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| 1 | microRNAs: Fad or future of liver disease显示文摘microRNAs (miRs) are small non-coding RNAs that regulate both mRNA and protein expression of target genes, which results in alterations in mRNA stability or translation inhibition. miRs influence at least one third of all human transcripts and are known regulators of various important cellular growth and differentiation factors. miRs have recently emerged as key regulatory molecules in chronic liver disease. This review details recent contributions to the field of miRs that influence liver development and the broad spectrum of disease, from non-alcoholic fatty liver disease to fibrosis/cirrhosis, with particular emphasis on hepatic stellate cells and potential use of miRs as therapeutic tools. | Ashley M Lakner Herbert L Bonkovsky Laura W Schrum | 2011 | World Journal of Gastroenterology2011，17，20： | 13 |
| 2 | Genetic factors that affect nonalcoholic fatty liver disease: A systematic clinical review显示文摘AIM: To investigate roles of genetic polymorphisms in non-alcoholic fatty liver disease(NAFLD) onset, severity, and outcome through systematic literature review. METHODS: The authors conducted both systematic and specific searches of Pub Med through December 2015 with special emphasis on more recent data(from 2012 onward) while still drawing from more historical data for background. We identified several specific genetic polymorphisms that have been most researched and, at this time, appear to have the greatest clinical significance on NAFLD and similar hepatic diseases. These were further investigated to assess their specific effects on disease onset and progression and the mechanisms by which these effects occur. RESULTS: We focus particularly on genetic polymorphisms of the following genes: PNPLA3, particularly the p. I148 M variant, TM6SF2, particularly the p. E167 K variant, and on variants in FTO, LIPA, IFNλ4, and iron metabolism, specifically focusing on HFE, and HMOX-1. We discuss the effect of these genetic variations and their resultant protein variants on the onset of fatty liver disease and its severity, including the effect on likelihood of progression to cirrhosis and hepatocellular carcinoma. While our principal focus is on NAFLD, we also discuss briefly effects of some of the variants on development and severity of other hepatic diseases, including hepatitis C and alcoholic liver disease. These results are briefly discussed in terms of clinical application and future potential for personalized medicine. CONCLUSION: Polymorphisms and genetic factors of several genes contribute to NAFLD and its end results. These genes hold keys to future improvements in diagnosis and management. | Tyler J Severson Siddesh Besur Herbert L Bonkovsky | 2016 | World Journal of Gastroenterology2016，22，29： | 12 |
| 3 | Hepatitis B and liver transplantation: Molecular and clinical features that influence recurrence and outcome显示文摘Hepatitis B virus(HBV) continues to be a major cause of morbidity and mortality worldwide. It is estimated that about 350 million people throughout the world are chronically infected with HBV. Some of these people will develop hepatic cirrhosis with decompensation and/or hepatocellular carcinoma. For such patients, liver transplantation may be the only hope for cure or real improvement in quality and quantity of life. Formerly, due to rapidity of recurrence of HBV infection after liver transplantation, usually rapidly progressive, liver transplantation was considered to be contraindicated. This changed dramatically following the demonstration that hepatitis B immune globulin(HBIG), could prevent recurrent HBV infection. HBIG has been the standard of care for the past two decades or so. Recently, with the advent of highly active inhibitors of the ribose nucleic acid polymerase of HBV(entecavir, tenofovir), there has been growing evidence that HBIG needs to be given for shorter lengths of time; indeed, it may no longer be necessary at all. In this review, we describe genetic variants of HBV and past, present, and future prophylaxis of HBV infection during and after liver transplantation. We have reviewed the extant medical literature on the subject of infection with the HBV, placing particular emphasis upon the prevention and treatment of recurrent HBV during and after liver transplantation. For the review, we searched PubMed for all papers on the subject of 'hepatitis B virus AND liver transplantation'. We describe some of the more clinically relevant and important genetic variations in the HBV. We also describe current practices at our medical centers, provide a summary and analysis of comparative costs for alternative strategies for prevention of recurrent HBV, and pose important still unanswered questions that are in need of answers during the next decade or two. We conclude that it is now rational and cost-effective to decrease and, perhaps, cease altogether, the routine use of HBIG during and following liver transplantation for HBV infection. Here we propose an individualized prophylaxis regimen, based on an integrated approach and risk-assessment. | Tahereh Ghaziani Hossein Sendi Saeid Shahraz Philippe Zamor Herbert L Bonkovsky | 2014 | World Journal of Gastroenterology2014，20，39： | 7 |
| 4 | Non-coding RNAs in hepatitis C-induced hepatocellular carcinoma:Dysregulation and implications for early detection,diagnosis and therapy显示文摘Hepatitis C virus(HCV)infection is one of main causes of hepatocellular carcinoma(HCC)and the prevalence of HCV-associated HCC is on the rise worldwide.It is particularly important and helpful to identify potential markers for screening and early diagnosis of HCC among high-risk individuals with chronic hepatitis C,and to identify target molecules for the prevention and treatment of HCV-associated-HCC.Small noncoding RNAs,mainly microRNAs(miRNAs),and long non-coding RNAs(lncRNAs)with size greater than 200nucleotides,are likely to play important roles in a variety of biological processes,including development and progression of HCC.For the most part their underlying mechanisms of action remain largely unknown.In recent years,with the advance of high-resolution of microarray and application of next generation sequencing techniques,a significant number of non-coding RNAs(ncRNAs)associated with HCC,particularly caused by HCV infection,have been found to be differentially expressed and to be involved in pathogenesis of HCVassociated HCC.In this review,we focus on recent studies of ncRNAs,especially miRNAs and lncRNAs related to HCV-induced HCC.We summarize those ncRNAs aberrantly expressed in HCV-associated HCC and highlight the potential uses of ncRNAs in early detection,diagnosis and therapy of HCV-associated HCC.We also discuss the limitations of recent studies,and suggest future directions for research in the field.miRNAs,lncRNAs and their target genes may represent new candidate molecules for the prevention,diagnosis and treatment of HCC in patients with HCV infection.Studies of the potential uses of miRNAs and lncRNAs as diagnostic tools or therapies are still in their infancy. | Weihong Hou Herbert L Bonkovsky | 2013 | World Journal of Gastroenterology2013，19，44： | 6 |
| 5 | Iron increases HMOX1 and decreases hepatitis C viral expression in HCV-expressing cells显示文摘AIM:To investigate effects of iron on oxidative stress, heme oxygenase-1(HMOX1)and hepatitis C viral(HCV) expression in human hepatoma cells stably expressing HCV proteins. METHODS:Effects of iron on oxidative stress,HMOX1, and HCV expression were assessed in CON1 cells. Measurements included mRNA by quantitative reverse transcription-polymerase chain reaction,and protein levels by Western blots. RESULTS:Iron,in the form of ferric nitrilotriacetate,increased oxidative stress and up-regulated HMOX1 gene expression.Iron did not affect mRNA or protein levels of Bach1,a repressor of HMOX1.Silencing the up-regulation of HMOX1 nuclear factor-erythroid 2-related factor 2(Nrf2)by Nrf2-siRNA decreased FeNTA-mediated up-regulation of HMOX1 mRNA levels.These iron effects were completely blocked by deferoxamine(DFO).Iron also significantly decreased levels of HCV core mRNA and protein by 80%-90%, nonstructural 5A mRNA by 90%and protein by about 50%in the Con1 full length HCV replicon cells, whereas DFO increased them. CONCLUSION:Excess iron up-regulates HMOX1 and down-regulates HCV gene expression in hepatoma cells.This probably mitigates liver injury caused by combined iron overload and HCV infection. | Wei-Hong Hou Lisa Rossi Ying Shan Jian-Yu Zheng Richard W Lambrecht Herbert L Bonkovsky | 2009 | World Journal of Gastroenterology2009，15，36： | 5 |
| 6 | Maintenance Peginterferon Therapy and Other Factors Associated With Hepatocellular Carcinoma in Patients With Advanced Hepatitis C显示文摘 | Anna S. Lok James E. Everhart Elizabeth C. Wright Adrian M. Di Bisceglie Hae–Young Kim Richard K. Sterling Gregory T. Everson Karen L. Lindsay William M. Lee Herbert L. Bonkovsky Jules L. Dienstag Marc G. Ghany Chihiro Morishima Timothy R. Morgan | 2011 | Gastroenterology2011，，3： | 4 |
| 7 | Incidence of Hepatocellular Carcinoma and Associated Risk Factors in Hepatitis C-Related Advanced Liver Disease显示文摘 | Anna S. Lok Leonard B. Seeff Timothy R. Morgan Adrian M. di Bisceglie Richard K. Sterling Teresa M. Curto Gregory T. Everson Karen L. Lindsay William M. Lee Herbert L. Bonkovsky Jules L. Dienstag Marc G. Ghany Chihiro Morishima Zachary D. Goodman | 2009 | Gastroenterology2009，，1： | 3 |
| 8 | Legalon-SIL downregulates HCV core and NS5A in human hepatocytes expressing full-length HCV显示文摘AIM: To determine the effect of Legalon-SIL (LS) on hepatitis C virus (HCV) core and NS5A expression and on heme oxygenase-1 (HMOX-1) and its transcriptional regulators in human hepatoma cells expressing full length HCV genotype 1b. METHODS: CON1 cells were treated with 50 μmol/L or 200 μmol/L LS. Cells were harvested after 2, 6 and 24 h. HCV RNA and protein levels were determined by quantitative real-time polymerase chain reaction and Western blotting, respectively. RESULTS: HCV RNA (core and NS5A regions) wasdecreased after 6 h with LS 200 μmol/L (P < 0.05). Both 50 and 200 μmol/L LS decreased HCV RNA levels [core region (by 55% and 88%, respectively) and NS5A region (by 62% and 87%, respectively) after 24 h compared with vehicle (dimethyl sulphoxide) control (P < 0.01). Similarly HCV core and NS5A protein were decreased (by 85%, P < 0.01 and by 65%, P < 0.05, respectively) by LS 200 μmol/L. Bach1 and HMOX-1 RNA were also downregulated by LS treatment (P < 0.01), while Nrf2 protein was increased (P < 0.05).CONCLUSION: Our results demonstrate that treatment with LS downregulates HCV core and NS5A expression in CON1 cells which express full length HCV genotype 1b, and suggests that LS may prove to be a valuable alternative or adjunctive therapy for the treatment of HCV infection. | Marjan Mehrab-Mohseni Hossein Sendi Nury Steuerwald Sriparna Ghosh Laura W Schrum Herbert L Bonkovsky | 2011 | World Journal of Gastroenterology2011，17，13： | 3 |
| 9 | Non-alcoholic steatohepatitis and iron: increased prevalence of mutations of the HFE gene in non-alcoholic steatohepatitis显示文摘 | Herbert L Bonkovsky Qaiser Jawaid Kristina Tortorelli Paula LeClair Joseph Cobb Richard W Lambrecht Barbara F Banner | 1999 | Journal of Hepatology1999，，3： | 2 |
| 10 | 草药和膳食补充剂伴随肝损伤风险显示文摘正在受健身者和试图减肥的中年妇女热捧的草药或膳食补充剂(herbals and dietary supplements, HDS)乱用情况泛滥,尽管很多美国人都相信膳食补充剂是安全的,但实际上政府相关条例(1994年膳食补充剂健康与教育法)对此类产品上市监管较松,相较传统药品缺少上市安全性证据。由于这种对草药等膳食补充剂不太严格的监督,造成发生包括危及生命在内的较大潜在有害后果。在过去10年中已逐渐成为导致肝损伤越来越重要的原因。 | Navarro VJ Barnhart H Bonkovsky HL | 2014 | 中华普通外科学文献(电子版)2014，8，5： | 2 |
| 11 | Drug-Induced Liver Injury Network (DILIN) Prospective Study: Rationale, Design and Conduct显示文摘 | Fontana Robert J Watkins Paul B Bonkovsky Herbert L Chalasani Naga Davern Timothy Serrano Jose Rochon James | 2009 | Drug Safety2009，，1： | 2 |
| 12 | Causes, Clinical Features, and Outcomes From a Prospective Study of Drug-Induced Liver Injury in the United States显示文摘 | Naga Chalasani Robert J. Fontana Herbert L. Bonkovsky Paul B. Watkins Timothy Davern Jose Serrano Hongqiu Yang James Rochon | 2008 | Gastroenterology2008，，6： | 2 |
| 13 | Reciprocal Effects of Micro-RNA-122 on Expression of Heme Oxygenase-1 and Hepatitis C Virus Genes in Human Hepatocytes显示文摘 | Ying Shan Jianyu Zheng Richard W. Lambrecht Herbert L. Bonkovsky | 2007 | Gastroenterology2007，，4： | 2 |
| 14 | Causes, Clinical Features, and Outcomes From a Prospective Study of Drug-Induced Liver Injury in the United States显示文摘 | Naga Chalasani Robert J. Fontana Herbert L. Bonkovsky Paul B. Watkins Timothy Davern Jose Serrano Hongqiu Yang James Rochon | 2008 | Gastroenterology2008，，6： | 2 |
| 15 | Des-γ-Carboxy Prothrombin and α-Fetoprotein as Biomarkers for the Early Detection of Hepatocellular Carcinoma显示文摘 | Anna S. Lok Richard K. Sterling James E. Everhart Elizabeth C. Wright John C. Hoefs Adrian M. Di Bisceglie Timothy R. Morgan Hae–Young Kim William M. Lee Herbert L. Bonkovsky Jules L. Dienstag | 2010 | Gastroenterology2010，，2： | 2 |
| 16 | Drug Induced Liver Injury Network Causes, clinical features, and outcomes from a prospective study of drug-induced liver injury in the United States显示文摘 | Chalasani N Fontana PJ Bonkovsky HL | 2008 | Gastroenterology2008，135，6： | 1 |
| 17 | Herbal and dietary supplement induced bepatotoxicity in the US 显示文摘 | Navarro VJ Barnhart HX Bonkovsky HL | 2012 | Gastroenterology2012，142，51： | 1 |
| 18 | Causes, clinical features, and outcomes from a prospective study of drug-induced liver injury in the United States 显示文摘 | Chalasani N Fontana R J Bonkovsky HL | 2008 | Gastroenterology2008，135，6： | 1 |
| 19 | ACG clinical guideline: the diagnosis and management of idiosyncratic drug -induced liver injury显示文摘 | CHALASANI NP HAYASHI PH BONKOVSKY HL | 2014 | Am J Gastroenterology2014，109，7： | 1 |
| 20 | Causes,clinical features,and outcomes from a frospective study of drug-induced liver injury in the United States显示文摘 | Chalasani N Fontana RJ Bonkovsky HL | | 0，，： | 1 |
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