30 December 2003

Malek Louha, Jérome Nicolet, Herve Zylberberg, Abdelmajid Sabile, Corinne Vons, Giovanna Vona, Karine Poussin, Monique Tournebize, Frédérique Capron, Stanislas Pol, Dominique Franco, Bernard Lacour, Christian Bréchot, Patrizia Paterlini‐Bréchot – 30 December 2003 – We have investigated whether liver resection and needle liver biopsy cause dissemination of liver cells into peripheral blood circulation, using a reverse‐transcription polymerase chain reaction (RT‐PCR)‐based assay targeted against α‐fetoprotein (AFP) mRNA.

Yasuo Yamaguchi, Kazutoshi Okabe, Fujio Matsumura, Eiji Akizuki, Teishi Matsuda, Hajime Ohshiro, Jian Liang, Shinwa Yamada, Katsutaka Mori, Michio Ogawa – 30 December 2003 – The role of nitric oxide (NO) on tissue injury of hepatic allografts during rejection remains controversial. We investigated inducible nitric oxide synthase (iNOS) expression and formation of peroxynitrite in ACI rat liver grafts implanted in recipients.

David L. Thomas – 30 December 2003

Charles‐Henry Cottart, Louis Do, Marie‐Céline Blanc, Michel Vaubourdolle, Geneviève Descamps, Dominique Durand, François‐Xavier Galen, Jean‐Pierre Clot – 30 December 2003 – The aim of this study was to evaluate the protective or deleterious effects of endogenous nitric oxide (NO) on liver cells during hepatic ischemia‐reperfusion (IR) in the rat. Injury to hepatocytes and endothelial cells was evaluated by determining cytolysis‐marker activity in plasma (alanine transaminase [ALT]; aspartate transaminase [AST]) and plasma hyaluronic acid (HA) concentration.

Marina Baptista, Anna Kramvis, Michael C. Kew – 30 December 2003 – The purpose of this study was to identify mutations in the basic core promoter and enhancer II region of the hepatitis B virus (HBV) that might cause the HBV e antigen (HBeAg)‐negative phenotype and contribute to hepatocarcinogenesis in black African carriers of the virus. The basic core promoter/enhancer II overlaps with the X gene. HBV DNA from serum of 47 asymptomatic carriers and 50 patients with hepatocellular carcinoma and from 28 tumor and 10 nontumor liver tissues was amplified and sequenced directly.

Elena R. García‐Trevijano, María J. Iraburu, Luis Fontana, José A. Domínguez‐Rosales, Anitra Auster, Amador Covarrubias‐Pinedo, Marcos Rojkind – 30 December 2003 – Oxidative stress plays a key role in liver fibrosis. Both inflammatory cells and activated Kupffer cells produce H2O2, an oxidant involved in the activation of hepatic stellate cells (HSC). Increased production of reactive oxygen intermediates (ROIs) in fibrotic livers is associated in part with the up‐regulation of transforming growth factor β (TGF‐β), and this cytokine enhances collagen production by cultured HSC.

Vincent M. Christoffels, Habib Sassi, Jan M. Ruijter, Antoon F. Moorman, Thierry Grange, Wouter H. Lamers – 30 December 2003 – In the liver, genes are expressed along a portocentral gradient. Based on their adaptive behavior, a gradient versus compartment type, and a dynamic versus stable type of gradient have been recognized. To understand at least in principle the development and maintenance of these gradients in gene expression in relation to the limited number of signal gradients, we propose a simple and testable model.

Dae‐Ghon Kim, Dae‐yeol Lee, Baik‐Hwan Cho, Kyung‐Ran You, Mi‐Young Kim, Deuk‐Soo Ahn – 30 December 2003 – We observed that all‐trans‐retinoic acid (RA) down‐regulated insulin‐like growth factor binding proteins (IGFBPs) in cultured human hepatoma cells (Hep 3B, PLC/PRF/5, and Hep G2); therefore, we characterized the role of this down‐regulation in cell growth. Treatment with 10 μmol/L RA revealed a rapid decrease in IGFBP‐3 within 2 days, and continued treatment with RA for 6 days resulted in a time‐dependent stimulation of Hep 3B cell growth.

Claus‐Thomas Bock, Stefan Kubicka, Michael Peter Manns, Christian Trautwein – 30 December 2003 – Natural occurring mutations in the preS‐region are frequently found during chronic hepatitis B virus (HBV) infection. Here we used the mutated preS‐region from a patient to study the transcriptional regulation of the S‐promoter. The mutations were a CCAAT‐box (MUT1) point mutation, a 6‐base pair (bp) deletion (MUT2) 3′ of the CCAAT‐box, and a 153 bp deletion (MUT3) in the preS2 genome.