Paul J. Pockros, Eugene R. Schiff, Mitchell L. Shiffman, John G. McHutchison, Robert G. Gish, Nezam H. Afdhal, Manana Makhviladze, Mira Huyghe, David Hecht, Tilman Oltersdorf, David A. Shapiro – 27 July 2007 – Increased rates of apoptosis (programmed cell death) have been demonstrated in many hepatic diseases including chronic hepatitis C. IDN‐6556 is a potent inhibitor of caspases, the proteases that execute apoptosis. In a prior phase 1 study, IDN‐6556 lowered aminotransferase activity in a small number of patients with liver impairment.

Eike Steinmann, Thomas Whitfield, Stephanie Kallis, Raymond A. Dwek, Nicole Zitzmann, Thomas Pietschmann, Ralf Bartenschlager – 27 July 2007 – Current therapy of chronic hepatitis C is based on the combination of pegylated interferon‐α and ribavirin. In spite of 50% sustained virological response, therapy is still limited by unsatisfying success rates with genotype 1 infections and adverse side effects. One attempt to increase success rates is triple combination therapy of interferon and ribavirin with amantadine, a drug assumed to interfere with HCV p7 ion channel function.

Stanley D.W. Miller, Catherine M. Greene, Caitriona McLean, Matthew W. Lawless, Clifford C. Taggart, Shane J. O'Neill, Noel G. McElvaney – 27 July 2007 – Z alpha‐1 antitrypsin (AAT) deficiency is a genetic disease associated with accumulation of misfolded AAT in the endoplasmic reticulum (ER) of hepatocytes. ZAAT‐expressing cells display ER stress responses including nuclear factor kappaB activation and apoptosis. Using an in vitro model of ZAAT ER accumulation, we investigated the mechanism of ZAAT‐mediated ER‐induced apoptosis and evaluated methods to inhibit this process.

Jason S. Soden, Michael W. Devereaux, Joel E. Haas, Eric Gumpricht, Rolf Dahl, Jane Gralla, Maret G. Traber, Ronald J. Sokol – 27 July 2007 – Several genetic metabolic liver diseases share the pathological features of combined steatosis and cholestasis, or steatocholestasis. The aims of this study were to develop and characterize an in vivo model for steatocholestasis and to evaluate the effects of an antioxidant treatment on liver injury, oxidative stress, and mitochondrial perturbations in this model.

Kenichi Harada, Yasunori Sato, Keita Itatsu, Kumiko Isse, Hiroko Ikeda, Mitsue Yasoshima, Yoh Zen, Akira Matsui, Yasuni Nakanuma – 27 July 2007 – Infections of Reoviridae consisting of a double‐stranded RNA (dsRNA) genome are a possible cause of biliary atresia (BA). The aim of the present study is to clarify the pathophysiological function of dsRNA viruses in the pathogenesis of BA.

Daniel Gatti, Akira Maki, Elissa J. Chesler, Roumyana Kirova, Oksana Kosyk, Lu Lu, Kenneth F. Manly, Robert W. Williams, Andy Perkins, Michael A. Langston, David W. Threadgill, Ivan Rusyn – 27 July 2007 – The liver is the primary site for the metabolism of nutrients, drugs, and chemical agents. Although metabolic pathways are complex and tightly regulated, genetic variation among individuals, reflected in variations in gene expression levels, introduces complexity into research on liver disease.

Pierre Bedossa, Rami Moucari, Emna Chelbi, Tarik Asselah, Valerie Paradis, Michel Vidaud, Dominique Cazals‐Hatem, Nathalie Boyer, Dominique Valla, Patrick Marcellin – 27 July 2007 – Although steatosis is a common histological feature in chronic hepatitis C (CHC), nonalcoholic steatohepatitis (NASH) has not yet been clearly characterized in this context. The aim of this prospective study was to investigate the characteristics of patients with NASH and CHC. Biopsies were categorized as CHC alone (178 patients [57%]), CHC+steatosis (94 patients [34%]), or CHC+NASH (24 patients [9%]).

Anna S. F. Lok, Brian J. McMahon – 27 July 2007

Francesco P. Russo, Yiannis N. Kallis, Malcolm R. Alison, Stuart J. Forbes – 27 July 2007

Jiun‐Ming Su, Xiang‐Me Lai, Keng‐Hsin Lan, Chung‐Pin Li, Yee Chao, Sang‐Hue Yen, Full‐Young Chang, Shou‐Dong Lee, Wei‐Ping Lee – 27 July 2007 – The X protein of hepatitis B virus (HBx) is essential for transactivation of hepatitis B viral and host cellular genes. It has been specifically implicated in the development of hepatocellular carcinoma; however, the molecular mechanism remains unknown.