Michelle Martinot‐Peignoux, Nathalie Boyer, Dominique Cazals‐Hatem, Bach‐Nga Pham, Anne Gervais, Véronique Le Breton, Stéphane Levy, Claude Degott, Dominique‐Charles Valla, Patrick Marcellin – 30 December 2003 – A significant proportion of patients with detectable antibodies to hepatitis C virus have normal serum alanine transaminase levels. Our aim was to study the outcome of this group.

Satheesh Nair, Robert P. Perrillo – 30 December 2003 – During interferon treatment of chronic hepatitis B, an alanine aminotransferase (ALT) flare may herald a sustained loss of viral replication, but the relationship between virologic response, the extent of a flare, and pretreatment hepatitis B virus (HBV) DNA level has not been defined. We retrospectively examined the impact of an ALT flare on sustained virologic response in 121 interferon‐treated patients and 42 untreated controls with either low‐level (<100 pg/mL) or high‐level (≥100 pg/mL) viremia.

Patricia Boya, Esther Larrea, Iosu Sola, Pedro‐Lorenzo Majano, Carlos Jiménez, María‐Pilar Civeira, Jesús Prieto – 30 December 2003 – The mechanisms of liver damage in chronic hepatitis C virus (HCV) infection are poorly understood. The transcription factor, nuclear factor‐κB (NF‐κB), regulates the expression of genes involved in apoptosis, inflammation, and antiviral response. It plays a protective role in several forms of liver damage.

Carmen Peralta, Ramón Bartrons, Anna Serafin, Cristina Blázquez, Manuel Guzmán, Neus Prats, Carme Xaus, Blanca Cutillas, Emilio Gelpí, Joan Roselló‐Catafau – 30 December 2003 – Hepatic ischemia‐reperfusion (I/R) injury associated with liver transplantation and hepatic resections are an unresolved problem in the clinical practice. Preconditioning is known to preserve energy metabolism in liver during sustained ischemia, but the molecular mechanisms underlying this effect are still unclear.

Diana M. Toivola, Mikko I. Nieminen, Michael Hesse, Tao He, Hélène Baribault, Thomas M. Magin, M. Bishr Omary, John E. Eriksson – 30 December 2003 – Simple epithelial tissues such as liver and pancreas express keratins 8 (K8) and 18 (K18) as their major intermediate filament proteins. K8 and K1 null mice and transgenic mice that express mutant K18 (K18C) manifest several hepatocyte abnormalities and demonstrate that K8/18 are important in maintaining liver tissue and cell integrity, although other potential functions remain uncharacterized.

Anna S. F. Lok, Brian J. McMahon – 30 December 2003

Javier Crespo, Amalía Cayón, Pedro Fernández‐Gil, Manuel Hernández‐Guerra, Marta Mayorga, Agustín Domínguez‐Díez, José Carlos Fernández‐Escalante, Fernando Pons‐Romero – 30 December 2003 – The main objective of this study was to analyze the pathogenic role of the tumor necrosis factor α (TNF‐α) system in the development of nonalcoholic steatohepatitis (NASH). Fifty‐two obese patients were studied.

Yoshiya Tahashi, Koichi Matsuzaki, Masataka Date, Katsunori Yoshida, Fukiko Furukawa, Yasushi Sugano, Masanori Matsushita, Yasuo Himeno, Yutaka Inagaki, Kyoichi Inoue – 30 December 2003 – During chronic liver injury, transforming growth factor β (TGF‐β) plays a prominent role in stimulating liver fibrogenesis by myofibroblast‐like cells derived from hepatic stellate cells (HSCs). On the other hand, Smad 7 was recently shown to antagonize the TGF‐β–induced activation of signal‐transducing Smads (2 and 3).

Satheesh Nair, Sumita Verma, Paul J. Thuluvath – 30 December 2003 – Studies assessing morbidity and mortality in obese patients undergoing orthotopic liver transplantation (OLT) have produced conflicting results, mainly because of the small sample size. The objective of our study was to determine graft and patient survival in obese adults receiving OLT in the U.S. between 1988 through 1996 using the United Network for Organ Sharing (UNOS) database. Among the 23,675 transplantations performed during the 9‐year study period, 18,172 (75%) patients fulfilled the inclusion criteria.

Toshiaki Ninomiya, Koichiro Mihara, Kazuo Fushimi, Yoshitake Hayashi, Tomoko Hashimoto‐Tamaoki, Taiki Tamaoki – 30 December 2003 – We investigated mechanisms regulating expression of α‐fetoprotein (AFP) in 3 human hepatoma cell lines, HuH‐7, HepG2, and huH‐1, producing high, medium, and low levels of AFP, respectively. The silencer, a negative cis‐acting element of the AFP gene, was highly activated in huH‐1 and HepG2 to repress AFP enhancer activity by 91%, whereas only 26% repression was observed in HuH‐7.