E B Keeffe, F B Hollinger – 30 December 2003 – Chronic hepatitis C is an insidious disease associated with significant morbidity and mortality. Currently, the only approved therapies for chronic hepatitis C are the α interferons. Consensus interferon (CIFN) is a nonnatural, synthetic, recombinant type I interferon derived by assigning the most commonly observed amino acid in each position of several α interferon nonallelic subtypes to generate a consensus sequence. The efficacy and safety of CIFN in the treatment of chronic hepatitis C were assessed in two large phase 3 trials.

Jane Collier, Jenny Heathcote – 30 December 2003

Motoko Sasaki, Yasuni Nakanuma, Young S. Kim – 30 December 2003 – Mucin plays an important role in the development of hepatoliths, which are formed within the intrahepatic large bile ducts. To date, eight apomucins, components of mucin, have been identified.

Masahiro Arai, Satoshi Mochida, Akihiko Ohno, Shin Arai, Kenji Fujiwara – 30 December 2003 – Gut‐derived substances can activate Kupffer cells to provoke hepatic necrosis after partial hepatectomy in rats. A similar situation may occur during orthotopic liver transplantation (OLT), as congestion in the intestinal wall, caused by portal vein occlusion, is inevitable during the operation. The contribution of such substances to liver injury following OLT was investigated in rats.

Toshiyuki Maruyama, Shoji Kuwata, Kazuhiko Koike, Shiro Iino, Kiyomi Yasuda, Hiroshi Yotsuyanagi, Kyoji Moriya, Hisato Maekawa, Haruki Yamada, Yoichi Shibata, David R. Milich – 30 December 2003 – Precore hepatitis B virus (HBV) mutants may gradually prevail during or after seroconversion (SC) from hepatitis B e antigen (HBeAg) to hepatitis B e antigen antibody (anti‐HBe) status in many chronic hepatitis B (CH‐B) patients.

Nader Ghebranious, Stewart Sell – 30 December 2003 – The major risk factors for human liver cancer: hepatitis B virus (HBV) related liver injury, male gender, aflatoxin exposure, and p53 expression, are evaluated and compared in experimental transgenic mouse models. Transgenic mice that express hepatitis B surface antigen (HBsAg) in their liver and develop liver tumors at 18 months of age (HBV+ mice) were bred to p53 null mice (p53−/−) to produce mice p53+/−, HBV+ mice.

Alex B. Lentsch, Hiroyuki Yoshidome, William G. Cheadle, Frederick N. Miller, Michael J. Edwards – 30 December 2003 – Hepatic injury induced by ischemia and reperfusion is an important clinical problem after liver resection or transplantation. Neutrophils are known to mediate the organ injury, but the precise mechanisms leading to hepatic neutrophil recruitment are undefined. Two CXC chemokines, macrophage inflammatory protein‐2 (MIP‐2) and KC, are potently chemotactic for neutrophils in vitro and have been reported to be involved in neutrophil‐dependent inflammatory tissue injury.

Alexander Swidsinski, Michael Khilkin, Hartmut Pahlig, Sonja Swidsinski, Friedrich Priem – 30 December 2003 – The role of bacteria in gallstone formation could not be conclusively evaluated until bacterial presence or absence in a stone was consistently shown. Cultural bacteriologic investigations at the time of cholecystectomy, however, led to the assumption that cholesterol gallstones were free of bacteria.

Rebecca A. Schroeder, Jian S. Gu, Paul C. Kuo – 30 December 2003 – The multiple interlocking regulatory mechanisms that underlie induction of hepatocyte inducible nitric oxide synthase (iNOS) expression are largely unknown. Although previous work has indicated the requirement for multiple proinflammatory cytokines to induce hepatocyte NO production, investigators have recently shown that interleukin‐1β (IL‐1β) alone can initiate iNOS expression. In contrast, interferon gamma (IFN‐γ) serves as the sole initiating factor in other cell systems.

Jacob Wanon, France Guertin, Sylvain Brunet, Edgard Delvin, Victor Gavino, Daniel Bouthillier, Denis Lairon, Wagner Yotov, Emile Levy – 30 December 2003 – High‐density lipoprotein (HDL) participates in the transfer of cholesterol to the liver, in which it is subsequently excreted into bile as bile acid and cholesterol. In this study, the effect of essential fatty‐acid (EFA) deficiency on cholesterol contribution from HDL subfractions to bile was investigated. Rats that were rendered EFA‐deficient over 4 weeks displayed changes in their plasma HDL subfractions and liver tissue fatty acids.