Makoto Asamoto, Naomi Hokaiwado, Toshiya Murasaki, Tomoyuki Shirai – 30 June 2004 – Connexins are subunits of gap junction channels, which allow direct transfer of ions, secondary messenger molecules, and other metabolites between contacting cells. Gap junctions are believed to be involved in tissue homeostasis, embryonic development, and control of cell proliferation. Several studies have shown that cell damage signals are transmitted through gap junctions when cells are irradiated or when cells bearing the herpes simplex virus‐thymidine kinase (HSV‐TK) gene are treated with ganciclovir.

Ariel E. Feldstein, Nathan W. Werneburg, Ali Canbay, Maria Eugenia Guicciardi, Steven F. Bronk, Robert Rydzewski, Laurence J. Burgart, Gregory J. Gores – 30 June 2004 – Nonalcoholic fatty liver disease (NAFLD) is a serious health problem. Although NAFLD represents a form of lipotoxicity, its pathogenesis remains poorly understood. The aim of this study was to examine the cellular mechanisms involved in free fatty acid (FFA)‐mediated hepatic lipotoxicity.

Neil Kaplowitz – 30 June 2004

Barry H. Rumack – 30 June 2004 – Examination of the pharmacokinetics of acetaminophen can decrease misconceptions involved in clinical evaluation. Enzyme patterns and acetaminophen levels must be related to time and known metabolic phenomena. A careful look at ethanol and nutrition, especially fasting demonstrates that therapeutic doses of acetaminophen do not place patients at a greater risk in either of these instances. An overdose of acetaminophen in a chronic alcohol abuser may result in more severe hepatotoxicity than in the nonalcoholic.

Johannes Wiegand, Elmar Jäckel, Markus Cornberg, Holger Hinrichsen, Manfred Dietrich, Julian Kroeger, Wolfgang P. Fritsch, Anne Kubitschke, Nuray Aslan, Hans L. Tillmann, Michael Peter Manns, Heiner Wedemeyer – 30 June 2004 – Early treatment of acute hepatitis C infection with interferon alfa‐2b (IFN‐α‐2b) prevents chronicity in almost all patients. So far, no data are available on the long‐term outcome after interferon (IFN) therapy of acute hepatitis C.

Michael Schepke, Gerhard Kleber, Dieter Nürnberg, Jörg Willert, Lydia Koch, Wilfried Veltzke‐Schlieker, Claus Hellerbrand, Johannes Kuth, Stefan Schanz, Stefan Kahl, Wolfgang E. Fleig, Tilman Sauerbruch – 30 June 2004 – In this randomized controlled multicenter trial, we compared endoscopic variceal banding ligation (VBL) with propranolol (PPL) for primary prophylaxis of variceal bleeding. One hundred fifty‐two cirrhotic patients with 2 or more esophageal varices (diameter >5 mm) without prior bleeding were randomized to VBL (n = 75) or PPL (n = 77).

Patrick Marcellin, Herve Mommeja‐Marin, Stephen L. Sacks, George K. K. Lau, Daniel Sereni, Jean‐Pierre Bronowicki, Brian Conway, Christian Trepo, M. Robert Blum, Byung Chul Yoo, Elsa Mondou, Jeff Sorbel, Andrea Snow, Franck Rousseau, Hyo‐Suk Lee – 30 June 2004 – Current therapies available for the treatment of chronic hepatitis B are limited in their ability to result in a cure. Clevudine is a new pyrimidine analog with potent anti‐hepatitis B virus (HBV) activity in vitro. A multicenter dose‐escalation study evaluated clevudine at 10, 50, 100, and 200 mg once daily for 28 days.

James G. Orr, Val Leel, Gary A. Cameron, Carylyn J. Marek, Emma L. Haughton, Lucy J. Elrick, Julie E. Trim, Gabrielle M. Hawksworth, Andrew P. Halestrap, Matthew C. Wright – 30 June 2004 – Gliotoxin has been shown to promote a reversal of liver fibrosis in an animal model of the disease although its mechanism of action in the liver is poorly defined. The effects of gliotoxin on activated hepatic stellate cells (HSCs) and hepatocytes have therefore been examined.

30 June 2004

Gavin E. Arteel – 30 June 2004 – Angiotensin II (AngII) is a pro‐oxidant and fibrogenic cytokine. We investigated the role of NADPH oxidase in AngII‐induced effects in hepatic stellate cells (HSCs), a fibrogenic cell type. Human HSCs express mRNAs of key components of nonphagocytic NADPH oxidase. AngII phosphorylated p47phox, a regulatory subunit of NADPH oxidase, and induced reactive oxygen species formation via NADPH oxidase activity. AngII phosphorylated AKT and MAPKs and increased AP‐1 DNA binding in a redox‐sensitive manner.