Giovanni Corrao, Sarino Aricò – 30 December 2003 – Although alcohol intake and hepatitis C virus (HCV) infection are the major determinants of liver cirrhosis (LC) in Western countries, the joint effect of these two factors on LC risk has not yet been adequately studied. We used data from two hospital‐based case‐control studies performed in Italy. Cases were 285 cirrhotic patients admitted for the first time to district hospitals for liver decompensation.

Sheng‐Li Zhou, Ronald E. Gordon, Michael Bradbury, Decherd Stump, Chih‐Li Kiang, Paul D. Berk – 30 December 2003 – To explain the increased plasma mitochondrial aspartate aminotransferase (mAspAT) observed in alcoholics, we cultured HepG2 hepatoma cells in ethanol. Acute (24 hour) exposure to 0, 20, 40, or 80 mmol/L ethanol produced a dose‐dependent (r = .98) increase in mAspAT messenger RNA (mRNA) of ≤ thirteen‐fold, with no significant change in the cellular content of mAspAT or of several other enzymes.

Arno Kalkuhl, Jacob Troppmair, Albrecht Buchmann, Stefan Stinchcombe, Christoph Lars Buenemann, Ulf R. Rapp, Klaus Kaestner, Michael Schwarz – 30 December 2003 – Mouse liver tumors frequently harbor activating ras gene mutations. Downstream effector molecules of p21Ras include Raf‐1 kinase which mediates external signals via kinase signaling pathways to nuclear transcription factors including c‐Fos and c‐Jun. Mouse liver tumors with differing ras‐mutational status were analyzed for alterations in Ras/Raf‐1 signal transduction.

Richard A. Weisiger – 30 December 2003

Pablo R. Ros, Gary L. Davis – 30 December 2003

Hidetsugu Saito, Hirotoshi Ebinuma, Masahiko Takahashi, Fumihiko Kaneko, Kanji Wakabayashi, Mitsuyasu Nakamura, Hiromasa Ishii – 30 December 2003 – We have demonstrated that sodium butyrate induces differentiation in human hepatoma cells; however, recent studies have shown that this agent causes apoptosis in some types of cancer cells. In this study, we examined whether sodium butyrate causes apoptosis in the human hepatoma cell lines, HCC‐M and HCC‐T. The growth of human hepatoma cells was dose‐dependently reduced by sodium butyrate.

Timothy S. Walsh, Patrick Hopton, Barbara J. Philips, Simon J. Mackenzie, Alistair Lee – 30 December 2003 – We have investigated the effect of N‐acetylcysteine on hemodynamic variables, oxygen delivery (Do2), oxygen consumption (Vo2), and oxygen extraction in patients with fulminant hepatic failure using independent methods of determining Do2 and Vo2, thereby eliminating the effect of mathematical coupling, which may have biased previous studies.

Kenneth L. Tyler, Ronald J. Sokol, Stephanie M. Oberhaus, Mysan Le, Frederick M. Karrer, Michael R. Narkewicz, R. Weslie Tyson, James R. Murphy, Robert Low, William R. Brown – 30 December 2003 – Extrahepatic biliary atresia (EHBA) and choledochal cysts (CDC) are important causes of obstructive jaundice in pediatric patients. Viruses in general, and reoviruses in particular, have long been considered as possible etiologic agents responsible for inciting the inflammatory process that leads to these infantile obstructive cholangiopathies.

Sabrina Brambilla, Giorgio Bellati, Margherita Asti, Antonella Lisa, Maria Elena Candusso, Maria D'Amico, Gabriele Grassi, Mauro Giacca, Angelo Franchini, Savino Bruno, Gaetano Ideo, Mario U. Mondelli, Enrico M. Silini – 30 December 2003 – Hepatitis C virus (HCV) infection is a dynamic process during which molecular variants are continously selected as the result of virus adaptation to the host. Understanding the nature of HCV genetic variation is central to current theories of pathogenesis and immune response.

Masaki Hattori, Kentaro Yoshioka, Toshiyuki Aiyama, Kazuo Iwata, Yasuyuki Terazawa, Masatoshi Ishigami, Motoyoshi Yano, Shinichi Kakumu – 30 December 2003 – To clarify the nature of serum anti‐hypervariable region 1 (HVR1) antibodies in patients infected with hepatitis C virus (HCV), we assessed the reactivity of 21 patients' sera with 42 HVR1 proteins by Western blot. HVR1 was expressed as fusion proteins with glutathione S‐transferase (GST). The patients' sera reacted with variable percentages of the HVR1 proteins, and always reacted with HVR1 proteins of the different genotype.