Different lobular distributions of altered hepatocyte tight junctions in rat models of intrahepatic and extrahepatic cholestasis

Takumi Kawaguchi, Shotaro Sakisaka, Michio Sata, Michio Mori, Kyuichi Tanikawa – 30 December 2003 – Hepatocyte tight junctions (TJs), the only intercellular barrier between the sinusoidal and the canalicular spaces, play a key role in bile formation. Although hepatocyte TJs are impaired in cholestasis, attempts to localize the precise site of hepatocyte TJ damage by freeze‐fracture electron microscopy have produced limited information. Recently, several TJ‐associated proteins like ZO‐1 and 7H6 have been identified and characterized.

Hepatitis C virus RNA profiles in chronically infected individuals: Do they relate to disease activity?

Patrizia Pontisso, Giorgio Bellati, Maurizia Brunetto, Liliana Chemello, Guido Colloredo, Rosellina Di Stefano, Massimo Nicoletti, Maria Grazia Rumi, Maria Grazia Ruvoletto, Roberta Soffredini, Lilli Mario Valenza, Giuseppe Colucci – 30 December 2003 – Fluctuations of hepatitis C virus (HCV)‐RNA serum levels were monitored in a multicenter study in 76 chronic HCV carriers who had been followed longitudinally without receiving antiviral therapy to assess their relation with the course of liver disease activity.

Efficacy of lamivudine in patients with hepatitis B e antigen–negative/hepatitis B virus DNA–positive (precore mutant) chronic hepatitis befficacy of lamivudine in patients with hepatitis B e antigen–negative/hepatitis B virus DNA–positive (precore mutant

Nicolaos C. Tassopoulos, Riccardo Volpes, Giuseppe Pastore, Jenny Heathcote, Maria Buti, Robert D. Goldin, Sasha Hawley, Judy Barber, Lynn Condreay, D. Fraser Gray – 30 December 2003 – This placebo controlled, double‐blind study evaluated the efficacy and safety of lamivudine in patients with hepatitis B e antigen (HBeAg)‐negative/hepatitis B virus (HBV) DNA–positive chronic hepatitis B. Patients were randomized to receive 100 mg lamivudine orally once daily for 52 weeks (n = 60) or placebo for 26 weeks (n = 65). Patients who were HBV DNA positive at week 24 were withdrawn at week 26.

DNA hypermethylation at the D17S5 locus and reduced HIC‐1mRNA expression are associated with hepatocarcinogenesis

Yae Kanai, Ai‐Min Hui, Lin Sun, Saori Ushijima, Michiie Sakamoto, Hitoshi Tsuda, Setsuo Hirohashi – 30 December 2003 – To examine the significance of aberrant DNA methylation in hepatocarcinogenesis, the DNA methylation status at the D17S5 locus and mRNA expression of a candidate tumor suppressor gene, HIC‐1(hypermethylated‐in‐cancer), which was identified at the D17S5 locus, in primary hepatocellular carcinomas (HCCs) and their corresponding noncancerous liver tissues were assessed.

Anti‐idiotypic antibodies to anti–PDC‐E2 in primary biliary cirrhosis and normal subjects

Qiao‐yi Chen, Merrill J. Rowley, Ian R. Mackay – 30 December 2003 – Anti‐idiotypic antibodies may regulate the immune system and influence pathogenic autoimmunity. We investigated idiotype–anti‐idiotype interactions in sera of patients with primary biliary cirrhosis (PBC), normal subjects and animals immunized with pyruvate dehydrogenase complex (PDC) or its derivatives. IgG autoantibody to the E2 subunit of PDC (PDC‐E2) was derived by affinity‐purification from sera of 12 patients with PBC, and F(ab)2 was prepared (anti–PDC‐E2‐F[ab]2).

Gadolinium blocks rat kupffer cell calcium channels: Relevance to calcium‐dependent prostaglandin E2 synthesis and septic mortality

Claude R. Roland, Bashoo Naziruddin, T. Mohanakumar, M. Wayne Flye – 30 December 2003 – Hepatic Kupffer cells (KC), the major tissue macrophage population, produce the septic response mediators, tumor necrosis factor α (TNF‐α) and prostaglandin E2 (PGE2 ), and have been shown to internalize gadolinium chloride (GD), a rare earth metal of the lanthanide series.

Characterization of the overlap syndrome of primary biliary cirrhosis (PBC) and autoimmune hepatitis: Evidence for it being a hepatitic form of PBC in genetically susceptible individuals

Ansgar W. Lohse, Karl‐Hermann Meyer zum Büschenfelde, Beate Franz, Stephan Kanzler, Guido Gerken, Hans‐Peter Dienes – 30 December 2003 – Some patients with autoimmune liver disease present with a clinical and/or histological picture showing characteristic findings of both autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC). Various names, mostly overlap syndrome, have been used to describe these cases, which have thus far not been more closely characterized.

The long‐term outcomes of patients with compensated hepatitis C virus–related cirrhosis and history of parenteral exposure in the united states

Ke‐Qin Hu, Myron J. Tong – 30 December 2003 – It is well known that hepatitis C virus (HCV) infection may progress to cirrhosis and is linked to the development of hepatocellular carcinoma (HCC). Previous studies have shown that compensated HCV‐cirrhosis is related to a certain morbidity and mortality in European patients, but little is known in regard to the clinical outcomes of a similar group of patients in the United States.

Histopathological study of primary biliary cirrhosis and the effect of ursodeoxycholic acid treatment on histology progression

Claude Degott, Elie Serge Zafrani, Patrice Callard, Beverley Balkau, Renée Eug Poupon, Raoul Poupon – 30 December 2003 – The semiquantitative histopathological analysis of the liver biopsies obtained before and after 4 years of ursodeoxycholic acid (UDCA) therapy in a cohort of primary biliary cirrhosis (PBC) patients is reported. The relationships between elementary histological lesions before treatment and their progression under therapy were assessed.

Influence of human immunodeficiency virus infection on chronic hepatitis B in homosexual men

Jean‐François Colin, Dominique Cazals‐Hatem, Marie Anne Loriot, Michèle Martinot‐Peignoux, Bach Nga Pham, Anne Auperin, Claude Degott, Jean‐Pierre Benhamou, Serge Erlinger, Dominique Valla, Patrick Marcellin – 30 December 2003 – The aim of this study was to assess the influence of human immunodeficiency virus (HIV) infection on chronic hepatitis B.

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