantly greater at 3.0-T MRP than at 1.5-T MRP (P < 0.001).
Conclusions: The MRP at 3.0 T was superior to 1.5-T MRP for demonstrating MPD abnormalities in AIP, with better image contrast and fewer image artifacts. Consequently, 3.0-T MRP may be useful for the diagnosis and management of patients with AIP.
C1 [Kim, Jin Hee; Byun, Jae Ho; Kim, Hyoung Jung; Lee, Seung Soo; Kim, So Yeon; Lee, Moon-Gyu] Univ Ulsan, Coll Med, Dept Radiol, Seoul, South Korea.
[Kim, Jin Hee; Byun, Jae Ho; Kim, Hyoung Jung; Lee, Seung Soo; Kim, So Yeon; Lee, Moon-Gyu] Univ Ulsan, Coll Med, Res Inst Radiol, Seoul, South Korea.
[Kim, Myung-Hwan; Lee, Sung Koo] Univ Ulsan, Coll Med, Dept Internal Med, Seoul, South Korea.
[Kim, Song Cheol] Univ Ulsan, Coll Med, Dept Surg, Seoul, South Korea.
C3 University of Ulsan; University of Ulsan; University of Ulsan;
University of Ulsan
RP Byun, JH (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Dept Radiol, 88 Olymp Ro, Seoul 05505, South Korea.; Byun, JH (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Res Inst Radiol, 88 Olymp Ro, Seoul 05505, South Korea.
EM jhbyun@amc.seoul.kr
RI Kim, Seongman/N-6910-2014; Lee, Seung/AAP-3250-2020; Kim,
Sung/G-4114-2014; ZHANG, GUO/D-2556-2014
FU Guerbet Korea (Seoul, South Korea)
FX This study (J.H.B.) has received funding from Guerbet Korea (Seoul,
South Korea).
CR Chari ST, 2009, CLIN GASTROENTEROL H, V7, P1097, DOI 10.1016/j.cgh.2009.04.020
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U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD AUG
PY 2017
VL 46
IS 7
BP 921
EP 926
DI 10.1097/MPA.0000000000000853
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FA5YE
UT WOS:000405519400012
PM 28697133
DA 2025-01-07
ER
PT J
AU Talangescu, A
Calenic, B
Mihailescu, DF
Tizu, M
Maruntelu, I
Constantinescu, AE
Constantinescu, I
AF Talangescu, Adriana
Calenic, Bogdan
Mihailescu, Dan Florin
Tizu, Maria
Maruntelu, Ion
Constantinescu, Alexandra E.
Constantinescu, Ileana
TI Molecular Analysis of HLA Genes in Romanian Patients with Chronic
Hepatitis B Virus Infection
SO CURRENT ISSUES IN MOLECULAR BIOLOGY
LA English
DT Article
DE next-generation sequencing (NGS); human leukocyte antigens (HLAs);
hepatitis B virus (HBV); amino acid residues
ID GENOME-WIDE ASSOCIATION; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS;
ALLELES; RISK; SUSCEPTIBILITY; POLYMORPHISM; CLEARANCE; OUTCOMES;
VACCINE
AB Hepatitis B, a persistent inflammatory liver condition, stands as a significant global health issue. In Romania, the prevalence of chronic hepatitis B virus (CHB) infection ranks among the highest in the European Union. The HLA genotype significantly impacts hepatitis B virus infection progression, indicating that certain HLA variants can affect the infection's outcome. The primary goal of the present work is to identify HLA alleles and specific amino acid residues linked to hepatitis B within the Romanian population. The study enrolled 247 patients with chronic hepatitis B; HLA typing was performed using next-generation sequencing. This study's main findings include the identification of certain HLA alleles, such as DQB1*06:03:01, DRB1*13:01:01, DQB1*06:02:01, DQA1*01:03:01, DRB5*01:01:01, and DRB1*15:01:01, which exhibit a significant protective effect against HBV. Additionally, the amino acid residue alanine at DQB1_38 is associated with a protective role, while valine presence may signal an increased risk of hepatitis B. The present findings are important in addressing the urgent need for improved methods of diagnosing and managing CHB, particularly when considering the disease's presence in diverse population groups and geographical regions.
C1 [Talangescu, Adriana; Calenic, Bogdan; Tizu, Maria; Maruntelu, Ion; Constantinescu, Alexandra E.; Constantinescu, Ileana] Carol Davila Univ Med & Pharm, Immunol & Transplant Immunol, 258 Fundeni Ave, Bucharest 022328, Romania.
[Talangescu, Adriana; Tizu, Maria; Maruntelu, Ion; Constantinescu, Ileana] Fundeni Clin Inst, Ctr Immunogenet & Virol, 258 Fundeni Ave, Bucharest 022328, Romania.
[Mihailescu, Dan Florin] Univ Bucharest, Dept Anat Anim Physiol & Biophys, Fac Biol, Splaiul Independentei St 91-95, Bucharest 050095, Romania.
C3 Carol Davila University of Medicine & Pharmacy; Institutul Clinic
Fundeni; University of Bucharest
RP Calenic, B (corresponding author), Carol Davila Univ Med & Pharm, Immunol & Transplant Immunol, 258 Fundeni Ave, Bucharest 022328, Romania.
EM adriana.oprea@drd.umfcd.ro; bcalenic@yahoo.co.uk;
d.f.mihailescu@gmail.com; maria.tizu@drd.umfcd.ro;
ionutz.marion@gmail.com; alexandra.constantinescu08@gmail.com;
ileana.constantinescu@imunogenetica.ro
RI Maruntelu, Ion/IAM-2516-2023; Constantinescu, Ileana/AAE-2194-2022;
Maruntelu, Ion/LMP-5161-2024; Mihailescu, Dan/AAG-2975-2021
OI Maruntelu, Ion/0000-0002-4284-8654; Mihailescu, Dan/0000-0001-6398-5837
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NR 59
TC 4
Z9 4
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1467-3037
EI 1467-3045
J9 CURR ISSUES MOL BIOL
JI Curr. Issues Mol. Biol.
PD FEB
PY 2024
VL 46
IS 2
BP 1064
EP 1077
DI 10.3390/cimb46020067
PG 14
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA JH2X7
UT WOS:001172219600001
PM 38392185
OA gold
DA 2025-01-07
ER
PT J
AU Nakazawa, T
Naitoh, I
Hayashi, K
Okumura, F
Miyabe, K
Yoshida, M
Yamashita, H
Ohara, H
Joh, T
AF Nakazawa, Takahiro
Naitoh, Itaru
Hayashi, Kazuki
Okumura, Fumihiro
Miyabe, Katsuyuki
Yoshida, Michihiro
Yamashita, Hiroaki
Ohara, Hirotaka
Joh, Takashi
TI Diagnostic criteria for IgG4-related sclerosing cholangitis based on
cholangiographic classification
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune pancreatitis; Diagnostic criteria; IgG4-related sclerosing
cholangitis; Primary sclerosing cholangitis: IgG4-SC
ID AUTOIMMUNE PANCREATITIS; EXTRAPANCREATIC LESIONS
AB IgG4-related sclerosing cholangitis (IgG4-SC) needs to be differentiated from pancreatic cancer (PCa), primary sclerosing cholangitis (PSC), and cholangiocarcinoma (CC). We attempted to establish diagnostic criteria for IgG4-SC based on cholangiographic classification by comparison with several diagnostic modalities.
We classified 62 IgG4-SC patients into three groups on the basis of cholangiographic findings to allow differentiation from PCa, PSC, and CC: Group A IgG4-SC showed features similar to PCa (Type 1, n = 32), Group B showed similarity to PSC (Type 2, n = 15), and Group C showed similarity to CC (Type 3, 4, n = 15). Thirty-five patients with PCa, 40 with PSC, and 32 CC were enrolled as controls. We retrospectively compared the clinical, imaging, serological, and histopathological features and involvement of other organs between Group A and PCa, Group B and PSC, and Group C and CC.
Association with autoimmune pancreatitis (AIP) (P < 0.001) and involvements with other organs (specificity 100%) were common useful diagnostic parameters in all three IgG4-SC groups. A high serum IgG4 level was a useful parameter in Groups A and B (P < 0.001). Discriminant analysis of cholangiograms (P < 0.001), liver biopsy (specificity 100%), and exclusion of inflammatory bowel disease (specificity 100%) were useful parameters in Group B. Intraductal ultrasonography findings (P < 0.001) and exclusion of malignancy by bile duct biopsy (specificity 100%) were useful parameters in Group C. We established diagnostic criteria for IgG4-SC (sensitivity 100%, specificity 96.3%) by incorporating parameters that showed P < 0.001 or 100% specificity.
Diagnostic criteria for IgG4-SC based on cholangiographic classification are useful for distinguishing it from PCa, PSC, and CC.
C1 [Nakazawa, Takahiro; Naitoh, Itaru; Hayashi, Kazuki; Okumura, Fumihiro; Miyabe, Katsuyuki; Yoshida, Michihiro; Yamashita, Hiroaki; Joh, Takashi] Nagoya City Univ, Grad Sch Med Sci, Dept Gastroenterol & Metab, Mizuho Ku, Nagoya, Aichi 4678601, Japan.
[Ohara, Hirotaka] Nagoya City Univ, Grad Sch Med Sci, Dept Community Based Med Educ, Nagoya, Aichi 4678601, Japan.
C3 Nagoya City University; Nagoya City University
RP Nakazawa, T (corresponding author), Nagoya City Univ, Grad Sch Med Sci, Dept Gastroenterol & Metab, Mizuho Ku, 1 Kawasumi,Mizuho Cho, Nagoya, Aichi 4678601, Japan.
EM tnakazaw@med.nagoya-cu.ac.jp
RI ; Naitoh, Itaru/AAB-7252-2020
OI Miyabe, Katsuyuki/0000-0002-4915-9835; Naitoh, Itaru/0000-0001-8342-886X
FU Ministry of Culture and Science of Japan [23591015, 23790803]; Ministry
of Health, Labor and Welfare of Japan; Grants-in-Aid for Scientific
Research [23591015, 23790803] Funding Source: KAKEN
FX This study was partly supported by a Grant-in-Aid for Scientific
Research from the Ministry of Culture and Science of Japan (23591015,
23790803) and a Grant-in-Aid for the "Research for Intractable Disease"
Program from the Ministry of Health, Labor and Welfare of Japan.
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NR 19
TC 88
Z9 99
U1 0
U2 6
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JAN
PY 2012
VL 47
IS 1
BP 79
EP 87
DI 10.1007/s00535-011-0465-z
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 892NC
UT WOS:000300291900010
PM 21947649
DA 2025-01-07
ER
PT J
AU Kamisawa, T
Okazaki, K
Kawa, S
Shimosegawa, T
Tanaka, M
AF Kamisawa, Terumi
Okazaki, Kazuichi
Kawa, Shigeyuki
Shimosegawa, Tooru
Tanaka, Masao
CA Res Comm Intractable Pancreatic
Japan Pancreas Soc
TI Japanese consensus guidelines for management of autoimmune pancreatitis:
III. Treatment and prognosis of AIP
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Autoimmune pancreatitis; Steroid therapy; IgG4
ID LYMPHOPLASMACYTIC SCLEROSING PANCREATITIS; LONG-TERM PROGNOSIS;
STEROID-THERAPY; CORTICOSTEROID TREATMENT; DIABETES-MELLITUS; EXOCRINE
FUNCTION; CANCER; ENDOCRINE; REMISSION; PROPOSAL
AB Steroid therapy appeared to be a standard treatment for autoimmune pancreatitis (AIP), although some AIP patients improve spontaneously. The indications for steroid therapy in AIP patients are symptoms such as obstructive jaundice, abdominal pain, and back pain, and the presence of symptomatic extrapancreatic lesions. Before steroid therapy, jaundice should be managed by biliary drainage in patients with obstructive jaundice, and blood glucose levels should be controlled in patients with diabetes mellitus. For the initial oral prednisolone dose for induction of remission, 0.6 mg/kg/day is recommended. The initial dose is administered for 2-4 weeks, and the dose is tapered by 5 mg every 1-2 weeks, based on changes in the clinical manifestations, biochemical blood tests (such as liver enzymes and IgG or IgG4 levels), and repeated imaging findings (US, CT, MRCP, ERCP, etc.). The dose is tapered to a maintenance dose (2.5-5 mg/day) over a period of 2-3 months. Steroid therapy should be stopped based on the disease activity in each case. Stopping of maintenance therapy should be planned within at least 3 years in cases with radiological and serological improvement. Re-administration or dose-up of steroid is effective for treating AIP relapses. The prognosis of AIP appears to be good over the short-term with steroid therapy. It is unclear whether the long-term outcome is good because there are many unknown factors, such as relapse, pancreatic exocrine or endocrine dysfunction, and associated malignancy.
C1 [Kamisawa, Terumi] Tokyo Metropolitan Komagome Hosp, Dept Internal Med, Bunkyo Ku, Tokyo 1138677, Japan.
[Okazaki, Kazuichi] Kansai Med Univ, Dept Gastroenterol & Hepatol, Osaka, Japan.
[Kawa, Shigeyuki] Shinshu Univ, Ctr Hlth Safety & Environm Management, Matsumoto, Nagano 390, Japan.
[Shimosegawa, Tooru] Tohoku Univ, Grad Sch Med, Div Gastroenterol, Sendai, Miyagi 980, Japan.
[Tanaka, Masao] Kyushu Univ, Grad Sch Med Sci, Dept Surg & Oncol, Fukuoka 812, Japan.
C3 Tokyo Metropolitan Cancer & Infectious Diseases Center Komagome
Hospital; Kansai Medical University; Shinshu University; Tohoku
University; Kyushu University
RP Kamisawa, T (corresponding author), Tokyo Metropolitan Komagome Hosp, Dept Internal Med, Bunkyo Ku, 3-18-22 Honkomagome, Tokyo 1138677, Japan.
EM kamisawa@cick.jp
FU Ministry of Labor, Health, and Welfare of Japan
FX This study was supported by the grant-in-aid for the Refractory
Pancreatic Disease from the Ministry of Labor, Health, and Welfare of
Japan.
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NR 39
TC 200
Z9 243
U1 0
U2 12
PU SPRINGER TOKYO
PI TOKYO
PA 1-11-11 KUDAN-KITA, CHIYODA-KU, TOKYO, 102-0073, JAPAN
SN 0944-1174
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD MAY
PY 2010
VL 45
IS 5
BP 471
EP 477
DI 10.1007/s00535-010-0221-9
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 595IB
UT WOS:000277602800001
PM 20213336
DA 2025-01-07
ER
PT J
AU Jin, BF
Shen, HX
Lin, SB
Li, JL
Chen, ZR
Griffin, JD
Wu, LZ
AF Jin, Baofeng
Shen, Huangxuan
Lin, Shuibin
Li, Jian-Liang
Chen, Zirong
Griffin, James D.
Wu, Lizi
TI The Mastermind-like 1 (MAML1) Co-activator Regulates Constitutive NF-κB
Signaling and Cell Survival
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TRANSCRIPTIONAL COACTIVATORS; NOTCH RECEPTORS; EMBRYONIC LETHALITY;
LIVER-REGENERATION; MICE LACKING; CROSS-TALK; APOPTOSIS; ALPHA;
EXPRESSION; PATHWAY
AB Nuclear factor-kappa B (NF-kappa B)-based signaling regulates diverse biological processes, and its deregulation is associated with various disorders including autoimmune diseases and cancer. Identification of novel factors that modulate NF-kappa B function is therefore of significant importance. The Mastermind-like 1 (MAML1) transcriptional co-activator regulates transcriptional activity in the Notch pathway and is emerging as a co-activator of other pathways. In this study, we found that MAML1 regulates NF-kappa B signaling via two mechanisms. First, MAML1 coactivates the NF-kappa B subunit RelA (p65) in NF-kappa B-dependent transcription. Second, MAML1 causes degradation of the inhibitor of NF-kappa B (I kappa B alpha). Maml1-deficient mouse embryonic fibroblasts showed impaired tumor necrosis factor-alpha (TNF alpha)-induced NF-kappa B responses. Moreover, MAML1 expression level directly influences cellular sensitivity to TNF alpha-induced cytotoxicity. In vivo, mice deficient in the Maml1 gene exhibited spontaneous cell death in the liver, with a large increase in the number of apoptotic hepatic cells. These findings indicate that MAML1 is a novel modulator for NF-kappa B signaling and regulates cellular survival.
C1 Univ Florida, Shands Canc Ctr, Dept Mol Genet & Microbiol, Gainesville, FL 32610 USA.
[Li, Jian-Liang] Univ Florida, Interdisciplinary Ctr Biotechnol Res, Gainesville, FL 32610 USA.
[Griffin, James D.] Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Griffin, James D.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
C3 State University System of Florida; University of Florida; State
University System of Florida; University of Florida; Harvard University;
Dana-Farber Cancer Institute; Brigham & Women's Hospital; Harvard
University; Harvard Medical School
RP Wu, LZ (corresponding author), 2033 Mowry Rd, Gainesville, FL 32610 USA.
EM lzwu@ufl.edu
RI Li, Jian-Liang/AAE-9315-2019; lin, shuibin/F-6015-2015; Chen,
Zirong/S-4042-2016
OI Li, Jian-Liang/0000-0002-6487-081X; Wu, Lizi/0000-0002-0076-2617
FU National Institutes of Health [R01 CA097148, R01 CA036167]; University
of Florida Shands Cancer Center
FX This work was supported, in whole or in part, by National Institutes of
Health Grant R01 CA097148. This work was also supported by the
University of Florida Shands Cancer Center startup fund (to L. W.) and
National Institutes of Health Grant R01 CA036167 (to J. D. G.).
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NR 36
TC 31
Z9 35
U1 0
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 7
PY 2010
VL 285
IS 19
BP 14356
EP 14365
DI 10.1074/jbc.M109.078865
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 591KQ
UT WOS:000277299700033
PM 20231278
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Yosri, M
Dokhan, M
Aboagye, E
Al Moussawy, M
Abdelsamed, HA
AF Yosri, Mohammed
Dokhan, Mohamed
Aboagye, Elizabeth
Al Moussawy, Mouhamad
Abdelsamed, Hossam A.
TI Mechanisms governing bystander activation of T cells
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE T cells; bystander; activation; cytokines; peptide/MHC complex;
cross-reactivity
ID MEMORY CD8(+) T; PRIMARY BILIARY-CIRRHOSIS; MHC CLASS-I; HOMEOSTATIC
PROLIFERATION; CUTTING EDGE; ATHEROSCLEROTIC PLAQUES;
LIVER-TRANSPLANTATION; AUTOIMMUNE ARTHRITIS; DISEASE RECURRENCE; COGNATE
ANTIGEN
AB The immune system is endowed with the capacity to distinguish between self and non-self, so-called immune tolerance or "consciousness of the immune system." This type of awareness is designed to achieve host protection by eliminating cells expressing a wide range of non-self antigens including microbial-derived peptides. Such a successful immune response is associated with the secretion of a whole spectrum of soluble mediators, e.g., cytokines and chemokines, which not only contribute to the clearance of infected host cells but also activate T cells that are not specific to the original cognate antigen. This kind of non-specific T-cell activation is called "bystander activation." Although it is well-established that this phenomenon is cytokine-dependent, there is evidence in the literature showing the involvement of peptide/MHC recognition depending on the type of T-cell subset (naive vs. memory). Here, we will summarize our current understanding of the mechanism(s) of bystander T-cell activation as well as its biological significance in a wide range of diseases including microbial infections, cancer, auto- and alloimmunity, and chronic inflammatory diseases such as atherosclerosis.
C1 [Yosri, Mohammed] Al Azhar Univ, Reg Ctr Mycol & Biotechnol, Cairo, Egypt.
[Dokhan, Mohamed; Aboagye, Elizabeth; Abdelsamed, Hossam A.] Augusta Univ, MCG, Immunol Ctr Georgia IMMCG, Augusta, GA 30912 USA.
[Al Moussawy, Mouhamad] Univ Pittsburgh, Sch Med, Starzl Transplantat Inst, Pittsburgh, PA 15238 USA.
[Abdelsamed, Hossam A.] Augusta Univ, Dept Physiol, Augusta, GA 30904 USA.
C3 Egyptian Knowledge Bank (EKB); Al Azhar University; University System of
Georgia; Augusta University; Pennsylvania Commonwealth System of Higher
Education (PCSHE); University of Pittsburgh; University System of
Georgia; Augusta University
RP Abdelsamed, HA (corresponding author), Augusta Univ, MCG, Immunol Ctr Georgia IMMCG, Augusta, GA 30912 USA.; Al Moussawy, M (corresponding author), Univ Pittsburgh, Sch Med, Starzl Transplantat Inst, Pittsburgh, PA 15238 USA.; Abdelsamed, HA (corresponding author), Augusta Univ, Dept Physiol, Augusta, GA 30904 USA.
EM mmoussawy@gmail.com; habdelsamed@augusta.edu
FU Medical College of Georgia; Augusta University; IMMCG
FX The author(s) declare financial support was received for the research,
authorship, and/or publication of this article. IMMCG, Medical College
of Georgia, Augusta University start up funds were used for publication
fees.
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NR 210
TC 0
Z9 0
U1 1
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD NOV 27
PY 2024
VL 15
AR 1465889
DI 10.3389/fimmu.2024.1465889
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA P0H4O
UT WOS:001374828300001
PM 39669576
DA 2025-01-07
ER
PT J
AU Zhang, YN
Yu, SF
Li, XM
Yang, BY
Wu, CY
AF Zhang, Yannan
Yu, Sifei
Li, Xiaomin
Yang, Binyan
Wu, Changyou
TI The ligands of translocator protein inhibit human Th1 responses and the
rejection of murine skin allografts
SO CLINICAL SCIENCE
LA English
DT Article
DE CD4(+) T-cells; skin allografts; TCR signal transduction; Th1 responses;
TSPO ligands
ID PERIPHERAL BENZODIAZEPINE-RECEPTOR; HEPATOCELLULAR-CARCINOMA CELLS;
POSITRON-EMISSION-TOMOGRAPHY; DIAZEPAM-BINDING INHIBITOR; HUMAN
MONONUCLEAR-CELLS; 18 KDA TSPO; MULTIPLE-SCLEROSIS; ALZHEIMERS-DISEASE;
CYCLE ARREST; HELPER T
AB The translocator protein (TSPO) ligands affected inflammatory and immune responses. However, the exact effects of TSPO ligands on Th1 responses in vitro and in vivo are still unclear. In the present study, we found that TSPO ligands, FGIN1-27 and Ro5-4864, suppressed the cytokine production in a dose-dependent manner by purified human CD4(+) T-cells from peripheral blood mononuclear cells (PBMCs) after stimulation. TSPO ligands inhibited the production of interferon gamma (IFN-gamma) by memory CD4+ T-cells and the differentiation of naive CD4+ T-cells into Th1 cells via suppressing the activity of the corresponding transcription factors as indicated by reduced expression of T-bet and down-regulation of STAT1, STAT4 and STAT5 phosphorylation. TSPO ligands suppressed cell proliferation and activation of CD4+ T-cells by the inhibition of TCR signal transduction including membrane proteins: Zap, Lck, Src; cytoplasm proteins: Plc gamma 1, Slp-76, ERK, JNK and the nucleoproteins: c-Jun and c-Fos. In addition, FGIN1-27 inhibited mixed lymphocyte reactions by human or murine cells. After the transplantation of allogeneic murine skin, injection of FGIN1-27 into mice prevented graft rejection by inhibition of cell infiltration and IFN-gamma production. Taken together, our data suggest that TSPO ligands inhibit Th1 cell responses and might be novel therapeutic medicine for the treatment of autoimmune diseases and prevention of transplant rejection.
C1 [Zhang, Yannan; Yu, Sifei; Li, Xiaomin; Yang, Binyan; Wu, Changyou] Sun Yat Sen Univ, Zhongshan Sch Med, Guangdong Prov Key Lab Organ Donat & Transplant I, Inst Immunol, Guangzhou 510080, Guangdong, Peoples R China.
C3 Sun Yat Sen University
RP Wu, CY (corresponding author), Sun Yat Sen Univ, Zhongshan Sch Med, Guangdong Prov Key Lab Organ Donat & Transplant I, Inst Immunol, Guangzhou 510080, Guangdong, Peoples R China.
EM changyou_wu@yahoo.com
FU Guangdong Provincial Key Laboratory Construction Projection on Organ
Donation and Transplant Immunology [2013A061401007]; National Natural
Science Foundation of China [31470888]
FX This work was supported by the Guangdong Provincial Key Laboratory
Construction Projection on Organ Donation and Transplant Immunology
[grant number 2013A061401007]; and the National Natural Science
Foundation of China [grant number 31470888].
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NR 31
TC 6
Z9 7
U1 0
U2 8
PU PORTLAND PRESS LTD
PI LONDON
PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND
SN 0143-5221
EI 1470-8736
J9 CLIN SCI
JI Clin. Sci.
PD FEB 1
PY 2017
VL 131
IS 4
BP 297
EP 308
DI 10.1042/CS20160547
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA EK9KU
UT WOS:000394244200004
PM 27923881
DA 2025-01-07
ER
PT J
AU Yin, HB
Tian, Y
Luo, RY
Deng, YP
AF Yin, Hongbo
Tian, Yan
Luo, Rongying
Deng, Yingping
TI Thymic Stromal Lymphopoietin Is Expressed in Human Corneal Stromal Cells
and Secreted upon Protease-Activated Receptor 1 Activation
SO IUBMB LIFE
LA English
DT Article
DE thymic stromal lymphopoietin; human corneal stromal cell;
protease-activated receptor 1; matrix metalloprotease
ID EPITHELIAL-CELLS; MOLECULAR-CLONING; TSLP; KERATOCONUS; CYTOKINE;
THROMBIN
AB Thymic stromal lymphopoietin (TSLP) is an interleukin-7 (IL-7) like cytokine that triggers inflammatory responses through activating dendritic cell. It is demonstrated to be involved in a number of disorders, including cancer, gastrointestinal diseases, and autoimmune diseases. In addition, TSLP is also found to be able to induce itch sensation by directly activating the itch sensory neurons. The expression of human TSLP is detected in various tissues such as heart, liver, testis, and prostate. In this study, we report that TSLP was expressed in the human corneal stromal cells, the highly specialized cells that are critical for the function of the cornea. Furthermore, we found that activation of the protease-activated receptor 1 (PAR1) induced secretion of TSLP by the corneal stromal cells. Beside the canonical activator thrombin, PAR1 can also be activated by a few matrix metalloproteases (MMPs) such as MMP1 and MMP13. Since MMPs including MMP1 and MMP13 are upregulated in many corneal diseases as well as the corneal wound healing process, we proposed that TSLP might function as the link between increased protease activity and inflammatory responses or itch sensation in the corneas. (C) 2017 IUBMB Life
C1 [Yin, Hongbo; Tian, Yan; Luo, Rongying; Deng, Yingping] Sichuan Univ, West China Hosp, Dept Ophthalmol, 37 Guo Xue Xiang, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University
RP Deng, YP (corresponding author), Sichuan Univ, West China Hosp, Dept Ophthalmol, 37 Guo Xue Xiang, Chengdu 610041, Sichuan, Peoples R China.
EM ypd_wch@163.com
RI Yin, Hongbo/KVY-9590-2024
FU China National Natural Science [31200711]
FX This study was supported by China National Natural Science (Grant No.
31200711).
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NR 29
TC 1
Z9 1
U1 0
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1521-6543
EI 1521-6551
J9 IUBMB LIFE
JI IUBMB Life
PD AUG
PY 2017
VL 69
IS 8
BP 606
EP 610
DI 10.1002/iub.1644
PG 5
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA FC5ZS
UT WOS:000406920800005
PM 28631887
OA Bronze
DA 2025-01-07
ER
PT J
AU Liu, CJ
Chang, YS
Teng, CJ
Chen, TJ
Ou, SM
Tzeng, CH
Wang, SJ
AF Liu, C. -J.
Chang, Y. -S.
Teng, C. -J.
Chen, T. -J.
Ou, S. -M.
Tzeng, C. -H.
Wang, S. -J.
TI Risk of extrathymic cancer in patients with myasthenia gravis in Taiwan:
a nationwide population-based study
SO EUROPEAN JOURNAL OF NEUROLOGY
LA English
DT Article
DE autoimmune disease; cancer risk; extrathymic malignancy;
immunosuppressant; myasthenia gravis
ID THYMOMA; MALIGNANCIES; AZATHIOPRINE; AUTOIMMUNITY
AB Background and purpose: The relationship between myasthenia gravis (MG) and extrathymic malignancies has not been determined. This study aimed to explore the risk of extrathymic malignancy in patients with MG based on a nationwide population-based dataset.
Methods: We identified 2614 patients with MG from the Taiwan National Health Insurance database between 1997 and 2005 and compared the incidence rates of extrathymic malignancies with 15 684 randomly selected age-, sex-, and comorbidity-matched subjects without MG. Both cohorts were followed until the end of 2009. Cox proportional hazard model was used to evaluate the predictors of extrathymic malignancy in the MG cohort, including age, sex, comorbidities, and prescription drugs.
Results: After an average follow-up of 8 years, the MG cohort had a higher risk of extrathymic cancers with an incidence rate ratio (IRR) of 1.38 (95% CI 1.12-1.68, P = 0.002) than the control cohort. Although breast cancer was the most common cancer found, no statistically significant relationship between MG and any specific malignancy was observed. Cox multivariate proportional hazards analysis showed that only age (HR = 1.05, 95% CI 1.04-1.06, P < 0.001) and liver cirrhosis (IRR = 3.85, 95% CI 1.22-12.14, P = 0.021) were predictors of extrathymic cancers in the MG cohort.
Conclusions: Our study showed that patients with MG had an increased risk of extrathymic malignancy in a follow-up of 8 years, but no specific susceptibility to certain malignancies was found.
C1 [Wang, S. -J.] Taipei Vet Gen Hosp, Dept Neurol, Neurol Inst, Taipei 112, Taiwan.
[Liu, C. -J.; Tzeng, C. -H.] Taipei Vet Gen Hosp, Dept Med, Div Hematol & Oncol, Taipei 112, Taiwan.
[Liu, C. -J.; Chang, Y. -S.; Teng, C. -J.; Chen, T. -J.; Tzeng, C. -H.; Wang, S. -J.] Natl Yang Ming Univ, Sch Med, Taipei 112, Taiwan.
[Chang, Y. -S.] Taipei Vet Gen Hosp, Dept Med, Div Allergy Immunol & Rheumatol, Taipei 112, Taiwan.
[Teng, C. -J.] Natl Yang Ming Univ Hosp, Dept Med, Div Hematol & Oncol, Yilan, Taiwan.
[Chen, T. -J.] Taipei Vet Gen Hosp, Dept Family Med, Taipei 112, Taiwan.
[Ou, S. -M.] Taipei Vet Gen Hosp, Dept Med, Div Nephrol, Taipei 112, Taiwan.
C3 Taipei Veterans General Hospital; Taipei Veterans General Hospital;
National Yang Ming Chiao Tung University; Taipei Veterans General
Hospital; Taipei Veterans General Hospital; Taipei Veterans General
Hospital
RP Wang, SJ (corresponding author), Taipei Vet Gen Hosp, Dept Neurol, Neurol Inst, 201 Shih Pai Rd,Sec 2, Taipei 112, Taiwan.
EM sjwang@vghtpe.gov.tw
RI Chen, TJ/AAH-8430-2021; Chen, Wei-Yu/ABH-4523-2020; Shou Ming,
Ou/GPJ-9589-2022; Liu, Chen-Hua/F-6608-2018
OI Wang, Shuu-Jiun/0000-0001-5179-5358; Teng, Chung-Jen/0000-0003-3517-3131
FU Taipei Veterans General Hospital [VGHUST 100-G7-1-1, V100D-002-3];
National Science Council support for the Center for Dynamical Biomarkers
and Translational Medicine, National Central University, Taiwan [NSC
99-2911-I-008-100]; Ministry of Education, Taipei, Taiwan
FX The study was supported in part by a grant from Taipei Veterans General
Hospital (VGHUST 100-G7-1-1 and V100D-002-3), the National Science
Council support for the Center for Dynamical Biomarkers and
Translational Medicine, National Central University, Taiwan (NSC
99-2911-I-008-100), and the Ministry of Education (Aim for the Top
University Plan), Taipei, Taiwan. These funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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TC 22
Z9 22
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1351-5101
EI 1468-1331
J9 EUR J NEUROL
JI Eur. J. Neurol.
PD MAY
PY 2012
VL 19
IS 5
BP 746
EP 751
DI 10.1111/j.1468-1331.2011.03621.x
PG 6
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 927LL
UT WOS:000302908900017
PM 22221515
DA 2025-01-07
ER
PT J
AU Choi, SY
Lee-Kwon, W
Kwon, HM
AF Choi, Soo Youn
Lee-Kwon, Whaseon
Kwon, Hyug Moo
TI The evolving role of TonEBP as an immunometabolic stress protein
SO NATURE REVIEWS NEPHROLOGY
LA English
DT Review
ID ENHANCER-BINDING PROTEIN; DAMAGE-INDUCIBLE KINASE; NACL-INDUCED
ACTIVATION; T-CELLS; ANTIBACTERIAL DEFENSE; NUCLEAR-LOCALIZATION;
TRANSCRIPTION; TONICITY; EXPRESSION; NFAT5
AB Tonicity-responsive enhancer-binding protein (TonEBP), which is also known as nuclear factor of activated T cells 5 (NFAT5), was discovered 20 years ago as a transcriptional regulator of the cellular response to hypertonic (hyperosmotic salinity) stress in the renal medulla. Numerous studies since then have revealed that TonEBP is a pleiotropic stress protein that is involved in a range of immunometabolic diseases. Some of the single-nucleotide polymorphisms (SNPs) in TONEBP introns are cis-expression quantitative trait loci that affect TONEBP transcription. These SNPs are associated with increased risk of type 2 diabetes mellitus, diabetic nephropathy, inflammation, high blood pressure and abnormal plasma osmolality, indicating that variation in TONEBP expression might contribute to these phenotypes. In addition, functional studies have shown that TonEBP is involved in the pathogenesis of rheumatoid arthritis, atherosclerosis, diabetic nephropathy, acute kidney injury, hyperlipidaemia and insulin resistance, autoimmune diseases (including type 1 diabetes mellitus and multiple sclerosis), salt-sensitive hypertension and hepatocellular carcinoma. These pathological activities of TonEBP are in contrast to the protective actions of TonEBP in response to hypertonicity, bacterial infection and DNA damage induced by genotoxins. An emerging theme is that TonEBP is a stress protein that mediates the cellular response to a range of pathological insults, including excess caloric intake, inflammation and oxidative stress.
TonEBP is a DNA-binding protein with multiple roles, via transcription regulation and other mechanisms, in both protective and pathological responses to stress. In this Review, Kwon and colleagues discuss these multiple roles in various stress responses.
C1 [Choi, Soo Youn; Lee-Kwon, Whaseon; Kwon, Hyug Moo] Ulsan Natl Inst Sci & Technol, Sch Life Sci, Ulsan, South Korea.
C3 Ulsan National Institute of Science & Technology (UNIST)
RP Kwon, HM (corresponding author), Ulsan Natl Inst Sci & Technol, Sch Life Sci, Ulsan, South Korea.
EM hmkwon@unist.ac.kr
OI Choi, Soo Youn/0000-0002-3149-5590; CHOI, SOO YOUN/0009-0008-3645-3040
FU National Research Foundation [2018R1A5A1024340, 2017R1E1A1A01074673,
NRF-2019R1A2C1089260]
FX Work in the laboratory of H.M.K. was supported by the National Research
Foundation grants 2018R1A5A1024340, 2017R1E1A1A01074673 and
NRF-2019R1A2C1089260.
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NR 78
TC 54
Z9 54
U1 0
U2 24
PU NATURE RESEARCH
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1759-5061
EI 1759-507X
J9 NAT REV NEPHROL
JI Nat. Rev. Nephrol.
PD JUN
PY 2020
VL 16
IS 6
BP 352
EP 364
DI 10.1038/s41581-020-0261-1
EA MAR 2020
PG 13
WC Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Urology & Nephrology
GA LQ2KM
UT WOS:000518883600001
PM 32157251
DA 2025-01-07
ER
PT J
AU Ye, Z
Xu, J
Li, SK
Cai, C
Li, TJ
Sun, LS
AF Ye, Zhao
Xu, Juan
Li, Shukui
Cai, Cheng
Li, Tiejun
Sun, Lishan
TI Lnc-IL7R promotes the growth of fibroblast-like synoviocytes through
interaction with enhancer of zeste homolog 2 in rheumatoid arthritis
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE fibroblast-like synoviocytes; enhancer of zeste homolog 2; rheumatoid
arthritis; long noncoding-interleukin-7 receptor; long noncoding RNA
ID LONG NONCODING RNA; DNA METHYLOME SIGNATURE; SYNOVIAL FIBROBLASTS;
HEPATOCELLULAR-CARCINOMA; INCREASE LEVELS; EXPRESSION; CELL;
INFLAMMATION; APOPTOSIS; REVEALS
AB Rheumatoid arthritis (RA) is an inflammatory and autoimmune disease that affects 1% of the world's population. Although the precise mechanism of RA has yet to be elucidated, accumulating evidence suggests that fibroblast-like synoviocytes (FLSs) serve critical roles in the initiation and progression of RA. However, the underlying molecular mechanisms of FLS proliferation have yet to be elucidated. Long noncoding-interleukin-7 receptor (Inc-IL7R) has been recently identified, which is activated by lipopolysaccharide (LPS) stimulation and diminishes the LPS-induced inflammatory response. In the present study, gain-and loss-of-function assays were performed in order to investigate the role of Inc-IL7R in FLS. It is demonstrated, to the best of the authors' knowledge for the first time, that Lnc-IL7R promotes cell proliferation, cell cycle progression and inhibits apoptosis in FLS. Further investigation identified that lnc-IL7 interacts with enhancer of zeste homolog 2 (EZH2) and is required for polycomb repressive complex 2 (PRC2)-mediated suppression, including cyclin-dependent kinase inhibitor IA and cyclin-dependent kinase inhibitor 2A. Lnc-IL7R may be a promising therapeutic target for the treatment of RA.
C1 [Ye, Zhao; Li, Shukui; Cai, Cheng; Sun, Lishan] Cangzhou Cent Hosp, Dept Orthoped, 16 West Xinhua Rd, Cangzhou 061000, Hebei, Peoples R China.
[Xu, Juan] Cangzhou Cent Hosp, Dept Ultrasound, Cangzhou 061000, Hebei, Peoples R China.
[Li, Tiejun] Cangzhou Cent Hosp, Dept Teaching, Cangzhou 061000, Hebei, Peoples R China.
RP Sun, LS (corresponding author), Cangzhou Cent Hosp, Dept Orthoped, 16 West Xinhua Rd, Cangzhou 061000, Hebei, Peoples R China.
EM sunlishanmyc@126.com
RI li, jinsong/HJH-9559-2023
FU Support Project of Hebei province science and technology [1123038ZD]
FX This study was supported by a grant from the Support Project of Hebei
province science and technology (grant no. 1123038ZD).
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NR 41
TC 22
Z9 24
U1 0
U2 12
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD MAR
PY 2017
VL 15
IS 3
BP 1412
EP 1418
DI 10.3892/mmr.2017.6150
PG 7
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA EP1VS
UT WOS:000397173000056
PM 28138707
OA Bronze
DA 2025-01-07
ER
PT J
AU Tybl, E
Shi, FD
Kessler, SM
Tierling, S
Walter, J
Bohle, RM
Wieland, S
Zhang, JY
Tan, EM
Kiemer, AK
AF Tybl, Elisabeth
Shi, Fu-Dong
Kessler, Sonja M.
Tierling, Sascha
Walter, Joern
Bohle, Rainer M.
Wieland, Stefan
Zhang, Jianying
Tan, Eng M.
Kiemer, Alexandra K.
TI Overexpression of the IGF2-mRNA binding protein p62 in
transgenic mice induces a steatotic phenotype
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE PTEN; IMP; NAFLD; NASH; CMV promoter activity; p65
ID NONALCOHOLIC FATTY LIVER; GENE-EXPRESSION; METABOLIC SYNDROME; IGF2
EXPRESSION; UP-REGULATION; H19 GENE; KAPPA-B; PTEN; STEATOHEPATITIS;
MODEL
AB Background & Aims: The insulin-like growth-factor 2 (IGF2) mRNA binding protein p62 is highly expressed in hepatocellular carcinoma tissue. Still, its potential role in liver disease is largely unknown. In this study, we investigated pathophysiological implications of p62 overexpression in mice.
Methods: We generated mice overexpressing p62 under a LAP-promotor. mRNA expression levels and stability were examined by real-time RT-PCR. Allele-specific expression of Igf2 and H19 was assessed after crossing mice with SD7 animals. The Igf2 downstream mediators pAKT and PTEN were determined by Western blot.
Result: Hepatic p62 overexpression neither induced inflammatory processes nor liver damage. However, 2.5 week old transgenic animals displayed a steatotic phenotype and improved glucose tolerance. p62 overexpression induced the expression of the imprinted genes Igf2 and H19 and their transcriptional regulator Aire (autoimmune regulator). Neither monoallelic expression nor mRNA stability of Igf2 and H19 was affected. Investigating Igf2 downstream signalling pathways showed increased AKT activation and attenuated PTEN expression.
Conclusions: The induction of a steatotic phenotype implies that p62 plays a role in hepatic pathophysiology. (C) 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Tybl, Elisabeth; Kessler, Sonja M.; Kiemer, Alexandra K.] Univ Saarland, Dept Pharm, D-66041 Saarbrucken, Germany.
[Shi, Fu-Dong] St Josephs Hosp, Barrow Neurol Inst, Phoenix, AZ USA.
[Tierling, Sascha; Walter, Joern] Univ Saarland, Inst Genet Epigenet, D-66041 Saarbrucken, Germany.
[Bohle, Rainer M.] Univ Saarland, Dept Pathol, D-6650 Homburg, Germany.
[Wieland, Stefan; Tan, Eng M.] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA.
[Zhang, Jianying] Univ Texas El Paso, Dept Biol, El Paso, TX 79968 USA.
C3 Saarland University; St. Joseph's Hospital and Medical Center; Barrow
Neurological Institute; Saarland University; Saarland University;
Scripps Research Institute; University of Texas System; University of
Texas El Paso
RP Kiemer, AK (corresponding author), Univ Saarland, Dept Pharm, POB 15 11 50, D-66041 Saarbrucken, Germany.
EM pharm.bio.kiemer@mx.uni-saarland.de
RI Zhang, Jianying/F-3798-2010; Kessler, Sonja/AAC-9195-2021; Walter,
Jörn/AFN-6428-2022; Kiemer, Alexandra K./I-9300-2012
OI Kiemer, Alexandra K./0000-0002-7224-9900; Kessler, Sonja
M./0000-0002-8591-851X; Shi, Fu-Dong/0000-0002-9675-4637
FU Deutsche Krebshilfe [107751]; National Institutes of Health, USA [CA
56956]; Alexander von Humboldt foundation
FX The project was funded by the Deutsche Krebshilfe (#107751) and by grant
CA 56956 from the National Institutes of Health, USA A.K.K. was
supported by the Alexander von Humboldt foundation.
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NR 49
TC 52
Z9 55
U1 2
U2 17
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD MAY
PY 2011
VL 54
IS 5
BP 994
EP 1001
DI 10.1016/j.jhep.2010.08.034
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 756LJ
UT WOS:000290012400024
PM 21145819
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Chitsamankhun, C
Siritongtaworn, N
Fournier, BPJ
Sriwattanapong, K
Theerapanon, T
Samaranayake, L
Porntaveetus, T
AF Chitsamankhun, Chakriya
Siritongtaworn, Nutwara
Fournier, B. P. J.
Sriwattanapong, Kanokwan
Theerapanon, Thanakorn
Samaranayake, Lakshman
Porntaveetus, Thantrira
TI Cathepsin C in health and disease: from structural insights to
therapeutic prospects
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Cathepsin C; Atherosclerosis; Inflammation; Palmoplantar hyperkeratosis;
Papillon-Lefevre syndrome; Periodontitis; Protease
ID PAPILLON-LEFEVRE-SYNDROME; DIPEPTIDYL-PEPTIDASE-I; COMPOUND HETEROZYGOUS
MUTATIONS; SYNDROME CLINICAL PRESENTATION; HAIM-MUNK-SYNDROME;
OF-THE-LITERATURE; CTSC GENE; PREPUBERTAL PERIODONTITIS; CYSTEINE
CATHEPSINS; ALLELIC MUTATIONS
AB Cathepsin C (CTSC) is a lysosomal cysteine protease constitutively expressed at high levels in the lung, kidney, liver, and spleen. It plays a key role in the activation of serine proteases in cytotoxic T cells, natural killer cells (granzymes A and B), mast cells (chymase and tryptase) and neutrophils (cathepsin G, neutrophil elastase, proteinase 3) underscoring its pivotal significance in immune and inflammatory defenses. Here, we comprehensively review the structural attributes, synthesis, and function of CTSC, with a focus on its variants implicated in the etiopathology of several syndromes associated with neutrophil serine proteases, including Papillon-Lefevre syndrome (PLS), Haim-Munk Syndrome (HMS), and aggressive periodontitis (AP). These syndromes are characterized by palmoplantar hyperkeratosis, and early-onset periodontitis (severe gum disease) resulting in premature tooth loss. Due to the critical role played by CTSC in these and several other conditions it is being explored as a potential therapeutic target for autoimmune and inflammatory disorders. The review also discusses in depth the gene variants of CTSC, and in particular their postulated association with chronic obstructive pulmonary disease (COPD), COVID-19, various cancers, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, sudden cardiac death (SCD), atherosclerotic vascular disease, and neuroinflammatory disease. Finally, the therapeutic potential of CTSC across a range of human diseases is discussed.
C1 [Chitsamankhun, Chakriya; Siritongtaworn, Nutwara; Sriwattanapong, Kanokwan; Theerapanon, Thanakorn; Porntaveetus, Thantrira] Chulalongkorn Univ, Fac Dent, Ctr Excellence Genom & Precis Dent, Dept Physiol, Bangkok 10330, Thailand.
[Fournier, B. P. J.] Univ Paris Cite, Rothschild Hosp, Reference Ctr Oral & Dent Rare Dis, Dent Fac,Oral Biol Dept, Paris, France.
[Samaranayake, Lakshman] Univ Hong Kong, Fac Dent, Hosp Rd, Hong Kong, Peoples R China.
[Porntaveetus, Thantrira] Chulalongkorn Univ, Fac Dent, Grad Program Geriatr & Special Patients Care, Bangkok, Thailand.
[Samaranayake, Lakshman] Chulalongkorn Univ, Fac Dent, Off Res Affairs, Bangkok, Thailand.
C3 Chulalongkorn University; Universite Paris Cite; Assistance Publique
Hopitaux Paris (APHP); Sorbonne Universite; Hopital Universitaire
Rothschild - APHP; University of Hong Kong; Chulalongkorn University;
Chulalongkorn University
RP Porntaveetus, T (corresponding author), Chulalongkorn Univ, Fac Dent, Ctr Excellence Genom & Precis Dent, Dept Physiol, Bangkok 10330, Thailand.; Porntaveetus, T (corresponding author), Chulalongkorn Univ, Fac Dent, Grad Program Geriatr & Special Patients Care, Bangkok, Thailand.
EM thantrira.p@chula.ac.th
RI Porntaveetus, Thantrira/ABF-6854-2020; Fournier, Benjamin/E-1791-2011
OI Fournier, Benjamin/0000-0003-4383-7524
FU Thailand Science Research and Innovation Fund; Chulalongkorn University,
second century high potential professoriate fund at the Faculty of
Dentistry
FX LS was supported by Chulalongkorn University, second century high
potential professoriate fund at the Faculty of Dentistry.
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NR 137
TC 0
Z9 0
U1 9
U2 9
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD AUG 20
PY 2024
VL 22
IS 1
AR 777
DI 10.1186/s12967-024-05589-7
PG 25
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA D2I6S
UT WOS:001294478800001
PM 39164687
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Panday, A
Sahoo, MK
Osorio, D
Batra, S
AF Panday, Arvind
Sahoo, Malaya K.
Osorio, Diana
Batra, Sanjay
TI NADPH oxidases: an overview from structure to innate immunity-associated
pathologies
SO CELLULAR & MOLECULAR IMMUNOLOGY
LA English
DT Review
DE alcohol; COPD; NLRs; NOX; TLRs
ID ADENINE-DINUCLEOTIDE PHOSPHATE; CHRONIC GRANULOMATOUS-DISEASE; MONOCYTE
CHEMOATTRACTANT PROTEIN-1; NEUTROPHIL RESPIRATORY BURST;
SMOOTH-MUSCLE-CELLS; OBSTRUCTIVE PULMONARY-DISEASE;
SUPEROXIDE-GENERATING OXIDASE; ALCOHOLIC LIVER-INJURY; TOLL-LIKE
RECEPTOR-4; SMALL GTPASE RAC
AB Oxygen-derived free radicals, collectively termed reactive oxygen species (ROS), play important roles in immunity, cell growth, and cell signaling. In excess, however, ROS are lethal to cells, and the overproduction of these molecules leads to a myriad of devastating diseases. The key producers of ROS in many cells are the NOX family of NADPH oxidases, of which there are seven members, with various tissue distributions and activation mechanisms. NADPH oxidase is a multisubunit enzyme comprising membrane and cytosolic components, which actively communicate during the host responses to a wide variety of stimuli, including viral and bacterial infections. This enzymatic complex has been implicated in many functions ranging from host defense to cellular signaling and the regulation of gene expression. NOX deficiency might lead to immunosuppression, while the intracellular accumulation of ROS results in the inhibition of viral propagation and apoptosis. However, excess ROS production causes cellular stress, leading to various lethal diseases, including autoimmune diseases and cancer. During the later stages of injury, NOX promotes tissue repair through the induction of angiogenesis and cell proliferation. Therefore, a complete understanding of the function of NOX is important to direct the role of this enzyme towards host defense and tissue repair or increase resistance to stress in a timely and disease-specific manner.
C1 [Panday, Arvind; Osorio, Diana; Batra, Sanjay] Louisiana State Univ, Sch Vet Med, Dept Pathobiol Sci, Baton Rouge, LA 70803 USA.
[Sahoo, Malaya K.] Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA.
[Batra, Sanjay] Southern Univ & A&M Coll, Dept Environm Toxicol, Baton Rouge, LA 70813 USA.
C3 Louisiana State University School of Veterinary Medicine; Louisiana
State University System; Louisiana State University; Stanford
University; Southern University System; Southern University & A&M
College
RP Batra, S (corresponding author), Southern Univ & A&M Coll, Dept Environm Toxicol, Baton Rouge, LA 70813 USA.
EM sanjaybatra100@gmail.com
RI Sahoo, Malaya/AAS-6907-2020; Batra, Sanjay/C-3040-2009; Panday,
Arvind/K-5439-2017
FU Flight Attendant Medical Research Award [YCSA-123253]; National
Institutes of Health [R15-1R15ES023151-01]; SVM Corp [LAV-3383]
FX This work was supported through funding from the Flight Attendant
Medical Research Award YCSA-123253, the National Institutes of Health
(grant R15-1R15ES023151-01) and a SVM Corp LAV-3383 grant to SB.
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NR 291
TC 531
Z9 545
U1 5
U2 111
PU CHIN SOCIETY IMMUNOLOGY
PI BEING
PA 5 DONGDAN SANTIAO, DONGCHEN DISTRICT, BEING, 100005, PEOPLES R CHINA
SN 1672-7681
EI 2042-0226
J9 CELL MOL IMMUNOL
JI Cell. Mol. Immunol.
PD JAN
PY 2015
VL 12
IS 1
DI 10.1038/cmi.2014.89
PG 19
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AY2AX
UT WOS:000347392000002
OA Bronze, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Shi, HL
Xu, XT
Wang, SS
Chen, QL
Zhang, F
Guo, HY
Lu, WT
Qiao, F
AF Shi, Huilian
Xu, Xiangtao
Wang, Shuangshuang
Chen, Qinlei
Zhang, Fan
Guo, Haiyan
Lu, Weiting
Qiao, Fei
TI The relationship between CXCR6+CD8+T cells and clinicopathological
parameters in patients with primary biliary cholangitis
SO HEPATOLOGY INTERNATIONAL
LA English
DT Article
DE Primary biliary cirrhosis; CXCR6+CD8+T cell; Autoimmune liver disease;
Clinical and pathological data
ID T-CELLS; METASTASIS; DIAGNOSIS; CANCER; CXCR6
AB Background CXCR6+CD8+T cells have been implicated in the pathogenesis of various liver and autoimmune diseases. However, their involvement in primary biliary cholangitis (PBC) has not been elucidated. Methods We used immunohistochemistry and flow cytometry to quantify CXCR6+CD8+T cells in hepatic tissue and peripheral blood samples obtained from CXCR6+CD8+T cells obtained from PBC patients. Then, we performed comprehensive statistical analyses to access the correlation between the abundance of these cells and clinical as well as pathological data across different stages of PBC. Results Our research revealed that CXCR6+ cell frequencies in CD3+CD8+T cells from PBC patients significantly exceeded that of healthy controls (HCs) (2.24 vs. 0.61%, p < 0.01). A similar pattern emerged for hepatic CXCR6+CD8+T cell counts, which were notably higher in the PBC cohort compared to HCs. Our cohort consisted of 118 PBC patients, categorized into 62 early-stage (E-PBC) and 56 late-stage (L-PBC) cases. Notably, significant disparities existed between these groups in terms of liver enzyme and lipid profile levels (p < 0.05), with no notable differences observed in gender, age, blood counts, cholesterol levels, or autoantibodies (p > 0.05). Intriguingly, the quantity of hepatic CXCR6+CD8+T cells per high power field (HPF) was significantly elevated in both E-PBC and L-PBC patients as opposed to normal liver samples, indicating a substantial increase in these cells across all stages of PBC (p = 0.000). Spearman's rank correlation analysis showed a positive correlation between CXCR6+CD8+T cell counts and serum levels of Alkaline Phosphatase (AKP) and Gamma-Glutamyl Transferase (GGT), ANA, IgG and IgM, while revealing a negligible correlation with Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST). Subsequent findings indicated significant variances in CXCR6+ cell numbers not only among different PBC stages but also across various degrees of inflammation and fibrosis (p <= 0.007). In a follow-up study post-Ursodeoxycholic Acid (UDCA) treatment, stark differences were identified in biochemical and immunohistochemical profiles between responder (31 patients) and non-responder (33 patients) groups (p < 0.05). A Wilcoxon rank-sum test further demonstrated a significant difference in the level of hepatic CXCR6+CD8+T cells between these two response groups (p = 0.002). Conclusion CXCR6+CD8+T cells play a vital role in the pathogenesis of PBC, exhibiting correlations with the extent of inflammation, staging of liver fibrosis, and response to pharmacological interventions in PBC patients.
C1 [Shi, Huilian; Xu, Xiangtao; Chen, Qinlei; Zhang, Fan; Guo, Haiyan; Lu, Weiting; Qiao, Fei] Nanjing Univ Chinese Med, Affiliated Hosp, Dept Infect Dis, 155 Hanzhong Rd,Qinhuai Ave, Nanjing 210000, Jiangsu, Peoples R China.
[Wang, Shuangshuang] Nanjing Univ Chinese Med, Affiliated Hosp, Dept Pathol, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
Medicine
RP Shi, HL; Guo, HY; Lu, WT; Qiao, F (corresponding author), Nanjing Univ Chinese Med, Affiliated Hosp, Dept Infect Dis, 155 Hanzhong Rd,Qinhuai Ave, Nanjing 210000, Jiangsu, Peoples R China.
EM shihuilian820@163.com; guohaiyan1980@163.com; 20221772@qq.com;
qiaofeidata@aliyun.com
RI guo, haiyan/KGM-7631-2024; Wang, Shuangshuang/ACG-6635-2022
OI Shi, Huilian/0000-0003-2437-2573
FU Natural Science Foundation of Jiangsu Province
FX The authors especially thank Dr. Weiting Lu for her assistance in
observing and choosing the microphotographs, and Dr. Shuangshuang Wang
for her help in the immunohistochemistry experiment.
CR Chen S, 2022, HEPATOL INT, V16, P195, DOI 10.1007/s12072-021-10267-7
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NR 33
TC 0
Z9 0
U1 3
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1936-0533
EI 1936-0541
J9 HEPATOL INT
JI Hepatol. Int.
PD OCT
PY 2024
VL 18
IS 5
BP 1555
EP 1565
DI 10.1007/s12072-024-10715-0
EA AUG 2024
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA I6K3M
UT WOS:001289939200001
PM 39134906
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Falcone, M
Concia, E
Iori, I
Lo Cascio, G
Mazzone, A
Pea, F
Violi, F
Venditti, M
AF Falcone, Marco
Concia, Ercole
Iori, Ido
Lo Cascio, Giuliana
Mazzone, Antonino
Pea, Federico
Violi, Francesco
Venditti, Mario
TI Identification and management of invasive mycoses in internal medicine:
a road-map for physicians
SO INTERNAL AND EMERGENCY MEDICINE
LA English
DT Review
DE Invasive mycoses; Candidemia; Aspergillosis; Antifungal therapy;
Echinocandins; Internal medicine
ID OBSTRUCTIVE PULMONARY-DISEASE; INTENSIVE-CARE-UNIT; CRITICALLY-ILL
PATIENTS; ESCMID-ASTERISK GUIDELINE; NON-NEUTROPENIC PATIENTS;
FUNGAL-INFECTIONS; PROSPECTIVE MULTICENTER; ANTIMANNAN ANTIBODIES;
CLINICAL-EXPERIENCE; ELDERLY-PATIENTS
AB Invasive mycoses are a rising problem, not only in traditional categories of patients like hematologic or neutropenic ones, but also in elderly non-neutropenic patients admitted to internal medicine wards. Patients being admitted to medical wards are usually older, have multiple comorbidities, e.g., liver cirrhosis or chronic obstructive respiratory disease, may be malnourished or receive peripheral or total parenteral nutrition, and frequently are undergoing chronic corticosteroid therapy, chemotherapy for cancer or monoclonal antibodies for autoimmune diseases. Such risk factors may be contemporarily present in a single patient increasing the risk for the development of invasive mycoses. Diagnosis of candidemia and invasive aspergillosis is particularly difficult in patients hospitalized on medical wards, since symptoms and signs have low specificity, and most diagnostic tests have been only validated in neutropenic hematologic patients, but not in those without neutropenia. Both candidemia and invasive aspergillosis carry significant morbidity and mortality. The aim of this paper is to provide a simple guide to physicians for a prompt identification and treatment of patients with possible or suspected invasive mycoses.
C1 [Falcone, Marco; Venditti, Mario] Univ Roma La Sapienza, Policlin Umberto I, Dept Publ Hlth & Infect Dis, I-00185 Rome, Italy.
[Concia, Ercole] Azienda Osped Univ Integrata, Policlin GB Rossi, Dept Pathol & Diagnost, Infect Dis Sect, Verona, Italy.
[Iori, Ido] Azienda Osped ASMN Reggio Emilia, Ctr Emostasi & Trombosi, Stroke Unit, Reggio Emilia, Italy.
[Lo Cascio, Giuliana] Azienda Osped Univ Integrata Verona, Serv Microbiol & Virol, Dept Pathol & Diagnost, I-37100 Verona, Italy.
[Mazzone, Antonino] Hosp Legnano, Dept Internal Med, Legnano, Italy.
[Pea, Federico] Azienda Osped Univ Santa Maria Misericordia, Inst Clin Pharmacol, Udine, Italy.
[Violi, Francesco] Univ Roma La Sapienza, Dept Internal Med & Med Specialties, Med Clin 1, I-00185 Rome, Italy.
C3 Sapienza University Rome; University Hospital Sapienza Rome; University
of Verona; Azienda Ospedaliera Universitaria Integrata Verona; IRCCS
Arcispedale S. Maria Nuova; University of Verona; Azienda Ospedaliera
Universitaria Integrata Verona; Hospital Santa Maria della Misericordia;
Sapienza University Rome
RP Falcone, M (corresponding author), Univ Roma La Sapienza, Policlin Umberto I, Dept Publ Hlth & Infect Dis, Piazzale Aldo Moro 5, I-00185 Rome, Italy.
EM marcofalc@libero.it
RI Pea, Federico/O-3636-2019; Falcone, Marco/K-7614-2016; Violi,
Francesco/K-1509-2016
OI Falcone, Marco/0000-0003-3813-8796; VENDITTI, Mario/0000-0003-2639-0281;
Violi, Francesco/0000-0002-6610-7068; Pea, Federico/0000-0002-6966-7167
FU Pfizer
FX The authors have served as members of an advisory board on infections in
Internal Medicine funded by an unrestricted grant by Pfizer. Dr. A. M.
ARUC provided assistance in the preparation of manuscript.
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NR 71
TC 20
Z9 20
U1 0
U2 8
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 1828-0447
EI 1970-9366
J9 INTERN EMERG MED
JI Intern. Emerg. Med.
PD AUG
PY 2014
VL 9
IS 5
BP 501
EP 511
DI 10.1007/s11739-014-1077-4
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA AM4JO
UT WOS:000339820100004
PM 24871636
OA Bronze
DA 2025-01-07
ER
PT J
AU Bao, T
Liu, J
Leng, JY
Cai, L
AF Bao, Terigen
Liu, Jia
Leng, Jiyan
Cai, Lu
TI The cGAS-STING pathway: more than fighting against viruses and cancer
SO CELL AND BIOSCIENCE
LA English
DT Review
DE Anti-virus inflammation; cGAS-STING pathway; Diabetes; Insulin
resistance; Diabetes complications
ID CYCLIC GMP-AMP; ENDOPLASMIC-RETICULUM STRESS; CYTOSOLIC DNA SENSOR;
INSULIN-RESISTANCE; MITOCHONDRIAL DAMAGE; MICE LACKING; ADIPOSE-TISSUE;
PROTEIN-KINASE; ISLET INFLAMMATION; LIVER-INJURY
AB In the classic Cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS)-stimulator of interferon genes (STING) pathway, downstream signals can control the production of type I interferon and nuclear factor kappa-light-chain-enhancer of activated B cells to promote the activation of pro-inflammatory molecules, which are mainly induced during antiviral responses. However, with progress in this area of research, studies focused on autoimmune diseases and chronic inflammatory conditions that may be relevant to cGAS-STING pathways have been conducted. This review mainly highlights the functions of the cGAS-STING pathway in chronic inflammatory diseases. Importantly, the cGAS-STING pathway has a major impact on lipid metabolism. Different research groups have confirmed that the cGAS-STING pathway plays an important role in the chronic inflammatory status in various organs. However, this pathway has not been studied in depth in diabetes and diabetes-related complications. Current research on the cGAS-STING pathway has shown that the targeted therapy of diseases that may be caused by inflammation via the cGAS-STING pathway has promising outcomes.
C1 [Bao, Terigen; Liu, Jia; Leng, Jiyan] First Hosp Jilin Univ, Dept Geriatr, Changchun 130021, Peoples R China.
[Bao, Terigen; Cai, Lu] Univ Louisville, Sch Med, Pediat Res Inst, Dept Pediat, Louisville, KY 40292 USA.
[Cai, Lu] Univ Louisville, Sch Med, Dept Pharmacol, Louisville, KY 40292 USA.
[Cai, Lu] Univ Louisville, Sch Med, Dept Toxicol, Louisville, KY 40292 USA.
C3 Jilin University; University of Louisville; University of Louisville;
University of Louisville
RP Leng, JY (corresponding author), First Hosp Jilin Univ, Dept Geriatr, Changchun 130021, Peoples R China.
EM lengjy@jlu.edu.cn
RI bao, terigen/KPA-6122-2024
FU China Jilin Province Science and Technology Department Project
[20190701067GH]
FX This work was supported in part by the China Jilin Province Science and
Technology Department Project (20190701067GH).
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NR 194
TC 32
Z9 33
U1 7
U2 65
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2045-3701
J9 CELL BIOSCI
JI Cell Biosci.
PD DEC 14
PY 2021
VL 11
IS 1
AR 209
DI 10.1186/s13578-021-00724-z
PG 20
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA XO4UO
UT WOS:000730182500002
PM 34906241
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Mani, H
Kleiner, DE
AF Mani, Haresh
Kleiner, David E.
TI Liver Biopsy Findings in Chronic Hepatitis B
SO HEPATOLOGY
LA English
DT Article; Proceedings Paper
CT NIH Consensus Development Conference on Management of Hepatitis B Virus
CY OCT 20-22, 2008
CL Bethesda, MD
SP Natl Inst Hlth
ID FIBROSING CHOLESTATIC HEPATITIS; CHRONIC VIRAL-HEPATITIS; ALANINE
AMINOTRANSFERASE LEVELS; HISTOLOGY ACTIVITY INDEX; PERSISTENTLY NORMAL
ALT; VIRUS PRECORE MUTANT; LARGE-CELL CHANGE; HEPATOCELLULAR-CARCINOMA;
E-ANTIGEN; CORE ANTIGEN
AB Liver biopsy plays a central role in treatment algorithms in patients with hepatitis B and remains the gold standard for evaluating hepatic pathology. The pathology of hepatitis B is diverse and reflects the natural history of infection. An acute hepatitic pattern with lobular disarray is seen in acute infection, during acute flares of disease, and with acute hepatitis D superinfection. In chronic hepatitis B, inflammation is less pronounced in the immune-tolerant phase and is prominent during immune-mediated viral clearance. Active inflammation appears to be the driving force for development of fibrosis. Inflammatory grades and fibrosis stage are assigned as is done for hepatitis C. Although current management guidelines recommend liver biopsies only in select patients based on age, viral levels, and hepatitis B e antigen status, these clinical and biochemical parameters do not show consistent correlations with liver histology. Liver biopsy also helps identify preneoplastic lesions including large cell and small cell change. Unlike in other causes of chronic hepatitis, immunostains are widely used and can help determine the phase of infection. Liver biopsies can also identify additional pathology that may contribute to liver disease such as steatohepatitis, iron overload, autoimmune hepatitis, and drug-induced injury. Thus, liver biopsy can play an important role in staging and grading chronic hepatitis B and should be more widely used in assessing the need for therapy. (HEPATOLOGY 2009;49:S61-S71.)
C1 [Mani, Haresh; Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI)
RP Kleiner, DE (corresponding author), NCI, Pathol Lab, NIH, Bldg 10,Room 2B50,MSC 1500,10 Ctr Dr, Bethesda, MD 20892 USA.
EM kleinerd@mail.nih.gov
RI Kleiner, David/N-2770-2013
OI Kleiner, David/0000-0003-3442-4453
FU Intramural NIH HHS Funding Source: Medline
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NR 108
TC 91
Z9 100
U1 2
U2 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD MAY
PY 2009
VL 49
IS 5
SU S
BP S61
EP S71
DI 10.1002/hep.22930
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology
GA 439ZZ
UT WOS:000265668700009
PM 19399798
OA Bronze
DA 2025-01-07
ER
PT J
AU Zhang, M
Wang, YZ
Wang, YT
Bai, Y
Gu, DQ
AF Zhang, Min
Wang, Yizhou
Wang, Yutong
Bai, Ye
Gu, Dongqing
TI Association Between Systemic Lupus Erythematosus and Cancer Morbidity
and Mortality: Findings From Cohort Studies
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE systemic lupus erythematosus; cancer; meta-analysis; cohort study;
Mendelian randomization
ID CYCLOPHOSPHAMIDE THERAPY; MENDELIAN RANDOMIZATION; MULTIPLE-SCLEROSIS;
RHEUMATIC-DISEASES; BLADDER-CANCER; RISK; AUTOIMMUNE; LYMPHOMA;
SUSCEPTIBILITY; EPIDEMIOLOGY
AB Background:& nbsp;Observational studies suggested that systemic lupus erythematosus (SLE) might be associated with increased cancer incidence and cancer-related death, however, the results are inconsistent. We aim to comprehensively estimate the causal relationships between SLE and cancer morbidity and mortality using a meta-analysis of cohort studies and Mendelian randomization.& nbsp;Methods:& nbsp;A systematic search was conducted using PubMed to identify cohort studies published before January 21, 2021. Meta-analysis was performed to calculate relative risk (RR) and corresponding 95% confidence intervals (CI). In addition, we further evaluated the potentially causal relationships identified by cohort studies using two-sample Mendelian randomization.& nbsp;Results:& nbsp;A total of 48 cohort studies involving 247,575 patients were included. We performed 31 main meta-analysis to assess the cancer risk and three meta-analyses to evaluate cancer mortality in SLE patients. Through meta-analyses, we observed an increased risk of overall cancer (RR=1.62, 95%CI, 1.47-1.79, P < 0.001) and cancer-related death (RR=1.52, 95%CI, 1.36-1.70, P < 0.001) in patients with SLE. Subgroup analysis by site-specific cancer showed that SLE was a risk factor for 17 site-specific cancers, including six digestive cancers (esophagus, colon, anus, hepatobiliary, liver, pancreatic), five hematologic cancers (lymphoma, Hodgkin's lymphoma, non-Hodgkin lymphoma, leukemia, multiple myeloma), as well as cancer in lung, larynx, cervical, vagina/vulva, renal, bladder, skin, and thyroid. In addition, further mendelian randomization analysis verified a weakly association between genetically predisposed SLE and lymphoma risk (odds ratio=1.0004, P=0.0035).& nbsp;Conclusions:& nbsp;Findings from our study suggest an important role of SLE in carcinogenesis, especially for lymphoma.
C1 [Zhang, Min; Bai, Ye] Chongqing Med Univ, Sch Publ Hlth & Management, Chongqing, Peoples R China.
[Wang, Yizhou] Sichuan Mental Hlth Ctr, Hosp Mianyang 3, Dept Pathol, Mianyang, Peoples R China.
[Wang, Yutong] Sichuan Univ, West China Sch Publ Hlth, Dept Epidemiol & Med, Chengdu, Peoples R China.
[Gu, Dongqing] Army Med Univ, Affiliated Hosp 1, Dept Infect Dis, Chongqing, Peoples R China.
[Wang, Yutong] Sichuan Univ, West China Hosp 4, Chengdu, Peoples R China.
C3 Chongqing Medical University; Sichuan University; Army Medical
University; Sichuan University
RP Gu, DQ (corresponding author), Army Med Univ, Affiliated Hosp 1, Dept Infect Dis, Chongqing, Peoples R China.
EM dongqing.gu@vip.163.com
RI WANG, YUANYUAN/IQR-4295-2023; wang, wy/JDD-3603-2023
FU National Natural Science Foundation of China [81903393]; Chongqing
Natural Science Foundation Program [cstc2020jcyj-msxmX0021]
FX Funding This study was supported by the National Natural Science
Foundation of China (81903393), and Chongqing Natural Science Foundation
Program (cstc2020jcyj-msxmX0021). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 55
TC 25
Z9 25
U1 5
U2 19
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD MAY 4
PY 2022
VL 12
AR 860794
DI 10.3389/fonc.2022.860794
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 1I9IG
UT WOS:000797539900001
PM 35600353
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Le Daré, B
Lagente, V
Gicquel, T
AF Le Dare, Brendan
Lagente, Vincent
Gicquel, Thomas
TI Ethanol and its metabolites: update on toxicity, benefits, and focus on
immunomodulatory effects
SO DRUG METABOLISM REVIEWS
LA English
DT Review
DE Ethanol; alcohol; acetaldehyde; metabolism; toxicity; immunomodulation
ID MODERATE ALCOHOL-CONSUMPTION; BONE-MINERAL DENSITY; HUMAN ALDEHYDE
DEHYDROGENASES; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RETINOIC ACID
BIOSYNTHESIS; DOSE-RESPONSE METAANALYSIS; CARDIOVASCULAR-DISEASE;
HEART-FAILURE; BREAST-CANCER; RHEUMATOID-ARTHRITIS
AB This article summarizes recent experimental and epidemiological data on the toxic and beneficial effects of ethanol and its metabolites (acetaldehyde), and focuses on their immunomodulatory effects. The section dealing with the toxic effects of alcohol focuses on its chronic toxicity (liver disorders, carcinogenic effects, cardiovascular disorders, neuropsychic disorders, addiction and withdrawal syndrome, hematologic disorders, reprotoxicity, osteoporosis) although acute toxicity is considered. The role of oxidative metabolism of ethanol by alcohol dehydrogenase, cytochrome P450 2E1, and aldehyde dehydrogenase, as well as the impact of genetic polymorphism in its physiopathology are also highlighted. The section dealing with the beneficial effects of low to moderate alcohol consumption (on cardiovascular system, diabetes, the nervous system and sensory organs, autoimmune diseases, and rheumatology) highlights the importance of anti-inflammatory and immunomodulatory effects in these observations. This knowledge, enriched by a focus on the immunomodulatory effects of ethanol and its metabolites, in particular on the NLRP3 inflammasome pathway, might facilitate the development of treatments that can reduce ethanol's harmful effects or accentuate its beneficial effects.
C1 [Le Dare, Brendan; Gicquel, Thomas] Univ Rennes, INSERM, INRA, Inst NuMeCan Nutr Metab & Canc, F-35000 Rennes, France.
[Le Dare, Brendan; Lagente, Vincent] Pontchaillou Univ Hosp, Pharm Unit, Rennes, France.
[Le Dare, Brendan; Gicquel, Thomas] Pontchaillou Univ Hosp, Forens & Toxicol Lab, Rennes, France.
C3 INRAE; Universite de Rennes; Institut National de la Sante et de la
Recherche Medicale (Inserm); Universite de Rennes; CHU Rennes; CHU
Rennes; Universite de Rennes
RP Le Daré, B (corresponding author), Univ Rennes, INSERM, INRA, Inst NuMeCan Nutr Metab & Canc, F-35000 Rennes, France.
EM brendan.le.dare@chu-rennes.fr
RI Lagente, Vincent/Y-8870-2019; Le Daré, Brendan/AAL-7050-2020; Gicquel,
Thomas/Q-1880-2019
OI LE DARE, Brendan/0000-0002-5907-2450; Lagente,
Vincent/0000-0003-4920-009X; Gicquel, Thomas/0000-0002-2354-1884
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NR 163
TC 89
Z9 91
U1 0
U2 43
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0360-2532
EI 1097-9883
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD DEC
PY 2019
VL 51
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BP 545
EP 561
DI 10.1080/03602532.2019.1679169
EA OCT 2019
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Pharmacology & Pharmacy
GA QK9NA
UT WOS:000492105500001
PM 31646907
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Hahn, U
AF Hahn, Ulrich
TI Charomers-Interleukin-6 Receptor Specific Aptamers for Cellular
Internalization and Targeted Drug Delivery
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE aptamers; charomers; targeted drug delivery; targeted chemotherapy;
photodynamic therapy; interleukin-6 receptor
ID ALPHA-6-BETA-4 INTEGRIN; PHOTODYNAMIC THERAPY; PROSTATE-CANCER;
NANOPARTICLES; 5-FLUOROURACIL; THERAPEUTICS; CHIMERAS; PROGRESS; DESIGN;
BIND
AB Interleukin-6 (IL-6) is a key player in inflammation and the main factor for the induction of acute phase protein biosynthesis. Further to its central role in many aspects of the immune system, IL-6 regulates a variety of homeostatic processes. To interfere with IL-6 dependent diseases, such as various autoimmune diseases or certain cancers like multiple myeloma or hepatocellular carcinoma associated with chronic inflammation, it might be a sensible strategy to target human IL-6 receptor (hIL-6R) presenting cells with aptamers. We therefore have selected and characterized different DNA and RNA aptamers specifically binding IL-6R. These IL-6R aptamers, however, do not interfere with the IL-6 signaling pathway but are internalized with the receptor and thus can serve as vehicles for the delivery of different cargo molecules like therapeutics. We succeeded in the construction of a chlorin e6 derivatized aptamer to be delivered for targeted photodynamic therapy (PDT). Furthermore, we were able to synthesize an aptamer intrinsically comprising the cytostatic 5-Fluoro-2'-deoxy-uridine for targeted chemotherapy. The alpha 6 beta 4 integrin specific DNA aptamer IDA, also selected in our laboratory is internalized, too. All these aptamers can serve as vehicles for targeted drug delivery into cells. We call them charomers-in memory of Charon, the ferryman in Greek mythology, who ferried the deceased into the underworld.
C1 [Hahn, Ulrich] Univ Hamburg, MIN Fac, Inst Biochem & Mol Biol, Chem Dept, Martin Luther King Pl 6, D-20146 Hamburg, Germany.
C3 University of Hamburg
RP Hahn, U (corresponding author), Univ Hamburg, MIN Fac, Inst Biochem & Mol Biol, Chem Dept, Martin Luther King Pl 6, D-20146 Hamburg, Germany.
EM uli.hahn@uni-hamburg.de
RI Hahn, Ulrich/E-8069-2010
OI Hahn, Ulrich/0000-0002-6526-0693
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NR 49
TC 10
Z9 11
U1 1
U2 27
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD DEC
PY 2017
VL 18
IS 12
AR 2641
DI 10.3390/ijms18122641
PG 10
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA FR2KU
UT WOS:000418896700145
PM 29211023
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Arsentieva, NA
Korobova, ZR
Batsunov, OK
Lyubimova, NE
Basina, VV
Esaulenko, EV
Totolian, AA
AF Arsentieva, Natalia A.
Korobova, Zoia R.
Batsunov, Oleg K.
Lyubimova, Natalia E.
Basina, Valentina V.
Esaulenko, Elena V.
Totolian, Areg A.
TI CX3CL1/Fractalkine: A Potential Biomarker for Liver Fibrosis in Chronic
HBV Infection
SO CURRENT ISSUES IN MOLECULAR BIOLOGY
LA English
DT Article
DE CX3CL1/Fractalkine; chemokines; hepatitis B virus; hepatitis C virus;
liver fibrosis
ID B-VIRUS REPLICATION; FRACTALKINE RECEPTOR CX(3)CR1; EXPRESSION;
CONTRIBUTE; MIGRATION; DISEASE; CX3CL1; CELLS
AB A hepatitis B virus (HBV) infection can progress to chronic hepatitis, leading to liver fibrosis, cirrhosis, and hepatocellular carcinoma. CX3CL1/Fractalkine plays a crucial role in recruiting immune cells that are responsible for protecting against HBV infection. The aim of this study was to measure CX3CL1/Fractalkine concentrations in the blood plasma of individuals infected with HBV and to evaluate the role of this chemokine in the development of liver tissue fibrosis. Our study included patients infected with HBV, patients infected with HCV, autoimmune hepatitis, and healthy donors. We analyzed the CX3CL1/Fractalkine concentrations in blood plasma using the xMAP technology. Our results showed that HBV-infected patients had lower concentrations of CX3CL1/Fractalkine. Furthermore, in HBV-infected patients with severe fibrosis/cirrhosis, we observed significantly lower concentrations of CX3CL1/Fractalkine compared to those with no/mild fibrosis. Our study revealed that CX3CL1/Fractalkine concentrations are significantly associated with the stage of fibrosis in HBV infection. We demonstrated that lowered CX3CL1/Fractalkine concentrations might have prognostic value for predicting fibrosis development in liver tissue. Our findings suggest that decreased concentrations of CX3CL1/Fractalkine are associated with an increased risk of progressive liver fibrosis, indicating the potential of this chemokine as a prognostic biomarker for the development of liver fibrosis.
C1 [Arsentieva, Natalia A.; Korobova, Zoia R.; Batsunov, Oleg K.; Lyubimova, Natalia E.; Esaulenko, Elena V.; Totolian, Areg A.] St Petersburg Pasteur Inst, Lab Mol Immunol, Mira St 14, St Petersburg 197101, Russia.
[Korobova, Zoia R.; Batsunov, Oleg K.; Totolian, Areg A.] Pavlov First State Med Univ St Petersburg, Dept Immunol, Lva Tolstogo St 6-8, St Petersburg 197022, Russia.
[Basina, Valentina V.; Esaulenko, Elena V.] St Petersburg State Pediat Med Univ, Dept Infect Dis Adults & Epidemiol, Litovskaya St,Bldg 2, St Petersburg 194100, Russia.
C3 Saint-Petersburg Pasteur Institute; Saint Petersburg State Pediatric
Medical University
RP Arsentieva, NA (corresponding author), St Petersburg Pasteur Inst, Lab Mol Immunol, Mira St 14, St Petersburg 197101, Russia.
EM arsentieva_n.a@bk.ru; zoia-korobova@yandex.ru; batsunov@gmail.com;
natelu@mail.ru; v.basina@mail.ru; eve-gpmu@mail.ru; totolian@spbraaci.ru
RI Arsentieva, Natalia/M-6557-2018; Totolian, Areg/ITV-7106-2023; Korobova,
Zoia/AAB-8213-2022; Totolian, Areg/J-3513-2014
OI Korobova, Zoia/0000-0003-0535-5014; Totolian, Areg/0000-0003-4571-8799
FU Saint Petersburg Pasteur Institute; [121021600217-1]
FX This research was funded by the Saint Petersburg Pasteur Institute
within the framework of a State Task (Registration No. 121021600217-1).
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WHO, US
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NR 38
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1467-3037
EI 1467-3045
J9 CURR ISSUES MOL BIOL
JI Curr. Issues Mol. Biol.
PD SEP
PY 2024
VL 46
IS 9
BP 9948
EP 9957
DI 10.3390/cimb46090593
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA H4C6J
UT WOS:001322941800001
PM 39329945
OA gold
DA 2025-01-07
ER
PT J
AU Zhou, H
Sun, LH
Li, J
Xu, CY
Yu, F
Liu, YH
Ji, CN
He, JH
AF Zhou, Huan
Sun, Lihua
Li, Jian
Xu, Chunyan
Yu, Feng
Liu, Yahui
Ji, Chaoneng
He, Jianhua
TI The crystal structure of human GDP-L-fucose synthase
SO ACTA BIOCHIMICA ET BIOPHYSICA SINICA
LA English
DT Article
DE gdp-L-fucose synthase; gdp-L-fucose; fx
ID UDP-GALACTOSE 4-EPIMERASE; MANNOSE 4,6-DEHYDRATASE; ESCHERICHIA-COLI;
HEPATOCELLULAR-CARCINOMA; FX ENZYME; FUCOSYLATION; BIOSYNTHESIS;
EXPRESSION; MECHANISM; BINDING
AB Human GDP-L-fucose synthase, also known as FX protein, synthesizes GDP-L-fucose from its substrate GDP-4-keto-6-deoxy-D-mannose. The reaction involves epimerization at both C-3 and C-5 followed by an NADPH-dependent reduction of the carbonyl at C-4. In this paper, the first crystal structure of human FX protein was determined at 2.37 A degrees resolution. The asymmetric unit of the crystal structure contains four molecules which form two homodimers. Each molecule consists of two domains, a Rossmann-fold NADPH-binding motif and a carboxyl terminal domain. Compared with the Escherichia coli GDP-L-fucose synthase, the overall structures of these two enzymes have four major differences. There are four loops in the structure of human FX protein corresponding to two alpha-helices and two beta-sheets in that of the E. coli enzyme. Besides, there are seven different amino acid residues binding with NAPDH comparing human FX protein with that from E. coli. The structure of human FX reveals the key catalytic residues and could be useful for the design of drugs for the treatment of inflammation, autoimmune diseases, and possibly certain types of cancer.
C1 [Zhou, Huan; Sun, Lihua; Li, Jian; Xu, Chunyan; Yu, Feng; Liu, Yahui; He, Jianhua] Chinese Acad Sci, Shanghai Inst Appl Phys, Dept Biol Sci, Shanghai 201204, Peoples R China.
[Ji, Chaoneng] Fudan Univ, Sch Life Sci, Inst Genet, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
C3 Chinese Academy of Sciences; Shanghai Institute of Applied Physics, CAS;
Fudan University
RP He, JH (corresponding author), Chinese Acad Sci, Shanghai Inst Appl Phys, Dept Biol Sci, Shanghai 201204, Peoples R China.
EM hejh@sinap.ac.cn
RI zhou, huan/GYJ-4398-2022; Yu, Feng/U-9998-2019; Sun, Lihua/A-3874-2009
OI Sun, Lihua/0000-0002-7555-7941
FU Ministry of Science and Technology of China [2011CB911102]; National
Natural Science Foundation of China [31100528]
FX This work was supported by grants from the Ministry of Science and
Technology of China (No. 2011CB911102) and the National Natural Science
Foundation of China (No. 31100528).
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NR 32
TC 11
Z9 14
U1 0
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1672-9145
EI 1745-7270
J9 ACTA BIOCH BIOPH SIN
JI Acta Biochim. Biophys. Sin.
PD SEP
PY 2013
VL 45
IS 9
BP 720
EP 725
DI 10.1093/abbs/gmt066
PG 6
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 206XD
UT WOS:000323558400002
PM 23774504
DA 2025-01-07
ER
PT J
AU Bartsch, O
Schneider, E
Damatova, N
Weis, R
Tufano, M
Iorio, R
Ahmed, A
Beyer, V
Zechner, U
Haaf, T
AF Bartsch, Oliver
Schneider, Eberhard
Damatova, Natalja
Weis, Roger
Tufano, Maria
Iorio, Raffaele
Ahmed, Alischo
Beyer, Vera
Zechner, Ulrich
Haaf, Thomas
TI Fulminant Hepatic Failure Requiring Liver Transplantation in 22q13.3
Deletion Syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE 22q13.3 deletion syndrome; fulminant hepatic failure; liver
transplantation; PIM3; SHANK3/PROSAP2; PPARA
ID HEPATOCELLULAR-CARCINOMA DEVELOPMENT; MOLECULAR CHARACTERIZATION; PIM-3;
MICE; ASSOCIATION; EXPRESSION; DISORDERS; DEFICIENT; AUTISM; GENE
AB We report on a 4-year-old girl with severe developmental delay, absent speech, and chromosome 22q13.3 deletion (Phelan-McDermid syndrome), karyotype 46,XX.ish del(22)(q13.31qter) (ARSA-,N85A-,SHANK3-). At the age of 3 years, she needed an emergency liver transplantation because of fulminant hepatic failure, most likely caused by hyperacute autoimmune hepatitis triggered by a viral infection. This is the second report of a patient with 22q13.3 deletion and fulminant liver failure. By array-CGH we identified in this patient a 5.675 Mb terminal deletion (22q13.31 -> qter; including similar to 55 genes; from NUP50 to RABL2B) and in the previous patient a 1.535 Mb deletion (22q13.32 -> qter, including similar to 39 genes; from BRD1 to RABL2B). PIM3 is a prime candidate gene for the fulminant hepatic failure in the two patients; SHANK3/PROSAP2 could be another candidate gene. We recommend liver function tests and array-CGH in the management of patients with Phelan-McDermid syndrome. This patient showed a developmental catch-up following the liver transplantation, possibly suggesting that chronic hepatic disease could contribute to the developmental delay in a subset of these patients. (C) 2010 Wiley-Liss, Inc.
C1 [Bartsch, Oliver] Johannes Gutenberg Univ Mainz, Inst Human Genet, Univ Med, D-55101 Mainz, Germany.
[Schneider, Eberhard; Damatova, Natalja; Haaf, Thomas] Univ Wurzburg, Inst Human Genet, D-8700 Wurzburg, Germany.
[Weis, Roger] Kinderneurol Zentrum, Mainz, Germany.
[Tufano, Maria; Iorio, Raffaele] Univ Naples Federico II, Dept Pediat, Naples, Italy.
[Ahmed, Alischo] Max Planck Inst Mol Genet, Dept Human Mol Genet, Berlin, Germany.
C3 Johannes Gutenberg University of Mainz; University of Wurzburg;
University of Naples Federico II; Max Planck Society
RP Bartsch, O (corresponding author), Johannes Gutenberg Univ Mainz, Inst Human Genet, Univ Med, Langenbeckstr 1, D-55101 Mainz, Germany.
EM bartsch@humgen.klinik.uni-mainz.de
RI Zechner, Ulrich/G-2116-2010; Iorio, Raffaele/J-2137-2012; Bartsch,
Oliver/ABE-2681-2020
OI schneider, eberhard/0000-0003-4320-3652; IORIO,
RAFFAELE/0000-0002-7483-234X
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NR 22
TC 12
Z9 13
U1 0
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD AUG
PY 2010
VL 152A
IS 8
BP 2099
EP 2102
DI 10.1002/ajmg.a.33542
PG 4
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 638VO
UT WOS:000280925800035
PM 20635403
DA 2025-01-07
ER
PT J
AU Slimen, IB
Najar, T
Ghram, A
Dabbebi, H
Ben Mrad, M
Abdrabbah, M
AF Slimen, Imen Belhadj
Najar, Taha
Ghram, Abdeljelil
Dabbebi, Hajer
Ben Mrad, Moncef
Abdrabbah, Manef
TI Reactive oxygen species, heat stress and oxidative-induced mitochondrial
damage. A review
SO INTERNATIONAL JOURNAL OF HYPERTHERMIA
LA English
DT Review
DE Apoptosis; heat stress; mitochondria; oxidative stress; reactive oxygen
species (ROS)
ID SUPEROXIDE RADICAL PRODUCTION; CYTOCHROME-C RELEASE; BROWN
ADIPOSE-TISSUE; NITRIC-OXIDE; CELL-DEATH; HYDROGEN-PEROXIDE;
PERMEABILITY TRANSITION; UNCOUPLING PROTEIN; SKELETAL-MUSCLE; RAT-LIVER
AB In recent years there has been enormous interest in researching oxidative stress. Reactive oxygen species (ROS) are derived from the metabolism of oxygen as by-products of cell respiration, and are continuously produced in all aerobic organisms. Oxidative stress occurs as a consequence of an imbalance between ROS production and the available antioxidant defence against them. Nowadays, a variety of diseases and degenerative processes such as cancer, Alzheimer's and autoimmune diseases are mediated by oxidative stress. Heat stress was suggested to be an environmental factor responsible for stimulating ROS production because of similarities in responses observed following heat stress compared with that occurring following exposure to oxidative stress. This manuscript describes the main mitochondrial sources of ROS and the antioxidant defences involved to prevent oxidative damage in all the mitochondrial compartments. It also deals with discussions concerning the cytotoxic effect of heat stress, mitochondrial heat-induced alterations, as well as heat shock protein (HSP) expression as a defence mechanism.
C1 [Slimen, Imen Belhadj; Najar, Taha; Abdrabbah, Manef] Preparatory Inst Sci & Tech Studies, Lab Mat Mol & Applicat, Tunis, Tunisia.
[Slimen, Imen Belhadj; Najar, Taha; Dabbebi, Hajer; Ben Mrad, Moncef] Natl Agron Inst Tunisia, Dept Anim Food & Halieut Resources, Tunis 1082, Tunisia.
[Ghram, Abdeljelil] Pasteur Inst Tunisia, Microbiol Lab, Tunis, Tunisia.
C3 Universite de Carthage; Pasteur Network; Universite de Tunis-El-Manar;
Institut Pasteur Tunis
RP Slimen, IB (corresponding author), Natl Agron Inst Tunisia, Dept Anim Food & Halieut Resources, Tunis 1082, Tunisia.
EM belhadj_slimen_imen@yahoo.fr
RI Slimen, Imen/AAI-7410-2020; Abderrabba, Manef/AAD-6206-2021
OI Abderrabba, Manef/0000-0002-1129-0539; DEBBABI,
Hajer/0000-0001-5825-6744; Belhadj Slimen, Imen/0000-0002-9492-7899
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NR 174
TC 543
Z9 592
U1 27
U2 323
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0265-6736
EI 1464-5157
J9 INT J HYPERTHER
JI Int. J. Hyperthermia
PD NOV
PY 2014
VL 30
IS 7
BP 513
EP 523
DI 10.3109/02656736.2014.971446
PG 11
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA AS8AG
UT WOS:000344472300011
PM 25354680
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Azzi, J
Sayegh, MH
AF Azzi, Jamil
Sayegh, Mohamed H.
TI Clinical Transplantation Tolerance: A Myth No More, But ...
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
ID DONOR LIVER-TRANSPLANTATION; RENAL-ALLOGRAFT TOLERANCE;
IMMUNOLOGICAL-TOLERANCE; T-CELLS; OPERATIONAL TOLERANCE; COSTIMULATORY
BLOCKADE; HUMAN KIDNEY; BONE-MARROW; IMMUNOSUPPRESSION; RECIPIENTS
AB More than 55 years after the description of the phenomenon of acquired immunologic tolerance to transplant antigens by Medawar and colleagues, the holy grail of transplantation is a myth no more. Establishment of the Immune Tolerance Network in 1999 changed the approach used to achieve clinical tolerance by translating advances in the field of immunology in general and in tolerance in particular from experimental animal strategies into human clinical trials, and initial results have been promising. Despite these advances, scientific and operational challenges still face the transplantation community and affect progress. Overcoming those challenges is a shared responsibility of scientists, transplant professionals, and general nephrologists alike. Achieving tolerance could not only revolutionize the field of transplantation through avoidance of toxicity associated with immunosuppressive agents, but also influence the treatment of autoimmune diseases, in which the immune system attacks self, as well as cancer, in which tolerance of the immune system toward malignant cells may permit disease development and progression. Am J Kidney Dis 54:1005-1011. (C) 2009 by the National Kidney Foundation, Inc.
C1 [Sayegh, Mohamed H.] Harvard Univ, Transplant Res Ctr, Brigham & Womens Hosp, Sch Med,Childrens Hosp Boston, Boston, MA 02115 USA.
Brigham & Womens Hosp, Transplantat Res Ctr, Div Renal, Boston, MA 02115 USA.
C3 Harvard University; Harvard Medical School; Boston Children's Hospital;
Brigham & Women's Hospital; Harvard University; Brigham & Women's
Hospital
RP Sayegh, MH (corresponding author), Harvard Univ, Transplant Res Ctr, Brigham & Womens Hosp, Sch Med,Childrens Hosp Boston, 221 Longwood Ave, Boston, MA 02115 USA.
EM msayegh@rics.bwh.harvard.edu
OI Sayegh, Mohamed/0000-0002-2847-588X
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NR 44
TC 9
Z9 11
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
EI 1523-6838
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD DEC
PY 2009
VL 54
IS 6
BP 1005
EP 1011
DI 10.1053/j.ajkd.2009.08.005
PG 7
WC Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Urology & Nephrology
GA 524LF
UT WOS:000272144100008
PM 19819055
DA 2025-01-07
ER
PT J
AU Hsieh, YC
Lin, CL
Hung, CH
Chen, CH
Tung, SY
Lin, CY
Hu, TH
Lu, SN
Chien, RN
Sheen, IS
AF Hsieh, Yi-Chung
Lin, Chih-Lang
Hung, Chao-Hung
Chen, Chien-Hung
Tung, Shui-Yi
Lin, Chun-Yen
Hu, Tsung-Hui
Lu, Sheng-Nan
Chien, Rong-Nan
Sheen, I-Shyan
TI Real-world experience of elbasvir/grazoprevir in Taiwan: This study was
focused on liver and renal adverse effects
SO JOURNAL OF VIRAL HEPATITIS
LA English
DT Article
DE adverse effect; elbasvir; grazoprevir; hepatitis C; real-world
experience
ID HEPATITIS-C VIRUS; GENOTYPE 1 INFECTION; GRAZOPREVIR MK-5172; ELBASVIR
MK-8742; TREATMENT-NAIVE; EFFICACY; SAFETY; COMBINATION; RIBAVIRIN;
THERAPY
AB Elbasvir/grazoprevir with or without ribavirin has excellent efficacy and safety for the treatment of hepatitis C virus (HCV) genotype 1 and 4 patients. The real-world experience has been reported but the detailed analysis of liver and renal adverse effects is lacking. This study evaluated the real-world experience relating to the effectiveness and liver/renal safety of elbasvir/grazoprevir in HCV genotype 1 patients with compensated liver disease. In the four medical centres of Chang Gung Medical System, 350 HCV genotype 1 patients with compensated liver disease who were treated with elbasvir/grazoprevir were enrolled. Clinical characteristics and laboratory data were collected. The effectiveness (sustained virologic response 12 weeks after end of treatment, SVR12) and safety were assessed. A consecutive series of 350 patients with a mean age of 68.8 +/- 10.0 years old were enrolled. The majority were treatment-naive (72.3%), genotype 1b (97.7%) and advanced fibrosis/cirrhosis (94.3%). Seventy-nine (22.6%) had hepatocellular carcinoma and 23 (6.6%) had coinfection with hepatitis B. The effectiveness of SVR12 was 94.6% (95% CI: 92.2%-97.0%) in the full analysis set and 99.1% (95% CI: 98.1%-100.1%) in the per-protocol set. There were two relapses and one nonresponder. Seven (2.0%) patients had adverse events resulting in premature discontinuation of treatment. Five of them were considered drug-related. One was due to autoimmune hepatitis. Contrary to previous reports, around 49% of ALT elevation was observed after 8 weeks, and in two patients was due to hepatitis B flares. As to the renal function during the course of therapy, a minor deterioration of eGFR was observed in patients with baseline eGFR >= 60 mL/min/1.73 m(2), but not in those with baseline eGFR <60, <60-30 or <30 mL/min/1.73 m(2). In this real-world data, elbasvir/grazoprevir was effective with few liver/renal adverse effects. One patient developed autoimmune hepatitis.
C1 [Hsieh, Yi-Chung; Lin, Chun-Yen; Sheen, I-Shyan] Linkou Chang Gung Mem Hosp, Div Hepatogastroenterol, Taoyuan, Taiwan.
[Lin, Chih-Lang; Chien, Rong-Nan] Keelung Chang Gung Mem Hosp, Div Hepatogastroenterol, Keelung, Taiwan.
[Hung, Chao-Hung; Tung, Shui-Yi; Lu, Sheng-Nan] Chiayi Chang Gung Mem Hosp, Div Hepatogastroenterol, Chiayi, Taiwan.
[Hung, Chao-Hung; Chen, Chien-Hung; Tung, Shui-Yi; Lin, Chun-Yen; Hu, Tsung-Hui; Lu, Sheng-Nan; Chien, Rong-Nan; Sheen, I-Shyan] Chang Gung Univ, Coll Med, Taoyuan, Taiwan.
[Chen, Chien-Hung; Hu, Tsung-Hui] Kaohsiung Chang Gung Mem Hosp, Div Hepatogastroenterol, Kaohsiung, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung Memorial Hospital; Chang Gung
Memorial Hospital; Chang Gung University; Chang Gung Memorial Hospital
RP Chen, CH (corresponding author), Kaohsiung Chang Gung Mem Hosp, Div Hepatogastroenterol, Dept Internal Med, 123 Dapi Rd, Kaohsiung 83301, Taiwan.; Tung, SY (corresponding author), Chiayi Chang Gung Mem Hosp, Dept Internal Med, Div Hepatogastroenterol, 6,Sec W,Jiapu Rd, Puzi 61363, Chiayi, Taiwan.
EM e580306@ms31.hinet.net; ma1898@cloud.cgmh.org.tw
RI Lin, Chiu-Yue/AFE-3858-2022; Chen, Chien-Hung/X-4596-2019
OI Lin, Chih-Lang/0000-0002-1225-3895; Lin, Chun-Yen/0000-0003-3007-3190
FU Chang Gung Memory Research Grant
FX This study was supported by the Chang Gung Memory Research Grant. We
thank all patients, their medical providers, and collectors of clinical
data enrolled in this study, and all authors for their contributions to
the manuscript.
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NR 33
TC 1
Z9 1
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1352-0504
EI 1365-2893
J9 J VIRAL HEPATITIS
JI J. Viral Hepatitis
PD MAY
PY 2020
VL 27
IS 5
BP 505
EP 513
DI 10.1111/jvh.13262
EA FEB 2020
PG 9
WC Gastroenterology & Hepatology; Infectious Diseases; Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Infectious Diseases; Virology
GA KZ2VD
UT WOS:000512181900001
PM 32039536
DA 2025-01-07
ER
PT J
AU Bayarsaikhan, G
Bayarsaikhan, D
Lee, J
Lee, B
AF Bayarsaikhan, Govigerel
Bayarsaikhan, Delger
Lee, Jaewon
Lee, Bonghee
TI Targeting Scavenger Receptors in Inflammatory Disorders and Oxidative
Stress
SO ANTIOXIDANTS
LA English
DT Review
DE AGEs; AOPPs; ALEs; scavenger receptors; oxidative stress; inflammation;
gene knockout
ID GLYCATION END-PRODUCTS; INDUCED GLOMERULAR INJURY; PROTEIN PRODUCTS;
ADVANCED GLYCOXIDATION; SYSTEMIC INFLAMMATION; PROTECTIVE ROLE;
LIVER-INJURY; RAGE; ACTIVATION; AGES
AB Oxidative stress and inflammation cannot be considered as diseases themselves; however, they are major risk factors for the development and progression of the pathogenesis underlying many illnesses, such as cancer, neurological disorders (including Alzheimer's disease and Parkinson's disease), autoimmune and metabolic disorders, etc. According to the results obtained from extensive studies, oxidative stress-induced biomolecules, such as advanced oxidation protein products, advanced glycation end products, and advanced lipoxidation end products, are critical for an accelerated level of inflammation and oxidative stress-induced cellular damage, as reflected in their strong affinity to a wide range of scavenger receptors. Based on the limitations of antioxidative and anti-inflammatory molecules in practical applications, targeting such interactions between harmful molecules and their cellular receptors/signaling with advances in gene engineering technology, such as CRISPR or TALEN, may prove to be a safe and effective alternative. In this review, we summarize the findings of recent studies focused on the deletion of scavenger receptors under oxidative stress as a development in the therapeutic approaches against the diseases linked to inflammation and the contribution of advanced glycation end products (AGEs), advanced lipid peroxidation products (ALEs), and advanced oxidation protein products (AOPPs).
C1 [Bayarsaikhan, Govigerel; Bayarsaikhan, Delger; Lee, Jaewon; Lee, Bonghee] Gachon Univ, Lee Gil Ya Canc & Diabet Inst, Incheon 406840, South Korea.
[Lee, Bonghee] Gachon Univ, Grad Sch Med, Dept Anat & Cell Biol, Incheon 405760, South Korea.
C3 Gachon University; Gachon University
RP Lee, B (corresponding author), Gachon Univ, Lee Gil Ya Canc & Diabet Inst, Incheon 406840, South Korea.; Lee, B (corresponding author), Gachon Univ, Grad Sch Med, Dept Anat & Cell Biol, Incheon 405760, South Korea.
EM govio888@gachon.ac.kr; degii07@gachon.ac.kr; jwlee169@gachon.ac.kr;
bhlee@gachon.ac.kr
FU National Institute of Health, Korea [2021ER130101, 2021ER100901]
FX This research was supported by the grant No. 2021ER130101 and
2021ER100901 by the National Institute of Health, Korea.
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NR 164
TC 9
Z9 10
U1 3
U2 23
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-3921
J9 ANTIOXIDANTS-BASEL
JI Antioxidants
PD MAY
PY 2022
VL 11
IS 5
AR 936
DI 10.3390/antiox11050936
PG 21
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Food Science &
Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Food Science
& Technology
GA 1T7PH
UT WOS:000804919600001
PM 35624800
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Spandole, S
Cimponeriu, D
Berca, LM
Mihaescu, G
AF Spandole, Sonia
Cimponeriu, Danut
Berca, Lavinia Mariana
Mihaescu, Grigore
TI Human anelloviruses: an update of molecular, epidemiological and
clinical aspects
SO ARCHIVES OF VIROLOGY
LA English
DT Review
ID TT-VIRUS-INFECTION; TORQUE-TENO-VIRUS; BLOOD MONONUCLEAR-CELLS;
TRANSFUSION-TRANSMITTED VIRUS; POSTTRANSFUSION NON-A; BONE-MARROW-CELLS;
FULMINANT HEPATIC-FAILURE; TO-INFANT TRANSMISSION; CHRONIC
LIVER-DISEASE; HUMAN DNA VIRUS
AB Human torque teno viruses (TTVs) are new, emerging infectious agents, recently assigned to the family Anelloviridae. The first representative of the genus, torque teno virus (TTV), was discovered in 1997, followed by torque teno mini virus (TTMV) in 2000, and torque teno midi virus (TTMDV) in 2007. These viruses are characterized by an extremely high prevalence, with relatively uniform distribution worldwide and a high level of genomic heterogeneity, as well as an apparent pan-tropism at the host level. Although these viruses have a very high prevalence in the general population across the globe, neither their interaction with their hosts nor their direct involvement in the etiology of specific diseases are fully understood. Since their discovery, human anelloviruses, and especially TTV, have been suggested to be associated with various diseases, such as hepatitis, respiratory diseases, cancer, hematological and autoimmune disorders, with few arguments for their direct involvement. Recent studies have started to reveal interactions between TTVs and the host's immune system, leading to new hypotheses for potential pathological mechanisms of these viruses. In this review article, we discuss the most important aspects and current status of human TTVs in order to guide future studies.
C1 [Spandole, Sonia; Cimponeriu, Danut] Univ Bucharest, Dept Genet, Bucharest 060101, Romania.
[Berca, Lavinia Mariana] Natl Inst Res & Dev Food Bioresources, Mol Biol Lab, Bucharest 020323, Romania.
[Mihaescu, Grigore] Univ Bucharest, Dept Microbiol, Bucharest 060101, Romania.
C3 University of Bucharest; National Research & Development Institute for
Food Bioresources - IBA Bucharest; Cantacuzino Institute Bucharest;
University of Bucharest
RP Spandole, S (corresponding author), Univ Bucharest, Dept Genet, 1-3 Intrarea Portocalelor, Bucharest 060101, Romania.
EM sonia.spandole@gmail.com
RI Cimponeriu, Danut/AAT-4687-2021; Berca, Lavinia/Q-7400-2016;
Spandole-Dinu, Sonia/F-9946-2013
OI Spandole-Dinu, Sonia/0000-0002-7370-1911
FU Romanian Ministry of Education [PN 12 48]
FX This paper was written in the framework of project PN 12 48, funded by
the Romanian Ministry of Education and granted to the National Institute
of Research and Development for Food Bioresources.
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NR 199
TC 193
Z9 208
U1 0
U2 27
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0304-8608
EI 1432-8798
J9 ARCH VIROL
JI Arch. Virol.
PD APR
PY 2015
VL 160
IS 4
BP 893
EP 908
DI 10.1007/s00705-015-2363-9
PG 16
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA CE0RW
UT WOS:000351514100002
PM 25680568
OA Bronze
DA 2025-01-07
ER
PT J
AU Krishnan, K
AF Krishnan, Kannabiran
TI A Systematic Review on the Impact of Micro-Nanoplastics Exposure on
Human Health and Diseases
SO BIOINTERFACE RESEARCH IN APPLIED CHEMISTRY
LA English
DT Review
DE microplastics; nanoplastics; micro-nanoplastics; environmental
pollution; ecotoxicity; inflammation; human health
ID MICROPLASTICS; BIODEGRADATION; TRANSLOCATION; DISSEMINATION;
NANOPARTICLES; PARTICLES; FIBERS; WATER
AB Plastic production is continuously increasing worldwide for daily use. Micro-plastics and nano-plastics remain major emerging pollutants and threaten the environment, ecosystem, human health, and well-being. Micro-nanoplastics (MNPs) are also exposed to humans through cosmetics, inhalation, ingestion, drinking water, dietary sources, and drug formulations. Oral uptake is the major among the different exposure routes of MNPs to humans. After entry, it gets absorbed due to its nano size (<100 nm) and easily distributed to all parts of the body through blood, affecting multiple organs, especially vital organs of the human body leading to severe diseases. It causes cancer, heart, liver, and kidney diseases, crosses the blood-brain barrier, and affects the brain. Its adsorption with protein leads to multi-layered corona formation in human blood plasma. MNPs interact with immune cells and induce pro-inflammatory mediators, inflammatory reactions, reactive oxygen species (ROS) production, and associated cytotoxicity. MNPs suppress T lymphocyte activity which results in a lack of immune regulation leading to autoimmune diseases. Hence, it is necessary to understand the impact of MNPs exposure on humans. Strict control measures for the production and use of plastics and developing appropriate strategies for safe disposal would prevent MNPs-mediated toxicity in humans.
C1 [Krishnan, Kannabiran] Vellore Inst Technol, Sch Biosci & Technol, Dept Biomed Sci, Vellore 632014, Tamil Nadu, India.
C3 Vellore Institute of Technology (VIT); VIT Vellore
RP Krishnan, K (corresponding author), Vellore Inst Technol, Sch Biosci & Technol, Dept Biomed Sci, Vellore 632014, Tamil Nadu, India.
EM kkb@vit.ac.in
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NR 71
TC 8
Z9 8
U1 14
U2 143
PU AMG TRANSCEND ASSOC
PI BUCHAREST
PA POLIZU ST 1-7, BUILDING I, ROOM, I-102, BUCHAREST, ROMANIA
SN 2069-5837
J9 BIOINTERFACE RES APP
JI Biointerface Res. Appl. Chem.
PD AUG 15
PY 2023
VL 13
IS 4
AR 381
DI 10.33263/BRIAC134.381
PG 12
WC Chemistry, Applied
WE Emerging Sources Citation Index (ESCI)
SC Chemistry
GA 6H6BP
UT WOS:000885522800019
OA gold
DA 2025-01-07
ER
PT J
AU Asao, H
AF Asao, Hironobu
TI Interleukin-21 in Viral Infections
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE interleukin (IL)-21; CD4(+) T cell; follicular helper T (Tfh) cell; B
cell; CD8(+) T cell; T cell exhaustion
ID FOLLICULAR-HELPER-CELLS; COMMON GAMMA-CHAIN; CD8(+) T-CELLS; IMMUNE
ACTIVATION; VIRUS-INFECTION; HIV-1 INFECTION; LIVER-CIRRHOSIS;
EFFECTOR-CELLS; IL-21 RECEPTOR; CUTTING EDGE
AB Interleukin (IL)-21 is a cytokine that affects the differentiation and function of lymphoid and myeloid cells and regulates both innate and adaptive immune responses. In addition to regulating the immune response to tumor and viral infections, IL-21 also has a profound effect on the development of autoimmune and inflammatory diseases. IL-21 is produced mainly from CD4(+) T cells-in particular, follicular helper T (Tfh) cells-which have a great influence on the regulation of antibody production. It is also an important cytokine for the activation of CD8(+) T cells, and its role in recovering the function of CD8(+) T cells exhausted by chronic microbial infections and cancer has been clarified. Thus, IL-21 plays an extremely important role in viral infections, especially chronic viral infections. In this review, I will introduce the findings to date on how IL-21 is involved in some typical viral infections and the potential of treating viral diseases with IL-21.
C1 [Asao, Hironobu] Yamagata Univ, Dept Immunol, Fac Med, 2-2-2 Iida Nishi, Yamagata 9909585, Japan.
C3 Yamagata University
RP Asao, H (corresponding author), Yamagata Univ, Dept Immunol, Fac Med, 2-2-2 Iida Nishi, Yamagata 9909585, Japan.
EM asao-h@med.id.yamagata-u.ac.jp
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NR 154
TC 13
Z9 13
U1 1
U2 20
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2021
VL 22
IS 17
AR 9521
DI 10.3390/ijms22179521
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA UO0GN
UT WOS:000694383100001
PM 34502427
OA gold, Green Published
DA 2025-01-07
ER
PT S
AU Devaux, J
Fykkolodziej, B
Gow, A
AF Devaux, Jerome
Fykkolodziej, Bozena
Gow, Alexander
BE Yu, ASL
TI Claudin Proteins and Neuronal Function
SO CLAUDINS
SE Current Topics in Membranes
LA English
DT Review; Book Chapter
ID OLIGODENDROCYTE-SPECIFIC PROTEIN; EXPERIMENTAL AUTOIMMUNE
ENCEPHALOMYELITIS; PATHOGENIC T-CELLS; MAJOR DENSE LINE; TIGHT
JUNCTIONS; MULTIPLE-SCLEROSIS; MYELIN SHEATHS; WHITE-MATTER; CNS MYELIN;
OSP/CLAUDIN-11-INDUCED EAE
AB OVERVIEW
The identification and characterization of the claudin family of tight junction (TJ) proteins in the late 1990s ushered in a new era for research into the molecular and cellular biology of intercellular junctions. Since that time, TJs have been studied in the contexts of many diseases including deafness, male infertility, cancer, bacterial invasion, and liver and kidney disorders. In this review, we consider the role of claudins in the nervous system focusing on the mechanisms by which TJs in glial cells are involved in neuronal function. Electrophysiological evidence suggests that claudins may operate in the central nervous system (CS) in a manner similar to polarized epithelia. We also evaluate hypotheses that TJs are the gatekeepers of an immune-privileged myelin compartment and that us emerged during evolution to form major adhesive forces within the myelin sheath. Finally, we consider the implications of disrupted CNS myelin TJs in the contexts of behavioral disorders (schizophrenia) and demyelinating or hypomyelinating diseases (multiple sclerosis and the leukodystrophies), and explore evidence of a possible mechanism governing affective disorder symptoms in patients with white matter abnormalities.
C1 [Devaux, Jerome] Univ Mediterranee Univ Paul Cezanne, CRN2M, CNRS, Dept Signalisat Neuronale,UMR,IFR Jean Roche, Marseille, France.
[Fykkolodziej, Bozena; Gow, Alexander] Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI USA.
[Gow, Alexander] Wayne State Univ, Sch Med, Carman & Ann Adams Dept Pediat, Detroit, MI USA.
[Gow, Alexander] Wayne State Univ, Sch Med, Dept Neurol, Detroit, MI USA.
C3 Centre National de la Recherche Scientifique (CNRS); Aix-Marseille
Universite; Wayne State University; Wayne State University; Wayne State
University
RP Devaux, J (corresponding author), Univ Mediterranee Univ Paul Cezanne, CRN2M, CNRS, Dept Signalisat Neuronale,UMR,IFR Jean Roche, Marseille, France.
RI ; Devaux, jerome/X-8581-2019
OI gow, alexander/0000-0001-7446-8990; Devaux, jerome/0000-0001-6383-4334
FU NIDCD NIH HHS [R01 DC006262] Funding Source: Medline; NINDS NIH HHS [R01
NS043783] Funding Source: Medline
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U1 0
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PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1063-5823
BN 978-0-12-381039-7
J9 CURR TOP MEMBR
JI Curr. Top. Membr.
PY 2010
VL 65
BP 229
EP 253
DI 10.1016/S1063-5823(10)65010-7
PG 25
WC Biochemistry & Molecular Biology; Biophysics
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA BPZ47
UT WOS:000280437500010
PM 25013353
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Chalaris, A
Schmidt-Arras, D
Yamamoto, K
Rose-John, S
AF Chalaris, Athena
Schmidt-Arras, Dirk
Yamamoto, Kosuke
Rose-John, Stefan
TI Interleukin-6 Trans-Signaling and Colonic Cancer Associated with
Inflammatory Bowel Disease
SO DIGESTIVE DISEASES
LA English
DT Article; Proceedings Paper
CT Falk Workshop on Inflammation and Cancer
CY JAN 26-27, 2012
CL Hamburg, GERMANY
DE Cancer; IL-6; IL-6R; Inflammation; Shedding; Soluble receptor;
Trans-signaling
ID SOLUBLE IL-6 RECEPTOR; CYTOKINE-INDEPENDENT GROWTH;
NECROSIS-FACTOR-ALPHA; STAT3 ACTIVATION; EPITHELIAL-CELLS; TNF-ALPHA;
GP130; MICE; BLOCKADE; PROGRESSION
AB Interleukin-6 (IL-6) is a cytokine largely induced during infection, inflammation, and cancer. In the liver, IL-6 induces the synthesis of acute-phase proteins, which are believed to support the response of the body during infection and inflammation. Moreover, IL-6 has been reported to be a growth factor in multiple myeloma. IL-6 on cells binds to an IL-6 receptor (IL-6R) forming an IL-6/IL-6R complex, which associates with a homodimer of a second receptor subunit, gp130, to initiate signaling. Gp130 is present on all cells of the body, whereas IL-6R is only expressed on hepatocytes, some leukocytes, and some epithelial cells. Since gp130 has no measurable affinity for IL-6, cells which do not express IL-6R are unresponsive to the cytokine. A soluble form of IL-6R, which is found in the blood, can still bind IL-6 and the complex of IL-6/sIL-6R can bind to cellular gp130 also on cells without IL6R expression. This signaling mechanism has been called trans-signaling. Interestingly, a soluble form of gp130 (sgp130) blocks IL-6 trans-signaling without affecting classic IL-6 signaling via the membrane-bound IL-6R. We used a dimerized version of sgp130 fused to the Fc portion of an IgG1 antibody (sgp130Fc) to discriminate between classic and trans-signaling of IL-6. It turned out that proinflammatory activities of IL-6 are mediated via trans-signaling, whereas anti-inflammatory or regenerative activities are mediated via classic signaling. These results are important for strategies to inhibit IL-6 signaling in autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease, and inflammation-associated colorectal cancer. Copyright (c) 2012 S. Karger AG, Basel
C1 [Chalaris, Athena; Schmidt-Arras, Dirk; Yamamoto, Kosuke; Rose-John, Stefan] Univ Kiel, Inst Biochem, DE-24098 Kiel, Germany.
C3 University of Kiel
RP Rose-John, S (corresponding author), Univ Kiel, Inst Biochem, Olshausenstr 40, DE-24098 Kiel, Germany.
EM rosejohn@biochem.uni-kiel.de
RI Schmidt-Arras, Dirk/ABB-6644-2020; Rose-John, Stefan/A-7998-2010;
Schmidt-Arras, Dirk/J-6688-2014
OI Rose-John, Stefan/0000-0002-7519-3279; Schmidt-Arras,
Dirk/0000-0002-1072-7495; Yamamoto, Kosuke/0000-0001-6837-3549
FU German Academic Exchange Service (DAAD); Deutsche
Forschungsgemeinschaft, Bonn [SFB841, SFB877]; Cluster of Excellence
'Inflammation at Interfaces'
FX Dr. Kosuke Yamamoto was supported by a postdoctoral fellowship from the
German Academic Exchange Service (DAAD). The work described in this
article was funded by the Deutsche Forschungsgemeinschaft, Bonn,
(SFB841, project C1; SFB877, project A1) and by the Cluster of
Excellence 'Inflammation at Interfaces'.
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NR 73
TC 27
Z9 33
U1 0
U2 9
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PY 2012
VL 30
IS 5
BP 492
EP 499
DI 10.1159/000341698
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology
GA 030IE
UT WOS:000310563600007
PM 23108305
DA 2025-01-07
ER
PT J
AU Ma, Q
AF Ma, Qiang
TI Influence of light on aryl hydrocarbon receptor signaling and
consequences in drug metabolism, physiology and disease
SO EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY
LA English
DT Review
DE AH receptor; AHR ligand; CYP1A1 induction; FICZ; tryptophan
photoreaction; UV response
ID CYP1A1 GENE-EXPRESSION; NF-KAPPA-B; PROTEIN-TYROSINE PHOSPHATASES;
MESSENGER-RNA EXPRESSION; GROWTH-FACTOR RECEPTOR; LIVER-CELL CULTURE;
REGULATORY T-CELLS; AH-RECEPTOR; ULTRAVIOLET-B; HEMATOPOIETIC STEM
AB Introduction: A key to understanding the biological function(s) of the aryl hydrocarbon receptor (AHR) - a xenobiotic-activated receptor - is to identify its endogenous ligand(s). The discovery of a tryptophan photoproduct 6-formylindolo[3,2-b]carbazole (FICZ) as an endogenous, high affinity agonist of AHR filled this knowledge gap in the context of skin physiology and pathology in response to light and opened several new directions for research on AHR.
Area covered: This paper reviews major developments in the study of light-elicited AHR signaling and its impact on drug metabolism, skin physiology and disease with a focus on the identification of AHR ligands from Trp photoproducts and the AHR-mediated UV response. This review consists of material obtained from Medline and PubMed literature searches up to May 2011.
Expert opinion: The recognition of FICZ as a potent, endogenous ligand of AHR provided a molecular link between light exposure and AHR signaling and function. The uncovering of the bifurcated signaling pathway of AHR in the mammalian UV response - that is, activation of the cytoplasmic AHR by light via FICZ leads to: i) AHR/AH response element-dependent transcription to induce CYP1A1 and ii) activation of the AHR-pp60(src)-EGFR pathway to induce Cox-2 - put forward a working model for the multiple roles of AHR in skin function and disease that include drug metabolism, circadian oscillation, melanogenesis, inflammation, immunosuppression and cancer. Such findings suggest AHR as a therapeutic target for cancer, autoimmune dysfunction, inflammatory disease and stem cell therapy.
C1 Ctr Dis Control & Prevent, Receptor Biol Lab, Toxicol & Mol Biol Branch, Hlth Effects Lab Div,NIOSH, Morgantown, WV 26505 USA.
C3 Centers for Disease Control & Prevention - USA; National Institute for
Occupational Safety & Health (NIOSH)
RP Ma, Q (corresponding author), Ctr Dis Control & Prevent, Receptor Biol Lab, Toxicol & Mol Biol Branch, Hlth Effects Lab Div,NIOSH, Mailstop 3014,1095 Willowdale Rd, Morgantown, WV 26505 USA.
EM qam1@cdc.gov
RI Ma, Qiang/AAD-2446-2021
FU National Institute for Occupational Safety and Health, Centers for
Disease Control and Prevention
FX This research was supported by the National Institute for Occupational
Safety and Health, Centers for Disease Control and Prevention. The
author declares no other conflicts of interest. The findings and
conclusions in this report are those of the authors and do not
necessarily represent the views of the National Institute for
Occupational Safety and Health.
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NR 181
TC 45
Z9 51
U1 0
U2 28
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1742-5255
EI 1744-7607
J9 EXPERT OPIN DRUG MET
JI Expert Opin. Drug Metab. Toxicol.
PD OCT
PY 2011
VL 7
IS 10
BP 1267
EP 1293
DI 10.1517/17425255.2011.614947
PG 27
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA 821IB
UT WOS:000294967200006
PM 21883026
DA 2025-01-07
ER
PT J
AU An, K
Xue, MJ
Zhong, JY
Yu, SN
Lan, TS
Qi, ZQ
Xia, JJ
AF An, Ke
Xue, Meng-Jiao
Zhong, Jia-Ying
Yu, Sheng-Nan
Lan, Tian-Shu
Qi, Zhong-Quan
Xia, Jun-Jie
TI Arsenic trioxide ameliorates experimental autoimmune encephalomyelitis
in C57BL/6 mice by inducing CD4+ T cell apoptosis
SO JOURNAL OF NEUROINFLAMMATION
LA English
DT Article
DE Experimental autoimmune encephalomyelitis; Arsenic trioxide; CD4(+) T
cells; Apoptosis
ID ACUTE PROMYELOCYTIC LEUKEMIA; TRANS-RETINOIC ACID; MULTIPLE-SCLEROSIS;
ALLOGRAFT SURVIVAL; CARDIAC ALLOGRAFTS; CANCER; MECHANISMS; LYMPHOCYTES;
ACTIVATION; INHIBITION
AB Background Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system characterized by severe white matter demyelination. Because of its complex pathogenesis, there is no definite cure for MS. Experimental autoimmune encephalomyelitis (EAE) is an ideal animal model for the study of MS. Arsenic trioxide (ATO) is an ancient Chinese medicine used for its therapeutic properties with several autoimmune diseases. It is also used to inhibit acute immune rejection due to its anti-inflammatory and immunosuppressive properties. However, it is unclear whether ATO has a therapeutic effect on EAE, and the underlying mechanisms have not yet been clearly elucidated. In this study, we attempted to assess whether ATO could be used to ameliorate EAE in mice. Methods ATO (0.5 mg/kg/day) was administered intraperitoneally to EAE mice 10 days post-immunization for 8 days. On day 22 post-immunization, the spinal cord, spleen, and blood were collected to analyze demyelination, inflammation, microglia activation, and the proportion of CD4(+) T cells. In vitro, for mechanistic studies, CD4(+) T cells were sorted from the spleen of naive C57BL/6 mice and treated with ATO and then used for an apoptosis assay, JC-1 staining, imaging under a transmission electron microscope, and western blotting. Results ATO delayed the onset of EAE and alleviated the severity of EAE in mice. Treatment with ATO also attenuated demyelination, alleviated inflammation, reduced microglia activation, and decreased the expression levels of IL-2, IFN-gamma, IL-1 beta, IL-6, and TNF-alpha in EAE mice. Moreover, the number and proportion of CD4(+) T cells in the spinal cord, spleen, and peripheral blood were reduced in ATO-treated EAE mice. Finally, ATO induced CD4(+) T cell apoptosis via the mitochondrial pathway both in vitro and in vivo. Additionally, the administration of ATO had no adverse effect on the heart, liver, or kidney function, nor did it induce apoptosis in the spinal cord. Conclusions Overall, our findings indicated that ATO plays a protective role in the initiation and progression of EAE and has the potential to be a novel drug in the treatment of MS.
C1 [An, Ke; Xue, Meng-Jiao; Zhong, Jia-Ying; Yu, Sheng-Nan; Xia, Jun-Jie] Xiamen Univ, Organ Transplantat Inst, Sch Med, Fujian Prov Key Lab Organ & Tissue Regenerat, Xiamen, Fujian, Peoples R China.
[Yu, Sheng-Nan] Xiamen Univ, Zhongshan Hosp, Dept Obstet & Gynecol, Xiamen, Fujian, Peoples R China.
[Lan, Tian-Shu] Fujian Prov Univ, Xiamen Med Coll, Key Lab Funct & Clin Translat Med, Xiamen, Fujian, Peoples R China.
[Qi, Zhong-Quan] Guangxi Univ, Sch Med, Nanning, Guangxi, Peoples R China.
C3 Xiamen University; Xiamen University; Xiamen Medical College; Fuzhou
University; Guangxi University
RP Xia, JJ (corresponding author), Xiamen Univ, Organ Transplantat Inst, Sch Med, Fujian Prov Key Lab Organ & Tissue Regenerat, Xiamen, Fujian, Peoples R China.; Qi, ZQ (corresponding author), Guangxi Univ, Sch Med, Nanning, Guangxi, Peoples R China.
EM yxyyz@gxu.edu.cn; xia@xmu.edu.cn
RI Xia, Junjie/C-9726-2012; An, Ke/JPX-5153-2023; Lan,
Tianshu/GQZ-6939-2022; wang, chenxi/HMD-9902-2023
OI Xia, Junjie/0000-0001-9714-7065
FU National Natural Science Foundation of China [81671583, 81971505,
81771271, 81971506]; National Key R&D Program of China [2018YFA0108304];
Fujian Provincial Health Education Joint Research Project
[WKJ2016-2-20]; key laboratory of functional and clinical translational
medicine, Fujian province university [JNYLC1813]
FX This study was supported by grants from the National Natural Science
Foundation of China (81671583), the National Key R&D Program of China
(2018YFA0108304), the National Natural Science Foundation of China
(81971505, 81771271, 81971506), the Fujian Provincial Health Education
Joint Research Project (WKJ2016-2-20), and the key laboratory of
functional and clinical translational medicine, Fujian province
university (JNYLC1813).
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NR 61
TC 20
Z9 22
U1 0
U2 19
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1742-2094
J9 J NEUROINFLAMM
JI J. Neuroinflamm.
PD MAY 6
PY 2020
VL 17
IS 1
AR 147
DI 10.1186/s12974-020-01829-x
PG 14
WC Immunology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Neurosciences & Neurology
GA LS1XU
UT WOS:000536185300008
PM 32375831
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Huggett, MT
Culver, EL
Kumar, M
Hurst, JM
Rodriguez-Justo, M
Chapman, MH
Johnson, GJ
Pereira, SP
Chapman, RW
Webster, GJM
Barnes, E
AF Huggett, Matthew T.
Culver, E. L.
Kumar, M.
Hurst, J. M.
Rodriguez-Justo, M.
Chapman, M. H.
Johnson, G. J.
Pereira, S. P.
Chapman, R. W.
Webster, George J. M.
Barnes, E.
TI Type 1 Autoimmune Pancreatitis and IgG4-Related Sclerosing Cholangitis
Is Associated With Extrapancreatic Organ Failure, Malignancy, and
Mortality in a Prospective UK Cohort
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; DIAGNOSTIC-CRITERIA; SERUM
IGG4; IGG4-ASSOCIATED CHOLANGITIS; CLINICAL PROFILE; CONSENSUS; RISK;
MULTICENTER; SUBTYPES; G4
AB OBJECTIVES: Type I autoimmune pancreatitis (AIP) and IgG4-related sclerosing cholangitis (IgG4-related SC) are now recognized as components of a multisystem IgG4-related disease (IgG4-RD). We aimed to define the clinical course and long-term outcomes in patients with AIP/IgG4-SC recruited from two large UK tertiary referral centers.
METHODS: Data were collected from 115 patients identified between 2004 and 2013, and all were followed up prospectively from diagnosis for a median of 33 months (range 1-107), and evaluated for response to therapy, the development of multiorgan involvement, and malignancy. Comparisons were made with national UK statistics.
RESULTS: Although there was an initial response to steroids in 97%, relapse occurred in 50% of patients. IgG4-SC was an important predictor of relapse (P<0.01). Malignancy occurred in 11% shortly before or after the diagnosis of IgG4-RD, including three hepatopancreaticobiliary cancers. The risk of any cancer at diagnosis or during follow-up when compared with matched national statistics was increased (odds ratio=2.25, CI=1.12-3.94, P=0.02). Organ dysfunction occurred within the pancreas, liver, kidney, lung, and brain. Mortality occurred in 10% of patients during follow-up. The risk of death was increased compared with matched national statistics (odds ratio=2.07, CI=1.07-3.55, P=0.02).
CONCLUSIONS: Our findings suggest that AIP and IgG4-SC are associated with significant morbidity and mortality owing to extrapancreatic organ failure and malignancy. Detailed clinical evaluation for evidence of organ dysfunction and associated malignancy is required both at first presentation and during long-term follow-up.
C1 [Huggett, Matthew T.; Pereira, S. P.] UCL, Inst Liver & Digest Hlth, London, England.
[Huggett, Matthew T.; Kumar, M.; Chapman, M. H.; Johnson, G. J.; Pereira, S. P.; Webster, George J. M.] Univ Coll London Hosp, Dept Gastroenterol & Hepatol, London NW1 2PG, England.
[Culver, E. L.; Chapman, R. W.; Barnes, E.] John Radcliffe Hosp, Translat Gastroenterol Unit, Oxford OX3 9DU, England.
[Culver, E. L.; Chapman, R. W.; Barnes, E.] Univ Oxford, NDM, Oxford Martin Sch, Oxford, England.
[Hurst, J. M.] Univ Oxford, Oxford Martin Sch, Inst Emerging Dis, Oxford, England.
[Rodriguez-Justo, M.] Univ Coll London Hosp, Dept Pathol, London NW1 2PG, England.
[Barnes, E.] Univ Oxford, Oxford NIHR BRC, Oxford, England.
C3 University of London; University College London; University of London;
University College London; University College London Hospitals NHS
Foundation Trust; University of Oxford; University of Oxford; University
of Oxford; University of London; University College London; University
College London Hospitals NHS Foundation Trust; University of Oxford
RP Webster, GJM (corresponding author), Univ Coll London Hosp, Dept Gastroenterol & Hepatol, Ground Floor West,250 Euston Rd, London NW1 2PG, England.
EM george.webster@uclh.nhs.uk
RI Pereira, Stephen/C-5639-2009; Rodriguez-Justo, Manuel/C-6204-2009
OI Pereira, Stephen/0000-0003-0821-1809; Rodriguez-Justo,
Manuel/0000-0001-5007-1761; Culver, Emma/0000-0001-9644-8392; Barnes,
Eleanor/0000-0002-0860-0831
FU MRC [MR/K010239/1] Funding Source: UKRI
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NR 47
TC 177
Z9 198
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD OCT
PY 2014
VL 109
IS 10
BP 1675
EP 1683
DI 10.1038/ajg.2014.223
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AS7UM
UT WOS:000344460100024
PM 25155229
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Imam, MH
Eaton, JE
Puckett, JS
Loftus, EV
Mathis, KL
Gossard, AA
Talwalkar, JA
Lindor, KD
AF Imam, Mohamad H.
Eaton, John E.
Puckett, Jason S.
Loftus, Edward V., Jr.
Mathis, Keine L.
Gossard, Andrea A.
Talwalkar, Jayant A.
Lindor, Keith D.
TI Neoplasia in the ileoanal pouch following colectomy in patients with
ulcerative colitis and primary sclerosing cholangitis
SO JOURNAL OF CROHNS & COLITIS
LA English
DT Article
DE Colorectal cancer; Autoimmune liver disease; Inflammatory bowel disease
ID INFLAMMATORY-BOWEL-DISEASE; COLORECTAL NEOPLASIA; RESTORATIVE
PROCTOCOLECTOMY; NATURAL-HISTORY; INCREASED RISK; ILEAL POUCH;
DYSPLASIA; ADENOCARCINOMA; POPULATION; MANAGEMENT
AB Background Et Aims: Primary sclerosing cholangitis (PSC) is typically associated with inflammatory bowel disease (IBD), particularly ulcerative colitis (UC). PSC IBD patients are at an increased risk for colorectal neoplasia. The ileal pouch-anal anastomosis (IPM) is a treatment option for patients with medically refractory UC or neoplasia. However, little is known about the development of pouch neoplasia in PSC UC patients following an IPM. We aim to describe the incidence of pouch neoplasia in PSC UC patients after an IPM.
Methods: We conducted a retrospective chart review of patients with a confirmed diagnosis of PSC and IBD who underwent colectomy with IPAA followed by pouch surveillance between 1995 and 2012.
Results: Sixty-five patients were included in the cohort and were followed up from the time of colectomy/IPAA for a median of 6 years. The most common indications for surgery were low-grade dysplasia (LGD) and refractory colitis. Only 3 patients developed evidence of neoplasia (LGD n = 1, high-grade dysplasia n = 1, adenocarcinoma n = 1). The cumulative 5-year incidence of pouch neoplasia was 5.6% (95% confidence intervals [CI], 1.8%-16.1%).
Conclusion: Based on our short-term follow-up, surveying the pouch frequently appears to be an unnecessary practice in PSC-IBD patients. Longer follow-up will be needed to develop an optimal surveillance strategy for the development of dysplasia and cancer in such patients. (C) 2014 European Crohn's and Colitis Organisation. Published by Elsevier B.V. All rights reserved.
C1 [Imam, Mohamad H.; Eaton, John E.; Loftus, Edward V., Jr.; Gossard, Andrea A.; Talwalkar, Jayant A.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA.
[Puckett, Jason S.] Mayo Clin, Dept Med, Rochester, MN USA.
[Mathis, Keine L.] Mayo Clin, Div Colorectal Surg, Rochester, MN USA.
[Lindor, Keith D.] Arizona State Univ, Coll Hlth Solut, Phoenix, AZ 85004 USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic; Arizona State University; Arizona
State University-Downtown Phoenix
RP Lindor, KD (corresponding author), Arizona State Univ, Coll Hlth Solut, Mail Code 3020,550 N 3rd St, Phoenix, AZ 85004 USA.
EM Keith.Lindor@asu.edu
RI Loftus, Edward/E-8304-2011
OI Loftus, Edward/0000-0001-7199-6851
CR Bambha K, 2003, GASTROENTEROLOGY, V125, P1364, DOI 10.1016/j.gastro.2003.07.011
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NR 20
TC 20
Z9 20
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1873-9946
EI 1876-4479
J9 J CROHNS COLITIS
JI J. Crohns Colitis
PD OCT 1
PY 2014
VL 8
IS 10
BP 1294
EP 1299
DI 10.1016/j.crohns.2014.03.011
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AS2RU
UT WOS:000344128100017
PM 24768559
OA Bronze
DA 2025-01-07
ER
PT J
AU Relation, T
Yi, T
Guess, AJ
La Perle, K
Otsuru, S
Hasgur, S
Dominici, M
Breuer, C
Horwitz, EM
AF Relation, Theresa
Yi, Tai
Guess, Adam J.
La Perle, Krista
Otsuru, Satoru
Hasgur, Suheyla
Dominici, Massimo
Breuer, Christopher
Horwitz, Edwin M.
TI Intratumoral Delivery of Interferonγ-Secreting Mesenchymal Stromal Cells
Repolarizes Tumor-Associated Macrophages and Suppresses Neuroblastoma
Proliferation In Vivo
SO STEM CELLS
LA English
DT Article
DE Mesenchymal stem cells; Microenvironment; Immunotherapy; Cancer;
Cellular therapy
ID STEM-CELLS; MICROENVIRONMENT; THERAPY; BONE; MECHANISMS; RESPONSES;
CRITERIA; DISEASE; GROWTH; VITRO
AB Neuroblastoma, the most common extracranial solid tumor in childhood, remains a therapeutic challenge. However, one promising patient treatment strategy is the delivery of anti-tumor therapeutic agents via mesenchymal stromal cell (MSC) therapy. MSCs have been safely used to treat genetic bone diseases such as osteogenesis imperfecta, cardiovascular diseases, autoimmune diseases, and cancer. The pro-inflammatory cytokine interferon-gamma (IFN gamma) has been shown to decrease tumor proliferation by altering the tumor microenvironment (TME). Despite this, clinical trials of systemic IFN gamma therapy have failed due to the high blood concentration required and associated systemic toxicities. Here, we developed an intra-adrenal model of neuroblastoma, characterized by liver and lung metastases. We then engineered MSCs to deliver IFN gamma directly to the TME. In vitro, these MSCs polarized murine macrophages to the M1 phenotype. In vivo, we attained a therapeutically active TME concentration of IFN gamma without increased systemic concentration or toxicity. The TME-specific IFN gamma reduced tumor growth rate and increased survival in two models of T cell deficient athymic nude mice. Absence of this benefit in NOD SCID gamma (NSG) immunodeficient mouse model indicates a mechanism dependent on the innate immune system. IL-17 and IL-23p19, both uniquely M1 polarization markers, transiently increased in the tumor interstitial fluid. Finally, the MSC vehicle did not promote tumor growth. These findings reveal that MSCs can deliver effective cytokine therapy directly to the tumor while avoiding systemic toxicity. This method transiently induces inflammatory M1 macrophage polarization, which reduces tumor burden in our novel neuroblastoma murine model.
C1 [Relation, Theresa] Ohio State Univ, Med Scientist Training Program, Columbus, OH 43210 USA.
[Relation, Theresa; Guess, Adam J.; Otsuru, Satoru; Hasgur, Suheyla; Horwitz, Edwin M.] Nationwide Childrens Hosp, Res Inst, Ctr Childhood Canc & Blood Dis, Columbus, OH USA.
[Yi, Tai; Breuer, Christopher] Nationwide Childrens Hosp, Res Inst, Ctr Cardiovasc Res, Columbus, OH USA.
[La Perle, Krista] Ohio State Univ, Dept Vet Biosci, Columbus, OH 43210 USA.
[Dominici, Massimo] Univ Modena & Reggio Emilia, Dept Med & Surg Sci Children & Adults, Modena, Italy.
C3 University System of Ohio; Ohio State University; University System of
Ohio; Ohio State University; Nationwide Childrens Hospital; Research
Institute at Nationwide Children's Hospital; University System of Ohio;
Ohio State University; Nationwide Childrens Hospital; Research Institute
at Nationwide Children's Hospital; University System of Ohio; Ohio State
University; Universita di Modena e Reggio Emilia
RP Horwitz, EM (corresponding author), Emory Univ, Dept Pediat, Childrens Healthcare Atlanta, Aflac Canc & Blood Disorders Ctr, 2015 Uppergate Dr, Atlanta, GA 30322 USA.
EM edwin.horwitz@emory.edu
RI Dominici, Massimo/K-8014-2016; Otsuru, Satoru/HKN-3355-2023; Breuer,
Christoph/F-4482-2011; La Perle, Krista/B-3099-2015
OI Breuer, Christopher/0000-0003-0987-3898; Dominici,
Massimo/0000-0002-4007-1503
FU CancerFree Kids Foundation; Families for a Cure Foundation; Ohio State
Cancer Center; Research Institute at Nationwide Children's Hospital
FX This work was partially supported by the CancerFree Kids Foundation,
Families for a Cure Foundation, Ohio State Cancer Center Support Grant,
and the Research Institute at Nationwide Children's Hospital. E.M.H. is
currently affiliated with Aflac Cancer and Blood Disorders Center,
Children's Healthcare of Atlanta, Emory University Department of
Pediatrics, Atlanta, GA.
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NR 44
TC 55
Z9 59
U1 1
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PD JUN
PY 2018
VL 36
IS 6
BP 915
EP 924
DI 10.1002/stem.2801
PG 10
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA GI2BQ
UT WOS:000434175000011
PM 29430789
OA Bronze, Green Submitted
DA 2025-01-07
ER
PT S
AU Ilangumaran, S
Bobbala, D
Ramanathan, S
AF Ilangumaran, Subburaj
Bobbala, Diwakar
Ramanathan, Sheela
BE Yoshimura, A
TI SOCS1: Regulator of T Cells in Autoimmunity and Cancer
SO EMERGING CONCEPTS TARGETING IMMUNE CHECKPOINTS IN CANCER AND
AUTOIMMUNITY
SE Current Topics in Microbiology and Immunology
LA English
DT Review; Book Chapter
ID CYTOKINE SIGNALING 1; KINASE INHIBITORY REGION; JANUS TYROSINE KINASE;
DENDRITIC CELLS; IFN-GAMMA; IN-VIVO; NEGATIVE REGULATION;
HEPATOCELLULAR-CARCINOMA; FUNCTIONAL-DIFFERENTIATION;
NUCLEAR-LOCALIZATION
AB SOCS1 is a negative feedback regulator of cytokine and growth factor receptor signaling, and plays an indispensable role in attenuating interferon gamma signaling. Studies on SOCS1-deficient mice have established a crucial role for SOCS1 in regulating CD8(+) T cell homeostasis. In the thymus, SOCS1 prevents thymocytes that had failed positive selection from surviving and expanding, ensures negative selection and prevents inappropriate developmental skewing toward the CD8 lineage. In the periphery, SOCS1 not only controls production of T cell stimulatory cytokines but also attenuates the sensitivity of CD8(+) T cells to synergistic cytokine stimulation and antigen non-specific activation. As cytokine stimulation of CD8(+) T lymphocytes increases their sensitivity to low affinity TCR ligands, SOCS1 likely contributes to peripheral T cell tolerance by putting brakes on aberrant T cell activation driven by inflammatory cytokines. In addition, SOCS1 is critical to maintain the stability of T regulatory cells and control their plasticity to become pathogenic Th17 and Th1 cells under the harmful influence of inflammatory cytokines. SOCS1 also regulates T cell activation by dendritic cells via modulating their generation, maturation, antigen presentation, costimulatory signaling, and cytokine production. The above control mechanisms of SOCS1 on T cells, T regulatory cells and dendritic cells collectively contribute to immunological tolerance and prevent autoimmune manifestation. On other hand, silencing SOCS1 in dendritic cells or CD8(+) T cells stimulates efficient antitumor immunity. Thus, even though SOCS1 is not a cell surface checkpoint inhibitor, its regulatory functions on T cell responses qualify SOCS1as a "non-classical" checkpoint blocker. SOCS1 also functions as a tumor suppressor in cancer cells by regulating oncogenic signal transduction pathways. The loss of SOCS1 expression observed in many tumors may have an impact on classical checkpoint pathways. The potential to exploit SOCS1 to treat inflammatory/autoimmune diseases and elicit antitumor immunity is discussed.
C1 [Ilangumaran, Subburaj; Bobbala, Diwakar; Ramanathan, Sheela] Univ Sherbrooke, Fac Med & Hlth Sci, Dept Pediat, Immunol Div, 3001 North 12th Ave, Sherbrooke, PQ J1H 5N4, Canada.
C3 University of Sherbrooke
RP Ilangumaran, S (corresponding author), Univ Sherbrooke, Fac Med & Hlth Sci, Dept Pediat, Immunol Div, 3001 North 12th Ave, Sherbrooke, PQ J1H 5N4, Canada.
EM Subburaj.Ilangumaran@Usherbrooke.ca
OI Ilangumaran, Subburaj/0000-0002-7563-576X
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NR 167
TC 27
Z9 29
U1 0
U2 8
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 0070-217X
EI 2196-9965
BN 978-3-319-68929-6; 978-3-319-68928-9
J9 CURR TOP MICROBIOL
JI Curr.Top.Microbiol.Immunol.
PY 2017
VL 410
BP 159
EP 189
DI 10.1007/82_2017_63
D2 10.1007/978-3-319-68929-6
PG 31
WC Oncology; Immunology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA BI9XH
UT WOS:000416540000008
PM 28900678
DA 2025-01-07
ER
PT J
AU Stephens, C
Moreno-Casares, A
López-Nevot, MA
García-Cortés, M
Medina-Cáliz, I
Hallal, H
Soriano, G
Roman, E
Ruiz-Cabello, F
Romero-Gomez, M
Lucena, MI
Andrade, RJ
AF Stephens, Camilla
Moreno-Casares, Antonia
Lopez-Nevot, Miguel-Angel
Garcia-Cortes, Miren
Medina-Caliz, Inmaculada
Hallal, Hacibe
Soriano, German
Roman, Eva
Ruiz-Cabello, Francisco
Romero-Gomez, Manuel
Isabel Lucena, M.
Andrade, Raul J.
TI Killer Immunoglobulin-Like Receptor Profiles Are not Associated with
Risk of Amoxicillin-Clavulanate-Induced Liver Injury in Spanish Patients
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE hepatotoxicity; drug-induced liver injury,pharmacogenetics; immune
response; HLA; receptor/ligand
ID CELL-INHIBITORY RECEPTOR; HLA-C; CLASS-I; GENES; RECOGNITION;
POLYMORPHISM; LIGANDS; KIR2DL3; DISEASE; BINDING
AB Natural killer cells are an integral part of the immune system and represent a large proportion of the lymphocyte population in the liver. The activity of these cells is regulated by various cell surface receptors, such as killer Ig-like receptors (KIR) that bind to human leukocyte antigen (HLA) class I ligands on the target cell. The composition of KIR receptors has been suggested to influence the development of specific diseases, in particularly autoimmune diseases, cancer and reproductive diseases. The role played in idiosyncratic drug-induced liver injury (DILI) is currently unknown. In this study, we examined KIR gene profiles and HLA class I polymorphisms in amoxicillin-clavulanate (AC) DILI patients in search for potential risk associations. One hundred and two AC DILI patients and 226 controls were genotyped for the presence or absence of 16 KIR loci, including the two pseudogenes 2DP1 and 3DP1. No significant differences were found in the distribution of individual KIRs between patients and controls, which were comparable to previously reported KIR data from ethnically similar cohorts. The 21.6 and 21.2% of the patients and controls, respectively, were homozygous haplotype A carriers, while 78.4 and 78.8%, respectively, contained at least one B haplotype (Bx). The genotypes translated into 27 (AC DILI) and 46 (controls) different gene profiles, with 19 being present in both groups. The most frequent Bx gene profile containing KIRs 2DS2, 2DL2, 2DL3, 2DP1, 2DL1, 3DL1, 2DS4, 3DL2, 3DL3, 2DL4, and 3PD1 was present in 16% of the DILI patients and 14% of the controls. The distribution of HLA class I epitopes did not differ significantly between AC DILI patients and controls. The most frequent receptor-ligand combinations in the DILI patients were 2DL3 + epitope Cl (67%) and 3DL1 + Bw4 motif (67%), while 2DL1 + epitope C2 (69%) and 3DL1 + Bw4 motif (69%) predominated in the controls. This is to our knowledge the first analysis of KIR receptor-HLA ligand associations in DILI, although our findings do not support evidence of these genetic variations playing a major role in AC DILI development.
C1 [Stephens, Camilla; Garcia-Cortes, Miren; Medina-Caliz, Inmaculada; Isabel Lucena, M.; Andrade, Raul J.] Univ Malaga, Inst Invest Biomed Malaga, Hosp Univ Virgen de la Victoria,CIBERehd, Unidad Gest Clin Aparato Digest,Serv Farmacol Cli, Malaga, Spain.
[Moreno-Casares, Antonia; Lopez-Nevot, Miguel-Angel] Univ Granada, Inst Invest Biosanitario Granada, Complejo Hosp Granada, Dept Bioquim & Biol Mol Inmunol 3,Unidad Gest Cli, Granada, Spain.
[Hallal, Hacibe; Ruiz-Cabello, Francisco] Hosp Morales Meseguer, Serv Aparato Digest, Murcia, Spain.
[Soriano, German; Roman, Eva] Univ Autonoma Barcelona, Serv Gastroenterol, CIBERehd, Hosp Santa Creu & St Pau, Barcelona, Spain.
[Roman, Eva] Univ Autonoma Barcelona, Escola Univ Infermeria St Pau, Barcelona, Spain.
[Romero-Gomez, Manuel] Hosp Univ Virgen Macarena Virgen del Rocio, Unidad Gest Clin Aparato Digest Interctr, CIBERehd, Seville, Spain.
C3 CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD; Universidad
de Malaga; University of Granada; CIBER - Centro de Investigacion
Biomedica en Red; CIBEREHD; Autonomous University of Barcelona; Hospital
of Santa Creu i Sant Pau; Autonomous University of Barcelona; CIBER -
Centro de Investigacion Biomedica en Red; CIBEREHD
RP Lucena, MI (corresponding author), Univ Malaga, Inst Invest Biomed Malaga, Hosp Univ Virgen de la Victoria,CIBERehd, Unidad Gest Clin Aparato Digest,Serv Farmacol Cli, Malaga, Spain.
EM lucena@uma.es
RI Stephens, Camilla/JRP-4877-2023; Ruiz-Cabello, Francisco/ABG-8828-2020;
GARCIA, MIREN/ABC-2896-2020; Romero-Gomez, Manuel/L-8030-2014
OI Ruiz-Cabello, Francisco/0000-0002-2247-3293; Romero-Gomez,
Manuel/0000-0001-8494-8947; Soriano, German/0000-0002-9267-6811; Lopez
Nevot, Miguel Angel/0000-0002-3465-6062; Garcia Cortes,
Miren/0000-0003-0410-8273; Medina-Caliz, Inmaculada/0000-0003-0471-6658
FU Instituto de Salud Carlos III [PI12/00378, SAS-PI-0239/2012,
AC-0073-2013]; Agencia Espanola del Medicamento
FX The present study has been supported by grants of the Instituto de Salud
Carlos III co-founded by Fondo Europeo de Desarrollo Regional - FEDER
(contract numbers: PI12/00378, SAS-PI-0239/2012, AC-0073-2013) and by
the Agencia Espanola del Medicamento. CIBERehd is funded by Instituto de
Salud Carlos III. The funding sources had no involvement in the study
design; in the collection, analysis, and interpretation of data; in the
writing of the report or in the decision to submit the manuscript for
publication.
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NR 32
TC 3
Z9 3
U1 0
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD AUG 26
PY 2016
VL 7
AR 280
DI 10.3389/fphar.2016.00280
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DU3KE
UT WOS:000382108400001
PM 27616993
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Nakanuma, Y
Harada, K
Sasaki, M
Sato, Y
AF Nakanuma, Yasuni
Harada, Kenichi
Sasaki, Motoko
Sato, Yasunori
TI Proposal of a new disease concept "biliary diseases with pancreatic
counterparts". Anatomical and pathological bases
SO HISTOLOGY AND HISTOPATHOLOGY
LA English
DT Review
DE Biliary tract; Pancreas; Duct adenocarcinoma; Intraepithelial neoplasm;
Periductal glands
ID INTRAHEPATIC PERIBILIARY GLANDS; BILE-DUCT; INTRAEPITHELIAL NEOPLASIA;
LIVERS; CHOLANGIOCARCINOGENESIS; HEPATOLITHIASIS; EXPRESSION; AUTOPSY;
ORIGIN; CANCER
AB The biliary tract and pancreas are located closely anatomically, and both develop from the endoderm foregut almost at the same time. Interestingly, the lining epithelia of the bile duct and main pancreatic duct show similar morphologies and phenotypes, and both are accompanied by periductal glands. Furthermore, the exocrine pancreatic acini are remnantly found in the peribiliary glands. Based on these findings, it seems plausible that the biliary tract has features of pancreatic elements in addition to the duct system, which is specialized for the drainage of bile secreted by hepatic parenchyma, particularly, hepatocytes. Interestingly, some pancreatic and biliary diseases show similar pathological features and even biological behaviors. For example, extrahepatic cholangiocarcinoma and ductal adenocarcinoma of the pancreas share many clinicopathological features. Both of them are hypothesized to arise from similar preneoplastic and early neoplastic intraepithelial lesions. Intraductal papillary tumors, with frequent mucin hyperproduction, develop in the pancreas (intraductal papillary mucinous neoplasm) and also in the biliary tract (intraductal papillary neoplasm of the bile duct). IgG4-related disease affects the biliary tract (IgG4-related sclerosing cholangitis) and the pancreas (autoimmune pancreatitis) in the same patients, with both showing similar morphologies. Herein, we propose that these nonneoplastic and neoplastic biliary diseases showing similarities to corresponding pancreatic diseases could be included in a new disease concept "biliary diseases with pancreatic counterparts". Based on this new concept, information obtained in biliary tract diseases could be applied to the analysis of pancreatic disease and vice versa, and also novel therapeutical strategies and molecular and genetic studies on pancreatic and biliary diseases may be developed with a unified approach.
C1 [Nakanuma, Yasuni; Harada, Kenichi; Sasaki, Motoko; Sato, Yasunori] Kanazawa Univ, Grad Sch Med, Dept Human Pathol, Kanazawa, Ishikawa 9208640, Japan.
C3 Kanazawa University
RP Nakanuma, Y (corresponding author), Kanazawa Univ, Grad Sch Med, Dept Human Pathol, Kanazawa, Ishikawa 9208640, Japan.
EM pbcpsc@kenroku.kanazawa-u.ac.jp
RI Sasaki, Motoko/K-5913-2015
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NR 37
TC 42
Z9 42
U1 0
U2 8
PU F HERNANDEZ
PI MURCIA
PA PLAZA FUENSANTA 2-7 C, 30008 MURCIA, SPAIN
SN 0213-3911
EI 1699-5848
J9 HISTOL HISTOPATHOL
JI Histol. Histopath.
PD JAN
PY 2014
VL 29
IS 1
BP 1
EP 10
PG 10
WC Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Pathology
GA 281SW
UT WOS:000329122300001
PM 24108502
DA 2025-01-07
ER
PT J
AU Nair, S
Fang, M
Sigal, LJ
AF Nair, Savita
Fang, Min
Sigal, Luis J.
TI The natural killer cell dysfunction of aged mice is due to the bone
marrow stroma and is not restored by IL-15/IL-15Rα treatment
SO AGING CELL
LA English
DT Article
DE aging; natural killer cells; immunosenescence; cellular immunology;
immune cell development; mice
ID MURINE CYTOMEGALOVIRUS-INFECTION; NK-CELLS; MEDIATED RESISTANCE; INNATE
RESISTANCE; LYMPHOID ORGANS; IL-15; HOMEOSTASIS; COLLAGEN;
SUSCEPTIBILITY; MATURATION
AB Immune dysfunctions in the elderly result in increased susceptibility to infectious diseases, cancer, and autoimmune diseases. Natural killer (NK) cells are bone marrow-derived lymphocytes crucial for host defense against several infections and cancer. We have previously shown that compared to young, aged C57BL/6 mice have decreased numbers of mature NK cells in the blood, spleen, and bone marrow, resulting in susceptibility to mousepox, a lethal disease caused by ectromelia virus. Here, we describe further age-related defects in NK cells including reduced proliferationin vivo, additional signs of immaturity, and dysregulated expression of activating and inhibitory receptors. Aging also alters the expression of collagen-binding integrins in conventional NK cells and the frequency and phenotype of liver tissue-resident NK cells. We additionally show that the defect in NK maturation is the consequence of deficient maturational cues provided by bone marrow stromal cells. Moreover, we demonstrate that in aged mice, treatment with complexes of the cytokine IL-15 and IL-15R induce massive expansion of the NK cells, but most of these NK cells remain immature and are unable to restore resistance to mousepox. The use of rodent model to understand immunosenescence may help the development of treatments to improve the immune fitness of the aged. Our work with NK cells should contribute toward this goal.
C1 [Nair, Savita; Fang, Min; Sigal, Luis J.] Fox Chase Canc Ctr, Res Inst, Immune Cell Dev & Host Def Program, Philadelphia, PA 19111 USA.
C3 Fox Chase Cancer Center
RP Sigal, LJ (corresponding author), Fox Chase Canc Ctr, 333 Cottman Ave, Philadelphia, PA 19111 USA.
EM luis.sigal@fccc.edu
RI Sigal, Luis/AAL-1849-2021
OI Fang, Min/0000-0002-5278-1430; Sigal, Luis/0000-0001-6642-5472
FU NIH [R01AI065544, R01AG048602, P30CA006927]; Ellison/AFAR Postdoctoral
Fellowship in Aging Research
FX We thank Fox Chase Cancer Center (FCCC) Laboratory Animal, Flow
Cytometry and Tissue Culture Facilities, and Ms. Holly Gillin for
assistance in the preparation of the manuscript. This work was supported
by NIH grants R01AI065544 and R01AG048602 to L.J.S. and P30CA006927 to
the FCCC. A generous gift from Cathie and Pete Getchell through the FCCC
board of Associates also contributed to support this project. S.N. was
partially supported by an Ellison/AFAR Postdoctoral Fellowship in Aging
Research.
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NR 45
TC 30
Z9 37
U1 0
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1474-9718
EI 1474-9726
J9 AGING CELL
JI Aging Cell
PD APR
PY 2015
VL 14
IS 2
BP 180
EP 190
DI 10.1111/acel.12291
PG 11
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA CC9AN
UT WOS:000350659900004
PM 25399821
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Yang, NX
Yang, YT
Huang, ZH
Chen, HW
AF Yang, Nianxin
Yang, Yatian
Huang, Zenghong
Chen, Hong-Wu
TI Deregulation of Cholesterol Homeostasis by a Nuclear Hormone Receptor
Crosstalk in Advanced Prostate Cancer
SO CANCERS
LA English
DT Article
DE nuclear receptors; ROR gamma; LXRs; SREBP2; antagonists; inverse
agonists; agonists; cholesterol efflux
ID ROR-GAMMA-T; LIGANDS; METABOLISM; CELLS
AB Metastatic castration-resistant prostate cancer (mCRPC) features high intratumoral cholesterol levels, due to aberrant regulation of cholesterol homeostasis. However, the underlying mechanisms are still poorly understood. The retinoid acid receptor-related orphan receptor gamma (ROR gamma), an attractive therapeutic target for cancer and autoimmune diseases, is strongly implicated in prostate cancer progression. We demonstrate in this study that in mCRPC cells and tumors, ROR gamma plays a crucial role in deregulation of cholesterol homeostasis. First, we found that ROR gamma activates the expression of key cholesterol biosynthesis proteins, including HMGCS1, HMGCR, and SQLE. Interestingly, we also found that RORy inhibition induces cholesterol efflux gene program including ABCA1, ABCG1 and ApoA1. Our further studies revealed that liver X receptors (LXR alpha and LXR beta), the master regulators of cholesterol efflux pathway, mediate the function of ROR gamma in repression of cholesterol efflux. Finally, we demonstrated that ROR gamma antagonist in combination with statins has synergistic effect in killing mCRPC cells through blocking statin-induced feedback induction of cholesterol biosynthesis program and that the combination treatment also elicits stronger anti-tumor effects than either alone. Altogether, our work revealed that in mCRPC, ROR gamma contributes to aberrant cholesterol homeostasis by induction of cholesterol biosynthesis program and suppression of cholesterol efflux genes. Our findings support a therapeutic strategy of targeting ROR gamma alone or in combination with statin for effective treatment of mCRPC.
C1 [Yang, Nianxin; Yang, Yatian; Huang, Zenghong; Chen, Hong-Wu] Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Sacramento, CA 95817 USA.
[Chen, Hong-Wu] Univ Calif Davis, Natl Canc Inst, Designated Comprehens Canc Ctr, Sacramento, CA 95817 USA.
[Chen, Hong-Wu] Vet Affairs Northern Calif Hlth Care Syst, Mather, CA 95655 USA.
C3 University of California System; University of California Davis;
University of California System; University of California Davis;
National Institutes of Health (NIH) - USA; NIH National Cancer Institute
(NCI)
RP Chen, HW (corresponding author), Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Sacramento, CA 95817 USA.; Chen, HW (corresponding author), Univ Calif Davis, Natl Canc Inst, Designated Comprehens Canc Ctr, Sacramento, CA 95817 USA.; Chen, HW (corresponding author), Vet Affairs Northern Calif Hlth Care Syst, Mather, CA 95655 USA.
EM nxyang@ucdavis.edu; yatyang@ucdavis.edu; znhhuang@ucdavis.edu;
hwzchen@ucdavis.edu
RI Huang, Zenghong/M-6004-2018
OI Chen, Hongwu/0000-0003-0177-6989; Yang, Nianxin/0000-0002-6842-7874
FU NIH [R01CA224900]; US Department of Veterans Affairs, Office of Research
& Development BLD [I01 BX004271]; UCD Comprehensive Cancer Center
Support Grant (CCSG) awarded by the NCI [P30 CA093373]
FX This work was supported in part by grants from the NIH (R01CA224900),
and the US Department of Veterans Affairs, Office of Research &
Development BL&D (I01 BX004271) to H.-W. Chen. The UCDCCC Genomics
Shared Resource is funded by the UCD Comprehensive Cancer Center Support
Grant (CCSG) awarded by the NCI P30 CA093373.
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NR 49
TC 6
Z9 7
U1 2
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2022
VL 14
IS 13
AR 3110
DI 10.3390/cancers14133110
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2W4UT
UT WOS:000824521400001
PM 35804882
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Özdemir-Kumral, ZN
Erkek, BE
Karakus, B
Almaci, M
Fathi, R
Yüksel, M
Cumbul, A
Alican, I
AF Ozdemir-Kumral, Zarife N.
Erkek, Burak E.
Karakus, Buse
Almaci, Meslina
Fathi, Reza
Yuksel, Meral
Cumbul, Alev
Alican, Inci
TI Potential Effect of 1,25 Dihydroxyvitamin D3 on
Thioacetamide-Induced Hepatotoxicity in Rats
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE Apoptosis; 1,25(OH)(2)D-3; Hepatotoxicity; Oxidative stress; Rat;
Thioacetamide
ID INDUCED LIVER-INJURY; VITAMIN-D; HEPATIC-ENCEPHALOPATHY; NITRIC-OXIDE;
OXIDATIVE STRESS; APOPTOSIS; PROTECTS; INFLAMMATION; INVOLVEMENT; MODELS
AB Background: 1,25 Dihydroxyvitamin D-3 (1,25(OH)(2)D-3) modulates inflammation and immune responses. Deficiency of 1,25(OH)(2)D-3 was found to be associated with the risk of cancer, cardiovascular disease, osteoarthritis, infections, and autoimmune diseases. This study evaluated the effect of 1,25 dihydroxyvitamin D-3 1,25(OH)(2)D-3 on thioacetamide (TAA)-induced acute liver injury in rats.
Materials and methods: Rats were treated with either saline or 1,25(OH)(2)D-3 (0.30 mg/kg; orogastrically) for 15 d. Starting from day 13, TAA (200 mg/kg; intraperitoneally) was given for 3 d. On day 15, all rats were euthanized. Liver and blood samples were collected.
Results: TAA caused severe damage, increased lipid peroxidation with reductions in endogenous antioxidants, increased apoptosis, increased production of reactive oxygen species, and elevated inducible nitric oxide synthase (iNOS), and nuclear factor kappa B (NF-kappa B) expression in liver. Extent of damage was decreased by 1,25(OH)(2)D-3 (P < 0.01). 1,25(OH)(2)D-3 attenuated the increase in malondialdehyde (P < 0.01), increase in myeloper-oxidase (P < 0.01), increase in chemiluminescence levels (P < 0.05) and apoptotic activity (P < 0.001). Elevated liver iNOS and NF-kappa B expression in TAA group was also reduced by 1,25(OH)(2)D-3 (P < 0.001, for iNOS; P < 0.001, for NF-kappa B). TAA group revealed high serum aspartate transaminase and alanine transaminase (ALT) activities (P < 0.01, for aspartate transaminase; P = 0.08, for ALT) and reduced albumin levels (P < 0.01) compared with control. 1,25(OH)(2)D-3 had no statistically significant effect on these parameters.
Conclusions: 1,25(OH)(2)D-3 provides protection against hepatic injury in a rat model of TAA-induced hepatotoxicity via suppression of inflammatory reaction, oxidative stress, and apoptosis. (C) 2019 Elsevier Inc. All rights reserved.
C1 [Ozdemir-Kumral, Zarife N.; Erkek, Burak E.; Karakus, Buse; Almaci, Meslina; Fathi, Reza; Alican, Inci] Marmara Univ, Sch Med, Dept Physiol, Istanbul, Turkey.
[Yuksel, Meral] Marmara Univ, Vocat Sch Hlth Serv, Dept Med Lab Biochem, Istanbul, Turkey.
[Cumbul, Alev] Yeditepe Univ, Sch Med, Dept Histol & Embryol, Istanbul, Turkey.
C3 Marmara University; Marmara University; Yeditepe University
RP Alican, I (corresponding author), Marmara Univ, Sch Med, Dept Physiol, Physiol, TR-34854 Istanbul, Turkey.
EM incialican@yahoo.com
RI CUMBUL, Alev/H-3991-2011; Yüksel, Meral/Z-3692-2019; KUMRAL,
Zarife/AAG-1861-2020
OI Cumbul, Alev/0000-0002-9491-8220; Ozdemir Kumral, Zarife
Nigar/0000-0002-9485-0174
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NR 38
TC 10
Z9 13
U1 1
U2 9
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
EI 1095-8673
J9 J SURG RES
JI J. Surg. Res.
PD NOV
PY 2019
VL 243
BP 165
EP 172
DI 10.1016/j.jss.2019.05.020
PG 8
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA JA7SF
UT WOS:000488045900025
PM 31177036
DA 2025-01-07
ER
PT J
AU Yu-Rice, Y
Edassery, SL
Urban, N
Hellstrom, I
Hellstrom, KE
Deng, YP
Li, Y
Luborsky, JL
AF Yu-Rice, Yi
Edassery, Seby L.
Urban, Nicole
Hellstrom, Ingegerd
Hellstrom, Karl Erik
Deng, Youping
Li, Yan
Luborsky, Judith L.
TI Selenium-Binding Protein 1 (SBP1) autoantibodies in ovarian disorders
and ovarian cancer
SO REPRODUCTION
LA English
DT Article
ID TUMOR-ASSOCIATED ANTIGENS; GENE-EXPRESSION; LAYING HEN;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE-DISEASES; PREMATURE MENOPAUSE; P53
AUTOANTIBODIES; INFERTILE WOMEN; IN-VITRO; BIOMARKERS
AB Infertility is a risk factor for ovarian cancer (OvCa). The goal was to determine if antibodies to selenium-binding protein 1 (SBP1), an autoantibody we identified in patients with premature ovarian failure (POF), occurs in both infertility and OvCa patients, and thus could be associated with preneoplasia. Anti-SBP1 was measured by immunoassay against recombinant SBP1, in sera from OvCa (n = 41), infertility (n = 92) and control (n = 87) patients. Infertility causes were POF, unexplained, irregular ovulation or endometriosis. The percent of anti-SBP1-positive sera was higher in POF (P = 0.02), irregular ovulation (P = 0.001), unexplained causes (P = 0.02), late (III-IV)-stage OvCa (P = 0.02) but was not significant in endometriosis, benign ovarian tumors/cysts, early stage (I-II) OvCa or uterine cancer compared to healthy controls. Anti-SBP1 was significantly higher in women with serous (P = 0.04) but not non-serous (P = 0.33) OvCa compared to controls. Also, we determined if anti-SBP1 was associated with CA125 or anti-TP53, markers often studied in OvCa. Anti-TP53 and CA125 were measured by established immunoassays. The ability of anti-SBP1 alone to discriminate infertility or OvCa from controls or when combined with anti-TP53 and CA125, to identify OvCa was evaluated by comparing the area under the curve (AUC) in ROC analysis. Anti-SBP1 alone discriminated infertility (AUC = 0.7; P = 0.001) or OvCa (AUC = 0.67; P = 0.03) from controls. The sensitivity and specificity of OvCa identification was increased by combining CA125, anti-TP53 and anti-SBP1 (AUC = 0.96). Therefore, anti-SBP1 occurs in infertile women with POF, ovulatory disturbances or unexplained infertility and in serous OvCa. This suggests an autoimmune process is associated with the development of serous OvCa.
C1 [Yu-Rice, Yi; Edassery, Seby L.; Luborsky, Judith L.] Rush Univ, Med Ctr, Dept Pharmacol, Chicago, IL 60612 USA.
[Urban, Nicole] Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[Hellstrom, Ingegerd; Hellstrom, Karl Erik] Univ Washington, Harborview Med Ctr, Dept Pathol, Seattle, WA 98195 USA.
[Deng, Youping; Li, Yan] Rush Univ, Med Ctr, Dept Bioinformat & Biostat, Chicago, IL 60612 USA.
[Yu-Rice, Yi] Nutril Prod Inc, Buena Pk, CA USA.
[Luborsky, Judith L.] Woods Hole Oceanog Inst, Dept Biol, Woods Hole, MA 02543 USA.
C3 Rush University; Fred Hutchinson Cancer Center; Harborview Medical
Center; University of Washington; University of Washington Seattle; Rush
University; Woods Hole Oceanographic Institution
RP Luborsky, JL (corresponding author), Rush Univ, Med Ctr, Dept Pharmacol, Chicago, IL 60612 USA.
EM JLuborsky@whoi.edu
RI Li, Yuxiang/HNJ-4258-2023
FU National Institutes of Health [R01AI055060-01, P50CA083636,
R01CA134487]; Rush University Segal award; Fujirebio Diagnostics, Inc
FX The studies were supported by the National Institutes of Health
(R01AI055060-01 (J L); P50CA083636 (N U); R01CA134487 (I H, J L)), a
Rush University Segal award (J L) and a grant from Fujirebio
Diagnostics, Inc (I H, K E H).
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NR 74
TC 16
Z9 17
U1 1
U2 11
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 1470-1626
J9 REPRODUCTION
JI Reproduction
PD MAR
PY 2017
VL 153
IS 3
BP 277
EP 284
DI 10.1530/REP-16-0265
PG 8
WC Developmental Biology; Reproductive Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology; Reproductive Biology
GA EK8EQ
UT WOS:000394157100007
PM 27965399
OA Green Accepted, Bronze
DA 2025-01-07
ER
PT J
AU Buono, A
Lidbury, JA
Wood, C
Wilson-Robles, H
Dangott, LJ
Allenspach, K
Suchodolski, JS
Steiner, JM
AF Buono, A.
Lidbury, J. A.
Wood, C.
Wilson-Robles, H.
Dangott, L. J.
Allenspach, K.
Suchodolski, J. S.
Steiner, J. M.
TI Development, analytical validation, and initial clinical evaluation of a
radioimmunoassay for the measurement of soluble CD25 concentrations in
canine serum
SO VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY
LA English
DT Article
DE Canine; Interleukin 2 receptor alpha; Soluble CD25; Radioimmunoassay;
p55; tac
ID INTERLEUKIN-2-RECEPTOR ALPHA; REFERENCE INTERVALS; RECEPTOR-ALPHA;
T-LYMPHOCYTES; EXPRESSION; ACTIVATION; CHILDREN; GROWTH; GAMMA
AB During immune activation, CD25 is expressed by T cells, and its soluble form (sCD25) is released into the extracellular matrix and the bloodstream. In humans, serum sCD25 concentrations are used as a surrogate marker for autoimmune diseases, malignancies, and transplant rejection. However, a canine-specific assay for the measurement of sCD25 in dog serum has not previously been described. Therefore, the aims of this study were to develop and analytically validate a radioimmunoassay to measure sCD25 in canine serum, to establish a reference interval for canine sCD25, and to test the clinical utility of this assay with serum samples for dogs with various diseases. A competitive radioimmunoassay (RIA) was developed and analytically validated. Analytical validation consisted of lower limit of detection (LLOD), dilutional parallelism, spiking recovery, and intra- and inter-assay variability using pooled surplus canine serum samples. A reference interval was established in healthy dogs and serum samples from dogs with various types of neoplasia, IBD, liver disease, suspected pancreatitis, or suspected small intestinal disease and serum samples with an increased C-reactive protein concentration (CRP) were analyzed to test the clinical utility of the assay. LLOD was calculated to be 0.5 ng/mL. The mean (+/- SD) observed-to-expected ratio (O/E) for serial dilutions was 101.7 +/- 14.0%, and the mean (+/- SD) O/E for spiking recovery was 93.2 +/- 4.2%. Coefficients of variation (CVs) for intra-assay variability were <= 12.5% (mean +/- SD: 7.5 +/- 4.2%), and inter-assay CVs were <= 15.7% (mean +/- SD: 11 +/- 4.4%). A reference interval (RI) for canine sCD25 of 1.2-4.2 ng/mL was established from a population of 112 clinically healthy dogs. Dogs with neoplasia and dogs with suspected small intestinal disease had decreased concentrations of serum sCD25 when compared to healthy dogs (p < 0.0001, respectively). However, the majority of clinical samples used in this study were within the reference interval. Median concentrations of serum sCD25 were 1.9 ng/mL for healthy dogs. Dogs with cancer, IBD, liver disease, suspected pancreatitis, or suspected small intestinal disease, as well as sera with an increased serum CRP concentration, had median serum sCD25 concentrations of 1.6 ng/mL, 2.1 ng/mL, 2.2 ng/mL, 1.7 ng/mL, 1.5 ng/mL, and 1.8 ng/mL, respectively.
Thus, the RIA described here is linear, accurate, precise, and reproducible for measuring sCD25 in canine serum. However, this assay shows little clinical utility of sCD25 as a biomarker for dogs with inflammatory, autoimmune, and/or neoplastic conditions.
C1 [Buono, A.; Lidbury, J. A.; Suchodolski, J. S.; Steiner, J. M.] Texas A&M Univ, Coll Vet Med & Biomed Sci, Dept Small Anim Clin Sci, Gastrointestinal Lab, College Stn, TX 77843 USA.
[Wood, C.; Wilson-Robles, H.] Texas A&M Univ, Coll Vet Med & Biomed Sci, Dept Small Anim Med & Surg, College Stn, TX 77843 USA.
[Dangott, L. J.] Texas A&M Univ, Dept Biochem & Biophys, Prot Chem Lab, College Stn, TX 77843 USA.
[Allenspach, K.] Iowa State Univ, Dept Vet Clin Sci, Ames, IA 50011 USA.
C3 Texas A&M University System; Texas A&M University College Station; Texas
A&M University System; Texas A&M University College Station; Texas A&M
University System; Texas A&M University College Station; Iowa State
University
RP Buono, A (corresponding author), Texas A&M Univ, Coll Vet Med & Biomed Sci, Dept Small Anim Clin Sci, Gastrointestinal Lab, College Stn, TX 77843 USA.
EM ABuono@cvm.tamu.edu
RI ; Wilson-Robles, Heather/D-4209-2016
OI Buono, Agostino/0000-0002-1893-3787; Wilson-Robles,
Heather/0000-0002-6489-8468
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NR 43
TC 11
Z9 12
U1 1
U2 12
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0165-2427
EI 1873-2534
J9 VET IMMUNOL IMMUNOP
JI Vet. Immunol. Immunopathol.
PD SEP
PY 2019
VL 215
AR 109904
DI 10.1016/j.vetimm.2019.109904
PG 7
WC Immunology; Veterinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Veterinary Sciences
GA IU5SE
UT WOS:000483646800002
PM 31420068
DA 2025-01-07
ER
PT J
AU Cao, EY
Lindgren, A
Martinsson, S
Hu, LJ
Lindfors, L
Sigfridsson, K
Skantze, U
Michaëlsson, E
Trevaskis, NL
Porter, CJH
AF Cao, Enyuan
Lindgren, Anna
Martinsson, Sofia
Hu, Luojuan
Lindfors, Lennart
Sigfridsson, Kalle
Skantze, Urban
Michaelsson, Erik
Trevaskis, Natalie L.
Porter, Christopher J. H.
TI Promoting intestinal lymphatic transport targets a liver-X receptor
(LXR) agonist (WAY-252,623) to lymphocytes and enhances immunomodulation
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE Lymphocyte; Lymphatic transport; Drug targeting; Lipid based drug
delivery system; Lipophilic drugs; Atherosclerosis
ID AMORPHOUS DRUG NANOSUSPENSIONS; LIPID-METABOLISM; FATTY-ACIDS;
LOW-DENSITY; MODEL; DELIVERY; LXR-623; IMPACT; CANCER; GUT
AB Lymphocytes play a central role in the pathology of a range of chronic conditions such as autoimmune disease, transplant rejection, leukemia, lymphoma HIV/AIDS and cardiometabolic diseases such as atherosclerosis. Current treatments for lymphocyte-associated conditions are incompletely effective and/or complicated by a range of off-target toxicities. One major challenge is poor drug access to lymphocytes via the systemic blood and this may be attributed, at least in part, to the fact that lymphocytes are concentrated within lymph fluid and lymphoid tissues, particularly in gut-associated lymphatics. Here we demonstrate that promoting drug uptake into the intestinal lymphatics with a long chain fatty acid, thereby increasing lymphocyte access, enhances the pharmacodynamic effect of a highly lipophilic liver X receptor (LXR) agonist, WAY-252623, that has been suggested as a potential treatment for atherosclerosis. This has been exemplified by: (1) increased mRNA expression of key markers of LXR activation (ABCA1) and regulatory T cells (Foxp3) in local lymphatic lymphocytes and (2) enhanced numbers of CD4(+)CD25(+)Foxp3(+) regulatory T cells in the systemic circulation, after administration of a 5-fold lower dose with a lymph directing lipid formulation when compared with a non-lipid containing formulation. These data suggest that combining lipophilic, lyrnphotropic drug candidates such as WAY-252,623, with lymph-directing long chain lipid based formulations can enhance drug targeting to, and activity on, lymphocytes in lymph and that this effect persists through to the systemic circulation. This presents a promising approach to achieve more selective and effective therapeutic outcomes for the treatment of lymphocyte associated diseases.
C1 [Cao, Enyuan; Hu, Luojuan; Trevaskis, Natalie L.; Porter, Christopher J. H.] Monash Univ, Monash Inst Pharmaceut Sci, Drug Delivery Disposit & Dynam, Melbourne, Vic, Australia.
[Lindgren, Anna] AstraZeneca, IMED Biotech Unit, Precis Med & Genom, Gothenburg, Sweden.
[Martinsson, Sofia; Michaelsson, Erik] AstraZeneca, IMED Biotech Unit, Biosci Heart Failure Cardiovasc Renal & Metab, Gothenburg, Sweden.
[Lindfors, Lennart; Sigfridsson, Kalle; Skantze, Urban] AstraZeneca, Pharmaceut Sci, Adv Drug Delivery, IMED Biotech Unit, Gothenburg, Sweden.
[Cao, Enyuan; Hu, Luojuan; Porter, Christopher J. H.] Monash Univ, ARC Ctr Excellence Bionano Sci & Technol, Monash Inst Pharmaceut Sci, Melbourne, Vic, Australia.
C3 Monash University; AstraZeneca; AstraZeneca; AstraZeneca; Monash
University
RP Porter, CJH (corresponding author), Monash Univ, Monash Inst Pharmaceut Sci, Drug Delivery Disposit & Dynam, Melbourne, Vic, Australia.
EM chris.porter@monash.edu
RI Trevaskis, Natalie/C-6217-2008; Porter, Christopher/C-6333-2011
OI Porter, Christopher/0000-0003-3474-7551; Michaelsson,
Erik/0000-0001-8643-2821; Trevaskis, Natalie/0000-0001-9538-549X; Cao,
Enyuan/0000-0002-9689-4517
FU National Health and Medical Research Council of Australia [APP1100036];
Australian Research Council [CE140100036]
FX This work was financially supported by the National Health and Medical
Research Council of Australia (APP1100036) and the Australian Research
Council (CE140100036). The authors thank Dr Hanna Grindebacke
(AstraZeneca) and Sandy Fung (Monash University) for scientific and
technical advice on Treg cell flow cytometry experiments.
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NR 43
TC 12
Z9 14
U1 0
U2 20
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-3659
EI 1873-4995
J9 J CONTROL RELEASE
JI J. Control. Release
PD FEB 28
PY 2019
VL 296
BP 29
EP 39
DI 10.1016/j.jconrel.2019.01.002
PG 11
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA HL5JO
UT WOS:000458763000003
PM 30611901
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Zeidler, JD
Hogan, KA
Agorrody, G
Peclat, TR
Kashyap, S
Kanamori, KS
Gomez, LS
Mazdeh, DZ
Warner, GM
Thompson, KL
Chini, CCS
Chini, EN
AF Zeidler, Julianna D.
Hogan, Kelly A.
Agorrody, Guillermo
Peclat, Thais R.
Kashyap, Sonu
Kanamori, Karina S.
Gomez, Lilian Sales
Mazdeh, Delaram Z.
Warner, Gina M.
Thompson, Katie L.
Chini, Claudia C. S.
Chini, Eduardo Nunes
TI The CD38 glycohydrolase and the NAD sink: implications for pathological
conditions
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Review
DE CD38; diseases; NAD metabolism
ID CYCLIC-ADP-RIBOSE; ADENINE-DINUCLEOTIDE PHOSPHATE;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; CHRONIC LYMPHOCYTIC-LEUKEMIA; NICOTINAMIDE
N-METHYLTRANSFERASE; MITOCHONDRIAL OXIDATIVE STRESS; INNATE
IMMUNE-RESPONSE; DIET-INDUCED OBESITY; FATTY LIVER-DISEASE; CHRONIC
HEPATITIS-C
AB Nicotinamide adenine dinucleotide (NAD) acts as a cofactor in several oxidation-reduction (redox) reactions and is a substrate for a number of nonredox enzymes. NAD is fundamental to a variety of cellular processes including energy metabolism, cell signaling, and epigenetics. NAD homeostasis appears to be of paramount importance to health span and longevity, and its dysregulation is associated with multiple diseases. NAD metabolism is dynamic and maintained by synthesis and degradation. The enzyme CD38, one of the main NAD-consuming enzymes, is a key component of NAD homeostasis. The majority of CD38 is localized in the plasma membrane with its catalytic domain facing the extracellular environment, likely for the purpose of controlling systemic levels of NAD. Several cell types express CD38, but its expression predominates on endothelial cells and immune cells capable of infiltrating organs and tissues. Here we review potential roles of CD38 in health and disease and postulate ways in which CD38 dysregulation causes changes in NAD homeostasis and contributes to the pathophysiology of multiple conditions. Indeed, in animal models the development of infectious diseases, autoimmune disorders, fibrosis, metabolic diseases, and age-associated diseases including cancer, heart disease, and neurodegeneration are associated with altered CD38 enzymatic activity. Many of these conditions are modified in CD38-deficient mice or by blocking CD38 NADase activity. In diseases in which CD38 appears to play a role, CD38-dependent NAD decline is often a common denominator of pathophysiology. Thus, understanding dysregulation of NAD homeostasis by CD38 may open new avenues for the treatment of human diseases.
C1 [Zeidler, Julianna D.; Hogan, Kelly A.; Peclat, Thais R.; Kanamori, Karina S.; Gomez, Lilian Sales; Mazdeh, Delaram Z.; Warner, Gina M.; Thompson, Katie L.; Chini, Eduardo Nunes] Mayo Clin, Coll Med, Signal Transduct & Mol Nutr Lab, Kogod Aging Ctr,Dept Anesthesiol & Perioperat Med, Rochester, MN 55905 USA.
[Kashyap, Sonu; Chini, Claudia C. S.; Chini, Eduardo Nunes] Mayo Clin, Dept Anesthesiol & Perioperat Med, Jacksonville, FL 32224 USA.
[Agorrody, Guillermo] Hosp Clin Montevideo, Dept Fisiopatol, Montevideo, Uruguay.
[Agorrody, Guillermo] Inst Pasteur Montevideo, Lab Patol Metabolismo & Envejecimiento, Montevideo, Uruguay.
C3 Mayo Clinic; Mayo Clinic; Universidad de la Republica, Uruguay; Pasteur
Network; Institut Pasteur de Montevideo
RP Chini, EN (corresponding author), Mayo Clin, Coll Med, Signal Transduct & Mol Nutr Lab, Kogod Aging Ctr,Dept Anesthesiol & Perioperat Med, Rochester, MN 55905 USA.; Chini, EN (corresponding author), Mayo Clin, Dept Anesthesiol & Perioperat Med, Jacksonville, FL 32224 USA.
EM chini.eduardo@mayo.edu
OI Zeidler, Julianna D./0000-0003-3168-1518; Sales Gomez,
Lilian/0000-0002-5309-7438; Agorrody, Guillermo/0000-0002-9241-6681;
Peclat, Thais/0000-0002-8907-5548
FU Helen Diller Family Foundation; Glenn Foundation for Medical Research
via the Paul F. Glenn Laboratories for the Biology of Aging; Calico Life
Sciences LLC; National Institute on Aging [AG-26094, AG58812]; National
Cancer Institute [CA233790]; National Institute on Aging [R01AG058812]
Funding Source: NIH RePORTER
FX This work was supported by the Helen Diller Family Foundation, the Glenn
Foundation for Medical Research via the Paul F. Glenn Laboratories for
the Biology of Aging, Calico Life Sciences LLC, National Institute on
Aging Grants AG-26094 and AG58812, and National Cancer Institute Grant
CA233790 to E.N.C.
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NR 318
TC 34
Z9 38
U1 4
U2 26
PU AMER PHYSIOLOGICAL SOC
PI Rockville
PA 6120 Executive Blvd, Suite 600, Rockville, MD, UNITED STATES
SN 0363-6143
EI 1522-1563
J9 AM J PHYSIOL-CELL PH
JI Am. J. Physiol.-Cell Physiol.
PD MAR
PY 2022
VL 322
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BP C521
EP C545
DI 10.1152/ajpcell.00451.2021
PG 25
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA 3G1PU
UT WOS:000831128500008
PM 35138178
OA Green Published
DA 2025-01-07
ER
PT J
AU He, XA
Xia, L
Tumas, KC
Wu, J
Su, XZ
AF He, Xiao
Xia, Lu
Tumas, Keyla C.
Wu, Jian
Su, Xin-Zhuan
TI Type I Interferons and Malaria: A Double-Edge Sword Against a Complex
Parasitic Disease
SO FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
LA English
DT Review
DE IFN-Is; Plasmodium; immune response; signaling pathways; virulence
ID TOLL-LIKE RECEPTOR; PLASMACYTOID DENDRITIC CELLS; CYCLIC GMP-AMP;
PATTERN-RECOGNITION RECEPTORS; EXPERIMENTAL CEREBRAL MALARIA; INNATE
IMMUNE-RESPONSES; NF-KAPPA-B; PLASMODIUM-FALCIPARUM; RIG-I; ADAPTER
PROTEIN
AB Type I interferons (IFN-Is) are important cytokines playing critical roles in various infections, autoimmune diseases, and cancer. Studies have also shown that IFN-Is exhibit 'conflicting' roles in malaria parasite infections. Malaria parasites have a complex life cycle with multiple developing stages in two hosts. Both the liver and blood stages of malaria parasites in a vertebrate host stimulate IFN-I responses. IFN-Is have been shown to inhibit liver and blood stage development, to suppress T cell activation and adaptive immune response, and to promote production of proinflammatory cytokines and chemokines in animal models. Different parasite species or strains trigger distinct IFN-I responses. For example, a Plasmodium yoelii strain can stimulate a strong IFN-I response during early infection, whereas its isogenetic strain does not. Host genetic background also greatly influences IFN-I production during malaria infections. Consequently, the effects of IFN-Is on parasitemia and disease symptoms are highly variable depending on the combination of parasite and host species or strains. Toll-like receptor (TLR) 7, TLR9, melanoma differentiation-associated protein 5 (MDA5), and cyclic GMP-AMP synthase (cGAS) coupled with stimulator of interferon genes (STING) are the major receptors for recognizing parasite nucleic acids (RNA/DNA) to trigger IFN-I responses. IFN-I levels in vivo are tightly regulated, and various novel molecules have been identified to regulate IFN-I responses during malaria infections. Here we review the major findings and progress in ligand recognition, signaling pathways, functions, and regulation of IFN-I responses during malaria infections.
C1 [He, Xiao; Xia, Lu; Tumas, Keyla C.; Wu, Jian; Su, Xin-Zhuan] NIAID, Malaria Funct Genom Sect, Lab Malaria & Vector Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Xia, Lu] Cent South Univ, Ctr Med Genet, Sch Life Sci, Changsha, Peoples R China.
C3 National Institutes of Health (NIH) - USA; NIH National Institute of
Allergy & Infectious Diseases (NIAID); Central South University
RP Wu, J; Su, XZ (corresponding author), NIAID, Malaria Funct Genom Sect, Lab Malaria & Vector Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jian.wu2@nih.gov; xsu@niaid.nih.gov
RI HE, XIAO/LFS-5307-2024
OI He, Xiao/0009-0004-9727-467X
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases (NIAID), National Institutes of Health (NIH), USA
FX This work was supported by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases (NIAID), National
Institutes of Health (NIH), USA.
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Zhu JZ, 2005, J BIOL CHEM, V280, P8617, DOI 10.1074/jbc.M413539200
Zhu SJ, 2019, ELIFE, V8, DOI 10.7554/eLife.40845
NR 213
TC 22
Z9 24
U1 1
U2 9
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2235-2988
J9 FRONT CELL INFECT MI
JI Front. Cell. Infect. Microbiol.
PD DEC 2
PY 2020
VL 10
AR 594621
DI 10.3389/fcimb.2020.594621
PG 18
WC Immunology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology
GA PF1RT
UT WOS:000598840600001
PM 33344264
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Tanaka, A
Tazuma, S
Okazaki, K
Nakazawa, T
Inui, K
Chiba, T
Takikawa, H
AF Tanaka, Atsushi
Tazuma, Susumu
Okazaki, Kazuichi
Nakazawa, Takahiro
Inui, Kazuo
Chiba, Tsutomu
Takikawa, Hajime
TI Clinical Features, Response to Treatment, and Outcomes of IgG4-Related
Sclerosing Cholangitis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Inflammation; Natural History; Cancer; Liver Transplantation
ID AUTOIMMUNE PANCREATITIS; IGG4-ASSOCIATED CHOLANGITIS;
DIAGNOSTIC-CRITERIA; DISEASE; JAPAN; CHOLANGIOGRAPHY; STATEMENT;
THERAPY; SYSTEM
AB BACKGROUND & AIMS: Immunoglobulin G4 sclerosing cholangitis (IgG4-SC) is a biliary tract manifestation of IgG4-related systemic disease. We investigated the demographics, clinical features at presentation, treatment response, and outcomes of IgG4-SC using data from a large-scale survey in Japan.
METHODS: We performed a retrospective cohort study of 527 patients with IgG4-SC (436 female; median age, 66.2 years; range, 23-89 years) in Japan from 2000 to 2015. Data on patient demographics, presentation, treatment response, and outcomes were collected from questionnaires given to patients at 211 referral centers in Japan in 2015. Patients were diagnosed with IgG4-SC based on the clinical diagnostic criteria established by the Japanese Biliary Association in 2012. Patients were followed for a median of 4.1 +/- 3.1 years. Survival was assessed using the Kaplan-Meier curve and log-rank test.
RESULTS: Symptoms at presentation included jaundice (35% of patients) and pruritus (13% of patients); 28% of patients were asymptomatic. It was extremely rare for patients with IgG4-SC to present with symptoms of decompensated cirrhosis. At presentation, serum levels of IgG4 were increased (> 135 mg/dL) in 84% of patients. Response to prednisolone was excellent in 90% of patients. No patients received liver transplants, and cholangiocarcinoma was found in only 4 patients (0.7%). Restenosis of bile ducts was observed in 19% of patients but did not affect overall survival.
CONCLUSIONS: In a retrospective cohort study of 527 patients with IgG4-SC in Japan, we found the disease to be benign. Most patients (90%) respond to treatment with prednisolone and few develop decompensated cirrhosis or cholangiocarcinoma.
C1 [Tanaka, Atsushi; Takikawa, Hajime] Teikyo Univ, Dept Med, Sch Med, Tokyo, Japan.
[Tazuma, Susumu] Hiroshima Univ, Grad Sch Med Sci, Dept Gen Med, Hiroshima, Japan.
[Okazaki, Kazuichi] Kansai Med Univ, Dept Internal Med 3, Hirakata, Osaka, Japan.
[Nakazawa, Takahiro] Japanese Red Cross Nagoya Daini Hosp, Dept Gastroenterol, Nagoya, Aichi, Japan.
[Inui, Kazuo] Fujita Hlth Univ, Teaching Hosp 2, Dept Internal Med, Nagoya, Aichi, Japan.
[Chiba, Tsutomu] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Kyoto, Japan.
C3 Teikyo University; Hiroshima University; Kansai Medical University;
Japanese Red Cross Nagoya Daini Hospital; Fujita Health University;
Kyoto University
RP Tanaka, A (corresponding author), Teikyo Univ, Sch Med, Itabashi Ku, 2-11-1 Kaga, Tokyo 1758605, Japan.
EM a-tanaka@med.teikyo-u.ac.jp
FU Intractable Hepatobiliary Disease Study Group in Japan; Ministry of
Health, Labor, and Welfare of Japan
FX This study was supported by the Intractable Hepatobiliary Disease Study
Group in Japan, and by the Research Committee to establish diagnostic
criteria and development of treatment for systemic IgG4-related
sclerosing disease, supported by the Research Program of Intractable
Disease, both of which were provided by the Ministry of Health, Labor,
and Welfare of Japan.
CR Beuers U, 2015, DIGEST DIS, V33, P176, DOI 10.1159/000440830
Chari ST, 2006, CLIN GASTROENTEROL H, V4, P1010, DOI 10.1016/j.cgh.2006.05.017
Deshpande V, 2012, MODERN PATHOL, V25, P1181, DOI 10.1038/modpathol.2012.72
Doorenspleet ME, 2016, HEPATOLOGY, V64, P501, DOI 10.1002/hep.28568
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Okazaki K, 2006, J GASTROENTEROL, V41, P626, DOI 10.1007/s00535-006-1868-0
Okazaki K, 2013, J GASTROENTEROL, V48, P303, DOI 10.1007/s00535-012-0744-3
Stone JH, 2012, ARTHRITIS RHEUM-US, V64, P3061, DOI 10.1002/art.34593
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Zen Y, 2016, J GASTROENTEROL, V51, P295, DOI 10.1007/s00535-016-1163-7
NR 28
TC 67
Z9 82
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD JUN
PY 2017
VL 15
IS 6
BP 920
EP +
DI 10.1016/j.cgh.2016.12.038
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EW3XV
UT WOS:000402437500028
PM 28111336
DA 2025-01-07
ER
PT J
AU Quraishi, MN
Acharjee, A
Beggs, AD
Horniblow, R
Tselepis, C
Gkoutos, G
Ghosh, S
Rossiter, AE
Loman, N
van Schaik, W
Withers, D
Walters, JRF
Hirschfield, GM
Iqbal, TH
AF Quraishi, Mohammed Nabil
Acharjee, Animesh
Beggs, Andrew D.
Horniblow, Richard
Tselepis, Chris
Gkoutos, Georgios
Ghosh, Subrata
Rossiter, A. E.
Loman, Nicholas
van Schaik, Willem
Withers, David
Walters, Julian R. F.
Hirschfield, Gideon M.
Iqbal, Tariq H.
TI A Pilot Integrative Analysis of Colonic Gene Expression, Gut Microbiota,
and Immune Infiltration in Primary Sclerosing Cholangitis-Inflammatory
Bowel Disease: Association of Disease With Bile Acid Pathways
SO JOURNAL OF CROHNS & COLITIS
LA English
DT Article
DE Autoimmune liver disease; dysbiosis; bioinformatics; colitis
ID GENOME-WIDE ASSOCIATION; RISK LOCI; CELLS; LIVER; TH17; ACTIVATION;
COLITIS
AB Background: Although a majority of patients with PSC have colitis [PSC-IBD; primary sclerosing cholangitis-inflammatory bowel disease], this is phenotypically different from ulcerative colitis [UC]. We sought to define further the pathophysiological differences between PSC-IBD and UC, by applying a comparative and integrative approach to colonic gene expression, gut microbiota and immune infiltration data.
Methods: Colonic biopsies were collected from patients with PSC-IBD [n = 10], UC [n = 10], and healthy controls [HC; n = 10]. Shotgun RNA-sequencing for differentially expressed colonic mucosal genes [DEGs], 16S rRNA analysis for microbial profiling, and immunophenotyping were performed followed by multi-omic integration.
Results: The colonic transcriptome differed significantly between groups [p = 0.01]. Colonic transcriptomes from HC were different from both UC [1343 DEGs] and PSC-IBD [4312 DEGs]. Of these genes, only 939 had shared differential gene expression in both UC and PSC-IBD compared with HC. Imputed pathways were predominantly associated with upregulation of immune response and microbial defense in both disease cohorts compared with HC. There were 1692 DEGs between PSCIBD and UC. Bile acid signalling pathways were upregulated in PSC-IBD compared with UC [p = 0.02]. Microbiota profiles were different between the three groups [p = 0.01]; with inferred function in PSCIBD also being consistent with dysregulation of bile acid metabolism. Th17 cells and IL17-producing CD4 cells were increased in both PSC-IBD and UC when compared with HC [p < 0.05]. Multi-omic integration revealed networks involved in bile acid homeostasis and cancer regulation in PSC-IBD.
Conclusions: Colonic transcriptomic and microbiota analysis in PSC-IBD point toward dysregulation of colonic bile acid homeostasis compared with UC. This highlights important mechanisms and suggests the possibility of novel approaches in treating PSC-IBD.
C1 [Quraishi, Mohammed Nabil; Acharjee, Animesh; Beggs, Andrew D.; Horniblow, Richard; Tselepis, Chris; Gkoutos, Georgios; Iqbal, Tariq H.] Univ Birmingham, Inst Canc & Genom Sci, Birmingham, W Midlands, England.
[Quraishi, Mohammed Nabil; Ghosh, Subrata; Iqbal, Tariq H.] Univ Hosp Birmingham, Queen Elizabeth Hosp, Dept Gastroenterol, Birmingham, W Midlands, England.
[Quraishi, Mohammed Nabil; Iqbal, Tariq H.] Univ Birmingham, Microbiome Treatment Ctr, Birmingham, W Midlands, England.
[Quraishi, Mohammed Nabil; Gkoutos, Georgios; Ghosh, Subrata; Hirschfield, Gideon M.; Iqbal, Tariq H.] Univ Birmingham, Ctr Liver & Gastroenterol Res, NIHR Birmingham Biomed Res Ctr, Birmingham, W Midlands, England.
[Acharjee, Animesh; Gkoutos, Georgios; Ghosh, Subrata] Univ Hosp Birmingham, Inst Translat Med, Birmingham, W Midlands, England.
[Gkoutos, Georgios] Wellcome Trust Res Labs, MRC Hlth Data Res UK HDR UK, London, England.
[Gkoutos, Georgios] NIHR Surg Reconstruct & Microbiol Res Ctr, NIHR Expt Canc Med Ctr, Birmingham, W Midlands, England.
[Rossiter, A. E.; Loman, Nicholas; van Schaik, Willem] Univ Birmingham, Inst Microbiol & Infect, Birmingham, W Midlands, England.
[Withers, David] Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham, W Midlands, England.
[Walters, Julian R. F.] Imperial Coll London, Div Digest Dis, London, England.
[Hirschfield, Gideon M.] Univ Toronto, Toronto Gen Hosp, Toronto Ctr Liver Dis, Toronto, ON, Canada.
C3 University of Birmingham; University of Birmingham; University of
Birmingham; University of Birmingham; University of Birmingham;
University of Birmingham; University of Birmingham; Imperial College
London; University of Toronto; University Health Network Toronto;
Toronto General Hospital
RP Hirschfield, GM (corresponding author), Univ Hlth Network, Toronto Ctr Liver Dis, Toronto, ON, Canada.; Hirschfield, GM (corresponding author), Univ Toronto, Toronto, ON, Canada.
EM gideon.hirschfield@uhn.ca
RI Gkoutos, Georgios/AAS-9936-2020; Loman, Nicholas/AFM-0891-2022; Beggs,
Andrew/A-6912-2013; Acharjee, Animesh/AAC-7637-2019; Ghosh,
Subrata/AAC-2676-2021; Walters, Julian/D-5189-2009; Withers,
David/C-7055-2015; Horniblow, Richard/F-8577-2014
OI Acharjee, Animesh/0000-0003-2735-7010; iqbal, tariq/0000-0002-6681-9882;
Beggs, Andrew/0000-0003-0784-2967; Withers, David/0000-0003-3757-7594;
van Schaik, Willem/0000-0001-5832-0988; Horniblow,
Richard/0000-0002-3996-9236; Gkoutos, Georgios/0000-0002-2061-091X
FU NIHR Birmingham Biomedical Research Centre at UHB; University of
Birmingham; Wellcome Trust [102732/Z/13/Z]; Cancer Research UK
[C31641/A23923]; Medical Research Council [MR/M016587/1]; Lily and Terry
Horner Chair in Autoimmune Liver Disease Research; Wellcome Trust
[102732/Z/13/Z] Funding Source: Wellcome Trust; MRC [MR/M016587/1,
MR/M009157/1, MR/M501621/1, MR/L015080/1] Funding Source: UKRI
FX This paper presents independent research supported by the NIHR
Birmingham Biomedical Research Centre at UHB and University of
Birmingham. The views expressed are those of the author[s] and not
necessarily those of NHS, the NIHR, or Department of Health and Social
Care. ADB acknowledges funding from the Wellcome Trust [102732/Z/13/Z],
Cancer Research UK [C31641/A23923], and the Medical Research Council
[MR/M016587/1]. GMH is supported by the Lily and Terry Horner Chair in
Autoimmune Liver Disease Research.
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NR 46
TC 87
Z9 87
U1 1
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1873-9946
EI 1876-4479
J9 J CROHNS COLITIS
JI J. Crohns Colitis
PD JUL
PY 2020
VL 14
IS 7
BP 935
EP 947
DI 10.1093/ecco-jcc/jjaa021
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA OH1DG
UT WOS:000582311700009
PM 32016358
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Obara, N
Ueno, Y
Fukushima, K
Nakagome, Y
Kakazu, E
Kimura, O
Wakui, Y
Kido, O
Ninomiya, M
Kogure, T
Inoue, J
Kondo, Y
Shiina, M
Iwasaki, T
Yamamoto, T
Shimosegawa, T
AF Obara, Noriyuki
Ueno, Yoshiyuki
Fukushima, Koji
Nakagome, Yu
Kakazu, Eiji
Kimura, Osamu
Wakui, Yuta
Kido, Osamu
Ninomiya, Masashi
Kogure, Takayuki
Inoue, Jun
Kondo, Yasuteru
Shiina, Masaaki
Iwasaki, Takao
Yamamoto, Takeshi
Shimosegawa, Tooru
TI Transient elastography for measurement of liver stiffness measurement
can detect early significant hepatic fibrosis in Japanese patients with
viral and nonviral liver diseases
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE transient elastography; fibrosis; chronic liver disease; NAFLD
ID NONALCOHOLIC FATTY LIVER; PRIMARY BILIARY-CIRRHOSIS; VIRUS-RELATED
CIRRHOSIS; NATURAL-HISTORY; HEPATOCELLULAR-CARCINOMA; BIOCHEMICAL
MARKERS; STEATOHEPATITIS; BIOPSY; PREVALENCE; POPULATION
AB Background. Many studies have reported the efficiency of transient elastography, a noninvasive, reproducible, and reliable method for predicting liver fibrosis, in patients with chronic hepatitis C (CHC) and B (CHB), but there are few reports about nonviral chronic liver disease (CLD) such as primary biliary cirrhosis (PBC), nonalcoholic steatohepatitis (NAFLD), and autoimmune hepatitis (AIH). We therefore compared the efficiency of transient elastography between CHC and nonviral CLD. Methods. We assessed the accuracy of liver stiffness measurement (LSM) using Fibroscan, and compared these values with those of hyaluronic acid, type 4 collagen, platelet count, prothrombin index, and AST/platelet ratio index (APRI) as indices for the diagnosis of liver fibrosis in 114 patients with a variety of chronic liver diseases: CHC (n = 51), CHB (n = 11), NAFLD (n = 17), PBC (n = 20), and AIH (n = 15). The histology was assessed according to the METAVIR score by two pathologists. Results. The number of fibrosis stage (F0/1/2/3/4) with CHC was 9/15/12/6/10, and that with nonviral CLD was 10/21/11/4/6, respectively. The ability, assessed by area under receiver operating characteristic (AUROC) curve, to predict liver fibrosis F >= 2 for LSM, HA, type 4 collagen, platelet count, prothrombin index, and APRI, was 0.92, 0.81, 0.87, 0.85, 0.85, and 0.92 in CHC patients, respectively; and 0.88, 0.72, 0.81, 0.67, 0.81, and 0.77 in nonviral CLD patients, respectively. Conclusions. In patients with nonviral CLD, LSM was most helpful in predicting significant fibrosis (F >= 2). Transient elastography is a reliable method for predicting significant liver fibrosis, not only in CHC patients but also in nonviral CLD patients.
C1 [Obara, Noriyuki; Ueno, Yoshiyuki; Fukushima, Koji; Nakagome, Yu; Kakazu, Eiji; Kimura, Osamu; Wakui, Yuta; Kido, Osamu; Ninomiya, Masashi; Kogure, Takayuki; Inoue, Jun; Kondo, Yasuteru; Shiina, Masaaki; Iwasaki, Takao; Shimosegawa, Tooru] Tohoku Univ, Grad Sch Med, Div Gastroenterol, Aoba Ku, Sendai, Miyagi 9808574, Japan.
[Yamamoto, Takeshi] Tohoku Koseinenkin Hosp, Dept Gastroenterol, Sendai, Miyagi, Japan.
C3 Tohoku University
RP Ueno, Y (corresponding author), Tohoku Univ, Grad Sch Med, Div Gastroenterol, Aoba Ku, 1-1 Seiryo, Sendai, Miyagi 9808574, Japan.
RI obara, noriyuki/GLT-9922-2022; Kogure, Takayuki/AAI-3946-2021; Kondo,
Yasuteru/A-6893-2010; Ueno, Yoshiyuki/R-9242-2019; Inoue,
Jun/S-9282-2019
OI Kondo, Yasuteru/0000-0001-5935-4346; Inoue, Jun/0000-0003-1171-7835
FU Ministry of Health, Labour and Welfare of Japan
FX This work was supported in part by grants from Health and Labour
Sciences Research Grants for the Research on Measures for Intractable
Diseases (from the Ministry of Health, Labour and Welfare of Japan).
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NR 39
TC 67
Z9 79
U1 0
U2 8
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD SEP
PY 2008
VL 43
IS 9
BP 720
EP 728
DI 10.1007/s00535-008-2225-2
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 350RQ
UT WOS:000259371200010
PM 18807134
DA 2025-01-07
ER
PT J
AU Yang, L
Zhang, H
Jiang, YF
Jin, QL
Zhang, P
Li, X
Gao, PJ
Niu, JQ
AF Yang, Liu
Zhang, Hong
Jiang, Yan-Fang
Jin, Qing-Long
Zhang, Peng
Li, Xu
Gao, Pu-Jun
Niu, Jun-Qi
TI Association of Estrogen Receptor Gene Polymorphisms and Primary Biliary
Cirrhosis in a Chinese Population: A Case-Control Study
SO CHINESE MEDICAL JOURNAL
LA English
DT Article
DE Estrogen Receptor; Gene Polymorphism; Primary Biliary Cirrhosis
ID AUTOIMMUNE HEPATITIS; FINER BRANCHES; HUMAN LIVERS; CANCER RISK; TREE;
SUSCEPTIBILITY; PATHOPHYSIOLOGY; PROGRESSION; PROFILE; BETA
AB Background: Primary biliary cirrhosis (PBC) is a chronic and slowly progressive cholestatic liver disease characterized by destruction of the interlobular bile ducts and a striking female predominance. The aim of this study was to identify associations between estrogen receptor (ESR) gene polymorphisms with the risk of developing PBC and abnormal serum liver tests in a Chinese population.
Methods: Thirty-six patients with PBC (case group) and 35 healthy individuals (control group) from the First Hospital of Jilin University were studied. Whole genomic DNA was extracted from all the participants. Three single-nucleotide polymorphisms (rs2234693, rs2228480, and rs3798577) from ESR1 and two (rs1256030 and rs1048315) from ESR2 were analyzed by a pyrosequencing method. Demographic data and liver biochemical data were collected.
Results: Subjects with the T allele at ESR2 rs1256030 had 1.5 times higher risk of developing PBC than those with the C allele (odds ratio [OR] = 2.1277, 95% confidence interval [CI] = 1.1872-4.5517). Haplotypes TGC of ESR1 rs2234693, rs2228480, and rs3798577 were risk factors for having PBC. The C allele at ESR1 rs2234693 was associated with abnormal alkaline phosphatase (OR = 5.2469, 95% CI = 1.3704-20.0895) and gamma-glutamyl transferase (OR = 3.4286, 95% CI = 1.0083-13.6578) levels in PBC patients.
Conclusions: ESR2 rs1256030 T allele may be a significant risk factor for the development of PBC. Screening for patients with gene polymorphisms may help to make early diagnoses in patients with PBC.
C1 [Yang, Liu; Jiang, Yan-Fang; Jin, Qing-Long; Zhang, Peng; Li, Xu; Gao, Pu-Jun; Niu, Jun-Qi] Jilin Univ, Dept Hepatol, Hosp 1, Changchun 130021, Jilin, Peoples R China.
[Yang, Liu] Nanjing Univ, Sch Med, Natl Clin Res Ctr Kidney Dis, Jinling Hosp, Nanjing 210002, Jiangsu, Peoples R China.
[Zhang, Hong] Jilin Univ, Phase Clin Trials Unit 1, Hosp 1, Changchun 130021, Jilin, Peoples R China.
C3 Jilin University; Nanjing University; Jilin University
RP Niu, JQ (corresponding author), Jilin Univ, Dept Hepatol, Hosp 1, Changchun 130021, Jilin, Peoples R China.
EM junqiniu@126.com
RI Jiang, Yanfang/AEZ-9708-2022
OI Jiang, Yanfang/0000-0002-2478-1521
FU National Natural Science Foundation of China [30872174, 81300313]; Youth
Fund the First Hospital of Jilin University
FX This work was supported by grants from the National Natural Science
Foundation of China (Nos. 30872174, 81300313) and the Youth Fund the
First Hospital of Jilin University.
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NR 29
TC 6
Z9 7
U1 2
U2 8
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S NO 1498A-2
VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 0366-6999
J9 CHINESE MED J-PEKING
JI Chin. Med. J.
PD NOV 20
PY 2015
VL 128
IS 22
BP 3008
EP 3014
DI 10.4103/0366-6999.168964
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA CX5WO
UT WOS:000365773400005
PM 26608979
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Buc, E
Lesurtel, M
Belghiti, J
AF Buc, E.
Lesurtel, M.
Belghiti, J.
TI Is preoperative histological diagnosis necessary before referral to
major surgery for cholangiocarcinoma?
SO HPB
LA English
DT Review
ID PRIMARY SCLEROSING CHOLANGITIS; BILE-DUCT STENOSIS; BRUSH CYTOLOGY;
BILIARY STRICTURES; INFLAMMATORY PSEUDOTUMOR; MR
CHOLANGIOPANCREATOGRAPHY; DIFFERENTIAL-DIAGNOSIS; PORTAL BILIOPATHY;
LIVER METASTASES; SERUM CA-19-9
AB Major surgical resection is often the only curative treatment for cholangiocarcinoma. When imaging techniques fail to establish the accurate diagnosis, biopsy of the lesion is unavoidable. However, biopsy is not necessarily required for topography of the cholangiocarcinoma (intrahepatic or extrahepatic). 1) In extrahepatic cholangiocarcinoma (ECC), clinical features and radiological imaging relate to biliary obstruction. Provided that between 8% and 43% of bile duct strictures are not ECC, the lesions mimicking ECC that should be ruled out are gallbladder cancer, Mirizzi syndrome, primary sclerosing cholangitis (PSC), autoimmune pancreatitis and portal biliopathy. Systematic biopsy is usually difficult and has poor sensitivity, but a good knowledge of these mimicking ECC diseases, along with precise analysis of clinical and imaging semiology, may lead to a correct diagnosis without the need for biopsy. 2) Intrahepatic cholangiocarcinoma (ICC) developing in normal liver appears as a hypovascular tumour with fibrotic component and capsular retraction that can be confused with fibrous metastases such as breast and colorectal cancers. The lack of the primary site, a relatively large tumour size and ancillary findings such as bile duct dilatation may provide a clue to the diagnosis. If not, we advocate local resection with lymph node dissection, since ICC is the most likely diagnostis and surgery is the only curative treatment. In the event of adenocarcinoma from unknown primary, surgery is an effective treatment even if prognosis is poor.
C1 [Buc, E.; Lesurtel, M.; Belghiti, J.] Hop Beaujon, Dept HBP Surg, F-92110 Clichy, France.
C3 Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
Hopital Universitaire Beaujon - APHP
RP Belghiti, J (corresponding author), Hop Beaujon, Dept HBP Surg, 100 Bd Gen Leclerc, F-92110 Clichy, France.
EM jacques.belghiti@bjn.aphp.fr
RI Buc, Emmanuel/JEP-6444-2023; Lesurtel, Mickaël/J-3710-2019
OI Lesurtel, Mickael/0000-0003-2397-4599
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NR 94
TC 17
Z9 18
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1365-182X
EI 1477-2574
J9 HPB
JI HPB
PD APR
PY 2008
VL 10
IS 2
BP 98
EP 105
DI 10.1080/13651820802014585
PG 8
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA V15PH
UT WOS:000207813400008
PM 18773064
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Gong, FY
Gong, Z
Duo, CC
Wang, J
Hong, C
Gao, XM
AF Gong, Fang-Yuan
Gong, Zheng
Duo, Cui-Cui
Wang, Jun
Hong, Chao
Gao, Xiao-Ming
TI Aberrant Glycosylation Augments the Immuno-Stimulatory Activities of
Soluble Calreticulin
SO MOLECULES
LA English
DT Article
DE calreticulin eukaryotic; macrophage; glycosylation
ID PROTEIN-KINASE-C; RHEUMATOID-ARTHRITIS; HEAT-SHOCK; GLYCOPROTEINS;
ANGIOGENESIS; DIMERIZATION; FRAGMENT; RECEPTOR; CALCIUM; DISEASE
AB Calreticulin (CRT), a luminal resident calcium-binding glycoprotein of the cell, is a tumor-associated antigen involved in tumorigenesis and also an autoantigen targeted by autoantibodies found in patients with various autoimmune diseases. We have previously shown that prokaryotically expressed recombinant murine CRT (rCRT) exhibits strong stimulatory activities against monocytes/macrophages in vitro and potent immunogenicity in vivo, which is partially attributable to self-oligomerization of soluble rCRT. However, even in oligomerized form native CRT (nCRT) isolated from mouse liver is much less active than rCRT, arguing against the possibility that self-oligomerization alone would license potent pro-inflammatory properties to nCRT. Since rCRT differs from nCRT in its lack of glycosylation, we wondered if aberrant glycosylation of eukaryotically expressed CRT (eCRT) would significantly enhance its immunological activity. In the present study, tunicamycin, an N-glycosyltransferase inhibitor, was employed to treat CHO cells (CHO-CRT) stably expressing full-length recombinant mouse CRT in secreted form for preparation of aberrantly glycosylated eCRT (tun-eCRT). Our biochemical and immunological analysis results indicate that eCRT produced by CHO-CRT cells is similar to nCRT in terms of glycosylation level, lack of self-oligomerization, relatively poor immunogenicity and weak macrophage-stimulatory activity, while tun-eCRT shows reduced glycosylation yet much enhanced ability to elicit specific humoral responses in mice and TNF-alpha, and nitric oxide production by macrophages in vitro. Given that abberant glycosylation of proteins is a hallmark of cancer cells and also related to the development of autoimmune disorders in humans, our data may provide useful clues for better understanding of potentiating roles of dysregulated glycosylation of molecules such as CRT in tumorigenesis and autoimmunity.
C1 [Gong, Fang-Yuan; Gong, Zheng; Duo, Cui-Cui; Wang, Jun; Hong, Chao; Gao, Xiao-Ming] Soochow Univ, Inst Biol & Med Sci, Suzhou 215123, Jiangsu, Peoples R China.
C3 Soochow University - China
RP Gong, FY; Gao, XM (corresponding author), Soochow Univ, Inst Biol & Med Sci, Suzhou 215123, Jiangsu, Peoples R China.
EM gongfangyuan@suda.edu.cn; 20154221101@stu.suda.edu.cn; gfy0308@sina.com;
jwang79@suda.edu.cn; chaohong@suda.edu.cn; xmgao@suda.edu.cn
RI Wang, Jun/AGJ-1311-2022
OI Wang, Jun/0000-0002-4458-3741
FU Program for Changjiang Scholars and Innovative Research Team [IRT1075];
National Foundation of Nature Science [31370908/31570868]; Foundation
for Application and Fundamental Research of Healthcare of China
[SYS201667]
FX This study was supported by grants from the Program for Changjiang
Scholars and Innovative Research Team (IRT1075) and National Foundation
of Nature Science (31370908/31570868) and also Foundation for
Application and Fundamental Research of Healthcare (SYS201667) of China.
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Z9 5
U1 1
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD MAR
PY 2018
VL 23
IS 3
AR 523
DI 10.3390/molecules23030523
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA GA7KD
UT WOS:000428514100014
PM 29495436
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Ewees, MG
Abdelghany, TM
Abdel-Aziz, AAH
Abdel-Bakky, MS
AF Ewees, Mohamed G.
Abdelghany, Tamer M.
Abdel-Aziz, H. Abdel-Aziz
Abdel-Bakky, Mohamed S.
TI All-trans retinoic acid mitigates methotrexate-induced liver injury in
rats; relevance of retinoic acid signaling pathway
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Article
DE Retinoid X receptor; Retinoic acid receptor; All-trans retinoic acid;
Hepatotoxicity; Methotrexate
ID HEPATIC STELLATE CELLS; OXIDATIVE ORGAN INJURY; INDUCED HEPATOTOXICITY;
IN-VITRO; COLORIMETRIC METHOD; RXR HETERODIMERS; GENE-EXPRESSION;
RECEPTOR; ALPHA; ACTIVATION
AB Methotrexate (MTX) is a widely used drug for treatment of rheumatic and autoimmune diseases as well as different types of cancer. One of the major side effects of MTX is hepatotoxicity. Retinoid receptors, including retinoid X receptor (RXR), and retinoic acid receptor (RAR) are vitamin A receptors that are highly expressed in the liver and regulate important physiological processes through regulation of different genes. In this study, we investigated the effect of MTX on RXR-alpha and RAR-alpha expression in the liver and the potential protective effects of all-trans retinoic acid (ATRA) in MTX-induced hepatotoxicity. Rats were randomly divided into five groups: The rates were treated with saline, DMSO, MTX (20 mg/kg/IP; single dose), ATRA (7.5 mg/kg/day, I.P), or MTX and ATRA. Rats were killed 24 h after the last ATRA injection. The liver tissues were dissected out, weighed, and subjected to histological, immunohistochemical, and biochemical examinations. Our results demonstrated that treatment with MTX resulted in significant decrease in reduced glutathione (GSH) content and superoxide dismutase (SOD) activity, with concomitant increase in ALT, AST, and MDA levels. In addition, MTX markedly downregulated the expression of both RXR-alpha and RAR-alpha, and changed the appearance of RXR-alpha to be very small speckled droplets. Treatment with ATRA significantly ameliorated MTX-induced effects on GSH, ALT, and MDA. Moreover, ATRA administration increased the expression and nuclear translocation of RXR-alpha in rat hepatocytes. In conclusion, our study revealed, for the first time, that retinoid receptors may play an important role in the MTX-induced hepatotoxicity.
C1 [Ewees, Mohamed G.; Abdelghany, Tamer M.; Abdel-Aziz, H. Abdel-Aziz; Abdel-Bakky, Mohamed S.] Al Azhar Univ, Fac Pharm, Cairo, Egypt.
[Abdel-Bakky, Mohamed S.] Aljouf Univ, Coll Pharm, Aljouf 2014, Saudi Arabia.
C3 Egyptian Knowledge Bank (EKB); Al Azhar University; Al Jouf University
RP Abdelghany, TM (corresponding author), Al Azhar Univ, Fac Pharm, Cairo, Egypt.
EM tamer_ibrahim2@yahoo.com
RI Ewees, Mohamed/ABH-3386-2021; ABDELGHANY, Tamer/L-7347-2019;
ABdel-Bakky, Mohamed/AAD-3608-2019
OI Ewees, Mohamed Gomaa/0000-0003-4839-4291; Abdelghany,
Tamer/0000-0002-2568-9356; Abdel-Bakky, mohamed/0000-0002-0426-5458
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NR 35
TC 18
Z9 20
U1 0
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0028-1298
EI 1432-1912
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD SEP
PY 2015
VL 388
IS 9
BP 931
EP 938
DI 10.1007/s00210-015-1130-5
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CP3WB
UT WOS:000359812300003
PM 25971792
DA 2025-01-07
ER
PT J
AU Hegde, M
Girisa, S
BharathwajChetty, B
Vishwa, R
Kunnumakkara, AB
AF Hegde, Mangala
Girisa, Sosmitha
BharathwajChetty, Bandari
Vishwa, Ravichandran
Kunnumakkara, Ajaikumar B.
TI Curcumin Formulations for Better Bioavailability: What We Learned from
Clinical Trials Thus Far?
SO ACS OMEGA
LA English
DT Article
ID QUALITY-OF-LIFE; TYPE-2 DIABETES-MELLITUS; FATTY LIVER-DISEASE; CHRONIC
PULMONARY COMPLICATIONS; RHEUMATOID-ARTHRITIS PATIENTS;
OXIDANT-ANTIOXIDANT BALANCE; RANDOMIZED CONTROLLED-TRIAL; SYSTEMIC
OXIDATIVE STRESS; SOLID LIPID CURCUMIN; DOUBLE-BLIND
AB Curcumin has been credited with a wide spectrum of pharmacological properties for the prevention and treatment of several chronic diseases such as arthritis, autoimmune diseases, cancer, cardiovascular diseases, diabetes, hemoglobinopathies, hypertension, infectious diseases, inflammation, metabolic syndrome, neurological diseases, obesity, and skin diseases. However, due to its weak solubility and bioavailability, it has limited potential as an oral medication. Numerous factors including low water solubility, poor intestinal permeability, instability at alkaline pH, and fast metabolism contribute to curcumin's limited oral bioavailability. In order to improve its oral bioavailability, different formulation techniques such as coadministration with piperine, incorporation into micelles, micro/nanoemulsions, nanoparticles, liposomes, solid dispersions, spray drying, and noncovalent complex formation with galactomannosides have been investigated with in vitro cell culture models, in vivo animal models, and humans. In the current study, we extensively reviewed clinical trials on various generations of curcumin formulations and their safety and efficacy in the treatment of many diseases. We also summarized the dose, duration, and mechanism of action of these formulations. We have also critically reviewed the advantages and limitations of each of these formulations compared to various placebo and/or available standard care therapies for these ailments. The highlighted integrative concept embodied in the development of next-generation formulations helps to minimize bioavailability and safety issues with least or no adverse side effects and the provisional new dimensions presented in this direction may add value in the prevention and cure of complex chronic diseases.
C1 [Hegde, Mangala; Girisa, Sosmitha; BharathwajChetty, Bandari; Vishwa, Ravichandran; Kunnumakkara, Ajaikumar B.] Indian Inst Technol Guwahati, Dept Biosci & Bioengn, Gauhati 781039, Assam, India.
C3 Indian Institute of Technology System (IIT System); Indian Institute of
Technology (IIT) - Guwahati
RP Kunnumakkara, AB (corresponding author), Indian Inst Technol Guwahati, Dept Biosci & Bioengn, Gauhati 781039, Assam, India.
EM kunnumakkara@iitg.ac.in
RI Kunnumakkara, Ajaikumar/AAH-5214-2019; Girisa, Sosmitha/JGD-3270-2023;
Kunnumakkara, Ajaikumar/H-8566-2012
OI Kunnumakkara, Ajaikumar/0000-0001-9121-6816; BharathwajChetty,
Bandari/0000-0002-4147-3993; Vishwa, Ravichandran/0000-0001-5532-1387
FU Department of Biotechnology (DBT) , Government of India
[BT/556/NE/U-Excel/2016]
FX Funding This project was supported by BT/556/NE/U-Excel/2016 grant
awarded to A.B.K. by Department of Biotechnology (DBT) , Government of
India.
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NR 314
TC 72
Z9 74
U1 14
U2 47
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 2470-1343
J9 ACS OMEGA
JI ACS Omega
PD MAR 28
PY 2023
VL 8
IS 12
BP 10713
EP 10746
DI 10.1021/acsomega.2c07326
EA MAR 2023
PG 34
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA A5GQ2
UT WOS:000950581800001
PM 37008131
OA gold, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Prud'homme, GJ
Glinka, Y
Khan, AS
Draghia-Akli, R
AF Prud'homme, Gerald J.
Glinka, Yelena
Khan, Amir S.
Draghia-Akli, Ruxandra
TI Electroporation-enhanced nonviral gene transfer for the prevention or
treatment of immunological, endocrine and neoplastic diseases
SO CURRENT GENE THERAPY
LA English
DT Review
DE autoimmunity; cancer; diabetes; DNA vaccination; electroporation; gene
therapy; growth hormone releasing hormone; muscle; plasmid
ID IN-VIVO ELECTROPORATION; HORMONE-RELEASING-HORMONE; COLLAGEN-INDUCED
ARTHRITIS; SMALL INTERFERING RNA; BLEOMYCIN-MEDIATED
ELECTROCHEMOTHERAPY; DUCHENNE/BECKER MUSCULAR-DYSTROPHIES; ANTIGEN
POLYNUCLEOTIDE VACCINE; PLASMID DNA ELECTROTRANSFER; HER-2 TRANSGENIC
MICE; HEPATITIS-B-VIRUS
AB Nonviral gene transfer is markedly enhanced by the application of in vivo electroporation (also denoted electrogene transfer or electrokinetic enhancement). This approach is safe and can be used to deliver nucleic acid fragments, oligonucleotides, siRNA, and plasmids to a wide variety of tissues, such as skeletal muscle, skin and liver. In this review, we address the principles of electroporation and demonstrate its effectiveness in disease models. Electroporation has been shown to be equally applicable to small and large animals (rodents, dogs, pigs, other farm animals and primates), and this addresses one of the major problems in gene therapy, that of scalability to humans. Gene transfer can be optimized and tissue injury minimized by the selection of appropriate electrical parameters. We and others have applied this approach in preclinical autoimmune and/or inflammatory diseases to deliver either cytokines, anti-inflammatory agents or immunoregulatory molecules. Electroporation is also effective for the intratumoral delivery of therapeutic vectors. It strongly boost DNA vaccination against infectious agents (e.g., hepatitis B virus, human immunodeficiency virus-1) or tumor antigens (e.g., HER-2/neu, carcinoembryonic antigen). In addition; we found that electroporation-enhanced DNA vaccination against islet-cell antigens ameliorated autoimmune diabetes. One of the most likely future applications, however, may be in intramuscular gene transfer for systemic delivery of either endocrine hormones (e.g., growth hormone releasing hormone and leptin), hematopoietic factors (e.g., erythropoietin, GM-CSF), antibodies, enzymes, or numerous other protein drugs. In vivo electroporation has been performed in humans, and it seems likely it could be applied clinically for nonviral gene therapy.
C1 St Michaels Hosp, Dept Lab Med, Toronto, ON M5B 1W8, Canada.
Univ Turin, Toronto, ON M5B 1W8, Canada.
ADViSYS Inc, The Woodlands, TX 77381 USA.
C3 University of Toronto; Saint Michaels Hospital Toronto; University of
Turin; Advisys
RP Prud'homme, GJ (corresponding author), St Michaels Hosp, Dept Lab Med, Room 2013CC,30 Bond St, Toronto, ON M5B 1W8, Canada.
EM prudhommeg@smh.toronto.on.ca
RI khan, Amir/AAS-4269-2021
OI Draghia-Akli, Ruxandra/0000-0001-6372-4039
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2004, DRUGS R D, V5, P293
NR 319
TC 145
Z9 168
U1 0
U2 35
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1566-5232
EI 1875-5631
J9 CURR GENE THER
JI Curr. Gene Ther.
PD APR
PY 2006
VL 6
IS 2
BP 243
EP 273
DI 10.2174/156652306776359504
PG 31
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 046UY
UT WOS:000237837800006
PM 16611045
DA 2025-01-07
ER
PT J
AU Esmailbeig, M
Ghaderi, A
AF Esmailbeig, Maryam
Ghaderi, Abbas
TI Interleukin-18: a regulator of cancer and autoimmune diseases
SO EUROPEAN CYTOKINE NETWORK
LA English
DT Review
DE IL-18; cancer; autoimmunity
ID GENE PROMOTER POLYMORPHISMS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; TYPE-1
DIABETES-MELLITUS; GAMMA-INDUCING FACTOR; IL-18 SERUM-LEVEL;
HEPATOCELLULAR-CARCINOMA; MULTIPLE-SCLEROSIS; METABOLIC SYNDROME;
INTERFERON-GAMMA; PROSTATE-CANCER
AB Interleukin (IL)-18, structurally similar to IL-1 beta, is a member of IL-1 superfamily of cytokines. This cytokine, which is expressed by many human lymphoid and nonlymphoid cells, has an important role in inflammatory processes. The main function of IL-18 is mediated through induction of interferon-gamma (IFN-gamma) secretion from T helper (Th1) cells. This cytokine synergistically with IL-12 contributes to Thl differentiation and, therefore, is important in host defense mechanisms against intracellular bacteria, viruses, and fungi. Recent evidences showing the involvement of IL-18 in Th2 differentiation and ultimately IgE production from B cells have shed a new insight on the dual effects of IL-18 on Thl and Th2 inflammatory responses. IL-18 in combination with IL-12 can activate cytotoxic T cells (CTLs), as well as natural killer (NK) cells, to produce IFN-gamma, and, therefore, may contribute to tumor immunity. The biological activity of IL-18 is not limited to these cells, but it also plays a role in development of Th17 cell responses. IL-18 synergistically with IL-23 can induce IL-17 secretion from Th17 cells. The diverse biological activity of IL-18 on T-cell subsets and other immune cells has made this cytokine a good target for investigating its role in various inflammatory-based diseases. Lately, the discovery of IL-18 binding protein (IL-18BP), a physiological inhibitor of IL-18 and a hallmark of IL-18 biology, made this cytokine an attractive target for studying its pros and cons in the treatment of various diseases. In recent years, the biology, genetics, and pathological role of IL-18 have been studied in a number of diseases. In this article, we aimed to present an updated review on these aspects regarding the contribution of IL-18 to important diseases such as cancer, autoimmunity, and inflammatory mediated conditions including allergic diseases, metabolic syndrome, and atherosclerosis. Emerging data indicating prognostic, diagnostic, and therapeutic features of IL-18 and its related molecules will also be discussed.
C1 [Esmailbeig, Maryam; Ghaderi, Abbas] Shiraz Univ Med Sci, Shiraz Inst Canc Res, Sch Med, Shiraz, Iran.
[Ghaderi, Abbas] Shiraz Univ Med Sci, Dept Immunol, Sch Med, Shiraz, Iran.
C3 Shiraz University of Medical Science; Shiraz University of Medical
Science
RP Ghaderi, A (corresponding author), Shiraz Univ Med Sci, Shiraz Inst Canc Res, Sch Med, Shiraz, Iran.; Ghaderi, A (corresponding author), Shiraz Univ Med Sci, Dept Immunol, Sch Med, Shiraz, Iran.
EM ghaderia@sums.ac.ir
RI Ghaderi, Abbas/AGY-3479-2022; Ghaderi, Abbas/B-3874-2012
OI Ghaderi, Abbas/0000-0003-0849-3375
FU Shiraz University of Medical Sciences [1182]; Shiraz Institute for
Cancer Research [ICR-100-502]
FX This work was financially supported by Shiraz University of Medical
Sciences (grant number: 1182) and by grant from Shiraz Institute for
Cancer Research (grant number: ICR-100-502). Conflict of interest: none.
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NR 124
TC 68
Z9 71
U1 1
U2 18
PU JOHN LIBBEY EUROTEXT LTD
PI MONTROUGE
PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE
EI 1952-4005
J9 EUR CYTOKINE NETW
JI Eur. Cytokine Netw.
PD OCT-DEC
PY 2017
VL 28
IS 4
BP 127
EP 140
DI 10.1684/ecn.2018.0401
PG 14
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA GB6BF
UT WOS:000429151600001
PM 29478963
DA 2025-01-07
ER
PT J
AU Klussmeier, A
Massalski, C
Putke, K
Schäfer, G
Sauter, J
Schefzyk, D
Pruschke, J
Hofmann, J
Fürst, D
Carapito, R
Bahram, S
Schmidt, AH
Lange, V
AF Klussmeier, Anja
Massalski, Carolin
Putke, Kathrin
Schaefer, Gesine
Sauter, Juergen
Schefzyk, Daniel
Pruschke, Jens
Hofmann, Jan
Fuerst, Daniel
Carapito, Raphael
Bahram, Seiamak
Schmidt, Alexander H.
Lange, Vinzenz
TI High-Throughput MICA/B Genotyping of Over Two Million Samples:
Workflow and Allele Frequencies
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE MICA; MICB; hematopoietic stem cell transplantation; allele; genotyping;
next generation sequencing; NGS; high-throughput
ID CHAIN-RELATED GENE; HEPATOCELLULAR-CARCINOMA; MICA-129 POLYMORPHISM;
HUMAN NKG2D; HLA-B; MICB; DIVERSITY; ASSOCIATION; RECEPTOR; HAPLOTYPES
AB MICA and MICB are ligands of the NKG2D receptor and thereby influence NK and T cell activity. MICA/B gene polymorphisms, expression levels and the amount of soluble MICA/B in the serum have been linked to autoimmune diseases, infections, and cancer. In hematopoietic stem cell transplantation, MICA matching between donor and patient has been correlated with reduced acute and chronic graft-vs.-host disease and improved survival. Hence, we developed an extremely cost-efficient high-throughput workflow for genotyping MICA/B for newly registered potential stem cell donors. Since mid-2017, we have genotyped over two million samples using NGS amplicon sequencing for MICA/B exons 2-5. In donors of German origin, MICA*008 is the most common MICA allele with a frequency of 42.3%. It is followed by MICA*002 (11.7%) and MICA*009 (8.8%). The three most common MICB alleles are MICB*005 (43.9%), MICB*004 (21.7%), and MICB*002 (18.9%). In general, MICB is less diverse than MICA and only 6 alleles, instead of 15, account for a cumulative allele frequency of 99.5%. In 0.5% of the samples we observed at least one allele of MICA or MICB which has so far not been reported to the IPD/IMGT-HLA database. By providing MICA/B typed voluntary donors, clinicians become empowered to include MICA/B into their donor selection process to further improve unrelated hematopoietic stem cell transplantation.
C1 [Klussmeier, Anja; Massalski, Carolin; Putke, Kathrin; Schaefer, Gesine; Schmidt, Alexander H.; Lange, Vinzenz] DKMS Life Sci Lab, Dresden, Germany.
[Sauter, Juergen; Schefzyk, Daniel; Pruschke, Jens; Hofmann, Jan; Schmidt, Alexander H.] DKMS, Tubingen, Germany.
[Fuerst, Daniel] German Red Cross Blood Transfus Serv, Inst Clin Transfus Med & Immunogenet Ulm, Baden Wuerttemberg Hesse, Germany.
[Fuerst, Daniel] Univ Hosp Ulm, Ulm, Germany.
[Fuerst, Daniel] Univ Ulm, Inst Transfus Med, Ulm, Germany.
[Carapito, Raphael; Bahram, Seiamak] Univ Strasbourg, Lab ImmunoRhumatol Mol, Plateforme GENOMAX, LabEx TRANSPLANTEX,INSERM,UMR S 1109, Strasbourg, France.
C3 Eberhard Karls University of Tubingen; Eberhard Karls University
Hospital; Ulm University; Ulm University; Institut National de la Sante
et de la Recherche Medicale (Inserm); Universites de Strasbourg
Etablissements Associes; Universite de Strasbourg; Universite de
Lorraine
RP Klussmeier, A (corresponding author), DKMS Life Sci Lab, Dresden, Germany.
EM klussmeier@dkms-lab.de
RI Carapito, Raphael/ABG-5061-2020; Klussmeier, Anja/GRR-7916-2022; Bahram,
Seiamak/IXW-8227-2023; Carapito, Raphael/O-5317-2016; Lange,
Vinzenz/I-1077-2019
OI Klussmeier, Anja/0000-0002-2987-7071; Bahram,
Seiamak/0000-0002-6928-9952; Carapito, Raphael/0000-0002-7036-442X;
Lange, Vinzenz/0000-0002-6442-9573
FU Agence Nationale de la Recherche (ANR) [ANR-11-LABX-0070_TRANSPLANTEX];
MSD-Avenir grant AUTOGEN
FX RC and SB were supported by the Agence Nationale de la Recherche
(ANR)-ANR-11-LABX-0070_TRANSPLANTEX and MSD-Avenir grant AUTOGEN.
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NR 54
TC 27
Z9 27
U1 0
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD FEB 21
PY 2020
VL 11
AR 314
DI 10.3389/fimmu.2020.00314
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA KZ7CT
UT WOS:000523416300001
PM 32153595
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Chen, HW
Huang, HH
Lai, CH
Chang, WE
Shih, YL
Chang, WK
Hsieh, TY
Chu, HC
AF Chen, Hsuan-Wei
Huang, Hsin-Hung
Lai, Ching-Huang
Chang, Wei-En
Shih, Yu-Lueng
Chang, Wei-Kuo
Hsieh, Tsai-Yuan
Chu, Heng-Cheng
TI Hepatitis C virus infection in patients with primary binary cirrhosis
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Child-Pugh score; MELD score; Cirrhosis
ID PRIMARY BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; RISK-FACTORS;
INTERFERON THERAPY; LIVER-DISEASE; ANTI-HCV; PROGRESSION; AUTOIMMUNE;
ANTIBODIES
AB Background and aim. The aim of this study is to evaluate the role of hepatitis C virus (HCV) infection in patients with primary biliary cirrhosis (PBC). Material and methods. On the basis of a retrospective review of medical records, all patients consecutively diagnosed with PBC or HCV infection between 1999 and 2011 and who had a regular follow-up of at least 3 years were included in the study. Clinical characteristics, especially the severity of cirrhosis, were analyzed in PBC patients with HCV infection (PBC-HCV), PBC patients without HCV infection (PBC-only), and patients with only HCV infection (HCV-only). Results. A total of 76 patients with PBC, including 9 patients with HCV infection, were analyzed. Of the PBC-HCV patients, 7 (7/9, 77.8%) were women with a mean age of 55.11 +/- 14.29 years. Age- and sex-matched PBC-only patients (n = 36) and HCV-only patients (n = 36) were used as control groups. In comparison to the PBC-only controls, PBC-HCV patients had a greater severity of cirrhosis based on Child-Pugh (p = 0.019) and Model for End-Stage Liver Disease (MELD) (p = 0.01) scores. However, no significant difference in the severity of cirrhosis was found between the PBC-HCV and HCV-only control patients (p = 0.94 in Child-Pugh scores; p = 0.64 in MELD scores). Conclusions. In PBC patients with concomitant HCV infection, aggressive management may be warranted in view of the associated more severe liver cirrhosis.
C1 [Chen, Hsuan-Wei; Huang, Hsin-Hung; Shih, Yu-Lueng; Chang, Wei-Kuo; Hsieh, Tsai-Yuan; Chu, Heng-Cheng] Natl Def Med Ctr, Triserv Gen Hosp, Div Gastroenterol & Hepatol, Taipei, Taiwan.
[Lai, Ching-Huang] Natl Def Med Ctr, Sch Publ Hlth, Taipei, Taiwan.
[Chang, Wei-En] Hualien Armed Forces Gen Hosp, Dept Internal Med, Hualien, Taiwan.
C3 National Defense Medical Center; Tri-Service General Hospital; National
Defense Medical Center
RP Chu, HC (corresponding author), Natl Def Med Ctr, Triserv Gen Hosp, Dept Internal Med, Div Gastroenterol & Hepatol, 325,Sect 2,Cheng Kung Rd,Neihu 114, Taipei, Taiwan.
EM chu5583@ms55.hinet.net
RI Cheng, Ann-Lii/ACM-0936-2022; Lai, Ching-Huang/ABF-9274-2021
FU National Science Council [NSC94-2314-B-016-047]; Tri-Service General
Hospital, National Defense Medical Center [TSGH-C97-44, TSGH-C98-48,
TSGH-C99-61]; C.Y. Foundation for Advancement of Education, Sciences and
Medicine, Taiwan
FX This study was supported in parts by National Science Council
(NSC94-2314-B-016-047), Tri-Service General Hospital, National Defense
Medical Center (TSGH-C97-44, TSGH-C98-48 and TSGH-C99-61) and the C.Y.
Foundation for Advancement of Education, Sciences and Medicine, Taiwan.
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NR 33
TC 8
Z9 8
U1 0
U2 0
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD JAN-FEB
PY 2013
VL 12
IS 1
BP 78
EP 84
DI 10.1016/S1665-2681(19)31388-2
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 145PU
UT WOS:000319030100010
PM 23293197
OA hybrid
DA 2025-01-07
ER
PT J
AU Selmaj, I
Cichalewska, M
Namiecinska, M
Galazka, G
Horzelski, W
Selmaj, KW
Mycko, MP
AF Selmaj, Igor
Cichalewska, Maria
Namiecinska, Magdalena
Galazka, Grazyna
Horzelski, Wojciech
Selmaj, Krzysztof W.
Mycko, Marcin P.
TI Global Exosome Transcriptome Profiling Reveals Biomarkers for Multiple
Sclerosis
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID EXTRACELLULAR VESICLES; HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE
DEMYELINATION; CIRCULATING MICRORNAS; MIRNA EXPRESSION; DISEASE;
MIR-122; CANCER; DIFFERENTIATION; COMMUNICATION
AB Objective: Accumulating evidence supports a role for exosomes in immune regulation. In this study, we investigated the total circulating exosome transcriptome in relapsing-remitting multiple sclerosis (RRMS) patients and healthy controls (HC).
Methods: Next generation sequencing (NGS) was used to define the global RNA profile of serum exosomes in 19 RRMS patients (9 in relapse, 10 in remission) and 10 HC. We analyzed 5 million reads and >50,000 transcripts per sample, including a detailed analysis of microRNAs (miRNAs) differentially expressed in RRMS. The discovery set data were validated by quantification using digital quantitative polymerase chain reaction with an independent cohort of 63 RRMS patients (33 in relapse, 30 in remission) and 32 HC.
Results: Exosomal RNA NGS revealed that of 15 different classes of transcripts detected, 4 circulating exosomal sequences within the miRNA category were differentially expressed in RRMS patients versus HC: hsa-miR-122-5p, hsa-miR-196b-5p, hsa-miR-301a-3p, and hsa-miR-532-5p. Serum exosomal expression of these miRNAs was significantly decreased during relapse in RRMS. These miRNAs were also decreased in patients with a gadolinium enhancement on brain magnetic resonance imaging. In vitro secretion of these miRNAs by peripheral blood mononuclear cells was also significantly impaired in RRMS.
Interpretation: These data show that circulating exosomes have a distinct RNA profile in RRMS. Because putative targets for these miRNAs include the signal transducer and activator of transcription 3 and the cell cycle regulator aryl hydrocarbon receptor, the data suggest a disturbed cell-to-cell communication in this disease. Thus, exosomal miRNAs might represent a useful biomarker to distinguish multiple sclerosis relapse.
C1 [Selmaj, Igor; Cichalewska, Maria; Namiecinska, Magdalena; Galazka, Grazyna; Selmaj, Krzysztof W.; Mycko, Marcin P.] Univ Lodz, Dept Neurol, Lab Neuroimmunol, Lodz, Poland.
[Horzelski, Wojciech] Univ Lodz, Dept Math & Informat, Appl Comp Sci, Lodz, Poland.
C3 University of Lodz; University of Lodz
RP Mycko, MP (corresponding author), Med Univ Lodz, Lab Neuroimmunol, Dept Neurol, Kopcinskiego 22, PL-90153 Lodz, Poland.
EM mm@afazja.am.lodz.pl
RI Mycko, Marcin/S-9386-2016; Namiecinska, Magdalena/V-4363-2018; Galazka,
Grazyna/V-4379-2018; Horzelski, Wojciech/S-6773-2018
OI Namiecinska, Magdalena/0000-0002-6874-4992; Galazka,
Grazyna/0000-0002-4256-1610; Selmaj, Krzysztof/0000-0003-1213-7218;
Cichalewska-Studzinska, Maria/0000-0003-3051-4056; Horzelski,
Wojciech/0000-0002-3690-5368; Mycko, Marcin/0000-0002-2226-1784
FU National Science Center Poland [MAESTRO 2012/04/A/NZ6/00423, PRELUDIUM
2014/13/N/NZ6/03510, OPUS 2015/19/B/NZ6/02834, SONATA
2015/17/D/NZ6/04245]; Polish-Swiss Research Program [PSPB 007/2012];
Polish National Center for Research and Development [STRATEGMED
1/248672/14/MCBR/2015]; Medical University of Lodz
[502-03/1-033-01/502-14-225, 502-03/1-033-01/502-14-223]; Genzyme
[FRM-6429-A]
FX The research was supported by grants from the National Science Center
Poland (MAESTRO 2012/04/A/NZ6/00423, K.W.S.; PRELUDIUM
2014/13/N/NZ6/03510, I.S.; OPUS 2015/19/B/NZ6/02834, M.P.M.; SONATA
2015/17/D/NZ6/04245, M.C.), the Polish-Swiss Research Program (PSPB
007/2012, M.P.M.), the Polish National Center for Research and
Development (STRATEGMED 1/248672/14/MCBR/2015, K.W.S.), the Medical
University of Lodz (502-03/1-033-01/502-14-225, I.S.;
502-03/1-033-01/502-14-223, M.C.), and Genzyme (FRM-6429-A, M.N.).
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NR 45
TC 126
Z9 136
U1 1
U2 43
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD MAY
PY 2017
VL 81
IS 5
BP 703
EP 717
DI 10.1002/ana.24931
PG 15
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA EV6PM
UT WOS:000401891300011
PM 28411393
DA 2025-01-07
ER
PT J
AU Mair, SM
Weiss, G
AF Mair, Sabine M.
Weiss, Guenter
TI New Pharmacological Concepts for the Treatment of Iron Overload
Disorders
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Hepcidin; hemochromatosis; anaemia; erythropoietin; Friedreich ataxia;
divalent metal transporter 1; ferroportin
ID TRANSFERRIN RECEPTOR EXPRESSION; ANTIMICROBIAL PEPTIDE HEPCIDIN;
HEPATITIS-C; REGULATORY PROTEIN; DEFICIENCY ANEMIA; NONALCOHOLIC
STEATOHEPATITIS; HEREDITARY HEMOCHROMATOSIS; HEPATOCELLULAR-CARCINOMA;
OXIDATIVE STRESS; SERINE-PROTEASE
AB Imbalances of iron homeostasis cause frequent clinical syndromes. Iron deficiency affects almost 25% of the global population and approximately one billion people suffer from iron deficiency anaemia. Moreover, the anaemia of chronic disease, which develops primarily in subjects suffering from malignancies, infections and autoimmune disorders is pivotally caused by an iron-limited erythropoiesis, which arises from iron retention within cells of the reticulo endothelial system. In contrast, one of the most frequent inherited disorders in people of Northern-Western European origin is hereditary hemochromatosis (HH). HH leads to progressive iron overload in parenchymal organs with subsequent organ failure. In addition, secondary iron overload develops in patients receiving repetitive blood transfusion for the treatment of genetic hemoglobinopathies or for the correction of anaemia in cancer or myelodysplastic syndromes. Due to the discovery of new genes, our knowledge on the regulation of iron homeostasis has dramatically expanded which offers avenues for new treatment options. This is of importance, since some of these clinical syndromes (e. g. anaemia of chronic disease or secondary iron overload) are not sufficiently treatable with current medications (e. g. iron chelators, iron, erythropoietin) in many patients. In addition, some patients with iron deficiency face side effects from iron therapy or refuse phlebotomy for treatment of HH. Thus, new treatment strategies for iron metabolism disorders or improvement of existing concepts are necessary. This review discusses established, approaching and future putative treatment strategies and concepts for combating iron metabolism disorders.
C1 [Mair, Sabine M.; Weiss, Guenter] Med Univ Innsbruck, Dept Gen Internal Med Clin Immunol & Infect Dis, A-6020 Innsbruck, Austria.
C3 Medical University of Innsbruck
RP Weiss, G (corresponding author), Med Univ Innsbruck, Dept Gen Internal Med Clin Immunol & Infect Dis, Anichstr 35, A-6020 Innsbruck, Austria.
EM guenter.weiss@i-med.ac.at
OI Weiss, Guenter/0000-0003-0709-2158
FU Austrian research Funds FWF [P 19664]; European Union; 6th
framework-Euroiron 1
FX This work was supported by the Austrian research Funds FWF, P 19664 and
the European Union, 6th framework-Euroiron 1.
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NR 219
TC 9
Z9 10
U1 0
U2 4
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PD FEB
PY 2009
VL 16
IS 5
BP 576
EP 590
DI 10.2174/092986709787458434
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 440EG
UT WOS:000265682400005
PM 19199923
DA 2025-01-07
ER
PT J
AU Zhang, Y
Zheng, TY
Huang, ZX
Song, B
AF Zhang, Yun
Zheng, Tianying
Huang, Zixing
Song, Bin
TI CT and MR imaging of primary biliary cholangitis: a pictorial review
SO INSIGHTS INTO IMAGING
LA English
DT Review
DE Primary biliary cholangitis; Computed tomography; Magnetic resonance
imaging; Diagnosis; Staging
ID GENOME-WIDE ASSOCIATION; RADIATION FORCE IMPULSE; MAGNETIC-RESONANCE;
URSODEOXYCHOLIC ACID; BIOCHEMICAL RESPONSE; AUTOIMMUNE HEPATITIS;
PORTAL-HYPERTENSION; LIVER FIBROSIS; GRADING SYSTEM; CIRRHOSIS
AB Primary biliary cholangitis (PBC) is a rare chronic autoimmune-mediated cholestatic liver disease involving medium and small bile ducts that can lead to liver fibrosis and cirrhosis. To date, the pathogenesis of PBC remains elusive, and there is currently no curative medical treatment. Computed tomography (CT) and magnetic resonance (MR) imaging, as common technical tools that allow non-invasive monitoring of liver tissue in vivo, play crucial roles in the diagnosis, staging, and prognosis prediction in PBC by enabling assessment of abnormalities in liver morphology and parenchyma, irregular configuration of bile ducts, lymphadenopathy, portal hypertension, and complications of cirrhosis. Moreover, CT and MRI can be used to monitor the disease progression after treatment of PBC (e.g. the onset of cirrhotic decompensation or HCC) to guide the clinical decisions for liver transplantation. With the optimization of imaging technology, magnetic resonance elastography (MRE) offers additional information on liver stiffness, allows for the identification of early cirrhosis in PBC and provides a basis for predicting prognosis. Gadoxetic acid-enhanced MRI enables the assessment of liver function in patients with PBC. The purpose of this review is to detail and illustrate the definition, pathological basis, and clinical importance of CT and MRI features of PBC to help radiologists and clinicians enhance their understanding of PBC.Critical Relevance StatementCharacteristic CT and MR imaging manifestations of primary biliary cholangitis may reflect the course of the disease and provide information associated with histological grading and altered cellular function.Key points center dot Imaging has become highly useful for differentiating PBC from other diseases.center dot Key pathological alterations of PBC can be captured by CT and MRI.center dot Characteristic manifestations provide information associated with histological grade and cellular function.center dot Despite this, the CT or MRI features of PBC are not specific.
C1 [Zhang, Yun; Zheng, Tianying; Huang, Zixing; Song, Bin] Sichuan Univ, West China Hosp, Dept Radiol, 37 Guoxue Alley, Chengdu 610041, Sichuan, Peoples R China.
[Huang, Zixing] Sichuan Univ, West China Tianfu Hosp, Dept Radiol, Chengdu, Peoples R China.
[Song, Bin] Sanya Peoples Hosp, Dept Radiol, Sanya, Hainan, Peoples R China.
C3 Sichuan University; Sichuan University
RP Song, B (corresponding author), Sichuan Univ, West China Hosp, Dept Radiol, 37 Guoxue Alley, Chengdu 610041, Sichuan, Peoples R China.; Song, B (corresponding author), Sanya Peoples Hosp, Dept Radiol, Sanya, Hainan, Peoples R China.
EM songlab_radiology@163.com
RI Sun, Bin/HMD-1646-2023
OI Zhang, Yun/0000-0001-9621-1408
FU Science and Technology Support Program of Sichuan Province
[2023NSFSC1617]
FX This work was funded by the Science and Technology Support Program of
Sichuan Province (No. 2023NSFSC1617).
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NR 84
TC 2
Z9 2
U1 2
U2 6
PU SPRINGER WIEN
PI Vienna
PA Prinz-Eugen-Strasse 8-10, A-1040 Vienna, AUSTRIA
SN 1869-4101
J9 INSIGHTS IMAGING
JI Insights Imaging
PD OCT 26
PY 2023
VL 14
IS 1
AR 180
DI 10.1186/s13244-023-01517-3
PG 18
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA W0UK3
UT WOS:001088865200002
PM 37880457
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Che, WI
Baecklund, F
Hellgren, K
Kuja-Halkola, R
Lundberg, IE
Westerlind, H
Holmqvist, M
AF Che, Weng Ian
Baecklund, Fredrik
Hellgren, Karin
Kuja-Halkola, Ralf
Lundberg, Ingrid E.
Westerlind, Helga
Holmqvist, Marie
TI Familial Co-Aggregation of Idiopathic Inflammatory Myopathies and
Cancer: A Swedish Population-Based Study
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; SUSCEPTIBILITY LOCI; RISK-FACTORS; IDENTIFIES
2; NATIONWIDE; DERMATOMYOSITIS; POLYMYOSITIS; AUTOIMMUNE; MYOSITIS;
PREVALENCE
AB Objective. To examine if idiopathic inflammatory myopathies (IIMs) share familial susceptibility with cancer, we estimated the familial co-aggregation of these diseases.Methods. This Swedish population-based family study with data from national registers included 8,460 first-degree relatives of patients with IIM and 41,127 relatives of matched individuals without IIM. We modeled the adjusted odds ratios (ORs) of familial co-aggregation of IIM and cancer using conditional logistic regressions and adjusted for sex and birth year of index individuals and their first-degree relatives. We examined the associations for cancer overall and stratified by several factors of interest. We also performed exploratory analyses for specific cancer types.Results. We observed no statistically significant familial associations between IIM and cancer overall. However, there was a familial association in male relative pairs of patients with dermatomyositis (adjusted OR for familial association 1.39 [95% confidence interval (95% CI) 1.15-1.68]). The association remained statistically significant after controlling for multiple testing. Moreover, this finding was consistent between kinships. Familial co-aggregation of IIM and cancer diagnosed before 50 years of age was only observed in offspring. In exploratory analyses, only the familial associations for myeloid malignancies (adjusted OR 2.27 [95% CI 1.43-3.60]) and liver cancer (adjusted OR 2.01 [95% CI 1.21-3.33]) in male relative pairs remained significant after controlling for multiple testing.Conclusion. We found little evidence of shared familial susceptibility as a major pathologic mechanism contributing to the co-occurrence of IIM and cancer overall. There could be subsets of patients and cancer types for which familial factors including genetics and shared environments are of more importance, but these findings need replication.
C1 [Che, Weng Ian; Westerlind, Helga] Karolinska Inst, Dept Med Solna, Clin Epidemiol Div, Stockholm, Sweden.
[Baecklund, Fredrik] Karolinska Inst, Karolinska Univ Hosp, Pediat Oncol Unit, Stockholm, Sweden.
[Baecklund, Fredrik] Karolinska Inst, Dept Womens & Childrens Hlth, Childhood Canc Res Unit, Stockholm, Sweden.
[Hellgren, Karin; Holmqvist, Marie] Karolinska Inst, Clin Epidemiol Div, Stockholm, Sweden.
[Hellgren, Karin; Lundberg, Ingrid E.; Holmqvist, Marie] Karolinska Inst, Div Rheumatol, Dept Med Solna, Stockholm, Sweden.
[Kuja-Halkola, Ralf] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Lundberg, Ingrid E.] Karolinska Univ Hosp, ME Gastro Derm & Rheuma Theme Inflammat & Aging, Stockholm, Sweden.
C3 Karolinska Institutet; Karolinska Institutet; Karolinska University
Hospital; Karolinska Institutet; Karolinska Institutet; Karolinska
Institutet; Karolinska Institutet; Karolinska Institutet; Karolinska
University Hospital
RP Che, WI (corresponding author), Karolinska Inst, Dept Med Solna, Clin Epidemiol Div, Stockholm, Sweden.
EM weng.ian.che@ki.se
RI Westerlind, Helga/T-6191-2018; Hellgren, karin/KFB-8213-2024; Che, Weng
Ian/ABM-5982-2022; Kuja-Halkola, Ralf/ABA-5061-2020; Holmqvist,
Marie/D-4508-2017
OI Lundberg, Ingrid/0000-0002-6068-9212; Kuja-Halkola,
Ralf/0000-0002-3765-2067; Che, Weng Ian/0000-0002-8355-2024; Holmqvist,
Marie/0000-0001-8996-5260; Westerlind, Helga/0000-0003-3380-5342
FU Swedish Research Council
FX Supported by the Swedish Research Council.
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NR 48
TC 0
Z9 0
U1 2
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2326-5191
EI 2326-5205
J9 ARTHRITIS RHEUMATOL
JI Arthritis Rheumatol.
PD AUG
PY 2023
VL 75
IS 8
BP 1445
EP 1455
DI 10.1002/art.42493
EA MAY 2023
PG 11
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA Q0LL3
UT WOS:000984593100001
PM 36908049
OA hybrid
DA 2025-01-07
ER
PT J
AU Mason, AL
Zhang, G
AF Mason, A. L.
Zhang, G.
TI Linking human beta retrovirus infection with primary biliary cirrhosis
SO GASTROENTEROLOGIE CLINIQUE ET BIOLOGIQUE
LA English
DT Review
ID MAMMARY-TUMOR VIRUS; ENV GENE-SEQUENCES; NOD.C3C4 MOUSE MODEL;
BREAST-CANCER; EXPRESSION; CELLS; LIVER; TRIAL; IDENTIFICATION;
ANTIBODIES
AB Several environmental agents have been linked with primary biliary cirrhosis (PBC) that include bacteria, xenobiotics and viruses. A human beta retrovirus (HBRV) related to mouse mammary tumor virus has been cloned and characterized from patients with PBC. This agent can be detected in the majority of patients' perihepatic lymph nodes by immunochemistry and RT-PCR. The HBRV has recently been isolated in culture and integration sites have been identified in the genome of patients to provide convincing evidence of beta retrovirus infection in patients. Three lines of evidence support a role for the virus in PBC. First, the beta retrovirus is linked with aberrant expression of mitochondrial protein(s) on the biliary epithelium cell (BEC) surface, a disease specific phenotype. Second, the related agent, mouse mammary tumor virus has been linked with autoimmune biliary disease in the NOD.c3c4 mouse model for PBC. In this mouse model, the virus is localized to diseased biliary epithelium that also display aberrant expression of the mitochondrial autoantigens. In translational studies, both patients with PBC and NOD.c3c4 mice demonstrate significant improvement in biliary disease with combination antiviral therapy. An overview of the biological relevance of the beta retrovirus infection in PBC will be discussed in this review. (c) 2010 Elsevier Masson SAS. All rights reserved.
C1 [Mason, A. L.; Zhang, G.] Univ Alberta, Div Gastroenterol, KGR, Edmonton, AB T6G 2E1, Canada.
C3 University of Alberta
RP Mason, AL (corresponding author), Univ Alberta, Div Gastroenterol, KGR, 7-142J, Edmonton, AB T6G 2E1, Canada.
EM andrew.mason@ualberta.ca
RI Mason, Andrew/D-2938-2013
OI Mason, Andrew/0000-0002-0470-9522
FU Alberta Heritage Foundation for Medical Research; Canadian Association
of Gastroenterology; Canadian Institutes for Health Research; Canadian
Liver Foundation; GlaxoSmithKline; Axcan Pharma
FX The research was supported by Alberta Heritage Foundation for Medical
Research, Canadian Association of Gastroenterology, Canadian Institutes
for Health Research and the Canadian Liver Foundation. The clinical
trials were supported by GlaxoSmithKline and Axcan Pharma. Andrew Mason
was principal investigator on the antiviral clinical trials that were
supported by GlaxoSmithKline and Axcan Pharma. The authors express their
gratitude to Gina Mason for assistance with manuscript review and
preparation.
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Z9 20
U1 0
U2 6
PU MASSON EDITEUR
PI MOULINEAUX CEDEX 9
PA 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE
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J9 GASTROEN CLIN BIOL
JI Gastroenterol. Clin. Biol.
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IS 6-7
BP 359
EP 366
DI 10.1016/j.gcb.2010.04.014
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 636OU
UT WOS:000280748300006
PM 20580176
DA 2025-01-07
ER
PT J
AU Kosar, M
Mach, L
Carreira, EM
Nazaré, M
Pacher, P
Grether, U
AF Kosar, Miroslav
Mach, Leonard
Carreira, Erick M.
Nazare, Marc
Pacher, Pal
Grether, Uwe
TI Patent review of cannabinoid receptor type 2 (CB2R)
modulators (2016-present)
SO EXPERT OPINION ON THERAPEUTIC PATENTS
LA English
DT Review
DE Agonist; antagonist; cannabinoid receptor type 2; fibrosis; G
protein-coupled receptor; inflammation
ID ACETYL-11-KETO-BETA-BOSWELLIC ACID AKBA; BOSWELLIC ACIDS; ANTIMICROBIAL
ACTIVITY; CANCER CELLS; IN-VITRO; APOPTOSIS; ANTITUMOR; PROLIFERATION;
EXTRACT; SERRATA
AB Introduction: Cannabinoid receptor type 2 (CB2R), predominantly expressed in immune tissues, is believed to play a crucial role within the body's protective mechanisms. Its modulation holds immense therapeutic promise for addressing a wide spectrum of dysbiotic conditions, including cardiovascular, gastrointestinal, liver, kidney, neurodegenerative, psychiatric, bone, skin, and autoimmune diseases, as well as lung disorders, cancer, and pain management. Areas covered: This review is an account of patents from 2016 up to 2023 which describes novel CB2R ligands, therapeutic applications, synthesis, as well as formulations of CB2R modulators. Expert opinion: The patents cover a vast, structurally diverse chemical space. The focus of CB2R ligand development has shifted from unselective dual-cannabinoid receptor type 1 (CB1R) and 2 agonists toward agonists with high selectivity over CB1R, particularly for indications associated with inflammation and tissue injury. Currently, there are at least eight CB2R agonists and one antagonist in active clinical development. A better understanding of the endocannabinoid system (ECS) and in particular of CB2R pharmacology is required to unlock the receptor's full therapeutic potential.
C1 [Kosar, Miroslav; Carreira, Erick M.] Eidgenoss TH Zurich, Lab Organ Chem, Zurich, Switzerland.
[Mach, Leonard; Nazare, Marc] Leibniz Forschungsinst Mol Pharmakol FMP Berlin, Med Chem, Berlin, Germany.
[Pacher, Pal] Natl Inst Alcohol Abuse & Alcoholism, NIH, Rockville, MD USA.
[Grether, Uwe] F Hoffmann La Roche Ltd, Roche Innovat Ctr Basel, Roche Pharm Res & Early Dev, Basel, Switzerland.
C3 National Institutes of Health (NIH) - USA; NIH National Institute on
Alcohol Abuse & Alcoholism (NIAAA); Roche Holding
RP Grether, U (corresponding author), F Hoffmann La Roche Ltd, Roche Innovat Ctr Basel, Pharm Res & Early Dev pRED, Grenzacherstr 124, CH-4070 Basel, Switzerland.
EM uwe.grether@roche.com
RI Nazare, Marc/X-4996-2018; Grether, Uwe/LKL-8415-2024
OI Kosar, Miroslav/0000-0003-0166-7571
FU Swiss Chemical Industry; Intramural program of the NIH/NIAAA
FX This paper was funded by a fellowship by the scholarship fund of the
Swiss Chemical Industry to M. Kosar and the intramural program of the
NIH/NIAAA to P. Pacher.
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NR 287
TC 1
Z9 1
U1 6
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3776
EI 1744-7674
J9 EXPERT OPIN THER PAT
JI Expert Opin. Ther. Patents
PD AUG 2
PY 2024
VL 34
IS 8
BP 665
EP 700
DI 10.1080/13543776.2024.2368745
EA JUL 2024
PG 36
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA YN1O0
UT WOS:001261040100001
PM 38886185
DA 2025-01-07
ER
PT J
AU Li, ZH
Wang, X
Lin, Y
Wang, YJ
Wu, SW
Xia, KJ
Xu, C
Ma, HK
Zheng, JY
Luo, LS
Zhu, F
He, SD
Zhang, XH
AF Li, Zhanhui
Wang, Xu
Lin, Yu
Wang, Yujie
Wu, Shuwei
Xia, Kaijiang
Xu, Chen
Ma, Haikuo
Zheng, Jiyue
Luo, Lusong
Zhu, Fang
He, Sudan
Zhang, Xiaohu
TI Design, synthesis, and evaluation of pyrrolidine based CXCR4 antagonists
with in vivo anti-tumor metastatic activity
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Antagonist; Chemokine; CXCL12; CXCR4; GPCR
ID CHEMOKINE RECEPTOR; DISCOVERY; INHIBITORS; MICROENVIRONMENT;
DERIVATIVES; NICOTINE; AMD3100; AMD070; ENTRY
AB The chemokine receptor CXCR4 has been proposed as a drug target based on its important functions in HIV infection, inflammation/autoimmune diseases and cancer metastasis. Herein we report the design, synthesis and evaluation of novel CXCR4 antagonists based on a pyrrolidine scaffold. The structural exploration/optimization identified numerous potent CXCR4 antagonists, represented by compound 46, which displayed potent binding affinity to CXCR4 receptor (IC50 = 79 nM competitively displacing fluorescent 12G5 antibody) and inhibited CXCL12 induced cytosolic calcium flux (IC50 = 0.25 nM). Moreover, in a transwell invasion assay, compound 46 significantly mitigated CXCL12/CXCR4 mediated cell migration. Compound 46 exhibited good physicochemical properties (MW 367, logD(7.4) 1.12, pKa 8.2) and excellent in vitro safety profiles (e.g., hERG patch clamp IC50 > 30 mu M and minimal CYP isozyme inhibition). Importantly, 46 displayed much improved metabolic stability in human and rat liver microsomes. Lastly, 46 demonstrated marked efficacy in a cancer metastasis model in mice. These results strongly support 46 as a prototypical lead for the development of promising CXCR4 antagonists as clinical candidates. (C) 2020 Elsevier Masson SAS. All rights reserved.
C1 [Li, Zhanhui; Wang, Xu; Lin, Yu; Wang, Yujie; Wu, Shuwei; Xia, Kaijiang; Xu, Chen; Ma, Haikuo; Zheng, Jiyue; Zhang, Xiaohu] Soochow Univ, Jiangsu Key Lab Neuropsychiat Dis, Suzhou 215123, Jiangsu, Peoples R China.
[Li, Zhanhui; Wang, Xu; Lin, Yu; Wang, Yujie; Wu, Shuwei; Xia, Kaijiang; Xu, Chen; Ma, Haikuo; Zheng, Jiyue; Zhang, Xiaohu] Soochow Univ, Coll Pharmaceut Sci, Suzhou 215123, Jiangsu, Peoples R China.
[Luo, Lusong] BeiGene Beijing Co Ltd, 30 Sci Pk Rd,Zhongguancun Life Sci Pk, Beijing 102206, Peoples R China.
[Zhu, Fang; He, Sudan] Soochow Univ, Cyrus Tang Hematol Ctr, Jiangsu Inst Hematol, Suzhou 215123, Peoples R China.
[Zhu, Fang; He, Sudan] Soochow Univ, Collaborat Innovat Ctr Hematol, Suzhou 215123, Peoples R China.
[Zhu, Fang; He, Sudan] Chinese Acad Med Sci & Peking Union Medial Coll, Ctr Syst Med, Inst Basic Med Sci, Beijing, Peoples R China.
[Zhu, Fang; He, Sudan] Suzhou Inst Syst Med, Suzhou 215123, Jiangsu, Peoples R China.
C3 Soochow University - China; Soochow University - China; Soochow
University - China; Soochow University - China
RP Zhang, XH (corresponding author), Soochow Univ, Jiangsu Key Lab Neuropsychiat Dis, Suzhou 215123, Jiangsu, Peoples R China.; Zhang, XH (corresponding author), Soochow Univ, Coll Pharmaceut Sci, Suzhou 215123, Jiangsu, Peoples R China.; Luo, LS (corresponding author), BeiGene Beijing Co Ltd, 30 Sci Pk Rd,Zhongguancun Life Sci Pk, Beijing 102206, Peoples R China.; He, SD (corresponding author), Soochow Univ, Cyrus Tang Hematol Ctr, Jiangsu Inst Hematol, Suzhou 215123, Peoples R China.; He, SD (corresponding author), Soochow Univ, Collaborat Innovat Ctr Hematol, Suzhou 215123, Peoples R China.
EM lusong.luo@beigene.com; hesudan2018@163.com; xiaohuzhang@suda.edu.cn
OI Yu, Lin/0009-0004-4321-8015
FU National Natural Science Foundation of China [81973161, 81773561,
21502133]; Priority Academic Program Development of the Jiangsu Higher
Education Institutes (PAPD); Jiangsu Key Laboratory of Neuropsychiatric
Diseases [BM2013003]; CAMS Innovation Fund for Medical Sciences (CIFMS)
[2019-I2M-1e004, 2016-I2M1e005, 2019-I2M-1e003]
FX This work was supported by National Natural Science Foundation of China
(Grant No. 81973161, 81773561, 21502133), the Priority Academic Program
Development of the Jiangsu Higher Education Institutes (PAPD) and the
Jiangsu Key Laboratory of Neuropsychiatric Diseases (BM2013003). The
CAMS Innovation Fund for Medical Sciences (CIFMS; 2019-I2M-1e004,
2016-I2M1e005 and 2019-I2M-1e003).
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NR 40
TC 12
Z9 15
U1 2
U2 33
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD NOV 1
PY 2020
VL 205
AR 112537
DI 10.1016/j.ejmech.2020.112537
PG 18
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Pharmacology & Pharmacy
GA OC2JM
UT WOS:000578986400005
PM 32768738
DA 2025-01-07
ER
PT J
AU Semwal, R
Semwal, RB
Lehmann, J
Semwal, DK
AF Semwal, Ravindra
Semwal, Ruchi Badoni
Lehmann, Joerg
Semwal, Deepak Kumar
TI Recent advances in immunotoxicity and its impact on human health:
causative agents, effects and existing treatments
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE Immunotoxicity; Validation; Development; Testing model; Immune system;
Nanoparticles
ID BIFENTHRIN CAUSES IMMUNOTOXICITY; OXIDATIVE STRESS; RISK-ASSESSMENT;
NECROSIS-FACTOR; TOPICAL APPLICATION; IMMUNE FUNCTION; NANOPARTICLE;
VALIDATION; EXPOSURE; LIVER
AB Background: A strong immune system is a primary requirement to keep the body safe from different ailments and infections. A human knowingly or unknowingly often comes to the exposure of many foreign substances such as pollutants, chemicals, metals and drugs that affect the immune system. Though some of these substances are known to exert immunotoxicity, their precise role as immunotoxicant is still unidentified, hence, the testing of these substances has to be taken into account. The present manuscript aimed to explore the mechanism behind immunotoxicity, biomarkers involved, manifestations, testing of immunotoxicity and its management.
Methods: Relevant literature on immunotoxicity, collected from online scientific databases like Scopus, PubMed and Google Scholar, was rigorously reviewed.
Results: Earlier reports showed that immunotoxic effects of chemicals and pharmaceuticals may cause various health problems including allergic reactions, skin disorders, respiratory infections, gastrointestinal problems, and autoimmune disorders. If diagnosed in time, many of these conditions can be managed with the help of existing treatments although the complete treatment is sometimes a big challenge.
Conclusion: Based on the review of available literature, it can be concluded that immunotoxicity is one of the key factors responsible for several infectious diseases, autoimmune disorders and even cancers. Hence, the requirement of advanced diagnostic tools and established treatments for immunotoxicity is highly recommended.
C1 [Semwal, Ravindra] Uttarakhand Ayurved Univ, Fac Biomed Sci, Res & Dev Ctr, Dehra Dun 248001, Uttarakhand, India.
[Semwal, Ruchi Badoni] Govt Postgrad Coll, Dept Chem, Dehra Dun, Uttarakhand, India.
[Lehmann, Joerg] Fraunhofer Inst Cell Therapy & Immunol, Perlickstr 1, D-04103 Leipzig, Germany.
[Semwal, Deepak Kumar] Uttarakhand Ayurved Univ, Fac Biomed Sci, Dept Phytochem, Dehra Dun 248001, Uttarakhand, India.
C3 Fraunhofer Gesellschaft
RP Semwal, DK (corresponding author), Uttarakhand Ayurved Univ, Fac Biomed Sci, Dept Phytochem, Dehra Dun 248001, Uttarakhand, India.
EM dr_dks.1983@yahoo.co.in
RI Semwal, Deepak/K-4380-2016
OI Semwal, Deepak/0000-0003-3105-0759
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NR 120
TC 2
Z9 2
U1 4
U2 11
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD JUL
PY 2022
VL 108
AR 108859
DI 10.1016/j.intimp.2022.108859
PG 16
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA CN5M0
UT WOS:001125940800005
PM 35598397
DA 2025-01-07
ER
PT J
AU Lin, B
Liu, K
Wang, WT
Li, W
Dong, X
Chen, Y
Lu, Y
Guo, JL
Zhu, MY
Li, MS
AF Lin, Bo
Liu, Kun
Wang, Wenting
Li, Wei
Dong, Xu
Chen, Yi
Lu, Yan
Guo, Junli
Zhu, Mingyue
Li, Mengsen
TI Expression and bioactivity of human α-fetoprotein in a Bac-to-Bac system
SO BIOSCIENCE REPORTS
LA English
DT Article
ID PURIFICATION; BINDING; AGGLUTININ; MECHANISM; RECEPTOR
AB alpha-fetoprotein (AFP) is an early serum growth factor in foetal embryonic development and hepatic oncogenesis. A growing number of investigations of AFP as a tumour-specific biomarker have concluded that AFP is an important target for cancer treatment. AFP also plays an immunomodulatory role in the treatment of several autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, myasthenia gravis and thyroiditis. In an effort to support biochemical screening and drug design and discovery, we attempted to express and purify human AFP in a Bac-to-Bac system. Two key factors affecting the expression of recombinant human AFP (R-AFP), namely the infectious baculovirus inoculum volume and the culturing time post-infection, were optimized to maximize the yield. We achieved a high yield of approximately 1.5 mg/l of harvested medium with a 72-96 h incubation period after infection and an inoculum volume ratio of 1: 100. We also assessed the role of R-AFP in the proliferation of the human liver cancer cell line Bel 7402, and the results indicated that R-AFP promoted the growth of hepatoma cells. We concluded that this method can produce high yields of R-AFP, which can be used for studies related to AFP.
C1 [Lin, Bo; Liu, Kun; Wang, Wenting; Li, Wei; Dong, Xu; Chen, Yi; Lu, Yan; Guo, Junli; Zhu, Mingyue; Li, Mengsen] Hainan Med Coll, Hainan Prov Key Lab Carcinogenesis & Intervent, Haikou 571199, Hainan Province, Peoples R China.
[Lin, Bo; Liu, Kun; Li, Wei; Dong, Xu; Chen, Yi; Lu, Yan; Guo, Junli; Zhu, Mingyue; Li, Mengsen] Hainan Med Coll, Key Lab Mol Biol, Haikou 571199, Peoples R China.
[Li, Mengsen] Hainan Med Coll, Inst Tumor, Haikou 570102, Hainan Province, Peoples R China.
[Wang, Wenting] Hainan Med Coll, Affiliated Hosp 2, Dept Anesthesiol, Haikou 570311, Peoples R China.
C3 Hainan Medical University; Hainan Medical University; Hainan Medical
University; Hainan Medical University
RP Zhu, MY; Li, MS (corresponding author), Hainan Med Coll, Hainan Prov Key Lab Carcinogenesis & Intervent, Haikou 571199, Hainan Province, Peoples R China.; Zhu, MY; Li, MS (corresponding author), Hainan Med Coll, Key Lab Mol Biol, Haikou 571199, Peoples R China.; Li, MS (corresponding author), Hainan Med Coll, Inst Tumor, Haikou 570102, Hainan Province, Peoples R China.
EM mingyuezhu2002@163.com; mengsenli@163.com
RI Zhu, Mingyue/D-1338-2017; 林, 波/GWN-2449-2022; Liu, Kun/I-4874-2016
FU National Natural Science Foundation of China [81660463, 81560450,
31560243, 81360307, 81260306, 81160261]; Project of Hainan Province
Innovative Team [2016CXTD008]; Key Projects of Science and Technology,
Hainan Province [ZDXM 20110038]; New Century Excellent Talents in China
[NCET-10-0124]; Natural Science Foundation of Hainan Province [814293,
20168263]; Fund of Hainan Provincial Society Development [2015SF03];
Hainan Provincial Association for Science and Technology program of
Youth Science Talent and Academic Innovation [201514]; Hainan Provincial
Department of Education [HjKj 2013-21]
FX This work was supported by the National Natural Science Foundation of
China [grant numbers 81660463, 81560450, 31560243, 81360307, 81260306
and 81160261]; Project of Hainan Province Innovative Team [grant number
2016CXTD008]; Key Projects of Science and Technology, Hainan Province
[grant number ZDXM 20110038]; New Century Excellent Talents in China
[grant number NCET-10-0124]; Natural Science Foundation of Hainan
Province [grant numbers 814293 and 20168263]; Fund of Hainan Provincial
Society Development [grant number 2015SF03]; Hainan Provincial
Association for Science and Technology program of Youth Science Talent
and Academic Innovation [grant number 201514]; and Hainan Provincial
Department of Education [grant number HjKj 2013-21].
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Z9 9
U1 0
U2 16
PU PORTLAND PRESS LTD
PI LONDON
PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND
SN 0144-8463
EI 1573-4935
J9 BIOSCIENCE REP
JI Biosci. Rep.
PD FEB 28
PY 2017
VL 37
AR BSR20160161
DI 10.1042/BSR20160161
PN 1
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA EM1SA
UT WOS:000395096100001
PM 27913752
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Yuan, XD
Qin, JW
Zheng, H
Qi, C
Guo, YF
Zhu, ZB
Wu, W
Xu, ZJ
Li, XF
Wang, N
Chai, XQ
Xie, YH
Tao, XG
Liu, HH
Liu, WY
Liu, GY
Ye, L
Deng, KX
Li, Y
Ji, XB
Hou, CL
Yao, ZQ
Huang, Q
Song, RP
Zhang, SG
Wang, JZ
Liu, LX
Nashan, B
AF Yuan, Xiaodong
Qin, Jiwei
Zheng, Hao
Qi, Can
Guo, Yafei
Zhu, Zebin
Wu, Wei
Xu, Zhijun
Li, Xuefeng
Wang, Ning
Chai, Xiaoqing
Xie, Yanhu
Tao, Xiaogen
Liu, Haihua
Liu, Weiyong
Liu, Guoyan
Ye, Lei
Deng, Kexue
Li, Yi
Ji, Xuebing
Hou, Changlong
Yao, Zhiqin
Huang, Qiang
Song, Ruipeng
Zhang, Shugeng
Wang, Jizhou
Liu, Lianxin
Nashan, Bjoern
TI Enhanced recovery after liver transplantation-a prospective analysis
focusing on quality assessment
SO HEPATOBILIARY SURGERY AND NUTRITION
LA English
DT Article; Early Access
DE Enhanced Recovery After Surgery (ERAS); liver transplantation (LTx);
quality management; IQTIG benchmarks
ID INVASIVE FUNGAL-INFECTIONS; INTENSIVE-CARE-UNIT; PERIOPERATIVE CARE;
FAST-TRACKING; RISK-FACTORS; SURGERY; GUIDELINES; ANESTHESIA;
EXTUBATION; EVOLUTION
AB Background: Enhanced Recovery After Surgery (ERAS) is a multimodal approach for almost all types of surgical procedures, including liver transplantation (LTx). We developed an ERAS protocol for LTx based on previous experience and assessed it using benchmarks from the German Institute for Quality Management and Transparency in Healthcare (IQTIG). Methods: An ERAS protocol was developed and implemented in our center since 2018 for LTx, including preoperative, intraoperative, and postoperative procedures. From January 2021 to December 31st 2022, we conducted a prospective analysis including donor and recipient demographics, Model for End-Stage Liver Disease (MELD) score and medical history. Perioperative management, such as operative time, anhepatic phase time, intensive care unit (ICU) stay, morbidity and mortality as well as postoperative hospitalization, readmission and 1-year patient survival, were collected as outcome measures. Results: Sixty-eight consecutive liver transplant recipients were included. Mean age of the donors was 47 (36-55.5) years old, type of donation was in 41 donation after brain death (DBD), 26 donation after controlled circulatory death (DCD) and 1 donation after brain and cardiac death (DBCD). Mean age of the patients was 49.6 years (range, 26-68 years), 81% were male. The mean body mass index (BMI) of the recipients was 24 kg/m(2) (range, 15-37 kg/m(2)), mean MELD score was 15 (range, 6-39), 3 patients had a MELD score higher than 30. Fifty-three patients suffered from hepatitis B virus (HBV) related cirrhosis. Twenty-eight patients had hepatocellular carcinoma (HCC); 5 patients were diagnosed with alcohol related cirrhosis and primary biliary cirrhosis, autoimmune disease and drug induced cirrhosis, undefined cirrhosis, respectively. The mean operation time in our cohort was 6.73 hours, and the average anhepatic phase time was 68 minutes. No patient had intraoperative hypothermia. Tracheal extubation was performed in the ICU department within 6 hours post operation and the average ICU/intermediate care (IMC) unit stay was 4.5 days (range, 2-14 days). None of the patients required re-intubation. Postoperative complications with a CDC classification > II were seen in 16 patients (23.5%). Mean hospital stay was 21.7 days and readmission rate was 13 (19%). Neither acute rejection nor postoperative mortality during the hospital stay was recorded. One patient died from acute myocardial infarction after discharge. Conclusions: We developed an ERAS protocol in LTx, consisting of preoperative, perioperative and postoperative management and assessed the quality using benchmarks from IQTIG. Our study revealed that the proposed ERAS approach in LTx is feasible offering the opportunities of enhanced recovery and quality management.
C1 [Yuan, Xiaodong; Qin, Jiwei; Zheng, Hao; Qi, Can; Guo, Yafei; Zhu, Zebin; Wu, Wei; Xu, Zhijun; Li, Xuefeng; Wang, Ning; Nashan, Bjoern] Univ Sci & Technol China, Affiliated Hosp USTC 1, Transplantat Ctr, Div Life Sci & Med, Tianehu 1, Hefei 230071, Peoples R China.
[Chai, Xiaoqing; Xie, Yanhu] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Anesthesia, Div Life Sci & Med, Hefei, Peoples R China.
[Tao, Xiaogen; Liu, Haihua] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Intens Care Unit, Div Life Sci & Med, Hefei, Peoples R China.
[Liu, Weiyong; Liu, Guoyan; Ye, Lei] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Ultrasound Med, Div Life Sci & Med, Hefei, Peoples R China.
[Deng, Kexue] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Radiol, Div Life Sci & Med, Hefei, Peoples R China.
[Li, Yi] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Infect Dis, Div Life Sci & Med, Hefei, Peoples R China.
[Ji, Xuebing; Hou, Changlong] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Intervent, Div Life Sci & Med, Hefei, Peoples R China.
[Yao, Zhiqin] Univ Sci & Technol China, Affiliated Hosp USTC 1, Organ Procurement Org, Div Life Sci & Med, Hefei, Peoples R China.
[Huang, Qiang] Univ Sci & Technol China, Affiliated Hosp USTC 1, Div Life Sci & Med, Dept Gen Surg,Anhui Prov Key Lab Hepatopancreatobi, Hefei, Peoples R China.
[Song, Ruipeng; Zhang, Shugeng; Wang, Jizhou; Liu, Lianxin] Univ Sci & Technol China, Affiliated Hosp USTC 1, Div Life Sci & Med, Dept Hepatobiliary Surg,Anhui Prov Key Lab Hepatop, Hefei, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
China, CAS; Chinese Academy of Sciences; University of Science &
Technology of China, CAS; Chinese Academy of Sciences; University of
Science & Technology of China, CAS; Chinese Academy of Sciences;
University of Science & Technology of China, CAS; Chinese Academy of
Sciences; University of Science & Technology of China, CAS; Chinese
Academy of Sciences; University of Science & Technology of China, CAS;
Chinese Academy of Sciences; University of Science & Technology of
China, CAS; Chinese Academy of Sciences; University of Science &
Technology of China, CAS; Chinese Academy of Sciences; University of
Science & Technology of China, CAS; Chinese Academy of Sciences;
University of Science & Technology of China, CAS
RP Nashan, B (corresponding author), Univ Sci & Technol China, Affiliated Hosp USTC 1, Transplantat Ctr, Div Life Sci & Med, Tianehu 1, Hefei 230071, Peoples R China.
EM bjoern.nashan@gmail.com
RI Guo, Yafei/AAK-1635-2021; 刘, 国彦/KPA-5019-2024
FU Anhui Provincial Natural Science Foundation [2108085MH256]; Fundamental
Research Funds for the Central Universities [WK9110000055, WK9110000131]
FX Funding: This work was supported by the Anhui Provincial Natural Science
Foundation (No. 2108085MH256 to X.Y.) and the Fundamental Research Funds
for the Central Universities (No. WK9110000055 to B.N., No. WK9110000131
to X.Y.) .
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NR 65
TC 0
Z9 0
U1 2
U2 2
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2304-3881
EI 2304-389X
J9 HEPATOBIL SURG NUTR
JI Hepatobil. Surg. Nutr.
PD 2024 SEP 23
PY 2024
DI 10.21037/hbsn-24-349
EA SEP 2024
PG 21
WC Gastroenterology & Hepatology; Nutrition & Dietetics; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Nutrition & Dietetics; Surgery
GA G9E3V
UT WOS:001319583100001
OA gold
DA 2025-01-07
ER
PT J
AU Thuluvath, AJ
Chen, PH
Thuluvath, PJ
Kantsevoy, S
Savva, Y
AF Thuluvath, Avesh J.
Chen, Po-Hung
Thuluvath, Paul J.
Kantsevoy, Sergey
Savva, Yulia
TI Poor Survival After Retransplantation in NASH Cirrhosis
SO TRANSPLANTATION
LA English
DT Article
ID LIVER-TRANSPLANTATION; NONALCOHOLIC STEATOHEPATITIS; HEPATITIS-C;
PERFORMANCE STATUS; OUTCOMES; MORTALITY; IMPACT; DONOR
AB Background. Nonalcoholic steatohepatitis (NASH) cirrhosis is a common indication for liver transplantation (LT) in the United States. There is a paucity of data on retransplantation (re-LT) in those who were initially transplanted for NASH. Methods. We queried the United Network for Organ Sharing data sets from 2002 to 2016 to analyze the outcomes of adults with NASH (n = 128) and compared them with groups that received re-LT for cryptogenic cirrhosis (n = 189), alcoholic cirrhosis (n = 300) or autoimmune hepatitis cirrhosis (n = 118) after excluding multiple-organ re-LT and individuals with hepatocellular carcinoma. We estimated survival probabilities using a Kaplan-Meier estimator, and a relative risk of patient and graft mortality using proportional hazards regression. Results. The NASH group was older and had a higher prevalence of obesity, type II diabetes mellitus, renal insufficiency, portal vein thrombosis, and poor performance status. The median interval between the first and the second LT was shorter in the NASH group (27 days). The graft and patient 5-year survival rates were lower for the NASH group after re-LT compared with the other 3 groups. After adjusting for demographic and disease complication factors, the factors that increased a risk of patient or graft failure were a poor performance status (hazard ratio [HR], 1.64; 1.19-2.26), Donor Risk Index (HR, 1.51; 1.08-2.12), and a high Model for End-stage Liver Disease score (HR, 1.02; 1.00-1.04). Conclusions. Despite the comparable outcomes reported for initial LTamong the various etiologies, the outcome of re-LT is significantly worse for NASH cirrhosis.
C1 [Thuluvath, Avesh J.; Chen, Po-Hung] Johns Hopkins Univ, Sch Med, Dept Med, 4940 Eastem Ave, Baltimore, MD 21224 USA.
[Thuluvath, Paul J.; Kantsevoy, Sergey; Savva, Yulia] Mercy Med Ctr, Inst Digest Hlth & Liver Dis, Baltimore, MD USA.
[Thuluvath, Paul J.; Kantsevoy, Sergey] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
C3 Johns Hopkins University; Mercy Medical Center - Maryland; University
System of Maryland; University of Maryland Baltimore
RP Thuluvath, AJ (corresponding author), Johns Hopkins Univ, Sch Med, Dept Med, 4940 Eastem Ave, Baltimore, MD 21224 USA.
EM athuluv1@jhmi.edu
RI Chen, Po-Hung/ABD-1749-2020
FU NCATS NIH HHS [KL2 TR001077] Funding Source: Medline
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NR 22
TC 10
Z9 11
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD JAN
PY 2019
VL 103
IS 1
BP 101
EP 108
DI 10.1097/TP.0000000000002135
PG 8
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA HG5UH
UT WOS:000455044100026
PM 29470354
OA Bronze
DA 2025-01-07
ER
PT J
AU Lin, L
Piao, MY
Jiang, XH
Lv, HN
Zhao, NN
Yang, F
Sun, C
AF Lin, Lin
Piao, Meiyu
Jiang, Xihui
Lv, Houning
Zhao, Ningning
Yang, Fang
Sun, Chao
TI Does neutrophil-to-lymphocyte ratio predict 1-year mortality in patients
with primary biliary cholangitis? Results from a retrospective study
with validation cohort
SO BMJ OPEN
LA English
DT Article
ID AUTOIMMUNE LIVER-DISEASES; ACUTE-PANCREATITIS; CIRRHOSIS; CANCER;
MARKER; MODEL
AB Objectives Neutrophil-to-lymphocyte ratio (NLR) has been used to predict prognosis in various liver diseases, but its role in primary biliary cholangitis (PBC) is not clarified. We aimed to investigate the prognostic usefulness of NLR for 1-year mortality in PBC.
Methods The study recruited a retrospective cohort with 88 patients with PBC and a prospective validation cohort with 63 participants who were followed-up for 1 year. NLR and other laboratory measurements were analysed by multivariate regression model for identifying independent factors for early mortality. The cut-off threshold of NLR was determined by calculating the area under the receiver operating characteristics curve (AUROC) and used in a subsequent Kaplan-Meier survival analysis.
Results Univariate and multivariate analyses showed that Mayo Risk Score (MRS), serum creatinine and NLR were independent indicators for mortality. NLR yielded significantly higher AUROC (0.86) than those of platelet-to-lymphocyte ratio (0.58, p=0.03), but comparable with MRS (0.87, p=0.88). Spearman's correlation analysis represented a positive correlation between escalating NLR and aggravating Child-Pugh grade (r=0.44, p<0.001). Patients with NLR <2.18 exhibited higher survival (with 100% sensitivity and 67.1% specificity) within 1 year follow-up duration, and NLR >= 2.18 was indicative of higher mortality (log-rank test, p<0.001). In addition, these results were internally confirmed by a validation cohort.
Conclusion NLR is closely related to short-term mortality in patients with PBC.
C1 [Lin, Lin; Piao, Meiyu; Jiang, Xihui; Lv, Houning; Zhao, Ningning; Yang, Fang; Sun, Chao] Tianjin Med Univ, Gen Hosp, Dept Gastroenterol & Hepatol, Tianjin, Peoples R China.
[Lin, Lin; Piao, Meiyu; Jiang, Xihui; Lv, Houning; Zhao, Ningning; Yang, Fang; Sun, Chao] Tianjin Med Univ, Gen Hosp, Tianjin Inst Digest Dis, Tianjin, Peoples R China.
C3 Tianjin Medical University; Tianjin Medical University
RP Sun, C (corresponding author), Tianjin Med Univ, Gen Hosp, Dept Gastroenterol & Hepatol, Tianjin, Peoples R China.; Sun, C (corresponding author), Tianjin Med Univ, Gen Hosp, Tianjin Inst Digest Dis, Tianjin, Peoples R China.
EM chaosun@tmu.edu.cn
RI Sun, Chao/AAL-4920-2021; zhao, ningning/A-8721-2013
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Zimmermann HW, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0021381
NR 33
TC 12
Z9 14
U1 0
U2 6
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 2044-6055
J9 BMJ OPEN
JI BMJ Open
PD JUL
PY 2017
VL 7
IS 7
AR e015304
DI 10.1136/bmjopen-2016-015304
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA FG4HQ
UT WOS:000410203700084
PM 28706093
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Li, SD
Zhao, CL
Zhang, GZ
Xu, QF
Liu, Q
Zhao, W
Chou, CJ
Zhang, YJ
AF Li, Shunda
Zhao, Chunlong
Zhang, Guozhen
Xu, Qifu
Liu, Qian
Zhao, Wei
Chou, C. James
Zhang, Yingjie
TI Development of selective HDAC6 inhibitors with in vitro and in vivo
anti-multiple myeloma activity
SO BIOORGANIC CHEMISTRY
LA English
DT Article
DE Histone deacetylase 6; Selective inhibitor; Multiple myeloma;
Anticancer; Pyrrolo[2; 3-d]pyrimidine
ID DEACETYLASE; DISCOVERY; DESIGN; PROTEASOME; POTENT
AB Histone deacetylase 6 (HDAC6) is a promising therapeutic target for the treatment of cancers, neurodegenerative diseases and autoimmune disorders. Herein a novel series of pyrrolo[2,3-d]pyrimidine-based HDAC inhibitors were designed, synthesized and biologically evaluated, among which compounds 7a, 12a1, and 16a1 exhibited potent inhibitory activities and selectivities against HDAC6. Notably, compared with the well-known HDAC6 inhibitor Tubastatin A, our pyrrolo[2,3-d]pyrimidine-based HDAC6 inhibitors showed superior in vitro antiproliferative activity against human multiple myeloma cell lines RPMI 8226, U266 and MM.1S, while maintaining the low cytotoxicity against human breast cancer cell line MDA-MB-231 and two normal cell lines. The HDAC6 selective inhibition of one representative compound 12a1 in RPMI 8226 cells was confirmed by western blot analysis. Although pyrrolo[2,3-d]pyrimidine is a privileged structure in many kinase inhibitors, compound 12a1 showed negligible inhibition against several kinases including JAK family members and Akt1, indicating its acceptable off-target profile. Besides, compound 12a1 exhibited desirable metabolic stability in mouse liver microsome. The in vivo anti-multiple myeloma potency of 12a1, alone and in combination with bortezomib, was demonstrated in a RPMI 8226 xenograft model.
C1 [Li, Shunda; Zhao, Chunlong; Zhang, Guozhen; Xu, Qifu; Liu, Qian; Zhao, Wei; Zhang, Yingjie] Shandong Univ, Cheeloo Coll Med, Sch Pharmaceut Sci, Dept Med Chem,Key Lab Chem Biol,Minist Educ, 44 West Wenhua Rd, Jinan 250012, Shandong, Peoples R China.
[Chou, C. James] Med Univ South Carolina, South Carolina Coll Pharm, Dept Drug Discovery & Biomed Sci, Charleston, SC 29425 USA.
C3 Shandong University; Medical University of South Carolina
RP Zhang, YJ (corresponding author), Shandong Univ, Cheeloo Coll Med, Sch Pharmaceut Sci, Dept Med Chem,Key Lab Chem Biol,Minist Educ, 44 West Wenhua Rd, Jinan 250012, Shandong, Peoples R China.
EM zhangyingjie@sdu.edu.cn
RI Liu, Qian/GZG-3496-2022; Xu, Qifu/HGU-6669-2022; ZHAO, WEI/C-9163-2011;
Zhang, Yingjie/V-6712-2019
OI Zhang, Yingjie/0000-0001-6118-6695; Zhao, Chunlong/0000-0001-7920-8231
FU Natural Science Foundation of Shandong Province [ZR2018QH007]; Key
Research and Development Program of Shandong Province [2017CXGC1401];
Young Scholars Program of Shandong University (YSPSDU) [2016WLJH33]
FX This work was supported by Natural Science Foundation of Shandong
Province (Grant No. ZR2018QH007), Key Research and Development Program
of Shandong Province (2017CXGC1401), Young Scholars Program of Shandong
University (YSPSDU, 2016WLJH33).
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NR 27
TC 17
Z9 19
U1 2
U2 28
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0045-2068
EI 1090-2120
J9 BIOORG CHEM
JI Bioorganic Chem.
PD NOV
PY 2021
VL 116
AR 105278
DI 10.1016/j.bioorg.2021.105278
EA AUG 2021
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Biochemistry & Molecular Biology; Chemistry
GA UY7FG
UT WOS:000701684500002
PM 34474303
DA 2025-01-07
ER
PT J
AU Brandhorst, S
Levine, ME
Wei, M
Shelehchi, M
Morgan, TE
Nayak, KS
Dorff, T
Hong, KR
Crimmins, EM
Cohen, P
Longo, VD
AF Brandhorst, Sebastian
Levine, Morgan E.
Wei, Min
Shelehchi, Mahshid
Morgan, Todd E.
Nayak, Krishna S.
Dorff, Tanya
Hong, Kurt
Crimmins, Eileen M.
Cohen, Pinchas
Longo, Valter D.
TI Fasting-mimicking diet causes hepatic and blood markers changes
indicating reduced biological age and disease risk
SO NATURE COMMUNICATIONS
LA English
DT Article
ID NONALCOHOLIC FATTY LIVER; HEMATOPOIETIC STEM-CELLS;
MOLECULAR-MECHANISMS; METABOLIC SYNDROME; LIFE-SPAN; REGENERATION;
MORTALITY; HEALTH; CANCER; QUANTIFICATION
AB In mice, periodic cycles of a fasting mimicking diet (FMD) protect normal cells while killing damaged cells including cancer and autoimmune cells, reduce inflammation, promote multi-system regeneration, and extend longevity. Here, we performed secondary and exploratory analysis of blood samples from a randomized clinical trial (NCT02158897) and show that 3 FMD cycles in adult study participants are associated with reduced insulin resistance and other pre-diabetes markers, lower hepatic fat (as determined by magnetic resonance imaging) and increased lymphoid to myeloid ratio: an indicator of immune system age. Based on a validated measure of biological age predictive of morbidity and mortality, 3 FMD cycles were associated with a decrease of 2.5 years in median biological age, independent of weight loss. Nearly identical findings resulted from a second clinical study (NCT04150159). Together these results provide initial support for beneficial effects of the FMD on multiple cardiometabolic risk factors and biomarkers of biological age.
Fasting mimicking diets (FMDs) can promote healthy aging in animal models but effects on human healthspan remain elusive. Here the authors provide support for beneficial effects of the FMD on cardiometabolic risk factors and biological age biomarkers.
C1 [Brandhorst, Sebastian; Wei, Min; Shelehchi, Mahshid; Morgan, Todd E.; Crimmins, Eileen M.; Cohen, Pinchas; Longo, Valter D.] Univ Southern Calif, Leonard Davis Sch Gerontol, Los Angeles, CA 90089 USA.
[Levine, Morgan E.] Yale Sch Med, Dept Pathol, New Haven, CT 06519 USA.
[Nayak, Krishna S.] Univ Southern Calif, Viterbi Sch Engn, Ming Hsieh Dept Elect Engn, Los Angeles, CA 90089 USA.
[Dorff, Tanya] Univ Southern Calif, Norris Comprehens Canc Ctr, Keck Sch Med, Dept Pathol, Los Angeles, CA 90033 USA.
[Hong, Kurt] Keck Sch Med USC, Ctr Clin Nutr & Appl Hlth Res, Los Angeles, CA 90033 USA.
[Crimmins, Eileen M.] Univ Calif Los Angeles, Ctr Biodemog & Populat Hlth, Los Angeles, CA 90089 USA.
[Crimmins, Eileen M.] Univ Southern Calif, Los Angeles, CA 90089 USA.
[Longo, Valter D.] Italian Fdn Canc Res Inst Mol Oncol, AIRC Inst Mol Oncol, Milan 20139, Italy.
C3 University of Southern California; Yale University; University of
Southern California; University of Southern California; University of
California System; University of California Los Angeles; University of
Southern California; IFOM - FIRC Institute of Molecular Oncology
RP Longo, VD (corresponding author), Univ Southern Calif, Leonard Davis Sch Gerontol, Los Angeles, CA 90089 USA.; Longo, VD (corresponding author), Italian Fdn Canc Res Inst Mol Oncol, AIRC Inst Mol Oncol, Milan 20139, Italy.
EM vlongo@usc.edu
RI Longo, Valter D./JXM-3545-2024
OI Nayak, Krishna/0000-0001-5735-3550; Cohen, Pinchas/0000-0002-0035-8366
FU University of Southern California: Edna Jones Chair Fund; USC Edna Jones
chair fund [4R00AG052604-02, NIH/NIA 1R01AG060110-01]; NIH/NIA
[P30AG021342]; Yale PEPPER Center
FX We thank Dr. Annunziata "Nancy" Crupi for help with the study design and
for the initial processing of the data related to the clinical trial
NCT04150159. Funding was provided by the USC Edna Jones chair fund to
V.D.L., in addition to NIH/NIA 4R00AG052604-02 (Levine), NIH/NIA
1R01AG060110-01 (Levine & Crimmins), and the Yale PEPPER Center
P30AG021342 (Levine). The funding sources had no involvement in study
design; collection, analysis, and interpretation of data; writing of the
report; or decision to submit the article for publication.
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Z9 4
U1 6
U2 16
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
EI 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD FEB 20
PY 2024
VL 15
IS 1
AR 1309
DI 10.1038/s41467-024-45260-9
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA JW0G1
UT WOS:001176075200022
PM 38378685
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Correa, P
Piazuelo, MB
AF Correa, Pelayo
Piazuelo, M. Blanca
TI Evolutionary History of the Helicobacter pylori Genome:
Implications for Gastric Carcinogenesis
SO GUT AND LIVER
LA English
DT Review
DE Helicobacter pylori; Genome; Gastric carcinogenesis
ID VACUOLATING CYTOTOXIN; BIOLOGICAL-ACTIVITY; GENETIC DIVERSITY; CANCER
INCIDENCE; ETHNIC-GROUPS; CAGA; STRAINS; INFECTION; VIRULENCE; VACA
AB The genome of the bacterium Helicobacter pylori has evolved over the millennia since its migration out of Africa along with its human host approximately 60,000 years ago. Human migrations, after thousands of years of permanent settlement in those lands, resulted in seven prototypes of genetic populations of H. pylori with distinct geographical distributions. In all continents, present day isolates of H. pylori have molecular markers that reflect population migrations. The colonization of the Americas as well as the slave trade introduced European and African strains to the New World. The relationship between H. pylori genome and gastric cancer rates is linked to the presence of the cagA gene, but the knowledge on this subject is incomplete because other genes may be involved in certain populations. A new situation for Homo sapiens is the absence of H. pylori colonization in certain, mostly affluent, populations, apparently brought about by improved home sanitation and widespread use of antibiotics during the last decades. The disappearance of H. pylori from the human microbiota may be linked to emerging epidemics of esophageal adenocarcinoma, some allergic diseases such as asthma and some autoimmune disorders. (Gut Liver 2012;6:21-28)
C1 [Correa, Pelayo; Piazuelo, M. Blanca] Vanderbilt Univ, Med Ctr, Dept Med, Div Gastroenterol, Nashville, TN 37232 USA.
C3 Vanderbilt University
RP Correa, P (corresponding author), Vanderbilt Univ, Med Ctr, Dept Med, Div Gastroenterol, 2215 Garland Ave,1030 MRB 4, Nashville, TN 37232 USA.
EM pelayo.correa@vanderbilt.edu
FU U.S. National Cancer Institute [P01-CA28842]
FX This work was supported by the grant P01-CA28842 from the U.S. National
Cancer Institute.
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NR 71
TC 32
Z9 44
U1 0
U2 5
PU EDITORIAL OFFICE GUT & LIVER
PI SEOUL
PA 305 LOTTE GOLD ROSE II, 890-59, DAECHI 4-DONG, GANGNAM-GU, SEOUL,
135-839, SOUTH KOREA
SN 1976-2283
EI 2005-1212
J9 GUT LIVER
JI Gut Liver
PD JAN
PY 2012
VL 6
IS 1
BP 21
EP 28
DI 10.5009/gnl.2012.6.1.21
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 879XY
UT WOS:000299367400003
PM 22375167
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Krel, C
Piko, N
Tomazic, J
Bevc, S
AF Krel, Cvetka
Piko, Nejc
Tomazic, Jozica
Bevc, Sebastjan
TI Bioelectrical impedance analysis as a marker of nutritional status in
chronically ill patients
SO AUSTRALIAN JOURNAL OF ADVANCED NURSING
LA English
DT Article
DE nutritional risk; albumin; phase angle; chronic disease
ID PHASE-ANGLE; CANCER CACHEXIA; MALNUTRITION; DISEASE; RISK
AB Objective
The aim of the study was to evaluate different methods of nutritional status analysis like basic anthropometric data, laboratory data and bioelectrical impedance analysis (BIA) with phase angle (PA) in patients with chronic diseases.
Setting
Clinic for Internal Medicine, Department of Nephrology, University Clinical Centre Maribor, a tertiary referral centre in Slovenia, Europe.
Subjects
Patients with chronic disease and increased nutritional risk (>= 1 fulfilled NRS 2002 criterion) at the time of inclusion in the study.
Results
Patients had chronic kidney disease (93%), arterial hypertension (80%), active infection (33.3%), heart failure (23.3%), diabetes mellitus (20%), active malignancy (10%), autoimmune disease (6.6%), history of stroke (6.6%), chronic obstructive pulmonary disease (3.3%) and/or liver cirrhosis (3.3%). Mean serum albumin was 33.6 +/- 5.7 g/L, mean BMI 25.6 +/- 4.4 kg/m(2) and mean PA 4.4 +/- 1.2 degrees. No correlation between serum albumin and BMI was found. Lower PA was associated with lower serum albumin (p=0.045) and advanced age (p=0.043). The department nurses conducted nutritional education for all patients included in the study. Study was performed in accordance with the Strengthening the reporting of observational studies in epidemiology.
Conclusion
Results of the study show the importance of nutritional risk assessment in all chronically ill patients. BIA is a promising method of determining nutritional status. PA values have important diagnostic, therapeutic and prognostic implications as they are a marker of body cell mass, membrane function and metabolic health. A multifaceted approach to assess malnutrition in patients with chronic diseases is important, followed by a prompt nutritional intervention.
C1 [Krel, Cvetka; Piko, Nejc; Bevc, Sebastjan] Univ Med Ctr Maribor, Dept Nephrol, Clin Internal Med, Maribor, Slovenia.
[Tomazic, Jozica] Univ Med Ctr Maribor, Clin Internal Med, Maribor, Slovenia.
C3 University of Maribor; University of Maribor
RP Krel, C (corresponding author), Univ Med Ctr Maribor, Dept Nephrol, Clin Internal Med, Maribor, Slovenia.
EM cvetka.krel@gmail.com; Nejc.piko@gmail.com; jozefa.tomazic@ukc-mb.si;
sebastjan.bevc@gmail.com
RI Piko, Nejc/HOA-9880-2023
CR Abad S, 2011, NEFROLOGIA, V31, P670, DOI 10.3265/Nefrologia.pre2011.Sep.10999
Allard JP, 2016, CLIN NUTR, V35, P144, DOI 10.1016/j.clnu.2015.01.009
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NR 31
TC 1
Z9 1
U1 0
U2 2
PU AUSTRALIAN NURSING FEDERATION
PI KINGSTON
PA PO BOX 4239, KINGSTON, ACT 2604, AUSTRALIA
SN 0813-0531
EI 1447-4328
J9 AUST J ADV NURS
JI Aust. J. Adv. Nurs.
PD MAR-MAY
PY 2019
VL 36
IS 3
BP 14
EP 21
PG 8
WC Nursing
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Nursing
GA HP9VB
UT WOS:000462040000002
DA 2025-01-07
ER
PT J
AU Abdulkarim, M
Zenouzi, R
Sebode, M
Schulz, L
Quaas, A
Lohse, AW
Schramm, C
Weiler-Normann, C
AF Abdulkarim, Mosaab
Zenouzi, Roman
Sebode, Marcial
Schulz, Lisa
Quaas, Alexander
Lohse, Ansgar W.
Schramm, Christoph
Weiler-Normann, Christina
TI Sex differences in clinical presentation and prognosis in patients with
primary biliary cholangitis
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune liver disease; male; primary biliary cholangitis; prognosis;
sex differences
ID QUALITY-OF-LIFE; NATURAL-HISTORY; RISK-FACTORS; CIRRHOSIS; GENDER; MEN;
EPIDEMIOLOGY; PREVALENCE; DIAGNOSIS; FATIGUE
AB Objectives: Primary biliary cholangitis (PBC) is a chronic inflammatory disease of the small intrahepatic bile ducts disproportionally affecting women. Timely diagnosis and treatment can often prevent progression to liver cirrhosis. We hypothesized PBC diagnosis in male patients is delayed and prognosis impaired. We, therefore, conducted a case-control study and compared clinical and prognostic features among male and female patients with PBC. Materials and methods: 49 male patients with PBC treated at a German tertiary care center between 2006 and 2017 were identified and compared to 98 age-matched female controls. Prospectively collected clinical/biochemical data were analyzed retrospectively. Liver biopsies were scored in a blinded fashion. Prognostic parameters were calculated using established prognostic scores (GLOBE, PBC-UKE). Statistical analysis was performed using Mann-Whitney test and Fisher ' s exact test. Results: At PBC diagnosis, male patients reported significantly less PBC-associated symptoms as compared to female controls (34 versus 71%, p < .01). Compared to female patients, median time from onset of PBC-related symptoms and/or first reported elevated cholestatic biochemical parameters to PBC diagnosis was significantly increased in men (36 versus 12 months, p = .02). In addition, male patients underwent liver biopsy to establish PBC diagnosis more frequently, tended to show more advanced fibrosis and showed significantly poorer prognostic PBC score results. Hepatocellular carcinoma was only observed in male patients (n = 3). Conclusions: When compared to women, men with PBC suffer from less PBC-related symptoms, receive PBC diagnosis delayed and have a worse prognosis. Despite its rarity, the diagnosis of PBC should be considered in men with elevated cholestatic parameters.
C1 [Abdulkarim, Mosaab; Zenouzi, Roman; Sebode, Marcial; Schulz, Lisa; Lohse, Ansgar W.; Schramm, Christoph; Weiler-Normann, Christina] Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Martinistr 52, D-20246 Hamburg, Germany.
[Abdulkarim, Mosaab] Tripoli Univ, Al Khadra Teaching Hosp, Fac Med, Tripoli, Libya.
[Zenouzi, Roman; Sebode, Marcial; Schulz, Lisa; Lohse, Ansgar W.; Schramm, Christoph; Weiler-Normann, Christina] European Reference Network Hepatol Dis ERN RARE L, Hamburg, Germany.
[Quaas, Alexander] Univ Med Ctr Hamburg Eppendorf, Inst Pathol, Hamburg, Germany.
[Quaas, Alexander] Univ Med Ctr Cologne, Dept Pathol, Cologne, Germany.
[Schramm, Christoph; Weiler-Normann, Christina] Univ Med Ctr Hamburg Eppendorf, Martin Zeitz Ctr Rare Dis, Hamburg, Germany.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf;
University of Tripoli; University of Hamburg; University Medical Center
Hamburg-Eppendorf; University of Cologne; University of Hamburg;
University Medical Center Hamburg-Eppendorf
RP Weiler-Normann, C (corresponding author), Univ Med Ctr Hamburg Eppendorf, Dept Med 1, Martinistr 52, D-20246 Hamburg, Germany.
EM cweiler@uke.de
RI Schramm, Christoph/X-6915-2019
FU Deutsche Forschungsgemeinschaft [SFB 841, CRU306]; Hannelore and Helmut
Greve Foundation
FX R. Z., C. S., A. W. L., and C. W. N. are supported by the Deutsche
Forschungsgemeinschaft (SFB 841 and CRU306). C. S. is supported by the
Hannelore and Helmut Greve Foundation.
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NR 47
TC 8
Z9 8
U1 0
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD NOV 2
PY 2019
VL 54
IS 11
BP 1391
EP 1396
DI 10.1080/00365521.2019.1683226
EA NOV 2019
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA JQ2HF
UT WOS:000494716700001
PM 31692389
DA 2025-01-07
ER
PT J
AU Unal, A
Pinar, Y
Murat, Z
Murat, K
AF Unal, Aydin
Pinar, Yazici
Murat, Zeytunlu
Murat, Kilic
TI Management of hemorrhage of retro hepatic inferior vena cava injury
during piggy-back technique for liver transplantation
SO INDIAN JOURNAL OF SURGERY
LA English
DT Article
DE Retrohepatic inferior vena cava; Approach to vena cava injury; Surgical
technique; Digital compression
ID TOTAL VASCULAR EXCLUSION; RESECTION
AB Background Injury to large abdominal vessels is still one of the most terrifying results of trauma or intraoperative faults, as the management of the hemorrhage is hardly difficult due to being torrentially and unaware of the proper reparation. The controversial problem is which technique should be preferred in case of injury to RHIVC and how can it be managed with minimal risk.
Patients and Methods Over two-year period, we retrospectively analyzed the patients who had undergone adult-to-adult liver transplantation and collected data about the injuries to RHIVC during recipient hepatectomy. All patients were treated with the same surgical technique including digital compression and continuous suturing the tear.
Results Twenty five patients (21 male, 4 female) were detected. The causative factors for end stage liver disease included hepatitis B, hepatitis C with or without hepatocellular carcinoma, autoimmune hepatitis, alcoholic hepatitis, cryptogenic hepatitis, Wilson disease, and nonalcoholic steatohepatitis. Mean diameter of the injury was measured 0.5 cm (range: 0.2-1.6). Only three patients (12%) had more than one injury. Mean amount of blood loss between injury and repair was 130 cc (40-350 cc). There was no operative mortality.
Conclusion Calmness of the operative team followed by the appropriate surgical approach is the key of the success in case of any injury to RHIVC. Digital compression technique can be enough to prevent massive bleeding and repair the injury tract without any vascular exclusion that may result with serious postoperative complications. We proposed this technique because of its ability by most surgeon and easy to perform in a safe way.
C1 [Unal, Aydin; Pinar, Yazici; Murat, Zeytunlu; Murat, Kilic] Ege Univ, Sch Med, Organ Transplantat & Res Ctr, TR-35100 Izmir, Turkey.
C3 Ege University
RP Pinar, Y (corresponding author), Ege Univ, Sch Med, Organ Transplantat & Res Ctr, TR-35100 Izmir, Turkey.
EM pinar.yazici@ege.edu.tr
RI yazici, pinar/ABH-2934-2020
OI kilic, murat/0000-0002-2887-1487; yazici, pinar/0000-0002-3445-5084
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NR 9
TC 0
Z9 0
U1 5
U2 13
PU SPRINGER INDIA
PI NEW DELHI
PA 7TH FLOOR, VIJAYA BUILDING, 17, BARAKHAMBA ROAD, NEW DELHI, 110 001,
INDIA
SN 0972-2068
EI 0973-9793
J9 INDIAN J SURG
JI Indian J. Surg
PD FEB
PY 2008
VL 70
IS 1
BP 19
EP 24
DI 10.1007/s12262-008-0004-1
PG 6
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA 449UZ
UT WOS:000266357100004
PM 23133010
OA Green Published
DA 2025-01-07
ER
PT J
AU Simon, P
Omokoko, TA
Breitkreuz, A
Hebich, L
Kreiter, S
Attig, S
Konur, A
Britten, CM
Paret, C
Dhaene, K
Türeci, Ö
Sahin, U
AF Simon, Petra
Omokoko, Tana A.
Breitkreuz, Andrea
Hebich, Lisa
Kreiter, Sebastian
Attig, Sebastian
Konur, Abdo
Britten, Cedrik M.
Paret, Claudia
Dhaene, Karl
Tuereci, Oezlem
Sahin, Ugur
TI Functional TCR Retrieval from Single Antigen-Specific Human T Cells
Reveals Multiple Novel Epitopes
SO CANCER IMMUNOLOGY RESEARCH
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; IMMUNE-RESPONSES; RECEPTOR-ALPHA; BETA-CHAINS;
GENE; IDENTIFICATION; LYMPHOCYTES; REPERTOIRE; NY-ESO-1; CANCER
AB The determination of the epitope specificity of disease-associated T-cell responses is relevant for the development of biomarkers and targeted immunotherapies against cancer, autoimmune, and infectious diseases. The lack of known T-cell epitopes and corresponding T-cell receptors (TCR) for novel antigens hinders the efficient development and monitoring of new therapies. We developed an integrated approach for the systematic retrieval and functional characterization of TCRs from single antigen-reactive T cells that includes the identification of epitope specificity. This is accomplished through the rapid cloning of full-length TCR-alpha and TCR-beta chains directly from single antigen-specific CD8(+) or CD4(+) T lymphocytes. The functional validation of cloned TCRs is conducted using in vitro-transcribed RNA transfer for expression of TCRs in T cells and HLA molecules in antigen-presenting cells. This method avoids the work and bias associated with repetitive cycles of in vitro T-cell stimulation, and enables fast characterization of antigen-specific T-cell responses. We applied this strategy to viral and tumor-associated antigens (TAA), resulting in the retrieval of 56 unique functional antigen-specific TCRs from human CD8(+) and CD4(+) T cells (13 specific for CMV-pp65, 16 specific for the well-known TAA NY-ESO-1, and 27 for the novel TAA TPTE), which are directed against 39 different epitopes. The proof-of-concept studies with TAAs NY-ESO-1 and TPTE revealed multiple novel TCR specificities. Our approach enables the rational development of immunotherapy strategies by providing antigen-specific TCRs and immunogenic epitopes. (C) 2014 AACR.
C1 [Simon, Petra; Omokoko, Tana A.; Breitkreuz, Andrea; Hebich, Lisa; Kreiter, Sebastian; Attig, Sebastian; Konur, Abdo; Britten, Cedrik M.; Sahin, Ugur] Johannes Gutenberg Univ Mainz, Dept Med 3, Div Translat & Expt Oncol, D-55122 Mainz, Germany.
[Simon, Petra; Breitkreuz, Andrea; Hebich, Lisa; Kreiter, Sebastian; Attig, Sebastian; Paret, Claudia; Sahin, Ugur] Johannes Gutenberg Univ Mainz, Mainz gGmbH, Univ Med Ctr, D-55122 Mainz, Germany.
[Dhaene, Karl] Algemeen Stedelijk Ziekenhuis Aalst, Dept Pathol, Aalst, Belgium.
[Tuereci, Oezlem] Ganymed Pharmaceut AG, Mainz, Germany.
C3 Johannes Gutenberg University of Mainz; Johannes Gutenberg University of
Mainz
RP Sahin, U (corresponding author), TRON gGmbH, Langenbeckstr 1,VFG 708 3 OG, D-55131 Mainz, Germany.
EM front-office@tron-mainz.de
RI Paret, Claudia/T-2913-2019; Sahin, Ugur/L-4818-2017
OI Oehm, Petra/0000-0002-1086-2726; Sahin, Ugur/0000-0003-0363-1564
FU BioNTech Cell & Gene Therapies GmbH
FX P. Simon is Head of Immunoreceptor Validation at BioNTech Cell & Gene
Therapies GmbH and has ownership interest in a patent application. T.
Omokoko is a senior scientist at BioNTech Cell & Gene Therapies GmbH and
has ownership interest (including patents) in a patent application. A.
Breitkreuz is an engineer at BioNTech Cell & Gene Therapies GmbH. L.
Hebich is a technician at BioNTech Cell & Gene Therapies GmbH. O. Tureci
has ownership interest in a patent. U. Sahin is a cofounder of BioNTech
Cell & Gene Therapies GmbH, reports receiving a commercial research
grant from BioNTech Cell & Gene Therapies GmbH, and has ownership
interest (including patents) in TRON and BioNTech Cell & Gene Therapies
GmbH. No potential conflicts of interest were disclosed by the other
authors.
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NR 50
TC 36
Z9 43
U1 0
U2 11
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2326-6066
EI 2326-6074
J9 CANCER IMMUNOL RES
JI Cancer Immunol. Res.
PD DEC
PY 2014
VL 2
IS 12
BP 1230
EP 1244
DI 10.1158/2326-6066.CIR-14-0108
PG 15
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA AW2RE
UT WOS:000346135500012
PM 25245536
OA Green Submitted, Bronze
DA 2025-01-07
ER
PT J
AU Xu, FP
Zhang, H
Chen, JM
Zhan, JY
Liu, P
Liu, W
Qi, SL
Mu, YP
AF Xu, Feipeng
Zhang, Hua
Chen, Jiamei
Zhan, Junyi
Liu, Ping
Liu, Wei
Qi, Shenglan
Mu, Yongping
TI Recent progress on the application of compound formulas of traditional
Chinese medicine in clinical trials and basic research in
vivo for chronic liver disease
SO JOURNAL OF ETHNOPHARMACOLOGY
LA English
DT Article
DE Chronic liver disease; Compound formula of TCM; Clinical trial; Basic
research in vivo; Research scheme; Efficacy and mechanism
ID CHRONIC HEPATITIS-B; INTESTINAL MICROBIOTA; PRACTICE GUIDELINES;
NOURISHING-SHEN; FATTY-ACIDS; PHASE-II; TANG; FIBROSIS; THERAPY; CAPSULE
AB Ethnopharmacological relevance: Chronic liver diseases mainly include chronic viral liver disease, metabolic liver disease, cholestatic liver disease (CLD), autoimmune liver disease, and liver fibrosis or cirrhosis. Notably, the compound formulas of traditional Chinese medicine (TCM) is effective for chronic liver diseases in clinical trials and basic research in vivo, which provide evidence of chronic liver disease treatment with integrated TCM and traditional Western medicine. Aim of the review: This paper aims to provide a comprehensive review of the compound formulas of TCM for treating different chronic liver diseases to elucidate the composition, main curative effects, and mechanisms of these formulas and research methods. Materials and methods: Different keywords related to chronic liver diseases and keywords related to the compound formulas of TCM were used to search the literature. PubMed, Scopus, Web of Science, and CNKI were searched to screen out original articles about the compound formulas of TCM related to the treatment of chronic liver diseases, mainly including clinical trials and basic in vivo research related to Chinese patent drugs, classic prescriptions, proven prescriptions, and hospital preparations. We excluded review articles, meta-analysis articles, in vitro experiments, articles about TCM monomers, articles about single-medicine extracts, and articles with incomplete or uncertain description of prescription composition. Plant names were checked with MPNS (http://mpns.kew.org). Results: In this review, the clinical efficacy and mechanism of compound formulas of TCM were summarized for the treatment of chronic viral hepatitis, nonalcoholic fatty liver disease, CLD, and liver fibrosis or cirrhosis developed from these diseases and other chronic liver diseases. For each clinical trial and basic research in vivo, this review provides a detailed record of the specific composition of the compound formulas of TCM, type of clinical research, modeling method of animal experiments, grouping methods, medication administration, main efficacy, and mechanisms. Conclusion: The general development process of chronic liver disease can be summarized as chronic hepatitis, liver fibrosis or cirrhosis, and hepatocellular carcinoma. The compound formulas of TCM have some applications in these stages of chronic liver diseases. Owing to the continuous progress of medical technology, the benefits of the compound formulas of TCM in the treatment of chronic liver diseases are constantly changing and developing.
C1 [Xu, Feipeng; Zhang, Hua; Chen, Jiamei; Zhan, Junyi; Liu, Ping; Liu, Wei; Qi, Shenglan; Mu, Yongping] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Shanghai Key Lab Tradit Chinese Clin Med, Key Lab Liver & Kidney Dis,Minist Educ,Inst Liver, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.
[Liu, Wei; Qi, Shenglan] Shanghai Univ Tradit Chinese Med, Dept Pharm, SATCM Grade Lab Tradit Chinese Med Preparat 3, Shuguang Hosp, Shanghai 201203, Peoples R China.
[Qi, Shenglan] Shanghai Univ Tradit Chinese Med, Inst Interdisciplinary Complex Res, Shanghai 201203, Peoples R China.
[Liu, Wei; Qi, Shenglan; Mu, Yongping] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine; Shanghai University
of Traditional Chinese Medicine; Shanghai University of Traditional
Chinese Medicine; Shanghai University of Traditional Chinese Medicine
RP Liu, W; Qi, SL; Mu, YP (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.
EM lwhzayl@163.com; qsl_7018@163.com; ypmu8888@126.com
FU National Natural Science Foundation of China [82130120, U23A20516];
Young Elite Scientists Sponsorship Program by CAST [2020QNRC001];
Shanghai Municipal Education Commission; Shanghai Education Development
Foundation [20CG50]
FX This work was supported by the National Natural Science Foundation of
China (No. 82130120, U23A20516), Young Elite Scientists Sponsorship
Program by CAST (No. 2020QNRC001), "Chen Guang" project supported by
Shanghai Municipal Education Commission and Shanghai Education
Development Foundation (No. 20CG50).
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NR 179
TC 4
Z9 5
U1 10
U2 26
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0378-8741
EI 1872-7573
J9 J ETHNOPHARMACOL
JI J. Ethnopharmacol.
PD MAR 1
PY 2024
VL 321
AR 117514
DI 10.1016/j.jep.2023.117514
EA DEC 2023
PG 26
WC Plant Sciences; Chemistry, Medicinal; Integrative & Complementary
Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary
Medicine
GA DU0P5
UT WOS:001134477000001
PM 38042388
DA 2025-01-07
ER
PT J
AU Wang, J
Liu, YQ
Zhao, JY
Xu, JJ
Li, S
Qin, X
AF Wang, Jian
Liu, Yanqiong
Zhao, Jiangyang
Xu, Juanjuan
Li, Shan
Qin, Xue
TI P-glycoprotein gene MDR1 polymorphisms and susceptibility to systemic
lupus erythematosus in Guangxi population: a case-control study
SO RHEUMATOLOGY INTERNATIONAL
LA English
DT Article
DE P-glycoprotein; MDR1; Polymorphisms; Systemic lupus erythematosus
ID MULTIDRUG-RESISTANCE GENE; HEPATOCELLULAR-CARCINOMA; C3435T
POLYMORPHISM; CLINICAL-RELEVANCE; ASSOCIATION; ABCB1; EXPRESSION;
DISEASE; CANCER; RISK
AB The multidrug resistance 1 gene (MDR1) encodes for P-glycoprotein (P-gp), which plays a pathophysiological role in the development of autoimmune diseases, including systemic lupus erythematosus (SLE). Herein, we aimed to investigate the relationship between MDR1 gene polymorphisms and SLE susceptibility in the Chinese Guangxi population. The genotypes of rs1128503 and rs1045642 in MDR1 gene were analyzed using the polymerase chain reaction-restriction fragment length polymorphism method in 283 SLE patients and 247 healthy controls from Guangxi. Direct sequencing method was used to verify the results. Binary logistic regression analyses adjusting for gender and age indicated that subjects carrying the rs1128503 T-allele and TT genotype were at increased risk of SLE when compared to carriers of the C allele and CC genotype, with adjusted ORs of 1.36 (95% CI 1.07-1.74; P = 0.014) and 1.77 (95% CI 1.08-2.88; P = 0.022), respectively. In addition, the risk allele T had a recessive effect (OR 1.49, 95% CI 1.04-2.14, P = 0.029). Subgroup analyses revealed effect modification by age for the presence of the rs1128503 T allele, yielding a significant positive association with SLE in older (ae40 years) subjects (T vs. C allele: OR 1.41, 95% CI 1.01-1.96; P = 0.041; TT vs. CC genotype: OR 1.74, 95% CI 1.07-2.79; P = 0.021). For the first time, we demonstrated that MDR1 rs1128503 polymorphisms were associated with SLE susceptibility in Chinese Guangxi population.
C1 [Wang, Jian; Liu, Yanqiong; Xu, Juanjuan; Li, Shan; Qin, Xue] Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, Nanning, Guangxi, Peoples R China.
[Zhao, Jiangyang] Maternal & Child Hlth Hosp Guangxi Zhuang Autonom, Dept Clin Lab, Nanning, Guangxi, Peoples R China.
C3 Guangxi Medical University
RP Li, S; Qin, X (corresponding author), Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, Nanning, Guangxi, Peoples R China.
EM lis8858@126.com; qinxue919@126.com
RI qin, xue/KQV-3701-2024
FU Guangxi Health Department [Z2013022]
FX This research was supported by Guangxi Health Department self-funded
research projects (Z2013022).
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NR 37
TC 7
Z9 9
U1 0
U2 5
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0172-8172
EI 1437-160X
J9 RHEUMATOL INT
JI Rheumatol. Int.
PD APR
PY 2017
VL 37
IS 4
BP 537
EP 545
DI 10.1007/s00296-017-3652-2
PG 9
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA ER1YR
UT WOS:000398591600008
PM 28154898
DA 2025-01-07
ER
PT J
AU Koay, LB
Feng, IC
Sheu, MJ
Kuo, HT
Lin, CY
Chen, JJ
Wang, SL
Tang, LY
Tsai, SL
AF Koay, Lok-Beng
Feng, I-Che
Sheu, Ming-Jen
Kuo, Hsing-Tao
Lin, Chin-Yih
Chen, Jyh-Jou
Wang, Shih-Ling
Tang, Ling-Yu
Tsai, Sun-Lung
TI Hepatitis B virus (HBV) core antigen-specific regulatory T cells confer
sustained remission to anti-HBV therapy in chronic hepatitis B with
acute exacerbation
SO HUMAN IMMUNOLOGY
LA English
DT Article
DE Chronic hepatitis B; Gene profiling; HLA-class II tetramer; SYFPEITHI
score; Regulatory T-cell clone
ID LAMIVUDINE THERAPY; IMMUNE-RESPONSE; HEPATOCELLULAR-CARCINOMA;
VIRAL-HEPATITIS; NATURAL-HISTORY; SURFACE-ANTIGEN; INFECTION; PEPTIDE;
DISEASE; SEROCONVERSION
AB Acute exacerbations (AEs) of chronic hepatitis B (CH-B) are thought to be the result of breakdown of immune tolerance on the natural history of chronic hepatitis B virus (HBV) infection. Immune tolerance to HBV maintained in CU-B patients without hepatitis is under the control of the host's forkhead box p3-expressing regulatory T cells (Tregs). Its breakdown mimics the occurrence of autoimmune diseases. Severe AEs may lead to liver decompensation and mortalities. Consequently, AEs are currently the major therapeutic targets in patient treatment. In this study, we employed the SYFPEITHI scoring system to identify epitopes on HBV core antigen (HBcAg) for the construction of human leukocyte antigen class II tetramers to measure HBcAg-specific Treg frequencies (Tregf). Upregulation of Treg gene profiling accompanied by increased HBcAg-specific Tregf was detected in AE patients with sustained remission (SR) to anti-HBV therapy. Depletion of Tregs from peripheral blood mononuclear cells enhanced proliferation to HBcAg. HBcAg-specific Treg clones inhibited the killing capacity of cytotoxic T lymphocyte clones in an antigen-independent manner. A greater posttherapy increase in HBcAg-specific Tregf correlated with a higher SR rate to anti-HBV therapy. These results suggest that HBcAg-specific Tregs function as suppressor effectors and confer SR to anti-HBV therapy. (C) 2011 Published by Elsevier Inc. on behalf of American Society for Histocompatibility and Immunogenetics.
C1 [Koay, Lok-Beng; Feng, I-Che; Sheu, Ming-Jen; Kuo, Hsing-Tao; Lin, Chin-Yih; Tsai, Sun-Lung] Chi Mei Med Ctr, Dept Internal Med, Div Hepatogastroenterol, Tainan, Taiwan.
[Chen, Jyh-Jou] Chi Mei Hosp Liouying, Dept Internal Med, Tainan, Taiwan.
[Wang, Shih-Ling; Tang, Ling-Yu; Tsai, Sun-Lung] Chi Mei Med Ctr, Dept Med Res, Liver Res Unit, Tainan, Taiwan.
C3 Chi Mei Hospital; Chi Mei Hospital
RP Tsai, SL (corresponding author), Chi Mei Med Ctr, Dept Internal Med, Div Hepatogastroenterol, Tainan, Taiwan.
EM 860316@mail.chimei.org.tw
FU Chi Mei Foundation, Tainan, Taiwan [CMFHT 9102, 9401, 9701, CMFHR9557]
FX This work was supported by grants from the Chi Mei Foundation (CMFHT
9102, 9401, and 9701 and CMFHR9557), Tainan, Taiwan. The authors are
grateful to Miss Chin-Li Lu, statistician, Department of Medical
Research, Chi Mei Medical Center, Tainan, Taiwan, for statistical
analysis of the data.
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NR 62
TC 11
Z9 13
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0198-8859
EI 1879-1166
J9 HUM IMMUNOL
JI Hum. Immunol.
PD SEP
PY 2011
VL 72
IS 9
BP 687
EP 698
DI 10.1016/j.humimm.2010.11.001
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 816EM
UT WOS:000294581500001
PM 21215784
DA 2025-01-07
ER
PT J
AU Ashizawa, T
Matsuno, N
Yokoyama, T
Kihara, Y
Kuzuoka, K
Taira, S
Konno, O
Jyojima, Y
Akashi, I
Nakamura, Y
Hama, K
Iwamoto, H
Iwahori, T
Nagao, T
Kasahara, M
Tanaka, K
AF Ashizawa, T.
Matsuno, N.
Yokoyama, T.
Kihara, Y.
Kuzuoka, K.
Taira, S.
Konno, O.
Jyojima, Y.
Akashi, I.
Nakamura, Y.
Hama, K.
Iwamoto, H.
Iwahori, T.
Nagao, T.
Kasahara, M.
Tanaka, K.
TI The role of plasmapheresis therapy for perioperative management in
ABO-incompatible adult living donor liver transplantation
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article; Proceedings Paper
CT 1st World Transplant Congress (WTC 2006)
CY JUL 23-27, 2006
CL Boston, MA
SP Transplantat Soc, Amer Soc Transplantat, Amer Soc Transplan Surg
ID BLOOD-GROUP BARRIERS; KIDNEY-TRANSPLANTATION; PROSTAGLANDIN-E1;
REJECTION; RECIPIENT; SURVIVAL
AB Background. Although living donor liver transplantation (LDLT) was established as a treatment for end-stage liver disease in Japan, the indication for LDLT across an ABO-incompatible barrier remains controversial. The purpose of this study was to elucidate the role of plasmapheresis in incompatible LDLT.
Methods. Eleven adult patients (seven men and four women) who underwent incompatible LDLT were enrolled in this study. Of these three patients had hepatocellular carcinoma, three chronic hepatitis C, one Wilson's disease, one autoimmune hepatitis, one chronic hepatitis B, one hemochromatosis, and one fulminant hepatic failure. The immunosuppressive regimen consisted of tacrolimus, prednisolone, mycophenolate mofetil (or cyclophosphamide), and prostaglandin El in all patients. Multiple plasmapheresis was performed perioperatively to reduce the recipient's antibody titers against the donor's blood type.
Results. Plasmapheresis was useful for the reduction of the recipient's antibody titers to X16 or lower before and after transplantation. There was no difference in transplant outcome between the 11 patients with incompatible blood group and 30 patients with identical or compatible blood groups.
Discussion. Major postoperative complications such as intrahepatic biliary complications and hepatic necrosis may occur in incompatible transplantation. Several investigators suggested that anti-imunoglobulin (Ig) M and anti-IgG antibody titers sustained these complications. The antibody titers must be decreased sufficiently with plasmapheresis. An elevation of anti-ABO titers after transplantation may be a predictive risk factor for increased mortality and morbidity. In order to perform LDLT in a safer manner, plasmapheresis is an indispensable treatment to improve the outcome of ABO-incompatible cases.
C1 Tokyo Med Univ, Hachioji Med Ctr, Dept Surg, Hachioji, Tokyo 1930998, Japan.
C3 Tokyo Medical University
RP Ashizawa, T (corresponding author), Tokyo Med Univ, Hachioji Med Ctr, Dept Surg, 1163 Tate Machi, Hachioji, Tokyo 1930998, Japan.
RI Kasahara, Mureo/AAB-8496-2020
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NR 13
TC 8
Z9 11
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0041-1345
J9 TRANSPLANT P
JI Transplant. Proc.
PD DEC
PY 2006
VL 38
IS 10
SI SI
BP 3629
EP 3632
DI 10.1016/j.transproceed.2006.10.122
PG 4
WC Immunology; Surgery; Transplantation
WE Conference Proceedings Citation Index - Science (CPCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA 120PY
UT WOS:000243098400139
PM 17175351
DA 2025-01-07
ER
PT J
AU Silina, K
Rulle, U
Kalnina, Z
Line, A
AF Silina, Karina
Rulle, Undine
Kalnina, Zane
Line, Aija
TI Manipulation of tumour-infiltrating B cells and tertiary lymphoid
structures: a novel anti-cancer treatment avenue?
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Review
DE Tumour-infiltrating B cells; Tertiary lymphoid structures; Cancer
immunotherapy; Cancer therapy
ID BREAST-CANCER METASTASIS; CELLULAR IMMUNE-RESPONSE; IMMUNOGLOBULIN-KAPPA
C; NODE-LIKE STRUCTURES; SECRETE GRANZYME-B; T-CELL; FAVORABLE
PROGNOSIS; LUNG-CANCER; HEPATOCELLULAR-CARCINOMA; LYMPHOTOXIN-ALPHA
AB Combining different standard therapies with immunotherapy for the treatment of solid tumours has proven to yield a greater clinical benefit than when each is applied separately; however, the percentage of complete responses is still far from optimal, and there is an urgent need for improved treatment modalities. The latest literature data suggest that tertiary lymphoid structures (TLS), previously shown to correlate with the severity of autoimmune diseases or transplant rejection, are also formed in tumours, have a significant beneficial effect on survival and might reflect the generation of an effective immune response in close proximity to the tumour. Thus, the facilitation of TLS formation in tumour stroma could provide novel means to improve the efficiency of immunotherapy and other standard therapies. However, little is known about the mechanisms regulating the formation of tumour-associated TLS. Studies of chronic inflammatory diseases and transplant rejection have demonstrated that TLS formation and/or function requires the presence of B cells. Additionally, the infiltration of B cells into the tumour stroma has been demonstrated to be a significant prognostic factor for improved survival in different human tumours. This suggests that B cells could play a beneficial role in antitumour immune response not only in the context of antibody production, antigen presentation and Th1-promoting cytokine production, but also TLS formation. This review focuses on the latest discoveries in tumour-infiltrating B cell functions, their role in TLS formation and relevance in human tumour control, revealing novel opportunities to improve cancer therapies.
C1 [Silina, Karina; Rulle, Undine; Kalnina, Zane; Line, Aija] Latvian Biomed Res & Study Ctr, LV-1067 Riga, Latvia.
C3 Latvian Biomedical Research & Study Centre
RP Silina, K (corresponding author), Latvian Biomed Res & Study Ctr, Ratsupites 1, LV-1067 Riga, Latvia.
EM karina@biomed.lu.lv
RI Linē, Aija/AAH-9999-2021; Kalnina, Zane/AAH-9884-2021
OI Silina, Karina/0000-0003-3947-2710; Kalnina, Zane/0000-0001-9002-3131;
Line, Aija/0000-0002-8492-4758
FU European Regional Development Fund (ERDF) [2010/0231/2DP/2.1.
1.1.0/10/APIA/VIAA/044]
FX This work was supported by the European Regional Development Fund (ERDF)
project No 2010/0231/2DP/2.1. 1.1.0/10/APIA/VIAA/044.
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NR 179
TC 56
Z9 57
U1 0
U2 28
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0340-7004
EI 1432-0851
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD JUL
PY 2014
VL 63
IS 7
BP 643
EP 662
DI 10.1007/s00262-014-1544-9
PG 20
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA AM5CN
UT WOS:000339873300001
PM 24695950
OA Green Published
DA 2025-01-07
ER
PT J
AU Yamada, S
Kakuta, H
AF Yamada, Shoya
Kakuta, Hiroki
TI Retinoid X receptor ligands: a patent review (2007-2013)
SO EXPERT OPINION ON THERAPEUTIC PATENTS
LA English
DT Review
DE Alzheimer's disease; atherosclerosis; cancer; diabetes; permissive
mechanism; revival drug discovery; rexinoids; retinoid X receptor
heterodimers; retinoid X receptors; western-style Chinese medicine
ID PROLIFERATOR-ACTIVATED RECEPTOR; UNION-OF-PHARMACOLOGY; LINOLEIC-ACID;
PPAR-GAMMA; POTENTIAL TREATMENT; INSULIN-RESISTANCE; APOLIPOPROTEIN-E;
RXR AGONISTS; FATTY-ACIDS; IMPROVES
AB Introduction: Retinoid X receptors (RXRs) are nuclear receptors that act as ligand-dependent transcription factors. RXRs function as homodimers or as heterodimers with other nuclear receptors, such as retinoic acid receptors, PPARs, liver X receptors, farnesoid X receptor, vitamin D receptor or thyroid hormone receptors. RXR ligands (agonists or antagonists) show various physiological effects, depending on their partner receptors. RXR agonist bexarotene (Targretin (R)) is used for the treatment of cutaneous T-cell lymphoma in clinical practice. RXR agonists were also reported to be useful for treatment of type 2 diabetes, autoimmune disease and Alzheimer's disease. RXR antagonists were also reported to be effective in type 2 diabetes treatment.
Areas covered: Here patent applications (2007 - 2013) concerning RXR ligands are summarized, and the usefulness of RXR ligands as pharmaceutical agents is discussed.
Expert opinion: RXR agonists show a wide variety of biological effects. However, they cause serious side effects, such as blood triglyceride elevation, hypothyroidism and others. Thus, for clinical application of RXR agonists, abrogation of these side effects is required. RXR heterodimer-selective agonists and RXR partial agonists exhibiting desired effects without side effects are expected to find clinical application.
C1 [Yamada, Shoya; Kakuta, Hiroki] Okayama Univ, Grad Sch Med, Div Pharmaceut Sci Dent & Pharmaceut Sci, Kita Ku, Okayama 7008530, Japan.
[Yamada, Shoya] Japan Soc Promot Sci, Res Fellowship Div, Chiyoda Ku, Tokyo 1028472, Japan.
C3 Okayama University; Japan Society for the Promotion of Science
RP Kakuta, H (corresponding author), Okayama Univ, Grad Sch Med, Div Pharmaceut Sci Dent & Pharmaceut Sci, Kita Ku, 1-1-1 Tsushima Naka, Okayama 7008530, Japan.
EM kakuta-h@cc.okayama-u.ac.jp
RI Kakuta, Hiroki/X-6328-2018
OI Kakuta, Hiroki/0000-0002-3633-8121
FU Okayama Medical Foundation; Japan Society for the Promotion of Science;
Grants-in-Aid for Scientific Research [12J06716] Funding Source: KAKEN
FX The authors thank the Okayama Medical Foundation and Japan Society for
the Promotion of Science for financial support. The authors declare no
other conflicts of interest.
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NR 112
TC 30
Z9 50
U1 0
U2 40
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3776
EI 1744-7674
J9 EXPERT OPIN THER PAT
JI Expert Opin. Ther. Patents
PD APR
PY 2014
VL 24
IS 4
BP 443
EP 452
DI 10.1517/13543776.2014.880692
PG 10
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA AD2WW
UT WOS:000333098200005
PM 24456080
DA 2025-01-07
ER
PT J
AU Eisman, S
Sinclair, R
AF Eisman, Samantha
Sinclair, Rodney
TI Ritlecitinib: an investigational drug for the treatment of moderate to
severe alopecia areata
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Article
DE Alopecia areata; alopecia totalis; alopecia universalis; hair diseases;
JAK inhibitors/janus kinase inhibitors; JAK 3 and 'tyrosine kinase
expressed in hepatocellular carcinoma' family inhibitor; PF-06651600;
ritlecitinib; safety; SALT score
ID INTERNATIONAL EXPERT OPINION; JANUS KINASE INHIBITORS; TOFACITINIB; JAK;
CONSENSUS; VARIANTS; PATIENT; PATHWAY; ACE
AB Introduction: Alopecia areata (AA) is an inflammatory and autoimmune form of hair loss, which can present with one patch of hair loss, but in more extreme cases can lead to total body hair loss. There are limited therapeutic options and no cure, but medication can sometimes induce sustained remission. Disease control cannot be guaranteed; even those who regrow all hair on treatment can experience relapse. There are no FDA approved systemic treatments; therefore, an unmet need for safe, and effective treatments exists. Few treatments have been evaluated by randomized controlled trials. Case reports and series indicate oral Janus Kinase (JAK) inhibitors as a potential therapy. Ritlecitinib is a novel oral JAK3-selective inhibitor being investigated as an AA treatment.
Areas covered: This article introduces ritlecitinib as treatment for AA and considers the mechanism of action, pharmacodynamics, pharmacokinetics, clinical efficacy, and safety [reporting data from a 24-week, phase 2a double-blinded placebo-controlled trial of ritlecitinib in patients with AA who have more than 50% scalp hair loss].
Expert opinion: Ritlecitinib offers a novel mode of action, rapid onset, and the capacity for a superior safety profile over other JAK inhibitors. If approved, ritlecitinib will be widely prescribed by physicians overseeing the more severe AA patients for the foreseeable future. As JAK inhibitors regulate the hair growth cycle and have anti-inflammatory effects, the implementation of ritlecitinib in hair loss disorders other than AA, may prove beneficial.
C1 [Eisman, Samantha] Sinclair Dermatol & Investigator Sinclair Direct, Sinclair Dermatol, 2-2 Wellington Parade, East Melbourne, Vic 3002, Australia.
[Sinclair, Rodney] Epworth Dermatol, Richmond, VA USA.
[Sinclair, Rodney] Univ Melbourne, Dept Med, Sinclair Dermatol, East Melbourne, Vic, Australia.
C3 Sinclair Dermatology; University of Melbourne; Sinclair Dermatology
RP Eisman, S (corresponding author), Sinclair Dermatol & Investigator Sinclair Direct, Sinclair Dermatol, 2-2 Wellington Parade, East Melbourne, Vic 3002, Australia.
EM Samantha.Eisman@sinclairdermatology.com.au
RI Sinclair, Rodney/AAI-8355-2020
OI Sinclair, Rodney/0000-0001-6751-1428; Eisman,
Samantha/0000-0003-0111-6403
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NR 43
TC 9
Z9 9
U1 1
U2 22
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3784
EI 1744-7658
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD DEC 2
PY 2021
VL 30
IS 12
BP 1169
EP 1174
DI 10.1080/13543784.2021.2012149
EA DEC 2021
PG 6
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA YM0IW
UT WOS:000734241100001
PM 34826225
DA 2025-01-07
ER
PT J
AU Solá, S
Amaral, JD
Aranha, MM
Steer, CJ
Rodrigues, CMP
AF Sola, S.
Amaral, J. D.
Aranha, M. M.
Steer, C. J.
Rodrigues, C. M. P.
TI Modulation of hepatocyte apoptosis:: Cross-talk between bile acids and
nuclear steroid receptors
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE apoptosis; Bcl-2 family; bile acids; E2F/p53; liver; TGF-beta 1; nuclear
steroid receptors; nuclear trafficking
ID GROWTH-FACTOR-BETA; CYTOCHROME-C RELEASE; MITOCHONDRIAL PERMEABILITY
TRANSITION; GLUCOCORTICOID-INDUCED APOPTOSIS; FACTOR-KAPPA-B;
INTRACELLULAR SIGNALING PATHWAYS; FACTOR BETA(1)-INDUCED APOPTOSIS;
CHOLESTATIC LIVER-DISEASE; PRIMARY BILIARY-CIRRHOSIS; PRIMARY RAT
HEPATOCYTES
AB The efficient removal of unwanted cells, such as senescent, damaged, mutated or infected cells is crucial for the maintenance of normal liver function. In fact, apoptosis has emerged as a potential contributor to the pathogenesis of a number of hepatic disorders, such as viral hepatitis, autoimmune diseases, ethanol-induced injury, cholestasis, and hepatocellular carcinoma. In contrast to the effect of cytotoxic bile acids in the liver, ursodeoxycholic acid (UDCA) has increasingly been used for the treatment of various liver disorders. The clinical efficacy of this hydrophilic bile acid was first recognized by its use in traditional Asian medicine. However, many studies have subsequently confirmed that UDCA improves liver function by three major mechanisms of action, including protection of cholangiocytes against the cytotoxicity of hydrophobic bile acids, stimulation of hepatobiliary secretion, and inhibition of liver cell apoptosis. UDCA acts as a potent inhibitor of the classical mitochondrial pathway of apoptosis, but also interferes with alternate and upstream molecular targets such as the E2F-1/p53 pathway. Together, there is growing evidence that this hydrophilic bile acid may modulate gene expression to prevent cell death. Curiously, as a cholesterol-derived molecule, UDCA interacts with nuclear steroid receptors, such as the glucocorticoid receptor. Nuclear steroid receptors play crucial roles in mediating steroid hormone signaling involved in many biological processes, including apoptosis. Here, we review the anti-apoptotic mechanisms of UDCA in hepatic cells, and discuss a potential involvement of nuclear steroid receptors in mediating the survival effects of UDCA.
C1 Univ Lisbon, Fac Pharm, Ctr Patogenese Mol, P-1600083 Lisbon, Portugal.
Univ Minnesota, Sch Med, Dept Med, Minneapolis, MN 55455 USA.
Univ Minnesota, Sch Med, Dept Genet, Minneapolis, MN 55455 USA.
Univ Minnesota, Sch Med, Dept Cell Biol, Minneapolis, MN 55455 USA.
Univ Minnesota, Sch Med, Dept Dev, Minneapolis, MN 55455 USA.
C3 Universidade de Lisboa; University of Minnesota System; University of
Minnesota Twin Cities; University of Minnesota System; University of
Minnesota Twin Cities; University of Minnesota System; University of
Minnesota Twin Cities; University of Minnesota System; University of
Minnesota Twin Cities
RP Rodrigues, CMP (corresponding author), Univ Lisbon, Fac Pharm, Ctr Patogenese Mol, Av Forcas Armadas, P-1600083 Lisbon, Portugal.
EM cmprodrigues@ff.ul.pt
RI Aranha, Marcia/AAO-7240-2021; Pereira Rodrigues, Cecilia
Maria/M-3572-2013; Amaral, Joana/M-4660-2013; Sola, Susana/M-5251-2013
OI Pereira Rodrigues, Cecilia Maria/0000-0002-4829-754X; Amaral,
Joana/0000-0001-9504-5102; Sola, Susana/0000-0003-2036-797X; Aranha,
Marcia/0000-0001-9842-4335
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NR 209
TC 27
Z9 32
U1 0
U2 11
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2006
VL 13
IS 25
BP 3039
EP 3051
DI 10.2174/092986706778521823
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 083KD
UT WOS:000240453900005
PM 17073645
DA 2025-01-07
ER
PT J
AU Pisarska, MM
Dunne, MR
O'Shea, D
Hogan, AE
AF Pisarska, Marta M.
Dunne, Margaret R.
O'Shea, Donal
Hogan, Andrew E.
TI Interleukin-17 producing mucosal associated invariant T cells - emerging
players in chronic inflammatory diseases?
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Review
DE chronic inflammation; IL-17; mucosal-associated invariant T cells
ID MAIT CELLS; PERIPHERAL-BLOOD; IL-17; INNATE; TCR; ACTIVATION; ALPHA;
HETEROGENEITY; INVOLVEMENT; CONTRIBUTE
AB Mucosal associated invariant T (MAIT) cells are a population of evolutionarily conserved T cells, which express an invariant T cell receptor (TCR) and represent a significant subset of innate-like T cells in humans, yet their role in immunity is still emerging. Unlike conventional alpha beta T cells, MAIT cells are not restricted by MHC molecules, but instead uniquely recognize microbially derived vitamin metabolites presented by the MHC-I like molecule MR1. MAIT cells are enriched in mucosal sites and tissues including liver and adipose tissue where they are thought to play an important role in immunosurveillance and immunity against microbial infection. In addition to their putative role in antimicrobial immunity, recent research on MAIT cells, in particular IL-17 producing MAIT cells, has demonstrated their involvement in numerous chronic inflammatory conditions. In this review, we give an overview of the work to date on the function and subsets of MAIT cells. We also examine the role of IL-17 producing MAIT cells in chronic inflammatory diseases ranging from autoimmune conditions, metabolic diseases to cancer. Furthermore, we discuss the most recent findings from the clinic that might help deepen our understanding about the biology of MAIT cells.
C1 [Pisarska, Marta M.; Hogan, Andrew E.] Maynooth Univ, Kathleen Lonsdale Inst Human Hlth Res, Maynooth, Kildare, Ireland.
[Pisarska, Marta M.; Hogan, Andrew E.] Natl Childrens Res Ctr, Dublin, Ireland.
[Dunne, Margaret R.] St James Hosp, Trinity Translat Med Inst, Dept Surg, Dublin, Ireland.
[Dunne, Margaret R.] St Jamess Hosp Dublin, Trinity St Jamess Canc Inst, Dublin, Ireland.
[O'Shea, Donal; Hogan, Andrew E.] Univ Coll, St Vincents Univ Hosp, Educ & Res Ctr, Obes Immunol Grp, Dublin, Ireland.
C3 Maynooth University; Trinity College Dublin; National Children's
Research Centre (NCRC); Trinity College Dublin; Trinity College Dublin;
University College Dublin; Saint Vincent's University Hospital
RP Hogan, AE (corresponding author), Maynooth Univ, Kathleen Lonsdale Inst Human Hlth Res, Maynooth, Kildare, Ireland.; Hogan, AE (corresponding author), Natl Childrens Res Ctr, Dublin, Ireland.; Hogan, AE (corresponding author), Univ Coll, St Vincents Univ Hosp, Educ & Res Ctr, Obes Immunol Grp, Dublin, Ireland.
EM Andrew.E.Hogan@mu.ie
RI Dunne, Margaret/AAE-9152-2020; Hogan, Andrew/K-1521-2013
OI Dunne, Margaret/0000-0002-2816-5064; O'Shea, Donal/0000-0002-1408-5274;
Hogan, Andrew/0000-0001-5875-230X
FU Health Research Board; National Children's Research Centre
FX A.E.H. and D.O.S. are supported by the Health Research Board. A.E.H. and
M.P. are supported by the National Children's Research Centre.
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NR 107
TC 20
Z9 22
U1 3
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD AUG
PY 2020
VL 50
IS 8
BP 1098
EP 1108
DI 10.1002/eji.202048645
EA JUL 2020
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA MT5ZV
UT WOS:000548587900001
PM 32617963
OA Bronze, Green Accepted
DA 2025-01-07
ER
PT J
AU Ko, PY
Lin, SD
Hsieh, MC
Chen, YC
AF Ko, Po-Yen
Lin, Shi-Dou
Hsieh, Ming-Chia
Chen, Yu-Cheng
TI Diabetes mellitus increased all-cause mortality rate among
newly-diagnosed tuberculosis patients in an Asian population: A
nationwide population-based study
SO DIABETES RESEARCH AND CLINICAL PRACTICE
LA English
DT Article
DE Diabetes mellitus; Mortality; Tuberculosis; Taiwan
ID HEALTH-INSURANCE; RISK-FACTORS; TAIWAN; MANIFESTATIONS; PREVALENCE;
IMPACT
AB Aims: To investigate the effect of diabetes mellitus (DM) on all-cause mortality among patients with newly-diagnosed tuberculosis (TB) in an Asian population. We also identified risk factors for mortality in these patients.
Methods: The data were obtained from the National Health Insurance Research Database and included 9831 newly-diagnosed TB individuals and 1627 TB mortality cases in the period of 2000-2010. The mortality data were divided into a DM group and a non-DM group. We measured the incidence density of mortality and identified the risk factors of mortality.
Results: The all-cause mortality of newly-diagnosed TB patients progressively increased with an average rate of 16.5% during 2000-2010. DM is an independent risk factor for all-cause mortality with HRs 1.17-1.27 by various models. TB patients with ages above 75 years had the highest risk of mortality (HR = 11.93) compared with those under 45 years. TB patients with heart failure, peripheral vascular disease, ischemic heart disease, cerebral vascular disease, hypertension, chronic kidney disease, pulmonary disease, liver disease, cancer, peptic ulcer disease, gout, and autoimmune disease had higher mortality compared to those without the aforementioned factors.
Conclusions: The one-year all-cause mortality after TB diagnosis was high among TB patients in Taiwan and it tended to increase in the past decade. While treating these newly-diagnosed TB patients, it is crucial to detect the factors predisposing to death, such as old age, male gender, certain kinds of aforementioned factors and diabetes. (C) 2017 Elsevier B.V. All rights reserved.
C1 [Ko, Po-Yen] China Med Univ Hosp, Div Cardiol, Dept Med, 2 Yuh Der Rd, Taichung 40447, Taiwan.
[Ko, Po-Yen] China Med Univ, Taichung, Taiwan.
[Lin, Shi-Dou; Hsieh, Ming-Chia; Chen, Yu-Cheng] Changhua Christian Hosp, Div Endocrinol & Metab, Dept Internal Med, Changhua, Taiwan.
[Hsieh, Ming-Chia; Chen, Yu-Cheng] Changhua Christian Hosp, Div Endocrinol & Metab, Dept Internal Med, Yuanlin Branch, Yuanlin, Taiwan.
[Ko, Po-Yen] Asia Univ, Dept Bioinformat & Med Engn, Taichung, Taiwan.
[Hsieh, Ming-Chia] China Med Univ, Grad Inst Integrated Med, Taichung, Taiwan.
[Hsieh, Ming-Chia] Changhua Christian Hosp, Dept Internal Med, Yuanlin Branch, 456 Juguang Rd, Changhua 510, Taiwan.
[Lin, Shi-Dou] Changhua Christian Hosp, Dept Internal Med, 135 Nanxiao St, Changhua 500, Changhua, Taiwan.
C3 China Medical University Taiwan; China Medical University Hospital -
Taiwan; China Medical University Taiwan; Changhua Christian Hospital;
Changhua Christian Hospital; Asia University Taiwan; China Medical
University Taiwan; Changhua Christian Hospital; Changhua Christian
Hospital
RP Chen, YC (corresponding author), Changhua Christian Hosp, Dept Internal Med, Yuanlin Branch, 456 Juguang Rd, Changhua 510, Taiwan.
EM 1520004@cch.org.tw
RI chen, yu-cheng/IQT-1648-2023; Ko, PoYen/LWK-4310-2024
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NR 29
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Z9 12
U1 0
U2 7
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0168-8227
EI 1872-8227
J9 DIABETES RES CLIN PR
JI Diabetes Res. Clin. Pract.
PD NOV
PY 2017
VL 133
BP 115
EP 123
DI 10.1016/j.diabres.2017.08.011
PG 9
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA FM9WU
UT WOS:000415623700016
PM 28934668
DA 2025-01-07
ER
PT J
AU Subramanian, M
Wojtusciszyn, A
Favre, L
Boughorbel, S
Shan, JX
Letaief, KB
Pitteloud, N
Chouchane, L
AF Subramanian, Murugan
Wojtusciszyn, Anne
Favre, Lucie
Boughorbel, Sabri
Shan, Jingxuan
Letaief, Khaled B.
Pitteloud, Nelly
Chouchane, Lotfi
TI Precision medicine in the era of artificial intelligence: implications
in chronic disease management
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Exposome; Chronic inflammation; Chronic diseases; Precision medicine;
Personalized treatment; Deep phenotyping; Big-data analytics; Machine
leaning; Artificial intelligence
ID CHRONIC INFLAMMATION; LIFE-STYLE; ENVIRONMENTAL EXPOSURE; GENETIC
ARCHITECTURE; AIR-POLLUTION; IMMUNE-SYSTEM; BIG DATA; CANCER;
PREVENTION; NUTRITION
AB Aberrant metabolism is the root cause of several serious health issues, creating a huge burden to health and leading to diminished life expectancy. A dysregulated metabolism induces the secretion of several molecules which in turn trigger the inflammatory pathway. Inflammation is the natural reaction of the immune system to a variety of stimuli, such as pathogens, damaged cells, and harmful substances. Metabolically triggered inflammation, also called metaflammation or low-grade chronic inflammation, is the consequence of a synergic interaction between the host and the exposome-a combination of environmental drivers, including diet, lifestyle, pollutants and other factors throughout the life span of an individual. Various levels of chronic inflammation are associated with several lifestyle-related diseases such as diabetes, obesity, metabolic associated fatty liver disease (MAFLD), cancers, cardiovascular disorders (CVDs), autoimmune diseases, and chronic lung diseases. Chronic diseases are a growing concern worldwide, placing a heavy burden on individuals, families, governments, and health-care systems. New strategies are needed to empower communities worldwide to prevent and treat these diseases. Precision medicine provides a model for the next generation of lifestyle modification. This will capitalize on the dynamic interaction between an individual's biology, lifestyle, behavior, and environment. The aim of precision medicine is to design and improve diagnosis, therapeutics and prognostication through the use of large complex datasets that incorporate individual gene, function, and environmental variations. The implementation of high-performance computing (HPC) and artificial intelligence (AI) can predict risks with greater accuracy based on available multidimensional clinical and biological datasets. AI-powered precision medicine provides clinicians with an opportunity to specifically tailor early interventions to each individual. In this article, we discuss the strengths and limitations of existing and evolving recent, data-driven technologies, such as AI, in preventing, treating and reversing lifestyle-related diseases.
C1 [Subramanian, Murugan; Chouchane, Lotfi] Weill Cornell Med, Dept Microbiol & Immunol, New York, NY 10021 USA.
[Wojtusciszyn, Anne; Favre, Lucie; Pitteloud, Nelly] Lausanne Univ Hosp, Serv Endocrinol Diabetol & Metab, Lausanne, Switzerland.
[Subramanian, Murugan; Shan, Jingxuan; Chouchane, Lotfi] Qatar Fdn, Genet Intelligence Lab, Weill Cornell Med Qatar, Doha, Qatar.
[Boughorbel, Sabri] Sidra Med, Res Div, Clin Bioinformat Sect, Doha, Qatar.
[Chouchane, Lotfi] Weill Cornell Med, Dept Genet Med, 45 F 69th St,Suite 432, New York, NY 10021 USA.
[Letaief, Khaled B.] Hong Kong Univ Sci & Technol, Dept Elect & Comp Engn, Kowloon, Hong Kong, Peoples R China.
C3 Cornell University; Weill Cornell Medicine; University of Lausanne;
Centre Hospitalier Universitaire Vaudois (CHUV); Qatar Foundation (QF);
Weill Cornell Medical College Qatar; Sidra Medical & Research Center;
Cornell University; Weill Cornell Medicine; Hong Kong University of
Science & Technology
RP Chouchane, L (corresponding author), Weill Cornell Med, Dept Microbiol & Immunol, New York, NY 10021 USA.; Pitteloud, N (corresponding author), Lausanne Univ Hosp, Serv Endocrinol Diabetol & Metab, Lausanne, Switzerland.; Chouchane, L (corresponding author), Qatar Fdn, Genet Intelligence Lab, Weill Cornell Med Qatar, Doha, Qatar.; Chouchane, L (corresponding author), Weill Cornell Med, Dept Genet Med, 45 F 69th St,Suite 432, New York, NY 10021 USA.
EM Nelly.Pitteloud@chuv.ch; loc2008@med.cornell.edu
RI Letaief, Khaled/LSJ-2311-2024; Chouchane, Lotfi/ABF-1360-2020
OI Wojtusciszyn, Anne/0000-0002-9410-9909; Letaief,
Khaled/0000-0003-2519-6401
FU BMRP Funding of Weill Cornell Medicine-Qatar
FX This work was supported by the BMRP Funding of Weill Cornell
Medicine-Qatar.
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NR 148
TC 95
Z9 101
U1 12
U2 82
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD DEC 9
PY 2020
VL 18
IS 1
AR 472
DI 10.1186/s12967-020-02658-5
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA PH0FO
UT WOS:000600100200008
PM 33298113
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Abi-Rafeh, J
Safran, T
Al-Halabi, B
Dionisopolous, T
AF Abi-Rafeh, Jad
Safran, Tyler
Al-Halabi, Becher
Dionisopolous, Tassos
TI Death by Implants: Critical Analysis of the FDA-MAUDE Database on Breast
Implant-related Mortality
SO PLASTIC AND RECONSTRUCTIVE SURGERY-GLOBAL OPEN
LA English
DT Article
ID LARGE-CELL LYMPHOMA; SURGICAL-SITE INFECTION; HEALTH OUTCOMES; RISK;
FOOD; RECONSTRUCTION; WOMEN
AB Introduction: Since the 1992 moratorium by the Food and Drug Administration (FDA), the debate on the association of breast implants with systemic illnesses has been ongoing. Breast implant-associated anaplastic large cell lymphoma has also raised significant safety concerns in recent years.
Methods: A systematic search of the Manufacturer and User Facility Device Experience (MAUDE) database was performed to identify all cases of breast implant associated deaths reported to the FDA.
Results: The search identified 50 reported cases of apparent implant-related mortality; breast implant-associated anaplastic large cell lymphoma comprised the majority of fatal outcomes (n = 21, 42%), followed by lymphoma (n = 4, 8%), breast cancer (n = 3, 6%), pancreatic cancer (n = 2, 4%), implant rupture (n = 2, 4%), and postoperative infections (n = 2, 4%). Single cases (n = 1, 2% each) of leukemia, small bowel cancer, lung disease, pneumonia, autoimmune and joint disease, amyotrophic lateral sclerosis, liver failure, and sudden death, and 2 cases (4%) of newborn deaths, to mothers with breast implants, were also identified. A literature review demonstrated that 54% of alleged implant-related deaths were not truly associated with breast implant use: the majority of these reports (82%) originated from the public and third-party sources, rather than evidence-based reports by health-care professionals and journal articles.
Conclusions: Although there exists a need for more comprehensive reporting in federal databases, the information available should be considered for a more complete understanding of implant-associated adverse outcomes. With only 46% of FDA-reported implant-related deaths demonstrated to be truly associated with breast implant use, there exists a need for public awareness and education on breast implant safety.
C1 [Abi-Rafeh, Jad] McGill Univ, Dept Med, Montreal, PQ, Canada.
[Safran, Tyler; Al-Halabi, Becher; Dionisopolous, Tassos] McGill Univ, Div Plast & Reconstruct Surg, Montreal, PQ, Canada.
C3 McGill University; McGill University
RP Dionisopolous, T (corresponding author), McGill Univ, Div Plast & Reconstruct Surg, Jewish Gen Hosp, 3755 Chemin Cote St Catherine, Montreal, PQ H3T 1E2, Canada.
RI Alhalabi, Becher/H-2935-2019
OI Alhalabi, Becher/0000-0001-9690-8977
CR Administration USFD, MAUDE MAN US FAC DEV
[Anonymous], 2011, AN LARG CELL LYMPH A
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NR 34
TC 12
Z9 12
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 2169-7574
J9 PRS-GLOB OPEN
JI PRS-GLOB. OPEN
PD DEC
PY 2019
VL 7
IS 12
AR e2554
DI 10.1097/GOX.0000000000002554
PG 10
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA KK4FU
UT WOS:000512700800010
PM 32537301
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Karash, A
Mazzoni, MR
Gilchrist, A
AF Karash, Angela
Mazzoni, Maria R.
Gilchrist, Annette
TI Pharmacological Intervention at CCR1 and CCR5 as an Approach for Cancer:
Help or Hindrance
SO CURRENT TOPICS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Cancer; CCL3; CCL5; CCR1; CCR5; chemokine receptor; G protein; G protein
coupled receptor; metastasis; polypharmacology
ID CHEMOKINE RECEPTOR EXPRESSION; MONOCYTE CHEMOATTRACTANT PROTEIN-1;
MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; SIGNAL-TRANSDUCTION PATHWAY;
CELL LUNG-CANCER; FUNCTIONAL EXPRESSION; MOLECULAR-CLONING; SPIROCYCLIC
COMPOUNDS; HEPATOCELLULAR-CARCINOMA; RHEUMATOID-ARTHRITIS
AB While a number of agents directed at chemokine receptors have entered clinic trials, the vast majority of these have failed, and the enthusiasm for this class of drugs has been attenuated. To date, there are two drugs that inhibit chemokine receptors approved by the FDA. The first to be approved in 2007 was maraviroc (brand name Selzentry, or Celsentri outside the US) which targets CCR5 and is used for the treatment of HIV infection. The second is plerixafor (Mozobil) which was approved in 2008, targets CXCR4, and is used for the mobilization of hematopoietic stem cells. This review will focus on the CC chemokine receptors CCR1 and CCR5. These G protein coupled receptors are both activated by a relatively large number of chemokines, most of which overlap. While most of the drugs for CCR1 have been assessed in the context of autoimmune diseases like multiple sclerosis and rheumatoid arthritis, and those for CCR5 were examined for HIV-infection, we review the role of these receptors in relation to cancer. Recently introduced pharma-cophores that serve as agonists or antagonists for the receptors are presented. Efforts to exploit polypharmacology approaches using promiscuous compounds that target more than one receptor are also considered.
C1 [Karash, Angela; Gilchrist, Annette] Midwestern Univ, Chicago Coll Pharm, Downers Grove, IL 60515 USA.
[Mazzoni, Maria R.] Univ Pisa, Dept Pharm, I-56126 Pisa, Italy.
C3 Midwestern University; Midwestern University - Chicago College of
Pharmacy; University of Pisa
RP Gilchrist, A (corresponding author), Midwestern Univ, Dept Pharmaceut Sci, 555 31st St, Downers Grove, IL 60515 USA.
EM agilch@midwestern.edu
RI Mazzoni, Maria/AAA-2366-2022; Gilchrist, Annette/I-4465-2014
OI Gilchrist, Annette/0000-0003-2386-7646; Mazzoni, Maria
Rosa/0000-0003-2612-432X
FU Chicago College of Pharmacy at Midwestern University; University of Pisa
FX Funding has been received from the Chicago College of Pharmacy at
Midwestern University in the form of research grants for Dr. Annette
Gilchrist and Dr. Maria Mazzoni has received grants from the University
of Pisa. The authors would like to thank Timothy Gauntner who assisted
with the initial outline of the work to be presented.
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NR 215
TC 10
Z9 10
U1 7
U2 20
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1568-0266
EI 1873-4294
J9 CURR TOP MED CHEM
JI Curr. Top. Med. Chem.
PY 2014
VL 14
IS 13
BP 1553
EP 1573
DI 10.2174/1568026614666140827144440
PG 21
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA AP3IW
UT WOS:000341969900005
PM 25159162
DA 2025-01-07
ER
PT J
AU Fischer, U
Schulze-Osthoff, K
AF Fischer, U
Schulze-Osthoff, K
TI New approaches and therapeutics targeting apoptosis in disease
SO PHARMACOLOGICAL REVIEWS
LA English
DT Review
ID TUMOR-NECROSIS-FACTOR; SMALL-MOLECULE INHIBITORS; INTERLEUKIN-1-BETA
CONVERTING-ENZYME; X-LINKED INHIBITOR; DIPEPTIDYL ASPARTYL
FLUOROMETHYLKETONES; REVERSIBLE CASPASE-3 INHIBITOR;
MITOCHONDRIA-DERIVED ACTIVATOR; PERMEABILITY TRANSITION PORE;
UBIQUITIN-PROTEIN LIGASE; MONOCLONAL-ANTIBODY CA2
AB Apoptosis, the major form of cellular suicide, is central to various physiological processes and the maintenance of homeostasis in multicellular organisms. Presumably, even more important is a causative or contributing role of apoptosis to various human diseases. These include situations with unwanted cell accumulation (cancer) and failure to eradicate aberrant cells (autoimmune diseases) or disorders with an inappropriate loss of cells (heart failure, stroke, AIDS, neurodegenerative diseases, and liver injury). The past decade has witnessed a tremendous progress in the knowledge of the molecular mechanisms that regulate apoptosis and the mediators that either prevent or trigger cell death. Consequently, apoptosis regulators have emerged as key targets for the design of therapeutic strategies aimed at modulating cellular life-and-death decisions. Numerous novel approaches are currently being followed employing gene therapy and antisense strategies, recombinant biologics, or classical organic and combinatorial chemistry to target specific apoptotic regulators. Convincing proof-of-principle evidence obtained in several animal models confirms the validity of strategies targeting apoptosis and revealed an enormous potential for therapeutic intervention in a variety of illnesses. Although numerous apoptotic drugs are currently being developed, several therapeutics have progressed to clinical testing or are already approved and marketed. Here we review the recent progress of apoptosis-based therapies and survey some highlights in a very promising field of drug development.
C1 Univ Dusseldorf, Inst Mol Med, D-40225 Dusseldorf, Germany.
C3 Heinrich Heine University Dusseldorf
RP Univ Dusseldorf, Inst Mol Med, Bldg 23-12,Univ Str 1, D-40225 Dusseldorf, Germany.
EM kso@uni-duesseldorf.de
RI Schulze-Osthoff, Klaus/N-9025-2013
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NR 219
TC 212
Z9 258
U1 0
U2 32
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0031-6997
EI 1521-0081
J9 PHARMACOL REV
JI Pharmacol. Rev.
PD JUN
PY 2005
VL 57
IS 2
BP 187
EP 215
DI 10.1124/pr.57.2.6
PG 29
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 928XR
UT WOS:000229305700004
PM 15914467
DA 2025-01-07
ER
PT J
AU Cao, WT
Qian, G
Luo, W
Liu, X
Pu, YJ
Hu, GL
Han, LL
Yuan, LM
Xiao, A
Deng, DQ
AF Cao, Wenting
Qian, Ge
Luo, Wen
Liu, Xin
Pu, Yunjing
Hu, Guilan
Han, Lulu
Yuan, Limei
Xiao, A.
Deng, Danqi
TI miR-125b is downregulated in systemic lupus erythematosus patients and
inhibits autophagy by targeting UVRAG
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Ultraviolet B; miR-125b; Systemic lupus erythematosus; UV radiation
resistance associated gene; Autophagy
ID HUMAN HEPATOCELLULAR-CARCINOMA; T-LYMPHOCYTES; CELLS; EXPRESSION
AB Systemic lupus erythematosus (SLE) is a severe autoimmune disease and the pathogenesis remains incompletely understood. This study aimed to investigate the role of miR-125b in the pathogenesis of SLE and explore the underlying mechanism. Compared to healthy controls, the expression of miR-125b decreased in peripheral blood mononuclear cells (PBMCs) of SLE patients. In addition, PBMCs exposed to ultraviolet B had lower miR-125b level compared to those unexposed to radiation. We identified UV radiation resistance associated gene (UVRAG) as a target of miR-125b. Jurkat cells treated with miR-125b-5p agomir showed reduced levels of ATG7, Beclin-1 and LC3 II and decreased autophagy. In contrast, Jurkat cells treated with miR-125b-5p antagomir showed increased levels of ATG7, Beclin-1 and LC3 II and increased autophagy. Furthermore, Jurkat cells transfected with UVRAG expression vector showed higher expression of ATG7, Beclin-1 and LC3 II and increased autophagy. Conversely, cells transfected with UVRAG siRNA had lower expression of ATG7, Beclin-1 and LC3 II and decreased autophagy. Taken together, our data demonstrate that Ultraviolet B radiation can downregulate miR-125b-5p and increase UVRAG expression and autophagy activity in PBMCs of SLE patients. These findings help explain how ultraviolet B exacerbates SLE and suggest that UVRAG is a potential therapeutic target for SLE.
C1 [Cao, Wenting; Qian, Ge; Luo, Wen; Liu, Xin; Pu, Yunjing; Hu, Guilan; Han, Lulu; Yuan, Limei; Xiao, A.; Deng, Danqi] Kunming Med Univ, Dept Dermatol, Affiliated Hosp 2, Kunming 650101, Yunnan, Peoples R China.
C3 Kunming Medical University
RP Deng, DQ (corresponding author), Kunming Med Univ, Dept Dermatol, Affiliated Hosp 2, Kunming 650101, Yunnan, Peoples R China.
EM danqid128@sina.com
FU National Natural Science Foundation of China [81460472]; Yunnan Applied
Basic Research Projects-Union Foundation [2014FB050]
FX This study was funded by National Natural Science Foundation of China
(No. 81460472) and Yunnan Applied Basic Research Projects-Union
Foundation (No. 2014FB050).
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NR 21
TC 34
Z9 40
U1 1
U2 7
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD MAR
PY 2018
VL 99
BP 791
EP 797
DI 10.1016/j.biopha.2018.01.119
PG 7
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA FZ2TR
UT WOS:000427436800100
PM 29710477
DA 2025-01-07
ER
PT J
AU Khan, M
Arooj, S
Wang, H
AF Khan, Muhammad
Arooj, Sumbal
Wang, Hua
TI Soluble B7-CD28 Family Inhibitory Immune Checkpoint Proteins and
Anti-Cancer Immunotherapy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE soluble immune checkpoints (SIC); alternative splice variants (ASV);
immunotherapy (IT); immune checkpoint blockade (ICB); gene therapy;
cancer vaccination (CVax)
ID DEATH-LIGAND 1; T-LYMPHOCYTE ATTENUATOR; ENHANCES ANTITUMOR IMMUNITY;
CELL LUNG-CANCER; B7 FAMILY; COSTIMULATORY MOLECULE;
HEPATOCELLULAR-CARCINOMA; PD-L1 EXPRESSION; SPLICE VARIANT;
GASTRIC-CANCER
AB Co-inhibitory B7-CD28 family member proteins negatively regulate T cell responses and are extensively involved in tumor immune evasion. Blockade of classical CTLA-4 (cytotoxic T lymphocyte-associated antigen-4) and PD-1 (programmed cell death protein-1) checkpoint pathways have become the cornerstone of anti-cancer immunotherapy. New inhibitory checkpoint proteins such as B7-H3, B7-H4, and BTLA (B and T lymphocyte attenuator) are being discovered and investigated for their potential in anti-cancer immunotherapy. In addition, soluble forms of these molecules also exist in sera of healthy individuals and elevated levels are found in chronic infections, autoimmune diseases, and cancers. Soluble forms are generated by proteolytic shedding or alternative splicing. Elevated circulating levels of these inhibitory soluble checkpoint molecules in cancer have been correlated with advance stage, metastatic status, and prognosis which underscore their broader involvement in immune regulation. In addition to their potential as biomarker, understanding their mechanism of production, biological activity, and pathological interactions may also pave the way for their clinical use as a therapeutic target. Here we review these aspects of soluble checkpoint molecules and elucidate on their potential for anti-cancer immunotherapy.
C1 [Khan, Muhammad; Wang, Hua] Anhui Med Univ, Dept Oncol, Affiliated Hosp 1, Hefei, Peoples R China.
[Khan, Muhammad; Wang, Hua] Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Hefei, Peoples R China.
[Arooj, Sumbal] Univ Sialkot, Dept Biochem, Sialkot, Pakistan.
C3 Anhui Medical University; Anhui Medical University
RP Wang, H (corresponding author), Anhui Med Univ, Dept Oncol, Affiliated Hosp 1, Hefei, Peoples R China.; Wang, H (corresponding author), Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Hefei, Peoples R China.
EM wanghua@ahmu.edu.cn
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NR 259
TC 56
Z9 63
U1 2
U2 26
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD AUG 31
PY 2021
VL 12
AR 651634
DI 10.3389/fimmu.2021.651634
PG 21
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA UU1NM
UT WOS:000698569800001
PM 34531847
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Gomaa, MS
Lim, AST
Lau, SCW
Watts, AM
Illingworth, NA
Bridgens, CE
Veal, GJ
Redfern, CPF
Brancale, A
Armstrong, JL
Simons, C
AF Gomaa, Mohamed S.
Lim, Andrew S. T.
Lau, S. C. Wilson
Watts, Ann-Marie
Illingworth, Nicola A.
Bridgens, Caroline E.
Veal, Gareth J.
Redfern, Christopher P. F.
Brancale, Andrea
Armstrong, Jane L.
Simons, Claire
TI Synthesis and CYP26A1 inhibitory activity of novel methyl
3-[4-(arylamino)phenyl]-3-(azole)-2,2-dimethylpropanoates
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE CYP26A1; Methyl 3-[4-(arylamino)phenyl]-3-(azole)-2,2-dimethylpropanoate
derivatives; IC50 enzyme inhibition; MCF-7; Molecular modeling
ID TRANS-RETINOIC ACID; PROTEIN TRANSFERASE INHIBITORS; SMALL-MOLECULE
INHIBITORS; BIOLOGICAL EVALUATION; METABOLISM; CANCER; NEUROBLASTOMA;
DERIVATIVES
AB The role of all-trans-retinoic acid (ATRA) in the development and maintenance of many epithelial and neural tissues has raised great interest in the potential of ATRA and related compounds (retinoids) as pharmacological agents, particularly for the treatment of cancer, skin, neurodegenerative and autoimmune diseases. The use of ATRA or prodrugs as pharmacological agents is limited by a short half-life in vivo resulting from the activity of specific ATRA hydroxylases, CYP26 enzymes, induced by ATRA in liver and target tissues. For this reason retinoic acid metabolism blocking agents (RAMBAs) have been developed for treating cancer and a wide range of other diseases.
The synthesis, CYP26A1 inhibitory activity and molecular modeling studies of novel methyl 3-[4-(arylamino)phenyl]-3-(azole)-2,2-dimethylpropanoates are presented. From this series of compounds clear SAR can be derived for 4-substitution of the phenyl ring with electron-donating groups more favourable for inhibitory activity. Both the methylenedioxyphenyl imidazole (17, IC50 = 8 nM) and triazole (18, IC50 = 6.7 nM) derivatives were potent inhibitors with additional binding interactions between the methylenedioxy moiety and the CYP26 active site likely to be the main factor. The 6-bromo-3-pyridine imidazole 15 (IC50 = 5.7 nM) was the most active from this series compared with the standards liarozole (IC50 = 540 nM) and R116010 (IC50 = 10 nM). (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Gomaa, Mohamed S.; Lim, Andrew S. T.; Lau, S. C. Wilson; Watts, Ann-Marie; Brancale, Andrea; Simons, Claire] Cardiff Univ, Div Med Chem, Welsh Sch Pharm, Cardiff CF10 3NB, S Glam, Wales.
[Illingworth, Nicola A.; Bridgens, Caroline E.; Veal, Gareth J.; Redfern, Christopher P. F.] Newcastle Univ, No Inst Canc Res, Sch Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
[Armstrong, Jane L.] Newcastle Univ, Inst Cellular Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
C3 Cardiff University; Newcastle University - UK; Newcastle University - UK
RP Simons, C (corresponding author), Cardiff Univ, Div Med Chem, Welsh Sch Pharm, King Edward VII Ave, Cardiff CF10 3NB, S Glam, Wales.
EM SimonsC@Cardiff.ac.uk
RI Gomaa, Mohamed/AAF-5079-2019; Simons, Claire/ABD-7192-2021; Illingworth,
Nicola/AAP-2138-2021; Simons, Claire/N-5788-2014; Brancale,
Andrea/N-9445-2014
OI Simons, Claire/0000-0002-9487-1100; Veal, Gareth/0000-0002-1897-8678;
Armstrong, Jane/0000-0002-5822-0597; gomaa, Mohamed/0000-0003-2112-9092;
Redfern, Christopher/0000-0002-1833-8048; Brancale,
Andrea/0000-0002-9728-3419
FU Cancer Research UK [C7735/A9612]; Nuffield Foundation
FX We acknowledge Cancer Research UK (M.S.G. and C.E.B., Grant Ref.
C7735/A9612) and the Nuffield Foundation (A.S.T.L.) for funding and the
EPSRC Mass Spectrometry Centre, Swansea, UK for mass spectroscopy data.
CR Alvarez S, 2011, EXPERT OPIN THER PAT, V21, P55, DOI 10.1517/13543776.2011.536531
[Anonymous], MOL OP ENV MOE
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NR 28
TC 11
Z9 11
U1 0
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
EI 1464-3391
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD OCT 15
PY 2012
VL 20
IS 20
BP 6080
EP 6088
DI 10.1016/j.bmc.2012.08.044
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 017MN
UT WOS:000309594200009
PM 22989911
DA 2025-01-07
ER
PT J
AU Fortes, P
Morris, KV
AF Fortes, Puri
Morris, Kevin V.
TI Long noncoding RNAs in viral infections
SO VIRUS RESEARCH
LA English
DT Article
DE IncRNAs; Proviral; Antiviral; IFN response; IncRNA processing;
Transcription regulation; RNA interference
ID DOUBLE-STRANDED-RNA; HEPATITIS-C VIRUS; HEPATOCELLULAR-CARCINOMA; RIG-I;
VA-RNA; TRANSCRIPTION FACTOR; ANTIVIRAL RESPONSES; INTERFERING RNAS;
IMMUNE-RESPONSE; GENE-EXPRESSION
AB Viral infections induce strong modifications in the cell transcriptome. Among the RNAs whose expression is altered by infection are long noncoding RNAs (IncRNAs). LncRNAs are transcripts with potential to function as RNA molecules. Infected cells may express viral incRNAs, cellular lncRNAs and chimeric IncRNAs formed by viral and cellular sequences. Some viruses express viral IncRNAs whose function is essential for viral viability. They are transcribed by polymerase II or III and some of them can be processed by unique maturation steps performed by host cell machineries. Some viral IncRNAs control transcription, stability or translation of cellular and viral genes. Surprisingly, similar functions can be exerted by cellular lncRNAs induced by infection. Expression of cellular incRNAs may be altered in response to viral replication or viral protein expression. However, many cellular IncRNAs respond to the antiviral pathways induced by infection. In fact, many lncRNAs function as positive or negative regulators of the innate antiviral response. Our current knowledge about the identity and function of lncRNAs in infected cells is very limited. However, research into this field has already helped in the identification of novel cellular pathways and may help in the development of therapeutic tools for the treatment of viral infections, autoimmune diseases, neurological disorders and cancer. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Fortes, Puri] Univ Navarra, Dept Gene Therapy & Hepatol, Ctr Appl Med Res CIMA, E-31080 Pamplona, Spain.
[Fortes, Puri] Univ Navarra, Dept Gene Therapy & Hepatol, Navarra Inst Hlth Res IdiSNA, E-31080 Pamplona, Spain.
[Morris, Kevin V.] Scripps Res Inst, Dept Mol & Expt Med, 10666 N Torrey Pines Rd, La Jolla, CA 92037 USA.
[Morris, Kevin V.] Univ New S Wales, Sch Biotechnol & Biomed Sci, POB 1, Kensington, NSW 2033, Australia.
C3 University of Navarra; University of Navarra; Scripps Research
Institute; University of New South Wales Sydney
RP Fortes, P (corresponding author), CIMA, Pio 12 55, Pamplona 31008, Spain.
EM pfortes@unav.es
RI morris, kevin/B-5481-2011; Fortes, Puri/J-7872-2016
OI Fortes, Puri/0000-0001-7571-6220; Morris, Kevin/0000-0002-0157-0553
FU Ministry of Economy and Competitivity [BIO2009/09295, SAF2012-40003,
BFU2013-50517-EXP]; Fondo de Investigation Sanitaria [PI13/01989];
Fundacio La Marato de TV3 [20132130-31-32]; Caja Navarra Foundation
[70020]; FEDER funding; UTE project CIMA; project RNAREG
[CSD2009-00080]; Ministry of Economy and Competitivity under the program
CONSOLIDER INGENIO; NIAID [PO1 AI099783-01, R01 AI111139-01, R01
DK104681-01]; Australian Research Council [FT1300100572]; Instituto de
Salud Carlos III
FX We want to apologize to all the scientists whose work has not been
mentioned due to space limitations. This study was supported by grants
from the Ministry of Economy and Competitivity (BIO2009/09295,
SAF2012-40003, BFU2013-50517-EXP), Fondo de Investigation Sanitaria
(PI13/01989), financed by the Instituto de Salud Carlos III, Fundacio La
Marato de TV3 (20132130-31-32), Caja Navarra Foundation (70020), FEDER
funding, funds from the "UTE project CIMA" and by the project RNAREG
[CSD2009-00080], funded by the Ministry of Economy and Competitivity
under the program CONSOLIDER INGENIO 2010. Support for KVM is
acknowledged from NIAID PO1 AI099783-01, R01 AI111139-01, R01
DK104681-01 and Australian Research Council FT1300100572. The authors
declare no conflict of interest.
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NR 147
TC 90
Z9 97
U1 0
U2 18
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-1702
EI 1872-7492
J9 VIRUS RES
JI Virus Res.
PD JAN 2
PY 2016
VL 212
SI SI
BP 1
EP 11
DI 10.1016/j.virusres.2015.10.002
PG 11
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA DE6VE
UT WOS:000370770900001
PM 26454188
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Fu, YS
Chen, TH
Weng, LB
Huang, LY
Lai, D
Weng, CF
AF Fu, Yaw-Syan
Chen, Ting-Hsu
Weng, Lebin
Huang, Liyue
Lai, Dong
Weng, Ching-Feng
TI Pharmacological properties and underlying mechanisms of curcumin and
prospects in medicinal potential
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Curcumin; Turmeric; Anti-virus; Anti-hyperglycemia; Anti-inflammation;
Anti-oxidation
ID OXIDATIVE STRESS; VIRUS-INFECTION; NATURAL-PRODUCTS; INFLAMMATION;
ACTIVATION; LIVER; CHIKUNGUNYA; ANTICANCER; EXPRESSION; AUTOPHAGY
AB Curcumin, isolated from Curcuma longa L., is a fat-soluble natural compound that can be obtained from ginger plant tuber roots, which accumulative evidences have demonstrated that it can resist viral and microbial infection and has anti-tumor, reduction of blood lipid and blood glucose, antioxidant and removal of free rad-icals, and is active against numerous disorders various chronic diseases including cardiovascular, pulmonary, neurological and autoimmune diseases. In this article is highlighted the recent evidence of curcuminoids applied in sevral aspects of medical problem particular in COVID-19 pandemics. We have searched several literature databases including MEDLINE (PubMed), EMBASE, the Web of Science, Cochrane Library, Google Scholar, and the ClinicalTrials.gov website via using curcumin and medicinal properties as a keyword. All studies published from the time when the database was established to May 2021 was retrieved. This review article summarizes the growing confirmation for the mechanisms related to curcumin's physiological and pharmacological effects with related target proteins interaction via molecular docking. The purpose is to provide deeper insight and un-derstandings of curcumin's medicinal value in the discovery and development of new drugs. Curcumin could be used in the prevention or therapy of cardiovascular disease, respiratory diseases, cancer, neurodegeneration, infection, and inflammation based on cellular biochemical, physiological regulation, infection suppression and immunomodulation.
C1 [Fu, Yaw-Syan; Chen, Ting-Hsu; Weng, Lebin; Huang, Liyue; Weng, Ching-Feng] Xiamen Med Coll, Sch Basic Med, Dept Physiol, Xiamen 361023, Fujian, Peoples R China.
[Lai, Dong] Xiamen Med Coll, Affiliated Hosp 2, Dept Transfus, Xiamen 361021, Fujian, Peoples R China.
C3 Xiamen Medical College; Xiamen Medical College
RP Weng, CF (corresponding author), Xiamen Med Coll, Sch Basic Med, Dept Physiol, Xiamen 361023, Fujian, Peoples R China.
EM yawsyan@gmail.com; 410613031@gms.ndhu.edu.tw; annycat202006@outlook.com;
hly0915@163.com; ld727476@163.com; cfweng@gms.ndhu.edu.tw
OI Chen, Ting-Hsu/0000-0002-5596-3600
FU Xiamen Medical College, Fujian, China [K201903]
FX The financial support received from Xiamen Medical College, Fujian,
China, grant ID: K201903.
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NR 115
TC 114
Z9 118
U1 6
U2 55
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD SEP
PY 2021
VL 141
AR 111888
DI 10.1016/j.biopha.2021.111888
EA JUL 2021
PG 9
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA UM0BV
UT WOS:000693006700006
PM 34237598
OA gold
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Zhang, HY
Liu, Y
Bian, ZL
Huang, SS
Han, XF
You, ZR
Wang, QX
Qiu, DK
Miao, Q
Peng, YS
Li, XY
Invernizzi, P
Ma, X
AF Zhang, Haiyan
Liu, Yuan
Bian, Zhaolian
Huang, Shanshan
Han, Xiaofeng
You, Zhengrui
Wang, Qixia
Qiu, Dekai
Miao, Qi
Peng, Yanshen
Li, Xiaoying
Invernizzi, Pietro
Ma, Xiong
TI The critical role of myeloid-derived suppressor cells and FXR activation
in immune-mediated liver injury
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Autoimmunity; FXR activation; Lymphoid subpopulations; Myeloid-derived
suppressor cells
ID PIR-B; TUMOR PROGRESSION; HEPATOCELLULAR-CARCINOMA; RECEPTOR;
ACCUMULATION; INFLAMMATION; MICE; RESPONSES; EXPRESSION; SUBSETS
AB The immunobiology of FXR has attracted significant attention in immune regulation and innate immunity. We have studied the mechanism of action of FXR activation on two models of acute hepatitis, inflammation mediated by Con A and alpha-GalCer and focused on the interactions of FXR activation and expression of PIR-B, both in vivo and in vitro using luciferase reporter and CHIP assays. In addition, based upon our data, we studied the role of FXR activation on the immunobiology of myeloid-derived suppressor cells (MDSCs). Importantly, we report herein that FXR activation reduces the inflammatory insult induced by either alpha-GalCer or Con A; such treatment expands CD11b(+)Ly6C(+) MDSCs. The protective effect of FXR activation is dependent on expansion of MDSCs, particularly liver CD11b(+)Ly6C(high) cells. Indeed, FXR activation enhances the suppressor function of MDSCs through upregulation of PIR-B by binding the PIR-B promoter. FXR activation drives the accumulation of MDSCs to liver through upregulation of S100A8. FXR activation facilitates homing and function of MDSCs, which function as a critical negative feedback loop in immune-mediated liver injury. The novel mechanisms defined herein emphasize not only the importance of liver lymphoid subpopulations, but also the potential roles of modulating FXR in autoimmune liver disease. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Zhang, Haiyan; Liu, Yuan; Bian, Zhaolian; Huang, Shanshan; Han, Xiaofeng; You, Zhengrui; Wang, Qixia; Qiu, Dekai; Miao, Qi; Peng, Yanshen; Ma, Xiong] Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Digest Dis, Ren Ji Hosp,Div Gastroenterol & Hepatol, Shanghai 200001, Peoples R China.
[Zhang, Haiyan; Liu, Yuan; Bian, Zhaolian; Huang, Shanshan; Han, Xiaofeng; You, Zhengrui; Wang, Qixia; Qiu, Dekai; Miao, Qi; Peng, Yanshen; Ma, Xiong] Shanghai Jiao Tong Univ, Minist Hlth, Key Lab Gastroenterol & Hepatol, Shanghai 200001, Peoples R China.
[Li, Xiaoying] Shanghai Jiao Tong Univ, Shanghai Inst Endocrinol & Metab, Shanghai Clin Ctr Endocrine & Metab Dis, Dept Endocrine & Metab Dis,Ruijin Hosp,Sch Med, Shanghai 200001, Peoples R China.
[Invernizzi, Pietro] Humanitas Clin & Res Ctr, Liver Unit, Milan, Italy.
[Invernizzi, Pietro] Humanitas Clin & Res Ctr, Ctr Autoimmune Liver Dis, Milan, Italy.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University; Shanghai
Jiao Tong University
RP Ma, X (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Digest Dis, Ren Ji Hosp, 145 Shandong Middle Rd, Shanghai 200001, Peoples R China.
EM maxiongmd@hotmail.com
RI Invernizzi, Pietro/AAB-8367-2022; Li, Xianzhi/IUO-5698-2023; Zhang,
Haiyan/KWT-8071-2024; you, zhengrui/JYP-7419-2024
OI Ma, Xiong/0000-0001-9616-4672; Zhang, Haiyan/0009-0002-6401-7090;
Invernizzi, Pietro/0000-0003-3262-1998; you,
zhengrui/0000-0003-0765-5141; Li, Xiaoying/0000-0002-9383-5757
FU National Natural Science Foundation of China [81170380, 81325002,
81100271]; Program of Shanghai Innovative Research Team in Immunity of
Non-viral Liver Diseases; Science and Technology Commission of Shanghai
Municipality [12XD1403300]
FX This work was supported by grants from the National Natural Science
Foundation of China (Nos. 81170380 and 81325002 to X.M., 81100271 to Q.
W.), the Program of Shanghai Innovative Research Team in Immunity of
Non-viral Liver Diseases (to X.M.) and the program of excellent academic
leader from the Science and Technology Commission of Shanghai
Municipality (12XD1403300).
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NR 36
TC 32
Z9 37
U1 1
U2 19
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD SEP
PY 2014
VL 53
BP 55
EP 66
DI 10.1016/j.jaut.2014.02.010
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AQ1HM
UT WOS:000342532500006
PM 24721598
DA 2025-01-07
ER
PT J
AU Gurr, W
Shaw, M
Li, YX
Sherwin, R
AF Gurr, Werner
Shaw, Margaret
Li, Yanxia
Sherwin, Robert
TI RegII is a β-cell protein and autoantigen in diabetes of NOD mice
SO DIABETES
LA English
DT Article
ID REGULATORY T-CELLS; TNF-ALPHA; REGENERATION FACTOR; EXPRESSION; GENE;
PATHWAY; DISEASE; ISLETS; LITHOSTATHINE; PANCREATITIS
AB The Reg family of proteins has been studied in the context of growth and regeneration in several organs including pancreatic islets. We previously suggested that Reg proteins act as autoantigens in type I diabetes, based on evidence that a member of the Reg family (hepatocellular carcinoma intestine pancreas [HIP]/pancreatitis-associated protein [PAP]) was overexpressed in the islets of a patient who died after sudden onset of type 1 diabetes, and that, in NOD mice, Reg-specific T-cells adoptively transferred diabetes. In the current study, we developed antisera to detect individual Reg members in mouse islets and found that RegIII alpha was present in the non-beta-cell portion of the islets, while RegII was predominantly expressed in beta-cells. Vaccination of NOD mice with the separately expressed N-terminal (NtfrII) or C-terminal (CtfrII) portion of RegII revealed a dichotomy: NtfrII vaccination accelerated and CtfrII vaccination delayed type 1 diabetes. Vaccination with CtfrII was more effective when given at later stages in the pathogenesis of type 1 diabetes, a time dependency different from that seen with other antigen-dependent vaccine strategies in NOD mice, which might have therapeutic implications. In conclusion, RegII is a novel beta-cell-derived autoantigen in NOD mice. The autoimmune response against this protein may convert a regenerative into an islet-destructive process accelerating development of type 1 diabetes.
C1 Yale Univ, Sch Med, Endocrinol Sect, New Haven, CT 06520 USA.
C3 Yale University
RP Gurr, W (corresponding author), Yale Univ, Sch Med, Endocrinol Sect, 333 Cedar St, New Haven, CT 06520 USA.
EM werner.gurr@yale.edu
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NR 27
TC 36
Z9 45
U1 0
U2 4
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD JAN
PY 2007
VL 56
IS 1
BP 34
EP 40
DI 10.2337/db06-0669
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 125TY
UT WOS:000243466900006
PM 17192462
OA Bronze
DA 2025-01-07
ER
PT J
AU Zeng, T
Deng, GH
Zhong, WC
Gao, ZW
Ma, SY
Mo, C
Li, YJ
Huang, S
Zhou, CY
Lai, YQ
Xie, SW
Xie, ZP
Chen, YY
He, SQ
Lv, ZP
Gao, L
AF Zeng, Ting
Deng, Guanghui
Zhong, Weichao
Gao, Zhuowei
Ma, Shuoyi
Mo, Chan
Li, Yunjia
Huang, Sha
Zhou, Chuying
Lai, Yuqi
Xie, Shuwen
Xie, Zeping
Chen, Yuyao
He, Songqi
Lv, Zhiping
Gao, Lei
TI Indoleamine 2, 3-dioxygenase 1enhanceshepatocytes ferroptosis in acute
immune hepatitis associated with excess nitrative stress
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Acute immune hepatitis; Ferroptosis; Indoleamine 2; 3-Dioxygenase 1;
Nitrative stress
ID CELL-DEATH; AUTOIMMUNE HEPATITIS; 2,3-DIOXYGENASE; INJURY; INFLAMMATION;
DISEASE; CANCER; LIVER; TOLERANCE; MICE
AB Ferroptosis is a recently recognized form of regulated cell death that is characterized by lipid peroxidation. However, the molecular mechanisms of ferroptosis in acute immune hepatitis (AIH) are largely unknown. In this study, we investigated the classical ferroptotic events in the livers of mice with concanavalin A (ConA) to induce AIH. The dramatically upregulated gene indoleamine 2, 3-dioxygenase 1 (IDO1) was identi fied with AIH, and its role in generation of ferroptosis and reactive nitrogen species (RNS) was assessed both in vitro and in vivo by genetic deletion or pharmacologic inhibition of IDO1. We observed that ferroptosis contributed to the ConA- induced hepatic damage, which was con firmed by the therapeutical e ffects of ferroptosis inhibitor (ferrostatin- 1). Noteworthy, upregulation of hepatic IDO1 and nitrative stress in ConA-induced hepatic damage were also remarkably inhibited by the ferroptosis abolishment. Additionally, IDO1 de ficiency contributed to ferroptosis resistance by activating solute carrier family 7 member 11 (SLC7A11; also known as xCT) expression, accom- panied with the reductions of murine liver lesions and RNS. Meanwhile, IDO inhibitor 1 -methyl tryptophan alleviated murine liver damage with the reduction of inducible nitric oxide synthase and 3-nitrotyrosine ex- pression. Consistent with the results in vivo , hepatocytes-speci fic knockdown of IDO1 led to ferroptosis resistance upon exposure to ferroptosis-inducing compound (Erastin) in vitro , whereas IDO1 overexpression aggravated the classical ferroptotic events, and the RNS stress. Overall, these results revealed a novel molecular mechanism of ferroptosis with the key feature of nitrative stress in ConA-induced liver injury, and also identi fied IDO1-de- pendent ferroptosis as a potential target for the treatment of AIH.
C1 [Zeng, Ting; Deng, Guanghui; Gao, Zhuowei; Mo, Chan; Li, Yunjia; Huang, Sha; Zhou, Chuying; Lai, Yuqi; Xie, Shuwen; Xie, Zeping; Chen, Yuyao; He, Songqi; Lv, Zhiping; Gao, Lei] Southern Med Univ, Sch Tradit Chinese Med, Guangzhou, Guangdong, Peoples R China.
[Zhong, Weichao] Shenzhen Tradit Chinese Med Hosp, 1 Fuhua Rd, Shenzhen, Guangdong, Peoples R China.
[Ma, Shuoyi] South China Univ Technol, Guangzhou First Peoples Hosp, Sch Med, Guangzhou, Guangdong, Peoples R China.
C3 Southern Medical University - China; Shenzhen Traditional Chinese
Medicine Hospital; South China University of Technology
RP He, SQ; Lv, ZP; Gao, L (corresponding author), Southern Med Univ SMU, Sch Tradit Chinese Med, Sha Tai Nan Rd 1063, Guangzhou 510515, Guangdong, Peoples R China.
EM hesongqijz@126.com; lzp48241@126.com; raygaolei@smu.edu.cn
RI li, fangyu/KCY-0521-2024; GAO, LEI/HZJ-6990-2023; mo, chan/HJB-4184-2022
OI Zhiping, Lv/0000-0003-2796-526X; Gao, Lei/0000-0001-9030-390X
FU National Natural Science Foundation of China [81774170, 81603501,
81673774, 81804011]; Natural Science Foundation of Guangdong Province
[2018B030306012]; Science and Technology Planning Project of Guangdong
Province [2014A020221097]; Science and Technology Planning Project of
Guangzhou city [201707010080]; Scientific Research Program of Southern
Medical University [CX2017N001]
FX This work was supported by the National Natural Science Foundation of
China (Grants No. 81774170, 81603501, 81673774 and 81804011), Natural
Science Foundation of Guangdong Province (Grants No. 2018B030306012),
the Science and Technology Planning Project of Guangdong Province
(Grants No. 2014A020221097), the Science and Technology Planning Project
of Guangzhou city (Grants No. 201707010080), and the Scientific Research
Program of Southern Medical University (Grants No. CX2017N001).
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NR 67
TC 51
Z9 54
U1 6
U2 55
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD MAY 20
PY 2020
VL 152
BP 668
EP 679
DI 10.1016/j.freeradbiomed.2020.01.009
PG 12
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA MB9XG
UT WOS:000542950200001
PM 31945497
DA 2025-01-07
ER
PT J
AU Gyurkovska, V
Ivanovska, N
Saso, L
Dimitrova, P
AF Gyurkovska, V.
Ivanovska, N.
Saso, L.
Dimitrova, P.
TI EFFECT OF TYROSINE KINASE INHIBITOR AG-490 ON THE DEVELOPMENT OF ASEPTIC
SHOCK
SO BIOTECHNOLOGY & BIOTECHNOLOGICAL EQUIPMENT
LA English
DT Article
DE hepatocytes; tyrphostin AG-490; SCID mice; zymosan
AB Recently, protein kinase inhibitors are used to limit the uncontrolled immune responses in cancer and autoimmune diseases. Tyrphostin AG-490 is a novel benzylidine malononitrile analogue that inhibits the activity of Janus activation kinase 2 (JAK2). In the present study we investigate the effect of the drug on the development of aseptic shock. The acute inflammation was provoked in mice with severe combined immunodeficiency (SCID) by intraperitoneal injection of 0.8 mg/g body weight of zymosan. Tyrphostin AG-490 was administrated intraperitoneally in a dose of 5 mg/kg. Blood, liver and spleens were collected on day 21 of shock. The white blood cell differential count showed that the percentage of polymorphonuclear cells in peripheral blood was not affected by AG-490 administration. The proportion of blood monocytes increased 2 times in shock mice and returned to the baseline value in AG-490-treated mice. At the late phase of zymosan-induced inflammation SCID mice had enlarged spleens and increased numbers of splenocytes that were significantly reduced by AG-490 administration. Interestingly, the elevated number of hepatocytes and the enhanced ability of hepatocytes to produce nitric oxide (NO) in response to zymosan restimulation in vitro were observed in the group of AG-490-treated mice with shock. These data suggest that the inhibition of JAK2 kinase can stimulate the NO inflammatory pathway in liver when functional T and B cells are missing. Our study has performed an evidence for the decisive role of T and B cells for the resolution of inflammation and cell repair in the liver.
C1 [Gyurkovska, V.; Ivanovska, N.; Dimitrova, P.] Bulgarian Acad Sci, Inst Microbiol, Dept Immunol, Sofia, Bulgaria.
[Saso, L.] Sapienza Univ, Dept Human Physiol & Pharmacol, Rome, Italy.
C3 Bulgarian Academy of Sciences; Medical University Sofia; Sapienza
University Rome
RP Gyurkovska, V (corresponding author), Bulgarian Acad Sci, Inst Microbiol, Dept Immunol, Sofia, Bulgaria.
EM vali_lqs@yahoo.com
RI Dimitrova, Petya/AFW-8031-2022
OI Dimitrova, Petya/0000-0003-0920-3712; Dimitrova,
Albena/0009-0000-6124-607X; gyurkovska, valeriya/0000-0001-6564-0066
FU Reintegration NATO Grant [RIG 982937]
FX This work was supported by a Reintegration NATO Grant RIG 982937
CR Burdelya L, 2005, J IMMUNOL, V174, P3925, DOI 10.4049/jimmunol.174.7.3925
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NR 22
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1310-2818
EI 1314-3530
J9 BIOTECHNOL BIOTEC EQ
JI Biotechnol. Biotechnol. Equip.
PY 2009
VL 23
SU 1
BP 713
EP 717
DI 10.1080/13102818.2009.10818524
PG 5
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA VH2OZ
UT WOS:000451691400174
OA Bronze
DA 2025-01-07
ER
PT J
AU Bian, ZL
Miao, Q
Zhong, W
Zhang, HY
Wang, QX
Peng, YS
Chen, XY
Guo, CJ
Shen, L
Yang, F
Xu, J
Qiu, DK
Fang, JY
Friedman, S
Tang, RQ
Gershwin, ME
Ma, X
AF Bian, Zhaolian
Miao, Qi
Zhong, Wei
Zhang, Haiyan
Wang, Qixia
Peng, Yanshen
Chen, Xiaoyu
Guo, Canjie
Shen, Li
Yang, Fan
Xu, Jie
Qiu, Dekai
Fang, Jingyuan
Friedman, Scott
Tang, Ruqi
Gershwin, M. Eric
Ma, Xiong
TI Treatment of cholestatic fibrosis by altering gene expression of Cthrc1:
Implications for autoimmune and non-autoimmune liver disease
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Hepatic fibrosis; Cholestatic liver fibrosis; Hepatic stellate cell;
Anti-fibrotic treatment; TGF-beta pathway
ID PRIMARY BILIARY-CIRRHOSIS; TRANSFORMING-GROWTH-FACTOR; TRIPLE-HELIX
REPEAT; GASTRIC-CANCER; HEPATIC FIBROGENESIS; COLLAGEN EXPRESSION;
CELLS; PROTEIN; ACTIVATION; IDENTIFICATION
AB Collagen triple helix repeat containing-1 (Cthrc1) is a documented specific inhibitor of TGF-beta. signaling. Based on this observation, we developed the hypothesis that knocking in/knocking out the Cthrc1 gene in murine models of cholestasis would alter the natural history of cholestatic fibrosis. To study this thesis, we studied two murine models of fibrosis, first, common bile duct ligation (CBDL) and second, feeding of 3, 5-diethoxy-carbonyl-1, 4-dihydrocollidine (DDC). In both models, we administered well-defined adenoviral vectors that expressed either Cthrc1 or, alternatively, a short hairpin RNA (shRNA)-targeting Cthrc1 either before or after establishment of fibrosis. Importantly, when Cthrc1 gene expression was enhanced, we noted a significant improvement of hepatic fibrosis, both microscopically and by analysis of fibrotic gene expression. In contrast, when Cthrc1 gene expression was deleted, there was a significant exacerbation of fibrosis. To identify the mechanism of action of these significant effects produced by knocking in/knocking out Cthrc gene expression, we thence studied the interaction of Cthrc1 gene expression using hepatic stellate cells (HSCs) and human LX-2 cells. Importantly, we demonstrate that Cthrc1 is induced by TGF-beta 1 via phospho-Smad3 binding to the promoter with subsequent transcription activation. In addition, we demonstrate that Cthrc1 inhibits TGF-beta signaling by accelerating degradation of phospho-Smad3 through a proteosomal pathway. Importantly, the anti-fibrotic effects can be recapitulated with a truncated fragment of Cthrc1. In conclusion, our findings uncover a critical negative feedback regulatory loop in which TGF-beta 1 induces Cthrc1, which can attenuate fibrosis by accelerating degradation of phospho-Smad3. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Bian, Zhaolian; Miao, Qi; Zhong, Wei; Zhang, Haiyan; Wang, Qixia; Peng, Yanshen; Chen, Xiaoyu; Guo, Canjie; Shen, Li; Yang, Fan; Xu, Jie; Qiu, Dekai; Fang, Jingyuan; Tang, Ruqi; Ma, Xiong] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes,Minist Hl, Key Lab Gastroenterol & Hepatol,Ren Ji Hosp,Shang, Div Gastroenterol & Hepatol,Sch Med,Shanghai Inst, Shanghai 200001, Peoples R China.
[Friedman, Scott] Icahn Sch Med Mt Sinai, Div Liver Dis, New York, NY 10029 USA.
[Gershwin, M. Eric] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
C3 Shanghai Jiao Tong University; Icahn School of Medicine at Mount Sinai;
University of California System; University of California Davis
RP Ma, X (corresponding author), Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes,Minist Hl, Key Lab Gastroenterol & Hepatol,Ren Ji Hosp,Shang, Div Gastroenterol & Hepatol,Sch Med,Shanghai Inst, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.
EM bianzhaolian1998@163.com; miaoqi0730@126.com; rjzhongwei@163.com;
heidi0509@163.com; wqx0221155@126.com; pengyanshen@yahoo.com.cn;
1621508481@qq.com; guocanjie@yahoo.com.cn; shirleypear@126.com;
flyingfish_yf@163.com; jiexu@yahoo.com; qiudekai2008@126.com;
fangjingyuan_new@163.com; scott.friedman@mssm.edu; ruqi_tang@126.com;
megershwin@ucdavis.edu; maxiongmd@hotmail.com
RI FANG, Jing-Yuan/JOZ-1388-2023; liu, yuchen/GYQ-6286-2022; Xu,
Jie/K-3712-2019; Zhang, Haiyan/KWT-8071-2024; Xu, Jie/C-4283-2016
OI Xu, Jie/0000-0001-9163-3898; Ma, Xiong/0000-0001-9616-4672; Zhang,
Haiyan/0009-0002-6401-7090
FU National Natural Science Foundation of China [81170380, 81325002,
81421001, 81400608, 81200309, 81200293, 81100296]; National Institutes
of Health [DK090019, DK56621]; Doctoral Innovation Fund Projects from
Shanghai Jiaotong University School of Medicine [BXJ201321]
FX Financial Support: This work was supported by grants from the National
Natural Science Foundation of China (# 81170380 and # 81325002 to Xiong
Ma, #81421001 to Jingyuan Fang, #81400608 to Ruqi Tang, #81200309 to Wei
Zhong, #81200293 to Qi Miao and # 81100296 to Canjie Guo); National
Institutes of Health grants DK090019 (M. Eric Gershwin) and DK56621
(Scott Friedman); Doctoral Innovation Fund Projects from Shanghai
Jiaotong University School of Medicine BXJ201321 (Zhaolian Bian).
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NR 50
TC 33
Z9 33
U1 4
U2 25
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD SEP
PY 2015
VL 63
BP 76
EP 87
DI 10.1016/j.jaut.2015.07.010
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CS2UM
UT WOS:000361927500008
PM 26238209
OA Green Accepted, Green Submitted
DA 2025-01-07
ER
PT J
AU Figueroa-Sanchez, M
Nuno-Guzman, CM
Alvarez-Lopez, MC
Ordonez-Cardenas, M
Montano-Rodriguez, LJ
AF Figueroa-Sanchez, Mauricio
Nuno-Guzman, Carlos M.
Alvarez-Lopez, M. Carmen
Ordonez-Cardenas, Mariana
Montano-Rodriguez, Leidy J.
TI Case Report: Splanchnic Vein Thrombosis as a Complication of Necrotizing
Acute Pancreatitis in a Pediatric Patient
SO FRONTIERS IN SURGERY
LA English
DT Article
DE splanchnic vein thrombosis; portosplenomesenteric venous thrombosis;
acute pancreatitis; pediatric patients; vascular complications
ID VENOUS THROMBOSIS; ANTICOAGULATION; MANAGEMENT
AB Splanchnic vein thrombosis is an unusual manifestation of venous thromboembolism and includes portal vein thrombosis, mesenteric veins thrombosis, splenic vein thrombosis, and the Budd-Chiari syndrome. The most common risk factors include hematologic and autoimmune disorders, hormonal therapy, liver cirrhosis, solid abdominal cancer, recent abdominal surgery, and abdominal infections or inflammatory conditions, such as pancreatitis. Splanchnic vein thrombosis in acute pancreatitis is most commonly associated with the severe form of the disease and pancreatic necrosis. This report describes a case of splanchnic vein thrombosis as a complication of necrotizing acute pancreatitis in a pediatric patient. Splanchnic vein thrombosis was incidentally detected on contrast-enhanced computed tomography to assess the pancreas. There was no evidence of prior risk factors for the thrombotic condition. The patient was treated with anticoagulation and showed complete resolution after recovery from necrotizing acute pancreatitis, at a 16-month follow-up. The complication of necrotizing acute pancreatitis with splanchnic vein thrombosis in pediatric age is a rare presentation.
C1 [Figueroa-Sanchez, Mauricio; Montano-Rodriguez, Leidy J.] Hosp Civil Guadalajara Fray Antonio Alcalde, Dept Radiol & Imaging, Guadalajara, Mexico.
[Figueroa-Sanchez, Mauricio; Nuno-Guzman, Carlos M.] Univ Guadalajara, Ctr Univ Ciencias Salud, Guadalajara, Mexico.
[Nuno-Guzman, Carlos M.] Hosp Civil Guadalajara Fray Antonio Alcalde, Dept Gen Surg, Guadalajara, Mexico.
[Alvarez-Lopez, M. Carmen; Ordonez-Cardenas, Mariana] Hosp Civil Guadalajara Fray Antonio Alcalde, Dept Pediat Gastroenterol, Guadalajara, Mexico.
C3 Universidad de Guadalajara
RP Nuno-Guzman, CM (corresponding author), Univ Guadalajara, Ctr Univ Ciencias Salud, Guadalajara, Mexico.; Nuno-Guzman, CM (corresponding author), Hosp Civil Guadalajara Fray Antonio Alcalde, Dept Gen Surg, Guadalajara, Mexico.
EM carlosnunoguzman@hotmail.com
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Pant C, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0095552
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Xu WD, 2015, GASTROENT RES PRACT, V2015, DOI 10.1155/2015/245460
NR 31
TC 2
Z9 2
U1 0
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-875X
J9 FRONT SURG
JI Front. Surg.
PD APR 1
PY 2022
VL 9
AR 747671
DI 10.3389/fsurg.2022.747671
PG 6
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA 0W6MV
UT WOS:000789139100001
PM 35433812
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Yoshimura, A
Aki, D
Ito, M
AF Yoshimura, Akihiko
Aki, Daisuke
Ito, Minako
TI SOCS, SPRED, and NR4a: Negative regulators of cytokine signaling and
transcription in immune tolerance
SO PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL
SCIENCES
LA English
DT Review
DE immune tolerance; cytokine signal; regulatory T cells; autoimmunity;
anergy
ID T-CELLS; ACTIVATION; LIVER; CANCER; DIFFERENTIATION; SUPPRESSION;
INHIBITION; DELETION; BINDING; PROTEIN
AB Cytokines are important intercellular communication tools for immunity. Most cytokines utilize the JAK-STAT and Ras-ERK pathways to promote gene transcription and proliferation; however, this signaling is tightly regulated. The suppressor of cytokine signaling (SOCS) family and SPRED family are a representative negative regulators of the JAK-STAT pathway and the Ras-ERK pathway, respectively. The SOCS family regulates the differentiation and function of CD4(+) T cells, CD8(+) T cells, and regulatory T cells, and is involved in immune tolerance, anergy, and exhaustion. SPRED family proteins have been shown to inactivate Ras by recruiting the Ras-GTPase neurofibromatosis type 1 (NF1) protein. Human genetic analysis has shown that SOCS family members are strongly associated with autoimmune diseases, allergies, and tumorigenesis, and SPRED1 is involved in NF1-like syndromes and tumors. We also identified the NR4a family of nuclear receptors as a key transcription factor for immune tolerance that suppresses cytokine expression and induces various immuno-regulatory molecules including SOCS1.
C1 [Yoshimura, Akihiko; Aki, Daisuke] Keio Univ, Dept Microbiol & Immunol, Sch Med, Tokyo, Japan.
[Ito, Minako] Kyushu Univ, Med Inst Bioregulat, Fukuoka, Japan.
C3 Keio University; Kyushu University
RP Yoshimura, A (corresponding author), Keio Univ, Dept Microbiol & Immunol, Sch Med, Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan.
EM yoshimura@keio.jp
FU JSPS KAKENHI [JP17H06175, 17K15667, 19H04817, 19K16618]; AMED-CREST [JP
20gm1110009]; Princess Takamatsu Cancer Research Found; Yasuda Medical
Foundation; Kishimoto Foun-dation; Tomizawa Jun-ichi & Keiko Fund of
Molecular Biology Society of Japan for Young Scientist; Mitsubishi
Foundation; Mochida Memorial Foundation for Medical and Pharmaceutical
Research; Takeda Science Foundation; Uehara Memorial Foundation; Naito
Memorial Foundation; Kanae Foundation; SENSHIN Medical Research
Foundation; Astellas Foundation for Research on Metabolic Disorders, an
Inoue Research Award; Life Science Research Award; Keio Gijuku Academic
Developmental Funds; AMED-PRIME [20gm6210012]; Grants-in-Aid for
Scientific Research [19H04817, 19K16618, 17K15667] Funding Source: KAKEN
FX We would like to thank Mari Ikeda, Yasuko Hirata, and Yukiko Tokifuji
(Keio University) for their technical assistance. This work was
supported by JSPS KAKENHI (S) JP17H06175, 17K15667, 19H04817, and
19K16618, AMED-CREST JP 20gm1110009 grants, AMED-PRIME 20gm6210012,
Princess Takamatsu Cancer Research Found and Yasuda Medical Foundation,
the Kishimoto Foun-dation, the Tomizawa Jun-ichi & Keiko Fund of
Molecular Biology Society of Japan for Young Scientist, The Mitsubishi
Foundation, the Mochida Memorial Foundation for Medical and
Pharmaceutical Research, the Takeda Science Foundation, the Uehara
Memorial Foundation, the Naito Memorial Foundation, the Kanae
Foundation, the SENSHIN Medical Research Foundation, the Astellas
Foundation for Research on Metabolic Disorders, an Inoue Research Award,
a Life Science Research Award, and Keio Gijuku Academic Developmental
Funds.
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NR 117
TC 12
Z9 12
U1 0
U2 9
PU JAPAN ACAD
PI TOKYO
PA 7-32, UENO PARK, TAITO-KU, TOKYO, 110-0007, JAPAN
SN 0386-2208
EI 1349-2896
J9 P JPN ACAD B-PHYS
JI Proc. Jpn. Acad. Ser. B-Phys. Biol. Sci.
PD JUN
PY 2021
VL 97
IS 6
BP 277
EP 291
DI 10.2183/pjab.97.016
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA SR8MN
UT WOS:000661299700001
PM 34121041
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Waddington, KE
Jury, EC
AF Waddington, Kirsty E.
Jury, Elizabeth C.
TI Manipulating membrane lipid profiles to restore T-cell function in
autoimmunity
SO BIOCHEMICAL SOCIETY TRANSACTIONS
LA English
DT Article
DE autoimmunity; cholesterol; glycosphingolipids; lipid rafts; plasma
membrane; T-cells
ID LIVER-X-RECEPTOR; CD4(+) T; RAFTS; ACTIVATION; TRAFFICKING; EXPRESSION;
DIFFERENTIATION; MICRODOMAINS; CHOLESTEROL; GANGLIOSIDE
AB Plasma membrane lipid rafts are heterogeneous cholesterol and glycosphingolipid (GSL)-enriched microdomains, within which the tight packing of cholesterol with the saturated-acyl chains of GSLs creates a region of liquid-order relative to the surrounding disordered membrane. Thus lipid rafts govern the lateral mobility and interaction of membrane proteins and regulate a plethora of signal transduction events, including T-cell antigen receptor (TCR) signalling. The pathways regulating homoeostasis of membrane cholesterol and GSLs are tightly controlled and alteration of these metabolic processes coincides with immune cell dysfunction as is evident in atherosclerosis, cancer and autoimmunity. Indeed, membrane lipid composition is emerging as an important factor influencing the ability of cells to respond appropriately to microenvironmental stimuli. Consequently, there is increasing interest in targeting membrane lipids or their metabolic control as a novel therapeutic approach to modulate immune cell behaviour and our recent work demonstrates that this is a promising strategy in T-cells from patients with the autoimmune disease systemic lupus erythematosus (SLE).
C1 [Waddington, Kirsty E.] UCL, Ctr Clin Pharmacol, London WC1E 6JF, England.
[Waddington, Kirsty E.; Jury, Elizabeth C.] UCL, Ctr Rheumatol, London WC1E 6JF, England.
C3 University of London; University College London; University of London;
University College London
RP Jury, EC (corresponding author), UCL, Ctr Rheumatol, Rayne Bldg,5 Univ St, London WC1E 6JF, England.
EM e.jury@ucl.ac.uk
RI Waddington, Kirsty/AAL-5710-2020
OI Waddington, Kirsty/0000-0001-8762-6548
FU Arthritis Research UK [18106, 19607]; Lupus UK; British Heart Foundation
PhD studentship
FX This work was supported by the Arthritis Research UK [grant numbers
18106 and 19607 (to E.C.J.)]; and the Lupus UK (to E.C.J.); and the
British Heart Foundation PhD studentship (to K.E.W.).
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NR 50
TC 8
Z9 8
U1 0
U2 11
PU PORTLAND PRESS LTD
PI LONDON
PA 5TH FLR, 90 HIGH HOLBORN, LONDON WC1V 6LJ, ENGLAND
SN 0300-5127
EI 1470-8752
J9 BIOCHEM SOC T
JI Biochem. Soc. Trans.
PD AUG
PY 2015
VL 43
BP 745
EP 751
DI 10.1042/BST20150111
PN 4
PG 7
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA CO2QJ
UT WOS:000359001400035
PM 26551723
DA 2025-01-07
ER
PT J
AU Petersen, DMS
Weiss, RM
Hajj, KA
Yerneni, SS
Chaudhary, N
Newby, AN
Arral, ML
Whitehead, KA
AF Petersen, Daria M. Strelkova
Weiss, Ryan M.
Hajj, Khalid A.
Yerneni, Saigopalakrishna S.
Chaudhary, Namit
Newby, Alexandra N.
Arral, Mariah L.
Whitehead, Kathryn A.
TI Branched-Tail Lipid Nanoparticles for Intravenous mRNA Delivery to Lung
Immune, Endothelial, and Alveolar Cells in Mice
SO ADVANCED HEALTHCARE MATERIALS
LA English
DT Article
DE extrahepatocellular; helper lipids; ionizable lipids; IVIS; lipid
nanoparticles; LNPs; lung delivery; mRNA delivery
ID IN-VIVO; SIRNA DELIVERY; OPTIMIZATION; EXPRESSION; EFFICIENCY;
EVOLUTION; GENE
AB Lipid nanoparticles (LNPs) are proven safe and effective delivery systems on a global scale. However, their efficacy has been limited primarily to liver and immune cell targets. To extend the applicability of mRNA drugs, 580 ionizable lipidoids are synthesized and tested for delivery to extrahepatocellular targets. Of these, over 40 enabled protein expression in mice, with the majority transfecting the liver. Beyond the liver, several LNPs containing new, branched-tail ionizable lipidoids potently delivered mRNA to the lungs, with cell-level specificity depending on helper lipid chemistry. Incorporation of the neutral helper lipid 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine (DOPE) at 16 mol% enabled highly specific delivery to natural killer and dendritic cells within the lung. Although inclusion of the cationic lipid 1,2-di-(9Z-octadecenoyl)-3-trimethylammonium-propane (DOTAP) improved lung tropism, it decreased cell specificity, resulting in equal transfection of endothelial and lymphoid cells. DOTAP formulations are also less favorable than DOPE formulations because they elevated liver enzyme and cytokine levels. Together, these data identify a new branched-tailed LNP with a unique ability to selectively transfect lung immune cell populations without the use of toxicity-prone cationic helper lipids. This novel vehicle may unlock RNA therapies for lung diseases associated with immune cell dysregulation, including cancer, viral infections, and autoimmune disorders.
This paper describes several new and efficacious ionizable lipids for mRNA delivery to the liver, spleen, and/or lungs in mice when administered by intravenous injection. The most potent lipid nanoparticles contain branched tails and preferentially targeted natural killer and dendritic cells in the lungs without the use of toxicity-prone cationic lipids such as DOTAP. image
C1 [Petersen, Daria M. Strelkova; Whitehead, Kathryn A.] Carnegie Mellon Univ, Dept Biomed Engn, 5000 Forbes Ave, Pittsburgh, PA 15213 USA.
[Weiss, Ryan M.; Hajj, Khalid A.; Yerneni, Saigopalakrishna S.; Chaudhary, Namit; Newby, Alexandra N.; Arral, Mariah L.; Whitehead, Kathryn A.] Carnegie Mellon Univ, Dept Chem Engn, 5000 Forbes Ave, Pittsburgh, PA 15213 USA.
C3 Carnegie Mellon University; Carnegie Mellon University
RP Whitehead, KA (corresponding author), Carnegie Mellon Univ, Dept Biomed Engn, 5000 Forbes Ave, Pittsburgh, PA 15213 USA.; Whitehead, KA (corresponding author), Carnegie Mellon Univ, Dept Chem Engn, 5000 Forbes Ave, Pittsburgh, PA 15213 USA.
EM kawhite@cmu.edu
RI Whitehead, Kathryn/ABF-3857-2020; Whitehead, Kathryn/G-7001-2012
OI Whitehead, Kathryn/0000-0002-0100-7824
FU Defense Advanced Research Projects Agency (DARPA) [D16AP00143,
HR0011-19-2-0007]; National Institutes of Health (NIH) Award
[DP2-HD098860]; NSF [CHE-0130903, CHE-1039870, CHE-1726525, DGE1745016]
FX This research was funded by Defense Advanced Research Projects Agency
(DARPA) Grant Nos. D16AP00143 and HR0011-19-2-0007 and National
Institutes of Health (NIH) Award No. DP2-HD098860. The NMR
instrumentation at Carnegie Mellon University was partially supported by
the NSF Grant Nos. CHE-0130903, CHE-1039870, and CHE-1726525. M.L.A. was
supported by an NSF Graduate Research Fellowship Program award number
DGE1745016. The authors are thankful to R. Petersen for his feedback on
the manuscript.
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NR 68
TC 1
Z9 1
U1 28
U2 30
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2192-2640
EI 2192-2659
J9 ADV HEALTHC MATER
JI Adv. Healthc. Mater.
PD SEP
PY 2024
VL 13
IS 22
DI 10.1002/adhm.202400225
EA JUL 2024
PG 11
WC Engineering, Biomedical; Nanoscience & Nanotechnology; Materials
Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Science & Technology - Other Topics; Materials Science
GA E6V2R
UT WOS:001259844400001
PM 38888972
DA 2025-01-07
ER
PT J
AU Lee, TK
Gereige, JD
Maglione, PJ
AF Lee, Theodore K.
Gereige, Jessica D.
Maglione, Paul J.
TI State-of-the-art diagnostic evaluation of common variable
immunodeficiency
SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY
LA English
DT Review
ID LUNG-DISEASE; IMMUNE DYSREGULATION; EUROPEAN-SOCIETY; LRBA DEFICIENCY;
CELLS; DISORDERS; CANCER; COMPLICATIONS; AUTOIMMUNE; MANAGEMENT
AB Objective: To summarize the current understanding of diagnostic and postdiagnostic evaluation of common variable immunodeficiency (CVID).
Data Sources: PubMed Central database. Study Selections: Original research articles and review articles from 2015 to 2020 including seminal articles that shaped the diagnostic and postdiagnostic evaluation of CVID were incorporated. This work focuses on initial diagnosis of CVID, genetic evaluations, and postdiagnostic assessment of respiratory, gastrointestinal, and hepatobiliary diseases including spleen and lymph node enlargement.
Results: CVID presents not only with frequent infections but also with noninfectious complications such as auto immunity, gastrointestinal disease, chronic lung disease, granulomas, liver disease, lymphoid hyperplasia, splenomegaly, or malignancy. The risk of morbidity and mortality is higher in patients with CVID and noninfectious complications. Detailed diagnostic approaches, which may incorporate genetic testing, can aid characterization of individual CVID cases and shape treatment in some instances. Moreover, continued evaluation after CVID diagnosis is key to optimal management of this complex disorder. These postdiagnostic evaluations include pulmonary function testing, radiologic studies, and laboratory evaluations that may be conducted at frequencies determined by disease activity.
Conclusion: Although the diagnosis can be achieved similarly in all patients with CVID, those with noninfectious complications have distinct concerns during clinical evaluation. State-of-the-art workup of CVID with noninfectious complications typically includes genetic analysis, which may shape precision therapy, and thoughtful application of postdiagnostic tests that monitor the presence and progression of disease in the myriad of tissues that may be affected. Even with recent advancements, knowledge gaps in diagnosis, prognosis, and treatment of CVID persist, and continued research efforts are needed. (C) 2021 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
C1 [Lee, Theodore K.; Gereige, Jessica D.; Maglione, Paul J.] Boston Univ, Sch Med, Dept Med, Sect Pulm Allergy Sleep & Crit Care Med,Boston Me, Boston, MA 02118 USA.
C3 Boston University
RP Maglione, PJ (corresponding author), Boston Univ, Sch Med, Dept Med, Sect Pulm Allergy Sleep & Crit Care Med,Pulm Ctr, 72 East Concord St,R304, Boston, MA 02118 USA.
EM pmaglion@bu.edu
OI Maglione, Paul J./0000-0001-6805-7271; Gereige,
Jessica/0000-0003-0755-1131
FU National Institute of Allergy and Infectious Diseases [R21AI151486]
Funding Source: NIH RePORTER
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NR 77
TC 23
Z9 23
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1081-1206
EI 1534-4436
J9 ANN ALLERG ASTHMA IM
JI Ann. Allergy Asthma Immunol.
PD JUL
PY 2021
VL 127
IS 1
BP 19
EP 27
DI 10.1016/j.anai.2021.03.005
EA JUN 2021
PG 9
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA SX2PX
UT WOS:000665053500006
PM 33716149
OA Green Accepted, Bronze
DA 2025-01-07
ER
PT J
AU Quinn, MA
Xu, XJ
Ronfani, M
Cidlowski, JA
AF Quinn, Matthew A.
Xu, Xiaojiang
Ronfani, Melania
Cidlowski, John A.
TI Estrogen Deficiency Promotes Hepatic Steatosis via a Glucocorticoid
Receptor-Dependent Mechanism in Mice
SO CELL REPORTS
LA English
DT Article
ID ADIPOSE-TISSUE; FATTY LIVER; AUTOIMMUNE HEPATITIS; GENE-EXPRESSION;
WOMENS HEALTH; KNOCKOUT MICE; BREAST-CANCER; HEART-DISEASE; PPAR-ALPHA;
FSH
AB Glucocorticoids (GCs) are master regulators of systemic metabolism. Intriguingly, Cushing's syndrome, a disorder of excessive GCs, phenocopies several menopause-induced metabolic pathologies. Here, we show that the glucocorticoid receptor (GR) drives steatosis in hypogonadal female mice because hepatocyte-specific GR knockout mice are refractory to developing ovariectomy-induced steatosis. Intriguingly, transcriptional profiling revealed that ovariectomy elicits hepatic GC hypersensitivity globally. Hypogonadism-induced GC hypersensitivity results from a loss of systemic but not hepatic estrogen (E2) signaling, given that hepatocyte-specific E2 receptor deletion does not confer GC hypersensitivity. Mechanistically, enhanced chromatin recruitment and ligand-dependent hyperphosphorylation of GR underlie ovariectomy-induced glucocorticoid hypersensitivity. The dysregulated glucocorticoid-mediated signaling present in hypogonadal females is a product of increased follicle-stimulating hormone (FSH) production because FSH treatment in ovary-intact mice recapitulates glucocorticoid hypersensitivity similar to hypogonadal female mice. Our findings uncover a regulatory axis between estradiol, FSH, and hepatic glucocorticoid receptor signaling that, when disrupted, as in menopause, promotes hepatic steatosis.
C1 [Quinn, Matthew A.; Ronfani, Melania; Cidlowski, John A.] NIEHS, Signal Transduct Lab, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
[Xu, Xiaojiang] NIEHS, Lab Integrat Bioinformat, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Institute of
Environmental Health Sciences (NIEHS); National Institutes of Health
(NIH) - USA; NIH National Institute of Environmental Health Sciences
(NIEHS)
RP Cidlowski, JA (corresponding author), NIEHS, Signal Transduct Lab, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
EM cidlows1@niehs.nih.gov
RI xu, Xiaojiang/AAT-3851-2020; Cidlowski, John/G-2548-2019
OI Xu, Xiaojiang/0000-0001-5758-6581; Cidlowski, John/0000-0003-1420-0516
FU Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences [1ZIAES090057]
FX We would like to acknowledge the NIEHS Epigenomics core for assistance
with RNA sequencing experiments. We thank Dr. Robert Oakley, Dr.
Xiaoling Li, and Dr. Michael Fessler for critical reading of the
manuscript. We would also like to thank the Pathology Support Group at
NIEHS for assistance with histological examinations. This research was
supported by the Intramural Research Program of the NIH, National
Institute of Environmental Health Sciences (1ZIAES090057 to J.A.C.).
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NR 53
TC 63
Z9 68
U1 4
U2 10
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD MAR 6
PY 2018
VL 22
IS 10
BP 2690
EP 2701
DI 10.1016/j.celrep.2018.02.041
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FY7ZI
UT WOS:000427081800018
PM 29514097
OA Green Accepted, gold
DA 2025-01-07
ER
PT J
AU Ergin, AD
Oltulu, C
Türker, NP
Demirbolat, GM
AF Ergin, Ahmet Dogan
Oltulu, Cagatay
Turker, Nebiye Pelin
Demirbolat, Gulen Melike
TI In vitro hepatotoxicity evaluation of methotrexate-loaded niosome
formulation: fabrication, characterization and cell culture studies
SO TURKISH JOURNAL OF MEDICAL SCIENCES
LA English
DT Article
DE Methotrexate; niosomes; hepatotoxicity; oxidative stress; apoptosis
ID INDUCED APOPTOSIS; DELIVERY
AB Background/aim: Methotrexate (MTX) is a folic acid antagonist that is widely used to treat osteosarcoma, leukemia, breast cancer, and autoimmune and inflammatory diseases. The most important concerns with MTX are its poor solubility and high toxicity, particularly in liver cells. To enhance its solubility and to minimize its toxicity, we encapsulated MTX in niosomes and investigated its hepatotoxicity mechanisms using genetic biomarkers.
Materials and methods: Niosomes were successfully prepared using a modified thin film method, and the prepared monodisperse smallsized formulation was subsequently characterized. In vitro cytotoxicity studies were performed both in hepatocarcinoma (HEP3G) and healthy liver (AML12) cell lines. Specifically, immunofluorescence assay and evaluation of the expression levels of apoptotic, antioxidant, heat shock protein, and oxidative stress genes were performed.
Results: The formulation had a particle size of 117.1 +/- 33 nm, a surface charge of -38.41 +/- 0.7 mV, and an encapsulation efficiency of 59.7% +/- 2.3%. The results showed that the niosomal formulation exhibited significantly higher cytotoxic effects in HEP3G than in AML12. The immunofluorescence and genetic analyses showed that the increased cytotoxicity of niosomes resulted mainly from oxidative stress and slight apoptosis.
Conclusion: These results demonstrated that niosomal drug delivery systems could be a new potential formulation for minimizing MTX-related hepatotoxicity.
C1 [Ergin, Ahmet Dogan] Univ Torino, Dept Neurosci, Turin, Italy.
[Ergin, Ahmet Dogan] Trakya Univ, Dept Pharmaceut Technol, Fac Pharm, Edirne, Turkiye.
[Oltulu, Cagatay] Trakya Univ, Dept Pharmaceut Toxicol, Fac Pharm, Edirne, Turkiye.
[Turker, Nebiye Pelin] Trakya Univ, Technol Res Dev Applicat & Res Ctr, Edirne, Turkiye.
[Demirbolat, Gulen Melike] Acibadem Mehmet Ali Aydinlar Univ, Dept Pharmaceut Technol, Fac Pharm, Istanbul, Turkiye.
C3 University of Turin; Trakya University; Trakya University; Trakya
University; Acibadem University
RP Demirbolat, GM (corresponding author), Acibadem Mehmet Ali Aydinlar Univ, Dept Pharmaceut Technol, Fac Pharm, Istanbul, Turkiye.
EM gulenmelikedemir@gmail.com
RI DEMİRBOLAT, Gülen Melike/B-2807-2017; Ergin, Ahmet Dogan/AAO-1876-2021;
Turker, Nebiye/AAH-3197-2021; Oltulu, Cagatay/V-1823-2018
OI TURKER, N.Pelin/0000-0001-6060-3557; DEMIRBOLAT, Gulen
Melike/0000-0001-5621-5818; Oltulu, Cagatay/0000-0002-6051-3479; Ergin,
Ahmet Dogan/0000-0002-9387-0085
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NR 35
TC 1
Z9 1
U1 1
U2 3
PU Tubitak Scientific & Technological Research Council Turkey
PI ANKARA
PA ATATURK BULVARI NO 221, KAVAKLIDERE, TR-06100 ANKARA, TURKIYE
SN 1300-0144
EI 1303-6165
J9 TURK J MED SCI
JI Turk. J. Med. Sci.
PY 2023
VL 53
IS 4
BP 872
EP 882
DI 10.55730/1300-0144.5651
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA IM3T3
UT WOS:001166710900004
PM 38031943
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Haruki, H
Hovius, R
Pedersen, MG
Johnsson, K
AF Haruki, Hirohito
Hovius, Ruud
Pedersen, Miriam Gronlund
Johnsson, Kai
TI Tetrahydrobiopterin Biosynthesis as a Potential Target of the Kynurenine
Pathway Metabolite Xanthurenic Acid
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SEPIAPTERIN REDUCTASE; TRYPTOPHAN-HYDROXYLASE; PLASMA PHENYLALANINE;
BRAIN; INHIBITION; DEGRADATION; TRANSPORT; REVEALS; LIVER
AB Tryptophan metabolites in the kynurenine pathway are up-regulated by pro-inflammatory cytokines or glucocorticoids, and are linked to anti-inflammatory and immunosuppressive activities. In addition, they are up-regulated in pathologies such as cancer, autoimmune diseases, and psychiatric disorders. The molecular mechanisms of how kynurenine pathway metabolites cause these effects are incompletely understood. On the other hand, pro-inflammatory cytokines also up-regulate the amounts of tetrahydrobiopterin (BH4), an enzyme cofactor essential for the synthesis of several neurotransmitter and nitric oxide species. Here we show that xanthurenic acid is a potent inhibitor of sepiapterin reductase (SPR), the final enzyme in de novo BH4 synthesis. The crystal structure of xanthurenic acid bound to the active site of SPR reveals why among all kynurenine pathway metabolites xanthurenic acid is the most potent SPR inhibitor. Our findings suggest that increased xanthurenic acid levels resulting from up-regulation of the kynurenine pathway could attenuate BH4 biosynthesis and BH4-dependent enzymatic reactions, linking two major metabolic pathways known to be highly up-regulated in inflammation.
C1 [Haruki, Hirohito; Hovius, Ruud; Pedersen, Miriam Gronlund; Johnsson, Kai] Ecole Polytech Fed Lausanne, Natl Ctr Competence Res NCCR Chem Biol, Inst Bioengn, Inst Chem Sci & Engn, CH-1015 Lausanne, Switzerland.
C3 Swiss Federal Institutes of Technology Domain; Ecole Polytechnique
Federale de Lausanne
RP Johnsson, K (corresponding author), Ecole Polytech Fed Lausanne, Natl Ctr Competence Res NCCR Chem Biol, Inst Bioengn, Inst Chem Sci & Engn, CH-1015 Lausanne, Switzerland.
EM kai.johnsson@epfl.ch
RI johnsson, kai/P-4222-2014
FU EPFL; Swiss National Science Foundation; NCCR in Chemical Biology
FX This work was supported by the EPFL, the Swiss National Science
Foundation, and the NCCR in Chemical Biology. The authors declare that
they have no conflicts of interest with the contents of this article.
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NR 39
TC 53
Z9 56
U1 1
U2 16
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD JAN 8
PY 2016
VL 291
IS 2
BP 652
EP 657
DI 10.1074/jbc.C115.680488
PG 6
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA DA5GF
UT WOS:000367830500013
PM 26565027
OA Green Published
DA 2025-01-07
ER
PT J
AU Kuttkat, N
Mohs, A
Ohl, K
Hooiveld, G
Longerich, T
Tenbrock, K
Cubero, FJ
Trautwein, C
AF Kuttkat, Nadine
Mohs, Antje
Ohl, Kim
Hooiveld, Guido
Longerich, Thomas
Tenbrock, Klaus
Javier Cubero, Francisco
Trautwein, Christian
TI Hepatic overexpression of cAMP-responsive element modulator a induces a
regulatory T-cell response in a murine model of chronic liver disease
SO GUT
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; IMMUNE-MEDIATED HEPATITIS; RETINOIC ACID;
IL-2 PRODUCTION; HEPATOCELLULAR-CARCINOMA; TH17 CELLS;
HEPATOCARCINOGENESIS; MICE; INFLAMMATION; FIBROSIS
AB Objective Th17 cells are a subset of CD4(+) T-helper cells characterised by interleukin 17 (IL-17) production, a cytokine that plays a crucial role in inflammation-associated diseases. The cyclic AMP-responsive element modulator-alpha (CREM alpha) is a central mediator of T-cell pathogenesis, which contributes to increased IL-17 expression in patients with autoimmune disorders. Since an increased Th17 response is associated with a poor prognosis in patients with chronic liver injury, we investigated the relevance of Th17 cells for chronic liver disease (CLD) and hepatocarcinogenesis.
Design Transgenic mice overexpressing CREM alpha were crossed with hepatocyte-specific Nemo knockout mice (Nemo(Delta hepa)) to generate Nemo(Delta hepa)/CREM alpha(Tg) mice. The impact of CREM alpha(Tg) on CLD progression was examined. Additionally, soft agar colony formation assays, in vitro studies, adoptive transfer of bone marrow-derived cells (BMDCs) and T cells, and gene arrays in T cells were performed.
Results 8-week-old Nemo(Delta hepa)/CREM alpha(Tg) mice presented significantly decreased transaminase levels, concomitant with reduced numbers of CD11b(+) dendritic cells and CD8(+) T cells. CREM alpha(Tg) overexpression in Nemo(Delta hepa) mice was associated with significantly reduced hepatic fibrogenesis and carcinogenesis at 52 weeks. Interestingly, hepatic stellate cell-derived retinoic acid induced a regulatory T-cell (Treg) phenotype in CREM alpha(Tg) hepatic T cells. Moreover, simultaneous adoptive transfer of BMDCs and T cells from CREM alpha(Tg) into Nemo(Delta hepa) mice ameliorated markers of liver injury and hepatitis.
Conclusions Our results demonstrate that overexpression of CREM alpha in T cells changes the inflammatory milieu, attenuating initiation and progression of CLD. Unexpectedly, our study indicates that CREM alpha transgenic T cells shift chronic inflammation in Nemo(Delta hepa) livers towards a protective Treg response.
C1 [Kuttkat, Nadine; Mohs, Antje; Javier Cubero, Francisco; Trautwein, Christian] Univ Hosp RWTH Aachen, Dept Internal Med 3, Pauwelsstr 30, D-52074 Aachen, Germany.
[Ohl, Kim; Tenbrock, Klaus] Univ Hosp RWTH Aachen, Dept Pediat, Aachen, Germany.
[Hooiveld, Guido] Wageningen Univ Res Ctr, Inst Nutr Metab & Genom, Wageningen, Netherlands.
[Longerich, Thomas] RWTH Univ Hosp Aachen, Inst Pathol, Aachen, Germany.
C3 RWTH Aachen University; RWTH Aachen University Hospital; RWTH Aachen
University; RWTH Aachen University Hospital; Wageningen University &
Research; RWTH Aachen University; RWTH Aachen University Hospital
RP Cubero, FJ (corresponding author), Univ Hosp RWTH Aachen, Dept Internal Med 3, Pauwelsstr 30, D-52074 Aachen, Germany.; Trautwein, C (corresponding author), Univ Complutense, Sch Med, Dept Immunol, Plaza Ramon & Cajal S-N, Madrid 28040, Spain.
EM fcubero@ucm.es; ctrautwein@ukaachen.de
RI Tenbrock, Klaus/AEB-8213-2022; Hooiveld, Guido/F-4912-2010
OI Cubero, Francisco Javier/0000-0003-1499-650X; Mohs,
Antje/0000-0001-5937-0696; Hooiveld, Guido/0000-0003-1954-3542
FU IZKF (UKA); IZKF (RWTH Aachen); START-Program of the Faculty of Medicine
(RWTH Aachen) [691405]; DFG [TR 285/10-1]; [SFB \TRR57]
FX This work was supported by the IZKF (UKA, RWTH Aachen), the SFB \TRR57
and the START-Program of the Faculty of Medicine (#691405, RWTH Aachen)
DFG grant (TR 285/10-1).
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NR 41
TC 10
Z9 10
U1 0
U2 19
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD MAY
PY 2017
VL 66
IS 5
BP 908
EP 919
DI 10.1136/gutjnl-2015-311119
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ER1QH
UT WOS:000398566800017
PM 27686093
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Suzuki, G
Izumi, S
Hakoda, M
Takahashi, N
AF Suzuki, G
Izumi, S
Hakoda, M
Takahashi, N
TI LTA 252G allele containing haplotype block is associated with
high serum C-reactive protein levels
SO ATHEROSCLEROSIS
LA English
DT Article
DE inflammation; interleukins; risk factors; atherosclerosis; genetics
ID CORONARY-HEART-DISEASE; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION;
CHLAMYDIA-PNEUMONIAE; LYMPHOTOXIN-ALPHA; RISK; GENE; INFLAMMATION;
STRESS; ATHEROSCLEROSIS
AB C-reactive protein (CRP), an inflammatory biomarker, is a predictor of future risk for cardiovascular disease. Hypothetically, the levels of inflammatory response to microbial and lifestyle-related factors are influenced by genetic factors. LT-alpha. is a proinflammatory cytokine that plays an important role in the pathogenesis of atherosclerosis in mice. We examined the association between gene polymorphism of the LT-alpha coding gene, LTA A252G, and CRP based on a case-control study. The top 149 and bottom 151 subjects in terms of CRP levels were selected for genotyping from among 1000 A-bomb survivors free from acute infection, chronic liver diseases, uremia, autoimmune diseases, and cancers. The genotype of LTA was determined by fluorescence resonance energy transfer-polymerase chain reaction (FRET-PCR) and subsequent melting curve analysis. The values of traditional risk factors such as body mass index (BMI), white blood cell (WBC) Count, hemoglobin (Hb) concentration, and glycated Hb (HbA1c) differed significantly between the low and high CRP groups. After adjusting for the effect of sex, age, BMI, WBC, Hb, and HbA1c, the LTA 252G allele was found to be associated with high CRP levels (odds ratio = 1.93, P = 0.007) by multiple logistic regression analysis. Thus, CRP levels are influenced not only by environmental factors but also by the polymorphism, of LTA or other genes in the same haplotype block. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
C1 Radiat Effects Res Fdn, Dept Clin Studies, Minami Ku, Hiroshima 7320815, Japan.
Radiat Effects Res Fdn, Dept Stat, Minami Ku, Hiroshima 7320815, Japan.
Radiat Effects Res Fdn, Dept Genet, Minami Ku, Hiroshima 7320815, Japan.
C3 Radiation Effects Research Foundation - Japan; Radiation Effects
Research Foundation - Japan; Radiation Effects Research Foundation -
Japan
RP Suzuki, G (corresponding author), Radiat Effects Res Fdn, Dept Clin Studies, Minami Ku, 5-2 Hijiyama Pk, Hiroshima 7320815, Japan.
EM gsuzuki@rerf.or.jp
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NR 22
TC 17
Z9 21
U1 0
U2 2
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0021-9150
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD SEP
PY 2004
VL 176
IS 1
BP 91
EP 94
DI 10.1016/j.atherosclerosis.2003.12.013
PG 4
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA 869FJ
UT WOS:000224968500011
PM 15306179
DA 2025-01-07
ER
PT J
AU Kiriyama, Y
Nochi, H
AF Kiriyama, Yoshimitsu
Nochi, Hiromi
TI The Role of Gut Microbiota-Derived Lithocholic Acid, Deoxycholic Acid
and Their Derivatives on the Function and Differentiation of Immune
Cells
SO MICROORGANISMS
LA English
DT Review
DE bile acids; DCA; LCA; isoalloLCA; isoDCA; FXR; ROR gamma t; FOXP3; TGR5;
Th1; Th17; Treg
ID BILE-SALT BIOTRANSFORMATIONS; T-CELLS; HYDROLASE ACTIVITY; NUCLEAR
RECEPTOR; MECHANISM; TH17; INHIBITION; INDUCTION; TOLERANCE; BETA
AB A wide variety and large number of bacterial species live in the gut, forming the gut microbiota. Gut microbiota not only coexist harmoniously with their hosts, but they also induce significant effects on each other. The composition of the gut microbiota can be changed due to environmental factors such as diet and antibiotic intake. In contrast, alterations in the composition of the gut microbiota have been reported in a variety of diseases, including intestinal, allergic, and autoimmune diseases and cancer. The gut microbiota metabolize exogenous dietary components ingested from outside the body to produce short-chain fatty acids (SCFAs) and amino acid metabolites. Unlike SCFAs and amino acid metabolites, the source of bile acids (BAs) produced by the gut microbiota is endogenous BAs from the liver. The gut microbiota metabolize BAs to generate secondary bile acids, such as lithocholic acid (LCA), deoxycholic acid (DCA), and their derivatives, which have recently been shown to play important roles in immune cells. This review focuses on current knowledge of the role of LCA, DCA, and their derivatives on immune cells.
C1 [Kiriyama, Yoshimitsu; Nochi, Hiromi] Tokushima Bunri Univ, Kagawa Sch Pharmaceut Sci, Sanuki 7692193, Japan.
[Kiriyama, Yoshimitsu] Tokushima Bunri Univ, Inst Neurosci, Sanuki 7692193, Japan.
C3 Tokushima Bunri University; Tokushima Bunri University
RP Kiriyama, Y (corresponding author), Tokushima Bunri Univ, Kagawa Sch Pharmaceut Sci, Sanuki 7692193, Japan.; Kiriyama, Y (corresponding author), Tokushima Bunri Univ, Inst Neurosci, Sanuki 7692193, Japan.
EM kiriyamay@kph.bunri-u.ac.jp; nochi@kph.bunri-u.ac.jp
OI , Yoshimitsu/0000-0002-7653-483X; Nochi, Hiromi/0000-0003-2352-8716
FU Tokushima Bunri University
FX No Statement Available
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NR 101
TC 8
Z9 8
U1 7
U2 20
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-2607
J9 MICROORGANISMS
JI Microorganisms
PD NOV
PY 2023
VL 11
IS 11
AR 2730
DI 10.3390/microorganisms11112730
PG 14
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA CE1S2
UT WOS:001123486800001
PM 38004742
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Madan, K
Madan, M
Sharma, S
Paliwal, S
AF Madan, Kirtika
Madan, Mansi
Sharma, Swapnil
Paliwal, Sarvesh
TI Chitinases: Therapeutic Scaffolds for Allergy and Inflammation
SO RECENT PATENTS ON INFLAMMATION & ALLERGY DRUG DISCOVERY
LA English
DT Review
DE Acidic Mammalian Chitinases (AMCase); allergy; allosamidin (Allo);
chitinases; chitotriosidase (CHIT1); inflammatory disorders
ID PLASMA CHITOTRIOSIDASE ACTIVITY; ACIDIC MAMMALIAN CHITINASE; DISEASE;
PROTEINS; PURIFICATION; INHIBITORS; SERUM; GENE; IDENTIFICATION;
ASSOCIATION
AB Background: Chitinases are the evolutionary conserved glycosidic enzymes that are characterized by their ability to cleave the naturally abundant polysaccharide chitin. The potential role of chitinases has been identified in the manifestation of various allergies and inflammatory diseases. In recent years, chitinases inhibitors are emerging as an alluring area of interest for the researchers and scientists and there is a dire need for the development of potential and safe chitinase antagonists for the prophylaxis and treatment of several diseases.
Objective: The present review expedites the role of chitinases and their inhibitors in inflammation and related disorders.
Methods: At first, an exhaustive survey of literature and various patents available related to chitinases were carried out. Useful information on chitinases and their inhibitor was gathered from the authentic scientific databases namely SCOPUS, EMBASE, PUBMED, GOOGLE SCHOLAR, MEDLINE, EMBASE, EBSCO, WEB OF SCIENCE, etc. This information was further analyzed and compiled up to prepare the framework of the review article. The search strategy was conducted by using queries with key terms " chitin", "chitinase", "chitotrisidase", "acidic mammalian chitinase", "chitinase inhibitors", "asthma" and "chitinases associated inflammatory disorders", etc. The patents were searched using the key terms "chitinases and uses thereof", "chitinase inhibitors", "chitin-chitinase associated pathological disorders" etc. from www.google.com/patents, www.freepatentsonline.com, and www-scopus-com.a8.sjuku.top.
Results: The present review provides a vision for apprehending human chitinases and their participation in several diseases. The patents available also signify the extended role and effectiveness of chitinase inhibitors in the prevention and treatment of various diseases viz. asthma, acute and chronic inflammatory diseases, autoimmune diseases, dental diseases, neurologic diseases, metabolic diseases, liver diseases, polycystic ovary syndrome, endometriosis, and cancer. In this regard, extensive pre-clinical and clinical investigations are required to develop some novel, potent and selective drug molecules for the treatment of various inflammatory diseases, allergies and cancers in the foreseeable future.
Conclusion: In conclusion, chitinases can be used as potential biomarkers in prognosis and diagnosis of several inflammatory diseases and allergies and the design of novel chitinase inhibitors may act as key and rational scaffolds in designing some novel therapeutic agents in the treatment of variety of inflammatory diseases.
C1 [Madan, Kirtika; Sharma, Swapnil; Paliwal, Sarvesh] Banasthali Vidyapith, Dept Pharm, Banasthali 304022, Rajasthan, India.
[Madan, Mansi] Dr Ulhas Patil Med Coll & Hosp, Jalgaon 425309, Maharashtra, India.
C3 Banasthali Vidyapith
RP Sharma, S (corresponding author), Banasthali Univ, Dept Pharm, PO Banasthali Vidyapith, Banasthali 304022, Rajasthan, India.
EM skspharmacology@gmail.com
RI Paliwal, Sarvesh/GQQ-1555-2022; Sharma, Swapnil/AAV-4850-2020
OI paliwal, sarvesh/0000-0002-5247-2021; Sharma,
Swapnil/0000-0003-2639-7096
FU Indian Council of Medical Research (ICMR), India [45/74/2018/PHA/BMS/OL]
FX Authors are grateful to Indian Council of Medical Research (ICMR),
India, (45/74/2018/PHA/BMS/OL) for providing the financial support.
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NR 105
TC 6
Z9 8
U1 5
U2 14
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1872-213X
EI 2212-2710
J9 RECENT PATENTS INFLA
JI Recent Patents Inflamm. Allergy Drug Discov.
PY 2020
VL 14
IS 1
BP 46
EP 57
DI 10.2174/1872213X14666200114184054
PG 12
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA KY6LP
UT WOS:000522685000004
PM 31934842
OA Green Published
DA 2025-01-07
ER
PT J
AU Floranovic, MP
Velickovic, LJ
AF Floranovic, Milena Potic
Velickovic, Ljubinka Jankovic
TI Effect of CXCL12 and Its Receptors on Unpredictable Renal Cell Carcinoma
SO CLINICAL GENITOURINARY CANCER
LA English
DT Review
DE Chemokine signaling; CXCR4; CXCR7; Immunochemistry; Prognosis
ID CHEMOKINE RECEPTOR; CXCR4 EXPRESSION; CANCER; HYPOXIA; SDF-1;
HIF-1-ALPHA; METASTASIS; ADHESION; THERAPY; GROWTH
AB Chemokines are chemotactic cytokines that participate in numerous cell functions during hematopoiesis, morphogenesis, inflammation, neovascularization, and autoimmune diseases and cancer. They achieve their functions on binding to their G protein-coupled receptors. CXCL12, or stromal cell-derived factor-1, is a homeostatic chemokine secreted by fibroblasts, macrophages, and endothelial cells. It binds to CXC receptor 4 (CXCR4), also known as fusin (CD184), and alternate CXC receptor 7 (CXCR7), also known as atypical chemokine receptor 3. The CXCL12/CXCR4 axis participates in homing of hematopoietic stem cells and the development and production of B and T lymphocytes, plasmacytoid dendritic cells, and natural killer cells. It has been examined in > 20 different malignancies. CXCL12 plays an important role in tumor metastasis because it mediates the migration of tumor cells through the endothelial vessel wall and extracellular matrix. Its expression has been highest in common metastatic sites such as the brain, bone marrow, lymph nodes, and liver. CXCR4 is expressed by tumor cells in prostate, breast, lung, and other malignancies. Numerous studies have shown its correlation with a poor prognosis, recurrence-free survival, and poor overall survival. The present review has addressed the structure and function of CXCL12 and its receptors and the effect CXCL12/CXCR4 axis has on the pathogenesis and clinical development of renal cell carcinoma, one of the most aggressive cancers in urology, with limited therapeutic options.
C1 [Floranovic, Milena Potic] Univ Nis, Fac Med, Sci Res Ctr Biomed, Zoran Djindjic Blvd 81, Nish 18000, Serbia.
[Velickovic, Ljubinka Jankovic] Clin Ctr Nis, Pathol & Pathol Anat Ctr, Nish, Serbia.
C3 University of Nis
RP Floranovic, MP (corresponding author), Univ Nis, Fac Med, Sci Res Ctr Biomed, Zoran Djindjic Blvd 81, Nish 18000, Serbia.
EM milenapotic@yahoo.com
OI Potic Floranovic, Milena/0000-0003-1002-8296
FU Ministry of Education and Science of the Republic of Serbia [175092]
FX The present study was supported by the Ministry of Education and Science
of the Republic of Serbia (grant 175092).
CR [Anonymous], 2011, J CLIN ONCOL S
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NR 62
TC 21
Z9 23
U1 0
U2 6
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1558-7673
EI 1938-0682
J9 CLIN GENITOURIN CANC
JI Clin. Genitourin. Cancer
PD AUG
PY 2020
VL 18
IS 4
BP E337
EP E342
DI 10.1016/j.clgc.2019.11.004
PG 6
WC Oncology; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Urology & Nephrology
GA MV3QV
UT WOS:000556276800014
PM 31882334
DA 2025-01-07
ER
PT J
AU Yoshimura, N
Okajima, H
Ushigome, H
Sakamoto, S
Fujiki, M
Okamoto, M
AF Yoshimura, Norio
Okajima, Hideaki
Ushigome, Hidetaka
Sakamoto, Seisuke
Fujiki, Masato
Okamoto, Masahiko
TI Current status of organ transplantation in Japan and worldwide
SO SURGERY TODAY
LA English
DT Review
DE Organ transplantation; Deceased donor; Immunosuppression
ID PRIMARY BILIARY-CIRRHOSIS; DONOR LIVER-TRANSPLANTATION; HEPATITIS-C
VIRUS; PANCREATIC ALLOGRAFT THROMBOSIS; MESENTERIC VENOUS THROMBOSIS;
SUCCESSFUL SURGICAL SALVAGE; HEPATOCELLULAR-CARCINOMA; INTESTINAL
TRANSPLANTATION; LIVING DONOR; KIDNEY-TRANSPLANTATION
AB Recent advances in immunosuppressant therapy have dramatically reduced the frequency of acute rejection of organ transplants. Subsequently, the short-term graft survival rate has been improved, and ABO blood type-incompatible and existing anti-HLA antibody-positive kidney transplantation has been enabled, which has increased the availability of living kidney donors. Japan has a unique history and strategies of liver transplantation (LT) for various liver diseases. The outcomes of living donor liver transplantation (LDLT) in Japan is comparable to that of deceased donor liver transplantation (DDLT) in Western countries despite the relatively short history of LT. The main disadvantage of LT in Japan is donor shortage mainly due to the small number of available deceased donors. There are some disadvantages with LDLT in autoimmune liver diseases because of the dependence on blood relative donors. The first brain-dead pancreas transplantation (PTx) was performed in 2000. Since that time, 42 brain-dead PTx, 2 non-heart beating PTx, and 14 living donor PTx had been performed by the end of 2007. One of the 44 recipients of deceased donor PTx died of unknown causes 11 months after transplantation. Although most of the deceased donors in Japan were marginal and their condition was not favorable, the results of these cases were comparable to those of Western countries. Fourteen intestinal transplantations (ITx) had been performed by the end of 2007 in four transplant centers. There were 3 deceased donor and 11 live donor transplants. The original diseases included short bowel syndrome (n = 6), intestinal function disorder (n = 6), and retransplantation (n = 2). The graft and patient survival rate are 60% and 69%, respectively. Eight recipients survived and stopped parenteral nutrition with full-functioning grafts. Amendment of the Japanese law for the utilization of deceased donors should increase the number available donors in the future.
C1 [Yoshimura, Norio; Okajima, Hideaki; Ushigome, Hidetaka; Sakamoto, Seisuke; Fujiki, Masato; Okamoto, Masahiko] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Organ Transplant & Regenerat Surg, Kamigyo Ku, Kyoto 6020841, Japan.
[Yoshimura, Norio; Fujiki, Masato; Okamoto, Masahiko] Kyoto Prefectural Univ Med, Dept Organ Interact Res Med, Kyoto 6020841, Japan.
[Sakamoto, Seisuke] Natl Ctr Child Hlth & Dev, Dept Transplant Surg, Tokyo, Japan.
[Fujiki, Masato] Cleveland Clin, Dept Gen Surg, Transplantat Ctr, Cleveland, OH 44106 USA.
C3 Kyoto Prefectural University of Medicine; Kyoto Prefectural University
of Medicine; National Center for Child Health & Development - Japan;
Cleveland Clinic Foundation
RP Yoshimura, N (corresponding author), Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Organ Transplant & Regenerat Surg, Kamigyo Ku, 465 Hirokoji Kawaramachi, Kyoto 6020841, Japan.
RI Fujiki, Masato/ABB-8738-2021
OI Fujiki, Masato/0000-0002-1118-0081
FU Japanese Society for Intestinal Transplantation
FX The author of this section thanks the members of the working group for
clinical intestinal transplantation, supported by the Japanese Society
for Intestinal Transplantation, especially Takehisa Ueno MD and Motoshi
Wada MD.
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NR 59
TC 27
Z9 30
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0941-1291
EI 1436-2813
J9 SURG TODAY
JI Surg. Today
PD JUN
PY 2010
VL 40
IS 6
BP 514
EP 525
DI 10.1007/s00595-009-4214-3
PG 12
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA 600CC
UT WOS:000277959900005
PM 20496132
DA 2025-01-07
ER
PT J
AU Mukherjee, S
Patra, R
Behzadi, P
Masotti, A
Paolini, A
Sarshar, M
AF Mukherjee, Suprabhat
Patra, Ritwik
Behzadi, Payam
Masotti, Andrea
Paolini, Alessandro
Sarshar, Meysam
TI Toll-like receptor-guided therapeutic intervention of human cancers:
molecular and immunological perspectives
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE toll-like receptors (TLRs); human cancers; therapeutic interventions;
immunotherapy; chemotherapy; agonists; antagonists
ID NF-KAPPA-B; PLASMACYTOID DENDRITIC CELLS; WORLD-HEALTH-ORGANIZATION;
BACILLUS-CALMETTE-GUERIN; HEPATOCELLULAR-CARCINOMA; TUMOR
MICROENVIRONMENT; COLORECTAL-CANCER; GASTRIC-CANCER; X-CHROMOSOME;
INFLAMMATORY RESPONSES
AB Toll-like receptors (TLRs) serve as the body's first line of defense, recognizing both pathogen-expressed molecules and host-derived molecules released from damaged or dying cells. The wide distribution of different cell types, ranging from epithelial to immune cells, highlights the crucial roles of TLRs in linking innate and adaptive immunity. Upon stimulation, TLRs binding mediates the expression of several adapter proteins and downstream kinases, that lead to the induction of several other signaling molecules such as key pro-inflammatory mediators. Indeed, extraordinary progress in immunobiological research has suggested that TLRs could represent promising targets for the therapeutic intervention of inflammation-associated diseases, autoimmune diseases, microbial infections as well as human cancers. So far, for the prevention and possible treatment of inflammatory diseases, various TLR antagonists/inhibitors have shown to be efficacious at several stages from pre-clinical evaluation to clinical trials. Therefore, the fascinating role of TLRs in modulating the human immune responses at innate as well as adaptive levels directed the scientists to opt for these immune sensor proteins as suitable targets for developing chemotherapeutics and immunotherapeutics against cancer. Hitherto, several TLR-targeting small molecules (e.g., Pam3CSK4, Poly (I:C), Poly (A:U)), chemical compounds, phytocompounds (e.g., Curcumin), peptides, and antibodies have been found to confer protection against several types of cancers. However, administration of inappropriate doses of such TLR-modulating therapeutics or a wrong infusion administration is reported to induce detrimental outcomes. This review summarizes the current findings on the molecular and structural biology of TLRs and gives an overview of the potency and promises of TLR-directed therapeutic strategies against cancers by discussing the findings from established and pipeline discoveries.
C1 [Mukherjee, Suprabhat; Patra, Ritwik] Kazi Nazrul Univ, Dept Anim Sci, Integrat Biochem & Immunol Lab, Asansol, West Bengal, India.
[Behzadi, Payam] Islamic Azad Univ, Dept Microbiol, Shahr E Qods Branch, Tehran, Iran.
[Masotti, Andrea; Paolini, Alessandro; Sarshar, Meysam] Bambino Gesu Childrens Hosp IRCCS, Res Labs, Rome, Italy.
C3 Islamic Azad University; IRCCS Bambino Gesu
RP Mukherjee, S (corresponding author), Kazi Nazrul Univ, Dept Anim Sci, Integrat Biochem & Immunol Lab, Asansol, West Bengal, India.; Behzadi, P (corresponding author), Islamic Azad Univ, Dept Microbiol, Shahr E Qods Branch, Tehran, Iran.; Sarshar, M (corresponding author), Bambino Gesu Childrens Hosp IRCCS, Res Labs, Rome, Italy.
EM suprabhat.mukherjee@knu.ac.in; behzadipayam@yahoo.com;
meysam.sarshar@uniroma1.it
RI BEHZADI, Payam/GPW-6289-2022; Patra, Ritwik/AAN-7386-2021; Sarshar,
Meysam/K-4347-2018; Paolini, Alessandro/H-2905-2016
OI Sarshar, Meysam/0000-0002-5726-2090; Paolini,
Alessandro/0000-0003-4354-9100; Patra, Ritwik/0000-0003-1450-1589
FU DST-SERB-CRG; Italian Ministry of Health with Current Research funds [5
x 1,000, SG-2018-12365432]; Italian Ministry of Health
FX SM and RP acknowledge DST-SERB-CRG, Govt. of India (Sanction no.
CRG/2021/002605) for awarding the research grant to SM and Junior
Research Fellowship to RP. This work was supported by the Italian
Ministry of Health with Current Research funds. We would also like to
thank the Italian Ministry of Health for funding (Ricerca 5 x 1,000 to
AM and AP and Ricerca Finalizzata Starting Grant SG-2018-12365432 to
MS).
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NR 349
TC 40
Z9 43
U1 3
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 26
PY 2023
VL 14
AR 1244345
DI 10.3389/fimmu.2023.1244345
PG 33
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA T4WM8
UT WOS:001078007600001
PM 37822929
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Gürses, D
Akpinar, F
Dogan, M
AF Gurses, Dolunay
Akpinar, Funda
Dogan, Mustafa
TI Mean Platelet Volume and the Ratio of Mean Platelet Volume/Platelet
Count in Acute Rheumatic Fever
SO JOURNAL OF PEDIATRIC RESEARCH
LA English
DT Article
DE Acute rheumatic fever; mean platelet volume; platelet count
ID PARAMETERS; CHILDREN; DISEASE
AB Aim: Acute rheumatic fever (ARF) is an endemic disease especially in developing countries. Due to an autoimmune response to group B streptococcus throat infection, ARF develops in susceptible children. Mean platelet volume (MPV) reflects the platelet size and the rate of platelet production. It is important in cardiovascular events and rheumatic diseases. The MPV/platelet count ratio was determined to be more sensitive than MPV alone in patients with hepatocellular carcinoma, deep vein thrombosis and myocardial infarction. The aim of this study was to investigate changes in MPV and the MPV/platelet count ratio during the active and remission periods of ARF compared with healthy subjects.
Materials and Methods: This study population consisted with 70 ARF patients and 70 age and gender matched healthy controls. In all subjects, complete blood count; including haemoglobin, white blood cell count (WBC), platelet count, MPV and C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were measured during the active stage and during the remission period and compared with healthy individuals.
Results: There was no statistically significant difference between the ARF and control groups in terms of the sex and age (p>0.05). Forty-one patients in the ARF group had carditis. The ARF patients in the active stage had significantly higher WBC, CRP and ESR values (p<0.05). Although no significant difference was observed in MPV between the groups (p>0.05); the MPV/platelet count ratio was low during the active stage but increased during the remission period and reached the same values as the healthy controls (p<0.001).
Conclusion: We did not find any relationship between MPV and ARF. However, a decreased MPV/platelet count ratio was detected during the active stage of ARF. The present findings emphasize the association between the MPV/platelet count ratio and ARF. The MPV/platelet count ratio may be used to determine the activity of ARF.
C1 [Gurses, Dolunay] Pamukkale Univ, Dept Pediat Cardiol, Fac Med, Denizli, Turkey.
[Akpinar, Funda] Ankara Univ, Dept Dev & Behav Pediat, Fac Med, Ankara, Turkey.
[Dogan, Mustafa] Avcilar Hosp, Clin Child Hlth & Dis, Istanbul, Turkey.
C3 Pamukkale University; Ankara University
RP Akpinar, F (corresponding author), Ankara Univ, Dept Dev & Behav Pediat, Fac Med, Ankara, Turkey.
EM fundaozgurler@gmail.com
RI Akpinar, Funda/GSE-3820-2022
OI Dogan, MUSTAFA/0000-0001-5799-426X; Akpinar, Funda/0000-0002-4624-1382
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who, 2004, WHO TECH REP SER, V923, P1
NR 24
TC 0
Z9 0
U1 1
U2 9
PU GALENOS YAYINCILIK
PI FINDIKZADE
PA MOLLA GURANI MAHALLESI KACAMAK SOKAK NO 21, FINDIKZADE, ISTANBUL 34093,
TURKEY
SN 2147-9445
J9 J PEDIATR RES
JI J. Pediatr. Res.
PD JUN
PY 2021
VL 8
IS 2
BP 176
EP 180
DI 10.4274/jpr.galenos.2020.57614
PG 5
WC Pediatrics
WE Emerging Sources Citation Index (ESCI)
SC Pediatrics
GA SK2MY
UT WOS:000656055300012
OA gold
DA 2025-01-07
ER
PT J
AU Lankarani, KB
Honarvar, B
Seif, MA
Anushiravani, A
Nikeghbalian, S
Motazedian, N
Janghorban, P
Foroutanifard, E
Akbari, M
Malekhosseini, SA
AF Lankarani, Kamran Bagheri
Honarvar, Behnam
Seif, Mozhgan Assadat
Anushiravani, Amir
Nikeghbalian, Saman
Motazedian, Nasrin
Janghorban, Parisa
Foroutanifard, Elaheh
Akbari, Maryam
Malekhosseini, Sayed Ali
TI Outcome of Liver Transplant Patients With Intraoperative-Detected Portal
Vein Thrombosis: A Retrospective Cohort Study in Shiraz, Iran
SO EXPERIMENTAL AND CLINICAL TRANSPLANTATION
LA English
DT Article
DE Hazards model; Model for End-Stage Liver Disease score; Mortality;
Survival
ID RISK-FACTORS; EXPERIENCE
AB Objectives: We aimed to determine outcomes and predictors of intraoperative-detected portal vein thrombosis in liver transplant recipients.
Materials and Methods: We retrospectively analyzed 806 adult liver transplant recipients from Shiraz, Iran, to determine those with intraoperative-detected portal vein thrombosis. Patients with this complication were compared with age- and sex-matched patients without this complication. Background diseases, surgery parameters, hospital admission, reoperation, rethrombosis, acute rejection, and use of anticoagulants were assessed. Cox proportional hazards, logistic regression, and random classification forest and random survival forest plots were used for data analyses.
Results: Mean age of patients was 44.7 +/- 13.2 years. Patients with intraoperative-detected portal vein thrombosis (n = 91; 11.3%) had mortality ratio of 2.9 (range, 1.0-8.6) and 2- year survival of 78% versus 2-year survival rate of 92% in patients without this disease. Median time of survival in patients with this complication who died was 2 weeks versus 10 months in patients who died and did not have this complication. Random classification forest plots showed that high fasting blood sugar, autoimmune hepatitis, low prothrombin time, and cryptogenic cirrhosis were (in order) the main predictors of this complication. Random survival forest plots revealed that low prothrombin time, having intraoperative- detected portal vein thrombosis, Model for End Stage Liver Disease score, primary sclerosing cholangitis, diabetes mellitus, and hepatocellular carcinoma were (in order) the main predictors of death in liver transplant recipients. Low body mass index was associated with mortality in patients with intraoperative-detected portal vein thrombosis (by Cox proportional hazards).
Conclusions: One of every 9 liver transplant patients had intraoperative-detected portal vein thrombosis. Hazard of death was 2.9, and death occurred far earlier in patients with this complication. Improvements in diabetes mellitus care, prothrombin time, Model for End-Stage Liver Disease score, and body mass index may improve outcomes of these patients.
C1 [Lankarani, Kamran Bagheri; Honarvar, Behnam; Foroutanifard, Elaheh; Akbari, Maryam] Shiraz Univ Med Sci, Hlth Policy Res Ctr, Inst Hlth, POB 71348532135, Shiraz, Iran.
[Seif, Mozhgan Assadat] Shiraz Univ Med Sci, Dept Epidemiol, Sch Hlth, Shiraz, Iran.
[Anushiravani, Amir] Shiraz Univ Med Sci, Nemazee Hosp, Dept Internal Med, Shiraz, Iran.
[Nikeghbalian, Saman; Janghorban, Parisa; Malekhosseini, Sayed Ali] Shiraz Univ Med Sci, Shiraz Organ Transplant Ctr, Shiraz, Iran.
[Motazedian, Nasrin] Shiraz Univ Med Sci, Shiraz Transplant Res Ctr, Shiraz, Iran.
C3 Shiraz University of Medical Science; Shiraz University of Medical
Science; Shiraz University of Medical Science; Shiraz University of
Medical Science; Shiraz University of Medical Science
RP Honarvar, B (corresponding author), Shiraz Univ Med Sci, Hlth Policy Res Ctr, Inst Hlth, POB 71348532135, Shiraz, Iran.
EM honarvarbh32@yahoo.com
RI Honarvar, Behnam/K-1623-2013; Malek-Hosseini, Seyed/AAQ-9080-2021;
Nikeghbalian, Saman/T-6992-2019; Akbari, Ali/G-6044-2016; Seif,
Mozhgan/A-1073-2019
OI Anushiravani, Amir/0000-0002-9196-1901
CR Bakthavatsalam R, 2001, AM J TRANSPLANT, V1, P284, DOI 10.1034/j.1600-6143.2001.001003284.x
Bertelli R, 2005, TRANSPL P, V37, P1119, DOI 10.1016/j.transproceed.2005.01.031
Charco R, 2005, TRANSPLANT P, V37, P3904, DOI 10.1016/j.transproceed.2005.09.120
Chen H, 2016, LIVER TRANSPLANT, V22, P352, DOI 10.1002/lt.24387
CHERQUI D, 1993, WORLD J SURG, V17, P669, DOI 10.1007/BF01659140
Cho JY, 2008, WORLD J SURG, V32, P1731, DOI 10.1007/s00268-008-9651-4
Fouzas I, 2012, TRANSPL P, V44, P2734, DOI 10.1016/j.transproceed.2012.09.024
Ghabril M, 2016, TRANSPLANTATION, V100, P126, DOI 10.1097/TP.0000000000000785
Gimeno FA, 2005, TRANSPL P, V37, P3899, DOI 10.1016/j.transproceed.2005.10.085
Hernández-Conde M, 2016, REV ESP ENFERM DIG, V108, P716, DOI 10.17235/reed.2016.4211/2016
Hosseini SAM, 2017, HEPAT MON, V17, DOI 10.5812/hepatmon.60745
Janousek L, 2011, Rozhl Chir, V90, P114
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Kakaei F, 2010, INT J TRANSPLANT MED, V1, P44
Lankarani KB, 2015, HEPAT MON, V15, DOI 10.5812/hepatmon.26407
Manzanet G, 2001, LIVER TRANSPLANT, V7, P125, DOI 10.1053/jlts.2001.21295
Pan C, 2009, TRANSPL P, V41, P3761, DOI 10.1016/j.transproceed.2009.06.215
Ponziani FR, 2014, TRANSPLANT REV-ORLAN, V28, P92, DOI 10.1016/j.trre.2014.01.003
Ramos AP, 2010, TRANSPL P, V42, P498, DOI 10.1016/j.transproceed.2010.01.038
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Artacho GS, 2010, TRANSPL P, V42, P3156, DOI 10.1016/j.transproceed.2010.05.057
Wu Gang, 2009, Zhonghua Wai Ke Za Zhi, V47, P590
Yerdel MA, 2000, TRANSPLANTATION, V69, P1873, DOI 10.1097/00007890-200005150-00023
You Shen, 2008, Zhonghua Wai Ke Za Zhi, V46, P176
NR 24
TC 3
Z9 3
U1 0
U2 5
PU BASKENT UNIV
PI ANKARA
PA TASKENT CADDESI NO 77, KAT 4, BAHCELIEVLER, ANKARA, 06490, TURKEY
SN 1304-0855
EI 2146-8427
J9 EXP CLIN TRANSPLANT
JI Exp. Clin. Transplant.
PD APR
PY 2021
VL 19
IS 4
BP 324
EP 330
DI 10.6002/ect.2018.0295
PG 7
WC Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Transplantation
GA RG7HV
UT WOS:000635706100006
PM 30995894
DA 2025-01-07
ER
PT J
AU Dou, B
Ma, FZ
Jiang, ZY
Zhao, L
AF Dou, Bin
Ma, Fuzhe
Jiang, Zhenyu
Zhao, Ling
TI Blood HDAC4 Variation Links With Disease Activity and Response to Tumor
Necrosis Factor Inhibitor and Regulates CD4+T Cell Differentiation in
Ankylosing Spondylitis
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE Histone deacetylase 4; ankylosing spondylitis; disease activity;
treatment outcome; T-helper 17 polarization
ID HISTONE DEACETYLASE HDAC4; HEPATOCELLULAR-CARCINOMA; EXPRESSION
AB PurposeHistone deacetylase 4 (HDAC4) regulates the progression of autoimmune diseases. This study aimed to further investigate the correlation between HDAC4 and Th cells, inflammation, disease activity, and treatment response in patients with ankylosing spondylitis (AS). MethodsA total of 132 active patients with AS were enrolled, of whom 54 patients received TNF inhibitor (TNFi) and 78 patients received NSAID. Serum HDAC4 was measured by ELISA in patients with AS before treatment (W0) and at week (W)4, W8, and W12 after treatment. Meanwhile, serum HDAC4 was detected in 30 patients with osteoarthritis and in 30 healthy controls (HCs) by ELISA. Besides, naive CD4(+) T cells from patients with AS were isolated, followed by modulation of HDAC4 and then polarization toward Th1, Th2, and Th17. ResultsHistone deacetylase 4 was reduced in patients with AS compared with HCs and patients with osteoarthritis (both P < 0.01). In patients with AS, HDAC4 was negatively correlated with TNF (P < 0.001), IL-1 beta (P = 0.003), Th17 proportion (P = 0.008), C-reactive protein (P < 0.001), and ASDAS (P = 0.038), but not with IL-6, Th1 proportion, or other characteristics. Meanwhile, HDAC4 increased from W0 to W12 (P < 0.001); HDAC4 at W8 (P = 0.014) and W12 (P = 0.006) was raised in ASAS40-response patients than ASAS40-non-response patients; further subgroup analysis showed that HDAC4 at W12 was higher in ASAS40-response patients than ASAS40-non-response patients (P = 0.016) in the TNFi-treated group, but not in the NSAID-treated group. In addition, HDAC4 negatively regulated the polarization of naive CD4(+) T cells toward Th17 (P < 0.01), but not Th1 or Th2. ConclusionHistone deacetylase 4 is associated with lower inflammation, and the disease activity negatively regulates Th17 polarization, whose increment after treatment reflects favorable outcomes in patients with AS.
C1 [Dou, Bin; Jiang, Zhenyu; Zhao, Ling] First Hosp Jilin Univ, Dept Rheumatol, Changchun, Peoples R China.
[Ma, Fuzhe] First Hosp Jilin Univ, Dept Nephrol, Changchun, Peoples R China.
C3 Jilin University; Jilin University
RP Jiang, ZY; Zhao, L (corresponding author), First Hosp Jilin Univ, Dept Rheumatol, Changchun, Peoples R China.
EM jiangzy@jlu.edu.cn; zhaoling17@jlu.edu.cn
RI Zhao, Ling/JEF-2376-2023
FU Jilin Province Direct Health Special Project [JLSWSRCZX2020-038];
National Natural Science Foundation of China [81501343]; Bethune Plan
Project of Jilin University [2015410]; Jilin Scientific and
Technological Development Program [20170520010JH, 20150101152JC];
Postdoctoral Science Foundation of China [801181010432]
FX Funding We thank the staff of the Division of Clinical Research and the
Genetic Diagnosis Center in our hospital for their assistance during
this study. This work was supported by Jilin Province Direct Health
Special Project (JLSWSRCZX2021-062); Jilin Province Direct Health
Special Project (JLSWSRCZX2020-038); the National Natural Science
Foundation of China (Grant Number 81501343); the Bethune Plan Project of
Jilin University (Grant Number 2015410); the Jilin Scientific and
Technological Development Program (Grant Number 20170520010JH;
20150101152JC); the Postdoctoral Science Foundation of China (Grant
Number 801181010432).
CR Chang LH, 2021, J INFLAMM RES, V14, P6157, DOI 10.2147/JIR.S336099
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Dean LE, 2014, RHEUMATOLOGY, V53, P650, DOI 10.1093/rheumatology/ket387
Demyanenko SV, 2020, BRAIN RES BULL, V162, P151, DOI 10.1016/j.brainresbull.2020.06.010
Ebrahimiadib N, 2021, J OPHTHAL VIS RES, V16, P462, DOI 10.18502/jovr.v16i3.9440
Gaston JSH, 2017, BEST PRACT RES CL RH, V31, P777, DOI 10.1016/j.berh.2018.07.010
Guo KL, 2021, J IMMUNOL RES, V2021, DOI 10.1155/2021/6693542
Hao JY, 2022, INFLAMMATION, V45, P196, DOI 10.1007/s10753-021-01538-4
Hou F, 2020, J CELL BIOCHEM, V121, P930, DOI 10.1002/jcb.29365
Jafarnezhad-Ansariha F, 2018, INFLAMMOPHARMACOLOGY, V26, P375, DOI 10.1007/s10787-017-0386-4
Jansen JP, 2011, INT J RHEUMATOL, V2011, DOI 10.1155/2011/160326
Jin SW, 2018, ANN RHEUM DIS, V77, P1644, DOI 10.1136/annrheumdis-2018-213511
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Li MW, 2021, INFLAMMOPHARMACOLOGY, V29, P1371, DOI 10.1007/s10787-021-00854-3
Li QM, 2021, CELL DEATH DISCOV, V7, DOI 10.1038/s41420-021-00601-1
Liu D, 2021, FRONT IMMUNOL, V12, DOI 10.3389/fimmu.2021.696973
Lu W, 2015, NAT IMMUNOL, V16, P1185, DOI 10.1038/ni.3292
Ma QX, 2021, CANCER LETT, V520, P243, DOI 10.1016/j.canlet.2021.07.049
Mauro D, 2021, NAT REV RHEUMATOL, V17, P387, DOI 10.1038/s41584-021-00625-y
Park JS, 2018, SCI REP-UK, V8, DOI 10.1038/s41598-018-25933-4
Pei XF, 2018, PATHOL RES PRACT, V214, P1095, DOI 10.1016/j.prp.2018.04.009
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Shao CJ, 2021, TRANSL LUNG CANCER R, V10, P4558, DOI 10.21037/tlcr-21-982
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Wang ZH, 2019, ANN CLIN LAB SCI, V49, P189
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Zeybel M, 2016, CLIN EPIGENETICS, V8, DOI 10.1186/s13148-016-0218-1
Zhang F, 2021, BMC CARDIOVASC DISOR, V21, DOI 10.1186/s12872-021-01980-0
Zhao JL, 2020, RHEUMATOL INT, V40, P859, DOI 10.1007/s00296-020-04537-0
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Zhou XJ, 2022, MOD RHEUMATOL, V32, P613, DOI 10.1093/mr/roab039
NR 40
TC 6
Z9 6
U1 1
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD MAY 6
PY 2022
VL 9
AR 875341
DI 10.3389/fmed.2022.875341
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 1K3AO
UT WOS:000798478200001
PM 35602496
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Saracco, GM
Evangelista, A
Fagoonee, S
Ciccone, G
Bugianesi, E
Caviglia, GP
Abate, ML
Rizzetto, M
Pellicano, R
Smedile, A
AF Saracco, Giorgio Maria
Evangelista, Andrea
Fagoonee, Sharmila
Ciccone, Giovannino
Bugianesi, Elisabetta
Caviglia, Gian Paolo
Abate, Maria Lorena
Rizzetto, Mario
Pellicano, Rinaldo
Smedile, Antonina
TI Etiology of chronic liver diseases in the Northwest of Italy, 1998
through 2014
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Chronic liver diseases; Cirrhosis; Hepatitis C virus; Hepatitis B virus;
Nonalcoholic steatohepatitis
ID HEPATOCELLULAR-CARCINOMA; CHRONIC HEPATITIS; LIFE-STYLE; DIAGNOSIS;
WEIGHT; EPIDEMIOLOGY; POPULATION
AB AIM
To assess the etiology of chronic liver diseases (CLD) from 1998 to 2014 at the outpatient clinic of Gastroenterology of the main hospital in Northwest of Italy among those dedicated to hepatology.
METHODS
A random sample of charts of patients referred to for increased liver enzymes between January 1998 and December 2006, and between January 2012 and December 2014 were reviewed. Etiology search included testing for hepatitis B virus (HBV), hepatitis C virus (HCV), autoimmune hepatitis, primary biliary cirrhosis, Wilson's disease and hereditary hemocromatosis. A risky alcohol consumption was also considered. Nonalcoholic fatty liver disease (NAFLD) was diagnosed in patients with histological and/or ultrasound evidence of steatosis/steatohepatitis, and without other causes of CLD.
RESULTS
The number of patients included was 1163. Of them, 528 (45%) had positivity for HCV and 85 (7%) for HBV. Among the virus-free patients, 417 (36%) had metabolic disorders whereas the remaining had history of alcohol abuse, less prevalent causes of CLD or concomitant conditions. In comparison to 1998-2000 (41%), a reduction of HCV alone-related cases was detected during the periods 2001-2003 (35%, OR = 0.75, 95% CI: 0.53-1.06), 2004-2006 (33%, OR = 0.70, 95% CI: 0.50-0.97) and 2012-2014 (31%, OR = 0.64, 95% CI: 0.46-0.91). On the contrary, in comparison to 1998-2000 (31%), metabolic-alone disorders increased in the period 2004-2006 (39%, OR = 1.37, 95% CI: 0.99-1.91) and 2012-2014 (41%, OR = 1.53, 95% CI: 1.09-2.16). The other etiologies remained stable. The increase of incidence of metabolic-alone etiology during the period 2004-2006 and 2012-2014 tended to be higher in older patients (>= 50 years) compared to younger (P = 0.058).
CONCLUSION
In the Northwest of Italy, during this study period, the prevalence of HCV infection decreased notably whereas that of NAFLD increased.
C1 [Saracco, Giorgio Maria] Univ Turin, Dept Oncol, I-10123 Turin, Italy.
[Evangelista, Andrea; Ciccone, Giovannino] Univ Turin, Unit Canc Epidemiol CPO Piemonte, I-10123 Turin, Italy.
[Fagoonee, Sharmila] Univ Turin, Inst Biostruct & Bioimages, CNR, Ctr Mol Biotechnol, I-10126 Turin, Italy.
[Bugianesi, Elisabetta; Caviglia, Gian Paolo; Abate, Maria Lorena; Rizzetto, Mario; Smedile, Antonina] Univ Turin, Dept Med Sci, I-10123 Turin, Italy.
[Saracco, Giorgio Maria; Bugianesi, Elisabetta; Rizzetto, Mario; Pellicano, Rinaldo; Smedile, Antonina] Molinette Mauriziano Hosp, Gastroenterol Unit, I-10123 Turin, Italy.
C3 University of Turin; University of Turin; University of Turin; Consiglio
Nazionale delle Ricerche (CNR); Istituto di Biostrutture e Bioimmagini
(IBB-CNR); University of Turin; A.O.U. Citta della Salute e della
Scienza di Torino; AOU San Giovanni Battista-Molinette
RP Pellicano, R (corresponding author), Molinette Mauriziano Hosp, Gastroenterol Unit, Outpatient Clin, Corso Bramante 88, I-10123 Turin, Italy.
EM rinaldo_pellican@hotmail.com
RI Saracco, Guido/C-9834-2013; Pellicano, Rinaldo/K-2575-2016; Caviglia,
Gian/H-6076-2012; Fagoonee, Sharmila/L-1940-2019; Bugianesi,
Elisabetta/K-8008-2016; evangelista, andrea/A-7802-2013
OI evangelista, andrea/0000-0003-1901-2805; Caviglia, Gian
Paolo/0000-0002-0529-9481; FAGOONEE, SHARMILA/0000-0001-6070-6716;
PELLICANO, RINALDO/0000-0003-3438-0649; Saracco, Giorgio
Maria/0000-0001-5310-4143
FU Regione Piemonte [R01 DK090317, R01 DA031095]; Bando Ricerca Scientifica
Applicata Anno
FX Supported by Regione Piemonte grants, No. R01 DK090317 and No. R01
DA031095 (in part); Bando Ricerca Scientifica Applicata Anno 2003.
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NR 26
TC 56
Z9 58
U1 1
U2 3
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD SEP 28
PY 2016
VL 22
IS 36
BP 8187
EP 8193
DI 10.3748/wjg.v22.i36.8187
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DW9LY
UT WOS:000383982700013
PM 27688660
OA Green Published, Green Submitted, hybrid
DA 2025-01-07
ER
PT J
AU De Nardi, L
Natale, MF
Messia, V
Tomà, P
De Benedetti, F
Insalaco, A
AF De Nardi, Laura
Natale, Marco Francesco
Messia, Virginia
Toma, Paolo
De Benedetti, Fabrizio
Insalaco, Antonella
TI A child with polyarthritis and chronic lung disease: a case report of
ataxia-telangiectasia
SO ITALIAN JOURNAL OF PEDIATRICS
LA English
DT Article
DE Ataxia-telangiectasia; Juvenile idiopathic arthritis; Bronchiectasis;
Interstitial lung disease; Granulomatosis; Immunodeficiency; Case
report.
ID MUTATIONS
AB BackgroundAtaxia-telangiectasia (A-T) is a rare autosomal recessive DNA repair disorder, characterized by progressive cerebellar degeneration, telangiectasia, immunodeficiency, recurrent sinopulmonary infections, radiation sensitivity, premature aging and predisposition to cancer. Although the association with autoimmune and chronic inflammatory conditions such as vitiligo, thrombocytopenia and arthritis has occasionally been reported, an onset with articular involvement at presentation is rare.Case presentationWe herein report the case of a 7-year-old Caucasian girl who was admitted to the Rheumatology Department with a history of febrile chough and polyarthritis which led initially to the suspicion of an autoinflammatory disease. She had overt polyarthritis with knees deformities and presented with severe pneumonia. A chest Computed Tomography (CT) scan showed bilateral bronchiectasis, parenchymal consolidation and interstitial lung disease; rheumatoid factor and type I interferon signature resulted negative, therefore excluding COatomer Protein subunit Alpha (COPA) syndrome. A diagnosis of sarcoidosis had been suspected based on histological evidence of granulomatous liver inflammation, but ruled out after detecting normal angiotensin converting enzyme and chitotriosidase blood levels. Based on her past medical history characterized by at least six episodes of pneumonia in the previous 4 years, immunological phenotyping was performed. This showed complete IgA and IgE deficiency with defective antigen-specific antibodies to Pneumococcal, Tetanus toxin and Hemophilus Influenzae B vaccines. Additionally, low numbers of B cells and recent thymic emigrants (RTE) were found (CD4Ra 1.4%), along with a low CD4+/CD8 + T cells ratio (< 1). Finally, based on gait disturbances (wobbly wide-based walking), serum alfa-fetoprotein was dosed, which resulted increased at 276 ng/ml (normal value < 7 ng/ml). A diagnosis of Ataxia-Telangiectasia was made, strengthened by the presence of bulbar telangiectasia, and then confirmed by Whole Exome Sequencing (WES).ConclusionsAlthough rare, A-T should always be ruled out in case of pulmonary bronchiectasis and gait disturbances even in the absence of bulbar or skin telangiectasia. Autoimmune and granulomatous disorders must to be considered as differential diagnosis.
C1 [De Nardi, Laura] Univ Trieste, Piazzale Europa 1, I-34127 Trieste, Italy.
[Natale, Marco Francesco; Messia, Virginia; Toma, Paolo; De Benedetti, Fabrizio; Insalaco, Antonella] Bambino Gesu Pediat Hosp, IRCCS, Rome, Italy.
C3 University of Trieste; IRCCS Bambino Gesu
RP De Nardi, L (corresponding author), Univ Trieste, Piazzale Europa 1, I-34127 Trieste, Italy.
EM laura.denardi1993@gmail.com
RI De Nardi, Laura/GYJ-0849-2022; Natale, marco francesco/GYD-4544-2022
OI De Nardi, Laura/0000-0002-8141-3389
FU Italian Ministry of Health
FX This work was supported also by the Italian Ministry of Health with
"Current Research funds" .
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NR 21
TC 1
Z9 1
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1720-8424
EI 1824-7288
J9 ITAL J PEDIATR
JI Ital. J. Pediatr.
PD SEP 4
PY 2023
VL 49
IS 1
AR 111
DI 10.1186/s13052-023-01509-5
PG 5
WC Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics
GA FH0T4
UT WOS:001144760900001
PM 37667293
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Teschke, R
Danan, G
AF Teschke, Rolf
Danan, Gaby
TI Idiosyncratic DILI and RUCAM under One Hat: The Global View
SO LIVERS
LA English
DT Review
DE DILI; drug-induced liver injury; original RUCAM; updated RUCAM; Roussel
Uclaf Causality Assessment Method; DILI causality assessment methods
ID INDUCED LIVER-INJURY; CORTICOSTEROID PLUS GLYCYRRHIZIN; CAUSALITY
ASSESSMENT METHODS; CLINICAL-FEATURES; INDUCED HEPATOTOXICITY;
CHECKPOINT INHIBITORS; AUTOIMMUNE HEPATITIS; ADVERSE REACTIONS;
RISK-FACTORS; DRUG
AB Drugs are prescribed worldwide to treat diseases but with the risk of idiosyncratic drug-induced liver injury (iDILI). The most important difficulty is how best to establish causality. Based on strong evidence and principles of artificial intelligence (AI) to solve complex processes through quantitative algorithms using scored elements, progress was achieved with the Roussel Uclaf Causality Assessment Method (RUCAM) in its original and updated versions, often viewed now as the gold standard. As a highly appreciated diagnostic algorithm, the RUCAM is in global use with around 100,000 iDILI cases published worldwide using RUCAM to assess causality, largely outperforming any other specific causality assessment tool in terms of case numbers. Consequently, the RUCAM helps to establish a list of top-ranking drugs worldwide implicated in iDILI and to describe clinical and mechanistic features of iDILI caused by various drugs. In addition, the RUCAM was recently applied in iDILI cases of patients treated for coronavirus disease 2019 (COVID-19) infections or cancer patients treated with immune checkpoint inhibitors (ICIs), as well as in the search for new treatment options with conventional drugs in iDILI. Analyses of RUCAM-based iDILI cases are helpful to support pathogenetic steps like immune reactions, genetic predisposition as evidenced by human leucocyte antigens (HLA) genotypes for selected drugs, and the role of the gut microbiome. To achieve consistency in data collection, analysis, and specific clinical and pathogenetic presentation, researchers, regulatory agencies, and pharmaceutical firms should place iDILI and the updated RUCAM as the causality tool under one and the same hat in review articles and clinical guidelines for the diagnosis and treatment of iDILI.
C1 [Teschke, Rolf] Klinikum Hanau, Dept Internal Med 2, Div Gastroenterol & Hepatol, D-63450 Hanau, Germany.
[Teschke, Rolf] Goethe Univ Frankfurt Main, Acad Teaching Hosp, Med Fac, D-60590 Frankfurt, Germany.
[Danan, Gaby] Pharmacovigilance Consultancy, Rue Ormeaux, F-75020 Paris, France.
C3 Goethe University Frankfurt
RP Teschke, R (corresponding author), Klinikum Hanau, Dept Internal Med 2, Div Gastroenterol & Hepatol, D-63450 Hanau, Germany.; Teschke, R (corresponding author), Goethe Univ Frankfurt Main, Acad Teaching Hosp, Med Fac, D-60590 Frankfurt, Germany.
EM rolf.teschke@gmx.de; gaby.danan@gmail.com
OI teschke, rolf/0000-0001-8910-1200
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NR 244
TC 2
Z9 2
U1 2
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2673-4389
J9 LIVERS-BASEL
JI Livers
PD SEP
PY 2023
VL 3
IS 3
BP 397
EP 433
DI 10.3390/livers3030030
PG 37
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA WI4M3
UT WOS:001254227400001
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Rostved, AA
Lundgren, JD
Hillingso, J
Peters, L
Mocroft, A
Rasmussen, A
AF Rostved, Andreas A.
Lundgren, Jens D.
Hillingso, Jens
Peters, Lars
Mocroft, Amanda
Rasmussen, Allan
TI MELD score measured day 10 after orthotopic liver transplantation
predicts death and re-transplantation within the first year
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Alanine transaminase; bilirubin; creatinine; graft survival;
international normalized ratio; liver transplantation; mortality;
postoperative complications; retrospective studies
ID EARLY ALLOGRAFT DYSFUNCTION; DONOR RISK INDEX; SHORT-TERM; DISEASE
SCORE; MODEL; SURVIVAL; MORTALITY; FAILURE; DEFINITION; VALIDATION
AB Objective: The impact of early allograft dysfunction on the outcome after liver transplantation is yet to be established. We explored the independent predictive value of the Model for End-Stage Liver Disease (MELD) score measured in the post-transplant period on the risk of mortality or re-transplantation.Material and methods: Retrospective cohort study on adults undergoing orthotopic deceased donor liver transplantation from 2004 to 2014. The MELD score was determined prior to transplantation and daily until 21 days after. The risk of mortality or re-transplantation within the first year was assessed according to quartiles of MELD using unadjusted and adjusted stepwise Cox regression analysis.Results: We included 374 consecutive liver transplant recipients of whom 60 patients died or were re-transplanted. The pre-transplant MELD score was comparable between patients with good and poor outcome, but from day 1 the MELD score significantly diversified and was higher in the poor outcome group (MELD score quartile 4 versus quartile 1-3 at day 10: HR 5.1, 95% CI: 2.8-9.0). This association remained after adjustment for non-identical blood type, autoimmune liver disease and hepatocellular carcinoma (adjusted HR 5.3, 95% CI: 2.9-9.5 for MELD scores at day 10). The post-transplant MELD score was not associated with pre-transplant MELD score or the Eurotransplant donor risk index.Conclusion: Early determination of the MELD score as an indicator of early allograft dysfunction after liver transplantation was a strong independent predictor of mortality or re-transplantation and was not influenced by the quality of the donor, or preoperative recipient risk factors.
C1 [Rostved, Andreas A.; Hillingso, Jens; Rasmussen, Allan] Rigshosp, Dept Surg & Liver Transplantat, Copenhagen, Denmark.
[Lundgren, Jens D.; Peters, Lars] CHIP, Dept Infect Dis, Rigshosp, Sect 2100, Copenhagen, Denmark.
[Mocroft, Amanda] UCL, Dept Infect & Populat Hlth, London, England.
C3 University of Copenhagen; Rigshospitalet; Rigshospitalet; University of
Copenhagen; University of London; University College London
RP Rasmussen, A (corresponding author), Copenhagen Univ Hosp, Liver Transplantat, Rigshosp, Dept Surg & Transplantat, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.
EM allan.rasmussen@dadlnet.dk
RI Lundgren, Jens/AAE-6876-2019
OI Mocroft, Amanda/0000-0001-8316-1122; Lundgren, Jens/0000-0001-8901-7850;
Hillingsoe, Jens G./0000-0002-2381-7836; Rostved, Andreas
A./0000-0002-3359-7734; Rasmussen, Allan/0000-0002-9550-4767
FU Research council at Rigshospitalet; University of Copenhagen; Danish
National Research Foundation [126]
FX Funding was obtained from the Research council at Rigshospitalet,
University of Copenhagen and from the Danish National Research
Foundation [Grant 126].
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NR 30
TC 12
Z9 13
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PY 2016
VL 51
IS 11
BP 1360
EP 1366
DI 10.1080/00365521.2016.1196497
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DZ1EH
UT WOS:000385581200014
PM 27319374
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Zaremba, A
Chorti, E
Jockenhöfer, F
Bolz, S
Sirin, S
Glas, M
Becker, JC
Ugurel, S
Boesch, A
Schadendorf, D
Livingstone, E
Hagenacker, T
Zimmer, L
AF Zaremba, Anne
Chorti, Eleftheria
Jockenhoefer, Finja
Bolz, Saskia
Sirin, Selma
Glas, Martin
Becker, Juergen C.
Ugurel, Selma
Boesch, Alexander
Schadendorf, Dirk
Livingstone, Elisabeth
Hagenacker, Tim
Zimmer, Lisa
TI Metastatic Merkel cell carcinoma and myasthenia gravis: contraindication
for therapy with immune checkpoint inhibitors?
SO JOURNAL FOR IMMUNOTHERAPY OF CANCER
LA English
DT Article
DE Merkel cell carcinoma; Myasthenia gravis; Immune checkpoint inhibitor;
Adverse events; Immunotherapy
ID NONMELANOMA SKIN-CANCER; ADVANCED MELANOMA; CHEMOTHERAPY; TOXICITY;
BLOCKADE; RISK
AB Background: PD-1/PD-L1 inhibitors are promising approaches for advanced Merkel cell carcinoma (MCC). Nevertheless, these inhibitors bear a high risk for induction of immune-related adverse events (irAEs), particularly flares of preexisting autoimmune diseases. Neurological irAEs of PD-1/PD-L1 inhibitors are possibly underestimated and potentially fatal toxicities. Additionally, exacerbations of preexisting myasthenia gravis (MG) with a high MG-specific-related mortality have been reported.
Case presentation: A 61-year-old woman with a history of MG since 2005 was treated with azathioprine and pyridostigmine after thymectomy. In March 2016, she was diagnosed with MCC. Six months later the tumor had progressed to stage IV and metastases were detected in lymph nodes and the pancreas. The immunosuppressive therapy was therefore changed to mycophenolatmofetil (MMF) and an immune checkpoint blockade with the PD-1 inhibitor pembrolizumab was initiated in November 2016. Due to MMF-induced liver toxicity, MMF was switched to cyclosporine A (CsA) with normalized liver transaminases six weeks later. After six cycles of pembrolizumab the patient achieved a partial response. Follow up analysis sixty-five weeks later revealed a long-lasting tumor response with a partial remission of pancreatic and inguinal metastases and no flare of MG.
Conclusions: Patients with a preexisting MG can be considered for treatment with immune checkpoint inhibitors if they have a life-threatening cancer and if other effective, long-lasting treatment options are not available. The risks and benefits of therapy should be weighed in a multidisciplinary setting and should be discussed thoroughly with the patient. Exacerbation of underlying MG can be potentially life-threatening and requires close monitoring in collaboration with neuromuscular specialists.
C1 [Zaremba, Anne; Chorti, Eleftheria; Jockenhoefer, Finja; Becker, Juergen C.; Ugurel, Selma; Boesch, Alexander; Schadendorf, Dirk; Livingstone, Elisabeth; Zimmer, Lisa] Univ Hosp Essen, Dept Dermatol, Essen, Germany.
[Bolz, Saskia; Hagenacker, Tim] Univ Hosp Essen, Dept Neurol, Essen, Germany.
[Sirin, Selma] Univ Hosp Essen, Dept Diagnost & Intervent Radiol & Neuroradiol, Essen, Germany.
[Glas, Martin] Univ Hosp Essen, Dept Neurol, Div Clin Neurooncol, Essen, Germany.
[Becker, Juergen C.] German Canc Consortium DKTK, Translat Skin Canc Res, Partner Site Essen Dusseldorf, Essen, Germany.
C3 University of Duisburg Essen; University of Duisburg Essen; University
of Duisburg Essen; University of Duisburg Essen; Helmholtz Association;
German Cancer Research Center (DKFZ)
RP Zaremba, A; Zimmer, L (corresponding author), Univ Hosp Essen, Dept Dermatol, Essen, Germany.
EM anne.zaremba@uk-essen.de; lisa.zimmer@uk-essen.de
RI Hagenacker, Tim/HNQ-4582-2023; Livingstone, Elisabeth/AHE-9171-2022;
Zimmer, Lisa/AAP-8495-2021; Schadendorf, Dirk/AAE-8206-2019
OI Schadendorf, Dirk/0000-0003-3524-7858; Livingstone,
Elisabeth/0000-0001-8279-9239
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NR 21
TC 11
Z9 11
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2051-1426
J9 J IMMUNOTHER CANCER
JI J. Immunother. Cancer
PD MAY 29
PY 2019
VL 7
AR 141
DI 10.1186/s40425-019-0626-9
PG 6
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA IA3DH
UT WOS:000469442700001
PM 31142383
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Sohrab, SS
Raj, R
Nagar, A
Hawthorne, S
Paiva-Santos, AC
Kamal, MA
El-Daly, MM
Azhar, EI
Sharma, A
AF Sohrab, Sayed Sartaj
Raj, Riya
Nagar, Amka
Hawthorne, Susan
Paiva-Santos, Ana Claudia
Kamal, Mohammad Amjad
El-Daly, Mai M. M.
Azhar, Esam I. I.
Sharma, Ankur
TI Chronic Inflammation's Transformation to Cancer: A Nanotherapeutic
Paradigm
SO MOLECULES
LA English
DT Review
DE cancer; inflammation; nanoparticles; drug delivery; inflammatory
pathways
ID NF-KAPPA-B; BREAST-CANCER; HEPATITIS-B; HEPATOCELLULAR-CARCINOMA; SILVER
NANOPARTICLES; TUMOR MICROENVIRONMENT; GOLD NANOPARTICLES;
COLORECTAL-CANCER; BOWEL-DISEASE; ACTIVATION
AB The body's normal immune response against any invading pathogen that causes infection in the body results in inflammation. The sudden transformation in inflammation leads to the rise of inflammatory diseases such as chronic inflammatory bowel disease, autoimmune disorders, and colorectal cancer (different types of cancer develop at the site of chronic infection and inflammation). Inflammation results in two ways: short-term inflammation i.e., non-specific, involves the action of various immune cells; the other results in long-term reactions lasting for months or years. It is specific and causes angiogenesis, fibrosis, tissue destruction, and cancer progression at the site of inflammation. Cancer progression relies on the interaction between the host microenvironment and tumor cells along with the inflammatory responses, fibroblast, and vascular cells. The two pathways that have been identified connecting inflammation and cancer are the extrinsic and intrinsic pathways. Both have their own specific role in linking inflammation to cancer, involving various transcription factors such as Nuclear factor kappa B, Activator of transcription, Single transducer, and Hypoxia-inducible factor, which in turn regulates the inflammatory responses via Soluble mediators cytokines (such as Interleukin-6, Hematopoietin-1/Erythropoietin, and tumor necrosis factor), chemokines (such as Cyclooxygenase-2, C-X-C Motif chemokines ligand-8, and IL-8), inflammatory cells, cellular components (such as suppressor cells derived from myeloid, tumor-associated macrophage, and acidophils), and promotes tumorigenesis. The treatment of these chronic inflammatory diseases is challenging and needs early detection and diagnosis. Nanotechnology is a booming field nowadays for its rapid action and easy penetration inside the infected destined cells. Nanoparticles are widely classified into different categories based on their different factors and properties such as size, shape, cytotoxicity, and others. Nanoparticles emerged as excellent with highly progressive medical inventions to cure diseases such as cancer, inflammatory diseases, and others. Nanoparticles have shown higher binding capacity with the biomolecules in inflammation reduction and lowers the oxidative stress inside tissue/cells. In this review, we have overall discussed inflammatory pathways that link inflammation to cancer, major inflammatory diseases, and the potent action of nanoparticles in chronic inflammation-related diseases.
C1 [Sohrab, Sayed Sartaj; Kamal, Mohammad Amjad; El-Daly, Mai M. M.; Azhar, Esam I. I.] King Abdulaziz Univ, King Fahd Med Res Ctr, Special Infect Agents Unit, Jeddah 21589, Saudi Arabia.
[Sohrab, Sayed Sartaj; El-Daly, Mai M. M.; Azhar, Esam I. I.] King Abdulaziz Univ, Fac Appl Med Sci, Dept Med Lab Sci, Jeddah 21589, Saudi Arabia.
[Raj, Riya] Bangalore Univ, Dept Biochem, Bangalore 560056, India.
[Nagar, Amka] Sharda Univ, Sch Basic Sci & Res, Dept Life Sci, Greater Noida 201310, India.
[Hawthorne, Susan] Ulster Univ, Sch Pharm & Pharmaceut Sci, Coleraine BT52 1SA, North Ireland.
[Paiva-Santos, Ana Claudia] Univ Coimbra, Fac Pharm, Dept Pharmaceut Technol, P-3000548 Coimbra, Portugal.
[Paiva-Santos, Ana Claudia] Univ Coimbra, Fac Pharm, Dept Pharmaceut Technol, LAQV,REQUIMTE, P-3000548 Coimbra, Portugal.
[Kamal, Mohammad Amjad] Enzymoics Inc, Hebersham, NSW 2770, Australia.
[Kamal, Mohammad Amjad] Novel Global Community Educ Fdn, Hebersham, NSW 2770, Australia.
[Sharma, Ankur] Univ Strathclyde, Strathclyde Inst Pharmaceut & Biomed Sci, Glasgow G1 0RE, Scotland.
C3 King Abdulaziz University; King Abdulaziz University; Bangalore
University; Sharda University; Ulster University; Universidade de
Coimbra; Universidade de Coimbra; University of Strathclyde
RP Sharma, A (corresponding author), Univ Strathclyde, Strathclyde Inst Pharmaceut & Biomed Sci, Glasgow G1 0RE, Scotland.
EM ssohrab@kau.edu.sa; asharma.nanotechnologist@gmail.com
RI Azhar, Esam/ABI-1044-2020; SOHRAB, SAYED/ABA-2305-2021; Sharma,
Ankur/R-2991-2019; Kamal, Mohammad Amjad/J-2918-2014; El-Daly,
Mai/C-4704-2013; Paiva-Santos, Ana Claudia/B-5780-2019
OI Kamal, Mohammad Amjad/0000-0003-0088-0565; Hawthorne,
Susan/0000-0003-4693-0513; SOHRAB, SAYED SARTAJ/0000-0002-0663-0324;
Sharma, Dr Ankur/0000-0003-3058-760X; El-Daly, Mai/0000-0002-3864-523X;
Paiva-Santos, Ana Claudia/0000-0003-2710-6000; Azhar, Esam
Ibraheem/0000-0002-1736-181X
FU Institutional Fund Projects [IFPIP:513-141-1443]; APC; ministry of
Education; King Abdulaziz University, DSR, Jeddah, Saudi
[IFPIP:513-141-1443]
FX This review work was funded by Institutional Fund Projects under grant
No. (IFPIP:513-141-1443) and the APC was funded from this grant. The
authors gratefully acknowledge the financial support provided by the
ministry of Education and King Abdulaziz University, DSR, Jeddah, Saudi:
IFPIP:513-141-1443.
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NR 117
TC 23
Z9 24
U1 6
U2 21
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD MAY 29
PY 2023
VL 28
IS 11
AR 4413
DI 10.3390/molecules28114413
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA I7RC8
UT WOS:001004712300001
PM 37298889
OA Green Published, gold, Green Accepted
DA 2025-01-07
ER
PT J
AU Liu, Y
Chen, H
Hao, JH
Li, ZC
Hou, TZ
Hao, HQ
AF Liu, Yang
Chen, Hao
Hao, Jianheng
Li, Zhencheng
Hou, Tiezheng
Hao, Huiqin
TI Characterization and functional prediction of the microRNAs
differentially expressed in a mouse model of concanavalin A-induced
autoimmune hepatitis
SO INTERNATIONAL JOURNAL OF MEDICAL SCIENCES
LA English
DT Article
DE autoimmune hepatitis; concanavalin A; microRNA; microarray; Gene
Ontology; KEGG
ID KUPFFER CELLS; LIVER; BIOLOGY; FERROPTOSIS; MECHANISMS; TARGETS; TYPE-1;
CANCER
AB In order to investigate the altered expression of microRNAs (miRNAs) in the development of autoimmune hepatitis (AIH), the aberrantly expressed miRNAs in the concanavalin A (Con A)-induced AIH mouse model were identified for the first time with microarray in this study. A total of 49 miRNAs (31 upand 18 down-regulated) were screened out, and the qRT-PCR validation results of 12 chosen miRNAs were consistent with the microarray data. Combined with the profiling of differently expressed mRNAs in the same model (data not shown), 959 predicted target genes (601 for upand 358 for down-regulated miRNAs) were obtained according to the intersection of databases miRWalk and miRDB, and several hub genes were obtained from the regulatory networks, including Cadm1 and Mier3. These target genes were significantly enriched in the Gene ontology (GO) terms of "transcription, DNA-templated", and were annotated in 47 signaling pathways, comprising "Wnt signaling pathway", "Hippo signaling pathway", "Ferroptosis" and "mitogen-activated protein kinase (MAPK) signaling pathway", according to the GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. In the miRNA-GO-network, mmu-miR-193b-3p were exhibited in 33 GO terms of biological processes (BP), and the most significantly regulated GO term in BP categories was "regulation of transcription, DNA-templated". While in the miRNA-pathway-network, mmu-miR-7005-5p were enriched in 37 pathways, which was more than the other specifically expressed miRNAs, and the most significantly enriched pathways were "Endocytosis" and "MAPK signaling pathway". In conclusion, these differently expressed miRNAs seemed to be associated with the onset of AIH, and have the potential to serve as the new targets on the treatment of this disease.
C1 [Liu, Yang; Chen, Hao; Hao, Jianheng; Li, Zhencheng; Hou, Tiezheng; Hao, Huiqin] Shanxi Univ Chinese Med, Coll Basic Med Sci, Jinzhong 030619, Peoples R China.
[Liu, Yang; Chen, Hao; Hao, Jianheng; Li, Zhencheng; Hou, Tiezheng; Hao, Huiqin] Shanxi Univ Chinese Med, Basic Lab Integrated Tradit Chinese & Western Med, Jinzhong 030619, Peoples R China.
C3 Shanxi University of Chinese Medicine; Shanxi University of Chinese
Medicine
RP Hou, TZ; Hao, HQ (corresponding author), Shanxi Univ Chinese Med, Coll Basic Med Sci, Jinzhong 030619, Peoples R China.; Hou, TZ; Hao, HQ (corresponding author), Shanxi Univ Chinese Med, Basic Lab Integrated Tradit Chinese & Western Med, Jinzhong 030619, Peoples R China.
EM houtiezheng@sina.com; hhq@sxtcm.edu.cn
OI Liu, Yang/0000-0002-6627-5002
FU Basic applied study of Shanxi Province [201901D111333, 201801D121228];
Shanxi Provincial Key Research and Development Project [201803D31084];
Shanxi Key Laboratory of Innovative Drug for the Treatment of Serious
Diseases Basing on the Chronic Inflammation (Shanxi University of
Chinese Medicine) [SXIDL-2018-07]; Research projects of Health
Commission of Shanxi Province [2018002]; Science and Technology
Innovation Program of Shanxi University of Chinese Medicine
[2020PY-JC-07]; Basic Laboratory of Integrated Traditional Chinese and
Western Medicine, Shanxi University of Chinese Medicine
FX This study was funded by Basic applied study of Shanxi Province (Grant
Number: 201901D111333; Grant Recipient: Yang Liu and Grant Number:
201801D121228; Grant Recipient: Huiqin Hao); Shanxi Provincial Key
Research and Development Project (Grant Number: 201803D31084; Grant
Recipient: Huiqin Hao); Shanxi Key Laboratory of Innovative Drug for the
Treatment of Serious Diseases Basing on the Chronic Inflammation (Shanxi
University of Chinese Medicine) (Grant Number: SXIDL-2018-07, Grant
Recipient: Yang Liu); Research projects of Health Commission of Shanxi
Province (Grant Number: 2018002, Grant Recipient: Yang Liu); Science and
Technology Innovation Program of Shanxi University of Chinese Medicine
(Grant Number: 2020PY-JC-07, Grant Recipient: Yang Liu); The Basic
Laboratory of Integrated Traditional Chinese and Western Medicine,
Shanxi University of Chinese Medicine.
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NR 68
TC 14
Z9 16
U1 1
U2 9
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-1907
J9 INT J MED SCI
JI Int. J. Med. Sci.
PY 2020
VL 17
IS 15
BP 2312
EP 2327
DI 10.7150/ijms.47766
PG 16
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA NT6TF
UT WOS:000573070000011
PM 32922197
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Yuzhalin, AE
Kutikhin, AG
AF Yuzhalin, Arseniy E.
Kutikhin, Anton G.
TI Interleukin-12: Clinical usage and molecular markers of cancer
susceptibility
SO GROWTH FACTORS
LA English
DT Article
DE Interleukin-12; IL-12; SNP; cancer; carcinogenesis
ID RECOMBINANT HUMAN INTERLEUKIN-12; RENAL-CELL CARCINOMA;
NON-HODGKINS-LYMPHOMA; VASOACTIVE-INTESTINAL-PEPTIDE; IFN-GAMMA
PRODUCTION; PHASE-II TRIAL; HUMAN T-CELLS; GASTRIC-CANCER;
HEPATOCELLULAR-CARCINOMA; MAMMARY CARCINOGENESIS
AB The last decade has seen the emergence of immunomodulators as therapeutic agents in cancer treatment. Interleukins (ILs) are a category of small cell-signaling molecules that organize communication and interaction between immune cells and therefore they could be used as perfect immunomodulators. IL-12 is a promising candidate for cancer immunotherapy since it plays a major role in development of antitumor immune response. Numerous studies report that IL-12 promotes an effective destruction of cancer cells both in vivo and in vitro. In addition, IL-12 has anti-angiogenic activity and it is able to dramatically decrease tumor-supportive activities of tumor-associated macrophages. The first part of the review is devoted to immunobiology of IL-12. Signaling pathways of IL-12 as well as clinical trials of this cytokine are discussed. The second part of the review is concerned on the inherited variations in IL-12A and IL-12B genes that could modulate cancer susceptibility, and as a consequence, possess predictive, therapeutic, or prognostic significance. It is known that functional single nucleotide polymorphisms (SNPs) in IL-12A and IL-12B genes may dramatically affect on protein expression level, or alter its functions, which may lead to immune disorders, autoimmune diseases, and eventually contribute to cancer occurrence. The list of genetic polymorphisms for further investigations might include the following: IL-12B_ + 1188A/C (rs3212227), IL-12A_ + 277G/A (rs568408), IL-12A_-798T/A (rs582054), IL-12A_-504T/G (rs190533), IL-12A_-1148T/C (rs2243123), and IL-12B_ + 16974 A/C. Perhaps, some of these SNPs may become an attractive target for oncogenomics and possibly could be used in programs of early cancer diagnosis as well as cancer prevention in the nearest future.
C1 [Yuzhalin, Arseniy E.] Kemerovo State Univ, Dept Genet, Kemerovo 650000, Russia.
[Yuzhalin, Arseniy E.; Kutikhin, Anton G.] Kemerovo State Med Acad, Cent Res Lab, Kemerovo, Russia.
[Kutikhin, Anton G.] Kemerovo State Med Acad, Dept Epidemiol, Kemerovo, Russia.
C3 Kemerovo State University; Kemerovo State Medical Academy; Kemerovo
State Medical Academy
RP Yuzhalin, AE (corresponding author), Kemerovo State Univ, Dept Genet, Krasnaya Str 6, Kemerovo 650000, Russia.
EM yuzhalin@gmail.com; antonkutikhin@gmail.com
RI Kutikhin, Anton/B-9397-2012; Yuzhalin, Arseniy/J-3951-2013
OI Kutikhin, Anton G/0000-0001-8679-4857; Yuzhalin,
Arseniy/0000-0001-7454-6653
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NR 127
TC 58
Z9 65
U1 0
U2 24
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0897-7194
EI 1029-2292
J9 GROWTH FACTORS
JI Growth Factors
PD JUN
PY 2012
VL 30
IS 3
BP 176
EP 191
DI 10.3109/08977194.2012.678843
PG 16
WC Cell Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Endocrinology & Metabolism
GA 945IC
UT WOS:000304265300005
PM 22515181
DA 2025-01-07
ER
PT J
AU Tannoury, J
de Mestier, L
Hentic, O
Ruszniewski, P
Créange, A
Sobhani, I
AF Tannoury, Jenny
de Mestier, Louis
Hentic, Olivia
Ruszniewski, Philippe
Creange, Alain
Sobhani, Iradj
TI Contribution of Immune-Mediated Paraneoplastic Syndromes to Neurological
Manifestations of Neuroendocrine Tumours: A Retrospective Study
SO NEUROENDOCRINOLOGY
LA English
DT Article
DE Neuroendocrine tumours; Paraneoplastic neurological syndromes;
Onconeural antibodies; Gut
ID CANCER
AB Introduction: Neurological symptoms associated with neuroendocrine tumours (NETs) may be related to metastatic disease or paraneoplastic syndromes (PNSs); these last are often associated with autoantibodies targeting various onconeural antigens. To better characterize neurological PNSs related to NETs, we report the largest case-series study to date. Methods: We retrospectively reviewed the charts of all patients diagnosed with NETs of the gastrointestinal tract who presented with neurological symptoms at either of 2 tertiary academic hospitals (Henri Mondor and Beaujon, France) between 1994 and 2016. All patients underwent extensive neurological tests including clinical, laboratory, and radiological investigations. The clinical response to immunomodulating agents was recorded. Results: In the 13 identified patients, the most common presentations were peripheral neuropathy (46.2%) and encephalopathy (26.6%). Of the 6 (53.3%) patients whose serum anti-neuronal antibodies were assayed, 5 had high titres. Short-term oral corticosteroid and immunosuppressant drug therapy was given to 4 of these patients, of whom 3 had a clinical response and 1 no response. Repeated high-dose intravenous immunoglobulin therapy induced a complete clinical response in 1 patient. Encephalopathy resolved fully after hepatectomy or intrahepatic chemoembolization for liver metastases in another 2 patients. Discussion: The neurological symptoms associated with NETs may be due in part to autoimmune PNS. Based on experience at our 2 centres, we estimate that autoimmune PNS occurs in about 1% of patients with NETs. Early symptom recognition allows the initiation of effective treatments including corticosteroids, immunosuppressive drugs, and/or intravenous immunoglobulins.
C1 [Tannoury, Jenny; Sobhani, Iradj] Henri Mondor Univ Hosp, Dept Gastroenterol, 51 Ave Marechal de Lattre de Tassigny, FR-94010 Creteil, France.
[de Mestier, Louis; Hentic, Olivia; Ruszniewski, Philippe] Paris Diderot Univ, Beaujon Univ Hosp, ENETS Ctr Excellence, Dept Gastroenterol Pancreatol, Clichy, France.
[Creange, Alain] Paris Est Creteil Univ UPEC, Henri Mondor Univ Hosp, Dept Neurol, Creteil, France.
[Tannoury, Jenny; Sobhani, Iradj] Paris Est Creteil Univ UPEC, EC2M3 EA7375, Creteil, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite
Paris-Est-Creteil-Val-de-Marne (UPEC); Hopital Universitaire
Henri-Mondor - APHP; Universite Paris Cite; Assistance Publique Hopitaux
Paris (APHP); Hopital Universitaire Beaujon - APHP; Assistance Publique
Hopitaux Paris (APHP); Universite Paris-Est-Creteil-Val-de-Marne (UPEC);
Hopital Universitaire Henri-Mondor - APHP; Universite
Paris-Est-Creteil-Val-de-Marne (UPEC)
RP Sobhani, I (corresponding author), Henri Mondor Univ Hosp, Dept Gastroenterol, 51 Ave Marechal de Lattre de Tassigny, FR-94010 Creteil, France.
EM iradj.sobhani@aphp.fr
RI SOBHANI, Iradj/A-3973-2013; de Mestier, Louis/HKO-6167-2023
OI de Mestier, Louis/0000-0001-9715-9189; TANNOURY,
Jenny/0000-0001-6439-1782
FU EC2M3-EA7375 Paris Est Creteil University (UPEC)
FX This study was supported by EC2M3-EA7375 Paris Est Creteil University
(UPEC).
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NR 22
TC 2
Z9 2
U1 0
U2 3
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0028-3835
EI 1423-0194
J9 NEUROENDOCRINOLOGY
JI Neuroendocrinology
PD DEC
PY 2020
VL 111
IS 1-2
BP 123
EP 128
DI 10.1159/000506400
PG 6
WC Endocrinology & Metabolism; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA PG4NU
UT WOS:000599714500009
PM 32040952
DA 2025-01-07
ER
PT J
AU Zhang, YM
Hosaka, N
Cui, YZ
Shi, M
Ikehara, S
AF Zhang, Yuming
Hosaka, Naoki
Cui, Yunze
Shi, Ming
Ikehara, Susumu
TI Effects of Allogeneic Hematopoietic Stem Cell Transplantation Plus
Thymus Transplantation on Malignant Tumors: Comparison Between Fetal,
Newborn, and Adult Mice
SO STEM CELLS AND DEVELOPMENT
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; VERSUS-HOST-DISEASE; AUTOIMMUNE-DISEASES;
DONOR; LYMPHOCYTES; INDUCTION; CARCINOMA; SUBSETS; BMT
AB We have recently shown that allogeneic intrabone marrow-bone marrow transplantation+adult thymus transplantation (TT) is effective for hosts with malignant tumors. However, since thymic and hematopoietic cell functions differ with age, the most effective age for such intervention needed to be determined. We performed hematopoietic stem cell transplantation (HSCT) using the intrabone marrow method with or without TT from fetal, newborn, and adult B6 mice (H-2(b)) into BALB/c mice (H-2(d)) bearing Meth-A sarcoma (H-2(d)). The mice treated with all types of HSCT+TT showed more pronounced regression and longer survival than those treated with HSCT alone in all age groups. Those treated with HSCT+TT showed increased numbers of CD4(+) and CD8(+) T cells but decreased numbers of Gr-1/Mac-1 myeloid suppressor cells and decreased percentages of FoxP3 cells in CD4(+) T cells, compared with those treated with HSCT alone. In all mice, those treated with fetal liver cell (as fetal HSCs) transplantation+fetal TT or with newborn liver cell (as newborn HSCs) transplantation (NLT)+newborn TT (NTT) showed the most regression, and the latter showed the longest survival. The number of Gr-1/Mac-1 cells was the lowest, whereas the percentage of CD62L(-)CD44(+) effector memory T cells and the production of interferon gamma (IFN-gamma) were highest in the mice treated with NLT+NTT. These findings indicate that, at any age, HSCT+TT is more effective against cancer than HSCT alone and that NLT+NTT is most effective.
C1 [Cui, Yunze; Shi, Ming; Ikehara, Susumu] Kansai Med Univ, Dept Stem Cell Disorders, Osaka 5708506, Japan.
[Zhang, Yuming; Hosaka, Naoki] Kansai Med Univ, Dept Pathol 1, Osaka 5708506, Japan.
[Zhang, Yuming] Nanfang Hosp, Dept Pediat, Guangzhou, Guangdong, Peoples R China.
[Cui, Yunze] JIMRO Co Ltd, Gunma, Japan.
C3 Kansai Medical University; Kansai Medical University; Southern Medical
University - China
RP Ikehara, S (corresponding author), Kansai Med Univ, Dept Stem Cell Disorders, 10-15 Fumizono Cho, Osaka 5708506, Japan.
EM ikehara@takii.kmu.ac.jp
RI zhang, yu/HNS-5948-2023
FU Haiteku Research Center of the Ministry of Education; Ministry of
Education, Culture, Sports, Science, and Technology; The 21st Century
Center of Ministry of Education, Culture, Sports, Science, and
Technology; Kansai Medical University, Health and Labor Sciences;
Department of Transplantation for Regeneration Therapy (sponsored by
Otsuka Pharmaceutical Co., Ltd.); Molecular Medical Science Institute
(Otsuka Pharmaceutical Co., Ltd.); Japan Immunoresearch Laboratories
Co., Ltd. (JIMRO)
FX This work was supported by a grant from Haiteku Research Center of the
Ministry of Education, a grant from the Millennium Program of the
Ministry of Education, Culture, Sports, Science, and Technology, a grant
from the Science Frontier Program of the Ministry of Education, Culture,
Sports, Science, and Technology, a grant from The 21st Century Center of
Excellence Program of the Ministry of Education, Culture, Sports,
Science, and Technology, a Research Grant B from Kansai Medical
University, Health and Labor Sciences research grants (Research on Human
Genome, Tissue Engineering Food Biotechnology), a grant from the
Department of Transplantation for Regeneration Therapy (sponsored by
Otsuka Pharmaceutical Co., Ltd.), a grant from the Molecular Medical
Science Institute (Otsuka Pharmaceutical Co., Ltd.), and a grant from
Japan Immunoresearch Laboratories Co., Ltd. (JIMRO). We wish to thank
Ms. Y. Tokuyama and Ms. A. Kitajima for their technical assistance and
Mr. Hilary Eastwick-Field and Ms. K. Ando for their help in the
preparation of the manuscript.
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NR 34
TC 6
Z9 9
U1 0
U2 5
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1547-3287
EI 1557-8534
J9 STEM CELLS DEV
JI Stem Cells Dev.
PD APR
PY 2011
VL 20
IS 4
BP 599
EP 607
DI 10.1089/scd.2010.0230
PG 9
WC Cell & Tissue Engineering; Hematology; Medicine, Research &
Experimental; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Hematology; Research & Experimental Medicine;
Transplantation
GA 743XO
UT WOS:000289053000005
PM 20672991
OA Green Published
DA 2025-01-07
ER
PT J
AU Goraça, A
Huk-Kolega, H
Piechota, A
Kleniewska, P
Ciejka, E
Skibska, B
AF Goraca, Anna
Huk-Kolega, Halina
Piechota, Aleksandra
Kleniewska, Paulina
Ciejka, Elzbieta
Skibska, Beata
TI Lipoic acid - biological activity and therapeutic potential
SO PHARMACOLOGICAL REPORTS
LA English
DT Review
DE lipoic acid; antioxidant activity; therapeutic application
ID NF-KAPPA-B; INDUCED OXIDATIVE STRESS; MITOCHONDRIAL-FUNCTION;
DIHYDROLIPOIC ACID; THIOCTIC ACID; NITRIC-OXIDE; GLYCEMIC CONTROL;
BEAGLE DOG; ALPHA; ANTIOXIDANT
AB alpha-Lipoic acid (LA; 5-(1,2-dithiolan-3-yl)pentanoic acid) was originally isolated from bovine liver by Reed et al. in 1951. LA was once considered a vitamin. Subsequently, it was found that LA is not a vitamin and is synthesized by plants and animals. LA is covalently bound to the c-amino group of lysine residues and functions as a cofactor for mitochondrial enzymes by catalyzing the oxidative decarboxylation of pyruvate, alpha-ketoglutarate and branched-chain alpha-keto acids. LA and its reduced form dihydrolipoic acid (DHLA), meet all the criteria for an ideal antioxidant because they can easily quench radicals, can chelate metals, have an amphiphlic character and they do not exhibit any serious side effects. They interact with other antioxidants and can regenerate them. For this reason, LA is called an antioxidant of antioxidants. LA has an influence on the second messenger nuclear factor kappa B (NF-kappa B) and attenuates the release of free radicals and cytotoxic cytokincs. The therapeutic action of LA is based on its antioxidant properties. Current studies support its use in the ancillary treatment of many diseases, such as diabetes, cardiovascular, neurodegenerative, autoimmune diseases, cancer and AIDS. This review was undertaken to gather the most recent information regarding the therapeutic properties of LA and its possible utility in disease treatment.
C1 [Skibska, Beata] Med Univ Lodz, Dept Appl Pharm, Dept Pharm, PL-90151 Lodz, Poland.
[Goraca, Anna; Huk-Kolega, Halina; Piechota, Aleksandra; Kleniewska, Paulina] Med Univ Lodz, Chair Expt & Clin Physiol, Dept Cardiovasc Physiol, PL-92215 Lodz, Poland.
[Ciejka, Elzbieta] Hlth Care Sch Bialystok, Dept Physiotherapy & Cosmetol, PL-15875 Bialystok, Poland.
C3 Medical University Lodz; Medical University Lodz
RP Skibska, B (corresponding author), Med Univ Lodz, Dept Appl Pharm, Dept Pharm, Muszynskiego 1, PL-90151 Lodz, Poland.
EM beata.skibska@umed.lodz.pl
RI Skibska, Beata/AAM-9077-2021; Kleniewska, Paulina/S-9840-2016;
Piechota-Polanczyk, Aleksandra/IAN-9244-2023
OI Piechota-Polanczyk, Aleksandra/0000-0001-8062-4435
FU Medical University of Lodz [503/0-079-03/503-01]
FX The study was supported by grant 503/0-079-03/503-01 from the Medical
University of Lodz.
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NR 88
TC 337
Z9 368
U1 3
U2 107
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1734-1140
EI 2299-5684
J9 PHARMACOL REP
JI Pharmacol. Rep.
PD JUL-AUG
PY 2011
VL 63
IS 4
BP 849
EP 858
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 854YL
UT WOS:000297530600001
PM 22001972
DA 2025-01-07
ER
PT J
AU Desole, C
Gallo, S
Vitacolonna, A
Vigna, E
Basilico, C
Montarolo, F
Zuppini, F
Casanova, E
Miggiano, R
Ferraris, DM
Bertolotto, A
Comoglio, PM
Crepaldi, T
AF Desole, Claudia
Gallo, Simona
Vitacolonna, Annapia
Vigna, Elisa
Basilico, Cristina
Montarolo, Francesca
Zuppini, Francesca
Casanova, Elena
Miggiano, Riccardo
Ferraris, Davide Maria
Bertolotto, Antonio
Comoglio, Paolo Maria
Crepaldi, Tiziana
TI Engineering, Characterization, and Biological Evaluation of an Antibody
Targeting the HGF Receptor
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE HGF; MET; PSI domains; antibody engineering; regenerative medicine;
anti-cancer therapy; multiple sclerosis; experimental autoimmune
encephalomyelitis
ID HEPATOCYTE GROWTH-FACTOR; TYROSINE KINASE RECEPTOR; C-MET PROTOONCOGENE;
SCATTER FACTOR; HIGH-AFFINITY; MONOCLONAL-ANTIBODIES; DOMAIN-STRUCTURE;
HEPARAN-SULFATE; SERINE-PROTEASE; LIVER FIBROSIS
AB The Hepatocyte growth factor (HGF) and its receptor (MET) promote several physiological activities such as tissue regeneration and protection from cell injury of epithelial, endothelial, neuronal and muscle cells. The therapeutic potential of MET activation has been scrutinized in the treatment of acute tissue injury, chronic inflammation, such as renal fibrosis and multiple sclerosis (MS), cardiovascular and neurodegenerative diseases. On the other hand, the HGF-MET signaling pathway may be caught by cancer cells and turned to work for invasion, metastasis, and drug resistance in the tumor microenvironment. Here, we engineered a recombinant antibody (RDO24) and two derived fragments, binding the extracellular domain (ECD) of the MET protein. The antibody binds with high affinity (8 nM) to MET ECD and does not cross-react with the closely related receptors RON nor with Semaphorin 4D. Deletion mapping studies and computational modeling show that RDO24 binds to the structure bent on the Plexin-Semaphorin-Integrin (PSI) domain, implicating the PSI domain in its binding to MET. The intact RDO24 antibody and the bivalent Fab2, but not the monovalent Fab induce MET auto-phosphorylation, mimicking the mechanism of action of HGF that activates the receptor by dimerization. Accordingly, the bivalent recombinant molecules induce HGF biological responses, such as cell migration and wound healing, behaving as MET agonists of therapeutic interest in regenerative medicine. In vivo administration of RDO24 in the murine model of MS, represented by experimental autoimmune encephalomyelitis (EAE), delays the EAE onset, mitigates the early clinical symptoms, and reduces inflammatory infiltrates. Altogether, these results suggest that engineered RDO24 antibody may be beneficial in multiple sclerosis and possibly other types of inflammatory disorders.
C1 [Desole, Claudia; Gallo, Simona; Vitacolonna, Annapia; Vigna, Elisa; Basilico, Cristina; Zuppini, Francesca; Crepaldi, Tiziana] Univ Turin, Dept Oncol, Candiolo, Italy.
[Gallo, Simona; Vitacolonna, Annapia; Vigna, Elisa; Casanova, Elena; Crepaldi, Tiziana] FPO IRCCS, Candiolo Canc Inst, Candiolo, Italy.
[Montarolo, Francesca; Bertolotto, Antonio] Neurosci Inst Cavalieri Ottolenghi NICO, Orbassano, Italy.
[Montarolo, Francesca] Univ Turin, Dept Mol Biotechnol & Hlth Sci, Turin, Italy.
[Miggiano, Riccardo; Ferraris, Davide Maria] Univ Piemonte Orientale, Dept Pharmaceut Sci, Novara, Italy.
[Miggiano, Riccardo; Ferraris, Davide Maria] IXTAL Srl, Novara, Italy.
[Comoglio, Paolo Maria] IFOM, FIRC Inst Mol Oncol, Milan, Italy.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia;
University of Turin; University of Eastern Piedmont Amedeo Avogadro;
IFOM - FIRC Institute of Molecular Oncology
RP Crepaldi, T (corresponding author), Univ Turin, Dept Oncol, Candiolo, Italy.; Crepaldi, T (corresponding author), FPO IRCCS, Candiolo Canc Inst, Candiolo, Italy.
EM tiziana.crepaldi@unito.it
RI Gallo, Simona/IQS-8032-2023; Comoglio, Paolo/G-6323-2011; Ferraris,
Davide/AAP-7110-2020; Miggiano, Riccardo/AAO-7887-2020; CREPALDI,
TIZIANA/AAY-7207-2020; Casanova, Elena/AAC-1186-2021; Montarolo,
F/K-3331-2018; Vigna, Elisa/JWO-5055-2024
OI Crepaldi, Tiziana/0000-0003-3410-947X; Montarolo,
Francesca/0000-0002-3633-8746; MIGGIANO, Riccardo/0000-0002-2159-3314;
Casanova, Elena/0000-0002-0262-244X; Ferraris, Davide
Maria/0000-0001-5112-9910; Vitacolonna, Annapia/0000-0002-7492-6100
FU Fondazione Italiana Sclerosi Multipla (FISM); AIRC 5permille Program
[N.21719]; AIRC IG [23820, 2017/R/9]; Italian Ministry of Health Ricerca
Corrente 2021
FX Funding This work was supported by Fondazione Italiana Sclerosi Multipla
(FISM), AIRC 5permille Program N.21719, AIRC IG N. 23820 (grant number
2017/R/9) and by Italian Ministry of Health Ricerca Corrente 2021.
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NR 76
TC 4
Z9 5
U1 3
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD DEC 3
PY 2021
VL 12
AR 775151
DI 10.3389/fimmu.2021.775151
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA XQ3KN
UT WOS:000731447200001
PM 34925346
OA Green Published
DA 2025-01-07
ER
PT J
AU Hytiroglou, P
Theise, ND
AF Hytiroglou, Prodromos
Theise, Neil D.
TI Regression of human cirrhosis: an update, 18 years after the pioneering
article by Wanless et al.
SO VIRCHOWS ARCHIV
LA English
DT Review
DE Regression; Cirrhosis; Incomplete septal cirrhosis; Vascular lesions
ID CHRONIC HEPATITIS-B; HISTOLOGICAL IMPROVEMENT; VIROLOGICAL RESPONSE;
FIBROSIS; LIVER; THERAPY; CLASSIFICATION; REVERSIBILITY; DISEASE; SYSTEM
AB Cirrhosis has been traditionally viewed as an irreversible, end-stage condition. Eighteen years ago, Wanless, Nakashima, and Sherman published a study that was based on the concept that hepatic architecture is under constant remodeling in the course of chronic liver diseases, even during their most advanced stages; depending on the balance between injury and repair, the histologic changes might be progressing or regressing. These authors described in detail the morphologic features of regressing cirrhosis, identified a set of histologic features of regression that they called the "hepatic repair complex," and provided convincing morphologic evidence that incomplete septal cirrhosis represents regressed cirrhosis. In the years that followed publication of this pioneering article, a number of clinical studies with performance of pre- and post-treatment liver biopsies provided abundant evidence that cirrhosis can regress after successful therapy of chronic hepatitis B, chronic hepatitis C, autoimmune hepatitis, and genetic hemochromatosis. Evidence for other chronic liver diseases may also be provided in the future, pending ongoing studies. Successful therapy allows resorption of fibrous septa, which can be followed by loss of nodularity and architectural improvement; however, many vascular lesions of cirrhotic livers are not thought to regress. Cases of cirrhosis that are considered more likely to improve than others include those of recent onset, with relatively thin fibrous septa and mild vascular changes. Histologic examination of liver biopsy specimens from patients with chronic liver diseases provides the opportunity to appreciate the features of the hepatic repair complex on a routine diagnostic basis; however, interpretation is often difficult, and can be aided by immunohistochemical stains. Clinicopathologic correlation is essential for a meaningful assessment of such cases. For many patients, cirrhosis is not an end-stage condition anymore; therefore, use of the term "cirrhosis" has been challenged, almost 200 years after its invention. However, regression of cirrhosis does not imply regression of molecular changes involved in hepatocarcinogenesis; therefore, surveillance for hepatocellular carcinoma should be continued in these patients.
C1 [Hytiroglou, Prodromos] Aristotle Univ Thessaloniki, Sch Med, Dept Pathol, Thessaloniki 54006, Greece.
[Theise, Neil D.] NYU, Sch Med, Dept Pathol, 550 First Ave,TH415, New York, NY 10016 USA.
C3 Aristotle University of Thessaloniki; New York University
RP Hytiroglou, P (corresponding author), Aristotle Univ Thessaloniki, Sch Med, Dept Pathol, Thessaloniki 54006, Greece.
EM phitir@med.auth.gr; Neil.Theise@nyumc.com
CR [Anonymous], 1819, AUSCULTATION MEDIATE
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NR 50
TC 38
Z9 42
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0945-6317
EI 1432-2307
J9 VIRCHOWS ARCH
JI Virchows Arch.
PD JUL
PY 2018
VL 473
IS 1
BP 15
EP 22
DI 10.1007/s00428-018-2340-2
PG 8
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA GK9JO
UT WOS:000436563100003
PM 29589101
DA 2025-01-07
ER
PT J
AU Shi, W
Shao, T
Li, JY
Fan, DD
Lin, AF
Xiang, LX
Shao, JZ
AF Shi, Wei
Shao, Tong
Li, Jiang-yuan
Fan, Dong-dong
Lin, Ai-fu
Xiang, Li-xin
Shao, Jian-zhong
TI BTLA-HVEM Checkpoint Axis Regulates Hepatic Homeostasis and Inflammation
in a ConA-Induced Hepatitis Model in Zebrafish
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID HERPESVIRUS ENTRY MEDIATOR; T-CELL-ACTIVATION; B-LYMPHOCYTE;
LIVER-INJURY; RECEPTOR; LIGHT; EXPRESSION; GENE; STIMULATION; MECHANISMS
AB The BTLA-HVEM checkpoint axis plays extensive roles in immunomodulation and diseases, including cancer and autoimmune disorders. However, the functions of this checkpoint axis in hepatitis remain limited. In this study, we explored the regulatory role of the Btla(-)Hvem axis in a ConA-induced hepatitis model in zebrafish. Results showed that Btla and Hvem were differentially expressed on intrahepatic Cd8(+) T cells and hepatocytes. Knockdown of Btla or Hvem significantly promoted hepatic inflammation. Btla was highly expressed in Cd8(+) T cells in healthy liver but was downregulated in inflamed liver, as evidenced by a disparate proportion of Cd8(+)Btla(+) and Cd8(+)Btla(-) T cells in individuals without or with ConA stimulation. Cd8(+)Btla(+) T cells showed minimal cytotoxicity to hepatocytes, whereas Cd8(+)Btla(-) T cells were strongly reactive. The depletion of Cd8(+)Btla(-) T cells reduced hepatitis, whereas their transfer enhanced hepatic inflammation. These observations indicate that Btla endowed Cd8(+)Btla(+) T cells with self-tolerance, thereby preventing them from attacking hepatocytes. Btla downregulation deprived this tolerization. Mechanistically, Btla-Hvem interaction contributed to Cd8(+)Btla(+) T cell tolerization, which was impaired by Hvem knockdown but rescued by soluble Hvem protein administration. Notably, Light was markedly upregulated on Cd8(+)Btla(-) T cells, accompanied by the transition of Cd8(+)Btla(+) Light(-) to Cd8(+)Btla(-)Light(+) T cells during hepatitis, which could be modulated by Cd4(+) T cells. Light blockade attenuated hepatitis, thereby suggesting the positive role of Light in hepatic inflammation. These findings provide insights into a previously unrecognized Btla-Hvem-Light regulatory network in hepatic homeostasis and inflammation, thus adding a new potential therapeutic intervention for hepatitis.
C1 [Shi, Wei; Shao, Tong; Li, Jiang-yuan; Fan, Dong-dong; Lin, Ai-fu; Xiang, Li-xin; Shao, Jian-zhong] Zhejiang Univ, Coll Life Sci, Key Lab Cell & Gene Engn Zhejiang Prov, Hangzhou 310058, Zhejiang, Peoples R China.
[Shao, Jian-zhong] Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266071, Shandong, Peoples R China.
C3 Zhejiang University; Laoshan Laboratory
RP Xiang, LX; Shao, JZ (corresponding author), Zhejiang Univ, Coll Life Sci, 866 YuHangTang Rd, Hangzhou 310058, Zhejiang, Peoples R China.
EM xianglx@zju.edu.cn; shaojz@zju.edu.cn
OI Li, Jiang-Yuan/0000-0002-2147-5908; SHI, Wei/0000-0002-2236-4708
FU National Natural Science Foundation of China [31630083, 31572641];
National Key Research and Development Program of China [2018YFD0900503,
2018YFD0900505, 2016YFA0101001]; Open Fund of the Laboratory for Marine
Biology and Biotechnology; Qingdao National Laboratory for Marine
Science and Technology, Qingdao, China [OF2017NO02]; Open Funding
Project of the State Key Laboratory of Bioreactor Engineering; Zhejiang
Major Special Program of Breeding [2016C02055-4]
FX This work was supported by grants from the National Natural Science
Foundation of China (31630083, 31572641), the National Key Research and
Development Program of China (2018YFD0900503, 2018YFD0900505,
2016YFA0101001), the Open Fund of the Laboratory for Marine Biology and
Biotechnology, the Qingdao National Laboratory for Marine Science and
Technology, Qingdao, China (OF2017NO02), the Open Funding Project of the
State Key Laboratory of Bioreactor Engineering, and the Zhejiang Major
Special Program of Breeding (2016C02055-4).
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NR 62
TC 12
Z9 14
U1 0
U2 19
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD NOV 1
PY 2019
VL 203
IS 9
BP 2425
EP 2442
DI 10.4049/jimmunol.1900458
PG 18
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA JG3GK
UT WOS:000491962200009
PM 31562209
OA Bronze
DA 2025-01-07
ER
PT J
AU Riveiro-Barciela, M
Barreira-Díaz, A
Callejo-Pérez, A
Muñoz-Couselo, E
Díaz-Mejía, N
Díaz-González, A
Londoño, MC
Salcedo, MT
Buti, M
AF Riveiro-Barciela, Mar
Barreira-Diaz, Ana
Callejo-Perez, Ana
Munoz-Couselo, Eva
Diaz-Mejia, Nely
Diaz-Gonzalez, Alvaro
Londono, Maria-Carlota
Salcedo, Maria-Teresa
Buti, Maria
TI Retreatment With Immune Checkpoint Inhibitors After a Severe
Immune-Related Hepatitis: Results From a Prospective Multicenter Study
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Immune -Related Hepatitis; Immunotherapy; Hepatotoxicity; Immune
checkpoint inhibitors
ID ADVERSE EVENTS; MONOTHERAPY; IPILIMUMAB; EFFICACY; CANCER; SAFETY
AB BACKGROUND & AIMS: Liver injury related to immunotherapy is a relatively frequent immune-related adverse event that requires permanent discontinuation of immune checkpoint inhibitors (ICIs) in severe cases. We present the outcome of a cohort of patients who were retreated with immunotherapy after resolution of severe immune-related hepatitis. METHODS: We performed a prospective, multicenter, noninterventional study that included all consecutive patients with cancer and previous grade 3 or 4 immune-related hepatitis who were retreated with ICIs in 3 academic hospitals. RESULTS: Twenty-three patients who developed severe immune-related hepatitis were included: 20 of 23 (87.0%) received a single ICI and 3 of 23 (13.0%) received anti-programmed cell death protein-1 plus an anti-cytotoxic T-lymphocyte-associated antigen. The most frequent cancers were lung cell and urinary tract (7 and 6 cases, respectively). Immunotherapy was discontinued in all cases. Nineteen patients (82.6%) also received corticoids. Patients mainly were retreated with the same ICI (18 of 23; 78.3%) after a median time of 10 weeks (range, 1-54 wk) from the severe immune -related hepatitis. Fifteen patients (65.2%) did not have recurrence of the immune-related hepa-titis after retreatment. Among the 8 (34.8%) subjects with recurrence, 5 of 8 were grade 3 and 3 of 8 were grade 4. Six (75%) had either an underlying autoimmune disease or antinuclear antibodies double dagger 1/80 (75% vs 26.7%; P [ .037). None of the patients with previously grade 4 hepatitis had a recurrence, and those patients who had a recurrence tended to present with a better oncological prognosis. Overall, 19 (82.6%) subjects required permanent discontinuation of ICIs, with cancer progression the main reason for discontinuation (9 of 19; 47.8%). CONCLUSIONS: Retreatment with ICIs is a feasible option after a severe immune-related hepatitis, even with the same ICIs, without recurrence of the liver injury retreatment in up to 65% of patients.
C1 [Riveiro-Barciela, Mar; Barreira-Diaz, Ana; Buti, Maria] Hosp Univ Vall dHebron, Internal Med Dept, Liver Unit, Vall dHebron Barcelona Hosp Campus, Barcelona, Spain.
[Riveiro-Barciela, Mar; Londono, Maria-Carlota; Buti, Maria] Inst Salud Carlos III, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Madrid, Spain.
[Riveiro-Barciela, Mar; Barreira-Diaz, Ana; Buti, Maria] Univ Autonoma Barcelona, Dept Med, Barcelona, Spain.
[Callejo-Perez, Ana; Munoz-Couselo, Eva; Diaz-Mejia, Nely] Hosp Univ Vall dHebron, Oncol Dept, Inst Oncol Vall dHebron, Vall dHebron Barcelona Hosp Campus, Barcelona, Spain.
[Diaz-Gonzalez, Alvaro] Hosp Univ Marques de Valdecilla, Gastroenterol Dept, Inst Invest Sanitaria Valdecilla, Santander, Spain.
[Londono, Maria-Carlota] Hosp Clin Barcelona, Liver Unit, Barcelona, Spain.
[Salcedo, Maria-Teresa] Hosp Univ Vall dHebron, Pathol Dept, Vall dHebron Barcelona Hosp Campus, Barcelona, Spain.
C3 Hospital Universitari Vall d'Hebron; CIBER - Centro de Investigacion
Biomedica en Red; CIBEREHD; Instituto de Salud Carlos III; Autonomous
University of Barcelona; Hospital Universitari Vall d'Hebron; Hospital
Universitario Marques de Valdecilla (HUMV); University of Barcelona;
Hospital Clinic de Barcelona; Hospital Universitari Vall d'Hebron
RP Riveiro-Barciela, M (corresponding author), Hosp Univ Vall dHebron, Dept Internal Med, Liver Unit, Barcelona 08035, Spain.
EM mar.riveiro@gmail.com
RI Díaz-González, Álvaro/KCY-2906-2024; Londono, Maria/KMA-4581-2024; Buti,
MARIA/A-5327-2019
OI Londono, Maria-Carlota/0000-0002-6533-1586; Riveiro-Barciela,
Mar/0000-0001-9309-2052; Callejo, Ana/0000-0003-2556-8412;
Diaz-Gonzalez, Alvaro/0000-0003-3610-2263; Diaz Mejia,
Nely/0000-0001-5006-2929
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NR 24
TC 24
Z9 25
U1 3
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD MAR
PY 2023
VL 21
IS 3
BP 732
EP 740
DI 10.1016/j.cgh.2022.03.050
EA FEB 2023
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 9Q0KU
UT WOS:000944664000001
PM 35487453
DA 2025-01-07
ER
PT J
AU Pacher, P
Mechoulam, R
AF Pacher, P.
Mechoulam, R.
TI Is lipid signaling through cannabinoid 2 receptors part of a protective
system?
SO PROGRESS IN LIPID RESEARCH
LA English
DT Review
DE Endocannabinoids; Cannabinoid 1 and 2 receptors; Disease; Inflammation;
Immune function; Disease
ID ACID AMIDE HYDROLASE; HEPATIC ISCHEMIA/REPERFUSION INJURY;
ISCHEMIA-REPERFUSION INJURY; CEREBRAL ISCHEMIC/REPERFUSION INJURY;
ACTIVATED ENDOCANNABINOID SYSTEM; AMYOTROPHIC-LATERAL-SCLEROSIS; HUMAN
MONOCYTE MIGRATION; FOS PROTEIN EXPRESSION; LONG-TERM DEPRESSION; CB2
RECEPTOR
AB The mammalian body has a highly developed immune system which guards against continuous invading protein attacks and aims at preventing, attenuating or repairing the inflicted damage. It is conceivable that through evolution analogous biological protective systems have been evolved against non-protein attacks. There is emerging evidence that lipid endocannabinoid signaling through cannabinoid 2 (CB2) receptors may represent an example/part of such a protective system/armamentarium. Inflammation/tissue injury triggers rapid elevations in local endocannabinoid levels, which in turn regulate signaling responses in immune and other cells modulating their critical functions. Changes in endocannabinoid levels and/or CB2 receptor expressions have been reported in almost all diseases affecting humans, ranging from cardiovascular, gastrointestinal, liver, kidney, neurodegenerative, psychiatric, bone, skin, autoimmune, lung disorders to pain and cancer, and modulating CB2 receptor activity holds tremendous therapeutic potential in these pathologies. While CB2 receptor activation in general mediates immunosuppressive effects, which limit inflammation and associated tissue injury in large number of pathological conditions, in some disease states activation of the CB2 receptor may enhance or even trigger tissue damage, which will also be discussed alongside the protective actions of the CB2 receptor stimulation with endocannabinoids or synthetic agonists, and the possible biological mechanisms involved in these effects. Published by Elsevier Ltd.
C1 [Pacher, P.] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Mechoulam, R.] Hebrew Univ Jerusalem, Fac Med, Inst Drug Res, Jerusalem, Israel.
C3 National Institutes of Health (NIH) - USA; NIH National Institute on
Alcohol Abuse & Alcoholism (NIAAA); Hebrew University of Jerusalem
RP Pacher, P (corresponding author), NIAAA, Lab Physiol Studies, NIH, 5625 Fishers Lane,MSC 9413, Bethesda, MD 20892 USA.
EM Pacher@mail.nih.gov; mechou@cc.huji.ac.il
RI Pacher, Pal/B-6378-2008
OI Pacher, Pal/0000-0001-7036-8108
FU NIH/NIAAA; NIDA [9789]
FX This study was supported by the Intramural Research Program of NIH/NIAAA
(to P.P.) and by NIDA grant #9789 (to R.M.). The authors are indebted to
Dr. George Kunos for providing key resources and support and apologize
to colleagues whose important work could not be cited because of the
size limitations of this review.
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NR 286
TC 333
Z9 376
U1 0
U2 56
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7827
EI 1873-2194
J9 PROG LIPID RES
JI Prog. Lipid Res.
PD APR
PY 2011
VL 50
IS 2
BP 193
EP 211
DI 10.1016/j.plipres.2011.01.001
PG 19
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA 750KA
UT WOS:000289543800004
PM 21295074
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Huotari, A
Herzig, KH
AF Huotari, Anne
Herzig, Karl-Heinz
TI Vitamin D and living in northern latitudes - An endemic risk area for
vitamin D deficiency
SO INTERNATIONAL JOURNAL OF CIRCUMPOLAR HEALTH
LA English
DT Review
DE vitamin D; northern latitudes; vitamin D deficiency
ID 25-HYDROXYVITAMIN D CONCENTRATIONS; BONE-MINERAL DENSITY;
PROSTATE-CANCER RISK; D SUPPLEMENTATION; PARATHYROID-HORMONE;
DIETARY-INTAKE; 1,25-DIHYDROXYVITAMIN D-3; SERUM 25-HYDROXYVITAMIN-D;
CALCIUM SUPPLEMENTATION; MULTIPLE-SCLEROSIS
AB Objectives. To review the current literature on the health effects of vitamin D, especially the effects on inhabitants living in the northern latitudes.
Study Design. Literature review.
Methods The scientific literature concerning health effects of vitamin D was reviewed and the current dietary recommendations for inhabitants living in northern latitudes were discussed.
Results. Vitamin D is a steroid-structured hormone produced in the skin upon exposure to UVB-radiation or obtained from certain,food products (for example, liver). Its production,is mediated by the vitamin D receptor, which belongs to the nuclear receptor family, and exerts its function as a transcription factor regulating several target genes. Active metabolites of vitamin D play an important role in calcium and phosphate homeostasis. Deficiency of vitamin D results in diminished bone mineralization and an increased risk of fractures. In addition, vitamin D is connected to a variety of other diseases that include different cancer types, muscular weakness, hypertension, autoimmune diseases, multiple sclerosis, type 1 diabetes, schizophrenia and depression.
Conclusions. Vitamin D plays a fundamental role in calcium and phosphate homeostasis. A deficiency of vitamin D has been attributed to several diseases. Since its production in the skin depends on exposure to UVB-radiation via the sunlight, the level of vitamin D is of crucial importance for the health of inhabitants who live in the Nordic latitudes where there is diminished exposure to sunlight during the winter season. Therefore, fortification or supplementation of vitamin D is necessary for most of the people living in the northern latitudes during the winter season to maintain adequate levels of circulating 25(OH)D-3 to maintain optimal body function and prevent diseases.
C1 [Herzig, Karl-Heinz] Oulu Univ, Sch Med, Dept Physiol, Inst Biomed, Oulu 90014, Finland.
[Huotari, Anne; Herzig, Karl-Heinz] Univ Kuopio, AI Virtanen Inst Mol Sci, FIN-70211 Kuopio, Finland.
[Herzig, Karl-Heinz] Kuopio Univ Hosp, Dept Internal Med, SF-70210 Kuopio, Finland.
[Herzig, Karl-Heinz] Oulu Univ, Sch Med, Bioctr Oulu, Oulu 90014, Finland.
C3 University of Oulu; University of Eastern Finland; Kuopio University
Hospital; University of Eastern Finland; University of Oulu
RP Herzig, KH (corresponding author), Oulu Univ, Sch Med, Dept Physiol, Inst Biomed, Aapistie 7, Oulu 90014, Finland.
EM karl-heinz.herzig@oulu.fi
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NR 101
TC 93
Z9 107
U1 0
U2 23
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1239-9736
EI 2242-3982
J9 INT J CIRCUMPOL HEAL
JI Int. J. Circumpolar Health
PD JUN
PY 2008
VL 67
IS 2-3
BP 164
EP 178
DI 10.3402/ijch.v67i2-3.18258
PG 15
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA 328CW
UT WOS:000257776200002
PM 18767337
OA gold
DA 2025-01-07
ER
PT J
AU Vanderschaeghe, D
Meuris, L
Raes, T
Grootaert, H
Van Hecke, A
Verhelst, X
Van de Velde, F
Lapauw, B
Van Vlierberghe, H
Callewaert, N
AF Vanderschaeghe, Dieter
Meuris, Leander
Raes, Tom
Grootaert, Hendrik
Van Hecke, Annelies
Verhelst, Xavier
Van de Velde, Frederique
Lapauw, Bruno
Van Vlierberghe, Hans
Callewaert, Nico
TI Endoglycosidase S Enables a Highly Simplified Clinical Chemistry
Procedure for Direct Assessment of Serum IgG Undergalactosylation in
Chronic Inflammatory Disease
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID STREPTOCOCCUS-PYOGENES; N-GLYCOSYLATION; LIVER FIBROSIS;
GALACTOSYLATION; PROTEIN; BIOMARKER; ENDOS; GLYCOME; CANCER; FAB
AB Over the past 30 years, it has been firmly established that a wide spectrum of (autoimmune) diseases such as rheumatoid arthritis, Crohn's and lupus, but also other pathologies like alcoholic and non-alcoholic steatohepatitis (ASH and NASH) are driven by chronic inflammation and are hallmarked by a reduced level of serum IgG galactosylation. IgG (under)galactosylation is a promising biomarker to assess disease severity, and monitor and adjust therapy. However, this biomarker has not been implemented in routine clinical chemistry because of a complex analytical procedure that necessitates IgG purification, which is difficult to perform and validate at high throughput. We addressed this issue by using endo-beta-N-acetyl-glucosaminidase from Streptococcus pyogenes (endoS) to specifically release Fc N-glycans in whole serum. The entire assay can be completed in a few hours and only entails adding endoS and labeling the glycans with APTS. Glycans are then readily analyzed through capillary electrophoresis. We demonstrate in two independent patient cohorts that IgG undergalactosylation levels obtained with this assay correlate very well with scores calculated from PNGaseF-released glycans of purified antibodies. Our new assay allows to directly and specifically measure the degree of IgG galactosylation in serum through a fast and completely liquid phase protocol, without the requirement for antibody purification. This should help advancing this biomarker toward clinical implementation.
C1 [Vanderschaeghe, Dieter; Meuris, Leander; Raes, Tom; Grootaert, Hendrik; Van Hecke, Annelies; Callewaert, Nico] VIB Ctr Med Biotechnol, Technol Pk 927, B-9052 Ghent, Belgium.
[Vanderschaeghe, Dieter; Meuris, Leander; Raes, Tom; Grootaert, Hendrik; Van Hecke, Annelies; Callewaert, Nico] Univ Ghent, Dept Biochem & Microbiol, Ledeganckstr 35, B-9000 Ghent, Belgium.
[Verhelst, Xavier; Van Vlierberghe, Hans] Ghent Univ Hosp, Dept Hepatol & Gastroenterol, Lab Hepatol, Corneel Heymanslaan 10, B-9000 Ghent, Belgium.
[Van de Velde, Frederique; Lapauw, Bruno] Ghent Univ Hosp, Dept Endocrinol, Corneel Heymanslaan 10, B-9000 Ghent, Belgium.
C3 Flanders Institute for Biotechnology (VIB); Ghent University; Ghent
University; Ghent University Hospital; Ghent University; Ghent
University Hospital
RP Callewaert, N (corresponding author), VIB UGhent Univ, Ctr Med Biotechnol, Unit Med Biotechnol, Technol Pk 927, B-9052 Ghent, Belgium.
EM Nico.Callewaert@ugent.vib.be
RI Verhelst, Xavier/ABF-6965-2021; Vanderschaeghe, Dieter/A-5577-2011;
Lapauw, Bruno/AAB-4463-2021; Meuris, Leander/B-6988-2015
OI Grootaert, Hendrik/0000-0002-1411-8195; Van Vlierberghe,
Hans/0000-0003-0647-9238; Verhelst, Xavier/0000-0002-2798-5415; Meuris,
Leander/0000-0001-8940-3022; Van Hecke, Annelies/0000-0002-3010-8034;
Lapauw, Bruno/0000-0002-1584-4965
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NR 39
TC 15
Z9 16
U1 0
U2 17
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI ROCKVILLE
PA 11200 ROCKVILLE PIKE, SUITE 302, ROCKVILLE, MD, UNITED STATES
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD DEC
PY 2018
VL 17
IS 12
BP 2508
EP 2517
DI 10.1074/mcp.TIR118.000740
PG 10
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA HD4DC
UT WOS:000452476000016
PM 30190373
OA Green Published, Green Submitted, hybrid
DA 2025-01-07
ER
PT J
AU Shekari, F
Nazari, A
Kashani, SA
Hajizadeh-Saffar, E
Lim, R
Baharvand, H
AF Shekari, Faezeh
Nazari, Abdoreza
Kashani, Sara Assar
Hajizadeh-Saffar, Ensiyeh
Lim, Rebecca
Baharvand, Hossein
TI Pre-clinical investigation of mesenchymal stromal cell-derived
extracellular vesicles: a systematic review
SO CYTOTHERAPY
LA English
DT Review
DE animal models; exosomes; extracellular vesicles; mesenchymal stromal
cells; pre-clinical studies
ID EXOSOMES; MODELS
AB The therapeutic potential of naturally secreted micro-and nanoscale extracellular vesicles (EVs) makes them attractive candidates for regenerative medicine and pharmaceutical science applications. To date, the results of numerous publications have shown the practicality of using EVs to replace mesenchymal stromal cells (MSCs) or liposomes. This article presents a systematic review of pre-clinical studies conducted over the past decade of MSC-derived EVs (MSC-EVs) used in animal models of disease. The authors searched the relevant literature in the PubMed and Scopus databases (9358 articles), and 690 articles met the inclusion criteria. The eligible articles were placed in the following disease categories: autoimmune, brain, cancer, eye, gastrointestinal, heart, inflammation/transplantation, liver, musculoskeletal, pancreas, spinal cord and peripheral nervous system, respiratory system, reproductive system, skin, urinary system and vascular-related diseases. Next, the eligible articles were assessed for the rate of publication and global distribution, methodology of EV isolation and characterization, route of MSC-EV administration, length of follow-up, source of MSCs and animal species. The current review classifies and critically discusses the technical aspects of these MSC-EV animal studies and discusses potential relationships between methodological details and the effectiveness of MSC-EVs as reported by these pre-clinical studies.
Crown Copyright (c) 2021. Published by Elsevier Inc. on behalf of International Society for Cell & Gene Therapy. All rights reserved.
C1 [Shekari, Faezeh; Nazari, Abdoreza; Kashani, Sara Assar; Baharvand, Hossein] Acad Ctr Educ Culture & Res, Royan Inst Stem Cell Biol & Technol, Dept Stem Cells & Dev Biol, Cell Sci Res Ctr, Banihashem Sq,Banihashem St,Resalat Highway, Tehran 1665659911, Iran.
[Shekari, Faezeh; Baharvand, Hossein] Univ Sci & Culture, Dept Biol, Tehran, Iran.
[Hajizadeh-Saffar, Ensiyeh] Acad Ctr Educ Culture & Res, Cell Sci Res Ctr, Royan Inst Stem Cell Biol & Technol, Dept Regenerat Med, Tehran, Iran.
[Shekari, Faezeh; Nazari, Abdoreza; Hajizadeh-Saffar, Ensiyeh] Acad Ctr Educ Culture & Res, Adv Therapy Med Prod Technol Dev Ctr, Royan Inst Stem Cell Biol & Technol, Tehran, Iran.
[Lim, Rebecca] Monash Univ, Ritchie Ctr, Hudson Inst Med Res, Dept Obstet & Gynecol, Clayton, Vic, Australia.
C3 Academic Center for Education, Culture & Research (ACECR); Academic
Center for Education, Culture & Research (ACECR); Academic Center for
Education, Culture & Research (ACECR); Monash University; Hudson
Institute of Medical Research
RP Shekari, F; Baharvand, H (corresponding author), Acad Ctr Educ Culture & Res, Royan Inst Stem Cell Biol & Technol, Dept Stem Cells & Dev Biol, Cell Sci Res Ctr, Banihashem Sq,Banihashem St,Resalat Highway, Tehran 1665659911, Iran.
EM faezehshekari@gmail.com; baharvand@royaninstitute.org
RI Sheakri, Faezeh/AEL-2145-2022; Nazari, Abdoreza/AAH-8821-2019;
Baharvand, Hossein/IVV-0758-2023
OI Nazari, Abdolreza/0009-0001-0315-3534; Assar Kashani,
Sara/0009-0001-8161-9571; Baharvand, Hossein/0000-0001-6528-3687;
Shekari, Faezeh/0000-0001-6026-5412
FU Royan Institute
FX This study was funded by grants provided by the Royan Institute.
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NR 33
TC 29
Z9 30
U1 0
U2 15
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1465-3249
EI 1477-2566
J9 CYTOTHERAPY
JI Cytotherapy
PD APR
PY 2021
VL 23
IS 4
BP 277
EP 284
DI 10.1016/j.jcyt.2020.12.0091465-3249/
PG 8
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology; Hematology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research
& Experimental Medicine
GA RC2YB
UT WOS:000632669600001
PM 33541780
DA 2025-01-07
ER
PT J
AU Tafech, B
Mohabatpour, F
Hedtrich, S
AF Tafech, Belal
Mohabatpour, Fatemeh
Hedtrich, Sarah
TI Surface modification of lipid nanoparticles for gene therapy
SO JOURNAL OF GENE MEDICINE
LA English
DT Review
DE conjugation; gene therapy; lipid nanoparticles; selective targeting;
surface engineering
ID MESSENGER-RNA; TARGETED DELIVERY; IN-VIVO; PLGA NANOPARTICLES;
CANCER-CELLS; HB-EGF; PEPTIDE; SIRNA; THERAPEUTICS; APTAMERS
AB Gene therapies have the potential to target and effectively treat a variety of diseases including cancer as well as genetic, neurological, and autoimmune disorders. Although we have made significant advances in identifying non-viral strategies to deliver genetic cargo, certain limitations remain. In general, gene delivery is challenging for several reasons including the instabilities of nucleic acids to enzymatic and chemical degradation and the presence of restrictive biological barriers such as cell, endosomal and nuclear membranes. The emergence of lipid nanoparticles (LNPs) helped overcome many of these challenges. Despite its success, further optimization is required for LNPs to yield efficient gene delivery to extrahepatic tissues, as LNPs favor accumulation in the liver after systemic administration. In this mini-review, we provide an overview of current preclinical approaches in that LNP surface modification was leveraged for cell and tissue targeting by conjugating aptamers, antibodies, and peptides among others. In addition to their cell uptake and efficiency-enhancing effects, we outline the (dis-)advantages of the different targeting moieties and commonly used conjugation strategies.
Surface modifications of lipid nanoparticles have the potential to overcome the current limitation of low targeting efficacies of extrahepatic tissues. Here, a variety of targeting moieties can be employed such as peptides, small-molecule ligands and aptamers among others.image
C1 [Tafech, Belal; Mohabatpour, Fatemeh; Hedtrich, Sarah] Univ British Columbia, Fac Pharmaceut Sci, Vancouver, BC, Canada.
[Hedtrich, Sarah] Univ Med Berlin, Berlin Inst Hlth Charite, Ctr Biol Design, Berlin, Germany.
[Hedtrich, Sarah] Charite Univ Med Berlin, Dept Infect Dis & Resp Med, Berlin, Germany.
[Hedtrich, Sarah] Free Univ Berlin, Berlin, Germany.
[Hedtrich, Sarah] Humboldt Univ, Berlin, Germany.
[Hedtrich, Sarah] Max Delbruck Ctr Mol Med, Helmholtz Assoc, Berlin, Germany.
[Hedtrich, Sarah] Charite, Berlin Inst Hlth, Lindenberger Weg 80, D-13125 Berlin, Germany.
C3 University of British Columbia; Berlin Institute of Health; Free
University of Berlin; Humboldt University of Berlin; Charite
Universitatsmedizin Berlin; Berlin Institute of Health; Free University
of Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
Berlin; Free University of Berlin; Humboldt University of Berlin;
Helmholtz Association; Max Delbruck Center for Molecular Medicine;
Berlin Institute of Health; Free University of Berlin; Humboldt
University of Berlin; Charite Universitatsmedizin Berlin
RP Hedtrich, S (corresponding author), Charite, Berlin Inst Hlth, Lindenberger Weg 80, D-13125 Berlin, Germany.
EM sarah.hedtrich@bih-charite.de
OI Hedtrich (nee Kuchler), Sarah/0000-0001-6770-3657
FU Mitacs Canada [IT19059]; Providence Healthcare; Canadian Institute of
Health Research [CIHR PJT-166035]; LEO Foundation [LF-OC-22-000954];
Foundation Charite
FX Mitacs Canada, Grant/Award Number: IT19059; Providence Healthcare;
Canadian Institute of Health Research, Grant/Award Number: CIHR
PJT-166035; LEO Foundation, Grant/Award Number: LF-OC-22-000954;
Foundation Charite
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NR 120
TC 2
Z9 2
U1 14
U2 28
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1099-498X
EI 1521-2254
J9 J GENE MED
JI J. Gene. Med.
PD JAN
PY 2024
VL 26
IS 1
DI 10.1002/jgm.3642
EA DEC 2023
PG 18
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA KB9V8
UT WOS:001112416900001
PM 38043928
DA 2025-01-07
ER
PT J
AU Silva, MF
Ribeiro, C
Gonçalves, VMF
Tiritan, ME
Lima, A
AF Silva, Monica Francisco
Ribeiro, Claudia
Goncalves, Virginia M. F.
Tiritan, Maria Elizabeth
Lima, Aurea
TI Liquid chromatographic methods for the therapeutic drug monitoring of
methotrexate as clinical decision support for personalized medicine: A
brief review
SO BIOMEDICAL CHROMATOGRAPHY
LA English
DT Review
DE 7-hydroxymethotrexate; liquid chromatography; methotrexate; methotrexate
polyglutamates; personalized medicine; therapeutic drug monitoring
ID LOW-DOSE METHOTREXATE; RHEUMATOID-ARTHRITIS PATIENTS; HPLC METHOD;
OSTEOSARCOMA PATIENTS; MASS-SPECTROMETRY; HUMAN PLASMA; LC-MS/MS;
POLYGLUTAMATES; METABOLITES; TOXICITY
AB Methotrexate (MTX) is an antifolate drug used for several diseases. Depending on the disease, MTX can be administered at low dose (LDMTX) in some autoimmune diseases, like rheumatoid arthritis, or at high dose (HDMTX) in some cancers, such as acute lymphoblastic leukemia. After absorption, MTX is metabolized in the liver to 7-hydroxymethotrexate and in the intestine to 2,4-diamino-N10-methylpteroic acid(DAMPA). Moreover, inside red blood cells, MTX is converted to active metabolites, MTX polyglutamates (MTXPGs), contributing to its pharmacodynamics. Owing to its narrow therapeutic range, and inter- and intra-patient variability, either noneffectiveness and/or toxicity may occur. Because of the existence of a relationship between drug therapeutic outcome and its systemic concentration, therapeutic drug monitoring (TDM) may ensure the effectiveness and safety of MTX use. In order to monitor the optimization of patient clinical response profile, several analytical methods have been described for TDM in biological samples. These include liquid chromatography (LC) coupled with ultraviolet detection, fluorescence detection or mass spectrometry, each one presenting advantages and drawbacks. This paper reviews the most commonly used techniques for sample preparation and critically discusses the current LC methods applied for the TDM of MTX in biological samples, at LDMTX and HDMTX.
C1 [Silva, Monica Francisco; Ribeiro, Claudia; Goncalves, Virginia M. F.; Tiritan, Maria Elizabeth; Lima, Aurea] Inst Invest & Formacao Avancada Ciencias & Tecnol, CESPU, Rua Cent Gandra, Gandra, Prd, Portugal.
[Silva, Monica Francisco] Univ Coimbra, Fac Med, Coimbra, Portugal.
[Ribeiro, Claudia; Tiritan, Maria Elizabeth] Univ Porto, Ctr Interdisciplinar Invest Marinha & Ambiental, Porto, Portugal.
[Tiritan, Maria Elizabeth] Univ Porto, Dept Ciencias Quim, Lab Quim Organ & Farmaceut, Fac Farm, Rua Jorge Viterbo Ferreira, Porto, Portugal.
[Lima, Aurea] Inst Portugues Oncol Porto, Ctr Invest, Grp Oncol Mol & Patol Viral, Rua Dr Antonio Bernardino de Almeida, Porto, Portugal.
[Lima, Aurea] Ctr Hosp Porto, Hosp Santo Antonio, EPE Largo Prof Abel Salazar, Porto, Portugal.
C3 Universidade de Coimbra; Universidade do Porto; Universidade do Porto
RP Ribeiro, C; Lima, A (corresponding author), Inst Invest & Formacao Avancada Ciencias & Tecnol, CESPU, Rua Cent Gandra, Gandra, Prd, Portugal.
EM claudia.ribeiro@iucs.cespu.pt; aurealima1010@hotmail.com
RI Gonçalves, Virginia/ABH-5466-2020; Tiritan, Maria/K-2243-2019; Ribeiro,
Cláudia/AGL-8265-2022
OI Ferreira Goncalves, Virginia Maria/0000-0002-9151-516X; Tiritan, Maria
Elizabeth/0000-0003-3320-730X; Ribeiro, Claudia/0000-0001-7245-4552;
Lima, Aurea/0000-0002-9779-0584
FU CESPU through project PGx_MTX_RA-CESPU; CESPU through project
PHARMADRUGS-CESPU; CESPU through project ChiralDrugs_CESPU
FX This work was financially supported by CESPU through projects
PGx_MTX_RA-CESPU-2014, PHARMADRUGS-CESPU-2014 and
ChiralDrugs_CESPU_2017.
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NR 66
TC 24
Z9 26
U1 0
U2 39
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-3879
EI 1099-0801
J9 BIOMED CHROMATOGR
JI Biomed. Chromatogr.
PD MAY
PY 2018
VL 32
IS 5
AR e4159
DI 10.1002/bmc.4159
PG 13
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Pharmacology & Pharmacy
GA GD4HO
UT WOS:000430464400001
PM 29226354
DA 2025-01-07
ER
PT J
AU Pezone, A
Olivieri, F
Napoli, MV
Procopio, A
Avvedimento, EV
Gabrielli, A
AF Pezone, Antonio
Olivieri, Fabiola
Napoli, Maria Vittoria
Procopio, Antonio
Avvedimento, Enrico Vittorio
Gabrielli, Armando
TI Inflammation and DNA damage: cause, effect or both
SO NATURE REVIEWS RHEUMATOLOGY
LA English
DT Review
ID HOMOLOGY-DIRECTED REPAIR; CELLULAR SENESCENCE; AIM2 INFLAMMASOME;
TRANSPOSABLE ELEMENTS; OXIDATIVE STRESS; CANCER; DISEASE; NAD(+); CELLS;
LIVER
AB Inflammation is a biological response involving immune cells, blood vessels and mediators induced by endogenous and exogenous stimuli, such as pathogens, damaged cells or chemicals. Unresolved (chronic) inflammation is characterized by the secretion of cytokines that maintain inflammation and redox stress. Mitochondrial or nuclear redox imbalance induces DNA damage, which triggers the DNA damage response (DDR) that is orchestrated by ATM and ATR kinases, which modify gene expression and metabolism and, eventually, establish the senescent phenotype. DDR-mediated senescence is induced by the signalling proteins p53, p16 and p21, which arrest the cell cycle in G1 or G2 and promote cytokine secretion, producing the senescence-associated secretory phenotype. Senescence and inflammation phenotypes are intimately associated, but highly heterogeneous because they vary according to the cell type that is involved. The vicious cycle of inflammation, DNA damage and DDR-mediated senescence, along with the constitutive activation of the immune system, is the core of an evolutionarily conserved circuitry, which arrests the cell cycle to reduce the accumulation of mutations generated by DNA replication during redox stress caused by infection or inflammation. Evidence suggests that specific organ dysfunctions in apparently unrelated diseases of autoimmune, rheumatic, degenerative and vascular origins are caused by inflammation resulting from DNA damage-induced senescence.
In this Review, the authors describe the relationships between persistent DNA damage, inflammation and cellular senescence, which represent a common pathway that contributes to the pathology of many conditions, including rheumatic diseases.
C1 [Pezone, Antonio] Univ Federico II, Dipartimento Biol, Naples, Italy.
[Olivieri, Fabiola; Napoli, Maria Vittoria; Procopio, Antonio] Univ Politecn Marche, Dipartimento Sci Clin & Molecolari, DISCLIMO, Ancona, Italy.
[Olivieri, Fabiola; Procopio, Antonio] IRCCS, Clin Med Lab & Precis, INRCA, Ancona, Italy.
[Avvedimento, Enrico Vittorio] Univ Federico II, Ist Endocrinol Oncol Sperimentale, Dipartimento Med Mol & Biotecnol Med, CNR, Naples, Italy.
[Gabrielli, Armando] Univ Politecn Marche, Fdn Med Mol & Terapia Cellulare, Ancona, Italy.
C3 University of Naples Federico II; Marche Polytechnic University; IRCCS
INRCA; University of Naples Federico II; Consiglio Nazionale delle
Ricerche (CNR); Istituto per Endocrinologia e Oncologia "Gaetano
Salvatore" (IEOS-CNR); Marche Polytechnic University
RP Pezone, A (corresponding author), Univ Federico II, Dipartimento Biol, Naples, Italy.; Avvedimento, EV (corresponding author), Univ Federico II, Ist Endocrinol Oncol Sperimentale, Dipartimento Med Mol & Biotecnol Med, CNR, Naples, Italy.; Gabrielli, A (corresponding author), Univ Politecn Marche, Fdn Med Mol & Terapia Cellulare, Ancona, Italy.
EM antonio.pezone@unina.it; avvedim@unina.it; a.gabrielli@staff.univpm.it
RI Olivieri, Fabiola/K-6465-2016; Pezone, Antonio/AAL-3765-2021
OI Avvedimento, Vittorio Enrico/0000-0001-6087-3442; Pezone,
Antonio/0000-0002-0068-6212
FU PON RI 2014-2020 [E65F21002850007]; POR Campania FESR 2014-2020 "SATIN"
grant; Fondazione di Medicina Molecolare e Terapia Cellulare
(Ancona-Italy)
FX A. Pezone is supported by the PON R&I 2014-2020 [E65F21002850007],
E.V.A. is supported by the POR Campania FESR 2014-2020 "SATIN" grant,
and A.G. is supported by Fondazione di Medicina Molecolare e Terapia
Cellulare (Ancona-Italy).
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Z9 65
U1 26
U2 116
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1759-4790
EI 1759-4804
J9 NAT REV RHEUMATOL
JI Nat. Rev. Rheumatol.
PD APR
PY 2023
VL 19
IS 4
BP 200
EP 211
DI 10.1038/s41584-022-00905-1
EA FEB 2023
PG 12
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA A3AQ2
UT WOS:000928883900004
PM 36750681
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Zheng, N
Wei, AL
Wu, T
Long, L
Yang, HY
Li, H
Wang, LL
AF Zheng, Nan
Wei, Aili
Wu, Tong
Long, Long
Yang, Haiying
Li, Hua
Wang, Lili
TI Triptolide and atorvastatin synergistically promote hepatotoxicity in
cultured hepatocytes and female Sprague-Dawley rats by inhibiting
pregnane X receptor-mediated transcriptional activation of CYP3A4
SO TOXICOLOGY LETTERS
LA English
DT Article
DE Triptolide; Atorvastatin; Synergistic hepatotoxicity; Progesterone X
receptor; CYP3A4; RNAPIIi
ID NUCLEAR RECEPTORS; PXR; TARGET; CYTOCHROME-P450; METABOLISM; PREDICTION;
TOXICITY; TFIIH; CAR
AB Triptolide (TP), an active component of Tripterygium wilfordii Hook. F, has been widely used in China for treating autoimmune and inflammatory diseases, and has also been validated by modern science and developed as a candidate anti-cancer treatment. However, liver toxicity of TP has seriously hindered its use and development, the clinical features and primary toxicological mechanism have been unclear. Considering the major target regulation mechanism of TP is the suppression of global transcription regulated by RNAPII, which is closed related with the detoxification of drugs. This paper tries to verify the synergistic liver injury and its mechanism of TP when co-administered with CYP3A4 substrate drug. The experiments showed that TP dose-dependently blocked transcriptional activation of CYP3A4 in both hPXR and hPXR-CYP3A4 reporter cell lines, lowered the mRNA and protein expression of PXR target genes such as CYP3A1, CYP2B1, and MDR1, and inhibited the functional activity of CYP3A in a time- and concentration-dependent manner in sandwich-cultured rat hepatocytes (SCRH) and female Sprague-Dawley (f-SD) rats. Furthermore, TP combined with atorvastatin (ATR), the substrate of CYP3A4, synergistically enhanced hepatotoxicity in cultured HepG2 and SCRH cells (CI is 0.38 and 0.29, respectively), as well as in f-SD rats, with higher exposure levels of both drugs. These results clearly indicate that TP inhibits PXR-mediated transcriptional activation of CYP3A4, leading to a blockade on the detoxification of itself and ATR, thereby greatly promoting liver injury. This study may implies the key cause of TP related liver injury and provides experimental data for the rational use of TP in a clinical scenario. (C) 2021 Published by Elsevier B.V.
C1 [Zheng, Nan; Wei, Aili; Wu, Tong; Long, Long; Yang, Haiying; Li, Hua; Wang, Lili] Beijing Inst Pharmacol & Toxicol, State Key Lab Toxicol & Med Countermeasures, Beijing 100850, Peoples R China.
[Zheng, Nan] Chinese Acad Med Sci, Beijing Hosp, Natl Ctr Gerontol,Dept Pharm, Inst Geriatr Med,Beijing Key Lab Assessment Clin, Beijing 100730, Peoples R China.
[Wang, Lili] Guizhou Med Univ, State Key Lab Funct & Applicat Med Plants, Guiyang 550014, Peoples R China.
C3 Academy of Military Medical Sciences - China; Chinese Academy of Medical
Sciences - Peking Union Medical College; Beijing Hospital; Guizhou
Medical University
RP Li, H; Wang, LL (corresponding author), Beijing Inst Pharmacol & Toxicol, State Key Lab Toxicol & Med Countermeasures, Beijing 100850, Peoples R China.
EM amms_hli@126.com; wangll63@126.con
RI Li, Hua/Q-5308-2016
OI Zheng, Nan/0000-0003-3565-3100
FU National Key Research & Development Program [2018YFC1602405]; National
Natural Science Foundation of China [81803836]; State Key Laboratory of
Functions and Applications of Medicinal Plants project, Guizhou Medical
University [FAMP201708K]
FX This work was financially supported by the National Key Research &
Development Program (2018YFC1602405), the National Natural Science
Foundation of China (Grant No. 81803836), and partially supported by the
State Key Laboratory of Functions and Applications of Medicinal Plants
project, Guizhou Medical University (FAMP201708K).
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NR 48
TC 14
Z9 16
U1 0
U2 27
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0378-4274
EI 1879-3169
J9 TOXICOL LETT
JI Toxicol. Lett.
PD MAY 15
PY 2021
VL 342
BP 85
EP 94
DI 10.1016/j.toxlet.2021.02.008
EA FEB 2021
PG 10
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA QU6RZ
UT WOS:000627409800009
PM 33600922
DA 2025-01-07
ER
PT J
AU Petryk, N
Shevchenko, O
AF Petryk, Nataliia
Shevchenko, Oleksandr
TI Mesenchymal Stem Cells Anti-Inflammatory Activity in Rats:
Proinflammatory Cytokines
SO JOURNAL OF INFLAMMATION RESEARCH
LA English
DT Article
DE chronic inflammation; mesenchymal stem cells; carrageenan; tumor
necrosis; factor-alpha; interleukin-6; C-reactive protein
ID TNF-ALPHA; IMMUNOSUPPRESSION; RECEPTORS; CANCER; BLOOD; LIVER
AB Introduction: Many widespread intractable diseases are caused or supported by chronic inflammation. Such conditions include the 2nd type of diabetes mellitus, atherosclerosis, neurodegenerative diseases, chronic inflammatory diseases of the connective tissue - anky-losing spondylitis, rheumatoid arthritis, autoimmune myositis, etc. Therefore, the search for targeted treatment of these illnesses is extremely in high demand. Immunomodulatory activity of mesenchymal stem cells is one of their remarkable properties. Several biomarkers (cytokines and nonspecific proteins) are known to be associated with chronic inflammation.
Methods: Our study aimed to investigate the serum levels of tumor necrosis factor-alpha, interleukin 6 and C-reactive protein in carrageenan myositis in rats, because there is more and more evidence of the significance of these markers in the course and resolution of the diseases mentioned above. For the first time in our experiment, it was shown and evaluated using analysis of variance, how MSCs influence the indicators of proinflammatory cytokines on the model of carrageenan myositis. The levels of alpha-TNF, IL-6 and CRP in the plasma of rats were studied in groups with chronic carrageenan inflammation and chronic inflammation with local injection of MSCs into the affected area.
Results: Our study proved the effectiveness of MSCs by showing a significant decrease in the levels of inflammatory mediators in the plasma of the studied animals.
Discussion and Conclusions: Thus, the administration of MSCs is a promising tool in the pathogenic treatment of chronic inflammation and concomitant conditions.
C1 [Petryk, Nataliia; Shevchenko, Oleksandr] Kharkiv Natl Med Univ, Dept Pathol, Kharkiv, Ukraine.
C3 Kharkiv National Medical University
RP Petryk, N (corresponding author), Kharkiv Natl Med Univ, Dept Pathol, Kharkiv, Ukraine.
EM perfectgynecologist@gmail.com
RI Shevchenko, Oleksandr/LTF-5352-2024; Petryk, Nataliia/JXX-2201-2024
OI Sevcenko, Oleksandr Mikolaiovic/0000-0001-5456-8652; Petryk,
Nataliia/0000-0001-6427-0155
FU Kharkiv National Medical University, Kharkiv, Ukraine
FX This project was supported by Kharkiv National Medical University,
Kharkiv, Ukraine.
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NR 46
TC 14
Z9 14
U1 0
U2 2
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-7031
J9 J INFLAMM RES
JI J. Inflamm. Res.
PY 2020
VL 13
BP 293
EP 301
DI 10.2147/JIR.S256932
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA MJ7JB
UT WOS:000548262400001
PM 32753930
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Barrow, F
Khan, S
Wang, HG
Revelo, XS
AF Barrow, Fanta
Khan, Saad
Wang, Haiguang
Revelo, Xavier S.
TI The Emerging Role of B Cells in the Pathogenesis of NAFLD
SO HEPATOLOGY
LA English
DT Review
ID FATTY LIVER-DISEASE; PROMOTE INSULIN-RESISTANCE; NONALCOHOLIC
STEATOHEPATITIS; T-CELLS; ACTIVATING FACTOR; KUPFFER CELLS; PROGRESSION;
INFLAMMATION; FIBROSIS; MICE
AB NAFLD is one of the leading causes of abnormal liver function worldwide. NAFLD refers to a group of liver conditions ranging from nonalcoholic fatty liver to NASH, which involves inflammation, hepatocellular damage, and fibrosis. Triggering of inflammation in NASH is a key event in the progression of the disease, and identifying the factors that initiate or dysregulate this process is needed to develop strategies for its prevention or treatment. B cells have been implicated in several autoimmune and inflammatory diseases. However, their role in the pathogenesis of NAFLD and NASH is less clear. This review discusses the emerging evidence implicating intrahepatic B cells in the progression of NAFLD. We highlight the potential mechanisms of B-cell activation during NAFLD, such as increased hepatic expression of B-cell-activating factor, augmented oxidative stress, and translocation of gut-derived microbial products. We discuss the possible effector functions by which B cells promote NAFLD, including the production of proinflammatory cytokines and regulation of intrahepatic T cells and macrophages. Finally, we highlight the role of regulatory and IgA(+) B cells in the pathogenesis of NASH-associated HCC. In this review, we make the case that future research is needed to investigate the potential of B-cell-targeting strategies for the treatment of NAFLD.
C1 [Barrow, Fanta; Wang, Haiguang; Revelo, Xavier S.] Univ Minnesota, Dept Integrat Biol & Physiol, Minneapolis, MN USA.
[Khan, Saad] Univ Toronto, Dept Immunol, Toronto, ON, Canada.
[Revelo, Xavier S.] Univ Minnesota, Ctr Immunol, Minneapolis, MN USA.
C3 University of Minnesota System; University of Minnesota Twin Cities;
University of Toronto; University of Minnesota System; University of
Minnesota Twin Cities
RP Revelo, XS (corresponding author), Univ Minnesota, Sch Med, Dept Integrat Biol & Physiol, 3-145 CCRB 2231 6th St Southeast, Minneapolis, MN 55455 USA.; Revelo, XS (corresponding author), Univ Minnesota, Sch Med, Ctr Immunol, 3-145 CCRB 2231 6th St Southeast, Minneapolis, MN 55455 USA.
EM xrevelo@umn.edu
RI Revelo, Xavier/AAQ-9094-2020
OI Barrow, Fanta/0000-0002-6025-1210; Revelo, Xavier/0000-0002-2754-509X
FU NIH [DK122056]
FX Supported by NIH grant DK122056 (to X.R.).
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NR 84
TC 66
Z9 67
U1 0
U2 27
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2021
VL 74
IS 4
BP 2277
EP 2286
DI 10.1002/hep.31889
EA JUN 2021
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA UU4QH
UT WOS:000662974400001
PM 33961302
OA Green Published
DA 2025-01-07
ER
PT J
AU Nicastro, E
Verdoni, L
Bettini, LR
Zuin, G
Balduzzi, A
Montini, G
Biondi, A
D'Antiga, L
AF Nicastro, Emanuele
Verdoni, Lucio
Bettini, Laura Rachele
Zuin, Giovanna
Balduzzi, Adriana
Montini, Giovanni
Biondi, Andrea
D'Antiga, Lorenzo
TI COVID-19 in Immunosuppressed Children
SO FRONTIERS IN PEDIATRICS
LA English
DT Review
DE SARS-CoV-2; kidney transplant; rheumatologic diseases; liver transplant;
cancer; immunosuppression; autoimmune disease; innate immunity
ID JUVENILE IDIOPATHIC ARTHRITIS; ACUTE RESPIRATORY SYNDROME; T-CELL
RESPONSES; SARS-COV-2 INFECTION; SARS CORONAVIRUS; DISEASE 2019;
RECOMBINATION; PROGRESSION; EXPRESSION; PNEUMONIA
AB Following the spread of the SARS-CoV-2 infection and coronavirus disease 2019 (COVID-19) to a global pandemic, concerns have arisen for the disease impact in at-risk populations, especially in immunocompromised hosts. On the other hand, clinical studies have clarified that the COVID-19 clinical burden is mostly due to over-inflammation and immune-mediated multiorgan injury. This has led to downsizing the role of immunosuppression as a determinant of outcome, and early reports confirm the hypothesis that patients undergoing immunosuppressive treatments do not have an increased risk of severe COVID-19 with respect to the general population. Intriguingly, SARS-CoV-2 natural reservoirs, such as bats and mice, have evolved mechanisms of tolerance involving selection of genes optimizing viral clearance through interferon type I and III responses and also dampening inflammasome response and cytokine expression. Children exhibit resistance to COVID-19 severe manifestations, and age-related features in innate and adaptive response possibly explaining this difference are discussed. A competent recognition by the innate immune system and controlled pro-inflammatory signaling seem to be the pillars of an effective response and the premise for pathogen clearance in SARS-CoV-2 infection. Immunosuppression-if not associated with other elements of fragility-do not represent per se an obstacle to this competent/tolerant phenotype in children. Several reports confirm that children receiving immunosuppressive medications have similar clinical involvement and outcomes as the pediatric general population, indicating that maintenance treatments should not be interrupted in suspect or confirmed SARS-CoV-2 infection.
C1 [Nicastro, Emanuele; D'Antiga, Lorenzo] Hosp Papa Giovanni XXIII, Pediat Hepatol Gastroenterol & Transplantat Unit, Bergamo, Italy.
[Verdoni, Lucio; D'Antiga, Lorenzo] Hosp Papa Giovanni XXIII, Pediat Unit, Bergamo, Italy.
[Bettini, Laura Rachele; Zuin, Giovanna; Balduzzi, Adriana; Biondi, Andrea] Univ Milano Bicocca, MBBM Fdn, Dept Pediat, Hosp San Gerardo, Monza, Italy.
[Montini, Giovanni] Osped Maggiore Policlin Milano, Pediat Nephrol Dialysis & Transplant Unit, Fdn Ist Ricovero & Cura Carattere Sci Ca Granda, Milan, Italy.
C3 ASST Papa Giovanni XXIII; ASST Papa Giovanni XXIII; University of
Milano-Bicocca; IRCCS Ca Granda Ospedale Maggiore Policlinico
RP Nicastro, E (corresponding author), Hosp Papa Giovanni XXIII, Pediat Hepatol Gastroenterol & Transplantat Unit, Bergamo, Italy.
EM enicastro@asst-pg23.it
RI Biondi, Andrea/AAX-1865-2020; Nicastro, Emanuele/K-1260-2018; D Antiga,
Lorenzo/HZK-1269-2023; BALDUZZI, Adriana/AAC-1033-2019; Montini,
Giovanni/AGI-8385-2022; BETTINI, LAURA RACHELE/LSK-6378-2024
OI BETTINI, LAURA RACHELE/0000-0002-0280-1704; D'Antiga,
Lorenzo/0000-0001-7150-3148; Biondi, Andrea/0000-0002-6757-6173;
Montini, Giovanni/0000-0002-7350-4475
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NR 141
TC 31
Z9 31
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-2360
J9 FRONT PEDIATR
JI Front. Pediatr.
PD APR 29
PY 2021
VL 9
AR 629240
DI 10.3389/fped.2021.629240
PG 12
WC Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics
GA SA8HX
UT WOS:000649545100001
PM 33996683
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Schomburg, L
AF Schomburg, Lutz
TI Selenoprotein P - Selenium transport protein, enzyme and biomarker of
selenium status
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Review
DE Micronutrient; Redox cycling; Autoimmune disease; COVID-19; Biomarker
ID HYDROPEROXIDE GLUTATHIONE-PEROXIDASE; LOW-DENSITY-LIPOPROTEIN; 3
UNTRANSLATED REGION; HUMAN PLASMA; TRANSFER-RNA; LIPID-PEROXIDATION;
ENDOTHELIAL-CELLS; DIETARY SELENIUM; THYROID-DISEASE; BINDING-PROTEIN
AB The habitual intake of selenium (Se) varies strongly around the world, and many people are at risk of inadequate supply and health risks from Se deficiency. Within the human organism, efficient transport mechanisms ensure that organs with a high demand and relevance for reproduction and survival are preferentially supplied. To this end, selenoprotein P (SELENOP) is synthesized in the liver and mediates Se transport to essential tissues such as the endocrine glands and the brain, where the "SELENOP cycle" maintains a privileged Se status. Mouse models indicate that SELENOP is not essential for life, as supplemental Se supply was capable of preventing the development of severe symptoms. However, knockout mice died under limiting supply, arguing for an essential role of SELENOP in Se deficiency. Many clinical studies support this notion, pointing to close links between health risks and low SELENOP levels. Accordingly, circulating SELENOP concentrations serve as a functional biomarker of Se supply, at least until a saturated status is achieved and SELENOP levels reach a plateau. Upon toxic intake, a further increase in SELENOP is observed, i.e., SELENOP provides information about possible selenosis. The SELENOP transcripts predict an insertion of ten selenocysteine residues. However, the decoding is imperfect, and not all these positions are ultimately occupied by selenocysteine. In addition to the selenocysteine residues near the C-terminus, one selenocysteine resides central within an enzyme-like environment. SELENOP proved capable of catalyzing peroxide degradation in vitro and protecting e.g. LDL particles from oxidation. An enzymatic activity in the intact organism is unclear, but an increasing number of clinical studies provides evi-dence for a direct involvement of SELENOP-dependent Se transport as an important and modifiable risk factor of disease. This interaction is particularly strong for cardiovascular and critical disease including COVID-19, cancer at various sites and autoimmune thyroiditis. This review briefly highlights the links between the growing knowledge of Se in health and disease over the last 50 years and the specific advances that have been made in our understanding of the physiological and clinical contribution of SELENOP to the current picture.
C1 [Schomburg, Lutz] Charite Univ Med Berlin, Inst Expt Endocrinol, Cardiovasc Metab Renal CMR Res Ctr, Hesische Str 3-4, D-10115 Berlin, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
University of Berlin; Charite Universitatsmedizin Berlin
RP Schomburg, L (corresponding author), Charite Univ Med Berlin, Inst Expt Endocrinol, Cardiovasc Metab Renal CMR Res Ctr, Hesische Str 3-4, D-10115 Berlin, Germany.
EM lutz.schomburg@charite.de
OI Schomburg, Lutz/0000-0001-9445-1555
FU Deutsche Forschungsgemeinschaft (DFG) [FOR-2558, Scho849/6-2, CRC/TR
296]
FX Research in the author's lab is supported by the Deutsche
Forschungsgemeinschaft (DFG), Research Unit FOR-2558 "TraceAge"
(Scho849/6-2) and CRC/TR 296 "Local control of TH action" (LocoTact,
P17). The author is deeply grateful to Prof. Josef Kohrle and Prof.
Ulrich Schweizer for a highly constructive and delightful journey into
the science of selenoproteins, several great colleagues in the Se
research field and from the ISSR, many highly motivated students working
on specific aspects of SELENOP biology, and for the constant support of
Anja Fischbach, Gabriele Boehm and Vartit ' er Seher during the last two
decades of research. Parts of Figs. 3-5 were generated using Servier
Medical Art, provided by Servier, licensed under a Creative Commons
Attribution 3.0 unported license.
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NR 170
TC 39
Z9 41
U1 6
U2 29
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD OCT
PY 2022
VL 191
BP 150
EP 163
DI 10.1016/j.freeradbiomed.2022.08.022
EA SEP 2022
PG 14
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 4W9NA
UT WOS:000860480200003
PM 36067902
DA 2025-01-07
ER
PT J
AU Li, DC
Ma, DH
Liu, Y
Liu, LH
Chen, YH
Liu, HI
Zhang, L
Lu, J
Chen, KX
You, J
Li, W
AF Li, Dingchun
Ma, Dehong
Liu, Ye
Liu, Lihui
Chen, Yihui
Liu, Huaie
Zhang, Lu
Lu, Jie
Chen, Kexuan
You, Jing
Li, Wu
TI Extracts of Periplaneta americana alleviate hepatic fibrosis by
affecting hepatic TGF-β and NF-κB expression in rats with pig
serum-induced liver fibrosis
SO FOLIA HISTOCHEMICA ET CYTOBIOLOGICA
LA English
DT Article
DE Rat; pig-serum hepatic fibrosis; Periplaneta americana; NF-kappa B;
alpha-SMA; TGF-beta 1;; TIMP-1; IHC
ID STELLATE CELLS; CANCER; GENE; PATHOGENESIS; INFLAMMATION; ACTIVATION;
DISEASE
AB Introduction. Liver fibrosis is caused by continuous wound healing responses to various harmful stimuli, including viral infection, drugs, alcohol, and autoimmune liver disease. The purpose of this study was to examine the effects of extracts of Periplaneta americana (EPA) in rats with pig serum-induced liver fibrosis to preliminarily assess the antifibrotic effect of EPA.
Material and methods. Seventy rats were randomly divided into 7 groups (10 rats in each group): HC, the healthy control group; FC, the fibrotic control group; TL, low-dose EPA treatment group group; TM, medium-dose EPA group; TH, high-dose EPA treatment group; TC1, Panax notoginseng/Salvia mitiorrhiza treatment control group 1; TC2, colchicine treatment control group 2. TC1 and TC2 were used as the positive control to demonstrate the difference between EPA and the effects of other compounds. The liver fibrosis model was induced by intraperitoneal injection of 0.5 mL pig serum twice a week for 13 weeks in all groups except for the HC group. The hepatic fibrosis model was established at the 7th week, and followingly, the corresponding compounds were administered once a day in all groups for 6 weeks. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity was determined in rat blood serum. We also measured liver fibrosis-related serum markers, including hyaluronic acid (HA), laminin (LN), type III pre-collagen (PC-III) and type IV collagen (IV-C). Hematoxylin and eosin (H&E) and Masson stainings were used to assess liver morphology and determine the stage of fibrosis. Immunohistochemistry was used to detect the protein expression of NF-kappa B, alpha-smooth muscle actin (alpha-SMA), transforming growth factor-beta 1 (TGF-beta 1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in rat liver tissue.
Results. Compared with that of the HC group, the liver tissue of the FC group presented obvious liver damage and collagen deposition. The serum levels of ALT, AST, HA, LN, PC-III and IV-C and the expression of NF-kappa B, alpha-SMA, TGF-beta 1 and TIMP-1 in the FC group were significantly higher than those in the HC group, the EPA treatment groups, the TC1 group and the TC2 group (P < 0.01). The levels of serum ALT, AST, HA, LN, PC-III and IV-C and the expression of alpha-SMA, NF-kappa B, TGF-beta 1 and TIMP-1 in the TL, TC1 and TC2 groups were significantly higher than those TM and TH groups (P < 0.05). EPA treatment significantly improved liver function, decreased collagen deposition and reversed the pathological changes related to liver fibrosis.
Conclusions. We found that EPA could reduce liver inflammation, suppress liver cell degeneration and necrosis, and reduce the formation of liver fibrous tissue. Its mechanism might be associated with inhibiting the expression of TGF-beta 1, TIMP-1, NF-kappa B and alpha-SMA to block signal transduction pathways in the hepatic fibrosis process. Therefore, EPA, as a traditional Chinese medicine, might be potentially used to prevent and treat hepatic fibrosis in the future. However, further more experiments are necessary to verify its effectiveness and possible signaling pathways.
C1 [Li, Dingchun; Liu, Ye; Liu, Lihui; Chen, Yihui; Liu, Huaie; Zhang, Lu; Lu, Jie; Chen, Kexuan; You, Jing; Li, Wu] Kunming Med Univ, Affiliated Hosp 1, Kunming, Yunnan, Peoples R China.
[Ma, Dehong] Xishuangbanna Dai Natl Minor Autonomous Prefectur, Jinghong 666100, Peoples R China.
C3 Kunming Medical University
RP You, J; Li, W (corresponding author), Kunming Med Univ, Affiliated Hosp 1, 295 Xichang Rd, Kunming 650032, Yunnan, Peoples R China.
EM liwu_893624@163.com
RI Liu, Lihui/HGU-0114-2022
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NR 52
TC 5
Z9 6
U1 4
U2 18
PU VIA MEDICA
PI GDANSK
PA UL SWIETOKRZYSKA 73, 80-180 GDANSK, POLAND
SN 0239-8508
EI 1897-5631
J9 FOLIA HISTOCHEM CYTO
JI Folia Histochem. Cytobiol.
PY 2022
VL 60
IS 2
BP 125
EP 135
DI 10.5603/FHC.a2022.0011
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 8X5GF
UT WOS:000932040300001
PM 35575220
OA gold
DA 2025-01-07
ER
PT J
AU Chang, JA
Coskun, MD
Kim, J
AF Chang, JuOae
Debreli Coskun, Melis
Kim, Jonghan
TI Inflammation alters iron distribution in bone and spleen in mice
SO METALLOMICS
LA English
DT Article
DE anemia of inflammation; erythropoiesis; hepcidin; ferroportin;
turpentine oil; tracer kinetics
ID CHRONIC DISEASE; ANEMIA; HEPCIDIN; FERROPORTIN; EXPRESSION;
ERYTHROPOIESIS; HOMEOSTASIS; TRANSPORT; THERAPY
AB Anemia of inflammation (or inflammation-associated anemia) decreases the quality of life in billions of patients suffering from various inflammatory diseases, such as infection, autoimmune diseases, and cancer, associated with a prolonged state of immune activation. While proper utilization of iron, a nutrient metal essential for erythropoiesis, is important for the prevention of anemia, the alteration of body iron homeostasis upon inflammation, which can contribute to the development of anemia, is not completely understood. Thus, we sought to examine temporal and spatial changes in the distribution of iron and iron-associated molecules during inflammation in mice. To induce inflammation, C57BL/6J mice were injected with turpentine oil weekly for 3 weeks, which resulted in anemia, decreased protein expression of ferroportin, a cellular iron exporter, in the spleen, duodenum, and liver, and increased iron stores in the duodenum and spleen. Tracer kinetic studies after oral administration of 59Fe revealed that more iron was found in the spleen and less in the femur bone in turpentine oil-injected mice compared to the saline-injected mice, indicating tissue-specific abnormalities in iron distribution during inflammation. However, there was no difference in the utilization of iron for red blood cell production after turpentine oil injection; instead, serum hemopexin level and lactate dehydrogenase activity were increased, suggesting increased red blood cell destruction upon inflammation. Our findings provide an improved understanding of temporal and spatial changes in the distribution and utilization of iron during inflammation.
Graphical Abstract Inflammation induces downregulation of ferroportin (Fpn) in the liver, duodenum, and spleen, which is accompanied by iron accumulation in tissues. In addition, inflammation causes dysregulation of iron transport, specifically by decreasing and increasing iron transport into the bone and spleen, respectively. Impaired tissue distribution of iron may result in anemia of inflammation.
C1 [Chang, JuOae; Debreli Coskun, Melis; Kim, Jonghan] Northeastern Univ, Dept Pharmaceut Sci, Boston, MA 02115 USA.
[Chang, JuOae] Sungkyunkwan Univ, Sch Pharm, 2066 Seobu Ro, Suwon, Gyeonggi Do, South Korea.
[Debreli Coskun, Melis; Kim, Jonghan] Univ Massachusetts Lowell, Dept Biomed & Nutr Sci, 3 Solomont Way,Suite 4, Lowell, MA 01854 USA.
C3 Northeastern University; Sungkyunkwan University (SKKU); University of
Massachusetts System; University of Massachusetts Lowell
RP Chang, JA; Kim, J (corresponding author), Northeastern Univ, Dept Pharmaceut Sci, Boston, MA 02115 USA.; Chang, JA (corresponding author), Sungkyunkwan Univ, Sch Pharm, 2066 Seobu Ro, Suwon, Gyeonggi Do, South Korea.; Kim, J (corresponding author), Univ Massachusetts Lowell, Dept Biomed & Nutr Sci, 3 Solomont Way,Suite 4, Lowell, MA 01854 USA.
EM joc123@skku.edu; jonghan_kim@uml.edu
RI Coskun, Melis/AAF-3992-2020
FU This study was supported in part by the National Institutes of Health
(HL140526 to J.K.). We thank Angela Nocera from Dr. Mansoor Amiji group
for the help in cytokine measurement. We also thank HaYoung Nam, Shirley
Zipei Liang, Elham Davoudi, and other lab [HL140526]; National
Institutes of Health
FX This study was supported in part by the National Institutes of Health
(HL140526 to J.K.). We thank Angela Nocera from Dr. Mansoor Amiji group
for the help in cytokine measurement. We also thank HaYoung Nam, Shirley
Zipei Liang, Elham Davoudi, and other lab members for their help in
conducting experiments.
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NR 46
TC 0
Z9 0
U1 1
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1756-5901
EI 1756-591X
J9 METALLOMICS
JI Metallomics
PD OCT 4
PY 2023
VL 15
IS 10
AR mfad055
DI 10.1093/mtomcs/mfad055
EA OCT 2023
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA T5DQ6
UT WOS:001078194100001
PM 37738439
OA Green Published
DA 2025-01-07
ER
PT J
AU Morcos, PN
Moreira, SA
Brennan, BJ
Blotner, S
Shulman, NS
Smith, PF
AF Morcos, P. N.
Moreira, S. A.
Brennan, B. J.
Blotner, S.
Shulman, N. S.
Smith, P. F.
TI Influence of chronic hepatitis C infection on cytochrome P450 3a4
activity using midazolam as an in vivo probe substrate
SO EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY
LA English
DT Article
DE Hepatitis C; Inflammation; Cytochrome P450; Pharmacokinetics
ID REVERSE-TRANSCRIPTASE INHIBITORS; HUMAN HEPATOCYTES; HEALTHY-VOLUNTEERS;
VIRUS-INFECTION; CLINICAL PHARMACOKINETICS; RHEUMATOID-ARTHRITIS;
PROTEASE INHIBITOR; ANTIVIRAL ACTIVITY; RAT HEPATOCYTES; GENE-EXPRESSION
AB Inflammation-related changes in pharmacokinetics have been described for a number of disease-states including cancer, infection, and autoimmune disorders. This study examined the impact of chronic hepatitis C infection (CHC) on the pharmacokinetics of the cytochrome P450 3A probe midazolam in patients without significant liver disease who were either treatment na < ve or prior interferon null-responders.
Data were pooled from three studies which compared the pharmacokinetics of oral midazolam in healthy volunteers (n = 107) and in treatment-naive patients (n = 35) and interferon-null responders (n = 24) with CHC but without significant liver disease. Oral midazolam was administered as a single 2 mg oral dose, followed by frequent pharmacokinetic sampling and determination of the pharmacokinetics of midazolam and its alpha-hydroxy metabolite. CYP3A activity was determined by the metabolic ratio (MR) of the AUC metabolite/AUC parent and compared across groups as the mean effect ratio (test/reference).
The midazolam MR was lower in treatment-na < ve patients with CHC than in health volunteers with a mean effect ratio of 0.63 [90 % confidence interval (CI) 0.56-0.72]. The effect was more pronounced in null-responders, who demonstrated a mean MR effect ratio of 0.46 (90 % CI 0.39-0.53) compared to volunteers. The mean area under the concentration-time curve (AUC(inf)) for midazolam in healthy volunteers, na < ve patients, and null-responders was 32.3 [coefficient of variation (CV%) 41], 36.5 (CV% 33.5), and 55.3 (CV% 36.9) ng.h/mL, respectively.
The results of this study demonstrate a reduction in CYP3A4 activity between healthy volunteers and patients with CHC, with interferon null-responders demonstrating the most substantial difference. These results may have implications for the pharmacotherapy of patients infected with CHC.
C1 [Morcos, P. N.; Moreira, S. A.; Brennan, B. J.] Hoffmann La Roche Inc, Dept Clin Pharmacol Pharma Res & Early Dev, Nutley, NJ 07110 USA.
[Blotner, S.] Hoffmann La Roche Inc, Dept Biometr, Pharma Dev, Nutley, NJ 07110 USA.
[Shulman, N. S.] Hoffmann La Roche Inc, Virol, Pharma Dev, San Francisco, CA USA.
[Smith, P. F.] SUNY Buffalo, Sch Pharm, Dept Pharm Practice, Buffalo, NY 14215 USA.
[Smith, P. F.] d3 Med, Montville, NJ USA.
C3 Roche Holding; Roche Holding; State University of New York (SUNY)
System; University at Buffalo, SUNY
RP Smith, PF (corresponding author), d3 Med, Montville, NJ USA.
EM patrick.smith@d3medicine.com
OI Smith, Patrick/0000-0002-6003-0805
FU Roche
FX The authors are indebted to Edward Gane, Catherine Stedman, Dennis Riff,
and Thomas Hunt for participating in the success of the clinical trials,
in addition to the site investigational staff and, most importantly, the
patients and volunteers. The funding for this work was provided by
Roche.
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NR 45
TC 38
Z9 42
U1 0
U2 14
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0031-6970
J9 EUR J CLIN PHARMACOL
JI Eur. J. Clin. Pharmacol.
PD OCT
PY 2013
VL 69
IS 10
BP 1777
EP 1784
DI 10.1007/s00228-013-1525-5
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 217CI
UT WOS:000324333800006
PM 23765407
DA 2025-01-07
ER
PT J
AU Landau, DA
Scerra, S
Sene, D
Resche-Rigon, M
Saadoun, D
Cacoub, P
AF Landau, Dan-Avi
Scerra, Samy
Sene, Damien
Resche-Rigon, Mathieu
Saadoun, David
Cacoub, Patrice
TI Causes and Predictive Factors of Mortality in a Cohort of Patients with
Hepatitis C Virus-related Cryoglobulinemic Vasculitis Treated with
Antiviral Therapy
SO JOURNAL OF RHEUMATOLOGY
LA English
DT Article
DE HEPATITIS C VIRUS; MIXED CRYOGLOBULINEMIA; VASCULITIS; MORTALITY
ID SYSTEMIC WEGENERS-GRANULOMATOSIS; CHURG-STRAUSS-SYNDROME;
NON-HODGKINS-LYMPHOMA; MIXED CRYOGLOBULINEMIA; POLYARTERITIS-NODOSA;
INFECTIOUS COMPLICATIONS; INTERFERON-ALPHA; RITUXIMAB; SURVIVAL;
RIBAVIRIN
AB Objective. Hepatitis C Virus (HCV)-associated mixed cryoglobulinemia (MC) vasculitis is,in autoimmune disorder with significant morbidity and mortality. Renal involvement was associated with an increased mortality, and was the most common cause of death; these data were obtained before effective antiviral treatment was available. We studied causes of death and predictive factors in patients with HCV-associated MC vasculitis treated with antivirals.
Methods. Case histories of 85 patients with HCV-associated MC vasculitis treated in a single center between 1990 and 2006 were retrospectively reviewed. Prognostic factors affecting mortality were studied by comparing 23 patients who died with 62 survivors, using the Cox model regression analysis.
Results. The most common cause of death was infection, accounting for 34.7%, followed by end-stage liver disease in 30.4% (including 4 patients with hepatocellular carcinoma), and cardiovascular disease in 17.4% of patients. Endstage renal disease accounted for only 8.7% of deaths, as did central nervous system vasculitis and nonhepatic malignancy. Increased mortality was strongly associated with immunosuppressive treatment [hazard ratio (HR) 6.51, 95% CI 2.75-15.37], cutaneous ulcers (HR 5.37, 95% CI 1.79-16.14), and renal insufficiency (HR 3.25, 95% CI 1.37-7.72). A 2 log] 0 decrease in HCV viral load at month 3 after starting antiviral treatment was associated with decreased mortality (HR 0.39, 95% CI 0.16-0.95).
Conclusion. While renal involvement is still associated with poorer prognosis, infectious processes are now the most common Cause of death in HCV cryoglobulinemia vasculitis. Immunosuppressive treatment is associated with an increased risk of death, independently from disease severity. Response to antiviral treatment is associated with significantly reduced mortality risk. (First Release Feb 1 2010; J Rheumatol 2010;37:615-21; doi:10.3899/jrheum.090790)
C1 [Landau, Dan-Avi; Scerra, Samy; Sene, Damien; Saadoun, David; Cacoub, Patrice] Univ Paris 06, Hop La Pitie Salpetriere, AP HP, Serv Med Interne, Paris, France.
[Resche-Rigon, Mathieu] Hop St Louis, INSERM, U717, Dept Biostat & Med Data Proc, Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
Pitie-Salpetriere - APHP; Sorbonne Universite; Universite Paris Cite;
Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
Saint-Louis - APHP; Institut National de la Sante et de la Recherche
Medicale (Inserm)
RP Cacoub, P (corresponding author), Grp Hosp Pitie Salpetriere, Serv Med Interne, 47-83 Blvd Hop, F-75013 Paris, France.
EM patrice.cacoub@psl.aphp.fr
RI Resche-Rigon, Matthieu/ABA-5374-2021; sene, damien/R-3970-2017
OI Cacoub, Patrice/0000-0002-6727-4992; saadoun, david/0000-0003-3628-9996;
SENE, Damien/0000-0001-8640-4580; resche-rigon,
matthieu/0000-0003-2220-5085
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NR 49
TC 45
Z9 47
U1 0
U2 0
PU J RHEUMATOL PUBL CO
PI TORONTO
PA 365 BLOOR ST E, STE 901, TORONTO, ONTARIO M4W 3L4, CANADA
SN 0315-162X
EI 1499-2752
J9 J RHEUMATOL
JI J. Rheumatol.
PD MAR
PY 2010
VL 37
IS 3
BP 615
EP 621
DI 10.3899/jrheum.090790
PG 7
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 563MD
UT WOS:000275135700023
PM 20110523
OA Bronze
DA 2025-01-07
ER
PT J
AU Deneau, MR
Mack, C
Perito, ER
Ricciuto, A
Valentino, PL
Amin, M
Amir, AZ
Aumar, M
Auth, M
Broderick, A
DiGuglielmo, M
Draijer, LG
Fagundes, EDT
El-Matary, W
Ferrari, F
Furuya, KN
Gupta, N
Hochberg, JT
Homan, M
Horslen, S
Iorio, R
Jensen, MK
Jonas, MM
Kamath, BM
Kerkar, N
Kim, KM
Kolho, KL
Koot, BGP
Laborda, TJ
Lee, CK
Loomes, KM
Martinez, M
Miethke, A
Miloh, T
Mogul, D
Mohammad, S
Mohan, P
Moroz, S
Ovchinsky, N
Palle, S
Papadopoulou, A
Rao, G
Ferreira, AR
Sathya, P
Schwarz, KB
Shah, U
Shteyer, E
Singh, R
Smolka, V
Soufi, N
Tanaka, A
Varier, R
Vitola, B
Woynarowski, M
Zerofsky, M
Zizzo, A
Guthery, SL
AF Deneau, Mark R.
Mack, Cara
Perito, Emily R.
Ricciuto, Amanda
Valentino, Pamela L.
Amin, Mansi
Amir, Achiya Z.
Aumar, Madeleine
Auth, Marcus
Broderick, Annemarie
DiGuglielmo, Matthew
Draijer, Laura G.
Fagundes, Eleonora Druve Tavares
El-Matary, Wael
Ferrari, Federica
Furuya, Katryn N.
Gupta, Nitika
Hochberg, Jessica T.
Homan, Matjaz
Horslen, Simon
Iorio, Raffaele
Jensen, M. Kyle
Jonas, Maureen M.
Kamath, Binita M.
Kerkar, Nanda
Kim, Kyung Mo
Kolho, Kaija-Leena
Koot, Bart G. P.
Laborda, Trevor J.
Lee, Christine K.
Loomes, Kathleen M.
Martinez, Mercedes
Miethke, Alexander
Miloh, Tamir
Mogul, Douglas
Mohammad, Saeed
Mohan, Parvathi
Moroz, Stacy
Ovchinsky, Nadia
Palle, Sirish
Papadopoulou, Alexandra
Rao, Girish
Ferreira, Alexandre Rodrigues
Sathya, Pushpa
Schwarz, Kathleen B.
Shah, Uzma
Shteyer, Eyal
Singh, Ruchi
Smolka, Vratislav
Soufi, Nisreen
Tanaka, Atsushi
Varier, Raghu
Vitola, Bernadette
Woynarowski, Marek
Zerofsky, Melissa
Zizzo, Andreanne
Guthery, Stephen L.
TI The Sclerosing Cholangitis Outcomes in Pediatrics (SCOPE) Index: A
Prognostic Tool for Children
SO HEPATOLOGY
LA English
DT Article
ID NATURAL-HISTORY; AUTOIMMUNE HEPATITIS; RISK; VALIDATION; SURVIVAL;
MODEL; CHOLANGIOCARCINOMA
AB Background and Aims Disease progression in children with primary sclerosing cholangitis (PSC) is variable. Prognostic and risk-stratification tools exist for adult-onset PSC, but not for children. We aimed to create a tool that accounts for the biochemical and phenotypic features and early disease stage of pediatric PSC.
Approach and Results We used retrospective data from the Pediatric PSC Consortium. The training cohort contained 1,012 patients from 40 centers. We generated a multivariate risk index (Sclerosing Cholangitis Outcomes in Pediatrics [SCOPE] index) that contained total bilirubin, albumin, platelet count, gamma glutamyltransferase, and cholangiography to predict a primary outcome of liver transplantation or death (TD) and a broader secondary outcome that included portal hypertensive, biliary, and cancer complications termed hepatobiliary complications (HBCs). The model stratified patients as low, medium, or high risk based on progression to TD at rates of <1%, 3%, and 9% annually and to HBCs at rates of 2%, 6%, and 13% annually, respectively (P < 0.001). C-statistics to discriminate outcomes at 1 and 5 years were 0.95 and 0.82 for TD and 0.80 and 0.76 for HBCs, respectively. Baseline hepatic fibrosis stage was worse with increasing risk score, with extensive fibrosis in 8% of the lowest versus 100% with the highest risk index (P < 0.001). The model was validated in 240 children from 11 additional centers and performed well.
Conclusions The SCOPE index is a pediatric-specific prognostic tool for PSC. It uses routinely obtained, objective data to predict a complicated clinical course. It correlates strongly with biopsy-proven liver fibrosis. SCOPE can be used with families for shared decision making on clinical care based on a patient's individual risk, and to account for variable disease progression when designing future clinical trials.
C1 [Deneau, Mark R.; Jensen, M. Kyle; Laborda, Trevor J.; Guthery, Stephen L.] Univ Utah, Salt Lake City, UT 84113 USA.
[Deneau, Mark R.; Jensen, M. Kyle; Laborda, Trevor J.; Guthery, Stephen L.] Intermt Primary Childrens Hosp, Salt Lake City, UT USA.
[Mack, Cara] Univ Colorado, Sch Med, Aurora, CO USA.
[Perito, Emily R.; Zerofsky, Melissa] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Ricciuto, Amanda; Kamath, Binita M.] Univ Toronto, Toronto, ON, Canada.
[Valentino, Pamela L.] Yale Univ, Sch Med, New Haven, CT USA.
[Amin, Mansi] Phoenix Childrens Hosp, Phoenix, AZ USA.
[Amir, Achiya Z.] Tel Aviv Univ, Dana Dwek Childrens Hosp, Tel Aviv Med Ctr, Tel Aviv, Israel.
[Aumar, Madeleine] Univ Lille, CHU Lille, Lille, France.
[Auth, Marcus] Alder Hey Childrens Hosp, Liverpool, Merseyside, England.
[Broderick, Annemarie] Childrens Hlth Ireland Crumlin, Dublin, Ireland.
[Broderick, Annemarie] Univ Coll Dublin, Dublin, Ireland.
[DiGuglielmo, Matthew] Nemours Alfred I duPont Hosp Children, Wilmington, DE USA.
[Draijer, Laura G.; Koot, Bart G. P.] Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
[Fagundes, Eleonora Druve Tavares; Ferreira, Alexandre Rodrigues] Univ Fed Minas Gerais, Belo Horizonte, MG, Brazil.
[El-Matary, Wael] Univ Manitoba, Winnipeg, MB, Canada.
[Ferrari, Federica] Sapienza Univ Rome, Rome, Italy.
[Furuya, Katryn N.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
[Gupta, Nitika] Emory Univ, Sch Med, Atlanta, GA USA.
[Hochberg, Jessica T.; Miloh, Tamir] Univ Miami, Miami, FL USA.
[Homan, Matjaz] Univ Ljubljana, Ljubljana, Slovenia.
[Horslen, Simon] Univ Washington, Seattle, WA 98195 USA.
[Iorio, Raffaele] Univ Naples Federico II, Naples, Italy.
[Jonas, Maureen M.; Lee, Christine K.] Boston Childrens Hosp, Boston, MA USA.
[Jonas, Maureen M.; Lee, Christine K.] Harvard Med Sch, Boston, MA 02115 USA.
[Kerkar, Nanda] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
[Kim, Kyung Mo] Univ Ulsan, Seoul, South Korea.
[Kolho, Kaija-Leena] Univ Helsinki Hosp, Helsinki, Finland.
[Kolho, Kaija-Leena] Tampere Univ, Helsinki, Finland.
[Loomes, Kathleen M.] Childrens Hosp Philadelphia, Philadelphia, PA USA.
[Martinez, Mercedes] Columbia Univ, New York, NY USA.
[Miethke, Alexander; Singh, Ruchi] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Mogul, Douglas; Schwarz, Kathleen B.] Johns Hopkins Univ, Baltimore, MD USA.
[Mohammad, Saeed] Lurie Childrens Hosp, Chicago, IL USA.
[Mohan, Parvathi] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Moroz, Stacy; Soufi, Nisreen] Univ Southern Calif, Los Angeles, CA 90007 USA.
[Ovchinsky, Nadia] Albert Einstein Coll Med, Childrens Hosp Montefiore, Bronx, NY 10467 USA.
[Palle, Sirish] Oklahoma Univ, Oklahoma City, OK USA.
[Papadopoulou, Alexandra] Univ Athens, Childrens Hosp Agia Sofia, Dept Pediat 1, Athens, Greece.
[Rao, Girish] Indiana Univ, Indianapolis, IN 46204 USA.
[Sathya, Pushpa] Mem Univ, St John, NF, Canada.
[Schwarz, Kathleen B.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Shah, Uzma] Harvard Med Sch, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Shteyer, Eyal] Shaare Zedek Med Ctr, Jerusalem, Israel.
[Smolka, Vratislav] Palacky Univ, Olomouc, Czech Republic.
[Tanaka, Atsushi] Teikyo Univ, Sch Med, Tokyo, Japan.
[Varier, Raghu] Northwest Pediat Gastroenterol LLC, Portland, OR USA.
[Vitola, Bernadette] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Woynarowski, Marek] UJK Kielce, Fac Med & Hlth Sci, Kielce, Poland.
[Zizzo, Andreanne] Western Univ, London Hlth Sci Ctr, London, ON, Canada.
C3 Utah System of Higher Education; University of Utah; University of
Colorado System; University of Colorado Anschutz Medical Campus;
University of California System; University of California San Francisco;
University of Toronto; Yale University; Phoenix Children's Hospital; Tel
Aviv University; Universite de Lille; CHU Lille; Alder Hey Children's
NHS Foundation Trust; Alder Hey Children's Hospital; University College
Dublin; Nemours Alfred I. duPont Hospital for Children; University of
Amsterdam; Universidade Federal de Minas Gerais; University of Manitoba;
Sapienza University Rome; University of Wisconsin System; University of
Wisconsin Madison; Emory University; University of Miami; University of
Ljubljana; University of Washington; University of Washington Seattle;
University of Naples Federico II; Harvard University; Boston Children's
Hospital; Harvard University; Harvard Medical School; University of
Rochester; University of Ulsan; University of Helsinki; Helsinki
University Central Hospital; Tampere University; University of
Pennsylvania; Pennsylvania Medicine; Childrens Hospital of Philadelphia;
Columbia University; Cincinnati Children's Hospital Medical Center;
Johns Hopkins University; Ann & Robert H. Lurie Children's Hospital of
Chicago; Children's National Health System; University of Southern
California; Yeshiva University; Montefiore Medical Center; Albert
Einstein College of Medicine; Childrens Hospital at Montefiore;
University of Oklahoma System; University of Oklahoma Health Sciences
Center; National & Kapodistrian University of Athens; Indiana University
System; Indiana University Indianapolis; Memorial University
Newfoundland; University of California System; University of California
San Diego; Harvard University; Massachusetts General Hospital; Harvard
Medical School; Hebrew University of Jerusalem; Shaare Zedek Medical
Center; Palacky University Olomouc; Teikyo University; Medical College
of Wisconsin; Western University (University of Western Ontario); London
Health Sciences Centre
RP Deneau, MR (corresponding author), Univ Utah, Intermt Primary Childrens Hosp, Div Gastroenterol Hepatol & Nutr, 81 North Mario Capecchi Dr, Salt Lake City, UT 84113 USA.
EM mark.deneau@hsc.utah.edu
RI Homan, Matjaž/AAO-7198-2020; Ricciuto, Amanda/JUF-0278-2023; Aumar,
Madeleine/M-3129-2018; Ferreira, Alexandre/AAK-2601-2021; Singh,
Ruchi/IQU-8464-2023; Valentino, Pamela/AGF-2466-2022; Woynarowski,
Marek/AAQ-7188-2020; vitola, Bernadette/K-6242-2019; Jonas,
Maureen/E-6712-2017; Horslen, Simon/ABB-9076-2021; Palle,
Sirish/K-4572-2017; Iorio, Raffaele/J-2137-2012
OI Aumar, Madeleine/0000-0002-2908-6931; IORIO,
RAFFAELE/0000-0002-7483-234X; Ricciuto, Amanda/0000-0001-9538-3005;
Vitola, Bernadette/0000-0002-6438-2648; Valentino,
Pamela/0000-0002-8227-2004; Deneau, Mark/0000-0003-0459-9404; Horslen,
Simon/0000-0001-5949-7363; Marek, Woynarowski/0000-0003-4533-4699
FU PSC Partners Seeking A Cure; Primary Children's Hospital Foundation;
National Center for Advancing Translational Sciences of the National
Institutes of Health [KL2TR001065, 8UL1TR000105]
FX Research reported in this publication was supported by PSC Partners
Seeking A Cure, the Primary Children's Hospital Foundation, and the
National Center for Advancing Translational Sciences of the National
Institutes of Health under Award Numbers KL2TR001065 and 8UL1TR000105
(formerly UL1RR025764). The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institutes of Health.
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NR 39
TC 25
Z9 28
U1 0
U2 17
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD MAR
PY 2021
VL 73
IS 3
BP 1074
EP 1087
DI 10.1002/hep.31393
EA DEC 2020
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA QX7PS
UT WOS:000600028900001
PM 32464706
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Park, JS
Choi, SY
Lee, JH
Lee, M
Nam, ES
Jeong, AL
Lee, S
Han, S
Lee, MS
Lim, JS
Yoon, DY
Kwon, Y
Yang, Y
AF Park, Jeong Su
Choi, Su Yun
Lee, Jeong-Hyung
Lee, Maria
Nam, Eun Sook
Jeong, Ae Lee
Lee, Sunyi
Han, Sora
Lee, Myeong-Sok
Lim, Jong-Seok
Yoon, Do Young
Kwon, Yongil
Yang, Young
TI Interleukin-32β stimulates migration of MDA-MB-231 and MCF-7cells via
the VEGF-STAT3 signaling pathway
SO CELLULAR ONCOLOGY
LA English
DT Article
DE Interleukin-32; VEGF; STAT3; Breast cancer
ID BREAST-CANCER CELLS; NF-KAPPA-B; PROINFLAMMATORY CYTOKINE;
GROWTH-FACTOR; HEPATOCELLULAR-CARCINOMA; RHEUMATOID-ARTHRITIS; OXIDATIVE
STRESS; IL-32; EXPRESSION; ACTIVATION
AB Background IL-32 is known to play an important role in inflammatory and autoimmune disease responses. In addition to its role in these responses, IL-32 and its different isoforms have in recent years been implicated in the development of various cancers. As of yet, the role of IL-32 in breast cancer has remained largely unknown.
Results By performing immunohistochemical assays on primary breast cancer samples, we found that the level of IL-32 beta expression was positively correlated with tumor size, number of lymph node metastases and tumor stage. In addition, we found that breast cancer-derived MDA-MB-231 cells exogenously expressing IL-32 beta exhibited increased migration and invasion capacities. These increased capacities were found to be associated with an increased expression of the epithelial mesenchymal transition (EMT) markers vimentin and Slug, the latter of which is responsible for the increase in vimentin transcription. To next investigate whether IL-32 beta enhances migration and invasion through a soluble factor, we determined the levels of several migration-stimulating ligands, and found that the production of VEGF was increased by IL-32 beta. In addition, we found that IL-32 beta-induced VEGF increased migration and invasion through STAT3 activation.
Conclusion The IL-32 beta-VEGF-STAT3 pathway represents an additional pathway that mediates the migration and invasion of breast cancer cells under the conditions of normoxia and hypoxia.
C1 [Park, Jeong Su; Jeong, Ae Lee; Lee, Sunyi; Han, Sora; Lee, Myeong-Sok; Lim, Jong-Seok; Yang, Young] Sookmyung Womens Univ, Res Ctr Womens Dis, Seoul 140742, South Korea.
[Choi, Su Yun] Hallym Univ, Coll Med, Dept Surg, Seoul, South Korea.
[Lee, Jeong-Hyung] Kangwon Natl Univ, Dept Biochem, Chunchon 200701, South Korea.
[Lee, Maria; Kwon, Yongil] Hallym Univ, Dept Obstet & Gynecol, Seoul, South Korea.
[Nam, Eun Sook] Hallym Univ, Coll Med, Dept Pathol, Seoul, South Korea.
[Yoon, Do Young] Konkuk Univ, Dept Biosci & Biotechnol, Seoul, South Korea.
C3 Sookmyung Women's University; Hallym University; Kangwon National
University; Hallym University; Hallym University; Konkuk University
RP Yang, Y (corresponding author), Sookmyung Womens Univ, Res Ctr Womens Dis, Seoul 140742, South Korea.
EM yyang@sm.ac.kr
RI Lee, Maria/AAQ-2558-2020
OI Lim, Jong-Seok/0000-0003-4024-6868; Yang, Young/0000-0003-4239-0804;
Lee, Maria/0000-0002-8017-3176
FU Sookmyung Women's University
FX This Research was supported by the Sookmyung Women's University Research
Grants 2012.
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NR 41
TC 48
Z9 51
U1 0
U2 14
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 2211-3428
EI 2211-3436
J9 CELL ONCOL
JI Cell. Oncol.
PD DEC
PY 2013
VL 36
IS 6
BP 493
EP 503
DI 10.1007/s13402-013-0154-4
PG 11
WC Oncology; Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Pathology
GA 269UT
UT WOS:000328268400006
PM 24114327
DA 2025-01-07
ER
PT J
AU Egberts, JH
Cloosters, V
Noack, A
Schniewind, B
Thon, L
Klose, S
Kettler, B
von Forstner, C
Kneitz, C
Tepel, J
Adam, D
Wajant, H
Kalthoff, H
Trauzold, A
AF Egberts, Jan-Hendrik
Cloosters, Vera
Noack, Andreas
Schniewind, Bodo
Thon, Lutz
Klose, Stefanie
Kettler, Bastian
von Forstner, Corinna
Kneitz, Christian
Tepel, Juergen
Adam, Dieter
Wajant, Harald
Kalthoff, Holger
Trauzold, Anna
TI Anti-tumor necrosis factor therapy inhibits pancreatic tumor growth and
metastasis
SO CANCER RESEARCH
LA English
DT Article
ID NF-KAPPA-B; FACTOR-ALPHA; CANCER CELLS; DUCTAL ADENOCARCINOMA;
CARCINOMA-CELLS; ENDOTHELIAL-CELLS; GENE-EXPRESSION; TNF-ALPHA;
RESECTION; CYTOKINES
AB Chronic inflammation has been implicated in the pathogenesis of many severe autoimmune disorders, as well as in diabetes, pulmonary diseases, and cancer. Inflammation accompanies most solid cancers including pancreatic ductal adenocarcinoma (PDAC), one of the most fatal cancers with surgery being the only curative therapeutic approach currently available. In the present work, we investigated the role of the major proinflammatory cytokine tumor necrosis factor alpha (TNF alpha) in the malignancy of PDAC cells in vitro and in vivo. In vitro, TNF alpha strongly increased invasiveness of Colo357, BxPc3, and PancTuI cells and showed only moderate antiproliferative effect. TNF alpha. treatment of mice bearing orthotopically growing PDAC tumors led to dramatically enhanced tumor growth and metastasis. Notably, we found that PDAC cells themselves secrete TNF alpha. Although inhibition of TNF alpha with infliximab or etanercept only marginally affected proliferation and invasiveness of PDAC cells in vitro, both reagents exerted strong antitumoral effects in vivo. In severe combined immunodeficient mice with orthotopically growing Colo357, BxPc3, or PancTul tumors, human-specific anti-TNF antibody infliximab reduced tumor growth and metastasis by about 30% and 50%, respectively. Importantly, in a PDAC resection model performed with PancTul cells, we found an even stronger therapeutic effect for both anti-TNF compounds. Infliximab and etanercept reduced the number of liver metastases by 69% and 42%, respectively, as well as volumes of recurrent tumors by 73% and 51%. Thus, tumor cell-derived TNF alpha plays a profound role in malignancy of PDAC, and inhibition of TNF alpha represents a promising therapeutic option particularly in adjuvant therapy after subtotal pancreatectomy.
C1 [Kneitz, Christian; Wajant, Harald] Univ Wurzburg, Med Clin & Polyclin 2, Dept Mol Internal Med, D-97070 Wurzburg, Germany.
[Thon, Lutz; Adam, Dieter] Univ Hosp Schleswig Holstein, Dept Nucl Med, Inst Immunol, Kiel, Germany.
[Egberts, Jan-Hendrik; Cloosters, Vera; Noack, Andreas; Schniewind, Bodo; Klose, Stefanie; Kettler, Bastian; Tepel, Juergen; Kalthoff, Holger; Trauzold, Anna] Univ Hosp Schleswig Holstein, Dept Gen Surg, Div Mol Oncol, Kiel, Germany.
C3 University of Wurzburg; University of Kiel; Schleswig Holstein
University Hospital; University of Kiel; Schleswig Holstein University
Hospital
RP Wajant, H (corresponding author), Univ Wurzburg, Med Clin & Polyclin 2, Dept Mol Internal Med, Rontgenring 2, D-97070 Wurzburg, Germany.
EM harald.wajant@mail.uni-wuerzburg.de; hkalthoff@email.uni-kiel.de
RI Egberts, Jan-Hendrik/E-3211-2015; Trauzold, Anna/P-4398-2014; Kalthoff,
Holger/B-1618-2010; von Forstner, Corinna/A-8489-2010; Adam,
Dieter/E-9763-2010; Wajant, Harald/A-3020-2017
OI Trauzold, Anna/0000-0003-4697-556X; Adam, Dieter/0000-0002-5668-5032;
Wajant, Harald/0000-0002-2005-3949
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NR 47
TC 212
Z9 238
U1 2
U2 15
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAR 1
PY 2008
VL 68
IS 5
BP 1443
EP 1450
DI 10.1158/0008-5472.CAN-07-5704
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 271PW
UT WOS:000253802200025
PM 18316608
OA Green Submitted
DA 2025-01-07
ER
PT J
AU Chen, MH
Hsiao, LT
Chen, MH
Tsai, CY
Huang, YH
Chou, CT
AF Chen, Ming-Han
Hsiao, Liang-Tsai
Chen, Ming-Huang
Tsai, Chang-Youh
Huang, Yi-Hsiang
Chou, Chung-Tei
TI Clinical significance of chronic hepatitis B virus infection in patients
with primary Sjogren's syndrome
SO CLINICAL RHEUMATOLOGY
LA English
DT Article
DE Hepatitis B virus; Sjogren's syndrome
ID CHRONIC ACTIVE HEPATITIS; LABIAL SALIVARY-GLANDS; C VIRUS;
HEPATOCELLULAR-CARCINOMA; IMMUNOSUPPRESSIVE THERAPY; ALLERGIC DISEASES;
AUTOIMMUNE; HYDROXYCHLOROQUINE; ALPHA; CRYOGLOBULINEMIA
AB The role of hepatitis B virus (HBV) infection in patients with primary Sjogren's syndrome (pSS) remains unclear. Therefore, we investigated the prevalence and clinical significance of HBV infection in Taiwanese patients with pSS. One hundred seventy-five patients with pSS who fulfilled the 2002 American-European Revised Classification Criteria were enrolled. Eighteen (10.3%) patients were positive for hepatitis B surface antigen (HBsAg). There were 4 males and 14 females, with the mean age of 54.4 years. The main immunological feature was rheumatoid factor (13 of 18, 72.2%), which was significantly higher than those negative for HBsAg (28.1%, p < 0.001). Twelve (66.7%) patients developed liver dysfunction, which was significantly different from the 15.3% of patients who were negative for HBsAg (p < 0.001). There was no significant difference in extraglandular features between patients positive and negative for HBsAg, except patients positive for HBsAg had a lower rate to develop pulmonary involvement than those negative for HBsAg (5.6% vs. 29.9%, p = 0.027). The mortality rate of pSS patients positive for HBsAg during follow-up was 12.0% and the presence of HBV infection did not influence the survival rate (p = 0.730). pSS patients with liver cirrhosis presented shorter median overall survival compared to those with without liver cirrhosis (p < 0.001). Our findings suggest that HBV infection may protect individuals from pSS and reduce pulmonary involvement.
C1 [Chen, Ming-Han; Tsai, Chang-Youh; Chou, Chung-Tei] Taipei Vet Gen Hosp, Dept Med, Div Allergy Immunol & Rheumatol, Taipei 11217, Taiwan.
[Chen, Ming-Han; Hsiao, Liang-Tsai; Chen, Ming-Huang; Tsai, Chang-Youh; Huang, Yi-Hsiang; Chou, Chung-Tei] Natl Yang Ming Univ, Dept Med, Inst Clin Med, Taipei 112, Taiwan.
[Huang, Yi-Hsiang] Taipei Vet Gen Hosp, Dept Med, Div Gastroenterol, Taipei 11217, Taiwan.
C3 Taipei Veterans General Hospital; National Yang Ming Chiao Tung
University; Taipei Veterans General Hospital
RP Chou, CT (corresponding author), Taipei Vet Gen Hosp, Dept Med, Div Allergy Immunol & Rheumatol, 201,Sect 2,Shipai Rd, Taipei 11217, Taiwan.
EM ctchou@vghtpe.gov.tw
RI CHAO, TZE-FAN/JAX-3231-2023; Huang, Yi-Hsiang/ADX-9119-2022; Tsai,
Chang-Youh/G-1747-2013
OI Huang, Yi-Hsiang/0000-0001-5241-5425
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NR 48
TC 12
Z9 13
U1 0
U2 4
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0770-3198
EI 1434-9949
J9 CLIN RHEUMATOL
JI Clin. Rheumatol.
PD FEB
PY 2012
VL 31
IS 2
BP 309
EP 315
DI 10.1007/s10067-011-1814-2
PG 7
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 885GZ
UT WOS:000299768300015
PM 21809004
DA 2025-01-07
ER
PT J
AU Hu, CX
Zhao, LF
Zhang, LJ
Bao, QL
Li, LJ
AF Hu, Chenxia
Zhao, Lingfei
Zhang, Lingjian
Bao, Qiongling
Li, Lanjuan
TI Mesenchymal stem cell-based cell-free strategies: safe and effective
treatments for liver injury
SO STEM CELL RESEARCH & THERAPY
LA English
DT Review
DE Mesenchymal stem cell; Cell-free; Treatment; Liver injury; Cell death
ID EXTRACELLULAR VESICLES; CONDITIONED MEDIUM; PROTEOMIC ANALYSIS; STROMAL
CELLS; EXOSOMES; APOPTOSIS; HYPOXIA; REGENERATION; AUTOPHAGY; FAILURE
AB Various hepatoxic factors, such as viruses, drugs, lipid deposition, and autoimmune responses, induce acute or chronic liver injury, and 3.5% of all worldwide deaths result from liver cirrhosis, liver failure, or hepatocellular carcinoma. Liver transplantation is currently limited by few liver donors, expensive surgical costs, and severe immune rejection. Cell therapy, including hepatocyte transplantation and stem cell transplantation, has recently become an attractive option to reduce the overall need for liver transplantation and reduce the wait time for patients. Recent studies showed that mesenchymal stem cell (MSC) administration was a promising therapeutic approach for promoting liver regeneration and repairing liver injury by the migration of cells into liver sites, hepatogenic differentiation, immunoregulation, and paracrine mechanisms. MSCs secrete a large number of molecules into the extracellular space, and soluble proteins, free nucleic acids, lipids, and extracellular vesicles (EVs) effectively repair tissue injury in response to fluctuations in physiological states or pathological conditions. Cell-free-based therapies avoid the potential tumorigenicity, rejection of cells, emboli formation, undesired differentiation, and infection transmission of MSC transplantation. In this review, we focus on the potential mechanisms of MSC-based cell-free strategies for attenuating liver injury in various liver diseases. Secretome-mediated paracrine effects participate in the regulation of the hepatic immune microenvironment and promotion of hepatic epithelial repair. We look forward to completely reversing liver injury through an MSC-based cell-free strategy in regenerative medicine in the near future.
C1 [Hu, Chenxia; Zhang, Lingjian; Bao, Qiongling; Li, Lanjuan] Zhejiang Univ, State Key Lab Diag & Treatment Infect Dis, Collaborat Innovat Ctr Diag & Treatment Infect Di, Sch Med,Affiliated Hosp 1, Hangzhou, Peoples R China.
[Hu, Chenxia; Zhang, Lingjian; Bao, Qiongling; Li, Lanjuan] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Natl Clin Res Ctr Infect Dis, Hangzhou, Zhejiang, Peoples R China.
[Zhao, Lingfei] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Kidney Dis Ctr, Hangzhou, Peoples R China.
[Zhao, Lingfei] Key Lab Kidney Dis Prevent & Control Technol, Hangzhou, Zhejiang, Peoples R China.
[Zhao, Lingfei] Zhejiang Univ, Inst Nephrol, Hangzhou, Zhejiang, Peoples R China.
C3 Collaborative Innovation Center for Diagnosis & Treatment of Infectious
Diseases; Zhejiang University; Zhejiang University; Zhejiang University;
Zhejiang University
RP Li, LJ (corresponding author), Zhejiang Univ, State Key Lab Diag & Treatment Infect Dis, Collaborat Innovat Ctr Diag & Treatment Infect Di, Sch Med,Affiliated Hosp 1, Hangzhou, Peoples R China.; Li, LJ (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 1, Natl Clin Res Ctr Infect Dis, Hangzhou, Zhejiang, Peoples R China.
EM ljli@zju.edu.cn
RI li, li/HJY-8663-2023
FU National Natural Science Foundation of China [81700553]; Zhejiang basic
public welfare research program [LGF20H030008]; Independent Fund of
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases,
Zhejiang University
FX This work was supported by the National Natural Science Foundation of
China (no. 81700553), Zhejiang basic public welfare research program
(no. LGF20H030008), and the Independent Fund of State Key Laboratory for
Diagnosis and Treatment of Infectious Diseases, Zhejiang University.
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NR 102
TC 87
Z9 91
U1 6
U2 45
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1757-6512
J9 STEM CELL RES THER
JI Stem Cell Res. Ther.
PD SEP 3
PY 2020
VL 11
IS 1
AR 377
DI 10.1186/s13287-020-01895-1
PG 12
WC Cell & Tissue Engineering; Cell Biology; Medicine, Research &
Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA NN1PP
UT WOS:000568563000001
PM 32883343
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Maeda, N
Maenaka, K
AF Maeda, Naoyoshi
Maenaka, Katsumi
TI The Roles of Matricellular Proteins in Oncogenic Virus-Induced Cancers
and Their Potential Utilities as Therapeutic Targets
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE matricellular proteins; oncogenic viruses; osteopontin (OPN); periostin
(POSTN); secreted protein acidic and rich in cysteine (SPARC);
tenascin-C (TNC); thrombospondin (TSP); tumor microenvironment
ID EPITHELIAL-MESENCHYMAL TRANSITION; SARCOMA-ASSOCIATED HERPESVIRUS;
ENDOTHELIAL GROWTH-FACTOR; CELL LUNG-CANCER; LATENT-TGF-BETA;
TENASCIN-C; HUMAN-PAPILLOMAVIRUS; HEPATOCELLULAR-CARCINOMA;
MYOCARDIAL-INFARCTION; PLASMA OSTEOPONTIN
AB Matricellular proteins differ from other classical extracellular matrix proteins; for instance, they are transiently expressed as soluble proteins rather than being constitutively expressed in pathological conditions, such as acute viral infections. Accumulating studies have revealed that matricellular proteins, including osteopontin and tenascin-C, both of which interact with integrin heterodimers, are involved in inflammatory diseases, autoimmune disorders, and cancers. The concentrations of these matricellular proteins are elevated in the plasma of patients with certain types of cancers, indicating that they play important roles in oncogenesis. Chronic viral infections are associated with certain cancers, which are distinct from non-viral cancers. Viral oncogenes play critical roles in the development and progression of such cancers. It is vital to investigate the mechanisms of tumorigenesis and, particularly, the mechanism by which viral proteins induce tumor progression. Viral proteins have been shown to influence not only the viral-infected cancer cells, but also the stromal cells and matricellular proteins that constitute the extracellular matrix that surrounds tumor tissues. In this review, we summarize the recent progress on the involvement of matricellular proteins in oncogenic virus-induced cancers to elucidate the mechanism of oncogenesis and consider the possible role of matricellular proteins as therapeutic targets in virus-induced cancers.
C1 [Maeda, Naoyoshi; Maenaka, Katsumi] Hokkaido Univ, Fac Pharmaceut Sci, Ctr Res & Educ Drug Discovery, Kita Ku, Kita 12,Nishi 6, Sapporo, Hokkaido 0600812, Japan.
[Maenaka, Katsumi] Hokkaido Univ, Fac Pharmaceut Sci, Lab Biomol Sci, Kita Ku, Kita 12,Nishi 6, Sapporo, Hokkaido 0600812, Japan.
C3 Hokkaido University; Hokkaido University
RP Maeda, N (corresponding author), Hokkaido Univ, Fac Pharmaceut Sci, Ctr Res & Educ Drug Discovery, Kita Ku, Kita 12,Nishi 6, Sapporo, Hokkaido 0600812, Japan.
EM nmaeda@pharm.hokudai.ac.jp; maenaka@pharm.hokudai.ac.jp
FU Ministry of Education, Culture, Sports, Science and Technology (MEXT);
Japan Agency for Medical Research and Development (AMED); Hokkaido
University, Global Facility Center (GFC); Pharma Science Open Unit
(PSOU) - MEXT; Grants-in-Aid for Scientific Research [17K08848] Funding
Source: KAKEN
FX We sincerely thank Dr. Toshimitsu Uede, a professor emeritus of Hokkaido
University, for supporting our research. This research is partially
supported by the Platform Project for Supporting in Drug Discovery and
Life Science Research (Platform for Drug Discovery, Informatics, and
Structural Life Science) from the Ministry of Education, Culture,
Sports, Science and Technology (MEXT), and Japan Agency for Medical
Research and Development (AMED), and Hokkaido University, Global
Facility Center (GFC), Pharma Science Open Unit (PSOU), funded by MEXT
under "Support Program for Implementation of New Equipment Sharing
System".
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NR 122
TC 15
Z9 15
U1 1
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2017
VL 18
IS 10
AR 2198
DI 10.3390/ijms18102198
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA FM0QL
UT WOS:000414671800181
PM 29065446
OA gold, Green Submitted, Green Published
DA 2025-01-07
ER
PT J
AU Todoric, J
Antonucci, L
Karin, M
AF Todoric, Jelena
Antonucci, Laura
Karin, Michael
TI Targeting Inflammation in Cancer Prevention and Therapy
SO CANCER PREVENTION RESEARCH
LA English
DT Review
ID NF-KAPPA-B; TUMOR-ASSOCIATED MACROPHAGES; ADIPOSE-TISSUE INFLAMMATION;
HIGH-FAT DIET; HEPATOCELLULAR-CARCINOMA; CIGARETTE-SMOKE; INTESTINAL
MICROBIOME; PANCREATIC-CANCER; OXIDATIVE STRESS; DOWN-REGULATION
AB Inflammation is associated with the development and malignant progression of most cancers. As most of the cell types involved in cancer-associated inflammation are genetically stable and thus are not subjected to rapid emergence of drug resistance, the targeting of inflammation represents an attractive strategy both for cancer prevention and for cancer therapy. Tumor-extrinsic inflammation is caused by many factors, including bacterial and viral infections, autoimmune diseases, obesity, tobacco smoking, asbestos exposure, and excessive alcohol consumption, all of which increase cancer risk and stimulatemalignant progression. In contrast, cancer-intrinsic or cancer-elicited inflammation can be triggered by cancer-initiating mutations and can contribute to malignant progression through the recruitment and activation of inflammatory cells. Both extrinsic and intrinsic inflammation can result in immunosuppression, thereby providing a preferred background for tumor development. In clinical trials, lifestyle modifications including healthy diet, exercise, alcohol, and smoking cessation have proven effective in ameliorating inflammation and reducing the risk of cancer-related deaths. In addition, consumption of certain anti-inflammatory drugs, including aspirin, can significantly reduce cancer risk, suggesting that common nonsteroidal anti-inflammatory drugs (NSAID) and more specific COX2 inhibitors can be used in cancer prevention. In addition to being examined for their preventative potential, both NSAIDs and more potent anti-inflammatory antibody-based drugs need to be tested for their ability to augment the efficacy of more conventional therapeutic approaches on the basis of tumor resection, radiation, and cytotoxic chemicals.
C1 [Todoric, Jelena; Antonucci, Laura; Karin, Michael] Univ Calif San Diego, Sch Med, Dept Pharmacol, Lab Gene Regulat & Signal Transduct, La Jolla, CA 92093 USA.
[Todoric, Jelena] Med Univ Vienna, Dept Lab Med, Vienna, Austria.
[Karin, Michael] Univ Calif San Diego, Sch Med, Dept Pathol, La Jolla, CA 92093 USA.
C3 University of California System; University of California San Diego;
Medical University of Vienna; University of California System;
University of California San Diego
RP Karin, M (corresponding author), Univ Calif San Diego, Dept Pharmacol, 9500 Gilman Dr,M-C 0723, La Jolla, CA 92093 USA.
EM karinoffice@ucsd.edu
FU Erwin Schroedinger Fellowship from the Austrian Science Fund [J3233];
Austrian Association for Laboratory Medicine and Clinical Chemistry
(OGLMKC); Austrian Program for Advanced Research and Technology of the
Austrian Academy of Sciences; International Cancer Research Fellowship
(iCARE); NIH [CA163798]; Lustgarten Foundation [RFP-B-007]; AIRC
(Associazione Italiana per la ricerca sul cancro); Austrian Science Fund
(FWF) [J3233] Funding Source: Austrian Science Fund (FWF)
FX J. Todoric was supported by the Erwin Schroedinger Fellowship from the
Austrian Science Fund (J3233) and Univ. Prof. Dr. 17 Matthias M. Muller
Fellowship from the Austrian Association for Laboratory Medicine and
Clinical Chemistry (OGLMKC) and the Austrian Program for Advanced
Research and Technology of the Austrian Academy of Sciences. L.
Antonucci was supported by the International Cancer Research Fellowship
(iCARE), AIRC (Associazione Italiana per la ricerca sul cancro)
co-founded by the European Union. M. Karin was supported by grants from
the NIH grants (CA163798) and the Lustgarten Foundation (RFP-B-007). who
holds the Ben and Wanda Hildyard Chair for Mitochondrial and Metabolic
Diseases and is an American Cancer Society Research Professor.
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NR 147
TC 292
Z9 314
U1 1
U2 97
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2016
VL 9
IS 12
BP 895
EP 905
DI 10.1158/1940-6207.CAPR-16-0209
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EF1NS
UT WOS:000390092200002
PM 27913448
OA Green Accepted, Green Submitted, Bronze
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Göbel, A
Rachner, TD
Hoffmann, O
Klotz, DM
Kasimir-Bauer, S
Kimmig, R
Hofbauer, LC
Bittner, AK
AF Goebel, Andy
Rachner, Tilman D.
Hoffmann, Oliver
Klotz, Daniel Martin
Kasimir-Bauer, Sabine
Kimmig, Rainer
Hofbauer, Lorenz C.
Bittner, Ann-Kathrin
TI High serum levels of leucine-rich α-2 glycoprotein 1 (LRG-1) are
associated with poor survival in patients with early breast cancer
SO ARCHIVES OF GYNECOLOGY AND OBSTETRICS
LA English
DT Article
DE LRG-1; Early breast cancer; Prognostic marker; Serum marker; Minimal
residual disease; Disseminated tumor cells
ID COLORECTAL-CANCER; ALPHA-2-GLYCOPROTEIN; EXPRESSION; BIOMARKER; DISEASE;
IDENTIFICATION; MARKER
AB Background: Leucine-rich alpha-2 glycoprotein 1 (LRG-1) is a secreted glycoprotein that is mainly produced in the liver. Elevated levels of LRG-1 are found in a multitude of pathological conditions including eye diseases, diabetes, infections, autoimmune diseases, and cancer. In patients with early breast cancer (BC), high intratumoral LRG-1 protein expression levels are associated with reduced survival. In this study, we assessed serum levels of LRG-1 in patients with early BC and investigated its correlation with the presence of disseminated tumor cells (DTCs) in the bone marrow and survival outcomes. Methods: Serum LRG-1 levels of 509 BC patients were determined using ELISA and DTCs were assessed by immunocytochemistry using the pan-cytokeratin antibody A45-B/B3. We stratified LRG-1 levels according to selected clinical parameters. Using the log-rank (Mantel-Cox) test and multivariate Cox regression analysis, Kaplan-Meier survival curves and prognostic relevance were assessed. Results: Mean serum levels of LRG-1 were 29.70 +/- 8.67 mu g/ml. Age was positively correlated with LRG-1 expression (r = 0.19; p < 0.0001) and significantly higher LRG-1 levels were found in patients over 60 years compared to younger ones (30.49 +/- 8.63 mu g/ml vs. 28.85 +/- 8.63 mu g/ml; p = 0.011) and in postmenopausal patients compared to premenopausal patients (30.15 +/- 8.34 mu g/ml vs. 26.936.94 mu g/ml; p = 0.002). Patients with no DTCs showed significantly elevated LRG-1 levels compared to the DTC-positive group (30.51 +/- 8.69 mu g/ml vs. 28.51 +/- 8.54 mu g/ml; p = 0.004). Overall and BC-specific survival was significantly lower in patients with high serum LRG-1 levels (above a cut-off of 33.63 mu g/ml) compared to patients with lower LRG-1 levels during a mean follow-up of 8.5 years (24.8% vs. 11.1% BC-specific death; p = 0.0003; odds ratio 2.63, 95%CI: 1.56-4.36). Multivariate analyses revealed that LRG-1 is an independent prognostic marker for BC-specific survival (p = 0.001; hazard ratio 2.61). Conclusions: This study highlights the potential of LRG-1 as an independent prognostic biomarker in patients with early BC.
C1 [Goebel, Andy; Rachner, Tilman D.; Hofbauer, Lorenz C.] Tech Univ Dresden, Dept Med 3, Div Endocrinol & Metab Bone Dis, Dresden, Germany.
[Goebel, Andy; Rachner, Tilman D.; Hofbauer, Lorenz C.] Tech Univ Dresden, Ctr Hlth Ageing, Dept Med 3, Dresden, Germany.
[Goebel, Andy; Rachner, Tilman D.; Klotz, Daniel Martin; Hofbauer, Lorenz C.] German Canc Consortium DKTK, Dresden, Germany.
[Goebel, Andy; Rachner, Tilman D.; Klotz, Daniel Martin; Hofbauer, Lorenz C.] German Canc Res Ctr, Heidelberg, Germany.
[Hoffmann, Oliver; Kasimir-Bauer, Sabine; Kimmig, Rainer; Bittner, Ann-Kathrin] Univ Duisburg Essen, Univ Hosp Essen, Dept Gynecol & Obstet, Essen, Germany.
[Hoffmann, Oliver; Kasimir-Bauer, Sabine; Kimmig, Rainer; Bittner, Ann-Kathrin] Natl Ctr Tumor Dis NCT, Heidelberg, Germany.
[Klotz, Daniel Martin] Tech Univ Dresden, Fac Med, Dept Gynecol & Obstet, Dresden, Germany.
[Klotz, Daniel Martin] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dresden, Germany.
[Klotz, Daniel Martin] Natl Ctr Tumor Dis NCT, Dresden, Germany.
[Klotz, Daniel Martin] Helmholtz Zentrum Dresden Rossendorf HZDR, Dresden, Germany.
C3 Technische Universitat Dresden; Technische Universitat Dresden;
Helmholtz Association; German Cancer Research Center (DKFZ); Helmholtz
Association; German Cancer Research Center (DKFZ); University of
Duisburg Essen; Helmholtz Association; German Cancer Research Center
(DKFZ); Ruprecht Karls University Heidelberg; Technische Universitat
Dresden; Technische Universitat Dresden; Carl Gustav Carus University
Hospital; Helmholtz Association; German Cancer Research Center (DKFZ);
Ruprecht Karls University Heidelberg; Helmholtz Association;
Helmholtz-Zentrum Dresden-Rossendorf (HZDR)
RP Göbel, A (corresponding author), Tech Univ Dresden, Dept Med 3, Div Endocrinol & Metab Bone Dis, Dresden, Germany.; Göbel, A (corresponding author), Tech Univ Dresden, Ctr Hlth Ageing, Dept Med 3, Dresden, Germany.; Göbel, A (corresponding author), German Canc Consortium DKTK, Dresden, Germany.; Göbel, A (corresponding author), German Canc Res Ctr, Heidelberg, Germany.
EM andy.goebel@uniklinikum-dresden.de
RI Klotz, Daniel/LFV-5666-2024; Hofbauer, Lorenz C./G-2490-2010
OI Hofbauer, Lorenz C./0000-0002-8691-8423
FU Deutsche Forschungsgemeinschaft
FX No Statement Available
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NR 53
TC 2
Z9 2
U1 4
U2 5
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0932-0067
EI 1432-0711
J9 ARCH GYNECOL OBSTET
JI Arch. Gynecol. Obstet.
PD JUN
PY 2024
VL 309
IS 6
BP 2789
EP 2798
DI 10.1007/s00404-024-07434-0
EA FEB 2024
PG 10
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA SZ4S9
UT WOS:001171859400002
PM 38413424
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Radosavljevic, G
Volarevic, V
Jovanovic, I
Milovanovic, M
Pejnovic, N
Arsenijevic, N
Hsu, DK
Lukic, ML
AF Radosavljevic, Gordana
Volarevic, Vladislav
Jovanovic, Ivan
Milovanovic, Marija
Pejnovic, Nada
Arsenijevic, Nebojsa
Hsu, Daniel K.
Lukic, Miodrag L.
TI The roles of Galectin-3 in autoimmunity and tumor progression
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Galectin-3; Con-A-induced hepatitis; Multiple low-dose
streptozotocin-induced diabetes; Experimental autoimmune
encephalomyelitis; Melanoma metastasis
ID GALACTOSIDE-BINDING PROTEIN; T-CELL GROWTH; HUMAN BREAST;
CONCANAVALIN-A; CANCER-CELLS; DECREASED SUSCEPTIBILITY; OVEREXPRESSION
PROTECTS; TARGETED DISRUPTION; MELANOMA PATIENT; EPITHELIAL-CELLS
AB Galectin-3, a unique chimera-type member of the beta-galactoside-binding soluble lectin family, is widely expressed in numerous cells. Here, we discuss the role of Galectin-3 in T-cell-mediated inflammatory (auto) immunity and tumor rejection by using Galectin-3-deficient mice and four disease models of human pathology: experimental autoimmune encephalomyelitis (EAE), Con-A-induced hepatitis, multiple low-dose streptozotocin-induced diabetes (MLD-STZ diabetes) and metastatic melanoma. We present evidence which suggest that Galectin-3 plays an important pro-inflammatory role in Con-A-induced hepatitis by promoting the activation of T lymphocytes, NKT cells and DCs, cytokine secretion, prevention of M2 macrophage polarization and apoptosis of mononuclear cells, and it leads to severe liver injury. In addition, experiments in Galectin-3-"knock-out" mice indicate that Galectin-3 is also involved in immune-mediated beta-cell damage and is required for diabetogenesis in MLD-STZ model by promoting the expression of IFN-gamma, TNF-alpha, IL-17 and iNOS in immune and accessory effector cells. Next, our data demonstrated that Galectin-3 plays an important disease-exacerbating role in EAE through its multifunctional roles in preventing cell apoptosis and increasing IL-17 and IFN-gamma synthesis, but decreasing IL-10 production. Finally, based on our findings, we postulated that expression of Galectin-3 in the host may also facilitate melanoma metastasis by affecting tumor cell adhesion and modulating anti-melanoma immune response, in particular innate antitumor immunity. Taken together, we discuss the evidence of pro-inflammatory and antitumor activities of Galectin-3 and suggest that Galectin-3 may be an important therapeutic target.
C1 [Radosavljevic, Gordana; Volarevic, Vladislav; Jovanovic, Ivan; Milovanovic, Marija; Pejnovic, Nada; Arsenijevic, Nebojsa; Lukic, Miodrag L.] Univ Kragujevac, Fac Med, Ctr Mol Med & Stem Cell Res, Kragujevac 34000, Serbia.
[Hsu, Daniel K.] Univ Calif Davis, Sch Med, Dept Dermatol, Sacramento, CA 95817 USA.
C3 University of Kragujevac; University of California System; University of
California Davis
RP Lukic, ML (corresponding author), Univ Kragujevac, Fac Med, Ctr Mol Med & Stem Cell Res, Svetozara Markovica 69, Kragujevac 34000, Serbia.
EM miodrag.lukic@medf.kg.ac.rs
RI Volarevic, Vladislav/ABH-8934-2020; Milovanovic, Marija/HPB-6090-2023;
Lukic, Miodrag/U-8848-2019
OI Volarevic, Vladislav/0000-0002-9057-9460; Arsenijevic,
Nebojsa/0000-0002-2107-3490; Volarevic, Vladislav/0000-0001-5948-9902;
Jovanovic, Ivan/0000-0002-1169-2378; Milovanovic,
Marija/0000-0002-6894-1275; Lukic, Miodrag/0000-0002-3563-632X;
Radosavljevic, Gordana/0000-0001-6016-0725; Pejnovic,
Nada/0000-0002-2279-9197
FU Ministry of Education and Science, Republic of Serbia [ON175069,
ON175071, ON175103]
FX This study is supported by grants ON175069, ON175071 and ON175103 from
Ministry of Education and Science, Republic of Serbia. We thank Milan
Milojevic for excellent technical assistance.
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NR 113
TC 96
Z9 109
U1 1
U2 27
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD APR
PY 2012
VL 52
IS 1-2
SI SI
BP 100
EP 110
DI 10.1007/s12026-012-8286-6
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 929JN
UT WOS:000303057600011
PM 22418727
DA 2025-01-07
ER
PT J
AU Villaseñor-Altamirano, AB
Watson, JD
Prokopec, SD
Yao, CQ
Boutros, PC
Pohjanvirta, R
Valdés-Flores, J
Elizondo, G
AF Villasenor-Altamirano, Ana B.
Watson, John D.
Prokopec, Stephenie D.
Yao, Cindy Q.
Boutros, Paul C.
Pohjanvirta, Raimo
Valdes-Flores, Jesus
Elizondo, Guillermo
TI 2,3,7,8-Tetrachlorodibenzo-p-dioxin modifies alternative splicing
in mouse liver
SO PLOS ONE
LA English
DT Article
ID ARYL-HYDROCARBON RECEPTOR; AH RECEPTOR; BINDING DOMAIN; EXPRESSION;
TCDD; EXON; IDENTIFICATION; DISRUPTION; MECHANISMS; REPRESSOR
AB Alternative splicing is a co-transcriptional mechanism that generates protein diversity by including or excluding exons in different combinations, thereby expanding the diversity of protein isoforms of a single gene. Abnormalities in this process can result in deleterious effects to human health, and several xenobiotics are known to interfere with splicing regulation through multiple mechanisms. These changes could lead to human diseases such as cancer, neurological disorders, autoimmune diseases, and developmental disorders. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant generated as a byproduct of various industrial activities. Exposure to this dioxin has been linked to a wide range of pathologies through the alteration of multiple cellular processes. However, the effects of TCDD exposure on alternative splicing have not yet been studied. Here, we investigated whether a single po. dose of 5 mu g/kg or 500 mu g/kg TCDD influence hepatic alternative splicing in adult male C57BL/6Kou mouse. We identified several genes whose alternative splicing of precursor messenger RNAs was modified following TCDD exposure. In particular, we demonstrated that alternative splicing of Cyp1a1, Ahrr, and Actn1 was significantly altered after TCDD treatment. These findings show that the exposure to TCDD has an impact on alternative-splicing, and suggest a new avenue for understanding TCDD-mediated toxicity and pathogenesis.
C1 [Villasenor-Altamirano, Ana B.; Elizondo, Guillermo] IPN, CINVESTAN, Natl Polytech Inst, Cell Biol Dept,Ctr Res & Adv Studies, Mexico City, DF, Mexico.
[Villasenor-Altamirano, Ana B.] Univ Nacl Autonoma Mexico, Int Lab Human Genome Res, Queretaro, Mexico.
[Watson, John D.; Prokopec, Stephenie D.; Yao, Cindy Q.; Boutros, Paul C.] Ontario Inst Canc Res, Toronto, ON, Canada.
[Yao, Cindy Q.; Boutros, Paul C.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
[Boutros, Paul C.] Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA.
[Pohjanvirta, Raimo] Natl Inst Hlth & Welf, Lab Toxicol, Kuopio, Finland.
[Pohjanvirta, Raimo] Univ Helsinki, Dept Food Hyg & Environm Hlth, Helsinki, Finland.
[Valdes-Flores, Jesus] IPN, CINVESTAV, Natl Polytech Inst, Biochem Dept,Ctr Res & Adv Studies, Mexico City, DF, Mexico.
C3 CINVESTAV - Centro de Investigacion y de Estudios Avanzados del
Instituto Politecnico Nacional; Instituto Politecnico Nacional - Mexico;
Universidad Nacional Autonoma de Mexico; University of Toronto; Ontario
Institute for Cancer Research; University of Toronto; University of
California System; University of California Los Angeles; Finland
National Institute for Health & Welfare; University of Helsinki;
CINVESTAV - Centro de Investigacion y de Estudios Avanzados del
Instituto Politecnico Nacional; Instituto Politecnico Nacional - Mexico
RP Elizondo, G (corresponding author), IPN, CINVESTAN, Natl Polytech Inst, Cell Biol Dept,Ctr Res & Adv Studies, Mexico City, DF, Mexico.
EM gazuela@cinvestav.mx
RI Pohjanvirta, Raimo/I-4509-2019; Boutros, Paul/A-1084-2009
OI Pohjanvirta, Raimo/0000-0003-0952-5746; Villasenor Altamirano, Ana
Beatriz/0000-0002-3940-5617
FU Terry Fox Research Institute; CIHR New Investigator Awards; Consejo
Nacional de Ciencia y Tecnologia [153377, 280897]
FX This study was supported by Terry Fox Research Institute and CIHR New
Investigator Awards, to PCB; and Consejo Nacional de Ciencia y
Tecnologia grant 153377 and 280897, GE. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 48
TC 5
Z9 5
U1 0
U2 15
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 6
PY 2019
VL 14
IS 8
AR e0219747
DI 10.1371/journal.pone.0219747
PG 18
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA IW5CU
UT WOS:000484997100009
PM 31386671
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Blinova, VG
Zhdanov, DD
AF Blinova, Varvara G.
Zhdanov, Dmitry D.
TI Many Faces of Regulatory T Cells: Heterogeneity or Plasticity?
SO CELLS
LA English
DT Review
DE regulatory T cells; heterogeneity; plasticity; phenotype switch;
treg-based therapy
ID TRANSCRIPTION FACTOR FOXP3; CD127 EXPRESSION; TREG CELLS; SUPPRESSIVE
FUNCTION; PHENOTYPE; THERAPY; DISEASE; TIGIT; LIVER; DIFFERENTIATION
AB Regulatory T cells (Tregs) are essential for maintaining the immune balance in normal and pathological conditions. In autoimmune diseases and transplantation, they restrain the loss of self-tolerance and promote engraftment, whereas in cancer, an increase in Treg numbers is mostly associated with tumor growth and poor prognosis. Numerous markers and their combinations have been used to identify Treg subsets, demonstrating the phenotypic diversity of Tregs. The complexity of Treg identification can be hampered by the unstable expression of some markers, the decrease in the expression of a specific marker over time or the emergence of a new marker. It remains unclear whether such phenotypic shifts are due to new conditions or whether the observed changes are due to initially different populations. In the first case, cellular plasticity is observed, whereas in the second, cellular heterogeneity is observed. The difference between these terms in relation to Tregs is rather blurred. Considering the promising perspectives of Tregs in regenerative cell-based therapy, the existing confusing data on Treg phenotypes require further investigation and analysis. In our review, we introduce criteria that allow us to distinguish between the heterogeneity and plasticity of Tregs normally and pathologically, taking a closer look at their diversity and drawing the line between two terms.
C1 [Blinova, Varvara G.; Zhdanov, Dmitry D.] Inst Biomed Chem, Lab Med Biotechnol, Pogodinskaya St 10-8, Moscow 119121, Russia.
[Zhdanov, Dmitry D.] Peoples Friendship Univ Russia, Dept Biochem, RUDN Univ, 6 Miklukho Maklaya St, Moscow 117198, Russia.
C3 Russian Academy of Medical Sciences; Institute of Biomedical Chemistry;
Peoples Friendship University of Russia
RP Zhdanov, DD (corresponding author), Inst Biomed Chem, Lab Med Biotechnol, Pogodinskaya St 10-8, Moscow 119121, Russia.; Zhdanov, DD (corresponding author), Peoples Friendship Univ Russia, Dept Biochem, RUDN Univ, 6 Miklukho Maklaya St, Moscow 117198, Russia.
EM v.02.blinova@gmail.com; zhdanovdd@gmail.com
RI Blinova, Varvara/JED-8413-2023; Zhdanov, Dmitry/ABD-2524-2020; Zhdanov,
Dmitry/S-4921-2017
OI Blinova, Varvara/0000-0002-3290-9839; Zhdanov,
Dmitry/0000-0003-4753-7588
FU Russian Science Foundation
FX No Statement Available
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NR 217
TC 1
Z9 1
U1 4
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD JUN
PY 2024
VL 13
IS 11
AR 959
DI 10.3390/cells13110959
PG 34
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA UB9H8
UT WOS:001245714600001
PM 38891091
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Niu, XK
Bhetuwal, A
Das, S
Xiao, YQ
Sun, F
Zeng, LC
Yang, HF
AF Niu, Xiang-ke
Bhetuwal, Anup
Das, Sushant
Xiao, Ying-quan
Sun, Feng
Zeng, Li-chuan
Yang, Han-feng
TI Meta-analysis of quantitative diffusion-weighted MR imaging in
differentiating benign and malignant pancreatic masses
SO JOURNAL OF HUAZHONG UNIVERSITY OF SCIENCE AND TECHNOLOGY-MEDICAL
SCIENCES
LA English
DT Article
DE apparent diffusion coefficient; diffusion-weighted imaging; magnetic
resonance imaging; meta-analysis; pancreatic tumor; pancreatic
adenocarcinoma
ID FORMING CHRONIC-PANCREATITIS; AUTOIMMUNE PANCREATITIS; DIAGNOSTIC-TEST;
CARCINOMA; LESIONS; CURVE; TUMOR; CANCER; LIVER; CT
AB There have been numerous studies done to explore the diagnostic performance of quantitative diffusion-weighted (DW) MR imaging to differentiate between benign and malignant pancreatic masses. However, the results have been inconsistent. We performed a meta-analysis to investigate whether DW-MR imaging can differentiate between these two diseases. Databases including MEDLINE, EMBASE and Cochrane Library were utilized to find relevant articles published between January 2001 and January 2014. A Stata version 12.0 and a Meta-Disc version 1.4 were used to describe primary results. Twelve studies with 594 patients, which fulfilled the inclusion criteria, were enrolled for the analysis. The pooled sensitivity and specificity of DW imaging was 0.91 (95% CI: 0.84, 0.95) and 0.86 (95% CI: 0.76, 0.93) respectively. The area under the curve of the summary receiver operating characteristic was 0.95 (95% CI: 0.93, 0.96). The results indicated that DW imaging might be a valuable tool for differentiating benign and malignant pancreatic masses.
C1 [Niu, Xiang-ke] Chengdu Univ, Affiliated Hosp, Dept Radiol, Chengdu 610000, Peoples R China.
[Bhetuwal, Anup; Das, Sushant; Xiao, Ying-quan; Sun, Feng; Zeng, Li-chuan; Yang, Han-feng] North Sichuan Med Coll, Affiliated Hosp, Sichuan Key Lab Med Imaging, Nanchong 637000, Peoples R China.
[Bhetuwal, Anup; Das, Sushant; Xiao, Ying-quan; Sun, Feng; Zeng, Li-chuan; Yang, Han-feng] North Sichuan Med Coll, Affiliated Hosp, Dept Radiol, Nanchong 637000, Peoples R China.
C3 Chengdu University; North Sichuan Medical University; North Sichuan
Medical University
RP Yang, HF (corresponding author), North Sichuan Med Coll, Affiliated Hosp, Sichuan Key Lab Med Imaging, Nanchong 637000, Peoples R China.
EM 862639224@qq.com; niu19850519@163.com
RI Bhetuwal, Anup/KIG-6037-2024
FU Science Foundation for Distinguished Young Scholars of Sichuan Province,
China [2012JQ0060]
FX This project was supported by the Science Foundation for Distinguished
Young Scholars of Sichuan Province, China (No. 2012JQ0060).
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NR 34
TC 5
Z9 8
U1 0
U2 10
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1672-0733
EI 1993-1352
J9 J HUAZHONG U SCI-MED
JI J. Huazhong Univ. Sci. Tech.-Med.
PD DEC
PY 2014
VL 34
IS 6
BP 950
EP 956
DI 10.1007/s11596-014-1379-9
PG 7
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA AW1JK
UT WOS:000346045600026
PM 25480596
DA 2025-01-07
ER
PT J
AU Baldo, BA
Pham, NH
AF Baldo, Brian A.
Pham, Nghia H.
TI Adverse reactions to targeted and non-targeted chemotherapeutic drugs
with emphasis on hypersensitivity responses and the invasive metastatic
switch
SO CANCER AND METASTASIS REVIEWS
LA English
DT Review
DE Chemotherapy-induced hypersensitivities; Cancer drug hypersensitivities;
Cancer drug adverse effects; Hypersensitivities to chemotherapy drugs;
Drug allergies; Drug hypersensitivities; Drugs and metastatic switch
ID AUTOIMMUNE HEMOLYTIC-ANEMIA; IMMUNE-MEDIATED THROMBOCYTOPENIA; CHRONIC
LYMPHOCYTIC-LEUKEMIA; HISTONE DEACETYLASE INHIBITORS; ANTI-ANGIOGENIC
DRUGS; CUTANEOUS VASCULITIS; ALLERGIC REACTIONS; PHASE-I; TUMOR
ANGIOGENESIS; IMATINIB MESYLATE
AB More than 100 drugs are used to treat the many different cancers. They can be divided into agents with relatively broad, non-targeted specificity and targeted drugs developed on the basis of a more refined understanding of individual cancers and directed at specific molecular targets on different cancer cells. Individual drugs in both groups have been classified on the basis of their mechanism of action in killing cancer cells. The targeted drugs include proteasome inhibitors, toxic chimeric proteins and signal transduction inhibitors such as tyrosine kinase (non-receptor and receptor), serine/threonine kinase, histone deacetylase and mammalian target of rapamycin inhibitors. Increasingly used targeted vascular (VEGF) and platelet-derived endothelial growth factor blockade can provoke a range of pathological consequences. Many of the non-targeted drugs are cytotoxic, suppressing haematopoiesis as well as provoking cutaneous eruptions and vascular, lung and liver injury. Cytotoxic side effects of the targeted drugs occur less often and usually with less severity, but they show their own unusual adverse effects including, for example, a lengthened QT interval, a characteristic papulopustular rash, nail disorders and a hand-foot skin reaction variant. The term hypersensitivity is widely used across a number of disciplines but not always with the same definition in mind, and the terminology needs to be standardised. This is particularly apparent in cancer chemotherapy where anti-neoplastic drug-induced thrombocytopenia, neutropenia, anaemia, vascular disorders, liver injury and lung disease as well as many dermatological manifestations sometimes have an immune basis. The most insidious of all adverse consequences of targeted therapies, however, are tumour adaptation, increased malignancy and the invasive metastatic switch seen with anti-angiogenic drugs that inhibit the VEGF-A pathway. Adverse reactions to 44 non-targeted and 33 targeted, frequently used, chemotherapeutic drugs are presented together with discussions of diagnosis, premedications, desensitizations and importance of understanding the mechanisms underlying the various drug-induced reactions. There is need for wide-ranging acceptance of what constitutes a hypersensitivity reaction and for allergists to be more involved in the diagnosis, treatment and prevention of chemotherapeutic drug-induced hypersensitivity reactions.
C1 [Baldo, Brian A.; Pham, Nghia H.] Royal N Shore Hosp, Kolling Inst Med Res, Mol Immunol Unit, Sydney, NSW, Australia.
[Baldo, Brian A.; Pham, Nghia H.] Univ Sydney, Dept Med, Sydney, NSW 2006, Australia.
C3 Royal North Shore Hospital; University of Sydney; Kolling Institute of
Medical Research; University of Sydney
RP Baldo, BA (corresponding author), 11 Bent St, Lindfield, NSW 2070, Australia.
EM babaldo@iinet.net.au
OI Baldo, Brian/0000-0001-9401-4865
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NR 256
TC 55
Z9 62
U1 0
U2 43
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-7659
EI 1573-7233
J9 CANCER METAST REV
JI Cancer Metastasis Rev.
PD DEC
PY 2013
VL 32
IS 3-4
SI SI
BP 723
EP 761
DI 10.1007/s10555-013-9447-3
PG 39
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 263ZD
UT WOS:000327845700026
PM 24043487
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Tauzin, S
Debure, L
Moreau, JF
Legembre, P
AF Tauzin, Sebastien
Debure, Laure
Moreau, Jean-Francois
Legembre, Patrick
TI CD95-mediated cell signaling in cancer: mutations and post-translational
modulations
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
DE Fas; Oncogene; Tumor suppressor; Lipid rafts; ALPS
ID AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME; FAS GENE-MUTATIONS; NF-KAPPA-B;
CONFER IMMUNE PRIVILEGE; VERSUS-HOST-DISEASE; DEATH RECEPTOR; LIPID
RAFTS; CD95 LIGAND; SOMATIC MUTATIONS; INDUCED APOPTOSIS
AB Apoptosis has emerged as a fundamental process important in tissue homeostasis, immune response, and during development. CD95 (also known as Fas), a member of the tumor necrosis factor receptor (TNF-R) superfamily, has been initially cloned as a death receptor. Its cognate ligand, CD95L, is mainly found at the plasma membrane of activated T-lymphocytes and natural killer cells where it contributes to the elimination of transformed and infected cells. According to its implication in the immune homeostasis and immune surveillance, and since several malignant cells of various histological origins exhibit loss-of-function mutations, which cause resistance towards the CD95-mediated apoptotic signal, CD95 has been classified as a tumor suppressor gene. Nevertheless, this assumption has been recently challenged, as in certain pathophysiological contexts, CD95 engagement transmits non-apoptotic signals that promote inflammation, carcinogenesis or liver/peripheral nerve regeneration. The focus of this review is to discuss these apparent contradictions of the known function(s) of CD95.
C1 [Debure, Laure; Legembre, Patrick] Univ Rennes 1, IRSET, Team Death Receptors & Tumor Escape, F-35043 Rennes, France.
[Moreau, Jean-Francois] Univ Bordeaux 2, UMR CNRS 5164, F-33076 Bordeaux, France.
C3 Universite de Rennes; Centre National de la Recherche Scientifique
(CNRS); CNRS - National Institute for Biology (INSB); Universite de
Bordeaux
RP Legembre, P (corresponding author), Univ Rennes 1, IRSET, Team Death Receptors & Tumor Escape, 2 Av Prof Leon Bernard, F-35043 Rennes, France.
EM patrick.legembre@inserm.fr
RI DEBURE, Laure/AAE-7358-2021; legembre, patrick/U-1882-2019; legembre,
patrick/L-3475-2016
OI Debure, Laure/0000-0001-6613-1108; legembre, patrick/0000-0001-6649-8049
FU ANR [JC07_183182]; INCa; Region Bretagne; Ligue Contre le Cancer
(Comites d'Ille-et-Vilaine, Comite du Morbihan, Comites de la Dordogne,
Comites des Pyrenees-Atlantiques); Ligue Contre le Cancer; Rennes
Metropole
FX This work was supported by Grants from ANR (JC07_183182), INCa (projets
libres recherche biomedicale), Region Bretagne, Rennes Metropole and
Ligue Contre le Cancer (Comites d'Ille-et-Vilaine, Comite du Morbihan,
Comites de la Dordogne, Comites des Pyrenees-Atlantiques). S.T. is
supported by Ligue Contre le Cancer (postdoctoral fellowships).
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NR 116
TC 45
Z9 48
U1 0
U2 7
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
EI 1420-9071
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD APR
PY 2012
VL 69
IS 8
BP 1261
EP 1277
DI 10.1007/s00018-011-0866-4
PG 17
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 918OD
UT WOS:000302258700002
PM 22042271
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Barnea, ER
Almogi-Hazan, O
Or, R
Mueller, M
Ria, F
Weiss, L
Paidas, MJ
AF Barnea, E. R.
Almogi-Hazan, O.
Or, R.
Mueller, M.
Ria, F.
Weiss, L.
Paidas, M. J.
TI Immune regulatory and neuroprotective properties of preimplantation
factor: From newborn to adult
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE PreImplantation Factor (PIF); Neuroprotection; Immune regulation
ID T-CELL SUBSETS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; QUINONE
REDUCTASE-ACTIVITY; CENTRAL-NERVOUS-SYSTEM; PROTEIN-KINASE-C; FACTOR
PIF; MULTIPLE-SCLEROSIS; 1ST TRIMESTER; VIRUS-INFECTION; BRAIN-INJURY
AB Embryonic-maternal interaction from the earliest stages of gestation has a key, sustained role in neurologic development, persisting into adulthood. Early adverse events may be detrimental in adulthood. Protective factors present during gestation could significantly impact post-natal therapy. The role of PreImplantation Factor (PIF) within this context is herein examined. Secreted by viable early embryos, PIF establishes effective embryonic-maternal communication and exerts essential trophic and protective roles by reducing oxidative stress and protein misfolding and by blunting the nocive let-7 microRNA related pathway. PIFs effects on systemic immunity lead to comprehensive immune modulation, not immune suppression. We examine PIF's role in protecting embryos from adverse maternal environment, which can lead to neurological disorders that may only manifest postnataly: Synthetic PIF successfully translates endogenous PIF features in both pregnant and non-pregnant clinically relevant models. Specifically PIF has neuroprotective effects in neonatal prematurity. In adult relapsing-remitting neuroinflammation, PIF reverses advanced paralysis while promoting neurogenesis. PIF reversed Mycobacterium smegmatis induced brain infection. In graft-vs.-host disease, PIF reduced skin ulceration, liver inflammation and colon ulceration while maintaining beneficial anti-cancer, graft-vs.-leukemia effect. Clinical-grade PIF has high-safety profile even at supraphysiological doses. The FDA awarded FAST-TRACK designation, and university-sponsored clinical trials for autoimmune disorder are ongoing. Altogether, PIF properties point to its determining regulatory role in immunity, inflammation and transplant acceptance. Specific plans for using PIF for the treatment of complex neurological disorders (ie. traumatic brain injury, progressive paralysis), including neuroprotection from newborn to adult, are presented. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Barnea, E. R.] SIEP, Cherry Hill, NJ USA.
[Barnea, E. R.] BioIncept LLC, Cherry Hill, NJ USA.
[Almogi-Hazan, O.; Or, R.; Weiss, L.] Hebrew Univ Jerusalem, Hadassah Univ Hosp Ein Kerem, Dept Bone Marrow Transplantat & Canc Immunotherap, Jerusalem, Israel.
[Mueller, M.] Yale Univ, Sch Med, Dept Obstet Gynecol & Reprod Sci, New Haven, CT USA.
[Mueller, M.] Univ Hosp Bern, Dept Obstet & Gynecol, CH-3010 Bern, Switzerland.
[Ria, F.] Univ Cattolica Sacro Cuore, Inst Gen Pathol, I-00168 Rome, Italy.
[Paidas, M. J.] Yale Univ, Yale Women & Childrens Ctr Blood Disorders, Sch Med, Dept Obstet Gynecol & Reprod Sci, New Haven, CT USA.
C3 Hebrew University of Jerusalem; Yale University; University of Bern;
University Hospital of Bern; Catholic University of the Sacred Heart;
IRCCS Policlinico Gemelli; Yale University
RP Barnea, ER (corresponding author), 1697 Lark Lane, Cherry Hill, NJ USA.
EM barnea@earlypregnancy.org
RI Barnea, Eytan/AAC-9910-2021; Ria, Francesco/AAD-1174-2022; Mueller,
Martin/J-9682-2019
OI Ria, Francesco/0000-0001-7455-4290; Mueller, Martin/0000-0001-5594-0532
CR Almogi-Hazan O., 2014, ROLE NITRIC OXIDE TO
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NR 177
TC 28
Z9 30
U1 0
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
EI 1879-016X
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD DEC
PY 2015
VL 156
BP 10
EP 25
DI 10.1016/j.pharmthera.2015.10.008
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CZ2RP
UT WOS:000366952600002
PM 26546485
DA 2025-01-07
ER
PT J
AU Cheung, V
Gupta, T
Payne, M
Middleton, MR
Collier, JD
Simmons, A
Klenerman, P
Brain, O
Cobbold, JF
AF Cheung, Vincent
Gupta, Tarun
Payne, Miranda
Middleton, Mark R.
Collier, Jane D.
Simmons, Alison
Klenerman, Paul
Brain, Oliver
Cobbold, Jeremy F.
TI Immunotherapy-related hepatitis: real-world experience from a tertiary
centre
SO FRONTLINE GASTROENTEROLOGY
LA English
DT Article
ID IMMUNE CHECKPOINT INHIBITORS; PREEXISTING AUTOIMMUNE; CELL-CARCINOMA;
OPEN-LABEL; CANCER; PEMBROLIZUMAB; TREMELIMUMAB; MANAGEMENT; NIVOLUMAB;
BLOCKADE
AB Objective Immune checkpoint inhibitors like anti-programmed cell death protein 1 (PD-1) drugs Nivolumab and Pembrolizumab and anti-cytotoxic T-lymphocyte associated (CTLA-4) drug Ipilimumab have become standard of care in many metastatic cancers. Immunotherapy-related hepatitis and cholangitis present a diagnostic and management challenge, being rare and incompletely characterised. We aim to report the incidence, features and treatments used for this in a real-world setting and to identify useful biomarkers, which can be used to predict effective use of steroids.
Design Retrospective review of 453 patients started on immunotherapy over 7 years.
Setting Tertiary hepatology and oncology centre.
Patients 21 patients identified with immunotherapy-related hepatotoxicity.
Results Hepatitis was most common in those receiving dual therapy (incidence 20%), with 75% of Grade 4 hepatitis cases occurring with ipilimumab-containing regimens. Corticosteroid monotherapy is first line treatment, but doses above 60 mg OD prednisolone do not demonstrate any additional benefit in time to hepatitis resolution. The alanine transaminase (ALT) reduction in steroid-responsive hepatitis is typically rapid (with a halving of ALT within 11 days). The commencement of additional immunosuppression (typically mycophenolate) appears safe and prompts a more rapid fall in ALT than corticosteroid use alone. Infliximab was safely used twice as hepatitis treatment. We also describe one patient with rare immunotherapy-induced biliary disease.
Conclusions Vigilance is required for detection of immunotherapy-associated liver disease as, other than dual immunotherapy, we can identify no predictive factors for its development. Our data suggest that corticosteroid response is not dependent on the higher dosing regimens. Early escalation of immunosuppression may be of benefit in the absence of a rapid response to corticosteroids.
C1 [Cheung, Vincent; Gupta, Tarun; Simmons, Alison; Klenerman, Paul; Brain, Oliver] Translat Gastroenterol Unit, Gastroenterol, Oxford OX3 9DU, England.
[Cheung, Vincent; Gupta, Tarun; Collier, Jane D.; Simmons, Alison; Klenerman, Paul; Brain, Oliver; Cobbold, Jeremy F.] NIHR Oxford Biomed Res Ctr, Oxford OX3 9DU, England.
[Payne, Miranda; Middleton, Mark R.] Churchill Hosp, Oncol, Oxford, England.
[Collier, Jane D.; Cobbold, Jeremy F.] Translat Gastroenterol Unit, Hepatol, Oxford, England.
C3 University of Oxford; University of Oxford
RP Cheung, V (corresponding author), Translat Gastroenterol Unit, Gastroenterol, Oxford OX3 9DU, England.; Cheung, V (corresponding author), NIHR Oxford Biomed Res Ctr, Oxford OX3 9DU, England.
EM vincent.cheung@doctors.org.uk
RI Cheung, Vincent/AAF-9833-2019; klenerman, paul/LGZ-0523-2024
OI Gupta, Tarun/0000-0002-9235-8717; Simmons, Alison/0000-0003-3454-0710;
klenerman, paul/0000-0003-4307-9161; Cheung, Vincent/0000-0003-1715-2281
FU National Institute for Health Research (NIHR) Oxford Biomedical Research
Centre (BRC); NIHR Research Capability Funding; MRC [MC_UU_12010/7,
MC_UU_00008/7] Funding Source: UKRI; SPF [MR/S036377/1] Funding Source:
UKRI
FX The research was supported by funds from the National Institute for
Health Research (NIHR) Oxford Biomedical Research Centre (BRC) and NIHR
Research Capability Funding.
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DI 10.1136/flgastro-2018-101146
PG 8
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA JG2PD
UT WOS:000491916800007
PM 31656561
OA Green Submitted, Green Published
DA 2025-01-07
ER
PT J
AU Yu, CW
Hsiao, JK
Hsu, CY
Shih, TTF
AF Yu, CW
Hsiao, JK
Hsu, CY
Shih, TTF
TI Bacterial pyomyositis: MRI and clinical correlation
SO MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE pyomyositis; MRI; infection; muscle
ID BASEMENT-MEMBRANE WIDTH; DIAGNOSIS; MYOSITIS; CT
AB Objective: To characterize the findings of magnetic resonance imaging (MRI) of bacterial pyomyositis (PM) and correlate these data with the clinical information.
Materials and Methods: Eighty-one patients were diagnosed with PM in our institute between 1997 and 2003. Of these, 40 patients (21 male, 19 female; mean age, 53 years) also underwent MRI examination. The clinical manifestation underlying medical problems and the characteristics of MRI were analyzed. Thirty of the patients received surgical intervention or image-guided drainage/aspiration of the abscess along with administration of antibiotics, while the remaining 10 patients were promptly treated solely with antibiotics.
Results: Thirty-one of 40 patients had underlying medical problems. These involved diabetes mellitus (DM, n=16), malignancies including cervical cancer, prostate cancer, non-Hodgkin's lymphoma and acute lymphocytic leukemia (n=10, one case also had DM), autoimmune disease or asthma with long-term steroid usage (n=4, one case also had DM), liver cirrhosis (n=2) and chronic renal insufficiency (n=1). Four patients had no abscess formation at presentation (invasive or early purulent stage), while the remaining 36 cases presented with at least one abscess (purulent stage). Patients older than 40 years or DM patients tended to have larger abscess(s) (P<.05). Gadolinium-enhanced images demonstrated either thick (n=12) or thin rim enhancement (n=24) of the abscess wall. For those 10 patients promptly treated solely with antibiotics, nine demonstrated thin rim enhancement of the abscess (P<.05).
Conclusion: Magnetic resonance imaging plays an important role in the early recognition of bacterial PM. By precisely demarcating the extent of the disease, MRI can allow planning prompt antibiotic treatment combined with or without interventional procedures. (C) 2004 Elsevier Inc. All rights reserved.
C1 Natl Taiwan Univ, Dept Med Imaging, Coll Med, Taipei 100, Taiwan.
Natl Taiwan Univ, Dept Med Imaging, Taiwan Hosp, Taipei 100, Taiwan.
C3 National Taiwan University; National Taiwan University
RP Natl Taiwan Univ, Dept Med Imaging, Coll Med, Taipei 100, Taiwan.
EM ttfshih@ha.me.ntu.edu.tw
RI Yu, Chih-Wei/GRX-2332-2022
OI YU, CHIH-WEI/0000-0002-8648-8419; SHIH, TIFFANY
TING-FANG/0000-0002-3292-9688; HSU, CHAO-YU/0000-0003-3731-2748
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NR 19
TC 46
Z9 49
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0730-725X
EI 1873-5894
J9 MAGN RESON IMAGING
JI Magn. Reson. Imaging
PD NOV
PY 2004
VL 22
IS 9
BP 1233
EP 1241
DI 10.1016/j.mri.2004.08.005
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 884DP
UT WOS:000226065100008
PM 15607094
DA 2025-01-07
ER
PT J
AU Palomer, X
Salvador, JM
Griñán-Ferré, C
Barroso, E
Pallàs, M
Vázquez-Carrera, M
AF Palomer, Xavier
Salvador, Jesus M.
Grinan-Ferre, Christian
Barroso, Emma
Pallas, Merce
Vazquez-Carrera, Manuel
TI GADD45A: With or without you
SO MEDICINAL RESEARCH REVIEWS
LA English
DT Review
DE cancer; cell cycle control; cell metabolism; GADD45A; inflammation
ID NF-KAPPA-B; VASCULAR SMOOTH-MUSCLE; DAMAGE-INDUCIBLE GENE; ACTIVE DNA
DEMETHYLATION; MESSENGER-RNA EXPRESSION; GROWTH-ARREST; INDUCED
APOPTOSIS; OXIDATIVE STRESS; MEDIATED REPRESSION; HEMATOPOIETIC-CELLS
AB The growth arrest and DNA damage inducible (GADD)45 family includes three small and ubiquitously distributed proteins (GADD45A, GADD45B, and GADD45G) that regulate numerous cellular processes associated with stress signaling and injury response. Here, we provide a comprehensive review of the current literature investigating GADD45A, the first discovered member of the family. We first depict how its levels are regulated by a myriad of genotoxic and non-genotoxic stressors, and through the combined action of intricate transcriptional, posttranscriptional, and even, posttranslational mechanisms. GADD45A is a recognized tumor suppressor and, for this reason, we next summarize its role in cancer, as well as the different mechanisms by which it regulates cell cycle, DNA repair, and apoptosis. Beyond these most well-known actions, GADD45A may also influence catabolic and anabolic pathways in the liver, adipose tissue and skeletal muscle, among others. Not surprisingly, GADD45A may trigger AMP-activated protein kinase activity, a master regulator of metabolism, and is known to act as a transcriptional coregulator of numerous nuclear receptors. GADD45A has also been reported to display a cytoprotective role by regulating inflammation, fibrosis and oxidative stress in several organs and tissues, and is regarded an important contributor for the development of heart failure. Overall data point to that GADD45A may play an important role in metabolic, neurodegenerative and cardiovascular diseases, and also autoimmune-related disorders. Thus, the potential mechanisms by which dysregulation of GADD45A activity may contribute to the progression of these diseases are also reviewed below.
C1 [Palomer, Xavier; Grinan-Ferre, Christian; Barroso, Emma; Pallas, Merce; Vazquez-Carrera, Manuel] Univ Barcelona, Fac Pharm & Food Sci, Dept Pharmacol Toxicol & Therapeut Chem, Barcelona, Spain.
[Palomer, Xavier; Barroso, Emma; Vazquez-Carrera, Manuel] Univ Barcelona, Inst Biomed Univ Barcelona IBUB, Barcelona, Spain.
[Palomer, Xavier; Barroso, Emma; Vazquez-Carrera, Manuel] Spanish Biomed Res Ctr Diabet & Associated Metab D, Madrid, Spain.
[Palomer, Xavier; Barroso, Emma; Vazquez-Carrera, Manuel] Hosp St Joan Deu, Pediat Res Inst, Esplugas de Llobregat, Barcelona, Spain.
[Salvador, Jesus M.] Ctr Nacl Biotecnol CSIC, Dept Immunol & Oncol, Madrid, Spain.
[Grinan-Ferre, Christian; Pallas, Merce] Univ Barcelona NeuroUB, Inst Neurociencies, Barcelona, Spain.
[Grinan-Ferre, Christian; Pallas, Merce] Inst Salud Carlos III, Spanish Biomed Res Ctr Neurodegenerat Dis CIBERNED, Madrid, Spain.
[Palomer, Xavier; Vazquez-Carrera, Manuel] Univ Barcelona, Fac Pharm & Food Sci, Dept Pharmacol Toxicol & Therapeut Chem, Ave Joan 2327-31, E-08028 Barcelona, Spain.
C3 University of Barcelona; University of Barcelona; Consejo Superior de
Investigaciones Cientificas (CSIC); CSIC - Centro Nacional de
Biotecnologia (CNB); Instituto de Salud Carlos III; University of
Barcelona
RP Palomer, X; Vázquez-Carrera, M (corresponding author), Univ Barcelona, Fac Pharm & Food Sci, Dept Pharmacol Toxicol & Therapeut Chem, Ave Joan 2327-31, E-08028 Barcelona, Spain.
EM xpalomer@ub.edu
RI Barroso, Emma/JXY-3878-2024; Pallàs, Mercè/H-3129-2016; Barroso,
Emma/G-9305-2018; Vazquez-Carrera, Manuel/H-2612-2015
OI Salvador, Jesus Maria/0000-0002-1087-9675; Barroso,
Emma/0000-0003-4551-4825; Vazquez-Carrera, Manuel/0000-0001-7138-8207
FU CIBER de Diabetes y Enfermedades Metabolicas Asociadas [CB07/08/0003,
PID2021-122116OB-100]; MCIN/AEI; ERDF A way of making Europe
FX CIBER de Diabetes y Enfermedades Metabolicas Asociadas,Grant/Award
Number: CB07/08/0003;PID2021-122116OB-100;
MCIN/AEI/10.13039/501100011033; ERDF A way of making Europe
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NR 162
TC 10
Z9 10
U1 7
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0198-6325
EI 1098-1128
J9 MED RES REV
JI Med. Res. Rev.
PD JUL
PY 2024
VL 44
IS 4
BP 1375
EP 1403
DI 10.1002/med.22015
EA JAN 2024
PG 29
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA TQ3U5
UT WOS:001147524800001
PM 38264852
OA hybrid
DA 2025-01-07
ER
PT J
AU Zhang, W
Modén, O
Mannervik, B
AF Zhang, Wei
Moden, Olof
Mannervik, Bengt
TI Differences among allelic variants of human glutathione transferase A2-2
in the activation of azathioprine
SO CHEMICO-BIOLOGICAL INTERACTIONS
LA English
DT Article
DE Azathioprine; Glutathione transferase; Bioactivation; Thiopurine
methyltransferase; Allelic variants
ID INFLAMMATORY-BOWEL-DISEASE; THIOPURINE S-METHYLTRANSFERASE;
GENETIC-POLYMORPHISM; CANCER; 6-MERCAPTOPURINE; THERAPY; DRUG;
PHARMACOGENETICS; SUSCEPTIBILITY; DERIVATIVES
AB Azathioprine has been clinically used for decades in connection with organ transplantation, autoimmune disease, and treatment of cancer. Toxic side-reactions are common and have been linked to the liberation of excessively high concentrations of 6-mercaptopurine and corresponding toxic metabolites. An allelic variant of thiopurine methyltransferase with low activity is associated with elevated concentrations of 6-mercaptopurine. However, other genetic markers remain to be identified in order to fully account for adverse reactions and efficacy failure. In the present study, we studied the five known allelic variants of human glutathione transferase A2-2 (GST A2-2) (EC2.5.1.18), abundantly expressed in liver and efficiently catalyzing the bioactivation of azathioprine to release 6-mercaptopurine. All five variants exhibited high activity with azathioprine, but allelic variant E of GST A2-2 displayed a 3-4-fold elevated catalytic efficiency compared to the other variants. High GST activity can lead to overproduction of 6-mercaptopurine, and the nature of the multiple forms of GSTs in a patient will obviously affect the metabolism of azathioprine. In addition to GST A2-2, the polymorphic GST M1-1 is also highly active with azathioprine. Considering our findings, it appears that the genotypic and phenotypic variations in the GST complement may influence the presentation of adverse reactions in patients treated with azathioprine. Clinical trials will be required to clarify the impact of the GST expression in comparison with the established biomarker thiopurine methyltransferase as predictors of adverse reactions. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Mannervik, Bengt] Uppsala Univ, Dept Biochem & Organ Chem, BMC, SE-75123 Uppsala, Sweden.
C3 Uppsala University
RP Mannervik, B (corresponding author), Uppsala Univ, Dept Biochem & Organ Chem, BMC, Box 576, SE-75123 Uppsala, Sweden.
EM Wei.Zhang@biorg.uu.se; Olof.Moden@biorg.uu.se;
Bengt.Mannervik@biorg.uu.se
OI Wei, Zhang/0009-0007-5347-417X
FU Swedish Cancer Society
FX This work was supported by the Swedish Cancer Society. We thank Dr.
Sanela Kurtovic and Dr. Leif Grehn for providing NPTI and Birgit Olin
for valuable advice on enzyme purification.
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NR 38
TC 22
Z9 25
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0009-2797
EI 1872-7786
J9 CHEM-BIOL INTERACT
JI Chem.-Biol. Interact.
PD JUL 30
PY 2010
VL 186
IS 2
BP 110
EP 117
DI 10.1016/j.cbi.2010.04.028
PG 8
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA 622EW
UT WOS:000279644900002
PM 20434437
DA 2025-01-07
ER
PT J
AU Longhi, MS
Moss, A
Jiang, ZG
Robson, SC
AF Longhi, Maria Serena
Moss, Alan
Jiang, Zhenghui Gordon
Robson, Simon C.
TI Purinergic signaling during intestinal inflammation
SO JOURNAL OF MOLECULAR MEDICINE-JMM
LA English
DT Review
DE Adaptive immunity; Adenosine; AHR; ATP; CD39; CD73; ENPP; ENTPD;
Extracellular nucleotides; Inflammation; Inflammatory bowel disease;
Innate immunity; Lymphocytes; Macrophages; P1 receptors; P2 receptors
ID ARYL-HYDROCARBON RECEPTOR; REGULATORY T-CELLS; BOWEL-DISEASE; ADENOSINE
RECEPTORS; ECTO-ATPASE; EPITHELIAL-CELLS; CROHNS-DISEASE;
NERVOUS-SYSTEM; IMMUNE-SYSTEM; GLIAL-CELLS
AB Inflammatory bowel disease (IBD) is a devastating disease that is associated with excessive inflammation in the intestinal tract in genetically susceptible individuals and potentially triggered by microbial dysbiosis. This illness markedly predisposes patients to thrombophilia and chronic debility as well as bowel, lymphatic, and liver cancers. Development of new therapies is needed to re-establish long-term immune tolerance in IBD patients without increasing the risk of opportunistic infections and cancer. Aberrant purinergic signaling pathways have been implicated in disordered thromboregulation and immune dysregulation, as noted in the pathogenesis of IBD and other gastrointestinal/hepatic autoimmune diseases. Expression of CD39 on endothelial or immune cells allows for homeostatic integration of hemostasis and immunity, which are disrupted in IBD. Our focus in this review is on novel aspects of the functions of CD39 and related NTPDases in IBD. Regulated CD39 activity allows for scavenging of extracellular nucleotides, the maintenance of P2-receptor integrity and coordination of adenosinergic signaling responses. CD39 together with CD73, serves as an integral component of the immunosuppressive machinery of dendritic cells, myeloid cells, T and B cells. Genetic inheritance and environental factors closely regulate the levels of expression and phosphohydrolytic activity of CD39, both on immune cells and released microparticles. Purinergic mechanisms associated with T regulatory and supressor T helper type 17 cells modulate disease activity in IBD, as can be modeled in experimental colitis. As a recent example, upregulation of CD39 is dependent upon ligation of the aryl hydrocarbon receptor (AHR), as with natural ligands such as bilirubin and 2-(1' H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE). Decreased expression of CD39 and/or dysfunctional AHR signaling, however, abrogates the protective effects of immunosuppressive AHR ligands. These factors could also serve as biomarkers of disease activity in IBD. Heightened thrombosis, inflammation, and immune disturbances as seen in IBD appear to be associated with aberrant purinergic signaling. Ongoing development of therapeutic strategies augmenting CD39 ectonucleotidase bioactivity via cytokines or AHR ligands offers promise for management of thrombophilia, disordered inflammation, and aberrant immune reactivity in IBD.
C1 [Longhi, Maria Serena; Moss, Alan; Jiang, Zhenghui Gordon; Robson, Simon C.] Harvard Univ, Beth Israel Deaconess Med Ctr, Div Gastroenterol, E CLS 612,3 Blackfan Circle, Boston, MA 02215 USA.
[Longhi, Maria Serena; Moss, Alan; Jiang, Zhenghui Gordon; Robson, Simon C.] Harvard Univ, Beth Israel Deaconess Med Ctr, Liver Ctr, Dept Med, E CLS 612,3 Blackfan Circle, Boston, MA 02215 USA.
[Longhi, Maria Serena; Moss, Alan; Jiang, Zhenghui Gordon; Robson, Simon C.] Harvard Univ, Harvard Med Sch, E CLS 612,3 Blackfan Circle, Boston, MA 02215 USA.
C3 Harvard University; Beth Israel Deaconess Medical Center; Harvard
University; Beth Israel Deaconess Medical Center; Harvard University;
Harvard Medical School
RP Longhi, MS; Robson, SC (corresponding author), Harvard Univ, Beth Israel Deaconess Med Ctr, Div Gastroenterol, E CLS 612,3 Blackfan Circle, Boston, MA 02215 USA.; Longhi, MS; Robson, SC (corresponding author), Harvard Univ, Beth Israel Deaconess Med Ctr, Liver Ctr, Dept Med, E CLS 612,3 Blackfan Circle, Boston, MA 02215 USA.; Longhi, MS; Robson, SC (corresponding author), Harvard Univ, Harvard Med Sch, E CLS 612,3 Blackfan Circle, Boston, MA 02215 USA.
EM mlonghi@bidmc.harvard.edu; srobson@bidmc.harvard.edu
RI Jiang, Z./U-5256-2017; Robson, Simon/AAA-8537-2021; Jiang,
Zhenghui/R-4366-2016; Moss, Alan/B-9192-2019
OI Jiang, Zhenghui/0000-0003-0495-9940; Moss, Alan/0000-0003-0179-5477
FU National Institute of Health [R01 HL094400, R01 DK108894, P01HL107152,
P01 HL087203]; Clinical Research Award from the American
Gastroenterology Association; Alan Holfman Clinical and Translational
Research Award from the American Association for the Study of Liver
Disease
FX The work summarized in this review article was supported by the National
Institute of Health grants to SCR and MSL; R01 HL094400; R01 DK108894;
P01HL107152, and P01 HL087203 as well as the generosity of the family of
Jane O. Siegel; as well as a Clinical Research Award from the American
Gastroenterology Association and the Alan Holfman Clinical and
Translational Research Award from the American Association for the Study
of Liver Disease to ZGJ. We thank Eliza Robson for the graphic design
for figures.
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NR 72
TC 73
Z9 74
U1 0
U2 28
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0946-2716
EI 1432-1440
J9 J MOL MED
JI J. Mol. Med.
PD SEP
PY 2017
VL 95
IS 9
BP 915
EP 925
DI 10.1007/s00109-017-1545-1
PG 11
WC Genetics & Heredity; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Research & Experimental Medicine
GA FC8QU
UT WOS:000407106700003
PM 28547076
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Onwuzo, S
Boustany, A
Abou Zeid, HK
Hitawala, A
Almomani, A
Onwuzo, C
Lawrence, F
Monteiro, JM
Ndubueze, C
Asaad, I
AF Onwuzo, Somtochukwu
Boustany, Antoine
Abou Zeid, Hadi Khaled
Hitawala, Asif
Almomani, Ashraf
Onwuzo, Chidera
Lawrence, Favour
Monteiro, Jessy Mascarenhas
Ndubueze, Chidera
Asaad, Imad
TI Prevalence and Risk Factors Associated With Inflammatory Bowel Disease
in Patients Using Proton-Pump Inhibitors: A Population-Based Study
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE database; population-based study; inflammatory bowel disease; crohn?s
disease; ulcerative colitis; proton pump inhibitor
AB Background and aim Proton pump inhibitor (PPI) is a heavily prescribed medication in the United States that is used to treat several gastrointestinal disorders. Although it has been considered to be safe compared to other medications, multiple gastrointestinal side effects have been reported. These effects of PPIs might stem from the progressive alteration of the intestinal microbiome. Patients with inflammatory bowel disease (IBD) using PPI are also seen to be less likely to achieve remission. However, in the current literature, there is very little evidence of the risk of developing IBD in patients who have been using PPIs. Therefore, our aim was to perform a cross-sectional population-based study with in-depth analysis to assess the prevalence and risk factors of IBD amongst PPI users in the United States. Methodology A validated multicenter and research platform database of more than 360 hospitals from 26 different healthcare systems across the United States was utilized to construct this study. A cohort of patients with a diagnosis of ulcerative colitis (UC) and Crohn's disease (CD) between 1999-2022 was identified using the Systematized Nomenclature of Medicine-Clinical Terms (SNOMED-CT). Patients aged 18 to 65 years were included. We excluded any individual who had a diagnosis of chronic liver disease, autoimmune disease (excluding IBD), or cancer. The risk of IBD was calculated using a multivariate regression analysis to account for potential confounders including non-steroidal anti-inflammatory drugs (NSAIDs) use, smoking, patients who have had a diagnosis of alcoholism, gastroesophageal reflux disease (GERD), irritable bowel syndrome (IBS), and metabolic syndrome. A two-sided P-value <0.05 was considered statistically significant, and all statistical analyses were performed using R version 4.0.2 (R Foundation for Statistical Computing, Vienna, Austria, 2008). Results A total of 79,984,328 individuals were screened in the database and 45,586,150 patients were selected in the final analysis after accounting for inclusion and exclusion criteria. Using multivariate regression analysis, the risk of developing UC and CD was calculated. The odds of having UC amongst patients on PPI was 2.02 (95%CI 1.98-2.06), P-value <0.001. Similarly, the odds of having CD were high amongst PPI users (OR 2.79, 95%CI 2.75-2.84), P-value <0.001 Conclusion Our study demonstrates that patients on PPIs are frequently found to have UC and CD even when adjusting for common risk factors. Hence, we urge clinicians to be aware of this association in order to limit unnecessary prescriptions of PPIs, especially for patients who are at risk for autoimmune diseases.
C1 [Onwuzo, Somtochukwu; Boustany, Antoine; Hitawala, Asif; Almomani, Ashraf; Asaad, Imad] Cleveland Clin Fdn, Internal Med, Cleveland, OH 44195 USA.
[Abou Zeid, Hadi Khaled] Univ Balamand, Internal Med, Koura, Lebanon.
[Onwuzo, Chidera; Lawrence, Favour] Gen Hosp Lagos Isl, Internal Med, Lagos, Nigeria.
[Monteiro, Jessy Mascarenhas] Ross Univ, Sch Med, Internal Med, Bridgetown, Barbados.
[Ndubueze, Chidera] Univ Port Harcourt, Internal Med, Teaching Hosp, Port Harcourt, Nigeria.
C3 Cleveland Clinic Foundation; University Balamand; University of Port
Harcourt
RP Onwuzo, S (corresponding author), Cleveland Clin Fdn, Internal Med, Cleveland, OH 44195 USA.
EM onwuzos@ccf.org
RI Boustany, Antoine/ACC-9168-2022
OI Abou Zeid, Hadi Khaled/0000-0002-5111-3043
CR BOYKO EJ, 1989, AM J GASTROENTEROL, V84, P530
BOYKO EJ, 1987, NEW ENGL J MED, V316, P707, DOI 10.1056/NEJM198703193161202
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NR 17
TC 3
Z9 4
U1 0
U2 4
PU CUREUS INC
PI PALO ALTO
PA PO BOX 61002, PALO ALTO, CA 94306 USA
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD JAN 23
PY 2023
VL 15
IS 1
DI 10.7759/cureus.34088
PG 6
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 9A5HK
UT WOS:000934088700044
PM 36843811
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Clarke, AE
Pooley, N
Marjenberg, Z
Langham, J
Nicholson, L
Langham, S
Embleton, N
Wang, X
Desta, B
Barut, V
Hammond, ER
AF Clarke, Ann E.
Pooley, Nick
Marjenberg, Zoe
Langham, Julia
Nicholson, Lindsay
Langham, Sue
Embleton, Nina
Wang, Xia
Desta, Barnabas
Barut, Volkan
Hammond, Edward R.
TI Risk of malignancy in patients with systemic lupus erythematosus:
Systematic review and meta-analysis
SO SEMINARS IN ARTHRITIS AND RHEUMATISM
LA English
DT Review
DE Systemic Lupus Erythematosus; Systematic Review With Meta-Analysis;
Cancer; Malignancy
ID AUTOIMMUNE-DISEASES; CANCER-RISK; HEMATOLOGIC MALIGNANCIES;
RHEUMATIC-DISEASES; HODGKINS-LYMPHOMA; OXIDATIVE STRESS; REVISED
CRITERIA; FEMALE-PATIENTS; BREAST-CANCER; FOLLOW-UP
AB Background: Malignancy is a potential comorbidity in patients with systemic lupus erythematosus (SLE). However, risk by malignancy type remains to be fully elucidated. We evaluated the risk of malignancy type in SLE patients in a systematic review and meta-analysis.
Methods: MEDLINE and EMBASE were searched from inception to July 2018 to identify observational studies that evaluated malignancy risk in adult SLE patients compared with the general population. Random-effects models were used to calculate pooled risk ratios (RRs) and 95% confidence intervals (CIs). Heterogeneity was quantified using the I-2 test.
Findings: Forty-one studies reporting on 40 malignancies (one overall, 39 site-specific) were included in the meta-analysis. The pooled RR for all malignancies from 3694 events across 80 833 patients was 1.18 (95% CI: 1.00-1.38). The risk of 24 site-specific malignancies (62%) was increased in SLE patients. For malignancies with >= 6 studies, non-Hodgkin lymphoma and Hodgkin lymphoma risk was increased >3-fold; myeloma and liver >2-fold; cervical, lung, bladder, and thyroid >= 1.5-fold; stomach and brain >1.3-fold. The risk of four malignancies (breast, uterine, melanoma, prostate) was decreased, whereas risk of 11 other malignancies did not differ between SLE patients and the general population. Heterogeneity ranged between 0% and 96%, and 63% were non-significant.
Interpretation: The risk of overall and some site-specific malignancies is increased in SLE compared with the general population. However, the risk for some site-specific malignancies is decreased or did not differ. Further examination of risk profiles and SLE patient phenotypes may support guidelines aimed at reducing malignancy risk. (C) 2021 The Authors. Published by Elsevier Inc.
C1 [Clarke, Ann E.] Univ Calgary, Dept Med, Div Rheumatol, Calgary, AB, Canada.
[Pooley, Nick; Marjenberg, Zoe; Nicholson, Lindsay] Maverex Ltd, Systemat Review Grp, Manchester, Lancs, England.
[Langham, Julia] Maverex Ltd, Epidemiol Grp, Manchester, Lancs, England.
[Langham, Sue] Maverex Ltd, Hlth Econ Grp, Manchester, Lancs, England.
[Embleton, Nina] Maverex Ltd, Stat Grp, Manchester, Lancs, England.
[Wang, Xia] AstraZeneca, BioPharmaceut Med, Data Sci & AI, Gaithersburg, MD USA.
[Desta, Barnabas] AstraZeneca, BioPharmaceut Med, Global Pricing & Market Access, Gaithersburg, MD USA.
[Barut, Volkan] AstraZeneca, BioPharmaceut Med, Global Med Affairs, Gaithersburg, MD USA.
[Hammond, Edward R.] AstraZeneca, BioPharmaceut Med, Gaithersburg, MD USA.
C3 University of Calgary; AstraZeneca; AstraZeneca; AstraZeneca;
AstraZeneca
RP Clarke, AE (corresponding author), Univ Calgary, Cumm Sch Med, Div Rheumatol, Calgary, AB, Canada.
EM aeclarke@ucalgary.ca
RI wang, xia/HJI-5034-2023
OI langham, julia/0000-0003-1046-7598
FU AstraZeneca
FX This work was supported by funding from AstraZeneca. Writing and editing
assistance was provided by Rebecca S. Jones, PhD, of JK Associates Inc.,
part of Fishawack Health. This study was funded by AstraZeneca.
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NR 84
TC 37
Z9 39
U1 1
U2 7
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0049-0172
EI 1532-866X
J9 SEMIN ARTHRITIS RHEU
JI Semin. Arthritis Rheum.
PD DEC
PY 2021
VL 51
IS 6
BP 1230
EP 1241
DI 10.1016/j.semarthrit.2021.09.009
EA OCT 2021
PG 12
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA WS3GE
UT WOS:000715072700005
PM 34710720
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Javid, J
Mir, R
Elfaki, I
Almotairi, R
Barnawi, J
Algehainy, NA
Jalal, MM
Altayar, MA
Alanazi, MA
Albalawi, SO
Bhat, T
Hussain, E
Abuduhier, FM
AF Javid, Jamsheed
Mir, Rashid
Elfaki, Imadeldin
Almotairi, Reema
Barnawi, Jameel
Algehainy, Naseh A.
Jalal, Mohammed M.
Altayar, Malik A.
Alanazi, Mohammad A.
Albalawi, Salem Owaid
Bhat, Tanzeela
Hussain, Eram
Abuduhier, Faisel M.
TI Dysregulated Vitamin D, CYP2R1, TCF7L2, and CCR5 △32 Gene Variations are
Associated with Coronary Artery Disease
SO DISCOVERY MEDICINE
LA English
DT Article
DE coronary artery disease; vitamin D; C-C chemokine receptor type 5;
transcription factor 7-like 2; amplification-refractory mutation
system-PCR
ID TYPE-2 DIABETES-MELLITUS; CARDIOVASCULAR-DISEASE; 25-HYDROXYVITAMIN D;
RISK; ATHEROSCLEROSIS; POLYMORPHISMS; PREVENTION
AB Background: Insufficient vitamin D (vit D) levels are associated with various chronic conditions such as cancers, autoimmune diseases, diabetes, and cardiovascular diseases, notably coronary artery disease (CAD). The enzyme 25-hydroxylase, cytochrome P450 2R1 (CYP2R1), catalyzes the hydroxylation of vitamin D in the liver, producing the 25-hydroxyvitamin D, which is then activated in the kidney by cytochrome P450 27B1 (CYP27B1) to form 1,25-dihydroxyvitamin D. Mutations in the CYP2R1 gene can impair vitamin D production. The C-C chemokine receptor type 5 (CCR5) supports endothelial repair and angiogenesis, with its mutation (CCR5 59029 G to A) being linked to insulin resistance and type 2 diabetes (T2D). Additionally, the transcription factor 7-like 2 (TCF7L2), part of the Wnt signaling pathway, regulates glucose homeostasis and the development of tissues, brain, liver and muscles and has been linked to obesity, insulin insensitivity, and elevated blood sugar levels. Materials and Methods: We evaluated the association of reduced serum vitamin D levels with CAD using enzyme-linked immunosorbent assay (ELISA). Genotyping of the CYP2R1 rs1562902 C > T, TCF7L2 rs12255372 G > T, and CCR5 triangle 32 bp deletion mutation were performed using amplification-refractory mutation system polymerase chain reaction (PCR) and allelespecific PCR to evaluate their association with CAD risk. Results: The CYP2R1 rs1562902 C > T single nucleotide polymorphism (SNP) genotypes CT and TT were significantly associated with CAD, with odds ratios (ORs) of 4.1 and 7.6 and p-values of 0.0001 and 0.0008, respectively. The +/triangle genotype of the CCR5 triangle 32 bp (ins/del) mutation was also associated with CAD (OR = 2.51, p = 0.006). Additionally, the T allele of the TCF7L2 rs12255372 G > T SNP was linked to an increased risk of CAD (OR = 1.89, p = 0.006). Conclusion: The CYP2R1 rs1562902 C > T, CCR5 triangle 32 (rs333), and TCF7L2 rs12255372 G > T polymorphisms are potential genetic loci associated with increased CAD risk. Furthermore, CYP2R1 variants are associated with vitamin D deficiency, predisposing carriers of CYP2R1 to associated pathologies. These findings warrant further validation through larger case-control studies and functional protein analysis.
C1 [Javid, Jamsheed; Mir, Rashid; Almotairi, Reema; Barnawi, Jameel; Algehainy, Naseh A.; Jalal, Mohammed M.; Altayar, Malik A.; Alanazi, Mohammad A.; Bhat, Tanzeela; Hussain, Eram; Abuduhier, Faisel M.] Univ Tabuk, Fac Appl Med Sci, Prince Fahad Bin Sultan Chair Biomed Res, Dept Med Lab Technol, Tabuk 71491, Saudi Arabia.
[Elfaki, Imadeldin] Univ Tabuk, Fac Sci, Dept Biochem, Tabuk 71491, Saudi Arabia.
[Albalawi, Salem Owaid] King Fahd Specialist Hosp, Dept Cardiol, Tabuk 71491, Saudi Arabia.
C3 University of Tabuk; University of Tabuk
RP Mir, R (corresponding author), Univ Tabuk, Fac Appl Med Sci, Prince Fahad Bin Sultan Chair Biomed Res, Dept Med Lab Technol, Tabuk 71491, Saudi Arabia.; Elfaki, I (corresponding author), Univ Tabuk, Fac Sci, Dept Biochem, Tabuk 71491, Saudi Arabia.
EM rashidmirut@gmail.com; elfakiimadeldin@gmail.com
RI mohammed, reema/HKO-6472-2023; Barnawi, Jameel/HSH-8111-2023; Jalal,
Mohammed/HSE-4694-2023; Javid, Dr. Jamsheed/ABA-5434-2021; MIR,
RASHID/AAH-1895-2019; Abuduhier, Faisel/J-7958-2013; Elfaki,
Imadeldin/AER-0062-2022
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NR 72
TC 0
Z9 0
U1 0
U2 0
PU DISCOVERY MEDICINE
PI TIMONIUM
PA 10 GERARD AVE, STE 201, TIMONIUM, MD 21093 USA
SN 1539-6509
EI 1944-7930
J9 DISCOV MED
JI Discov. Med.
PD NOV
PY 2024
VL 36
IS 190
BP 2287
EP 2299
DI 10.24976/Discov.Med.202436190.210
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA M9X7C
UT WOS:001360989800015
PM 39600283
DA 2025-01-07
ER
PT J
AU Nagarkatti, P
Pandey, R
Rieder, SA
Hegde, VL
Nagarkatti, M
AF Nagarkatti, Prakash
Pandey, Rupal
Rieder, Sadiye Amcaoglu
Hegde, Venkatesh L.
Nagarkatti, Mitzi
TI Cannabinoids as novel anti-inflammatory drugs
SO FUTURE MEDICINAL CHEMISTRY
LA English
DT Review
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; HEPATIC ISCHEMIA/REPERFUSION
INJURY; LEGIONELLA-PNEUMOPHILA INFECTION; COLLAGEN-INDUCED ARTHRITIS;
NECROSIS-FACTOR-ALPHA; NITRIC-OXIDE RELEASE; MULTIPLE-SCLEROSIS;
CANCER-CELLS; ENDOCANNABINOID SYSTEM; RECEPTOR AGONIST
AB Cannabinoids are a group of compounds that mediate their effects through cannabinoid receptors. The discovery of Delta(9)-tetrahydrocannabinol (THC) as the major psychoactive principle in marijuana, as well as the identification of cannabinoid receptors and their endogenous ligands, has led to a significant growth in research aimed at understanding the physiological functions of cannabinoids. Cannabinoid receptors include CBI, which is predominantly expressed in the brain, and CB2, which is primarily found on the cells of the immune system. The fact that both CBI and CB2 receptors have been found on immune cells suggests that cannabinoids play an important role in the regulation of the immune system. Recent studies demonstrated that administration of THC into mice triggered marked apoptosis in T cells and dendritic cells, resulting in immunosuppression. In addition, several studies showed that cannabinoids downregulate cytokine and chemokine production and, in some models, upregulate T-regulatory cells (Tregs) as a mechanism to suppress inflammatory responses. The endocannabinoid system is also involved in immunoregulation. For example, administration of endocannabinoids or use of inhibitors of enzymes that break down the endocannabinoids, led to immunosuppression and recovery from immune-mediated injury to organs such as the liver. Manipulation of endocannabinoids and/or use of exogenous cannabinoids in vivo can constitute a potent treatment modality against inflammatory disorders. This review will focus on the potential use of cannabinoids as a new class of anti-inflammatory agents against a number of inflammatory and autoimmune diseases that are primarily triggered by activated T cells or other cellular immune components.
C1 [Nagarkatti, Prakash; Pandey, Rupal; Rieder, Sadiye Amcaoglu; Hegde, Venkatesh L.; Nagarkatti, Mitzi] Univ S Carolina, Sch Med, Dept Pathol Microbiol & Immunol, Columbia, SC 29208 USA.
C3 University of South Carolina System; University of South Carolina
Columbia
RP Nagarkatti, P (corresponding author), Univ S Carolina, Sch Med, Dept Pathol Microbiol & Immunol, Columbia, SC 29208 USA.
EM pnagark@uscmed.sc.edu
RI Hegde, Venkatesh/E-8519-2014
OI Nagarkatti, Prakash/0000-0003-2663-0759
FU NIH [R01AI053703, R01ES09008, R01AI058300, R01DA016545, R01HL058641,
P01AT003961]
FX This work was supported in part by NIH grants R01AI053703, R01ES09008,
R01AI058300, R01DA016545, R01HL058641 and P01AT003961. The authors have
no other relevant affiliations or financial involvement with any
organization or entity with a financial interest in or financial
conflict with the subject matter or materials discussed in the
manuscript. This includes employment, consultancies, honoraria, stock
ownership or options, expert testimony, grants or patents received or
pending, or royalties.
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NR 130
TC 349
Z9 396
U1 0
U2 40
PU FUTURE SCI LTD
PI LONDON
PA UNITED HOUSE, 2 ALBERT PL, LONDON, N3 1QB, ENGLAND
SN 1756-8919
EI 1756-8927
J9 FUTURE MED CHEM
JI Future Med. Chem.
PD OCT
PY 2009
VL 1
IS 7
BP 1333
EP 1349
DI 10.4155/FMC.09.93
PG 17
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 575UI
UT WOS:000276094000018
PM 20191092
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Eduin, B
Roubille, C
Badiou, S
Cristol, JP
Fesler, P
AF Eduin, Benjamin
Roubille, Camille
Badiou, Stephanie
Cristol, Jean Paul
Fesler, Pierre
TI Association between Elevated Plasma Vitamin B12 and Short-Term Mortality
in Elderly Patients Hospitalized in an Internal Medicine Unit
SO INTERNATIONAL JOURNAL OF CLINICAL PRACTICE
LA English
DT Article
ID PROTON PUMP INHIBITORS; HYPERVITAMINEMIA B12; DEPARTMENTS; PHYSIOLOGY;
COBALAMIN; CUBILIN
AB Background: The prognostic value of vitamin B12 blood levels remains controversial. An association between elevated vitamin B12 and mortality has been reported, particularly among elderly patients with cancers and liver or blood diseases. The present study explored the relationship between mortality and elevated vitamin B12 levels in a population of unscheduled inpatients in an internal medicine unit. Methods: This retrospective observational analysis was conducted between August 2014 and December 2018. We compared 165 patients with elevated plasma vitamin B12 levels (>600 pmol/l) with a random sample of 165 patients with normal B12 levels who were hospitalized during the same period. Demographic, clinical, and biological characteristics were assessed during hospitalization. The primary endpoint was all-cause death at 1 year.Results: Patients with elevated B12 were younger, with a lower body mass index and lower plasma albumin than those with normal B12 (75 +/- 16 years vs 79 +/- 13 years, p = 0.047; 23 +/- 5 vs 26 +/- 7 kg/m(2), p < 0.001; and 33 +/- 5 vs 35 +/- 5 g/l, p < 0.001, respectively). The prevalence of auto-immune disease and referral from an intensive care unit was higher among patients with elevated B12 (11% vs 5%, p = 0.043 and 36% vs 10%, p < 0.001, respectively). After 1 year of follow-up, 64 (39%) patients with elevated B12 had died compared to 43 (26%) patients with normal B12 (p = 0.018). Multivariate analysis using the Cox proportional hazards regression model adjusted for age, gender, body mass index, intensive care unit hospitalization, albumin level, and the presence of solid cancer or autoimmune disease revealed elevated B12 to be associated with a significant risk of death in the first year of follow-up (hazard ratio: 1.71 [1.08-2.7], p = 0.022). Conclusion: Elevated B12 is an early warning indicator of increased short-term mortality, such as independently of age, cancer, or comorbidities, in patients hospitalized in an internal medicine department.
C1 [Eduin, Benjamin; Roubille, Camille; Fesler, Pierre] Univ Hosp Montpellier, Dept Internal Med, Montpellier, France.
[Roubille, Camille; Badiou, Stephanie; Cristol, Jean Paul; Fesler, Pierre] Univ Montpellier, Univ Hosp Montpellier, PhyMedExp, INSERM,CNRS, Montpellier, France.
[Badiou, Stephanie; Cristol, Jean Paul] Univ Hosp Montpellier, Dept Biochem & Hormonol, Montpellier, France.
C3 Universite de Montpellier; CHU de Montpellier; Centre National de la
Recherche Scientifique (CNRS); Universite de Montpellier; CHU de
Montpellier; Institut National de la Sante et de la Recherche Medicale
(Inserm); Universite de Montpellier; CHU de Montpellier
RP Fesler, P (corresponding author), Univ Hosp Montpellier, Dept Internal Med, Montpellier, France.; Fesler, P (corresponding author), Univ Montpellier, Univ Hosp Montpellier, PhyMedExp, INSERM,CNRS, Montpellier, France.
EM benjamin.eduin@gmail.com; c-roubille@chu-montpellier.fr;
s-badiou@chu-montpellier.fr; jp-cristol@chu-montpellier.fr;
p-fesler@chu-montpellier.fr
RI Fesler, Pierre/O-7620-2018
OI Fesler, Pierre/0000-0002-7831-6545; , Jean-Paul
Cristol/0000-0001-8563-7278
FU COUPERIN CY23
FX Open Access funding was enabled and organized by COUPERIN CY23.
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NR 38
TC 2
Z9 2
U1 1
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1368-5031
EI 1742-1241
J9 INT J CLIN PRACT
JI Int. J. Clin. Pract.
PD DEC 18
PY 2023
VL 2023
AR 6652671
DI 10.1155/2023/6652671
PG 7
WC Medicine, General & Internal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Pharmacology & Pharmacy
GA DK4D2
UT WOS:001131911000002
PM 38146346
OA gold
DA 2025-01-07
ER
PT J
AU Rivkees, SA
AF Rivkees, S. A.
TI Controversies in the management of Graves' disease in children
SO JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
LA English
DT Review
DE Thyroid; Hyperthyroidism; Methimazole; Propylthiouracil; Radioactive
iodine; Thyroidectomy; Hepatotoxicity
ID ANTITHYROID DRUG-TREATMENT; RADIOACTIVE IODINE I-131; RADIOIODINE
THERAPY; AUTOIMMUNE HYPERTHYROIDISM; PREPUBERTAL CHILDREN; ECONOMIC
OUTCOMES; THYROID-DISEASE; RAI THERAPY; CANCER-RISK; LONG
AB Graves' disease (GD) is the most prevalent cause of thyrotoxicosis in children. Because spontaneous and lasting resolution of this condition occurs in only a minority of patients, most pediatric patients with GD will need radioactive iodine treatment (I-131) or thyroidectomy. Whereas the medication propylthiouracil (PTU) had been used in the past, only methimazole (MMI) should be now used in children, as PTU is associated with an unacceptable risk of liver failure. However, MMI may be associated minor and major side effects, which may be minimized using lower doses. An area of controversy involves the optimal duration of antithyroid drug (ATD) therapy. For some children, the prolonged use of antithyroid drugs is a valid approach, but for most, this will not increase the chance of remission. When I-131 is administered, dosages should be greater than 150 uCi/gm of thyroid tissue, with higher dosages needed for larger glands. Considering that there will be low-level whole body radiation exposure associated with I-131, this treatment is viewed as controversial by some and should be avoided in young children. When surgery is performed, near-total or total thyroidectomy is the recommended procedure. Complications for thyroidectomy in children are considerably higher than in adults. Thus, an experienced thyroid surgeon is needed when children have surgery. Overall, when different treatment options for GD are considered, the benefits, risks and viewpoints of the family need to be considered and discussed in full.
C1 [Rivkees, S. A.] Univ Florida, Dept Pediat, Coll Med, Pediat Chairmans Off, 1600 SW Archer Rd,Room R1-118, Gainesville, FL 32610 USA.
C3 State University System of Florida; University of Florida
RP Rivkees, SA (corresponding author), Univ Florida, Dept Pediat, Coll Med, Pediat Chairmans Off, 1600 SW Archer Rd,Room R1-118, Gainesville, FL 32610 USA.
EM srivkees@ufl.edu
FU NIH [7R01FD003707]
FX This study was supported in part by NIH grant 7R01FD003707.
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NR 114
TC 48
Z9 57
U1 0
U2 13
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0391-4097
EI 1720-8386
J9 J ENDOCRINOL INVEST
JI J. Endocrinol. Invest.
PD NOV
PY 2016
VL 39
IS 11
BP 1247
EP 1257
DI 10.1007/s40618-016-0477-x
PG 11
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA EA4RK
UT WOS:000386601500004
PM 27153850
DA 2025-01-07
ER
PT J
AU Rodríguez-Torres, M
Ríos-Bedoya, CF
Ortiz-Lasanta, G
Marxuach-Cuétara, AM
Jiménez-Rivera, J
AF Rodriguez-Torres, Maribel
Rios-Bedoya, Carlos F.
Ortiz-Lasanta, Grisell
Marxuach-Cuetara, Acisclo M.
Jimenez-Rivera, Josselyn
TI Thyroid dysfunction (TD) among chronic hepatitis C patients with mild
and severe hepatic fibrosis
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE autoimmune thyroid dysfunction; HCV; fibrosis
ID INTERFERON-ALPHA THERAPY; CHRONIC VIRAL-HEPATITIS; PROSPECTIVE COHORT;
HIGH PREVALENCE; HCV; DISORDERS; INFECTION; AUTOANTIBODIES; DISEASES;
CANCER
AB Background: Thyroid dysfunction (TD) is associated to chronic hepatitis C (HCV) and interferon (IFN) therapy. The prevalence of TD at baseline and during IFN therapy among stages of hepatic fibrosis is unknown. Goals: To examine the frequency of TD at baseline and during Peg-IFN therapy among patients with severe and mild fibrosis. Study: 100 patients were treated with Peg-IFN and divided in 2 groups (50 each), according to liver histology; Metavir 0-2 (mild fibrosis) and Metavir 3-4 (severe fibrosis). Baseline TD was defined as history of TD, or abnormal thyroid stimulating hormone (TSH) or antiperoxidase thyroid auto-antibodies (TPO-Ab). Frequency of TD during therapy was defined as TD that required treatment. Results: 20% in the severe fibrosis group and 10% in the mild fibrosis group, had TD at baseline. Most of the cases, 31.4% were female as compared to 6.25% males. During therapy, 24% of patients in the severe fibrosis group, compared to 12% in the mild fibrosis, had TD. Most patients had biochemical hypothyroidism, and 66% were female, compared to 33.33% male. TPO-Ab predicted TD during therapy in 50% of cases while those negative only had 16.6% TD during IFN therapy. Conclusions: Patients with severe fibrosis have more TD events at baseline and during treatment with Peg IFN alfa-2a. Patients with more hepatic fibrosis require careful attention to diagnose and manage TD. More research in the immune mechanisms of hepatic fibrosis progression and autoimmune complications is needed.
C1 [Rodriguez-Torres, Maribel; Ortiz-Lasanta, Grisell; Marxuach-Cuetara, Acisclo M.; Jimenez-Rivera, Josselyn] Fdn Invest Diego, San Juan, PR USA.
[Rodriguez-Torres, Maribel] Ponce Sch Med, Ponce, PR USA.
[Rios-Bedoya, Carlos F.] Michigan State Univ, Dept Epidemiol, E Lansing, MI 48824 USA.
C3 Michigan State University
RP Rodríguez-Torres, M (corresponding author), Fdn Invest Diego, Ave Diego 359,Suite 302, Santurce, PR 00909 USA.
EM rodztorres@coqui.net
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U1 0
U2 0
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD JAN-MAR
PY 2008
VL 7
IS 1
BP 72
EP 77
DI 10.1016/S1665-2681(19)31891-5
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 278BA
UT WOS:000254257200010
PM 18376370
OA hybrid
DA 2025-01-07
ER
PT J
AU Ahmed, W
Kyle, D
Khanna, A
Devlin, J
Reffitt, D
Zeino, Z
Webster, G
Phillpotts, S
Gordon, R
Corbett, G
Gelson, W
Nayar, M
Khan, H
Cramp, M
Potts, J
Fateen, W
Miller, H
Paranandi, B
Huggett, M
Everett, SM
Hegade, VS
O'Kane, R
Scott, R
McDougall, N
Harrison, P
Joshi, D
AF Ahmed, Wafaa
Kyle, Dave
Khanna, Amardeep
Devlin, John
Reffitt, David
Zeino, Zeino
Webster, George
Phillpotts, Simon
Gordon, Robert
Corbett, Gareth
Gelson, William
Nayar, Manu
Khan, Haider
Cramp, Matthew
Potts, Jonathan
Fateen, Waleed
Miller, Hamish
Paranandi, Bharat
Huggett, Matthew
Everett, Simon M.
Hegade, Vinod S.
O'Kane, Rebecca
Scott, Ryan
McDougall, Neil
Harrison, Phillip
Joshi, Deepak
TI Intraductal fully covered self-expanding metal stents in the management
of post-liver transplant anastomotic strictures: a UK wide experience
SO THERAPEUTIC ADVANCES IN GASTROENTEROLOGY
LA English
DT Article
DE biliary stricture; ERCP; intra-ductal fully covered metal stent; liver
transplant
ID BENIGN BILIARY STRICTURES; MULTIPLE PLASTIC STENTS;
ANTIBIOTIC-PROPHYLAXIS; ENDOSCOPIC TREATMENT; COMPLICATIONS; RESOLUTION;
EFFICACY; ERCP
AB Background: Fully covered intraductal self-expanding metal stents (IDSEMS) have been well described in the management of post-liver transplant (LT) anastomotic strictures (ASs). Their antimigration waists and intraductal nature make them suited for deployment across the biliary anastomosis.
Objectives: We conducted a multicentre study to analyse their use and efficacy in the management of AS.
Design: This was a retrospective, multicentre observational study across nine tertiary centres in the United Kingdom.
Methods: Consecutive patients who underwent endoscopic retrograde cholangiopancreatography with IDSEMS insertion were analysed retrospectively. Recorded variables included patient demographics, procedural characteristics, response to therapy and follow-up data.
Results: In all, 162 patients (100 males, 62%) underwent 176 episodes of IDSEMS insertion for AS. Aetiology of liver disease in this cohort included hepatocellular carcinoma (n=35, 22%), followed by alcohol-related liver disease (n=29, 18%), non-alcoholic steatohepatitis (n=20, 12%), primary biliary cholangitis (n=15, 9%), acute liver failure (n=13, 8%), viral hepatitis (n=13, 8%) and autoimmune hepatitis (n=12, 7%). Early AS occurred in 25 (15%) cases, delayed in 32 (20%) cases and late in 95 (59%) cases. Age at transplant was 54 years (range, 12-74), and stent duration was 15weeks (range, 3 days-78weeks). In total, 131 (81%) had complete resolution of stricture at endoscopic re-evaluation. Stricture recurrence was observed in 13 (10%) cases, with a median of 19weeks (range, 4-88weeks) after stent removal. At removal, there were 21 (12%) adverse events, 5 (3%) episodes of cholangitis and 2 (1%) of pancreatitis. In 11 (6%) cases, the removal wires unravelled, and 3 (2%) stents migrated. All were removed endoscopically.
Conclusion: IDSEMS appears to be safe and highly efficacious in the management of post-LT AS, with low rates of AS recurrence.
C1 [Ahmed, Wafaa; Kyle, Dave; Khanna, Amardeep; Devlin, John; Reffitt, David; Harrison, Phillip; Joshi, Deepak] Kings Coll Hosp NHS Fdn Trust, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
[Zeino, Zeino] Southmead Hosp North Bristol NHS Trust, Bristol, Avon, England.
[Webster, George; Phillpotts, Simon] Univ Coll Hosp, Hepatopancreatobiliary Unit, London, England.
[Gordon, Robert; Corbett, Gareth; Gelson, William] Addenbrookes Hosp, Cambridge Liver Unit, Cambridge, England.
[Nayar, Manu] Freeman Rd Hosp, Newcastle Upon Tyne, Tyne & Wear, England.
[Khan, Haider; Cramp, Matthew] Southwest Liver Unit, Plymouth, Devon, England.
[Khan, Haider; Cramp, Matthew] Plymouth Univ, Peninsula Sch Med, Plymouth, Devon, England.
[Khan, Haider; Cramp, Matthew] Plymouth Univ, Peninsula Sch Dent, Plymouth, Devon, England.
[Potts, Jonathan; Fateen, Waleed; Miller, Hamish] Royal Free Hosp, Royal Free Sheila Sherlock Liver Ctr, London, England.
[Potts, Jonathan; Fateen, Waleed; Miller, Hamish] UCL Inst Liver & Digest Hlth, London, England.
[Paranandi, Bharat; Huggett, Matthew; Everett, Simon M.; Hegade, Vinod S.] Leeds Teaching Hosp NHS Trust, Leeds, W Yorkshire, England.
[O'Kane, Rebecca; Scott, Ryan; McDougall, Neil] Belfast Hlth & Social Care Trust, Belfast, Antrim, North Ireland.
C3 King's College Hospital NHS Foundation Trust; North Bristol NHS Trust;
University of London; University College London; University of
Cambridge; Cambridge University Hospitals NHS Foundation Trust;
Addenbrooke's Hospital; Newcastle University - UK; Newcastle Freeman
Hospital; University of Plymouth; University of Plymouth; University of
London; University College London; UCL Medical School; Royal Free London
NHS Foundation Trust; University of London; University College London;
University of Leeds
RP Ahmed, W (corresponding author), Kings Coll Hosp NHS Fdn Trust, Inst Liver Studies, Denmark Hill, London SE5 9RS, England.
EM Wafaa.ahmed@nhs.net
RI Nayar, Manu/AAO-1414-2021; Corbett, Gareth/GOK-1289-2022
OI Gordon, Robert James/0009-0008-7071-6545
CR Aepli P, 2017, SURG ENDOSC, V31, P1558, DOI 10.1007/s00464-016-5138-9
Ahmed W, 2021, GUT, V70, DOI 10.1136/gutjnl-2021-324105
Arhan M, 2009, SURG ENDOSC, V23, P769, DOI 10.1007/s00464-008-0067-x
Bagul Atul, 2010, Ann R Coll Surg Engl, V92, pW27, DOI 10.1308/147870810X12659688852239
Cantù P, 2019, LIVER INT, V39, P1355, DOI 10.1111/liv.14010
Coté GA, 2016, JAMA-J AM MED ASSOC, V315, P1250, DOI 10.1001/jama.2016.2619
Cotton PB, 2008, GASTROINTEST ENDOSC, V67, P471, DOI 10.1016/j.gie.2007.06.065
Devière J, 2014, GASTROENTEROLOGY, V147, P385, DOI 10.1053/j.gastro.2014.04.043
Dumonceau JM, 2020, ENDOSCOPY, V52, P127, DOI 10.1055/a-1075-4080
Graziadei IW, 2006, LIVER TRANSPLANT, V12, P718, DOI 10.1002/lt.20644
Huszár O, 2017, PLOS ONE, V12, DOI 10.1371/journal.pone.0169618
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Kaffes A, 2014, THER ADV GASTROENTER, V7, P64, DOI 10.1177/1756283X13503614
Kao DN, 2013, GASTROINTEST ENDOSC, V77, P679, DOI 10.1016/j.gie.2013.01.015
Keane MG, 2021, TRANSPLANT REV-ORLAN, V35, DOI 10.1016/j.trre.2020.100593
Khan MA, 2017, ENDOSCOPY, V49, P682, DOI 10.1055/s-0043-109865
Khashab MA, 2015, GASTROINTEST ENDOSC, V81, P81, DOI 10.1016/j.gie.2014.08.008
Landi F, 2018, TRANSPL INT, V31, P131, DOI 10.1111/tri.13089
Larghi A, 2019, LIVER TRANSPLANT, V25, P323, DOI 10.1002/lt.25358
Lee DW, 2016, CLIN ENDOSC, V49, P457, DOI 10.5946/ce.2016.130
Martinez NS, 2021, ENDOSC INT OPEN, V09, pE888, DOI 10.1055/a-1388-6964
Nayar M., 2021, UEG WEEK VIRTUAL 202
Sharma S, 2008, LIVER TRANSPLANT, V14, P759, DOI 10.1002/lt.21509
Tal AO, 2017, GASTROINTEST ENDOSC, V86, P1038, DOI 10.1016/j.gie.2017.03.009
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Verdonk RC, 2006, LIVER TRANSPLANT, V12, P726, DOI 10.1002/lt.20714
Villa Nicolas A, 2015, Gastroenterol Hepatol (N Y), V11, P316
von Elm E, 2007, PREV MED, V45, P247, DOI 10.1016/j.ypmed.2007.08.012
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Zheng X, 2017, DIGEST ENDOSC, V29, P198, DOI 10.1111/den.12742
NR 30
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1756-283X
EI 1756-2848
J9 THER ADV GASTROENTER
JI Ther. Adv. Gastroenterol.
PD SEP
PY 2022
VL 15
DI 10.1177/17562848221122473
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 4X9XU
UT WOS:000861190000001
PM 36187366
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Manangeeswaran, M
Jacques, J
Tami, C
Konduru, K
Amharref, N
Perrella, O
Casasnovas, JM
Umetsu, DT
Dekruyff, RH
Freeman, GJ
Perrella, A
Kaplan, GG
AF Manangeeswaran, Mohanraj
Jacques, Jerome
Tami, Cecilia
Konduru, Krishnamurthy
Amharref, Nadia
Perrella, Oreste
Casasnovas, Jose M.
Umetsu, Dale T.
Dekruyff, Rosemarie H.
Freeman, Gordon J.
Perrella, Alessandro
Kaplan, Gerardo G.
TI Binding of Hepatitis A Virus to Its Cellular Receptor 1 Inhibits
T-Regulatory Cell Functions in Humans
SO GASTROENTEROLOGY
LA English
DT Article
DE Hepatitis A Virus Cellular Receptor 1; Viral Clearance; TGF-beta; Immune
Regulation
ID AUTOIMMUNE-DISEASES; IDENTIFICATION; ACTIVATION; INFECTION;
AUTOANTIBODIES; INDIVIDUALS; EXPRESSION; FAMILY; DEATH
AB BACKGROUND & AIMS: CD4+ T-regulatory (Treg) cells suppress immune responses and control self-tolerance and immunity to pathogens, cancer, and alloantigens. Most pathogens activate Treg cells to minimize immune-mediated tissue damage and prevent clearance, which promotes chronic infections. However, hepatitis A virus (HAV) temporarily inhibits Treg-cell functions. We investigated whether the interaction of HAV with its cellular receptor 1 (HAVCR1), a T-cell co-stimulatory molecule, inhibits the function of Treg cells to control HAV infection. METHODS: We studied the effects of HAV interaction with HAVCR1 on human T cells using binding, signal transduction, apoptosis, activation, suppression, cytokine production, and confocal microscopy analyses. Cytokines were analyzed in sera from 14 patients with HAV infection using bead arrays. RESULTS: Human Treg cells constitutively express HAVCR1. Binding of HAV to HAVCR1 blocked phosphorylation of Akt, prevented activation of the T-cell receptor, and inhibited function of Treg cells. At the peak viremia, patients with acute HAV infection had no Treg-cell suppression function, produced low levels of transforming growth factor-beta, which limited leukocyte recruitment and survival, and produced high levels of interleukin-22, which prevented liver damage. CONCLUSIONS: Interaction between HAV and its receptor HAVCR1 inhibits Treg-cell function, resulting in an immune imbalance that allows viral expansion with limited hepatocellular damage during early stages of infection-a characteristic of HAV pathogenesis. The mechanism by which HAV is cleared in the absence of Treg-cell function could be used as a model to develop anticancer therapies, modulate autoimmune and allergic responses, and prevent transplant rejection.
C1 [Manangeeswaran, Mohanraj; Jacques, Jerome; Tami, Cecilia; Konduru, Krishnamurthy; Amharref, Nadia; Kaplan, Gerardo G.] Ctr Biol Evaluat & Res Food & Drug Adm, Bethesda, MD 20892 USA.
[Perrella, Oreste; Perrella, Alessandro] Hosp D Cotugno, Div Infect Dis & Immunol 7, Naples, Italy.
[Casasnovas, Jose M.] CSIC, Ctr Nacl Biotecnol, Madrid, Spain.
[Umetsu, Dale T.; Dekruyff, Rosemarie H.] Harvard Univ, Childrens Hosp, Boston, MA 02115 USA.
[Freeman, Gordon J.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
C3 US Food & Drug Administration (FDA); Center For Biologics & Evaluation
Research - Bacterial Products; Consejo Superior de Investigaciones
Cientificas (CSIC); CSIC - Centro Nacional de Biotecnologia (CNB);
Harvard University; Boston Children's Hospital; Harvard University;
Harvard Medical School
RP Kaplan, GG (corresponding author), Ctr Biol Evaluat & Res Food & Drug Adm, 8800 Rockville Pike,Bldg 29 NIH,HFM 325, Bethesda, MD 20892 USA.
EM gk@helix.nih.gov
RI Casasnovas, Jose/L-6299-2014; Manangeeswaran, Mohanraj/JXN-5616-2024; ,
Gordon/ADF-6477-2022; amharref, nadia/Y-6498-2018; Perrella,
Alessandro/AAS-1534-2020
OI Perrella, Alessandro/0000-0003-2812-8500; kaplan,
gerardo/0000-0003-3303-7259
FU Food and Drug Administration; National Institutes of Health
[1P01AI54456-01 NIAID, 2P01AI054456-06A1 NIAID, R01 AI089955]
FX Jerome Jacques and Nadia Amharref are Research Fellows of the Oak Ridge
Institute for Science and Education. This work was supported by Food and
Drug Administration Intramural Funding, and National Institutes of
Health grants 1P01AI54456-01 NIAID and 2P01AI054456-06A1 NIAID (to
D.T.U, R.H.D., J.M.C., G.J.F., and G.G.K.) and R01 AI089955 (to G.J.F.
and R.H.D.).
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NR 32
TC 36
Z9 40
U1 0
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD JUN
PY 2012
VL 142
IS 7
BP 1516
EP +
DI 10.1053/j.gastro.2012.02.039
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 952GF
UT WOS:000304778700030
PM 22430395
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Enriquez, J
Mims, BM
Trasti, S
Furr, KL
Grisham, MB
AF Enriquez, Josue
Mims, Brianyell Mc Daniel
Trasti, Scott
Furr, Kathryn L.
Grisham, Matthew B.
TI Genomic, microbial and environmental standardization in animal
experimentation limiting immunological discovery
SO BMC IMMUNOLOGY
LA English
DT Review
DE Outbred mice; Infection; Inflammation; Microbiota; Obesity; GVHD;
Steatohepatitis; Atherosclerosis; Autoimmune disease; Colorectal cancer
ID VERSUS-HOST-DISEASE; SEGMENTED FILAMENTOUS BACTERIA; STREPTOCOCCUS-SUIS
SEROTYPE-2; CD4(+) T-LYMPHOCYTE; FATTY LIVER-DISEASE; GUT MICROBIOTA;
MOUSE MODELS; HOUSING TEMPERATURE; INTESTINAL INFLAMMATION;
COLLABORATIVE CROSS
AB Background The use of inbred mice housed under standardized environmental conditions has been critical in identifying immuno-pathological mechanisms in different infectious and inflammatory diseases as well as revealing new therapeutic targets for clinical trials. Unfortunately, only a small percentage of preclinical intervention studies using well-defined mouse models of disease have progressed to clinically-effective treatments in patients. The reasons for this lack of bench-to-bedside transition are not completely understood; however, emerging data suggest that genetic diversity and housing environment may greatly influence muring immunity and inflammation. Results Accumulating evidence suggests that certain immune responses and/or disease phenotypes observed in inbred mice may be quite different than those observed in their outbred counterparts. These differences have been thought to contribute to differing immune responses to foreign and/or auto-antigens in mice vs. humans. There is also a growing literature demonstrating that mice housed under specific pathogen free conditions possess an immature immune system that remarkably affects their ability to respond to pathogens and/or inflammation when compared with mice exposed to a more diverse spectrum of microorganisms. Furthermore, recent studies demonstrate that mice develop chronic cold stress when housed at standard animal care facility temperatures (i.e. 22-24 degrees C). These temperatures have been shown alter immune responses to foreign and auto-antigens when compared with mice housed at their thermo-neutral body temperature of 30-32 degrees C. Conclusions Exposure of genetically diverse mice to a spectrum of environmentally-relevant microorganisms at housing temperatures that approximate their thermo-neutral zone may improve the chances of identifying new and more potent therapeutics to treat infectious and inflammatory diseases.
C1 [Enriquez, Josue; Mims, Brianyell Mc Daniel; Trasti, Scott; Furr, Kathryn L.; Grisham, Matthew B.] Texas Tech Univ, Hlth Sci Ctr, Dept Immunol & Mol Microbiol, 3601 4th St STOP 6591, Lubbock, TX 79430 USA.
[Trasti, Scott] Texas Tech Univ, Lab Anim Res Ctr, Hlth Sci Ctr, Lubbock, TX 79430 USA.
C3 Texas Tech University System; Texas Tech University Health Science
Center; Texas Tech University System; Texas Tech University Health
Science Center
RP Grisham, MB (corresponding author), Texas Tech Univ, Hlth Sci Ctr, Dept Immunol & Mol Microbiol, 3601 4th St STOP 6591, Lubbock, TX 79430 USA.
EM matthew.grisham@ttuhsc.edu
FU National Institute of Allergy and Infectious Disease [F31AI145077]
FX National Institute of Allergy and Infectious Disease; F31AI145077
(Brianyell McDaniel Mims).
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NR 143
TC 11
Z9 11
U1 0
U2 12
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2172
J9 BMC IMMUNOL
JI BMC Immunol.
PD SEP 2
PY 2020
VL 21
IS 1
AR 50
DI 10.1186/s12865-020-00380-x
PG 19
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA NM6MX
UT WOS:000568210800001
PM 32878597
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Nesslinger, NJ
Sahota, RA
Stone, B
Johnson, K
Chima, N
King, C
Rasmussen, D
Bishop, D
Rennie, PS
Gleave, M
Blood, P
Pai, H
Ludgate, C
Nelson, BH
AF Nesslinger, Nancy J.
Sahota, Robert A.
Stone, Brad
Johnson, Kayli
Chima, Navraj
King, Caitlin
Rasmussen, Devon
Bishop, Darcy
Rennie, Paul S.
Gleave, Martin
Blood, Paul
Pai, Howard
Ludgate, Charles
Nelson, Brad H.
TI Standard treatments induce antigen-specific immune responses in prostate
cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID TUMOR-INFILTRATING LYMPHOCYTES; HUMAN HEPATOCELLULAR-CARCINOMA;
DENDRITIC CELL IMMUNOTHERAPY; COLON-CANCER; T-CELLS;
PROGNOSTIC-SIGNIFICANCE; ANDROGEN SUPPRESSION; SEROLOGICAL CLONING;
IONIZING-RADIATION; AUTOIMMUNE-DISEASE
AB Purpose: Prostate tumors express antigens that are recognized by the immune system in a significant proportion of patients; however, little is known about the effect of standard treatments on tumor-specific immunity. Radiation therapy induces expression of inflammatory and immune-stimulatory molecules, and neoadjuvant hormone therapy causes prominent T-cell infiltration of prostate tumors. We therefore hypothesized that radiation therapy and hormone therapy may initiate tumor-specific immune responses.
Experimental Design: Pretreatment and posttreatment serum samples from 73 men with nonmetastatic prostate cancer and 50 cancer-free controls were evaluated by Western blotting and SEREX (serological identification of antigens by recombinant cDNA expression cloning) antigen arrays to examine whether autoantibody responses to tumor proteins arose during the course of standard treatment.
Results: Western blotting revealed the development of treatment-associated autoantibody responses in patients undergoing neoadjuvant hormone therapy (7 of 24, 29.2%), external beam radiation therapy (4 of 29,13.8%), and brachytherapy (5 of 20, 25%), compared with 0 of 14 patients undergoing radical prostatectomy and 2 of 36 (5.6%) controls. Responses were seen within 4 to 9 months of initiation of treatment and were equally prevalent across different disease risk groups. Similarly, in the murine Shionogi tumor model, hormone therapy induced tumor-associated autoantibody responses in 5 of 10 animals. In four patients, SEREX immunoscreening of a prostate cancer c DNA expression library identified several antigens recognized by treatment-associated autoantibodies, including PARP1, ZNF707 + PTMA, CEP78, SDCCAG1, and ODF2.
Conclusion: We show for the first time that standard treatments induce antigen-specific immune responses in prostate cancer patients. Thus, immunologic mechanisms may contribute to clinical outcomes after hormone and radiation therapy, an effect that could potentially be exploited as a practical, personalized form of immunotherapy.
C1 British Columbia Canc Agcy, Vancouver Isl Ctr, Trev & Joyce Deeley Res Ctr, Victoria, BC V8R 6V5, Canada.
British Columbia Canc Agcy, Vancouver Isl Ctr, Radiat Oncol Program, Victoria, BC V8R 6V5, Canada.
Virginia Mason, Benaroya Res Inst, Seattle, WA USA.
Vancouver Gen Hosp, Jack Bell Res Ctr, Prostate Ctr, Vancouver, BC, Canada.
C3 British Columbia Cancer Agency; British Columbia Cancer Agency; Benaroya
Research Institute; Virginia Mason Medical Center; University of British
Columbia
RP Nelson, BH (corresponding author), British Columbia Canc Agcy, Vancouver Isl Ctr, Trev & Joyce Deeley Res Ctr, 2410 Lee Ave, Victoria, BC V8R 6V5, Canada.
EM bnelson@bccancer.bc.ca
RI Nelson, Brad/K-2622-2014; Evans, Devon/ABF-4939-2021
OI Evans, Devon/0000-0002-2326-5090; Nelson, Brad/0000-0002-4445-5539
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NR 83
TC 137
Z9 151
U1 0
U2 11
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD MAR 1
PY 2007
VL 13
IS 5
BP 1493
EP 1502
DI 10.1158/1078-0432.CCR-06-1772
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 144CL
UT WOS:000244772800021
PM 17332294
DA 2025-01-07
ER
PT J
AU Mann, BK
Bhandohal, JS
Cobos, E
Chitturi, C
Eppanapally, S
AF Mann, Baldeep Kaur
Bhandohal, Janpreet Singh
Cobos, Everardo
Chitturi, Chandrika
Eppanapally, Sabitha
TI LECT-2 amyloidosis: what do we know?
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Review
DE amyloidosis; kidney failure; chronic
ID LEUKOCYTE CHEMOTACTIC FACTOR-2; CELL-DERIVED CHEMOTAXIN-2; RENAL
AMYLOIDOSIS; HEPATOCELLULAR-CARCINOMA; HEPATIC AMYLOIDOSIS;
MOLECULAR-CLONING; BETA-CATENIN; ALECT2; EXPRESSION; PREVALENCE
AB Amyloidosis is a rare group of diseases characterized by abnormal folding of proteins and extracellular deposition of insoluble fibrils. It can be localized to one organ system or can have systemic involvement. The kidney is the most common organ to be involved in systemic amyloidosis often leading to renal failure and the nephrotic syndrome. The two most common types of renal amyloidosis are immunoglobulin light chain-derived amyloidosis (AL) and reactive amyloidosis (AA). A novel form of amyloidosis (ALECT2) derived from leukocyte chemotactic factor 2 (LECT-2) and primarily involving the kidneys was first described by Benson et al in 2008. The liver was subsequently identified as the second most common organ involved in ALECT2 amyloidosis. LECT-2 is a unique protein that can form amyloid deposits even in its unmutated form. Patients with ALECT2 present with minimal proteinuria in contrast to other forms of amyloidosis especially AL and AA. They may present with slightly elevated serum creatinine. Nephrotic syndrome and hematuria are rare. ALECT2 can be found in association with other types of amyloidosis as well as malignancies or autoimmune diseases. ALECT2 may be confused with amyloidosis associated with light and heavy chain monoclonal gammopathy if the immunofluorescence is positive with anti-light chain and anti-AA sera. The other organs involved are the duodenum, adrenal gland, spleen, prostate, gall bladder, pancreas, small bowel, parathyroid gland, heart, and pulmonary alveolar septa, but consistently uninvolved organs included brain and fibroadipose tissue. A renal biopsy along with characteristic features found on immunohistochemistry and mass spectrometry is diagnostic of ALECT2. ALECT2 should be suspected when all markers for AL and AA are negative. Proper diagnosis of ALECT2 can determine need for supportive care versus more aggressive interventions.
C1 [Mann, Baldeep Kaur; Bhandohal, Janpreet Singh; Chitturi, Chandrika; Eppanapally, Sabitha] Kern Med Ctr, Internal Med, Bakersfield, CA 93306 USA.
[Cobos, Everardo] Kerm Med, Med, Bakersfield, CA USA.
RP Mann, BK (corresponding author), Kern Med Ctr, Internal Med, Bakersfield, CA 93306 USA.
EM USAbaldeep.sippi@gmail.com
RI COBOS, EVERARDO/LRU-2001-2024
OI cobos, everardo/0000-0001-5799-0074; Mann, Baldeep/0000-0001-8006-2479
CR An N, 2017, Zhonghua Nei Ke Za Zhi, V56, P298, DOI 10.3760/cma.j.issn.0578-1426.2017.04.012
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NR 47
TC 10
Z9 15
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1081-5589
EI 1708-8267
J9 J INVEST MED
JI J. Investigative Med.
PD FEB
PY 2022
VL 70
IS 2
BP 348
EP 353
DI 10.1136/jim-2021-002149
EA NOV 2021
PG 6
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA YX3DR
UT WOS:000725042000001
PM 34848562
OA Bronze
DA 2025-01-07
ER
PT J
AU Bozek, A
Zajac, M
AF Bozek, Andrzej
Zajac, Magdalena
TI Impact of comorbidities on risk of angioedema without urticaria in
elderly patients
SO ALLERGY ASTHMA AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Angioedema; Elderly; IgE; Hyperuricemia; Hashimoto
ID URIC-ACID; HEREDITARY
AB Background: Angioedema without urticaria (AWU) is a disease found in the elderly population but is still poorly studied. The aim of this study was to investigate potential factors, especially comorbidities, that may affect the induction of angioedema without urticaria in patients over 60 years of age.
Methods: This was an observational, retrospective study of 242 patients with a diagnosis of AWU and 263 controls. The inclusion criteria were as follows: at least one episode of confirmed AWU based on the ICD-10 code (T78.3) that required treatment in the last 15 years (2004-2019); age above 60 years; detailed medical history of comorbidities; and details regarding the use of drugs at that time. Serum functional and quantitative C1 inhibitor assays were performed, and serum C4 was measured. Comorbidities were grouped into the following panels: autoimmune, cancer, cardiac, metabolic, respiratory and allergic, liver failure and renal failure. Individual diseases were checked according to ICD code and treatment.
Results: In 1 (0.4%) patient, hereditary angioedema was confirmed. Decreased levels of C1INH were observed in 4 (1.65%) patients, dysfunction of C1INH was observed in 5 (1.76%) patients, and low levels of C4 were observed in 9 (3.71%) patients in the study group. The multiple logistic regression model revealed that patients with hyperuricemia or Hashimoto's disease had a significantly higher chance of angioedema (OR = 3.21, 95% CI 2.92-3.66, p = 0.002; OR = 1.78 95% CI 1.37-2.21, p = 0.034, respectively).
Conclusion: The obtained results may indicate a significant influence of hyperuricemia or Hashimoto's disease on angioedema manifestations.
C1 [Bozek, Andrzej] Med Univ Silesia, Clin Dept Internal Dis Dermatol & Allergol, Katowice, Poland.
[Zajac, Magdalena] Wroclaw Med Univ, Wroclaw, Poland.
[Bozek, Andrzej] MC Sklodowskiej 10, PL-41800 Zabrze, Poland.
C3 Medical University Silesia; Wroclaw Medical University
RP Bozek, A (corresponding author), Med Univ Silesia, Clin Dept Internal Dis Dermatol & Allergol, Katowice, Poland.; Bozek, A (corresponding author), MC Sklodowskiej 10, PL-41800 Zabrze, Poland.
EM andrzejbozek@o2.pl
OI Bozek, Andrzej/0000-0003-2263-2263; Zajac, Magdalena/0000-0001-5744-3230
FU Medical University of Silesia, Katowice, Poland
FX Medical University of Silesia, Katowice, Poland.
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Bhupendra, 2020, STATPEARLS
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NR 15
TC 2
Z9 2
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1710-1492
J9 ALLERGY ASTHMA CL IM
JI Allerg Asthma Clin. Immunol.
PD DEC 14
PY 2021
VL 17
IS 1
AR 133
DI 10.1186/s13223-021-00637-z
PG 6
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA XO4WG
UT WOS:000730186900001
PM 34906225
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Boyd, S
Tenca, A
Jokelainen, K
Mustonen, H
Krogerus, L
Arola, J
Färkkilä, MA
AF Boyd, Sonja
Tenca, Andrea
Jokelainen, Kalle
Mustonen, Harri
Krogerus, Leena
Arola, Johanna
Farkkila, Martti A.
TI Screening primary sclerosing cholangitis and biliary dysplasia with
endoscopic retrograde cholangiography and brush cytology: risk factors
for biliary neoplasia
SO ENDOSCOPY
LA English
DT Article
ID IMMUNOGLOBULIN G4-ASSOCIATED CHOLANGITIS; AUTOIMMUNE HEPATITIS;
CHOLANGIOCARCINOMA; MALIGNANCY; DIAGNOSIS; EPIDEMIOLOGY; STRICTURES;
CANCER; G4
AB Background and study aims: Primary sclerosing cholangitis (PSC) is associated with increased risk of biliary dysplasia and cholangiocarcinoma (CCA). The aim of this study was to evaluate the role of early endoscopic retrograde cholangiography (ERC) with systematic brush cytology to identify risk factors associated with biliary neoplasia.
Patients and methods: Patients who were referred for their first ERC for suspicion of PSC between January 2006 and October 2011 were included in the study. Brush cytology specimens were scored as benign, suspicious, or malignant. End points were CCA, biliary dysplasia, benign histology, or benign disease course for >= 2 years.
Results: PSC was diagnosed in 261 patients (125 men, 136 women), most of whom were asymptomatic (n = 211). Cholangiographic changes were mild in 57.1%. Men presented with advanced disease more often than women. Brush cytology was benign in 243, suspicious in 16, and malignant in 2 patients. Follow-up completed in 249 patients indicated a benign disease course in 232 patients. Seven patients were diagnosed with CCA and eight had biliary dysplasia in the explanted liver. Thus, 15 patients had biliary neoplasia, and suspicious or malignant brush cytology had been detected in 8 of them at initial brushing. Advanced extrahepatic cholangiographic changes with elevated aminotransferases at diagnosis seemed to be associated with increased risk of biliary neoplasia.
Conclusions: Even in mostly asymptomatic patients with PSC, 42.9% had advanced disease and 6.9% presented with suspicious or malignant brush cytology at first ERC. Advanced extrahepatic ERC changes with elevated aminotransferases at diagnosis might be risk factors for biliary neoplasia.
C1 [Boyd, Sonja; Tenca, Andrea; Jokelainen, Kalle; Krogerus, Leena; Arola, Johanna; Farkkila, Martti A.] Univ Helsinki, Helsinki, Finland.
[Boyd, Sonja; Arola, Johanna] Helsinki Univ Hosp, HUSLAB Dept Pathol, Helsinki, Finland.
[Tenca, Andrea; Farkkila, Martti A.] Helsinki Univ Hosp, Gastroenterol Clin, Helsinki, Finland.
[Tenca, Andrea; Jokelainen, Kalle] Univ Milan, Fdn IRCCS Ca Granda Osped Maggiore Policlin, Dept Pathophysiol & Transplantat, Gastroenterol & Endoscopy Unit, Milan, Italy.
[Mustonen, Harri] Univ Helsinki, Dept Surg, Helsinki, Finland.
[Mustonen, Harri] Helsinki Univ Hosp, Biomedicum, Helsinki, Finland.
[Krogerus, Leena] Helsinki Univ Hosp Jorvi, Espoo, Finland.
C3 University of Helsinki; University of Helsinki; Helsinki University
Central Hospital; University of Helsinki; Helsinki University Central
Hospital; University of Milan; IRCCS Ca Granda Ospedale Maggiore
Policlinico; University of Helsinki; University of Helsinki; Helsinki
University Central Hospital
RP Boyd, S (corresponding author), HUSLAB Meilahti Labs Pathol, PB 400, Helsinki 00029, Finland.
EM sonja.boyd@hus.fi
RI Färkkilä, Martti/AAG-6970-2021; Boyd, Sonja/H-9981-2016
OI Mustonen, Harri Kalevi/0000-0001-5632-6796; Farkkila,
Martti/0000-0002-0250-8559
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NR 26
TC 38
Z9 39
U1 0
U2 1
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0013-726X
EI 1438-8812
J9 ENDOSCOPY
JI Endoscopy
PD MAY
PY 2016
VL 48
IS 5
BP 432
EP 439
DI 10.1055/s-0041-110792
PG 8
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA DK6QG
UT WOS:000375049000005
PM 26808393
DA 2025-01-07
ER
PT J
AU Aydogdu, S
Arikan, C
Kilic, M
Ozgenc, F
Akman, S
Unal, F
Yagci, RV
Tokat, Y
AF Aydogdu, S
Arikan, C
Kilic, M
Ozgenc, F
Akman, S
Unal, F
Yagci, RV
Tokat, Y
TI Outcome of pediatric liver transplant recipients in Turkey: Single
center experience
SO PEDIATRIC TRANSPLANTATION
LA English
DT Article
DE chronic liver disease; pediatric liver transplantation; survival;
surgical complication; pediatric end-stage liver disease score
ID CHRONIC REJECTION; RISK
AB To summarize the evolution of the pediatric liver transplant program in a developing country. Between April 1997, and September 2003, 32 cadaveric (CD) and 35 living donor (LD) liver transplantations were performed on 61 children (median age 3.8 yr, range 0.5-16) at Ege University Organ Transplantation and Research Center. The patient's charts were reviewed retrospectively. The outcome of patient and graft survival was analyzed and the incidence of graft loss, complications and rejections was calculated. Indications for liver transplantation were metabolic liver disease (n = 17), biliary atresia (n = 14), viral hepatitis (n = 4), autoimmune hepatitis (n = 6), cryptogenic cirrhosis (n = 11), fulminant liver failure (n = 5) and others (n = 5). Seven of 61 children with chronic liver disease had hepatocellular carcinoma concomitantly. Median pediatric end-stage liver disease score was 23 (range 1-54). Seven children (11.4%) were UNOS status I, 44 (72%) were UNOS status II and 10 (16.6%) were UNOS status III. The median follow-up of the study population was 3.6 yr (range 0.5-6). Actuarial patient survival rates at 1, 2, 3 and 4 yr were 86, 86, 71.3 and 65% in the CD group vs. 80, 76, 67 and 67% in the LR group, respectively (p = NS). Patients listed as UNOS status 1 had lower survival rates than patients listed as UNOS status 2 and 3 (p < 0.05). The mortality rate was 26.2%. Graft survival rates were 81, 81, 75 and 64% at 1, 2, 3 and 4-yr respectively. Six patients (9%) underwent retransplantation. The main complications were infections (64.7%) and surgical complications (43.2%) (including biliary complication, vascular problems, postoperative bleeding, small for size and large for size). The incidence of acute cellular rejection was 39.3%, whereas chronic rejection was 7.4%. The result of liver transplantation in Turkish children was slightly inferior to those reported for North American and European children. However, an important characteristic of these patients that distinguishes them from Europe and North America is that most were UNOS status IIa and UNOS status I (44%). Despite technical and medical progress, infectious and biliary problems have continued to be an important cause of mortality in these patients.
C1 Ege Univ Sch Med, Dept Pediat, Div Gastroenterol, Izmir, Turkey.
Ege Univ Sch Med, Dept Pediat, Div Hepatol, Izmir, Turkey.
Ege Univ Sch Med, Dept Pediat, Div Nutr, Izmir, Turkey.
Ege Univ Sch Med, Dept Gen Surg, Izmir, Turkey.
C3 Ege University; Ege University; Ege University; Ege University
RP 250 Sok 6 D-1, TR-35040 Izmir, Turkey.
EM arikan@med.ege.edu.tr
RI arikan, cigdem/ABF-2764-2020
OI Kilic, Murat/0009-0007-5052-2279; ARIKAN, Cigdem/0000-0002-0794-2741;
kilic, murat/0000-0002-2887-1487
CR ARIKAN C, 2002, TRANSPLANTATION S, V74, P3526
Emre S, 2002, PEDIATR TRANSPLANT, V6, P43, DOI 10.1034/j.1399-3046.2002.1r072.x
Goss JA, 1998, ANN SURG, V228, P411, DOI 10.1097/00000658-199809000-00014
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Jain A, 2002, TRANSPLANT P, V34, P1968, DOI 10.1016/S0041-1345(02)03143-3
Jain A, 2001, LIVER TRANSPLANT, V7, P623, DOI 10.1053/jlts.2001.25364
Kam I, 2002, LIVER TRANSPLANT, V8, P347, DOI 10.1053/jlts.2002.33194
Mazariegos GV, 2002, AM J TRANSPLANT, V2, P260, DOI 10.1034/j.1600-6143.2002.20311.x
McDiarmid SV, 2003, PEDIATR CLIN N AM, V50, P1335, DOI 10.1016/S0031-3955(03)00150-0
MCDIARMID SV, 1999, GRAFT S2, V2, pS86
Miller CM, 2001, ANN SURG, V234, P301, DOI 10.1097/00000658-200109000-00004
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NR 17
TC 27
Z9 28
U1 5
U2 22
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1397-3142
EI 1399-3046
J9 PEDIATR TRANSPLANT
JI Pediatr. Transplant.
PD DEC
PY 2005
VL 9
IS 6
BP 723
EP 728
DI 10.1111/j.1399-3046.2005.00366.x
PG 6
WC Pediatrics; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics; Transplantation
GA 980FG
UT WOS:000232999000006
PM 16269042
DA 2025-01-07
ER
PT J
AU Fleig, SV
Konen, FF
Schröder, C
Schmitz, J
Gingele, S
Bräsen, JH
Lovric, S
Schmidt, BMW
Haller, H
Skripuletz, T
von Vietinghoff, S
AF Fleig, Susanne V.
Konen, Franz F.
Schroeder, Christoph
Schmitz, Jessica
Gingele, Stefan
Braesen, Jan H.
Lovric, Svjetlana
Schmidt, Bernhard M. W.
Haller, Hermann
Skripuletz, Thomas
von Vietinghoff, Sibylle
TI Long-term B cell depletion associates with regeneration of kidney
function
SO IMMUNITY INFLAMMATION AND DISEASE
LA English
DT Article
DE cancer; cell migration; liver; hepatocytes
ID IDIOPATHIC MEMBRANOUS NEPHROPATHY; LOW-DOSE RITUXIMAB;
MOLECULAR-MECHANISMS; CYCLOSPORINE; INFLAMMATION; LYMPHOTOXIN;
SENESCENCE; THERAPY
AB Background Chronic kidney disease (CKD) is a common condition that increases mortality and the risk of cardiovascular and other morbidities regardless of underlying renal condition. Chronic inflammation promotes renal fibrosis. Recently, renal B cell infiltrates were described in chronic kidney disease of various etiologies beyond autoimmunity. Methods We here investigated B cells and indicators of tertiary lymphoid structure formation in human renal biopsies. Renal function was studied during long-term B cell depletion in human patients with membranous nephropathy and with CKD of unknown origin. Results Cytokine profiles of tertiary lymphoid structure formation were detected in human renal interstitium in a range of kidney diseases. Complex B cell structures consistent with tertiary lymphoid organ formation were evident in human membranous nephropathy. Here, B cell density did not significantly associate with proteinuria severity, but with worse excretory renal function. Proteinuria responses mostly occurred within the first 6 months of B cell depletion. In contrast, recovery of excretory kidney function was observed only after 18 months of continuous therapy, consistent with a structural process. Renal tertiary lymphatic structures were also detected in the absence of autoimmune kidney disease. To start to address whether B cell depletion may affect CKD in a broader population, we assessed kidney function in neurologic patients with CKD of unknown origin. In this cohort, eGFR significantly increased within 24 months of B cell depletion. Conclusion Long-term B cell depletion associated with significant improvement of excretory kidney function in human CKD. Kinetics and mechanisms of renal B cell aggregation should be investigated further to stratify the impact of B cells and their aggregates as therapeutic targets.
C1 [Fleig, Susanne V.; Schroeder, Christoph; Lovric, Svjetlana; Schmidt, Bernhard M. W.; Haller, Hermann; von Vietinghoff, Sibylle] Dept Internal Med, Div Nephrol & Hypertens, Bonn, Germany.
[Fleig, Susanne V.; von Vietinghoff, Sibylle] Rhein Friedrich Wilhelms Univ, Univ Hosp Bonn, Med Clin 1, Nephrol Sect, Venusberg Campus 1, D-53127 Bonn, Germany.
[Konen, Franz F.; Skripuletz, Thomas] Dept Neurol, Bonn, Germany.
[Konen, Franz F.; Schroeder, Christoph; Gingele, Stefan; Lovric, Svjetlana; Skripuletz, Thomas; von Vietinghoff, Sibylle] Interdisciplinary Day Clin, Bonn, Germany.
[Schmitz, Jessica; Braesen, Jan H.] Hannover Med Sch, Inst Pathol, Nephropathol Unit, Hannover, Germany.
C3 University of Bonn; Hannover Medical School
RP von Vietinghoff, S (corresponding author), Rhein Friedrich Wilhelms Univ, Univ Hosp Bonn, Med Clin 1, Nephrol Sect, Venusberg Campus 1, D-53127 Bonn, Germany.
EM Sibylle.von_Vietinghoff@ukbonn.de
RI Fleig, Susanne/AHA-7209-2022; Bräsen, Jan Hinrich/AER-1685-2022;
Schmitz, Jessica/KGL-5663-2024; Skripuletz, Thomas/AFE-8226-2022
OI Brasen, Jan Hinrich/0000-0002-2863-3067; Fleig,
Susanne/0000-0002-2886-2222; Skripuletz, Thomas/0000-0001-8550-335X;
Schmitz, Jessica/0000-0001-9843-7339
FU Deutsche Forschungsgemeinschaft
FX Deutsche Forschungsgemeinschaft
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NR 46
TC 3
Z9 3
U1 1
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2050-4527
J9 IMMUN INFLAMM DIS
JI IMMUN. INFLAMM. DIS.
PD DEC
PY 2021
VL 9
IS 4
BP 1479
EP 1488
DI 10.1002/iid3.499
EA JUL 2021
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA WW2EN
UT WOS:000678755700001
PM 34324242
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Valentine, C
AF Valentine, Cleo
TI The impact of architectural form on physiological stress: a systematic
review
SO FRONTIERS IN COMPUTER SCIENCE
LA English
DT Article
DE architecture; architectural health; physiological stress; clinical
biomarkers; architectural form; neuroarchitecture
ID SENSORY OVERLOAD; BRAIN; NEUROINFLAMMATION; JUDGMENTS; DESIGN; BEAUTY
AB Technological advancements in physiological body sensor networks (i.e., biometric tracking wearables) and simulated environments (i.e., VR) have led to increased research in the field of neuroarchitecture, specifically investigating the effects of architectural forms, defined here as subtle variations in the shape or configuration of the interior built environment, on neurological responses. While this research field is still in its nascent stages, early findings suggest that certain architectural forms may impact physiological stress responses. Physiological stress has, in turn, been implicated in the development of certain diseases, including cardiovascular disease, cancer, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. To aid future research, particularly into the relationship between media architecture and physiological stress, this paper conducts a systematic review following PRISMA-P guidelines on studies that evaluated physiological stress responses to architectural form using clinical biomarkers. The review identifies the specific clinical biomarkers used to evaluate physiological stress responses to architectural forms and the distinct categories of architectural forms that have, to date, been correlated with elevated stress responses: curvature, enclosure and proportion. Although these studies' findings imply that the identified architectural forms influence physiological stress, their generalisability is arguably constrained by several factors. These constraints include the paucity of research in this area, the lack of uniformity in the definition and measurement of these architectural forms, the varying contextual settings, the unisensory approach of research methodologies, and the duration of exposure under evaluation. The review concludes that clinical biomarkers may be used to measure the impact of architectural form on physiological stress; however, future research should strive for standardized approaches in defining and measuring architectural forms in order to increase the transferability and robustness of results.
C1 [Valentine, Cleo] Univ Cambridge, Dept Architecture, Cambridge, England.
C3 University of Cambridge
RP Valentine, C (corresponding author), Univ Cambridge, Dept Architecture, Cambridge, England.
EM crv29@cam.ac.uk
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NR 62
TC 2
Z9 2
U1 6
U2 16
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2624-9898
J9 FRONT COMP SCI-SWITZ
JI Front. Comput. Sci.-Switz
PD JAN 4
PY 2024
VL 5
AR 1237531
DI 10.3389/fcomp.2023.1237531
PG 11
WC Computer Science, Interdisciplinary Applications
WE Emerging Sources Citation Index (ESCI)
SC Computer Science
GA FF6S3
UT WOS:001144392900001
OA Green Published, gold
DA 2025-01-07
ER
EF
FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Tremblay, S
Boutin, J
Perreault, M
Coté, MF
Gobei, S
Gaudreault, RC
AF Tremblay, Sebastien
Boutin, Joel
Perreault, Martin
Cote, Marie-France
Gobei, Stephane
Gaudreault, Rene C.
TI Synthesis and evaluation of substituted phenyl cycloalkylureas and
bioisosteres as IL-6 expression inhibitors
SO MEDICINAL CHEMISTRY RESEARCH
LA English
DT Article
DE Interleukine-6 expression inhibitors; Phenyl cycloalkylureas; Phenyl
cycloalkylthioureas; Phenyl cycloalkylsquaramides
ID BIOLOGICS; ALKYLATION; HEALTH; DISEASE; PHASE; UREA
AB Inflammation is an important, normal, and complex host defense response to injury, autoimmune responses or infectious agents. However, chronic inflammation is associated with diseases like rheumatoid arthritis, cancers, cardiovascular diseases, diabetes, and obesity, and over 60% of deaths worldwide. Interleukine-6 is one of the key proinflammatory cytokines involved in inflammation processes and therefore considered as a valuable drug target. We have prepared three series of new drugs referred to as substituted phenyl cycloalkylureas (PcAUs), phenyl cycloalkylthioureas (PcATUs) and phenyl cycloalkylsquaramides (PcASs), respectively. PcAUs and PcATUs were prepared by nucleophilic addition of 3 or 4-tert-butyl, 3- or 4-cyclohexyl and 3- or 4-iodoaniline to a suitable cycloalkylisocyanate or cycloalkylisothiocyanate. PcASs were prepared by nucleophilic addition of the aforementioned anilines to diethoxysquarate. The resulting alkoxysquarates were further reacted with selected cycloalkylamines to produce the desired PcASs. The antiproliferative activity of PcAUs, PcATUs and PcASs was evaluated in human keratinocytes and human skin fibroblasts. Most compounds at the exception of 4f, 4f ', 4f '', 5f, 5f ', 5f '', 6f, and 6f ', 6f '' that are bearing a 3-cyclohexyl group did not exhibit significant antiproliferative activities at concentration <30 mu M. At 10 mu M, PcAUs 4b-4e, 5b, 5e, and 6e inhibited IL-6 expression by more than 70% in HaCaT cells, which is equivalent to or greater than ibuprofen used as a positive control. These PcAUs showed a good metabolic stability in presence of human liver microsomes. Our results are suggesting PcAUs as a new molecular template for the development of potentially useful IL-6 expression inhibitors for the treatment of inflammation-related diseases.
C1 [Tremblay, Sebastien; Cote, Marie-France; Gaudreault, Rene C.] Univ Laval, CRCHU Quebec, Hop St Francois Assise, 10 Rue Espinay, Quebec City, PQ G1L 3L5, Canada.
[Boutin, Joel; Perreault, Martin; Cote, Marie-France; Gobei, Stephane] CHU Laval CHUL, CRCHU Quebec Univ Laval, 2705 Blvd Laurier, Quebec City, PQ G1V 4G2, Canada.
[Gobei, Stephane; Gaudreault, Rene C.] Univ Laval, Fac Med, Dept Med Mol, Quebec City, PQ G1V 0A6, Canada.
C3 Laval University; Laval University; Laval University
RP Gaudreault, RC (corresponding author), Univ Laval, CRCHU Quebec, Hop St Francois Assise, 10 Rue Espinay, Quebec City, PQ G1L 3L5, Canada.; Gaudreault, RC (corresponding author), Univ Laval, Fac Med, Dept Med Mol, Quebec City, PQ G1V 0A6, Canada.
EM rene.c-gaudreault@crsfa.ulaval.ca
FU Canadian Institute for Health Research [MOP-142186, MOP-156019]; Fond de
Recherche du Quebec-Nature et Technologies (FRQNT) [209618]
FX This work was supported by the Canadian Institute for Health Research
(R.C.-G; Grant #MOP-142186 and #MOP-156019). S.T. is a recipient of a
studentship from the Fond de Recherche du Quebec-Nature et Technologies
(FRQNT) (Scholarship #209618).
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PU SPRINGER BIRKHAUSER
PI NEW YORK
PA 233 SPRING STREET, 6TH FLOOR, NEW YORK, NY 10013 USA
SN 1054-2523
EI 1554-8120
J9 MED CHEM RES
JI Med. Chem. Res.
PD AUG
PY 2020
VL 29
IS 8
BP 1424
EP 1437
DI 10.1007/s00044-020-02557-w
EA MAY 2020
PG 14
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA ME9NW
UT WOS:000534196600001
DA 2025-01-07
ER
PT J
AU Dasgupta, S
Kumar, V
AF Dasgupta, Suryasarathi
Kumar, Vipin
TI Type II NKT cells: a distinct CD1d-restricted immune regulatory NKT cell
subset
SO IMMUNOGENETICS
LA English
DT Review
DE NKT cells; CD1d; Antigen presenting cells; Lipids; Sulfatide; LPC
ID KILLER T-CELLS; ALPHA-GALACTOSYLCERAMIDE PRESENTATION; ANTIGEN
PRESENTATION; CD1D EXPRESSION; DENDRITIC CELLS; LIPID ANTIGENS; CUTTING
EDGE; MEDIATED ACTIVATION; NEGATIVE SELECTION; MULTIPLE DEFECTS
AB Type II natural killer T cells (NKT) are a subset of the innate-like CD1d-restricted lymphocytes that are reactive to lipid antigens. Unlike the type I NKT cells, which express a semi-invariant TCR, type II NKT cells express a broader TCR repertoire. Additionally, other features, such as their predominance over type I cells in humans versus mice, the nature of their ligands, CD1d/lipid/TCR binding, and modulation of immune responses, distinguish type II NKT cells from type I NKT cells. Interestingly, it is the self-lipid-reactivity of type II NKT cells that has helped define their physiological role in health and in disease. The discovery of sulfatide as one of the major antigens for CD1d-restricted type II NKT cells in mice has been instrumental in the characterization of these cells, including the TCR repertoire, the crystal structure of the CD1d/lipid/TCR complex, and their function. Subsequently, several other glycolipids and phospholipids from both endogenous and microbial sources have been shown to activate type II NKT cells. The activation of a specific subset of type II NKT cells following administration with sulfatide or lysophosphatidylcholine (LPC) leads to engagement of a dominant immunoregulatory pathway associated with the inactivation of type I NKT cells, conventional dendritic cells, and inhibition of the proinflammatory Th1/Th17 cells. Thus, type II NKT cells have been shown to be immunosuppressive in autoimmune diseases, inflammatory liver diseases, and in cancer. Knowing their relatively higher prevalence in human than type I NKT cells, understanding their biology is imperative for health and disease.
C1 [Dasgupta, Suryasarathi; Kumar, Vipin] Univ Calif San Diego, Div Gastroenterol, Dept Med, 9500 Gilman Dr, La Jolla, CA 92037 USA.
C3 University of California System; University of California San Diego
RP Kumar, V (corresponding author), Univ Calif San Diego, Div Gastroenterol, Dept Med, 9500 Gilman Dr, La Jolla, CA 92037 USA.
EM vckumar@ucsd.edu
FU National Institutes of Health, USA [R01 CA100660, R01 AA020864]
FX This work was supported by grants from the National Institutes of
Health, USA, R01 CA100660 and R01 AA020864 (to VK). We thank the other
members of the Kumar laboratory and Dr. Randle Ware for a critical
reading of the manuscript.
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NR 105
TC 50
Z9 52
U1 0
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0093-7711
EI 1432-1211
J9 IMMUNOGENETICS
JI Immunogenetics
PD AUG
PY 2016
VL 68
IS 8
BP 665
EP 676
DI 10.1007/s00251-016-0930-1
PG 12
WC Genetics & Heredity; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Immunology
GA DU7OJ
UT WOS:000382404100015
PM 27405300
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Woon, PY
Chien, JY
Wang, JH
Chou, YY
Lin, MC
Huang, SP
AF Woon, Peng Yeong
Chien, Jia-Ying
Wang, Jen-Hung
Chou, Yu-Yau
Lin, Mei-Chen
Huang, Shun-Ping
TI Prevalence and associated relating factors in patients with hereditary
retinal dystrophy: a nationwide population-based study in Taiwan
SO BMJ OPEN
LA English
DT Article
DE OPHTHALMOLOGY; EPIDEMIOLOGY; HEALTH SERVICES ADMINISTRATION & MANAGEMENT
ID CYSTOID MACULAR EDEMA; OPTICAL COHERENCE TOMOGRAPHY;
RETINITIS-PIGMENTOSA PATIENTS; CATARACT-SURGERY; DIABETES-MELLITUS;
VISUAL-ACUITY; ATROPHY; LESIONS; TRENDS; COMMON
AB Objective To investigate the prevalence, incidence and relating factors that are associated with hereditary retinal dystrophy (HRD) in Taiwan from 2000 to 2013. Design, setting and participants This is a nationwide, population-based, retrospective case-control study using National Health Insurance Database. Study groups are patients with HRD as case group; age-matched patients without any diagnosis of HRD as control group. We enrolled 2418 study subjects, of which 403 were HRD patients. Important relating factors such as hypertension, diabetes, coronary artery disease, autoimmune disease, cancer, liver cirrhosis, chronic kidney disease, stroke, hyperlipidaemia, asthma, depression and dementia are also included. Exposure Patients diagnosed with HRD were retrieved from National Health Insurance Database. Main outcomes and measures OR calculated between the relating factors and HRD for objects and stratified by age and sex group between 2000 and 2013. Results Four hundred and three patients were included in the study group and 2015 in the control group. The incidence of HRD was 3.29/100 000, and the prevalence of HRD was 40.5/100 000 persons. The tendency of study group to have more cataract, cystoid macula oedema (CME) as compared with the control group. Among the subgroup with comorbidities, the relating factors such as hypertension, diabetes and chronic kidney disease was significantly higher among HRD patients with age 55 and above. Conclusions 74% of the diagnosed HRD are retinitis pigmentosa. Population-based data suggested an increased incidence of cataract in younger patients, whereas older HRD patients are more susceptible to develop CME. Further work is needed to elucidate the mechanism between these ophthalmological disorders and HRD.
C1 [Woon, Peng Yeong; Chou, Yu-Yau; Huang, Shun-Ping] Tzu Chi Univ, Dept Mol Biol & Human Genet, Hualien, Taiwan.
[Chien, Jia-Ying; Huang, Shun-Ping] Tzu Chi Univ, Inst Med Sci, Hualien, Taiwan.
[Wang, Jen-Hung] Hualien Tzu Chi Med Ctr, Dept Med Res, Hualien, Taiwan.
[Lin, Mei-Chen] China Med Univ, Coll Med, Taichung, Taiwan.
[Lin, Mei-Chen] China Med Univ Hosp, Management Off Hlth Data, Taichung, Taiwan.
[Huang, Shun-Ping] Taichung Tzu Chi Hosp, Dept Ophthalmol, Taichung, Taiwan.
C3 Tzu Chi University; Tzu Chi University; Buddhist Tzu Chi General
Hospital; China Medical University Taiwan; China Medical University
Taiwan; China Medical University Hospital - Taiwan; Buddhist Tzu Chi
General Hospital; Taichung Tzu Chi Hospital
RP Huang, SP (corresponding author), Tzu Chi Univ, Dept Mol Biol & Human Genet, Hualien, Taiwan.; Huang, SP (corresponding author), Tzu Chi Univ, Inst Med Sci, Hualien, Taiwan.; Huang, SP (corresponding author), Taichung Tzu Chi Hosp, Dept Ophthalmol, Taichung, Taiwan.
EM sphophdoc1688@gms.tcu.edu.tw
RI Huang, SP/ITU-1519-2023
OI Chien, Jia-Ying/0000-0001-8631-0832; Chien,
Jia-Ying/0009-0006-8732-2097; zhou, yu yao/0000-0001-9030-2173; Chien,
Jia-Ying/0000-0002-3438-9435
FU Tzu Chi Medical Foundation; Tzu Chi University To: S-PH [TCAS-107-02];
Taiwan Ministry of Health and Welfare Clinical Trial Center
[MOHW109-TDU-B-212-114004]; MOST Clinical Trial Consortium for Stroke
[MOST 109-2321-B-039-002]; Tseng-Lien Lin Foundation, Taichung, Taiwan
FX This study was supported in part by Collaborative Grant by Tzu Chi
Medical Foundation and Tzu Chi University To: S-PH TCAS-107-02, Taiwan
Ministry of Health and Welfare Clinical Trial Center
(MOHW109-TDU-B-212-114004), MOST Clinical Trial Consortium for Stroke
(MOST 109-2321-B-039-002), Tseng-Lien Lin Foundation, Taichung, Taiwan.
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PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 2044-6055
J9 BMJ OPEN
JI BMJ Open
PD APR
PY 2022
VL 12
IS 4
AR e054111
DI 10.1136/bmjopen-2021-054111
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 0L1PM
UT WOS:000781254200019
PM 35396285
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Newman, RG
Ross, DB
Barreras, H
Herretes, S
Podack, ER
Komanduri, KV
Perez, VL
Levy, RB
AF Newman, Robert G.
Ross, Duncan B.
Barreras, Henry
Herretes, Samantha
Podack, Eckhard R.
Komanduri, Krishna V.
Perez, Victor L.
Levy, Robert B.
TI The allure and peril of hematopoietic stem cell transplantation:
overcoming immune challenges to improve success
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Allogeneic HSCT; Autologous HSCT; GVHD; Cyclophosphamide; gp96; IL-2
complex
ID VERSUS-HOST-DISEASE; BONE-MARROW-TRANSPLANTATION; HEAT-SHOCK PROTEINS;
HIGH-DOSE CYCLOPHOSPHAMIDE; MINIMAL RESIDUAL DISEASE; CYTOTOXIC
T-LYMPHOCYTES; CUTTING EDGE; SELECTIVE STIMULATION; VACCINE THERAPY;
DENDRITIC CELLS
AB Since its inception in the mid-twentieth century, the complication limiting the application and utility of allogeneic hematopoietic stem cell transplantation (allo-HSCT) to treat patients with hematopoietic cancer is the development of graft-versus-host disease (GVHD). Ironically, GVHD is induced by the cells (T lymphocytes) transplanted for the purpose of eliminating the malignancy. Damage ensuing to multiple tissues, e.g., skin, GI, liver, and others including the eye, provides the challenge of regulating systemic and organ-specific GVH responses. Because the immune system is also targeted by GVHD, this both: (a) impairs reconstitution of immunity post-transplant resulting in patient susceptibility to lethal infection and (b) markedly diminishes the individual's capacity to generate anti-cancer immunity-the raison d'etre for undergoing allo-HSCT. We hypothesize that deleting alloreactive T cells ex vivo using a new strategy involving antigen stimulation and alkylation will prevent systemic GVHD thereby providing a platform for the generation of anti-tumor immunity. Relapse also remains the major complication following autologous HSCT (auto-HSCT). While GVHD does not complicate auto-HSCT, its absence removes significant grant anti-tumor responses (GVL) and raises the challenge of generating rapid and effective anti-tumor immunity early post-transplant prior to immune reconstitution. We hypothesize that effective vaccine usage to stimulate tumor-specific T cells followed by their amplification using targeted IL-2 can be effective in both the autologous and allogeneic HSCT setting. Lastly, our findings support the notion that the ocular compartment can be locally targeted to regulate visual complications of GVHD which may involve both alloreactive and self-reactive (i.e., autoimmune) responses.
C1 [Newman, Robert G.; Ross, Duncan B.; Barreras, Henry; Podack, Eckhard R.; Levy, Robert B.] Univ Miami, Dept Microbiol & Immunol, Miller Sch Med, Miami, FL 33131 USA.
[Herretes, Samantha; Perez, Victor L.; Levy, Robert B.] Univ Miami, Dept Ophthalmol, Miller Sch Med, Miami, FL 33131 USA.
[Komanduri, Krishna V.; Levy, Robert B.] Univ Miami, Dept Med, Miller Sch Med, Miami, FL 33131 USA.
C3 University of Miami; University of Miami; University of Miami
RP Levy, RB (corresponding author), Univ Miami, Dept Microbiol & Immunol, Miller Sch Med, Miami, FL 33131 USA.
EM rlevy@med.miami.edu
RI Perez, Victor/AAY-8633-2020
FU Sylvester Comprehensive Cancer Center; Sheila and David Fuente Graduate
Program in Cancer Biology; National Institutes of Health [R01CA120776,
R01AI046689]
FX We thankfully acknowledge the support of the Sylvester Comprehensive
Cancer Center and the Sheila and David Fuente Graduate Program in Cancer
Biology. The authors also thank the Sylvester Comprehensive Cancer
Center for their continuous support as well as the Flow Cytometry
Facility. We also wish to gratefully acknowledge the excellent studies
performed by many of our departmental colleagues as well as our
collaborators, Drs. Sudipto Ganguly and Leo Luznik at Johns Hopkins
University. The work was supported by Grants from the National
Institutes of Health (R01CA120776 and R01AI046689) (R.B.L.).
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NR 98
TC 11
Z9 15
U1 0
U2 6
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD DEC
PY 2013
VL 57
IS 1-3
SI SI
BP 125
EP 139
DI 10.1007/s12026-013-8450-7
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 269RK
UT WOS:000328259400014
PM 24272856
OA Green Submitted, Green Accepted
DA 2025-01-07
ER
PT J
AU Mollinedo, F
Gajate, C
AF Mollinedo, Faustino
Gajate, Consuelo
TI Fas/CD95 death receptor and lipid rafts: New targets for
apoptosis-directed cancer therapy
SO DRUG RESISTANCE UPDATES
LA English
DT Review
DE Fas/CD95; FasL-independent Fas activation; lipid rafts : apoptosis :
cancer chemotherapy : antitumor drugs : edelfosine
ID DRUG-INDUCED APOPTOSIS; FAS-MEDIATED APOPTOSIS; CELL-SURFACE ANTIGEN;
NH2-TERMINAL KINASE ACTIVATION; LIGAND-INDEPENDENT ACTIVATION;
PROTEIN-TYROSINE-PHOSPHATASE; INHIBITORY MOLECULE FAIM; NF-KAPPA-B;
C-JUN; ET-18-OCH3 EDELFOSINE
AB The development of new drugs able to directly activate the apoptotic machinery in tumors is a promising approach in the treatment of cancer as it is independent of sensors and checkpoints. which are frequently mutated in cancer hampering current anti-proliferative chemotherapy. The Fas death receptor (CD95 or APO-1) conveys apoptotic signals through binding to its cognate ligand. FasL (CD95L). Unfortunately, the putative clinical antitumor action of FasL cannot be realized because of severe liver toxicity due to the high presence of Fas in hepatocytes. However, recent evidence for FasL-independent activation of Fas Suggests that the death receptor can also be activated intracellularly. in the absence of its ligand. Unraveling the mechanisms that underlie the intracellular activation of Fas call provide the basis for novel therapeutic strategies and for the development of new compounds able to exploit cytoplasmic triggers of apoptosis. This is of importance in apoptosis deficient disorders such as cancer and autoimmune diseases. Fas-mediated apoptosis involves translocation of Fas - and downstream signaling molecules - into lipid rafts, a process that call be pharmacologically modulated. FasL-independent clustering of Fas in membrane rafts generates high local concentrations of death receptor providing scaffolds for coupling adaptor and effector proteins involved in Fas-mediated apoptosis. Thus, lipid rafts act as the linchpin from which a potent death Signal is launched. becoming a new promising anticancer target. These findings set a novel framework for the development of more targeted therapies leading to intracellular Fas activation and recruitment of downstream signaling molecules into Fas-enriched lipid rafts. (c) 2006 Elsevier Ltd. All rights reserved.
C1 Univ Salamanca, Ctr Invest Canc, Inst Biol Mol & Celular Canc, CSIC, E-37007 Salamanca, Spain.
Univ Salamanca, Unidad Invest, Hosp Univ Salamanca, E-37007 Salamanca, Spain.
C3 Consejo Superior de Investigaciones Cientificas (CSIC); CSIC - Centro de
Investigacion del Cancer (CIC); CSIC-USAL - Instituto de Biologia
Molecular y Celular del Cancer de Salamanca (IBMCC); University of
Salamanca; University of Salamanca
RP Mollinedo, F (corresponding author), Univ Salamanca, Ctr Invest Canc, Inst Biol Mol & Celular Canc, CSIC, Campus Miguel Unamuno, E-37007 Salamanca, Spain.
EM fmollin@usal.es
RI Mollinedo, Faustino/M-9024-2016
OI Gajate, Consuelo/0000-0003-0604-6459
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NR 173
TC 125
Z9 140
U1 0
U2 14
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1368-7646
EI 1532-2084
J9 DRUG RESIST UPDATE
JI Drug Resist. Update
PD FEB-APR
PY 2006
VL 9
IS 1-2
BP 51
EP 73
DI 10.1016/j.drup.2006.04.002
PG 23
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 064YF
UT WOS:000239125900005
PM 16687251
DA 2025-01-07
ER
PT J
AU Groth, C
Wupper, S
Gnouamozi, GE
Böttcher, K
Cerwenka, A
AF Groth, Christopher
Wupper, Svea
Gnouamozi, Gnimah Eva
Boettcher, Katrin
Cerwenka, Adelheid
TI Intrinsic Immune Response of HBV/HDV-Infected Cells and Corresponding
Innate (Like) Immune Cell Activation
SO LIVERS
LA English
DT Review
DE hepatitis virus; HBV; HDV; innate immunity; NK cells; gamma delta T
cells; NKT cells; MAIT cells
ID HEPATITIS-B-VIRUS; NATURAL-KILLER-CELLS; COLONY-STIMULATING FACTOR;
AUTOIMMUNE LIVER-DISEASE; CD56(BRIGHT) NK CELLS; DELTA T-CELLS;
LYMPHOID-CELLS; DENDRITIC CELLS; PERIPHERAL-BLOOD; HEPARAN-SULFATE
AB Infection of hepatitis B (HBV) patients with hepatitis D (HDV) can cause the most severe form of viral hepatitis, leading to liver fibrosis, liver failure, and hepatocellular carcinoma. HDV relies on simultaneous infection with HBV for the generation of infectious viral particles. The innate immune response, which is weakly induced in HBV infection, becomes strongly activated upon HDV co-infection. In HBV/HDV co-infection, the immune system comprises a cell-intrinsic strong IFN response, which leads to the induction of interferon-stimulated genes (ISGs), the local activation of liver-resident innate immune cells, and additional immune cell recruitment from the blood. Efficient innate immune responses are indispensable for successful viral control and spontaneous viral clearance. Despite this fact, innate immune cell activation can also contribute to adaptive immune cell inhibition and accelerate liver damage in HBV/HDV infection. While the intrinsic IFN response in HDV-infected cells is well characterized, far less is known about the cellular innate immune cell compartment. In this review, we summarize HBV/HDV replication characteristics and decipher the role of innate immune cell subsets in the anti-viral response in HBV/HDV infections. We further review the impact of epigenetic and metabolic changes in infected heptatocytes on the innate anti-viral response. Moreover, we discuss the potential of exploiting the innate immune response for improving vaccination strategies and treatment options, which is also discussed in this review.
C1 [Groth, Christopher; Wupper, Svea; Cerwenka, Adelheid] Heidelberg Univ, Mannheim Inst Innate Immunosci MI3, Med Fac Mannheim, Dept Immunobiochem, D-68167 Mannheim, Germany.
[Gnouamozi, Gnimah Eva] Univ Hosp Heidelberg, Dept Infect Dis, Mol Virol, D-69120 Heidelberg, Germany.
[Boettcher, Katrin] Tech Univ Munich, TUM Univ Hosp, Sch Med & Hlth, Clin Dept Internal Med 2, Ismaninger Str 22, D-81675 Munich, Germany.
[Cerwenka, Adelheid] Heidelberg Univ, Med Fac Mannheim, European Ctr Angiosci ECAS, D-68167 Mannheim, Germany.
RP Cerwenka, A (corresponding author), Heidelberg Univ, Mannheim Inst Innate Immunosci MI3, Med Fac Mannheim, Dept Immunobiochem, D-68167 Mannheim, Germany.; Cerwenka, A (corresponding author), Heidelberg Univ, Med Fac Mannheim, European Ctr Angiosci ECAS, D-68167 Mannheim, Germany.
EM christopher.groth@medma.uni-heidelberg.de;
gnimaheva.gnouamozi@med.uni-heidelberg.de;
adelheid.cerwenka@medma.uni-heidelberg.de
FU German Research Foundation; German Cancer Aid translational oncology
program "NK fit against AML [74114180]; [TRR179]; [272983813];
[TP07]; [TP06/TP25]; [TP15]; [SFB1366]; [394046768-SFB 1366]; [SPP
1937 (CE 140/2-2)]; [SFB-TRR156 (B10N)]; [RTG2727-445549683 (B1.2)];
[RTG 2099]; [259332240-RTG2099]; [ExU 6.1.11]
FX The project was supported by the German Research Foundation: TRR179
(Project No. 272983813; TP07 to A.C., TP06/TP25 to K.B., TP15 to
G.E.G.), SFB1366 (Project No. 394046768-SFB 1366; C02 to A.C.), SPP 1937
(CE 140/2-2 to A.C.), SFB-TRR156 (B10N to A.C.), RTG2727-445549683 (B1.2
to A.C.), RTG 2099 (Project No. 259332240-RTG2099; P9 to A.C.), and ExU
6.1.11 (to A.C.), and by the German Cancer Aid translational oncology
program "NK fit against AML" (74114180) (to A.C.).
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NR 273
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2673-4389
J9 LIVERS-BASEL
JI Livers
PD DEC
PY 2024
VL 4
IS 4
BP 562
EP 593
DI 10.3390/livers4040040
PG 32
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA Q7T2R
UT WOS:001386648500001
OA gold
DA 2025-01-07
ER
PT J
AU Ioannidis, M
Cerundolo, V
Salio, M
AF Ioannidis, Melina
Cerundolo, Vincenzo
Salio, Mariolina
TI The Immune Modulating Properties of Mucosal-Associated Invariant T Cells
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE MAIT cells; TCR-dependent; TCR-independent; dendritic cell maturation;
inflammation; tissue repair
ID HUMAN MAIT CELLS; NKT CELLS; IN-VIVO; ANTIGEN PRESENTATION; RECEPTOR
HETEROGENEITY; DENDRITIC CELLS; TISSUE-REPAIR; LIVER-DISEASE;
ACTIVATION; TCR
AB Mucosal-associated invariant T (MAIT) cells are unconventional T lymphocytes that express a semi-invariant T cell receptor (TCR) recognizing microbial vitamin B metabolites presented by the highly conserved major histocompatibility complex (MHC) class I like molecule, MR1. The vitamin B metabolites are produced by several commensal and pathogenic bacteria and yeast, but not viruses. Nevertheless, viral infections can trigger MAIT cell activation in a TCR-independent manner, through the release of pro-inflammatory cytokines by antigen-presenting cells (APCs). MAIT cells belong to the innate like T family of cells with a memory phenotype, which allows them to rapidly release Interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and in some circumstances Interleukin (IL)-17 and IL-10, exerting an immunomodulatory role on the ensuing immune response, akin to iNKT cells and gamma delta T cells. Recent studies implicate MAIT cells in a variety of inflammatory, autoimmune diseases, and in cancer. In addition, through the analysis of the transcriptome of MAIT cells activated in different experimental conditions, an important function in tissue repair and control of immune homeostasis has emerged, shared with other innate-like T cells. In this review, we discuss these recent findings, focussing on the understanding of the molecular mechanisms underpinning MAIT cell activation and effector function in health and disease, which ultimately will aid in clinically harnessing this unique, not donor-restricted cell subtype.
C1 [Ioannidis, Melina; Cerundolo, Vincenzo; Salio, Mariolina] Univ Oxford, Med Res Council, Weatherall Inst Mol Med, Human Immunol Unit, Oxford, England.
C3 UK Research & Innovation (UKRI); Medical Research Council UK (MRC);
University of Oxford
RP Salio, M (corresponding author), Univ Oxford, Med Res Council, Weatherall Inst Mol Med, Human Immunol Unit, Oxford, England.
EM mariolina.salio@imm.ox.ac.uk
OI Ioannidis, Melina/0000-0001-7142-428X
FU Cancer Research UK [C399/A2291]; Medical Research Council (MRC Human
Immunology Unit Core funding); MRC [MR/K021222/1] Funding Source: UKRI
FX This work was supported by Cancer Research UK (Programme Grant
C399/A2291 to VC) and the Medical Research Council (MRC Human Immunology
Unit Core funding).
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NR 111
TC 30
Z9 35
U1 0
U2 12
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD AUG 13
PY 2020
VL 11
AR 1556
DI 10.3389/fimmu.2020.01556
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA NJ3YF
UT WOS:000565982300001
PM 32903532
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Uraz, S
Aygun, C
Sonsuz, A
Ozbay, G
AF Uraz, S
Aygun, C
Sonsuz, A
Ozbay, G
TI Serum iron levels and hepatic iron overload in nonalcoholic
steatohepatitis and chronic viral hepatitis
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE nonalcoholic steatohepatitis; serum iron levels; hepatic iron overload
ID HEMOCHROMATOSIS GENE-MUTATIONS; FATTY LIVER-DISEASE; HFE GENE;
HEPATOCELLULAR-CARCINOMA; INSULIN-RESISTANCE; NATURAL-HISTORY; FIBROSIS;
ASSOCIATION; PREVALENCE; POPULATION
AB Our objective was to determine the effect of serum iron levels and hepatic iron overload on hepatocellular damage in nonalcoholic steatohepatitis (NASH) and to compare this with chronic viral hepatitis. Twenty-five patients who had elevated transaminase levels on at least two occasions, without any evidence of viral and autoimmune hepatitis and diabetes, without a history of significant alcohol use, and with a liver biopsy consistent with NASH were enrolled in the study. Twenty-five patients with chronic viral hepatitis (13 patients with chronic hepatitis C and 12 with chronic hepatitis B) who were not under any antiviral treatment were taken as controls. Metabolic factors were studied in the NASH and chronic hepatitis groups. Biopsy specimens were stained with hematoxylin-eosin, and the grade of steatosis and the stage of fibrosis were evaluated as I, II, or III, I being mild and III being severe. Iron overload in the hepatic tissue was studied by Prussian blue staining. Serum ALT, AST, ALP, GGT, globulin, and ferritin levels were comparable in both steatohepatitis and chronic viral hepatitis groups. However, patients with chronic hepatitis had a lower albumin level and a higher serum iron level, with higher transferrin saturation. Among patients with NASH, mild, moderate, and severe steatosis was found in 7, 10, and 8 patients, respectively. Inflammatory infiltration was grade I in 24 patients and grade III in 1 patient. Fibrosis was mild in 12 patients and 13 patients had no fibrosis. Among patients with chronic viral hepatitis, inflammatory infiltration of grade I was seen in 11 patients, grade II in 11 patients, and grade III in 3 patients. Fibrosis was mild in 9 patients, moderate in 13 patients, and severe in 2 patients; 1 patient had no fibrosis. Compared to patients with NASH, those with chronic viral hepatitis cases had more severe inflammatory infiltration and fibrosis (P < 0.01). While five patients with chronic viral hepatitis had mild iron overload, patients with NASH had no hepatic paranchymal iron overload. Neither NASH nor chronic viral hepatitis revealed a relationship between hepatic iron overload and disease activity. This suggests that the iron overload actually may be a result of hemachromatosis gene mutation. The absence of hepatic parenchymal iron overload in the NASH group and only mild iron accumulation in the chronic hepatitis group may be explained by a lower frequency of the gene mutation in our country.
C1 Kocaeli Univ Hosp, Dept Internal Med & Gastroenterol, Kocaeli, Turkey.
Istanbul Univ, Cerrahpasa Med Fac, Dept Internal Med, Istanbul, Turkey.
Istanbul Univ, Cerrahpasa Med Fac, Div Gastroenterol, Istanbul, Turkey.
Istanbul Univ, Cerrahpasa Med Fac, Dept Pathol, Istanbul, Turkey.
C3 Kocaeli University; Istanbul University; Istanbul University -
Cerrahpasa; Istanbul University; Istanbul University - Cerrahpasa;
Istanbul University; Istanbul University - Cerrahpasa
RP Uraz, S (corresponding author), Kocaeli Univ, Fac Med, Dept Gastroenterol, Ibni Sina Mah Fatih Cad 75, TR-41900 Derince, Kocaeli, Turkey.
RI Uraz, Suleyman/ABF-5624-2020; Sonsuz, Abdullah/U-2295-2018
OI Sonsuz, Abdullah/0000-0002-8336-5472
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NR 31
TC 14
Z9 16
U1 0
U2 10
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD MAY
PY 2005
VL 50
IS 5
BP 964
EP 969
DI 10.1007/s10620-005-2672-z
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 923AB
UT WOS:000228879900029
PM 15906776
DA 2025-01-07
ER
PT J
AU Wei, YQ
He, W
Sun, W
Wu, CJ
Ren, DH
Wang, XM
Zhang, MS
Huang, M
Ji, NF
AF Wei, Yanqiu
He, Wei
Sun, Wei
Wu, Chaojie
Ren, Denghua
Wang, Xinmin
Zhang, Mingshun
Huang, Mao
Ji, Ningfei
TI Hemophagocytic lymphohistiocytosis in two patients following treatment
with pembrolizumab: two case reports and a literature review
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Review
DE Hemophagocytic lymphohistiocytosis (HLH); pembrolizumab; predisposing
factors; immune checkpoint inhibitors (ICIs); case report
ID SECONDARY
AB Background: Hemophagocytic lymphohistiocytosis (HLH) is a rare and life-threatening state of immune hyperactivation. It has the highest mortality rate among all hematological immune-related adverse events (irAEs) of immune checkpoint inhibitors (ICIs) when treating various cancers. However, the predisposing factors of HLH have rarely been mentioned in previous research. Case Description: Herein, we report 2 cases of HLH following treatment with pembrolizumab. A patient was diagnosed with thymic carcinoma (TC) and possible Sjogren's syndrome (SS), while another was diagnosed with non-small cell lung cancer (NSCLC) and Epstein-Barr virus (EBV) infection, and both were positive for antinuclear antibodies. Both cases experienced transient immune-related fever on day 7 after pembrolizumab administration and splenomegaly on day 10. Then recurrent high-grade fever appeared, and liver function impairment, highly elevated ferritin, and hypertriglyceridemia were tested. After the diagnosis of HLH, both patients were treated with dexamethasone and etoposide without relapse in our follow-up. Conclusions: Considering the widespread use of ICIs and the high mortality rate of HLH, the immune related fever, splenomegaly, and other signs of hyperinflammation after the infusion of ICIs, are worthy of attention to the presence of HLH. Preexisting autoimmune diseases (ADs) or positive antibodies, concomitant infection, and the setting of thymic epithelial tumors (TET) may be predisposing factors for HLH. And increased caution is needed before the initiation of ICIs for patients with 2 or more predisposing factors.
C1 [Wei, Yanqiu; He, Wei; Wu, Chaojie; Huang, Mao; Ji, Ningfei] Nanjing Med Univ, Affiliated Hosp 1, Dept Resp & Crit Care Med, Nanjing 210029, Peoples R China.
[Sun, Wei; Ren, Denghua] Xishan Peoples Hosp Wuxi City, Dept Resp & Crit Care Med, Wuxi, Jiangsu, Peoples R China.
[Wang, Xinmin] Shuyang Hosp Tradit Chinese Med, Dept Resp & Crit Care Med, Suqian, Peoples R China.
[Zhang, Mingshun] Nanjing Med Univ, Dept Immunol, NHC Key Lab Antibody Tech, Nanjing, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University
RP Huang, M; Ji, NF (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Dept Resp & Crit Care Med, Nanjing 210029, Peoples R China.
EM hm6114@163.com; jiningfei@163.com
RI 王, 新/HHS-1436-2022
FU National Natural Science Foundation of China [81770031, 81970031];
Natural Science Foundation of Jiangsu Province [BK20181497]; Key
Research and Development Project of Jiangsu Province [BE2020616];
General Projects of Jiangsu Province Commission of Health [M2020069]
FX This work was supported by the National Natural Science Foundation of
China (Nos. 81770031, 81970031), the Natural Science Foundation of
Jiangsu Province (No. BK20181497), the Key Research and Development
Project of Jiangsu Province (No. BE2020616), and the General Projects of
Jiangsu Province Commission of Health (No. M2020069).
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NR 25
TC 7
Z9 8
U1 0
U2 3
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD AUG
PY 2022
VL 11
IS 8
BP 2960
EP 2966
DI 10.21037/tcr-22-154
EA MAY 2022
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5F7ZA
UT WOS:000803247600001
PM 36093533
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Ma, SC
Ming, YN
Wu, JX
Cui, GL
AF Ma, Sicong
Ming, Yanan
Wu, Jingxia
Cui, Guoliang
TI Cellular metabolism regulates the differentiation and function of T-cell
subsets
SO CELLULAR & MOLECULAR IMMUNOLOGY
LA English
DT Review
DE Metabolism; Immunometabolism; T cell differentiation; CD4+T cells; CD8+T
cells
ID PROLIFERATOR-ACTIVATED RECEPTOR; HMG-COA REDUCTASE; LIVER X RECEPTOR;
ELEMENT-BINDING PROTEINS; OVARIAN-CANCER CELLS; FATTY-ACID SYNTHESIS;
GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; PYRUVATE-DEHYDROGENASE;
MESSENGER-RNA; EFFECTOR FUNCTION
AB T cells are an important component of adaptive immunity and protect the host from infectious diseases and cancers. However, uncontrolled T cell immunity may cause autoimmune disorders. In both situations, antigen-specific T cells undergo clonal expansion upon the engagement and activation of antigens. Cellular metabolism is reprogrammed to meet the increase in bioenergetic and biosynthetic demands associated with effector T cell expansion. Metabolites not only serve as building blocks or energy sources to fuel cell growth and expansion but also regulate a broad spectrum of cellular signals that instruct the differentiation of multiple T cell subsets. The realm of immunometabolism research is undergoing swift advancements. Encapsulating all the recent progress within this concise review in not possible. Instead, our objective is to provide a succinct introduction to this swiftly progressing research, concentrating on the metabolic intricacies of three pivotal nutrient classes-lipids, glucose, and amino acids-in T cells. We shed light on recent investigations elucidating the roles of these three groups of metabolites in mediating the metabolic and immune functions of T cells. Moreover, we delve into the prospect of "editing" metabolic pathways within T cells using pharmacological or genetic approaches, with the aim of synergizing this approach with existing immunotherapies and enhancing the efficacy of antitumor and antiinfection immune responses.
C1 [Ma, Sicong; Ming, Yanan; Wu, Jingxia; Cui, Guoliang] Univ Sci & Technol China, Ctr Adv Interdisciplinary Sci & Biomed IHM, Sch Basic Med Sci, Div Life Sci & Med,Key Lab Immune Response & Immun, Hefei 230601, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
China, CAS
RP Wu, JX; Cui, GL (corresponding author), Univ Sci & Technol China, Ctr Adv Interdisciplinary Sci & Biomed IHM, Sch Basic Med Sci, Div Life Sci & Med,Key Lab Immune Response & Immun, Hefei 230601, Peoples R China.
EM jingxia.wu@ihm.ac.cn; g.cui@ihm.ac.cn
RI Ming, Yanan/HZI-6563-2023; wu, Jingxia/AFR-6587-2022; Ma,
Sicong/JYP-8908-2024
OI Wu, Jingxia/0009-0001-2559-0065; Ma, Sicong/0000-0001-7569-2177
FU National Natural Science Foundation of China [82303187]; Huatuo
postdoctoral research fellowship; Institute of Health and Medicine,
Hefei Comprehensive National Science Center; CRI Lloyd J. Old STAR Award
[3914]
FX Sicong Ma is supported by the National Natural Science Foundation of
China (#82303187). Yanan Ming is supported by a Huatuo postdoctoral
research fellowship. Jingxia Wu and Guoliang Cui are supported by
funding from the Institute of Health and Medicine, Hefei Comprehensive
National Science Center. Guoliang Cui is also supported by a CRI Lloyd
J. Old STAR Award (#3914).
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NR 281
TC 12
Z9 12
U1 9
U2 14
PU CHIN SOCIETY IMMUNOLOGY
PI BEING
PA 5 DONGDAN SANTIAO, DONGCHEN DISTRICT, BEING, 100005, PEOPLES R CHINA
SN 1672-7681
EI 2042-0226
J9 CELL MOL IMMUNOL
JI Cell. Mol. Immunol.
PD MAY
PY 2024
VL 21
IS 5
BP 419
EP 435
DI 10.1038/s41423-024-01148-8
EA APR 2024
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA OY4J1
UT WOS:001195297100001
PM 38565887
OA hybrid
DA 2025-01-07
ER
PT J
AU Karabasz, A
Lachowicz, D
Karewicz, A
Mezyk-Kopec, R
Stalinska, K
Werner, E
Cierniak, A
Dyduch, G
Bereta, J
Bzowska, M
AF Karabasz, Alicja
Lachowicz, Dorota
Karewicz, Anna
Mezyk-Kopec, Renata
Stalinska, Krystyna
Werner, Ewa
Cierniak, Agnieszka
Dyduch, Grzegorz
Bereta, Joanna
Bzowska, Monika
TI Analysis of toxicity and anticancer activity of micelles of sodium
alginate-curcumin
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE curcumin; alginate conjugates; in vivo toxicity; antitumor activity
ID POLYMERIC MICELLES; HYALURONIC-ACID; CANCER; AUTOIMMUNE; INHIBITION;
STABILITY; THERAPY; DISEASE; AGENT; CELLS
AB Background: Curcumin is a natural polyphenol with anti-inflammatory, chemopreventive and anticancer activity. However, its high hydrophobicity and poor bioavailability limit its medical application. The development of nanocarriers for curcumin delivery is an attractive approach to overcome its low bioavailability and fast metabolism in the liver. We synthesized a blood compatible alginate-curcumin conjugate, AA-Cur, which formed colloidally stable micelles of approximately 200 nm and, as previously shown, exerted strong cytotoxicity against mouse cancer cell lines. Here we analyze in vivo toxicity and antitumor activity of AA-Cur in two different mouse tumor models.
Method: Potential toxicity of intravenously injected AA-Cur was evaluated by: i) analyses of blood parameters (morphology and biochemistry), ii) histology, iii) DNA integrity (comet assay), and iv) cytokine profiling (flow cytometry). Antitumor activity of AA-Cur was evaluated by measuring the growth of subcutaneously inoculated colon MC38-CEA- or orthotopically injected breast 4T1 tumor cells in control mice vs mice treated with AA-Cur.
Results: Injections of four doses of AA-Cur did not reveal any toxicity of the conjugate, thus indicating the safety of its use. AA-Cur elicited moderate anti-tumor activity toward colon MC38-CEA or breast 4T1 carcinomas.
Conclusion: The tested conjugate of alginate and curcumin, AA-Cur, is non-toxic and safe, but exhibits limited anticancer activity.
C1 [Karabasz, Alicja; Mezyk-Kopec, Renata; Stalinska, Krystyna; Bereta, Joanna; Bzowska, Monika] Jagiellonian Univ, Fac Biochem Biophys & Biotechnol, Dept Cell Biochem, 7 Gronostajowa St, PL-30387 Krakow, Poland.
[Lachowicz, Dorota] AGH Univ Sci & Technol, Acad Ctr Mat & Nanotechnol, Krakow, Poland.
[Karewicz, Anna] Jagiellonian Univ, Fac Chem, Krakow, Poland.
[Werner, Ewa] Jagiellonian Univ, Fac Biochem Biophys & Biotechnol, Dept Med Biotechnol, Krakow, Poland.
[Werner, Ewa] Univ Agr, Fac Anim Sci, Dept Anim Reprod & Anat, Krakow, Poland.
[Cierniak, Agnieszka] Jagiellonian Univ, Fac Biochem Biophys & Biotechnol, Dept Gen Biochem, Krakow, Poland.
[Dyduch, Grzegorz] Jagiellonian Univ, Coll Med, Dept Pathomorphol, Krakow, Poland.
C3 Jagiellonian University; AGH University of Krakow; Jagiellonian
University; Jagiellonian University; University of Agriculture in
Krakow; Jagiellonian University; Jagiellonian University; Collegium
Medicum Jagiellonian University
RP Bzowska, M (corresponding author), Jagiellonian Univ, Fac Biochem Biophys & Biotechnol, Dept Cell Biochem, 7 Gronostajowa St, PL-30387 Krakow, Poland.
EM monika.bzowska@uj.edu.pl
RI Monika, Bzowska/KYQ-0424-2024; Cierniak, Agnieszka/O-3139-2019;
Karewicz, Anna/IAS-0588-2023; Hinz, Alicja/IAN-4434-2023; Lachowicz,
Dorota/AAV-9221-2020; Cierniak, Agnieszka/M-1757-2018
OI Mezyk-Kopec, Renata/0000-0002-0239-0589; Cierniak,
Agnieszka/0000-0001-6537-2954; Hinz, Alicja/0000-0001-8781-8427; Bereta,
Joanna/0000-0001-7930-2770; Bzowska, Monika/0000-0003-1921-0334;
Karewicz, Anna/0000-0001-9769-6240; Werner, Ewa/0000-0003-4316-1683;
Stalinska, Krystyna/0000-0002-6258-6110; Lachowicz,
Dorota/0000-0001-9394-5297
FU Faculty of Biochemistry, Biophysics and Biotechnology of the
Jagiellonian University in Krakow [35p/4/2016, BMN 9/2018]; Polish
Ministry of Science and Higher Education
FX This work was supported by the Grant for employees over 35 - "Program
35+" no. 35p/4/2016 to MB and The Grant for Young Researchers no. BMN
9/2018 to AK funded by the Faculty of Biochemistry, Biophysics and
Biotechnology of the Jagiellonian University in Krakow. The Faculty of
Biochemistry, Biophysics and Biotechnology of the Jagiellonian
University in Krakow was partner of the Leading National Research Center
(KNOW) supported by the Polish Ministry of Science and Higher Education.
Agnieszka Cierniak's present affiliation is now the Department of
Biochemistry, Faculty of Medicine and Health Sciences, Andrzej Frycz
Modrzewski Krakow University, Krakow, Poland.
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NR 55
TC 21
Z9 21
U1 2
U2 23
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2019
VL 14
BP 7249
EP 7262
DI 10.2147/IJN.S213942
PG 14
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA IU9TV
UT WOS:000483924300002
PM 31564877
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Zhang, LH
Zhang, W
Chen, JL
AF Zhang, Linhu
Zhang, Wei
Chen, Jianling
TI Regulatory mechanism of immune-related genes in patients with
hypertension
SO MEDICINE
LA English
DT Article
DE cardiovascular disease; genomics; hub genes; hypertension;
immune-related
ID GROWTH-FACTOR RECEPTOR; RESISTANT HYPERTENSION; SOCS1; CANCER
AB Hypertension (HT) is among the most common cardiovascular diseases in the world and is an important risk factor for stroke, myocardial infarction, heart failure, and kidney failure. Recent studies have demonstrated that activation of the immune system plays an important role in the occurrence and maintenance of HT. Thus, this research aimed to determine the immune-related biomarkers in HT. In this study, RNA sequencing data of the gene expression profiling datasets (GSE74144) were downloaded from the Gene Expression Omnibus database. Differentially expressed genes between HT and normal samples were identified using the software limma. The immune-related genes associated with HT were screened. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using the program "clusterProfiler" of the R package. The protein-protein interaction network of these differentially expressed immune-related genes (DEIRGs) was constructed based on the information from the STRING database. Finally, the TF-hub and miRNA-hub gene regulatory networks were predicted and constructed using the miRNet software. Fifty-nine DEIRGs were observed in HT. The Gene Ontology analysis indicated that DEIRGs were mainly enriched in the positive regulation of cytosolic calcium ions, peptide hormones, protein kinase B signaling, and lymphocyte differentiation. The Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated that these DEIRGs were significantly involved in the intestinal immune network for IgA production, autoimmune thyroid disease, JAK-STAT signaling pathway, hepatocellular carcinoma, and Kaposi sarcoma-associated herpesvirus infection, among others. From the protein-protein interaction network, 5 hub genes (insulin-like growth factor 2, cytokine-inducible Src homology 2-containing protein, suppressor of cytokine signaling 1, cyclin-dependent kinase inhibitor 2A, and epidermal growth factor receptor) were identified. The receiver operating characteristic curve analysis was performed in GSE74144, and all genes with an area under the curve of > 0.7 were identified as the diagnostic genes. Moreover, miRNA-mRNA and TF-mRNA regulatory networks were constructed. Our study identified 5 immune-related hub genes in patients with HT and demonstrated that they were potential diagnostic biomarkers for HT.
C1 [Zhang, Linhu; Zhang, Wei; Chen, Jianling] Zunyi Med Univ, Affiliated Hosp, Dept Cardiol, Zunyi, Guizhou, Peoples R China.
[Chen, Jianling] Zunyi Med Univ, Affiliated Hosp, Dept Cardiol, Zunyi 563000, Guizhou, Peoples R China.
C3 Zunyi Medical University; Zunyi Medical University
RP Chen, JL (corresponding author), Zunyi Med Univ, Affiliated Hosp, Dept Cardiol, Zunyi 563000, Guizhou, Peoples R China.
EM 22549697@qq.com; 22549697@qq.com; 2871766504@qq.com
RI Wei, Zhang/JSK-6014-2023
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NR 34
TC 0
Z9 0
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD MAR 3
PY 2023
VL 102
IS 9
DI 10.1097/MD.0000000000032627
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 9M7IZ
UT WOS:000942400000027
PM 36862882
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Huang, HK
Chen, HY
Hsu, YC
AF Huang, Hsu-Kai
Chen, Hung-Yu
Hsu, Yin-Chou
TI Comparing the Prognosis of Patient with Alcohol and
Nonalcohol-Associated Cirrhosis with Bacteremia
SO ALCOHOL AND ALCOHOLISM
LA English
DT Article
ID SHORT-TERM PROGNOSIS; HEPATOCELLULAR-CARCINOMA; BACTERIAL-INFECTIONS;
AUTOIMMUNE HEPATITIS; LIVER-CIRRHOSIS; RISK; EPIDEMIOLOGY; SEPSIS; MODEL
AB Aims: Patients with liver cirrhosis are more susceptible to bacteremia and more likely to have a poor prognosis in comparison to healthy individuals. Studies on the role of alcohol in cirrhotic patients with bacteremia are limited. Our study aimed to investigate the clinical characteristics and prognostic differences between the patients with alcohol and non-alcohol-associated cirrhosis with bacteremia.
Methods: A single-center, retrospective cohort study was conducted among adult patients who presented to the emergency department from January 2015 to December 2018. All patients diagnosed with liver cirrhosis and bacteremia were enrolled and divided into alcohol-associated and non-alcohol-associated groups according to the etiology of their cirrhosis. We compared their clinical characteristics, laboratory results, microbiological data, and infection source as well as outcome measurements between the two groups.
Results: A total of 112 cirrhotic patients with bacteremia (alcohol-associated: 67; non-alcohol-associated: 45) were eligible for this study. In comparison with the non-alcohol-associated group, patients in the alcohol-associated group had a significantly higher rate of intensive care unit transfer (41.8% vs. 22.2%, P = 0.04), septic shock occurrence (56.7% vs. 35.6%, P = 0.04) and 30-day mortality risk (37.3% vs. 15.6%, P = 0.02). Moreover, alcohol-associated cirrhosis and Model for End-Stage Liver Disease score were independent predictors of 30-day mortality in cirrhotic patients with bacteremia.
Conclusions: The etiology of liver cirrhosis influences the outcomes of patients with bacteremia as well as the severity of their cirrhosis.
C1 [Huang, Hsu-Kai; Chen, Hung-Yu; Hsu, Yin-Chou] I Shou Univ, E Da Hosp, Dept Emergency Med, 1 Yida Rd, Kaohsiung 82445, Taiwan.
[Hsu, Yin-Chou] I Shou Univ, Coll Med, Sch Med, 8 Yida Rd, Kaohsiung 82445, Taiwan.
C3 E-Da Hospital; I Shou University; I Shou University
RP Hsu, YC (corresponding author), I Shou Univ, E Da Hosp, Dept Emergency Med, 1 Yida Rd, Kaohsiung 82445, Taiwan.
EM yinchou0406@gmail.com
OI Hsu, YinChou/0000-0001-5334-6484
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NR 34
TC 6
Z9 6
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0735-0414
EI 1464-3502
J9 ALCOHOL ALCOHOLISM
JI Alcohol Alcohol.
PD SEP
PY 2020
VL 55
IS 5
BP 512
EP 517
DI 10.1093/alcalc/agaa057
PG 6
WC Substance Abuse
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Substance Abuse
GA OF1JG
UT WOS:000580972700006
PM 32599621
DA 2025-01-07
ER
PT J
AU Chi, KW
Liu, SD
Li, CP
Kuo, HP
Wang, YS
Chao, Y
Hsieh, SL
AF Chi, KW
Liu, SD
Li, CP
Kuo, HP
Wang, YS
Chao, Y
Hsieh, SL
TI Combination of conformal radiotherapy and intratumoral injection of
adoptive dendritic cell immunotherapy in refractory hepatoma
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE hepatoma; dendritic cell; immunotherapy; conformal radiotherapy
ID CYTOTOXIC T-CELLS; HEPATOCELLULAR-CARCINOMA; GAMMA-IRRADIATION; TUMOR
VACCINES; CLASS-I; ANTIGEN; CANCER; RADIATION; VACCINATION; APOPTOSIS
AB A phase I study was conducted to assess the safety and immunologic response induced by direct injection of autologous immature dendritic cells (DCs) into tumor under radiotherapy in advanced hepatoma patients. Patients with advanced/rnetastatic stage hepatoma not suitable for surgery or transarterial embolization were enrolled. Groups of patients received two vaccinations. Each vaccination consisted of intratumoral injections of autologous immature DCs in four dose cohorts of 5 X 10(6), 1.5 X 10(7) 3 X 10(7), and 5 X 10(7) cells 2 days after a single fraction of conformal radiotherapy of 8 Gy. The second vaccination was performed 3 weeks later. Of the 14 patients entered, 12 completed two cycles of vaccination. The treatment was well tolerated at any of the dose levels. Six patients had mild transient fever (grade 1-2) with chill reactions, three patients developed grade I fatigue, and one patient developed mild myalgia and arthralgia after DC injections. There was no evidence of clinically manifested autoimmune disease. There were two partial responses and four minor responses. A decrease in the alpha-fetoprotein (AFP) level of more than 50% was found in three patients. Ten patients had completed immunologic response evaluation 2 weeks after the second cycle of vaccination. The AFP-specific immune response was evident in eight patients examined by cytokine release assay and in seven patients by ELISPOT assay. Six patients showed an increased NK cell cytotoxic activity after vaccination. These data suggest that the combination of intraturnoral injection of DCs and conformal radiotherapy is safe and can induce tumor-specific and innate immunity.
C1 Shin Kong Wu Ho Su Mem Hosp, Dept Radiat Therapy & Oncol, Taipei 111, Taiwan.
Natl Yang Ming Univ, Vet Gen Hosp, Ctr Canc, Taipei 112, Taiwan.
Anawratha Biotech Co, Taipei, Taiwan.
Natl Hlth Res Inst, Vaccine Res & Dev Ctr, Taipei, Taiwan.
Natl Yang Ming Univ, Vet Gen Hosp, Dept Internal Med, Taipei 112, Taiwan.
Natl Yang Ming Univ, Inst Microbiol & Immunol, Taipei 112, Taiwan.
C3 Shin Kong Wu Ho Su Memorial Hospital; National Yang Ming Chiao Tung
University; National Health Research Institutes - Taiwan; National Yang
Ming Chiao Tung University; National Yang Ming Chiao Tung University
RP Shin Kong Wu Ho Su Mem Hosp, Dept Radiat Therapy & Oncol, 95 Wen Chang Rd, Taipei 111, Taiwan.
EM M006565@ms.skli.org.tw
RI Liu, Shih-Jen/AAV-1931-2021; Hsieh, Shie-Liang/ABA-9184-2021
OI Liu, Shih-Jen/0000-0002-8736-1452
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NR 47
TC 147
Z9 168
U1 0
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1524-9557
EI 1537-4513
J9 J IMMUNOTHER
JI J. Immunother.
PD MAR-APR
PY 2005
VL 28
IS 2
BP 129
EP 135
DI 10.1097/01.cji.0000154248.74383.5e
PG 7
WC Oncology; Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology; Research & Experimental Medicine
GA 902YG
UT WOS:000227392000002
PM 15725956
DA 2025-01-07
ER
PT J
AU Fischer, CR
Müller, C
Reber, J
Müller, A
Krämer, SD
Ametamey, SM
Schibli, R
AF Fischer, Cindy R.
Mueller, Cristina
Reber, Josefine
Mueller, Adrienne
Kraemer, Stefanie D.
Ametamey, Simon M.
Schibli, Roger
TI [18F]Fluoro-Deoxy-Glucose Folate: A Novel PET Radiotracer
with Improved in Vivo Properties for Folate Receptor Targeting
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID TUMOR-BEARING MICE; POSITIVE TUMORS; PRECLINICAL EVALUATION; CLICK
CHEMISTRY; IMAGING AGENTS; RHEUMATOID-ARTHRITIS; MONOCLONAL-ANTIBODY;
TERMINAL ALKYNES; NORMAL-TISSUES; TC-99M-EC20
AB The folate receptor (FR) is upregulated in various cancer types (FR-alpha isoform) and in activated macrophages (FR-beta isoform) which are involved in inflammatory and autoimmune diseases, but its expression in healthy tissues and organs is highly restricted to only a few sites (e.g kidneys). Therefore, the FR is a promising target for imaging and therapy of cancer and inflammation using folate-based radiopharmaceuticals. Herein, we report the synthesis and evaluation of a novel folic acid conjugate with improved properties suitable for positron emission tomography (PET). [F-18]-fluoro-deoxy-glucose folate ([F-18]3) was synthesized based on the click chemistry approach using 2-deoxy-2-[F-18]fluoroglucopyranosyl azide and a folate alkyne derivative. The novel radiotracer [F-18]3 was produced in good radiochemical yields (25% d.c.) and high specific radioactivity (90 GBq/mu mol). Compared to previously published F-18-folic acid derivatives, an increase in hydrophilicity was achieved by using a glucose entity as a prosthetic group. Biodistribution and PET imaging studies in KB tumor-bearing mice showed a high and specific uptake of the radiotracer in FR-positive tumors (10.03 +/- 1.12%ID/g, 60 min p.i.) and kidneys (42.94 +/- 2.04%ID/g, 60 min p.i.). FR-unspecific accumulation of radioactivity was only found in the liver (9.49 +/- 1.13%ID/g, 60 min p.i.) and gallbladder (17.59 +/- 7.22%ID/g, 60 min p.i.). No radiometabolites were detected in blood, urine, and liver tissue up to 30 min after injection of [F-18]3.[F-18]-fluoro-deoxy-glucose-folate [F-18]3 is thus a promising PET radioligand for imaging FR-positive tumors.
C1 [Fischer, Cindy R.; Mueller, Adrienne; Kraemer, Stefanie D.; Ametamey, Simon M.; Schibli, Roger] ETH, PSI, Ctr Radiopharmaceut Sci, Zurich, Switzerland.
[Fischer, Cindy R.; Mueller, Adrienne; Kraemer, Stefanie D.; Ametamey, Simon M.; Schibli, Roger] ETH, Inst Pharmaceut Sci, USZ, Zurich, Switzerland.
[Mueller, Cristina; Reber, Josefine; Schibli, Roger] ETH, Ctr Radiopharmaceut Sci, PSI, CH-5232 Villigen, Switzerland.
[Mueller, Cristina; Reber, Josefine; Schibli, Roger] USZ, Villigen, Switzerland.
C3 Swiss Federal Institutes of Technology Domain; ETH Zurich; Paul Scherrer
Institute; Swiss Federal Institutes of Technology Domain; ETH Zurich;
Swiss Federal Institutes of Technology Domain; ETH Zurich; Paul Scherrer
Institute
RP Schibli, R (corresponding author), ETH Honggerberg, ETH, Ctr Radiopharmaceut Sci, PSI, Wolfgang Pauli Str 10, CH-8093 Zurich, Switzerland.
EM roger.schibli@pharma.ethz.ch
OI Reber, Josefine/0000-0003-4932-8990; Kramer, Stefanie
D./0000-0002-0426-4340; Schibli, Roger/0000-0002-1537-3833; Mueller,
Cristina/0000-0001-9357-9688
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NR 39
TC 63
Z9 72
U1 1
U2 37
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD APR
PY 2012
VL 23
IS 4
BP 805
EP 813
DI 10.1021/bc200660z
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 927BG
UT WOS:000302881300015
PM 22372827
DA 2025-01-07
ER
PT J
AU Lozano, T
Gorraiz, M
Lasarte-Cía, A
Ruiz, M
Rabal, O
Oyarzabal, J
Hervás-Stubbs, S
Llopiz, D
Sarobe, P
Prieto, J
Casares, N
Lasarte, JJ
AF Lozano, Teresa
Gorraiz, Marta
Lasarte-Cia, Aritz
Ruiz, Marta
Rabal, Obdulia
Oyarzabal, Julen
Hervas-Stubbs, Sandra
Llopiz, Diana
Sarobe, Pablo
Prieto, Jesus
Casares, Noelia
Lasarte, Juan Jose
TI Blockage of FOXP3 transcription factor dimerization and FOXP3/AML1
interaction inhibits T regulatory cell activity: sequence optimization
of a peptide inhibitor
SO ONCOTARGET
LA English
DT Article
DE Foxp3; Treg; peptide inhibitor; cancer; immunomodulation
ID TUMOR-IMMUNITY; STRUCTURE PREDICTION; SUPPRESSIVE FUNCTION; DENILEUKIN
DIFTITOX; PERIPHERAL-BLOOD; FUSION PROTEIN; AMINO-ACID; COMPLEX;
ANTIGEN; MICE
AB Although T regulatory cells (Treg) are essential for the prevention of autoimmune diseases, their immunoregulatory function restrains the induction of immune responses against cancer. Thus, development of inhibitors of FOXP3, a key transcription factor for the immunosuppressive activity of Treg, might give new therapeutic opportunities. In a previous work we identified a peptide (named P60) able to enter into the cells, bind to FOXP3, and impair Treg activity in vitro and in vivo. Here we show that P60 binds to the intermediate region of FOXP3 and inhibits its homodimerization as well as its interaction with the transcription factor AML1. Alanine-scanning of P60 revealed the relevance of each position on FOXP3 binding, homodimerization, association with AML1 and inhibition of Treg activity. Introduction of alanine at positions 2, 5 and 11 improved the activity of the original P60, whereas alanine mutations at positions 1, 7, 8, 9, 10 and 12 were detrimental. Multiple mutation experiments allowed us to identify peptides with higher FOXP3 binding affinity and stronger biological activity than the original P60. Head to tail macrocyclization of peptide P60-D2A-S5A improved Treg inhibition and enhanced anti-tumor activity of anti-PD1 antibodies in a model of hepatocellular carcinoma. Introduction of a D-aminoacid at position 2 augmented significantly microsomal stability while maintained FOXP3 binding capacity and Treg inhibition in vitro. In vivo, when combined with the cytotoxic T-cell epitope AH1, it induced protection against CT26 tumor implantation. This study provides important structure-function relationships essential for further drug design to inhibit Treg cells in cancer.
C1 [Lozano, Teresa; Gorraiz, Marta; Lasarte-Cia, Aritz; Ruiz, Marta; Hervas-Stubbs, Sandra; Llopiz, Diana; Sarobe, Pablo; Prieto, Jesus; Casares, Noelia; Lasarte, Juan Jose] Univ Navarra, Immunol & Immunotherapy Program, Pamplona 31008, Spain.
[Rabal, Obdulia; Oyarzabal, Julen] Univ Navarra, Ctr Appl Med Res CIMA, Mol Therapeut Program, Small Mol Discovery Platform, Pamplona 31008, Spain.
C3 University of Navarra; University of Navarra
RP Casares, N; Lasarte, JJ (corresponding author), Univ Navarra, Immunol & Immunotherapy Program, Pamplona 31008, Spain.
EM ncasares@unav.es; jjlasarte@unav.es
RI Llopiz, Diana Isabel/KLC-7890-2024; Sarobe, Pablo/D-6976-2017; Casares,
Noelia/HSC-2243-2023; Hervas-Stubbs, Sandra/C-9053-2018; RUIZ EGOZCUE,
MARTA/KLC-7919-2024; Lasarte, Juan J/AAN-6548-2020
OI Casares, Noelia/0000-0003-3817-6434; Lasarte-Cia,
Aritz/0000-0003-4758-7542; Hervas-Stubbs, Sandra/0000-0003-3391-1516;
RUIZ EGOZCUE, MARTA/0000-0002-8757-0932; Lasarte, Juan
J/0000-0003-1641-3881; Lozano, Teresa/0000-0001-7122-5475
FU Ministerio de Educacion y Ciencia [SAF2013-42772-R, SAF2016-78568-R];
Fundacion Ramon Areces; FPU grant (Ministerio de Educacion, Cultura y
Deporte, Spain)
FX This work was supported by grants from Ministerio de Educacion y Ciencia
(SAF2013-42772-R and SAF2016-78568-R to J.J.L.) and Fundacion Ramon
Areces. Teresa Lozano is a recipient of a FPU grant (Ministerio de
Educacion, Cultura y Deporte, Spain).
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NR 46
TC 27
Z9 29
U1 1
U2 11
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD SEP 22
PY 2017
VL 8
IS 42
BP 71709
EP 71724
DI 10.18632/oncotarget.17845
PG 16
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FH9DW
UT WOS:000411509400028
PM 29069740
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Chen, MH
Chen, MH
Tsai, CY
Chou, CT
Lin, HY
Huang, DF
Huang, YH
AF Chen, M-H
Chen, M-H
Tsai, C-Y
Chou, C-T
Lin, H-Y
Huang, D-F
Huang, Y-H
TI Incidence and antiviral response of hepatitis C virus reactivation in
lupus patients undergoing immunosuppressive therapy
SO LUPUS
LA English
DT Article
DE Systemic lupus erythematosus; HCV reactivation; immunosuppression;
interferon; virological response; late relapse
ID SUSTAINED VIROLOGICAL RESPONSE; NON-HODGKINS-LYMPHOMA; TERM-FOLLOW-UP;
HEPATOCELLULAR-CARCINOMA; B-VIRUS; PEGYLATED-INTERFERON; LIVER
DYSFUNCTION; INFECTION; RIBAVIRIN; CHEMOTHERAPY
AB Objective: Systemic lupus erythematosus (SLE) is a systemic autoimmune disease and usually requires immunosuppressive therapy, which is a major cause of viral reactivation. The incidence and antiviral response in SLE patients with hepatitis C virus (HCV) reactivation is unclear and needs to be investigated. Methods: One hundred and sixty-six SLE patients with antibody to HCV (anti-HCV) status were retrospectively reviewed regarding the events of HCV reactivation. Patients with HCV reactivation were treated with pegylated interferon plus ribavirin treatment. The virological response and relapse rate were evaluated. Results: Twenty-six patients were positive for anti-HCV. During a mean 8.4 years of follow-up, 10 (38.5%) cases developed HCV reactivation. No clear relationship was noted between immunosuppressive therapy and the HCV reactivation. Eight patients underwent antiviral therapy and the rapid virological response (RVR), early virological response, and sustained virological response (SVR) rates were 37.5%, 87.5%, and 75.0%, respectively. However, late relapse (reappearance of HCV RNA in serum after archiving SVR) was found in two (33.3%) of six patients achieving SVR. The two cases were HCV genotype 1 b concurrent with corticosteroid treatment. Conclusions: HCV reactivation in anti-HCV-positive SLE patients was possibly associated with glucocorticoids. The virological response to interferon plus ribavirin treatment is not inferior to the general population. However, monitoring HCV RNA after SVR is necessary for patients concurrent with corticosteroid treatment due to the risk of late relapse.
C1 [Chen, M-H; Tsai, C-Y; Chou, C-T; Lin, H-Y; Huang, D-F] Taipei Vet Gen Hosp, Dept Med, Div Allergy Immunol Rheumatol, Taipei 11217, Taiwan.
[Chen, M-H] Taipei Vet Gen Hosp, Dept Med, Hematol, Taipei 11217, Taiwan.
[Huang, Y-H] Taipei Vet Gen Hosp, Dept Med, Gastroenterol, Taipei 11217, Taiwan.
[Chen, M-H; Tsai, C-Y; Chou, C-T; Lin, H-Y; Huang, D-F] Natl Yang Ming Univ, Fac Med, Taipei 112, Taiwan.
[Huang, Y-H] Natl Yang Ming Univ, Inst Clin Med, Taipei 112, Taiwan.
C3 Taipei Veterans General Hospital; Taipei Veterans General Hospital;
Taipei Veterans General Hospital; National Yang Ming Chiao Tung
University; National Yang Ming Chiao Tung University
RP Huang, YH (corresponding author), Taipei Vet Gen Hosp, Dept Med, Div Gastroenterol, 201,Sect 2,Shipai Rd, Taipei 11217, Taiwan.
EM dfhuang@vghtpe.gov.tw; yhhuang@vghtpe.gov.tw
RI Huang, Yi-Hsiang/ADX-9119-2022; Chen, MuHong/ACJ-6131-2022; Tsai,
Chang-Youh/G-1747-2013; Huang, David/JTS-8033-2023
OI Huang, Yi-Hsiang/0000-0001-5241-5425
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NR 34
TC 15
Z9 16
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0961-2033
EI 1477-0962
J9 LUPUS
JI Lupus
PD SEP
PY 2015
VL 24
IS 10
BP 1029
EP 1036
DI 10.1177/0961203315571465
PG 8
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA CO8FQ
UT WOS:000359402200003
PM 25691509
DA 2025-01-07
ER
PT J
AU Ge, W
Wang, Y
Cao, YJ
Xie, M
Ding, YT
Zhang, M
Yu, DC
AF Ge, Wei
Wang, Yi
Cao, Ya-Juan
Xie, Min
Ding, Yi-Tao
Zhang, Ming
Yu, De-Cai
TI Radiological score for hemorrhage in the patients with portal
hypertension
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE Portal hypertension; radiological; hemorrhage; risk assessment; risk
factors
ID VENOUS-PRESSURE GRADIENT; MULTIDETECTOR-ROW CT; ESOPHAGEAL-VARICES;
CIRRHOTIC-PATIENTS; PHARMACOLOGICAL THERAPY; COMPUTED-TOMOGRAPHY; LIVER;
DIAGNOSIS; RISK
AB Goal: To analyze the risk factors from radiological indices for hemorrhage in the patients with portal hypertension and weight risk factors. Method: We retrospectively analyzed all cases of portal hypertension with hepatitis B from June 2008 to June 2014 in Nanjing Drum Tower hospital. Patients with hepatocellular carcinoma, portal vein thrombosis, or portal hypertension with other causes, such as autoimmune hepatitis, pancreatitis, or hematological diseases were excluded. Results: Ninety-eight patients were recruited and divided into hemorrhage and non-hemorrhage groups. There were no statistical differences in clinical indexes such as age, prothrombin time, serum albumin, serum creatinine, serum sodium, hemameba, and blood platelet count. However, the differences were statistically significant in total bilirubin, hemoglobin, and liver function with the p values of 0.023, 0.000, and 0.039 respectively. For radiological indices, hemorrhage was correlated with diameter of inferior mesenteric vein (P=0.0528), posterior gastric vein (P=0.0283), and esophageal varices scores (P=0.0221). Logistic procedure was used to construct the model with stepwise selection and finally inferior mesenteric vein, posterior gastric vein, esophageal varices, and short gastric vein were enrolled into the model. These veins were scored according to the diameters and the rates of hemorrhage were increased with the score. We then validated the model with 26 patents from July 2014 to December 2014. The AUC value was 0.8849 in ROC curves for this radiological model. Conclusions: A risk model was constructed including inferior mesenteric vein, esophageal varices, posterior gastric vein, and short gastric vein. This radiological scoring model may be a valuable indicator for hemorrhage of portal hypertension.
C1 [Ge, Wei; Cao, Ya-Juan; Xie, Min; Ding, Yi-Tao; Yu, De-Cai] Nanjing Univ, Sch Med, Affiliated Drum Tower Hosp, Dept Gen Surg, Nanjing 210008, Jiangsu, Peoples R China.
[Wang, Yi; Zhang, Ming] Nanjing Univ, Sch Med, Affiliated Drum Tower Hosp, Dept Digest Surg, Nanjing 210008, Jiangsu, Peoples R China.
C3 Nanjing University; Nanjing University
RP Yu, DC (corresponding author), Nanjing Univ, Sch Med, Affiliated Drum Tower Hosp, Dept Gen Surg, Nanjing 210008, Jiangsu, Peoples R China.
EM mg0923@163.com; dryudecai@qq.com
RI YU, De-cai/D-4129-2009; XIE, MIN/JKJ-0132-2023; D, Yi/JJC-2699-2023
OI Zhang, Ming/0009-0009-7742-3128; YU, Decai/0000-0002-3006-2531
FU grants for key clinical center of institutes of Health in Jiangsu
province; outstanding young medical scientists in Jiangsu Province
FX This study was supported by grants for key clinical center of institutes
of Health in Jiangsu province, and outstanding young medical scientists
in Jiangsu Province.
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NR 20
TC 3
Z9 4
U1 0
U2 1
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2015
VL 8
IS 9
BP 11517
EP 11523
PG 7
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA DA4ZX
UT WOS:000367812800201
PM 26617884
DA 2025-01-07
ER
PT J
AU Diaz, JA
Sanchez, L
Diaz, LA
Murillo, MF
Poveda, L
Suescun, OF
Castro, L
AF Diaz, Jairo A.
Sanchez, Liliana
Diaz, Luis A.
Murillo, Mauricio F.
Poveda, Laura
Suescun, Oscar F.
Castro, Laura
TI Sequential development of embryoblast-like memory entities in human
cancer tissues: an evolutionary self-repair structure with
pluripotentiality
SO AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
LA English
DT Article
DE Cancer; self-assembly structures; embryoblast-like entities
ID HEPATOCELLULAR-CARCINOMA; CELL; DIFFERENTIATION; PROLIFERATION; GROWTH
AB Hidden collective organization of cancer cells can partially or completely return to embryoid genotype -phenotype with the plasticity to transform their morphology on cell embryoblast-like memory entities by expression of dormant genes that arise from embryogenesis. After hundreds of driver mutations, cancer cells gain new abilities or attributes and recapitulate early stages of embryogenesis. Our findings document how malignant tissues reactivated ancestral storage memory and elaborate inside tumor glands spiral-pyramidal-fractal chiral crystals (Tc) as geometric attractor proteins and biomimicry the primitive cellular blastocyst embryoblast fluid-filled cavity. The resultant evolutionary embryoblast-like entity has higher survivability and spatial cephalic-caudal growth organization with pluripotentiality that carry the correct DNA instructions to repair, and regenerate. The isolation and manipulation of these order structures can guide and control the regenerative pathway mechanism in human tumors as follows: modify and reprogram the phenotype of the tumor where these entities are generated, establish a reverse primordial microscopic mold to use the swirlonic collective behavior of cellular building blocks to regenerate injured tissues, convert cancer cells to a normal phenotype through regeneration using the organizational level and scale properties of reverse genetic guidance, global control of mitotic activity and morphogenetic movements avoiding their spread and metastasis, determining a better life prognosis for patients who incubate these entities in their tumors compared to those who do not express them. An emergent self-repair order structure, biological template can develop targeted therapeutic alternatives not only in cancer but also in treatment of autoimmune, viral diseases, and in regenerative medicine and rejuvenation.
C1 [Diaz, Jairo A.; Sanchez, Liliana; Diaz, Luis A.; Poveda, Laura; Suescun, Oscar F.] Cooperat Univ Colombia, Fac Med, Villavicencio, Colombia.
[Diaz, Jairo A.; Diaz, Luis A.; Murillo, Mauricio F.] Dept Hosp Villavicencio, Lab Pathol, Villavicencio, Colombia.
[Diaz, Jairo A.; Castro, Laura] Hosp Reg Granada, Meta, Colombia.
[Diaz, Jairo A.] Lab Pathol, Liga Colombiana Contra el Canc, Villavicencio, Colombia.
[Diaz, Jairo A.] Empresa Social Estado ESE, Villavicencio, Colombia.
[Diaz, Jairo A.] Dept Hosp Villavicencio, Villavicencio, Colombia.
C3 Universidad Cooperativa de Colombia
RP Diaz, JA (corresponding author), Dept Hosp Villavicencio, Villavicencio, Colombia.
EM jaditod@hot-mail.com
RI Diaz, Luis/A-6018-2008
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NR 35
TC 0
Z9 0
U1 0
U2 0
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1943-8141
J9 AM J TRANSL RES
JI Am. J. Transl. Res.
PY 2022
VL 14
IS 9
BP 6011
EP 6028
PG 18
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA 5U4DW
UT WOS:000876500600004
PM 36247292
DA 2025-01-07
ER
PT J
AU Yang, Y
Wu, XQ
Li, WX
Huang, HM
Li, HD
Pan, XY
Li, XF
Huang, C
Meng, XM
Zhang, L
Lv, XW
Wang, H
Li, J
AF Yang, Yang
Wu, Xiao-qin
Li, Wan-xia
Huang, Hui-min
Li, Hai-di
Pan, Xue-yin
Li, Xiao-feng
Huang, Cheng
Meng, Xiao-ming
Zhang, Lei
Lv, Xiong-wen
Wang, Hua
Li, Jun
TI PSTPIP2 connects DNA methylation to macrophage polarization in
CCL4-induced mouse model of hepatic fibrosis
SO ONCOGENE
LA English
DT Article
ID CHRONIC MULTIFOCAL OSTEOMYELITIS; CHRONIC ACTIVE HEPATITIS;
AUTOINFLAMMATORY DISEASE; AUTOIMMUNE HEPATITIS; IN-VIVO;
HEPATOCELLULAR-CARCINOMA; PSTPIP2-DEFICIENT MICE;
CORTICOSTEROID-THERAPY; LIVER FIBROSIS; ACTIVATION
AB Macrophages play a crucial role in the progression of hepatic fibrosis (HF). In macrophages, epigenetic mechanisms are increasingly being recognized as crucial controllers of their phenotype. However, the functions of macrophage DNA methylation in experimental models of hepatic fibrosis have not been fully addressed. Here, we analyzed isolated hepatic macrophages DNA methylation from CCL4-induced (4 weeks) mice using reduced representation bisulfite sequencing (RRBS). We identified and validated the methylation status of 26 gene promoter regions associated with CpG islands. We further investigated the function of PSTPIP2 in HF by hepatic-adeno-associated virus (AAV9)-PSTPIP2 overexpression. The molecular mechanisms underlying PSTPIPS2-regulated HF were further explored in mice and RAW264.7 cell line. RRBS results show hypermethylation of PSTPIP2 (chr18: 77,843,840-77,843,968) in the 5'-UTR region. PSTPIP2 expression was significantly decreased in isolated hepatic macrophages from CCL4-induced mice. PSTPIP2 hypermethylation is mediated by the methyltransferases DNMT3a and DNMT3b in LPS-induced RAW264.7 cell line. Further investigation indicated that specific overexpression of PSTPIP2 in C57BL/6 mice reduced the inflammatory response and ameliorated liver fibrosis. These data indicated that hypermethylation of PSTPIP2 caused a mixed induction of hepatic classical macrophage (M1) and alternative macrophage (M2) biomarkers in CCL4-induced HF mice. Furthermore, overexpression of PSTPIP2 inhibited the expression of M1 markers by suppressing STAT1 activity, and enhanced the expression of M2 markers by promoting STAT6 activity. In contrast, knockdown of PSTPIP2 promoted M1 polarization and suppressed M2 polarization in vitro. Adding PSTPIP2 expression alleviates liver fibrosis and hepatic inflammation in mice by regulating macrophage polarization.
C1 [Yang, Yang; Wu, Xiao-qin; Li, Wan-xia; Huang, Hui-min; Li, Hai-di; Pan, Xue-yin; Li, Xiao-feng; Huang, Cheng; Meng, Xiao-ming; Zhang, Lei; Lv, Xiong-wen; Wang, Hua; Li, Jun] Anhui Med Univ, Sch Pharm, Anhui Key Lab Bioact Nat Prod, Hefei 230032, Anhui, Peoples R China.
[Yang, Yang; Wu, Xiao-qin; Li, Wan-xia; Huang, Hui-min; Li, Hai-di; Pan, Xue-yin; Li, Xiao-feng; Huang, Cheng; Meng, Xiao-ming; Zhang, Lei; Lv, Xiong-wen; Wang, Hua; Li, Jun] Anhui Med Univ, Key Lab Antiinflammatory & Immune Med, Minist Educ, Hefei 230032, Anhui, Peoples R China.
[Yang, Yang; Wu, Xiao-qin; Li, Wan-xia; Huang, Hui-min; Li, Hai-di; Pan, Xue-yin; Li, Xiao-feng; Huang, Cheng; Meng, Xiao-ming; Zhang, Lei; Lv, Xiong-wen; Wang, Hua; Li, Jun] Anhui Med Univ, Inst Liver Dis, Hefei 230032, Anhui, Peoples R China.
[Yang, Yang; Wu, Xiao-qin; Li, Wan-xia; Huang, Hui-min; Li, Hai-di; Pan, Xue-yin; Li, Xiao-feng; Huang, Cheng; Meng, Xiao-ming; Zhang, Lei; Lv, Xiong-wen; Wang, Hua; Li, Jun] Anhui Med Univ, Anhui Inst Innovat Drugs, Hefei 230032, Anhui, Peoples R China.
C3 Anhui Medical University; Anhui Medical University; Anhui Medical
University; Anhui Medical University
RP Li, J (corresponding author), Anhui Med Univ, Sch Pharm, Anhui Key Lab Bioact Nat Prod, Hefei 230032, Anhui, Peoples R China.; Li, J (corresponding author), Anhui Med Univ, Key Lab Antiinflammatory & Immune Med, Minist Educ, Hefei 230032, Anhui, Peoples R China.; Li, J (corresponding author), Anhui Med Univ, Inst Liver Dis, Hefei 230032, Anhui, Peoples R China.; Li, J (corresponding author), Anhui Med Univ, Anhui Inst Innovat Drugs, Hefei 230032, Anhui, Peoples R China.
EM lj@ahmu.edu.cn
RI wang, hua/E-5028-2013; Yang, Yang/AAB-5926-2021; lv,
xiongwen/ABE-6452-2021
OI Yang, Yang/0000-0002-0942-1800; Meng, Xiao-ming/0000-0002-1166-561X
FU National Natural Science Foundation of China [81770609]
FX This work was supported by grants from the National Natural Science
Foundation of China (81770609).
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NR 54
TC 55
Z9 60
U1 2
U2 34
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD NOV 22
PY 2018
VL 37
IS 47
BP 6119
EP 6135
DI 10.1038/s41388-018-0383-0
PG 17
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA HB2PG
UT WOS:000450883000002
PM 29993036
DA 2025-01-07
ER
PT J
AU Asl, MH
Khelejani, FP
Mahdavi, SZB
Emrahi, L
Jebelli, A
Mokhtarzadeh, A
AF Asl, Mohammad Heydarnezhad
Khelejani, Faezeh Pasban
Mahdavi, Seyedeh Zahra Bahojb
Emrahi, Leila
Jebelli, Asiyeh
Mokhtarzadeh, Ahad
TI The various regulatory functions of long noncoding RNAs in apoptosis,
cell cycle, and cellular senescence
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Review
DE apoptosis; cell cycle; cellular senescence; lncRNA
ID EPITHELIAL-MESENCHYMAL TRANSITION; MAMMALIAN MITOCHONDRIAL FISSION;
COLORECTAL-CANCER; EMERGING ROLES; POOR-PROGNOSIS; GASTRIC-CANCER;
TRANSCRIPTIONAL REGULATION; HEPATOCELLULAR-CARCINOMA; DOWN-REGULATION;
OVARIAN-CANCER
AB Long noncoding RNAs (lncRNAs) are a group of noncoding cellular RNAs involved in significant biological phenomena such as differentiation, cell development, genomic imprinting, adjusting the enzymatic activity, regulating chromosome conformation, apoptosis, cell cycle, and cellular senescence. The misregulation of lncRNAs interrupting normal biological processes has been implicated in tumor formation and metastasis, resulting in cancer. Apoptosis and cell cycle, two main biological phenomena, are highly conserved and intimately coupled mechanisms. Hence, some cell cycle regulators can influence both programmed cell death and cell division. Apoptosis eliminates defective and unwanted cells, and the cell cycle enables cells to replicate themselves. The improper regulation of apoptosis and cell cycle contributes to numerous disorders such as neurodegenerative and autoimmune diseases, viral infection, anemia, and mainly cancer. Cellular senescence is a tumor-suppressing response initiated by environmental and internal stress factors. This phenomenon has recently attained more attention due to its therapeutic implications in the field of senotherapy. In this review, the regulatory roles of lncRNAs on apoptosis, cell cycle, and senescence will be discussed. First, the role of lncRNAs in mitochondrial dynamics and apoptosis is addressed. Next, the interaction between lncRNAs and caspases, pro/antiapoptotic proteins, and also EGFR/PI3K/PTEN/AKT/mTORC1 signaling pathway will be investigated. Furthermore, the effect of lncRNAs in the cell cycle is surveyed through interaction with cyclins, cdks, p21, and wnt/beta-catenin/c-myc pathway. Finally, the function of essential lncRNAs in cellular senescence is mentioned.
C1 [Asl, Mohammad Heydarnezhad] Univ Tabriz, Fac Nat Sci, Dept Biol, Tabriz, Iran.
[Khelejani, Faezeh Pasban] Univ Maragheh, Fac Basic Sci, Dept Cell & Mol Biol, Maragheh, Iran.
[Mahdavi, Seyedeh Zahra Bahojb] Azarbaijan Shahid Madani Univ, Fac Basic Sci, Dept Biol, Tabriz, Iran.
[Emrahi, Leila] Tarbiat Modares Univ, Fac Med Sci, Dept Med Genet, Tehran, Iran.
[Jebelli, Asiyeh] Higher Educ Inst Rab Rashid, Fac Basic Sci, Dept Biol Sci, Tabriz, Iran.
[Jebelli, Asiyeh] Tabriz Univ Med Sci, TB & Lung Dis Res Ctr, Tabriz, Iran.
[Mokhtarzadeh, Ahad] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
C3 University of Tabriz; University of Maragheh; Azarbaijan Shahid Madani
University; Tarbiat Modares University; Tabriz University of Medical
Science; Tabriz University of Medical Science
RP Jebelli, A (corresponding author), Higher Educ Inst Rab Rashid, Fac Basic Sci, Dept Biol Sci, Tabriz, Iran.; Mokhtarzadeh, A (corresponding author), Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
EM jebelli.a@raberashidi.ac.ir; mokhtarzadehah@tbzmed.ac.ir
RI Mokhtarzadeh, Ahad/V-3748-2017; Jebelli, Asiyeh/IAP-3359-2023
OI jebelli, asiyeh/0000-0001-9494-2207
FU Immunology Research Center, Tabriz University of Medical Sciences
[67252, 67255]
FX The authors are grateful for the financial support from the Immunology
Research Center, Tabriz University of Medical Sciences (Grant numbers:
67252 and 67255).
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NR 209
TC 35
Z9 35
U1 4
U2 28
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0730-2312
EI 1097-4644
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD JUN
PY 2022
VL 123
IS 6
BP 995
EP 1024
DI 10.1002/jcb.30221
EA FEB 2022
PG 30
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 2C9JI
UT WOS:000749470100001
PM 35106829
DA 2025-01-07
ER
PT J
AU Balkan, A
Alkan, S
Barutçu, S
Konduk, BT
Yildirim, AE
Er, RE
Gulsen, MT
AF Balkan, Ayhan
Alkan, Samet
Barutcu, Sezgin
Konduk, Bugra Tolga
Yildirim, Abdullah Emre
Er, Ramazan Erdem
Gulsen, Murat Taner
TI ETIOLOGICAL DISTRIBUTION AND CLINICAL FEATURES OF CIRRHOTIC PATIENTS:
SINGLE TERTIARY REFERRAL CENTER EXPERIENCE
SO ACTA MEDICA MEDITERRANEA
LA English
DT Article
DE Cirrhosis; etiology; viral hepatitis
ID LIVER-CIRRHOSIS
AB Introduction: Cirrhosis has various etiologies, and the etiologic distribution differs from center to center. Our aim is to reveal the etiological distribution and clinical features of cirrhotic patients.
Materials and methods: We retrospectively recruited 1144 patients. Of patients, 480 were cirrhotic, 664 were non-cirrhotic. Patients were diagnosed by means of clinical features, laboratory values, radiologic imaging and biopsy when required.
Results: Of the 480 cirrhotic patients, 250 were male (52%), and the mean age was 57.6 years. In cirrhotics, 289 (60.2%) patients were decompensated. However, hepatitis B virus (HBV) - hepatitis C virus (HCV) coinfection and Budd-Chiari syndrome were found to have highest tendency of decompensation (85.7%, 84.6% respectively). Child-Pugh classification was evaluated: 243 (50.6%) class A, 164 (34.2%) class B and73 (15.2%) class C patients were analyzed. Ascites in 206 (42.9%), hepatic encephalopathy in 55 (11.4%), hepatocellular carcinoma in 23 (4.7%), and spontaneous bacterial peritonitis in 17 (3.5%) of the patients were determined. In the group of patients with viral etiology, while 160 (53.9%) of 297 cirrhotic patients were HCV, 137 (46.1%) were HBV, 503 (75.8%) out of 664 non-cirrhotics were HBV and 161 (24.2%) were HCV infected.
Conclusion: Although HBV was more common in chronic hepatitides, cirrhosis was mostly caused by HCV infection. The reason of this may be due to anti-viral use for HBV. We found that decompensation rate was higher for Budd-Chiari syndrome and HBV-HCV coinfected patients. Cryptogenic cirrhosis still continues to have high prevalence. The reason for this may be undiagnosed autoimmune liver disease, non-alcoholic steatohepatitis, occult HBV or gluten enteropathy.
C1 [Balkan, Ayhan; Barutcu, Sezgin; Konduk, Bugra Tolga; Yildirim, Abdullah Emre; Er, Ramazan Erdem; Gulsen, Murat Taner] Gaziantep Univ, Fac Med, Dept Gastroenterol, Univ Bulvari Sehitkamil, TR-27310 Gaziantep, Turkey.
[Alkan, Samet] Gaziantep Univ, Fac Med, Dept Internal Med, TR-27310 Gaziantep, Turkey.
C3 Gaziantep University; Gaziantep University
RP Balkan, A (corresponding author), Gaziantep Univ, Fac Med, Dept Gastroenterol, Univ Bulvari Sehitkamil, TR-27310 Gaziantep, Turkey.
RI Barutçu, Sezgin/AAD-4552-2019; er, ramazan/AAA-6063-2021; YILDIRIM,
Abdullah/AAG-6561-2020; alkan, samet/AAA-1025-2020; Gülşen,
Murat/AAH-1097-2020
OI Barutcu, Sezgin/0000-0003-0823-3215
CR Anderson Robert N, 2003, Natl Vital Stat Rep, V52, P1
[Anonymous], 2009, EPIDEMIOLOGY CHRONIC
Bayan K, 2007, HEPATO-GASTROENTEROL, V54, P2198
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NR 19
TC 1
Z9 2
U1 0
U2 1
PU CARBONE EDITORE
PI PALERMO
PA VIA QUINTINO SELLA, 68, PALERMO, 90139, ITALY
SN 0393-6384
EI 2283-9720
J9 ACTA MEDICA MEDITERR
JI Acta Medica Mediterr.
PY 2016
VL 32
IS 3
BP 669
EP 674
DI 10.19193/0393-6384_2016_3_73
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DM9NQ
UT WOS:000376693400002
DA 2025-01-07
ER
PT J
AU Burke, BP
Miranda, CS
Lee, RE
Renard, I
Nigam, S
Clemente, GS
D'Huys, T
Ruest, T
Domarkas, J
Thompson, JA
Hubin, TJ
Schols, D
Cawthorne, CJ
Archibald, SJ
AF Burke, Benjamin P.
Miranda, Cecilia S.
Lee, Rhiannon E.
Renard, Isaline
Nigam, Shubhanchi
Clemente, Goncalo S.
D'Huys, Thomas
Ruest, Torsten
Domarkas, Juozas
Thompson, James A.
Hubin, Timothy J.
Schols, Dominique
Cawthorne, Christopher J.
Archibald, Stephen J.
TI 64Cu PET Imaging of the CXCR4 Chemokine Receptor Using a
Cross-Bridged Cyclam Bis-Tetraazamacrocyclic Antagonist
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE CXCR4; Cu-64; azamacrocycle; cyclam; AMD3100
ID HUMAN CANCER XENOGRAFTS; 4 EXPRESSION; COMPLEXES; COPPER(II); BINDING;
CELLS; INHIBITORS; CHEMISTRY; BEHAVIOR; CXCL12
AB Expression of the chemokine receptor chemokine C-X-C motif receptor 4 (CXCR4) plays an important role in cancer metastasis, in autoimmune diseases, and during stem cell-based repair processes after stroke and myocardial infarction. Previously reported PET imaging agents targeting CXCR4 suffer from either high nonspecific uptake or bind only to the human form of the receptor. The objective of this study was to develop a high-stability Cu-64-labeled small-molecule PET agent for imaging both human and murine CXCR4 chemokine receptors. Methods: Synthesis, radiochemistry, stability and radioligand binding assays were performed for the novel tracer Cu-64-CuCB-bicyclam. In vivo dynamic PET studies were performed on mice bearing U87 (CXCR4 low-expressing) and U87.CXCR4 (human-CXCR4 high-expressing) tumors. Biodistribution and receptor blocking studies were performed on CD1-IGS immunocompetent mice. CXCR4 expression on tumor and liver disaggregates was confirmed using a combination of immunohistochemistry, quantitative polymerase chain reaction, and Western blot. Results: Cu-64-CuCB-bicyclam has a high affinity for both the human and the murine variants of the CXCR4 receptor (half-maximal inhibitory concentration, 8 nM [human]/2 nM [murine]) and can be obtained from the parent chelator that has low affinity. In vitro and in vivo studies demonstrate specific uptake in CXCR4-expressing cells that can be blocked by more than 90% using a higher-affinity antagonist, with limited uptake in non-CXCR4-expressing organs and high in vivo stability. The tracer was also able to selectively displace the CXCR4 antagonists AMD3100 and AMD3465 from the liver. Conclusion: The tetraazamacrocyclic small molecule Cu-64-CuCB-bicyclam has been shown to be an imaging agent for the CXCR4 receptor that is likely to be applicable across a range of species. It has high affinity and stability and is suitable for preclinical research in immunocompetent murine models.
C1 [Burke, Benjamin P.; Lee, Rhiannon E.; Renard, Isaline; Domarkas, Juozas; Archibald, Stephen J.] Univ Hull, Dept Chem, Kingston Upon Hull, N Humberside, England.
[Burke, Benjamin P.; Miranda, Cecilia S.; Lee, Rhiannon E.; Renard, Isaline; Nigam, Shubhanchi; Clemente, Goncalo S.; Domarkas, Juozas; Thompson, James A.; Cawthorne, Christopher J.; Archibald, Stephen J.] Univ Hull, Positron Emiss Tomog Res Ctr, Kingston Upon Hull, N Humberside, England.
[Burke, Benjamin P.; Miranda, Cecilia S.; Nigam, Shubhanchi; Clemente, Goncalo S.; Ruest, Torsten; Cawthorne, Christopher J.; Archibald, Stephen J.] Univ Hull, Dept Biomed Sci, Kingston Upon Hull, N Humberside, England.
[D'Huys, Thomas; Schols, Dominique] Katholieke Univ Leuven, Rega Inst Med Res, Leuven, Belgium.
[Thompson, James A.] Univ Hull, Hull York Med Sch, Kingston Upon Hull, N Humberside, England.
[Hubin, Timothy J.] Southwestern Oklahoma State Univ, Dept Chem & Phys, Weatherford, OK USA.
C3 University of Hull; University of Hull; University of Hull; KU Leuven;
University of Hull; University of York - UK
RP Archibald, SJ (corresponding author), Univ Hull, Cottingham Rd, Kingston Upon Hull HU6 7RX, N Humberside, England.
EM s.j.archibald@hull.ac.uk
RI Hubin, Timothy/A-9399-2009; Cawthorne, Christopher/AAC-1018-2022;
Renard, Isaline/GZB-0219-2022; Burke, Benjamin/L-6151-2016; Carrondo,
Manuel/C-8155-2011; Archibald, Steve/I-8723-2012; Cawthorne,
Christopher/Q-5512-2018; Schols, Dominique/S-9057-2017; D'huys,
Thomas/F-5936-2018
OI Hubin, Tim/0000-0003-2277-1191; Cawthorne,
Christopher/0000-0002-5975-0354; Schols, Dominique/0000-0003-3256-5850;
D'huys, Thomas/0000-0002-0871-5604
FU Daisy Appeal Charity [DAhul0211]; Yorkshire Cancer Research [HEND376];
University of Hull
FX Funding was provided by the Daisy Appeal Charity (grant DAhul0211 and
BPB fellowship) and by Yorkshire Cancer Research (HEND376). The
University of Hull provided studentship funding to Rhiannon Lee and
Cecilia Miranda. No other potential conflict of interest relevant to
this article was reported.
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NR 52
TC 24
Z9 26
U1 2
U2 44
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD JAN 1
PY 2020
VL 61
IS 1
BP 123
EP 128
DI 10.2967/jnumed.118.218008
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA JZ6IA
UT WOS:000505203800022
PM 31201250
OA Bronze, Green Published, Green Accepted
DA 2025-01-07
ER
PT J
AU Kavanagh, DO
O'Riain, C
Ridgway, PF
Neary, P
Crotty, TC
Geoghegan, JG
Traynor, O
AF Kavanagh, D. O.
O'Riain, C.
Ridgway, P. F.
Neary, P.
Crotty, T. C.
Geoghegan, J. G.
Traynor, O.
TI Radical Pancreaticoduodenectomy for Benign Disease
SO THESCIENTIFICWORLDJOURNAL
LA English
DT Article
DE pancreaticoduodenectomy; endoscopic ultrasound; chronic pancreatitis;
choledochal cyst; Whipple's
ID FINE-NEEDLE-ASPIRATION; PANCREATIC-CANCER; DIFFERENTIAL-DIAGNOSIS;
PERITONEAL CYTOLOGY; AUTOIMMUNE PANCREATITIS; COMPUTED-TOMOGRAPHY; FOCAL
PANCREATITIS; SURGICAL-TREATMENT; BRUSH CYTOLOGY; ADENOCARCINOMA
AB Whipple's procedure is the treatment of choice for pancreatic and periampullary malignancies. Preoperative histological confirmation of malignancy is frequently unavailable and some patients will subsequently be found to have benign disease. Here, we review our experience with Whipple's procedure for patients ultimately proven to have benign disease. The medical records of all patients who underwent Whipple's procedure during a 15-year period (1987-2002) were reviewed; 112 patients underwent the procedure for suspected malignancy. In eight cases, the final histology was benign (7.1%). One additional patient was known to have benign disease at resection. The mean age was 50 years (range: 30-75). The major presenting features included jaundice (five), pain (two), gastric outlet obstruction (one), and recurrent gastrointestinal haemorrhage (one). Investigations included ultrasound (eight), computerised tomography (eight), endoscopic retrograde cholangiopancreatography (seven; of these, four patients had a stent inserted and three patients had sampling for cytology), and endoscopic ultrasound (two). The pathological diagnosis included benign biliary stricture (two), chronic pancreatitis (two), choledochal cyst (one), inflammatory pseudotumour (one), cystic duodenal wall dysplasia (one), duodenal angiodysplasia (one), and granular cell neoplasm (one). There was no operative mortality. Morbidity included intra-abdominal collection (one), anastomotic leak (one), liver abscess (one), and myocardial infarction (one). All patients remain alive and well at mean follow-up of 41 months. Despite recent advances in diagnostic imaging, 8% of the patients undergoing Whipple's procedure had benign disease. A range of unusual pathological entities can mimic malignancy. Accurate preoperative histological diagnosis may have allowed a less radical operation to be performed. Endoscopic ultrasound-guided fine needle aspirate (EUS-FNA) may reduce the need for Whipple's operation in benign pancreaticobiliary disease in the future.
C1 [Kavanagh, D. O.; Ridgway, P. F.; Neary, P.; Geoghegan, J. G.; Traynor, O.] St Vincents Univ Hosp, Liver Unit, Dublin, Ireland.
[O'Riain, C.; Crotty, T. C.] St Vincents Univ Hosp, Dept Pathol, Dublin, Ireland.
C3 University College Dublin; Saint Vincent's University Hospital;
University College Dublin; Saint Vincent's University Hospital
RP Kavanagh, DO (corresponding author), St Vincents Univ Hosp, Liver Unit, Dublin, Ireland.
EM dara_kav@hotmail.com
RI Alemanno, Giovanni/AAC-1759-2022
OI Ridgway, Paul/0000-0002-8500-8532
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NR 55
TC 11
Z9 11
U1 0
U2 0
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1537-744X
J9 THESCIENTIFICWORLDJO
JI TheScientificWorldJOURNAL
PY 2008
VL 8
BP 1156
EP 1167
DI 10.1100/tsw.2008.147
PG 12
WC Environmental Sciences; Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology; Science & Technology - Other Topics
GA 380QE
UT WOS:000261479500051
PM 19030761
OA gold, Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Zárate, R
el Jaber-Vazdekis, N
Tejera, N
Pérez, JA
Rodríguez, C
AF Zarate, Rafael
el Jaber-Vazdekis, Nabil
Tejera, Noemi
Perez, Jose A.
Rodriguez, Covadonga
TI Significance of long chain polyunsaturated fatty acids in human health
SO CLINICAL AND TRANSLATIONAL MEDICINE
LA English
DT Review
DE Disease; Health; Inflammation; Lipidomics; Lipids; Long chain
polyunsaturated fatty acids; Omega-3; Resolvins
ID SOLUBLE EPOXIDE HYDROLASE; DOCOSAHEXAENOIC ACID; CARDIOVASCULAR-DISEASE;
EICOSAPENTAENOIC ACID; LIPID-METABOLISM; OMEGA-3-FATTY-ACID
SUPPLEMENTATION; NEURODEGENERATIVE DISEASES; ALZHEIMERS-DISEASE;
HEART-DISEASE; DOUBLE-BLIND
AB In the last decades, the development of new technologies applied to lipidomics has revitalized the analysis of lipid profile alterations and the understanding of the underlying molecular mechanisms of lipid metabolism, together with their involvement in the occurrence of human disease. Of particular interest is the study of omega-3 and omega-6 long chain polyunsaturated fatty acids (LC-PUFAs), notably EPA (eicosapentaenoic acid, 20:5n-3), DHA (docosahexaenoic acid, 22:6n-3), and ARA (arachidonic acid, 20:4n-6), and their transformation into bioactive lipid mediators. In this sense, new families of PUFA-derived lipid mediators, including resolvins derived from EPA and DHA, and protectins and maresins derived from DHA, are being increasingly investigated because of their active role in the "return to homeostasis" process and resolution of inflammation. Recent findings reviewed in the present study highlight that the omega-6 fatty acid ARA appears increased, and omega-3 EPA and DHA decreased in most cancer tissues compared to normal ones, and that increments in omega-3 LC-PUFAs consumption and an omega-6/omega-3 ratio of 2-4:1, are associated with a reduced risk of breast, prostate, colon and renal cancers. Along with their lipid-lowering properties, omega-3 LC-PUFAs also exert cardioprotective functions, such as reducing platelet aggregation and inflammation, and controlling the presence of DHA in our body, especially in our liver and brain, which is crucial for optimal brain functionality. Considering that DHA is the principal omega-3 FA in cortical gray matter, the importance of DHA intake and its derived lipid mediators have been recently reported in patients with major depressive and bipolar disorders, Alzheimer disease, Parkinson's disease, and amyotrophic lateral sclerosis. The present study reviews the relationships between major diseases occurring today in the Western world and LC-PUFAs. More specifically this review focuses on the dietary omega-3 LC-PUFAs and the omega-6/omega-3 balance, in a wide range of inflammation disorders, including autoimmune diseases. This review suggests that the current recommendations of consumption and/or supplementation of omega-3 FAs are specific to particular groups of age and physiological status, and still need more fine tuning for overall human health and well being.
C1 [Zarate, Rafael] Canary Isl Canc Res Inst ICIC, Ave La Trinidad 61,Torre A Arevalo,7th Floor, Tenerife 38204, Spain.
[el Jaber-Vazdekis, Nabil] Acad Sci Czech Republ, Inst Microbiol, Ctr Algatech, Trebon, Czech Republic.
[Tejera, Noemi] Univ East Anglia, Norwich Med Sch, Dept Nutr & Prevent Med, Norwich NR4 7UQ, Norfolk, England.
[Perez, Jose A.; Rodriguez, Covadonga] Univ La Laguna, Fac Sci, Anim Physiol Unit, Dept Anim Biol Soil Sci & Geol, Ave Astrofis Francisco Sanchez S-N, E-38206 Tenerife, Spain.
[Rodriguez, Covadonga] Univ La Laguna, Inst Biomed Technol ITB, Campus Ofra, Tenerife 38071, Spain.
C3 Czech Academy of Sciences; Institute of Microbiology of the Czech
Academy of Sciences; University of East Anglia; Universidad de la
Laguna; Universidad de la Laguna
RP Zárate, R (corresponding author), Canary Isl Canc Res Inst ICIC, Ave La Trinidad 61,Torre A Arevalo,7th Floor, Tenerife 38204, Spain.
EM rzarate@icic.es
RI Tejera, Noemi/O-1558-2016; vazdekis, nabil/J-8108-2014; Rodriguez
Gonzalez, Covadonga/L-5173-2014; Perez Perez, Jose Antonio/L-4293-2014
OI Rodriguez Gonzalez, Covadonga/0000-0002-2805-0048; Tejera,
Noemi/0000-0001-8100-6022; Zarate, Rafael/0000-0001-7288-8481; Perez
Perez, Jose Antonio/0000-0002-5662-7246
FU project Macbioblue [MAC/1.1b/086]; program Interreg Mac; project
Macbioblue; project PROPUFAW3, Spanish National Program [AGL2015 70994
R]; project DIVERSIFY, European Program FP7 [603121]; National Programme
of Sustainability I, Czech Republic [LO1416]
FX RZ thanks funding from project Macbioblue (MAC/1.1b/086), program
Interreg Mac 2014-2020. CR and JAP were also supported by project
Macbioblue and projects PROPUFAW3, Spanish National Program (AGL2015
70994 R) and DIVERSIFY, European Program FP7 (KBBE-2013-GA No 603121).
NJV was supported by a grant from The National Programme of
Sustainability I, ID: LO1416, Czech Republic. We thanks Dr. G.
McNaughton-Smith for his comments and improvement of the English style
of the manuscript.
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NR 154
TC 370
Z9 394
U1 12
U2 233
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 2001-1326
J9 CLIN TRANSL MED
JI Clin. Transl. Med.
PD JUL 27
PY 2017
VL 6
AR 25
DI 10.1186/s40169-017-0153-6
PG 19
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA FC2IY
UT WOS:000406662300001
PM 28752333
OA Green Published, gold, Green Accepted
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Khoury, T
Chen, S
Adar, T
Jacob, EO
Mizrahi, M
AF Khoury, Tawfik
Chen, Shmuel
Adar, Tomer
Jacob, E. Ollech
Mizrahi, Meir
TI Hepatitis C infection and lymphoproliferative disease: Accidental
comorbidities?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Blood; Hepatitis C infection; Non-Hodgkin's lymphoma; Pathogenesis;
Treatment
ID NON-HODGKINS-LYMPHOMA; B-CELL LYMPHOMAS; VIRUS-INFECTION; SOLUBLE
INTERLEUKIN-2-RECEPTOR; MIXED CRYOGLOBULINEMIA; VILLOUS LYMPHOCYTES;
MALIGNANT-LYMPHOMA; SPLENIC LYMPHOMA; VIRAL-INFECTION; HIGH PREVALENCE
AB Chronic hepatitis C virus (HCV) infection has been associated with liver cancer and cirrhosis, autoimmune disorders such as thyroiditis and mixed cryoglobulinema, and alterations in immune function and chronic inflammation, both implicated in B cell lymphoproliferative diseases that may progress to non-Hodgkin lymphoma (NHL). HCV bound to B cell surface receptors can induce lymphoproliferation, leading to DNA mutations and/or lower antigen response thresholds. These findings and epidemiological reports suggest an association between HCV infection and NHL. We performed a systematic review of the literature to clarify this potential relationship. We searched the English-language literature utilizing Medline, Embase, Paper First, Web of Science, Google Scholar, and the Cochrane Database of Systematic Reviews, with search terms broadly defined to capture discussions of HCV and its relationship with NHL and/or lymphoproliferative diseases. References were screened to further identify relevant studies and literature in the basic sciences. A total of 62 reports discussing the relationship between HCV, NHL, and lymphoproliferative diseases were identified. Epidemiological studies suggest that at least a portion of NHL may be etiologically attributable to HCV, particularly in areas with high HCV prevalence. Studies that showed a lack of association between HCV infection and lymphoma may have been influenced by small sample size, short follow-up periods, and database limitations. The association appears strongest with the B-cell lymphomas relative to other lymphoproliferative diseases. Mechanisms by which chronic HCV infection promotes lymphoproliferative disease remains unclear. Lymphomagenesis is a multifactorial process involving genetic, environmental, and infectious factors. HCV most probably have a role in the lymphomagenesis but further study to clarify the association and underlying mechanisms is warranted. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
C1 [Khoury, Tawfik; Chen, Shmuel; Adar, Tomer; Jacob, E. Ollech; Mizrahi, Meir] Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Internal Med, IL-91120 Jerusalem, Israel.
[Mizrahi, Meir] Hebrew Univ Jerusalem, Hadassah Med Ctr, Inst Gastroenterol & Liver Dis, IL-91120 Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hadassah University Medical Center;
Hebrew University of Jerusalem; Hadassah University Medical Center
RP Mizrahi, M (corresponding author), Hebrew Univ Jerusalem, Hadassah Med Ctr, Inst Gastroenterol & Liver Dis, POB 12000, IL-91120 Jerusalem, Israel.
EM mizrahim@hadassah.org.il
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NR 63
TC 7
Z9 8
U1 0
U2 6
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 21
PY 2014
VL 20
IS 43
BP 16197
EP 16202
DI 10.3748/wjg.v20.i43.16197
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AW1LI
UT WOS:000346050500027
PM 25473174
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Qiu, FF
Fan, P
Nie, GD
Liu, HZ
Liang, CL
Yu, WL
Dai, ZH
AF Qiu, Feifei
Fan, Ping
Nie, Golay D.
Liu, Huazhen
Liang, Chun-Ling
Yu, Wanlin
Dai, Zhenhua
TI Effects of Cigarette Smoking on Transplant Survival: Extending or
Shortening It?
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE cigarette smoking; adaptive immunity; innate immunity; allograft
survival; transplant tolerance
ID REGULATORY T-CELLS; DENDRITIC CELLS; ALLOGRAFT SURVIVAL;
CARBON-MONOXIDE; HEME OXYGENASE-1; INDOLEAMINE 2,3-DIOXYGENASE;
ALLOANTIBODIES PREVENT; LIVER-TRANSPLANTATION; HEART-TRANSPLANTATION;
LUNG TRANSPLANTATION
AB Cigarette smoking (CS) regulates both innate and adaptive immunity and causes numerous diseases, including cardiovascular, respiratory, and autoimmune diseases, allergies, cancers, and transplant rejection. Therefore, smoking poses a serious challenge to the healthcare system worldwide. Epidemiological studies have always shown that CS is one of the major risk factors for transplant rejection, even though smoking plays redundant roles in regulating immune responses. The complex roles for smoking in immunoregulation are likely due to molecular and functional diversities of cigarette smoke components, including carbon monoxide (CO) and nicotine. Especially, CO has been shown to induce immune tolerance. Although CS has been shown to impact transplantation by causing complications and subsequent rejection, it is overlooked whether CS interferes with transplant tolerance. We have previously demonstrated that cigarette smoke exposure reverses long-term allograft survival induced by costimulatory blockade. Given that CS impacts both adaptive and innate immunity and that it hinders long-term transplant survival, our perspective is that CS impacts transplant tolerance. Here, we review impacts of CS on major immune cells that are critical for transplant outcomes and propose the cellular and molecular mechanisms underlying its effects on alloimmunity and transplant survival. Further investigations are warranted to fully understand why CS exerts deleterious rather than beneficial effects on transplant survival even if some of its components are immunosuppressive.
C1 [Qiu, Feifei; Liu, Huazhen; Liang, Chun-Ling; Yu, Wanlin; Dai, Zhenhua] Guangdong Prov Acad Chinese Med Sci, Immunol Sect, Guangzhou, Guangdong, Peoples R China.
[Fan, Ping] Shaanxi Prov Hosp Chinese Med, Dept Nephrol, Xian, Peoples R China.
[Nie, Golay D.] Univ Texas Med Branch, Sch Med, Galveston, TX 77555 USA.
C3 Guangzhou University of Chinese Medicine; Xi'an Medical University;
University of Texas System; University of Texas Medical Branch Galveston
RP Dai, ZH (corresponding author), Guangdong Prov Acad Chinese Med Sci, Immunol Sect, Guangzhou, Guangdong, Peoples R China.
EM zdai2009@outlook.com
FU National Natural Science Foundation of China (NSFC) [81471550]
FX This work was supported by National Natural Science Foundation of China
(NSFC 81471550).
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NR 60
TC 8
Z9 8
U1 0
U2 14
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015,
SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD FEB 10
PY 2017
VL 8
AR 127
DI 10.3389/fimmu.2017.00127
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA EK2EG
UT WOS:000393740000001
PM 28239383
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Liby, KT
Sporn, MB
AF Liby, Karen T.
Sporn, Michael B.
TI Synthetic Oleanane Triterpenoids: Multifunctional Drugs with a Broad
Range of Applications for Prevention and Treatment of Chronic Disease
SO PHARMACOLOGICAL REVIEWS
LA English
DT Review
ID PROLIFERATOR-ACTIVATED RECEPTOR; CDDO-METHYL ESTER; NF-KAPPA-B;
TRANSGENIC MOUSE MODEL; TRANSCRIPTION FACTOR NRF2; BREAST-CANCER CELLS;
2-CYANO-3,12-DIOXOOLEANA-1,9-DIEN-28-OIC ACID CDDO; ACUTE MYELOGENOUS
LEUKEMIA; NITRIC-OXIDE PRODUCTION; SMOKE-INDUCED EMPHYSEMA
AB We review the rationale for the use of synthetic oleanane triterpenoids (SOs) for prevention and treatment of disease, as well as extensive biological data on this topic resulting from both cell culture and in vivo studies. Emphasis is placed on understanding mechanisms of action. SOs are noncytotoxic drugs with an excellent safety profile. Several hundred SOs have now been synthesized and in vitro have been shown to: 1) suppress inflammation and oxidative stress and therefore be cytoprotective, especially at low nanomolar doses, 2) induce differentiation, and 3) block cell proliferation and induce apoptosis at higher micromolar doses. Animal data on the use of SOs in neurodegenerative diseases and in diseases of the eye, lung, cardiovascular system, liver, gastrointestinal tract, and kidney, as well as in cancer and in metabolic and inflammatory/autoimmune disorders, are reviewed. The importance of the cytoprotective Kelch-like erythroid cell-derived protein with CNC homology-associated protein 1/nuclear factor (erythroid-derived 2)-like 2/antioxidant response element (Keap1/Nrf2/ARE) pathway as a mechanism of action is explained, but interactions with peroxisome proliferator-activated receptor gamma (PARP gamma), inhibitor of nuclear factor-kappa B kinase complex (IKK), janus tyrosine kinase/signal transducer and activator of transcription (JAK/STAT), human epidermal growth factor receptor 2 (HER2)/ErbB2/neu, phosphatase and tensin homolog (PTEN), the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway, mammalian target of rapamycin (mTOR), and the thiol proteome are also described. In these interactions, Michael addition of SOs to reactive cysteine residues in specific molecular targets triggers biological activity. Ultimately, SOs are multifunctional drugs that regulate the activity of entire networks. Recent progress in the earliest clinical trials with 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid (CDDO) methyl ester (bardoxolone methyl) is also summarized.
C1 [Liby, Karen T.] Dartmouth Med Sch, Dept Med, Hanover, NH 03755 USA.
[Liby, Karen T.] Dartmouth Med Sch, Dept Pharmacol, Hanover, NH 03755 USA.
C3 Dartmouth College; Dartmouth College
RP Liby, KT (corresponding author), Dartmouth Med Sch, Dept Med, Remsen 524,HB7650, Hanover, NH 03755 USA.
EM karen.liby@dartmouth.edu
OI Liby, Karen/0000-0003-3317-3437
FU National Institutes of Health National Cancer Institute [R01-CA78814];
National Foundation for Cancer Research; Breast Cancer Research
Foundation; Reata Pharmaceuticals
FX This work was supported by National Institutes of Health National Cancer
Institute [Grant R01-CA78814]; the National Foundation for Cancer
Research; the Breast Cancer Research Foundation; and Reata
Pharmaceuticals. Many colleagues have contributed greatly to this work
over the past 15 years. Special thanks are due to the following: for
chemistry, G. Gribble, T. Honda, H. Finlay, L. Bore, B. Rounds, F.
Favaloro, T. Janosik, J. Han, H. Yoshizawa, C. Sundararajan, E. David,
M. Lajoie, E. Padegimas, X. Jiang, E. Anderson and M. Visnick. For
biology, N. Suh, Y. Wang, A. Place, M. Rendi, E. Heiss, K. Mix, M. Yore,
I. Pitha-Rowe, E. Kim, K. Tran, C. Williams, R. Risingsong, D. Royce, P.
Talalay, A. Dinkova-Kostova, T. Kensler, M. Yates, S. Biswal, R.
Thimmulappa, J. Letterio, J. Handa, E. Duh, F. Beal, A. Albini, M.
Konopleva, M. Andreeff, J. Reed, C. Meyer, C. Wigley, D. Ferguson, S.
Ruiz, and I. Dulubova. Special appreciation is owed to C. Nathan and the
late A. Roberts for their inspiration and assistance in starting this
project and to G. Gribble and T. Honda for their leadership with the
synthetic chemistry. G. Tuson has provided helpful assistance with the
manuscript and figures.
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NR 299
TC 344
Z9 388
U1 1
U2 102
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0031-6997
EI 1521-0081
J9 PHARMACOL REV
JI Pharmacol. Rev.
PD OCT
PY 2012
VL 64
IS 4
BP 972
EP 1003
DI 10.1124/pr.111.004846
PG 32
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 016WW
UT WOS:000309551500006
PM 22966038
OA Green Published
DA 2025-01-07
ER
PT J
AU Malnick, SDH
Abdullah, A
Neuman, MG
AF Malnick, Stephen D. H.
Abdullah, Ali
Neuman, Manuela G.
TI Checkpoint Inhibitors and Hepatotoxicity
SO BIOMEDICINES
LA English
DT Review
DE checkpoint inhibitors; hepatotoxicity; drug induced liver injury; tumor
cells; immunological escape; malignant cells; cytokines
ID CANCER; EXPRESSION; TIM-3; TOXICITIES; IPILIMUMAB; ACTIVATION;
RECEPTORS; NIVOLUMAB; ANTI-PD-1; SURVIVAL
AB Uncontrolled immune response to a pathogen or any protein can lead to tissue damage and autoimmune diseases, that represent aberrant immune responses of the individual to its own cells and/or proteins. The immune checkpoint system is the regulatory mechanism that controls immune responses. Tumor cells escape the immune surveillance mechanism, avoiding immune detection and elimination by activating these checkpoints and suppressing the anti-tumor response, thus allowing formation of tumors. Antigenic modulation facilitates masking and contributes to the escape of tumor cells. In addition, there are growing cell promoters, like transforming growth factor beta (TGF-beta), contributing to escape mechanisms. Targeting the immunological escape of malignant cells is the basis of immune oncology. Checkpoint inhibitors, cytokines and their antibodies may enhance the immune system's response to tumors. Currently, immunomodulatory agents have been designed, evaluated in clinical trials and have been approved by both European and United States Drug Agencies. The present review is a reflection of the increasingly important role of the checkpoint inhibitors. Our aim is to review the side effects with the emphasis on hepatic adverse reactions of these novel biological drug interventions.
C1 [Malnick, Stephen D. H.; Abdullah, Ali] Kaplan Med Ctr, Dept Internal Med C, IL-76100 Rehovot, Israel.
[Neuman, Manuela G.] Vitro Drug Safety & Biotechnol, Toronto, ON M5G IL5, Canada.
[Neuman, Manuela G.] Univ Toronto, Dept Pharmacol & Toxicol, Fac Med, Toronto, ON M5G 1L5, Canada.
C3 Hebrew University of Jerusalem; Kaplan Medical Center; University of
Toronto
RP Malnick, SDH (corresponding author), Kaplan Med Ctr, Dept Internal Med C, IL-76100 Rehovot, Israel.
EM steve_m@clalit.org.il; aliah@clalit.org.il; m_neuman@rogers.com
RI Almutawa, Abdullah/GYQ-5973-2022
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PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD FEB
PY 2021
VL 9
IS 2
AR 101
DI 10.3390/biomedicines9020101
PG 18
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA QM9OE
UT WOS:000622101900001
PM 33494227
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Jafarirad, S
Siassi, F
Harirchian, MH
Amani, R
Bitarafan, S
Saboor-Yaraghi, A
AF Jafarirad, Sima
Siassi, Fereydoon
Harirchian, Mohammad-Hossein
Amani, Reza
Bitarafan, Sama
Saboor-Yaraghi, Aliakbar
TI The Effect of Vitamin A Supplementation on Biochemical Parameters in
Multiple Sclerosis Patients
SO IRANIAN RED CRESCENT MEDICAL JOURNAL
LA English
DT Article
DE Vitamin A; Multiple Sclerosis; C-reactive Protein
ID C-REACTIVE PROTEIN; ACUTE-PHASE PROTEINS; RETINOID-X-RECEPTOR;
GENE-EXPRESSION; ACID; PLASMA; ISOTRETINOIN; CHOLESTEROL; ETRETINATE;
MECHANISMS
AB Background: Vitamin A has different functions in the body and after being converted to acid form; it can play many roles in immune system regulation. Therefore, this vitamin can be used as a supplement in the treatment of diseases, such as cancer and autoimmune diseases. Vitamin A is a fat-soluble compound and its long-term consumption in high doses can have some adverse effects.
Objective: The current study aimed to investigate the possible complications and find solutions to minimize the adverse effects.
Patients and Methods: This study was a double blind randomized clinical trial. In the main study, vitamin A (as retinyl palm itate) was given to 35 multiple sclerosis (MS) patients in order to regulate their immune system with a dose of 250 0 0 IU/day for a period of six months. To investigate the possible biochemical complications, lipid profiles, fasting blood sugar (FBS), liver enzymes, and C-reactive protein (CRP) were tested.
Results: Vitamin A did not have a significant difference in lipid profiles, FBS and liver enzymes between the two groups receiving vitamin A and the placebo, but CRP increased in patients who were taking vitamin A, 1.65 +/- 0.43 (mg/L) and 2.88 +/- 0.67, (Mean +/- SEM), before and after the intervention respectively (P=0.029), and statistical analysis showed significant differences with the group receiving placebo (P=0.011) and CRP level in vitamin A group was 1.3 mg/L more than those of the placebo group after intervention (P=0.011).
Conclusions: Considering that no significant difference was found in the proven vitamin A side effects, due to the increase in CRP, frequent clinical and biochemical controls are required along with vitamin A supplementation.
C1 [Jafarirad, Sima; Siassi, Fereydoon; Bitarafan, Sama; Saboor-Yaraghi, Aliakbar] Univ Tehran Med Sci, Dept Biochem & Nutr, Sch Publ Hlth, Tehran, Iran.
[Harirchian, Mohammad-Hossein] Univ Tehran Med Sci, Iranian Ctr Neurol Res, Tehran, Iran.
[Amani, Reza] Jundishapour Univ Med Sci, Dept Nutr, Sch Paramed, Ahvaz, Iran.
C3 Tehran University of Medical Sciences; Tehran University of Medical
Sciences
RP Saboor-Yaraghi, A (corresponding author), Univ Tehran Med Sci, Dept Biochem & Nutr, Sch Publ Hlth, BP 141613151, Tehran, Iran.
EM asaboor@sina.tums.ac.ir
RI Harirchian, Mohammad/AAW-7087-2020; Siassi, Fereydoun/D-4991-2018;
Amani, Reza/U-7483-2017; Jafarirad, Sima/I-3688-2018
OI Siassi, Fereydoun/0000-0002-2591-9406; Amani, Reza/0000-0002-0074-4080;
Jafarirad, Sima/0000-0002-3161-5329
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NR 34
TC 20
Z9 20
U1 0
U2 5
PU ZAMENSALAMATI PUBL CO
PI MASHHAD
PA KHORASAN, MASHHAD, SANABAD-EBNE SINA ST, MASHHAD, IRAN
SN 2074-1804
EI 2074-1812
J9 IRAN RED CRESCENT ME
JI Iran. Red Crescent Med. J.
PD MAR
PY 2013
VL 15
IS 3
BP 194
EP 198
DI 10.5812/ircmj.3480
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 268CC
UT WOS:000328144600004
PM 23983997
OA Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Scully, M
Cataland, S
Coppo, P
de la Rubia, J
Friedman, KD
Hovinga, JK
Lämmle, B
Matsumoto, M
Pavenski, K
Sadler, E
Sarode, R
Wu, H
AF Scully, M.
Cataland, S.
Coppo, P.
de la Rubia, J.
Friedman, K. D.
Hovinga, J. Kremer
Laemmle, B.
Matsumoto, M.
Pavenski, K.
Sadler, E.
Sarode, R.
Wu, H.
CA Int Working Grp Thrombotic
TI Consensus on the standardization of terminology in thrombotic
thrombocytopenic purpura and related thrombotic microangiopathies
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE ADAMTS-13 protein, human; diagnosis, differential; thrombocytopenia;
thrombotic microangiopathy; thrombotic thrombocytopenic purpura
ID HEMOLYTIC-UREMIC-SYNDROME; FACTOR-CLEAVING PROTEASE; UPSHAW-SCHULMAN
SYNDROME; ADAMTS13 ACTIVITY; PLASMA-EXCHANGE; ANTI-ADAMTS13 ANTIBODIES;
IGG ANTIBODIES; ACUTE EPISODES; RITUXIMAB; MANAGEMENT
AB Background: Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS) are two important acute conditions to diagnose. Thrombotic microangiopathy (TMA) is a broad pathophysiologic process that leads to microangiopathic hemolytic anemia and thrombocytopenia, and involves capillary and smallvessel platelet aggregates. The most common cause is disseminated intravascular coagulation, which may be differentiated by abnormal coagulation. Clinically, a number of conditions present with microangiopathic hemolytic anemia and thrombocytopenia, including cancer, infection, transplantation, drug use, autoimmune disease, and preeclampsia and hemolysis, elevated liver enzymes and low platelet count syndrome in pregnancy. Despite overlapping clinical presentations, TTP and HUS have distinct pathophysiologies and treatment pathways. Objectives: To present a consensus document from an International Working Group on TTP and associated thrombotic microangiopathies (TMAs). Methods: The International Working Group has proposed definitions and terminology based on published information and consensus-based recommendations. Conclusion: The consensus aims to aid clinical decisions, but also future studies and trials, utilizing standardized definitions. It presents a classification of the causes of TMA, and criteria for clinical response, remission and relapse of congenital and immune-mediated TTP.
C1 [Scully, M.] NIHR UCLH UCL BRC, Dept Haematol, Cardiometab Programme, UCLH, London, England.
[Cataland, S.] Ohio State Univ Hosp, Dept Internal Med, Columbus, OH 43210 USA.
[Coppo, P.] St Antoine Univ Hosp, Dept Hematol, Paris, France.
[de la Rubia, J.] Univ Hosp Dr Peset, Dept Hematol, Valencia, Spain.
[Friedman, K. D.] Med Coll Wisconsin, Div Benign Hematol, Milwaukee, WI 53226 USA.
[Hovinga, J. Kremer] Univ Hosp Bern, Dept Hematol, Bern, Switzerland.
[Laemmle, B.] Univ Med Ctr, Ctr Thrombosis & Hemostasis, Mainz, Germany.
[Matsumoto, M.] Nara Med Univ, Dept Blood Transfus Med, Nara, Japan.
[Pavenski, K.] St Michaels Hosp, Res Inst, Dept Lab Med, Toronto, ON, Canada.
[Sadler, E.] Washington Univ, Dept Hematol, Sch Med, St Louis, MO USA.
[Sarode, R.] UT Southwestern Med Ctr, Dept Pathol, Dallas, TX USA.
[Wu, H.] Ohio State Univ Hosp, Dept Pathol, Columbus, OH 43210 USA.
C3 University College London Hospitals NHS Foundation Trust; University of
London; University College London; University System of Ohio; Ohio State
University; Assistance Publique Hopitaux Paris (APHP); Sorbonne
Universite; Hopital Universitaire Saint-Antoine - APHP; Medical College
of Wisconsin; University of Bern; University Hospital of Bern; Johannes
Gutenberg University of Mainz; Nara Medical University; University of
Toronto; Saint Michaels Hospital Toronto; Washington University (WUSTL);
University of Texas System; University of Texas Southwestern Medical
Center Dallas; University System of Ohio; Ohio State University
RP Scully, M (corresponding author), UCLH, Dept Haematol, London W1T 4EU, England.
EM m.scully@ucl.ac.uk
RI De Las Rivas, Javier/G-5936-2014; Pavenski, Katerina/ABM-9349-2022;
Kremer Hovinga, Johanna A./M-3482-2013; Gale, Daniel/D-5594-2013;
Lammle, Bernhard/AAJ-1216-2020
OI Kremer Hovinga, Johanna A./0000-0002-1300-7135; Gale,
Daniel/0000-0002-9170-1579; Peyvandi, Flora/0000-0001-7423-9864; Lammle,
Bernhard/0000-0003-4538-5154
FU EHA-SWG platelet group; MRC [G0800671] Funding Source: UKRI
FX The development of this document involved key international, primarily
clinical, experts involved with TTP, HUS, and related disorders. The
concept was supported by the EHA-SWG platelet group, chaired by the late
R. Stasi (Rome, Italy and London, UK). We thank H. M. Tsai, Taiwan, for
his valuable contribution and review of the manuscript.
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NR 75
TC 334
Z9 357
U1 3
U2 50
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1538-7933
EI 1538-7836
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD FEB
PY 2017
VL 15
IS 2
BP 312
EP 322
DI 10.1111/jth.13571
PG 11
WC Hematology; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Cardiovascular System & Cardiology
GA EK5ON
UT WOS:000393975800013
PM 27868334
OA Green Submitted, Green Published, Bronze
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Akmal, A
Javaid, A
Hussain, R
Kanwal, A
Zubair, M
Ashfaq, UA
AF Akmal, Arina
Javaid, Anam
Hussain, Riaz
Kanwal, Asma
Zubair, Muhammad
Ashfaq, Usman Ali
TI Screening of phytochemicals against KEAP1-NRF2 interaction to reactivate
NRF2 Functioning: Pharmacoinformatics based approach
SO PAKISTAN JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Article
DE Medicinal plants; phytochemicals; molecular docking; KEAP1; NRF2
ID SMALL-MOLECULE; IDENTIFICATION; INHIBITOR
AB The transcription factor NF- E2 p45-related factor 2 (NRF2; encoded by NFE2L2) and its principal negative regulator, the E3 ligase adaptor Kelch- like ECH-associated protein 1 (KEAP1), significantly contribute to regulation of redox, metabolic and protein homeostasis, as well as inflammation. Therefore, activation of NRF2 imparts cytoprotective effect in numerous pathophysiological conditions including chronic diseases of the lung and liver; autoimmune, neurodegenerative and metabolic disorders and cancer initiation. The objective of this study was to screen library of phytochemicals to identify phytochemicals for direct inhibition of the Keapl-Nrf2 interaction using molecular docking approach. As a result, natural compounds such as 3-(Dimethylamino)-3-imino-N-(4-methylphenyl) propanamide, Phlorizin, Diffutin, Liquiritin and Dihydrogenistin were identified as direct inhibitors of the Keap1-Nrf2 interaction, as evident from its high binding affinity and occupancy of specific binding sites of Klech domain Thus these phytochemical could be proposed to improve cell resistance to oxidative stress, suggesting their potential as antioxidants. Moreover, the selected compounds fulfilled the Lipinksi rule and appropriate ADMET properties potentiating its efficacy. However, these need to be validated through experimental approaches to ensure its safety profile and efficacy.
C1 [Akmal, Arina; Javaid, Anam; Kanwal, Asma; Zubair, Muhammad; Ashfaq, Usman Ali] Govt Coll Univ, Dept Bioinformat & Biotechnol, Faisalabad, Pakistan.
[Hussain, Riaz] Aziz Fatima Teaching Hosp Faisalabad, Faisalabad, Pakistan.
C3 Government College University Faisalabad
RP Ashfaq, UA (corresponding author), Govt Coll Univ, Dept Bioinformat & Biotechnol, Faisalabad, Pakistan.
EM usmancemb@gmail.com
RI Kanwal, Asma/JHT-5232-2023; Hussain, Riaz/AAZ-9294-2021; Ashfaq,
Prof.Dr. Usman Ali/D-7792-2013; Zubair, Muhammad/HGA-4479-2022
OI Ashfaq, Prof.Dr. Usman Ali/0000-0002-5495-805X; Zubair,
Muhammad/0000-0003-4534-0968
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NR 29
TC 12
Z9 12
U1 2
U2 9
PU UNIV KARACHI
PI KARACHI
PA UNIV CAMPUS, FAC PHARMACY, KARACHI, 75270, PAKISTAN
SN 1011-601X
J9 PAK J PHARM SCI
JI Pak. J. Pharm. Sci.
PD NOV
PY 2019
VL 33
IS 6
SU S
BP 2823
EP 2828
DI 10.36721/PJPS.2019.32.6.SUP.2823-2828.1
PG 6
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA KD4UK
UT WOS:000507861200008
PM 32024620
DA 2025-01-07
ER
PT J
AU Telieps, T
Ewald, F
Gereke, M
Annemann, M
Rauter, Y
Schuster, M
Ueffing, N
von Smolinski, D
Gruber, AD
Bruder, D
Schmitz, I
AF Telieps, Tanja
Ewald, Frida
Gereke, Marcus
Annemann, Michaela
Rauter, Yvonne
Schuster, Marc
Ueffing, Nana
von Smolinski, Dorthe
Gruber, Achim D.
Bruder, Dunja
Schmitz, Ingo
TI Cellular-FLIP, Raji isoform (c-FLIPR) modulates cell death
induction upon T-cell activation and infection
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE Apoptosis; CD95; c-FLIP; Listeria monocytogenes; T cells
ID INHIBITORY PROTEIN; UP-REGULATION; FAS-LIGAND; CD95-MEDIATED APOPTOSIS;
IMMUNE-RESPONSES; EXPRESSION; FLIPSHORT; RESISTANCE; PROLIFERATION;
CONTRIBUTES
AB Dysregulation of apoptosis caused by an imbalance of pro- and anti-apoptotic protein expression can lead to cancer, neurodegenerative, and autoimmune diseases. Cellular-FLIP (c-FLIP) proteins inhibit apoptosis directly at the death-inducing signaling complex of death receptors, such as CD95, and have been linked to apoptosis regulation during immune responses. While the isoforms c-FLIPL and c-FLIPS are well characterized, the function of c-FLIPR remains poorly understood. Here, we demonstrate the induction of endogenous murine c-FLIPR in activated lymphocytes for the first time. To analyze c-FLIPR function in vivo, we generated transgenic mice expressing murine c-FLIPR specifically in hematopoietic cells. As expected, lymphocytes from c-FLIPR transgenic mice were protected against CD95-induced apoptosis in vitro. In the steady state, transgenic mice had normal cell numbers and unaltered frequencies of B cells and T-cell subsets in lymphoid organs. However, when challenged with Listeria monocytogenes, c-FLIPR transgenic mice showed less liver necrosis and better bacterial clearance compared with infected wild-type mice. We conclude that c-FLIPR expression in hematopoietic cells supports an efficient immune response against bacterial infections.
C1 [Telieps, Tanja; Ewald, Frida; Annemann, Michaela; Rauter, Yvonne; Schuster, Marc; Ueffing, Nana; Schmitz, Ingo] Otto Von Guericke Univ, Lab Syst Oriented Immunol & Inflammat Res, Inst Mol & Clin Immunol, Magdeburg, Germany.
[Telieps, Tanja; Ewald, Frida; Annemann, Michaela; Rauter, Yvonne; Schuster, Marc; Ueffing, Nana; Schmitz, Ingo] Helmholtz Ctr Infect Res, Dept Immune Control, Braunschweig, Germany.
[Gereke, Marcus; Bruder, Dunja] Univ Magdeburg, Dept Med Microbiol, Infect Immunol Grp, D-39106 Magdeburg, Germany.
[Gereke, Marcus; Bruder, Dunja] Helmholtz Ctr Infect Res, Immune Regulat Grp, Braunschweig, Germany.
[von Smolinski, Dorthe] Free Univ Berlin, Inst Vet Pathol, Deptartment Vet Med, Berlin, Germany.
C3 Otto von Guericke University; Helmholtz Association; Helmholtz-Center
for Infection Research; Otto von Guericke University; Helmholtz
Association; Helmholtz-Center for Infection Research; Free University of
Berlin
RP Schmitz, I (corresponding author), Otto Von Guericke Univ, Lab Syst Oriented Immunol & Inflammat Res, Inst Mol & Clin Immunol, Braunschweig, Germany.
EM ingo.schmitz@helmholtz-hzi.de
RI Gruber, Achim/ABA-4514-2021; Schmitz, Ingo/G-2093-2013
OI Schmitz, Ingo/0000-0002-5360-0419
FU Juergen Manchot Stiftung (Duesseldorf); Medical Faculty of the
Otto-von-Guericke University Magdeburg; President's Initiative and
Networking Fund of the Helmholtz Association of German Research Centers
[VH-GS-202, W2/W3029]; DFG [SCHM1586/2-1, SCHM1586/2-2]
FX We are grateful to Dominique Gollasch, Stephanie Grosch, and Sabrina
Schumann for excellent technical assistance and to Alisha Walker for
critically reading the manuscript. We thank Prof. Dr. Robert Klopfleisch
(Veterinary Pathology, FU Berlin) for help with histology. We are
grateful to the FACS facility, especially Dr. Lothar Groebe, and the
animal facility of the Helmholtz Centre for Infection Research for
excellent support. We thank Dr. Tarik Moroy (University of Montreal) for
vav-GFI1b Delta SNAG plasmid, Dr. Ulrich Ruther (University of
Duesseldorf) for generating vavFLIPR mice, as well as Drs.
Klaus Schulze-Osthoff (University of Tuebingen) and Klaus Pfeffer
(University of Duesseldorf) for critical discussion and support. T. T.
has been supported by stipends of the Juergen Manchot Stiftung
(Duesseldorf) and the Medical Faculty of the Otto-von-Guericke
University Magdeburg. F. E. and T. T. are supported by the President's
Initiative and Networking Fund of the Helmholtz Association of German
Research Centers (HGF) under contract number VH-GS-202. D. B. is
supported by the President's Initiative and Networking Fund of the
Helmholtz Association of German Research Centers (HGF) under contract
number W2/W3029. This project was funded by the DFG (SCHM1586/2-1 and
SCHM1586/2-2).
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NR 38
TC 11
Z9 11
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD JUN
PY 2013
VL 43
IS 6
BP 1499
EP 1510
DI 10.1002/eji.201242819
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 169MZ
UT WOS:000320785700018
PM 23505065
OA Bronze
DA 2025-01-07
ER
PT J
AU Ortiz, M
Alvarez, D
Muñoz, Y
Crisosto, N
Valenzuela, R
Maliqueo, M
AF Ortiz, Macarena
Alvarez, Daniela
Munoz, Yasna
Crisosto, Nicolas
Valenzuela, Rodrigo
Maliqueo, Manuel
TI Linoleic and Arachidonic Fatty Acids and their Potential Relationship
with Inflammation, Pregnancy, and Fetal Development
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Fatty acids; linoleic acid; arachidonic acid; obesity; pregnancy; fetal
development; inflammation
ID MATERNAL OBESITY; PUFA TRANSPORT; DIET; LIVER; RATIO; PROSTAGLANDINS;
METABOLISM; ALPHA; RICH; N-3
AB A healthy maternal diet must consider an appropriate supply of long-chain polyunsaturated fatty acids (LCPUFAs) precursors to ensure adequate growth and development of the fetus. In this regard, n-6 PUFAs, predominantly linoleic (C18:2 n-6, LA) and arachidonic acid (C20:4 n-6), have a central role in the development of the central nervous system because they are part of the membrane structure and participate in the metabolism and signal transduction of cells. Nevertheless, they can also be transformed into inflammatory metabolites promoting the pathogenesis of cardiovascular diseases, cancer, and autoimmune or inflammatory conditions. In modern westernized societies, there is a high dietary consumption of foods rich in n-6 PUFAs which could have detrimental consequences for the fetus and neonate due to excessive exposure to these fatty acids (FAs).Objective To summarize the evidence of maternal, placental, and fetal alterations that an excessive intake of n-6 polyunsaturated FAs (PUFAs), LA, and AA, could produce during pregnancy.Methods A thorough review of the literature regarding the effects of n-6 PUFAs during pregnancy and lactation including in vivo and in vitro models, was carried out using the PubMed database from the National Library of Medicine-National Institutes of Health.Results An elevated intake of n-6 PUFA, specifically LA, during pregnancy influences children's motor, cognitive, and verbal development during infancy and early childhood. Similarly, they could harm the placenta and the development of other fetal organs such as the fat tissue, liver, and cardiovascular system.Conclusion Maternal diet, specifically LA intake, could have significant repercussions on fetal development and long-term consequences in the offspring, including the possibility of future metabolic and mental diseases. It would be necessary to focus on the prevention of these alterations through timely dietary interventions in the target population.
C1 [Ortiz, Macarena; Alvarez, Daniela; Munoz, Yasna; Crisosto, Nicolas; Maliqueo, Manuel] Univ Chile, Lab Endocrinol & Metab, Dept Med, West Div, Santiago, Chile.
[Crisosto, Nicolas] Univ Desarrollo, Fac Med, Clin Alemana Santiago, Endocrinol Unit,Dept Med, Santiago, Chile.
[Valenzuela, Rodrigo] Univ Chile, Sch Med, Nutr Dept, Santiago, Chile.
C3 Universidad de Chile; Universidad del Desarrollo; Clinica Alemana;
Universidad de Chile
RP Maliqueo, M (corresponding author), Univ Chile, Sch Med, Dept Med West Div, Lab Endocrinol, Carlos Schachtebeck Las Palmeras 299,Interior Quin, Santiago 8320000, Chile.
EM mmaliqueo@med.uchile.cl
OI Munoz Carvajal, Yasna/0000-0003-3554-7543; Ortiz, Macarena
Paz/0000-0002-8243-8158; Valenzuela, Rodrigo/0000-0001-9298-6142;
Crisosto, Nicolas/0000-0001-9248-0264
FU Agencia Nacional de Investigacin y Desarrollo (FONDECYT) [1181798,
1221098]; Doctoral Scholarship CONICYT-PFCHA/Doctorado
[Nacional/2018-21180579]
FX This work was financially supported by the Agencia Nacional de
Investigacin y Desarrollo (ANID;M.M., FONDECYT grant number 1181798
(M.M), 1221098 (R.V) and Doctoral Scholarship CONICYT-PFCHA/Doctorado
Nacional/2018-21180579(M.O). ANID had no role in this article's design,
analysis, or writing
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NR 87
TC 5
Z9 5
U1 1
U2 5
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2024
VL 31
IS 31
BP 5046
EP 5060
DI 10.2174/0929867331666230706161144
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA A6B3K
UT WOS:001283362400005
PM 37415369
DA 2025-01-07
ER
PT J
AU Neurath, MF
AF Neurath, Markus F.
TI IL-36 in chronic inflammation and cancer
SO CYTOKINE & GROWTH FACTOR REVIEWS
LA English
DT Review
DE Cytokines; IL-36; Immune cells; Inflammation
ID GENERALIZED PUSTULAR PSORIASIS; INTERLEUKIN-36-RECEPTOR ANTAGONIST
DEFICIENCY; RECEPTOR ANTAGONIST; FAMILY CYTOKINES; EXPRESSION; CELLS;
SKIN; ACTIVATION; SECUKINUMAB; PATHWAY
AB IL-36 belongs to the IL-1 family of cytokines and activates target cells by binding to a specific cytokine receptor (IL-36R) followed by activation of intracellular regulators such as MAP kinases and NF-kappaB. Three subforms of IL-36, denoted IL-36alpha, IL-36beta and IL-36gamma, have been described that require N-terminal cleavage for activation. Functional studies have shown that IL-36 may activate a broad spectrum of immune and non-immune cells such as macrophages, T cells, keratinocytes and epithelial cells in an IL-1-independent fashion and thereby controls various inflammatory or oncogenic processes in the skin, the lung, the kidney, the liver and the intestine, respectively. Based on the presence of mutations of the IL-36RN in patients with generalized pustular psoriasis, successful clinical pilot trials with IL-36R blocking antibodies were conducted in these patients and further studies in patients with autoimmune or chronic inflammatory disorders such as inflammatory bowel diseases are under way. Collectively, these findings highlight a crucial regulatory role of IL-36 signaling in driving various inflammatory disorders that provide a rational basis for clinical targeting of this cytokine.
C1 [Neurath, Markus F.] Univ Erlangen Nurnberg, Univ Hosp Erlangen, Dept Med, Med Clin 1, Erlangen, Germany.
[Neurath, Markus F.] Deutsch Zentrum Immuntherapie DZI, Ulmenweg 18, D-91054 Erlangen, Germany.
C3 University of Erlangen Nuremberg
RP Neurath, MF (corresponding author), Univ Hosp Erlangen, Med Clin 1, Ulmenweg 18, D-91054 Erlangen, Germany.
EM Markus.Neurath@uk-erlangen.de
FU [DFGSFB 643]; [SFB1181]; [FOR2438]; [KFO257]
FX DFGSFB 643;SFB1181;FOR2438;KFO257.
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NR 126
TC 38
Z9 48
U1 1
U2 23
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6101
EI 1879-0305
J9 CYTOKINE GROWTH F R
JI Cytokine Growth Factor Rev.
PD OCT
PY 2020
VL 55
BP 70
EP 79
DI 10.1016/j.cytogfr.2020.06.006
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA OG8VF
UT WOS:000582153800007
PM 32540133
DA 2025-01-07
ER
PT J
AU Reis, LG
Ruiz, VLD
Kitamura, SMM
Andrade, AFC
Bussiman, FD
Poleti, MD
da Silveira, JC
Fukumasu, H
Faccioli, LH
Marzocchi-Machado, CM
Strefezzi, RD
Garcia, EN
Casey, T
Netto, AS
AF Reis, Leriana Garcia
Ruiz, Vera Letticie de Azevedo
Kitamura, Simone Maria Massami
Andrade, Andre Furugen Cesar
Bussiman, Fernando de Oliveira
Poleti, Mirele Daiana
da Silveira, Juliano Coelho
Fukumasu, Heidge
Faccioli, Lucia Helena
Marzocchi-Machado, Cleni Mara
Strefezzi, Ricardo de Francisco
Garcia, Edna Neves
Casey, Theresa
Netto, Arlindo Saran
TI Feeding sows milk biofortified with n-6 and n-3 modulates immune status
of sows and drives positive transgenerational effects
SO PLOS ONE
LA English
DT Article
ID POLYUNSATURATED FATTY-ACIDS; GENE-EXPRESSION; PREDICT COLOSTRUM;
MESSENGER-RNA; LITTER SIZE; FISH-OIL; RATIO; PERFORMANCE; LIVER;
INFLAMMATION
AB The risk of chronic diseases such as cardiovascular disease, cancer, inflammation, obesity, and autoimmune disease is linked to the quality of dietary fats, with lower intake of saturated and higher intake of n-6 and n-3 polyunsaturated fatty acids (PUFA) considered beneficial to health. This study investigated the effect of supplementing sows' diets with cow's milk biofortified with n-6 or n-3 PUFA, at varying n-6/n-3 ratios (8.26, 7.92, and 2.72) during their growing phase and throughout gestation and lactation on their reproductive performance and immune-inflammatory status. Specifically, we analyzed circulating cholesterol and fatty acid profiles of serum, colostrum and milk, sow body weight, and neonate colostrum intake, Apgar scores, muscle composition, and embryo viability. Analysis of circulating immunoglobulins (Ig), interleukins, and eicosanoids and complement system hemolytic activity were used to evaluate inflammatory and immune responses of sows and piglets. Expression of lipolysis and lipogenic genes in the liver were investigated in sows and piglets, with additional investigation of hypothalamus genes regulating appetite in sows. Feeding sows milk biofortified with n-6 and n-3 PUFA altered serum fatty acid profiles, reduced triglycerides (TG), increased embryo total number, increased early gestation backfat, and reduced colostrum IgG. Piglets of biofortified sow had higher circulating IgA, IgM and TNF-alpha, and lower IL-10. Sows fed n-3 biofortified milk had higher very low-density lipoproteins (VLDL) and TNF-alpha in circulation. Offspring from sows fed n-6 versus n-3 biofortified milk had lower IL-10 and expression levels of SREBP-1. N-3 versus n-6 also lowered arachidonic acid (ARA) levels in sow's milk and piglet viability 1. Findings offer insights into the potential health benefits of dietary supplementation with biofortified milk in swine, which serve as good model of diet-nutrition studies of humans, and therefore can potentially be considered in dietary recommendations both human and animal populations.
C1 [Reis, Leriana Garcia; Casey, Theresa] Purdue Univ, Dept Anim Sci, W Lafayette, IN 47907 USA.
[Ruiz, Vera Letticie de Azevedo; Poleti, Mirele Daiana; da Silveira, Juliano Coelho; Fukumasu, Heidge; Strefezzi, Ricardo de Francisco] Univ Sao Paulo, Sch Anim Sci & Food Engn, Dept Vet Med, Pirassununga, SP, Brazil.
[Kitamura, Simone Maria Massami; Garcia, Edna Neves; Netto, Arlindo Saran] Univ Sao Paulo, Sch Anim Sci & Food Engn, Dept Anim Sci, Sao Paulo, Brazil.
[Andrade, Andre Furugen Cesar] Univ Sao Paulo, Sch Anim Sci & Food Engn, Dept Anim Reprod, Sao Paulo, Brazil.
[Bussiman, Fernando de Oliveira] Univ Georgia, Dept Anim & Dairy Sci, Athens, GA USA.
[Faccioli, Lucia Helena; Marzocchi-Machado, Cleni Mara] Univ Sao Paulo, Sch Pharmaceut Sci Ribeirao Preto, Dept Clin Anal Toxicol & Food Sci, Ribeirao Preto, SP, Brazil.
C3 Purdue University System; Purdue University; Universidade de Sao Paulo;
Universidade de Sao Paulo; University System of Georgia; University of
Georgia; Universidade de Sao Paulo
RP Reis, LG (corresponding author), Purdue Univ, Dept Anim Sci, W Lafayette, IN 47907 USA.
EM lgarciar@purdue.edu
RI Reis, Leriana/X-5786-2019; Fukumasu, Heidge/B-3866-2013; Strefezzi,
Ricardo/B-8754-2010; Ruiz, Vera/F-8962-2012; Da Silveira,
Juliano/AAH-9784-2020; de Oliveira Bussiman, Fernando/P-7694-2015;
Poleti, Mirele/AAW-6907-2020; Faccioli, Lúcia/AGH-5297-2022; Martins,
Simone/M-7538-2013; Poleti, Mirele/M-4234-2013
OI Faccioli, Lucia Helena/0000-0002-4999-8305; Garcia Reis,
Leriana/0000-0001-9581-9235; Martins, Simone/0000-0002-5895-3678; de
Oliveira Bussiman, Fernando/0000-0001-5417-5816; Poleti,
Mirele/0000-0001-8651-8350
FU Sao Paulo Research Foundation (FAPESP) [2019/22764-9]
FX The authors would like to thank the Sao Paulo Research Foundation
(FAPESP) by the financial support (Grant n degrees 2019/22764-9). The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 88
TC 0
Z9 0
U1 2
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 27
PY 2024
VL 19
IS 8
AR e0306707
DI 10.1371/journal.pone.0306707
PG 35
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA E8L2O
UT WOS:001305453900026
PM 39190668
OA gold
DA 2025-01-07
ER
PT J
AU Trivedi, MK
Branton, A
Trivedi, D
Mondal, S
Jana, S
AF Trivedi, Mahendra Kumar
Branton, Alice
Trivedi, Dahryn
Mondal, Sambhu
Jana, Snehasis
TI Vitamin D3 supplementation improves spatial memory, muscle
function, pain score, and modulates different functional physiological
biomarkers in vitamin D3 deficiency diet (VDD)-induced rats
model
SO BMC NUTRITION
LA English
DT Article
DE Cholecalciferol; Vitamin d(3) deficiency diet; klotho; VDR; Spatial
memory
ID OXIDATIVE STRESS; GRIP STRENGTH; KLOTHO; ASSOCIATION; EXPRESSION; GENE
AB Background Vitamin D Deficiency is recognized as a pandemic, which is associated with high mortality. An inadequate level of vitamin D is associated with autoimmune diseases, hypertension, and cancer. The study was aimed to assess the pharmacological effects of chronic vitamin D-3 supplementation on the manipulation diet regiment of deprived cholecalciferol (vitamin D-3 deficient diet, VDD) rats.Methods Memory performance (Y-maze task), muscular function (muscle grip strength), and pain score (pressure application measurement meter) were measured. Functional biomarkers were measured using ELISA method in different matrix viz. in serum (parathyroid hormone; PTH, calcitonin, thyroxine, and C-reactive protein; CRP, 25-OH Vit D-3), and in CSF (klotho and beta-endorphin). 25-OH Vit D-3 was also estimated in liver and kidney homogenate using ELISA. Vitamin D receptor (VDR) was measured spectrophotometrically in liver and adipose tissue.Results VDD-induced rats showed a decrease in number of entries and time spent in the novel arm and spontaneous alternations in the Y-maze task. Significant improvements of neuromuscular function and pain score after addition of vitamin D-3. In comparison to the VDD group, VDR expression (liver) and active metabolites of vitamin D-3 (25-OH vit.D-3) in serum were significantly higher by 48.23% and 280%, respectively. The PTH and CRP levels were significantly reduced by 32.5% and 35.27%, respectively, whereas calcitonin was increased by 36.67% compared with the VDD group. Klotho and beta-endorphin expressions in cerebrospinal fluid were significantly elevated by 19.67% and 133.59%, respectively, compared to VDD group.Conclusions Overall, the results indicate that supplementation of cholecalciferol significantly improved spatial memory impairment, VDR expression, and may provide an opportunity to manage vitamin D deficiencies.
C1 [Trivedi, Mahendra Kumar; Branton, Alice; Trivedi, Dahryn] Trivedi Global Inc, Henderson, NV USA.
[Mondal, Sambhu; Jana, Snehasis] Trivedi Sci Res Lab Pvt Ltd, Thane W, Maharashtra, India.
RP Jana, S (corresponding author), Trivedi Sci Res Lab Pvt Ltd, Thane W, Maharashtra, India.
EM publication@trivedisrl.com
RI Branton, Alice/J-7074-2015; Trivedi, Dahryn/J-7053-2015; Kumar Trivedi,
Mahendra/J-4219-2015
OI Branton, Alice/0000-0002-3363-3520; Trivedi, Dahryn/0000-0002-3133-8675;
Kumar Trivedi, Mahendra/0000-0002-2548-780X
FU The authors extend their sincere thanks and gratitude to Dabur Research
Foundation, India, for providing the facilities and support that enabled
the successful completion of the work.; Dabur Research Foundation, India
FX The authors extend their sincere thanks and gratitude to Dabur Research
Foundation, India, for providing the facilities and support that enabled
the successful completion of the work.
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NR 44
TC 0
Z9 0
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2055-0928
J9 BMC NUTR
JI BMC Nutr.
PD SEP 25
PY 2023
VL 9
IS 1
AR 108
DI 10.1186/s40795-023-00767-0
PG 13
WC Nutrition & Dietetics
WE Emerging Sources Citation Index (ESCI)
SC Nutrition & Dietetics
GA T0NS6
UT WOS:001075046700003
PM 37749664
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Ramakrishnan, A
Velmurugan, G
Somasundaram, A
Mohanraj, S
Vasudevan, D
Vijayaragavan, P
Nightingale, P
Swaminathan, K
Neuberger, J
AF Ramakrishnan, Arulraj
Velmurugan, Ganesan
Somasundaram, Aravindh
Mohanraj, Sundaresan
Vasudevan, Dinakaran
Vijayaragavan, Paari
Nightingale, Peter
Swaminathan, Krishnan
Neuberger, James
TI Prevalence of abnormal liver tests and liver fibrosis among rural adults
in low and middle-income country: A cross-sectional study
SO ECLINICALMEDICINE
LA English
DT Article
DE Liver fibrosis; prevalence; Abnormal liver tests; Aetiological screening
for abnormal LFT's; Elastography screening; Metabolic syndrome; Low and
middle income country
ID NONALCOHOLIC FATTY LIVER; DISEASE; POPULATION; HEALTH
AB Background Liver disease is the only major chronic disease where the mortality is increasing. Earlier detection of liver fibrosis can reduce progression to cirrhosis and hepatocellular carcinoma. Many studies have reported an increased prevalence in liver fibrosis among adults in urban regions but there are few data in physically active rural populations without attributable metabolic risk factors. This aim of this study is to investigate the prevalence of abnormal liver functions tests (LFTs) and liver fibrosis among adults in a rural population.
Methods This cross-sectional study included observations from KMCH-NNCD-II (2017) study (n = 907) from a farming village, Nallampatti, located in South India. We assessed lifestyle (occupation, tobacco use and alcohol consumption using AUDIT-C questionnaire), markers for metabolic diseases (obesity, hypertension, diabetes, hypercholesterolemia), LFTs and markers for hepatitis viruses B and C. 901 participants had transient elastography to assess fibrosis. Participants with abnormal LFTs and significant liver fibrosis (F2-F4) underwent additional liver screening (caeruloplasmin, iron studies and autoimmune hepatitis panel). Multiple logistic regression analyses were performed to understand the association of liver fibrosis with lifestyle and metabolic risk factors after adjustment for co-variates.
Findings Significant liver fibrosis (F2-F4) was observed in 14.4%, and cirrhosis in 0.8%. There was an association of liver fibrosis with abnormal LFTs but no association between alcohol consumption, viral hepatitis, hepatic liver screening and liver fibrosis. Among metabolic risk factors, no association was observed for hypertension and hypercholesterolemia but diabetes [OR - 3.206 (95% CI: 1.792 - 5.736)], obesity [1.987 (1.341 - 2.944)] and metabolic syndrome [2.539 (1.680 - 3.836)] showed association with significant liver fibrosis (F2-F4) after adjustment for confounding factors.
Interpretation Our results suggest that the prevalence of liver fibrosis in rural population is similar to urban counterparts. The association of metabolic risk factors with liver fibrosis in physically active rural population warrants further investigations in future studies. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)
C1 [Ramakrishnan, Arulraj; Velmurugan, Ganesan; Mohanraj, Sundaresan; Vasudevan, Dinakaran; Swaminathan, Krishnan] Kovai Med Ctr & Hosp, KMCH Res Fdn, Coimbatore, Tamil Nadu, India.
[Ramakrishnan, Arulraj; Somasundaram, Aravindh; Vijayaragavan, Paari] Kovai Med Ctr & Hosp, Liver Unit, Coimbatore 641014, Tamil Nadu, India.
[Nightingale, Peter] Univ Hosp Birmingham, Birmingham B15 2TH, England.
[Neuberger, James] Univ Hosp Birmingham, Liver Unit, Birmingham B15 2TH, England.
C3 University of Birmingham; University of Birmingham
RP Ramakrishnan, A (corresponding author), Kovai Med Ctr & Hosp, KMCH Res Fdn, Liver Unit, Coimbatore 641014, Tamil Nadu, India.
EM arulraas@yahoo.com
RI Neuberger, James/ABG-3010-2020; Vasudevan, Dinakaran/AAE-1954-2020
OI Ramakrishnan, Arulraj/0000-0001-8133-224X; Sundaresan,
Mohanraj/0000-0001-6757-3194; Vasudevan, Dinakaran/0000-0003-0593-370X
FU KMCH Research Foundation, India
FX This study is funded by KMCH Research Foundation, India.
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U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2589-5370
J9 ECLINICALMEDICINE
JI EClinicalMedicine
PD SEP
PY 2022
VL 51
AR 101553
DI 10.1016/j.eclinm.2022.101553
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 7N4BQ
UT WOS:000907286800017
PM 35860452
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Jasyk, I
Siednienko, J
AF Jasyk, Izabella
Siednienko, Jakub
TI Type I interferon therapies of multiple sclerosis and hepatitis C virus
infection
SO POSTEPY HIGIENY I MEDYCYNY DOSWIADCZALNEJ
LA English
DT Article
DE interferon type I; multiple sclerosis; hepatitis C virus; MAP kinases;
NF-kappa B; STAT
ID BLOOD-BRAIN-BARRIER; MESSENGER-RNA TRANSLATION; VAV PROTOONCOGENE
PRODUCT; PLACEBO-CONTROLLED TRIAL; CENTRAL-NERVOUS-SYSTEM;
TUMOR-NECROSIS-FACTOR; DOUBLE-BLIND; MAGNETIC-RESONANCE; NON-A;
PHOSPHATIDYLINOSITOL 3-KINASE
AB Interferons type I (IFN-I), activated following a bacterial or viral infection, play a major role in the induction and regulation of the immune system. The immune response results in viral RNA and binds to receptors such as RIG-I-like receptors (RLRs) or Toll-like receptors, leading to the IFN-I signaling cascade. Thanks to its cellular function, IFN-I is widely used in therapies for such diseases as multiple sclerosis (MS) and hepatitis C disease (HCD).
MS is a neurological, autoimmune, chronic inflammatory disease of the central nervous system (CNS). During MS, nerve cell demyelination is observed due to the myelin heaths and oligodendrocyte damage. As a result, neuronal signal and neuron communication are attenuated. The mechanism of MS is still unknown. MS therapy applies interferon-beta (IFN-beta). IFN-beta therapy has been used since the last century, but the therapeutic mechanism of IFN-beta has not been completely understood. MS can lead to four syndromes: clinically isolated syndrome (CIS), relapsing-remitting MS (RRMS), primary progressive MS (PPMS), and secondary progressive MS (SPMS).
HCD occurs as a result of infection with the hepatitis C virus (HCV), belonging to the Flaviviridae family. HCV is a blood-borne virus with a positive single-stranded RNA. A vaccine for HCV is not available yet. HCD can lead to liver damage or cancer. In HCD interferon-alpha therapy (IFN-alpha) is applied. As with MS, the mechanism of IFN-alpha therapy is not completely known.
C1 [Jasyk, Izabella] Polish Acad Sci, Inst Immunol & Expt Therapy, Lab Microbiome Immunobiol, Wroclaw, Poland.
[Jasyk, Izabella; Siednienko, Jakub] Lukasiewicz Res Network PORT Polish Ctr Technol D, Bioengn Res Grp, Wroclaw, Poland.
C3 Polish Academy of Sciences; Hirszfeld Institute of Immunology &
Experimental Therapy of the Polish Academy of Sciences
RP Jasyk, I (corresponding author), Polish Acad Sci, Inst Immunol & Expt Therapy, Lab Microbiome Immunobiol, Wroclaw, Poland.; Jasyk, I (corresponding author), Lukasiewicz Res Network PORT Polish Ctr Technol D, Bioengn Res Grp, Wroclaw, Poland.
EM Izabella.jasyk@port.lukasiewicz.gov.pl
OI Siednienko, Jakub/0000-0003-2358-5876
FU National Science Centre, Poland [UMO-2015/18/E/NZ3/00695]
FX This work was supported by the grant No. UMO-2015/18/E/NZ3/00695 from
the National Science Centre, Poland.
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NR 119
TC 1
Z9 1
U1 0
U2 3
PU POLISH ACAD SCIENCES, INST IMMUNOL & EXP THERAPY
PI WROCLAW
PA RUDOLF WEIGL 12, WROCLAW, 53-114, POLAND
SN 0032-5449
EI 1732-2693
J9 POSTEP HIG MED DOSW
JI Postep. Hig. Med. Dosw.
PD OCT 21
PY 2021
VL 75
IS 1
BP 537
EP 547
DI 10.2478/ahem-2021-0001
PG 11
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA YJ5WR
UT WOS:000744603600003
OA gold
DA 2025-01-07
ER
PT J
AU Roberts, SB
Hirschfield, GM
Worobetz, LJ
Vincent, C
Flemming, JA
Cheung, A
Qumosani, K
Swain, M
Grbic, D
Ko, HH
Peltekian, K
Selzner, N
Abrahamyan, L
Aziz, B
Lytvyak, E
Tirona, K
Gulamhusein, AF
Janssen, HLA
Montano-Loza, AJ
Mason, AL
Hansen, BE
AF Roberts, Surain B.
Hirschfield, Gideon M.
Worobetz, Lawrence J.
Vincent, Catherine
Flemming, Jennifer A.
Cheung, Angela
Qumosani, Karim
Swain, Mark
Grbic, Dusanka
Ko, Hin Hin
Peltekian, Kevork
Selzner, Nazia
Abrahamyan, Lusine
Aziz, Bishoi
Lytvyak, Ellina
Tirona, Kattleya
Gulamhusein, Aliya F.
Janssen, Harry L. A.
Montano-Loza, Aldo J.
Mason, Andrew L.
Hansen, Bettina E.
CA Canadian Network Autoimmune Liver
TI Ethnicity, disease severity, and survival in Canadian patients with
primary biliary cholangitis
SO HEPATOLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; RHEUMATOID-ARTHRITIS; CIRRHOSIS; OUTCOMES; POPULATION;
VALIDATION; DISCOVERY; ALBERTA
AB Background and Aims We investigated associations between ethnicity, survival, and disease severity in a diverse Canadian cohort of patients with primary biliary cholangitis (PBC). Approach and Results Patients with PBC were included from the Canadian Network for Autoimmune Liver Disease. Ethnicity was defined using a modified list adopted from Statistics Canada, and ethnicities with small samples were grouped. Clinical events were defined as liver decompensation, HCC, liver transplantation, or death. Clinical event-free and liver transplantation-free survival were analyzed using Cox regression. Trajectories of serum liver function tests were assessed over time using mixed-effects regression. Health-related quality of life was assessed using the Short Form 36, the PBC-40 questionnaire, and the 5-D Itch scale and analyzed using mixed-effects regression. The cohort included 1538 patients with PBC from six sites and was comprised of 82% White, 4.7% Indigenous, 5.5% East Asian, 2.6% South Asian, and 5.1% miscellaneous ethnicities. Indigenous patients were the only ethnic group with impaired liver transplant-free and event-free survival compared to White patients (HR, 3.66; 95% CI, 2.23-6.01; HR, 3.09; 95% CI, 1.94-4.92). Indigenous patients were more likely to have a clinical event before diagnosis (10%) than all other ethnic groups despite similar age at diagnosis. Indigenous patients presented with higher alkaline phosphatase, total bilirubin, and GLOBE scores than White patients; and these relative elevations persisted during follow-up. Conclusions Indigenous Canadians with PBC present with advanced disease and have worse long-term outcomes compared to White patients.
C1 [Roberts, Surain B.; Hirschfield, Gideon M.; Tirona, Kattleya; Gulamhusein, Aliya F.; Janssen, Harry L. A.; Hansen, Bettina E.] Univ Hlth Network, Toronto Gen Hosp, Toronto Ctr Liver Dis, Toronto, ON, Canada.
[Roberts, Surain B.; Hirschfield, Gideon M.; Abrahamyan, Lusine; Gulamhusein, Aliya F.; Hansen, Bettina E.] Univ Toronto, Inst Hlth Policy Management & Evaluat, Toronto, ON, Canada.
[Worobetz, Lawrence J.] Univ Saskatchewan, Dept Med, Saskatoon, SK, Canada.
[Vincent, Catherine] Univ Montreal, Dept Med, Montreal, PQ, Canada.
[Flemming, Jennifer A.] Queens Univ, Dept Med, Kingston, ON, Canada.
[Cheung, Angela] Univ Ottawa, Dept Med, Ottawa, ON, Canada.
[Qumosani, Karim] Western Univ, Dept Med, London, ON, Canada.
[Swain, Mark] Univ Calgary, Dept Med, Calgary, AB, Canada.
[Grbic, Dusanka] Univ Sherbrooke, Dept Med, Sherbrooke, PQ, Canada.
[Ko, Hin Hin] Univ British Columbia, Dept Med, Vancouver, BC, Canada.
[Peltekian, Kevork] Dalhousie Univ, Dept Med, Halifax, NS, Canada.
[Selzner, Nazia; Abrahamyan, Lusine] Univ Hlth Network, Toronto Gen Hosp Res Inst, Toronto, ON, Canada.
[Aziz, Bishoi; Lytvyak, Ellina; Montano-Loza, Aldo J.; Mason, Andrew L.] Univ Alberta, Dept Med & Dent, Edmonton, AB, Canada.
C3 University of Toronto; University Health Network Toronto; Toronto
General Hospital; University of Toronto; University of Saskatchewan;
Universite de Montreal; Queens University - Canada; University of
Ottawa; Western University (University of Western Ontario); University
of Calgary; University of Sherbrooke; University of British Columbia;
Dalhousie University; University of Toronto; University Health Network
Toronto; University of Alberta
RP Hansen, BE (corresponding author), Univ Toronto, Toronto Gen Hosp, Toronto Ctr Liver Dis, Inst Hlth Policy, 200 Elizabeth St, Toronto, ON M5G 2C4, Canada.
EM bettina.hansen@utoronto.ca
RI Aziz, Bishoi/M-5984-2018; Hirschfield, Gideon/M-2143-2015; Kiemeney,
Lambertus/D-3357-2009; Selzner, Nazia/AAI-1469-2020; Montano-Loza,
Aldo/B-3092-2013; Mason, Andrew/D-2938-2013; Flemming,
Jennifer/L-4228-2018
OI Mason, Andrew/0000-0002-0470-9522; Flemming,
Jennifer/0000-0002-9911-0925; Roberts, Surain/0000-0001-8792-2240; Aziz,
Bishoi/0000-0002-8762-753X; Janssen, Harry/0000-0003-2398-8392; Lytvyak,
Ellina/0000-0001-5651-9010; Abrahamyan, Lusine/0000-0003-2788-4179; Ko,
Hin Hin/0000-0002-6433-5956
FU Canadian Liver Foundation; Intercept Pharma Canada Inc.; Toronto General
& Western Hospital Foundation
FX Supported in part by unrestricted financial support from the Canadian
Liver Foundation, Intercept Pharma Canada Inc., and the Toronto General
& Western Hospital Foundation. The funders had no influence on the study
design, data collection, analysis and interpretation of data, or the
decision to submit for publication.
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NR 35
TC 10
Z9 10
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD AUG
PY 2022
VL 76
IS 2
BP 303
EP 316
DI 10.1002/hep.32426
EA MAR 2022
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 2Y5VT
UT WOS:000768844900001
PM 35220609
DA 2025-01-07
ER
PT J
AU Hong, JW
Jing, SL
Zhang, YP
Chen, RG
Owusu, KG
Chen, BJ
Xie, HY
Zhou, L
Zheng, SS
Jiang, DH
AF Hong, Jiawei
Jing, Shilei
Zhang, Yanpeng
Chen, Ronggao
Owusu-Ansah, Kwabena Gyabaah
Chen, Bingjie
Xie, Haiyang
Zhou, Lin
Zheng, Shusen
Jiang, Donghai
TI Y-320, a novel immune-modulator, sensitizes multidrug-resistant tumors
to chemotherapy
SO AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
LA English
DT Article
DE Y-320; multidrug resistance; P glycoprotein; chemotherapy sensitizer;
combined therapy
ID CANCER LIVER METASTASES; IL-17; IMMUNOMODULATOR
AB Y-320, a novel immune-modulator, inhibits IL-17 production by CD4(+) T cells stimulated with IL-15. Its use in autoimmune diseases such as rheumatoid arthritis has been documented. However, no studies have be conducted to evaluate its application in cancer treatment either as mono or combined therapy. This study demonstrated that while Y-320 had little effect on multidrug resistance (MDR) cell lines, it induced remarkable injury to MDR tumor cells when concurrently administered with other chemotherapeutic agents. Concomitant use of Y-320 with a low dose of paclitaxel significantly sensitized MDR tumors by inducing G2/M phase arrest and apoptosis. Further analyses indicated that Y-320 was a substrate of P-glycoprotein (P-gp). It could inhibit P-gp efflux function without altering P-gp expression, and subsequently reverse P-gp mediated drug resistance in MDR cells. The co-administration of Y-320 and paclitaxel suppressed tumor growth remarkably with an inhibition rate of 77.1% compared to 6.5% in the paclitaxel monotherapy group in vivo. This co-treatment did not increase extra complications in MDR tumor xenograft models. Particularly, no significant changes in body weight and hepatorenal serology were observed with the co-treatment. In conclusion, our results confirm that Y-320 is a promising chemotherapy sensitizer for the first time. The co-administration of Y-320 and chemotherapeutic agents might be an effective and low-toxicity chemotherapeutic regime for the MDR tumor patients.
C1 [Hong, Jiawei; Jing, Shilei; Zhang, Yanpeng; Chen, Ronggao; Owusu-Ansah, Kwabena Gyabaah; Chen, Bingjie; Xie, Haiyang; Zhou, Lin; Zheng, Shusen; Jiang, Donghai] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Dept Surg,Div Hepatobiliary & Pancreat Surg, 79 Qingchun Rd, Hangzhou 310000, Zhejiang, Peoples R China.
[Hong, Jiawei; Jing, Shilei; Zhang, Yanpeng; Chen, Ronggao; Owusu-Ansah, Kwabena Gyabaah; Chen, Bingjie; Xie, Haiyang; Zhou, Lin; Zheng, Shusen; Jiang, Donghai] NHFPC Key Lab Combined Multiorgan Transplantat, Hangzhou 310000, Peoples R China.
[Xie, Haiyang; Zhou, Lin; Zheng, Shusen; Jiang, Donghai] CAMS, Key Lab Diag & Treatment Organ Transplantat, Beijing, Peoples R China.
[Xie, Haiyang; Zhou, Lin; Zheng, Shusen; Jiang, Donghai] Key Lab Organ Transplantat, Hangzhou 310003, Zhejiang, Peoples R China.
[Xie, Haiyang; Zhou, Lin; Zheng, Shusen; Jiang, Donghai] Collaborat Innovat Ctr Diag Treatment Infect Dis, Hangzhou 310000, Zhejiang, Peoples R China.
C3 Zhejiang University; Chinese Academy of Medical Sciences - Peking Union
Medical College; Collaborative Innovation Center for Diagnosis &
Treatment of Infectious Diseases
RP Zheng, SS; Jiang, DH (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 1, Dept Surg,Div Hepatobiliary & Pancreat Surg, 79 Qingchun Rd, Hangzhou 310000, Zhejiang, Peoples R China.
EM shu-senzheng@zju.edu; jdh8499@zju.edu.cn
RI Owusu-Ansah, Dr. Kwabena Gyabaah/R-7920-2019
OI Owusu-Ansah, Dr. Kwabena Gyabaah/0000-0002-6566-3222
FU Zhejiang Provincial Natural Science Foundation [LY18H160017];
Fundamental Research Funds for the Central Universities
[2019XZZX005-1-08]; Innovative Research Groups of National Natural
Science Foundation of China [81721091]; National ST Major Project
[2017ZX10203205]; Zhejiang International Science and Technology
Cooperation Project [2016C04003]
FX We thank Mrs. Rong Su for providing the flow cytometry technology. We
thank Mr. Cheng Jin and Mrs. Mengqiao Zhou for providing the xenograft
technology of athymic nude mice. We thank the support of Zhejiang
Provincial Natural Science Foundation (LY18H160017), Fundamental
Research Funds for the Central Universities (2019XZZX005-1-08),
Innovative Research Groups of National Natural Science Foundation of
China (No. 81721091), National S&T Major Project (No. 2017ZX10203205),
Zhejiang International Science and Technology Cooperation Project (NO.
2016C04003).
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NR 28
TC 10
Z9 11
U1 0
U2 3
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1943-8141
J9 AM J TRANSL RES
JI Am. J. Transl. Res.
PY 2020
VL 12
IS 2
BP 551
EP 562
PG 12
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA KS6DF
UT WOS:000518396700018
PM 32194903
DA 2025-01-07
ER
PT J
AU Simopoulos, C
Tsaroucha, AK
Asimakopoulos, B
Giatromanolaki, A
Gavriilidis, P
Polychronidis, A
Karayiannakis, A
AF Simopoulos, Constantinos
Tsaroucha, Alexandra K.
Asimakopoulos, Byron
Giatromanolaki, Alexandra
Gavriilidis, Paschalis
Polychronidis, Alexandros
Karayiannakis, Anastasios
TI Total and caspase-cleaved cytokeratin 18 in chronic cholecystitis: A
prospective study
SO BMC GASTROENTEROLOGY
LA English
DT Article
ID EPITHELIAL-CELL APOPTOSIS; LIVER; PATIENT; CANCER; SERUM; EXPRESSION;
HEPATITIS; FRAGMENTS; KINETICS; NECROSIS
AB Background: Cell death mode has been studied in cancer, autoimmune, and neurodegenerative diseases. In this study, apoptosis and necrosis are investigated for the first time in patients with chronic calculous cholecystitis.
Methods and materials: Thirty five (35) patients (27 women and 8 men, aged 55.65 +/- 13.48 years) with symptomatic chronic calculous cholecystitis underwent laparoscopic cholecystectomy. The early specific apoptotic tendency (caspase-cleaved cytokeratin 18) was studied in these patients with M30 Apoptosense ELISA and the total cytokerarin 18 (both derived from apoptosis and necrosis) with M65 ELISA. The ratio M30/M65 (caspase-cleaved to total cytokeratin 18) was also computed. According to the histopathological examination, the patients were divided in two groups: group A included patients with chronic inactive cholecystitis (n = 10), and group B those with chronic active cholecystitis (n = 25).
Results: The concentrations of caspase-cleaved cytokerarin 18 (CK18), and especially those of total CK18, were higher in bile samples than in serum samples. In group B, there were significant differences between serum and bile samples regarding both caspase-cleaved CK18 and total CK18. Cells staining positive for caspase-cleaved CK18 were present in the epithelial cells of the mucosa of the gallbladder.
Conclusion: CK18 is expressed in the gallbladder epithelial cells. The concentrations of both caspase-cleaved CK18 and total CK18 were higher in bile samples than in serum samples. The levels of total CK18, as well as caspase-cleaved CK18, do not seem to differ between active and inactive chronic cholecystitis.
C1 [Simopoulos, Constantinos; Tsaroucha, Alexandra K.; Gavriilidis, Paschalis; Polychronidis, Alexandros; Karayiannakis, Anastasios] Democritus Univ Thrace, Sch Med, Dept Surg 2, Alexandroupolis 68100, Greece.
[Asimakopoulos, Byron] Democritus Univ Thrace, Sch Med, Physiol Lab, Alexandroupolis 68100, Greece.
[Giatromanolaki, Alexandra] Democritus Univ Thrace, Sch Med, Dept Pathol, Alexandroupolis 68100, Greece.
C3 Democritus University of Thrace; Democritus University of Thrace;
Democritus University of Thrace
RP Tsaroucha, AK (corresponding author), Democritus Univ Thrace, Sch Med, Dept Surg 2, Alexandroupolis 68100, Greece.
EM simop@med.duth.gr; tsihrin@otenet.gr; byrona@panafonet.gr;
targ@her.forthnet.gr; pgav7461@yahoo.com; polych@med.duth.gr;
akarayan@usa.net
RI Asimakopoulos, Byron/AAK-4327-2021; Karayiannakis,
Anastasios/H-9801-2019; Gavriilidis, Paschalis/N-2440-2019
OI Gavriilidis, Pascal/0000-0001-7773-2291; Simopoulos,
Konstantinos/0000-0002-7994-3583; Karayiannakis,
Anastasios/0000-0002-9278-4273
CR Bantel H, 2004, HEPATOLOGY, V40, P1078, DOI 10.1002/hep.20411
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NR 25
TC 10
Z9 10
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD MAY 6
PY 2008
VL 8
AR 14
DI 10.1186/1471-230X-8-14
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 308FX
UT WOS:000256374800001
PM 18460214
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Niederseer, D
Wernly, S
Bachmayer, S
Wernly, B
Bakula, A
Huber-Schönauer, U
Semmler, G
Schmied, C
Aigner, E
Datz, C
AF Niederseer, David
Wernly, Sarah
Bachmayer, Sebastian
Wernly, Bernhard
Bakula, Adam
Huber-Schoenauer, Ursula
Semmler, Georg
Schmied, Christian
Aigner, Elmar
Datz, Christian
TI Diagnosis of Non-Alcoholic Fatty Liver Disease (NAFLD) Is Independently
Associated with Cardiovascular Risk in a Large Austrian Screening Cohort
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE NAFLD; cardiovascular risk; Framingham risk score; CVD; risk prediction;
secondary prevention; primary prevention; metabolic syndrome; NAFLD
fibrosis score
ID MORTALITY; FIBROSIS
AB Background: Many patients with non-alcoholic fatty liver disease (NAFLD) simultaneously suffer from cardiovascular (CV) disease and often carry multiple CV risk factors. Several CV risk factors are known to drive the progression of fibrosis in patients with NAFLD. Objectives: To investigate whether an established CV risk score, the Framingham risk score (FRS), is associated with the diagnosis of NAFLD and the degree of fibrosis in an Austrian screening cohort for colorectal cancer. Material and Methods: In total, 1965 asymptomatic subjects (59 +/- 10 years, 52% females, BMI 27.2 +/- 4.9 kg/m(2)) were included in this study. The diagnosis of NAFLD was present if (1) significantly increased echogenicity in relation to the renal parenchyma was present in ultrasound and (2) viral, autoimmune or hereditary liver disease and excess alcohol consumption were excluded. The FRS (ten-year risk of coronary heart disease) and NAFLD Fibrosis Score (NFS) were calculated for all patients. High CV risk was defined as the highest FRS quartile (>10%). Both univariable and multivariable logistic regression models were used to calculate associations of FRS with NAFLD and NFS. Results: Compared to patients without NAFLD (n = 990), patients with NAFLD (n = 975) were older (60 +/- 9 vs. 58 +/- 10 years; p < 0.001), had higher BMI (29.6 +/- 4.9 vs. 24.9 +/- 3.6 kg/m(2); p < 0.001) and suffered from metabolic syndrome more frequently (33% vs. 7%; p < 0.001). Cardiovascular risk as assessed by FRS was higher in the NAFLD-group (8.7 +/- 6.4 vs. 5.4 +/- 5.2%; p < 0.001). A one-percentage-point increase of FRS was independently associated with NAFLD (OR 1.04, 95%CI 1.02-1.07; p < 0.001) after correction for relevant confounders in multivariable logistic regression. In patients with NAFLD, NFS correlated with FRS (r = 0.29; p < 0.001), and FRS was highest in patients with significant fibrosis (F3-4; 11.7 +/- 5.4) compared to patients with intermediate results (10.9 +/- 6.3) and those in which advanced fibrosis could be ruled-out (F0-2, 7.8 +/- 5.9, p < 0.001). A one-point-increase of NFS was an independent predictor of high-risk FRS after correction for sex, age, and concomitant diagnosis of metabolic syndrome (OR 1.30, 95%CI 1.09-1.54; p = 0.003). Conclusion: The presence of NAFLD might independently improve prediction of long-term risk for CV disease and the diagnosis of NAFLD might be a clinically relevant piece in the puzzle of predicting long-term CV outcomes. Due to the significant overlap of advanced NAFLD and high CV risk, aggressive treatment of established CV risk factors could improve prognosis in these patients.
C1 [Niederseer, David; Bakula, Adam; Schmied, Christian] Univ Zurich, Univ Hosp Zurich, Univ Heart Ctr Zurich, Dept Cardiol, CH-8091 Zurich, Switzerland.
[Wernly, Sarah; Bachmayer, Sebastian; Huber-Schoenauer, Ursula; Semmler, Georg; Datz, Christian] Paracelsus Med Univ Salzburg, Teaching Hosp, Gen Hosp Oberndorf, Dept Internal Med, A-5110 Oberndorf, Austria.
[Wernly, Bernhard] Paracelsus Med Univ Salzburg, Dept Internal Med 2, A-5020 Salzburg, Austria.
[Aigner, Elmar] Paracelsus Med Univ Salzburg, Dept Internal Med 1, A-5020 Salzburg, Austria.
C3 University of Zurich; University Zurich Hospital; Paracelsus Private
Medical University; Paracelsus Private Medical University; Paracelsus
Private Medical University
RP Niederseer, D (corresponding author), Univ Zurich, Univ Hosp Zurich, Univ Heart Ctr Zurich, Dept Cardiol, CH-8091 Zurich, Switzerland.
EM david.niederseer@usz.ch; sarah_wernly@airpost.net;
S.Bachmayer@kh-oberndorf.at; bernhard@wernly.net; adam.bakula@usz.ch;
huber.schoenauer@gmail.com; georg.semmler@hotmail.com;
christian.schmied@usz.ch; e.aigner@salk.at; c.datz@kh-oberndorf.at
RI Schmied, Christian/JFJ-9105-2023; Wernly, Bernhard/AAA-8529-2020;
Semmler, Georg/O-3323-2019; Niederseer, David/X-7363-2018
OI Semmler, Georg/0000-0002-0411-166X; Wernly,
Bernhard/0000-0003-4024-0220; Huber-Schonauer,
Ursula/0000-0003-4674-6230; Niederseer, David/0000-0003-3089-1222
FU SPAR AG
FX Funding by SPAR AG to C.D. is greatly appreciated.
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NR 27
TC 19
Z9 20
U1 3
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD APR
PY 2020
VL 9
IS 4
AR 1065
DI 10.3390/jcm9041065
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA LL8RF
UT WOS:000531821000172
PM 32283679
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Hill, M
Havlílová, H
Vrbílová, J
Kancheva, R
Kancheva, L
Pouzar, V
Cerny, I
Stárka, L
AF Hill, M
Havlílová, H
Vrbílová, J
Kancheva, R
Kancheva, L
Pouzar, V
Cerny, I
Stárka, L
TI The identification and simultaneous quantification of 7-hydroxylated
metabolites of pregnenolone, dehydroepiandrosterone,
3β,17β-androstenediol, and testosterone in human serum using gas
chromatography-mass spectrometry
SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Article
DE 7-hydroxy steroids; GC-MS; neuroprotective steroids; immunomodulatory
steroids; ergosteroids
ID BREAST-CANCER PATIENTS; IN-VITRO; 7-HYDROXYDEHYDROEPIANDROSTERONE
EPIMERS; 7-ALPHA-HYDROXY DEHYDROEPIANDROSTERONE; ADRENAL ANDROGENS;
IMMUNE-RESPONSE; HAMSTER LIVER; RAT-LIVER; STEROIDS; ERGOSTEROIDS
AB 7-Hydroxy-metabolites of dehydroepiandrosterone (DHEA) and 3 beta,17 beta-androstenediol (AD) possess immunomodulatory and neuroprotective properties; therefore, the measurement of these steroids in patients with autoimmune diseases or disturbances in the CNS may be of interest. A gas chromatography-mass spectrometry (GC-MS) method for the determination of 7-hydroxy-metabolites of pregnenolone, DHEA, AD, and testosterone including the parent steroids was applied to serum samples from 12 adult men (27-66 years), 13 male adolescents (13-20 years), 5 boys (6-10 years), 15 women in the follicular phase of the menstrual cycle (22-45 years), 17 women in the luteal phase (22-45 years), and 4 girls (6-10 years)
The steroids were age and sex dependent, but independent of the menstrual cycle. The ratio of the 7 alpha-hydroxy-metabolites to their parent steroids were age dependent, exhibiting an increasing trend (p < 0.0001, ANOVA) from pregnenolone (5%) to AD (20%). The ratio of 7 beta- to 7 alpha-metabolites ranged from 0.6 to 1. These results are consistent with models suggesting 7 alpha-hydroxylation of the parent steroid, conversion to a 7-oxo-steroid and finally to the 7 beta-hydroxylated-metabolite. Partial correlations suggested that 7-hydroxylation might reduce the concentration of circulating androgens. Despite the three times lower concentration of AD-metabolites, their antiglucocorticoid, immunomodulatory, and neuroprotective effects may be comparable to that of DHEA based on their reported greater biological activity. (c) 2005 Elsevier Ltd. All rights reserved.
C1 Inst Endocrinol, Narodni Trida 8, CZ-11694 Prague, Czech Republic.
Acad Sci Czech Republic, Inst Organ Chem & Biochem, CR-16610 Prague, Czech Republic.
C3 Institute of Endocrinology - Prague; Czech Academy of Sciences;
Institute of Organic Chemistry & Biochemistry of the Czech Academy of
Sciences
RP Inst Endocrinol, Narodni Trida 8, CZ-11694 Prague, Czech Republic.
EM mhill@endo.cz; hhavlikova@endo.cz; jvrbikova@endo.cz; rkanceva@endo.cz;
lkanceva@endo.cz; pouzar@uochb.cas.cz; cerny@uochb.cas.cz;
lstarka@endo.cz
RI Hill, Martin/G-7699-2019
OI Starka, Luboslav/0000-0003-4589-6050; Hill, Martin/0000-0002-1705-0835
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NR 46
TC 23
Z9 23
U1 0
U2 15
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-0760
J9 J STEROID BIOCHEM
JI J. Steroid Biochem. Mol. Biol.
PD JUL
PY 2005
VL 96
IS 2
BP 187
EP 200
DI 10.1016/j.jsbmb.2005.02.009
PG 14
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 959JX
UT WOS:000231515100009
PM 15908198
DA 2025-01-07
ER
PT J
AU Goudarzi, M
Kalantar, M
Sadeghi, E
Karamallah, MH
Kalantar, H
AF Goudarzi, Mehdi
Kalantar, Mojtaba
Sadeghi, Elahe
Karamallah, Mojtaba Haghi
Kalantar, Hadi
TI Protective effects of apigenin on altered lipid peroxidation,
inflammation, and antioxidant factors in methotrexate-induced
hepatotoxicity
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Article
DE Methotrexate; Apigenin; Hepatotoxicity; Oxidative stress; Inflammation
ID INDUCED OXIDATIVE STRESS; INDUCED LIVER TOXICITY; CELL-CYCLE ARREST;
NITRIC-OXIDE; GLUCOSE-UPTAKE; FREE-RADICALS; CANCER-CELLS; IN-VITRO;
ACID; APOPTOSIS
AB Methotrexate (MTX) is used as an effective chemotherapeutic agent against autoimmune diseases and tumors. Oxidative stress and inflammation are involved in the pathogenesis of MTX-induced damage. This study aimed at examining the ameliorating effects of apigenin (API) as a natural antioxidant on MTX-induced hepatotoxicity. The rats were classified into four groups: group I: normal saline-treated, group II: MTX-treated (20 mg/kg, ip, single dose at day 7), group III: MTX + API-treated (20 mg/kg, po), and group IV: API-treated. API was administrated for 9 days. Alanine aminotransferase (ALT), alkaline phosphatase (ALP), and aspartate aminotransferase (AST) were used as biochemical factors of MTX-induced hepatic injury. In hepatic tissues, the levels of malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), and activities of antioxidant enzymes such as catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) as oxidative stress markers along with inflammatory factors such as tumor necrosis factor-alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta) were assessed. Our results showed that MTX administration significantly increased ALP, ASP, ALT, MDA, NO, TNF-alpha, and IL-1 beta levels and significantly decreased antioxidant factors such as GSH, CAT, GPx, and SOD. The API pretreatment group showed a significant rise in hepatic antioxidant markers, besides significant reductions in the serum levels of AST, ALT, and ALP and hepatic content of MDA, TNF-alpha, NO, and IL-1 beta. In addition, the hepatoprotective effect of API was confirmed by histological evaluation of the liver. API can prevent MTX-induced hepatotoxicity through mitigation of oxidative stress and inflammation.
C1 [Goudarzi, Mehdi; Kalantar, Hadi] Ahvaz Jundishapur Univ Med Sci, Med Plant Res Ctr, Ahvaz, Iran.
[Kalantar, Mojtaba; Karamallah, Mojtaba Haghi] Shoushtar Univ Med Sci, Fac Med, Shoushtar, Iran.
[Sadeghi, Elahe] Ahvaz Jundishapur Univ Med Sci, Toxicol Res Ctr, Ahvaz, Iran.
[Kalantar, Hadi] Ahvaz Jundishapur Univ Med Sci, Sch Pharm, Dept Toxicol, Ahvaz, Iran.
C3 Ahvaz Jundishapur University of Medical Sciences (AJUMS); Ahvaz
Jundishapur University of Medical Sciences (AJUMS); Ahvaz Jundishapur
University of Medical Sciences (AJUMS)
RP Kalantar, H (corresponding author), Ahvaz Jundishapur Univ Med Sci, Med Plant Res Ctr, Ahvaz, Iran.; Kalantar, H (corresponding author), Ahvaz Jundishapur Univ Med Sci, Sch Pharm, Dept Toxicol, Ahvaz, Iran.
EM kalantar-h@ajums.ac.ir
RI Goudarzi, Mehdi/AAZ-3027-2020; kalantar, mojtaba/H-6922-2018; Kalantar,
Hadi/X-5718-2018
OI Kalantar, Hadi/0000-0002-2765-3074; kalantar,
mojtaba/0000-0001-9490-4702
FU Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical
Sciences, Ahvaz, Iran [MPRC-9614]
FX This experiment was kindly supported by the Medicinal Plant Research
Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
(Grant No: MPRC-9614).
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NR 77
TC 44
Z9 45
U1 1
U2 11
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0028-1298
EI 1432-1912
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD MAR
PY 2021
VL 394
IS 3
BP 523
EP 531
DI 10.1007/s00210-020-01991-2
EA OCT 2020
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA QJ1RV
UT WOS:000577857400002
PM 33057777
DA 2025-01-07
ER
PT J
AU Chen, XR
Baker, SM
Chen, GP
AF Chen, XR
Baker, SM
Chen, GP
TI Methotrexate induction of human sulfotransferases in Hep G2 and Caco-2
cells
SO JOURNAL OF APPLIED TOXICOLOGY
LA English
DT Article
DE methotrexate; antifolate; folic acid; sulfotransferase;
drug-metabolizing enzyme; induction; regulation; Hep G2 cells; Caco-2
cells
ID MESSENGER-RNA EXPRESSION; RAT-LIVER; HYDROXYSTEROID SULFOTRANSFERASE;
ARYL SULFOTRANSFERASE; METABOLIZING-ENZYMES; GENE-EXPRESSION; DRUG;
SULT1A1; P450
AB Methotrexate (MTX) was the first antifolate drug developed for the treatment of cancer. It is also effective in treating inflammatory and autoimmune diseases. Sulfotransferases are phase II drug-metabolizing enzymes and their induction by hormones and endogenous molecules is relatively well known, although xenobiotic drug induction of sulfotransferases has not been well studied. In the present investigation, MTX is shown to be a xenobiotic inducer of human sulfotransferases in transformed human liver (Hep G2) and intestinal (Caco-2) cells. Following MTX treatment, various sulfotransferases were induced in both cell lines. Enzyme assay, Western blot and reverse-transcription polymerase chain reaction (RT-PCR) results demonstrated that protein and mRNA expressions of human simple phenol sulfotransferase (P-PST), human monoamine sulfotransferase (M-PST), human dehydroepiandrosterone sulfotransferase (DHEA-ST) and human estrogen sulfotransferase (EST) were induced in Hep G2 cells; M-PST and DHEA-ST were induced in Caco-2 cells. Inductions in both cell lines were dose dependent. Enzyme activity and Western blot results were in good agreement with RT-PCR results, suggesting that the induction is at the gene transcription level. Folic acid had a significantly lesser effect on sulfotransferases compared with MTX. Interestingly, the induction of different sulfotransferases by MTX was inhibited by high doses of folic acid at both protein and mRNA levels in Hep G2 cells. Methotrexate is the first antifolate and apoptosis-inducing drug to show induction of sulfotransferases in Hep G2 cells and Caco-2 cells. The inhibition by folic acid suggests a possible mechanism for MTX induction. Copyright (C) 2005 John Wiley & Sons, Ltd.
C1 Oklahoma State Univ, Coll Vet Med, Dept Physiol Sci, Stillwater, OK 74078 USA.
C3 Oklahoma State University System; Oklahoma State University - Stillwater
RP Oklahoma State Univ, Coll Vet Med, Dept Physiol Sci, 264 McElroy Hall, Stillwater, OK 74078 USA.
EM cguang@okstate.edu
FU NIGMS NIH HHS [GM59873] Funding Source: Medline
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NR 27
TC 21
Z9 24
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0260-437X
EI 1099-1263
J9 J APPL TOXICOL
JI J. Appl. Toxicol.
PD SEP-OCT
PY 2005
VL 25
IS 5
BP 354
EP 360
DI 10.1002/jat.1071
PG 7
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA 967WV
UT WOS:000232122800002
PM 15986412
DA 2025-01-07
ER
PT J
AU Naviaux, RK
AF Naviaux, Robert K.
TI Metabolic features of the cell danger response
SO MITOCHONDRION
LA English
DT Article
DE Oxidative stress; Oxidative shielding; Innate immunity; Inflammation;
Purinergic signaling; Mitochondria
ID CYSTINE/GLUTAMATE ANTIPORTER; MOLECULAR-MECHANISMS; IMPROVES RECOVERY;
STRESS-RESPONSE; ATP RELEASE; KAPPA-B; RECEPTOR; SURAMIN; MITOCHONDRIA;
DISEASE
AB The cell danger response (CDR) is the evolutionarily conserved metabolic response that protects cells and hosts from harm. It is triggered by encounters with chemical, physical, or biological threats that exceed the cellular capacity for homeostasis. The resulting metabolic mismatch between available resources and functional capacity produces a cascade of changes in cellular electron flow, oxygen consumption, redox, membrane fluidity, lipid dynamics, bioenergetics, carbon and sulfur resource allocation, protein folding and aggregation, vitamin availability, metal homeostasis, indole, pterin, 1-carbon and polyamine metabolism, and polymer formation. The first wave of danger signals consists of the release of metabolic intermediates like ATP and ADP, Krebs cycle intermediates, oxygen, and reactive oxygen species (ROS), and is sustained by purinergic signaling. After the danger has been eliminated or neutralized, a choreographed sequence of anti-inflammatoty and regenerative pathways is activated to reverse the CDR and to heal. When the CDR persists abnormally, whole body metabolism and the gut microbiome are disturbed, the collective performance of multiple organ systems is impaired, behavior is changed, and chronic disease results. Metabolic memory of past stress encounters is stored in the form of altered mitochondrial and cellular macromolecule content, resulting in an increase in functional reserve capacity through a process known as mitocellular hormesis. The systemic form of the CDR, and its magnified form, the purinergic life-threat response (PLTR), are under direct control by ancient pathways in the brain that are ultimately coordinated by centers in the brainstem. Chemosensory integration of whole body metabolism occurs in the brainstem and is a prerequisite for normal brain, motor, vestibular, sensory, social, and speech development. An understanding of the CDR permits us to reframe old concepts of pathogenesis for a broad array of chronic, developmental, autoimmune, and degenerative disorders. These disorders include autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), asthma, atopy, gluten and many other food and chemical sensitivity syndromes, emphysema, Tourette's syndrome, bipolar disorder, schizophrenia, post-traumatic stress disorder (PTSD), chronic traumatic encephalopathy (CTE), traumatic brain injury (TB!), epilepsy, suicidal ideation, organ transplant biology, diabetes, kidney, liver, and heart disease, cancer, Alzheimer and Parkinson disease, and autoimmune disorders like lupus, rheumatoid arthritis, multiple sclerosis, and primary sclerosing cholangitis. (C) 2013 The Author. Published by Elsevier B.V. and Mitochondria Research Society. All rights reserved.
C1 [Naviaux, Robert K.] Univ Calif San Diego, Sch Med, Mitochondrial & Metab Dis Ctr, Dept Med, San Diego, CA 92103 USA.
[Naviaux, Robert K.] Univ Calif San Diego, Sch Med, Mitochondrial & Metab Dis Ctr, Dept Pediat, San Diego, CA 92103 USA.
[Naviaux, Robert K.] Univ Calif San Diego, Sch Med, Mitochondrial & Metab Dis Ctr, Dept Pathol, San Diego, CA 92103 USA.
[Naviaux, Robert K.] Vet Affairs Ctr Excellence Stress & Mental Hlth C, La Jolla, CA USA.
C3 University of California System; University of California San Diego;
University of California System; University of California San Diego;
University of California System; University of California San Diego
RP Naviaux, RK (corresponding author), Univ Calif San Diego, Sch Med, Mitochondrial & Metab Dis Ctr, 214 Dickinson St,Bldg CTF,Rm C102, San Diego, CA 92103 USA.
EM Naviaux@ucsd.edu
FU UCSD Christini Fund; Jane Botsford Johnson Foundation; Wright
Foundation; Lennox Foundation; Takes Guts Foundation; UCSD Mitochondrial
Disease Research Foundation; Hailey's Wish Foundation
FX RKN thanks Jane Naviaux, Will Alaynick, Jim Adams, Steve Edelson, Kate
Crowley, and Vicki Kobliner for helpful comments on the manuscript. This
work was made possible by support from the UCSD Christini Fund, the Jane
Botsford Johnson Foundation, the Wright Foundation, the Lennox
Foundation, the It Takes Guts Foundation, the UCSD Mitochondrial Disease
Research Foundation, and the Hailey's Wish Foundation.
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NR 125
TC 150
Z9 161
U1 4
U2 104
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1567-7249
EI 1872-8278
J9 MITOCHONDRION
JI Mitochondrion
PD MAY
PY 2014
VL 16
SI SI
BP 7
EP 17
DI 10.1016/j.mito.2013.08.006
PG 11
WC Cell Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Genetics & Heredity
GA AH9OP
UT WOS:000336472000003
PM 23981537
OA hybrid
DA 2025-01-07
ER
PT J
AU Zhong, H
Liu, SY
Wang, YH
Xu, D
Li, MT
Zhao, Y
Zeng, XF
AF Zhong, Hui
Liu, Siyao
Wang, Yanhong
Xu, Dong
Li, Mengtao
Zhao, Yan
Zeng, Xiaofeng
TI Primary Sjogren's syndrome is associated with increased risk of
malignancies besides lymphoma: A systematic review and meta-analysis
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE Primary Sjogren's syndrome; Malignancy; Solid tumor; non-Hodgkin
lymphoma
ID NON-HODGKINS-LYMPHOMA; AUTOIMMUNE-DISEASES; CANCER; COHORT; LEUKEMIA;
PREDICTORS
AB Objective: Patients with primary Sjo spacing diaeresis gren's syndrome(pSS) have increased risk of non-Hodgkin lymphoma (NHL). However, whether pSS patients have increased risk of other malignancies is unclear. The aim of this study is to investigate the association between pSS and the risk of malignancy, with a focus on hematological malignancies besides lymphoma and solid tumors through a systematic review and meta-analysis. Method: We searched PubMed and EMBASE by March 21st 2021. Inclusion criteria were as follows: (1) pSS was the exposure of interest; (2) newly developed malignancies were the outcome of interest; (3) standardized incidence ratio or relative risk with 95% confidence interval or essential data to calculate them were reported. (4) Study design was cohort study. Patient with other connective diseases were excluded. Quality assessment was conducted according to Newcastle-Ottawa Scale for cohort study. Random or fixed effect models were used to calculate the pooled SIR according to heterogeneity measured by I2. Results: A total of 1003 articles were found by a comprehensive search in PubMed and EMBASE. Twenty-eight articles were eligible. Four of them were from the same database, and the one with longest observational span was chosen. Therefore, twenty-five articles were included for final analysis, which involved more than 47,607 pSS patients with the follow-up of more than 452,468 person-year. We found that pSS was significantly associated with increased risks of overall malignancy(pooled SIR 2.17, 95%1.57-3.00), hematological malignancy(pooled SIR 11.55, 95%CI 4.32-30.90) including NHL(pooled SIR 13.71, 95%CI 8.83-21.29), Hodgkin lymphoma(pooled SIR 8.84, 95%CI 5.00-15.61), multiple myeloma(pooled SIR 8.27, 95%CI 3.08-22.24), leukemia(pooled SIR 2.56, 95%CI 1.78-3.69) and solid tumors(pooled SIR 1.39, 95%CI 0.90-2.13) including lung cancer(pooled SIR 1.55, 95%CI 1.29-1.85), thyroid cancer(pooled SIR 2.05, 95%CI 1.20-3.48), non-melanoma skin cancer(pooled SIR 1.71, 95%CI 1.08-2.72), kidney/urinary tract cancer(pooled SIR 1.36, 95%CI 1.02; 1.81), liver cancer(pooled SIR 1.70, 95%CI 1.13-2.57) and prostate cancer(pooled SIR 1.50, 95%CI 1.02-2.22). Conclusion: This meta-analysis showed that pSS patients had increased risk of overall cancer, which not only contributed by NHL, but also by other hematological malignancies and solid tumors.
C1 [Zhong, Hui; Liu, Siyao; Xu, Dong; Li, Mengtao; Zhao, Yan; Zeng, Xiaofeng] Chinese Acad Med Sci & Peking Union Med Coll, Natl Clin Res Ctr Dermatol & Immunol Dis NCRC Did, Peking Union Med Coll Hosp PUMCH,Minist Educq, Dept Rheumatol & Clin Immunol,State Key Lab Compl, Beijing, Peoples R China.
[Wang, Yanhong] Chinese Acad Med Sci, Sch Basic Med, Dept Epidemiol & Biostat, Inst Basic Med Sci,Peking Union Med Coll, Beijing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
Peking Union Medical College; Institute of Basic Medical Sciences -
CAMS; Chinese Academy of Medical Sciences - Peking Union Medical
College; Peking Union Medical College
RP Xu, D; Li, MT (corresponding author), Peking Union Med Coll Hosp, Dept Rheumatol & Clin Immunol, Shuaifuyuan 1, Beijing 100730, Peoples R China.
EM xudong74@hotmail.com; mengtao.li@cstar.org.cn
FU Chinese National Key Technology R&D Program, Ministry of Science and
Technology [2017YFC0907601, 2017YFC0907605]; CAMS Innovation Fund for
Medical Sciences (CIFMS) [2021-I2M-1-005]
FX Funding This study was supported by the Chinese National Key Technology
R&D Program, Ministry of Science and Technology (2017YFC0907601,
2017YFC0907605) ,CAMS Innovation Fund for Medical Sciences (CIFMS)
(2021-I2M-1-005) .
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NR 48
TC 37
Z9 39
U1 1
U2 12
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD MAY
PY 2022
VL 21
IS 5
AR 103084
DI 10.1016/j.autrev.2022.103084
EA MAR 2022
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 1I2DF
UT WOS:000797043800009
PM 35341972
DA 2025-01-07
ER
PT J
AU Naldi, L
Venturuzzo, A
Invernizzi, P
AF Naldi, Luigi
Venturuzzo, Anna
Invernizzi, Pietro
TI Dermatological Complications After Solid Organ Transplantation
SO CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
LA English
DT Review
DE Solid organ transplantation; Dermatological complications; Neoplastic
complications; Adverse reactions; Immunosuppression; Drug toxicity
ID NONMELANOMA SKIN-CANCER; OF-THE-LITERATURE; SQUAMOUS-CELL CARCINOMA;
SARCOMA-ASSOCIATED HERPESVIRUS; RANDOMIZED CONTROLLED-TRIAL;
HUMAN-PAPILLOMAVIRUS DNA; DE-NOVO MALIGNANCIES; VERSUS-HOST-DISEASE;
LIVER-TRANSPLANTATION; KIDNEY-TRANSPLANTATION
AB Organ transplant recipients (OTRs) are a population at high risk for cutaneous adverse events. Their early recognition and appropriate treatment is an important component of the clinical management of OTRs and should be optimally dealt with by dermatologists working in the context of a transplant dermatology clinic. Skin examination should be a standard procedure before performing organ transplantation to assess conditions which may be difficult to manage after the transplant procedure has been performed or which may represent a contraindication to transplantation, e.g., malignant melanoma. It also offers an opportunity to educate patients on skin care after organ transplantation. Skin infections can occur at any time after organ transplantation and include viral, bacterial, and fungal opportunistic infections. The risk of reactivation of latent viruses, such as varicella-zoster virus (VZV) and cytomegalovirus (CMV), is high. Bacterial infections are frequent and may be caused by unusual agents such Actinomyces, Mycobacteria, Legionella, or Nocardia. A large spectrum of fungal infections may occur, ranging from superficial (e.g., dermatophytes) to deeper and more severe ones (Alternaria, Aspergillus, Cryptococcus, Histoplasma). Drug-related idiosyncratic reactions usually occur early after the introduction of the causative drug, e.g., hypersensitivity reaction to azathioprine. On the long-term run, cutaneous effects due to cumulative drug toxicity, e.g., sebaceous hyperplasia from cyclosporine, may appear. Rare immunologically driven inflammatory reactions may occur in OTRs such as GVH or autoimmune disease. Tumors are particularly frequent. Kaposi's sarcoma, associated with persistent human herpes virus 8 (HHV8) infection, and cutaneous anaplastic large-cell lymphoma (ALCL) occur early after transplantation. Other cancers, such as nonmelanoma skin cancer (NMSCs), associated with persistent human papillomavirus (HPV) infections, malignant melanoma, Merkel cell carcinoma, or adnexal tumors, manifest later with an incidence which is much higher than observed in the general population. The incidence increases further after a first NMSC occurs.
C1 [Naldi, Luigi] AULSS 8 Osped San Bortolo, Dept Dermatol, Viale Rodolfi 37, I-36100 Vicenza, Italy.
[Naldi, Luigi; Venturuzzo, Anna] Study Ctr, Italian Grp Epidemiol Res Dermatol GISED, Bergamo, Italy.
[Venturuzzo, Anna; Invernizzi, Pietro] Univ Milano Bicocca, Div Gastroenterol, Dept Med & Surg, Milan, Italy.
[Venturuzzo, Anna; Invernizzi, Pietro] Univ Milano Bicocca, Ctr Autoimmune Liver Dis, Dept Med & Surg, Milan, Italy.
C3 ULSS 8 Berica; Ospedale San Bortolo di Vicenza; University of
Milano-Bicocca; University of Milano-Bicocca
RP Naldi, L (corresponding author), AULSS 8 Osped San Bortolo, Dept Dermatol, Viale Rodolfi 37, I-36100 Vicenza, Italy.; Naldi, L (corresponding author), Study Ctr, Italian Grp Epidemiol Res Dermatol GISED, Bergamo, Italy.
EM luigi.naldi@aulss8.veneto.it
RI Invernizzi, Pietro/AAB-8367-2022; Naldi, Luigi/K-6343-2016
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NR 173
TC 37
Z9 39
U1 0
U2 11
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1080-0549
EI 1559-0267
J9 CLIN REV ALLERG IMMU
JI Clin. Rev. Allergy Immunol.
PD FEB
PY 2018
VL 54
IS 1
BP 185
EP 212
DI 10.1007/s12016-017-8657-9
PG 28
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA FV0LM
UT WOS:000424247300011
PM 29177692
DA 2025-01-07
ER
PT J
AU Lytras, D
Damink, SWMO
Amin, Z
Imber, CJ
Malagó, M
AF Lytras, Dimitrios
Damink, Steven W. M. Olde
Amin, Zahir
Imber, Charles J.
Malago, Massimo
TI Radical Surgery in the Presence of Biliary Metallic Stents: Revising the
Palliative Scenario
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Article
DE Self-expanding metallic stents; Cholangiocarcinoma; Bile duct; Hilar
tumours; Hepatic confluence
ID HILAR CHOLANGIOCARCINOMA; RESECTION; OBSTRUCTION; MORTALITY;
PANCREATICODUODENECTOMY; COMPLICATIONS; PLACEMENT; OUTCOMES; VOLUMES;
CANCER
AB Background The application of endobiliary self-expandable metallic stents (SEMS) is considered the palliative treatment of choice in patients with biliary obstruction in the setting of inoperable malignancies. In the presence of SEMS, however, radical surgery is the only curative option when the resectability status is revised in case of malignancies or for overcoming complications arising from their application in benign conditions that masquerade as inoperable tumours. The aim of our study was to report our surgical experience with patients who underwent an operation due to revision of the initial palliative approach, whilst they had already been treated with biliary SEMS exceeding the hilar bifurcation.
Methods Three patients with hilar cholangiocarcinoma that was considered inoperable and one patient with IgG4 autoimmune cholangio-pancreatopathy mimicking pancreatic cancer underwent radical resections in the presence of biliary SEMS.
Results After a detailed preoperative workup, two right trisectionectomies, one left extended hepatectomy and a radical extrahepatic biliary resection were performed. All cases demanded resection and reconstruction of the portal vein. R0 resection was achieved in all the malignant cases. Two patients required multiple biliodigestive anastomoses entailing three and seven bile ducts respectively. There was one perioperative death due to postoperative portal vein and hepatic artery thrombosis, whilst two patients developed grade III complications. At follow-up, one patient died at 13 months due to disease recurrence, whilst the remaining two are free of disease or symptoms at 21 and 12 months, respectively.
Conclusions Revising the initial palliative approach and operating in the setting of biliary metallic stents is extremely demanding and carries significant mortality and morbidity. Radical resection is the only option for offering cure in such complex cases, and this should only be attempted in advanced hepatopancreaticobiliary centres with active involvement in liver transplantation.
C1 [Lytras, Dimitrios; Damink, Steven W. M. Olde; Imber, Charles J.; Malago, Massimo] London Hosp NHS Fdn Trust, Univ Coll, Dept Surg, London NW1 2PG, England.
[Amin, Zahir] London Hosp NHS Fdn Trust, Univ Coll, Dept Radiol, London NW1 2PG, England.
C3 University of London; University College London; University of London;
University College London
RP Malagó, M (corresponding author), London Hosp NHS Fdn Trust, Univ Coll, Dept Surg, 250 Euston Rd, London NW1 2PG, England.
EM m.malago@ucl.ac.uk
RI Olde Damink, Steven/U-7919-2019
OI Olde Damink, Steven/0000-0002-5202-9345; Lytras,
Dimitrios/0000-0003-1172-2546
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NR 22
TC 8
Z9 10
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1091-255X
EI 1873-4626
J9 J GASTROINTEST SURG
JI J. Gastrointest. Surg.
PD MAR
PY 2011
VL 15
IS 3
BP 489
EP 495
DI 10.1007/s11605-010-1389-2
PG 7
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 740AA
UT WOS:000288762700017
PM 21246414
DA 2025-01-07
ER
PT J
AU Jiang, SW
Wang, P
Xiang, XG
Mo, RD
Lin, LY
Bao, SS
Lu, J
Xie, Q
AF Jiang, Shao-Wen
Wang, Peng
Xiang, Xiao-Gang
Mo, Rui-Dong
Lin, Lan-Yi
Bao, Shi-San
Lu, Jie
Xie, Qing
TI Serum soluble ST2 is a promising prognostic biomarker in HBV-related
acute-on-chronic liver failure
SO HEPATOBILIARY & PANCREATIC DISEASES INTERNATIONAL
LA English
DT Article
DE biomarker; HBV-related acute-on-chronic liver failure; interleukin-33;
prognosis; soluble ST2
ID CD8(+) T-CELLS; INTERLEUKIN-33; IL-33; OVEREXPRESSION; CHROMATIN;
RECEPTOR; PATIENT; INJURY
AB BACKGROUND: The IL-33/ST2 axis is involved in the pathogenesis of many diseases such as autoimmune diseases, cancer, and heart failure. However, studies of the IL-33/ST2 pathway in HBV-related acute-on-chronic liver failure (HBV-ACLF) are lacking. The present study aimed to determine the prognostic role of serum IL-33/soluble ST2 (sST2) in HBV-ACLF.
METHODS: Serum levels of IL-33 and sST2 in healthy controls (HC, n=18), chronic hepatitis B (CHB, n=27) and HBV-ACLF (n=51) patients at the 1st and 4th week after enrollment were detected using ELISA, and clinical data were collected. The follow-up of HBV-ACLF patients lasted for 6 months at least.
RESULTS: There was no significant difference of serum IL-33 level among HC, CHB and HBV-ACLF patients at week 1. However, serum sST2 level differed significantly among the three groups: highest in the HBV-ACLF group, moderate in the CHB group and lowest in the HC group. There was a reverse correlation between serum sST2 level and the survival of HBV-ACLF patients. The level of serum sST2 in HBV-ACLF survivors was significantly declined from week 1 to week 4 following the treatment, whereas that in HBV-ACLF non survivors remained at a high level during the same period. Furthermore, serum sST2 level was significantly correlated with laboratory parameters and the most updated prognostic scores (CLIF-C OF score, CLIF-C ACLF score and ACLF grades). The receiver operating characteristics curves demonstrated that serum sST2 level was a good diagnostic marker for predicting the 6-month mortality in HBV-ACLF patients, comparable to the most updated prognostic scores. Serum sST2 cut-off points for predicting prognosis in HBV-ACLF patients were 76 ng/mL at week 1 or 53 ng/mL at week 4, respectively. HBV-ACLF patients with serum sST2 level above the cut-off point often had a worse prognosis than those below the cut-off point.
CONCLUSION: Serum sST2 may act as a promising biomarker to assess severity and predict prognosis of patients with HBV-ACLF and help for the early identification and optimal treatment of HBV-ACLF patients at high risk of mortality.
C1 [Jiang, Shao-Wen; Wang, Peng; Xiang, Xiao-Gang; Mo, Rui-Dong; Lin, Lan-Yi; Lu, Jie; Xie, Qing] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Infect Dis, Sch Med, Shanghai 200025, Peoples R China.
[Bao, Shi-San] Univ Sydney, Sch Med Sci, Discipline Pathol, Sydney, NSW, Australia.
[Bao, Shi-San] Univ Sydney, Bosch Inst, Sydney, NSW, Australia.
C3 Shanghai Jiao Tong University; University of Sydney; University of
Sydney
RP Xie, Q (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Infect Dis, Sch Med, Shanghai 200025, Peoples R China.
EM xieqin-grjh@163.com
RI xiaogang, xiang/GXN-4124-2022; Bao, Shisan/C-6072-2014
FU National Natural Science Foundation of China [81300316, 81570535];
National Key Programs on Infectious Diseases of China
[2012ZX10002004-003]; National Clinical Key Speciality Construction
Project of China (Infectious Diseases); Shanghai Public Health
Three-Year Action Project [15GWZK0102]; Project of Shanghai Municipal
Health and Family Planning [20144329]
FX The study was supported by grants from the National Natural Science
Foundation of China (81300316 and 81570535), the National Key Programs
on Infectious Diseases of China (2012ZX10002004-003), the National
Clinical Key Speciality Construction Project of China (Infectious
Diseases), Shanghai Public Health Three-Year Action Project
(15GWZK0102), and Project of Shanghai Municipal Health and Family
Planning (20144329).
CR [Anonymous], 2015, IMMUNITY
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NR 30
TC 10
Z9 12
U1 0
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1499-3872
EI 2352-9377
J9 HEPATOB PANCREAT DIS
JI Hepatob. Pancreatic. Dis. Int.
PD APR
PY 2017
VL 16
IS 2
BP 181
EP 188
DI 10.1016/S1499-3872(16)60185-6
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ER7IH
UT WOS:000398984900010
PM 28381383
DA 2025-01-07
ER
PT J
AU Sylvester, JE
Buchanan, BK
Silva, TW
AF Sylvester, Jillian E.
Buchanan, Benjamin K.
Silva, Taran W.
TI Infectious Mononucleosis: Rapid Evidence Review
SO AMERICAN FAMILY PHYSICIAN
LA English
DT Article
ID EPSTEIN-BARR-VIRUS; SPLENIC RUPTURE; SPLEEN SIZE; VOLUME
AB Infectious mononucleosis is a viral syndrome characterized by fever, pharyngitis, and posterior cervical lymphadenopathy. It is usually caused by Epstein-Barr virus and most often affects adolescents and young adults 15 to 24 years of age. Primary transmission is through close personal contact with a person who is infected, particularly their saliva. Cost-effective, efficient initial laboratory testing for acute infectious mononucleosis'includes complete blood count with differential (to assess for greater than 40% lymphocytes and greater than 10% atypical lymphocytes) and a rapid heterophile antibody test. The heterophile antibody test has a sensitivity of 87% and specificity of 91% but can have a false-negative result in children younger than five years and in adults during the first week of illness. The presence of elevated liver enzymes increases clinical suspicion for infectious mononucleosis in the setting of a negative heterophile antibody test result. Epstein-Barr viral capsid antigen-antibody testing is more sensitive and specific but more expensive and takes longer to process than the rapid heterophile antibody test. Treatment of infectious mononucleosis is supportive; routine use of antivirals and corticosteroids is not recommended. Current guidelines recommend that patients with infectious mononucleosis not participate in athletic activity for three weeks from onset of symptoms. Shared decision-making should be used to determine the timing of return to activity. Immunosuppressed populations are at higher risk of severe disease and significant morbidity. Epstein-Barr virus infection has been linked to nine types of cancer, including Hodgkin lymphoma, non-Hodgkin lymphoma, and nasopharyngeal carcinoma, and some autoimmune diseases. (Copyright (C) 2023 American Academy of Family Physicians.)
C1 [Sylvester, Jillian E.] Univ N Carolina, Sch Med, Dept Orthoped, Chapel Hill, NC 27515 USA.
[Buchanan, Benjamin K.] Southwest Orthoped & Sports Med, Intermt Healthcare, St George, UT USA.
[Silva, Taran W.] David Grant Med Ctr, Travis AFB Calif Family Med Residency Program, Travis AFB, CA USA.
C3 University of North Carolina; University of North Carolina Chapel Hill;
University of North Carolina School of Medicine; Intermountain
Healthcare; Intermountain Medical Center
RP Sylvester, JE (corresponding author), UNC Orthoped, 3142 Bioinformat Bldg CB 7055, Chapel Hill, NC 27599 USA.
EM jillian_sylvester@med.unc.edu
RI Sylvester, Jillian/M-1129-2019
OI Sylvester, Jillian/0000-0002-3684-0963
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NR 45
TC 10
Z9 11
U1 2
U2 11
PU AMER ACAD FAMILY PHYSICIANS
PI KANSAS CITY
PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 USA
SN 0002-838X
EI 1532-0650
J9 AM FAM PHYSICIAN
JI Am. Fam. Physician
PD JAN
PY 2023
VL 107
IS 1
BP 71
EP 78
PG 8
WC Primary Health Care; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 8C2DF
UT WOS:000917424900014
PM 36689975
DA 2025-01-07
ER
PT J
AU Thorne, I
Stroud, J
Penn, H
AF Thorne, Iona
Stroud, Javier
Penn, Henry
TI A retrospective series of conditions and mortality associated with
extreme hyperferritinaemia in adults
SO INTERNATIONAL JOURNAL OF CLINICAL PRACTICE
LA English
DT Article
ID SERUM FERRITIN LEVELS; HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS; DIAGNOSIS;
PATHOGENESIS
AB Background: Serum ferritin is commonly used in the diagnosis of iron deficiency anaemia. However, extreme hyperferritinaemia suggests a significant illness, including the differential diagnosis of haemophagocytic lymphohistiocytosis (HLH), which is rare and associated with a high mortality, particularly if untreated. This series aims to identify the causes and associated mortality of severe hyperferritinaemia in patients seen at a teaching hospital in London, UK.
Method: Demographic and medical data were collected for all patients over 18years of age with extreme hyperferritinaemia (defined as serum ferritin levels of >= 4000mcg/L). Conditions associated with hyperferritinaemia and in-hospital mortality were identified from medical records, laboratory data and discharge and death notification.
Results: One hundred and fifty-five cases of extreme hyperferritinaemia in adults were identified. Associated conditions included iron overload (35%), malignancy (24%), infectious disease (21%) and hepatocellular disease (12%). Autoimmune disease and HLH resulted in significantly higher median peak ferritin levels compared with all cases (10616 mcg/L, P<.01 and 19138 mcg/L, P<.05, respectively). Patients with confirmed HLH had the highest median peak ferritin. Uncommon infections were identified in this series, and included such as dengue, syphilis, HIV and murine typhus. HLH had been confirmed in seven patients (5%). In five patients (3%) no clear cause for raised ferritin was identified. Overall mortality in the whole cohort was 14% (n=22), but there was a very high mortality of 80% in the group where no cause was found for the hyperferritinaemia, and these patients were significantly more likely to die during the index admission (P<.01).
Conclusion: Extreme hyperferritinaemia is associated with a broad differential diagnosis of significant medical conditions, including iron overload, infections, cancer and liver disease. Rare infectious causes were also identified, and this series reports a greater proportion of cases of HLH than has previously reported. Unexplained hyperferritinaemia was associated with significant mortality.
C1 [Thorne, Iona] Imperial Coll Healthcare NHS Trust Hammersmith Ho, London, England.
[Stroud, Javier] Wellington Reg Hosp, Capital & Coast Dist Hlth Board, Wellington, New Zealand.
[Penn, Henry] Northwick Pk Hosp & Clin Res Ctr, North West London NHS Hosp Trust, Harrow, Middx, England.
C3 Imperial College London
RP Thorne, I (corresponding author), Imperial Coll Healthcare NHS Trust Hammersmith Ho, Rheumatol Dept, London, England.
EM iona.thorne@nhs.net
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NR 15
TC 8
Z9 8
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1368-5031
EI 1742-1241
J9 INT J CLIN PRACT
JI Int. J. Clin. Pract.
PD SEP
PY 2018
VL 72
IS 9
AR e13215
DI 10.1111/ijcp.13215
PG 8
WC Medicine, General & Internal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Pharmacology & Pharmacy
GA GQ7AL
UT WOS:000441884600007
PM 29855115
OA gold
DA 2025-01-07
ER
PT J
AU Zabeau, L
Verhee, A
Catteeuw, D
Faes, L
Seeuws, S
Decruy, T
Elewaut, D
Peelman, F
Tavernier, J
AF Zabeau, Lennart
Verhee, Annick
Catteeuw, Dominiek
Faes, Liesbeth
Seeuws, Sylvie
Decruy, Tine
Elewaut, Dirk
Peelman, Frank
Tavernier, Jan
TI Selection of non-competitive leptin antagonists using a random
nanobody-based approach
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE body weight; leptin receptor (LR); nanobody; receptor activation;
signalling
ID BINDING-SITE-III; OBESE GENE; DB/DB MICE; OB-R; RECEPTOR;
IDENTIFICATION; ACTIVATION; HYPOTHALAMUS; EXPRESSION; CLONING
AB The adipocyte-derived cytokine leptin acts as a metabolic switch, connecting the body's metabolism to high-energy consuming processes such as reproduction and immune responses. Accumulating evidence suggests that leptin plays a role in human pathologies, such as autoimmune diseases and cancer, thus providing a rationale for the development of leptin antagonists. In the present study, we generated and evaluated a panel of neutralizing nanobodies targeting the LR (leptin receptor). A nanobody comprises the variable domain of the naturally occurring single-chain antibodies found in members of the Camelidae family. We identified three classes of neutralizing nanobodies targeting different LR subdomains: i.e. the CRH2 (cytokine receptor homology 2), Ig-like and FNIII (fibronectin type III) domains. Only nanobodies directed against the CRH2 domain inhibited leptin binding. We could show that a nanobody that targets the Ig-like domain potently interfered with leptin-dependent regulation of hypothalamic NPY (neuropeptide Y) expression. As a consequence, daily intraperitoneal injection increased body weight, body fat content, food intake, liver size and serum insulin levels. All of these characteristics resemble the phenotype of leptin and LR-deficient animals. The results of the present study support proposed models of the activated LR complex, and demonstrate that it is possible to block LR signalling without affecting ligand binding. These nanobodies form new tools to study the mechanisms of BBB (blood-brain barrier) leptin transport and the effect of LR inhibition in disease models.
C1 [Zabeau, Lennart; Verhee, Annick; Catteeuw, Dominiek; Faes, Liesbeth; Peelman, Frank; Tavernier, Jan] Univ Ghent, Dept Med Prot Res, Fac Med & Hlth Sci, Flanders Inst Biotechnol, B-9000 Ghent, Belgium.
[Seeuws, Sylvie; Decruy, Tine; Elewaut, Dirk] Univ Ghent, Ghent Univ Hosp, Dept Rheumatol, Lab Mol Immunol & Inflammat, B-9000 Ghent, Belgium.
C3 Flanders Institute for Biotechnology (VIB); Ghent University; Ghent
University; Ghent University Hospital
RP Tavernier, J (corresponding author), Univ Ghent, Dept Med Prot Res, Fac Med & Hlth Sci, Flanders Inst Biotechnol, A Baertsoenkaai 3, B-9000 Ghent, Belgium.
EM jan.tavernier@vib-ugent.be
RI Elewaut, Dirk/K-6831-2014; Tavernier, Jan/AAG-3636-2019
OI Elewaut, Dirk/0000-0002-7468-974X
FU Fund for Scientific Research Flanders [G.0164.O6N]; Ghent University;
Institute for the Promotion of Innovation through Science and Technology
in Flanders (IWT-Vlaanderen)
FX This work was supported by the Fund for Scientific Research Flanders
[grant number G.0164.O6N] and Ghent University. L.Z. is a postdoctoral
fellow of the Fund for Scientific Research, Flanders. S.S. is supported
by the Institute for the Promotion of Innovation through Science and
Technology in Flanders (IWT-Vlaanderen).
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NR 43
TC 34
Z9 39
U1 0
U2 19
PU PORTLAND PRESS LTD
PI LONDON
PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND
SN 0264-6021
EI 1470-8728
J9 BIOCHEM J
JI Biochem. J.
PD JAN 1
PY 2012
VL 441
BP 425
EP 434
DI 10.1042/BJ20110438
PN 1
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 874FN
UT WOS:000298940900041
PM 21851341
OA Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Shahab, O
Sayiner, M
Paik, J
Felix, S
Golabi, P
Younossi, ZM
AF Shahab, Omer
Sayiner, Mehmet
Paik, James
Felix, Sean
Golabi, Pegah
Younossi, Zobair M.
TI Burden of Primary Biliary Cholangitis Among Inpatient Population in the
United States
SO HEPATOLOGY COMMUNICATIONS
LA English
DT Article
ID URSODEOXYCHOLIC ACID; OBETICHOLIC ACID; ANTIMITOCHONDRIAL ANTIBODIES;
NATURAL-HISTORY; CIRRHOSIS; PROGRESSION; PREVALENCE; SURVIVAL; COHORT;
COST
AB Primary biliary cholangitis (PBC) is an autoimmune liver disease that can lead to cirrhosis and liver failure. Our aim was to assess the recent trends in the mortality rates and health care utilization of patients with PBC seen in the inpatient setting in the United States. We used the National (Nationwide) Inpatient Sample data (2005-2014). The study population included adults with PBC, using International Classification of Diseases, Ninth Revision codes. Trends in PBC-related discharges, total charges, length of stay (LoS), and in-hospital mortality were evaluated. Hierarchical generalized linear models were performed for determining predictors of mortality and total hospital charges. Between the study years of 2005 and 2014, a total of 22,665 hospitalized cases with PBC were identified (mean age 63 years; 84% female, 76% white). The number of PBC-related discharges increased from 3.24 per 100,000 in 2005 to 3.68 per 100,000 in 2014, with an average annual increase of 1.4% (95% confidence interval [CI]: 0.4%-2.4%). Fifty-seven percent had Medicare as their primary payer, 37% had cirrhosis, and 1.3% had hepatocellular carcinoma. Between 2005 and 2014, the average total charges for PBC increased from 53,901 to 57,613 (annual percent change [APC], 1.7%; 95% CI: -0.2%-3.5%), LoS decreased from 6.9 days to 5.4 days (APC, -2.2%; 95% CI: -3.2% to -1.1%), and mortality rate decreased from 3.8% to 2.8% (APC, -5.4%; 95% CI: -8.4% to -2.4%). Multivariable analysis revealed that ascites were independently associated with increased risk of in-hospital mortality (odds ratio: 1.77; 95% CI: 1.50-2.08), increased charge (percent change: 22.5%; 95% CI: 18.6%-26.7%), and increased LoS (percent change: 29.7%; 95% CI: 25.7%-33.9%). Conclusion: The number of PBC cases has increased in recent years. Mortality and LoS have decreased, and the total charges have remained the same.
C1 [Shahab, Omer; Sayiner, Mehmet; Younossi, Zobair M.] Inova Fairfax Hosp, Dept Med, Ctr Liver Dis, Falls Church, VA USA.
[Paik, James; Felix, Sean; Golabi, Pegah; Younossi, Zobair M.] Inova Hlth Syst, Betty & Guy Beatty Ctr Integrated Res, Falls Church, VA USA.
C3 Inova Fairfax Hospital; Inova Health System
RP Younossi, ZM (corresponding author), Betty & Guy Beatty Ctr Integrated Res, Claude Moore Hlth Educ & Res Bldg,3300 Gallows Rd, Falls Church, VA 22042 USA.
EM Zobair.Younossi@inova.org
RI Younossi, Zobair M./JRY-9916-2023
OI Shahab, Omer/0000-0001-9597-9175; Sayiner, Mehmet/0000-0002-3585-1564;
Golabi, Pegah/0000-0001-9818-0983
CR Ali AH, 2016, EXPERT OPIN PHARMACO, V17, P1809, DOI 10.1080/14656566.2016.1218471
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NR 38
TC 11
Z9 12
U1 0
U2 0
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
EI 2471-254X
J9 HEPATOL COMMUN
JI Hepatol. Commun.
PD MAR
PY 2019
VL 3
IS 3
BP 356
EP 364
DI 10.1002/hep4.1314
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HN1RV
UT WOS:000459965500005
PM 30859148
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Samur, S
Klebanoff, M
Banken, R
Pratt, DS
Chapman, R
Ollendorf, DA
Loos, AM
Corey, K
Hur, C
Chhatwal, J
AF Samur, Sumeyye
Klebanoff, Matthew
Banken, Reiner
Pratt, Daniel S.
Chapman, Rick
Ollendorf, Daniel A.
Loos, Anne M.
Corey, Kathleen
Hur, Chin
Chhatwal, Jagpreet
TI Long-Term Clinical Impact and Cost-Effectiveness of Obeticholic Acid for
the Treatment of Primary Biliary Cholangitis
SO HEPATOLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; URSODEOXYCHOLIC ACID; HEPATITIS-C;
LIVER-TRANSPLANTATION; FOLLOW-UP; CIRRHOSIS; PRURITUS; DISEASES; THERAPY
AB Primary biliary cholangitis (PBC) is a chronic, progressive autoimmune liver disease that mainly affects middle-aged women. Obeticholic acid (OCA), which was recently approved by the Food and Drug Administration for PBC treatment, has demonstrated positive effects on biochemical markers of liver function. Our objective was to evaluate the long-term clinical impact and cost-effectiveness of OCA as a second-line treatment for PBC in combination with ursodeoxycholic acid (UDCA) in adults with an inadequate response to UDCA. We developed a mathematical model to simulate the lifetime course of PBC patients treated with OCA+UDCA versus UDCA alone. Efficacy data were derived from the phase 3 PBC OCA International Study of Efficacy trial, and the natural history of PBC was informed by published clinical studies. Model outcomes were validated using the PBC Global Study. We found that in comparison with UDCA, OCAUDCA could decrease the 15-year cumulative incidences of decompensated cirrhosis from 12.2% to 4.5%, hepatocellular carcinoma from 9.1% to 4.0%, liver transplants from 4.5% to 1.2%, and liver-related deaths from 16.2% to 5.7% and increase 15-year transplant-free survival from 61.1% to 72.9%. The lifetime cost of PBC treatment would increase from $ 63,000 to $ 902,000 (1,330% increment). The discounted quality-adjusted life years with UDCA and OCA+UDCA were 10.74 and 11.78, respectively, and the corresponding costs were $ 142,300 and $ 633,900, resulting in an incremental costeffectiveness ratio of $ 473,400/quality-adjusted life year gained. The results were most sensitive to the cost of OCA. Conclusion: OCA is a promising new therapy to substantially improve the long-term outcomes of PBC patients, but at its current annual price of $ 69,350, it is not cost-effective using a willingness-to-pay threshold of $ 100,000/quality-adjusted life year; pricing below $ 18,450/year is needed to make OCA cost-effective.
C1 [Samur, Sumeyye; Klebanoff, Matthew; Hur, Chin; Chhatwal, Jagpreet] Massachusetts Gen Hosp, Inst Technol Assessment, 101 Merrimac St,10th, Boston, MA 02114 USA.
[Samur, Sumeyye; Pratt, Daniel S.; Hur, Chin; Chhatwal, Jagpreet] Harvard Med Sch, Boston, MA USA.
[Chapman, Rick; Ollendorf, Daniel A.; Loos, Anne M.] Inst Clin & Econ Review, Boston, MA USA.
[Corey, Kathleen; Hur, Chin] Massachusetts Gen Hosp, Gastroenterol, Boston, MA USA.
C3 Harvard University; Massachusetts General Hospital; Harvard University;
Harvard Medical School; Harvard University; Massachusetts General
Hospital
RP Hur, C (corresponding author), Massachusetts Gen Hosp, Inst Technol Assessment, 101 Merrimac St,10th, Boston, MA 02114 USA.
EM chur@mgh.harvard.edu
OI Hur, Chin/0000-0002-2819-7576; Loos, Anne/0009-0006-9920-8400;
Klebanoff, Matthew/0000-0002-5081-063X
FU Institute for Clinical and Economic Review
FX Supported by the Institute for Clinical and Economic Review.
CR Ali AH, 2016, EXPERT OPIN PHARMACO, V17, P1809, DOI 10.1080/14656566.2016.1218471
[Anonymous], 2016, Truven Health Analytics
[Anonymous], PHYS FEE SCHEDULE
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NR 33
TC 63
Z9 69
U1 1
U2 15
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD MAR
PY 2017
VL 65
IS 3
BP 920
EP 928
DI 10.1002/hep.28932
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EP3SF
UT WOS:000397301300017
PM 27906472
OA Bronze
DA 2025-01-07
ER
PT J
AU Muehler, A
Kohlhof, H
Groeppel, M
Vitt, D
AF Muehler, Andreas
Kohlhof, Hella
Groeppel, Manfred
Vitt, Daniel
TI The Selective Oral Immunomodulator Vidofludimus in Patients with Active
Rheumatoid Arthritis: Safety Results from the COMPONENT Study
SO DRUGS IN R&D
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; INFLAMMATORY-BOWEL-DISEASE; CANCER
RESISTANCE PROTEIN; TYROSINE KINASE-ACTIVITY; DIHYDROOROTATE
DEHYDROGENASE; IMMUNOSUPPRESSIVE AGENT; DOUBLE-BLIND; A77 1726; T-CELLS;
LEFLUNOMIDE
AB Introduction The dihydroorotate dehydrogenase (DHODH) inhibitors leflunomide and teriflunomide are immunomodulatory agents approved to treat rheumatoid arthritis (RA) and multiple sclerosis, respectively, and are actively being investigated as therapeutic agents for other immune-related diseases; however, both structurally related compounds have a number of potentially serious adverse effects. Vidofludimus, a new selective second-generation DHODH inhibitor, is chemically distinct from leflunomide/teriflunomide and appears to exhibit a distinct safety profile. Objective The aim of the COMPONENT study was to assess the efficacy, safety, and pharmacokinetics of vidofludimus in the treatment of patients with active RA on a background therapy of methotrexate. This report focuses solely on the safety results of the COMPONENT trial. Methods Patients received once-daily oral vidofludimus (N = 122) or placebo (N = 119) along with their standard of care methotrexate treatment for 13 weeks. Efficacy endpoints were assessed. Safety parameters were monitored throughout treatment and at follow-up. Plasma concentrations of vidofludimus were measured. Results The primary efficacy endpoint, American College of Rheumatology 20 (ACR(20)) responder rate at 13 weeks, demonstrated numerical superiority in the treatment group compared with placebo; however, it did not reach statistical significance. Nonetheless, the COMPONENT study yielded important safety and pharmacokinetic data that could provide important information regarding the use of vidofludimus in other clinical trials, not only for RA but also for other autoimmune diseases. A safety profile for vidofludimus similar to placebo was obtained in this RA patient population. This includes similar rates of the adverse events of diarrhea, alopecia, neutropenia, and elevated liver enzymes, all of which are known drug-related adverse events reported for leflunomide and teriflunomide. A potential pharmacokinetic interaction between vidofludimus and methotrexate was observed. Conclusions Vidofludimus demonstrated a positive safety profile, making it a promising candidate for the treatment of a variety of immune-related diseases.
C1 [Muehler, Andreas; Kohlhof, Hella; Groeppel, Manfred; Vitt, Daniel] Immunic AG, Klopferspitz 19, D-82152 Martinsried, Germany.
RP Muehler, A (corresponding author), Immunic AG, Klopferspitz 19, D-82152 Martinsried, Germany.
EM andreas.muehler@immunic.de
FU 4SC AG
FX The COMPONENT study was funded by 4SC AG, the original developer of
vidofludimus.
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NR 102
TC 19
Z9 22
U1 1
U2 14
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1174-5886
EI 1179-6901
J9 DRUGS R&D
JI Drugs R&D
PD DEC
PY 2019
VL 19
IS 4
BP 351
EP 366
DI 10.1007/s40268-019-00286-z
EA OCT 2019
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA KF2RP
UT WOS:000490882800001
PM 31621054
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Espíndola, MS
Frantz, FG
Soares, LS
Masson, AP
Tefé-Silva, C
Bitencourt, CS
Oliveira, SC
Rodrigues, V
Ramos, SG
Silva, CL
Faccioli, LH
AF Espindola, Milena Sobral
Frantz, Fabiani Gai
Soares, Luana Silva
Masson, Ana Paula
Tefe-Silva, Cristiane
Bitencourt, Claudia Silva
Oliveira, Sergio Costa
Rodrigues, Vanderlei
Ramos, Simone Gusmao
Silva, Celio Lopes
Faccioli, Lucia Helena
TI Combined immunization using DNA-Sm14 and DNA-Hsp65 increases CD8+memory
T cells, reduces chronic pathology and decreases egg viability during
Schistosoma mansoni infection
SO BMC INFECTIOUS DISEASES
LA English
DT Article
DE Schistosomiasis; DNA vaccines; DNA-Hsp65; DNA-Sm14
ID ACID-BINDING PROTEIN; DNA VACCINE; IMMUNE-RESPONSE; DEPENDENT PATHWAY;
PROTECTION; MICE; SM14; IMMUNOTHERAPY; TUBERCULOSIS; ACTIVATION
AB Background: Schistosomiasis is one of the most important neglected diseases found in developing countries and affects 249 million people worldwide. The development of an efficient vaccination strategy is essential for the control of this disease. Previous work showed partial protection induced by DNA-Sm14 against Schistosoma mansoni infection, whereas DNA-Hsp65 showed immunostimulatory properties against infectious diseases, autoimmune diseases, cancer and antifibrotic properties in an egg-induced granuloma model.
Methods: C57BL/6 mice received 4 doses of DNA-Sm14 (100 mu g/dose) and DNA-Hsp65 (100 mu g/dose), simultaneously administrated, or DNA-Sm14 alone, once a week, during four weeks. Three groups were included: 1-Control (no immunization); 2 DNA Sm14;3 DNA Sm14/DNA Hsp65. Two weeks following last immunization, animals were challenged subcutaneously with 30 cercariae. Fifteen, 48 and 69 days after infection splenocytes were collected to evaluate the number of CD8+ memory T cells (CD44(high)CD62(low)) using flow cytometry. Forty-eight days after challenge adult worms were collected by portal veins perfusion and intestines were collected to analyze the intestinal egg viability. Histological, immunohistochemical and soluble quantification of collagen and alpha-SMA accumulation were performed on the liver.
Results: In the current work, we tested a new vaccination strategy using DNA-Sm14 with DNA-Hsp65 to potentiate the protection against schistosomiasis. Combined vaccination increased the number of CD8+ memory T cells and decreased egg viability on the intestinal wall of infected mice. In addition, simultaneous vaccination with DNA-Sm14/DNA-Hsp65 reduced collagen and alpha-SMA accumulation during the chronic phase of granuloma formation.
Conclusion: Simultaneous vaccination with DNA- Sm14/ DNA- Hsp65 showed an immunostimulatory potential and antifibrotic property that is associated with the reduction of tissue damage on Schistosoma mansoni experimental infection.
C1 [Espindola, Milena Sobral; Frantz, Fabiani Gai; Soares, Luana Silva; Bitencourt, Claudia Silva; Faccioli, Lucia Helena] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Anal Clin Toxicol & Bromatol, BR-14040903 Sao Paulo, Brazil.
[Masson, Ana Paula; Rodrigues, Vanderlei; Silva, Celio Lopes] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Bioquim & Imunol, BR-14049900 Sao Paulo, Brazil.
[Tefe-Silva, Cristiane; Ramos, Simone Gusmao] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Patol, BR-14049900 Ribeirao Preto, SP, Brazil.
[Oliveira, Sergio Costa] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Bioquim & Imunol, BR-31270901 Belo Horizonte, MG, Brazil.
C3 Universidade de Sao Paulo; Universidade de Sao Paulo; Universidade de
Sao Paulo; Universidade Federal de Minas Gerais
RP Faccioli, LH (corresponding author), Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Anal Clin Toxicol & Bromatol, Av Cafe S-N, BR-14040903 Sao Paulo, Brazil.
EM faccioli@fcfrp.usp.br
RI Tefe-Silva, Cristiane/D-2493-2013; Faccioli, Lúcia/AGH-5297-2022;
Bitencourt, Claudia/JDD-2967-2023; Oliveira, Sergio/AAG-5408-2021;
Frantz, Fabiani/B-9204-2016; Masson, Ana Paula/T-2417-2018; Silva,
Celio/C-4639-2012
OI Ramos, Simone/0000-0002-1981-5248; Frantz, Fabiani/0000-0001-6960-2438;
Oliveira, Sergio/0000-0003-4062-5577; Masson, Ana
Paula/0000-0002-9081-8345; Faccioli, Lucia Helena/0000-0002-4999-8305;
Silva, Celio/0000-0002-0043-4568; Espindola, Milena
S/0000-0002-1079-8795
FU Sao Paulo Research Foundation (FAPESP) [2009/01501-8, 2009/07169-5];
Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq);
Forte [2009-01501] Funding Source: Forte; Formas [2009-01501] Funding
Source: Formas
FX We are grateful to Elaine Medeiros Floriano, Olinda Mara Brigoto and
Fabiana Rossetto de Morais for their technical assistance. This study
was supported by Sao Paulo Research Foundation (FAPESP, grant#
2009/01501-8 and 2009/07169-5) and Conselho Nacional de Desenvolvimento
Cientifico e Tecnologico (CNPq).
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NR 41
TC 7
Z9 7
U1 1
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2334
J9 BMC INFECT DIS
JI BMC Infect. Dis.
PD MAY 16
PY 2014
VL 14
AR 263
DI 10.1186/1471-2334-14-263
PG 9
WC Infectious Diseases
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases
GA AI3HQ
UT WOS:000336752100001
PM 24886395
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Biazzo, M
Deidda, G
AF Biazzo, Manuele
Deidda, Gabriele
TI Fecal Microbiota Transplantation as New Therapeutic Avenue for Human
Diseases
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE fecal microbiota transplantation; gut microbiome; neurological disorders
ID CLOSTRIDIUM-DIFFICILE INFECTION; INFLAMMATORY-BOWEL-DISEASE; INTESTINAL
BACTERIAL OVERGROWTH; RANDOMIZED CONTROLLED-TRIAL; ACTIVE
ULCERATIVE-COLITIS; GUT MICROBIOTA; DOUBLE-BLIND; GASTROINTESTINAL
SYMPTOMS; METABOLIC SYNDROME; SEVERE OBESITY
AB The human body is home to a variety of micro-organisms. Most of these microbial communities reside in the gut and are referred to as gut microbiota. Over the last decades, compelling evidence showed that a number of human pathologies are associated with microbiota dysbiosis, thereby suggesting that the reinstatement of physiological microflora balance and composition might ameliorate the clinical symptoms. Among possible microbiota-targeted interventions, pre/pro-biotics supplementations were shown to provide effective results, but the main limitation remains in the limited microbial species available as probiotics. Differently, fecal microbiota transplantation involves the transplantation of a solution of fecal matter from a donor into the intestinal tract of a recipient in order to directly change the recipient's gut microbial composition aiming to confer a health benefit. Firstly used in the 4th century in traditional Chinese medicine, nowadays, it has been exploited so far to treat recurrent Clostridioides difficile infections, but accumulating data coming from a number of clinical trials clearly indicate that fecal microbiota transplantation may also carry the therapeutic potential for a number of other conditions ranging from gastrointestinal to liver diseases, from cancer to inflammatory, infectious, autoimmune diseases and brain disorders, obesity, and metabolic syndrome. In this review, we will summarize the commonly used preparation and delivery methods, comprehensively review the evidence obtained in clinical trials in different human conditions and discuss the variability in the results and the pivotal importance of donor selection. The final aim is to stimulate discussion and open new therapeutic perspectives among experts in the use of fecal microbiota transplantation not only in Clostridioides difficile infection but as one of the first strategies to be used to ameliorate a number of human conditions.
C1 [Biazzo, Manuele] BioArte Ltd, Life Sci Pk, Sgn 3000, San Gwann, Malta.
[Biazzo, Manuele] Univ Siena, SienabioACTIVE, Via Aldo Moro 1, I-53100 Siena, Italy.
[Deidda, Gabriele] Univ Padua, Dept Biomed Sci, Via U Bassi 58-B, I-35131 Padua, Italy.
C3 University of Siena; University of Padua
RP Deidda, G (corresponding author), Univ Padua, Dept Biomed Sci, Via U Bassi 58-B, I-35131 Padua, Italy.
EM m.biazzo@thebioarte.com; gabriele.deidda@unipd.it
RI Deidda, Gabriele/GZH-0784-2022
OI DEIDDA, GABRIELE/0000-0002-0721-4971
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NR 266
TC 56
Z9 60
U1 5
U2 40
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD JUL
PY 2022
VL 11
IS 14
AR 4119
DI 10.3390/jcm11144119
PG 33
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 3G5PS
UT WOS:000831407000001
PM 35887883
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Park, JB
Peters, R
Pham, Q
Wang, TTY
AF Park, Jae B.
Peters, Renee
Quynhchi Pham
Wang, Thomas T. Y.
TI Javamide-II Inhibits IL-6 without Significant Impact on TNF-alpha and
IL-1beta in Macrophage-Like Cells
SO BIOMEDICINES
LA English
DT Article
DE Javamide-II (N-caffeoyltryptophan); Infection; COVID-19; IL-6
inhibition; p38/ATF-2; macrophage-like THP-1 cells
ID NF-KAPPA-B; INFLAMMATORY-BOWEL-DISEASE; TUMOR-NECROSIS-FACTOR;
SIGNAL-TRANSDUCTION; LIVER-DISEASES; MAP KINASE; INTERLEUKIN-6;
ARTHRITIS; PROFILE; CANCER
AB The main aim of this study is to find a therapeutic compound to inhibit IL-6, not TNF-alpha and IL-1beta, in macrophage-like cells, because the high-levels of IL-6 production by macrophages are reported to cause unfavorable outcomes under several disease conditions (e.g., autoimmune diseases, and acute viral infections, including COVID-19). In this study, the potential effects of javamide-II on IL-6, IL-1beta and TNF-alpha productions were determined using their ELISA kits in macrophage-like THP-1 cells. Western blots were also performed using the same cells, to determine its effects on signaling pathways (ERK, p38, JNK, c-Fos, ATF-2, c-Jun and NF-kappa B p65). At concentrations of 0.2-40 mu M, javamide-II inhibited IL-6 production significantly in the THP-1 cells (IC50 of 0.8 mu M) (P < 0.02). However, javamide-II did not inhibit IL-1beta or TNF-alpha productions much at the same concentrations. In addition, the treatment of javamide-II decreased the phosphorylation of p38 without significant effects on ERK and JNK phosphorylations in the THP-1 cells. Furthermore, the p38 inhibition, followed by the reduction of ATF-2 phosphorylation (not c-Fos, c-Jun or NF-kappa B p65), led to the suppression of IL-6 mRNA expression in the cells (P < 0.02). The data indicate that javamide-II may be a potent compound to inhibit IL-6 production via suppressing the p38 signal pathway, without significant effects on the productions of TNF-alpha and IL-1beta in macrophage-like THP-1 cells.
C1 [Park, Jae B.; Peters, Renee; Quynhchi Pham; Wang, Thomas T. Y.] ARS, Diet Genom & Immunol Lab, BHNRC, USDA, Bldg 307C,Rm 131, Beltsville, MD 20705 USA.
C3 United States Department of Agriculture (USDA)
RP Park, JB (corresponding author), ARS, Diet Genom & Immunol Lab, BHNRC, USDA, Bldg 307C,Rm 131, Beltsville, MD 20705 USA.
EM jae.park@usda.gov; renee.peters@usda.gov; quynhchi.pham@usda.gov;
tom.wang@usda.gov
FU USDA [1235-51000-054-00D]
FX This study was funded by USDA (project number 1235-51000-054-00D).
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NR 51
TC 10
Z9 10
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD JUN
PY 2020
VL 8
IS 6
AR 138
DI 10.3390/biomedicines8060138
PG 14
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA MO0NC
UT WOS:000551233000004
PM 32485858
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wang, H
Mengsteab, S
Tag, CG
Gao, CF
Hellerbrand, C
Lammert, F
Gressner, AM
Weiskirchen, R
AF Wang, Hao
Mengsteab, Senait
Tag, Carmen G.
Gao, Chun-Fang
Hellerbrand, Claus
Lammert, Frank
Gressner, Axel M.
Weiskirchen, Ralf
TI Transforming growth factor-β1 gene polymorphisms are associated with
progression of liver fibrosis in Caucasians with chronic hepatitis C
infection
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE TGF-beta 1; Gene polymorphism; LightCycler; Viral hepatitis; Fibrosis
ID BETA 1 GENE; DISEASE PROGRESSION; JAPANESE PATIENTS; NATURAL-HISTORY;
TGF-BETA; EXPRESSION; TGF-BETA-1; RECEPTOR; MICE; DYSFUNCTION
AB AIM: Considerable attention is focused on polymorphisms in the gene encoding transforming growth factor-beta 1 (TGF-beta 1), a multifunctional cytokine that is in turn a potent growth inhibitor involved in wound healing and differentiation. In humans, it promotes the pathogenesis of organ fibrosis, atherosclerosis, cancer, autoimmune and inflammatory diseases, keloid disease, and hypertrophic scarring. For this reason, much emphasis has been placed on studies elucidating the impact of TGF-beta 1 and its gene variations for the susceptibility and pathogenesis of these diseases. Unfortunately, some studies have serious limitations.
METHODS: We have recently described a high-throughput method for investigation the Arg25Pro polymorphism of human TGF-beta 1 gene and showed that the frequency of the Pro25 allele is significantly associated with hepatic fibrogenesis. In this report, we describe two novel LightCycler (LC) techniques that facilitate the examination of the two other known alterations in the coding region of TGF-beta 1. We investigated whether these polymorphisms contribute to hepatitis-induced progression of fibrogenesis in Chinese and Caucasians.
RESULTS: In the Chinese ancestry, the gene polymorphisms at codons 25 and 263 were not found and the genetic variant at codon 10 is unlikely to confer susceptibility to hepatic fibrosis. Contrarily, in Caucasians TGF-beta 1 allelic variations are more frequent and the presence of prolines either in codon 25 or 10 is associated with the interindividual variability in developing more severe fibrosis during chronic hepatitis C infection.
CONCLUSION: In summary, these results confirm the hypothesis that TGF-beta 1 polymorphisms are associated with fibrosis progression in Caucasians chronically infected with hepatitis C. (C) 2005 The WJG Press and Elsevier Inc. All rights reserved.
C1 [Mengsteab, Senait; Tag, Carmen G.; Gressner, Axel M.; Weiskirchen, Ralf] RWTH Univ Hosp, Inst Clin Chem & Pathobiochem, D-52074 Aachen, Germany.
[Wang, Hao; Gao, Chun-Fang] Second Mil Med Univ, Dept Lab Med, Changzheng Hosp, Shanghai, Peoples R China.
[Hellerbrand, Claus] Univ Regensburg, Dept Internal Med 1, D-8400 Regensburg, Germany.
[Lammert, Frank] RWTH Univ Hosp, Dept Med 3, D-52074 Aachen, Germany.
C3 RWTH Aachen University; RWTH Aachen University Hospital; Naval Medical
University; University of Regensburg; RWTH Aachen University; RWTH
Aachen University Hospital
RP Weiskirchen, R (corresponding author), RWTH Univ Hosp, Inst Clin Chem & Pathobiochem, D-52074 Aachen, Germany.
EM rweiskirchen@ukaachen.de
RI Weiskirchen, Ralf/O-1734-2018
OI Weiskirchen, Ralf/0000-0003-3888-0931
FU Federal Ministry of Education and Research of Germany (Network of
Competence in Medicine Hep-Net); Natural Science Foundation of China
[30270605]; Germany United Society of Clinical Chemistry and Laboratory
Medicine
FX Supported by the Grants From the Federal Ministry of Education and
Research of Germany (Network of Competence in Medicine Hep-Net) and the
Natural Science Foundation of China, No. 30270605 Dr. Hao Wang was
financed by a stipend from the Germany United Society of Clinical
Chemistry and Laboratory Medicine.
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NR 41
TC 73
Z9 86
U1 0
U2 1
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD APR 7
PY 2005
VL 11
IS 13
BP 1929
EP 1936
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA V19WM
UT WOS:000208102500007
PM 15800982
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Derbala, M
Elbadri, ME
Amer, AM
AlKaabi, S
Sultan, KH
Kamel, YM
Elsayed, EHS
Avades, TY
Chandra, P
Shebl, FM
AF Derbala, Moutaz
Elbadri, Mohammed Elshiekh
Amer, Aliaa Mohamed
AlKaabi, Saad
Sultan, Khaleel Hassan
Kamel, Yasser Medhat
Elsayed, Eman Hassan Satti
Avades, Tony Yervant
Chandra, Prem
Shebl, Fatma M.
TI Aspartate transaminase to platelet ratio index in hepatitis C virus and
Schistosomiasis coinfection
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Hepatitis C; Schistosomiasis; Aspartate transaminase to platelet ratio
index; Liver biopsy; Liver fibrosis
ID LIVER FIBROSIS; BIOPSY; PROGRESSION; INFECTION; EGYPT; COUNT; SCORE;
APRI
AB AIM: To assess the diagnostic accuracy, of amino-transferase-to-platelet ratio index (APRI) alone and with antischistosomal antibody (Ab) in patients with hepatitis C virus (HCV) and schistosomiasis coinfection.
METHODS: This retrospective study included medical records of three hundred and eighty three Egyptian men patients who had undergone percutaneous liver biopsy between January 2006 to April 2014 in tertiary care hospital in Qatar for diagnosis or monitoring purpose were selected. Data of patients > 18 years of age were included in the study. The values of HCV RNA titer and antischistosomal antibody titer were also taken into consideration. Patients were excluded from the study if they had any other concomitant chronic liver disease, including; history of previous antiviral or interferon therapy, immunosuppressive, therapy, chronic hepatitis B infection, human immunodeficiency virus co-infection, autoimmune hepatitis, decompensated liver disease, hepatocellular carcinoma, prior liver transplantation, and if no data about the liver biopsy present.
RESULTS: Median age of patients was 46 years. About 7.1% had no fibrosis, whereas 30.4%, 37.5%, 20.4%, and 4.6% had fibrosis of stage I, II, III, and. respectively. In bivariate analysis, APRI score, levels of AST, platelet count and age of patient showed statistically significant association with liver fibrosis (p < 0.0001); whereas antischistosomal antibody titer (p = 0.52) and HCV RNA titer (p = 0.79) failed to show a significant association. The respective AUC values for no fibrosis, significant fibrosis, severe fibrosis and cirrhosis of APRI score were 63%, 73.2%, 81.1% and 88.9% respectively. This showed good sensitivity and specificity of APRI alone for grading of liver fibrosis. But the inclusion of anti-Schistosoma antibody did not improve the prediction of fibrosis stage.
CONCLUSION: The study results suggest that noninvasive biochemical markers like APRI are sensitive and specific in diagnosing the degree of fibrosis and cirrhosis in patients with coinfection of HCV and schistosomiasis as compared to biopsy. The addition of antischistosomal Ab to APRI did not improve sensitivity for predicting the degree of cirrhosis.
C1 [Derbala, Moutaz; Elbadri, Mohammed Elshiekh; AlKaabi, Saad; Sultan, Khaleel Hassan; Kamel, Yasser Medhat] Hamad Gen Hosp, Hamad Med Corp, Gastroenterol & Hepatol, Doha 00974, Qatar.
[Derbala, Moutaz] Theodor Bilharz Res Inst, Gastroenterol & Hepatol, Giza 12411, Egypt.
[Derbala, Moutaz] Weill Cornell Med Coll, Dept Med, Doha 00974, Qatar.
[Amer, Aliaa Mohamed] Hamad Gen Hosp, Hamad Med Corp, Hematol Sect, Lab Med & Pathol, Doha 00974, Qatar.
[Elsayed, Eman Hassan Satti] Hamad Gen Hosp, Hamad Med Corp, Gen Med, Med Educ, Doha 00974, Qatar.
[Avades, Tony Yervant] Hamad Gen Hosp, Hamad Med Corp, Dept Lab Med & Pathol, Doha 00974, Qatar.
[Chandra, Prem] Hamad Gen Hosp, Hamad Med Corp, Med Res Ctr, Doha 00974, Qatar.
[Shebl, Fatma M.] Yale Univ, Sch Publ Hlth, Dept Epidemiol, Chron Dis, New Haven, CT 06510 USA.
C3 Hamad Medical Corporation; Hamad General Hospital; Egyptian Knowledge
Bank (EKB); Theodor Bilharz Research Institute (TBRI); Qatar Foundation
(QF); Weill Cornell Medical College Qatar; Hamad Medical Corporation;
Hamad General Hospital; Hamad Medical Corporation; Hamad General
Hospital; Hamad Medical Corporation; Hamad General Hospital; Hamad
Medical Corporation; Hamad General Hospital; Yale University
RP Derbala, M (corresponding author), Hamad Gen Hosp, Hamad Med Corp, Gastroenterol & Hepatol, Doha 00974, Qatar.
EM mod2002@qatar-med.cornell.edu
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World Health Organization, HEP C FACT SHEET
World Health Organization, HEP C GLOB RESP AL
NR 26
TC 10
Z9 10
U1 0
U2 7
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD DEC 14
PY 2015
VL 21
IS 46
BP 13132
EP 13139
DI 10.3748/wjg.v21.i46.13132
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CY1WY
UT WOS:000366200100016
PM 26674154
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Kawashima, H
Takatori, H
Suzuki, K
Iwata, A
Yokota, M
Suto, A
Minamino, T
Hirose, K
Nakajima, H
AF Kawashima, Hirotoshi
Takatori, Hiroaki
Suzuki, Kotaro
Iwata, Arifumi
Yokota, Masaya
Suto, Akira
Minamino, Tohru
Hirose, Koichi
Nakajima, Hiroshi
TI Tumor Suppressor p53 Inhibits Systemic Autoimmune Diseases by Inducing
Regulatory T Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID FOXP3 EXPRESSION; RHEUMATOID-ARTHRITIS; SELF-TOLERANCE; BREAST-CANCER;
GENE; DNA; MICE; INTERLEUKIN-6; ACTIVATION; MUTATIONS
AB The tumor suppressor p53 plays a central role in tumor suppression by inducing apoptosis, cell cycle arrest, senescence, and DNA repair. In addition to the antitumor functions of p53, accumulating evidence using systemic p53-deficient mice suggests that p53 suppresses autoimmunity. However, it remains unknown how p53 suppresses autoimmunity. In this study, we generated T cell-specific p53-deficient mice (CD4-Cre p53(fl/fl) mice, or p53 conditional knockout [cKO] mice) and found that aged p53-cKO mice spontaneously developed inflammatory lesions in various organs, including lung, liver, stomach, thyroid gland, submandibular gland, and kidney. Additionally, anti-nuclear Abs and autoantibodies against gastric parietal cells were detected in p53-cKO mice but not in control p53(fl/fl) mice (p53 wild-type mice). Importantly, the number of Foxp3(+)CD4(+) regulatory T cells (Tregs) in the spleen and lung as well as in vitro differentiation of induced Tregs was significantly reduced in p53-cKO mice as compared with that in p53 wild-type mice. Regarding the mechanisms underlying p53-mediated Treg induction, p53 enhanced the transcription of Foxp3 by binding to the promoter and the conserved noncoding DNA sequence-2 of the Foxp3 gene. Taken together, these results suggest that p53 expressed in T cells functions as a suppressor for autoimmunity by inducing Treg differentiation.
C1 [Kawashima, Hirotoshi; Takatori, Hiroaki; Suzuki, Kotaro; Iwata, Arifumi; Yokota, Masaya; Suto, Akira; Hirose, Koichi; Nakajima, Hiroshi] Chiba Univ, Grad Sch Med, Dept Allergy & Clin Immunol, Chiba 2608670, Japan.
[Minamino, Tohru] Niigata Univ, Grad Sch Med & Dent Sci, Dept Cardiovasc Biol & Med, Niigata 9518510, Japan.
C3 Chiba University; Niigata University
RP Takatori, H (corresponding author), Chiba Univ, Grad Sch Med, Dept Allergy & Clin Immunol, Chuo Ku, 1-8-1 Inohana, Chiba 2608670, Japan.
EM takatorih@faculty.chiba-u.jp; nakajimh@faculty.chiba-u.jp
RI Nakajima, Hiroshi/AFU-9313-2022; Hirose, Koichi/I-1506-2017; Minamino,
Tohru/P-8145-2018
OI Suto, Akira/0000-0002-2593-565X; Minamino, Tohru/0000-0003-1627-6151;
Nakajima, Hiroshi/0000-0001-8595-9381
FU Ministry of Education, Culture, Sports, Science and Technology; Japanese
Government; Global Centers of Excellence Program (Global Center for
Education and Research in Immune System Regulation and Treatment) of the
Ministry of Education, Culture, Sports, Science and Technology, Japan;
Grants-in-Aid for Scientific Research [23591432, 23591113, 24390207,
23591458, 24790989] Funding Source: KAKEN
FX This work was supported in part by grants-in-aids for scientific
research from the Ministry of Education, Culture, Sports, Science and
Technology, the Japanese Government, and by the Global Centers of
Excellence Program (Global Center for Education and Research in Immune
System Regulation and Treatment) of the Ministry of Education, Culture,
Sports, Science and Technology, Japan.
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NR 45
TC 72
Z9 81
U1 0
U2 22
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2013
VL 191
IS 7
BP 3614
EP 3623
DI 10.4049/jimmunol.1300509
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 221CH
UT WOS:000324634500017
PM 24006461
OA Bronze
DA 2025-01-07
ER
PT J
AU Schäck, LM
Buettner, M
Wirth, A
Neunaber, C
Krettek, C
Hoffmann, A
Noack, S
AF Schaeck, Luisa Marilena
Buettner, Manuela
Wirth, Alexander
Neunaber, Claudia
Krettek, Christian
Hoffmann, Andrea
Noack, Sandra
TI Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal
Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like Genotype
SO STEM CELLS INTERNATIONAL
LA English
DT Article
ID HEPATIC STELLATE CELLS; STEM-CELLS; LIVER FIBROSIS; ENGRAFTMENT;
MODULATION; CONTRIBUTE; INDUCTION
AB Human bone marrow-derived stromal cells (hBMSCs) derived from the adult organism hold great promise for diverse settings in regenerative medicine. Therefore a more complete understanding of hBMSC biology to fully exploit the cells' potential for clinical settings is important. The protein CD24 has been reported to be involved in a diverse range of processes such as cancer, adaptive immunity, inflammation, and autoimmune diseases in other cell types. Its expression in hBMSCs, which has not yet been analyzed, may add an important aspect in the understanding of hBMSC biology. The present study therefore analyzes the expression, regulation, and functional implication of the surface protein CD24 in hBMSCs. Methods used are stimulation studies with TGF beta as well as shRNA-mediated knockdown and overexpression of CD24 followed by microarray, immunocytochemistry, and flow cytometric analyses. To our knowledge, we demonstrate for the first time that the expression of CD24 is an inherent property of hBMSCs. Importantly, the data links the upregulation of CD24 to the adoption of a myofibroblast-like gene expression pattern in hBMSCs. We demonstrate that CD24 is an important modulator in transforming growth factor beta 3 (TGF beta 3) signaling with a reciprocal regulatory relationship between these two proteins.
C1 [Schaeck, Luisa Marilena; Neunaber, Claudia; Krettek, Christian; Hoffmann, Andrea; Noack, Sandra] Hannover Med Sch, Trauma Dept, D-30625 Hannover, Germany.
[Buettner, Manuela] Hannover Med Sch, Inst Lab Anim Sci, D-30625 Hannover, Germany.
[Wirth, Alexander] Hannover Med Sch, Cellular Neurophysiol, D-30625 Hannover, Germany.
C3 Hannover Medical School; Hannover Medical School; Hannover Medical
School
RP Neunaber, C (corresponding author), Hannover Med Sch, Trauma Dept, D-30625 Hannover, Germany.
EM neunaber.claudia@mh-hannover.de
RI Hoffmann, Andrea/AAG-4488-2020; Neunaber, Claudia/AAJ-1490-2021
OI Hoffmann, Andrea/0000-0003-2318-8985; Krettek,
Christian/0000-0001-9807-0020
FU Studienstiftung des Deutschen Volkes; DFG [PO732]
FX The skillful assistance of Annika Hamm was greatly appreciated.
Microarray data used or referred to in this publication were generated
by the Research Core Unit Transcriptomics of the Hannover Medical
School. The support of Professor Dr. Axel Schambach and Professor Dr.
Ralf Hass is gratefully acknowledged. Luisa Marilena Schack was
supported with a Ph.D. grant from the Studienstiftung des Deutschen
Volkes. This work was partly supported by the DFG through Grants PO732
and REBIRTH.
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NR 50
TC 16
Z9 20
U1 0
U2 9
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-966X
EI 1687-9678
J9 STEM CELLS INT
JI Stem Cells Int.
PY 2016
VL 2016
AR 1319578
DI 10.1155/2016/1319578
PG 13
WC Cell & Tissue Engineering
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA DB9MD
UT WOS:000368839400001
PM 26788063
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Urrata, V
Trapani, M
Franza, M
Moschella, F
Di Stefano, AB
Toia, F
AF Urrata, Valentina
Trapani, Marco
Franza, Mara
Moschella, Francesco
Di Stefano, Anna Barbara
Toia, Francesca
TI Analysis of MSCs' secretome and EVs cargo: Evaluation of functions and
applications
SO LIFE SCIENCES
LA English
DT Review
DE Mesenchymal stem cells; Extracellular vesicles; Secretome; miRNAs; 3D
cultures; Epigenetic
ID MESENCHYMAL STEM-CELLS; ANGIOGENESIS IN-VITRO; HUMAN FETAL LIVER;
EXTRACELLULAR VESICLES; INDUCE ANGIOGENESIS; BONE REGENERATION;
DIFFERENTIATION; IDENTIFICATION; PROLIFERATION; APOPTOSIS
AB Mesenchymal stem cells (MSCs) can exert different functions and can be used in several medical fields. In the last years, MSC properties have been attributed to their secreted factors such as soluble proteins, cytokines and growth factors. Moreover, a key role is played by the extracellular vesicles (EVs) which lead a heterogeneous cargo of proteins, lipids and small and long non-coding RNAs that interfere with the pathways of the recipient cells. Due to the safeness and easiness in obtaining the secretome, its use is becoming a turning point for the application in physiological and pathological fields. This review summarizes the most recent studies on the use of MSCs secretome, focusing on some physiological (angiogenesis and osteogenesis) and pathological (cancer, cardiovascular and autoimmune diseases) applications. The secreted analyzed factors are listed in a table. In addition, the different characteristics of the fetal MSCs derived secretome and the differences in the secretome composition of three-dimensionally (3D) cultured cells are discussed. As very innovative aspects, recent studies on some applications of engineered vesicles, embedded or not in three-dimensional structures, are treated and the influence of some epigenetic modifications on cells and EVs is investigated.
C1 [Urrata, Valentina; Trapani, Marco; Moschella, Francesco; Di Stefano, Anna Barbara; Toia, Francesca] Univ Palermo, Dept Surg Oncol & Oral Sci, Lab Biol & Regenerat Med PLAST Surg, BIOPLAST,Plast & Reconstruct Surg, I-90127 Palermo, Italy.
[Trapani, Marco; Franza, Mara; Toia, Francesca] Azienda Osped Univ Policlin Paolo Giaccone, Dept Oncol, Plast & Reconstruct Surg, I-90127 Palermo, Italy.
[Franza, Mara; Toia, Francesca] Univ Palermo, Dept Surg Oncol & Oral Sci, Plast & Reconstruct Surg, I-90127 Palermo, Italy.
C3 University of Palermo; University of Palermo; Policlinico Paolo
Giaccone; University of Palermo
RP Di Stefano, AB (corresponding author), Univ Palermo, Dept Surg Oncol & Oral Sci, Lab Biol & Regenerat Med PLAST Surg, BIOPLAST,Plast & Reconstruct Surg, I-90127 Palermo, Italy.
EM annabarbara.distefano@unipa.it
RI di stefano, anna barbara/ABA-2219-2021; Toia, Francesca/AAH-4246-2021;
franza, mara/JCE-6632-2023; di stefano, anna barbara/K-1447-2016
OI di stefano, anna barbara/0000-0003-4323-8564; Franza,
Mara/0000-0002-5799-1461
FU University of Palermo (IT), Doctoral Course of Experimental Oncology and
Surgery, Cycle XXXVI
FX Valentina Urrata, PhDst is supported, for this research, by the
University of Palermo (IT), Doctoral Course of Experimental Oncology and
Surgery, Cycle XXXVI.
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NR 105
TC 0
Z9 0
U1 0
U2 25
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD NOV 1
PY 2022
VL 308
AR 120990
DI 10.1016/j.lfs.2022.120990
EA SEP 2022
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 5C1UW
UT WOS:000864053100003
PM 36155182
DA 2025-01-07
ER
PT J
AU Lovelace, ES
Wagoner, J
MacDonald, J
Bammler, T
Bruckner, J
Brownell, J
Beyer, RP
Zink, EM
Kim, YM
Kyle, JE
Webb-Robertson, BJM
Waters, KM
Metz, TO
Farin, F
Oberlies, NH
Polyak, SJ
AF Lovelace, Erica S.
Wagoner, Jessica
MacDonald, James
Bammler, Theo
Bruckner, Jacob
Brownell, Jessica
Beyer, Richard P.
Zink, Erika M.
Kim, Young-Mo
Kyle, Jennifer E.
Webb-Robertson, Bobbie-Jo M.
Waters, Katrina M.
Metz, Thomas O.
Farin, Federico
Oberlies, Nicholas H.
Polyak, Stephen J.
TI Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress
Signaling
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID HEPATITIS-C VIRUS; ACTIVATED PROTEIN-KINASE; PROSTATE-CANCER
CHEMOPREVENTION; FOXO TRANSCRIPTION FACTORS; NF-KAPPA-B; T-CELLS;
QUANTITATIVE-ANALYSIS; MOLECULAR-MECHANISMS; AUTOIMMUNE-DISEASES;
PROTEOMICS DATA
AB Silymarin, a characterized extract of the seeds of milk thistle (Silybum marianum), suppresses cellular inflammation. To define how this occurs, transcriptional profiling; metabolomics, and signaling studies were performed in human liver and T cell lines. Cellular stress and metabolic pathways were modulated within 4 h of silymarin treatment: activation of Activating Transcription Factor 4 (ATF-4) and adenosine monophosphate protein kinase (AIVLPK) and inhibition of mammalian target of rapamycin (mTOR) signaling, the latter being associated with induction of DNA-damage-inducible transcript 4 (DDIT4). Metabolomics analyses revealed silymarin suppression of glycolytic, tricarboxylic acid (TCA) cycle, and amino acid metabolism. Anti-inflammatory effects arose with prolonged (i.e., 24 h) silymarin exposure, with suppression of multiple pro-inflammatory mRNAs and signaling pathways including nuclear factor kappa B (NF-kappa B) and forkhead box 0 (FOXO). Studies with murine knock out cells revealed that silymarin inhibition of both mTOR and NF-kappa B was partially AMPK dependent, whereas silymarin inhibition of mTOR required DDIT4. Other natural products induced similar stress responses, which correlated with their ability to suppress inflammation. Thus, natural products activate stress and repair responses that culminate in an anti-inflammatory cellular phenotype. Natural products like silymarin may be useful as tools to define how metabolic, stress, and repair pathways regulate cellular inflammation.
C1 [Lovelace, Erica S.; Wagoner, Jessica; Bruckner, Jacob; Polyak, Stephen J.] Univ Washington, Dept Lab Med, Seattle, WA 98104 USA.
[Polyak, Stephen J.] Univ Washington, Dept Global Hlth, Seattle, WA 98104 USA.
[Polyak, Stephen J.] Univ Washington, Dept Microbiol, Seattle, WA 98104 USA.
[MacDonald, James; Bammler, Theo; Beyer, Richard P.; Farin, Federico] Univ Washington, Dept Environm & Occupat Hlth Sci, Ctr Ecogenet & Environm Hlth, Seattle, WA 98104 USA.
[Brownell, Jessica] Seattle Biomed, Malaria Program, Seattle, WA 98109 USA.
[Zink, Erika M.; Kim, Young-Mo; Kyle, Jennifer E.; Webb-Robertson, Bobbie-Jo M.; Waters, Katrina M.; Metz, Thomas O.] Pacific NW Natl Lab, Div Biol Sci, Richland, WA 99352 USA.
[Oberlies, Nicholas H.] Univ N Carolina, Dept Chem & Biochem, Greensboro, NC 27402 USA.
C3 University of Washington; University of Washington Seattle; University
of Washington; University of Washington Seattle; University of
Washington; University of Washington Seattle; University of Washington;
University of Washington Seattle; Center for Infectious Disease
Research; United States Department of Energy (DOE); Pacific Northwest
National Laboratory; University of North Carolina; University of North
Carolina Greensboro
RP Polyak, SJ (corresponding author), Univ Washington, Dept Lab Med, Seattle, WA 98104 USA.
EM polyak@uw.edu
RI Webb-Robertson, Bobbie-Jo/K-8230-2019; Zink, Erika/E-2135-2014;
Oberlies, Nicholas/D-8162-2011; Kim, Young-Mo/D-3282-2009
OI Oberlies, Nicholas/0000-0002-0354-8464; Kim,
Young-Mo/0000-0002-8972-7593; Waters, Katrina/0000-0003-4696-5396;
Webb-Robertson, Bobbie-Jo/0000-0002-4744-2397
FU NIH from NCCIH [5R01AT006842, 3R01AT006842-03S1]; NIH Common Fund's
Metabolomics Program; National Institute Of Environmental Health
Sciences of the National Institutes of Health [P30ES007033]; DOE
[DE-AC05-76RLO 1830]
FX This work was supported by NIH grant 5R01AT006842 and 3R01AT006842-03S1
from NCCIH (formerly NCCAM), and the NIH Common Fund's Metabolomics
Program, respectively. Support was also provided by the National
Institute Of Environmental Health Sciences of the National Institutes of
Health under Award Number P30ES007033. Pacific Northwest National
Laboratory is a multiprogram national laboratory operated by Battelle
for the DOE under Contract DE-AC05-76RLO 1830.
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NR 77
TC 46
Z9 52
U1 0
U2 26
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
EI 1520-6025
J9 J NAT PROD
JI J. Nat. Prod.
PD AUG
PY 2015
VL 78
IS 8
BP 1990
EP 2000
DI 10.1021/acs.jnatprod.5b00288
PG 11
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy
GA CQ7HN
UT WOS:000360773700023
PM 26186142
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Mocchegiani, E
Malavolta, M
AF Mocchegiani, E
Malavolta, M
TI NK and NKT cell functions in immunosenescence
SO AGING CELL
LA English
DT Review
DE adaptive immunity; aging; cytokine production; cytotoxicity; innate
immunity; INK cell; NKT cells; successful aging
ID NATURAL-KILLER-CELLS; T-CELLS; CYTOKINE PRODUCTION; INNATE; IMMUNE;
LYMPHOCYTES; LIVER; ZINC; INTERPLAY; NONAGENARIANS
AB Immunosenescence is defined as the state of dysregulated immune function that contributes to the increased susceptibility to infection, cancer and autoimmune diseases observed in old organisms, including humans. However, dysregulations in the immune functions are normally counterbalanced by continuous adaptation of the body to the deteriorations that occur over time. These adaptive changes are likely to occur in healthy human centenarians. Both innate (natural) and adaptive (acquired) immune responses decline with advancing age. Natural killer (NK) and natural killer T (NKT) cells represent the best model to describe innate and adaptive immune response in aging. NK and NKT cell cytotoxicity decreases in aging as well as interferon-gamma (IFN-gamma) production by both activated cell types. Their innate and acquired immune responses are preserved in very old age. However, NKT cells bearing T-cell receptor (TCR) gammadelta also display an increased cytotoxicity and IFN-gamma production in very old age. This fact suggests that NKT cells bearing TCRgammadelta are more involved in maintaining innate and adaptive immune response in aging leading to successful aging. The role played by the neuroendocrine-immune network and by nutritional factors, such as zinc, in maintaining NK and NKT cell functions in aging is discussed.
C1 INRCA Ancona, Ctr Immunol, Res Dept, Sect Nutr Immun & Aging, I-60121 Ancona, Italy.
C3 IRCCS INRCA
RP INRCA Ancona, Ctr Immunol, Res Dept, Sect Nutr Immun & Aging, Via Birarelli 8, I-60121 Ancona, Italy.
EM e.mocchegiani@inrca.it
RI Malavolta, Marco/J-8215-2012
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NR 63
TC 138
Z9 160
U1 0
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1474-9718
EI 1474-9726
J9 AGING CELL
JI Aging Cell
PD AUG
PY 2004
VL 3
IS 4
BP 177
EP 184
DI 10.1111/j.1474-9728.2004.00107.x
PG 8
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA 844DT
UT WOS:000223138300006
PM 15268751
OA hybrid
DA 2025-01-07
ER
PT J
AU Szyk, P
Czarczynska-Goslinska, B
Mlynarczyk, DT
Slusarska, B
Kocki, T
Ziegler-Borowska, M
Goslinski, T
AF Szyk, Piotr
Czarczynska-Goslinska, Beata
Mlynarczyk, Dariusz T.
Slusarska, Barbara
Kocki, Tomasz
Ziegler-Borowska, Marta
Goslinski, Tomasz
TI Polymer-Based Nanoparticles as Drug Delivery Systems for Purines of
Established Importance in Medicine
SO NANOMATERIALS
LA English
DT Review
DE active pharmaceutical ingredients; drug delivery systems; nanoparticles;
pharmaceutical technology; polymers; purines
ID TENOFOVIR DISOPROXIL FUMARATE; IN-VITRO; PLGA NANOPARTICLES;
CONTROLLED-RELEASE; CHITOSAN NANOPARTICLES; GELATIN NANOPARTICLES;
EUDRAGIT RLPO; EX-VIVO; RS-PO; HIV
AB Many purine derivatives are active pharmaceutical ingredients of significant importance in the therapy of autoimmune diseases, cancers, and viral infections. In many cases, their medical use is limited due to unfavorable physicochemical and pharmacokinetic properties. These problems can be overcome by the preparation of the prodrugs of purines or by combining these compounds with nanoparticles. Herein, we aim to review the scientific progress and perspectives for polymer-based nanoparticles as drug delivery systems for purines. Polymeric nanoparticles turned out to have the potential to augment antiviral and antiproliferative effects of purine derivatives by specific binding to receptors (ASGR1-liver, macrophage mannose receptor), increase in drug retention (in eye, intestines, and vagina), and permeation (intranasal to brain delivery, PEPT1 transport of acyclovir). The most significant achievements of polymer-based nanoparticles as drug delivery systems for purines were found for tenofovir disoproxil in protection against HIV, for acyclovir against HSV, for 6-mercaptopurine in prolongation of mice ALL model life, as well as for 6-thioguanine for increased efficacy of adoptively transferred T cells. Moreover, nanocarriers were able to diminish the toxic effects of acyclovir, didanosine, cladribine, tenofovir, 6-mercaptopurine, and 6-thioguanine.
C1 [Szyk, Piotr; Mlynarczyk, Dariusz T.; Goslinski, Tomasz] Poznan Univ Med Sci, Chair & Dept Chem Technol Drugs, Rokietnicka 3, PL-60806 Poznan, Poland.
[Czarczynska-Goslinska, Beata] Poznan Univ Med Sci, Chair & Dept Pharmaceut Technol, Rokietnicka 3, PL-60806 Poznan, Poland.
[Slusarska, Barbara] Med Univ Lublin, Fac Hlth Sci, Dept Family & Geriatr Nursing, PL-20081 Lublin, Poland.
[Kocki, Tomasz] Med Univ Lublin, Dept Expt & Clin Pharmacol, PL-20081 Lublin, Poland.
[Ziegler-Borowska, Marta] Nicolaus Copernicus Univ Torun, Fac Chem, Dept Biomed Chem & Polymer Sci, Gagarina 7, PL-87100 Torun, Poland.
C3 Poznan University of Medical Sciences; Poznan University of Medical
Sciences; Medical University of Lublin; Medical University of Lublin;
Nicolaus Copernicus University
RP Szyk, P; Goslinski, T (corresponding author), Poznan Univ Med Sci, Chair & Dept Chem Technol Drugs, Rokietnicka 3, PL-60806 Poznan, Poland.
EM piotr.szyk@student.put.poznan.pl; bgoslinska@ump.edu.pl;
mlynarczykd@ump.edu.pl; barbara.slusarska@umlub.pl;
tomasz.kocki@umlub.pl; martaz@umk.pl; tomasz.goslinski@ump.edu.pl
RI Ziegler-Borowska, Marta/O-5764-2015; Mlynarczyk, Dariusz/AAA-7044-2021;
Slusarska, Barbara/U-8951-2018; GOSLINSKI, TOMASZ/A-4639-2010
OI Slusarska, Barbara/0000-0003-0101-9216; Kocki,
Tomasz/0000-0002-7587-2626; Ziegler-Borowska, Marta/0000-0002-0502-9932;
GOSLINSKI, TOMASZ/0000-0001-5705-5414
FU National Science Centre Poland [2022/47/O/NZ7/00925]
FX The authors gratefully acknowledge the National Science Centre Poland
for financial support (Grant no. 2022/47/O/NZ7/00925).
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NR 150
TC 1
Z9 1
U1 4
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2079-4991
J9 NANOMATERIALS-BASEL
JI Nanomaterials
PD OCT
PY 2023
VL 13
IS 19
AR 2647
DI 10.3390/nano13192647
PG 42
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
Science, Multidisciplinary; Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
Physics
GA U3SQ1
UT WOS:001084032600001
PM 37836288
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Abdel-Daim, MM
Khalifa, HA
Abushouk, AI
Dkhil, MA
Al-Quraishy, SA
AF Abdel-Daim, Mohamed M.
Khalifa, Hesham A.
Abushouk, Abdelrahman Ibrahim
Dkhil, Mohamed A.
Al-Quraishy, Saleh A.
TI Diosmin Attenuates Methotrexate-Induced Hepatic, Renal, and Cardiac
Injury: A Biochemical and Histopathological Study in Mice
SO OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
LA English
DT Article
ID OXIDATIVE STRESS; N-ACETYLCYSTEINE; CREATINE-KINASE; KIDNEY INJURY;
TNF-ALPHA; ACID; PROTECTS; LIVER; RAT; NEPHROTOXICITY
AB The current study was designed to investigate the beneficial role of diosmin, a biologically active flavonoid, against methotrexate (MTX-) induced hepatic, renal, and cardiac injuries in mice. Male Swiss albino mice received a single intraperitoneal injection of MTX (at 20 mg/kg, body weight) either alone or in combination with oral diosmin (at 50 or 100 mg/kg body weight, for 10 days). Serum was used to evaluate tissue injury markers, while hepatic, renal, and cardiac tissue samples were obtained for determination of antioxidant activity as well as histopathological examination. Diosmin treatment ameliorated the MTX-induced elevation of serum alkaline phosphatase, aminotransferases, urea, creatinine, lactate dehydrogenase, and creatine kinases as well as plasma proinflammatory cytokines (interleukin-1-beta, interleukin-6, and tumor necrosis factor-alpha). Additionally, both diosmin doses significantly reduced tissue levels of malondialdehyde and nitric oxide and increased those of glutathione, glutathione peroxidase, glutathione reductase, glutathione S-transferase, superoxide dismutase, and catalase, compared to the MTX-intoxicated group. Histopathological examination showed that diosmin significantly minimized the MTX-induced histological alterations and nearly restored the normal architecture of hepatic, renal, and cardiac tissues. Based on these findings, diosmin may be a promising agent for protection against MTX-induced cytotoxicity in patients with cancer and autoimmune diseases.
C1 [Abdel-Daim, Mohamed M.] Suez Canal Univ, Fac Vet Med, Pharmacol Dept, Ismailia, Egypt.
[Khalifa, Hesham A.] Zagazig Univ, Fac Vet Med, Dept Pharmacol, Zagazig, Egypt.
[Abushouk, Abdelrahman Ibrahim] Ain Shams Univ, Fac Med, Cairo, Egypt.
[Dkhil, Mohamed A.; Al-Quraishy, Saleh A.] King Saud Univ, Coll Sci, Dept Zool, Riyadh, Saudi Arabia.
[Dkhil, Mohamed A.] Helwan Univ, Coll Sci, Dept Zool & Entomol, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); Suez Canal University; Egyptian Knowledge
Bank (EKB); Zagazig University; Egyptian Knowledge Bank (EKB); Ain Shams
University; King Saud University; Egyptian Knowledge Bank (EKB); Helwan
University
RP Abdel-Daim, MM (corresponding author), Suez Canal Univ, Fac Vet Med, Pharmacol Dept, Ismailia, Egypt.
EM abdeldaim.m@vet.suez.edu.eg
RI Dkhil, Mohamed/F-8782-2011; Alquraishy, Saleh/R-3570-2016; Dkhil,
Mohamed/GWZ-8718-2022; Abdel-Daim, Mohamed/B-2545-2013; Abushouk,
Abdelrahman/I-9229-2018
OI Dkhil, Mohamed/0000-0003-1869-5800; Abdel-Daim,
Mohamed/0000-0002-4341-2713; Abushouk, Abdelrahman/0000-0003-1399-6487
FU King Saud University [RG-198]
FX The authors would like to thank Professor Amina A. Dessouki, the
professor of pathology, Faculty of Veterinary Medicine, Suez Canal
University, for her help in the histopathological evaluations of this
study. The authors would like to appreciate the Deanship of Scientific
Research at King Saud University for funding this study through the
research group project (no. RG-198).
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NR 64
TC 89
Z9 90
U1 0
U2 7
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1942-0900
EI 1942-0994
J9 OXID MED CELL LONGEV
JI Oxidative Med. Cell. Longev.
PY 2017
VL 2017
AR 3281670
DI 10.1155/2017/3281670
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FB7QB
UT WOS:000406334000001
OA Green Published, hybrid, Green Submitted
DA 2025-01-07
ER
PT J
AU Brown, B
Ojha, V
Fricke, I
Al-Sheboul, SA
Imarogbe, C
Gravier, T
Green, M
Peterson, L
Koutsaroff, IP
Demir, A
Andrieu, J
Leow, CY
Leow, CH
AF Brown, Brent
Ojha, Vanshika
Fricke, Ingo
Al-Sheboul, Suhaila A.
Imarogbe, Chinua
Gravier, Tanya
Green, Michael
Peterson, Lori
Koutsaroff, Ivoyl P.
Demir, Ayca
Andrieu, Jonatane
Leow, Chiuan Yee
Leow, Chiuan Herng
TI Innate and Adaptive Immunity during SARS-CoV-2 Infection: Biomolecular
Cellular Markers and Mechanisms
SO VACCINES
LA English
DT Review
DE COVID-19; B-cells; neutrophils; dendritic cells; T-cells; NK-cells;
monocytes; macrophages; innate; adaptive; cytokines; chemokines;
adhesion molecules; antibody; cluster of differentiation; receptors;
proteins; SARS-CoV-2; serology
ID PLASMACYTOID DENDRITIC CELLS; REGULATORY T-CELL; B-CELLS; NK CELLS;
ANTIBODY-RESPONSES; IMMUNOGLOBULIN-A; PERIPHERAL-BLOOD; CYTOKINE STORM;
COVID-19; EXPRESSION
AB The coronavirus 2019 (COVID-19) pandemic was caused by a positive sense single-stranded RNA (ssRNA) severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, other human coronaviruses (hCoVs) exist. Historical pandemics include smallpox and influenza, with efficacious therapeutics utilized to reduce overall disease burden through effectively targeting a competent host immune system response. The immune system is composed of primary/secondary lymphoid structures with initially eight types of immune cell types, and many other subtypes, traversing cell membranes utilizing cell signaling cascades that contribute towards clearance of pathogenic proteins. Other proteins discussed include cluster of differentiation (CD) markers, major histocompatibility complexes (MHC), pleiotropic interleukins (IL), and chemokines (CXC). The historical concepts of host immunity are the innate and adaptive immune systems. The adaptive immune system is represented by T cells, B cells, and antibodies. The innate immune system is represented by macrophages, neutrophils, dendritic cells, and the complement system. Other viruses can affect and regulate cell cycle progression for example, in cancers that include human papillomavirus (HPV: cervical carcinoma), Epstein-Barr virus (EBV: lymphoma), Hepatitis B and C (HB/HC: hepatocellular carcinoma) and human T cell Leukemia Virus-1 (T cell leukemia). Bacterial infections also increase the risk of developing cancer (e.g., Helicobacter pylori). Viral and bacterial factors can cause both morbidity and mortality alongside being transmitted within clinical and community settings through affecting a host immune response. Therefore, it is appropriate to contextualize advances in single cell sequencing in conjunction with other laboratory techniques allowing insights into immune cell characterization. These developments offer improved clarity and understanding that overlap with autoimmune conditions that could be affected by innate B cells (B1(+) or marginal zone cells) or adaptive T cell responses to SARS-CoV-2 infection and other pathologies. Thus, this review starts with an introduction into host respiratory infection before examining invaluable cellular messenger proteins and then individual immune cell markers.
C1 [Al-Sheboul, Suhaila A.] Jordan Univ Sci & Technol, Fac Appl Med Sci, Dept Med Lab Sci, Irbid 22110, Jordan.
[Al-Sheboul, Suhaila A.] Medipol Univ Istanbul, Int Sch Med, Dept Med Microbiol, TR-34810 Istanbul, Turkiye.
[Imarogbe, Chinua] UKHSA, Rosalind Franklin Lab, Royal Leamington Spa, England.
[Demir, Ayca] Afyonkarahisar Univ, Fac Med, TR-03030 Istanbul, Turkiye.
[Andrieu, Jonatane] Aix Marseille Univ, Fac Med, F-13005 Marseille, France.
[Leow, Chiuan Yee] Univ Sains Malaysia, Sch Pharmaceut Sci, George Town 11800, Malaysia.
[Leow, Chiuan Herng] Univ Sains Malaysia, Inst Res Mol Med, INFORMM, George Town 11800, Malaysia.
C3 Jordan University of Science & Technology; Istanbul Medipol University;
UK Health Security Agency (UKHSA); Afyonkarahisar Health Sciences
University; Aix-Marseille Universite; Universiti Sains Malaysia;
Universiti Sains Malaysia
RP Al-Sheboul, SA (corresponding author), Jordan Univ Sci & Technol, Fac Appl Med Sci, Dept Med Lab Sci, Irbid 22110, Jordan.
EM abrownbscmsc@gmail.com
RI Fricke, Ingo/HZL-1636-2023; Imarogbe, Chinua/IVH-6907-2023; Leow, Chiuan
Herng/F-8877-2014; Gravier, Tanya/HSH-9794-2023; Brown,
Brent/HIR-3281-2022; Koutsaroff, Ivoyl P./A-6992-2010
OI Leow, Chiuan Herng/0000-0003-0849-428X; Fricke,
Ingo/0000-0001-7638-3181; Gravier, Tanya/0000-0003-2996-5482; Leow,
Chiuan Yee/0000-0002-6919-5921; Brown, Brent/0000-0001-5238-6943;
Koutsaroff, Ivoyl P./0000-0003-0336-4101; Andrieu,
Jonatane/0000-0002-3603-0426
FU Biochem123 Ltd. [13519534]
FX This article was funded by Biochem123 Ltd. (13519534).
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NR 445
TC 15
Z9 16
U1 0
U2 26
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-393X
J9 VACCINES-BASEL
JI Vaccines
PD FEB
PY 2023
VL 11
IS 2
AR 408
DI 10.3390/vaccines11020408
PG 60
WC Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Research & Experimental Medicine
GA 9L1OL
UT WOS:000941325300001
PM 36851285
OA Green Submitted, gold, Green Published
DA 2025-01-07
ER
PT J
AU McCarty, MF
AF McCarty, Mark F.
TI GCN2 and FGF21 are likely mediators of the protection from cancer,
autoimmunity, obesity, and diabetes afforded by vegan diets
SO MEDICAL HYPOTHESES
LA English
DT Article
ID GROWTH-FACTOR 21; BONE-MINERAL DENSITY; IMPROVES INSULIN SENSITIVITY;
NONCARBONIC ACID PRODUCTION; CORONARY-ARTERY-DISEASE; FREE FATTY-ACIDS;
PROTEIN-INTAKE; FACTOR-I; IGF-I; RHEUMATOID-ARTHRITIS
AB Third World quasi-vegan cultures have been characterized by low risks for "Western" cancers, autoimmune disorders, obesity, and diabetes. The relatively low essential amino acid contents of many vegan diets may play a role in this regard. It is proposed that such diets modestly activate the kinase GCN2 - a physiological detector of essential amino acid paucity - within the liver, resulting in up-regulated production of fibroblast growth factor 21 (FGF21). FGF21, by opposing the stimulatory effect of growth hormone on hepatic IGF-I production, may be responsible for the down-regulation of plasma IGF-I observed in vegans consuming diets of modest protein content. Decreased IGF-I bioactivity throughout life can be expected to have a favorable impact on cancer risk, as observed in rodents that are calorie restricted or genetically defective in IGF-1 activity. Increased FGF21 in vegans might also contribute to their characteristic leanness and low LDL cholesterol by promoting hepatic lipid oxidation while inhibiting lipogenesis. Direct trophic effects of FGF21 on pancreatic beta-cells may help to explain the low risk for diabetes observed in vegans, and the utility of vegan diets in diabetes management. And up-regulation of GCN2 in immune cells, by boosting T regulatory activity, might play some role in the reduced risk for autoimmunity reported in some quasi-vegan cultures. The fact that bone density tends to be no greater in vegans than omnivores, despite consumption of a more "alkaline" diet, might be partially attributable to the fact that FGF21 opposes osteoblastogenesis and decreases IGF-I. If these speculations have merit, it should be possible to demonstrate that adoption of a vegan diet of modest protein content increases plasma FGF21 levels. (C) 2014 Elsevier Ltd. All rights reserved.
C1 Catalyt Longev, 7831 Rush Rose Dr,Apt 316, Carlsbad, CA 92009 USA.
RP McCarty, MF (corresponding author), Catalyt Longev, 7831 Rush Rose Dr,Apt 316, Carlsbad, CA 92009 USA.
EM markfmccarty@gmail.com
FU Catalytic Longevity
FX Financial support provided by Catalytic Longevity, a non-profit
organization.
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NR 123
TC 28
Z9 30
U1 0
U2 55
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0306-9877
EI 1532-2777
J9 MED HYPOTHESES
JI Med. Hypotheses
PD SEP
PY 2014
VL 83
IS 3
BP 365
EP 371
DI 10.1016/j.mehy.2014.06.014
PG 7
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA AP7PA
UT WOS:000342268000027
PM 25015767
DA 2025-01-07
ER
PT J
AU Wimalawansa, SJ
AF Wimalawansa, Sunil J.
TI Physiology of Vitamin D-Focusing on Disease Prevention
SO NUTRIENTS
LA English
DT Review
DE aging; 25(OH)D; calcifediol; calcitriol; cardiovascular diseases;
hypovitaminosis D; epidemiology; human diseases; morbidity and
mortality; prevention and treatment; public health
ID PARATHYROID-HORMONE LEVELS; BONE-MINERAL DENSITY; D-BINDING PROTEIN; D
DEFICIENCY; 25-HYDROXYVITAMIN D; D-RECEPTOR; D SUPPLEMENTATION;
CARDIOVASCULAR-DISEASE; HUMAN HEALTH; 1-ALPHA,25-DIHYDROXYVITAMIN D-3
AB Vitamin D is a crucial micronutrient, critical to human health, and influences many physiological processes. Oral and skin-derived vitamin D is hydroxylated to form calcifediol (25(OH)D) in the liver, then to 1,25(OH)2D (calcitriol) in the kidney. Alongside the parathyroid hormone, calcitriol regulates neuro-musculoskeletal activities by tightly controlling blood-ionized calcium concentrations through intestinal calcium absorption, renal tubular reabsorption, and skeletal mineralization. Beyond its classical roles, evidence underscores the impact of vitamin D on the prevention and reduction of the severity of diverse conditions such as cardiovascular and metabolic diseases, autoimmune disorders, infection, and cancer. Peripheral target cells, like immune cells, obtain vitamin D and 25(OH)D through concentration-dependent diffusion from the circulation. Calcitriol is synthesized intracellularly in these cells from these precursors, which is crucial for their protective physiological actions. Its deficiency exacerbates inflammation, oxidative stress, and increased susceptibility to metabolic disorders and infections; deficiency also causes premature deaths. Thus, maintaining optimal serum levels above 40 ng/mL is vital for health and disease prevention. However, achieving it requires several times more than the government's recommended vitamin D doses. Despite extensive published research, recommended daily intake and therapeutic serum 25(OH)D concentrations have lagged and are outdated, preventing people from benefiting. Evidence suggests that maintaining the 25(OH)D concentrations above 40 ng/mL with a range of 40-80 ng/mL in the population is optimal for disease prevention and reducing morbidities and mortality without adverse effects. The recommendation for individuals is to maintain serum 25(OH)D concentrations above 50 ng/mL (125 nmol/L) for optimal clinical outcomes. Insights from metabolomics, transcriptomics, and epigenetics offer promise for better clinical outcomes from vitamin D sufficiency. Given its broader positive impact on human health with minimal cost and little adverse effects, proactively integrating vitamin D assessment and supplementation into clinical practice promises significant benefits, including reduced healthcare costs. This review synthesized recent novel findings related to the physiology of vitamin D that have significant implications for disease prevention.
C1 [Wimalawansa, Sunil J.] Cardiometab & Endocrine Inst, North Brunswick, NJ 08902 USA.
RP Wimalawansa, SJ (corresponding author), Cardiometab & Endocrine Inst, North Brunswick, NJ 08902 USA.
EM suniljw@hotmail.com
OI Wimalawansa, Prof. Sunil/0000-0003-1096-8595
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NR 292
TC 5
Z9 5
U1 3
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD JUN
PY 2024
VL 16
IS 11
AR 1666
DI 10.3390/nu16111666
PG 31
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA UC2E0
UT WOS:001245788900001
PM 38892599
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Ciesla, A
Kusmider, M
Faron-Górecka, A
Dziedzicka-Wasylewska, M
Bociaga-Jasik, M
Owczarek, D
Ciecko-Michalska, I
Cibor, D
Mach, T
AF Ciesla, Andrzej
Kusmider, Maciej
Faron-Gorecka, Agata
Dziedzicka-Wasylewska, Marta
Bociaga-Jasik, Monika
Owczarek, Danuta
Ciecko-Michalska, Irena
Cibor, Dorota
Mach, Tomasz
TI Intrahepatic expression of genes related to metabotropic receptors in
chronic hepatitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Metabotropic receptors; Gene expression; DNA oligonucleotides;
Quantitative real-time polymerase chain reaction; Chronic hepatitis
ID CELL-ADHESION MOLECULE-1; LIVER-REGENERATION; RAT-LIVER; PROTEIN;
ACTIVATION; CHEMOKINES; INJURY; GAMMA; ANGIOTENSINOGEN; POLYMORPHISMS
AB AIM: To screen for genes related to metabotropic receptors that might be involved in the development of chronic hepatitis.
METHODS: Assessment of 20 genes associated with metabotropic receptors was performed in liver specimens obtained by punch biopsy from 12 patients with autoimmune and chronic hepatitis type B and C. For this purpose, a microarray with low integrity grade and with oligonucleotide DNA probes complementary to target transcripts was used. Evaluation of gene expression was performed in relation to transcript level, correlation between samples and grouping of clinical parameters used in chronic hepatitis assessment. Clinical markers of chronic hepatitis included alanine and aspartate aminotransferase, gamma-glutamyltranspeptidase, alkaline phosphatase and cholinesterase activity, levels of iron ions, total cholesterol, triglycerides, albumin, glucose, hemoglobin, platelets, histological analysis of inflammatory and necrotic status, fibrosis according to METAVIR score, steatosis, as well as anthropometric body mass index, waist/hip index, percentage of adipose tissue and liver size in ultrasound examination. Gender, age, concomitant diseases and drugs were also taken into account. Validation of oligonucleotide microarray gene expression results was done with the use of quantitative real-time polymerase chain reaction (qRT-PCR).
RESULTS: The highest (0.002 < P < 0.046) expression among genes encoding main components of metabotropic receptor pathways, such as the a subunit of G-coupled protein, phosphoinositol-dependent protein kinase or arrestin was comparable to that of angiotensinogen synthesized in the liver. Carcinogenesis suppressor genes, such as chemokine ligand 4, transcription factor early growth response protein 1 and lysophosphatidic acid receptor, were characterized by the lowest expression (0.002 < P < 0.046), while the factor potentially triggering hepatic cancer, transcription factor JUN-B, had a 20-fold higher expression. The correlation between expression of genes of protein kinases PDPK1, phosphoinositide 3-kinase and protein kinase A (Spearman's coefficient range: 0.762-0.769) confirmed a functional link between these enzymes. Gender (P = 0.0046) and inflammation severity, measured by alanine aminotransferase activity (P = 0.035), were characterized by diverse metabotropic receptor gene expression patterns. The Pearson's coefficient ranging from -0.35 to 0.99 from the results of qRT-PCR and microarray indicated that qRT-PCR had certain limitations as a validation tool for oligonucleotide microarray studies.
CONCLUSION: A microarray-based analysis of hepatocyte metabotropic G-protein-related gene expression can reveal the molecular basis of chronic hepatitis. (C) 2012 Baishideng. All rights reserved.
C1 [Ciesla, Andrzej; Bociaga-Jasik, Monika; Owczarek, Danuta; Ciecko-Michalska, Irena; Cibor, Dorota; Mach, Tomasz] Jagiellonian Univ, Coll Med, Dept Gastroenterol Hepatol & Infect Dis, PL-31521 Krakow, Poland.
[Kusmider, Maciej; Faron-Gorecka, Agata; Dziedzicka-Wasylewska, Marta] Polish Acad Sci, Inst Pharmacol, PL-31343 Krakow, Poland.
C3 Jagiellonian University; Collegium Medicum Jagiellonian University;
Polish Academy of Sciences
RP Ciesla, A (corresponding author), Jagiellonian Univ, Coll Med, Dept Gastroenterol Hepatol & Infect Dis, PL-31521 Krakow, Poland.
EM aciesla@su.krakow.pl
RI Mach, Tomasz/P-2216-2019; Faron-Górecka, Agata/AAG-2111-2020;
Dziedzicka-Wasylewska, Marta/AAD-3970-2020; Kusmider, Maciej/R-5309-2016
OI Kusmider, Maciej/0000-0002-2214-2283; Faron-Gorecka,
Agata/0000-0002-8202-190X; Dziedzicka-Wasylewska,
Marta/0000-0001-7030-7874
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NR 29
TC 2
Z9 3
U1 1
U2 8
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD AUG 21
PY 2012
VL 18
IS 31
BP 4156
EP 4161
DI 10.3748/wjg.v18.i31.4156
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 995CZ
UT WOS:000307986800012
PM 22919248
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Chavda, VP
Gogoi, NR
Vaghela, DA
Balar, PC
Dawre, S
Dave, DJ
AF Chavda, Vivek P.
Gogoi, Niva Rani
Vaghela, Dixa A.
Balar, Pankti C.
Dawre, Shilpa
Dave, Divyang J.
TI Parenteral microemulsions for drug delivery: Advances and update
SO JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
LA English
DT Review
DE Parenteral microemulsion; Formulation; Evaluation; Future challenges
ID IN-WATER MICROEMULSIONS; SITU PHASE-TRANSITION; BRUCEA-JAVANICA OIL;
LOADED MICROEMULSION; EX-VIVO; HEPATOCELLULAR-CARCINOMA; INJECTABLE
MICROEMULSION; TARGETING EFFICIENCY; LIPID NANOPARTICLES;
PROLONGED-RELEASE
AB Patients with chronic conditions often need to adhere to long-term medication regimens, requiring them to take medication daily for an extended period. Nevertheless, the requirement of daily dosing can contribute to treatment non-adherence, potentially leading to the reoccurrence of the underlying conditions. Moreover, the poor water solubility of certain molecules poses a significant challenge in the development of effective pharmaceutical drug formulations. It is also challenging that many newly developed drugs exhibit limited solubility in organic media as well. As a result, poorly water-soluble drugs often present problems such as unpredictable absorption patterns and low systemic bioavailability. In such cases parenteral drug delivery systems offer promising prospects such as an improved absorption profile of the drug, leading to enhanced bioavailability. Moreover, due to the limited solubility, it is impractical and potentially hazardous to administer them intravenously as solutions; because there is a risk of precipitation and vessel blockage. Additionally, formulating a suitable parenteral drug delivery system is already a challenging endeavor, and when combined with the presence of poorly water-soluble new chemical entities, the complexity of the task is further enhanced. Therefore, in designing of microemulsion (ME) for the parenteral delivery of the drug, utilizing an appropriate surfactant not only enhances the solubility of the drug but also facilitates improved permeability across cell membranes. Therefore, exploiting the advantages of ME opens new possibilities for harnessing the potential benefits of BCS-II, BCS-III and BCS-IV drugs. MEs are basically stable mixtures consisting of two immiscible liquids, stabilized by surfactants and potentially other compounds. They are thermodynamically stable, transparent, and isotropic, meaning they have a uniform composition throughout. Also, in the current scenario The ME has been applicable for ease of administration, spontaneous formulation, and easy manufacturing scale-up, to maintain the thermodynamic stability of the drug and improve drug solubilization without affecting the shelf-life and bioavailability of the drug. The sME following the parenteral route has a wide range of applications to treat prevalent diseases such as cancer, autoimmune disease, infectious disease, cardiovascular disease, and many more. In this review article, we have discussed applications of ME by emphasizing the focus on parenteral administration. Along with that, future challenges are also elucidated in the manuscript.
C1 [Chavda, Vivek P.] LM Coll Pharm, Dept Pharmaceut & Pharmaceut Technol, Ahmadabad 380009, Gujarat, India.
[Chavda, Vivek P.; Dave, Divyang J.] Kadi Sarva Vishwavidyalaya, KB Inst Pharmaceut Educ & Res, Dept Pharmaceut, Gandhinagar 382023, Gujarat, India.
[Gogoi, Niva Rani] Dibrugarh Univ, Fac Sci & Engn, Dept Pharmaceut Sci, Dibrugarh 786004, Assam, India.
[Vaghela, Dixa A.; Balar, Pankti C.] LM Coll Pharm, Pharm Sect, Ahmadabad 380009, India.
[Dawre, Shilpa] SVKMS NMIMS, Sch Pharm & Technol Management, Dept Pharmaceut, Shirpur, India.
C3 Dibrugarh University; SVKM's NMIMS (Deemed to be University)
RP Chavda, VP (corresponding author), LM Coll Pharm, Dept Pharmaceut & Pharmaceut Technol, Ahmadabad 380009, Gujarat, India.
EM vivek.chavda@lmcp.ac.in
RI Gogoi, Niva/JEO-8430-2023; Balar, Pankti/HTS-1474-2023; Chavda,
Vivek/ADR-8736-2022
OI Vaghela, Dixa/0000-0003-3129-6468; Chavda, Vivek/0000-0002-7701-8597;
Gogoi, Niva Rani/0000-0001-8900-6756
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NR 203
TC 6
Z9 6
U1 15
U2 27
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1773-2247
EI 2588-8943
J9 J DRUG DELIV SCI TEC
JI J. Drug Deliv. Sci. Technol.
PD NOV
PY 2023
VL 89
AR 104991
DI 10.1016/j.jddst.2023.104991
EA OCT 2023
PG 20
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA X5CO7
UT WOS:001098630000001
OA Bronze
DA 2025-01-07
ER
PT J
AU Li, J
Wang, LJ
Ying, X
Han, SX
Bai, E
Zhang, Y
Zhu, Q
AF Li, J.
Wang, L. J.
Ying, X.
Han, S. X.
Bai, E.
Zhang, Y.
Zhu, Q.
TI Immunodiagnostic Value of Combined Detection of Autoantibodies to
Tumor-associated Antigens as Biomarkers in Pancreatic Cancer
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; P53 ANTIBODIES; LUNG-CANCER; AUTOIMMUNE;
EXPRESSION; REPORTERS; RESPONSES; PROTEIN; DISEASE; P62
AB Previous studies demonstrated that cancer sera contain antibodies, which react with a unique group of autologous cellular antigens called tumour-associated antigens (TAAs). This study determines whether a panel of TAAs would enhance antibody detection and be a useful approach in pancreatic cancer (PC) detection and diagnosis. The panel of TAAs was composed of six TAAs including p53, p16, p62, survivin, Koc and IMP1 full-length recombinant proteins. Enzyme-linked immunosorbent assay (ELISA) was used to detect antibodies against these six TAAs in 23 sera from patients with PC and also 23 sera from normal individuals. Antibody frequency to any individual TAA in PC was variable and ranged from 14.7% to 30.4%. With the successive addition of TAAs to a final total of six antigens, there was a stepwise increase in positive antibody reactions reaching a sensitivity of 60.9% and a specificity of 87.0% in PC. Positive and negative likelihood ratio were 4.685 and 0.449, respectively. Positive and negative predictive values were, respectively, 82.4% and 69.0%. Agreement rate and Kappa value were 73.9% and 0.478, respectively. The data from this study support our previous hypothesis that using a panel of appropriately selected TAAs can enhance autoantibody detection in immunodiagnosis of PC. In 15 PC sera with carbohydrate antigen 19-9 (CA19-9) negative, 6 (40%) were found to have anti-TAA (anti-tumour associated antigens) antibodies. When CA19-9 and anti-TAAs were used together as markers in PC detection, the diagnostic sensitivity could be raised from 60.9% to 69.6%. Anti-TAA and CA19-9 were independent markers, and the simultaneous use of these two markers could raise the sensitivity of PC detection.
C1 [Li, J.; Wang, L. J.; Ying, X.; Han, S. X.; Bai, E.; Zhang, Y.; Zhu, Q.] Xi An Jiao Tong Univ, Hosp 1, Dept Med Oncol, Xian 710061, Shannxi, Peoples R China.
C3 Xi'an Jiaotong University
RP Zhu, Q (corresponding author), Xi An Jiao Tong Univ, Hosp 1, Dept Med Oncol, Xian 710061, Shannxi, Peoples R China.
EM newzhuqing1972@yahoo.com
OI Han, Suxia/0000-0002-1513-7427
FU University of Texas
FX The authors thank Dr Jianying Zhang at The University of Texas for his
help and support.
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NR 31
TC 15
Z9 15
U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAR
PY 2012
VL 75
IS 3
BP 342
EP 349
DI 10.1111/j.1365-3083.2011.02657.x
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 895MB
UT WOS:000300499200011
PM 22010875
OA Bronze
DA 2025-01-07
ER
PT J
AU Dedeepiya, VD
Terunuma, H
Deng, XW
Baskar, S
Manjunath, SR
Senthilkumar, R
Murugan, P
Thamaraikannan, P
Srinivasan, T
Preethy, S
Abraham, SJK
AF Dedeepiya, Vidyasagar Devaprasad
Terunuma, Hiroshi
Deng, Xuewen
Baskar, Subramani
Manjunath, Sadananda Rao
Senthilkumar, Rajappa
Murugan, Palanisamy
Thamaraikannan, Paramasivam
Srinivasan, Thangavelu
Preethy, Senthilkumar
Abraham, Samuel J. K.
TI A comparative analysis of in vitro expansion of natural killer
cells of a patient with autoimmune haemolytic anaemia and ovarian cancer
with patients with other solid tumours
SO ONCOLOGY LETTERS
LA English
DT Article
DE auto-immune hemolytic anemia; natural killer cells; CD3+CD56-cells; red
blood cell and natural killer cell antibodies; autologous immune
enhancement therapy
ID HEPATOCELLULAR-CARCINOMA; ADOPTIVE IMMUNOTHERAPY; RANDOMIZED-TRIAL;
NK-CELLS; LYMPHOCYTES; THERAPY; DISEASE
AB The functional profile of natural killer (NK) cells has been reported to be lower in auto-immune haemolytic anaemia (AIHA). In this study, we report a comparative analysis of peripheral blood mononuclear cells (PBMNCs) and the in vitro expansion of NK cells in a patient with AIHA and cancer, with that of other cancer patients without AI HA. PBMNCs and in vitro NK-cell expansion of a 64-year old female patient with ovarian cancer and AIHA was compared with that of four other patients with cancer without AIHA who underwent autologous immune enhancement therapy (AIET). The NK cells were cultured using autologous plasma without feeder layers. The quantities of PBMNCs, NK cells and CD3-CD56+ cells were compared. The average quantity of PBMNCs per ml in Cases I to V were 10.71, 39.2,49.26, 65.16 and 49.33x10(4), respectively, and the average maximum count of NK cells was 3.9, 1730.03, 1824.16, 1058.61 and 761x10(6), respectively. The average percentage of CD3-CD56+ cells in Cases I to V following in vitro expansion was 1.2, 65.7, 28.63, 65.9 and 40%, respectively. In the present study, probably the first in the literature, the in vitro expansion of NK cells was found to be significantly lower in the AIHA patient. Previously, only a lower NK-cell functional profile was reported. Further studies are required to establish the association between AIHA and NK-cell profile and in vitro expansion, and to find common antibodies between red blood cells (RBCs) and NK cells.
C1 [Dedeepiya, Vidyasagar Devaprasad; Baskar, Subramani; Manjunath, Sadananda Rao; Senthilkumar, Rajappa; Murugan, Palanisamy; Thamaraikannan, Paramasivam; Srinivasan, Thangavelu; Preethy, Senthilkumar; Abraham, Samuel J. K.] Vijaya Hlth Ctr Premises, Nichi In Ctr Regenerat Med, Madras 600026, Tamil Nadu, India.
[Terunuma, Hiroshi; Deng, Xuewen] Biotherapy Inst Japan, Tokyo, Japan.
[Preethy, Senthilkumar] Hope Fdn, Madras, Tamil Nadu, India.
[Abraham, Samuel J. K.] Yamanashi Univ, Sch Med, Chuo, Japan.
C3 University of Yamanashi
RP Abraham, SJK (corresponding author), Vijaya Hlth Ctr Premises, Nichi In Ctr Regenerat Med, C 16&17,175 NSK Salai, Madras 600026, Tamil Nadu, India.
EM drabrahamsj@ybb.ne.jp
RI Abraham, Samuel/GPK-1414-2022
FU M/S Hope Foundation (Trust), Chennai, India
FX The authors acknowledge the M/S Hope Foundation (Trust), Chennai, India
for providing funding for this study.
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NR 23
TC 6
Z9 6
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
J9 ONCOL LETT
JI Oncol. Lett.
PD FEB
PY 2012
VL 3
IS 2
BP 435
EP 440
DI 10.3892/ol.2011.498
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 880KL
UT WOS:000299405900038
PM 22740927
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wu, JW
Chen, WT
Huang, CG
Chen, YC
Hsu, CW
Chien, RN
Chang, ML
AF Wu, Jen-Wei
Chen, Wei-Ting
Huang, Chung-Guei
Chen, Yung-Chang
Hsu, Chao-Wei
Chien, Rong-Nan
Chang, Ming-Ling
TI Rheumatoid factor levels indicate cryoglobulinemia severity in hepatitis
B e antigen-negative hepatitis B virus carriers: a 7-year prospective
cohort study
SO HEPATOLOGY INTERNATIONAL
LA English
DT Article; Early Access
DE HBV; HBeAg; Cryoglobulinemia; Rheumatoid factor
ID MIXED CRYOGLOBULINEMIA; FLARES
AB Background The phenotype of cryoglobulinemia in hepatitis B virus (HBV) carriers remains elusive. Methods A 7-year prospective cohort of 648 hepatitis B e antigen (HBeAg)-negative Taiwanese HBV carriers [males: 344 (53%)] was conducted. Results Among 648, 189 (29.2%) had cryoglobulinemia, and 26 (4.0%) had cryoglobulinemic syndrome (CS). More females; higher levels of rheumatoid factor (RF), immunoglobulin M (IgM) and fibrosis-4 indices; higher proportions of proteinuria, hematuria and hepatocellular carcinoma; and lower levels of quantitative HBsAg, C3, C4 and eGFR were noted in patients with than in those without cryoglobulinemia. The associations were RF levels with cryoglobulinemia (cutoff > 12.55 IU/mL), and RF levels and baseline autoimmune diseases with CS. CS patients, symptomless cryoglobulinemia patients and patients without cryoglobulinemia had the highest, moderate, and lowest RF levels, respectively. A greater percentage of mixed cryoglobulins [IgG (2 +), IgM (2 +) and IgA (1 +)] was noted in cryoglobulinemia patients with than in those without CS (11.5% vs. 0.81%, p = 0.002). Among the 7 CS patients treated with nucleos(t)ide analogues (Nucs), cryoglobulinemia disappeared in 3 and symptoms improved in 5 during therapy. The CS prevalence was highest (6%) in patients with a baseline age of 31-40 years. Among the 26 CS patients, 23 (88.5%), 20 (76.9%), and 16 (61.5%) had peripheral neuropathy, articular and skin involvement, respectively. The cumulative incidences of major outcomes and mortality did not differ between patients with and without cryoglobulinemia. Conclusions The prevalence rates of cryoglobulinemia and CS in HBeAg-negative HBV carriers were 29.2% and 4.0%, respectively. RF levels correlate with cryoglobulinemia severity. Mixed cryoglobulins of IgG (2 +), IgM (2 +) and IgA (1 +) are likely linked to CS, which might be alleviated by Nucs in some patients. The impact of cryoglobulinemia on long-term outcomes might be negligible.
C1 [Wu, Jen-Wei; Chen, Wei-Ting; Hsu, Chao-Wei; Chien, Rong-Nan; Chang, Ming-Ling] Chang Gung Mem Hosp Linkou, Dept Gastroenterol & Hepatol, Div Hepatol, 5 Fu Hsing St,Kuei Shan, Taoyuan, Taiwan.
[Wu, Jen-Wei; Chen, Wei-Ting; Hsu, Chao-Wei; Chien, Rong-Nan; Chang, Ming-Ling] Chang Gung Univ, Coll Med, Dept Med, Taoyuan, Taiwan.
[Huang, Chung-Guei] Chang Gung Mem Hosp, Dept Lab Med, Linkou Branch, Taoyuan, Taiwan.
[Huang, Chung-Guei] Chang Gung Univ, Dept Med Biotechnol & Lab Sci, Taoyuan, Taiwan.
[Chen, Yung-Chang] Chang Gung Mem Hosp Linkou, Kidney Res Ctr, Dept Nephrol, Taoyuan, Taiwan.
RP Chang, ML (corresponding author), Chang Gung Mem Hosp Linkou, Dept Gastroenterol & Hepatol, Div Hepatol, 5 Fu Hsing St,Kuei Shan, Taoyuan, Taiwan.; Chang, ML (corresponding author), Chang Gung Univ, Coll Med, Dept Med, Taoyuan, Taiwan.
EM mlchang8210@gmail.com
FU Department of Gastroenterology and Hepatology, Chang Gung Memorial
Hospital, Taiwan
FX The authors thank Ms. Shu-Chun Chen from the Department of
Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Taiwan,
for his assistance with the data mining, as well as Ms. Chueh Wen Wang
and Ms. Chun Wan Fang from the Laboratory Center of Immunology, Chang
Gung Memorial Hospital, Linkou Branch, Taoyuan, Taiwan, for their
assistance with the cryoglobulin assessment.
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NR 42
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1936-0533
EI 1936-0541
J9 HEPATOL INT
JI Hepatol. Int.
PD 2024 DEC 19
PY 2024
DI 10.1007/s12072-024-10761-8
EA DEC 2024
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA P9Q7M
UT WOS:001381168400001
PM 39699792
DA 2025-01-07
ER
PT J
AU Castro-E-Silva, O
Sankarankutty, AK
Teixeira, AC
Mente, ED
Souza, FF
Pacheco, EG
Oliveira, GR
Cagnolatti, D
Correia, RB
Campos, W
Kemp, R
Miranda, A
Rondon, LZ
Rizzo, C
Mota, GA
Martinelli, ALC
Ramalho, FS
Ramalho, LNZ
Zucoloto, S
AF Castro-e-Silva, O.
Sankarankutty, A. K.
Teixeira, A. C.
Mente, E. D.
Souza, F. F.
Pacheco, E. G.
Oliveira, G. R.
Cagnolatti, D.
Correia, R. B.
Campos, W.
Kemp, R.
Miranda, A.
Rondon, L. Z.
Rizzo, C.
Mota, G. A.
Martinelli, A. L. C.
Ramalho, F. S.
Ramalho, L. N. Z.
Zucoloto, S.
TI Liver transplantation at a University Hospital, Faculty of the Medicine
of Ribeirao Preto, University of Sao Paulo: Results for the first 60
recipients
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article; Proceedings Paper
CT Joint Congress of the 10th Transplantation-Society-of-Brazil/19th
Latin-American-and-Caribbean-Transplantation-Society/6th
Luso-Brazilian-Transplantation-Society
CY SEP 02-05, 2007
CL Florianopolis, BRAZIL
SP Transplantat Soc Brazil, Latin Amer & Caribbean Transplantat Soc, Luso Brazilian Transplantat Soc
AB The purpose of the present article was to present the series operated by a Liver Transplant Group of the interior of the State of Sao Paulo, Brazil. Sixty patients were transplanted from May 2001 to May 2007. Thirty percent of the patients had alcoholic cirrhosis. 18.3% had C virus-induced cirrhosis, 10% had C virus- and alcohol-induced cirrhosis, 6% had B virus-induced cirrhosis, 13.3% had cryptogenic cirrhosis, 8.3% autoimmune cirrhosis, 13.3% had familial amyloidotic polyneuropathy (FAP), and 13.3% had hepatocellular carcinomas. The series was divided by a chronological criterion into two periods: A (n = 42) and B (n = 18) with the latter group operated based upon the Model for End-stage Liver Disease (MELD) criterion. Sixty-nine percent were men. Age ranged from 14 to 66 years. Period A included 12% Child A: 59.2%, Child B; 24%, Child C; and 4.8%, FAR Period B comprises 22.2% Child A: 11.1%, Child B: 33.3%, Child C: and 33.3%, FAP. MELD scores ranged from 8 to 35 for period A and from 14 to 31 for period B. Intraoperative mortality was 2/42 patients for period A and 0/18 for period B, overall postoperative mortality was 40% including for period A, 35% among Child B and C patients, and 5 % among FAP and Child A patients (P <.05) and 16.6% for period B among 11. 1 % Child B patients and 5.5 % FAP patients; 3.3 % of patients required retransplantation due to hepatic artery thrombosis. Real postoperative survival was 60% during period A and 83.3% during period B, with an overall survival rate of 67% for the two periods. The present results show levels of postoperative mortality, (especially during period B), and survival rates similar to those reported by several other centers in Brazil.
C1 [Castro-e-Silva, O.; Sankarankutty, A. K.; Teixeira, A. C.; Mente, E. D.; Souza, F. F.; Pacheco, E. G.; Oliveira, G. R.; Cagnolatti, D.; Correia, R. B.; Campos, W.; Kemp, R.; Miranda, A.; Rondon, L. Z.; Rizzo, C.; Mota, G. A.; Martinelli, A. L. C.; Ramalho, F. S.; Ramalho, L. N. Z.; Zucoloto, S.] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Surg, Special Liver Transplantat Unit, Sao Paulo, Brazil.
Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Anat, Special Liver Transplantat Unit, Sao Paulo, Brazil.
C3 Universidade de Sao Paulo; Universidade de Sao Paulo
RP Castro-E-Silva, O (corresponding author), Ribeirao Preto Med Sch, Surg & Anat Dept, Avenida Banderirantes 3900, BR-14049900 Ribeirao Preto, SP, Brazil.
EM orlando@fmrp.usp.br
RI Kemp, Rafael/H-7199-2012; MENTE, ENIO/P-7389-2015; Campos,
Walter/AAM-4778-2021; Ramalho, Leandra/A-3983-2010; Souza,
Fernanda/AHI-3546-2022; TEIXEIRA, ANDREZA/B-3318-2013; Sankarankutty,
Ajith/G-4605-2013; Ramalho, Fernando/G-3817-2012; Castro e Silva Junior,
Orlando/D-4646-2013
OI Ramalho, Leandra/0000-0002-3486-5294; Cagnolati, Daniel
Carlos/0000-0001-5928-128X; Sankarankutty, Ajith/0000-0002-2689-6242;
Ramalho, Fernando/0000-0002-7529-466X; Castro e Silva Junior,
Orlando/0000-0003-3912-0096
CR Ahmed Aijaz, 2007, Clin Liver Dis, V11, P227, DOI 10.1016/j.cld.2007.04.008
Bacchella T, 2004, TRANSPL P, V36, P929, DOI 10.1016/j.transproceed.2004.03.096
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NR 13
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0041-1345
EI 1873-2623
J9 TRANSPL P
JI Transplant. Proc.
PD APR
PY 2008
VL 40
IS 3
BP 785
EP 788
DI 10.1016/j.transproceed.2008.02.030
PG 4
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Immunology; Surgery; Transplantation
GA 296EZ
UT WOS:000255527600040
PM 18455017
DA 2025-01-07
ER
PT J
AU Urbani, L
Mazzoni, A
Catalano, G
De Simone, P
Vanacore, R
Pardi, C
Bortoli, M
Biancofiore, G
Campani, D
Perrone, V
Mosca, F
Scatena, F
Filipponi, F
AF Urbani, L
Mazzoni, A
Catalano, G
De Simone, P
Vanacore, R
Pardi, C
Bortoli, M
Biancofiore, G
Campani, D
Perrone, V
Mosca, F
Scatena, F
Filipponi, F
TI The use of extracorporeal photopheresis for allograft rejection in liver
transplant recipients
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article
ID PHOTOCHEMOTHERAPY
AB Background. Originally introduced for cutaneous T-cell lymphomas and autoimmune diseases, extracorporeal photopheresis (ECP) has been proven effective to reverse allograft rejection. The aim of the present work was to show the results of a single-center experience with ECP for the treatment of biopsy-proven rejection in selected liver transplant (LT) recipients.
Patients and methods. A retrospective review of five LT patients (M:F = 4:1; median age 51 years) undergoing ECP for biopsy-proven allograft rejection between January 1996 and December 2003. In this period 476 LT were performed on 441 patients.
Results. The indications for LT were three cases of HCV-related cirrhosis, complicated by hepatocellular carcinoma in two; one HBV-HDV-alcoholic cirrhosis; and one fulminant HBV hepatitis. All patients received calcineurin-inhibitor (CNI)-based immunosuppression with induction using anti-IL2R monoclonal antibodies. Indications for ECP were: ductopenic rejection in one patient with HCV recurrence; steroid-resistant acute rejection in two; acute rejection in a major ABO-mismatched liver graft; and one acute rejection in a patient with a proven allergy to steroids. The median interval from LT to inception of ECP was 43 days. The median number of ECP sessions per patient was 20. During the course of ECP, two patients tested positive for CMV antigenemia, associated in one case with bacterial pneumonia. All patients tolerated ECP and there were no procedure-related complications. At a median follow-up of 7.9 months after start of ECP, neither rejection relapses nor HCV/HBV recurrences have been observed. Three patients are off ECP with complete reversal and low-dose immunosuppression. Two patients are still receiving ECP with full-dose immunosuppression: one has achieved normal liver function but ECP is indicated due to a major ABO-incompatible liver graft, while the other patient's liver functions have not yet returned to baseline values.
C1 Univ Pisa, Liver Transplant Unit, I-56124 Pisa, Italy.
Univ Pisa, Ctr Blood, I-56124 Pisa, Italy.
Univ Pisa, Post Surg & Transplant Intens Care Unit, I-56124 Pisa, Italy.
Univ Pisa, Div Pathol, I-56124 Pisa, Italy.
C3 University of Pisa; University of Pisa; University of Pisa; University
of Pisa
RP Univ Pisa, Cisanello Hosp, Liver Transplant Unit, Via Paradisa 2, I-56124 Pisa, Italy.
EM f.filipponi@med.unipi.it
RI Biancofiore, Giandomenico/ABI-4414-2020; De Simone, Paolo/AAC-7412-2022
OI Urbani, Lucio/0000-0002-4075-6123; CAMPANI, DANIELA/0000-0001-5987-734X;
De Simone, Paolo/0000-0001-6713-6170; BIANCOFIORE, GIANDOMENICO
LUIGI/0000-0002-3755-1434
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NR 7
TC 34
Z9 40
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0041-1345
EI 1873-2623
J9 TRANSPL P
JI Transplant. Proc.
PD DEC
PY 2004
VL 36
IS 10
BP 3068
EP 3070
DI 10.1016/j.transproceed.2004.10.071
PG 3
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Surgery; Transplantation
GA 894BV
UT WOS:000226765800046
PM 15686696
DA 2025-01-07
ER
PT J
AU Liu, SQ
Guo, CM
Wang, JS
Wang, B
Qi, HB
Sun, MZ
AF Liu, Shuqing
Guo, Chunmei
Wang, Jiasheng
Wang, Bo
Qi, Houbao
Sun, Ming-Zhong
TI ANXA11 regulates the tumorigenesis, lymph node metastasis and
5-fluorouracil sensitivity of murine hepatocarcinoma Hca-P cells by
targeting c-Jun
SO ONCOTARGET
LA English
DT Article
DE Anxa11; hepatocarcinoma; lymphatic metastasis; chemoresistance; c-Jun
ID IN-VITRO PROLIFERATION; SYSTEMIC AUTOIMMUNE-DISEASES;
HEPATOCELLULAR-CARCINOMA; ANNEXIN-XI; LYMPHOGENOUS METASTASIS;
COLORECTAL-CANCER; SIGNALING PATHWAY; TUMOR MALIGNANCY; BREAST-CANCER;
PROTEIN
AB Annexin A11 (Anxa11) is associated with various cancers. Using a pair of syngeneic murine hepatocarcinoma cells, Hca-P with similar to 25% and Hca-F with similar to 75% lymph node metastatic (LNM) potentials, we demonstrated Anxa11 involvement in hepatocarcinoma lymphatic metastasis. Here, ANXA11 acted as a suppressor for the tumorigenicity, LNM and 5-FU resistance of Hca-P via c-Jun. We constructed monoclonal Hca-P cell line with stable ANXA11 knockdown. Although Bax and Bcl2 levels increased in shRNA-Anxa11-transfected Hca-P, ANXA11 downregulation showed no clear effect on Hca-P apoptosis. ANXA11 downregulation promoted in vitro migration and invasion capacities of Hca-P. In situ adhesion potential of Hca-P cells toward LN was significantly enhanced following ANXA11 downregulation. Consistently, ANXA11 downregulation promoted the in vivo tumor growth and LNM capacities of Hca-P cells. ANXA11 knockdown enhanced the chemoresistance of Hca-P cells specifically toward 5-FU instead of cisplatin. Its downregulation increased c-Jun (pSer73) and decreased c-Jun (pSer243) levels in Hca-P. c-Jun (pSer243) downregulation seemed to be only correlated with ANXA11 knockdown without the connection to 5-FU treatment. Interestingly, compared with scramble-Hca-P cells, the levels of c-Jun and c-Jun (pSer73) in shRNA-Anxa11-Hca-P cells were upregulated in the presences of 0.1 and 1.0 mg/L 5-FU. The levels changes from c-Jun and c-Jun (pSer73) in Hca-P cells showed a more obvious tendency with the combination of ANXA11 knockdown and 5-FU treatment. ANXA11 level regulates LNM and 5-FU resistance of Hca-P via c-Jun pathway. It might play an important role in hepatocarcinoma cell malignancy and be a therapeutic target for hepatocarcinoma.
C1 [Liu, Shuqing] Dalian Med Univ, Dept Biochem, Dalian 116044, Peoples R China.
[Guo, Chunmei; Wang, Jiasheng; Qi, Houbao; Sun, Ming-Zhong] Dalian Med Univ, Dept Biotechnol, Dalian 116044, Peoples R China.
[Wang, Bo] Dalian Med Univ, Dept Pathol, Dalian 116044, Peoples R China.
C3 Dalian Medical University; Dalian Medical University; Dalian Medical
University
RP Sun, MZ (corresponding author), Dalian Med Univ, Dept Biotechnol, Dalian 116044, Peoples R China.
EM smzlsq@163.com
RI Li, xiaolong/GRS-9148-2022; wang, wei/JYP-7819-2024
FU National Natural Science Foundation of China [81050010, 81171957,
81272186, 81100722]; Outstanding Youth Scholar Growth Project in
University and College of Liaoning [LJQ2011094]; Joint Fund of the
Provincial Natural Science Foundation of Liaoning [2014023047]
FX This work was supported by grants from National Natural Science
Foundation of China (No. 81050010, 81171957, 81272186 and 81100722),
Outstanding Youth Scholar Growth Project in University and College of
Liaoning (No. LJQ2011094) and Joint Fund of the Provincial Natural
Science Foundation of Liaoning (No. 2014023047). The funders had no role
in the study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
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NR 50
TC 10
Z9 14
U1 0
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD MAR 29
PY 2016
VL 7
IS 13
BP 16297
EP 16310
DI 10.18632/oncotarget.7484
PG 14
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DL5QW
UT WOS:000375692900077
PM 26908448
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Xu, WP
Wang, ZR
Zou, X
Zhao, C
Wang, R
Shi, PM
Yuan, ZL
Yang, F
Zeng, X
Wang, PQ
Sultan, S
Zhang, Y
Xie, WF
AF Xu, Wen Ping
Wang, Ze Rui
Zou, Xia
Zhao, Chen
Wang, Rui
Shi, Pei Mei
Yuan, Zong Li
Yang, Fang
Zeng, Xin
Wang, Pei Qin
Sultan, Sakhawat
Zhang, Yan
Xie, Wei Fen
TI Serum Wisteria floribunda agglutinin-positive Mac-2-binding
protein evaluates liver function and predicts prognosis in liver
cirrhosis
SO JOURNAL OF DIGESTIVE DISEASES
LA English
DT Article
DE decompensation; liver cirrhosis; liver reserve function; liver-related
death; Wisteria flori-bunda agglutinin-positive Mac-2-binding protein
ID MAC-2 BINDING-PROTEIN; CHRONIC HEPATITIS-C; CLINICAL-PRACTICE
GUIDELINES; PRIMARY BILIARY-CIRRHOSIS; SIMPLE NONINVASIVE INDEX;
HEPATOCELLULAR-CARCINOMA; AUTOIMMUNE HEPATITIS; SIGNIFICANT FIBROSIS;
MANAGEMENT; MORTALITY
AB OBJECTIVE: Wisteria floribunda agglutinin-positive Mac-2-binding protein (WFA(+)-M2BP) is a novel glycobiomarker for evaluating liver fibrosis, but less is known about its role in liver cirrhosis (LC). This study aimed to investigate the utility of WFA(+)-M2BP in evaluating liver function and predicting prognosis of cirrhotic patients.
METHODS: We retrospectively included 197 patients with LC between 2013 and 2016. Serum WFA(+)-M2BP and various biochemical parameters were measured in all patients. With a median follow-up of 23 months, liver-related complications and deaths of 160 patients were recorded. The accuracy of WFA(+)-M2BP in evaluating liver function, predicting decompensation and mortality were measured by the receiver operating characteristic (ROC) curve, logistic and Cox's regression analyses, respectively.
RESULTS: WFA(+)-M2BP levels increased with elevated Child-Pugh classification, especially in patients with hepatitis B virus (HBV) infection. ROC analysis confirmed the high reliability of WFA(+)-M2BP for the assessment of liver function using Child-Pugh classification. WFA(+)-M2BP was also significantly positively correlated with the model for end-stage liver disease (MELD) score. Multivariate logistic regression analysis indicated WFA(+)-M2BP as an independent predictor of clinical decompensation for compensated patients (odds ratio 11.958, 95% confidence interval [CI] 1.876-76.226, P = 0.009), and multivariate Cox's regression analysis verified WFA(+)-M2BP as an independent risk factor for liver-related death in patients with HBV infection (hazards ratio 10.596, 95% CI 1.356-82.820, P = 0.024).
CONCLUSION: Serum WFA(+)-M2BP is a reliable predictor of liver function and prognosis in LC and could be incorporated into clinical surveillance strategies for LC patients, especially those with HBV infection.
C1 [Xu, Wen Ping; Wang, Ze Rui; Zhao, Chen; Shi, Pei Mei; Yuan, Zong Li; Zeng, Xin; Wang, Pei Qin; Xie, Wei Fen] Second Mil Med Univ, Changzheng Hosp, Dept Gastroenterol, 415 Fengyang Rd, Shanghai 200003, Peoples R China.
[Zou, Xia; Yang, Fang; Zhang, Yan] Shanghai Jiao Tong Univ, Shanghai Ctr Syst Biomed, Minist Educ, Key Lab Syst Biomed, Shanghai, Peoples R China.
[Wang, Rui] Second Mil Med Univ, Fac Hlth Serv, Dept Hlth Stat, Shanghai, Peoples R China.
[Sultan, Sakhawat] Combined Mil Hosp, Dept Gastroenterol, Dhaka, Bangladesh.
C3 Naval Medical University; Shanghai Jiao Tong University; Naval Medical
University
RP Xie, WF (corresponding author), Second Mil Med Univ, Changzheng Hosp, Dept Gastroenterol, 415 Fengyang Rd, Shanghai 200003, Peoples R China.; Zhang, Y (corresponding author), Shanghai Jiao Tong Univ, Shanghai Ctr Syst Biomed, 800 Dong Chuan Rd, Shanghai 200240, Peoples R China.
EM yanzhang2006@sjtu.edu.cn; weifenxie@medmail.com.cn
RI WANG, ZERUI/AAU-3671-2021; wang, rui/JAC-6240-2023; Xu,
Wen-Ping/HNO-8776-2023; Yang, Fang/AAF-3024-2019
OI Zou, Xia/0000-0003-0295-0643; Xu, Wen-Ping/0000-0002-2062-4641
FU National Natural Science Foundation of China [81502077, 81400641];
Shanghai Municipal Education Commission; Shanghai Education Development
Foundation [15CG41]
FX This work was supported by grants from the National Natural Science
Foundation of China (nos. 81502077 and 81400641) and grant "Chen Guang'
projects from Shanghai Municipal Education Commission and Shanghai
Education Development Foundation (no. 15CG41).
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NR 47
TC 6
Z9 6
U1 0
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-2972
EI 1751-2980
J9 J DIGEST DIS
JI J. Dig. Dis.
PD APR
PY 2018
VL 19
IS 4
BP 242
EP 253
DI 10.1111/1751-2980.12596
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GF5MI
UT WOS:000432011200006
PM 29607614
DA 2025-01-07
ER
PT J
AU Ke, CZ
Chen, Y
Gong, ZL
Meng, ZJ
Liu, L
Ren, ZJ
Zhou, ZH
AF Ke, Chang-Zheng
Chen, Yue
Gong, Zuo-Liong
Meng, Zhong-Ji
Liu, Li
Ren, Ze-Jiu
Zhou, Zuo-Hua
TI Dynamic changes of HBV DNA in serum and peripheral blood mononuclear
cells of chronic hepatitis patients after lamivudine treatment
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE lamivudine; hepatitis B virus; DNA; peripheral blood mononuclear cells
ID B-VIRUS-DNA; CARCINOGEN METABOLIZING ENZYMES; LIVER-INJURY;
SURFACE-ANTIGEN; HEPATOCELLULAR-CARCINOMA; ALTERED EXPRESSION;
INFECTION; TRIAL; PATHOGENESIS; REPLICATION
AB AIM: To study the dynamic changes of hepatitis B virus (HBV) DNA in serum and peripheral blood mononuclear cells (PBMCs) of patients after lamivudine therapy.
METHODS: A total of 72 patients with chronic HBV infection were included in this study. All patients were confirmed to have the following conditions: above 16 years of age, elevated serum alanine amonotransferase (ALT), positive hepatitis B e antigen (HBeAg), positive HBV DNA in serum and PBMCs, negative antibodies against HAV, HCV, HDV, HEV. Other possible causes of chronic liver damages, such as drugs, alcohol and autoimmune diseases were excluded. Seventy-two cases were randomly divided into lamivudine treatment group (n = 42) and control group (n 30). HBV DNA was detected both in serum and in PBMCs by fluorescence quantitative polymerase chain reaction (PCR), during and after lamivudine treatment.
RESULTS: In the treatment group, HBV DNA became negative both in serum and in PBMC, of, 38 and 25 out of 42 cases respectively during the 48 wk oflamivudine treatment, the negative rate was 90.5% and 59.5% respectively. In the control group, the negative rate was 23.3% and 16.7% respectively. It was statistically significant at 12, 24 and 48 wk as compared with the control group (P < 0.005). The average conversion period of HBV DNA was 6 wk (2-8 wk) in serum and 16 wk (8-24 wk) in PBMC.
CONCLUSION: Lamivudine has remarkable inhibitory effects on HBV replication both in serum and in PBMCs. The inhibitory effect on HBV DNA in PBMCs is weaker than that in serum. (C) 2006 The WIG Press. All rights reserved.
C1 Wuhan Univ, Renmin Hosp, Dept Infect Dis, Wuhan 430060, Hubei Province, Peoples R China.
Yunyang Med Coll, Taihe Hosp, Dept Infect Dis, Shiyan 442000, Hubei Province, Peoples R China.
Yunyang Med Coll, Taihe Hosp, Clin Lab, Shiyan 442000, Hubei Province, Peoples R China.
C3 Wuhan University
RP Gong, ZL (corresponding author), Wuhan Univ, Renmin Hosp, Dept Infect Dis, Wuhan 430060, Hubei Province, Peoples R China.
EM zjgong@163.com
RI Gong, Zuojiong/S-1935-2019
OI Gong, Zuojiong/0000-0002-4676-5856; Meng, Zhongji/0000-0003-0401-535X
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NR 29
TC 7
Z9 8
U1 0
U2 1
PU W J G PRESS
PI BEIJING
PA PO BOX 2345, BEIJING 100023, PEOPLES R CHINA
SN 1007-9327
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUL 7
PY 2006
VL 12
IS 25
BP 4061
EP 4063
DI 10.3748/wjg.v12.i25.4061
PG 3
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 076JQ
UT WOS:000239954000021
PM 16810760
OA hybrid, Green Accepted, Green Published
DA 2025-01-07
ER
PT J
AU Autier, B
Gottstein, B
Millon, L
Ramharter, M
Gruener, B
Bresson-Hadni, S
Dion, S
Robert-Gangneux, F
AF Autier, Brice
Gottstein, Bruno
Millon, Laurence
Ramharter, Michael
Gruener, Beate
Bresson-Hadni, Solange
Dion, Sarah
Robert-Gangneux, Florence
TI Alveolar echinococcosis in immunocompromised hosts
SO CLINICAL MICROBIOLOGY AND INFECTION
LA English
DT Review
DE Alveolar echinococcosis; Cancer; Echinococcus multilocularis; HIV;
Immunosuppressive therapy; Malignant haemopathy; Primary immune de
ficiency; Transplantation
ID MULTILOCULARIS INFECTION; LIVER-TRANSPLANTATION; INVOLVEMENT;
CLASSIFICATION; PATIENT
AB Background: Alveolar echinococcosis (AE) results of an infection with the larval stage of Echinococcus multilocularis. It has been increasingly described in individuals with impaired immune responsiveness. Objectives: This narrative review aims at describing the presentation of AE according to the type of immune impairment, based on retrospective cohorts and case reports. Implications for patient man-agement and future research are proposed accordingly. Sources: Targeted search was conducted in PubMed using ((alveolar echinococcosis) OR (multilocularis)) AND ((immunosuppressive) OR (immunodeficiency) OR (AIDS) OR (solid organ transplant) OR (auto -immunity) OR (immune deficiency)). Only publications in English were considered. Content: Seventeen publications were found, including 13 reports of 55 AE in immunocompromised patients (AE/IS) and 4 retrospective studies of 755 AE immunocompetent patients and 115 AE/IS (13%). The cohorts included 9 (1%) solid organ transplantation (SOT) recipients, 2 (0.2%) HIV patients, 41 (4.7%) with chronic inflammatory/autoimmune diseases (I/AID) and 72 (8.3%) with malignancies. SOT, I/AID and malignancies, but not HIV infection, were significantly associated with AE (odds ratios of 10.8, 1.6, 5.9, and 1.3, respectively). Compared to AE immunocompetent patients, AE/IS was associated with earlier diagnosis (PNM stages I-II: 49/85 (58%) vs. 137/348 (39%), p < 0.001), high rate of atypical imaging (24/ 50 (48%) vs. 106/375 (28%), p < 0.01), and low sensitivity of serology (19/77 (25%) vs. 265/329 (81%), p < 0.001). Unusually extensive or disseminated infections were described in SOT and I/AID patients. Implications: Patients who live in endemic areas should benefit from serology before onset of a long-term immunosuppressive therapy, even if the cost-benefit ratio has to be evaluated. Physicians should explain AE to immunocompromised patients and think about AE when finding a liver lesion. Further research should address gaps in knowledge of AE/IS. Especially, extensive and accurate records of AE cases have to be collected by multinational registries. Brice Autier, Clin Microbiol Infect 2023;29:593 (c) 2022 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
C1 [Autier, Brice; Robert-Gangneux, Florence] Univ Rennes, CHU Rennes, INSERM, Irset Inst Rech Sante Environm & Travail,UMR S 108, Rennes, France.
[Gottstein, Bruno] Univ Bern, Inst Infect Dis, Fac Med, CH-3012 Bern, Switzerland.
[Millon, Laurence; Bresson-Hadni, Solange] Univ Hosp Besancon, Natl Reference Ctr Echinococcoses, Dept Parasitol Mycol, Besancon, France.
[Millon, Laurence] Univ Bourgogne Franche Comte, CNRS, UMR 6249, Lab Chronoenvironm, Besancon, France.
[Millon, Laurence; Ramharter, Michael; Robert-Gangneux, Florence] European Study Grp Clin Parasitol, ESCMID, Basel, Switzerland.
[Ramharter, Michael] Univ Med Ctr Hamburg Eppendorf, Bernhard Nocht Inst Trop Med, Ctr Trop Med, Hamburg, Germany.
[Gruener, Beate] Univ Hosp Ulm, Dept Internal Med 3, Div Infect Dis, Ulm, Germany.
[Bresson-Hadni, Solange] Univ Hosp Geneva, Fac Med, Div Trop & Humanitarian Med, Geneva, Switzerland.
[Dion, Sarah] Univ Rennes, INSERM, EHESP, Irset Inst Rech Sante Environm & Travail,UMR S 108, Rennes, France.
[Autier, Brice] Univ Rennes 1, INSERM, U1085, 2 Ave Pr Leon Bernard, F-35000 Rennes, Bretagne, France.
[Autier, Brice] CHU Rennes, Serv Parasitol Mycol, 2 Ave Pr Leon Bernard, F-35000 Rennes, Bretagne, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
Universite de Rennes; CHU Rennes; University of Bern; University of
Geneva; Universite de Franche-Comte; CHU Besancon; Universite de
Franche-Comte; Centre National de la Recherche Scientifique (CNRS); CNRS
- Institute of Ecology & Environment (INEE); Leibniz Association;
Bernhard Nocht Institut fur Tropenmedizin; University of Hamburg;
University Medical Center Hamburg-Eppendorf; Ulm University; University
of Geneva; Institut National de la Sante et de la Recherche Medicale
(Inserm); Ecole des Hautes Etudes en Sante Publique (EHESP); Universite
de Rennes; Institut National de la Sante et de la Recherche Medicale
(Inserm); Universite de Rennes; Universite de Rennes; CHU Rennes
RP Autier, B (corresponding author), Univ Rennes, CHU Rennes, INSERM, Irset Inst Rech Sante Environm & Travail,UMR S 108, Rennes, France.; Autier, B (corresponding author), Univ Rennes 1, INSERM, U1085, 2 Ave Pr Leon Bernard, F-35000 Rennes, Bretagne, France.; Autier, B (corresponding author), CHU Rennes, Serv Parasitol Mycol, 2 Ave Pr Leon Bernard, F-35000 Rennes, Bretagne, France.
EM brice.autier@univ-rennes1.fr
RI ROBERT-GANGNEUX, Florence/I-4692-2015; Autier, Brice/AAW-8446-2021;
Dion, Sarah/I-5656-2015; Ramharter, Michael/C-5273-2013
OI Dion, Sarah/0000-0002-7347-7462; Ramharter, Michael/0000-0002-9259-1885
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NR 60
TC 12
Z9 13
U1 2
U2 17
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1198-743X
EI 1469-0691
J9 CLIN MICROBIOL INFEC
JI Clin. Microbiol. Infect.
PD MAY
PY 2023
VL 29
IS 5
BP 593
EP 599
DI 10.1016/j.cmi.2022.12.010
EA APR 2023
PG 7
WC Infectious Diseases; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases; Microbiology
GA G1AM7
UT WOS:000986568300001
PM 36528295
OA Green Submitted, Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Trafford, AM
Parisi, R
Kontopantelis, E
Griffiths, CEM
Ashcroft, DM
AF Trafford, Alex M.
Parisi, Rosa
Kontopantelis, Evangelos
Griffiths, Christopher E. M.
Ashcroft, Darren M.
TI Association of Psoriasis With the Risk of Developing or Dying of Cancer
A Systematic Review and Meta-analysis
SO JAMA DERMATOLOGY
LA English
DT Review
ID POPULATION-BASED COHORT; NON-HODGKIN-LYMPHOMA; NONMELANOMA SKIN-CANCER;
CAUSE-SPECIFIC MORTALITY; AUTOIMMUNE-DISEASES; MALIGNANT-TUMORS;
PERSONAL HISTORY; INCIDENT CANCER; SQUAMOUS-CELL; MEDICAL CONDITIONS
AB Importance The risk of cancer developing in people with psoriasis has raised some concern, with little clarity regarding differentiation in risk according to psoriasis severity. Objective To conduct a systematic review and meta-analysis of observational studies on the risk of cancer incidence and mortality in people with psoriasis. Data Sources Six electronic databases (MEDLINE, Embase, MEDLINE in Process, Cochrane Central Register, Web of Science, and LILACS [Literatura Latino-Americana e do Caribe em Ciencias da Saude]) were searched from inception to November 15, 2017, for eligible studies. Study Selection Cohort and case-control studies that provided estimates of the risk of cancer incidence or cancer mortality associated with psoriasis were included. Data Extraction and Synthesis Data were extracted relating to study design, study population, and risk estimates. Study-specific estimates of the relative risk (RR) were combined using a random-effects model. Heterogeneity was quantified using the I-2 statistic. Data were analyzed from April 9, 2018, through February 22, 2019. Main Outcomes and Measures Pooled RR estimates for cancer incidence and cancer mortality for psoriasis cohorts compared with people without psoriasis. Results A total of 58 unique studies were included, with quality varying for the incidence and the mortality studies. Severe psoriasis (RR, 1.22; 95% CI, 1.08-1.39 [9 studies]) and all severities of psoriasis (RR, 1.18; 95% CI, 1.06-1.31 [7 studies]) were associated with an increased risk of cancer (overall), and associations were found for a range of site-specific cancers, including colon (RR, 1.18 [95% CI, 1.03-1.35]), colorectal (RR, 1.34 [95% CI, 1.06-1.70]), kidney (RR, 1.58 [95% CI, 1.11-2.24]), laryngeal (RR, 1.79 [95% CI, 1.06-3.01]), liver (RR, 1.83 [95% CI, 1.28-2.61]), lymphoma (RR, 1.40 [95% CI, 1.24-1.57]), non-Hodgkin lymphoma (RR, 1.28 [95% CI, 1.15-1.43]), keratinocyte cancers (RR, 1.71 [95% CI, 1.08-2.71]), esophageal (RR, 2.05 [95% CI, 1.04-4.07]), oral cavity (RR, 2.80 [95% CI, 1.99-3.93]), and pancreatic (RR, 1.41 [95% CI, 1.16-1.73]). Overall cancer mortality risk was higher in patients with severe psoriasis (RR, 1.22; 95% CI, 1.08-1.38 [4 studies]). Specifically, liver (RR, 1.43 [95% CI, 1.09-1.88]), esophageal (RR, 2.53 [95% CI, 1.87-3.41]), and pancreatic (RR, 1.31 [95% CI, 1.02-1.69]) cancer mortality were found to be elevated in those with severe psoriasis. The heterogeneity of estimates was often very high despite stratification. Marked attenuation of risk was found in those studies that adjusted estimates for smoking, alcohol consumption, and obesity. Conclusions and Relevance In this study, people with psoriasis appeared to have an increased risk of cancer incidence and cancer-related mortality involving a range of site-specific cancers. Future research examining specific lifestyle factors, treatments, and the inflammatory processes that contribute to psoriasis may help provide additional information on the underlying mechanisms for the apparent increased cancer risk.
Question What is the risk of cancer incidence and cancer mortality in people with psoriasis? Findings This systematic review and meta-analysis included 58 unique observational studies (50 reporting on cancer incidence and 15 on cancer mortality, including 7 reporting on both). The overall risk of developing cancer was significantly elevated in people with psoriasis and for a number of site-specific cancers; the risk of cancer mortality was found to be elevated in those with severe psoriasis. Meaning These findings suggest that cancer is an important comorbidity in people with psoriasis, and dermatologists should be aware of this increased risk; further studies are needed to improve our knowledge about the underlying mechanisms of this increased risk.
This systematic review and meta-analysis of 58 observational studies assessed the risks of cancer incidence and mortality among people with psoriasis.
C1 [Trafford, Alex M.; Parisi, Rosa; Ashcroft, Darren M.] Univ Manchester, Fac Biol Med & Hlth, Sch Hlth Sci, Div Pharm & Optometry, Oxford Rd,Stopford Bldg,Room 1-136, Manchester M13 9PT, Lancs, England.
[Kontopantelis, Evangelos] Univ Manchester, Fac Biol Med & Hlth, Natl Inst Hlth Res NIHR Sch Primary Care Res, Sch Hlth Sci,Div Populat Hlth,Hlth Serv Res & Pri, Manchester, Lancs, England.
[Griffiths, Christopher E. M.] Univ Manchester, Salford Royal NHS Fdn Trust, Fac Biol Med & Hlth, Dermatol Ctr,NIHR Manchester Biomed Res Ctr, Manchester, Lancs, England.
C3 University of Manchester; University of Manchester; University of
Manchester; Salford Royal NHS Foundation Trust
RP Trafford, AM (corresponding author), Univ Manchester, Fac Biol Med & Hlth, Sch Hlth Sci, Div Pharm & Optometry, Oxford Rd,Stopford Bldg,Room 1-136, Manchester M13 9PT, Lancs, England.
EM alex.trafford@postgrad.manchester.ac.uk
RI Trafford, Alex/AHB-3035-2022; Kontopantelis, Evangelos/H-2966-2019;
Ashcroft, Darren/G-3244-2015
OI Ashcroft, Darren/0000-0002-2958-915X; Trafford,
Alex/0000-0001-8145-8133; Kontopantelis, Evangelos/0000-0001-6450-5815
FU GPA Collaborating Organisations
FX We acknowledge the key role played by the GPA Collaborating
Organisations in the establishment and organisation of the Global
Psoriasis Atlas (GPA): International Federation of Psoriasis
Associations; International League of Dermatological Societies; and
International Psoriasis Council. The GPA is funded through contributions
from the GPA Collaborating Organisations and through supporters who are
listed on the GPA website
(https://globalpsoriasisatlas.com/supporters/).
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NR 75
TC 98
Z9 101
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6068
EI 2168-6084
J9 JAMA DERMATOL
JI JAMA Dermatol.
PD DEC
PY 2019
VL 155
IS 12
BP 1390
EP 1403
DI 10.1001/jamadermatol.2019.3056
PG 14
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA JZ6AX
UT WOS:000505184900010
PM 31617868
OA Bronze, Green Published
DA 2025-01-07
ER
PT J
AU Chen, QS
Meng, XJ
McQuade, P
Rubins, D
Lin, SA
Zeng, ZZ
Haley, H
Miller, P
Trotter, DG
Low, PS
AF Chen, Qingshou
Meng, Xiangjun
McQuade, Paul
Rubins, Daniel
Lin, Shu-An
Zeng, Zhizhen
Haley, Hyking
Miller, Patricia
Trotter, Dinko Gonzalez
Low, Philip S.
TI Folate-PEG-NOTA-Al18F: A New Folate Based Radiotracer for PET
Imaging of Folate Receptor-Positive Tumors
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE folate receptor; folate conjugate; (AlF)-F-18-NOTA; F-18-PET imaging;
cancer imaging
ID FOLIC-ACID DERIVATIVES; PRECLINICAL EVALUATION; IN-VIVO; CONTRAST AGENT;
CELL-LINES; F-18; CANCER; NANOPARTICLES; DENDRIMER; TISSUES
AB The folate receptor (FR) has been established as a promising target for imaging and therapy of cancer (FR-alpha), inflammation, and autoimmune diseases (FR-beta). Several folate based PET radiotracers have been reported in the literature, but an F-18-labeled folate-PET imaging agent with optimal properties for clinical translation is still lacking. In the present study, we report the design and preclinical evaluation of folate-PEG(12)-NOTA-(AlF)-F-18 (1), a new folate-PET agent with improved potential for clinical applications. Radiochemical synthesis of 1 was achieved via a one-pot labeling process by heating folate-PEG(12)-NOTA in the presence of in situ prepared (AlF)-F-18 for 15 min at 105 degrees C, followed by HPLC purification. Specific binding of 1 to FR was evaluated on homogenates of KB (FR-positive) and A549 (FR-deficient) tumor xenografts in the presence and absence of excess folate. In vivo tumor imaging with folate-PEG(12)-NOTA-(AlF)-F-18 was compared to imaging with Tc-99m-EC20 using nu/nu mice bearing either KB or A549 tumor xenografts. Specific accumulation of 1 in tumor and other tissues was assessed by high-resolution micro-PET and ex vivo biodistribution in the presence and absence of excess folate. Radiosynthesis of 1 was accomplished within similar to 35 min, affording pure radiotracer 1 in 8.4 +/- 1.3% (decay corrected) radiochemical yield with similar to 100% radiochemical purity after HPLC purification and a specific activity of 35.8 +/- 15.3 GBq/mmol. Further in vitro and in vivo examination of 1 demonstrated highly specific FR-mediated uptake in FR+ tumor, with K-d of similar to 0.4 nM (KB), and reduced accumulation in liver. Given its facile preparation and improved properties, the new radiotracer, folate-PEG(12)-NOTA-(AlF)-F-18 (1), constitutes a promising tool for identification and classification of patients with FR overexpressing cancers.
C1 [Chen, Qingshou; Low, Philip S.] Purdue Univ, Dept Chem, W Lafayette, IN 47907 USA.
[Chen, Qingshou; Low, Philip S.] Purdue Univ, Inst Drug Discovery, W Lafayette, IN 47907 USA.
[Meng, Xiangjun; McQuade, Paul; Rubins, Daniel; Lin, Shu-An; Zeng, Zhizhen; Haley, Hyking; Miller, Patricia; Trotter, Dinko Gonzalez] Merck & Co Inc, Merck Res Labs, Imaging, 770 Sumneytown Pike, West Point, PA 19486 USA.
C3 Purdue University System; Purdue University; Purdue University System;
Purdue University; Merck & Company; Merck & Company USA
RP Low, PS (corresponding author), Purdue Univ, Dept Chem, W Lafayette, IN 47907 USA.; Low, PS (corresponding author), Purdue Univ, Inst Drug Discovery, W Lafayette, IN 47907 USA.
EM plow@purdue.edu
OI Low, Philip/0000-0001-9042-5528
FU Endocyte, Inc.
FX This work was supported by a research grant from Endocyte, Inc.
Evaluations of compounds by nuclear magnetic resonance were accomplished
using the shared resources of the Purdue University Interdepartmental
NMR Facility at the Purdue University Center for Cancer Research (PCCR).
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NR 55
TC 25
Z9 28
U1 2
U2 42
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD DEC
PY 2017
VL 14
IS 12
BP 4353
EP 4361
DI 10.1021/acs.molpharmaceut.7b00415
PG 9
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA FP1AO
UT WOS:000417342400024
PM 29028357
DA 2025-01-07
ER
PT J
AU Zhou, SQ
Wen, H
Wang, B
Guan, SM
Fang, X
AF Zhou, Shaoqiong
Wen, Hui
Wang, Bin
Guan, Siming
Fang, Xin
TI Serum levels of soluble receptor activator for nuclear factor kB ligand
play a crucial role in the association of osteoprotegerin with coronary
artery disease
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE coronary artery disease; osteoprotegerin; receptor activator for nuclear
factor-kappa B ligand
ID KAPPA-B LIGAND; VASCULAR CALCIFICATION; CARDIOVASCULAR-DISEASE; BONE;
RISK; RANKL; ATHEROSCLEROSIS; EXPRESSION; PREVENTION; PREDICTOR
AB Osteoprotegerin (OPG) is a soluble decoy receptor for receptor activator of nuclear factor kB ligand (RANKL), and is implicated in the pathogenesis of atherosclerosis. The aim of the present study was to examine the hypothesis that serum OPG concentrations are increased in patients with stable coronary artery disease (CAD) at different serum levels of soluble RANKL (sRANKL). The study used a case-control design in which consecutively hospitalized individuals were recruited. Fasting blood samples were taken upon admission for serum testing. Participants with previously diagnosed CAD that was asymptomatic or had controlled symptoms constituted the stable CAD group, whereas patients with negative coronary computed tomography angiography results constituted the control non-CAD group. Exclusion criteria included recent acute coronary syndrome, severe heart failure, CAD-complicating autoimmune, blood or thyroid diseases, cancer, elevated temperature with or without infection, severe liver or kidney dysfunction, abnormal calcium metabolism, recent surgery and trauma history. A total of 118 individuals were included in the study. Smoothed plots generated using the recursive method and multivariate models showed that the incidence of stable CAD increased with serum OPG level up to the turning point of 18 pg/ml. This trend was observed at both high [odds ratio (OR), 1.61; 95% confidence interval (CI), 1.04-2.50; P=0.032) and low sRANKL concentrations (OR, 1.52; 95% CI, 1.06-2.17; P=0.022) after adjustment for cardiovascular risk factors. In conclusion, serum OPG levels <= 18 pg/ml are positively associated with stable CAD, regardless of sRANKL levels. In addition, at the same serum OPG level, higher sRANKL levels are associated with a greater incidence of stable CAD compared with lower sRANKL levels. This study identified the relationship between OPG, sRANKL, and stable CAD, and established the reference range for future clinical use.
C1 [Zhou, Shaoqiong; Wang, Bin; Guan, Siming; Fang, Xin] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Geriatr, 1277 Jiefang Ave, Wuhan 430022, Hubei, Peoples R China.
[Wen, Hui] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Gen Practice, Wuhan 430022, Hubei, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
Science & Technology
RP Guan, SM; Fang, X (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Geriatr, 1277 Jiefang Ave, Wuhan 430022, Hubei, Peoples R China.
EM 15972021296@163.com; smguan@163.com
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NR 45
TC 1
Z9 1
U1 1
U2 1
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD AUG
PY 2024
VL 28
IS 2
AR 325
DI 10.3892/etm.2024.12614
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA XY4T7
UT WOS:001265235300001
PM 38979019
OA gold
DA 2025-01-07
ER
PT J
AU Sunitha, K
Hemshekhar, M
Thushara, RM
Santhosh, MS
Yariswamy, M
Kemparaju, K
Girish, KS
AF Sunitha, K.
Hemshekhar, M.
Thushara, R. M.
Santhosh, M. Sebastin
Yariswamy, M.
Kemparaju, K.
Girish, K. S.
TI N-Acetylcysteine amide: a derivative to fulfill the promises of
N-Acetylcysteine
SO FREE RADICAL RESEARCH
LA English
DT Review
DE N-Acetylcysteine; N-Acetylcysteine amide; anti-inflammatory;
anti-apoptotic; neuroprotective
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; INDUCED OXIDATIVE STRESS;
BRAIN ENDOTHELIAL-CELLS; KAPPA-B ACTIVATION; THIOL ANTIOXIDANT;
FREE-RADICALS; INDUCED CYTOTOXICITY; INDUCED APOPTOSIS; ACETYL-CYSTEINE;
GENE-EXPRESSION
AB In the present human health scenario, implication of oxidative stress in numerous pathologies including neurodegenerative, cardiovascular, liver, renal, pulmonary disorders, and cancer has gained attention. N-Acetylcysteine (NAC), a popular thiol antioxidant, has been clinically used to treat various pathophysiological disorders. However, NAC therapy is routine only in paracetamol intoxication and as a mucolytic agent. Over six decades, numerous studies involving NAC therapy have yielded inconsistent results, and this could be due to low bioavailability. In order to overcome the limitations of NAC, an amide derivative N-Acetylcysteine amide (NACA) has been synthesized to improve the lipophilicity, membrane permeability, and antioxidant property. Recent studies have demonstrated the blood brain barrier permeability and therapeutic potentials of NACA in neurological disorders including Parkinson's disease, Alzheimer's disease, Multiple sclerosis, Tardive dyskinesia, and HIV-associated neurological disorders. In addition, NACA displays protective effect against pulmonary inflammation and antibiotic-induced apoptosis. Forthcoming research on the possible therapeutic properties of NACA and its generics in the management of pathologies associated with extracellular matrix degradation and oxidative stress-related inflammation is highly exiting. Superior bioavailability of NACA is likely to fulfill the promises of NAC as well as a molecule to improve the endurance and resident time of bioscaffolds and biomaterials. Till date, more than 800 reviews on NAC have been published. However, no comprehensive review is available on the therapeutic applications of NACA. Therefore, the current review would be the first to emphasize the therapeutic potentials of NACA and its derivatives.
C1 [Sunitha, K.; Hemshekhar, M.; Thushara, R. M.; Santhosh, M. Sebastin; Yariswamy, M.; Kemparaju, K.; Girish, K. S.] Univ Mysore, DOS Biochem, Mysore, Karnataka, India.
[Girish, K. S.] Tumkur Univ, DOS & Res Biochem, Tumkur 572102, Karnataka, India.
C3 University of Mysore; Tumkur University
RP Girish, KS (corresponding author), Tumkur Univ, DOS & Res Biochem, Tumkur 572102, Karnataka, India.
EM ksgbaboo@yahoo.com
RI KS, Girish/GWZ-7128-2022
OI KS, Girish/0000-0002-7284-3707; Hemshekhar,
Mahadevappa/0000-0002-5016-501X; Santhosh, Sebastin/0000-0003-0318-1233
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NR 53
TC 81
Z9 95
U1 0
U2 35
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-5762
EI 1029-2470
J9 FREE RADICAL RES
JI Free Radic. Res.
PD MAY
PY 2013
VL 47
IS 5
BP 357
EP 367
DI 10.3109/10715762.2013.781595
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 142XL
UT WOS:000318830800003
PM 23472882
DA 2025-01-07
ER
PT J
AU Bachhuka, A
Yadav, TC
Santos, A
Marsal, LF
Ergun, S
Karnati, S
AF Bachhuka, Akash
Yadav, Tara Chand
Santos, Abel
Marsal, Lluis F.
Ergun, Sueleyman
Karnati, Srikanth
TI Emerging nanomaterials for targeting peroxisomes
SO MATERIALS TODAY ADVANCES
LA English
DT Article
DE Peroxisomes; Nanomaterials; Arti ficial organelles; Metabolic disorders;
Nanozymes
ID PROLIFERATOR-ACTIVATED RECEPTORS; GLUTATHIONE-S-TRANSFERASE; RAT-LIVER
PEROXISOMES; ACID ALPHA-OXIDATION; BETA-OXIDATION; DOCOSAHEXAENOIC ACID;
CARBON NANOTUBES; PPAR-ALPHA; INTRACELLULAR DELIVERY; ANTIOXIDANT
ACTIVITY
AB Peroxisomes are single membrane-bound metabolic organelles whose dysfunction can lead to several metabolic disorders. In addition, they have been associated with the pathology of several diseases such as cancer, autoimmune diseases, diabetes, stroke, etc. In the last few decades, research has been focused on detecting peroxisomes in the physiological environment. However, the detection of these peroxisomes was based on fluorescent probes, which had limited success due to their toxicity, photobleaching, poor selectivity, and spontaneous oxidation. Moreover, research has been focused on mimicking the functionality of peroxisomes by fabricating artificial peroxisomes using synthetic materials, which have been limited due to poor stability and biocompatibility. Therefore, a new class of materials, "nanomaterials" has shown promise in overcoming the limitations underlying traditional techniques by providing better optical properties, stability and biocompatibility. Despite the advancement, the field remains in its infancy. Only a handful of studies have reported nanomaterials such as quantum dots, zeolites, liposomes, dendrimers, and nanoparticles to detect and fabricate peroxisomes. This review will provide a general description of peroxisomes and their role in different metabolic activities. The later part will focus on the challenges and progress related to nanomaterials-based peroxisome detection, fabrication, and delivery. This review will also provide insights into the critical research gaps and advances on different strategies utilized to explore peroxisomes, opening new avenues for future research in this field.(c) 2022 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Bachhuka, Akash; Marsal, Lluis F.] Rovira & Virgili Univ URV, Dept Elect Elect & Automat Engn, Tarragona 43003, Spain.
[Yadav, Tara Chand] Indian Inst Technol, Dept Biosci & Bioengn, Roorkee 247667, Uttar Pradesh, India.
[Yadav, Tara Chand] PP Savani Univ, Sch Sci, Surat 394125, India.
[Santos, Abel] Univ Adelaide, Sch Chem Engn, Adelaide, SA 5095, Australia.
[Ergun, Sueleyman; Karnati, Srikanth] Univ Wurzburg, Inst Anat & Cell Biol, Wurzburg, Germany.
C3 Universitat Rovira i Virgili; Indian Institute of Technology System (IIT
System); Indian Institute of Technology (IIT) - Roorkee; University of
Adelaide; University of Wurzburg
RP Bachhuka, A (corresponding author), Rovira & Virgili Univ URV, Dept Elect Elect & Automat Engn, Tarragona 43003, Spain.; Karnati, S (corresponding author), Univ Wurzburg, Inst Anat & Cell Biol, Wurzburg, Germany.
EM akash.bachhuka@urv.cat; srikanth.karnati@uni-wuerzburg.de
RI Bachhuka, Akash/AAA-6963-2022; Marsal, Lluis/G-8852-2011; Karnati,
Srikanth/AAP-9038-2021; YADAV, TARA/X-8840-2019; Santos,
Abel/U-7181-2017
OI Bachhuka, Akash/0000-0003-1253-8126
FU MICINN (Spain) [IJC-2019-042374-1]
FX AB thanks MICINN (Spain) for the Juan de la Cierva incorpora-tion
fellowship (IJC-2019-042374-1) .
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NR 139
TC 6
Z9 6
U1 2
U2 19
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2590-0498
J9 MATER TODAY ADV
JI Mater. Today Adv.
PD AUG
PY 2022
VL 15
AR 100265
DI 10.1016/j.mtadv.2022.100265
EA JUN 2022
PG 8
WC Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science
GA 2E4BY
UT WOS:000812174500001
OA gold
DA 2025-01-07
ER
PT J
AU Roche, B
Samuel, D
AF Roche, Bruno
Samuel, Didier
TI The difficulties of managing severe hepatitis B virus reactivation
SO LIVER INTERNATIONAL
LA English
DT Review
DE Liver failure; HBV; Nucleoside analogue
ID HBV REACTIVATION; CANCER-PATIENTS; CYTOTOXIC CHEMOTHERAPY; PREEMPTIVE
LAMIVUDINE; ADEFOVIR DIPIVOXIL; VIRAL-HEPATITIS; THERAPY; RISK;
MORTALITY; INFECTION
AB Reactivation of hepatitis B is characterized by a sudden increase in hepatitis B virus (HBV) replication in a patient with prior evidence of resolved or inactive HBV infection. Although HBV reactivation can occur spontaneously, it usually occurs after chemotherapy, immunosuppression (organ transplantation) or an alteration in immune function (therapy for autoimmune disease, human immunodeficiency virus infection). The clinical presentation cases can vary, ranging from a subclinical, asymptomatic course to severe acute hepatitis and even death. Although reactivation of HBV is mainly found in HBsAg-positive patients, it can be observed in serologically recovered anti-hepatitis B core antibody (HBc)-positive, HBsAg-negative patients. Serum HBV DNA typically increases during immune suppression, followed by a disease flare and HBV DNA clearance following immune restoration after immune suppression is stopped. In organ transplant recipients, without immune reconstitution, high HBV DNA levels can lead to fibrosing cholestatic hepatitis related to the direct cytopathic effect of HBV. Several randomized, controlled trials and meta-analyses have shown that reactivation can be prevented by lamivudine prophylaxis. Screening for HBsAg and anti-HBc should be performed before beginning immunosuppressive treatment and routine prophylaxis is recommended in HBsAg-positive patients. The optimal duration of prophylaxis remains to be determined. In anti-HBc-positive patients with or without anti-hepatitis B surface antigen, alanine transaminase and HBV DNA levels should be closely monitored and antiviral therapy should be started when HBV reactivation is confirmed. The use of new more potent nucleos(t)ides analogues with lower resistance rates would seem to be logical; however, experience with these drugs in the prophylaxis and treatment of severe HBV reactivation is limited.
C1 [Roche, Bruno; Samuel, Didier] Hop Paul Brousse, AP HP, Ctr Hepatobiliaire, F-94804 Villejuif, France.
[Roche, Bruno; Samuel, Didier] INSERM, U785, Villejuif, France.
[Roche, Bruno; Samuel, Didier] Univ Paris 11, UMR S 785, Villejuif, France.
C3 Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
Paul-Brousse - APHP; Universite Paris Saclay; Institut National de la
Sante et de la Recherche Medicale (Inserm); Universite Paris Saclay
RP Samuel, D (corresponding author), Hop Paul Brousse, AP HP, Ctr Hepatobiliaire, 14 Av PV Couturier, F-94804 Villejuif, France.
EM didier.samuel@pbr.aphp.fr
RI ROCHE, Bruno/T-7452-2018; Samuel, Didier/U-5265-2018
OI Samuel, Didier/0000-0001-9481-3616
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NR 48
TC 51
Z9 57
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD JAN
PY 2011
VL 31
SU 1
BP 104
EP 110
DI 10.1111/j.1478-3231.2010.02396.x
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 702FM
UT WOS:000285880000017
PM 21205146
OA Bronze
DA 2025-01-07
ER
PT J
AU Kline, J
Subbiah, S
Lazarus, HM
van Besien, K
AF Kline, J.
Subbiah, S.
Lazarus, H. M.
van Besien, K.
TI Autologous graft-versus-host disease: harnessing anti-tumor immunity
through impaired self-tolerance
SO BONE MARROW TRANSPLANTATION
LA English
DT Review
DE autologous GVHD; CsA; immunotherapy
ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION; PHASE-I TRIAL;
HIGH-DOSE CHEMOTHERAPY; CYCLOSPORINE-A; HODGKINS-DISEASE; TREATED RATS;
BLOOD; INDUCTION; CANCER
AB The absence of a graft-versus-malignancy (GVM) effect may be responsible for the higher relapse rate seen after autologous hematopoietic cell transplantation (auto-HCT) compared with allogeneic hematopoietic cell transplantation (allo-HCT). Acute GVHD developing after allo-HCT, however, is associated with signi. cant morbidity and mortality. An autoimmune syndrome similar to acute GVHD has been reported to occur after auto-HCT and has been termed the 'auto-aggression' syndrome or autologous GVHD (auto-GVHD). Auto-GVHD tends to be milder than classical GVHD, most commonly involves the skin ( rarely the gastrointestinal tract, liver or both) and often is self-limited. Auto-GVHD has been reported to occur both spontaneously and in subjects receiving post transplant immune modulation with CsA, IFN-gamma or the combination. The development of auto-GVHD depends upon the derangement of self tolerance either through administration of post transplant CsA, depletion of regulatory T cells following the preparative chemoradiotherapy or both. Self-reactive CD8(+) T cells paradoxically are able to recognize a self peptide antigen presented by MHC class II molecules and appear to mediate the syndrome. Many clinical trials have been performed using CsA with or without IFN-gamma in an attempt to induce auto-GVHD. While many patients do indeed develop the syndrome, any associated anti-tumor effect remains questionable to date. New strategies to exploit auto-GVHD and enhance a GVM effect such as through the depletion of regulatory T cells or through use of newer immunomodulatory agents may improve the efficacy of auto-HCT.
C1 [Kline, J.; van Besien, K.] Univ Chicago Hosp, Dept Med, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Subbiah, S.; Lazarus, H. M.] Univ Hosp Case Med Ctr, Div Hematol Oncol, Cleveland, OH USA.
C3 University of Chicago; University of Illinois System; University System
of Ohio; Case Western Reserve University; Case Western Reserve
University Hospital
RP Kline, J (corresponding author), Univ Chicago Hosp, Dept Med, Hematol Oncol Sect, MC 2115,5481 S Maryland Ave, Chicago, IL 60637 USA.
EM jkline@medicine.bsd.uchicago.edu
RI van Besien, Koen/G-4221-2012
OI van Besien, Koen/0000-0002-8164-6211
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NR 53
TC 40
Z9 44
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
EI 1476-5365
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD MAR
PY 2008
VL 41
IS 6
BP 505
EP 513
DI 10.1038/sj.bmt.1705931
PG 9
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 279DL
UT WOS:000254335100001
PM 18026144
DA 2025-01-07
ER
PT J
AU Esteghamati, A
Ashraf, H
Nakhjavani, M
Najafian, B
Hamidi, S
Abbasi, M
AF Esteghamati, A.
Ashraf, H.
Nakhjavani, M.
Najafian, B.
Hamidi, S.
Abbasi, M.
TI Insulin resistance is an independent correlate of increased urine
albumin excretion: a cross-sectional study in Iranian Type 2 diabetic
patients
SO DIABETIC MEDICINE
LA English
DT Article
DE Asian diabetes; insulin resistance; microalbuminuria
ID CARDIOVASCULAR RISK-FACTORS; METABOLIC SYNDROME; MICROALBUMINURIA;
HYPERTENSION; HOMEOSTASIS; DYSFUNCTION; GLUCOSE; PLASMA; NIDDM
AB To assess the association of insulin resistance with increased urinary albumin excretion (UAE) in a cohort of Iranian Type 2 diabetic patients.
Three hundred and sixty-one men and 472 women with Type 2 diabetes were enrolled from three different outpatient clinics (Tehran, Iran) during the period 2005-2008. Patients with obstructive uropathy, severe heart failure, liver disease, cancer, autoimmune disease and macroalbuminuria were not included. Microalbuminuria (MA; defined as UAE >= 30 mg/day) was found in 242 (29.1%) patients; 591 (70.9%) subjects had normoalbuminuria (UAE < 30 mg/day). Insulin resistance was assessed using homeostasis model assessment of insulin resistance (HOMA-IR).
HOMA-IR index values were higher in subjects with MA than those with normoalbuminuria (P < 0.00001). Adjusted values (for age, sex and duration of diabetes) of UAE and HOMA-IR were 11.81 +/- 7.51 (mg/day) and 3.30 +/- 2.21 in normoalbuminuric and 75.36 +/- 55.57 (mg/day) and 4.98 +/- 3.22 in the MA group, respectively (P < 0.00001 for all). Multiple regression analysis showed that UAE was predicted by HOMA-IR, independently of age, duration of diagnosed diabetes, triglycerides, waist circumference, metabolic control, blood pressure and related treatments (P < 0.00001). When patients were categorized into quartiles of HOMA-IR, those of the fourth quartile (i.e. the most insulin resistant) were at a higher risk of increased UAE than other quartiles [odds ratio (OR) 3.7 (95% confidence intervals 2.7-6.2)].
In Iranian Type 2 diabetic patients, albuminuria was strongly associated with insulin resistance. HOMA-IR is an independent predictor of UAE.
Diabet. Med. 26, 177-181 (2009).
C1 [Esteghamati, A.; Ashraf, H.; Nakhjavani, M.; Hamidi, S.; Abbasi, M.] Univ Tehran Med Sci, Dept Endocrinol, Endocrinol & Metab Res Ctr, Vali Asr Hosp, Tehran 1419733148, Iran.
[Najafian, B.] Univ Minnesota, Dept Paediat, Minneapolis, MN 55455 USA.
[Najafian, B.] Univ Minnesota, Dept Lab Med & Pathol, Sch Med, Minneapolis, MN 55455 USA.
C3 Tehran University of Medical Sciences; University of Minnesota System;
University of Minnesota Twin Cities; University of Minnesota System;
University of Minnesota Twin Cities
RP Esteghamati, A (corresponding author), Univ Tehran Med Sci, Dept Endocrinol, Endocrinol & Metab Res Ctr, Vali Asr Hosp, Keshavarz Blvd, Tehran 1419733148, Iran.
EM esteghamati@sina.tums.ac.ir
RI Nakhjavani, Manouchehr/J-3704-2019; Abbasi, Mehrshad/J-4064-2012
OI Ashraf, Haleh/0000-0001-6687-995X; Najafian, Behzad/0000-0002-0904-6721;
Abbasi, Mehrshad/0000-0001-5011-897X
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NR 22
TC 19
Z9 21
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0742-3071
EI 1464-5491
J9 DIABETIC MED
JI Diabetic Med.
PD FEB
PY 2009
VL 26
IS 2
BP 177
EP 181
DI 10.1111/j.1464-5491.2008.02653.x
PG 5
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 406NG
UT WOS:000263301600012
PM 19236623
DA 2025-01-07
ER
PT J
AU Khatami, M
AF Khatami, Mahin
TI Chronic Inflammation: Synergistic Interactions of Recruiting Macrophages
(TAMs) and Eosinophils (Eos) with Host Mast Cells (MCs) and
Tumorigenesis in CALTs. M-CSF, Suitable Biomarker for Cancer Diagnosis!
SO CANCERS
LA English
DT Review
DE Yin and Yang of acute inflammation; immune surveillance; conjunctival
associated lymphoid tissues (CALTS); mast cells; tumor-associated
macrophages (TAMs); cancer biomarkers; targeted therapies;
neurodegenerative and autoimmune diseases
ID FREE LIGHT-CHAINS; INTRATUMORAL MACROPHAGES; HEPATOCELLULAR-CARCINOMA;
UNRESOLVED INFLAMMATION; IMMUNE-RESPONSES; POOR-PROGNOSIS; T-CELLS;
DEGRANULATION; MECHANISMS; MICROENVIRONMENT
AB Ongoing debates, misunderstandings and controversies on the role of inflammation in cancer have been extremely costly for taxpayers and cancer patients for over four decades. A reason for repeated failed clinical trials (90% +/- 5 failure rates) is heavy investment on numerous genetic mutations (molecular false-flags) in the chaotic molecular landscape of site-specific cancers which are used for. targeted. therapies or. personalized. medicine. Recently, unresolved/chronic inflammation was defined as loss of balance between two tightly regulated and biologically opposing arms of acute inflammation ("Yin"-"Yang". or immune surveillance). Chronic inflammation could differentially erode architectural integrities in host immune-privileged or immune-responsive tissues as a common denominator in initiation and progression of nearly all age-associated neurodegenerative and autoimmune diseases and/or cancer. Analyses of data on our. accidental. discoveries in 1980s on models of acute and chronic inflammatory diseases in conjunctival-associated lymphoid tissues (CALTs) demonstrated at least three stages of interactions between resident (host) and recruited immune cells: (a), acute phase; activation of mast cells (MCs), IgE Abs, histamine and prostaglandin synthesis; (b), intermediate phase; down-regulation phenomenon, exhausted/degranulated MCs, heavy eosinophils (Eos) infiltrations into epithelia and goblet cells (GCs), tissue hypertrophy and neovascularization; and (c), chronic phase; induction of lymphoid hyperplasia, activated macrophages (M phi s), increased (irregular size) B and plasma cells, loss of integrity of lymphoid tissue capsular membrane, presence of histiocytes, follicular and germinal center formation, increased ratios of local IgG1/IgG2, epithelial thickening (growth) and/or thinning (necrosis) and angiogenesis. Results are suggestive of first evidence for direct association between inflammation and identifiable phases of immune dysfunction in the direction of tumorigenesis. Activated M Phi s (TAMs or M2) and Eos that are recruited by tissues (e. g., conjunctiva or perhaps lung airways) whose principal resident immune cells are MCs and lymphocytes are suggested to play crucial synergistic roles in enhancing growth promoting capacities of host toward tumorigenesis. Under oxidative stress, M-CSF may produce signals that are cumulative/synergistic with host mediators (e. g., low levels of histamine), facilitating tumor-directed expression of decoy receptors and immune suppressive factors (e. g., dTNFR, IL- 5, IL- 10, TGF-beta., PGE2). M-CSF, possessing superior sensitivity and specificity, compared with conventional markers (e. g., CA-125, CA-19-9) is potentially a suitable biomarker for cancer diagnosis and technology development. Systematic monitoring of interactions between resident and recruited cells should provide key information not only about early events in loss of immune surveillance, but it would help making informed decisions for balancing the inherent tumoricidal (Yin) and tumorigenic (Yang) properties of immune system and effective preventive and therapeutic approaches and accurate risk assessment toward improvement of public health.
C1 [Khatami, Mahin] Natl Canc Inst Ret, Natl Inst Hlth, Inflammat & Canc Biol, Bethesda, MD 20817 USA.
C3 National Institutes of Health (NIH) - USA
RP Khatami, M (corresponding author), Natl Canc Inst Ret, Natl Inst Hlth, Inflammat & Canc Biol, Bethesda, MD 20817 USA.
EM mkgoodness@aol.com
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NR 104
TC 25
Z9 26
U1 1
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2014
VL 6
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BP 297
EP 322
DI 10.3390/cancers6010297
PG 26
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA V47KK
UT WOS:000209950500016
PM 24473090
OA Green Submitted, Green Published, gold
DA 2025-01-07
ER
PT J
AU Younis, MYG
AF Younis, Mustafa Younis Gaballah
TI Prevalence of vitamin D deficiency in Libya and its relation to other
health disorders
SO METABOLISM AND TARGET ORGAN DAMAGE
LA English
DT Review
DE 25-hydroxycholecalciferol; Vitamin D deficiency prevalence; rickets;
osteomalacia
ID FATTY LIVER-DISEASE; SERUM 25-HYDROXYVITAMIN D; 1,25-DIHYDROXYVITAMIN
D-3; CALCIUM SUPPLEMENTATION; COLORECTAL-CANCER; MOLECULAR ACTIONS;
HYPOVITAMINOSIS D; PREGNANT-WOMEN; SAUDI-ARABIA; SUN EXPOSURE
AB Vitamin D (VD) has a potential role in calcium homeostasis in the human body. It is also considered a strong immunomodulator, affecting both arms of the immune system (Innate and adaptive immunity). VD can also lower the risk of diabetes, improve pregnancy outcomes, reduce the risk of acute respiratory infection (e.g., COVID-19), and decrease the risk of cancer. No doubt that VD deficiency (VDD) is a health condition that spreads out all over the globe. VDD is linked to many health problems ranging from fatigue and skeleton pain to serious conditions such as rickets, osteomalacia, diabetes, autoimmune disease, cardiovascular diseases, and cancer. This review aims to provide a whole picture of the status of 25hydroxycholecalciferol [25-(OH)D] as well as the frequency of 25(OH)D deficiency (VDD) among Libyans in various regions of the country and to discuss the correlation between VDD and other health problems. The prevalence of VDD reached up to 80% among healthy individuals in the Middle East region. Libya is a big Mediterranean country and is sunny most of the year. In the western part of Libya, particularly in Tripoli (the capital city), the prevalence of severe VDD [25-(OH)D < 10 ng/mL] was as high as 50.8%, whereas only 27.5% had moderate VDD [25-(OH)D; 10-20 ng/mL]. In Benghazi (second largest city), the VDD prevalence was also high (76%). The highest prevalence of VDD was reported at 79% in the biggest southern city of Sebha. In the whole country, the VDD prevalence was high (among males and females), ranging from 45.4% to 87%, with a mean of 55.58%. The mean prevalence of VDD among males was 54.3% and for females was 53.29%. As clear from these data, VDD prevalence was high in the entire country. However, the available data were obtained from small cross-sectional studies and it becomes a necessity to conduct nationally representative studies and establish national nutrition surveys to accurately assess the prevalence of VDD. Moreover, the data included in this review invites the health authorities in Libya to take preventive measures to reduce the high prevalence of VDD, which will decrease VDD-associated health problems in the future.
C1 [Younis, Mustafa Younis Gaballah] Univ Benghazi, Fac Med, Dept Biochem, Benghazi, Libya.
C3 University of Benghazi
RP Younis, MYG (corresponding author), Fac Med, Dept Biochem, Benghazi, Libya.
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NR 134
TC 0
Z9 0
U1 0
U2 0
PU OAE PUBLISHING INC
PI ALHAMBRA
PA 245 E MAIN ST, ST122, ALHAMBRA, CA 91801 USA
EI 2769-6375
J9 METAB TARGET ORGAN D
JI Metab. Target Organ Damage
PD JUN
PY 2024
VL 4
IS 2
AR 13
DI 10.20517/mtod.2023.36
PG 22
WC Endocrinology & Metabolism
WE Emerging Sources Citation Index (ESCI)
SC Endocrinology & Metabolism
GA G7L7V
UT WOS:001318414800003
OA gold
DA 2025-01-07
ER
PT J
AU Lenoir, C
Rollason, V
Desmeules, JA
Samer, CF
AF Lenoir, Camille
Rollason, Victoria
Desmeules, Jules A.
Samer, Caroline F.
TI Influence of Inflammation on Cytochromes P450 Activity in Adults: A
Systematic Review of the Literature
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE inflammation; cytochrome P450; pharmacokinetic; disease-drug
interaction; cytokines
ID CHRONIC HEPATITIS-C; PHARMACOKINETIC MODELING APPROACH; LIVER-TRANSPLANT
RECIPIENTS; CYCLOSPORINE TROUGH LEVELS; PROTEIN-DRUG INTERACTIONS;
URINARY-TRACT-INFECTION; CRITICALLY-ILL PATIENTS; CLOZAPINE
SERUM-LEVELS; ANTIPYRINE HALF-LIVES; PLASMA-CONCENTRATIONS
AB Background: Available in-vitro and animal studies indicate that inflammation impacts cytochromes P450 (CYP) activity via multiple and complex transcriptional and post-transcriptional mechanisms, depending on the specific CYP isoforms and the nature of inflammation mediators. It is essential to review the current published data on the impact of inflammation on CYP activities in adults to support drug individualization based on comorbidities and diseases in clinical practice.Methods: This systematic review was conducted in PubMed through 7th January 2021 looking for articles that investigated the consequences of inflammation on CYP activities in adults. Information on the source of inflammation, victim drugs (and CYPs involved), effect of disease-drug interaction, number of subjects, and study design were extracted.Results: The search strategy identified 218 studies and case reports that met our inclusion criteria. These articles were divided into fourteen different sources of inflammation (such as infection, autoimmune diseases, cancer, therapies with immunomodulator horizontal ellipsis ). The impact of inflammation on CYP activities appeared to be isoform-specific and dependent on the nature and severity of the underlying disease causing the inflammation. Some of these drug-disease interactions had a significant influence on drug pharmacokinetic parameters and on clinical management. For example, clozapine levels doubled with signs of toxicity during infections and the concentration ratio between clopidogrel's active metabolite and clopidogrel is 48-fold lower in critically ill patients. Infection and CYP3A were the most cited perpetrator of inflammation and the most studied CYP, respectively. Moreover, some data suggest that resolution of inflammation results in a return to baseline CYP activities.Conclusion: Convincing evidence shows that inflammation is a major factor to be taken into account in drug development and in clinical practice to avoid any efficacy or safety issues because inflammation modulates CYP activities and thus drug pharmacokinetics. The impact is different depending on the CYP isoform and the inflammatory disease considered. Moreover, resolution of inflammation appears to result in a normalization of CYP activity. However, some results are still equivocal and further investigations are thus needed.
C1 [Lenoir, Camille; Rollason, Victoria; Desmeules, Jules A.; Samer, Caroline F.] Univ Hosp Geneva, Dept Anesthesiol Pharmacol Intens Care & Emergenc, Div Clin Pharmacol & Toxicol, Geneva, Switzerland.
[Lenoir, Camille; Desmeules, Jules A.] Univ Geneva, Sch Pharmaceut Sci, Inst Pharmaceut Sci Western Switzerland IS, Geneva, Switzerland.
[Rollason, Victoria; Desmeules, Jules A.; Samer, Caroline F.] Univ Geneva, Fac Med, Geneva, Switzerland.
C3 University of Geneva; University of Geneva; University of Geneva
RP Lenoir, C (corresponding author), Univ Hosp Geneva, Dept Anesthesiol Pharmacol Intens Care & Emergenc, Div Clin Pharmacol & Toxicol, Geneva, Switzerland.; Lenoir, C (corresponding author), Univ Geneva, Sch Pharmaceut Sci, Inst Pharmaceut Sci Western Switzerland IS, Geneva, Switzerland.
EM Camille.Lenoir@hcuge.ch
RI ; Samer, Caroline/ABB-2447-2021
OI Lenoir, Camille/0000-0001-6506-8629; Samer, Caroline/0000-0001-8178-0616
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NR 233
TC 49
Z9 51
U1 1
U2 10
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD NOV 16
PY 2021
VL 12
AR 733935
DI 10.3389/fphar.2021.733935
PG 44
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XI4OD
UT WOS:000726092100001
PM 34867341
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Li, XY
Lin, X
Mei, XY
Chen, P
Liu, AN
Liang, WC
Chang, S
Li, J
AF Li, Xingyu
Lin, Xue
Mei, Xueyin
Chen, Pin
Liu, Anna
Liang, Weicheng
Chang, Shan
Li, Jian
TI HLA3D: an integrated structure-based computational toolkit for
immunotherapy
SO BRIEFINGS IN BIOINFORMATICS
LA English
DT Article
DE HLA structure; mutation; organ transplantation; neoantigen prediction
ID CLASS-I MOLECULES; IMMUNOGENICITY; MISMATCH; ALLELES; RISK;
IDENTIFICATION; PREDICTION; DATABASE; ANTIGEN; EPITOPE
AB Motivation: The human major histocompatibility complex (MHC), also known as human leukocyte antigen (HLA), plays an important role in the adaptive immune system by presenting non-self-peptides to T cell receptors. The MHC region has been shown to be associated with a variety of diseases, including autoimmune diseases, organ transplantation and tumours. However, structural analytic tools of HLA are still sparse compared to the number of identified HLA alleles, which hinders the disclosure of its pathogenic mechanism.
Result: To provide an integrative analysis of HLA, we first collected 1296 amino acid sequences, 256 protein data bank structures, 120 000 frequency data of HLA alleles in different populations, 73 000 publications and 39 000 disease-associated single nucleotide polymorphism sites, as well as 212 modelled HLA heterodimer structures. Then, we put forward two new strategies for building up a toolkit for transplantation and tumour immunotherapy, designing risk alignment pipeline and antigenic peptide prediction pipeline by integrating different resources and bioinformatic tools. By integrating 100 000 calculated HLA conformation difference and online tools, risk alignment pipeline provides users with the functions of structural alignment, sequence alignment, residue visualization and risk report generation of mismatched HLA molecules. For tumour antigen prediction, we first predicted 370 000 immunogenic peptides based on the affinity between peptides and MHC to generate the neoantigen catalogue for 11 common tumours. We then designed an antigenic peptide prediction pipeline to provide the functions of mutation prediction, peptide prediction, immunogenicity assessment and docking simulation. We also present a case study of hepatitis B virus mutations associated with liver cancer that demonstrates the high legitimacy of our antigenic peptide prediction process. HLA3D, including different HLA analytic tools and the prediction pipelines, is available at http://www.h1a34.56/.
C1 [Li, Xingyu; Mei, Xueyin; Chen, Pin; Liu, Anna; Liang, Weicheng; Li, Jian] Southeast Univ, Sch Life Sci & Technol, Key Lab DGHD, MOE, Nanjing 210096, Peoples R China.
[Lin, Xue] Nanjing Med Univ, Sch Biomed Engn & Informat, Dept Bioinformat, Nanjing, Peoples R China.
[Chang, Shan] Jiangsu Univ Technol, Sch Elect & Informat Engn, Inst Bioinformat & Med Engn, Changzhou, Peoples R China.
C3 Southeast University - China; Nanjing Medical University; Jiangsu
University of Technology
RP Li, J (corresponding author), Southeast Univ, Sch Life Sci & Technol, Key Lab DGHD, MOE, Nanjing 210096, Peoples R China.
EM jianli2014@seu.edu.cn
RI Li, Xingyu/AHE-0001-2022; Li, Chunyan/F-5309-2016
OI Chang, Shan/0000-0001-7169-9398; liang, wei cheng/0000-0002-8708-1143
FU National Natural Science Foundation of China [31871322, 31900473];
Fundamental Research Funds for the Central Universities [2242017K3DN23,
2242017 K41041]
FX National Natural Science Foundation of China (31871322, 31900473);
Fundamental Research Funds for the Central Universities (2242017K3DN23,
2242017 K41041). The funding bodies were not involved in the design of
the study, collection, analysis or interpretation of data.
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NR 43
TC 5
Z9 5
U1 1
U2 16
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1467-5463
EI 1477-4054
J9 BRIEF BIOINFORM
JI Brief. Bioinform.
PD MAY 13
PY 2022
VL 23
IS 3
DI 10.1093/bib/bbac076
EA MAR 2022
PG 13
WC Biochemical Research Methods; Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 1Z0DH
UT WOS:000769087700001
PM 35289353
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Ling, YY
Hu, HQ
Xu, XY
Feng, JL
Li, MZ
Li, H
Cheng, M
Wang, XL
AF Ling, Yanyan
Hu, Huaiqiang
Xu, Xiangyan
Feng, Jianli
Li, Mingzhe
Li, Huan
Cheng, Ming
Wang, Xiaoling
TI Paraneoplastic dermatomyositis and Hodgkin's lymphoma in a 14-year-old
girl: a case report and literature review
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE juvenile dermatomyositis; Hodgkin's lymphoma; paraneoplastic syndrome;
malignancy; nodular sclerosing Hodgkin's lymphoma
ID JUVENILE DERMATOMYOSITIS; INFLAMMATORY MYOPATHIES; POLYMYOSITIS;
DISEASES; CHILDREN
AB Background Juvenile dermatomyositis (JDM) is a rare autoimmune myopathy whose main clinical manifestations include a characteristic rash, symmetrical proximal muscle weakness, and elevated muscle enzymes. While approximately one-third of adult patients with dermatomyositis (DM) develop malignancies, typically within a year of diagnosis, this phenomenon is not commonly observed in patients with JDM. In this study, we present a rare case of both JDM and Hodgkin's lymphoma (HL) diagnosed in an adolescent female patient.Case description A 14-year-old girl with proximal muscle weakness and myalgia for 8 weeks was admitted to the hospital and ultimately received a diagnosis of DM. A thorough physical examination revealed enlarged lymph nodes on both sides of the cervical, and a lymph node biopsy was performed to diagnose HL. After she underwent radiotherapy and chemotherapy, her symptoms of both HL and DM were alleviated.Conclusion The phenomenon of JDM as a paraneoplastic syndrome associated with HL is very rare. Thus, routine cancer screening for DM in adolescents is currently not recommended. The diagnosis of JDM requires a detailed physical examination, and further tumor screening is necessary for patients with unusual physical findings, such as atypical rashes, enlarged lymph nodes, and enlargement of the spleen and/or liver. Even if no malignancy is detected when JDM is diagnosed, long-term follow-up is necessary.
C1 [Ling, Yanyan; Feng, Jianli] Shandong Second Prov Gen Hosp, Dept Neurol, Jinan, Peoples R China.
[Hu, Huaiqiang; Cheng, Ming; Wang, Xiaoling] 960th Hosp Joint Logist Force, Dept Neurol, PLA, Jinan, Peoples R China.
[Xu, Xiangyan] Shandong Second Prov Gen Hosp, Dept Traumat Orthoped, Jinan, Peoples R China.
[Li, Mingzhe] Shandong Second Prov Gen Hosp, Dept Emergency, Jinan, Peoples R China.
[Li, Huan] 970th Hosp Joint Logist Force, Dept Neurol, PLA, Yantai, Peoples R China.
RP Cheng, M; Wang, XL (corresponding author), 960th Hosp Joint Logist Force, Dept Neurol, PLA, Jinan, Peoples R China.
EM xwxy121213@163.com; CMCMLYY1990@163.com
RI Feng, jianli/KEJ-2030-2024
FX The author(s) declare that no financial support was received for the
research, authorship, and/or publication of this article.
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TC 0
Z9 0
U1 1
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PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
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PD AUG 7
PY 2024
VL 14
AR 1416083
DI 10.3389/fonc.2024.1416083
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D1V0G
UT WOS:001294119600001
PM 39169942
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Nedellec, V
Rabl, A
Dab, W
AF Nedellec, Vincent
Rabl, Ari
Dab, William
TI Public health and chronic low chlordecone exposures in Guadeloupe; Part
2: Health impacts, and benefits of prevention
SO ENVIRONMENTAL HEALTH
LA English
DT Article
DE Chlordecone; Low-dose; Threshold; Risk assessment; Non-mutagen agent;
Endocrine disrupter; Risk management; Exposure reduction program
ID TOXICOLOGY; MORTALITY; INFANTS; RISK; IQ
AB Background: Inhabitants of Guadeloupe are chronically exposed to low doses of chlordecone via local food due to its past use in banana plantations. The corresponding health impacts have not been quantified. We develop a quantitative method and present the results in two articles: 1. Hazard identification, exposure-response functions, and exposure, 2. Health impacts, and benefits of a program to reduce the exposure of the population. Here is the second article.
Methods: The exposure-response functions derived in Part 1 (for liver and prostate cancer, renal dysfunction and cognitive development) are combined with the exposure data to calculate the impacts. The corresponding costs are calculated via DALY's and VOLY. A no-effect threshold is included via the marginal fraction of the collective exposure above the reference dose. The health benefits are the impacts in 2002 (before the exposure reduction program) minus the impacts in 2006 (since the program). They are compared to the costs, namely the public annual expenditures for reducing the population exposure.
Results: Without threshold, estimated annual cases of liver cancer, prostate cancer and renal dysfunction are respectively 5.4, 2.8, 0.10 in 2002; and 2.0, 1.0, 0.04 in 2006. Annual IQ points lost (cognitive development) are respectively: 1 173 and 1 003. The annual cost of total impacts is 38.3 Million Euros (M(sic)) in 2002 and 23.7 M(sic) in 2006. Comparing the benefit of 14.6 M(sic) with the 3.25 M(sic) spent for prevention, the program appears well justified. With threshold, the costs of the impacts are lower, respectively: 26.5 M(sic) in 2002 and 12.8 M(sic) in 2006, but the benefit is not very different: 13.7 M(sic).
Conclusion: This is the first study that quantified chronic non genotoxic effects of chlordecone exposures in Guadeloupe. According to our results, preventive actions should be focused on pregnant women because of the high social cost of development impairment and also because their exposures decreased less rapidly than others. Prevention effort should be sustained as long as chlordecone remains in soils. Additional toxicological and epidemiological research would also be required for health endpoints that could not be taken into account (neurotoxicity of adults, autoimmune diseases and other developmental effects).
C1 [Nedellec, Vincent] Vincent Nedellec Conseil, 23 Rue Andre Massena, F-83000 Toulon, France.
[Rabl, Ari] Ecole Mines ARMINES, Paris, France.
[Rabl, Ari] Environm Impacts, 6 Ave Faidherbe, F-91440 Bures Sur Yvette, France.
[Dab, William] CNAM, Lab MESuRS Modelisat Epidemiol & Surveillance Ris, EA 4628, 292 Rue St Martin, F-75141 Paris 03, France.
C3 heSam Universite; Conservatoire National Arts & Metiers (CNAM)
RP Nedellec, V (corresponding author), Vincent Nedellec Conseil, 23 Rue Andre Massena, F-83000 Toulon, France.
EM vincent.nedellec3@gmail.com
FU French Ministry in charge of the environmental protection through the
"Programme National de Recherche sur les Perturbateurs Endocriniens"
PNRPE (The National Research Programme on Endocrine Disruptors)
[11-MRES-PNRPE-3CVS-029]
FX This work was done during the BAREPE project funded by grant from the
French Ministry in charge of the environmental protection (Grant number:
11-MRES-PNRPE-3CVS-029) through the "Programme National de Recherche sur
les Perturbateurs Endocriniens" PNRPE (The National Research Programme
on Endocrine Disruptors).
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NR 42
TC 7
Z9 7
U1 2
U2 14
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-069X
J9 ENVIRON HEALTH-GLOB
JI Environ. Health
PD JUL 19
PY 2016
VL 15
AR 78
DI 10.1186/s12940-016-0159-3
PG 13
WC Environmental Sciences; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health
GA DR6EK
UT WOS:000379994700001
PM 27430869
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Wood, KH
Zhou, ZL
AF Wood, Kathleen H.
Zhou, Zhaolan
TI Emerging Molecular and Biological Functions of MBD2, a Reader of DNA
Methylation
SO FRONTIERS IN GENETICS
LA English
DT Article
DE methyl-CpG binding domain protein; MBD2; MBD3; DNA methylation;
nucleosome remodeling and histone deacetylation complex (NuRD);
chromatin; mouse genetics; transcription regulation
ID CPG-BINDING DOMAIN; CHROMATIN REMODELING COMPLEXES;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; MESSENGER-RNA EXPRESSION; HISTONE
DEACETYLASE CORE; TUMOR-SUPPRESSOR GENE; TRANSCRIPTIONAL REPRESSION;
PREFERENTIAL BINDING; PROTEIN MBD2; SELF-RENEWAL
AB DNA methylation is an epigenetic mark that is essential for many biological processes and is linked to diseases such as cancer. Methylation is usually associated with transcriptional silencing, but new research has challenged this model. Both transcriptional activation and repression have recently been found to be associated with DNA methylation in a context-specific manner. How DNA methylation patterns are interpreted into different functional output remains poorly understood. One mechanism involves the protein 'readers' of methylation, which includes the methylCpG binding domain (MBD) family of proteins. This review examines the molecular and biological functions of MBD2, which binds to CpG methylation and is an integral part of the nucleosome remodeling and histone deacetylation (NuRD) complex. MBD2 has been linked to immune system function and tumorigenesis, yet little is known about its functions in vivo. Recent studies have found the MBD2 protein is ubiquitously expressed, with relatively high levels in the lung, liver, and colon. Mbd2 null mice surprisingly show relatively mild phenotypes compared to mice with loss of function of other MBD proteins. This evidence has previously been interpreted as functional redundancy between the MBD proteins. Here, we examine and contextualize research that suggests MBD2 has unique properties and functions among the MBD proteins. These functions translate to recently described roles in the development and differentiation of multiple cell lineages, including pluripotent stem cells and various cell types of the immune system, as well as in tumorigenesis. We also consider possible models for the dynamic interactions between MBD2 and NuRD in different tissues in vivo. The functions of MBD2 may have direct therapeutic implications for several areas of human disease, including autoimmune conditions and cancer, in addition to providing insights into the actions of NuRD and chromatin regulation.
C1 [Wood, Kathleen H.; Zhou, Zhaolan] Univ Penn, Dept Genet, Perelman Sch Med, Philadelphia, PA 19104 USA.
C3 University of Pennsylvania
RP Zhou, ZL (corresponding author), Univ Penn, Dept Genet, Perelman Sch Med, Philadelphia, PA 19104 USA.
EM zhaolan@mail.med.upenn.edu
OI Wood, Kathleen/0000-0001-6566-4885; Zhou, Zhaolan/0000-0003-1401-0296
FU Predoctoral Training Grant [T32GM008216]; US National Institutes of
Health [R01 MH091850]
FX This work was supported by a Predoctoral Training Grant T32GM008216 to
KW and US National Institutes of Health grant R01 MH091850 to ZZ. ZZ is
a Pew Scholar in the biomedical sciences. We thank all members of Zhou
lab for helpful discussion.
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NR 125
TC 53
Z9 57
U1 0
U2 17
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD MAY 26
PY 2016
VL 7
AR 93
DI 10.3389/fgene.2016.00093
PG 14
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA EW6JO
UT WOS:000402616700001
PM 27303433
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Betzel, T
Müller, C
Groehn, V
Müller, A
Reber, J
Fischer, CR
Krämer, SD
Schibli, R
Ametamey, SM
AF Betzel, Thomas
Mueller, Cristina
Groehn, Viola
Mueller, Adrienne
Reber, Josefine
Fischer, Cindy R.
Kraemer, Stefanie D.
Schibli, Roger
Ametamey, Simon M.
TI Radiosynthesis and Preclinical Evaluation of
3′-Aza-2′-[18F]fluorofolic Acid: A Novel PET Radiotracer for
Folate Receptor Targeting
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID FOLIC-ACID; MONOCLONAL-ANTIBODY; CANCER; F-18; PHOTODEGRADATION;
ARTHRITIS; KIDNEY; PHASE
AB The folate receptor (FR) has been identified as a valuable target for the imaging of cancer and activated macrophages, involved in inflammatory and autoimmune diseases via positron emission tomography (PET). Therefore, conjugates of folic acid have been synthesized by coupling of a radiolabeled prosthetic group to the glutamate part of folic acid (pendent approach). In this work, we present a novel class of folates, where the phenyl ring of folic acid was isosterically replaced by a pyridine moiety for direct labeling with [F-18]fluoride (integrated approach). 3'-Azafolic acid and its 2'-halogenated derivatives (2'-chloro and 2'-fluoro) were evaluated in vitro to determine their binding affinity. 3'-Aza-2'-[F-18]fluorofolic acid ([F-18]6) was obtained, starting from N-2-acetyl-3'-aza-2'-chlorofolic acid di-tert-butylester (2), in a maximum decay corrected radiochemical yield of about 9% in >= 98% radiochemical purity and high specific activities of 35-127 GBq/mu mol. Binding affinity to the FR was high (IC50 = 0.8 +/- 0.2 nM), and the radiotracer was stable in human plasma over 4 h at 37 degrees C. No degradation or defluorination was detected after incubation of the radiotracer for 1 h at 37 degrees C with human and murine liver microsomes and human S9-fraction. In vivo PET imaging and biodistribution studies with mice demonstrated a high and specific uptake in FR-positive KB tumor xenografts (12.59 +/- 1.77% ID/g, 90 min p.i.). A high and specific accumulation of radioactivity was observed in the kidneys (57.33 +/- 8.40% ID/g, 90 min p.i.) and salivary glands (14.09 +/- 0.93% ID/g, 90 min pi.), which are known to express the FR and nonspecific uptake found in the liver (10.31 +/- 2.37% ID/g, 90 min p.i.). Preinjection of folic acid resulted in a >85% reduced uptake of [F-18]6 in FR-positive tissues (xenografts, kidneys, and salivary glands). Furthermore, no radioactive metabolites were detected in the blood, urine, or tumor tissue, 30 min p.i. These characteristics indicate that this new F-18-labeled 3'-azafolate is an appropriate tool for imaging FR-positive (malignant) tissue.
C1 [Betzel, Thomas; Mueller, Adrienne; Fischer, Cindy R.; Kraemer, Stefanie D.; Schibli, Roger; Ametamey, Simon M.] ETH, Inst Pharmaceut Sci, Dept Chem & Appl Biosci, CH-8093 Zurich, Switzerland.
[Mueller, Cristina; Reber, Josefine; Schibli, Roger] Paul Scherrer Inst, ETH PSI USZ, Ctr Radiopharmaceut Sci, Villigen, Switzerland.
[Groehn, Viola] Merck & Cie, Schaffhausen, Switzerland.
C3 Swiss Federal Institutes of Technology Domain; ETH Zurich; Swiss Federal
Institutes of Technology Domain; ETH Zurich; Paul Scherrer Institute
RP Ametamey, SM (corresponding author), ETH, Wolfgang Pauli Str 10, CH-8093 Zurich, Switzerland.
EM simon.ametamey@pharma.ethz.ch
OI Schibli, Roger/0000-0002-1537-3833; Reber, Josefine/0000-0003-4932-8990;
Mueller, Cristina/0000-0001-9357-9688; Kramer, Stefanie
D./0000-0002-0426-4340
FU Commission of Technology and Innovation, Switzerland [CTI 11667.1
PFLS-LS]; Merck & Cie, Switzerland; Swiss National Foundation
[PZ00P3_121772]; Swiss National Science Foundation (SNF) [PZ00P3_121772]
Funding Source: Swiss National Science Foundation (SNF)
FX We thank Nadja Romano, Claudia Keller, and Dominique Leutwiler for
technical assistance. This work was financially supported by the
Commission of Technology and Innovation, Switzerland (CTI 11667.1
PFLS-LS), in collaboration with Merck & Cie, Switzerland, and by the
Swiss National Foundation (Ambizione Grant PZ00P3_121772).
CR Al Jammaz I, 2012, NUCL MED BIOL, V39, P864, DOI 10.1016/j.nucmedbio.2012.02.005
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Fischer CR, 2012, BIOCONJUGATE CHEM, V23, P805, DOI 10.1021/bc200660z
Fisher RE, 2008, J NUCL MED, V49, P899, DOI 10.2967/jnumed.107.049478
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Müller C, 2009, EUR J NUCL MED MOL I, V36, P938, DOI 10.1007/s00259-008-1058-9
Off MK, 2005, J PHOTOCH PHOTOBIO B, V80, P47, DOI 10.1016/j.jphotobiol.2005.03.001
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NR 33
TC 44
Z9 48
U1 0
U2 46
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD FEB
PY 2013
VL 24
IS 2
BP 205
EP 214
DI 10.1021/bc300483a
PG 10
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Biochemistry & Molecular Biology; Chemistry
GA 095HS
UT WOS:000315325900007
PM 23273015
DA 2025-01-07
ER
PT J
AU Tsimokha, AS
Artamonova, TO
Diakonov, EE
Khodorkovskii, MA
Tomilin, AN
AF Tsimokha, Anna S.
Artamonova, Tatiana O.
Diakonov, Egor E.
Khodorkovskii, Mikhail A.
Tomilin, Alexey N.
TI Post-Translational Modifications of Extracellular Proteasome
SO MOLECULES
LA English
DT Article
DE affinity purification; extracellular proteasome; fourier transform ion
cyclotron mass spectrometry (FT-ICR MS); human leukemia K562 cells;
matrix-assisted laser desorption; ionization (MALDI); post-translational
modifications (PTMs)
ID 26S PROTEASOME; 20S PROTEASOME; CIRCULATING PROTEASOMES; C-ABL;
UBIQUITIN; PHOSPHORYLATION; YEAST; SUBUNIT; ACETYLATION; DEGRADATION
AB The ubiquitin-proteasome system (UPS) is one of the major protein degradation pathways in eukaryotic cells. Abnormal functioning of this system has been observed in cancer and neurological diseases. The 20S proteasomes, essential components of the UPS, are present not only within the cells but also in the extracellular space, and their concentration in blood plasma has been found to be elevated and dependent upon the disease state, being of prognostic significance in patients suffering from cancer, liver diseases, and autoimmune diseases. However, functions of extracellular proteasomes and mechanisms of their release by cells remain largely unknown. The main mechanism of proteasome activity regulation is provided by modulation of their composition and post-translational modifications (PTMs). Moreover, diverse PTMs of proteins are known to participate in the loading of specific elements into extracellular vesicles. Since previous studies have revealed that the transport of extracellular proteasomes may occur via extracellular vesicles, we have set out to explore the PTMs of extracellular proteasomes in comparison to cellular counterparts. In this work, cellular and extracellular proteasomes were affinity purified and separated by SDS-PAGE for subsequent trypsinization and matrix-assisted laser desorption/ionization (MALDI) Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometry (MS) analysis. In total, we could identify 64 and 55 PTM sites in extracellular and cellular proteasomes, respectively, including phosphorylation, ubiquitination, acetylation, and succinylation. We observed novel sites of acetylation at K238 and K192 of the proteasome subunits beta 2 and beta 3, respectively, that are specific for extracellular proteasomes. Moreover, cellular proteasomes show specific acetylation at K227 of alpha 2 and ubiquitination at K201 of beta 3. Interestingly, succinylation of beta 6 at the residue K228 seems not to be present exclusively in extracellular proteasomes, whereas both extracellular and cellular proteasomes may also be acetylated at this site. The same situation takes place at K201 of the beta 3 subunit where ubiquitination is seemingly specific for cellular proteasomes. Moreover, crosstalk between acetylation, ubiquitination, and succinylation has been observed in the subunit alpha 3 of both proteasome populations. These data will serve as a basis for further studies, aimed at dissection of the roles of extracellular proteasome-specific PTMs in terms of the function of these proteasomes and mechanism of their transport into extracellular space.
C1 [Tsimokha, Anna S.; Artamonova, Tatiana O.; Diakonov, Egor E.; Khodorkovskii, Mikhail A.; Tomilin, Alexey N.] Russian Acad Sci, Inst Cytol, 4 Tikhoretsky Ave, St Petersburg 194064, Russia.
[Artamonova, Tatiana O.; Khodorkovskii, Mikhail A.] Peter Great St Petersburg Polytech Univ, Inst Nanobiotechnol, 29 Polytech Skaya Str, St Petersburg 195251, Russia.
C3 Russian Academy of Sciences; St. Petersburg Scientific Centre of the
Russian Academy of Sciences; Institute of Cytology RAS; Peter the Great
St. Petersburg Polytechnic University
RP Tsimokha, AS (corresponding author), Russian Acad Sci, Inst Cytol, 4 Tikhoretsky Ave, St Petersburg 194064, Russia.
EM atsimokha@incras.ru; artamonova@nanobio.spbstu.ru; e.diakonov@incras.ru;
nanobio@nanobio.spbstu.ru; a.tomilin@incras.ru
RI Tatyana, Artamonova/A-6235-2014; Tsimokha, Anna/D-2790-2014;
Khodorkovskii, Mikhail/G-2793-2011; Tomilin, Alexey/C-3361-2014
OI Artamonova, Tatiana/0000-0002-0069-0561; Tsimokha,
Anna/0000-0002-8261-2750; Khodorkovskii, Mikhail/0000-0003-0562-0156;
Tomilin, Alexey/0000-0002-1137-7167; Diakonov, Egor/0000-0002-5190-4531
FU Russian Foundation for Basic Research [18-04-01168]; Ministry of Science
and Higher Education
FX The study was supported by the Russian Foundation for Basic Research
(#18-04-01168). The mass-spectrometric experiments were carried out
using the equipment of the Center for Shared Usage, The Analytical
Center of Nano-and Biotechnologies of Peter the Great St-Petersburg
Polytechnic University, with financial support from the Ministry of
Science and Higher Education.
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NR 64
TC 8
Z9 8
U1 1
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD AUG
PY 2020
VL 25
IS 15
AR 3504
DI 10.3390/molecules25153504
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA MZ4DW
UT WOS:000559073200001
PM 32752045
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Moon, DB
Lee, SG
AF Moon, DB
Lee, SG
TI Adult-to-adult living donor liver transplantation at the Asan Medical
Center
SO YONSEI MEDICAL JOURNAL
LA English
DT Article
DE adult living donor liver transplantation; modified right lobe; dual
grafts
ID LOBE GRAFTS
AB Between February 1997 and December 2003, 580 adult-to-adult living donor liver transplants (A-A LDLTs) were performed at the Asan Medical Center for patients above 20 years of age. Indications for A-A LDLT were: chronic hepatitis B (309), chronic hepatitis C (18), hepatocellular carcinoma (144), alcoholic cirrhosis (20), Wilson's disease (4), autoimmune hepatitis (4), hepatic tuberculosis (1), cholangiocarcinoma (2), cryptogenic cirrhosis (5), secondary biliary cirrhosis (7), primary biliary cirrhosis (2), fulminant hepatic failure (18), primary sclerosing cholangitis (2), vanishing bile duct syndrome (1) and re-transplantation (4). Of 580 A-A LDLTs, 119 were of high medical urgency, 96 were for acute on chronic liver failure, 18 were for acute and subacute hepatic failure, I was for Wilson's disease, and 4 were for re-transplantation. Recipient age ranged from 20 to 69 years. The age of the donors ranged from 16 to 63 years. There was no donor mortality. Implanted liver grafts were categorized into seven types: 307 modified right lobes (MRL), 85 left lobes, 44 left lobe plus caudate lobes, 41 right lobes, 93 dual grafts, 5 extended right lobes, 4 posterior segments, and I extended left lateral segment. In the MRL, the tributaries of the middle hepatic vein were reconstructed by interpositioning a vein graft. Indication for dual graft implantation was the same as single graft A-A LDLT, and seventeen of 93 were emergency cases. As a right-sided graft, 47 received left lobes; 31 received a extended left lateral segment or a lateral segment; 13 received a right lobe with or without the reconstruction of middle hepatic vein tributaries; and 2 received a posterior segment. Graft volume ranged from 26.5% to 83% of the standard liver volume of the recipients. There were 46 (8.0%) one year mortalities among the 576 patients after 580 A-A LDLTs. Of the 119 patients who received emergency transplants, 108 (90.8%) survived. These encouraging results justify the expansion of A-A LDLT to adjust to increasing demands, even in urgent situations. We have aimed establish the efficacy of A-A LDLT in various end-stage chronic and acute liver diseases, as well as new technical advances to overcome the small-for-size graft syndrome by using dual-graft implantation and MRL, both of which were first developed in our department.
C1 Univ Ulsan, Coll Med, Asan Med Ctr,Dept Surg, Div Hepatobiliary Surg & Liver Transplantat, Seoul 138736, South Korea.
C3 University of Ulsan; Asan Medical Center
RP Univ Ulsan, Coll Med, Asan Med Ctr,Dept Surg, Div Hepatobiliary Surg & Liver Transplantat, 388-1 Pungnap Dong, Seoul 138736, South Korea.
EM sglee2@amc.seoul.kr
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Hwang S, 1999, J KOREAN SOC TRANSPL, V13, P213
Lee S, 2001, SURGERY, V129, P647, DOI 10.1067/msy.2001.114218
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NR 9
TC 37
Z9 41
U1 0
U2 0
PU YONSEI UNIV COLL MEDICINE
PI SEOUL
PA 50-1 YONSEI-RO, SEODAEMUN-GU, SEOUL 120-752, SOUTH KOREA
SN 0513-5796
EI 1976-2437
J9 YONSEI MED J
JI Yonsei Med. J.
PD DEC 31
PY 2004
VL 45
IS 6
BP 1162
EP 1168
DI 10.3349/ymj.2004.45.6.1162
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 885QN
UT WOS:000226172100029
PM 15627313
OA gold
DA 2025-01-07
ER
PT J
AU Bengmark, S
AF Bengmark, Stig
TI Gut microbiota, immune development and function
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Microbiota; Microbiome; Microbial translocation; Probiotic bacteria;
Lactobacillus; Lactobacillus plantarum; Lactobacillus paracasei;
Microbial translocation; Inflammation; Infection; Toll-like;
Neutrophils; Pharmaceuticals; Biological; Eco-biologicals;
Nutraceticals; Curcumin; Resveratrol; Antibiotics; Chemotherapeutics;
Barriers; Leakage; Gut; Airways; Oral cavity; Skin; Vagina; Placenta;
Amnion; Blood-brain barrier; Growth; Replication; Apoptosis; Mucosa;
Endothelium; Plaques; Cytokines; IL1; NF-kB; TNF; Growth factors;
Insulinogenic; IGF-1; Prebiotics; Plant fibers; Greens; Fruits;
Vegetables; Minerals; Fat diet; Refined carbohydrate diet; Advanced
glycation end products (AGEs); Advanced lipoxidation end products
(ALEs); Endotoxin; LPS; Proteotoxins; Casein; Gluten; Zein; Western
lifestyle; Paleolithic; Schimpanzee; ADHD; AIDS; Allergy; ALS;
Alzheimer; Arteriosclerosis; Atheroma; Autoimmune; Autism; Bipolar;
Cancer; Celiac disease; COPD; Coronary Heart Disease; Chronic Fatigue
Syndrome; Chronic Renal Disease; Cognitive; Diabetes; HIV-1;
Encephalopathy; Irritable Bowel Disease; Inflammatory Bowel Disease;
Liver cirrhosis; Liver steatosis; Obesity; Osteoarthritis; Osteoporosis;
Pancreatitis; Paradontosis ;Parkinson; Polycystic Ovary Disease;
Rheumatoid Disease; Schizophrenia; Stress; Stroke; Uveitis
ID GLYCATION END-PRODUCTS; INDUCED BACTERIAL TRANSLOCATION;
BLOOD-BRAIN-BARRIER; NF-KAPPA-B; MECHANICAL BOWEL PREPARATION;
RANDOMIZED CONTROLLED-TRIAL; EARLY ENTERAL NUTRITION; CRITICALLY-ILL
PATIENTS; FERMENTED OATMEAL SOUP; VITAMIN-D LEVELS
AB The microbiota of Westerners is significantly reduced in comparison to rural individuals living a similar lifestyle to our Paleolithic forefathers but also to that of other free-living primates such as the chimpanzee. The great majority of ingredients in the industrially produced foods consumed in the West are absorbed in the upper part of small intestine and thus of limited benefit to the microbiota. Lack of proper nutrition for microbiota is a major factor under-pinning dysfunctional microbiota, dysbiosis, chronically elevated inflammation, and the production and leakage of endotoxins through the various tissue barriers. Furthermore, the over-comsumption of insulinogenic foods and proteotoxins, such as advanced glycation and lipoxidation molecules, gluten and zein, and a reduced intake of fruit and vegetables, are key factors behind the commonly observed elevated inflammation and the endemic of obesity and chronic diseases, factors which are also likely to be detrimental to microbiota. As a consequence of this lifestyle and the associated eating habits, most barriers, including the gut, the airways, the skin, the oral cavity, the vagina, the placenta, the blood-brain barrier, etc., are increasingly permeable. Attempts to recondition these barriers through the use of so called 'probiotics', normally applied to the gut, are rarely successful, and sometimes fail, as they are usually applied as adjunctive treatments, e.g. in parallel with heavy pharmaceutical treatment, not rarely consisting in antibiotics and chemotherapy.
It is increasingly observed that the majority of pharmaceutical drugs, even those believed to have minimal adverse effects, such as proton pump inhibitors and anti-hypertensives, in fact adversely affect immune development and functions and are most likely also deleterious to microbiota. Equally, it appears that probiotic treatment is not compatible with pharmacological treatments. Eco-biological treatments, with plant-derived substances, or phytochemicals, e.g. curcumin and resveratrol, and pre-, pro- and synbiotics offers similar effects as use of biologicals, although milder but also free from adverse effects. Such treatments should be tried as alternative therapies; mainly, to begin with, for disease prevention but also in early cases of chronic diseases. Pharmaceutical treatment has, thus far, failed to inhibit the tsunami of endemic diseases spreading around the world, and no new tools are in sight. Dramatic alterations, in direction of a paleolithic-like lifestyle and food habits, seem to be the only alternatives with the potential to control the present escalating crisis. The present review focuses on human studies, especially those of clinical relevance. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Bengmark, Stig] UCL, Div Surg & Intervent Sci, London WC1E 6AU, England.
C3 University of London; University College London
RP Bengmark, S (corresponding author), 185 Barrier Point Rd, London E16 2SE, England.
EM stig@bengmark.se
OI Bengmark, Stig/0000-0003-1809-8889
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NR 333
TC 159
Z9 186
U1 8
U2 738
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD MAR
PY 2013
VL 69
IS 1
BP 87
EP 113
DI 10.1016/j.phrs.2012.09.002
PG 27
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 102FU
UT WOS:000315831100009
PM 22989504
DA 2025-01-07
ER
PT J
AU Wong, VWS
Petta, S
Hiriart, JB
Cammà, C
Wong, GLH
Marra, F
Vergniol, J
Chan, AWH
Tuttolomondo, A
Merrouche, W
Chan, HLY
Le Bail, B
Arena, U
Craxì, A
de Lédinghen, V
AF Wong, Vincent Wai-Sun
Petta, Salvatore
Hiriart, Jean-Baptiste
Camma, Calogero
Wong, Grace Lai-Hung
Marra, Fabio
Vergniol, Julien
Chan, Anthony Wing-Hung
Tuttolomondo, Antonino
Merrouche, Wassil
Chan, Henry Lik-Yuen
Le Bail, Brigitte
Arena, Umberto
Craxi, Antonio
de Ledinghen, Victor
TI Validity criteria for the diagnosis of fatty liver by M probe-based
controlled attenuation parameter
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE FibroScan; Liver stiffness measurement; Non-alcoholic fatty liver
disease; Hepatic steatosis; Liver biopsy; Diagnostic accuracy
ID MAGNETIC-RESONANCE SPECTROSCOPY; CHRONIC HEPATITIS-B; TRANSIENT
ELASTOGRAPHY; STIFFNESS MEASUREMENT; XL PROBE; HEPATOCELLULAR-CARCINOMA;
NONALCOHOLIC STEATOHEPATITIS; NONINVASIVE ASSESSMENT; OBESE-PATIENTS;
UNITED-STATES
AB Background & Aims: Controlled attenuation parameter (CAP) can be performed together with liver stiffness measurement (LSM) by transient elastography (TE) and is often used to diagnose fatty liver. We aimed to define the validity criteria of CAP.
Methods: CAP was measured by the M probe prior to liver biopsy in 754 consecutive patients with different liver diseases at three centers in Europe and Hong Kong (derivation cohort, n = 340; validation cohort, n = 414; 101 chronic hepatitis B, 154 chronic hepatitis C, 349 non-alcoholic fatty liver disease, 37 autoimmune hepatitis, 49 cholestatic liver disease, 64 others; 277 F3-4; age 52 +/- 14; body mass index 27.2 +/- 5.3 kg/m(2)). The primary outcome was the diagnosis of fatty liver, defined as steatosis involving >= 5% of hepatocytes.
Results: The area under the receiver-operating characteristics curve (AUROC) for CAP diagnosis of fatty liver was 0.85 (95% CI 0.82-0.88). The interquartile range (IQR) of CAP had a negative correlation with CAP (r = -0.32, p < 0.001), suggesting the IQR-to-median ratio of CAP would be an inappropriate validity parameter. In the derivation cohort, the IQR of CAP was associated with the accuracy of CAP (AUROC 0.86, 0.89 and 0.76 in patients with IQR of CAP <20 [15% of patients], 20-39 [51%], and >= 40 dB/m [33%], respectively). Likewise, the AUROC of CAP in the validation cohort was 0.90 and 0.77 in patients with IQR of CAp <40 and >= 40 dB/m, respectively (p = 0.004). The accuracy of CAP in detecting grade 2 and 3 steatosis was lower among patients with body mass index >= 30 kg/m(2) and F3-4 fibrosis.
Conclusions: The validity of CAP for the diagnosis of fatty liver is lower if the IQR of CAP is >= 40 dB/m.
Lay summary: Controlled attenuation parameter (CAP) is measured by transient elastography (TE) for the detection of fatty liver. In this large study, using liver biopsy as a reference, we show that the variability of CAP measurements based on its interquartile range can reflect the accuracy of fatty liver diagnosis. In contrast, other clinical factors such as adiposity and liver enzyme levels do not affect the performance of CAP. (C) 2017 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Wong, Vincent Wai-Sun; Wong, Grace Lai-Hung; Chan, Henry Lik-Yuen] Chinese Univ Hong Kong, Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China.
[Wong, Vincent Wai-Sun; Wong, Grace Lai-Hung; Chan, Henry Lik-Yuen] Chinese Univ Hong Kong, State Key Lab Digest Dis, Hong Kong, Hong Kong, Peoples R China.
[Petta, Salvatore; Camma, Calogero; Craxi, Antonio] Univ Palermo, Sez Gastroenterol, DiBiMIS, Palermo, Italy.
[Hiriart, Jean-Baptiste; Vergniol, Julien; Merrouche, Wassil; de Ledinghen, Victor] Bordeaux Univ Hosp, Ctr Invest Fibrose Hepat, Hop Haut Leveque, Pessac, France.
[Marra, Fabio; Arena, Umberto] Univ Firenze, Dipartimento Med Sperimentale & Clin, Florence, Italy.
[Chan, Anthony Wing-Hung] Chinese Univ Hong Kong, Dept Anat & Cellular Pathol, Hong Kong, Hong Kong, Peoples R China.
[Tuttolomondo, Antonino] Univ Palermo, Sez Med Interna & Cardioangiol, DiBiMIS, Palermo, Italy.
[Le Bail, Brigitte; de Ledinghen, Victor] Bordeaux Univ, INSERM U1053, Bordeaux, France.
[Le Bail, Brigitte] Bordeaux Univ Hosp, Hop Pellegrin, Serv Pathol, Bordeaux, France.
C3 Chinese University of Hong Kong; Chinese University of Hong Kong;
University of Palermo; Universite de Bordeaux; CHU Bordeaux; University
of Florence; Chinese University of Hong Kong; University of Palermo;
Institut National de la Sante et de la Recherche Medicale (Inserm);
Universite de Bordeaux; CHU Bordeaux; Universite de Bordeaux
RP de Lédinghen, V (corresponding author), Hop Haut Leveque, Ctr Invest Fibrose Hepat, Serv Hepatogastroenterol, F-33604 Pessac, France.; Wong, VWS (corresponding author), Prince Wales Hosp, Dept Med & Therapeut, 9/F,Clin Sci Bldg,30-32 Ngan Shing St, Shatin, Hong Kong, Peoples R China.
EM wongv@cuhk.edu.hk; victor.deledinghen@chu-bordeaux.fr
RI Chan, Henry/JKI-4211-2023; Wong, Vincent/K-3864-2014; Chan,
Anthony/N-6719-2016; Marra, Fabio/K-7263-2016; Wong, Grace
Lai-Hung/L-8586-2014
OI Marra, Fabio/0000-0001-8629-0878; Wong, Grace
Lai-Hung/0000-0002-2863-9389
FU Research Grant Council of the Hong Kong SAR Government [CUHK 477813]
FX This project was partially supported by a grant from the Research Grant
Council of the Hong Kong SAR Government (Project no. CUHK 477813).
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Younossi ZM, 2011, HEPATOLOGY, V53, P1874, DOI 10.1002/hep.24268
NR 37
TC 109
Z9 110
U1 0
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD SEP
PY 2017
VL 67
IS 3
BP 577
EP 584
DI 10.1016/j.jhep.2017.05.005
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FE0AP
UT WOS:000407883500021
PM 28506907
DA 2025-01-07
ER
PT J
AU Schoening, W
Helbig, M
Buescher, N
Andreou, A
Schmitz, V
Bahra, M
Puhl, G
Pascher, A
Pratschke, J
Seehofer, D
AF Schoening, Wenzel
Helbig, Michael
Buescher, Niklas
Andreou, Andreas
Schmitz, Volker
Bahra, Marcus
Puhl, Gero
Pascher, Andreas
Pratschke, Johann
Seehofer, Daniel
TI Eurotransplant donor-risk-index and recipient factors: influence on
long-term outcome after liver transplantation - A large single-center
experience
SO CLINICAL TRANSPLANTATION
LA English
DT Article
DE donor evaluation; liver transplantation; long-term graft survival
ID GRAFT-SURVIVAL; D-MELD; MODEL; RECURRENCE; ALLOCATION; CRITERIA;
QUALITY; SCORE
AB The organ shortage has led to increased use of marginal organs. The Eurotransplant Donor-Risk-Index (ET-DRI) was established to estimate outcome after Liver Transplantation (LT). Currently, data on impact of ET-DRI on long-term outcome for different indications and recipient conditions are missing. Retrospective, single-center analysis of long-term graft survival (GS) of 1767 adult primary LTs according to indication, labMELD category (1: <= 18; 2: >18-25; 3: >25-35; 4: >35), and ET-DRI. Mean ET-DRI in our cohort was 1.63 (+/- 0.43). One-, 10, and 15-yr GS was 83.5%, 63.3%, and 54.8%. Long-term GS was significantly influenced by ET-DRI. Accordingly, four ET-DRI categories were defined and analyzed with respect to underlying disease. Significant impact of these categories was observed for: Alcohol, cholestatic/autoimmune diseases (CD/AIH), and HCV, but not for HCC, HBV, cryptogenic cirrhosis, and acute liver failure. labMELD categories showed no significant influence on graft, but on patient survival. Matching ET-DRI categories with labMELD revealed significant differences in long-term GS for labMELDcategories 1, 2, and 3, but not 4. In multivariate analysis, HCV combined with ET-DRI > 2 and labMELDcategory 3 combined with ET-DRI > 2 emerged as negative predictors. To achieve excellent long-term graft survival, higher risk organs (ET-DRI > 1.4) should be used restrictively for patients with CD/AIH or HCV. Organs with ET-DRI > 2 should be avoided in patients with a labMELD of >25-35.
C1 [Schoening, Wenzel; Helbig, Michael; Buescher, Niklas; Andreou, Andreas; Schmitz, Volker; Bahra, Marcus; Puhl, Gero; Pascher, Andreas; Pratschke, Johann; Seehofer, Daniel] Charite, Dept Gen Visceral & Transplantat Surg, Berlin, Germany.
[Schoening, Wenzel] Rhein Westfal TH Aachen, Univ Hosp, Dept General Visceral & Transplantat Surg, Aachen, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
University of Berlin; Charite Universitatsmedizin Berlin; RWTH Aachen
University; RWTH Aachen University Hospital
RP Schoening, W (corresponding author), Charite, Abt F Allgemein Visceral & Transplantat Chirurg, Campus Virchow Klinikum,Augustenburger Pl 1, D-13353 Berlin, Germany.
EM wenzel.schoening@web.de
RI Seehofer, Daniel/X-1933-2019
OI Schoning, Wenzel/0000-0002-0446-5126
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NR 28
TC 17
Z9 17
U1 1
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0902-0063
EI 1399-0012
J9 CLIN TRANSPLANT
JI Clin. Transplant.
PD MAY
PY 2016
VL 30
IS 5
BP 508
EP 517
DI 10.1111/ctr.12714
PG 10
WC Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery; Transplantation
GA DL4LA
UT WOS:000375606100004
PM 26854873
DA 2025-01-07
ER
PT J
AU Plikus, MV
Van Spyk, EN
Pham, K
Geyfman, M
Kumar, V
Takahashi, JS
Andersen, B
AF Plikus, Maksim V.
Van Spyk, Elyse N.
Pham, Kim
Geyfman, Mikhail
Kumar, Vivek
Takahashi, Joseph S.
Andersen, Bogi
TI The Circadian Clock in Skin: Implications for Adult Stem Cells, Tissue
Regeneration, Cancer, Aging, and Immunity
SO JOURNAL OF BIOLOGICAL RHYTHMS
LA English
DT Review
DE skin; stem cells; regeneration; cancer; UV exposure; immunity; aging;
hair follicle; cell cycle; autoimmune diseases
ID TRANSEPIDERMAL WATER-LOSS; BETA-CATENIN ACTIVITY; HAIR CYCLE CLOCK;
DERMAL PAPILLA; SUPRACHIASMATIC NUCLEUS; COMPREHENSIVE GUIDE;
NONINVASIVE METHOD; BARRIER FUNCTION; PROTEIN-1 BMAL1; GENE-EXPRESSION
AB Historically, work on peripheral circadian clocks has been focused on organs and tissues that have prominent metabolic functions, such as the liver, fat, and muscle. In recent years, skin has emerged as a model for studying circadian clock regulation of cell proliferation, stem cell functions, tissue regeneration, aging, and carcinogenesis. Morphologically, skin is complex, containing multiple cell types and structures, and there is evidence for a functional circadian clock in most, if not all, of its cell types. Despite the complexity, skin stem cell populations are well defined, experimentally tractable, and exhibit prominent daily cell proliferation cycles. Hair follicle stem cells also participate in recurrent, long-lasting cycles of regeneration: the hair growth cycles. Among other advantages of skin is a broad repertoire of available genetic tools enabling the creation of cell type-specific circadian mutants. Also, due to the accessibility of skin, in vivo imaging techniques can be readily applied to study the circadian clock and its outputs in real time, even at the single-cell level. Skin provides the first line of defense against many environmental and stress factors that exhibit dramatic diurnal variations such as solar ultraviolet (UV) radiation and temperature. Studies have already linked the circadian clock to the control of UVB-induced DNA damage and skin cancers. Due to the important role that skin plays in the defense against microorganisms, it also represents a promising model system to further explore the role of the clock in the regulation of the body's immune functions. To that end, recent studies have already linked the circadian clock to psoriasis, one of the most common immune-mediated skin disorders. Skin also provides opportunities to interrogate the clock regulation of tissue metabolism in the context of stem cells and regeneration. Furthermore, many animal species feature prominent seasonal hair molt cycles, offering an attractive model for investigating the role of the clock in seasonal organismal behaviors.
C1 [Plikus, Maksim V.; Pham, Kim] Univ Calif Irvine, Dept Dev & Cell Biol, Irvine, CA 92697 USA.
[Plikus, Maksim V.; Pham, Kim] Univ Calif Irvine, Sue & Bill Gross Stem Cell Res Ctr, Irvine, CA 92697 USA.
[Plikus, Maksim V.; Van Spyk, Elyse N.; Andersen, Bogi] Univ Calif Irvine, Ctr Complex Biol Syst, Irvine, CA 92697 USA.
[Van Spyk, Elyse N.; Andersen, Bogi] Univ Calif Irvine, Dept Biol Chem, Irvine, CA 92697 USA.
[Van Spyk, Elyse N.; Andersen, Bogi] Univ Calif Irvine, Dept Med, Div Endocrinol, Irvine, CA 92697 USA.
[Geyfman, Mikhail] Kythera Biopharmaceut, Westlake Village, CA USA.
[Kumar, Vivek; Takahashi, Joseph S.] Univ Texas SW Med Ctr Dallas, Dept Neurosci, Dallas, TX 75390 USA.
[Kumar, Vivek; Takahashi, Joseph S.] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA.
C3 University of California System; University of California Irvine;
University of California System; University of California Irvine;
University of California System; University of California Irvine;
University of California System; University of California Irvine;
University of California System; University of California Irvine;
University of Texas System; University of Texas Southwestern Medical
Center Dallas; Howard Hughes Medical Institute; University of Texas
System; University of Texas Southwestern Medical Center Dallas
RP Andersen, B (corresponding author), Univ Calif Irvine, Sprague Hall,Room 206,839 Hlth Sci Rd, Irvine, CA 92697 USA.
EM bogi@uci.edu
RI Takahashi, Joseph/Y-2781-2019; Kumari, Priyanka/KCY-0528-2024;
Takahashi, Joseph/E-8482-2012
OI Plikus, Maksim/0000-0002-8845-2559; Takahashi,
Joseph/0000-0003-0384-8878
FU National Institutes of Health (NIH) National Institute of Arthritis and
Musculoskeletal and Skin Diseases (NIAMS) [R01-AR067273]; Edward
Mallinckrodt Jr. Foundation grant; National Science Foundation Graduate
Research Fellowship [DGE-1321846]; NIH-NIAMS [R01-AR056439]; National
Center for Advancing Translational Sciences [UL1TR001414] Funding
Source: NIH RePORTER; National Institute of Arthritis and
Musculoskeletal and Skin Diseases [R01AR056439] Funding Source: NIH
RePORTER; Direct For Biological Sciences; Div Of Biological
Infrastructure [1262049] Funding Source: National Science Foundation
FX M.V.P. is supported by National Institutes of Health (NIH) National
Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
grant R01-AR067273 and an Edward Mallinckrodt Jr. Foundation grant.
E.N.V.S. is supported by National Science Foundation Graduate Research
Fellowship DGE-1321846. B.A. is supported by R01-AR056439 from the
NIH-NIAMS.
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NR 143
TC 121
Z9 137
U1 3
U2 85
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0748-7304
EI 1552-4531
J9 J BIOL RHYTHM
JI J. Biol. Rhythms
PD JUN
PY 2015
VL 30
IS 3
BP 163
EP 182
DI 10.1177/0748730414563537
PG 20
WC Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Physiology
GA CI6KP
UT WOS:000354868200001
PM 25589491
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Balan, D
Vartolomei, MD
Magdás, A
Balan-Bernstein, N
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AF Balan, Daniel
Vartolomei, Mihai Dorin
Magdas, Annamaria
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Martha, Orsolya
TI Inflammatory Markers and Thromboembolic Risk in Patients with
Non-Muscle-Invasive Bladder Cancer
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE IMPROVE; neutrophil to lymphocyte ratio; complete blood count;
lymphocyte to monocyte ratio
ID TO-LYMPHOCYTE RATIO; MONOCYTE RATIO; PROGNOSTIC ROLE; NEUTROPHIL;
PROPHYLAXIS; PLATELET
AB Introduction: Patients with bladder cancer have a high risk of venous thrombosis that represents a key challenge for physicians in the decision-making for initiating anticoagulation therapy. Non-muscle-invasive bladder cancer (NMIBC) represents more than 70% of all diagnosed bladder malignancies; therefore, we aimed to evaluate the relationship of the neutrophil to lymphocyte ratio (NLR), lymphocyte to monocyte ratio (LMR), and risk of thrombosis by using the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE) score as well as the risk of bleeding by using the IMPROVE Bleeding Risk Assessment Score in a study cohort. Material and Methods: This was a retrospective observational study involving 130 patients who met the inclusion criteria: age > 18 years, stage pTa-pT1 NMIBC. The exclusion criteria were age < 18 years; stage pT2 or higher; or a presentation of metastasis, inflammatory, liver or autoimmune diseases, or other systemic neoplasms. In order to evaluate the risk of thromboembolic events as well as those of bleeding, the IMPROVE scores were calculated for each patient. Subjects were categorized in a Low IMPROVE group (< 4 points) or a High IMPROVE group. By using uni- and multivariate regression models, we analyzed CBC-derived parameters which could be associated with a higher risk of venous thrombosis in subjects with low or high IMPROVE scores. Results: Patients with IMPROVE score greater than 4 were associated with higher NLR, LMR and lymphocyte values (p < 0.05). In a multivariate regression model, the IMPROVE score was significantly influenced by lymphocyte count (p = 0.007) as well as the NLR value (p < 0.0001). Conclusions: In our study population, subjects with NMIBC with low lymphocytes and NLR > 3 were at a higher risk of developing venous thromboembolic events, reflected by an IMPROVE score of greater than 4. The IMPROVE and IMPROVE Bleeding Risk Assessment Scores are easy to use, and, complemented with the CBC-derived lymphocyte to monocyte ratio as a prothrombotic marker, could aid in the decision of prophylactic anticoagulation therapy during admission.
C1 [Balan, Daniel; Martha, Orsolya] Univ Med Pharm Sci & Technol GE Palade Targu Mure, Dept Urol, Targu Mures 540142, Romania.
[Vartolomei, Mihai Dorin] Vienna Gen Hosp, Urol Dept, A-1090 Vienna, Austria.
[Magdas, Annamaria] Univ Med Pharm Sci & Technol GE Palade Targu Mure, Dept Internal Med, Targu Mures 540142, Romania.
[Balan-Bernstein, Noemi] Mures Cty Hosp, Clin Pneumol, Targu Mures 540103, Romania.
[Voidazan, Septimiu Toader] GE Palade Univ Med Pharm Sci & Technol Targu Mure, Dept Epidemiol, Targu Mures 540142, Romania.
C3 George Emil Palade University of Medicine, Pharmacy, Science, &
Technology of Targu Mures; George Emil Palade University of Medicine,
Pharmacy, Science, & Technology of Targu Mures
RP Magdás, A (corresponding author), Univ Med Pharm Sci & Technol GE Palade Targu Mure, Dept Internal Med, Targu Mures 540142, Romania.
EM balan_dani@yahoo.com; mdvartolomei@yahoo.com; anamaria.magdas@umfst.ro;
b.noemi47@gmail.com; septimiu.voidazan@umfst.ro; orsim@hotmail.com
RI Magdas, Annamaria/AAB-9124-2020; Vartolomei, Mihai Dorin/AAJ-6864-2021;
Martha, Orsolya/AAG-1786-2020; voidazan, septimiu/GLR-2294-2022;
Vartolomei, Mihai Dorin/AAH-9338-2019
OI Vartolomei, Mihai Dorin/0000-0002-0359-8517; Balan,
Daniel/0000-0003-2331-2886; Lorand-Tibor, Reman/0009-0008-6311-8248
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NR 32
TC 2
Z9 2
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD NOV
PY 2021
VL 10
IS 22
AR 5270
DI 10.3390/jcm10225270
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA XF7YG
UT WOS:000724283400001
PM 34830552
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Magnadóttir, B
Hayes, P
Gísladóttir, B
Bragason, BD
Hristova, M
Nicholas, AP
Guomundsdóttir, S
Lange, S
AF Magnadottir, Bergljot
Hayes, Polly
Gisladottir, Berglind
Bragason, Birkir Thor
Hristova, Mariya
Nicholas, Anthony P.
Gudmundsdottir, Sigridur
Lange, Sigrun
TI Pentraxins CRP-I and CRP-II are post-translationally deiminated and
differ in tissue specificity in cod (Gadus morhua L.) ontogeny
SO DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY
LA English
DT Article
DE Pentraxin (CRP, SAP); Protein deimination; Mucosal immunity; Amyloid;
Autoimmunity; Cod (Gadus morhua L.); Ontogeny
ID C-REACTIVE-PROTEIN; AMYLOID-P-COMPONENT; ACUTE-PHASE RESPONSE; TROUT
ONCORHYNCHUS-MYKISS; SAP-LIKE PENTRAXIN; ARGININE DEIMINASES;
IMMUNE-RESPONSE; INNATE IMMUNITY; PEPTIDYLARGININE DEIMINASES; BINDING
CHARACTERISTICS
AB Pentraxins are fluid phase pattern recognition molecules that form an important part of the innate immune defence and are conserved between fish and human. In Atlantic cod (Gadus morhua L.), two pentraxin-like proteins have been described, CRP-I and CRP-II. Here we show for the first time that these two CRP forms are post-translationally deiminated (an irreversible conversion of arginine to citrulline) and differ with respect to tissue specific localisation in cod ontogeny from 3 to 84 days post hatching. While both forms are expressed in liver, albeit at temporally differing levels, CRP-I shows a strong association with nervous tissue while CRP-II is strongly associated to mucosal tissues of gut and skin. This indicates differing roles for the two pentraxin types in immune responses and tissue remodelling, also elucidating novel roles for CRP-I in the nervous system. The presence of deimination positive bands for cod CRPs varied somewhat between mucus and serum, possibly facilitating CRP protein moonlighting, allowing the same protein to exhibit a range of biological functions and thus meeting different functional requirements in different tissues. The presented findings may further current understanding of the diverse roles of pentraxins in teleost immune defences and tissue remodelling, as well as in various human pathologies, including autoimmune diseases, amyloidosis and cancer.
C1 [Magnadottir, Bergljot; Gisladottir, Berglind; Bragason, Birkir Thor; Gudmundsdottir, Sigridur] Univ Iceland, Inst Expt Pathol, Keldur v Vesturlandsveg 112, Reykjavik, Iceland.
[Hayes, Polly] Univ Westminster, Dept Biomed Sci, London W1W 6UW, England.
[Hristova, Mariya] UCL, EGA Inst Womens Hlth, Perinatal Brain Protect & Repair Grp, London WC1E 6HX, England.
[Nicholas, Anthony P.] Univ Alabama Birmingham, Dept Neurol, UAB Stn, Birmingham, AL 35294 USA.
[Lange, Sigrun] Univ Westminster, Dept Biomed Sci, Tissue Architecture & Regenerat Res Grp, London W1W 6UW, England.
C3 University of Iceland; University of Westminster; University of London;
University College London; University of Alabama System; University of
Alabama Birmingham; University of Westminster
RP Lange, S (corresponding author), Univ Westminster, Dept Biomed Sci, Tissue Architecture & Regenerat Res Grp, London W1W 6UW, England.
EM bergmagn@hi.is; P.Hayes@westminster.ac.uk; berglindg@gmail.com;
birkirbr@hi.is; m.hristova@ucl.ac.uk; anicholas@uabmc.edu; siggag@hi.is;
S.Lange@westminster.ac.uk
RI ; Bragason, Birkir THor (Thor)/L-7404-2015
OI Lange, Sigrun/0000-0002-7193-3102; Bragason, Birkir THor
(Thor)/0000-0002-3962-8036
FU Icelandic Research Council (RANNIS); EC grant Fishaid
[QLK2-CT-2000-01076]; University of Westminster
FX Thanks are due to Matthias Oddgeirsson, Agnar Steinarsson and other
staff the staff at the Marine Institutes Mariculture Laboratory, Staour
Grindavik, Iceland for providing sampling facilities and the fish. The
authors also thank Margret Jonsdottir, Keldur, Institute for
Experimental Pathology University of Iceland, for cod larvae sample
preparation. This work was partly supported by The Icelandic Research
Council (RANNIS), EC grant Fishaid QLK2-CT-2000-01076 and a University
of Westminster start-up grant to SL. The authors declare no competing
interest.
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Yasojima K, 2001, AM J PATHOL, V158, P1039, DOI 10.1016/S0002-9440(10)64051-5
NR 130
TC 30
Z9 30
U1 0
U2 5
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0145-305X
EI 1879-0089
J9 DEV COMP IMMUNOL
JI Dev. Comp. Immunol.
PD OCT
PY 2018
VL 87
BP 1
EP 11
DI 10.1016/j.dci.2018.05.014
PG 11
WC Fisheries; Immunology; Veterinary Sciences; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Fisheries; Immunology; Veterinary Sciences; Zoology
GA GQ9BB
UT WOS:000442059800001
PM 29777721
OA Green Published, Green Accepted, hybrid
DA 2025-01-07
ER
PT J
AU Vogt, J
Sheinson, D
Katavolos, P
Irimagawa, H
Tseng, M
Alatsis, KR
Proctor, WR
AF Vogt, Jennifer
Sheinson, Daniel
Katavolos, Paula
Irimagawa, Hiroko
Tseng, Min
Alatsis, Kathila R.
Proctor, William R.
TI Variance component analysis of circulating miR-122 in serum from healthy
human volunteers
SO PLOS ONE
LA English
DT Article
ID INDUCED LIVER-INJURY; EMERGING BIOMARKERS; STATISTICS NOTES; MICRORNAS;
EXPRESSION; INFLAMMATION; TRANSLATION; METABOLISM; MARKERS;
AMINOTRANSFERASE
AB Micro-RNA (miR)-122 is a promising exploratory biomarker for detecting liver injury in preclinical and clinical studies. Elevations in serum or plasma have been associated with viral and autoimmune hepatitis, non-alcoholic steatohepatitis (NASH), hepatocellular carcinoma, and drug-induced liver injury (DILI). However, these associations were primarily based upon population differences between the disease state and the controls. Thus, little is known about the variability and subsequent variance components of circulating miR-122 in healthy humans, which has implications for the practical use of the biomarker clinically. To address this, we set out to perform variance components analysis of miR-122 in a cohort of 40 healthy volunteers. Employing a quantitative real-time polymerase chain reaction (qRT-PCR) assay to detect miR-122 and other circulating miRNAs in human serum, the relative expression of miR-122 was determined using two different normalization approaches: to the mean expression of a panel of several endogenous miRNAs identified using an adaptive algorithm (miRA-Norm) and to the expression of an exogenous miRNA control (Caenorhabditis elegans miR-39). Results from a longitudinal study in healthy volunteers (N = 40) demonstrated high variability with 117- and 111-fold 95% confidence reference interval, respectively. This high variability of miR-122 in serum appeared to be due in part to ethnicity, as 95% confidence reference intervals were approximately three-fold lower in volunteers that identified as Caucasian relative to those that identified as Non-Caucasian. Variance analysis revealed equivalent contributions of intra- and inter-donor variability to miR-122. Surprisingly, miR-122 exhibited the highest variability compared to other 36 abundant miRNAs in circulation; the next variable miRNA, miR-133a, demonstrated a 45- to 62-fold reference interval depending on normalization approaches. In contrast, alanine aminotransferase (ALT) activity levels in this population exhibited a 5-fold total variance, with 80% of this variance due to inter-donor sources. In conclusion, miR-122 demonstrated higher than expected variability in serum from healthy volunteers, which has implications for its potential utility as a prospective biomarker of liver damage or injury.
C1 [Vogt, Jennifer; Katavolos, Paula; Irimagawa, Hiroko; Tseng, Min; Alatsis, Kathila R.; Proctor, William R.] Genentech Inc, Dept Safety Assessment, San Francisco, CA 94080 USA.
[Sheinson, Daniel] Genentech Inc, Nonclin Biostat, San Francisco, CA 94080 USA.
[Sheinson, Daniel] Genentech Inc, US Med Affairs, San Francisco, CA 94080 USA.
[Irimagawa, Hiroko] Theravance, Dept Pharmacol, San Francisco, CA USA.
C3 Roche Holding; Genentech; Roche Holding; Genentech; Roche Holding;
Genentech; Theravance
RP Proctor, WR (corresponding author), Genentech Inc, Dept Safety Assessment, San Francisco, CA 94080 USA.
EM proctorw@gene.com
OI Tseng, Min/0009-0007-1088-6510; Katavolos, Paula/0000-0001-7923-5328
FU Genentech, Inc.
FX Funding for this study was provided by Genentech, Inc., a member of the
Roche Group. All authors listed on this manuscript were employees of
Genentech during the planning, experimentation, and writing phases of
this manuscript. Hiroko Irimagawa is now a current employee of
Theravance Biopharma. Theravance did not provide funding in any manner
to this project/manuscript in regards to salaries, reagents, facilities,
or other means during the preparation, data generation, or writing of
this manuscript. The funding organization (e.g. Genentech, Inc.)
provided support in the form of salaries, instrumentation, facilities,
supplies, and other components of operations associated with this
manuscript. Genentech, Inc., did not have any additional role in the
study design, data collection and analysis, decision to publish, or
preparation of the manuscript. The specific roles of these authors are
articulated in the "author contributions" section.
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NR 62
TC 10
Z9 11
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD JUL 26
PY 2019
VL 14
IS 7
AR e0220406
DI 10.1371/journal.pone.0220406
PG 26
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA IW4WC
UT WOS:000484979500034
PM 31348817
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Crawford, JM
AF Crawford, JM
TI Evidence-based interpretation of liver biopsies
SO LABORATORY INVESTIGATION
LA English
DT Review
DE evidence based medicine; liver pathology; hepatitis; surgical pathology;
steatohepatitis; hepatopathology
ID CHRONIC HEPATITIS-C; INTERFERON-ALPHA-2B PLUS RIBAVIRIN;
INTERNATIONAL-AUTOIMMUNE-HEPATITIS; HUMAN-IMMUNODEFICIENCY-VIRUS;
NONALCOHOLIC FATTY LIVER; EVIDENCE-BASED MEDICINE; ANATOMIC PATHOLOGY;
HEPATOCELLULAR-CARCINOMA; QUALITY-ASSURANCE; INITIAL TREATMENT
AB Evidence based medicine' is a paradigm introduced in the 1990s in which collection of clinical data in a reproducible and unbiased way is intended to guide clinical decision-making. This paradigm has been promulgated across the spectrum of medicine, but with more limited critical analysis in the realm of pathology. The `evidence base' in support of our practices in Anatomic Pathology is a critical issue, given the key role that such diagnoses play in patient management decisions. The question is, 'On what basis are diagnostic opinions rendered in Anatomic Pathology?' The operative question becomes, 'What is the published literature that supports our anatomic pathology interpretations?' This second question was applied to the published literature in Hepatopathology, by identifying the 'citation classics' of this discipline. Specifically, the top 150 most-cited liver pathology articles were analyzed for: authorship; journal of publication; type of publication; and year of publication. Results are as follows. First, it is indeed true that the preeminent hepatopathologists of the age are the most cited authors in the 'top 150'. Second, the most cited articles in hepatopathology are not published in the pathology literature, but are instead published in much higher impact clinical journals. Third, the pathology of viral hepatitis is demonstrated to be extraordinarily well-grounded in 'evidence based medicine'. Much of the remainder of the hepatopathology literature falls into a 'narrative based' paradigm, which is the rigorous reporting of case experience without statistical clinical outcomes validation. Finally, the years of publication reflect, on the one hand, a vigorous recent literature in the pharmaceutical treatment of viral hepatitis, and on the other, a broadly distributed set of 'narrative' articles from the 1960s, 1970s, 1980s, and 1990s. In conclusion, the discipline of hepatopathology appears to be well-grounded in 'evidence based medicine' in the realm of viral hepatitis. The remainder of our discipline rests predominantly upon the time-honored identification of disease process through the publication of narrative case series.
C1 Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, Gainesville, FL 32610 USA.
C3 State University System of Florida; University of Florida
RP Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, POB 100275, Gainesville, FL 32610 USA.
EM crawford@pathology.ufl.edu
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NR 78
TC 16
Z9 17
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
EI 1530-0307
J9 LAB INVEST
JI Lab. Invest.
PD APR
PY 2006
VL 86
IS 4
BP 326
EP 334
DI 10.1038/labinvest.3700403
PG 9
WC Medicine, Research & Experimental; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pathology
GA 030WM
UT WOS:000236665900001
PM 16554749
OA Bronze
DA 2025-01-07
ER
PT J
AU Kasamatsu, T
AF Kasamatsu, Tetsuhiro
TI Implications of Senescent T Cells for Cancer Immunotherapy
SO CANCERS
LA English
DT Review
DE therapy-induced cellular senescence; T-cell senescence; PD-1
ID HEPATOCELLULAR-CARCINOMA; CELLULAR SENESCENCE; ANTITUMOR-ACTIVITY;
DNA-DAMAGE; B7 FAMILY; RECEPTOR; EXPRESSION; EXHAUSTION; SIGNATURE;
BLOOD
AB Simple Summary Senescent T cells are defective in proliferation and effector functions, and they accumulate owing to aging, chronic viral infections, and autoimmune diseases. Several DNA-damaging chemotherapeutic agents, such as melphalan and doxorubicin, induce senescence in cancer cells. However, it is unclear whether these agents induce senescence in T cells. We evaluated whether sublethal doses of melphalan and doxorubicin induce cellular senescence in human peripheral blood mononuclear cell-derived T cells from healthy donors. Our results demonstrate that therapy-induced cellular senescence is also induced in T cells and that PD-1 may be a biomarker for therapy-induced senescent T cells. In this review, we discuss the characteristics of senescent T-cells, including therapy-induced senescent T-cells. In addition, we investigate whether therapy-induced cellular senescence has positive and/or negative effects on T cells.Abstract T-cell senescence is thought to result from the age-related loss of the ability to mount effective responses to pathogens and tumor cells. In addition to aging, T-cell senescence is caused by repeated antigenic stimulation and chronic inflammation. Moreover, we demonstrated that T-cell senescence was induced by treatment with DNA-damaging chemotherapeutic agents. The characteristics of therapy-induced senescent T (TIS-T) cells and general senescent T cells are largely similar. Senescent T cells demonstrate an increase in the senescence-associated beta-galactosidase-positive population, cell cycle arrest, secretion of senescence-associated secretory phenotypic factors, and metabolic reprogramming. Furthermore, senescent T cells downregulate the expression of the co-stimulatory molecules CD27 and CD28 and upregulate natural killer cell-related molecules. Moreover, TIS-T cells showed increased PD-1 expression. However, the loss of proliferative capacity and decreased expression of co-stimulatory molecules associated with T-cell senescence cause a decrease in T-cell immunocompetence. In this review, we discuss the characteristics of senescent T-cells, including therapy-induced senescent T cells.
C1 [Kasamatsu, Tetsuhiro] Gunma Univ, Dept Lab Sci, Grad Sch Hlth Sci, 3-39-22 Showa Machi, Maebashi, Gunma 3718514, Japan.
C3 Gunma University
RP Kasamatsu, T (corresponding author), Gunma Univ, Dept Lab Sci, Grad Sch Hlth Sci, 3-39-22 Showa Machi, Maebashi, Gunma 3718514, Japan.
EM kasamatsu@gunma-u.ac.jp
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NR 110
TC 1
Z9 1
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD DEC
PY 2023
VL 15
IS 24
AR 5835
DI 10.3390/cancers15245835
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DH0H8
UT WOS:001131015700001
PM 38136380
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Hou, YL
Ding, WY
Wu, PS
Liu, CQ
Ding, LN
Liu, JJ
Wang, XL
AF Hou, Yanli
Ding, Wenyu
Wu, Peishan
Liu, Changqing
Ding, Lina
Liu, Junjun
Wang, Xiaolei
TI Adipose-derived stem cells alleviate liver injury induced by type 1
diabetes mellitus by inhibiting mitochondrial stress and attenuating
inflammation
SO STEM CELL RESEARCH & THERAPY
LA English
DT Article
DE Type 1 diabetes mellitus; Liver injury; Adipose-derived stem cells;
Mitochondrial stress; Inflammation; Immune regulation
ID OXIDATIVE STRESS; PERMEABILITY TRANSITION; HEPATIC STEATOSIS; PROTECTIVE
ROLE; DISEASE; FIBROSIS; STEATOHEPATITIS; PATHOGENESIS; NEPHROPATHY;
DAMAGE
AB Background Type 1 diabetes mellitus (T1D) is a worldwide health priority due to autoimmune destruction and is associated with an increased risk of multiorgan complications. Among these complications, effective interventions for liver injury, which can progress to liver fibrosis and hepatocellular carcinoma, are lacking. Although stem cell injection has a therapeutic effect on T1D, whether it can cure liver injury and the underlying mechanisms need further investigation. Methods Sprague-Dawley rats with streptozotocin (STZ)-induced T1D were treated with adipose-derived stem cell (ADSC) or PBS via the tail vein formed the ADSC group or STZ group. Body weights and blood glucose levels were examined weekly for 6 weeks. RNA-seq and PCR array were used to detect the difference in gene expression of the livers between groups. Results In this study, we found that ADSCs injection alleviated hepatic oxidative stress and injury and improved liver function in rats with T1D; potential mechanisms included cytokine activity, energy metabolism and immune regulation were potentially involved, as determined by RNA-seq. Moreover, ADSC treatment altered the fibroblast growth factor 21 (FGF21) and transforming growth factor beta (TGF-beta) levels in T1D rat livers, implying its repair capacity. Disordered intracellular energy metabolism, which is closely related to mitochondrial stress and dysfunction, was inhibited by ADSC treatment. PCR array and ingenuity pathway analyses suggested that the ADSC-induced suppression of mitochondrial stress is related to decreased necroptosis and apoptosis. Moreover, mitochondria-related alterations caused liver inflammation, resulting in liver injury involving the T lymphocyte-mediated immune response. Conclusions Overall, these results improve our understanding of the curative effect of ADSCs on T1D complications: ADSCs attenuate liver injury by inhibiting mitochondrial stress (apoptosis and dysfunctional energy metabolism) and alleviating inflammation (inflammasome expression and immune disorder). These results are important for early intervention in liver injury and for delaying the development of liver lesions in patients with T1D.
C1 [Hou, Yanli; Ding, Wenyu; Wu, Peishan; Liu, Changqing; Ding, Lina; Liu, Junjun; Wang, Xiaolei] Shandong First Med Univ, Shandong First Med Univ & Shandong Acad Med Sci, Endocrine & Metab Dis Hosp, Jinan, Peoples R China.
[Wu, Peishan] Shandong First Med Univ, Jinan, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
Sciences; Shandong First Medical University & Shandong Academy of
Medical Sciences
RP Wang, XL (corresponding author), Shandong First Med Univ, Shandong First Med Univ & Shandong Acad Med Sci, Endocrine & Metab Dis Hosp, Jinan, Peoples R China.
EM daturawing@163.com
OI Wang, Xiaolei/0000-0002-6950-4309; Hou, Yanli/0000-0002-6333-9453
FU China National Natural Science Foundation [81900736]; Shandong Province
"Double-HunInnovation Project of Shandong Academy of Medical Sciences
[2019-11]; Shandong Provincial Natural Science Foundation [ZR2016HP20,
WST2018004]
FX This work was funded by the China National Natural Science Foundation
(81900736), Shandong Province "Double-HunInnovation Project of Shandong
Academy of Medical Sciences (2019-11) and Shandong Provincial Natural
Science Foundation (ZR2016HP20).uction (WST2018004), the
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NR 75
TC 19
Z9 19
U1 1
U2 23
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1757-6512
J9 STEM CELL RES THER
JI Stem Cell Res. Ther.
PD APR 1
PY 2022
VL 13
IS 1
AR 132
DI 10.1186/s13287-022-02760-z
PG 16
WC Cell & Tissue Engineering; Cell Biology; Medicine, Research &
Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA 0G8OE
UT WOS:000778298400002
PM 35365229
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Nikolaev, B
Yakovleva, L
Fedorov, V
Yudintceva, N
Ryzhov, V
Marchenko, Y
Ischenko, A
Zhakhov, A
Dobrodumov, A
Combs, SE
Gao, HL
Shevtsov, M
AF Nikolaev, Boris
Yakovleva, Ludmila
Fedorov, Viacheslav
Yudintceva, Natalia
Ryzhov, Vyacheslav
Marchenko, Yaroslav
Ischenko, Alexander
Zhakhov, Alexander
Dobrodumov, Anatoliy
Combs, Stephanie E.
Gao, Huile
Shevtsov, Maxim
TI Magnetic Relaxation Switching Assay Using IFNα-2b-Conjugated
Superparamagnetic Nanoparticles for Anti-Interferon Antibody Detection
SO BIOSENSORS-BASEL
LA English
DT Article
DE interferon; IFN & alpha;-2b; anti-INF & alpha;-2b antibodies;
nanoparticles; SPIONs; magnetic resonance imaging; nanosensor; magnetic
relaxation switching assay
ID IRON-OXIDE NANOPARTICLES; ANTIVIRAL PEPTIDE NANOCOMPLEXES;
MONOCLONAL-ANTIBODIES; INTERFERON; AUTOANTIBODIES; THERAPY; DEXTRAN;
ANTIGEN; SYSTEM; TARGET
AB Type I interferons, particularly IFNa-2b, play essential roles in eliciting adaptive and innate immune responses, being implicated in the pathogenesis of various diseases, including cancer, and autoimmune and infectious diseases. Therefore, the development of a highly sensitive platform for analysis of either IFNa-2b or anti-IFNa-2b antibodies is of high importance to improve the diagnosis of various pathologies associated with the IFNa-2b disbalance. For evaluation of the anti-IFNa-2b antibody level, we have synthesized superparamagnetic iron oxide nanoparticles (SPIONs) coupled with the recombinant human IFNa-2b protein (SPIONs@IFNa-2b). Employing a magnetic relaxation switching assay (MRSw)-based nanosensor, we detected picomolar concentrations (0.36 pg/mL) of anti-INFa-2b antibodies. The high sensitivity of the real-time antibodies' detection was ensured by the specificity of immune responses and the maintenance of resonance conditions for water spins by choosing a high-frequency filling of short radio-frequency pulses of the generator. The formation of a complex of the SPIONs@IFNa-2b nanoparticles with the anti-INFa-2b antibodies led to a cascade process of the formation of nanoparticle clusters, which was further enhanced by exposure to a strong (7.1 T) homogenous magnetic field. Obtained magnetic conjugates exhibited high negative MR contrast-enhancing properties (as shown by NMR studies) that were also preserved when particles were administered in vivo. Thus, we observed a 1.2-fold decrease of the T2 relaxation time in the liver following administration of magnetic conjugates as compared to the control. In conclusion, the developed MRSw assay based on SPIONs@IFNa-2b nanoparticles represents an alternative immunological probe for the estimation of anti-IFNa-2b antibodies that could be further employed in clinical studies.
C1 [Nikolaev, Boris; Yakovleva, Ludmila; Fedorov, Viacheslav; Yudintceva, Natalia; Shevtsov, Maxim] Russian Acad Sci RAS, Lab Biomed Nanotechnol, Inst Cytol, Tikhoretsky Ave 4, St Petersburg 194064, Russia.
[Fedorov, Viacheslav; Yudintceva, Natalia; Shevtsov, Maxim] Almazov Natl Med Res Ctr, Personalized Med Ctr, Akkuratova Str 2, St Petersburg 197341, Russia.
[Fedorov, Viacheslav] St Petersburg State Univ Vet Med, Dept Inorgan Chem & Biophys, Chernigovskaya Str 5, St Petersburg 196084, Russia.
[Ryzhov, Vyacheslav; Marchenko, Yaroslav] Natl Res Ctr Kurchatov Inst, Petersburg Nucl Phys Inst, Gatchina 188300, Russia.
[Ischenko, Alexander; Zhakhov, Alexander] St Petersburg Pasteur Inst, Lab Hybridoma Technol, Mira Str 14, St Petersburg 197101, Russia.
[Dobrodumov, Anatoliy] Russian Acad Sci RAS, Dept Nucl Magnet Resonance, Inst Macromol Cpds, Bolshoi pr 31, St Petersburg 199004, Russia.
[Combs, Stephanie E.; Shevtsov, Maxim] Technishe Univ Munchen TUM, Dept Radiat Oncol, Klinikum Rechts Isar, Ismaninger Str 22, D-81675 Munich, Germany.
[Gao, Huile] Sichuan Univ, West China Sch Pharm, Key Lab Drug Targeting & Drug Delivery Syst, Educ Minist, Chengdu 610041, Peoples R China.
[Shevtsov, Maxim] Far Eastern Fed Univ, Lab Biomed Cell Technol, Vladivostok 690091, Russia.
C3 Russian Academy of Sciences; St. Petersburg Scientific Centre of the
Russian Academy of Sciences; Institute of Cytology RAS; Almazov National
Medical Research Centre; St. Petersburg State University of Veterinary
Medicine; National Research Centre - Kurchatov Institute; Petersburg
Nuclear Physics Institute; Saint-Petersburg Pasteur Institute; Russian
Academy of Sciences; Institute of Macromolecular Compounds of the
Russian Academy of Sciences; Technical University of Munich; Sichuan
University; Far Eastern Federal University
RP Shevtsov, M (corresponding author), Russian Acad Sci RAS, Lab Biomed Nanotechnol, Inst Cytol, Tikhoretsky Ave 4, St Petersburg 194064, Russia.; Shevtsov, M (corresponding author), Almazov Natl Med Res Ctr, Personalized Med Ctr, Akkuratova Str 2, St Petersburg 197341, Russia.; Shevtsov, M (corresponding author), Technishe Univ Munchen TUM, Dept Radiat Oncol, Klinikum Rechts Isar, Ismaninger Str 22, D-81675 Munich, Germany.; Shevtsov, M (corresponding author), Far Eastern Fed Univ, Lab Biomed Cell Technol, Vladivostok 690091, Russia.
EM yudintceva@mail.ru; ryzhov_va@pnpi.nrcki.ru; maxim.shevtsov@tum.de
RI Yudintceva, Natalia/N-5393-2016; Dobrodumov, Anatoliy/JCO-3292-2023;
gao, huile/G-8290-2012; Shevtsov, Maxim/U-8830-2019
FU Ministry of Science and Higher Education of the Russian Federation
[075-15-2022-301]
FX This work was financially supported by the Ministry of Science and
Higher Education of the Russian Federation (Agreement No.
075-15-2022-301).
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NR 71
TC 1
Z9 1
U1 17
U2 32
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2079-6374
J9 BIOSENSORS-BASEL
JI Biosensors-Basel
PD JUN
PY 2023
VL 13
IS 6
AR 624
DI 10.3390/bios13060624
PG 24
WC Chemistry, Analytical; Nanoscience & Nanotechnology; Instruments &
Instrumentation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Instruments &
Instrumentation
GA K7JS1
UT WOS:001018171100001
PM 37366989
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Srivastava, S
Rasool, M
AF Srivastava, Susmita
Rasool, Mahaboobkhan
TI Underpinning IL-6 biology and emphasizing selective JAK blockade as the
potential alternate therapeutic intervention for rheumatoid arthritis
SO LIFE SCIENCES
LA English
DT Review
DE Interleukin 6; Rheumatoid arthritis; JAK inhibitors; Momelotinib (CYT
387)
ID COLLAGEN-INDUCED ARTHRITIS; ANTI-INTERLEUKIN-6 MONOCLONAL-ANTIBODY;
NF-KAPPA-B; BREAST-CANCER; SYNOVIAL FIBROBLASTS; VX-509 DECERNOTINIB;
SIGNALING PATHWAY; ANIMAL-MODELS; OPEN-LABEL; INTERLEUKIN-6
AB Interleukin 6 (IL-6), a pleiotropic inflammatory cytokine, is produced transiently due to tissue damage and infections. Nonetheless, IL-6 contributes to the host regenerative defense mechanism via classical signaling at the basal physiological level. Although tightly regulated transcriptional and post-transcriptional mechanism modulates its expression, dysregulated continual production of IL-6 during inflammatory conditions negatively affects immune cells. Molecular evidence has substantiated the pernicious out-turn of IL-6 trans-signaling in developing one such autoimmune joint disorder, rheumatoid arthritis (RA). Significantly increased levels of IL-6 in RA, along with multiple growth factors mainly released by synovial-like fibroblasts (FLS) and macrophages, is crucial for clinical disease progression. Due to its pathogenicity, in mediating inflammation and context-driven signaling cassette, blockade of IL-6 could be a potent target in the therapeutic intervention of RA. The clinical trials of various humanized IL-6 and anti-IL-6 receptor antibodies have proved their efficacy. However, severe side effects like neutropenia, thrombocytopenia, and abnormal liver enzymes contributed to dysfunctional adaptive immunity. The JAK-STAT pathway has been majorly implicated in RA disease progression upon IL-6 stimulation, simultaneously paving the path for innovative therapeutic approaches. JAK inhibitors, namely Tofacitinib, Baricitinib, Decernotinib, Upadacitinib, Peficitinib, and Filgotinib, have demonstrated clinical efficacy in recent decades as an alternative therapeutic strategy to abrogate IL-6 mediated aberrant activity in RA. This approach substitutes for the side effects incurred due to the IL-6 targeted therapies. This review discusses the history of research into IL-6 biology and therapies that target the IL-6 driven JAK/STAT pathway, including the successes, challenges, and drawbacks, emphasizing RA.
C1 [Srivastava, Susmita; Rasool, Mahaboobkhan] Vellore Inst Technol VIT, Sch Biosci & Technol, Immunopathol Lab, SMV 240, Vellore 632014, Tamil Nadu, India.
C3 Vellore Institute of Technology (VIT); VIT Vellore
RP Rasool, M (corresponding author), Vellore Inst Technol VIT, Sch Biosci & Technol, Immunopathol Lab, SMV 240, Vellore 632014, Tamil Nadu, India.
EM rasool.m@vit.ac.in
OI Srivastava, Susmita/0000-0002-0707-8279
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NR 118
TC 17
Z9 17
U1 1
U2 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD JUN 1
PY 2022
VL 298
AR 120516
DI 10.1016/j.lfs.2022.120516
EA APR 2022
PG 14
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 1C6JW
UT WOS:000793223900002
PM 35367240
DA 2025-01-07
ER
PT J
AU Nanda, NK
AF Nanda, Navreet K.
TI Tissue-Resident Memory T Cells: Sheltering-in-Place for Host Defense
SO CRITICAL REVIEWS IN IMMUNOLOGY
LA English
DT Article
DE tissue-resident memory T cells; T-RM; memory T cells; immunity; host
defense; vaccine; autoimmunity; influenza; tuberculosis; leishmaniasis;
psoriasis; vitiligo; multiple sclerosis; MS
ID MULTIPLE-SCLEROSIS; LEISHMANIA-MAJOR; HUMAN NEURONS; RM CELLS; LUNG;
PROTECTION; INFECTION; VITILIGO; SKIN; VULNERABILITY
AB A silent revolution has occurred in our understanding of how T cell-mediated immunity protects the host from recrudescent pathogens and how it fits into occurrences of autoimmunity and allergies. Under the new paradigm, the hitherto unknown noncirculatory, tissue-resident memory T cells (T-RM) constitute the host defense sentinels posted in diverse anatomic compartments and they are the key actors in protection against reinfection, tissue surveillance, cancer, and in many cases in autoimmunity and allergy in both animal models and humans. This contrasts with the previously held view that circulating memory T cells (T-circM) transitioning through the peripheral tissue are the main defenders against reinfection and are underlying agents in autoimmune reactions. T-RM, elicited after primary pathogen encounter in a given tissue, are now known to be stably positioned in the respective bather (skin, lungs, gut, female reproductive tract mucosa, liver, etc.) or nonbanier (brain, kidneys, etc.) peripheral tissues. T-RM represent a rapid, tissue-autonomous, first line of robust adaptive immune defense against recurring infections. Following a discussion on the defining characteristics of T-RM, this review will focus on how T-RM seeding and induction at the site of recurrent pathogen invasion is now, and must continue to be, the governing principle in new vaccine designs. The review will also elaborate on the role of T-RM in relapsing and remitting autoimmunity by being prepositioned in the tissue as potent effectors. Many infectious disease vaccines targeted to establish and activate T-RM at the infection site in animal models are robustly more effective at host protection relative to their traditional, parenterally administered counterparts that only activate systemic T-circM. Likewise, T-RM-centered remedies are being successful in ameliorating T cell mediated autoimmunity in cases in which approaches based on circulatory T cells failed. Thus, the current and emerging T-RM discoveries are piloting a new era of T-RM-driven strategies focused on activation or inactivation of tissue-localized immunity in vaccines and therapies targeting infectious disease, cancer, autoimmunity, and allergies.
C1 [Nanda, Navreet K.] 12808 Sutherby Lane, Germantown, MD 20874 USA.
[Nanda, Navreet K.] NIH, Intracellular Parasite Biol Sect, Lab Parasit Dis, 4 Mem Dr, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA
RP Nanda, NK (corresponding author), 12808 Sutherby Lane, Germantown, MD 20874 USA.
EM Navreetn2000@yahoo.com
RI Nanda, Navreet/AAJ-5035-2021
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NR 86
TC 2
Z9 2
U1 1
U2 6
PU BEGELL HOUSE INC
PI DANBURY
PA 50 NORTH ST, DANBURY, CT 06810 USA
SN 1040-8401
EI 2162-6472
J9 CRIT REV IMMUNOL
JI Crit. Rev. Immunol.
PY 2020
VL 40
IS 5
SI SI
BP 423
EP 440
DI 10.1615/CritRevImmunol.2020035522
PG 18
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA PS3OZ
UT WOS:000607836300010
PM 33463954
DA 2025-01-07
ER
PT J
AU Desai, PN
Patel, CN
Kabrawala, MV
Mehta, RM
Nandwani, SK
Prajapati, R
Patel, N
Parekh, KK
AF Desai, Pankaj N.
Patel, Chintan N.
Kabrawala, Mayank V.
Mehta, Rajiv M.
Nandwani, Subhash K.
Prajapati, Ritesh
Patel, Nisharg
Parekh, Krishna K.
TI Use of n-Butyl 2 Cyanoacrylate without Lipiodol, Using a Modified
Protocol in Gastric Variceal Bleed Management: Retrospective Analysis of
2299 Patients
SO JOURNAL OF DIGESTIVE ENDOSCOPY
LA English
DT Article
DE cyanoacrylate glue; gastric varices; variceal bleed
AB Aim To assess the feasibility and amount of cyanoacrylate glue that can be injected safely per session, complications, and long-term results in GOV1, GOV2 and IGV1 varices, using a modified method.
Method All patients from October 2008 to December 2019 presenting to us with variceal bleeding were included. We injected 0.5 mL of cyanoacrylate glue followed by 1.5 mL to 3 mL distilled water in all GOV 1, GOV 2 and IGV varices. Number of glues used were not restricted. Esophageal variceal ligation (EVL) was done for esophageal varices. Follow-up was done at 4 weeks and 3 to 6 months and analyzed.
Results 2299 patients received therapy. Male:female, 69%:31%. Causes of varices-cirrhosis (84.9%) and extrahepatic portal vein obstruction (EHPVO) (15.1%). Causes of cirrhosis-alcohol (38.4%), nonalcoholic fatty liver disease (NAFLD) (29%), hepatitis B (19.9%), hepatitis C (10.1%), Wilson's disease (1.8%), and autoimmune diseases (0.9%). As much as 41.1% had blood in stomach and 10.2% had active spurt on index endoscopy. As much as 14.5% required endotracheal intubation (active bleed [53.1%], encephalopathy [40.5%], respiratory distress [6.6%]). As much as 30.9% had GOV1 + GOV2, 1.5% had GOV2 + IGV1, 21.3% had GOV1 + IGV1 and 16.4% had GOV1 + GOV2 + IGV1. Hemostasis could be achieved in 99.2% on index endoscopy. A total of 18 (0.8%) patients had uncontrolled bleed of whom 10 (55.6%) had hepatocellular carcinoma. Ongoing bleed was treated with transjugular intrahepatic portosystemic shunt (TIPSS) (61.1%) and endoscopic ultrasound (EUS)-guided coiling (38.8%). Amount of glue required for gastric variceal obturation was 3.6 on index endoscopy, 1.6 on follow-up at 4 to 6 weeks, and 1.2 at 3 months follow up. Glue extrusion with ulcers were seen in 6.4% at 4 to 6 weeks and 4.3% at 3 months. Rebleed occurred in 2.1% and 0.7% patients before 4 weeks and 3 months follow-up, respectively. As much as 1.3% and 1.2% patients were lost to follow-up before 4 weeks and 3 months follow-up sessions, respectively. Complications include pulmonary aspiration in 0.9% and bleeding from ulcers 2.8%. No evidence of pulmonary embolism was seen. In two endoscopic procedures, glue splashing into operator's eyes occurred. Incidents of needle getting stuck in the varix occurred in three patients.
Conclusions Our modified protocol for glue in gastric varices is safe and feasible, as it has less rebleed, no pulmonary embolism and less ulcers with glue extrusion as compared with available literature.
C1 [Desai, Pankaj N.; Patel, Chintan N.; Kabrawala, Mayank V.] Surat Inst Digest Sci SIDS, Dept Endoscopy & Endosonog, Ring Rd, Surat 395002, India.
[Mehta, Rajiv M.; Nandwani, Subhash K.; Prajapati, Ritesh; Patel, Nisharg] Surat Inst Digest Sci SIDS, Dept Gastroenterol, Surat, India.
[Parekh, Krishna K.] Surat Inst Digest Sci SIDS, Dept Clin Res, Surat, India.
RP Desai, PN (corresponding author), Surat Inst Digest Sci SIDS, Dept Endoscopy & Endosonog, Ring Rd, Surat 395002, India.
EM drp_desai@hotmail.com
RI Prajapati, Ritesh/JPX-1823-2023
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NR 17
TC 3
Z9 3
U1 0
U2 0
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0976-5042
EI 0976-5050
J9 J DIG ENDOSC
JI J. Dig. Endosc.
PD SEP
PY 2020
VL 11
IS 3
BP 187
EP 192
DI 10.1055/s-0040-1716447
PG 6
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA QF6XO
UT WOS:000617037500003
OA gold
DA 2025-01-07
ER
PT J
AU Bukhari, T
Jafri, L
Majid, H
Ahmed, S
Khan, AHH
Abid, S
Raza, A
Siddiqui, I
AF Bukhari, Tayyaba
Jafri, Lena
Majid, Hafsa
Ahmed, Sibtain
Khan, Aysha Habib H.
Abid, Shahab
Raza, Aniqa
Siddiqui, Imran
TI Diagnostic Accuracy of the Forns Score for Liver Cirrhosis in Patients
With Chronic Viral Hepatitis
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE liver; fibroscan; cirrhosis; hepatitis b; hepatitis c; bilirubin; forns
score
ID GLOBAL BURDEN; FIBROSIS; MARKERS; DISEASE; MORTALITY; INDEX
AB Introduction
Liver cirrhosis is an irreversible and end-stage disease. It results from chronic liver damage characterized by the replacement of normal liver tissue by fibrosis, leading to the progressive loss of liver function. Making an early diagnosis of cirrhosis is important for patients with chronic hepatitis because early antiviral therapy can prevent the progression of cirrhosis and even induce regression. There have been efforts to develop surrogate markers for liver cirrhosis as the biopsy is invasive, costly, and difficult to standardize.
Methods
This was a cross-sectional study conducted at the Section of Chemical Pathology, the Department of Pathology and Laboratory Medicine in Collaboration with the Section of Gastroenterology, Department of Medicine, the Aga Khan University, from January to December 2018. A total of 90 patients (>18 years of age) with a history of chronic viral hepatitis, who were attending the FibroScan (R) (Echosens, Paris, France) clinic were included. Patients with a history of autoimmune liver diseases and hepatocellular carcinoma were excluded from the study. Blood samples withdrawn were analyzed on ADVIA Centaur (R) (Siemens Healthineers, Erlangen, Germany), and Forns scores were calculated based on the following four parameters: patient age, total cholesterol, gamma-glutamyl transferase (GGT), and platelet count.
Results
The median age of the patients was 38.5 years [interquartile range (IQR): 21]. Among the study population, 59 (65.6%) were males and 31 (34.4%) were females; 26 patients showed reactivity for hepatitis B surface antigen (HBsAg), and 63 patients were found chronic with hepatitis C virus (HCV). The proportion of HCV was observed to be higher as compared with that of Hepatitis B virus (HBV). Nineteen patients were found to have jaundice and only one patient had ascites. An Area Under the Receiver Operating Curve (AUROC) was generated to determine the diagnostic accuracy of the Forns score. It was observed that the Forn score value of >7.110 had an AUROC of 0.9928 (95% CI: 0.9821-1.003, p-value: <0.001) with a sensitivity of 100% (95% CI: 91.19-100.0%) and specificity of 94% (95% CI: 83.45-98.75%), with a higher positive likelihood ratio of 16.67.
Conclusion
This study found the Forns score to be sensitive and specific in diagnosing liver cirrhosis in patients with chronic hepatitis. The Forns score at a cutoff of 7.11 is highly sensitive as well as a specific noninvasive method that can be used to ascertain the status of fibrosis in chronic hepatitis patients.
C1 [Bukhari, Tayyaba; Jafri, Lena; Majid, Hafsa; Ahmed, Sibtain; Khan, Aysha Habib H.; Raza, Aniqa; Siddiqui, Imran] Aga Khan Univ Hosp, Pathol & Lab Med, Karachi, Pakistan.
[Abid, Shahab] Aga Khan Univ Hosp, Gastroenterol, Karachi, Pakistan.
C3 Aga Khan University; Aga Khan University
RP Jafri, L (corresponding author), Aga Khan Univ Hosp, Pathol & Lab Med, Karachi, Pakistan.
EM lena.jafri@aku.edu
RI Khan, Abdul/B-1005-2010
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NR 23
TC 2
Z9 2
U1 0
U2 1
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD APR 13
PY 2021
VL 13
IS 4
AR e14477
DI 10.7759/cureus.14477
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA RN8AP
UT WOS:000640574200033
PM 33996335
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Overbye, A
Sætre, F
Hagen, LK
Johansen, HT
Seglen, PO
AF Overbye, Anders
Saetre, Frank
Hagen, Linda Korseberg
Johansen, Harald Thidemann
Seglen, Per O.
TI Autophagic activity measured in whole rat hepatocytes as the
accumulation of a novel BHMT fragment (p10), generated in amphisomes by
the asparaginyl proteinase, legumain
SO AUTOPHAGY
LA English
DT Article
DE AJN-230; ammonia; amphisome; autophagy; betaine:homocysteine
methyltransferase; liver; hepatocyte; legumain; leupeptin; lysosome;
proteinase; proteolytic processing; proteomics; rat
ID BETAINE-HOMOCYSTEINE METHYLTRANSFERASE; S-METHYLTRANSFERASE; MONITORING
AUTOPHAGY; ANTIGEN PRESENTATION; AGGREGATED PROTEINS; MAMMALIAN
LEGUMAIN; CATHEPSIN-L; DEGRADATION; LIVER; INHIBITION
AB To investigate the stepwise autophagic-lysosomal processing of hepatocellular proteins, the abundant cytosolic enzyme, betaine: homocysteine methyltransferase (BHMT) was used as a probe. Full-length (45 kDa) endogenous BHMT was found to be cleaved in an autophagy-dependent (3-methyladenine-sensitive) manner in isolated rat hepatocytes to generate a novel N-terminal 10-kDa fragment (p10) identified and characterized by mass spectrometry. The cleavage site was consistent with cleavage by the asparaginyl proteinase, legumain and indeed a specific inhibitor of this enzyme (AJN-230) was able to completely suppress p10 formation in intact cells, causing instead accumulation of a 42-kDa intermediate. To prevent further degradation of p10 or p42 by the cysteine proteinases present in autophagic vacuoles, the proteinase inhibitor leupeptin had to be present. Asparagine, an inhibitor of amphisome-lysosome fusion, did not detectably impede either p42 or p10 formation, indicating that BHMT processing primarily takes place in amphisomes rather than in lysosomes. Lactate dehydrogenase (LDH) was similarly degraded primarily in amphisomes by leupeptin-sensitive proteolysis, but some additional leupeptin-resistant LDH degradation in lysosomes was also indicated. The autophagic sequestration of BHMT appeared to be nonselective, as the accumulation of p10 (in the presence of leupeptin) or of its precursors (in the additional presence of AJN-230) proceeded at approximately the same rate as the model autophagic cargo, LDH. The complete lack of a cytosolic background makes p10 suitable for use in a "fragment assay" of autophagic activity in whole cells.
Incubation of hepatocytes with ammonium chloride, which neutralizes amphisomes as well as lysosomes, caused rapid, irreversible inhibition of legumain activity and stopped all p10 formation. The availability of several methods for selective targeting of legumain in intact cells may facilitate functional studies of this enigmatic enzyme, and perhaps suggest novel ways to reduce its contribution to cancer cell metastasis or autoimmune disease.
C1 [Overbye, Anders; Saetre, Frank; Hagen, Linda Korseberg; Seglen, Per O.] Oslo Univ Hosp, Norwegian Radium Hosp, Dept Cell Biol, Inst Canc Res, Oslo, Norway.
[Johansen, Harald Thidemann] Univ Oslo, Sch Pharm, Dept Pharmaceut Biosci, Oslo, Norway.
C3 University of Oslo; University of Oslo
RP Seglen, PO (corresponding author), Oslo Univ Hosp, Norwegian Radium Hosp, Dept Cell Biol, Inst Canc Res, Oslo, Norway.
EM Per.O.Seglen@rr-research.no
RI Hagen, Linda/KJK-9594-2024
OI Johansen, Harald Thidemann/0000-0001-6617-1732
FU Norwegian Cancer Society; South-Eastern Norway Regional Health Authority
FX This work has been generously supported by The Norwegian Cancer Society
and by the South-Eastern Norway Regional Health Authority. The excellent
technical assistance provided by Berit Elin Nedrebo and Abir Ahmad is
gratefully acknowledged.
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NR 86
TC 20
Z9 21
U1 0
U2 7
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD SEP
PY 2011
VL 7
IS 9
BP 1011
EP 1027
DI 10.4161/auto.7.9.16436
PG 17
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 814SI
UT WOS:000294477100008
PM 21610319
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Holzapfel, N
Zhang, AMY
Choi, WJ
Denroche, R
Jang, G
Dodd, A
Bucur, R
Wilson, J
Sapisochin, G
Notta, F
Grant, RC
Gallinger, S
Knox, JJ
O'Kane, GM
AF Holzapfel, Nicholas
Zhang, Amy
Choi, Woo-Jin
Denroche, Robert
Jang, Gunho
Dodd, Anna
Bucur, Roxana
Wilson, Julie
Sapisochin, Gonzalo
Notta, Faiyaz
Grant, Robert C.
Gallinger, Steven
Knox, Jennifer J.
O'Kane, Grainne M.
TI Whole-genome sequencing of 20 cholangiocarcinoma cases reveals unique
profiles in patients with cirrhosis and primary sclerosing cholangitis
br
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Cholangiocarcinoma (CCA); liver cirrhosis; primary sclerosing
cholangitis (PSC); whole genome sequencing (WGS)
ID MUTATIONAL SIGNATURES
AB Background: Cholangiocarcinoma (CCA) is a molecularly heterogenous disease that is often fatal. Whole genome sequencing (WGS) can provide additional knowledge of mutational spectra compared with panel sequencing. We describe the molecular landscape of CCA using whole-genome sequencing and compare the mutational landscape between short-term and long-term survivors. Methods: We explored molecular differences between short-term and long-term survivors by performing WGS on 20 patient samples from our biliary tract cancer database. Short-term survivors were enriched for cases with underlying primary sclerosing cholangitis (PSC) and patients with cirrhosis. All samples underwent tumour epithelial enrichment using laser capture microdissection (LCM).Results: Dominant single base substitution (SBS) signatures across the cohort included SBS1 and SBS5, with the latter more prevalent in long-term survivors. SBS17 was evident in 3 cases, all of whom had underlying ulcerative colitis (UC) with PSC. Additional rare signatures included SBS3 in a patient treated for prior mantle cell lymphoma and SBS26/SBS6 in a patient with a tumor mutational burden of 33 mutations/Mb and a pathogenic MLH1 germline mutation. Somatic TP53 inactivating mutations were present in 8/10 (80%) short-term survivors and in none of the long-term survivors. Additional mutations occurred in KRAS, SMAD4, CDKN2A, and chromatin remodelling genes. The long-term survivor group harboured predicted fusions in FGFR (n=2) and pathogenic mutations in BRAF and IDH1 (n=2).Conclusions:TP53 alterations are associated with poor outcomes in patients with CCA. Patients with underlying inflammatory/autoimmune conditions may be enriched for unique tumour mutational signatures
C1 [Holzapfel, Nicholas; Dodd, Anna; Bucur, Roxana; Grant, Robert C.; Knox, Jennifer J.; O'Kane, Grainne M.] Princess Margaret Canc Ctr, Dept Med Oncol & Hematol, Toronto, ON, Canada.
[Zhang, Amy; Denroche, Robert; Jang, Gunho; Wilson, Julie; Notta, Faiyaz; Gallinger, Steven] Ontario Inst Canc Res, Toronto, ON, Canada.
[Choi, Woo-Jin; Sapisochin, Gonzalo; Gallinger, Steven] Univ Toronto, Dept Surg, Toronto, ON, Canada.
[O'Kane, Grainne M.] Princess Margaret Canc Ctr, 610 Univ Ave, Toronto, ON M5G 2C1, Canada.
C3 University of Toronto; University Health Network Toronto; Princess
Margaret Cancer Centre; University of Toronto; Ontario Institute for
Cancer Research; University of Toronto; University of Toronto;
University Health Network Toronto; Princess Margaret Cancer Centre
RP O'Kane, GM (corresponding author), Princess Margaret Canc Ctr, 610 Univ Ave, Toronto, ON M5G 2C1, Canada.
EM Grainne.O'Kane@uhn.ca
RI Gallinger, Steven/E-4575-2013
OI O'Kane, Grainne M./0000-0002-8690-403X
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NR 40
TC 2
Z9 2
U1 0
U2 5
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD FEB 28
PY 2023
VL 14
IS 1
BP 379
EP +
DI 10.21037/jgo-22-676
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA G9XK0
UT WOS:000992597200012
PM 36915452
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Dar, AA
Fehaid, A
Alkhatani, S
Alarifi, S
Alqahtani, WS
Albasher, G
Almeer, R
Alfarraj, S
Moneim, AEA
AF Dar, A. A.
Fehaid, A.
Alkhatani, S.
Alarifi, S.
Alqahtani, W. S.
Albasher, G.
Almeer, R.
Alfarraj, S.
Moneim, A. E. Abdel
TI The protective role of luteolin against the methotrexate-induced
hepato-renal toxicity via its antioxidative, anti-inflammatory, and
anti-apoptotic effects in rats
SO HUMAN & EXPERIMENTAL TOXICOLOGY
LA English
DT Article
DE Methotrexate; luteolin; oxidative stress; apoptosis; inflammation;
hepato-renal toxicity
AB Methotrexate (MTX) is frequently used drug in treatment of cancer and autoimmune diseases. Unfortunately, MTX has many side effects including the hepato-renal toxicity. In this study, we hypothesized that Luteolin (Lut) exhibits protective effect against the MTX-induced hepato-renal toxicity. In order to investigate our hypothesis, the experiment was designed to examine the effect of exposure of male rats to MTX (20 mg/kg, i.p., at day 9) alone or together with Lut (50 mg/kg, oral for 14 days) compared to the control rats (received saline). The findings demonstrated that MTX treatment induced significant increases in the liver and kidney functions markers in serum samples including Aspartate transaminase (AST), Alanine transaminase (ALT), creatinine, urea and uric acid. MTX also mediated an oxidative stress expressed by elevated malondialdehyde (MDA) level and decreased level of reduced glutathione (GSH), antioxidant enzyme activities, and downregulation of the Nrf2 gene expression as an antioxidant trigger. Moreover, the inflammatory markers (NF-kappa B, TNF-alpha, and IL-1 beta) were significantly elevated upon MTX treatment. In addition, MTX showed an apoptotic response mediated by elevating the pro-apoptotic (Bax) and lowering the anti-apoptotic (Bcl-2) proteins. All of these changes were confirmed by the observed alterations in the histopathological examination of the hepatic and renal tissues. Lut exposure significantly reversed all the MTX-induced changes in the measured parameters suggesting its potential protective role against the MTX-induced toxicity. Finally, our findings concluded the antioxidative, anti-inflammatory and anti-apoptotic effects of Lut as a mechanism of its protective role against the MTX-induced hepato-renal toxicity in rats.
C1 [Dar, A. A.] Shaanxi Univ Sci & Technol, Sch Environm Sci & Engn, Xian, Peoples R China.
[Fehaid, A.] Mansoura Univ, Forens Med & Toxicol Dept, Fac Vet Med, Dakahlia, Egypt.
[Alkhatani, S.; Alarifi, S.; Alqahtani, W. S.; Albasher, G.; Almeer, R.; Alfarraj, S.] King Saud Univ, Coll Sci, Dept Zool, Riyadh, Saudi Arabia.
[Moneim, A. E. Abdel] Helwan Univ, Fac Sci, Dept Zool & Entomol, Cairo 11795, Egypt.
C3 Shaanxi University of Science & Technology; Egyptian Knowledge Bank
(EKB); Mansoura University; King Saud University; Egyptian Knowledge
Bank (EKB); Helwan University
RP Moneim, AEA (corresponding author), Helwan Univ, Fac Sci, Dept Zool & Entomol, Cairo 11795, Egypt.
EM aest1977@hotmail.com
RI Al-Qahtani, Wedad/ABH-7132-2020; Dar, Afzal/AAA-4297-2021; Alfarraj,
Saleh/AHE-7705-2022; ALARIFI, SAUD/N-4992-2015; fehaid,
alaa/P-4607-2018; Moneim, Ahmed/C-7461-2012
OI Abdel Moneim, Ahmed/0000-0002-2654-2591; ALARIFI,
SAUD/0000-0002-3613-5228; Dar, Afzal Ahmed/0000-0001-8823-4829; Fehaid,
Alaa/0000-0001-7759-663X; Al-Qahtani, Wedad Saeed/0000-0002-7347-9804
FU King Saud University, Riyadh, Saudi Arabia [RSP-2020/95]
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This work
was supported by King Saud University, Riyadh, Saudi Arabia (Research
Supporting Project number: RSP-2020/95).
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NR 40
TC 27
Z9 28
U1 1
U2 16
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0960-3271
EI 1477-0903
J9 HUM EXP TOXICOL
JI Hum. Exp. Toxicol.
PD JUL
PY 2021
VL 40
IS 7
BP 1194
EP 1207
AR 0960327121991905
DI 10.1177/0960327121991905
EA FEB 2021
PG 14
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA SN0FH
UT WOS:000636513200001
PM 33530773
DA 2025-01-07
ER
PT J
AU Shahoei, SH
Kim, YC
Cler, SJ
Ma, LQ
Anakk, S
Kemper, JK
Nelson, ER
AF Shahoei, Sayyed Hamed
Kim, Young-Chae
Cler, Samuel J.
Ma, Liqian
Anakk, Sayeepriyadarshini
Kemper, Jongsook K.
Nelson, Erik R.
TI Small Heterodimer Partner Regulates Dichotomous T Cell Expansion by
Macrophages
SO ENDOCRINOLOGY
LA English
DT Article
ID ORPHAN NUCLEAR RECEPTOR; NEGATIVE FEEDBACK-REGULATION; SHP; CHOLESTEROL;
METABOLISM; GENE; 27-HYDROXYCHOLESTEROL; MECHANISMS; REPRESSION;
EXPRESSION
AB The involvement of small heterodimer partner (SHP) in the inhibition of hepatic bile acid synthesis from cholesterol has been established. However, extrahepatic expression of SHP implies that SHP may have regulatory functions other than those in the liver. Here, we find that SHP mRNA expression is high in murine bone marrow cells, suggesting a physiological role within macrophages. Indeed, expression of SHP in macrophages decreases the transcriptional activity and nuclear localization of nuclear factor kappa B, whereas downregulation of SHP has the opposite effects. Expression of genes associated with macrophage-T cell crosstalk were altered by overexpression or downregulation of SHP. Intriguingly, increasing SHP expression in macrophages resulted in decreased T cell expansion, a hallmark of T cell activation, whereas knockdown of SHP resulted in increased expansion. Analyses of the expanded T cells revealed a dichotomous skewing between effector T cells and regulatory T cells (T-regs), with SHP overexpression reducing Tregs and downregulation of SHP increasing their expansion. The expanded T-regs were confirmed to be suppressive via adoptive transfers. IL-2 and TGF-beta, known inducers of T-reg differentiation, were found to be regulated by SHP. Furthermore, SHP occupancy at the promoter region of IL-2 was increased after macrophages were challenged with lipopolysaccharide. Neutralizing antibodies to IL-2 and TGF-b inhibited the expansion of T-regs mediated by downregulation of SHP. This study demonstrates that expression and activity of SHP within macrophages can alter T cell fate and identifies SHP as a potential therapeutic target for autoimmune diseases or solid cancers.
C1 [Shahoei, Sayyed Hamed; Kim, Young-Chae; Cler, Samuel J.; Ma, Liqian; Anakk, Sayeepriyadarshini; Kemper, Jongsook K.; Nelson, Erik R.] Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA.
[Anakk, Sayeepriyadarshini; Kemper, Jongsook K.; Nelson, Erik R.] Univ Illinois, Canc Ctr Illinois, Urbana, IL 61801 USA.
[Nelson, Erik R.] Univ Illinois, Div Nutr Sci, Urbana, IL 61801 USA.
[Nelson, Erik R.] Univ Illinois, Canc Ctr, Chicago, IL 60612 USA.
[Nelson, Erik R.] Univ Illinois, Carl R Woese Inst Genom Biol, Anticanc Discovery Pets People Theme, Urbana, IL 61801 USA.
C3 University of Illinois System; University of Illinois Urbana-Champaign;
University of Illinois System; University of Illinois Urbana-Champaign;
University of Illinois System; University of Illinois Urbana-Champaign;
University of Illinois System; University of Illinois Chicago;
University of Illinois Chicago Hospital; University of Illinois System;
University of Illinois Urbana-Champaign
RP Nelson, ER (corresponding author), Univ Illinois, 407 South Goodwin Ave,MC 114, Urbana, IL 61801 USA.
EM enels@illinois.edu
RI Nelson, Erik/U-2697-2019; Nelson, Erik Russell/B-5158-2013
OI Ma, Liqian/0000-0002-0264-9263; Nelson, Erik
Russell/0000-0002-8887-1905; Kim, Young-Chae/0000-0002-5130-4413
FU National Cancer Institute of the National Institutes of Health
[R00CA172357, R01CA234025]; Department of Defense Breast Cancer Research
Program [BC171214]; American Heart Association scientist development
award [16SDG27570006]; National Institutes of Health, National Institute
of Diabetes and Digestive and Kidney Diseases [R01DK62777, R01DK95842,
R01DK113080]; American Heart Association (AHA) [16SDG27570006] Funding
Source: American Heart Association (AHA)
FX This work was supported by grants to E.R.N. from the National Cancer
Institute of the National Institutes of Health (R00CA172357,
R01CA234025) and from the Department of Defense Breast Cancer Research
Program (BC171214). This study was also supported in part by an American
Heart Association scientist development award (16SDG27570006) to Y.-C.K.
and grants from the National Institutes of Health, National Institute of
Diabetes and Digestive and Kidney Diseases (R01DK62777 and R01DK95842 to
J.K.K., and R01DK113080 to S.A.).
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NR 57
TC 9
Z9 10
U1 0
U2 2
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD JUL
PY 2019
VL 160
IS 7
BP 1573
EP 1589
DI 10.1210/en.2019-00025
PG 17
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA IS7FV
UT WOS:000482316600002
PM 31050726
OA Bronze, Green Published
DA 2025-01-07
ER
PT J
AU Gatselis, NK
Goet, JC
Zachou, K
Lammers, WJ
Janssen, HLA
Hirschfield, G
Corpechot, C
Lindor, KD
Invernizzi, P
Mayo, MJ
Battezzati, PM
Floreani, A
Pares, A
Lygoura, V
Nevens, F
Mason, AL
Kowdley, KV
Ponsioen, CY
Bruns, T
Thorburn, D
Verhelst, X
Harms, MH
van Buuren, HR
Hansen, BE
Dalekos, GN
AF Gatselis, Nikolaos K.
Goet, Jorn C.
Zachou, Kalliopi
Lammers, Willem J.
Janssen, Harry L. A.
Hirschfield, Gideon
Corpechot, Christophe
Lindor, Keith D.
Invernizzi, Pietro
Mayo, Marlyn J.
Battezzati, Pier Maria
Floreani, Annarosa
Pares, Albert
Lygoura, Vasiliki
Nevens, Frederik
Mason, Andrew L.
Kowdley, Kris V.
Ponsioen, Cyriel Y.
Bruns, Tony
Thorburn, Douglas
Verhelst, Xavier
Harms, Maren H.
van Buuren, Henk R.
Hansen, Bettina E.
Dalekos, George N.
CA Global Primary Biliary Cholangitis
TI Factors Associated With Progression and Outcomes of Early Stage Primary
Biliary Cholangitis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Autoimmune Liver Disease; Prognostic Factor; Antimitochondrial
Antibodies; UDCA
ID URSODEOXYCHOLIC ACID; FOLLOW-UP; BIOCHEMICAL RESPONSE; RISK
STRATIFICATION; FREE SURVIVAL; CIRRHOSIS; COHORT; RATIO; PROGNOSIS;
BILIRUBIN
AB BACKGROUND & AIMS: Patients usually receive a diagnosis of primary biliary cholangitis (PBC) at an early stage, based on biochemical analyses. We investigated the proportion of patients who progress to moderate or advanced PBC and factors associated with progression and patient survival.
METHODS: We obtained data from 1615 patients (mean age, 55.4 y) with early stage PBC (based on their normal levels of albumin and bilirubin), collected at the time of initial evaluation or treatment, from the Global PBC Study Group database (comprising patients at 19 liver centers in North American and European countries). We collected data from health care evaluations on progression to moderate PBC (abnormal level of bilirubin or albumin) or advanced-stage PBC (abnormal level of both). The median follow-up time was 7.9 years. The composite end point was decompensation, hepatocellular carcinoma, liver transplantation, or death.
RESULTS: Of the 1615 patients identified with early stage PBC, 904 developed moderate PBC and 201 developed advanced disease over the study period. The proportions of patients who transitioned to moderate PBC at 1, 3, and 5 years were 12.9%, 30.2%, and 45.8%. The proportions of these patients who then transitioned to advanced PBC at 1, 3, and 5 years later were 3.4%, 12.5%, and 16.0%, respectively. During the follow-up period, 236 patients had a clinical event. The proportions of patients with moderate PBC and event-free survival were 97.9%, 95.1%, and 91.5% at 1, 3, and 5 years, respectively, and the proportions of patients with advanced PBC and event-free survival were 90.6%, 71.2%, and 58.3% at 1, 3, and 5 years later, respectively. Variables associated with transition from early to moderate PBC included baseline levels of bilirubin, albumin, and alkaline phosphatase; aspartate to alanine aminotransferase ratio; platelet count; and treatment with ursodeoxycholic acid. Transitions from early to moderate PBC and from moderate to advanced PBC were associated with higher probabilities of a clinical event (time-dependent hazard ratios, 3.0; 95% CI, 2.0-4.5; and 4.6; 95% CI, 3.5-6.2).
CONCLUSIONS: Approximately half of patients with early stage PBC progress to a more severe stage within 5 years. Progression is associated with an increased risk of a clinical event, so surveillance is important for patients with early stage PBC.
C1 [Gatselis, Nikolaos K.; Zachou, Kalliopi; Lygoura, Vasiliki; Dalekos, George N.] Thessaly Univ, Sch Med, Dept Med, Panepistimiou 3, Biopolis 41500, Larissa, Greece.
[Gatselis, Nikolaos K.; Zachou, Kalliopi; Lygoura, Vasiliki; Dalekos, George N.] Thessaly Univ, Sch Med, Res Lab Internal Med, Panepistimiou 3, Biopolis 41500, Larissa, Greece.
[Goet, Jorn C.; Lammers, Willem J.; Harms, Maren H.; van Buuren, Henk R.; Hansen, Bettina E.] Erasmus MC, Gastroenterol & Hepatol, Rotterdam, Netherlands.
[Janssen, Harry L. A.; Hansen, Bettina E.] Univ Toronto, Toronto Gen Hosp, Toronto Ctr Liver Dis, Toronto, ON, Canada.
[Hirschfield, Gideon] Univ Birmingham, NIHR, Biomed Res Unit, Birmingham, W Midlands, England.
[Hirschfield, Gideon] Univ Birmingham, Ctr Liver Res, Birmingham, W Midlands, England.
[Corpechot, Christophe] Hop St Antoine, Ctr Reference Malad Inflammatoires Voies Biliaire, Paris, France.
[Lindor, Keith D.] Mayo Clin, Dept Gastroenterol & Hepatol, Rochester, MN USA.
[Lindor, Keith D.] Arizona State Univ, Phoenix, AZ USA.
[Invernizzi, Pietro; Lygoura, Vasiliki] Univ Milano Bicocca, Div Gastroenterol, Milan, Italy.
[Invernizzi, Pietro; Lygoura, Vasiliki] Univ Milano Bicocca, Ctr Autoimmune Liver Dis, Dept Med & Surg, Milan, Italy.
[Mayo, Marlyn J.] Univ Texas Southwestern Med Ctr Dallas, Digest & Liver Dis, Dallas, TX 75390 USA.
[Battezzati, Pier Maria] Univ Milan, Dept Hlth Sci, Milan, Italy.
[Floreani, Annarosa] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
[Pares, Albert] Univ Barcelona, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Inst Invest Biomed August Pi i Sunyer IDIBAPS, Liver Unit,Hosp Clin, Barcelona, Spain.
[Nevens, Frederik] Katholieke Univ KU Leuven, Univ Hosp Leuven, Dept Hepatol, Leuven, Belgium.
[Mason, Andrew L.] Univ Alberta, Div Gastroenterol & Hepatol, Edmonton, AB, Canada.
[Kowdley, Kris V.] Swedish Med Ctr, Liver Care Network, Seattle, WA USA.
[Ponsioen, Cyriel Y.] Acad Med Ctr, Dept Gastroenterol & Hepatol, Amsterdam, Netherlands.
[Bruns, Tony] Friedrich Schiller Univ, Jena Univ Hosp, Dept Internal Med 4, Jena, Germany.
[Bruns, Tony] Rheinisch Westfalische Tech Hsch RWTH Aachen, Univ Hosp, Dept Med 3, Aachen, Germany.
[Thorburn, Douglas] Royal Free Hosp, Sheila Sherlock Liver Ctr, London, England.
[Verhelst, Xavier] Ghent Univ Hosp, Dept Gastroenterol & Hepatol, Ghent, Belgium.
[Hansen, Bettina E.] Univ Toronto, Inst Hlth Policy Management & Evaluat, Toronto, ON, Canada.
C3 Erasmus University Rotterdam; Erasmus MC; University of Toronto;
University Health Network Toronto; Toronto General Hospital; University
of Birmingham; University of Birmingham; Assistance Publique Hopitaux
Paris (APHP); Sorbonne Universite; Hopital Universitaire Saint-Antoine -
APHP; Mayo Clinic; Arizona State University; Arizona State
University-Downtown Phoenix; University of Milano-Bicocca; University of
Milano-Bicocca; University of Texas System; University of Texas
Southwestern Medical Center Dallas; University of Milan; University of
Padua; CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD;
University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; KU
Leuven; University Hospital Leuven; University of Alberta; Swedish
Medical Center; University of Amsterdam; Academic Medical Center
Amsterdam; Friedrich Schiller University of Jena; RWTH Aachen
University; RWTH Aachen University Hospital; University of London;
University College London; Royal Free London NHS Foundation Trust; UCL
Medical School; Ghent University; Ghent University Hospital; University
of Toronto
RP Gatselis, NK (corresponding author), Thessaly Univ, Sch Med, Dept Med, Panepistimiou 3, Biopolis 41500, Larissa, Greece.; Gatselis, NK (corresponding author), Thessaly Univ, Sch Med, Res Lab Internal Med, Panepistimiou 3, Biopolis 41500, Larissa, Greece.
EM gatselis@me.com
RI Kiemeney, Lambertus/D-3357-2009; Hirschfield, Gideon/M-2143-2015;
Verhelst, Xavier/ABF-6965-2021; Invernizzi, Pietro/AAB-8367-2022; Bruns,
Tony/C-5720-2011; Lammers, Willem/P-5456-2014; Pares, Albert/G-1328-2011
OI Bruns, Tony/0000-0002-5576-6914; Gatselis, Nikolaos/0000-0002-3715-8640;
Lammers, Willem/0000-0002-5455-5242; Pares, Albert/0000-0002-5413-9687;
Verhelst, Xavier/0000-0002-2798-5415; Janssen,
Harry/0000-0003-2398-8392; Goet, Jorn/0000-0002-6054-569X
FU Intercept Pharmaceuticals - Foundation for Liver and Gastrointestinal
Research (a not-for-profit foundation) in Rotterdam, The Netherlands
FX This investigator-initiated study was supported by unrestricted grants
from Intercept Pharmaceuticals and was funded by the Foundation for
Liver and Gastrointestinal Research (a not-for-profit foundation) in
Rotterdam, The Netherlands. The supporting parties had no influence on
the study design, data collection and analyses, writing of the
manuscript, or the decision to submit the manuscript for publication.
CR [Anonymous], 1987, Statistical analysis with missing data
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van der Meer AJ, 2017, HEPATOLOGY, V66, p155A
NR 28
TC 18
Z9 21
U1 0
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD MAR
PY 2020
VL 18
IS 3
BP 684
EP +
DI 10.1016/j.cgh.2019.08.013
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA KN2EJ
UT WOS:000514653800030
PM 31419573
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Drozd, M
Pujades-Rodriguez, M
Lillie, PJ
Straw, S
Morgan, AW
Kearney, MT
Witte, KK
Cubbon, RM
AF Drozd, Michael
Pujades-Rodriguez, Mar
Lillie, Patrick J.
Straw, Sam
Morgan, Ann W.
Kearney, Mark T.
Witte, Klaus K.
Cubbon, Richard M.
TI Non-communicable disease, sociodemographic factors, and risk of death
from infection: a UK Biobank observational cohort study
SO LANCET INFECTIOUS DISEASES
LA English
DT Article
ID SOCIAL DETERMINANTS; HEALTH; POPULATION; MORTALITY; COVID-19
AB Background Non-communicable diseases (NCDs) have been highlighted as important risk factors for COVID-19 mortality. However, insufficient data exist on the wider context of infectious diseases in people with NCDs. We aimed to investigate the association between NCDs and the risk of death from any infection before the COVID-19 pandemic (up to Dec 31, 2019).
Methods For this observational study, we used data from the UK Biobank observational cohort study to explore factors associated with infection death. We excluded participants if data were missing for comorbidities, body-mass index, smoking status, ethnicity, and socioeconomic deprivation, and if they were lost to follow-up or withdrew consent. Deaths were censored up to Dec 31, 2019. We used Poisson regression models including NCDs present at recruitment to the UK Biobank (obesity [defined by use of body-mass index] and self-reported hypertension, chronic heart disease, chronic respiratory disease, diabetes, cancer, chronic liver disease, chronic kidney disease, previous stroke or transient ischaemic attack, other neurological disease, psychiatric disorder, and chronic inflammatory and autoimmune rheumatological disease), age, sex, ethnicity, smoking status, and socioeconomic deprivation. Separate models were constructed with individual NCDs replaced by the total number of prevalent NCDs to define associations with multimorbidity. All analyses were repeated with non-infection-related death as an alternate outcome measure to establish differential associations of infection death and non-infection death. Associations are reported as incidence rate ratios (IRR) accompanied by 95% CIs.
Findings After exclusion of 9210 (1.8%) of the 502 505 participants in the UK Biobank cohort, our study sample comprised 493 295 individuals. During 5 273 731 person-years of follow-up (median 10.9 years [IQR 10.1-11.6] per participant), 27 729 deaths occurred, of which 1385 (5%) were related to infection. Advancing age, male sex, smoking, socioeconomic deprivation, and all studied NCDs were independently associated with the rate of both infection death and non-infection death. Compared with White ethnicity, a pooled Black, Asian, and minority ethnicity group was associated with a reduced risk of infection death (IRR 0.64, 95% CI 0.46-0.87) and non-infection death (0.80, 0.75-0.86). Stronger associations with infection death than with non-infection death were observed for advancing age (age 65 years vs 45 years: 7.59, 95% CI 5.92-9.73, for infection death vs 5.21, 4.97-5.48, for noninfection death), current smoking (vs never smoking: 3.69, 3.19-4.26, vs 2.52, 2.44-2.61), socioeconomic deprivation (most vs least deprived quintile: 2.13, 1.78-2.56, vs 1.38, 1.33-1.43), class 3 obesity (vs non-obese: 2.21, 1.74-2.82, vs 1.55, 1.44-1.66), hypertension (1.36, 1.22-1.53, vs 1.15, 1.12-1.18), respiratory disease (2.21, 1.96-2.50, vs 1.28, 1.24-1.32), chronic kidney disease (5.04, 4.28-7.31, vs 2.50, 2.20-2.84), psychiatric disease (1.56, 1.30-1.86, vs 1.23, 1.18-1.29), and chronic inflammatory and autoimmune rheumatological disease (2.45, 1.99-3.02, vs 1.41, 1.32-1.51). Accrual of multimorbidity was also more strongly associated with risk of infection death (five or more comorbidities vs none: 9.53, 6.97-13.03) than of non-infection death (5.26, 4.84-5.72).
Interpretation Several NCDs are associated with an increased risk of infection death, suggesting that some of the reported associations with COVID-19 mortality might be non-specific. Only a subset of NCDs, together with the accrual of multimorbidity, advancing age, smoking, and socioeconomic deprivation, were associated with a greater IRR for infection death than for other causes of death. Further research is needed to define why these risk factors are more strongly associated with infection death, so that more effective preventive strategies can be targeted to high-risk groups. Copyright (C) 2021 The Author(s). Published by Elsevier Ltd.
C1 [Drozd, Michael; Straw, Sam; Morgan, Ann W.; Kearney, Mark T.; Witte, Klaus K.; Cubbon, Richard M.] Univ Leeds, Sch Med, Leeds Inst Cardiovasc & Metab Med, Leeds, W Yorkshire, England.
[Pujades-Rodriguez, Mar] Univ Leeds, Sch Med, Leeds Inst Hlth Sci, Leeds, W Yorkshire, England.
[Pujades-Rodriguez, Mar] IQVIA, London, England.
[Lillie, Patrick J.] Hull Univ Hosp NHS Trust, Castle Hill Hosp, Dept Infect, Kingston Upon Hull, Yorks, England.
[Morgan, Ann W.] Leeds Teaching Hosp NHS Trust, NIHR Leeds Biomed Res Ctr, Leeds, W Yorkshire, England.
C3 University of Leeds; University of Leeds; IQVIA; University of Hull;
University of Leeds; Leeds Biomedical Research Centre
RP Cubbon, RM (corresponding author), Univ Leeds, LIGHT Labs 704, Leeds LS2 9JT, W Yorkshire, England.
EM r.cubbon@leeds.ac.uk
RI Pujades-Rodriguez, Mar/T-1129-2018; Drozd, Michael/GSN-3740-2022
OI Lillie, Patrick/0000-0002-4811-4774; Morgan, Ann/0000-0003-1109-624X;
Witte, Klaus/0000-0002-7146-7105; Drozd, Michael/0000-0003-0255-4624
FU British Heart Foundation Clinical Research Training Fellowship
[FS/18/44/33792]; British Heart Foundation Intermediate Clinical
Research Fellowship [FS/12/80/29821]; MRC [MR/N011775/1, MC_PC_19042]
Funding Source: UKRI
FX This research has been done with use of the UK Biobank resource, under
application 59585. MD is supported by a British Heart Foundation
Clinical Research Training Fellowship (FS/18/44/33792). AWM has received
salary support from the National Institute for Health Research and the
UK Medical Research Council. MTK is a British Heart Foundation
Professor. RMC was supported by a British Heart Foundation Intermediate
Clinical Research Fellowship (FS/12/80/29821). MPR is currently employed
by IQVIA, a contract research organisation. At no time did any authors,
nor their institutions, receive other payment or services from a third
party for any aspect of the submitted work.
CR Arvaniti V, 2010, GASTROENTEROLOGY, V139, P1246, DOI 10.1053/j.gastro.2010.06.019
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Drozd M, 2020, CIRC-HEART FAIL, V13, DOI 10.1161/CIRCHEARTFAILURE.119.006746
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NR 26
TC 29
Z9 30
U1 0
U2 14
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1473-3099
EI 1474-4457
J9 LANCET INFECT DIS
JI Lancet Infect. Dis.
PD AUG
PY 2021
VL 21
IS 8
BP 1184
EP 1191
DI 10.1016/S1473-3099(20)30978-6
EA JUL 2021
PG 8
WC Infectious Diseases
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases
GA TT0MQ
UT WOS:000680046200048
PM 33662324
OA Green Published, hybrid, Green Submitted
DA 2025-01-07
ER
PT J
AU Tanguy, Y
Falluel-Morel, A
Arthaud, S
Boukhzar, L
Manecka, DL
Chagraoui, A
Prevost, G
Elias, S
Dorval-Coiffec, I
Lesage, J
Vieau, D
Lihrmann, I
Jégou, B
Anouar, Y
AF Tanguy, Yannick
Falluel-Morel, Anthony
Arthaud, Sebastien
Boukhzar, Loubna
Manecka, Destiny-Love
Chagraoui, Abdeslam
Prevost, Gaetan
Elias, Salah
Dorval-Coiffec, Isabelle
Lesage, Jean
Vieau, Didier
Lihrmann, Isabelle
Jegou, Bernard
Anouar, Youssef
TI The PACAP-Regulated Gene Selenoprotein T Is Highly Induced in Nervous,
Endocrine, and Metabolic Tissues during Ontogenetic and Regenerative
Processes
SO ENDOCRINOLOGY
LA English
DT Article
ID CYCLASE-ACTIVATING POLYPEPTIDE; SELENIUM DEFICIENCY;
GLUTATHIONE-PEROXIDASE; SECRETOGRANIN-II; CHROMOGRANIN-A;
ADRENOCHROMAFFIN CELLS; EXPRESSION PATTERN; ANTERIOR-PITUITARY;
OXIDATIVE STRESS; MOUSE
AB Selenoproteins contain the essential trace element selenium whose deficiency leads to major disorders including cancer, male reproductive system failure, or autoimmune thyroid disease. Up to now, 25 selenoprotein-encoding genes were identified in mammals, but the spatiotemporal distribution, regulation, and function of some of these selenium-containing proteins remain poorly documented. Here, we found that selenoprotein T (SelT), a new thioredoxin-like protein, is regulated by the trophic neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) in differentiating but not mature adrenomedullary cells. In fact, our analysis revealed that, in rat, SelT is highly expressed in most embryonic structures, and then its levels decreased progressively as these organs develop, to vanish in most adult tissues. In the brain, SelT was abundantly expressed in neural progenitors in various regions such as the cortex and cerebellum but was undetectable in adult nervous cells except rostral migratory-stream astrocytes and Bergmann cells. In contrast, SelT expression was maintained in several adult endocrine tissues such as pituitary, thyroid, or testis. In the pituitary gland, SelT was found in secretory cells of the anterior lobe, whereas in the testis, the selenoprotein was present only in spermatogenic and Leydig cells. Finally, we found that SelT expression is strongly stimulated in liver cells during the regenerative process that occurs after partial hepatectomy. Taken together, these data show that SelT induction is associated with ontogenesis, tissue maturation, and regenerative mechanisms, indicating that this PACAP-regulated selenoprotein may play a crucial role in cell growth and activity in nervous, endocrine, and metabolic tissues. (Endocrinology 152: 4322-4335, 2011)
C1 [Tanguy, Yannick; Falluel-Morel, Anthony; Arthaud, Sebastien; Boukhzar, Loubna; Manecka, Destiny-Love; Chagraoui, Abdeslam; Prevost, Gaetan; Elias, Salah; Lihrmann, Isabelle; Anouar, Youssef] Univ Rouen, INSERM, Neuronal & Neuroendocrine Differentiat & Commun L, U982,Fac Sci, F-76821 Mont St Aignan, France.
[Prevost, Gaetan; Elias, Salah; Dorval-Coiffec, Isabelle; Lihrmann, Isabelle; Anouar, Youssef] Univ Rennes 1, INSERM, Inst Federatif Rech 140, Grp Etud Reprod Chez Homme & Mammifere,U625, F-35042 Rennes, France.
[Lesage, Jean; Vieau, Didier] Univ Lille Nord France, Maternal Perinatal Undernutr Team, Perinatal Environm & Growth Unit, EA4489, F-59000 Lille, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
Universite de Rouen Normandie; Universite de Rennes; Institut National
de la Sante et de la Recherche Medicale (Inserm); Universite de Lille
RP Anouar, Y (corresponding author), Univ Rouen, INSERM, Neuronal & Neuroendocrine Differentiat & Commun L, U982,Fac Sci, Pl Emile Blondel, F-76821 Mont St Aignan, France.
EM youssef.anouar@univ-rouen.fr
RI Jégou, Bernard/I-4742-2015; PREVOST, Gaetan/AAD-4865-2019; Anouar,
Youssef/F-9683-2017; Lihrmann, Isabelle/S-6464-2019; lesage,
jean/R-5019-2018
OI JEGOU, Bernard/0000-0003-0623-3609; Anthony,
FALLUEL-MOREL/0000-0002-4081-6704; Elias, Salah/0000-0003-1005-438X;
lesage, jean/0000-0002-6329-1613; Lihrmann,
Isabelle/0000-0002-4486-7074; Arthaud, Sebastien/0000-0001-7271-5468;
vieau, didier/0000-0002-3254-3662
FU INSERM [U982]; University of Rouen; Conseil Regional de Haute-Normandie;
Neuromed fellowship
FX This work was supported by grants from INSERM (U982), University of
Rouen, and the Conseil Regional de Haute-Normandie. Y.T. and D. L. M.
were supported by fellowships from the Conseil Regional de
Haute-Normandie. L. B. was a recipient of a Neuromed fellowship.
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NR 80
TC 44
Z9 55
U1 0
U2 13
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2011
VL 152
IS 11
BP 4322
EP 4335
DI 10.1210/en.2011-1246
PG 14
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 842GR
UT WOS:000296583900035
PM 21896670
OA Green Published, Bronze
DA 2025-01-07
ER
PT J
AU Soon, CF
Zhang, SH
Suneetha, PV
Antunes, DA
Manns, MP
Raha, S
Schultze-Florey, C
Prinz, I
Wedemeyer, H
Chen, MS
Cornberg, M
AF Soon, Chai Fen
Zhang, Shihong
Suneetha, Pothakamuri Venkata
Antunes, Dinler Amaral
Manns, Michael Peter
Raha, Solaiman
Schultze-Florey, Christian
Prinz, Immo
Wedemeyer, Heiner
Chen, Margaret Sallberg
Cornberg, Markus
TI Hepatitis E Virus (HEV)-Specific T Cell Receptor Cross-Recognition:
Implications for Immunotherapy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE CD8+T cells; cross-reactivity; T cell therapy; immunotherapy; T cell
receptor (TCR); TCR redirection; hepatitis E virus (HEV)
ID LIVER CHIMERIC MICE; EPSTEIN-BARR; ALPHA-CHAINS; TCR; INFECTION;
LYMPHOCYTES; ACTIVATION; RESPONSES; MODEL
AB T cell immunotherapy is a concept developed for the treatment of cancer and infectious diseases, based on cytotoxic T lymphocytes to target tumor- or pathogen-specific antigens. Antigen-specificity of the T cell receptors (TCRs) is an important selection criterion in the developmental design of immunotherapy. However, off-target specificity is a possible autoimmunity concern if the engineered antigen-specific T cells are cross-reacting to self-peptides in-vivo. In our recent work, we identified several hepatitis E virus (HEV)-specific TCRs as potential candidates to be developed into T cell therapy to treat chronic hepatitis E. One of the identified TCRs, targeting a HLA-A2-restricted epitope at the RNA-dependent RNA polymerase (HEV-1527: LLWNTVWNM), possessed a unique multiple glycine motif in the TCR-beta CDR3, which might be a factor inducing cross-reactivity. The aim of our study was to explore if this TCR could cross-recognize self-peptides to underlay autoimmunity. Indeed, we found that this HEV-1527-specific TCR could also cross-recognize an apoptosis-related epitope, Nonmuscle Myosin Heavy Chain 9 (MYH9-478: QLFNHTMFI). While this TCR had dual specificities to both viral epitope and a self-antigen by double Dextramer binding, it was selectively functional against HEV-1527 but not activated against MYH9-478. The consecutive glycine motif in beta chain may be the reason promoting TCR binding promiscuity to recognize a secondary target, thereby facilitating cross-recognition. In conclusion, candidate TCRs for immunotherapy development should be screened for autoimmune potential, especially when the TCRs exhibit unique sequence pattern.
C1 [Soon, Chai Fen; Zhang, Shihong; Suneetha, Pothakamuri Venkata; Manns, Michael Peter; Wedemeyer, Heiner; Cornberg, Markus] Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Hannover, Germany.
[Soon, Chai Fen; Manns, Michael Peter; Prinz, Immo; Cornberg, Markus] Hannover Med Sch, Cluster Excellence Resist EXC 2155, Hannover, Germany.
[Antunes, Dinler Amaral] Rice Univ, Dept Comp Sci, Houston, TX USA.
[Raha, Solaiman; Schultze-Florey, Christian; Prinz, Immo] Hannover Med Sch, Inst Immunol Hanover, Hannover, Germany.
[Schultze-Florey, Christian] Hannover Med Sch, Dept Hematol Hemostasis Oncol & Stem Cell Transpl, Hannover, Germany.
[Wedemeyer, Heiner; Cornberg, Markus] German Ctr Infect Res, Partner Site Hannover Braunschweig, Hannover, Germany.
[Wedemeyer, Heiner] Univ Clin Essen, Dept Gastroenterol & Hepatol, Essen, Germany.
[Chen, Margaret Sallberg] Karolinska Inst, Dept Dent Med, Stockholm, Sweden.
[Chen, Margaret Sallberg] Karolinska Inst, Dept Lab Med, Stockholm, Sweden.
[Chen, Margaret Sallberg] Tongji Univ, Shanghai Peoples Hosp 10, Shanghai, Peoples R China.
[Cornberg, Markus] Ctr Ind Individualised Infect Med, Hannover, Germany.
[Cornberg, Markus] Helmholtz Ctr Infect Res, Braunschweig, Germany.
C3 Hannover Medical School; Hannover Medical School; Rice University;
Hannover Medical School; Hannover Medical School; German Center for
Infection Research; University of Duisburg Essen; Karolinska Institutet;
Karolinska Institutet; Tongji University; Helmholtz Association;
Helmholtz-Center for Infection Research
RP Cornberg, M (corresponding author), Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Hannover, Germany.; Cornberg, M (corresponding author), Hannover Med Sch, Cluster Excellence Resist EXC 2155, Hannover, Germany.; Cornberg, M (corresponding author), German Ctr Infect Res, Partner Site Hannover Braunschweig, Hannover, Germany.; Cornberg, M (corresponding author), Helmholtz Ctr Infect Res, Braunschweig, Germany.
EM cornberg.markus@mh-hannover.de
RI chen, margaret/B-6757-2014; Cornberg, Markus/AAN-6939-2021; Manns,
Michael/AFG-3063-2022; Prinz, Immo/A-3026-2010; Antunes,
Dinler/Z-4437-2019
OI Sallberg Chen, Margaret/0000-0002-3793-4064; Schultze-Florey, Christian
R/0000-0002-3307-2639; Prinz, Immo/0000-0002-8789-9578; Antunes,
Dinler/0000-0001-7947-6455
FU Deutsche Forschungsgemeinschaft (DFG) [SU-888/1-1]; Swedish Cancer
Society (Cancerfonden); Hannover Biomedical Research School (HBRS);
Center for Infection Biology (ZIB); Deutsche Leberstiftung
[S163/10149/2018]; DZIF [TTU 05.702]; Deutsche Forschungsgemeinschaft
(DFG) under Germany's Excellence Strategy [EXC 2155 RESIST, 39087428]
FX This project was funded by Deutsche Forschungsgemeinschaft (DFG,
SU-888/1-1) and the Swedish Cancer Society (Cancerfonden). CS was
supported by the Hannover Biomedical Research School (HBRS), the Center
for Infection Biology (ZIB) and Deutsche Leberstiftung
(S163/10149/2018). MC was supported by DZIF (TTU 05.702). CS, MM, IP,
and MC are supported by the Deutsche Forschungsgemeinschaft (DFG) under
Germany's Excellence Strategy-EXC 2155 RESIST-Project ID 39087428.
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NR 48
TC 12
Z9 13
U1 2
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 4
PY 2019
VL 10
AR 2076
DI 10.3389/fimmu.2019.02076
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA IU7ND
UT WOS:000483769700001
PM 31552033
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Sun, B
Liu, K
Han, J
Zhao, LY
Su, X
Lin, B
Zhao, DM
Cheng, MS
AF Sun, Bin
Liu, Kai
Han, Jing
Zhao, Li-yu
Su, Xiao
Lin, Bin
Zhao, Dong-Mei
Cheng, Mao-Sheng
TI Design, synthesis, and biological evaluation of amide imidazole
derivatives as novel metabolic enzyme CYP26A1 inhibitors
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE All-trans-retinoic acid (ATRA); CYP26A1; Amide imidazole derivatives;
Binding model; Biological evaluation
ID TRANS-RETINOIC ACID; SMALL-MOLECULE INHIBITORS; R115866; NEUROBLASTOMA;
POTENT; AGENTS; RECOGNITION
AB All-trans-retinoic acid (ATRA) as a physiological metabolite of vitamin A is widely applied in the treatment of cancer, skin, neurodegenerative and autoimmune diseases. CYP26A1 enzyme, induced by ATRA in liver and target tissues, metabolizes ATRA into 4-hydroxyl-RA. Inhibition of CYP26A1 metabolic enzyme represents a promising strategy for discovery of new specific anticancer agents. Herein, we describe the design, synthesis and biological evaluation of a series of new amide imidazole derivatives as retinoic acid metabolism blocking agents (RAMBAs) toward CYP26A1 enzyme. First, based on the recent theoretical models (Sun et al., J. Mol. Graph. Model., 2015, 56, 10-19) a series of RAMBAs with novel scaffolds were designed using fragment-based drug discovery approach. Subsequently, the new RAMBAs were synthesized and evaluated for their biological activities. All the compounds demonstrated appropriate enzyme activities and cell activities. The promising inhibitors 20 and 23 with IC50 value of 0.22 mu M and 0.46 mu M toward CYP26A1, respectively, were further evaluated for CYP selectivity and the metabolic profile of ATRA. Both compounds 20 and 23 showed higher selectivity for CYP26A1 over other CYPs (CYP2D6, CYP3A4) when compared to liarozole. They also showed better inhibitory activities for the metabolism of ATRA when also compared to liarozole. These studies further validated the pharmacophore and structure-activity relationship models obtained about CYP26A1 inhibitors and highlighted the promising activities of the new series of CYP26A1 inhibitors designed from such models. They also paved the way for future development of those candidates as potential drugs. Published by Elsevier Ltd.
C1 [Sun, Bin; Liu, Kai; Han, Jing; Zhao, Li-yu; Su, Xiao; Lin, Bin; Zhao, Dong-Mei; Cheng, Mao-Sheng] Shenyang Pharmaceut Univ, Sch Pharmaceut Engn, Minist Educ, Key Lab Struct Based Drug Design & Discovery, Shenyang 110016, Peoples R China.
C3 Shenyang Pharmaceutical University
RP Zhao, DM (corresponding author), Shenyang Pharmaceut Univ, Sch Pharmaceut Engn, Minist Educ, Key Lab Struct Based Drug Design & Discovery, 103 Wenhua Rd, Shenyang 110016, Peoples R China.
EM medchemzhao@163.com
RI Lin, Binshan/A-9772-2009
OI Lin, Bin/0000-0003-2369-4765
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NR 37
TC 33
Z9 34
U1 1
U2 39
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
EI 1464-3391
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD OCT 15
PY 2015
VL 23
IS 20
BP 6763
EP 6773
DI 10.1016/j.bmc.2015.08.019
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA CS8ZT
UT WOS:000362379200025
PM 26365710
DA 2025-01-07
ER
PT J
AU Jorgensen, SF
Macpherson, ME
Skarpengland, T
Berge, RK
Fevang, B
Halvorsen, B
Aukrust, P
AF Jorgensen, Silje F.
Macpherson, Magnhild E.
Skarpengland, Tonje
Berge, Rolf K.
Fevang, Borre
Halvorsen, Bente
Aukrust, Pal
TI Disturbed lipid profile in common variable immunodeficiency - a
pathogenic loop of inflammation and metabolic disturbances
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE CVID; common variable immunodeficiency; antibody deficiencies; fatty
acids; metabolism; inflammation; HDL; cholesterol; triglycerid
ID HIGH-DENSITY-LIPOPROTEIN; TUMOR-NECROSIS-FACTOR; REGULATORY T-CELLS;
TRIGLYCERIDE-RICH LIPOPROTEINS; POLYUNSATURATED FATTY-ACIDS;
IMMUNE-RESPONSE; GUT MICROBIOTA; FACTOR-ALPHA; ACTIVATION; HDL
AB The relationship between metabolic and inflammatory pathways play a pathogenic role in various cardiometabolic disorders and is potentially also involved in the pathogenesis of other disorders such as cancer, autoimmunity and infectious diseases. Common variable immunodeficiency (CVID) is the most common primary immunodeficiency in adults, characterized by increased frequency of airway infections with capsulated bacteria. In addition, a large proportion of CVID patients have autoimmune and inflammatory complications associated with systemic inflammation. We summarize the evidence that support a role of a bidirectional pathogenic interaction between inflammation and metabolic disturbances in CVID. This include low levels and function of high-density lipoprotein (HDL), high levels of triglycerides (TG) and its major lipoprotein very low-density lipoprotein (VLDL), and an unfavorable fatty acid (FA) profile. The dysregulation of TG, VLDL and FA were linked to disturbed gut microbiota profile, and TG and VLDL levels were strongly associated with lipopolysaccharides (LPS), a marker of gut leakage in blood. Of note, the disturbed lipid profile in CVID did not include total cholesterol levels or high low-density lipoprotein levels. Furthermore, increased VLDL and TG levels in blood were not associated with diet, high body mass index and liver steatosis, suggesting a different phenotype than in patients with traditional cardiovascular risk such as metabolic syndrome. We hypothesize that these metabolic disturbances are linked to inflammation in a bidirectional manner with disturbed gut microbiota as a potential contributing factor.
C1 [Jorgensen, Silje F.; Macpherson, Magnhild E.; Fevang, Borre; Halvorsen, Bente; Aukrust, Pal] Oslo Univ Hosp, Res Inst Internal Med, Rikshosp, Oslo, Norway.
[Jorgensen, Silje F.; Macpherson, Magnhild E.; Skarpengland, Tonje; Fevang, Borre; Aukrust, Pal] Oslo Univ Hosp, Sect Clin Immunol & Infect Dis, Rikshosp, Oslo, Norway.
[Berge, Rolf K.] Univ Bergen, Dept Clin Sci, Bergen, Norway.
[Berge, Rolf K.] Haukeland Hosp, Dept Heart Dis, Bergen, Norway.
[Halvorsen, Bente; Aukrust, Pal] Univ Oslo, Inst Clin Med, Oslo, Norway.
C3 University of Oslo; National Hospital Norway; University of Oslo;
National Hospital Norway; University of Bergen; University of Bergen;
Haukeland University Hospital; University of Oslo
RP Jorgensen, SF (corresponding author), Oslo Univ Hosp, Res Inst Internal Med, Rikshosp, Oslo, Norway.; Jorgensen, SF (corresponding author), Oslo Univ Hosp, Sect Clin Immunol & Infect Dis, Rikshosp, Oslo, Norway.
EM s.f.jorgensen@medisin.uio.no
FU South-Eastern Norway Regional Health Authority [2019089, 2012/521]
FX Funding SJ (project number 2019089) and MM (project number 2012/521)
were funded by grants from the South-Eastern Norway Regional Health
Authority.
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NR 152
TC 4
Z9 4
U1 2
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUL 20
PY 2023
VL 14
AR 1199727
DI 10.3389/fimmu.2023.1199727
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA N8WB6
UT WOS:001039740100001
PM 37545531
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Leanza, L
Venturini, E
Kadow, S
Carpinteiro, A
Gulbins, E
Becker, KA
AF Leanza, Luigi
Venturini, Elisa
Kadow, Stephanie
Carpinteiro, Alexander
Gulbins, Erich
Becker, Katrin Anne
TI Targeting a mitochondrial potassium channel to fight cancer
SO CELL CALCIUM
LA English
DT Review
DE Potassium channel; Mitochondria; Cell death; Bax; Toxins
ID CYTOCHROME-C RELEASE; PERMEABILITY TRANSITION PORE; RAT-LIVER
MITOCHONDRIA; BAX-INDUCED APOPTOSIS; SENSITIVE K+ CHANNEL; MEMORY
T-CELLS; ION CHANNELS; OXIDATIVE-PHOSPHORYLATION; INTERNATIONAL-UNION;
AUTOIMMUNE-DISEASES
AB Although chemotherapy is able to cure many patients with malignancies, it still also often fails. Therefore, novel approaches and targets for chemotherapeutic treatment of malignancies are urgently required. Recent studies demonstrated the expression of several potassium channels in the inner mitochondrial membrane. Among them the voltage gated potassium channel Kv1.3 and the big-potassium (BK) channel were shown to directly function in cell death by serving as target for pro-apoptotic Bax and Bak proteins. Here, we discuss the role of mitochondrial potassium channel Kv1.3 (mitoKv1.3) in cell death and its potential function in treatment of solid tumors, leukemia and lymphoma. Box and Bak inhibit mitoKv1.3 by directly binding into the pore of the channel, by a toxin-like mechanism. Inhibition of mitoKv1.3 results in an initial hyperpolarization of the inner mitochondrial membrane that triggers the production of reactive oxygen species (ROS). ROS in turn induce a release of cytochrome c from the cristae of the inner mitochondrial membrane and an activation of the permeability transition pore, resulting in opening of the intrinsic apoptotic cell death. Since mitoKv1.3 functions downstream of pro-apoptotic Bax and Bak, compounds that directly inhibit mitoKv1.3 may serve as a new class of drugs for treatment of tumors, even with an altered expression of either pro- or anti-apoptotic Bcl-2 protein family members. This was successfully proven by the in vivo treatment of mouse melanoma and ex vivo human chronic leukemia B cells with inhibitors of mitoKv1.3. (C) 2014 Published by Elsevier Ltd.
C1 [Leanza, Luigi] Univ Padua, Dept Biol, I-35131 Padua, Italy.
[Venturini, Elisa; Kadow, Stephanie; Carpinteiro, Alexander; Gulbins, Erich; Becker, Katrin Anne] Univ Duisburg Essen, Dept Mol Biol, D-45122 Essen, Germany.
C3 University of Padua; University of Duisburg Essen
RP Becker, KA (corresponding author), Univ Duisburg Essen, Dept Mol Biol, Hufelandstr 55, D-45122 Essen, Germany.
EM erich.gulbins@uni-due.de; katrin.becker-flegler@uni-due.de
RI Becker, Katrin/KGL-8626-2024; LEANZA, LUIGI/K-3060-2016
OI LEANZA, LUIGI/0000-0002-5919-7114
FU Progetto Giovani Studiosi by University of Padua; EMBO Short Term
fellowship
FX The authors thank Bettina Peter for excellent editorial help. L.L. is a
recipient of a Progetto Giovani Studiosi 2012 by University of Padua and
of an EMBO Short Term fellowship.
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NR 96
TC 45
Z9 47
U1 0
U2 48
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0143-4160
EI 1532-1991
J9 CELL CALCIUM
JI Cell Calcium
PD JUL 1
PY 2015
VL 58
IS 1
SI SI
BP 131
EP 138
DI 10.1016/j.ceca.2014.09.006
PG 8
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA CL1YD
UT WOS:000356739900014
PM 25443654
DA 2025-01-07
ER
PT J
AU Kakehasi, AM
Radominski, SC
Baravalle, MD
Palazuelos, FCI
Garcia-Garcia, C
Arruda, MS
Curi, M
Liu, JH
Qiao, MH
Velez-Sanchez, P
Vargas, JI
AF Kakehasi, Adriana Maria
Radominski, Sebastiao Cezar
Baravalle, Marcos Daniel
Palazuelos, Fedra Consuelo Irazoque
Garcia-Garcia, Conrado
Arruda, Maysa Silva
Curi, Marco
Liu, John
Qiao, Meihua
Velez-Sanchez, Patricia
Vargas, Juan Ignacio
TI Safety of upadacitinib in Latin American patients with rheumatoid
arthritis: an integrated safety analysis of the SELECT phase 3 clinical
program
SO CLINICAL RHEUMATOLOGY
LA English
DT Article
DE Janus kinase inhibitor; Latin America; Rheumatoid arthritis; Safety;
Upadacitinib
ID VENOUS THROMBOEMBOLISM; JAK INHIBITORS; RISK; MANAGEMENT
AB Introduction/objectives Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by ongoing inflammation and degradation of synovial joints. The oral JAK inhibitor, upadacitinib, is approved for RA. We conducted an integrated safety analysis of upadacitinib 15 mg once daily (QD) in patients from Latin America (LATAM) versus the rest of the world (RoW).Methods Treatment-emergent adverse events (AEs) and laboratory data from six phase 3, randomized controlled trials, adjusted for upadacitinib 15 mg QD use in RA, were analyzed.Results Overall, 3209 patients received upadacitinib 15 mg QD for 7024 patient-years (PY). LATAM patients (n = 725) had a mean upadacitinib exposure of 1518 PY. Baseline characteristics were generally similar between LATAM and RoW populations. AE rates (including serious/opportunistic infections, tuberculosis, and herpes zoster) and deaths were comparable between populations. LATAM patients had lower serious AE rates per 100 PY (9.4 vs 14.0 E/100 PY) and discontinuation related AEs (3.9 vs 6.0 E/100 PY) versus RoW. Rates of cardiovascular events were low (<= 0.5 E/100 PY) and similar between populations. Malignancies, excluding non-melanoma skin cancer, were less common in the LATAM population versus RoW (0.2 vs 1.0 E/100 PY). Laboratory abnormalities were similar between populations, with decreases in hemoglobin, lymphocyte, and neutrophil counts, and elevations in liver enzymes and creatine phosphokinase. Mean change from baseline in low-and high-density lipoprotein cholesterol was generally comparable between LATAM and RoW populations.Conclusion Upadacitinib 15 mg QD demonstrated a consistent safety profile across LATAM and RoW patient populations, with no new safety risks observed.
C1 [Kakehasi, Adriana Maria] Univ Fed Minas Gerais, Hosp Clin, Belo Horizonte, MG, Brazil.
[Radominski, Sebastiao Cezar] Univ Fed Parana, Curitiba, PR, Brazil.
[Baravalle, Marcos Daniel] Inst Med Strusberg, Cordoba, Argentina.
[Palazuelos, Fedra Consuelo Irazoque] CINTRE Ctr Invest & Tratamiento Reumatol SC, Mexico City, Mexico.
[Garcia-Garcia, Conrado] Hosp Gen Mexico Dr Eduardo Liceaga, Rheumatol Unit, Mexico City, Mexico.
[Arruda, Maysa Silva; Curi, Marco] AbbVie Farmaceut Ltda, Sao Paulo, Brazil.
[Liu, John; Qiao, Meihua] AbbVie, N Chicago, IL USA.
[Velez-Sanchez, Patricia] Ctr Invest Reumatol & Especial Med SAS CIREEM SAS, Cundinamarca, Colombia.
[Vargas, Juan Ignacio] Quantum Res, Puerto Varas, Chile.
C3 Universidade Federal de Minas Gerais; Universidade Federal do Parana;
AbbVie
RP Kakehasi, AM (corresponding author), Univ Fed Minas Gerais, Hosp Clin, Belo Horizonte, MG, Brazil.
EM amkakehasi@gmail.com
RI Kakehasi, Adriana Maria/Y-9797-2018
OI Kakehasi, Adriana Maria/0000-0001-9411-7493
FU AbbVie
FX AbbVie funded this study and participated in the study design, research,
analysis, data collection, interpretation of data, review, and approval
of the publication. All authors had access to relevant data and
participated in the drafting, review, and approval of this publication.
No honoraria or payments were made for authorship.
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NR 41
TC 1
Z9 1
U1 0
U2 1
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0770-3198
EI 1434-9949
J9 CLIN RHEUMATOL
JI Clin. Rheumatol.
PD MAY
PY 2023
VL 42
IS 5
BP 1249
EP 1258
DI 10.1007/s10067-023-06513-y
EA JAN 2023
PG 10
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA D1AB4
UT WOS:000923618500001
PM 36715850
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Fard, LA
Malekinejad, H
Esmaeilzadeh, Z
Jafari, A
Khezri, MR
Ghasemnejad-Berenji, M
AF Afkhami Fard, Leila
Malekinejad, Hassan
Esmaeilzadeh, Zeinab
Jafari, Abbas
Khezri, Mohammad Rafi
Ghasemnejad-Berenji, Morteza
TI Protective effects of sitagliptin on methotrexate-induced nephrotoxicity
in rats
SO JOURNAL OF ENVIRONMENTAL SCIENCE AND HEALTH PART C-TOXICOLOGY AND
CARCINOGENESIS
LA English
DT Article
DE Methotrexate; sitagliptin; oxidative stress; nephrotoxicity;
nephroprotective
ID GLUCAGON-LIKE PEPTIDE-1; INDUCED KIDNEY DAMAGE; OXIDATIVE STRESS; RENAL
INJURY; INHIBITOR; APOPTOSIS; ACID; LIVER; GLP-1; DRUG
AB Methotrexate (MTX), a cytotoxic chemotherapeutic and immunosuppressant agent, is widely used in the treatment of autoimmune diseases and different types of cancers. However, its use has been limited by its life-threatening side effects, including nephrotoxicity and hepatotoxicity. The purpose of this study was to investigate the protective effect of sitagliptin on methotrexate (MTX)-induced nephrotoxicity in rats. Twenty-four rats were divided into four groups: control group, which received the vehicle for 6 days; MTX group, which received a single dose of MTX, followed by five daily doses of vehicle dosing; MTX + sitagliptin group, which received a single dose of MTX 1 h after the first sitagliptin treatment and six daily doses of sitagliptin; and sitagliptin group, which received sitagliptin for 6 days. Both MTX and sitagliptin were given as intraperitoneal injections at a dose of 20 mg/kg body weight. All rats were euthanized on the seventh day of the study. Kidney tissues were harvested and blood samples were collected. Serum levels of blood urea nitrogen (BUN) and creatinine were evaluated. Furthermore, catalase, glutathione peroxidase, superoxide dismutase activities, and malondialdehyde (MDA) levels were determined in kidney tissue. In addition, histopathological analysis was conducted. Histopathological evaluation showed that MTX-induced marked kidney injury. Biochemical analysis revealed a significant increase of BUN and creatinine in the serum of the MTX group. Furthermore, oxidative stress and depressed antioxidant system of the kidney tissues were evident in the MTX group. Sitagliptin did not affect these endpoints when administered alone, but it significantly attenuated the observed MTX-induced effects. These results suggest that sitagliptin exhibits potent anti-oxidant properties against the nephrotoxicity induced by MTX in rats.
C1 [Afkhami Fard, Leila; Khezri, Mohammad Rafi] Urmia Univ Med Sci, Student Res Comm, Orumiyeh, Iran.
[Malekinejad, Hassan; Ghasemnejad-Berenji, Morteza] Urmia Univ Med Sci, Expt & Appl Pharmaceut Res Ctr, Orumiyeh, Iran.
[Malekinejad, Hassan; Ghasemnejad-Berenji, Morteza] Urmia Univ Med Sci, Sch Pharm, Dept Pharmacol & Toxicol, Orumiyeh, Iran.
[Esmaeilzadeh, Zeinab] Urmia Univ Med Sci, Sch Med, Dept Nutr, Orumiyeh, Iran.
[Esmaeilzadeh, Zeinab] Urmia Univ Med Sci, Sch Med, Dept Biochem, Orumiyeh, Iran.
[Jafari, Abbas] Urmia Univ Med Sci, Cellular & Mol Med Inst, Cellular & Mol Res Ctr, Orumiyeh, Iran.
C3 Urmia University of Medical Sciences; Urmia University of Medical
Sciences; Urmia University of Medical Sciences; Urmia University of
Medical Sciences; Urmia University of Medical Sciences; Urmia University
of Medical Sciences
RP Ghasemnejad-Berenji, M (corresponding author), Urmia Univ Med Sci, Sch Pharm, Dept Pharmacol & Toxicol, Orumiyeh, Iran.
EM morteza.ghasemnejad@yahoo.com
RI Jafari, Abbas/C-8401-2016; Khezri, Mohammad Rafi/ABC-5317-2021;
Ghasemnejad-Berenji, Morteza/V-3882-2017
OI Ghasemnejad-Berenji, Morteza/0000-0001-5672-9202
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NR 70
TC 4
Z9 4
U1 2
U2 12
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 2689-6583
EI 2689-6591
J9 J ENV SCI HEAL C-TOX
JI J. Environ. Sci. Health Part C-Toxicol. Carcinogen.
PD APR 3
PY 2023
VL 41
IS 1-2
BP 22
EP 35
DI 10.1080/26896583.2023.2186683
EA MAR 2023
PG 14
WC Oncology; Environmental Sciences; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Environmental Sciences & Ecology; Toxicology
GA K3EZ6
UT WOS:000962037200001
PM 37010136
DA 2025-01-07
ER
PT J
AU Moscicki, AB
Flowers, L
Huchko, MJ
Long, ME
MacLaughlin, KL
Murphy, J
Spiryda, LB
Gold, MA
AF Moscicki, Anna-Barbara
Flowers, Lisa
Huchko, Megan J.
Long, Margaret E.
MacLaughlin, Kathy L.
Murphy, Jeanne
Spiryda, Lisa Beth
Gold, Michael A.
TI Guidelines for Cervical Cancer Screening in Immunosuppressed Women
Without HIV Infection
SO JOURNAL OF LOWER GENITAL TRACT DISEASE
LA English
DT Article
DE guidelines; cervical cancer; immunosuppressed
ID HUMAN-PAPILLOMAVIRUS INFECTION; HUMAN-IMMUNODEFICIENCY-VIRUS;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; SQUAMOUS INTRAEPITHELIAL LESIONS;
INFLAMMATORY-BOWEL-DISEASE; STEM-CELL TRANSPLANTATION; TYPE-1
DIABETES-MELLITUS; POPULATION-BASED COHORT; LONG-TERM SURVIVORS;
INCREASED RISK
AB Executive Summary The risk of cervical cancer (CC) among women immunosuppressed for a variety of reasons is well documented in the literature. Although there is improved organ function, quality of life and life expectancy gained through use of immunosuppressant therapy, there may be increased long-term risk of cervical neoplasia and cancer and the need for more intense screening, surveillance, and management. Although guidance for CC screening among HIV-infected women (see Table 1) has been supported by evidence from retrospective and prospective studies, recommendations for CC screening among non-HIV immunosuppressed women remains limited because quality evidence is lacking. Moreover, CC screening guidelines for HIV-infected women have changed because better treatments evolved and resulted in longer life expectancy. The objective of this report was to summarize current knowledge of CC, squamous intraepithelial lesions, and human papillomavirus (HPV) infection in non-HIV immunocompromised women to determine best practices for CC surveillance in this population and provide recommendations for screening. We evaluated those with solid organ transplant, hematopoietic stem cell transplant, and a number of autoimmune diseases. A panel of health care professionals involved in CC research and care was assembled to review and discuss existing literature on the subject and come to conclusions about screening based on available evidence and expert opinion. Literature searches were performed using key words such as CC, cervical dysplasia/squamous intraepithelial lesion, HPV, and type of immunosuppression resulting in an initial group of 346 articles. Additional publications were identified from review of citations in these articles. All generated abstracts were reviewed to identify relevant articles. Articles published within 10 years were considered priority for review. Reviews of the literature were summarized with relevant statistical comparisons. Recommendations for screening generated from each group were largely based on expert opinion. Adherence to screening, health benefits and risks, and available clinical expertise were all considered in formulating the recommendations to the degree that information was available. Results Solid Organ Transplant: Evidence specific for renal, heart/lung, liver, and pancreas transplants show a consistent increase in risk of cervical neoplasia and invasive CC, demonstrating the importance of long-term surveillance and treatment. Reports demonstrate continued risk long after transplantation, emphasizing the need for screening throughout a woman's lifetime. Hematopoietic Stem Cell Transplant: Although there is some evidence for an increase in CC in large cohort studies of these patients, conflicting results may reflect that many patients did not survive long enough to evaluate the incidence of slow-growing or delayed-onset cancers. Furthermore, history of cervical screening or previous hysterectomy was not included in registry study analysis, possibly leading to underestimation of CC incidence rates. Genital or chronic graft versus host disease is associated with an increase in high-grade cervical neoplasia and posttransplant HPV positivity. Inflammatory Bowel Disease: There is no strong evidence to support that inflammatory bowel disease alone increases cervical neoplasia or cancer risk. In contrast, immunosuppressant therapy does seem to increase the risk, although results of observational studies are conflicting regarding which type of immunosuppressant medication increases risk.
Moreover, misclassification of cases may underestimate CC risk in this population. Recently published preventive care guidelines for women with inflammatory bowel disease taking immunosuppressive therapy recommend a need for continued long-term CC screening. Systemic Lupus Erythematosus and Rheumatoid Arthritis: The risk of cervical high-grade neoplasia and cancer was higher among women with systemic lupus erythematosus than those with rheumatoid arthritis (RA), although studies were limited by size, inclusion of women with low-grade neoplasia in main outcomes, and variability of disease severity or exposure to immunosuppressants. In studies designed to look specifically at immunosuppressant use, however, there did seem to be an increase in risk, identified mostly in women with RA. Although the strength of the evidence is limited, the increase in risk is consistent across studies. Type 1 DM: There is a paucity of evidence-based reports associating type 1 DM with an increased risk of cervical neoplasia and cancer. Recommendations The panel proposed that CC screening guidelines for non-HIV immunocompromised women follow either the (1) guidelines for the general population or (2) current center for disease control guidelines for HIV-infected women. The following are the summaries for each group reviewed, and more details are noted in accompanying table: Solid Organ Transplant: The transplant population reflects a greater risk of CC than the general population and guidelines for HIV-infected women are a reasonable approach for screening and surveillance. Hematopoietic Stem Cell Transplant: These women have a greater risk of CC than the general population and guidelines for HIV-infected women are a reasonable approach for screening. A new diagnosis of genital or chronic graft versus host disease in a woman post-stem cell transplant results in a greater risk of CC than in the general population and should result in more intensive screening and surveillance. Inflammatory Bowel Disease: Women with inflammatory bowel disease being treated with immunosuppressive drugs are at greater risk of cervical neoplasia and cancer than the general population and guidelines for HIV-infected women are a reasonable approach for screening and surveillance. Those women with inflammatory bowel disease not on immunosuppressive therapy are not at an increased risk and should follow screening guidelines for the general population. Systemic Lupus Erythematosus and Rheumatoid Arthritis: All women with systemic lupus erythematosus, whether on immunosuppressant therapy or not and those women with RA on immunosuppressant therapy have a greater risk of cervical neoplasia and cancer than the general population and should follow CC screening guidelines for HIV-infected women. Women with RA not on immunosuppressant therapy should follow CC screening guidelines for the general population. Type 1 Diabetes Mellitus: Because of a lack of evidence of increased risk of cervical neoplasia and cancer among women with type 1 DM, these women should follow the screening guidelines for the general population.
C1 [Moscicki, Anna-Barbara] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
[Flowers, Lisa] Emory Univ, Sch Med, Dept Gynecol & Obstet, Atlanta, GA USA.
[Huchko, Megan J.] Duke Univ, Dept Obstet & Gynecol, Global Hlth Inst, Durham, NC USA.
[Long, Margaret E.] Mayo Clin, Dept Obstet & Gynecol, Rochester, MN USA.
[MacLaughlin, Kathy L.] Mayo Clin, Dept Family Med, Rochester, MN USA.
[Murphy, Jeanne] George Washington Univ, Sch Nursing, Ashburn, VA USA.
[Spiryda, Lisa Beth] Univ S Alabama, Coll Med, Dept Obstet & Gynecol, Mobile, AL USA.
[Gold, Michael A.] Univ Oklahoma, OU TU Sch Community Med, Dept Obstet & Gynecol, Tulsa, OK USA.
C3 University of California System; University of California Los Angeles;
Emory University; Duke University; Mayo Clinic; Mayo Clinic; George
Washington University; University of South Alabama; University of
Oklahoma System; University of Oklahoma - Tulsa
RP Moscicki, AB (corresponding author), Univ Calif Los Angeles, 10833 Conte Dr,Suite MD 22-432, Los Angeles, CA 90095 USA.
EM AMoscicki@mednet.ucla.edu
RI Murphy, Jeanne/AAK-9270-2020; Moscicki, Anna-Barbara/AAP-3806-2021;
Huchko, Megan/S-6063-2019; MacLaughlin, Kathy/AAH-7674-2020
OI Murphy, Jeanne/0000-0002-2460-7670; MacLaughlin,
Kathy/0000-0001-8241-7587
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NR 129
TC 75
Z9 82
U1 1
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1089-2591
EI 1526-0976
J9 J LOW GENIT TRACT DI
JI J. Low. Genit. Tract. Dis.
PD APR
PY 2019
VL 23
IS 2
BP 87
EP 101
DI 10.1097/LGT.0000000000000468
PG 15
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Obstetrics & Gynecology
GA HQ0LJ
UT WOS:000462086200001
PM 30907775
DA 2025-01-07
ER
PT J
AU Heidari, R
Ahmadi, A
Mohammadi, H
Ommati, MM
Azarpira, N
Niknahad, H
AF Heidari, Reza
Ahmadi, Asrin
Mohammadi, Hamidreza
Ommati, Mohammad Mehdi
Azarpira, Negar
Niknahad, Hossein
TI Mitochondrial dysfunction and oxidative stress are involved in the
mechanism of methotrexate-induced renal injury and electrolytes
imbalance
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Cancer chemotherapy; Energy metabolism; Fanconi syndrome; Mitochondria;
Oxidative stress
ID INDUCED HEPATOTOXICITY; INDUCED CYTOTOXICITY; LIVER-MITOCHONDRIA;
N-ACETYLCYSTEINE; PROXIMAL TUBULE; PROTECTIVE ROLE; DAMAGE;
NANOPARTICLES; METHIMAZOLE; TAURINE
AB Methotrexate is a folate analog used against a wide range of diseases including malignancies and autoimmune disorders. On the other hand, clinical use of the MTX is associated with kidney injury and renal failure. There is no clear mechanism for MTX-induced renal injury. The current investigation was designed to evaluate the role of mitochondrial dysfunction and oxidative stress in the pathogenesis of MTX-induced renal injury. Rats received MTX (a single dose of 20 or 30 mg/kg, i.p). Five days after MTX administration, serum biomarkers of kidney injury and tissue markers of oxidative stress were assessed. Moreover, kidney mitochondria were isolated, and several mitochondrial indices were determined. MTX-treated animals developed biochemical evidence of renal injury as judged by elevated serum blood urea nitrogen (BUN), creatinine (Cr) and along with hypokalemia, hypophosphatemia, hypocalcemia, and a decrease in serum glucose, and uric acid. Moreover, MTX caused an increase in kidney reactive oxygen species and lipid peroxidation. Renal glutathione reservoirs were also depleted, and tissue antioxidant capacity was decreased in MTX-treated animals. Kidney histopathological changes including interstitial inflammation, renal tubular degeneration, retraction glomeruli, and vascular congestion were also evident in MTX-treated rats. On the other hand, it was found that mitochondrial parameters including mitochondrial membrane potential, mitochondrial dehydrogenases activity, and mitochondrial glutathione and ATP content were decreased, while lipid peroxidation and mitochondrial permeabilization were increased with MTX treatment. These data suggest a role for mitochondrial dysfunction and oxidative stress in the mechanism of MTX nephrotoxicity.
C1 [Heidari, Reza; Ommati, Mohammad Mehdi; Niknahad, Hossein] Shiraz Univ Med Sci, Pharmaceut Sci Res Ctr, POB 1583,Karafarin St, Shiraz 71345, Fars, Iran.
[Ahmadi, Asrin; Mohammadi, Hamidreza; Niknahad, Hossein] Shiraz Univ Med Sci, Sch Pharm, Dept Pharmacol & Toxicol, Shiraz, Iran.
[Ommati, Mohammad Mehdi] Shiraz Univ, Sch Agr, Dept Anim Sci, Shiraz, Iran.
[Azarpira, Negar] Shiraz Univ Med Sci, Transplant Res Ctr, Shiraz, Iran.
C3 Shiraz University of Medical Science; Tehran University of Medical
Sciences; Shiraz University of Medical Science; Shiraz University;
Shiraz University of Medical Science
RP Heidari, R; Niknahad, H (corresponding author), Shiraz Univ Med Sci, Pharmaceut Sci Res Ctr, POB 1583,Karafarin St, Shiraz 71345, Fars, Iran.
EM rheidari@sums.ac.ir; niknahadh@sums.ac.ir
RI Azarpira, Negar/U-4784-2017; Ommati, Mohammad/AAQ-7091-2020; Heidari,
Reza/F-6625-2013; Ommati, Mohammad Mehdi/A-3037-2014; Niknahad,
Hossein/D-9783-2012
OI Mohammadi, Hamidreza/0000-0002-6467-523X; Heidari,
Reza/0000-0002-7038-9838; Ommati, Mohammad Mehdi/0000-0003-0514-2414;
Niknahad, Hossein/0000-0001-6211-5936
FU Shiraz University of Medical Sciences [95-01-36-12347]
FX This investigation was financially supported by the Vice Chancellor of
Research Affairs of Shiraz University of Medical Sciences (Grant number:
95-01-36-12347). Authors thank Pharmaceutical Sciences Research Center
of Shiraz University of Medical Sciences for providing technical
facilities to carry out this study.
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NR 55
TC 81
Z9 86
U1 0
U2 14
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD NOV
PY 2018
VL 107
BP 834
EP 840
DI 10.1016/j.biopha.2018.08.050
PG 7
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA GU1PC
UT WOS:000445036200091
PM 30142545
DA 2025-01-07
ER
PT J
AU Burda, P
Kuster, A
Hjalmarson, O
Suormala, T
Bürer, C
Lutz, S
Roussey, G
Christa, L
Asin-Cayuela, J
Kollberg, G
Andersson, BA
Watkins, D
Rosenblatt, DS
Fowler, B
Holme, E
Froese, DS
Baumgartner, MR
AF Burda, P.
Kuster, A.
Hjalmarson, O.
Suormala, T.
Buerer, C.
Lutz, S.
Roussey, G.
Christa, L.
Asin-Cayuela, J.
Kollberg, G.
Andersson, B. A.
Watkins, D.
Rosenblatt, D. S.
Fowler, B.
Holme, E.
Froese, D. S.
Baumgartner, M. R.
TI Characterization and review of MTHFD1 deficiency: four new patients,
cellular delineation and response to folic and folinic acid treatment
SO JOURNAL OF INHERITED METABOLIC DISEASE
LA English
DT Article
ID NEURAL-TUBE DEFECTS; RISK; POLYMORPHISMS; METABOLISM; SEQUENCE; ENZYME;
MUTATIONS; ALIGNMENT; CANCER; GENES
AB In the folate cycle MTHFD1, encoded by MTHFD1, is a trifunctional enzyme containing 5,10-methylenetetrahydrofolate dehydrogenase, 5,10-methenyltetrahydrofolate cyclohydrolase and 10-formyltetrahydrofolate synthetase activity. To date, only one patient with MTHFD1 deficiency, presenting with hyperhomocysteinemia, megaloblastic anaemia, hemolytic uremic syndrome (HUS) and severe combined immunodeficiency, has been identified (Watkins et al J Med Genet 48:590-2, 2011). We now describe four additional patients from two different families. The second patient presented with hyperhomocysteinemia, megaloblastic anaemia, HUS, microangiopathy and retinopathy; all except the retinopathy resolved after treatment with hydroxocobalamin, betaine and folinic acid. The third patient developed megaloblastic anaemia, infection, autoimmune disease and moderate liver fibrosis but not hyperhomocysteinemia, and was successfully treated with a regime that included and was eventually reduced to folic acid. The other two, elder siblings of the third patient, died at 9 weeks of age with megaloblastic anaemia, infection and severe acidosis and had MTFHD1 deficiency diagnosed retrospectively. We identified a missense mutation (c.806C > T, p.Thr296Ile) and a splice site mutation (c.1674G > A) leading to exon skipping in the second patient, while the other three harboured a missense mutation (c.146C > T, p.Ser49Phe) and a premature stop mutation (c.673G > T, p.Glu225*), all of which were novel. Patient fibroblast studies revealed severely reduced methionine formation from [C-14]-formate, which did not increase in cobalamin supplemented culture medium but was responsive to folic and folinic acid. These additional cases increase the clinical spectrum of this intriguing defect, provide in vitro evidence of disturbed methionine synthesis and substantiate the effectiveness of folic or folinic acid treatment.
C1 [Burda, P.; Suormala, T.; Buerer, C.; Lutz, S.; Fowler, B.; Froese, D. S.; Baumgartner, M. R.] Univ Childrens Hosp, Div Metab, CH-8032 Zurich, Switzerland.
[Burda, P.; Suormala, T.; Buerer, C.; Lutz, S.; Fowler, B.; Froese, D. S.; Baumgartner, M. R.] Univ Childrens Hosp, Childrens Res Ctr, CH-8032 Zurich, Switzerland.
[Kuster, A.; Roussey, G.] Univ Hosp Nantes, Dept Pediat Nephrol, Nantes, France.
[Hjalmarson, O.] Univ Gothenburg, Dept Pediat, Gothenburg, Sweden.
[Christa, L.] Univ Paris 05, Necker Hosp, AP HP, Metab Biochem Dept, Paris, France.
[Asin-Cayuela, J.; Kollberg, G.; Holme, E.] Sahlgrens Univ Hosp, Dept Clin Chem, SE-41345 Gothenburg, Sweden.
[Andersson, B. A.] Sahlgrens Univ Hosp, Dept Clin Immunol & Transfus Med, Gothenburg, Sweden.
[Watkins, D.; Rosenblatt, D. S.] McGill Univ, Dept Human Genet, Montreal, PQ, Canada.
[Rosenblatt, D. S.; Baumgartner, M. R.] Univ Zurich, Programfor Rare Dis, Clin Res Prior, Radiz Rare Dis Initiat Zurich, Zurich, Switzerland.
[Baumgartner, M. R.] Univ Zurich, Zurich Ctr Integrat Human Physiol, Zurich, Switzerland.
C3 University Children's Hospital Zurich; University Children's Hospital
Zurich; Nantes Universite; CHU de Nantes; University of Gothenburg;
Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
Hopital Universitaire Necker-Enfants Malades - APHP; Sahlgrenska
University Hospital; Sahlgrenska University Hospital; McGill University;
University of Zurich; University of Zurich; Zurich Center Integrative
Human Physiology (ZIHP)
RP Baumgartner, MR (corresponding author), Univ Childrens Hosp, Div Metab, Steinwiesstr 75, CH-8032 Zurich, Switzerland.
EM elisabeth.holme@clinchem.gu.se; matthias.baumgartner@kispi.uzh.ch
RI Froese, D. Sean/AAW-6899-2021; Andersson, Bengt/B-7295-2019;
Baumgartner, Matthias/JAC-6829-2023; Baumgartner, Matthias
R./Q-2855-2017; Froese, D. Sean/J-6665-2017
OI Baumgartner, Matthias R./0000-0002-9270-0826; Froese, D.
Sean/0000-0003-1557-3517
FU Swiss National Science Foundation [31003A_138521]; Rare Disease
Initiative Zurich (radiz), a clinical research priority program for rare
diseases of the University of Zurich, Switzerland; Swiss National
Science Foundation (SNF) [31003A_138521] Funding Source: Swiss National
Science Foundation (SNF)
FX This work was supported by the Swiss National Science Foundation [grant
number 31003A_138521 to M.R.B. and B.F.] and the Rare Disease Initiative
Zurich (radiz), a clinical research priority program for rare diseases
of the University of Zurich, Switzerland.
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NR 28
TC 33
Z9 39
U1 0
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0141-8955
EI 1573-2665
J9 J INHERIT METAB DIS
JI J. Inherit. Metab. Dis.
PD SEP
PY 2015
VL 38
IS 5
BP 863
EP 872
DI 10.1007/s10545-015-9810-3
PG 10
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA CQ2NC
UT WOS:000360436700010
PM 25633902
OA Green Published, Green Submitted
DA 2025-01-07
ER
PT J
AU Hartung, T
Corsini, E
AF Hartung, Thomas
Corsini, Emanuela
TI Immunotoxicology: Challenges in the 21st century and In Vitro
Opportunities
SO ALTEX-ALTERNATIVES TO ANIMAL EXPERIMENTATION
LA English
DT Article
DE immune system; xenobiotics; toxicity testing; alternative methods;
toxicology for the 21st century
ID HUMAN WHOLE-BLOOD; INTERNATIONAL VALIDATION; REPRODUCTIVE TOXICITY;
ALTERNATIVE METHODS; CYTOKINE PRODUCTION; DENDRITIC CELLS;
RISK-ASSESSMENT; ANIMAL-MODELS; LIVER-INJURY; IMMUNE
AB Over the last two decades, little has changed in the practice of immunotoxicity testing for regulatory purposes, especially for immunosuppression, and autoimmunity is still a challenge. Current guidelines still rely on animal tests, which include some immune endpoints in repeated dose tests and trigger dedicated tests only when certain alerts indicate a problem. At the same time, however, a wealth of in vitro approaches has been developed, but few have been adopted for routine testing. The extent to which immunotoxicity of chemicals represents a health problem for the human population at low levels of exposure is unclear: it appears that responses of healthy individuals to immunological challenges differ widely and most immunomodulators have few adverse effects except when they coincide with an infectious or malignant challenge or when early in life exposure is expected, in which cases the odds of progressing into infection, autoimmune diseases, or cancer can be changed. The enormous overcapacity of immune defense, the presence of compensatory mechanisms, and their fast restoration each contribute to limiting health threats for the individual, though on a population base also minor immunomodulation may result in increased morbidity. In vitro alternative approaches may allow screening for problematic substances and prioritize them for in vivo testing. New approaches are emerging from mapping pathways of immunotoxicity. Increasingly, the contribution of inflammatory and infectious components to the adverse outcome pathways of chemicals is recognized for various hazards, urging inclusion of tests for proinflammatory and immunomodulatory properties of chemicals into integrated testing strategies.
C1 [Hartung, Thomas] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, CAAT, Baltimore, MD USA.
[Hartung, Thomas] Univ Konstanz, CAAT Europe, Constance, Germany.
[Corsini, Emanuela] Univ Milan, Toxicol Lab, DiSFeB, Milan, Italy.
C3 Johns Hopkins University; Johns Hopkins Bloomberg School of Public
Health; University of Konstanz; University of Milan
RP Hartung, T (corresponding author), Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Alternat Anim Testing, 615 North Wolfe St,W7032, Baltimore, MD 21205 USA.
EM thartung@jhsph.edu
RI Corsini, Emanuela/B-5602-2011; Hartung, Thomas/Q-1076-2015
OI Corsini, Emanuela/0000-0002-6927-5956; Hartung,
Thomas/0000-0003-1359-7689
FU NIH [3R01ES018845-04S1, 1R01ES020750]
FX The discussions and work with the ECVAM taskforce on immunotoxicology
and the participants of the respective BC YAM workshop is gratefully
appreciated. TH holds patents on the whole blood pyrogen test and
cryopreserved blood mentioned above and is supported also by NIH
(3R01ES018845-04S1). The work on pathway of toxicity mapping referred to
is financed by NIH (1R01ES020750).
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NR 126
TC 37
Z9 43
U1 4
U2 17
PU SPEKTRUM AKADEMISCHER VERLAG-SPRINGER-VERLAG GMBH
PI HEILDEBERG
PA TIERGARTENSTRASSE 17, HEILDEBERG, 69121, GERMANY
SN 1868-596X
EI 1868-8551
J9 ALTEX-ALTERN ANIM EX
JI ALTEX-Altern. Anim. Exp.
PY 2013
VL 30
IS 4
BP 411
EP 426
DI 10.14573/altex.2013.4.411
PG 16
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 264TE
UT WOS:000327903100002
PM 24173166
OA Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Sulthana, S
Shrestha, D
Aryal, S
AF Sulthana, Shoukath
Shrestha, Dinesh
Aryal, Santosh
TI Maximizing liposome tumor delivery by hybridizing with tumor-derived
extracellular vesicles
SO NANOSCALE
LA English
DT Article
ID CELL; EXOSOME
AB Extracellular vesicles (EVs) have gained widespread interest due to their potential in the diagnosis and treatment of inflammation, autoimmune diseases, and cancers. EVs are lipidic vesicles comprising vesicles of endosomal origin called exosomes, microvesicles from membrane shedding, and apoptotic bodies from programmed cell death membrane blebbing that carry complex sets of cargo from their cells of origin, including proteins, lipids, mRNA, and DNA. EVs are rich in integrin proteins that facilitate intrinsic cellular communication to deliver their cargo contents and can also be used as biomarkers to study respective cellular conditions. Within this background, we hypothesized that when these EVs are hybridized with synthetic liposomes, it would help navigate the hybrid construct in the complex biological environment to find its target. Toward this endeavor, we have hybridized a synthetic liposome with EVs (herein called LEVs) derived from mouse breast cancer (4T1 tumors) cells and incorporated a rhodamine-B/near-infrared fluorescent dye to investigate their potential for cellular targeting and tumor delivery. Using membrane extrusion, we have successfully hybridized both entities resulting in the formation of LEVs and characterized their colloidal properties and stability over a period. While EVs are broadly dispersed nano- and micron-sized vesicles, LEVs are engineered as monodispersed with an average hydrodynamic size of 140 +/- 5. Using immunoblotting and ELISA, we monitored and quantified the EV-specific protein CD63 and other characteristic proteins such as CD9 and CD81, which were taken as a handle to ensure the reproducibility of EVs and thus LEVs. These LEVs were further challenged with mice bearing orthotopic 4T1 breast tumors and the LEV uptake was found to be maximum in tumors and organs like the liver, spleen, and lungs when compared to control PEGylated liposomes in live animal imaging. Likewise, the constructs were capable of finding lung metastasis as observed in ex vivo imaging. We anticipate that this study can open avenues for drug delivery solutions that are superior in target recognition.
This investigation highlights the maximizing of nanoparticle tumor delivery by hybridizing nanoparticles with tumor-derived-extracellular vesicles.
C1 [Sulthana, Shoukath; Shrestha, Dinesh; Aryal, Santosh] Univ Texas Tyler, Ben & Maytee Fisch Coll Pharm, Dept Pharmaceut Sci & Hlth Outcomes, Tyler, TX 75799 USA.
C3 University of Texas System; University of Texas at Tyler
RP Aryal, S (corresponding author), Univ Texas Tyler, Ben & Maytee Fisch Coll Pharm, Dept Pharmaceut Sci & Hlth Outcomes, Tyler, TX 75799 USA.
EM santosharyal@uttyler.edu
RI Aryal, Santosh/E-7310-2013
FU National Institute of Biomedical Imaging and Bioengineering; National
Institute of Health [7R15EB030815-02]; Research Office at the University
of Texas at Tyler
FX The authors acknowledge the support from the National Institute of
Biomedical Imaging and Bioengineering, the National Institute of Health
under grant no. 7R15EB030815-02. The authors thank Dr Ramakrishna
Vankayalapati, the University of Texas Health Science Center, University
of Texas at Tyler for reviewing the immunology section. The authors also
acknowledge the support from the Research Office at the University of
Texas at Tyler.
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NR 40
TC 0
Z9 0
U1 14
U2 14
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 2040-3364
EI 2040-3372
J9 NANOSCALE
JI Nanoscale
PD SEP 12
PY 2024
VL 16
IS 35
BP 16652
EP 16663
DI 10.1039/d4nr02191f
EA AUG 2024
PG 12
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
Science, Multidisciplinary; Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
Physics
GA F5M5O
UT WOS:001295519900001
PM 39171636
DA 2025-01-07
ER
PT J
AU Yin, LH
Zheng, LL
Xu, LN
Dong, DS
Han, X
Qi, Y
Zhao, YY
Xu, YW
Peng, JY
AF Yin, Lianhong
Zheng, Lingli
Xu, Lina
Dong, Deshi
Han, Xu
Qi, Yan
Zhao, Yanyan
Xu, Youwei
Peng, Jinyong
TI In-silico prediction of drug targets, biological
activities, signal pathways and regulating networks of dioscin based on
bioinformatics
SO BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
DE Dioscin; Inverse docking technology; Bioinformatics; Pathway; Network
ID DIVERSITY-ORIENTED SYNTHESIS; LIVER-DAMAGE; REVERSE DOCKING;
DOWN-REGULATION; SMALL-MOLECULE; PROTEIN; INHIBITION; APOPTOSIS; ASSAY
AB Background: Inverse docking technology has been a trend of drug discovery, and bioinformatics approaches have been used to predict target proteins, biological activities, signal pathways and molecular regulating networks affected by drugs for further pharmacodynamic and mechanism studies.
Methods: In the present paper, inverse docking technology was applied to screen potential targets from potential drug target database (PDTD). Then, the corresponding gene information of the obtained drug-targets was applied to predict the related biological activities, signal pathways and processes networks of the compound by using MetaCore platform. After that, some most relevant regulating networks were considered, which included the nodes and relevant pathways of dioscin.
Results: 71 potential targets of dioscin from humans, 7 from rats and 8 from mice were screened, and the prediction results showed that the most likely targets of dioscin were cyclin A2, calmodulin, hemoglobin subunit beta, DNA topoisomerase I, DNA polymerase lambda, nitric oxide synthase and UDP-N-acetylhexosamine pyrophosphorylase, etc. Many diseases including experimental autoimmune encephalomyelitis of human, temporal lobe epilepsy of rat and ankylosing spondylitis of mouse, may be inhibited by dioscin through regulating immune response alternative complement pathway, G-protein signaling RhoB regulation pathway and immune response antiviral actions of interferons, etc. The most relevant networks (5 from human, 3 from rat and 5 from mouse) indicated that dioscin may be a TOP1 inhibitor, which can treat cancer though the cell cycle-transition and termination of DNA replication pathway. Dioscin can down regulate EGFR and EGF to inhibit cancer, and also has anti-inflammation activity by regulating JNK signaling pathway.
Conclusions: The predictions of the possible targets, biological activities, signal pathways and relevant regulating networks of dioscin provide valuable information to guide further investigation of dioscin on pharmacodynamics and molecular mechanisms, which also suggests a practical and effective method for studies on the mechanism of other chemicals.
C1 [Yin, Lianhong; Xu, Lina; Han, Xu; Qi, Yan; Zhao, Yanyan; Xu, Youwei; Peng, Jinyong] Dalian Med Univ, Coll Pharm, Dalian 116044, Peoples R China.
[Zheng, Lingli; Dong, Deshi] Dalian Med Univ, Affiliated Hosp 1, Dalian 116022, Peoples R China.
[Peng, Jinyong] Dalian Med Univ, Res Inst Integrated Tradit & Western Med, Dalian 116011, Peoples R China.
C3 Dalian Medical University; Dalian Medical University; Dalian Medical
University
RP Peng, JY (corresponding author), Dalian Med Univ, Coll Pharm, Western 9 Lvshun South Rd, Dalian 116044, Peoples R China.
EM jinyongpeng2005@163.com
RI qi, Yan/KIC-1612-2024
FU National Natural Science Foundation of China [81274195]; Doctorate in
Higher Education Institutions of Ministry of Education [20122105110004];
Program for New Century Excellent Talents in University [NCET-11-1007];
Program for Liaoning Innovative Research Team in University [LT2013019];
National Science and Technology Major Special Project on Major New Drug
Innovation [2012ZX09503001-003]
FX This work was financially supported by National Natural Science
Foundation of China (No. 81274195), the Doctorate in Higher Education
Institutions of Ministry of Education (No. 20122105110004), the Program
for New Century Excellent Talents in University (NCET-11-1007), the
Program for Liaoning Innovative Research Team in University (LT2013019),
and the National Science and Technology Major Special Project on Major
New Drug Innovation (No. 2012ZX09503001-003).
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NR 42
TC 12
Z9 14
U1 1
U2 23
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1472-6882
J9 BMC COMPLEM ALTERN M
JI BMC Complement. Altern. Med.
PD MAR 5
PY 2015
VL 15
AR 41
DI 10.1186/s12906-015-0579-6
PG 17
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA CC8PL
UT WOS:000350630500001
PM 25879470
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Burris, RL
Ng, HP
Nagarajan, S
AF Burris, Ramona L.
Ng, Hang-Pong
Nagarajan, Shanmugam
TI Soy protein inhibits inflammation-induced VCAM-1 and inflammatory
cytokine induction by inhibiting the NF-κB and AKT signaling pathway in
apolipoprotein E-deficient mice
SO EUROPEAN JOURNAL OF NUTRITION
LA English
DT Article
DE Soy peptides; Inflammation; VCAM-1; Hyperlipidemia; Atherosclerosis
ID MICROVASCULAR ENDOTHELIAL-CELLS; SERUM AMYLOID-A; ATHEROSCLEROTIC
LESIONS; MONOCYTE ADHESION; EXPRESSION; ACTIVATION; ICAM-1; ISOLATE;
MECHANISMS; RECEPTORS
AB Inflammation is a hallmark of many diseases, such as atherosclerosis, autoimmune diseases, obesity, and cancer. Isoflavone-free soy protein diet (SPI-) has been shown to reduce atherosclerotic lesions in a hyperlipidemic mouse model compared to casein (CAS)-fed mice, despite unchanged serum lipid levels. However, possible mechanisms contributing to the athero-protective effect of soy protein remain unknown. Therefore, we investigated whether and how SPI- diet inhibits inflammatory responses associated with atherosclerosis.
Apolipoprotein E knockout (apoE-/-) mice (5-week) were fed CAS or SPI- diet for 1 or 5 week to determine LPS- and hyperlipidemia-induced acute and chronic inflammatory responses, respectively. Expression of NF-kappa B-dependent inflammation mediators such as VCAM-1, TNF-alpha, and MCP-1 were determined in aorta and liver. NF-kappa B, MAP kinase, and AKT activation was determined to address mechanisms contributing to the anti-inflammatory properties of soy protein/peptides.
Isoflavone-free soy protein diet significantly reduced LPS-induced VCAM-1 mRNA and protein expression in aorta compared to CAS-fed mice. Reduced VCAM-1 expression in SPI--fed mice also paralleled attenuated monocyte adhesion to vascular endothelium, a critical and primary processes during inflammation. Notably, VCAM-1 mRNA and protein expression in lesion-prone aortic arch was significantly reduced in apoE-/- mice fed SPI- for 5 weeks compared with CAS-fed mice. Moreover, dietary SPI- potently inhibited LPS-induced NF-kappa B activation and the subsequent upregulation of pro-inflammatory cytokines, including TNF-alpha, IL-6, IL-1 beta, and MCP-1. Interestingly, SPI- inhibited NF-kappa B-dependent inflammatory responses by targeting I-kappa B phosphorylation and AKT activation with no effect on MAP kinase pathway. Of the five putative soy peptides, four of the soy peptides inhibited LPS-induced VCAM-1, IL-6, IL-8, and MCP-1 protein expression in human vascular endothelial cells in vitro.
Collectively, our findings suggest that anti-inflammatory properties of component(s) of soy protein/peptides may be a possible mechanism for the prevention of chronic inflammatory diseases such as atherosclerosis.
C1 [Burris, Ramona L.; Nagarajan, Shanmugam] Arkansas Childrens Nutr Ctr, Little Rock, AR USA.
[Ng, Hang-Pong; Nagarajan, Shanmugam] Univ Arkansas Med Sci, Dept Microbiol & Immunol, Little Rock, AR 72202 USA.
[Ng, Hang-Pong; Nagarajan, Shanmugam] Univ Pittsburgh, Dept Pathol, Pittsburgh, PA 15261 USA.
[Ng, Hang-Pong; Nagarajan, Shanmugam] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA 15261 USA.
C3 University of Arkansas System; University of Arkansas Medical Sciences;
Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh
RP Nagarajan, S (corresponding author), Univ Pittsburgh, Dept Pathol, BST E1256,200 Lothrop St, Pittsburgh, PA 15261 USA.
EM nagarajans@upmc.edu
RI NG, Hang/AAB-2427-2020
FU U.S. Department of Agriculture [CRIS-6251-51000-005-02S]; Experimental
Pathology, Department of Pathology and Vascular Medicine Institute,
University of Pittsburgh, PA
FX This work was supported by a grant from U.S. Department of Agriculture
(CRIS-6251-51000-005-02S (SN) and SN was supported in part by intramural
funds from the Experimental Pathology, Department of Pathology and
Vascular Medicine Institute, University of Pittsburgh, PA. We thank John
Gregan for his help with manuscript preparation. We also thank Van
Goodwin III, Jessica Warden and Amy Greenway for technical assistance.
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NR 47
TC 39
Z9 41
U1 0
U2 24
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1436-6207
EI 1436-6215
J9 EUR J NUTR
JI Eur. J. Nutr.
PD FEB
PY 2014
VL 53
IS 1
BP 135
EP 148
DI 10.1007/s00394-013-0509-7
PG 14
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA AA4PZ
UT WOS:000331079500012
PM 23468309
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Gürbüz, Y
Tülek, NE
Tütüncü, EE
Koruk, ST
Aygen, B
Demirtürk, N
Kinikli, S
Kaya, A
Yildirmak, T
Süer, K
Korkmaz, F
Ural, O
Akhan, S
Günal, O
Tuna, N
Köse, S
Gönen, I
Örmen, B
Türker, N
Saltoglu, N
Batirel, A
Tuncer, G
Bulut, C
Sirmatel, F
Ulçay, A
Karagöz, E
Tosun, D
Sener, A
Aynioglu, A
Altunok, ES
AF Gurbuz, Yunus
Tulek, Necla Eren
Tutuncu, Emin Ediz
Koruk, Suda Tekin
Aygen, Bilgehan
Demirturk, Nese
Kinikli, Sami
Kaya, Ali
Yildirmak, Taner
Suer, Kaya
Korkmaz, Fatime
Ural, Onur
Akhan, Sila
Gunal, Ozgur
Tuna, Nazan
Kose, Sukran
Gonen, Ibak
Ormen, Bahar
Turker, Nesrin
Saltoglu, Nese
Batirel, Ayse
Tuncer, Gunay
Bulut, Cemal
Sirmatel, Fatma
Ulcay, Asim
Karagoz, Ergenekon
Tosun, Dervis
Sener, Alper
Aynioglu, Aynur
Altunok, Elif Sargin
TI Evaluation of Dual Therapy in Real Life Setting in Treatment-Naive
Turkish Patients with HCV Infection: A Multicenter, Retrospective Study
SO BALKAN MEDICAL JOURNAL
LA English
DT Article; Proceedings Paper
CT Conference of the Asian-Pacific-Association-for-the-Study-of-the-Liver
(APASL)
CY MAR 12-15, 2014
CL Brisbane, AUSTRALIA
SP Asian Pacific Assoc Study Liver
DE Hepatitis C; peginterferon alpha-2a; peginterferon alpha-2b; ribavirin;
therapy
ID CHRONIC HEPATITIS-C; SUSTAINED VIROLOGICAL RESPONSE; ALPHA-2B PLUS
RIBAVIRIN; PEGINTERFERON ALPHA-2A; HEPATOCELLULAR-CARCINOMA;
INSULIN-RESISTANCE; COMBINATION THERAPY; TOLERABILITY; MANAGEMENT;
DIAGNOSIS
AB Background: Before the introduction of direct-acting antivirals in the treatment of chronic hepatitis C patients, the combination of peginterferon alpha and ribavirin was the standard therapy. Observational studies that investigated sustained virological response (SVR) rates by these drugs yielded different outcomes.
Aims: The goal of the study was to demonstrate real life data concerning SVR rate achieved by peginterferon alpha plus ribavirin in patients who were treatment-naive.
Study Design: A multicenter, retrospective observational study.
Methods: The study was conducted retrospectively on 1214 treatment naive-patients, being treated with peginterferon alpha-2a or 2b plus ribavirin in respect of the current guidelines between 2005 and 2013. The patients' data were collected from 22 centers via a standard form, which has been prepared for this study. The data included demographic and clinical characteristics (gender, age, body weight, initial Hepatitis C virus RNA (HCV RNA) level, disease staging) as well as course of treatment (duration of treatment, outcomes, discontinuations and adverse events). Renal insufficiency, decompensated liver disease, history of transplantation, immunosuppressive therapy or autoimmune liver disease were exclusion criteria for the study. Treatment efficacy was assessed according to the patient's demographic characteristics, baseline viral load, genotype, and fibrosis scores.
Results: The mean age of the patients was 50.74 (+/- 0.64) years. Most of them were infected with genotype 1 (91.8%). SVR was achieved in 761 (62.7%) patients. SVR rate was 59.1% in genotype 1, 89.4% in genotype 2, 93.8% in genotype 3, and 33.3% in genotype 4 patients. Patients with lower viral load yielded higher SVR (65.8% vs. 58.4%, p=0.09). SVR rates according to histologic severity were found to be 69.3%, 66.3%, 59.9%, 47.3%, and 45.5% in patients with fibrosis stage 0, 1, 2, 3 and 4, respectively. The predictors of SVR were male gender, genotype 2/3, age less than 45 years, low fibrosis stage, low baseline viral load and presence of early virological response. SVR rates to each peginterferon were found to be similar in genotype 1/4 although SVR rates were found to be higher for peginterferon alpha-2b in patients with genotype 2/3. The number of patients who failed to complete treatment due to adverse effects was 33 (2.7%). The number of patients failed to complete treatment due to adverse effects was 33 (2.7%).
Conclusion: Our findings showed that the rate of SVR to dual therapy was higher in treatment-naive Turkish patients than that reported in randomized controlled trials. Also peginterferon alpha-2a and alpha-2b were found to be similar in terms of SVR in genotype 1 patients.
C1 [Gurbuz, Yunus; Tutuncu, Emin Ediz] Diskapi Yildirim Beyazit Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Ankara, Turkey.
[Tulek, Necla Eren; Kinikli, Sami; Tuncer, Gunay; Bulut, Cemal] Ankara Numune Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Ankara, Turkey.
[Koruk, Suda Tekin] Harran Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Sanliurfa, Turkey.
[Aygen, Bilgehan] Erciyes Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Kayseri, Turkey.
[Demirturk, Nese] Afyon Kocatepe Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Afyon, Turkey.
[Kaya, Ali] Mersin Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Mersin, Turkey.
[Yildirmak, Taner] Okmeydani Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Istanbul, Turkey.
[Suer, Kaya] Near East Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Nicosia, Cyprus.
[Korkmaz, Fatime] Konya Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Konya, Turkey.
[Ural, Onur] Selcuk Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Konya, Turkey.
[Akhan, Sila; Aynioglu, Aynur; Altunok, Elif Sargin] Kocaeli Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Kocaeli, Turkey.
[Gunal, Ozgur] Gaziosmanpasa Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Tokat, Turkey.
[Tuna, Nazan] Sakarya Univ, Fac Med, Dept Infect Dis & Clin Microbiol, Sakarya, Turkey.
[Kose, Sukran] Tepecik Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Izmir, Turkey.
Suleyman Demirel Univ, Dept Infect Dis & Clin Microbiol, Fac Med, Isparta, Turkey.
[Gonen, Ibak] Izmir Katip Celebi Univ, Ataturk Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Izmir, Turkey.
[Ormen, Bahar; Turker, Nesrin; Saltoglu, Nese] Istanbul Univ, Cerrahpasa Fac Med, Dept Infect Dis & Clin Microbiol, Istanbul, Turkey.
[Batirel, Ayse] Kartal Dr Lutfi Kirdar Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Istanbul, Turkey.
[Sirmatel, Fatma] Abant Izzet Baysal Univ, Dept Infect Dis & Clin Microbiol, Fac Med, Bolu, Turkey.
[Ulcay, Asim; Karagoz, Ergenekon] GATA Haydarpasa Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Istanbul, Turkey.
[Tosun, Dervis] Ulus State Hosp, Dept Infect Dis & Clin Microbiol, Ankara, Turkey.
[Sener, Alper] Canakkale Onsekiz Mart Univ, Dept Infect Dis & Clin Microbiol, Fac Med, Canakkale, Turkey.
C3 Diskapi Yildirim Beyazit Training & Research Hospital; Ankara Numune
Training & Research Hospital; Harran University; Erciyes University;
Afyon Kocatepe University; Mersin University; Istanbul Okmeydani
Training & Research Hospital; Near East University; Konya Egitim
Training & Research Hospital; Selcuk University; Kocaeli University;
Gaziosmanpasa University; Sakarya University; Izmir Tepecik Training &
Research Hospital; Suleyman Demirel University; Izmir Ataturk Training &
Research Hospital; Izmir Katip Celebi University; Istanbul University;
Istanbul University - Cerrahpasa; Istanbul Kartal Dr Lutfi Kirdar
Training & Research Hospital; Abant Izzet Baysal University; Istanbul
Haydarpasa Sultan Abdulhamid Training & Research Hospital; Gulhane
Military Medical Academy; Canakkale Onsekiz Mart University
RP Gürbüz, Y (corresponding author), Diskapi Yildirim Beyazit Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Ankara, Turkey.
EM yunusgurbuz@outlook.com
RI KAYA, Ali/KFA-9478-2024; bulut, cemal/AAB-5496-2022; Gürbüz,
Yunus/GPP-0781-2022; Saltoglu, Nese/E-2833-2019; SARGIN ALTUNOK,
Elif/GPT-3450-2022; Ertem, Gunay/GRJ-7397-2022; Örmen,
Bahar/ABA-1027-2021; sener, alper/F-6427-2011; KINIKLI,
Sami/IYJ-9555-2023; KOSE, SUKRAN/K-3936-2018; Batirel,
Ayse/KUC-6287-2024; Demirturk, Nese/ADZ-1979-2022; URAL,
Onur/KGL-7134-2024; Gunal, Ozgur/V-6314-2019; Süer, Kaya/GNM-8453-2022;
Tutuncu, Ediz/CAI-8025-2022; Tulek, Necla/M-3283-2017; Yildirmak,
Taner/AAK-4864-2021
OI Tuncer Ertem, Gunay/0000-0001-8760-0030; Yildirmak,
Taner/0000-0001-7006-7161; Gunal, Ozgur/0000-0002-7744-4123; ULCAY,
ASIM/0000-0003-0531-0668; Saltoglu, Nese/0000-0003-4239-9585; Ural,
Onur/0000-0003-1355-7572; Demirturk, Nese/0000-0002-6186-2494; Tulek,
Necla/0000-0002-3952-4982
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NR 42
TC 11
Z9 11
U1 0
U2 28
PU GALENOS PUBL HOUSE
PI ISTANBUL
PA MOLLA GURANI MAHALLESI KACAMAK SOKAK NO 21-1, ISTANBUL, TURKEY
SN 2146-3123
EI 2146-3131
J9 BALK MED J
JI Balk. Med. J.
PD JAN
PY 2016
VL 33
IS 1
BP 18
EP 26
DI 10.5152/balkanmedj.2015.15859
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC General & Internal Medicine
GA DE9ON
UT WOS:000370967500005
PM 26966614
OA Green Published, gold, Green Submitted
DA 2025-01-07
ER
PT J
AU Nagata, T
Yasuda, Y
Ando, M
Abe, T
Katsuno, T
Kato, S
Tsuboi, N
Matsuo, S
Maruyama, S
AF Nagata, Takanobu
Yasuda, Yoshinari
Ando, Masahiko
Abe, Tomoko
Katsuno, Takayuki
Kato, Sawako
Tsuboi, Naotake
Matsuo, Seiichi
Maruyama, Shoichi
TI Clinical Impact of Kidney Function on Presepsin Levels
SO PLOS ONE
LA English
DT Article
ID SOLUBLE CD14 SUBTYPE; SEVERE SEPSIS; SEPTIC SHOCK; EMERGENCY-DEPARTMENT;
PROCALCITONIN LEVELS; MULTICENTER; INTERLEUKIN-6; INHIBITION;
MANAGEMENT; DIAGNOSIS
AB Objective
Presepsin is highlighted as a diagnostic and prognostic marker of sepsis. Little information is available regarding the accurate association between presepsin levels and the degree of kidney function. We analyzed presepsin levels in patients with a glomerular filtration rate (GFR) in the categories G1 to G5, evaluated via inulin renal clearance test, and receiving hemodialysis (HD).
Methods
Patients who were not receiving HD were included if they had undergone inulin renal clearance measurements for the accurate measurement of GFR (measured GFR), and patients who were receiving hemodialysis (HD) were included if they had anuria. Exclusion criteria were infection, cancer, liver disease, autoimmune disorders, or steroid or immunosuppressant use. GFR category was defined as follows; G1: GFR >= 90 ml/min/1.73m(2), G2: GFR = 60 to 90 ml/min/1.73m(2), G3: GFR = 30 to 60 ml/min/1.73m(2), G4: GFR = 15 to 30 ml/min/1.73m(2), G5: GFR <= 15 ml/min/1.73m(2).
Results Seventy-one patients were included. The median (IQR) presepsin values of patients in each GFR category were as follows: G1 + G2: 69.8 (60.8-85.9) pg/ml; G3: 107.0 (68.7-150.0) pg/ml; G4: 171.0 (117.0-200.0) pg/ml; G5: 251.0 (213.0-297.5) pg/ml; and HD: 1160.0 (1070.0-1400.0) pg/ml. The log-transformed presepsin values, excluding patients receiving HD, inversely correlated with the measured GFR (Pearson's correlation coefficient = -0.687, P < 0.001). The multivariate analysis revealed that measured GFR and hemoglobin levels significantly correlated with elevated presepsin levels.
Conclusion
Presepsin levels were markedly high in patients receiving HD, similar to values seen in patients with severe sepsis or septic shock. In patients who were not receiving HD, presepsin levels increased as GFR decreased. Thus, the evaluation of presepsin levels in patients with chronic kidney disease requires further consideration, and a different cutoff value is needed for diagnosing sepsis in such patients.
C1 [Nagata, Takanobu; Yasuda, Yoshinari; Abe, Tomoko; Katsuno, Takayuki; Kato, Sawako; Tsuboi, Naotake; Matsuo, Seiichi; Maruyama, Shoichi] Nagoya Univ, Grad Sch Med, Dept Nephrol, Nagoya, Aichi 4648601, Japan.
[Ando, Masahiko] Nagoya Univ Hosp, Ctr Adv Med & Clin Res, Nagoya, Aichi, Japan.
C3 Nagoya University; Nagoya University
RP Maruyama, S (corresponding author), Nagoya Univ, Grad Sch Med, Dept Nephrol, Nagoya, Aichi 4648601, Japan.
EM marus@med.nagoya-u.ac.jp
RI ANDO, Masahiko/F-7035-2015; Tsuboi, Naotake/L-5960-2019; Kato,
Sawako/T-2422-2019
OI Tsuboi, Naotake/0000-0003-0760-845X
FU Kyowa Hakko Kirin Co., Ltd.; Otsuka Pharmaceutical Co., Ltd.; Dainippon
Sumitomo Pharma Co., Ltd.; Mochida Pharmaceutical Co., Ltd.;
Grants-in-Aid for Scientific Research [25460896, 25305029, 15H05291]
Funding Source: KAKEN
FX This work was supported by Kyowa Hakko Kirin Co., Ltd. Otsuka
Pharmaceutical Co., Ltd., Dainippon Sumitomo Pharma Co., Ltd., and
Mochida Pharmaceutical Co., Ltd. provided support in the form of
research grants for authors [TN, YY, MA, TA, TK, SK, NT, SM, SM], but
did not have any additional role in the study design, data collection
and analysis, decision to publish, or preparation of the manuscript. The
specific roles of these authors are articulated in the 'author
contributions' section.
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NR 36
TC 75
Z9 77
U1 0
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD JUN 1
PY 2015
VL 10
IS 6
AR e0129159
DI 10.1371/journal.pone.0129159
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CL0KF
UT WOS:000356630900212
PM 26030716
OA Green Published, Green Submitted, gold
DA 2025-01-07
ER
PT J
AU Burtea, C
Laurent, S
Lancelot, E
Ballet, S
Murariu, O
Rousseaux, O
Port, M
Elst, LV
Corot, C
Muller, RN
AF Burtea, Carmen
Laurent, Sophie
Lancelot, Eric
Ballet, Sebastien
Murariu, Oltea
Rousseaux, Olivier
Port, Marc
Elst, Luce Vander
Corot, Claire
Muller, Robert N.
TI Peptidic Targeting of Phosphatidylserine for the MRI Detection of
Apoptosis in Atherosclerotic Plaques
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE Phage display; peptide; apoptosis; atherosclerosis; MRI; molecular
imaging
ID PROGRAMMED CELL-DEATH; ANNEXIN-V; MAGNETIC-RESONANCE; PHAGE DISPLAY;
PHYSICOCHEMICAL CHARACTERIZATION; GADOLINIUM COMPLEX; IN-VIVO; CHANNEL;
PROTEIN; STABILITY
AB Molecular and cellular imaging of atherosclerosis has garnered more interest at the beginning of the 21st century, with aims to image in vivo biological properties of plaque lesions. Apoptosis seems an attractive target for the diagnosis of vulnerable atherosclerotic plaques prone to a thrombotic event. The aim of the present work was to screen for apoptosis peptide binders by phage display with the final purpose to detect apoptotic cells in atherosclerotic plaques by magnetic resonance imaging (MRI). A phosphatidylserine-specific peptide identified by phage display was thus used to design an MRI contrast agent (CA), which was evaluated as a potential in vivo reporter of apoptotic cells. A library of linear 6-mer random peptides was screened in vitro against immobilized phosphatidylserine. Phage DNA was isolated and sequenced, and the affinity of peptides for phosphatidylserine was evaluated by enzyme-linked immunosorbent assay. The phosphatidylserine-specific peptide and its scrambled homologue were attached to a linker and conjugated to DTPA-isothiocyanate. The products were purified by dialysis and by column chromatography and complexed with gadolinium chloride. After their evaluation using apoptotic cells and a mouse model of liver apoptosis, the phosphatidylserine-targeted CA was used to image atherosclerotic lesions on ApoE(-/-) transgenic mice. Apoptotic cells were detected on liver and aorta specimens by the immunostaining of phosphatidylserine and of active caspase-3. Sequencing of the phage genome highlighted nine different peptides. Their alignment with amino acid sequences of relevant proteins revealed a frequent homology with Ca2+ channels, reminiscent of the function of annexins. Alignment with molecules involved in apoptosis provides a direct correlation between peptide selection and utility. The in vivo MRI studies performed at 4.7 T provide proof of concept that apoptosis-related pathologies could be diagnosed by MRI with a low molecular weight paramagnetic agent. The new CA could have real potential in the diagnosis and therapy monitoring of atherosclerotic disease and of other apoptosis-associated pathologies, such as cancer, ischemia, chronic inflammation, autoimmune disorders, transplant rejection, neurodegenerative disorders, and diabetes mellitus. The phage display-derived peptide could also play a potential therapeutic role through anticoagulant activity by mimicking the role of annexin V, the endogenous ligand of phosphatidylserine.
C1 [Burtea, Carmen; Laurent, Sophie; Murariu, Oltea; Elst, Luce Vander; Muller, Robert N.] Univ Mons, Dept Gen Organ & Biomed Chem, NMR & Mol Imaging Lab, B-7000 Mons, Belgium.
[Lancelot, Eric; Ballet, Sebastien; Rousseaux, Olivier; Port, Marc; Corot, Claire] Guerbet, Res Ctr, F-93600 Aulnay Sous Bois, France.
C3 University of Mons; Guerbet Group
RP Muller, RN (corresponding author), Univ Mons, Dept Gen Organ & Biomed Chem, NMR & Mol Imaging Lab, 19 Ave Maistriau,Mendeleev Bldg, B-7000 Mons, Belgium.
EM robert.muller@umons.ac.be
RI Laurent, sophie/C-8095-2012; Burtea, Carmen/L-6223-2016
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NR 47
TC 74
Z9 83
U1 2
U2 38
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD NOV-DEC
PY 2009
VL 6
IS 6
BP 1903
EP 1919
DI 10.1021/mp900106m
PG 17
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 528QJ
UT WOS:000272461300024
PM 19743879
DA 2025-01-07
ER
PT J
AU Teschke, R
AF Teschke, Rolf
TI Hemochromatosis: Ferroptosis, ROS, Gut Microbiome, and Clinical
Challenges with Alcohol as Confounding Variable
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE hemochromatosis; iron overload; serum ferritin; fasting transferrin
saturation index; genetic testing; family screening; HFE genes;
phlebotomy; alcohol abuse; Haber-Weiss reaction; Fenton reaction; ROS;
ferroptosis; gut microbiome
ID MICROVILLOUS MEMBRANE-VESICLES; INTESTINAL IRON-ABSORPTION;
ETHANOL-OXIDIZING SYSTEM; HEREDITARY HEMOCHROMATOSIS; OXIDATIVE STRESS;
C282Y MUTATION; GENETIC HEMOCHROMATOSIS; LIVER-TRANSPLANTATION;
CAUSALITY ASSESSMENT; HFE HEMOCHROMATOSIS
AB Hemochromatosis represents clinically one of the most important genetic storage diseases of the liver caused by iron overload, which is to be differentiated from hepatic iron overload due to excessive iron release from erythrocytes in patients with genetic hemolytic disorders. This disorder is under recent mechanistic discussion regarding ferroptosis, reactive oxygen species (ROS), the gut microbiome, and alcohol abuse as a risk factor, which are all topics of this review article. Triggered by released intracellular free iron from ferritin via the autophagic process of ferritinophagy, ferroptosis is involved in hemochromatosis as a specific form of iron-dependent regulated cell death. This develops in the course of mitochondrial injury associated with additional iron accumulation, followed by excessive production of ROS and lipid peroxidation. A low fecal iron content during therapeutic iron depletion reduces colonic inflammation and oxidative stress. In clinical terms, iron is an essential trace element required for human health. Humans cannot synthesize iron and must take it up from iron-containing foods and beverages. Under physiological conditions, healthy individuals allow for iron homeostasis by restricting the extent of intestinal iron depending on realistic demand, avoiding uptake of iron in excess. For this condition, the human body has no chance to adequately compensate through removal. In patients with hemochromatosis, the molecular finetuning of intestinal iron uptake is set off due to mutations in the high-FE2+ (HFE) genes that lead to a lack of hepcidin or resistance on the part of ferroportin to hepcidin binding. This is the major mechanism for the increased iron stores in the body. Hepcidin is a liver-derived peptide, which impairs the release of iron from enterocytes and macrophages by interacting with ferroportin. As a result, iron accumulates in various organs including the liver, which is severely injured and causes the clinically important hemochromatosis. This diagnosis is difficult to establish due to uncharacteristic features. Among these are asthenia, joint pain, arthritis, chondrocalcinosis, diabetes mellitus, hypopituitarism, hypogonadotropic hypogonadism, and cardiopathy. Diagnosis is initially suspected by increased serum levels of ferritin, a non-specific parameter also elevated in inflammatory diseases that must be excluded to be on the safer diagnostic side. Diagnosis is facilitated if ferritin is combined with elevated fasting transferrin saturation, genetic testing, and family screening. Various diagnostic attempts were published as algorithms. However, none of these were based on evidence or quantitative results derived from scored key features as opposed to other known complex diseases. Among these are autoimmune hepatitis (AIH) or drug-induced liver injury (DILI). For both diseases, the scored diagnostic algorithms are used in line with artificial intelligence (AI) principles to ascertain the diagnosis. The first-line therapy of hemochromatosis involves regular and life-long phlebotomy to remove iron from the blood, which improves the prognosis and may prevent the development of end-stage liver disease such as cirrhosis and hepatocellular carcinoma. Liver transplantation is rarely performed, confined to acute liver failure.
In conclusion, ferroptosis, ROS, the gut microbiome, and concomitant alcohol abuse play a major contributing role in the development and clinical course of genetic hemochromatosis, which requires early diagnosis and therapy initiation through phlebotomy as a first-line treatment.
C1 [Teschke, Rolf] Dept Internal Med II, Div Gastroenterol & Hepatol, Klinikum Hanau, D-63450 Hanau, Germany.
[Teschke, Rolf] Goethe Univ Frankfurt Main, Acad Teaching Hosp, Med Fac, D-60590 Frankfurt, Germany.
C3 Goethe University Frankfurt
RP Teschke, R (corresponding author), Dept Internal Med II, Div Gastroenterol & Hepatol, Klinikum Hanau, D-63450 Hanau, Germany.; Teschke, R (corresponding author), Goethe Univ Frankfurt Main, Acad Teaching Hosp, Med Fac, D-60590 Frankfurt, Germany.
EM rolf.teschke@gmx.de
OI teschke, rolf/0000-0001-8910-1200
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NR 129
TC 5
Z9 5
U1 4
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD MAR
PY 2024
VL 25
IS 5
AR 2668
DI 10.3390/ijms25052668
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA KV9J5
UT WOS:001182852500001
PM 38473913
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Haitchi, S
Moliterno, P
Widhalm, K
AF Haitchi, Stefan
Moliterno, Paula
Widhalm, Kurt
TI Prevalence of vitamin D deficiency in seniors - A retrospective study
SO CLINICAL NUTRITION ESPEN
LA English
DT Article
DE Vitamin D deficiency; Geriatrics; Vitamin D supplementation; Nutrition
ID D SUPPLEMENTATION; METAANALYSIS; MASS
AB Background & aims: Vitamin D deficiency is a condition with different causes. It is associated with numerous comorbidities such as autoimmune diseases, bone diseases, cancer, cardiovascular diseases, neurodegenerative diseases, psychiatric diseases, and respiratory infections like COVID-19. Due to its high prevalence all over the world, it is a major task for health care systems worldwide. Through a combination of low sunlight exposure, insufficient nutrition, and age-related changes in skin, liver, and kidney function, especially seniors and nursing home residents, in particular, have a significantly increased risk of developing a vitamin D deficiency.Methods: This retrospective study analyzed the prevalence of vitamin D deficiency (serum 25-hydroxyvitamin D [25(OH)D] < 12 ng/ml) amongst selected Austrian nursing home seniors. It also examined whether demographic data and other laboratory values like calcium correlate with vitamin D levels by using the Pearson correlation coefficient. This correlation was graphically illustrated with a scatter plot and regression line. A total of 478 patients admitted to a nursing home in Vienna between January 3, 2017, and August 31, 2020, were included.Results: A total of 106 seniors (22,2%) suffered from a manifest vitamin D deficiency. The vitamin D level of the men was significantly lower than the level of the women (22.9 +/- 12.6 ng/ml vs. 26.2 +/- 14.8 ng/ml, p = 0.027). The vitamin D serum levels significantly correlated with the serum calcium levels of the participants (r = 0.19, p < 0.001). 39.5% (189 out of 478) of the nursing home residents had inadequate serum vitamin D levels.Conclusions: In summary, it can be said that the prevalence of vitamin D deficiency among nursing home residents is considerably high. Inadequate vitamin D levels were often associated with reduced calcium levels. Given the high prevalence, the numerous negative health consequences of inadequate levels, and the large therapeutic index, this risk group should get a general supplementation with a dose of 25 mg (1000 IU) vitamin D3 per day. In addition, a blood examination should be performed as early as three months after the start of the supplementation therapy. If some residents do not achieve an adequate vitamin D concentration, the substitution has to be adapted to the individual needs to treat them as precisely as possible.(c) 2023 The Author(s). Published by Elsevier Ltd on behalf of European Society for Clinical Nutrition and Metabolism. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
C1 [Haitchi, Stefan; Widhalm, Kurt] Med Univ Vienna, Spitalgasse 23, A-1090 Vienna, Austria.
[Moliterno, Paula] Univ Montevideo, Austrian Acad Inst Clin Nutr, Montevideo, Uruguay.
[Widhalm, Kurt] Austrian Acad Inst Clin Nutr, Alserstr 14-4a, A-1090 Vienna, Austria.
C3 Medical University of Vienna; Universidad de Montevideo
RP Widhalm, K (corresponding author), Med Univ Vienna, Spitalgasse 23, A-1090 Vienna, Austria.
EM stefan.haitchi@gmail.com; office@oeaie.org
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NR 35
TC 2
Z9 2
U1 8
U2 13
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2405-4577
J9 CLIN NUTR ESPEN
JI Clin. Nutr. ESPEN
PD OCT
PY 2023
VL 57
BP 691
EP 696
DI 10.1016/j.clnesp.2023.07.005
EA AUG 2023
PG 6
WC Nutrition & Dietetics
WE Emerging Sources Citation Index (ESCI)
SC Nutrition & Dietetics
GA T1VU0
UT WOS:001075938200001
PM 37739724
OA hybrid
DA 2025-01-07
ER
PT J
AU Zhou, GY
Yi, YX
Jin, LX
Lin, W
Fang, PP
Lin, XZ
Zheng, Y
Pan, CW
AF Zhou, Guang-Yao
Yi, Yong-Xiang
Jin, Ling-Xiang
Lin, Wei
Fang, Pei-Pei
Lin, Xiu-Zheng
Zheng, Yi
Pan, Chen-Wei
TI The protective effect of juglanin on fructose-induced hepatitis by
inhibiting inflammation and apoptosis through TLR4 and JAK2/STAT3
signaling pathways in fructose-fed rats
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Hepatitis; Juglanin; TLR4; Inflammation; JAK2/STAT3 signaling pathway
ID FATTY LIVER-DISEASE; TOLL-LIKE RECEPTORS; NF-KAPPA-B; AUTOIMMUNE
HEPATITIS; ANTIINFLAMMATORY ACTIVITY; JAPANESE PATIENTS; MYRICA-RUBRA;
TNF-ALPHA; P38; DIAGNOSIS
AB High fructose-feeding is an essential causative factor leading to the development and progression of hepatitis associated with high levels of endotoxin (LPS). Juglanin, as a natural compound extracted from the crude Polygonum aviculare, displayed inhibitory activity against inflammation response and cancer growth. However, researches about its role on anti-inflammation and apoptosis are far from available. Here, it is the first time that juglanin was administrated to investigate whether it inhibits fructose-feeding-induced hepatitis in rats and to elucidate the possible mechanism by which juglanin might recover it. Fructose-feeding rats were orally administrated with juglanin of 5, 10 and 20 mg/kg for 6 weeks, respectively. Juglanin exerted prevention of fructose-feeding-stimulated increased LPS levels, accelerated alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) and up-regulated inflammatory cytokines expression in serum, mainly including tumor necrosis factor-alpha (TNF-alpha), Interleukin 1beta (IL-1 beta), Interleukin 6 (IL-6) and Interleukin 18 (IL-18). Meanwhile, toll-like receptor 4 (TLR4)-modulated mitogen-activated protein kinase (MAPK)/nuclear factor kappa B (NF-kappa B) and apoptosis-related Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway are involved in the progression of hepatic injury and inflammation. And juglanin was found to suppress fructose-feeding-induced activation of these signaling pathways compared with the model group administrated only with fructose. These results indicate that juglanin represses inflammatory response and apoptosis via TLR4-regulated MAPK/NF-kappa B and JAK2/STAT3 signaling pathway respectively in rats with hepatitis induced by LPS for fructose-feeding. Treatment of juglanin might be an effective therapeutic strategy for preventing hepatitis. (C) 2016 Elsevier Masson SAS. All rights reserved.
C1 [Zhou, Guang-Yao; Jin, Ling-Xiang; Lin, Wei; Fang, Pei-Pei; Lin, Xiu-Zheng; Zheng, Yi; Pan, Chen-Wei] Wenzhou Med Univ, Affiliated Hosp 2, Dept Infect Dis, Wenzhou 325027, Zhejiang, Peoples R China.
[Zhou, Guang-Yao; Jin, Ling-Xiang; Lin, Wei; Fang, Pei-Pei; Lin, Xiu-Zheng; Zheng, Yi; Pan, Chen-Wei] Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou 325027, Zhejiang, Peoples R China.
[Yi, Yong-Xiang] Southeast Univ, Hosp Nanjing 2, Dept Hepatobiliary Surg, Nanjing 210003, Jiangsu, Peoples R China.
C3 Wenzhou Medical University; Wenzhou Medical University; Southeast
University - China
RP Pan, CW (corresponding author), Wenzhou Med Univ, Affiliated Hosp 2, Dept Infect Dis, Wenzhou 325027, Zhejiang, Peoples R China.; Pan, CW (corresponding author), Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou 325027, Zhejiang, Peoples R China.
EM panchenweigrk@126.com
FU Science and Technology Bureau, Public Welfare Projects of Science and
Technology of Wenzhou City [Y20150023]
FX This study was kindly supported by Science and Technology Bureau, Public
Welfare Projects of Science and Technology of Wenzhou City; No.
Y20150023.
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NR 32
TC 49
Z9 54
U1 0
U2 22
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD JUL
PY 2016
VL 81
BP 318
EP 328
DI 10.1016/j.biopha.2016.04.013
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA DN8RO
UT WOS:000377347300040
PM 27261609
DA 2025-01-07
ER
PT J
AU Baggott, JE
Tamura, T
AF Baggott, Joseph E.
Tamura, Tsunenobu
TI Folate-Dependent Purine Nucleotide Biosynthesis in Humans
SO ADVANCES IN NUTRITION
LA English
DT Review
DE folate; glycine; histidine; formate; serine; uric acid
ID URIC-ACID; BONE-MARROW; IN-VIVO; FORMATE; METABOLISM; PURIFICATION;
ENZYME; CARBON; AICA; 4-AMINO-5-IMIDAZOLECARBOXAMIDE
AB Purine nucleotide biosynthesis de novo (PNB) requires 2 folate-dependent transformylases-5'-phosphoribosyl-glycinamide (GAR) and 5'-phosphoribosyl-5-aminoimidazole-4-carboxamide (AICAR) transformylases-to introduce carbon 8 (C-8) and carbon 2 (C-2) into the purine ring. Both transformylases utilize 10-formyltetrahydrofolate (10-formyl-H(4)folate), where the formyl-carbon sources include ring-2-C of histidine, 3-C of serine, 2-C of glycine, and formate. Our findings in human studies indicate that glycine provides the carbon for GAR transformylase (exclusively C-8), whereas histidine and formate are the predominant carbon sources for AICAR transformylase (C-2). Contrary to the previous notion, these carbon sources may not supply a general 10-formyl-H(4)folate pool, which was believed to equally provide carbons to C-8 and C-2. To explain these phenomena, we postulate that GAR transformylase is in a complex with the trifunctional folate-metabolizing enzyme (TFM) and serine hydroxymethyltransferase to channel carbons of glycine and serine to C-8. There is no evidence for channeling carbons of histidine and formate to AICAR transformylase (C-2). GAR transformylase may require the TFM to furnish 10-formyl-H(4)folate immediately after its production from serine to protect its oxidation to 10-formyldihydrofolate (10-formyl-H(2)folate), whereas AICAR transformylase can utilize both 10-formyl-H(2)folate and 10-formyl-H(4)folate. Human liver may supply AICAR to AICAR transformylase in erythrocytes/erythroblasts. Incorporation of ring-2-C of histidine and formate into C-2 of urinary uric acid presented a circadian rhythm with a peak in the morning, which corresponds to the maximum DNA synthesis in the bone marrow, and it may be useful in the timing of the administration of drugs that block PNB for the treatment of cancer and autoimmune disease.
C1 [Baggott, Joseph E.; Tamura, Tsunenobu] Univ Alabama Birmingham, Dept Nutr Sci, Birmingham, AL 35294 USA.
C3 University of Alabama System; University of Alabama Birmingham
RP Tamura, T (corresponding author), Univ Alabama Birmingham, Dept Nutr Sci, Birmingham, AL 35294 USA.
EM tamurat@uab.edu
OI Tamura, Tsunenobu/0009-0006-5044-2474
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NR 55
TC 32
Z9 39
U1 0
U2 18
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 2161-8313
EI 2156-5376
J9 ADV NUTR
JI Adv. Nutr.
PD SEP
PY 2015
VL 6
IS 5
BP 564
EP 571
DI 10.3945/an.115.008300
PG 8
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA CR7CB
UT WOS:000361504400004
PM 26374178
OA Green Published, hybrid
DA 2025-01-07
ER
PT J
AU Sobczynska-Malefora, A
Sobczy, A
Katayev, A
Steed, D
O'Logbon, J
Crook, M
Harrington, DJ
AF Sobczynska-Malefora, Agata
Sobczy, Agata
Katayev, Alexander
Steed, David
O'Logbon, Jessica
Crook, Martin
Harrington, Dominic J.
TI Age- and ethnicity-related reference intervals for serum vitamin B12
SO CLINICAL BIOCHEMISTRY
LA English
DT Article
DE Reference intervals; Vitamin B 12; Ethnicity; Age; Haptocorrin;
Holotranscobalamin
ID HOLO-TRANSCOBALAMIN; WOMEN; MARKERS
AB Background: Age and ethnicity are known to influence serum vitamin B12 (B12) concentration, yet universal reference intervals (RIs) are typically applied by laboratories. Both lower and upper RI limits for B12 are clinically relevant. Low values suggest deficiency leading to anemia and/or neurological impairment, while high values are not always an innocuous consequence of high B12 intake but are associated with some cancers, autoimmune, liver, and renal diseases.This work aimed to establish age-and ethnicity-related RIs for B12 using a modified indirect method based on Hoffmann's approach.Methods: A total of 72,091 anonymized B12 results (Jan 2018-Nov 2019) were analyzed from an ethnically diverse South-East London general practice patient population. Patients belonged to five ethnic groups: Asian, Black, White, Mixed, or Other. Multiple records for the same patient and results with missing ethnicity were excluded from the analysis of adult RIs. B12 analyses were performed using ARCHITECT (R) (Abbott Diagnostics). Results: B12 was significantly higher in Black compared with Asian and White adults. There were no differences in B12 between Asian and White adults. Children (all ethnicities) between 2 and 5 years old had the highest B12. Because of the small number of children (up to the age of 13) in each ethnic-related age category, all ethnic groups were combined to obtain age-related RIs. The children's RIs ranged from 159 to 1025 pmol/L for 0-1 year-olds to 276-1102 pmol/L for 2-5-year-olds. The RIs for Black and White/Asian people >13 years of age were 166-805 pmol/L and 134-511 pmol/L respectively.Conclusions: The application of age-and ethnicity-appropriate RIs into diagnostic practice will provide a more accurate evaluation of B12 status when using the B12 test alone or in combination with other markers.
C1 [Sobczynska-Malefora, Agata; Harrington, Dominic J.] Guys & St Thomas Hosp NHS Trust, Nutristasis Unit, Guys & St, London, England.
[Sobczynska-Malefora, Agata; O'Logbon, Jessica; Harrington, Dominic J.] Kings Coll London, Fac Life Sci & Med, London, England.
[Katayev, Alexander] Lab Corp Amer Holdings, Elon, NC USA.
[Steed, David] Viapath Informat, London, England.
[O'Logbon, Jessica] Univ Cambridge, Dept Psychiat, Cambridge, England.
[Crook, Martin] Kings Coll London, Biochem Med, London, England.
[Crook, Martin] Guys & St Thomas Hosp NHS Trust, London, England.
[Crook, Martin] Lewisham & Greenwich NHS Trust, London, England.
C3 Guy's & St Thomas' NHS Foundation Trust; University of London; King's
College London; University of Cambridge; University of London; King's
College London
RP Sobczynska-Malefora, A (corresponding author), Kings Coll London, St Thomas Hosp, Nutristasis Unit, London SE1 7EH, England.; Sobczynska-Malefora, A (corresponding author), Kings Coll London, St Thomas Hosp, London SE1 7EH, England.
EM agata.malefora@kcl.ac.uk
RI Sobczynska-Malefora, Agata/ISA-8439-2023
OI Sobczynska-Malefora, Agata/0000-0001-7349-9517; O'Logbon,
Jessica/0000-0003-1216-9703; Harrington, Dominic/0000-0003-4786-9240
CR Arendt JFB, 2013, CLIN CHEM LAB MED, V51, P489, DOI 10.1515/cclm-2012-0545
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Sobczynska-Malefora A, 2022, J NUTR, V152, P163, DOI 10.1093/jn/nxab352
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Wolffenbuttel BHR, 2022, BMJ CASE REP, V15, DOI 10.1136/bcr-2021-247660
NR 29
TC 8
Z9 9
U1 0
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0009-9120
EI 1873-2933
J9 CLIN BIOCHEM
JI Clin. Biochem.
PD JAN
PY 2023
VL 111
BP 66
EP 71
DI 10.1016/j.clinbiochem.2022.10.007
EA DEC 2022
PG 6
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA 8C1DF
UT WOS:000917355900001
PM 36261053
OA hybrid
DA 2025-01-07
ER
PT J
AU Montano-Loza, AJ
Angulo, P
Meza-Junco, J
Prado, CMM
Sawyer, MB
Beaumont, C
Esfandiari, N
Ma, M
Baracos, VE
AF Montano-Loza, Aldo J.
Angulo, Paul
Meza-Junco, Judith
Prado, Carla M. M.
Sawyer, Michael B.
Beaumont, Crystal
Esfandiari, Nina
Ma, Mang
Baracos, Vickie E.
TI Sarcopenic obesity and myosteatosis are associated with higher mortality
in patients with cirrhosis
SO JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
LA English
DT Article
DE Lumbar skeletal muscle index; Muscle attenuation index; Overweight;
Muscle depletion; Myosteatosis; Cirrhosis
ID ADIPOSE-TISSUE; COMPUTED-TOMOGRAPHY; PROGNOSTIC-FACTOR; MUSCLE
DEPLETION; CANCER CACHEXIA; INFLAMMATION; NUTRITION; SURVIVAL; RISK;
EPIDEMIOLOGY
AB Background and aims Obesity is frequently associated with cirrhosis, and cirrhotic patients may develop simultaneous loss of skeletal muscle and gain of adipose tissue, culminating in the condition of sarcopenic obesity. Additionally, muscle depletion is characterized by both a reduction in muscle size and increased proportion of muscular fat, termed myosteatosis. In this study, we aimed to establish the frequency and clinical significance of sarcopenia, sarcopenic obesity and myosteatosis in cirrhotic patients.
Methods We analysed 678 patients with cirrhosis. Sarcopenia, sarcopenic obesity and myosteatosis were analysed by CT scan using the third lumbar vertebrae skeletal muscle and attenuation indexes, using previously validated gender-and body mass index-specific cutoffs.
Results Patients were predominately men (n = 457, 67%), and cirrhosis aetiology was hepatitis C virus in 269 patients (40%), alcohol in 153 (23%), non-alcoholic steatohepatitis/cryptogenic in 96 (14%), autoimmune liver disease in 55 (8%), hepatitis B virus in 43 (6%), and others in 5 patients (1%). Sarcopenia was present in 292 (43%), 135 had sarcopenic obesity (20%) and 353 had myosteatosis (52%). Patients with sarcopenia (22 +/- 3 vs. 95 +/- 22 months, P< 0.001), sarcopenic obesity (22 +/- 3 vs. 95 +/- 22 months, P< 0.001), and myosteatosis (28 +/- 5 vs. 95 +/- 22 months, P< 0.001) had worse median survival than patients without muscular abnormalities. By multivariate Cox regression analysis, both sarcopenia [hazard ratio (HR) 2.00, 95% confidence interval (CI) 1.44-2.77, P< 0.001], and myosteatosis (HR 1.42, 95% CI 1.02-1.07, P = 0.04) were associated with mortality.
Conclusions Sarcopenia, sarcopenic obesity and myosteatosis are often present in patients with cirrhosis, and sarcopenia and myosteatosis are independently associated with a higher long-term mortality in cirrhosis.
C1 [Montano-Loza, Aldo J.; Ma, Mang] Univ Alberta Hosp, Div Gastroenterol, Edmonton, AB T6G 2B7, Canada.
[Montano-Loza, Aldo J.; Ma, Mang] Univ Alberta Hosp, Liver Unit, Edmonton, AB T6G 2B7, Canada.
[Angulo, Paul] Univ Kentucky, Med Ctr, Div Digest Dis & Nutr, Lexington, KY USA.
[Meza-Junco, Judith; Sawyer, Michael B.; Beaumont, Crystal; Esfandiari, Nina; Baracos, Vickie E.] Cross Canc Inst, Dept Oncol, Edmonton, AB T6G 1Z2, Canada.
[Prado, Carla M. M.] Dept Agr Food & Nutr Sci, Edmonton, AB, Canada.
C3 University of Alberta; University of Alberta; University of Kentucky;
University of Alberta
RP Montano-Loza, AJ (corresponding author), Univ Alberta, Zeidler Ledcor Ctr, 130 Univ Campus, Edmonton, AB T6G 2X8, Canada.
EM montanol@ualberta.ca
RI Montano-Loza, Aldo/B-3092-2013; Prado, Carla/G-9365-2019
OI Prado, Carla/0000-0002-3609-5641; Montano-Loza, Aldo
J./0000-0002-2511-7980; Ma, Mang/0000-0003-2587-1788
FU American College of Gastroenterology Institute
FX This study has been funded by a Clinical Research Award from the
American College of Gastroenterology Institute 2011.
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NR 42
TC 379
Z9 387
U1 5
U2 32
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2190-5991
EI 2190-6009
J9 J CACHEXIA SARCOPENI
JI J. Cachexia Sarcopenia Muscle
PD MAY
PY 2016
VL 7
IS 2
BP 126
EP 135
DI 10.1002/jcsm.12039
PG 10
WC Geriatrics & Gerontology; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Geriatrics & Gerontology; General & Internal Medicine
GA DP0DU
UT WOS:000378159000003
PM 27493866
OA gold, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Mao, S
Shen, H
Zhang, JH
AF Mao, Song
Shen, Hua
Zhang, Jianhua
TI Systemic lupus erythematosus and malignancies risk
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Systemic lupus erythematosus; Malignancy; Meta-analysis
ID C VIRUS-INFECTION; AUTOIMMUNE-DISEASES; FEMALE-PATIENTS; CANCER-RISK;
COHORT; ASSOCIATION; LUNG; SLE; PREVALENCE; CARCINOMA
AB Objective To evaluate the risk of site-specific and overall malignancies after SLE and explore the potential influencing factors.
Methods We searched electronic databases for articles that assessed the risk of malignancies after SLE through February 2015. We extracted the incidence rates (IRs) and corresponding 95 % confidence intervals (CIs). We used random effects models to calculate the pooled IRs and assessed the impact of study designs, region, gender, age and duration of follow-up.
Results Eighteen studies were included, giving a pooled IR of 1.44 (95 % CI 1.23-1.69). Europeans, Americans and Asians showed a IR of 1.56 (95 % CI 1.07-2.28), 1.18 (95 % CI 1.01-1.39) and 1.62 (95 % CI 1.38-1.89), respectively. Males and females (eight studies) demonstrated a IR of 1.34 (95 % CI 1.07-1.67) and 1.51 (95 % CI 1.201.90), respectively. Prospective and retrospective studies showed a IR of 1.55 (95 % CI 0.97-2.47) and 1.44 (95 % CI 1.21-1.73), respectively. An increment of 10 years of colon/rectumage conferred a decrease in IR of 0.6. An increment of 5 years of SLE duration conferred a decrease in IR of 2.5. An increased IR of malignancies was observed in NHL, vagina/vulva, hematology, head/neck, leukemia, thyroid, liver/gallbladder, kidney, anal, cervix, esophagus, lung and pancreas. A decreased IR of malignancies was observed in ovary and colon/rectum.
Conclusions SLE patients had an increased risk of developing overall malignancies, particularly among Asians and females. Age and SLE duration are inversely associated with the risk of overall malignancies. SLE patients showed a different role in the onset of various site-specific malignancies.
C1 [Mao, Song; Zhang, Jianhua] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Pediat, Shanghai 200030, Peoples R China.
[Shen, Hua] Nanjing Med Univ, Affiliated Hosp 1, Dept Oncol, Nanjing, Jiangsu, Peoples R China.
C3 Shanghai Jiao Tong University; Nanjing Medical University
RP Mao, S (corresponding author), Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Pediat, Shanghai 200030, Peoples R China.
EM edjh123456@sina.com; zjh12195@sina.com
RI shen, hua/HTM-6972-2023
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NR 50
TC 38
Z9 41
U1 0
U2 19
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD JAN
PY 2016
VL 142
IS 1
BP 253
EP 262
DI 10.1007/s00432-015-2032-0
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DD8JN
UT WOS:000370172900026
PM 26319223
DA 2025-01-07
ER
PT J
AU Perrella, A
Esposito, C
Ioia, G
Campanella, L
Taglialatela, D
Cuomo, O
AF Perrella, A.
Esposito, C.
Ioia, G.
Campanella, L.
Taglialatela, D.
Cuomo, O.
TI Cytomegalovirus Infection After Liver Transplantation: Prophylaxis and
Preemptive Treatment-A Single-Center Experience
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article; Proceedings Paper
CT 33rd Congress of the Italian-Tranplantation-Society
CY DEC 13-15, 2009
CL Milan, ITALY
SP Italian Tranplantat Soc
ID ORAL GANCICLOVIR; RECIPIENTS; STRATEGIES; DISEASE; METAANALYSIS;
PREVENTION; EFFICACY
AB Background. Cytomegalovinrs (CMV) infection represents one of the most frequent opportunistic infections following solid-organ transplantation. The incidence and severity of CMV infection depend on the immunosuppressive regimen, the CMV serostatus of donor and recipient, and the type of transplant.
Methods. We evaluated CMV infection rates during the last 2 years in our center: March 2007 to March 2009. We enrolled 55 patients-13 females and 42 males-who underwent liver transplantation (OLT) due to hepatitis C virus (HCV) cirrhosis (n = 9), hepatitis B virus (HBV) cirrhosis (n = 5) HCC both on HCV and HBV cirrhosis (n. = 37), or autoimmune disease (n = 4). Fifty percent of the patients received tacrolimus (TRL) and the others cyclosporine (CsA), both dosed according to weight. All patients received oral acyclovir (400 mg/td or less, adapted to renal function) as herpes simplex prophylaxis for 6 months. CMV prophylaxis prescribed CMV- hyperimmunoglobulin on postoperative days 1 and 7. CMV infection was monitored using polymerase chain reaction (PCR <1000 IU/mL) according to the following schedule: every week for the first month, every 2 weeks from month 2 to 3 and monthly from month 4 to 6. Patients were treated when three positive PCR results not affected by immunosuppressive dose reduction or when the PCR showed DNA greater than three times the limit of detection. CMV treatment stipulated valgancyclovir (900 mg twice daily) until three consecutive PCRs were negative or for 3 months dosed according to renal function. PCR was measured every 2 weeks during treatment.
Results. Among the patients who were all D(+)/R(+) (CMV-Immunoglobulin G [IgG](+)/IgG(+)). 10 required treatment (18%) within 3 months from OLT. There subjects were prescribed TRL (n = 4) or CsA (n = 6). No renal impairment was observed among treated patients. Of those having the infection, one died due to other causes sepsis from candida at 5 months after OLT.
Conclusion. CMV-hyperimmunoglobulin on postoperative days 1 and 7 did not confer protection for CMV among OLT patients. Preemptive treatment with intravenous gancyclovir plus valgancyclovir per os seemed to be useful and safe in infected patients requiring treatment.
C1 [Perrella, A.; Esposito, C.; Ioia, G.; Campanella, L.; Cuomo, O.] AORN A Cardareli, Liver Transplant Ctr, I-80131 Naples, Italy.
[Taglialatela, D.] AORN A Cardareli, Virol Lab, I-80131 Naples, Italy.
RP Perrella, A (corresponding author), AORN A Cardareli, Liver Transplant Ctr, Via A Cardarelli 9, I-80131 Naples, Italy.
EM alex.perrel@virgilio.it
RI Perrella, Alessandro/AAS-1534-2020
OI Perrella, Alessandro/0000-0003-2812-8500
CR Kalil AC, 2005, ANN INTERN MED, V143, P870, DOI 10.7326/0003-4819-143-12-200512200-00005
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NR 9
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Z9 3
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0041-1345
J9 TRANSPL P
JI Transplant. Proc.
PD MAY
PY 2010
VL 42
IS 4
BP 1226
EP 1228
DI 10.1016/j.transproceed.2010.03.060
PG 3
WC Immunology; Surgery; Transplantation
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Immunology; Surgery; Transplantation
GA 607JH
UT WOS:000278498000058
PM 20534267
DA 2025-01-07
ER
PT J
AU Yoshiji, H
Nagoshi, S
Akahane, T
Asaoka, Y
Ueno, Y
Ogawa, K
Kawaguchi, T
Kurosaki, M
Sakaida, I
Shimizu, M
Taniai, M
Terai, S
Nishikawa, H
Hiasa, Y
Hidaka, H
Miwa, H
Chayama, K
Enomoto, N
Shimosegawa, T
Takehara, T
Koike, K
AF Yoshiji, Hitoshi
Nagoshi, Sumiko
Akahane, Takemi
Asaoka, Yoshinari
Ueno, Yoshiyuki
Ogawa, Koji
Kawaguchi, Takumi
Kurosaki, Masayuki
Sakaida, Isao
Shimizu, Masahito
Taniai, Makiko
Terai, Shuji
Nishikawa, Hiroki
Hiasa, Yoichi
Hidaka, Hisashi
Miwa, Hiroto
Chayama, Kazuaki
Enomoto, Nobuyuki
Shimosegawa, Tooru
Takehara, Tetsuo
Koike, Kazuhiko
TI Evidence-based clinical practice guidelines for Liver Cirrhosis 2020
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Liver cirrhosis; Guidelines; Diagnosis; Treatment; Complications
ID SPONTANEOUS BACTERIAL PERITONITIS; HEPATITIS-B IMMUNOGLOBULIN;
RETROGRADE TRANSVENOUS OBLITERATION; PORTAL-VEIN THROMBOSIS; ENDOSCOPIC
VARICEAL LIGATION; SUSTAINED VIROLOGICAL RESPONSE; PRIMARY SCLEROSING
CHOLANGITIS; AMINO-ACID SUPPLEMENTATION; ASIAN WORKING GROUP;
HEPATOCELLULAR-CARCINOMA
AB The first edition of the clinical practice guidelines for liver cirrhosis was published in 2010, and the second edition was published in 2015 by the Japanese Society of Gastroenterology (JSGE). The revised third edition was recently published in 2020. This version has become a joint guideline by the JSGE and the Japan Society of Hepatology (JSH). In addition to the clinical questions (CQs), background questions (BQs) are new items for basic clinical knowledge, and future research questions (FRQs) are newly added clinically important items. Concerning the clinical treatment of liver cirrhosis, new findings have been reported over the past 5 years since the second edition. In this revision, we decided to match the international standards as much as possible by referring to the latest international guidelines. Newly developed agents for various complications have also made great progress. In comparison with the latest global guidelines, such as the European Association for the Study of the Liver (EASL) and American Association for the Study of Liver Diseases (AASLD), we are introducing data based on the evidence for clinical practice in Japan. The flowchart for nutrition therapy was reviewed to be useful for daily medical care by referring to overseas guidelines. We also explain several clinically important items that have recently received focus and were not mentioned in the last editions. This digest version describes the issues related to the management of liver cirrhosis and several complications in clinical practice. The content begins with a diagnostic algorithm, the revised flowchart for nutritional therapy, and refracted ascites, which are of great importance to patients with cirrhosis. In addition to the updated antiviral therapy for hepatitis B and C liver cirrhosis, the latest treatments for non-viral cirrhosis, such as alcoholic steatohepatitis/non-alcoholic steatohepatitis (ASH/NASH) and autoimmune-related cirrhosis, are also described. It also covers the latest evidence regarding the diagnosis and treatment of liver cirrhosis complications, namely gastrointestinal bleeding, ascites, hepatorenal syndrome and acute kidney injury, hepatic encephalopathy, portal thrombus, sarcopenia, muscle cramp, thrombocytopenia, pruritus, hepatopulmonary syndrome, portopulmonary hypertension, and vitamin D deficiency, including BQ, CQ and FRQ. Finally, this guideline covers prognosis prediction and liver transplantation, especially focusing on several new findings since the last version. Since this revision is a joint guideline by both societies, the same content is published simultaneously in the official English journal of JSGE and JSH.
C1 [Yoshiji, Hitoshi; Nagoshi, Sumiko; Akahane, Takemi; Asaoka, Yoshinari; Ueno, Yoshiyuki; Ogawa, Koji; Kawaguchi, Takumi; Kurosaki, Masayuki; Sakaida, Isao; Shimizu, Masahito; Taniai, Makiko; Terai, Shuji; Nishikawa, Hiroki; Hiasa, Yoichi; Hidaka, Hisashi; Miwa, Hiroto; Enomoto, Nobuyuki; Shimosegawa, Tooru; Koike, Kazuhiko] Japanese Soc Gastroenterol, Guidelines Comm Creating & Evaluating Evidence Ba, Japan Soc Hepatol, Minato Ku, 6F Shimbashi I MARK Bldg,2-6-2 Shimbashi, Tokyo 1050004, Japan.
[Chayama, Kazuaki; Takehara, Tetsuo] Japan Soc Hepatol, Bunkyo Ku, Kashiwaya 2 Bldg 5F,3-28-10 Hongo, Tokyo 1130033, Japan.
[Yoshiji, Hitoshi] Nara Med Univ, Dept Gastroenterol, Shijo Cho 840, Kashihara, Nara 6348522, Japan.
C3 Nara Medical University
RP Yoshiji, H (corresponding author), Japanese Soc Gastroenterol, Guidelines Comm Creating & Evaluating Evidence Ba, Japan Soc Hepatol, Minato Ku, 6F Shimbashi I MARK Bldg,2-6-2 Shimbashi, Tokyo 1050004, Japan.; Yoshiji, H (corresponding author), Nara Med Univ, Dept Gastroenterol, Shijo Cho 840, Kashihara, Nara 6348522, Japan.
EM yoshijih@naramed-u.ac.jp
RI Asaoka, Yoshinari/ABC-5412-2021; Chayama, Kazuaki/B-2493-2016; Hiasa,
Yoichi/ABD-2759-2021; Akahane, Takemi/O-4509-2018; taniai,
makiko/HZH-7431-2023
OI Yoshiji, Hitoshi/0000-0002-5243-8544; Terai, Shuji/0000-0002-5439-635X
FU JSGE
FX This article was supported by a Grant-in-Aid fromJSGE. The authors thank
the investigators and supporters for participating in the studies. The
authors express special appreciation to Dr. Makoto Segawa (Yamaguchi
University) and Dr. Ryo Sakamaki (Niigata University).
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NR 207
TC 187
Z9 196
U1 7
U2 47
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JUL
PY 2021
VL 56
IS 7
BP 593
EP 619
DI 10.1007/s00535-021-01788-x
EA JUL 2021
PG 27
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA TJ4XD
UT WOS:000670157800001
PM 34231046
OA hybrid, Green Published
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Yoshiji, H
Nagoshi, S
Akahane, T
Asaoka, Y
Ueno, Y
Ogawa, K
Kawaguchi, T
Kurosaki, M
Sakaida, I
Shimizu, M
Taniai, M
Terai, S
Nishikawa, H
Hiasa, Y
Hidaka, H
Miwa, H
Chayama, K
Enomoto, N
Shimosegawa, T
Takehara, T
Koike, K
AF Yoshiji, Hitoshi
Nagoshi, Sumiko
Akahane, Takemi
Asaoka, Yoshinari
Ueno, Yoshiyuki
Ogawa, Koji
Kawaguchi, Takumi
Kurosaki, Masayuki
Sakaida, Isao
Shimizu, Masahito
Taniai, Makiko
Terai, Shuji
Nishikawa, Hiroki
Hiasa, Yoichi
Hidaka, Hisashi
Miwa, Hiroto
Chayama, Kazuaki
Enomoto, Nobuyuki
Shimosegawa, Tooru
Takehara, Tetsuo
Koike, Kazuhiko
TI Evidence-based clinical practice guidelines for liver cirrhosis 2020
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE complications; diagnosis; guidelines; liver cirrhosis; treatment
ID SPONTANEOUS BACTERIAL PERITONITIS; HEPATITIS-B IMMUNOGLOBULIN;
RETROGRADE TRANSVENOUS OBLITERATION; PORTAL-VEIN THROMBOSIS; ENDOSCOPIC
VARICEAL LIGATION; SUSTAINED VIROLOGICAL RESPONSE; PRIMARY SCLEROSING
CHOLANGITIS; AMINO-ACID SUPPLEMENTATION; ASIAN WORKING GROUP;
HEPATOCELLULAR-CARCINOMA
AB The first edition of the clinical practice guidelines for liver cirrhosis was published in 2010, and the second edition was published in 2015 by the Japanese Society of Gastroenterology (JSGE). The revised third edition was recently published in 2020. This version has become a joint guideline by the JSGE and the Japanese Society of Hepatology (JSH). In addition to the clinical questions (CQs), background questions (BQs) are new items for basic clinical knowledge, and future research questions (FRQs) are newly added clinically important items. Concerning the clinical treatment of liver cirrhosis, new findings have been reported over the past 5 years since the second edition. In this revision, we decided to match the international standards as much as possible by referring to the latest international guidelines. Newly developed agents for various complications have also made great progress. In comparison with the latest global guidelines, such as the European Association for the Study of the Liver (EASL) and American Association for the Study of Liver Diseases (AASLD), we are introducing data based on the evidence for clinical practice in Japan. The flowchart for nutrition therapy was reviewed to be useful for daily medical care by referring to overseas guidelines. We also explain several clinically important items that have recently received focus and were not mentioned in the last editions. This digest version describes the issues related to the management of liver cirrhosis and several complications in clinical practice. The content begins with a diagnostic algorithm, the revised flowchart for nutritional therapy, and refracted ascites, which are of great importance to patients with cirrhosis. In addition to the updated antiviral therapy for hepatitis B and C liver cirrhosis, the latest treatments for non-viral cirrhosis, such as alcoholic steatohepatitis/non-alcoholic steatohepatitis (ASH/NASH) and autoimmune-related cirrhosis, are also described. It also covers the latest evidence regarding the diagnosis and treatment of liver cirrhosis complications, namely gastrointestinal bleeding, ascites, hepatorenal syndrome and acute kidney injury, hepatic encephalopathy, portal thrombus, sarcopenia, muscle cramp, thrombocytopenia, pruritus, hepatopulmonary syndrome, portopulmonary hypertension, and vitamin D deficiency, including BQ, CQ and FRQ. Finally, this guideline covers prognosis prediction and liver transplantation, especially focusing on several new findings since the last version. Since this revision is a joint guideline by both societies, the same content is published simultaneously in the official English journal of JSGE and JSH.
C1 [Yoshiji, Hitoshi; Nagoshi, Sumiko; Akahane, Takemi; Asaoka, Yoshinari; Ueno, Yoshiyuki; Ogawa, Koji; Kawaguchi, Takumi; Kurosaki, Masayuki; Sakaida, Isao; Shimizu, Masahito; Taniai, Makiko; Terai, Shuji; Nishikawa, Hiroki; Hiasa, Yoichi; Hidaka, Hisashi; Miwa, Hiroto; Enomoto, Nobuyuki; Shimosegawa, Tooru; Koike, Kazuhiko] Japanese Soc Gastroenterol, Guidelines Comm Creating & Evaluating Evidence Ba, Tokyo, Japan.
[Yoshiji, Hitoshi] Nara Med Univ, Dept Gastroenterol, Shijo Cho 840, Kashihara, Nara 6348522, Japan.
[Chayama, Kazuaki; Takehara, Tetsuo] Japan Soc Hepatol, Tokyo, Japan.
C3 Nara Medical University
RP Yoshiji, H (corresponding author), Nara Med Univ, Dept Gastroenterol, Shijo Cho 840, Kashihara, Nara 6348522, Japan.
EM yoshijih@naramed-u.ac.jp
RI Asaoka, Yoshinari/ABC-5412-2021; Akahane, Takemi/O-4509-2018; taniai,
makiko/HZH-7431-2023; Chayama, Kazuaki/B-2493-2016; Hiasa,
Yoichi/ABD-2759-2021
OI Terai, Shuji/0000-0002-5439-635X; Akahane, Takemi/0000-0002-6675-0475;
Yoshiji, Hitoshi/0000-0002-5243-8544
FU Japanese Society of Gastroenterology
FX A Grant-in-aid from Japanese Society of Gastroenterology
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NR 208
TC 103
Z9 106
U1 1
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1386-6346
EI 1872-034X
J9 HEPATOL RES
JI Hepatol. Res.
PD JUL
PY 2021
VL 51
IS 7
BP 725
EP 749
DI 10.1111/hepr.13678
EA JUL 2021
PG 25
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA TJ0FM
UT WOS:000670004000001
PM 34228859
OA hybrid
DA 2025-01-07
ER
PT J
AU Wang, Y
Gu, Y
Shen, KL
Cui, XF
Min, R
Sun, SQ
Feng, CL
Chen, YB
Wang, L
Cao, M
Yang, J
Yao, J
Xu, J
Lin, D
Tao, YJ
Ma, GE
Shi, JX
Chen, BL
Ni, YY
Zhong, HH
Shi, Y
Su, X
AF Wang, Yu
Gu, Yu
Shen, Kunlu
Cui, Xuefan
Min, Rui
Sun, Siqing
Feng, Chunlai
Chen, Yanbin
Wang, Li
Cao, Min
Yang, Jian
Yao, Jian
Xu, Jing
Lin, Dang
Tao, Yujian
Ma, Guoer
Shi, Jiaxin
Chen, Bilin
Ni, Yueyan
Zhong, Huanhuan
Shi, Yi
Su, Xin
TI Clinical features of cryptococcosis in patients with different immune
statuses: a multicenter study in Jiangsu Province-China
SO BMC INFECTIOUS DISEASES
LA English
DT Article
DE Cryptococcosis; Immunocompetent; Immunodeficient; Clinical feature;
Mild-to-moderate
ID NON-AIDS PATIENTS; PULMONARY CRYPTOCOCCOSIS; EPIDEMIOLOGY; HIV
AB Background Current guidelines support different management of cryptococcosis between severely immunodeficient and immunocompetent populations. However, few studies have focused on cryptococcosis patients with mild-to-moderate immunodeficiency. We performed this study to determine the clinical features of pulmonary (PC) and extrapulmonary cryptococcosis (EPC) and compared them among populations with different immune statuses to support appropriate clinical management of this public health threat. Methods All cases were reported by 14 tertiary teaching hospitals in Jiangsu Province, China from January 2013 to December 2018. The trends in incidence, demographic data, medical history, clinical symptoms, laboratory test indicators, imaging characteristics and diagnostic method of these patients were then stratified by immune status, namely immunocompetent (IC, patients with no recognized underlying disease or those with an underlying disease that does not influence immunity, such as hypertension), mild-to-moderate immunodeficiency (MID, patients with diabetes mellitus, end-stage liver or kidney disease, autoimmune diseases treated with low-dose glucocorticoid therapy, and cancer treated with chemotherapy) and severe immunodeficiency (SID, patients with acquired immunodeficiency syndrome, haematologic malignancies, solid organ transplantation or haematologic stem cell transplantation, idiopathic CD4 lymphocytosis, agranulocytosis, aggressive glucocorticoid or immunosuppressive therapy and other conditions or treatments that result in severe immunosuppression). Results The clinical data of 255 cryptococcosis patients were collected. In total, 66.3% of patients (169) were IC, 16.9% (43) had MID, and 16.9% (43) had SID. 10.1% of the patients (17) with IC were EPC, 18.6% of the patients (8) with MID were EPC, and 74.4% of patients (32) were EPC (IC/MID vs. SID, p < 0.001). Fever was more common in the SID group than in the IC and MID groups (69.8% vs. 14.8% vs. 37.2%, p < 0.001). Of chest CT scan, most lesions were distributed under the pleura (72.7%), presenting as nodules/lumps (90.3%) or consolidations (10.7%). Pleural effusion was more common in SID group compared to IC group (33.3% vs. 2.4%, p < 0.001). Positivity rate on the serum capsular polysaccharide antigen detection (CrAg) test was higher in the SID group than in the other two groups [100.0% vs. 84.4% (MID) vs. 78.2% (IC), p = 0.013]. Positivity rate on the serum CrAg test was also higher in cryptococcal meningitis patients than in PC patients (100.0% vs. 79.5%, p = 0.015). Conclusions The clinical presentation of MID patients is intermediate between SID and IC patients and is similar to that of IC patients. The serum CrAg test is more sensitive for the identification of SID or EPC patients.
C1 [Wang, Yu; Chen, Bilin; Zhong, Huanhuan; Shi, Yi; Su, Xin] Nanjing Univ, Med Sch, Jinling Hosp, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.
[Gu, Yu; Ni, Yueyan; Su, Xin] Nanjing Med Univ, Jinling Hosp, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.
[Shen, Kunlu; Su, Xin] Southern Med Univ, Jinling Hosp, Dept Resp & Crit Care Med, Guangzhou 510000, Peoples R China.
[Cui, Xuefan; Min, Rui] Nanjing Med Univ, Jiangsu Prov Hosp, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.
[Sun, Siqing] Second Hosp Nanjing, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.
[Feng, Chunlai] Soochow Univ, Affiliated Hosp 3, Dept Resp & Crit Care Med, Changzhou 213000, Peoples R China.
[Chen, Yanbin] Soochow Univ, Affiliated Hosp 1, Dept Resp & Crit Care Med, Suzhou 215000, Peoples R China.
[Wang, Li] Nanjing Med Univ, Nanjing Hosp 1, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.
[Cao, Min] Nanjing Univ, Nanjing Drum Tower Hosp, Med Sch, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.
[Yang, Jian] Nanjing Med Univ, Affiliated Jiangning Hosp, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.
[Yao, Jian] First Peoples Hosp Nantong, Dept Resp & Crit Care Med, Nantong 226000, Peoples R China.
[Xu, Jing] Jiangsu Prov Hosp Chinese Med, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.
[Lin, Dang] Suzhou Municipal Hosp, Dept Resp & Crit Care Med, Suzhou 215000, Peoples R China.
[Tao, Yujian] Yangzhou Univ, Dept Resp & Crit Care Med, Affiliated Hosp, Yangzhou 225000, Jiangsu, Peoples R China.
[Ma, Guoer] Jiangsu Univ, Affiliated Hosp, Dept Resp & Crit Care Med, Zhenjiang 212000, Jiangsu, Peoples R China.
[Shi, Jiaxin] First Peoples Hosp Lianyungang, Dept Resp & Crit Care Med, Lianyungang 222000, Peoples R China.
C3 Nanjing University; Nanjing Medical University; Southern Medical
University - China; Nanjing Medical University; Soochow University -
China; Soochow University - China; Nanjing Medical University; Nanjing
University; Nanjing Medical University; Nanjing University of Chinese
Medicine; Yangzhou University; Jiangsu University
RP Su, X (corresponding author), Nanjing Univ, Med Sch, Jinling Hosp, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.; Su, X (corresponding author), Nanjing Med Univ, Jinling Hosp, Dept Resp & Crit Care Med, Nanjing 210002, Peoples R China.; Su, X (corresponding author), Southern Med Univ, Jinling Hosp, Dept Resp & Crit Care Med, Guangzhou 510000, Peoples R China.
EM suxinjs@163.com
RI MIN, Rui/GQP-9076-2022; Chen, Yan-Bin/ADS-3334-2022
OI TYAGI, SHILPA/0000-0001-7755-0324
FU Natural Science Foundation of China [82070011, 81873400]; Key Project of
Jiangsu Commission of Health [K2019004]; "333 project"of Jiangsu
Province [BRA2019339]
FX This work was supported by the Project of Natural Science Foundation of
China (82070011, 81873400), the Key Project of Jiangsu Commission of
Health (K2019004), and the "333 project"of Jiangsu Province
(BRA2019339).
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Xie XN, 2015, INT J CLIN EXP MED, V8, P3114
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Zhou Y, 2018, INFECT DRUG RESIST, V11, P2483, DOI 10.2147/IDR.S178391
NR 29
TC 12
Z9 13
U1 1
U2 11
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2334
J9 BMC INFECT DIS
JI BMC Infect. Dis.
PD OCT 8
PY 2021
VL 21
IS 1
AR 1043
DI 10.1186/s12879-021-06752-x
PG 11
WC Infectious Diseases
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases
GA WD9AO
UT WOS:000705225500002
PM 34625036
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Zahorchak, AF
DeRiggi, ML
Muzzio, JL
Sutherland, V
Humar, A
Lakkis, FG
Hsu, YMS
Thomson, AW
AF Zahorchak, Alan F.
DeRiggi, Misty L.
Muzzio, Jennifer L.
Sutherland, Veronica
Humar, Abhinav
Lakkis, Fadi G.
Hsu, Yen-Michael S.
Thomson, Angus W.
TI Manufacturing and validation of Good Manufacturing Practice-compliant
regulatory dendritic cells for infusion into organ transplant recipients
SO CYTOTHERAPY
LA English
DT Article
DE Cell therapy; Clinical trials; GMP manufacturing; Regulatory dendritic
cells; Release criteria
ID PROLONG ALLOGRAFT SURVIVAL; T-CELLS; TOLERANCE INDUCTION; STEADY-STATE;
IN-VIVO; THERAPY; IL-10
AB Background aims: Regulatory (or "tolerogenic") dendritic cells (DCregs) are a highly promising, innovative cell therapy for the induction or restoration of antigen-specific tolerance in immune-mediated inflammatory disorders. These conditions include organ allograft rejection, graft-versus-host disease following bone marrow transplantation and various autoimmune disorders. DCregs generated for adoptive transfer have potential to reduce patients' dependence on non-specific immunosuppressive drugs that can induce serious side effects and enhance the risk of infection and certain types of cancer. Here, our aim was to provide a detailed account of our experience manufacturing and validating comparatively large numbers of Good Manufacturing Practice-grade DCregs for systemic (intravenous) infusion into 28 organ (liver) transplant recipients and to discuss factors that influence the satisfaction of release criteria and attainment of target cell numbers. Results: DCregs were generated in granulocyte-macrophage colony stimulating factor and interleukin (IL)-4 from elutriated monocyte fractions isolated from non-mobilized leukapheresis products of consenting healthy adult prospective liver transplant donors. Vitamin D3 was added on day 0 and 4 and IL-10 on day 4 during the 7-day culture period. Release and post-release criteria included cell viability, purity, phenotype, sterility and functional assessment. The overall conversion rate of monocytes to DCregs was 28 +/- 8.2%, with 94 +/- 5.1% product viability. The mean cell surface T-cell co-inhibitory to co-stimulatory molecule (programmed death ligand-1:CD86) mean fluorescence intensity ratio was 3.9 +/- 2.2, and the mean ratio of anti-inflammatory:pro-inflammatory cytokine product (IL-10:IL-12p70) secreted upon CD40 ligation was 60 +/- 63 (median = 40). The mean total number of DCregs generated from a single leukapheresis product (n = 25 donors) and from two leukapheresis products (n = 3 donors) was 489 +/- 223 x 106 (n = 28). The mean total number of DCregs infused was 5.9 +/- 2.8 x 106 per kg body weight. DCreg numbers within a target cell range of 2.5-10 x 106/kg were achieved for 25 of 27 (92.6%) of products generated. Conclusions: High-purity DCregs meeting a range of quality criteria were readily generated from circulating blood monocytes under Good Manufacturing Practice conditions to meet target cell numbers for infusion into prospective organ transplant recipients. (c) 2022 International Society for Cell & Gene Therapy. Published by Elsevier Inc. All rights reserved.
C1 [Zahorchak, Alan F.; Humar, Abhinav; Lakkis, Fadi G.; Thomson, Angus W.] Univ Pittsburgh, Starzl Transplantat Inst, Dept Surg, Pittsburgh, PA USA.
[DeRiggi, Misty L.; Muzzio, Jennifer L.; Sutherland, Veronica; Hsu, Yen-Michael S.] Univ Pittsburgh, Immunol Monitoring & Cellular Prod Lab, Hillman Canc Ctr, Pittsburgh, PA USA.
[Lakkis, Fadi G.; Thomson, Angus W.] Univ Pittsburgh, Dept Immunol, Pittsburgh, PA USA.
[Lakkis, Fadi G.; Hsu, Yen-Michael S.] Univ Pittsburgh, Dept Med, Div Hematol & Oncol, Sch Med, Pittsburgh, PA USA.
[Thomson, Angus W.] Univ Pittsburgh, Clin & Translat Sci Inst, Pittsburgh, PA USA.
[Thomson, Angus W.] Univ Pittsburgh, Sch Med, W1544 Starzl Biomed Sci Tower,200 Lothrop St, Pittsburgh, PA 15213 USA.
[Hsu, Yen-Michael S.] Univ Pittsburgh, Hillman Canc Ctr, 5117 Ctr Ave, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh; Pennsylvania Commonwealth System of
Higher Education (PCSHE); University of Pittsburgh; Pennsylvania
Commonwealth System of Higher Education (PCSHE); University of
Pittsburgh; Pennsylvania Commonwealth System of Higher Education
(PCSHE); University of Pittsburgh; Pennsylvania Commonwealth System of
Higher Education (PCSHE); University of Pittsburgh; Pennsylvania
Commonwealth System of Higher Education (PCSHE); University of
Pittsburgh
RP Thomson, AW (corresponding author), Univ Pittsburgh, Sch Med, W1544 Starzl Biomed Sci Tower,200 Lothrop St, Pittsburgh, PA 15213 USA.; Hsu, YMS (corresponding author), Univ Pittsburgh, Hillman Canc Ctr, 5117 Ctr Ave, Pittsburgh, PA 15213 USA.
EM hsuys@upmc.edu; thomsonaw@upmc.edu
OI Hsu, Yen-Michael/0000-0001-9239-4980
FU University of Pittsburgh Medical Center (UPMC) Immune Tolerance and
Therapy Center (ITTC)/UPMC Enterprises [88906]; National Institutes of
Health [U01 AI 136779]; CCSG [P30 CA047904]
FX This work was supported by University of Pittsburgh Medical Center
(UPMC) Immune Tolerance and Therapy Center (ITTC)/UPMC Enterprises
(grant 88906) and by National Institutes of Health grant U01 AI 136779.
This work used the Hillman Cancer Center Immunologic Monitoring and
Cellular Products Laboratory, a shared resource at the University of
Pittsburgh supported by CCSG P30 CA047904.
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NR 61
TC 5
Z9 6
U1 0
U2 2
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1465-3249
EI 1477-2566
J9 CYTOTHERAPY
JI Cytotherapy
PD APR
PY 2023
VL 25
IS 4
BP 432
EP 441
DI 10.1016/j.jcyt.2022.11.005
EA MAR 2023
PG 10
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology; Hematology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research
& Experimental Medicine
GA C5SB9
UT WOS:000962500900001
PM 36639251
DA 2025-01-07
ER
PT J
AU Hokari, A
Ishikawa, T
Tajiri, H
Matsuda, T
Ishii, O
Matsumoto, N
Okuse, C
Takahashi, H
Kurihara, T
Kawahara, K
Maruyama, I
Zeniya, M
AF Hokari, Atsushi
Ishikawa, Tomohisa
Tajiri, Hisao
Matsuda, Takahide
Ishii, Osamu
Matsumoto, Nobuyuki
Okuse, Chiaki
Takahashi, Hideaki
Kurihara, Takeshi
Kawahara, Ko-ichi
Maruyama, Ikuro
Zeniya, Mikio
TI Efficacy of MK615 for the treatment of patients with liver disorders
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Prunus mume; MK615; Liver damage; Hepatitis C; Non-alcoholic fatty liver
disease
ID CHRONIC HEPATITIS-C; ALANINE AMINOTRANSFERASE LEVELS;
NECROSIS-FACTOR-ALPHA; PRUNUS-MUME-SIEB.; CELLS IN-VITRO;
HEPATOCELLULAR-CARCINOMA CELLS; OLEANOLIC ACID; JAPANESE APRICOT;
NONALCOHOLIC STEATOHEPATITIS; HEME OXYGENASE-1
AB AIM: To investigate the hepatoprotective effect of MK615, a Japanese apricot extract, in an animal model, and its clinical therapeutic effect.
METHODS: Wistar rats were administered physiological saline (4 mL/kg) or MK615 solution (4 ml./kg) for 7 d. On the sixth d, acute hepatic injury was induced by administering a single intraperitoneal injection (ip) of D-galactosamine hydrochloride (D-GaIN) (600 mg/kg). Plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined, and liver tissues were used for histopathological analysis. Fifty-eight patients with liver disorders [hepatitis C (n = 40), non-alcoholic fatty liver disease (n = 15), and autoimmune liver disease (n = 3)] were orally administered commercially available Misatol ME-containing MK615 (13 g/d) daily for 12 wk. Blood and urine were sampled immediately before and 6 wk, 12 wk, and 16 wk after the start of intake to measure various biochemical parameters. The percentage change in ALT and AST levels after 12 wk from the pre-intake baseline served as a primary endpoint.
RESULTS: D-GaIN effectively induced acute hepatic injury in the rats. At 48 h after the ip injection of D-GaIN, the plasma levels of ALT (475.6 +/- 191.5 IU/L vs 225.3 +/- 194.2 IU/L, P < 0.05) and AST (1253.9 +/- 223.4 IU/L vs 621.9 +/- 478.2 IU/L, P < 0.05) in the MK615 group were significantly lower than the control group. Scattered single cell necrosis, loss of hepatocytes, and extensive inflammatory cell infiltration were observed in hepatic tissue samples collected from the control group. However, these findings were less pronounced in the group receiving MK615. At the end of the clinical study, serum ALT and AST levels were significantly decreased compared with pre-intake baseline levels from 103.5 +/- 58.8 IU/L to 71.8 +/- 39.3 IU/L (P < 0.05) and from 93.5 +/- 55.6 IU/L to 65.5 +/- 34.8 IU/L (P < 0.05), respectively. A reduction of >= 30% from the pre-study baseline ALT level was observed in 26 (45%) of the 58 patients, while 25 (43%) patients exhibited similar AST level reductions. The chronic hepatitis C group exhibited significant ALT and AST level reductions from 93.4 +/- 51.1 IU/L to 64.6 +/- 35.1 IU/L (P < 0.05) and from 94.2 +/- 55.5 IU/L to 67.2 +/- 35.6 IU/L (P < 0.05), respectively. A reduction of >= 30% from the pre-study baseline ALT level was observed in 20 (50%) of the 40 patients. ALT levels in both the combined ursodeoxycholic acid (UDCA) treatment and the UDCA uncombined groups were significantly lower after Misatol ME administration. MK615 protected hepatocytes from D-GaIN-induced cytotoxicity in rats. Misatol ME decreased elevated ALT and AST levels in patients with liver disorders.
CONCLUSION: These results suggest that MK615 and Misatol ME are promising hepatoprotective agents for patients with liver disorders. (C) 2012 Baishideng. All rights reserved.
C1 [Zeniya, Mikio] Jikei Univ, Sch Med, Div Gastroenterol & Hepatol,Dept Internal Med, Minato Ku, Tokyo 1058471, Japan.
[Matsuda, Takahide; Ishii, Osamu] St Marianna Univ, Sch Med, Div Gen Internal Med, Dept Internal Med, Kawasaki, Kanagawa 2168511, Japan.
[Matsumoto, Nobuyuki; Okuse, Chiaki; Takahashi, Hideaki] St Marianna Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol, Kawasaki, Kanagawa 2168511, Japan.
[Kurihara, Takeshi] Keio Univ, Grad Sch Media & Governance, Fujisawa, Kanagawa 2520882, Japan.
[Kawahara, Ko-ichi] Osaka Inst Technol, Dept Biomed Engn, Osaka 5358585, Japan.
[Maruyama, Ikuro] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Syst Biol Thromboregulat, Kagoshima 8908580, Japan.
C3 Jikei University; Saint Marianna University; Saint Marianna University;
Keio University; Osaka Institute of Technology; Kagoshima University
RP Zeniya, M (corresponding author), Jikei Univ, Sch Med, Div Gastroenterol & Hepatol,Dept Internal Med, Minato Ku, Nishi Shimbashi 3-25-8, Tokyo 1058471, Japan.
EM zeniya@jikei.ac.jp
FU Grants-in-Aid for Scientific Research [24659804] Funding Source: KAKEN
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NR 47
TC 12
Z9 14
U1 0
U2 5
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD AUG 21
PY 2012
VL 18
IS 31
BP 4118
EP 4126
DI 10.3748/wjg.v18.i31.4118
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 995CZ
UT WOS:000307986800007
PM 22919243
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Al Safarjalani, ON
Zhou, XJ
Rais, RH
Shi, JX
Schinazi, RF
Naguib, FNM
el Kouni, MH
AF Al Safarjalani, ON
Zhou, XJ
Rais, RH
Shi, JX
Schinazi, RF
Naguib, FNM
el Kouni, MH
TI 5-(Phenylthio)acyclouridine: a powerful enhancer of oral uridine
bioavailability: relevance to chemotherapy with 5-fluorouracil and other
uridine rescue regimens
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE 5-(Phenylthio)acyclouridine; uridine; phosphorylase; inhibitor;
chemotherapy
ID HIGH-DOSE URIDINE; PERFUSED RAT-HEART; PHOSPHORYLASE INHIBITOR; PHASE-I;
PLASMA URIDINE; DIHYDROOROTATE DEHYDROGENASE; PYRIMIDINE NUCLEOSIDES;
ACID ACYCLONUCLEOSIDE; CIRCULATING URIDINE; CIRCADIAN-RHYTHM
AB Purpose: The purpose of this investigation was to evaluate the effectiveness of oral 5-(phenylthio)acyclouridine (PTAU) in improving the pharmacokinetics and bioavailability of oral uridine. PTAU is a potent and specific inhibitor of uridine phosphorylase (UrdPase, EC 2.4.2.3), the enzyme responsible for uridine catabolism. This compound was designed as a lipophilic inhibitor in order to facilitate its access to the liver and intestine, the main organs involved in uridine catabolism. PTAU is fully absorbed after oral administration with 100% oral bioavailability. Methods: Uridine (330, 660 or 1320 mg/kg) and/or PTAU (30, 45, 60, 120, 240 or 480 mg/kg) were orally administered to mice. The plasma levels of uridine, its catabolite uracil, and PTAU were measured using HPLC, and pharmacokinetic analysis was performed. Results: Oral PTAU up to 480 mg/kg per day is not toxic to mice. Oral PTAU at 30, 45, 60, 120 and 240 mg/kg has a prolonged plasma half-life of 2-3 h, and peak plasma PTAU concentrations (C-max) of 41, 51, 74, 126 and 161 mu M with AUCs of 70, 99, 122, 173 and 225 mu mol h/l, respectively. Coadministration of uridine with PTAU did not have a significant effect on the pharmacokinetic parameters of plasma PTAU at any of the doses tested. Coadministration of PTAU (30, 45, 60 and 120 or 240 mg/kg) with uridine (330, 660 or 1320 mg/kg) elevated the concentration of plasma uridine over that following the same dose of uridine alone, a result of reduced metabolic clearance of uridine as evidenced by decreased plasma exposure (C-max and AUC) to uracil. Plasma uridine was elevated with the increase of uridine dose at each PTAU dose tested and no plateau was reached. Coadministration of PTAU at 30, 45, 60, 120 and 240 mg/kg improved the low oral bioavailability (7.7%) of uridine administered at 1320 mg/kg by 4.3-, 5.9-, 9.9-, 11.7- and 12.5-fold, respectively, and reduced the AUC of plasma uracil (1227.8 mu mol h/l) by 5.7-, 6.8-, 8.2-, 6.3-, and 6.9-fold, respectively. Similar results were observed when PTAU was coadministered with lower doses of uridine. Oral PTAU at 30, 45, 60, 120 and 240 mg/kg improved the oral bioavailability of 330 mg/kg uridine by 1.7-, 2.4-, 2.6-, 5.2- and 4.3- fold, and that of 660 mg/kg uridine by 2.3-, 2.7-, 3.3-, 4.6- and 6.7-fold, respectively. Conclusion: The excellent pharmacokinetic properties of PTAU, and its extraordinary effectiveness in improving the oral bioavailability of uridine, could be useful to rescue or protect from host toxicities of 5-fluorouracil and various chemotherapeutic pyrimidine analogues used in the treatment of cancer and AIDS, as well as in the management of medical disorders that are remedied by the administration of uridine including CNS disorders (e.g. Huntington's disease, bipolar disorder), liver diseases, diabetic neuropathy, cardiac damage, various autoimmune diseases, and transplant rejection.
C1 Univ Alabama Birmingham, Ctr AIDS Res, Ctr Comprehens Canc, Dept Pharmacol & Toxicol, Birmingham, AL 35294 USA.
Pharmasset Inc, Tucker, GA 30084 USA.
Vet Affairs Med Ctr Atlanta, Decatur, GA 30033 USA.
Emory Univ, Sch Med, Dept Pediat, Biochem Pharmacol Lab, Atlanta, GA 30322 USA.
C3 University of Alabama System; University of Alabama Birmingham; Gilead
Sciences; Emory University
RP Univ Alabama Birmingham, Ctr AIDS Res, Ctr Comprehens Canc, Dept Pharmacol & Toxicol, Birmingham, AL 35294 USA.
EM m.elkouni@ccc.uab.edu
RI Schinazi, Raymond/B-6777-2017; Shi, Junxing/JRY-7814-2023
FU NCI NIH HHS [CA-94623] Funding Source: Medline
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NR 89
TC 62
Z9 68
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JUN
PY 2005
VL 55
IS 6
BP 541
EP 551
DI 10.1007/s00280-004-0967-y
PG 11
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 920XI
UT WOS:000228728400004
PM 15729584
DA 2025-01-07
ER
PT J
AU Parris, GE
AF Parris, GE
TI Hypothesis links emergence of chloroquine-resistant malaria and other
intracellular pathogens and suggests a new strategy for treatment of
diseases caused by intracellular parasites
SO MEDICAL HYPOTHESES
LA English
DT Article
ID NITRIC-OXIDE; IN-VITRO; PLASMODIUM-FALCIPARUM; HOST-DEFENSE; CPG MOTIFS;
APOPTOSIS; BCL-2; INFECTION; MECHANISMS; CELLS
AB Chloroquine and related anti-malarial drugs appear to promote apoptosis in T-cells by suppressing NF-kappa-B, which enhances the expression of anti-apoptotic proteins (e.g., Bcl-2). Thus, chloroquine has found applications in autoimmune diseases where it apparently facilitates apoptosis of abnormally persistent T-cell. clones. The mode of action of chloroquine in prevention of malaria is not known, but it may be to minimize replication of the parasite in the liver cells, which occurs before invasion of the erythrocytes, by facilitating premature apoptosis of the infected host cells. After introduction of chloroquine in the 1950s world-wide for prophylactic use, chloroquine-resistant malaria emerged. Here it is hypothesized that concurrent with emergence of chloroquine-resistant malaria (presumably with enhanced anti-apoptotic capabilities), other intracellular parasites have evolved to enhance their ability to prevent apoptosis in host cells. Two examples of viral diseases that have emerged from areas of high incidence of chloroquine-resistant malaria are AIDS from HIV and SARS from coronavirus. The hypothesis holds that prophylactic exposure to proapoptotic chloroquine drugs caused natural selection for strains of viruses and other parasites that have enhanced antiapoptotic abilities. When transmitted to host organisms that are not under the influence of the pro-apoptotic drug, the new "anti-apoptotic" strains may cause unexpected diseases. In the case of SARS, the coronavirus appears to have accessed a new niche where it proves to be Lethal to its host. In the case of AIDS, the HIV (which has had a long-term symbiotic relationship with primates) has run amuck because the infected cells are now substantially more tolerant to the toxins (i.e., resistant to apoptosis) that they secrete than the uninfected bystander cells, which are not unusually resistant to apoptosis. A corollary to the hypothesis is that if the level of resistance to apoptosis in the infected cells were no higher than the level of resistance in the bystander cells, then the infected cells would preferentially kill themselves through apoptosis. It appears that in the case of HIV, the increased resistance to apoptosis is provided by expression of Bcl-2 and suppression of p53. Hence, drugs that suppresses Bcl-2 or restore p53 function might be effective in restoring the parity of resistance to apoptosis between infected and uninfected cells. Currently, an antisense drug targeting Bcl-2 (G3139/Genasense(TM), Genta, Inc.) is in late-stage cancer trials and may be on the market for those indications in months. It would be interesting to try these drugs against various intracellular parasites including HIV. This approach to prevent or eliminate active infections might be particularly attractive against a range of parasites (virus, bacteria, protozoa, fungus) when safe and effective vaccines are not available. (C) 2003 Elsevier Ltd. All rights reserved.
RP 9601 Warfield Rd, Gaithersburg, MD 20882 USA.
EM antimony_121@hotmail.com
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NR 33
TC 13
Z9 15
U1 0
U2 3
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0306-9877
EI 1532-2777
J9 MED HYPOTHESES
JI Med. Hypotheses
PY 2004
VL 62
IS 3
BP 354
EP 357
DI 10.1016/j.mehy.2003.12.004
PG 4
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 805UR
UT WOS:000220391700006
PM 14975502
OA Green Accepted, Green Published
DA 2025-01-07
ER
PT J
AU Hung, JT
Huang, JR
Yu, AL
AF Hung, Jung-Tung
Huang, Jing-Rong
Yu, Alice L.
TI Tailored design of NKT-stimulatory glycolipids for polarization of
immune responses
SO JOURNAL OF BIOMEDICAL SCIENCE
LA English
DT Review
DE iNKT cell; alpha-galactosylceramide; Anergy; Myeloid-derived suppressive
cell
ID KILLER T-CELLS; LIGAND ALPHA-GALACTOSYLCERAMIDE; ANTIGEN-PRESENTING
CELLS; PHASE I/II TRIAL; SUPPRESSOR-CELLS; DENDRITIC CELLS;
RECEPTOR-ALPHA/BETA(+) CELLS; CRYSTAL-STRUCTURE; MOUSE CD1; EFFECTOR
FUNCTION
AB Natural killer T (NKT) cell is a distinct population of T lymphocytes that can rapidly release massive amount of Th1 and Th2 cytokines upon the engagement of their T cell receptor with glycolipids presented by CD1d. The secreted cytokines can promote cell-mediated immunity to kill tumor cells and intracellular pathogens, or suppress autoreactive immune cells in autoimmune diseases. Thus, NKT cell is an attractive target for developing new therapeutics to manipulate immune system. The best-known glycolipid to activate NKT cells is alpha-galactosylceramide (alpha-GalCer), which has been used as a prototype for designing new NKT stimulatory glycolipids. Many analogues have been generated by modification of the galactosyl moiety, the acyl chain or the phytosphingosine chain of alpha-GalCer. Some of the analogues showed greater abilities than alpha-GalCer in polarizing immune responses toward Th1 or Th2 dominance. Among them, several analogues containing phenyl groups in the lipid tails were more potent in inducing Th1-skewed cytokines and exhibited greater anticancer efficacy than alpha-GalCer. Analyses of the correlation between structure and activity of various alpha-GalCer analogues on the activation of iNKT cell revealed that CD1d-glycolipid complexes interacted with the same population of iNKT cell expressing similar T-cell receptor V beta as alpha-GalCer. On the other hand, those phenyl glycolipids with propensity for Th1 dominant responses showed greater binding avidity and stability than alpha-GalCer for iNKT T-cell receptor when complexed with CD1d. Thus, it is the avidity and stability of the ternary complexes of CD1d-glycolipid-iNKT TCR that dictate the polarity and potency of immune responses. These findings provide a key to the rationale design of immune modulating glycolipids with desirable Th1/Th2 polarity for clinical application. In addition, elucidation of alpha-GalCer-induced anergy, liver damage and accumulation of myeloid derived suppressor cells has offered explanation for its lacklustre anti-cancer activities in clinical trials. On other hand, the lack of such drawbacks in glycolipid analogues containing phenyl groups in the lipid tails of alpha-GalCer coupled with the greater binding avidity and stability of CD1d-glycolipid complex for iNKT T-cell receptor, account for their superior anti-cancer efficacy in tumor bearing mice. Further clinical development of these phenyl glycolipids is warranted.
C1 [Hung, Jung-Tung; Huang, Jing-Rong; Yu, Alice L.] Chang Gung Mem Hosp Linkou, Inst Stem Cell & Translat Canc Res, 5 Fu Shin St, Taoyuan 333, Taiwan.
[Hung, Jung-Tung; Huang, Jing-Rong; Yu, Alice L.] Chang Gung Univ, 5 Fu Shin St, Taoyuan 333, Taiwan.
[Yu, Alice L.] Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA.
C3 Chang Gung Memorial Hospital; Chang Gung University; Chang Gung Memorial
Hospital; University of California System; University of California San
Diego
RP Yu, AL (corresponding author), Chang Gung Mem Hosp Linkou, Inst Stem Cell & Translat Canc Res, 5 Fu Shin St, Taoyuan 333, Taiwan.; Yu, AL (corresponding author), Chang Gung Univ, 5 Fu Shin St, Taoyuan 333, Taiwan.; Yu, AL (corresponding author), Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA.
EM a1yu@ucsd.edu
RI Hung, JungTung/KHU-5937-2024
OI Hung, Jung-Tung/0000-0001-7161-1915; yu, alice/0000-0003-2444-0505
FU Ministry of Health and Welfare [DOH95-DC-1411]; Ministry of Science and
Technology [MOST 105-2320-B-182A-006]; Chang Gung Medical Foundation
[OMRPG3C0014, CMRPG3D1491-3]; Academia Sinica in Taiwan
FX This research was supported by grants from the Ministry of Health and
Welfare (DOH95-DC-1411), the Ministry of Science and Technology (MOST
105-2320-B-182A-006), the Chang Gung Medical Foundation (OMRPG3C0014 and
CMRPG3D1491-3) and Academia Sinica in Taiwan.
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NR 103
TC 31
Z9 35
U1 0
U2 20
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1021-7770
EI 1423-0127
J9 J BIOMED SCI
JI J. Biomed. Sci.
PD MAR 23
PY 2017
VL 24
AR 22
DI 10.1186/s12929-017-0325-0
PG 10
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA EQ0FQ
UT WOS:000397747500001
PM 28335781
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Samuels, J
Lawson, PJ
Morton, AP
Moore, HB
Hansen, KC
Sauaia, A
Schoen, JA
AF Samuels, Jason
Lawson, Peter J.
Morton, Alexander P.
Moore, Hunter B.
Hansen, Kirk C.
Sauaia, Angela
Schoen, Jonathan A.
TI Prospective assessment of fibrinolysis in morbid obesity: tissue
plasminogen activator resistance improves after bariatric surgery
SO SURGERY FOR OBESITY AND RELATED DISEASES
LA English
DT Article; Proceedings Paper
CT 11th Annual American Academic Surgical Congress (ASC) of the
Society-of-University-Surgeons / Association-for-Academic-Surgery
CY JAN 18-FEB 05, 2016
CL Jacksonville, FL
SP Soc Univ Surg, Assoc Acad Surg
DE Fibrinolysis; Thromboelastography; Venous thromboembolism; Thrombosis;
Coagulopathy; Morbid obesity; Bariatric surgery
ID TRAUMA-INDUCED COAGULOPATHY; HYPERCOAGULABLE STATE; METABOLIC SYNDROME;
RISK-FACTORS; THROMBOELASTOGRAPHY; RESUSCITATION; INFLAMMATION;
VITRONECTIN; PERSISTENCE; THROMBOSIS
AB Background: Morbid obesity is associated with an increased risk of thrombotic events, which has been attributed to increased thrombotic activity. Multiple mechanisms have been proposed to explain this increased risk, including an inflammatory state with upregulation of procoagul ant and antifibrinolytic proteins. We therefore hypothesize that patients with morbid obesity are hypercoagulable and will revert to normal after bariatric surgery.
Objectives: To evaluate changes in the hypercoagulable state after bariatric surgery.
Setting: University Hospital, Bariatric Center of Excellence, United States.
Methods: Thromboelastography (TEG) data were collected on 72 subjects with morbid obesity, with 36 who had 6 months of follow-up after bariatric surgery. TEG data of 75 healthy subjects (HS) without obesity, recent trauma or surgery, acute infection, or chronic conditions (e.g., liver, cardiovascular, or kidney disease; cancer; diabetes; autoimmune or inflammatory disorders; and disorders of coagulation) were used for comparison. TEG was performed alone and with the addition of 75 and 150 ng/mL tissue plasminogen activator (tPA) to quantify fibrinolysis resistance (tPA-challenged TEG).
Results: The bariatric surgery cohort had a median age of 40.5 years, a median body mass index of 44.6 kg/m(2), and 90% female patients. Median body mass index reduced significantly 6 months post surgery but remained elevated compared with the HS group (31.4 versus 25.4 kg/m(2), P < .0001). At 6 months post surgery, subjects had longer reaction time (mean difference, 1.3; P = .02), lower maximum amplitude (-2.4, P = .01), and increased fibrinolysis with low-dose (3.1, P < .0001) and high-dose tPA-challenged TEG (9, P < .0001). Compared with HS, the postsurgery TEG values were still more likely to be abnormal (all P < .05).
Conclusions: Patients with morbid obesity form stronger clots more rapidly and are more resistant to fibrinolysis than subjects without obesity. Bariatric surgery significantly improved the hypercoagulable profile and fibrinolysis resistance of morbid obesity. (C) 2019 Published by Elsevier Inc. on behalf of American Society for Bariatric Surgery.
C1 [Samuels, Jason; Lawson, Peter J.; Morton, Alexander P.; Moore, Hunter B.] Univ Colorado, Dept Surg, Trauma Res Ctr, Denver, CO USA.
[Morton, Alexander P.; Sauaia, Angela] Denver Hlth Med Ctr, Dept Surg, Denver, CO USA.
[Hansen, Kirk C.] Univ Colorado, Dept Biochem & Mol Genet, Denver, CO 80202 USA.
[Schoen, Jonathan A.] Univ Colorado, Div GI Trauma & Endocrine Surg, Dept Surg, Denver, CO USA.
C3 University of Colorado System; University of Colorado Denver; Denver
Health Medical Center; University of Colorado System; University of
Colorado Denver; University of Colorado System; University of Colorado
Denver
RP Schoen, JA (corresponding author), Trauma Res Ctr, Mail Stop C-320,RC2 Bldg,Room P15-6420 A-F, Aurora, CO 80045 USA.
EM Jason.Samuels@ucdenver.edu
RI Samuels, Jason/HGB-4341-2022; Samuels, Jason/LIC-2250-2024
OI Samuels, Jason/0000-0001-5427-3117
FU National Institute Of General Medical Sciences of the National
Institutes of Health [P50 GM049222, T32 GM008315-21]; National Heart,
Lung and Blood Institute [UM1 HL120877]
FX Research reported in this publication was supported by the National
Institute Of General Medical Sciences of the National Institutes of
Health (or other sponsors of the project) under Award Number P50
GM049222, and T32 GM008315-21, as well as funding from the National
Heart, Lung and Blood Institute grant UM1 HL120877. The content is
solely the responsibility of the authors and does not necessarily
represent the official views of the National Institutes of Health (or
other sponsors of the project).
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NR 39
TC 13
Z9 14
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1550-7289
EI 1878-7533
J9 SURG OBES RELAT DIS
JI Surg. Obes. Relat. Dis.
PD JUL
PY 2019
VL 15
IS 7
BP 1153
EP 1159
DI 10.1016/j.soard.2019.03.048
PG 7
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Surgery
GA IU3BF
UT WOS:000483453000018
PM 31128997
OA Green Accepted
DA 2025-01-07
ER
PT J
AU Tsunoda, T
Doi, K
Ishikura, S
Luo, H
Nishi, K
Matsuzaki, H
Koyanagi, M
Tanaka, Y
Okamura, T
Shirasawa, S
AF Tsunoda, Toshiyuki
Doi, Keiko
Ishikura, Shuhei
Luo, Hao
Nishi, Kensuke
Matsuzaki, Hiroshi
Koyanagi, Midori
Tanaka, Yoko
Okamura, Tadashi
Shirasawa, Senji
TI Zfat expression in ZsGreen reporter gene knock-in mice: Implications for
a novel function of Zfat in definitive erythropoiesis
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Article
DE Zfat; knock-in mouse; definitive erythropoiesis
ID GENOME-WIDE ASSOCIATION; FINGER PROTEIN ZFAT; AUTOIMMUNE
THYROID-DISEASE; PERIPHERAL T-CELLS; SUSCEPTIBILITY; IDENTIFICATION;
HOMEOSTASIS; CANCER; ROLES; DIFFERENTIATION
AB Zinc finger and AT-hook domain containing (Zfat) is a transcriptional regulator harboring an AT-hook domain and 18 repeats of a C2H2 zinc-finger motif, which binds directly to the proximal region of transcription start sites in Zfat-target genes. It was previously reported that deletion of the Zfat gene in mice yields embryonic lethality by embryonic day 8.5 and impairs primitive hematopoiesis in yolk sac blood islands. In addition, Zfat has been reported to be involved in thymic T-cell development and peripheral T-cell homeostasis. In the present study, in order to obtain a precise understanding of the expression and function of Zfat, a knock-in mouse strain (Zfat(ZsG/+) mice), which expressed ZsGreen in the Zfat locus, was established. ZsGreen signals in tissues and cells of Zfat(ZsG/+) mice were examined by flow cytometric and histological analyses. Consistent with our previous studies, ZsGreen signals in Zfat(ZsG/+) mice were detected in the embryo and yolk sac blood islands, as well as in thymocytes, B and T cells. In the Zfat(ZsG/+) thymus, ZsGreen(+) cells were identified not only in T-cell populations but also in thymic epithelial cells, suggesting the role of Zfat in antigen-presenting cells during thymic T-cell development. ZsGreen signals were observed in definitive erythroid progenitor cells in the fetal liver and adult bone marrow of Zfat(ZsG/+) mice. The proportion of ZsGreen(+) cells in these tissues was highest at the early stage of erythroid differentiation, suggesting that Zfat serves particular roles in definitive erythropoiesis. Histological studies demonstrated that ZsGreen signals were detected in the pyramidal cells in the hippocampal CA1 region and the Purkinje cells in the cerebellum, suggesting novel functions of Zfat in nervous tissues. Taken together, these results indicated that the Zfat(ZsG/+) reporter mouse may be considered a useful tool for elucidating the expression and function of Zfat.
C1 [Tsunoda, Toshiyuki; Doi, Keiko; Ishikura, Shuhei; Luo, Hao; Nishi, Kensuke; Matsuzaki, Hiroshi; Koyanagi, Midori; Tanaka, Yoko; Shirasawa, Senji] Fukuoka Univ, Fac Med, Dept Cell Biol, Fukuoka, Fukuoka 8140180, Japan.
[Tsunoda, Toshiyuki; Doi, Keiko; Ishikura, Shuhei; Shirasawa, Senji] Fukuoka Univ, Cent Res Inst Adv Mol Med, Fukuoka, Fukuoka 8140180, Japan.
[Okamura, Tadashi] Natl Ctr Global Hlth & Med, Res Inst, Dept Lab Anim Med, Tokyo 1628655, Japan.
[Okamura, Tadashi] Natl Ctr Global Hlth & Med, Res Inst, Sect Anim Models, Dept Infect Dis, Tokyo 1628655, Japan.
C3 Fukuoka University; Fukuoka University; National Center for Global
Health & Medicine - Japan; National Center for Global Health & Medicine
- Japan
RP Shirasawa, S (corresponding author), Fukuoka Univ, Fac Med, Dept Cell Biol, Jonan Ku, 7-45-1 Nanakuma, Fukuoka, Fukuoka 8140180, Japan.
EM sshirasa@fukuoka-u.ac.jp
RI Luo, Hao/KMY-0558-2024
OI Nishi, Kensuke/0000-0003-4052-0855
FU Ministry of Education, Culture, Sport, Science and Technology of Japan
FX The present study was supported, in part, by grants from the Ministry of
Education, Culture, Sport, Science and Technology of Japan.
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Gray DHD, 2002, J IMMUNOL METHODS, V260, P15, DOI 10.1016/S0022-1759(01)00493-8
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Ishikura S, 2016, BBA-GENE REGUL MECH, V1859, P1398, DOI 10.1016/j.bbagrm.2016.08.010
Ishikura S, 2016, J BIOL CHEM, V291, P15282, DOI 10.1074/jbc.M116.723734
Ishikura S, 2015, J CELL BIOCHEM, V116, P149, DOI 10.1002/jcb.24954
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Koyanagi M, 2008, GENOMICS, V91, P451, DOI 10.1016/j.ygeno.2008.01.009
Makvandi-Nejad S, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0039929
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Sabatino G, 2013, J BIOL REG HOMEOS AG, V27, P729
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Signer-Hasler H, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0037282
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Takeuchi F, 2009, J HUM GENET, V54, P749, DOI 10.1038/jhg.2009.99
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Tsunoda T, 2013, ANTICANCER RES, V33, P2833
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Yang SJ, 2006, INT IMMUNOL, V18, P729, DOI 10.1093/intimm/dxl010
NR 28
TC 4
Z9 5
U1 0
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD NOV
PY 2018
VL 42
IS 5
BP 2595
EP 2603
DI 10.3892/ijmm.2018.3806
PG 9
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA GX4LA
UT WOS:000447702700025
PM 30106088
OA hybrid, Green Submitted, Green Published
DA 2025-01-07
ER
PT J
AU Mahiout, S
Lindén, J
Esteban, J
Sánchez-Pérez, I
Sankari, S
Pettersson, L
Håkansson, H
Pohjanvirta, R
AF Mahiout, Selma
Linden, Jere
Esteban, Javier
Sanchez-Perez, Ismael
Sankari, Satu
Pettersson, Lars
Hakansson, Helen
Pohjanvirta, Raimo
TI Toxicological characterisation of two novel selective aryl hydrocarbon
receptor modulators in Sprague-Dawley rats
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE AH-receptor; Selective modulators; Ima-08401; Ima-07101; TCDD; Toxicity
ID 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD EXPOSURE; CATALYTIC ACTIVITY
CONCENTRATIONS; MESSENGER-RNA EXPRESSION; EQUIVALENCY FACTORS TEFS;
TRANS-RETINOIC ACID; T-CELLS; PHYSIOLOGICAL FUNCTIONS;
MOLECULAR-MECHANISMS; LABORATORY-ANIMALS; DIOXIN RECEPTOR
AB The aryl hydrocarbon receptor (AHR) mediates the toxicity of dioxins, but also plays important physiological roles. Selective AHR modulators, which elicit some effects imparted by this receptor without causing the marked toxicity of dioxins, are presently under intense scrutiny. Two novel such compounds are IMA-08401 (N-acetyl-N-phenyl-4-acetoxy-5-chloro-1,2-dihydro-1-methyl-2-oxo-quinoline-3-carboxamide) and IMA-07101 (N-acetyl-N-(4-trifluoromethylphenyl)-4-acetoxy-1,2-dihydro-5-methoxy-1-methyl-2-oxo-quinoline-3-carboxamide). They represent, as diacetyl prodrugs, AHR-active metabolites of the drug compounds laquinimod and tasquinimod, respectively, which are intended for the treatment of autoimmune diseases and cancer. Here, we toxicologically assessed the novel compounds in Sprague-Dawley rats, after a single dose (8.75-92.5 mg/kg) and 5-day repeated dosing at the highest doses achievable (IMA-08401: 100 mg/kg/day; and IMA-07101: 75 mg/kg/day). There were no overt clinical signs of toxicity, but body weight gain was marginally retarded, and the treatments induced minimal hepatic extramedullary haematopoiesis. Further, both the absolute and relative weights of the thymus were significantly decreased. Cyp1a1 gene expression was substantially increased in all tissues examined. The hepatic induction profile of other AHR battery genes was distinct from that caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The only marked alterations in serum clinical chemistry variables were a reduction in triglycerides and an increase in 3-hydroxybutyrate. Liver and kidney retinol and retinyl palmitate concentrations were affected largely in the same manner as reported for TCDD. In vitro, the novel compounds activated CYP1A1 effectively in H4IIE cells. Altogether, these novel compounds appear to act as potent activators of the AHR, but lack some major characteristic toxicities of dioxins. They therefore represent promising new selective AHR modulators. (C) 2017 Elsevier Inc. All rights reserved.
C1 [Mahiout, Selma; Pohjanvirta, Raimo] Univ Helsinki, Fac Vet Med, Dept Food Hyg & Environm Hlth, Mustialankatu 1, FI-00790 Helsinki, Finland.
[Linden, Jere] Univ Helsinki, Fac Vet Med, Dept Basic Vet Sci, Helsinki, Finland.
[Esteban, Javier; Sanchez-Perez, Ismael] Univ Miguel Hernandez Elche, Inst Bioingn, Alicante, Spain.
[Sankari, Satu] Univ Helsinki, Fac Vet Med, Dept Equine & Small Anim Med, Cent Lab, Helsinki, Finland.
[Pettersson, Lars] Immunahr AB, Lund, Sweden.
[Hakansson, Helen] Karolinska Inst, Inst Environm Med IMM, Stockholm, Sweden.
C3 University of Helsinki; University of Helsinki; Universidad Miguel
Hernandez de Elche; University of Helsinki; Karolinska Institutet
RP Mahiout, S (corresponding author), Univ Helsinki, Fac Vet Med, Dept Food Hyg & Environm Hlth, Mustialankatu 1, FI-00790 Helsinki, Finland.
EM selma.mahiout@helsinki.fi
RI Pohjanvirta, Raimo/I-4509-2019; Esteban, Javier/A-5640-2019
OI Hakansson, Helen/0000-0002-7524-8209; Esteban,
Javier/0000-0003-3760-8223; Linden, Jere/0000-0001-9872-3626; Mahiout,
Selma L/0000-0001-6405-1155
FU Academy of Finland [261232]; University of Helsinki Doctoral Programme
in Food Chain and Health of the Doctoral School in Environmental, Food
and Biological Sciences; Academy of Finland (AKA) [261232] Funding
Source: Academy of Finland (AKA)
FX The work was financially supported by Academy of Finland (Grant no.
261232; to RP) and University of Helsinki Doctoral Programme in Food
Chain and Health of the Doctoral School in Environmental, Food and
Biological Sciences (to SM). We further wish to acknowledge Susanna
Lukkarinen for her valuable technical contribution in processing samples
and performing RT-qPCR. The staff at Laboratory Animal Centre (LAC) of
the University of Helsinki is thanked for their cooperation and help
with practicalities; we especially thank Leena Liesirova, Anna Meller,
Virpi Ahokas and Lea Karvonen for having provided help whenever needed.
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NR 100
TC 20
Z9 22
U1 0
U2 18
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD JUL 1
PY 2017
VL 326
BP 54
EP 65
DI 10.1016/j.taap.2017.04.020
PG 12
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA EW6BH
UT WOS:000402589700007
PM 28433708
DA 2025-01-07
ER
PT J
AU Runken, MC
Noone, JM
Blanchette, CM
Zacherle, E
Howden, R
AF Runken, Michael C.
Noone, Joshua M.
Blanchette, Christopher M.
Zacherle, Emily
Howden, Reuben
TI Differences in Patient Demographics and Healthcare Costs of Patients
with PIDD Receiving Intravenous or Subcutaneous Immunoglobulin Therapies
in the United States
SO AMERICAN HEALTH AND DRUG BENEFITS
LA English
DT Article
DE healthcare costs; immunoglobulin therapies; intravenous therapy; IVIG;
primary immune-deficiency disease; SCIG; subcutaneous therapy
ID PRIMARY ANTIBODY DEFICIENCIES; REPLACEMENT THERAPY; PRIMARY
IMMUNODEFICIENCY; ECONOMIC-EVALUATION; GAMMA-GLOBULIN; SAFETY; EFFICACY;
INFUSION; CHILDREN; 10-PERCENT
AB BACKGROUND: Primary immune-deficiency disease (PIDD) is a rare, debilitating disease of the immune system that predisposes the affected individual to infection, autoimmune conditions, and neoplasm. A major component of the cost of treating PIDD is the high price of immunoglobulin drugs, which can be administered via an intravenous (IV) or subcutaneous (SC) route.
OBJECTIVE: To compare real-world costs for patients with PIDD who are receiving IV immunoglobulin (IVIG) or SC immunoglobulin (SCIG) treatment, from a US payer perspective, using a large claims database.
METHODS: Based on 2011 to 2013 data from the PharMetrics Plus database, a large national healthcare claims database, patients who were newly diagnosed with PIDD were included in the study if they had >= 2 claims for PIDD that were >= 90 days apart, and if they were treatment-naive for a minimum of 1 year before the study period. Patients who switched the route of immunoglobulin administration were excluded, with the exception of patients who received SCIG who could initially receive <= 2 IV-loading infusions, as directed by treatment guidelines. We used propensity score analysis to match the patients in the SCIG cohort to patients in the IVIG cohort based on age, sex, and all Elixhauser comorbidities. We compared the patient characteristics and direct medical costs (all-cause, PIDD-related, and pharmacy-related) before and after matching, using t-tests for continuous variables, chi-square test for categorical variables, and Wilcoxon rank-sum test for differences in medians.
RESULTS: A total of 1639 patients with PIDD (986 who received IVIG and 653 who received SCIG) met all the study inclusion criteria. Compared with the patients who received IVIG, the patients who received SCIG were predominantly female (58% vs 63%, respectively) and significantly younger (mean age, 49.1 vs 40.3 years, respectively). Significantly fewer patients who received SCIG than those receiving IVIG had claims with International Classification of Diseases, Ninth Revision codes for Elixhauser comorbidities, including cardiovascular and pulmonary conditions, diabetes, renal failure, liver disease, cancers, weight loss, fluid and electrolyte disorders, and psychoses (P <.05 for all), and their Charlson Comorbidity Index scores were lower than those receiving IVIG (1.74 vs 3.01, respectively; P <=.05 for all). After matching the 2 cohorts (N = 553 in each), the 1-year postindex median total PIDD-related costs were significantly lower in the IVIG group than in the SCIG group ($38,064 vs $43,266, respectively; P = .002).
CONCLUSIONS: In matched analyses, PIDD-related treatment costs were higher for patients who received SCIG than for those who received IVIG. Furthermore, patients who received SCIG were significantly younger and had significantly less comorbidities than their counterparts who received IVIG, suggesting that patient characteristics that reflect a desire and greater capacity for autonomy may affect physicians' choice of the route of administration for immunoglobulin.
C1 [Runken, Michael C.] Grifols SSNA, Global HEOR, Res Triangle Pk, NC 27709 USA.
[Noone, Joshua M.; Blanchette, Christopher M.; Zacherle, Emily; Howden, Reuben] Univ North Carolina Charlotte, Charlotte, NC USA.
C3 Grifols; University of North Carolina; University of North Carolina
Charlotte
RP Runken, MC (corresponding author), Grifols SSNA, Global HEOR, Res Triangle Pk, NC 27709 USA.
FU Grifols SSNA
FX Funding for this study was provided by Grifols SSNA.
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NR 52
TC 7
Z9 7
U1 0
U2 4
PU ENGAGE HEALTHCARE COMMUNICATIONS INC
PI HIGHLAND PARK
PA 318 CLEVELAND AVE, HIGHLAND PARK, NJ 08904 USA
SN 1942-2962
EI 1942-2970
J9 AM HEALTH DRUG BENEF
JI Am. Health Drug Benefits
PD OCT
PY 2019
VL 12
IS 6
BP 294
EP 303
PG 10
WC Health Care Sciences & Services; Health Policy & Services
WE Social Science Citation Index (SSCI)
SC Health Care Sciences & Services
GA JE3CM
UT WOS:000490571600005
PM 31908713
DA 2025-01-07
ER
PT J
AU Sanchez, LO
Zhan, CY
Cauduro, CGD
Crenier, L
Njimi, H
Englebert, G
Putignano, A
Lepida, A
Degré, D
Boon, N
Gustot, T
Deltenre, P
Marot, A
Devière, J
Moreno, C
Cnop, M
Trèpo, E
AF Sanchez, Lukas Otero
Zhan, Clara-Yongxiang
Cauduro, Carolina Gomes da Silveira
Crenier, Laurent
Njimi, Hassane
Englebert, Gael
Putignano, Antonella
Lepida, Antonia
Degre, Delphine
Boon, Nathalie
Gustot, Thierry
Deltenre, Pierre
Marot, Astrid
Deviere, Jacques
Moreno, Christophe
Cnop, Miriam
Trepo, Eric
TI A machine learning-based classification of adult-onset diabetes
identifies patients at risk of liver-related complications
SO JHEP REPORTS
LA English
DT Article
DE Liver fibrosis; Diabetes; Insulin-resistant; Clustering
ID INSULIN-RESISTANCE; FIBROSIS
AB Background & aims: Diabetes mellitus is a major risk factor for fatty liver disease development and progression. A novel machine learning method identified five clusters of patients with diabetes , with different characteristics and risk of diabetic complications using six clinical and biological variables. We evaluated whether this new classification could identify in-dividuals with an increased risk of liver-related complications. Methods: We used a prospective cohort of patients with a diagnosis of type 1 or type 2 diabetes without evidence of advanced fibrosis at baseline recruited between 2000 and 2020. We assessed the risk of each diabetic cluster of developing liver-related complications (i.e. ascites, encephalopathy, variceal haemorrhage, hepatocellular carcinoma), using competing risk analyses. Results: We included 1,068 patients , of whom 162 (15.2%) were determined to be in the severe autoimmune diabetes sub-group , 266 (24.9%) had severe insulin-deficient diabetes , 95 (8.9%) had severe insulin-resistant diabetes (SIRD) , 359 (33.6%) had mild obesity-related diabetes , and 186 (17.4%) were in the mild age-related diabetes subgroup. In multivariable analysis , patients in the SIRD cluster and those with excessive alcohol consumption at baseline had the highest risk for liver-related events. The SIRD cluster, excessive alcohol consumption , and hypertension were independently associated with clinically significant fibrosis, evaluated by liver biopsy or transient elastography. Using a simplified classification, patients assigned to the severe and mild insulin-resistant groups had a three-and twofold greater risk, respectively, of developing significant fibrosis compared with those in the insulin-deficient group. Conclusions: A novel clustering classification adequately stratifies the risk of liver-related events in a population with dia-betes. Our results also underline the impact of the severity of insulin resistance and alcohol consumption as key prognostic risk factors for liver-related complications. Impact and implications: Diabetes represents a major risk factor for NAFLD development and progression. This study examined the ability of a novel machine-learning approach to identify at-risk diabetes subtypes for liver-related complica-tions. Our results suggest that patients that had severe insulin resistance had the highest risk of liver-related outcomes and fibrosis progression. Moreover, excessive alcohol consumption at the diagnosis of diabetes was the strongest risk factor for developing liver-related events. & COPY; 2023 The Author(s). Published by Elsevier B.V. on behalf of European Association for the Study of the Liver (EASL). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Sanchez, Lukas Otero; Zhan, Clara-Yongxiang; Englebert, Gael; Putignano, Antonella; Lepida, Antonia; Degre, Delphine; Boon, Nathalie; Gustot, Thierry; Deltenre, Pierre; Deviere, Jacques; Moreno, Christophe; Trepo, Eric] Univ Libre Bruxelles, CUB Hop Erasme, Dept Gastroenterol Hepatopancreatol & Digest Oncol, Brussels, Belgium.
[Sanchez, Lukas Otero; Putignano, Antonella; Lepida, Antonia; Degre, Delphine; Boon, Nathalie; Gustot, Thierry; Deviere, Jacques; Moreno, Christophe; Trepo, Eric] Univ Libre Bruxelles, Lab Expt Gastroenterol, Brussels, Belgium.
[Cauduro, Carolina Gomes da Silveira; Crenier, Laurent; Cnop, Miriam] Univ Libre Bruxelles, CUB Hop Erasme, Dept Endocrinol, Brussels, Belgium.
[Cauduro, Carolina Gomes da Silveira; Cnop, Miriam] Univ Libre Bruxelles, Med Fac, ULB Ctr Diabet Res, Brussels, Belgium.
[Njimi, Hassane] Univ Libre Bruxelles, Biomed Stat, Brussels, Belgium.
[Gustot, Thierry] Ctr Rech Inflammat CRI, INSERM, Unite 1149, Paris, France.
[Gustot, Thierry] Univ Paris Diderot, UMR S 1149, Paris, France.
[Deltenre, Pierre] Clin St Luc, Dept Gastroenterol & Hepatol, Bouge, Belgium.
[Marot, Astrid] Catholic Univ Louvain, Dept Gastroenterol & Hepatol, CHU UCL Namur, Yvoir, Belgium.
[Sanchez, Lukas Otero; Trepo, Eric] CUB Hop Erasme, Dept Gastroenterol Hepatopancreatol & Digest Oncol, 808 Route Lennik, B-1070 Brussels, Belgium.
[Sanchez, Lukas Otero; Trepo, Eric] Univ Libre Bruxelles, Lab Expt Gastroenterol, Brussels, Belgium.
C3 Universite Libre de Bruxelles; Universite Libre de Bruxelles; Universite
Libre de Bruxelles; Universite Libre de Bruxelles; Universite Libre de
Bruxelles; Universite Paris Cite; Institut National de la Sante et de la
Recherche Medicale (Inserm); Universite Paris Cite; Universite
Catholique Louvain; Universite Libre de Bruxelles; Universite Libre de
Bruxelles
RP Sanchez, LO; Trèpo, E (corresponding author), CUB Hop Erasme, Dept Gastroenterol Hepatopancreatol & Digest Oncol, 808 Route Lennik, B-1070 Brussels, Belgium.; Sanchez, LO; Trèpo, E (corresponding author), Univ Libre Bruxelles, Lab Expt Gastroenterol, Brussels, Belgium.
EM Lukas.otero.sanchez@ulb.be; Eric.trepo@ulb.be
RI Trépo, Eric/ABD-9339-2021
OI Otero Sanchez, Lukas/0000-0002-8013-1371; Crenier,
Laurent/0000-0003-2326-4108
FU Fonds Erasme; Lucien Steinberg Prize; Collective Research Initiatives
consolidator grant from the Universite Libre de Bruxelles (EXPLORE
project)
FX LOS is a research fellow from Fund for Scientific Research (F.R.S-FNRS).
LOS is supported by Fonds Erasme. TG is supported by the Lucien
Steinberg Prize. This work is supported by a Collective Research
Initiatives consolidator grant from the Universite Libre de Bruxelles
(EXPLORE project). ET is a Research Associate of the FRS-FNRS in
Belgium.
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NR 34
TC 4
Z9 4
U1 0
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2589-5559
J9 JHEP REP
JI JHEP Rep.
PD AUG
PY 2023
VL 5
IS 8
AR 100791
DI 10.1016/j.jhepr.2023.100791
EA JUL 2023
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA P7FD5
UT WOS:001052286200001
PM 37456681
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Kamar, Z
El-Sahhar, M
Agena, H
Radwan, NA
Nelson, C
AF Kamar, Zeinab
El-Sahhar, Medhat
Agena, Hala
Radwan, Nehal A.
Nelson, Charles
TI Liver Transplantation: An Experience in Post-Operative Follow Up Of 80
Patients
SO LIFE SCIENCE JOURNAL-ACTA ZHENGZHOU UNIVERSITY OVERSEAS EDITION
LA English
DT Article
DE Orthotopic liver transplantation; Post operative follow up; Experience
ID FIBROSING CHOLESTATIC HEPATITIS; BIOPSY INTERPRETATION
AB Background: Orthotopic liver transplantation (OLT) is regarded as the only choice for treatment of patients with end stage liver disease (ESLD) and liver failure. Outcome for those patients is much better after liver transplantation resulting in reasonably good quality of life, provided complications are detected and treated promptly. Evaluation of needle liver graft biopsies and extensive clinicopathological correlation play an important role in the determination of liver allograft dysfunction after transplantation. Objective: To evaluate possible post-transplant outcome of patients underwent OLT. Methods: We analyzed 80 patients with liver cirrhosis who underwent deceased donor liver transplantation (DDLT) over a 10-year period in a cohort and observational study. The study was performed from June 2000 to June 2010 and included 75 men and 5 women. Results: Among all patients; origin of cirrhosis was post-viral in 76 patients, brimary biliary cirrhosis (PBC) in 2 cases, autoimmune hepatitis (AIH) in one case and cryptogenic cirrhosis in another case. The cases of post-viral cirrhosis were all of viral C etiology with 20 cases associated with hepatocellular carcinoma and 2 associated with hepatitis B viral infection. The patients are followed up for at least 18 months after enrolling in the study. They all had routine tests at the start of the study used as baseline for each patient. These tests are repeated according to the requirements of the individual patient. All patients had Tacrolimus (FK 506) as an immunosuppressive agent. Patients with hepatitis B viral infection had hepatitis B immunoglobulin, along with Lamivudine for relapse prophylaxis. Out of 80 patients, postoperative liver biopsy was performed, at least once, for 73 patients. The results of the biopsies revealed that recurrent HCV was detected in 46 (63.01%) cases, acute rejection in 14 (19.18%) cases, chronic rejection in 4 (5.48%) cases, cirrhosis in 2 (2.74%) cases, fibrosing cholestatic hepatitis in 2 (2.74%) cases, chronic active hepatitis with cholangitis and bile duct obstruction in 2 (2.74%) cases, recurrent primary biliary cirrhosis in 2 (2.74%) cases and one case (1.37%) with acquired schistosoma japonicum. A total of 24 (30%) patients died during follow up. Conclusion: The results of liver graft biopsies revealed that recurrent HCV is the prominent cause of organ dysfunction. Meanwhile; organ rejection was less frequently encountered. The complications of liver transplantation can be controlled and managed if diagnosed promptly and treated early. [Zeinab Kamar, Medhat El-Sahhar, Hala Agena, Nehal A. Radwan and Charles Nelson. Liver Transplantation: An Experience in Post-Operative Follow Up Of 80 Patients. Life Science Journal 2011;8(4):1088-1096]. (ISSN: 1097-8135). http://www.lifesciencesite.com. 135
C1 [Kamar, Zeinab; Radwan, Nehal A.] Ain Shams Univ, Fac Med, Dept Pathol, Cairo, Egypt.
[El-Sahhar, Medhat] Police Hosp, Giza, Egypt.
[Agena, Hala] Benha Univ, Fac Med, Dept Pathol, Cairo, Egypt.
[Nelson, Charles] Univ Leeds, St James Hosp, Dept Hepatol, Leeds LS2 9JT, W Yorkshire, England.
C3 Egyptian Knowledge Bank (EKB); Ain Shams University; Egyptian Knowledge
Bank (EKB); Benha University; University of Leeds; Saint James's
University Hospital
RP Kamar, Z (corresponding author), Ain Shams Univ, Fac Med, Dept Pathol, Cairo, Egypt.
EM zeinab_kamar@hotmail.com
CR Busuttil RW, 2004, TRANSPLANTATION, V77, pS44, DOI 10.1097/01.TP.0000126927.49589.3F
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NR 17
TC 0
Z9 0
U1 0
U2 1
PU MARSLAND PRESS
PI LANSING
PA PO BOX 21126, LANSING, MI 48909 USA
SN 1097-8135
J9 LIFE SCI J
JI Life Sci. J.
PY 2011
VL 8
IS 4
BP 1088
EP 1096
PG 9
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA 935NN
UT WOS:000303526000135
DA 2025-01-07
ER
PT J
AU Rodríguez-Tajes, S
Pocurull, A
Castillo, J
Casanova, G
Vega, L
Lens, S
Mariño, Z
Londoño, MC
Forner, A
Torres, F
Forns, X
AF Rodriguez-Tajes, Sergio
Pocurull, Anna
Castillo, Joaquin
Casanova, Gherzon
Vega, Laia
Lens, Sabela
Marino, Zoe
Londono, Maria-Carlota
Forner, Alejandro
Torres, Ferran
Forns, Xavier
TI Hepatitis C-related cirrhosis will be a marginal cause of hospital
admissions by 2025
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Hospitalization burden; Direct-acting antivirals; Decompensation; Viral
eradication
ID COMPENSATED CIRRHOSIS; PLUS SOFOSBUVIR; INTERFERON; THERAPY; VIRUS;
RECURRENCE; PROGRAM; COHORT; HCC
AB Background & Aims: Complications of cirrhosis are the main cause of hospital admissions in liver units. In areas where HCV is prevalent, most of these admissions are attributable to HCV-related cirrhosis (HCV-cirrhosis). This study assessed the impact of direct-acting antivirals (DAA) in the profile of patients with liver disease admitted to a referral liver unit from a university hospital.
Methods: We registered hospital admissions resulting from cirrhosis to the Liver Unit of the Hospital Clinic of Barcelona, from 2011 to 2014 (pre-DAA period) and from 2015 to 2019 (post-DAA period).
Results: From a total of 14,865 hospital admissions, 10,053 resulted from cirrhosis (corresponding to 6,272 patients). The number and proportion of hospital admissions because of HCV-cirrhosis remained stable during the period 2011-2014 (525 per year, 48.8% of the total), but decreased progressively after 2015 (p <0.001), reaching <300 (27.1%) admissions in 2019. Similarly, HCV-cirrhosis accounted for 3,885 inpatient days per year (44.9%) during the pre-DAA period and decreased steadily after 2015 (p >0.001), reaching only 1,909 inpatient days (22%) in 2019. The figures for intensive care unit admissions followed a similar pattern. By means of a slope analysis (binomial regression model), we predicted that HCV-cirrhosis hospital admissions will be residual by 2025 (2.3%, 95% CI 0-10.9%). By contrast, we observed a significant increase in hospital admissions because of metabolic-associated fatty liver disease (5-fold) and autoimmune hepatitis (4-fold) during the study period.
Conclusions: In summary, our data showed a profound reduction in HCV-cirrhosis hospitalisation burden since 2015, coincident with the wide use of DAAs in Spain. Our predictions suggest that, by 2025, HCV-cirrhosis will be a marginal cause of hospital admissions for patients with liver disease.
Lay summary: Over the past few years, the wide use of antiviral drugs that cure HCV has had a significant effect on patients being admitted to hospital. Most patients with HCV and cirrhosis are treated (and often cured) in the community and, thus, the number of hospital admissions because of severe forms of HCV has decreased drastically. HCV is no longer the first cause of admission into liver units and, in only a few years from now, it is likely to be only a residual cause of hospitalisation. (C) 2020 Published by Elsevier B.V. on behalf of European Association for the Study of the Liver.
C1 [Rodriguez-Tajes, Sergio; Pocurull, Anna; Castillo, Joaquin; Casanova, Gherzon; Vega, Laia; Lens, Sabela; Marino, Zoe; Londono, Maria-Carlota; Forner, Alejandro; Forns, Xavier] Univ Barcelona, Hosp Clin, Liver Unit, IDIBAPS, Barcelona, Spain.
[Rodriguez-Tajes, Sergio; Lens, Sabela; Marino, Zoe; Londono, Maria-Carlota; Forner, Alejandro; Forns, Xavier] Ctr Invest Biomed Red Enfermedades Hepat & Digest, Madrid, Spain.
[Torres, Ferran] Hosp Clin Barcelona, IDIBAPS, Med Stat Core Facil, Barcelona, Spain.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; CIBER -
Centro de Investigacion Biomedica en Red; CIBEREHD; University of
Barcelona; Hospital Clinic de Barcelona; IDIBAPS
RP Forns, X (corresponding author), Univ Barcelona, Hosp Clin, Liver Unit, IDIBAPS, Barcelona, Spain.
EM xforns@clinic.cat
RI Rodríguez-Tajes, Sergio/P-7895-2019; Torres, Ferran/D-1296-2011; Lens,
Sabela/L-4750-2018; Londono, Maria/KMA-4581-2024; Forner,
Alejandro/C-8884-2016
OI Torres, Ferran/0000-0002-7355-7913; Castillo-Iturra,
Joaquin/0000-0003-0639-1906; Londono, Maria-Carlota/0000-0002-6533-1586;
Lens, Sabela/0000-0003-4900-411X; Forns, Xavier/0000-0002-8188-1764;
Casanova Rimer, Gherzon/0000-0002-1543-5088; Rodriguez-Tajes,
Sergio/0000-0002-3189-7557; Forner, Alejandro/0000-0002-9014-4950
FU Instituto de Salud Carlos III, Ministry of Economy and Competitiveness,
Spain [PI18/00079]; Secretaria d'Universitats i Recerca del Departament
d'Economia i Coneixement [2017_SGR_1753]; CERCA Programme, Generalitat
de Catalunya, Spain; Rio Hortega program of the Instituto de Salud
Carlos III [CM17/00015]; Catalonian Society of Digestology; European
Fund of Regional Development, European Commission, Una Manera de Hacer
Europa; European Social Fund (ESF); Instituto de Salud Carlos III
[PI18/00542]
FX XF received support from Instituto de Salud Carlos III (PI18/00079),
Ministry of Economy and Competitiveness, Spain, cofunded by the European
Fund of Regional Development, European Commission, Una Manera de Hacer
Europa; Secretaria d'Universitats i Recerca del Departament d'Economia i
Coneixement (grant 2017_SGR_1753) and CERCA Programme, Generalitat de
Catalunya, Spain. SRT was supported by the Rio Hortega program
(Fellowship CM17/00015) of the Instituto de Salud Carlos III, both
co-funded by the European Social Fund (ESF) and by an initiation
research grant from the Catalonian Society of Digestology. AF received
support from Instituto de Salud Carlos III (PI18/00542).
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NR 26
TC 15
Z9 16
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD DEC
PY 2020
VL 73
IS 6
BP 1360
EP 1367
DI 10.1016/j.jhep.2020.07.018
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA OS6HS
UT WOS:000590263100014
PM 32697948
DA 2025-01-07
ER
PT J
AU Xu, L
Xia, H
Ni, DS
Hu, YX
Liu, JN
Qin, Y
Zhou, Q
Yi, QY
Xie, YJ
AF Xu, Lei
Xia, Hua
Ni, Dongsheng
Hu, Yanxia
Liu, Jianing
Qin, Yao
Zhou, Qin
Yi, Qiying
Xie, Yajun
TI High-Dose Dexamethasone Manipulates the Tumor Microenvironment and
Internal Metabolic Pathways in Anti-Tumor Progression
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE dexamethasone; FAO; FFA; glycolysis metabolism; Ppar alpha; Pparg; TG
synthesis; tumor progression
ID GLUCOCORTICOIDS; APOPTOSIS; ACCUMULATION; MECHANISMS; EXPRESSION;
SURVIVAL; TARGETS
AB High-dose dexamethasone (DEX) is used to treat chemotherapy-induced nausea and vomiting or to control immunotherapy-related autoimmune diseases in clinical practice. However, the underlying mechanisms of high-dose DEX in tumor progression remain unaddressed. Therefore, we explored the effects of high-dose DEX on tumor progression and the potential mechanisms of its anti-tumor function using immunohistochemistry, histological examination, real-time quantitative PCR (qPCR), and Western blotting. Tumor volume, blood vessel invasion, and levels of the cell proliferation markers Ki67 and c-Myc and the anti-apoptotic marker Bcl2 decreased in response to high-dose DEX. However, the cell apoptosis marker cleaved caspase 3 increased significantly in mice treated with 50 mg/kg DEX compared with controls. Some genes associated with immune responses were significantly downregulated following treatment with 50 mg/kg DEX e.g., Cxcl9, Cxcl10, Cd3e, Gzmb, Ifng, Foxp3, S100a9, Arg1, and Mrc1. In contrast, the M1-like tumor-associated macrophages (TAMs) activation marker Nos2 was shown to be increased. Moreover, the expression of peroxisome proliferator-activated receptors alpha and gamma (Ppar alpha and Pparg, respectively) was shown to be significantly upregulated in livers or tumors treated with DEX. However, high-dose DEX treatment decreased the expression of glucose and lipid metabolic pathway-related genes such as glycolysis-associated genes (Glut1, Hk2, Pgk1, Idh3a), triglyceride (TG) synthesis genes (Gpam, Agpat2, Dgat1), exogenous free fatty acid (FFA) uptake-related genes (Fabp1, Slc27a4, and CD36), and fatty acid oxidation (FAO) genes (Acadm, Acaa1, Cpt1a, Pnpla2). In addition, increased serum glucose and decreased serum TG and non-esterified fatty acid (NEFA) were observed in DEX treated-xenografted tumor mice. These findings indicate that high-dose DEX-inhibited tumor progression is a complicated process, not only activated by M1-like TAMs, but also decreased by the uptake and consumption of glucose and lipids that block the raw material and energy supply of cancer cells. Activated M1-like TAMs and inefficient glucose and lipid metabolism delayed tumor cell growth and promoted apoptosis. These findings have important implications for the application of DEX combined with drugs that target key metabolism pathways for tumor therapy in clinical practice.
C1 [Xu, Lei; Xia, Hua; Ni, Dongsheng; Hu, Yanxia; Liu, Jianing; Qin, Yao; Zhou, Qin; Xie, Yajun] Chongqing Med Univ, Sch Lab Med, Minist Educ, Key Lab Clin Diagnost, Chongqing 400016, Peoples R China.
[Yi, Qiying] Chongqing Med Univ, Lab Anim Ctr, Chongqing 400016, Peoples R China.
C3 Chongqing Medical University; Chongqing Medical University
RP Xie, YJ (corresponding author), Chongqing Med Univ, Sch Lab Med, Minist Educ, Key Lab Clin Diagnost, Chongqing 400016, Peoples R China.; Yi, QY (corresponding author), Chongqing Med Univ, Lab Anim Ctr, Chongqing 400016, Peoples R China.
EM xulei@stu.cqmu.edu.cn; xiahua@stu.cqmu.edu.cn;
dongshengni@stu.cqmu.edu.cn; yanxiahu@stu.cqmu.edu.cn;
keithliu@stu.cqmu.edu.cn; qinyao@stu.cqmu.edu.cn; zhouqin@cqmu.edu.cn;
qyi@cqmu.edu.cn; yjxie@cqmu.edu.cn
RI ; Zhou, Qin/HRP-6185-2023
OI Xie, Yajun/0000-0002-0943-5137; Zhou, Qin/0000-0003-3879-4021
FU National Science Foundation for Young Scientists of China [31701218];
Basic Science and Frontier Technology Research Program of Chongqing
Science and Technology Commission [cstc2017jcyjA0390]; National Natural
Science Foundation of China [81572076, 81873932]; Chongqing Municipal
Education Commission [KJQN201900411]
FX This work was funded by the National Science Foundation for Young
Scientists of China (Grant No. 31701218) and the Basic Science and
Frontier Technology Research Program of Chongqing Science and Technology
Commission (Grant No. cstc2017jcyjA0390). This work was also funded by
National Natural Science Foundation of China (grant numbers 81572076 and
81873932). Besides, this work was also supported by Chongqing Municipal
Education Commission (No. KJQN201900411).
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NR 50
TC 32
Z9 37
U1 5
U2 24
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD MAR
PY 2020
VL 21
IS 5
AR 1846
DI 10.3390/ijms21051846
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA LB8VL
UT WOS:000524908500297
PM 32156004
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Yen, HH
Shih, KL
Lin, TT
Su, WW
Soon, MS
Liu, CS
AF Yen, Hsu-Heng
Shih, Kai-Lun
Lin, Ta-Tsung
Su, Wei-Wen
Soon, Maw-Soan
Liu, Chin-San
TI Decreased mitochondrial deoxyribonucleic acid and increased oxidative
damage in chronic hepatitis C
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Hepatitis C; Mitochondria; Oxidative stress; Mitochondrial DNA;
Biomarker
ID DNA COPY NUMBER; HEPATOCELLULAR-CARCINOMA; VIRUS; STRESS; LIVER; HCV;
ASSOCIATION; INFECTION; DEPLETION
AB AIM: To determine whether alteration of the mitochondria DNA (mtDNA) copy number and its oxidative damage index (mtDNA(Delta CT)) can be detected by analysis of peripheral blood cells in hepatitis C virus (HCV)-infected patients.
METHODS: This study enrolled two groups of patients aged 40-60 years: a control group and an HCV-infected group in Department of Gastroenterology and Hepatology in Changhua Christian Hospital. Patients with co-infection with hepatitis B virus or human immunodeficiency virus, autoimmune disease, malignant neoplasia, pregnancy, thyroid disease, or alcohol consumption > 40 g/d were excluded. HCV-infected patients who met the following criteria were included: (1) positive HCV antibodies for > 6 mo; (2) alanine aminotransferase (ALT) levels more than twice the upper limit of normal on at least two occasions during the past 6 mo; and (3) histological fibrosis stage higher than F1. The mtDNA copy number and oxidative damage index of HCV mtDNA (mtDNA(Delta CT)) were measured in peripheral blood leukocytes. The association between mtDNA copy number and mtDNA(Delta CT) was further analyzed using clinical data.
RESULTS: Forty-seven normal controls (male/female: 26/21, mean age 50.51 +/- 6.15 years) and 132 HCV-infected patients (male/female: 76/61, mean age 51.65 +/- 5.50 years) were included in the study. The genotypes of HCV-infected patients include type 1a (n = 3), type 1b (n = 83), type 2a (n = 32), and type 2b (n = 14). Liver fibrosis stages were distributed as follows: F1/F2/F3/F4 = 1/61/45/25 and activity scores were A0/A1/A2/A3 = 7/45/55/25. There were no age or gender differences between the two groups. HCV-infected patients had higher hepatitis activity (aspartate transaminase levels 108.77 +/- 60.73 vs 23.19 +/- 5.47, P < 0.01; ALT levels 168.69 +/- 93.12 vs 23.15 +/- 9.45, P < 0.01) and lower platelet count (170.40 +/- 58.00 vs 251.24 +/- 63.42, P < 0.01) than controls. The mtDNA copy number was lower in HCV-infected patients than in controls (173.49 vs 247.93, P < 0.05). The mtDNA(Delta CT) was higher in HCV-infected patients than in controls (2.92 vs 0.64, P < 0.05). To clarify the clinical significance of these results in HCV-infected patients, their association with different clinical parameters among HCV-infected patients was analyzed. A negative association was found between mtDNA copy number and elevated aspartate transaminase levels (r = -0.17, P < 0.05). Changes in mtDNA copy number were not associated with HCV RNA levels, HCV genotypes, liver fibrosis severity, or inflammatory activity in the liver biopsy specimen. However, a correlation was observed between mtDNA(Delta CT) and platelet count (r = -0.22, P < 0.01), HCV RNA level (r = 0.36, P < 0.01), and hepatitis activity (r = 0.20, P = 0.02). However, no difference in the change in mtDNA(Delta CT) was observed between different fibrosis stages or HCV genotypes.
CONCLUSION: Oxidative stress and mtDNA damage are detectable in patient's peripheral leukocytes. Increased leukocyte mtDNA(Delta CT) correlates with higher HCV viremia, increased hepatitis activity, and lower platelet count. (c) 2012 Baishideng. All rights reserved.
C1 [Yen, Hsu-Heng; Shih, Kai-Lun; Su, Wei-Wen; Soon, Maw-Soan] Changhua Christian Hosp, Dept Gastroenterol & Hepatol, Changhua 500, Taiwan.
[Lin, Ta-Tsung; Liu, Chin-San] Changhua Christian Hosp, Vasc & Genom Res Ctr, Changhua 500, Taiwan.
C3 Changhua Christian Hospital; Changhua Christian Hospital
RP Yen, HH (corresponding author), Changhua Christian Hosp, Dept Gastroenterol & Hepatol, 135 Nanhsiao St, Changhua 500, Taiwan.
EM 91646@cch.org.tw
OI SHIH, KAI-LUN/0000-0003-4405-6033
FU Changhua Christian Hospital [99-CCH-IPR-12]
FX Supported by Changhua Christian Hospital, 99-CCH-IPR-12
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NR 29
TC 31
Z9 31
U1 0
U2 6
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD SEP 28
PY 2012
VL 18
IS 36
BP 5084
EP 5089
DI 10.3748/wjg.v18.i36.5084
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 019KM
UT WOS:000309738500015
PM 23049218
OA hybrid, Green Published
DA 2025-01-07
ER
PT J
AU Zhou, TN
Wei, HX
Wang, JJ
AF Zhou, Tiannan
Wei, Huixian
Wang, Jinjun
TI Research experimental design for the construction and identification of
the pGEX-BCKD-E4A recombinant point-mutant plasmid
SO PLOS ONE
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; ANTIMITOCHONDRIAL ANTIBODY; DIAGNOSIS; ACID;
AMA
AB Primary biliary cirrhosis (PBC) is an organ-specific autoimmune disease that eventually develops into cirrhosis and even liver cancer. In recent years, the incidence rate has been increasing, and the early diagnosis and treatment of PBC are crucial. In the early diagnosis method of PBC, anti-mitochondrial antibodies (AMAs) are an important diagnostic basis, especially the M2 subtype (AMA-M2) with almost 100% specificity. We selected the BCOADC-E2 protein, a mitochondrial autoantigen that reacts specifically with AMA-M2 antibodies, and carried out DNA recombination and protein mutation experiments by cloning in vitro the homologous target gene sequence BCKD that expresses the antigenic epitope of BCOADC-E2 protein, to provide experience for later exploring the effect of mutations of amino acids around the lysine in the active center of BCOADC-E2 protein on its specific binding to AMA-M2, and to lay the foundation for determining the key amino acids of BCOADC-E2 for the diagnosis and treatment of PBC. In addition, we apply this scientific research content to graduate course teaching. Experimental technology of microbial molecular ecology is a course with the cross-integration of multidisciplinary knowledge and experimental skills offered at our college since 2018. This article derives from the part of this course on the construction of recombinant plasmids. The students first constructed the recombinant plasmid pGEX-BCKD using the vector plasmid pGEX-4T1 and the target gene fragment BCKD provided by the laboratory and used this as a template to construct the pGEX-BCKD-E4A point mutation plasmid by the overlap extension PCR (SOE PCR) technique to achieve the effect of mutating the fifth amino acid glutamate in front of lysine, the active centre of the BCOADC-E2 lipid acyl binding domain, to alanine for subsequent studies. Through the research experiment, combining theoretical knowledge and experimental operation, we aim to deepen the student's understanding of DNA recombination technology, let them feel the practical application prospect of experimental technology, stimulate students' interest in professional knowledge learning, and cultivate students' scientific thinking and innovation consciousness. We examined the quality of the teaching through the process and summative evaluation of the students. In this study, the students successfully completed the construction of pGEX-BCKD-E4A point mutant plasmid, and the average test score increased from 40.4% before teaching to 91.1%. The teaching effect was remarkable. This kind of research experimental teaching mode has good application prospects, and other education and teachers can refer to and reference it.
C1 [Zhou, Tiannan; Wei, Huixian; Wang, Jinjun] Yangzhou Univ, Coll Environm Sci & Engn, Yangzhou, Peoples R China.
C3 Yangzhou University
RP Wang, JJ (corresponding author), Yangzhou Univ, Coll Environm Sci & Engn, Yangzhou, Peoples R China.
EM wangjinjun@yzu.edu.cn
OI Zhou, Tiannan/0000-0002-3553-6572; Wang, Jinjun/0000-0001-5723-1799
FU National Natural Science Foundation of China [81873877]; Scientific
Research Foundation for the Returned Overseas Chinese Scholars, State
Education Ministry of China [20151098]; Qing Lan Project of Yangzhou
University
FX We thank the University of California, Davis for providing the target
gene and plasmid vector and Professor Patrick S.C. Leung for the help
with our theoretical course. We thank many teaching assistants who have
guided students in the experiments. We also wish to thank KetengEdit for
its linguistic assistance during the preparation of this manuscript.
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NR 39
TC 0
Z9 0
U1 2
U2 14
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD FEB 24
PY 2023
VL 18
IS 2
AR e0279431
DI 10.1371/journal.pone.0279431
PG 19
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA D9QQ9
UT WOS:000972006100122
PM 36827343
OA Green Published, gold
DA 2025-01-07
ER
PT J
AU Bendik, I
Friedel, A
Roos, FF
Weber, P
Eggersdorfer, M
AF Bendik, Igor
Friedel, Angelika
Roos, Franz F.
Weber, Peter
Eggersdorfer, Manfred
TI Vitamin D: a critical and essential micronutrient for human health
SO FRONTIERS IN PHYSIOLOGY
LA English
DT Review
DE vitamin D; 25-hydroxyvitamin D; nutrition; micronutrients; hidden
hunger; nutrition security; nutritional pathways; nutrigenomics
ID NUTRITION EXAMINATION SURVEY; SERUM 25-HYDROXYVITAMIN D; LOWER-EXTREMITY
FUNCTION; 3RD NATIONAL-HEALTH; D DEFICIENCY; MULTIPLE-SCLEROSIS; CALCIUM
SUPPLEMENTATION; 1-ALPHA,25-DIHYDROXYVITAMIN D-3; SECONDARY
HYPERPARATHYROIDISM; MYOCARDIAL-INFARCTION
AB Vitamin D is a micronutrient that is needed for optimal health throughout the whole life. Vitamin D-3 (cholecalciferol) can be either synthesized in the human skin upon exposure to the UV light of the sun, or it is obtained from the diet. If the photoconversion in the skin due to reduced sun exposure (e.g., in wintertime) is insufficient, intake of adequate vitamin D from the diet is essential to health. Severe vitamin D deficiency can lead to a multitude of avoidable illnesses; among them are well-known bone diseases like osteoporosis, a number of autoimmune diseases, many different cancers, and some cardiovascular diseases like hypertension are being discussed. Vitamin D is found naturally in only very few foods. Foods containing vitamin D include some fatty fish, fish liver oils, and eggs from hens that have been fed vitamin D and some fortified foods in countries with respective regulations. Based on geographic location or food availability adequate vitamin D intake might not be sufficient on a global scale. The International Osteoporosis Foundation (IOF) has collected the 25-hydroxy-vitamin D plasma levels in populations of different countries using published data and developed a global vitamin D map. This map illustrates the parts of the world, where vitamin D did not reach adequate 25-hydroxyvitamin D plasma levels: 6.7% of the papers report 25-hydroxyvitamin D plasma levels below 25 nmol/L, which indicates vitamin D deficiency, 37.3% are below 50 nmol/Land only 11.9% found 25-hydroxyvitamin D plasma levels above 75 nmol/L target as suggested by vitamin D experts. The vitamin D map is adding further evidence to the vitamin D insufficiency pandemic debate, which is also an issue in the developed world. Besides malnutrition, a condition where the diet does not match to provide the adequate levels of nutrients including micronutrients for growth and maintenance, we obviously have a situation where enough nutrients were consumed, but lacked to reach sufficient vitamin D micronutrient levels. The latter situation is known as hidden hunger. The inadequate vitamin D status impacts on health care costs, which in turn could result in significant savings, if corrected. Since little is known about the effects on the molecular level that accompany the pandemic like epigenetic imprinting, the insufficiency-triggered gene regulations or the genetic background influence on the body to maintain metabolic resilience, future research will be needed. The nutrition community is highly interested in the molecular mechanism that underlies the vitamin D insufficiency caused effect. In recent years, novel large scale technologies have become available that allow the simultaneous acquisition of transcriptome, epigenome, proteome, or metabolome data in cells of organs. These important methods are now used for nutritional approaches summarized in emerging scientific fields of nutrigenomics, nutrigenetics, or nutriepigenetics. It is believed that with the help of these novel concepts further understanding can be generated to develop future sustainable nutrition solutions to safeguard nutrition security.
C1 [Bendik, Igor; Friedel, Angelika; Roos, Franz F.] DSM Nutr Prod Ltd, Human Nutr & Hlth, CH-4002 Basel, Switzerland.
[Weber, Peter; Eggersdorfer, Manfred] DSM Nutr Prod Ltd, Nutr Sci & Advocacy, CH-4002 Basel, Switzerland.
C3 DSM NV; DSM NV
RP Bendik, I (corresponding author), DSM Nutr Prod Ltd, Dept Human Nutr & Hlth, Bldg 201-219A,POB 2676, CH-4002 Basel, Switzerland.
EM igor.bendik@dsm.com
RI Weber, Peter/ABC-2705-2020
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NR 180
TC 164
Z9 177
U1 0
U2 24
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-042X
J9 FRONT PHYSIOL
JI Front. Physiol.
PD JUL 11
PY 2014
VL 5
AR 248
DI 10.3389/fphys.2014.00248
PG 14
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA AX7BH
UT WOS:000347071300001
PM 25071593
OA gold, Green Published
DA 2025-01-07
ER
PT J
AU Bignotto, M
Bianco, E
Centofanti, L
Russo, A
Dei Cas, M
Zermiani, P
Morano, C
Samartin, F
Bertolini, E
Bifari, F
Berra, C
Zuin, M
Paroni, R
Battezzati, PM
Folli, F
AF Bignotto, Monica
Bianco, Elena
Centofanti, Lucia
Russo, Antonio
Dei Cas, Michele
Zermiani, Paola
Morano, Camillo
Samartin, Federica
Bertolini, Emanuela
Bifari, Francesco
Berra, Cesare
Zuin, Massimo
Paroni, Rita
Battezzati, Pier Maria
Folli, Franco
TI Synergistic effects of glucose tolerance and BMI on cardiovascular
events and all-cause mortality in a healthy population: CA.ME.LI.A study
7 years follow-up
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE cardiovascular risk; type 1/type 2 diabetes mellitus; epidemiology;
impaired fasting glucose; obesity
ID INSULIN-RECEPTOR SUBSTRATE-1; BODY-MASS INDEX; SEX-DIFFERENCES;
PHOSPHATIDYLINOSITOL 3-KINASE; MULTIFACTORIAL INTERVENTION; DIABETES
PREVENTION; GENDER-DIFFERENCES; METABOLIC SYNDROME; RISK-FACTORS;
DISEASE
AB The CA.ME.LI.A (CArdiovascular risks, MEtabolic syndrome, LIver and Autoimmune disease) epidemiological study was conducted in Abbiategrasso (Milan, Italy) to identify risk factors for metabolic and cardiovascular disease in an apparently healthy population of northern Italy. The population (n = 2,545, 1,251 men, 1,254 women) was stratified according to body mass index [normal body weight (NBW): <25 kg/m(2); overweight-obese (OWO): >= 25 kg/m(2)] and according to fasting blood glucose [normal fasting glucose: <100 mg/dL; impaired fasting glucose (IFG): 100-125 mg/dL; diabetes mellitus (DM): >= 126 mg/dL]. The incidence of cardiovascular (CV) events and overall mortality were studied by the Kaplan-Meier method using the log rank test. Univariate analysis was conducted with time-dependent Cox models. During the 7-yr follow-up period, 80 deaths and 149 CV events occurred. IFG [hazard ratio (HR): 2.81; confidence interval (CI): 1.37-5.77; P = 0.005], DM (HR: 4.88; CI: 1.47-16; P = 0.010), or OWO (HR: 2.78; CI:1.68-4.59; P < 0.001) all produced significant increases in CV events and deaths. In the combination IFG/OWO (HR: 5.51; CI: 3.34-9.08; P < 0.001), there was an apparent additive effect of the two conditions, whereas in the combination DM/OWO (HR: 12.71; CI: 7.48-22; P < 0.001), there was an apparent multiplicative effect on the risk for CV events and deaths. In males, the DM/NBW group had a higher incidence of cardiovascular events and deaths than the IFG/OWO group. In contrast, in females, the IFG/OWO group had a higher incidence of cardiovascular events and deaths than the DM/NBW group. In women, there was a greater incidence of CV events in the IFG/OWO group (HR: 6.23; CI: 2.88-13; P < 0.001) than in men in the same group (HR: 4.27; CI: 2.15-8.47; P < 0.001). Consistent with these data, also all-cause mortality was progressively increased by IFG/DM and OWO, with an apparently exponential effect in the combination DM/OWO (HR: 11.78; CI: 6.11-23; P < 0.001). IFG/DM and OWO, alone or in combination, had major effects in increasing mortality for all causes and CV events. The relative contributions of hyperglycemia and overweight/obesity on cardiovascular events and deaths were apparently, to a certain extent, sex dependent. Females were more affected by overweight/obesity either alone or combined with IFG, as compared with males. NEW & NOTEWORTHY For the first time, the combined effects of glucose tolerance and BMI have been investigated in an apparently healthy large population sample of a city in the north of Italy. We found that there are synergistic effects of glucose levels with BMI to increase not only cardiovascular events and deaths but also cancer-related deaths and all-cause mortality.
C1 [Bignotto, Monica; Bianco, Elena; Zermiani, Paola; Samartin, Federica; Zuin, Massimo; Battezzati, Pier Maria] Univ Milan, Dept Hlth Sci, Liver & Gastroenterol Unit, Milan, Italy.
[Bianco, Elena; Samartin, Federica; Bertolini, Emanuela; Battezzati, Pier Maria] ASST Santi Paolo e Carlo, Med & Liver Unit, Milan, Italy.
[Centofanti, Lucia; Dei Cas, Michele; Morano, Camillo; Paroni, Rita] Univ Milan, Dept Hlth Sci, Clin Biochem & Mass Spectrometry Unit, Milan, Italy.
[Russo, Antonio] Agcy Hlth Protect Metropolitan City Milan, Epidemiol Unit, Milan, Italy.
[Bifari, Francesco] Univ Milan, Dept Med Biotechnol & Translat Med, Lab Cell Metab & Regenerat Med, LITA, Segrate, Italy.
[Berra, Cesare] IRCCS Multimed, Dipartimento Endocrino Metab, Milan, Italy.
[Folli, Franco] ASST Santi Paolo e Carlo, Dept Unit Diabet & Metab Dis, Milan, Italy.
[Folli, Franco] ASST Santi Paolo e Carlo, Dept Unit Diabet & Metab Dis, Milan, Italy.
C3 University of Milan; University of Milan; University of Milan; IRCCS
Multimedica
RP Folli, F (corresponding author), ASST Santi Paolo e Carlo, Dept Unit Diabet & Metab Dis, Milan, Italy.; Folli, F (corresponding author), ASST Santi Paolo e Carlo, Dept Unit Diabet & Metab Dis, Milan, Italy.
EM franco.folli@unimi.it
RI Morano, Camillo/ABB-5426-2021; Bifari, Francesco/M-3430-2014; bignotto,
monica/C-1024-2012; PARONI, RITA/AAC-6265-2020; PARONI,
RITA/C-2955-2012; Bifari, Francesco/M-5150-2016
OI Bignotto, Monica/0000-0002-2043-7846; Morano,
Camillo/0000-0003-0352-2819; PARONI, RITA/0000-0002-3186-8860; Bifari,
Francesco/0000-0003-2028-3012
FU Regione Lombardia [7364]; Italian Ministry for Education (MIUR)
[02350447]; Dipartimento di Scienze della Salute,Universita degli Studi
di Milano [PSR2020_DIP_013_PARONI]; European Union-NextGenerationEU;
[PNC0000001]; [B83C22006120001]
FX The CA.ME.LI.A project was supported by Regione Lombardia(DG Sanita
08/07/2008 n. 7364), Italian Ministry for Education (MIUR,GR-2011
02350447), and by Dipartimento di Scienze della Salute,Universita degli
Studi di Milano (LINEA 2 DEL PIANO DI SOSTEGNOALLA RICERCA
PSR2020_DIP_013_PARONI dal titolo: Looking forNovel Biomarkers of
Diabetes and Cardiovascular Diseases,"NODICARDIO"). The study was
approved by the Ethical Committeeof Ospedale San Paolo. L.C. is a PhD
student in"Scienze della nutri-zione - Universita degli Studi di
Milano"supported by Project PNC0000001 D3 4 Health-CUP
[B83C22006120001], The NationalPlan for Complementary Investments to the
NRRP, funded by the European Union-NextGenerationEU.
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NR 83
TC 0
Z9 0
U1 1
U2 1
PU AMER PHYSIOLOGICAL SOC
PI Rockville
PA 6120 Executive Blvd, Suite 600, Rockville, MD, UNITED STATES
SN 0193-1849
EI 1522-1555
J9 AM J PHYSIOL-ENDOC M
JI Am. J. Physiol.-Endocrinol. Metab.
PD OCT 28
PY 2024
VL 327
IS 4
BP E498
EP E511
DI 10.1152/ajpendo.00181.2024
PG 14
WC Endocrinology & Metabolism; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Physiology
GA J3W8H
UT WOS:001336409400002
PM 39196799
DA 2025-01-07
ER
PT J
AU Schmid, P
Rugo, HS
Adams, S
Schneeweiss, A
Barrios, CH
Iwata, H
Diéras, V
Henschel, V
Molinero, L
Chui, SY
Maiya, V
Husain, A
Winer, EP
Loi, S
Emens, LA
AF Schmid, Peter
Rugo, Hope S.
Adams, Sylvia
Schneeweiss, Andreas
Barrios, Carlos H.
Iwata, Hiroji
Dieras, Veronique
Henschel, Volkmar
Molinero, Luciana
Chui, Stephen Y.
Maiya, Vidya
Husain, Amreen
Winer, Eric P.
Loi, Sherene
Emens, Leisha A.
CA IMpassion130 Investigators
TI Atezolizumab plus nab-paclitaxel as first-line treatment for
unresectable, locally advanced or metastatic triple-negative breast
cancer (IMpassion130): updated efficacy results from a randomised,
double-blind, placebo-controlled, phase 3 trial
SO LANCET ONCOLOGY
LA English
DT Article
ID EXPRESSION; SURVIVAL
AB Background Immunotherapy in combination with chemotherapy has shown promising efficacy across many different tumour types. We report the prespecified second interim overall survival analysis of the phase 3 IMpassion130 study assessing the efficacy and safety of atezolizumab plus nab-paclitaxel in patients with unresectable, locally advanced or metastatic triple-negative breast cancer.
Methods In this randomised, placebo-controlled, double-blind, phase 3 trial, done in 246 academic centres and community oncology practices in 41 countries, patients aged 18 years or older, with previously untreated, histologically documented, locally advanced or metastatic triple-negative breast cancer, and Eastern Cooperative Oncology Group performance status of 0 or 1 were eligible. Patients were randomly assigned (1:1) using a permuted block method (block size of four) and an interactive voice-web response system. Randomisation was stratified by previous taxane use, liver metastases, and PD-L1 expression on tumour-infiltrating immune cells. Patients received atezolizumab 840 mg or matching placebo intravenously on day 1 and day 15 of every 28-day cycle and nab-paclitaxel 100 mg/m 2 of body surface area intravenously on days 1, 8, and 15 until progression or unacceptable toxicity. Investigators, patients, and the funder were masked to treatment assignment. Coprimary endpoints were investigator-assessed progression-free survival per Response Evaluation Criteria in Solid Tumors version 1.1 and overall survival, assessed in the intention-to-treat population and in patients with PD-L1 immune cell-positive tumours (tumours with >= 1% PD-L1 expression). The final progression-free survival results were previously reported at the first interim overall survival analysis. The prespecified statistical testing hierarchy meant that overall survival in the subgroup of PD-L1 immune cell-positive patients could only be formally tested if overall survival was significantly different between the treatment groups in the intention-to-treat population. This study is registered with ClinicalTrials.gov, NCT02425891.
Findings Between June 23, 2015, and May 24, 2017, 902 patients were enrolled, of whom 451 were randomly assigned to receive atezolizumab plus nab-paclitaxel and 451 were assigned to receive placebo plus nab-paclitaxel (the intention-to-treat population). Six patients from each group did not receive treatment. At the second interim analysis (data cutoff Jan 2, 2019), median follow-up was 18.5 months (IQR 9.6-22.8) in the atezolizumab group and 17.5 months (8.4-22.4) in the placebo group. Median overall survival in the intention-to-treat patients was 21.0 months (95% CI 19.0-22.6) with atezolizumab and 18.7 months (16.9-20.3) with placebo (stratified hazard ratio [HR] 0.86, 95% CI 0.72-1.02, p=0.078). In the exploratory overall survival analysis in patients with PD-L1 immune cell-positive tumours, median overall survival was 25.0 months (95% CI 19.6-30.7) with atezolizumab versus 18.0 months (13.6-20.1) with placebo (stratified HR 0.71, 0.54-0.94]). As of Sept 3, 2018 (the date up to which updated safety data were available), the most common grade 3-4 adverse events were neutropenia (38 [8%] of 453 patients in the atezolizumab group vs 36 [8%] of 437 patients in the placebo group), peripheral neuropathy (25 [6%] vs 12 [3%]), decreased neutrophil count (22 [5%] vs 16 [4%]), and fatigue (17 [4%] vs 15 [3%]). Treatment-related deaths occurred in two (<1%) patients in the atezolizumab group (autoimmune hepatitis related to atezolizumab [n=1] and septic shock related to nab-paclitaxel [n=1]) and one (<1%) patient in the placebo group (hepatic failure). No new treatment-related deaths have been reported since the primary clinical data cutoff date (April 17, 2018).
Interpretation Consistent with the first interim analysis, this second interim overall survival analysis of IMpassion130 indicates no significant difference in overall survival between the treatment groups in the intention-to-treat population but suggests a clinically meaningful overall survival benefit with atezolizumab plus nab-paclitaxel in patients with PD-L1 immune cell-positive disease. However, this positive result could not be formally tested due to the prespecified statistical testing hierarchy. For patients with PD-L1 immune cell-positive metastatic triple-negative breast cancer, atezolizumab plus nab-paclitaxel is an important therapeutic option in a disease with high unmet need. Copyright (C) 2019 Elsevier Ltd. All rights reserved.
C1 [Schmid, Peter] Queen Mary Univ London, Barts Canc Inst, London EC1M 6BQ, England.
[Rugo, Hope S.] Univ Calif San Francisco, Ctr Comprehens Canc, San Francisco, CA 94143 USA.
[Adams, Sylvia] NYU, Langone Med Ctr, Perlmutter Canc Ctr, New York, NY USA.
[Schneeweiss, Andreas] Heidelberg Univ Hosp, Natl Ctr Tumor Dis, Heidelberg, Germany.
[Schneeweiss, Andreas] German Canc Res Ctr, Heidelberg, Germany.
[Barrios, Carlos H.] Pontificia Univ Catolica Rio Grande do Sul, Hosp Sao Lucas, Ctr Pesquisa Clin, Porto Alegre, RS, Brazil.
[Barrios, Carlos H.] Latin Amer Cooperat Oncol Grp, Porto Alegre, RS, Brazil.
[Barrios, Carlos H.] Grp Oncoclin, Porto Alegre, RS, Brazil.
[Iwata, Hiroji] Aichi Canc Ctr Hosp, Nagoya, Aichi, Japan.
[Dieras, Veronique] Inst Curie, Dept Med Oncol, Paris, France.
[Dieras, Veronique] Ctr Eugene Marquis, Dept Med Oncol, Rennes, France.
[Henschel, Volkmar; Husain, Amreen] F Hoffmann La Roche, Basel, Switzerland.
[Molinero, Luciana; Chui, Stephen Y.; Maiya, Vidya] Genentech Inc, San Francisco, CA USA.
[Winer, Eric P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Loi, Sherene] Univ Melbourne, Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
[Emens, Leisha A.] Univ Pittsburgh, Med Ctr, Hillman Canc Ctr, Pittsburgh, PA USA.
C3 University of London; Queen Mary University London; University of
California System; University of California San Francisco; UCSF Medical
Center; UCSF Helen Diller Family Comprehensive Cancer Center; New York
University; NYU Langone Medical Center; Helmholtz Association; German
Cancer Research Center (DKFZ); Ruprecht Karls University Heidelberg;
Helmholtz Association; German Cancer Research Center (DKFZ); Pontificia
Universidade Catolica Do Rio Grande Do Sul; Aichi Cancer Center;
UNICANCER; Universite PSL; Institut Curie; UNICANCER; Centre Eugene
Marquis; Universite de Rennes; Roche Holding; Roche Holding; Genentech;
Harvard University; Dana-Farber Cancer Institute; Peter Maccallum Cancer
Center; University of Melbourne; Pennsylvania Commonwealth System of
Higher Education (PCSHE); University of Pittsburgh
RP Schmid, P (corresponding author), Queen Mary Univ London, Barts Canc Inst, London EC1M 6BQ, England.
EM p.schmid@qmul.ac.uk
RI Schneeweiss, Andreas/HHS-4098-2022; Loi, Sherene/ITT-3863-2023; Iwata,
Hiroji/AFO-7749-2022; Barrios, Carlos/HJG-7197-2022; Loi,
Sherene/H-1979-2016
OI Loi, Sherene/0000-0001-6137-9171; Adams, Sylvia/0000-0003-4737-1952
FU F Hoffmann-La Roche; Genentech
FX F Hoffmann-La Roche and Genentech.
CR Adams S, 2019, ANN ONCOL, V30, P405, DOI [10.1093/annonc/mdy518, 10.1093/annonc/mdy517]
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[Anonymous], SAN ANT BREAST CANC
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NR 28
TC 857
Z9 927
U1 10
U2 161
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD JAN
PY 2020
VL 21
IS 1
BP 44
EP 59
DI 10.1016/S1470-2045(19)30689-8
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JZ6KU
UT WOS:000505211900053
PM 31786121
HC Y
HP N
DA 2025-01-07
ER
PT J
AU Qiu, M
Shields, CL
AF Qiu, Mary
Shields, Carol L.
TI Choroidal Nevus in the United States Adult Population Racial
Disparities and Associated Factors in the National Health and Nutrition
Examination Survey
SO OPHTHALMOLOGY
LA English
DT Article
ID ULTRAVIOLET-LIGHT EXPOSURE; UVEAL MELANOMA; VISUAL IMPAIRMENT;
RISK-FACTORS; MELANOCYTIC NEVI; REFRACTIVE ERROR; PREVALENCE; EYE; AGE;
TRANSFORMATION
AB Purpose: To describe the prevalence of choroidal nevus in the US population and identify possible associated factors.
Design: Cross-sectional study.
Participants: A total of 5575 participants aged >= 40 years from the 2005-2008 National Health and Nutrition Examination Survey (NHANES) who underwent retinal imaging examination.
Methods: Predictor variables included a spectrum of demographic, ophthalmic, dermatologic, systemic, socioeconomic, or occupational factor variables available in NHANES.
Main Outcome Measures: Choroidal nevus on retinal imaging.
Results: The prevalence of choroidal nevus was 4.7% overall and increased with age (4.7%, 3.1%, 5.4%, 6.6%, and 7.5% in subjects aged 40-49, 50-59, 60-69, 70-79, and >= 80 years, respectively). The prevalence was 5.0% in men, 4.4% in women, 5.6% in whites, 2.7% in Hispanics, 0.6% in blacks, and 2.1% in others. After adjusting for age and race, the odds of choroidal nevus were 10-fold higher in whites than in blacks, 5-fold higher in Hispanics than in blacks, 4-fold higher in others than in blacks, and 2-fold higher in whites than in Hispanics. Choroidal nevus was associated with hypertension (odds ratio [OR], 1.40; 95% confidence interval [CI], 0.99-1.98); psoriasis (OR, 3.90; 95% CI, 1.57-9.66); lower high-density lipoprotein (OR, 0.99; 95% CI, 0.98-0.99); higher uric acid (OR, 1.13; 95% CI, 1.04-1.22); working in installation, maintenance, or repairs (OR,1.42; 95% CI, 1.03-1.96); and having never worked (OR, 1.56; 95% CI, 1.03-2.37; P = 0.04). There was no association with visual symptoms, visual functioning, visual acuity, refractive error, visual field, diabetic retinopathy, age-related macular degeneration, or elevated cup-to-disc ratio on retinal imaging. There was no association with skin melanoma, other cancers, lung/liver/kidney/thyroid disease, alcohol/drug use, income/education, hemoglobin A1C, C-reactive protein, lactate dehydrogenase, electrolytes, or urine albumin.
Conclusions: Among US adults, the prevalence of choroidal nevus located within two 45 degrees areas centered on the macula and optic disc is 4.7%. The prevalence increases with age, is highest among whites (5.6%), is lowest among blacks (0.6%), and has been previously under-recognized among Hispanics (2.7%). Extrapolating to the entire fundus, the true prevalence of choroidal nevus is even higher but difficult to accurately estimate. Possible associations with cardiovascular, renal, autoimmune, and occupational risk factors warrant further investigation. (C) 2015 by the American Academy of Ophthalmology.
C1 [Qiu, Mary] Johns Hopkins Univ, Wilmer Eye Inst, Baltimore, MD 21218 USA.
[Shields, Carol L.] Thomas Jefferson Univ, Wills Eye Hosp, Ocular Oncol Serv, Philadelphia, PA 19107 USA.
C3 Johns Hopkins University; Johns Hopkins Medicine; Jefferson University
RP Shields, CL (corresponding author), Wills Eye Hosp & Res Inst, Ocular Oncol Serv, 840 Walnut St,Suite 1440, Philadelphia, PA 19107 USA.
EM carolshields@gmail.com
RI shields, carol/AFV-8148-2022
OI Akyuz, Aydin/0000-0003-3304-4125; Qiu, Mary/0000-0002-0062-7386
FU Eye Tumor Research Foundation, Philadelphia, Pennsylvania
FX C.L.S.: Support - Eye Tumor Research Foundation, Philadelphia,
Pennsylvania The funders had no role in the design or conduct of the
study; in the collection, analysis, and interpretation of the data; and
in the preparation, review, or approval of the manuscript.
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NR 46
TC 51
Z9 57
U1 1
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0161-6420
EI 1549-4713
J9 OPHTHALMOLOGY
JI Ophthalmology
PD OCT
PY 2015
VL 122
IS 10
BP 2071
EP 2083
DI 10.1016/j.ophtha.2015.06.008
PG 13
WC Ophthalmology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Ophthalmology
GA CU4IP
UT WOS:000363491500024
PM 26255109
DA 2025-01-07
ER
PT J
AU Picciano, MF
AF Picciano, Mary Frances
TI Vitamin D Status and Health
SO CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION
LA English
DT Review
AB Vitamin D is a unique nutrient in that it is actually a prohormone obtained by endogenous synthesis from sun exposure on 7-dehydrocholesterol in skin and from certain foods and dietary supplements. Endogenous synthesis produces cholecalciferol (vitamin D3) and is transported to the liver bound to the vitamin D-binding protein (DBP). In foods and dietary supplements, vitamin D exists either as cholecalciferol or plant-derived ergocalciferol (vitamin D2). Both forms of the ingested vitamin are absorbed via the lymphatic system and transported to the liver. Vitamin D occurs naturally in a limited number of foods, and fish are found to have the highest amounts of the vitamin. Fortified foods provide the major dietary food sources of vitamin D (e.g., milk and milk products, margarines, and breakfast cereals) in the United States (Whiting and Calvo, 2006). In the liver, vitamin D is converted to 25(OH)D by the enzyme 25-hydroxylase. Conversion to the active form of vitamin D, 1,25-dihydroxyvitamin D [1,25(OH)2D], is achieved in renal tissue by the enzyme 1-hydroxylase (1-OHase). The 1,25(OH)2D form of vitamin D can depress the activity of 1-OHase, and the parathyroid hormone (PTH) can stimulate its activity. As such, 1,25(OH)2D exerts its effects by binding to a specific nuclear receptor (vitamin D receptor [VDR]), a ligand-dependent transcription factor that recognizes specific DNA sequences known as vitamin D response elements (DeLuca, 2004). The main circulating vitamin D metabolite is 25(OH)D, which is used as an indicator of vitamin D nutrition status. The appearance in the circulation of native vitamin D is brief because it is rapidly metabolized in the liver or stored in adipose tissue (Holick, 2007). DBP binds approximately 99% of circulating vitamin D and its metabolites and has a higher affinity for 25(OH)D than 1,25(OH)2D or native vitamin D. Vitamin D deficiency results in diseases such as rickets in infants and children, and osteomalacia in adults (Prentice et al., 2008). Investigations into possible non-bone-related functions of vitamin D are increasing because of the recognition that (1) expression of 1-OHase occurs in many extrarenal tissues and (2) the VDR appears not only in the target cells of enterocytes, osteoblasts, and distal renal tubule cells, but also in parathyroid gland cells, skin keratinocytes, promyelocytes, lymphocytes, colon cells, pituitary gland cells, and ovarian cells (Jones et al., 1998). Areas of promising research include osteoporosis, type-1 diabetes, some cancers, autoimmune diseases, and infectious diseases such as tuberculosis (Brannon et al., 2008). The most commonly used method for assessing Vitamin D status is the measurement of circulating 25(OH)D. There are major limitations of using 25(OH)D as a status biomarker, including the unknown extent of storage of vitamin D, potential dangers of its accumulation in adipose tissue, regulation of its mobilization from these stores, and the consequences of the saturation of this storage. Different methods are used to measure serum or plasma 25(OH)D concentration and comparisons have been complicated by a lack of a standardized reference material. Different laboratories and different methods yield different results using the same sample. The international Vitamin D Quality Assessment Scheme (DEQAS), established in 1989, monitors the performance of 25(OH)D assays and currently has over 100 registered participants from 18 countries (Carter et al., 2004).
The DEQAS has shown that samples analyzed by most commercially available methods are capable of providig results close to the target value for 25(OH)D3, but that results are highly dependent on the laboratory of analysis and the skill of the operator. The DEQAS has also shown that not all assay methods are capable of detecting 25(OH)D2 with the same efficiency as 25(OH)D3. The National Institute of Standards and Technology released standard reference materials (SRMS) for 25(OH)D2 and D3 in July 2009 (NIST, 2009). The availability of these SRMs should permit greater accuracy and precision for measuring 25(OH) D2 and D3 and enable meaningful comparison across laboratories. Vitamin D insufficiency or hypovitaminosis D is likely to be evident in individuals with 25(OH)D values less than 11 ng/mL or 27.5 nmol/L. However, there is no agreement for levels corresponding to sufficiency or ooptimalo vitamin D status. From associations between 25(OH) D concentrations with PTH concentrations and fractional calcium absorption rates, researchers have proposed that plasma 25(OH)D values greater than 50 and 75 nmol/L should define vitamin D sufficiency and ooptimalo concentrations (Dawson-Hughes, 2008; Heaney, 2008). Assessment of Vitamin D status in nationally representative samples from the National Health and Nutrition Examination Surveys (NHANES) 2000-2004 were compared with NHANES III 1988-1994 data (Looker et al., 2008). Mean serum 25(OH)D concentrations were significantly lower in 2000 to 2004 than in 1988 to 1994 in all of the groups examined. Adjustment for assay changes noticeably reduced the difference between surveys. This remaining difference likely represents a real decline in vitamin D status. Changes in body mass index, milk intake, and sun protection seemed to contribute to this decline. Ingested vitamin D is potentially toxic if taken in high amounts over long periods of time. Unfortunately, the available evidence on the quantitative aspects of the safety of vitamin D is very limited. Most of the available information is from studies of short duration. In the Women's Health Initiative, postmenopausal women supplemented with 10 g (400 IU) of vitamin D per day in combination with 1000 mg Ca/d exhibited a 17% increase in kidney stones (Jackson et al., 2006). Despite the considerable progress made in recent years, the available evidence on the relationship between vitamin D and health is far from complete. Investigations are needed that focus on understudied key population subgroups, such as dark-skinned individuals; reproductive-age, pregnant, and lactating women; infants; and adolescents. This article is not subject to US copyright law.
C1 NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA
RP Picciano, MF (corresponding author), NIH, Off Dietary Supplements, Bldg 10, Bethesda, MD 20892 USA.
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NR 12
TC 10
Z9 14
U1 0
U2 83
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1040-8398
EI 1549-7852
J9 CRIT REV FOOD SCI
JI Crit. Rev. Food Sci. Nutr.
PY 2010
VL 50
SU 1
BP 24
EP 25
AR PII 930669875
DI 10.1080/10408398.2010.526858
PG 2
WC Food Science & Technology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Nutrition & Dietetics
GA 689UL
UT WOS:000284955300009
OA Green Published
DA 2025-01-07
ER
PT J
AU Kallas, EG
Precioso, AR
Palacios, R
Thomé, B
Braga, PE
Vanni, T
Campos, LMA
Ferrari, L
Mondini, G
Salomao, MD
da Silva, A
Espinola, HM
Santos, JD
Santos, CLS
Timenetsky, MDST
Miraglia, JL
Gallina, NMF
Weiskopf, D
Sette, A
Goulart, R
Salles, RT
Maestri, A
Sallum, AME
Farhat, SCL
Sakita, NK
Ferreira, JCOA
Silveira, CGT
Costa, PR
Raw, I
Whitehead, SS
Durbin, AP
Kalil, J
AF Kallas, Esper G.
Precioso, Alexander Roberto
Palacios, Ricardo
Thome, Beatriz
Braga, Patricia Emilia
Vanni, Tazio
Campos, Lucia M. A.
Ferrari, Lilian
Mondini, Gabriella
Salomao, Maria da Graca
da Silva, Anderson
Espinola, Heloisa M.
Santos, Joane do Prado
Santos, Cecilia L. S.
Timenetsky, Maria do Carmo S. T.
Miraglia, Joao Luiz
Gallina, Neuza M. F.
Weiskopf, Daniela
Sette, Alessandro
Goulart, Raphaella
Salles, Rafael Tavares
Maestri, Alvino
Sallum, Adriana Maluf Elias
Farhat, Sylvia Costa Lima
Sakita, Neusa K.
Ferreira, Juliana C. O. A.
Silveira, Cassia G. T.
Costa, Priscilla R.
Raw, Isaias
Whitehead, Stephen S.
Durbin, Anna P.
Kalil, Jorge
TI Safety and immunogenicity of the tetravalent, live-attenuated dengue
vaccine Butantan-DV in adults in Brazil: a two-step, double-blind,
randomised placebo-controlled phase 2 trial
SO LANCET INFECTIOUS DISEASES
LA English
DT Article
ID T-CELL RESPONSES; VIRUS SEROTYPES; CANDIDATE; NAIVE; CHILDREN; HEALTHY
AB Background The Butantan Institute has manufactured a lyophilised tetravalent live-attenuated dengue vaccine Butantan-DV, which is analogous to the US National Institutes of Health (NIH) TV003 admixture. We aimed to assess the safety and immunogenicity of Butantan-DV.
Methods We did a two-step, double-blind, randomised placebo-controlled phase 2 trial at two clinical sites in Sao Paulo, Brazil. We recruited healthy volunteers aged 18-59 years; pregnant women, individuals with a history of neurological, heart, lung, liver or kidney disease, diabetes, cancer, or autoimmune diseases, and individuals with HIV or hepatitis C were excluded. Step A was designed as a small bridge-study between Butantan-DV and TV003 in DENV-naive participants. In step A, we planned to randomly assign 50 dengue virus (DENV)-naive individuals to receive two doses of Butantan-DV, TV003, or placebo, given 6 months apart. In step B, we planned to randomly assign 250 participants (DENV-naive and DENV-exposed) to receive one dose of Butantan-DV or placebo. Participants were randomly assigned, by computer-generated block randomisation (block sizes of five); participants in step A were randomly assigned (2:2:1) to receive Butantan-DV, TV003, or placebo and participants in step B were randomly assigned (4:1) to receive Butantan-DV or placebo. Participants and study staff were unaware of treatment allocation. The primary safety outcome was the frequency of solicited and unsolicited local and systemic adverse reactions within 21 days of the first vaccination, analysed by intention to treat. The primary immunogenicity outcome was seroconversion rates of the DENV-1-4 serotypes measured 91 days after the first vaccination, analysed in the per-protocol population, which included all participants in step A, and all participants included in step B who completed all study visits with serology sample collection. This trial is registered with ClinicalTrials. gov, NCT01696422.
Findings Between Nov 5, 2013, and Sept 21, 2015, 300 individuals were enrolled and randomly assigned: 155 (52%) DENV-naive participants and 145 (48%) DENV-exposed participants. Of the 155 DENV-naive participants, 97 (63%) received Butantan-DV, 17 (11%) received TV003, and 41 (27%) received placebo. Of the 145 DENV-exposed participants, 113 (78%) received Butantan-DV, three (2%) received TV003, and 29 (20%) received placebo. Butantan-DV and TV003 were both immunogenic, well-tolerated, and no serious adverse reactions were observed. In step A, rash was the most frequent adverse event (16 [845] of 19 participants in the Butantan-DV group and 13 [76%] of 17 participants in the TV003 group). Viraemia was similar between the Butantan-DV and TV003 groups. Of the 85 DENV-naive participants in the Butantan-DV group who attended all visits for sample collection for seroconversion analysis and thus were included in the per-protocol analysis population, 74 (87%) achieved seroconversion to DENV-1, 78 (92%) to DENV-2, 65 (76%) to DENV-3, and 76 (89%) to DENV-4. Of the 101 DENV-exposed participants in the Butantan-DV group who attended all visits for sample collection for seroconversion analysis, 82 (81%) achieved seroconversion to DENV-1, 79 (78%) to DENV-2, 83 (82%) to DENV-3, and 78 (77%) to DENV-4.
Interpretation Butantan-DV and TV003 were safe and induced robust, balanced neutralising antibody responses against the four DENV serotypes. Efficacy evaluation of the Butantan-DV vaccine is ongoing. Copyright (C) 2020 Elsevier Ltd. All rights reserved.
C1 [Kallas, Esper G.] Univ Sao Paulo, Sch Med, Dept Infect & Parasit Dis, Sao Paulo, Brazil.
[Precioso, Alexander Roberto; Campos, Lucia M. A.; Sallum, Adriana Maluf Elias; Farhat, Sylvia Costa Lima; Sakita, Neusa K.; Ferreira, Juliana C. O. A.] Univ Sao Paulo, Sch Med, Dept Pediat, Sao Paulo, Brazil.
[Ferrari, Lilian; Goulart, Raphaella; Salles, Rafael Tavares; Maestri, Alvino; Silveira, Cassia G. T.; Costa, Priscilla R.; Kalil, Jorge] Univ Sao Paulo, Sch Med, Div Clin Immunol & Allergy, Sao Paulo, Brazil.
[Precioso, Alexander Roberto; Palacios, Ricardo; Braga, Patricia Emilia; Vanni, Tazio; Mondini, Gabriella; Salomao, Maria da Graca; da Silva, Anderson; Espinola, Heloisa M.; Santos, Joane do Prado; Miraglia, Joao Luiz; Gallina, Neuza M. F.; Raw, Isaias] Inst Butantan, Div Clin Trials & Pharmacovigilance, BR-05503900 Sao Paulo, Brazil.
[Thome, Beatriz] Univ Fed Sao Paulo, Dept Prevent Med, Sao Paulo, Brazil.
[Santos, Cecilia L. S.; Timenetsky, Maria do Carmo S. T.] Adolfo Lutz Inst, Sao Paulo, Brazil.
[Weiskopf, Daniela; Sette, Alessandro] La Jolla Inst Allergy & Immunol, Div Vaccine Discovery, San Diego, CA USA.
[Whitehead, Stephen S.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Durbin, Anna P.] Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Immunizat Res, Baltimore, MD USA.
C3 Universidade de Sao Paulo; Universidade Federal de Sao Paulo (UNIFESP);
Universidade de Sao Paulo; Universidade de Sao Paulo; Instituto
Butantan; Universidade Federal de Sao Paulo (UNIFESP); Instituto Adolfo
Lutz; La Jolla Institute for Immunology; National Institutes of Health
(NIH) - USA; NIH National Institute of Allergy & Infectious Diseases
(NIAID); Johns Hopkins University; Johns Hopkins Bloomberg School of
Public Health
RP Precioso, AR (corresponding author), Inst Butantan, Div Clin Trials & Pharmacovigilance, BR-05503900 Sao Paulo, Brazil.
EM alexander.precioso@butantan.gov.br
RI Braga, Patricia/B-7806-2018; da Graca Salomao, Maria/A-4515-2014;
TIMENETSKY, MARIA/I-3956-2018; Maluf Elias, Adriana/H-4779-2013; Kallas,
Esper/C-9539-2012; Miraglia, Joao/H-5294-2013; Weiskopf,
Daniela/HCH-3338-2022; de Oliveira A, Juliana/AAC-9229-2019; Sette,
Alessandro/AFO-8916-2022; Campos, Maria/K-3998-2013; MONDINI,
GABRIELLA/B-7958-2018; Whitehead, Stephen/AAG-2787-2019; thome,
beatriz/B-7337-2018; campos, lucia/G-5800-2018; Terrassani Silveira,
Cassia Gisele/M-8057-2017; Salomao, Maria da Graca/L-1349-2014; KALIL,
JORGE/C-8029-2012; Precioso, Alexander/A-9712-2013; Palacios,
Ricardo/B-7248-2018
OI thome, beatriz/0000-0002-3941-3756; campos, lucia/0000-0001-9653-0468;
Terrassani Silveira, Cassia Gisele/0000-0002-0932-7769; Salomao, Maria
da Graca/0000-0001-8066-6774; Farhat, Sylvia/0000-0003-4036-5226;
Miraglia, Joao Luiz/0000-0002-4788-6254; SAMPAIO TAVARES TIMENETSKY,
MARIA DO CARMO/0000-0001-8317-0539; KALIL, JORGE/0000-0001-8415-4274;
Sallum, Adriana/0000-0003-0823-6459; Caires de Oliveira Achili Ferreira,
Juliana/0000-0002-9249-2318; Precioso, Alexander/0000-0001-8657-9292;
Palacios, Ricardo/0000-0002-1410-8579
FU Intramural Research Program US NIH National Institute of Allergy and
Infectious Diseases; Brazilian National Bank for Economic and Social
Development; Fundacao de Amparo a Pesquisa do Estado de Sao Paulo;
Fundacao Butantan
FX Intramural Research Program US NIH National Institute of Allergy and
Infectious Diseases, Brazilian National Bank for Economic and Social
Development, Fundacao de Amparo a Pesquisa do Estado de Sao Paulo, and
Fundacao Butantan.
CR Aguiar M, 2016, PLOS NEGLECT TROP D, V10, DOI 10.1371/journal.pntd.0005179
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NR 33
TC 53
Z9 62
U1 2
U2 13
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1473-3099
EI 1474-4457
J9 LANCET INFECT DIS
JI Lancet Infect. Dis.
PD JUL
PY 2020
VL 20
IS 7
BP 839
EP 850
DI 10.1016/S1473-3099(20)30023-2
PG 12
WC Infectious Diseases
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases
GA ME3PZ
UT WOS:000544572300041
PM 32220283
DA 2025-01-07
ER
PT J
AU Gopal, A
Kim, SJ
AF Gopal, Anjana
Kim, S.
TI Hemophagocytic Lymphohistiocytosis in a Remote Kidney Transplant
Recipient Triggered by HSV Infection With Complete Recovery: An
Educational Case Report
SO CANADIAN JOURNAL OF KIDNEY HEALTH AND DISEASE
LA English
DT Article
DE hemophagocytic lymphohistiocytosis; kidney transplant; herpes simplex
virus
ID CLINICAL-FEATURES; DIAGNOSIS; OUTCOMES; ADULTS
AB Rationale: Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening disease characterized by excessive immune activation. It is more commonly seen in children but increasingly recognized in adults. Primary HLH relies on a genetic predisposition, whereas secondary HLH develops in the context of infections, malignancies, or autoimmune diseases. Hemophagocytic lymphohistiocytosis has been rarely described in patients on immunosuppressive therapy after kidney transplant. Here, we describe a case of HLH in a patient with a remote history of kidney transplant, triggered by a viral infection.Presenting Concerns: A 45-year-old female, with a kidney transplant in 2009 for IgA nephropathy, presented with fever, vomiting, and back pain of 1-week duration. She was on triple immunosuppression consisting of daily doses of prednisone 5 mg, azathioprine 100 mg, and tacrolimus extended release 1 mg, and a baseline creatinine of 130 mu mol/L.Diagnosis: Initial investigations showed anemia, leukopenia, elevated serum creatinine, transaminitis, and markedly increased ferritin of 67 600 mu g/L which prompted a bone marrow biopsy to rule out HLH. The bone marrow showed an increased proportion of CD68+ cells (macrophages) with more than 5 in 1000 hemophagocytic macrophages. Her soluble IL-2 receptor (CD25) level was 3406 pg/mL (606-2299 pg/mL) which was mildly elevated. She fulfilled 4 of the 8 criteria for HLH and with an H score was 223 which suggested a diagnosis of HLH with 96.9% probability. An extensive secondary workup for possible triggers for HLH led to a swab from genital ulcers that was positive for herpes simplex virus (HSV) type 2. The polymerase chain reaction (PCR) in the blood for HSV type 2 was also positive.Interventions: Given the diagnosis of HSV type 2 as the putative trigger for HLH, she was started on parenteral acyclovir for 2 weeks followed by oral valacyclovir for 2 more weeks. In the context of infection, the azathioprine was stopped while low-dose steroid and tacrolimus were continued.Outcomes: With the initiation of treatment for HSV infection, leukopenia, creatinine, and transaminases improved along with ferritin levels. At her 6-month follow-up, her blood counts and liver enzymes had normalized, and ferritin was 566 mu g/L.Teaching points: Hemophagocytic lymphohistiocytosis is a rare disease in kidney transplant recipients with a high mortality rate. It can occur even in remote kidney transplant recipients so a high degree of suspicion is necessary to lead to a prompt diagnosis. Infections are common triggers for secondary HLH. Early identification and treatment of the triggering infection may improve outcomes.
Justification: La lymphohistiocytose hé mophagocytaire (HLH) est une maladie potentiellement mortelle caracté risé e par une activation excessive du systè me immunitaire. Elle est plus fré quente chez les enfants, mais de plus en plus observé e chez les adultes. La HLH primaire se manifeste en raison d'une pré disposition gé né tique, tandis que la HLH secondaire se dé veloppe dans le contexte d'une infection, d'un cancer ou d'une maladie auto-immune. La HLH a rarement é té dé crite chez les patients sous traitement immunosuppresseur à la suite d'une transplantation ré nale. Nous pré sentons un cas de HLH dé clenché par une infection virale chez une patiente avec des anté cé dents lointains de transplantation ré nale.Pré sentation du cas: Une femme de 45 ans, greffé e du rein en 2009 en raison d'une né phropathie à IgA, a consulté pour de la fiè vre, des vomissements et des douleurs dorsales depuis une semaine. Son triple traitement immunosuppresseur consistait en des doses quotidiennes de prednisone (5 mg), d'azathioprine (100 mg) et de tacrolimus à libé ration prolongé e (1 mg). Son taux de cré atinine usuel é tait de 130 umol/L.Diagnostic: Les premiè res investigations ont ré vé lé une ané mie, de la leucopé nie, un taux de cré atinine sé rique é levé, une transaminite et un taux de ferritine nettement é levé de 67 600 ug/L, ce qui a justifié une biopsie de la moelle osseuse pour exclure une HLH. Les ré sultats ont montré une plus grande proportion de cellules CD68+ (macrophages), avec plus de 5 macrophages hé mophagocytaires sur 1000. Le taux de ré cepteurs solubles de l'IL-2 (CD25) s'é tablissait à 3 406 pg/ml (606 à 2 299 pg/ml), ce qui est lé gè rement é levé. La patiente ré pondait à quatre des huit critè res de la HLH et pré sentait un score H de 223, ce qui suggé rait une probabilité de 96,9 % pour un diagnostic de HLH. L'examen secondaire approfondi des possibles dé clencheurs de la HLH a inclus un pré lè vement sur des ulcè res gé nitaux qui s'est avé ré positif pour le virus de l'herpè s simplex (HSV) de type 2. La PCR d'é chantillons sanguins é tait é galement positive pour HSV de type 2.Interventions: L'infection par HSV de type 2 ayant é té identifié e comme le dé clencheur pré sumé de la HLH, la patiente a reç u un traitement parenté ral d'acyclovir pendant deux semaines, suivi d'un traitement oral de valacyclovir pour deux semaines supplé mentaires. Dans le contexte de l'infection, l'azathioprine a é té cessé e, mais le tacrolinus et les sté roï des à faible dose ont é té maintenus.Ré sultats: L'amorce du traitement antiviral a entraî né une amé lioration de la leucopé nie, du taux de cré atinine et des transaminases, ainsi que des taux de ferritine. Lors du dernier suivi à 6 mois, la numé risation sanguine et les enzymes hé patiques de la patiente s'é taient normalisé es et son taux de ferritine é tait de 566 ug/L.
Enseignements tiré s: La lymphohistiocytose hé mophagocytaire est une maladie rare chez les greffé s ré naux et elle entraî ne un taux é levé de mortalité. La maladie peut survenir mê me chez des greffé s ré naux de longue date, de sorte qu'il est né cessaire d'exercer un degré é levé de vigilance afin de poser rapidement un diagnostic. Les infections sont de fré quents dé clencheurs de la HLH secondaire. Les ré sultats peuvent ê tre amé lioré s par l'identification et le traitement pré coces de l'infection ayant dé clenché la maladie.
C1 [Gopal, Anjana; Kim, S.] Univ Hlth Network, Toronto Gen Hosp, Ajmera Transplant Ctr, Toronto, ON M5G 2N2, Canada.
C3 University of Toronto; University Health Network Toronto; Toronto
General Hospital
RP Gopal, A (corresponding author), Univ Hlth Network, Toronto Gen Hosp, Ajmera Transplant Ctr, Toronto, ON M5G 2N2, Canada.
EM anjanagopal1988@gmail.com
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NR 15
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
EI 2054-3581
J9 CAN J KIDNEY HEALTH
JI Can. J. Kidney Health Dis.
PY 2024
VL 11
AR 20543581241253921
DI 10.1177/20543581241253921
PG 6
WC Urology & Nephrology
WE Emerging Sources Citation Index (ESCI)
SC Urology & Nephrology
GA RV1H3
UT WOS:001230338800001
PM 38799982
OA Green Published, gold
DA 2025-01-07
ER
EF