Hepatitis C virus core protein induces spontaneous and persistent activation of peroxisome proliferator-activated receptor alpha in transgenic mice: Implications for HCV-associated hepatocarcinogenesis

This is a preprint of an article published in INTERNATIONAL JOURNAL OF CANCER. Copyright (c) 2008 Wiley-Liss, Inc., A Wiley CompanyArticleINTERNATIONAL JOURNAL OF CANCER. 122(1): 124-131journal articl

Pancreatic exocrine insufficiency: a rare cause of nonalcoholic steatohepatitis

This is an electronic version of an Article published in the American Journal of Gastroenterology 2008; 103(1): 245-246.ArticleAmerican journal of gastroenterology. 103(1): 245-246 (2008)journal articl

Prevalence and distribution of extrapancreatic lesions complicating autoimmune pancreatitis

The original publication is available at www.springerlink.com.ArticleJOURNAL OF GASTROENTEROLOGY. 41(12): 1197-1205 (2006)journal articl

Possible relationship between Helicobacter pylori infection and cap polyposis of the colon

The definitive version is available at www.blackwell-synergy.com.ArticleHELICOBACTER. 9(6): 651-656 (2004)journal articl

Polyenephosphatidylcholine prevents alcoholic liver disease in PPARα-null mice through attenuation of increases in oxidative stress

Background/Aims: Alcoholic liver disease (ALD) is one of the leading causes of cirrhosis and yet efficient therapeutic strategies are lacking. Polyenephosphatidylcholine (PPC), a major component of essential phospholipids, prevented alcoholic liver fibrosis in baboons, but its precise mechanism remains uncertain. We aimed to explore the effects of PPC on ALD using ethanol-fed peroxisome proliferator-activated receptor α (Ppara)-null mice, showing several similarities to human ALD. Methods: Male wild-type and Ppara-null mice were pair-fed a Lieber-DeCarli control or 4% ethanol-containing diet with or without PPC (30 mg/kg/day) for 6 months. Results: PPC significantly ameliorated ethanol-induced hepatocyte damage and hepatitis in Ppara-null mice. These effects were likely a consequence of decreased oxidative stress through down-regulation of reactive oxygen species (ROS)-generating enzymes, including cytochrome P450 2E1, acyl-CoA oxidase, and NADPH oxidases, in addition to restoration of increases in Toll-like receptor 4 and CD14. PPC also decreased Bax and truncated Bid, thus inhibiting apoptosis. Furthermore, PPC suppressed increases in transforming growth factor-β1 expression and hepatic stellate cell activation, which retarded hepatic fibrogenesis. Conclusions: PPC exhibited anti-inflammatory, anti-apoptotic, and anti-fibrotic effects on ALD as a result of inhibition of the overexpression of ROS-generating enzymes. Our results demonstrate detailed molecular mechanisms of the anti-oxidant action of PPC.ArticleJournal of Hepatology 50(6): 1236-1246(2009)journal articl

Patients with and without loss of hepatitis B virus DNA after hepatitis B e antigen seroconversion have different virological characteristics

Copyright © 2006 Wiley-Liss, Inc., A Wiley CompanyArticleJOURNAL OF MEDICAL VIROLOGY. 78(1): 68-73 (2006)journal articl

Laparoscopic findings in patients with nonalcoholic steatohepatitis

ArticleLIVER INTERNATIONAL. 26(1): 32-38 (2006)journal articl

Association of Autoimmune Pancreatitis With Cytotoxic T-lymphocyte Antigen 4 Gene Polymorphisms in Japanese Patients

ArticleAMERICAN JOURNAL OF GASTROENTEROLOGY. 103(3):588-594 (2008)journal articl

Hepatitis B virus RNA is measurable in serum and can be a new marker for monitoring lamivudine therapy

The original publication is available at www.springerlink.comArticleJOURNAL OF GASTROENTEROLOGY. 41(8): 785-790 (2006)journal articl

Hepatitis B virus core and core-related antigen quantitation in Chinese patients with chronic genotype B and C hepatitis B virus infection

The definitive version is available at www.blackwell-synergy.com.ArticleJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY. 20(11): 1726-1730 (2005)journal articl