Akinori Kasahara, Norio Hayashi, Kiyoshi Mochizuki, Masahide Takayanagi, Kentaro Yoshioka, Shinichi Kakumu, Akihiro Iijima, Akihiko Urushihara, Kendo Kiyosawa, Michiari Okuda, Keisuke Hino, Kiwamu Okita, Osaka Liver Disease Study Group – 30 December 2003 – To elucidate the risk factors for liver carcinogenesis and to examine the incidence of hepatocellular carcinoma (HCC) after interferon therapy, 1,022 chronic hepatitis C patients treated with interferon were followed by ultrasonography for 13 to 97 months (median 36 months).

Rathnagiri Polavarapu, Douglas R. Spitz, Julia E. Sim, Mark H. Follansbee, Larry W. Oberley, Amir Rahemtulla, Amin A. Nanji – 30 December 2003 – Increased hepatic oxidative stress with ethanol administration is hypothesized to be caused either by enhanced pro‐oxidant production or decreased levels of antioxidants or both. We used the intragastric feeding rat model to assess the relationship between hepatic antioxidant enzymes and pathological liver injury in animals fed different dietary fats.

E. Jenny Heathcote, Emmet B. Keeffe, Samuel S. Lee, Saya V. Feinman, Myron J. Tong, K. R. Reddy, Karsten Witt, Lawrence M. Blatt, Consensus Interferon Study Group – 30 December 2003 – A multicenter, open‐label, phase 3 study was conducted in 337 patients with chronic hepatitis C virus (HCV) infection who had either not responded to previous interferon therapy or had relapsed after discontinuation of therapy with either consensus interferon (9 μg) or interferon α‐2b (3 million U) three times a week for 24 weeks.

Emmet B. Keeffe, Sten Iwarson, Brian J. McMahon, Karen L. Lindsay, Raymond S. Koff, Michael Manns, Renate Baumgarten, Manfred Wiese, Marc Fourneau, Assad Safary, Ralf Clemens, David S. Krause – 30 December 2003 – Acute hepatitis A superimposed on chronic liver disease (CLD) has been associated with severe or fulminant hepatitis. An open, multicenter study was performed to compare the safety and immunogenicity of an inactivated hepatitis A vaccine in patients with CLD with that in healthy subjects.

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.

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.

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.

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.

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.

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.