Hidenari Nagai, Katsuhiko Matsumaru, Guoping Feng, Neil Kaplowitz – 30 December 2003 – The effect of reduced glutathione (GSH) depletion by acetaminophen (APAP), diethylmaleate (DEM), or phorone on the mode of cell death and susceptibility to tumor necrosis factor (TNF)‐induced cell death was studied in cultured mouse hepatocytes. Dose‐dependent necrosis was the exclusive mode of cell death with APAP alone, but the addition of TNF‐α induced a switch to about half apoptosis without changing total loss of viability.

José Such, Rubén Francés, Carlos Muñoz, Pedro Zapater, Juan A. Casellas, Ana Cifuentes, Francisco Rodríguez‐Valera, Sonia Pascual, Javier Sola‐Vera, Fernando Carnicer, Francisco Uceda, José M. Palazón, Miguel Pérez‐Mateo – 30 December 2003 – The current pathogenic theory of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis and ascites suggests that repeated episodes of bacterial translocation (BT) from intestinal lumen to mesenteric lymph nodes followed by systemic seeding are the key steps for the final development of infectious events.

J. Donald Ostrow, Lorella Pascolo, Claudio Tiribelli – 30 December 2003

Akihide Kamiya, Nobuhiko Kojima, Taisei Kinoshita, Yasuyuki Sakai, Atsushi Miyaijma – 30 December 2003 – Previously, we described that embryonic day 14.5 (E14.5) mouse fetal hepatocytes differentiate to express tyrosine amino transferase (TAT) and glucose‐6‐phosphatase, which are expressed in the perinatal liver, in response to oncostatin M (OSM) or in high‐cell‐density culture. However, under such conditions, fetal hepatic cells failed to express genes for adult liver‐specific enzymes, such as tryptophan oxygenase (TO).

Ju‐Seog Lee, Snorri S. Thorgeirsson – 30 December 2003 – Global gene expression profiles in cancer have impacted both classification of tumors and definition of molecular pathways in neoplasia. To explore the possibility of employing human tumor cell lines to obtain information on the functional genomics of the early stages of tumorigenesis, we have characterized variation in gene‐expression patterns in a cytogenetically well‐defined series of cell lines derived from human hepatocellular carcinoma (HCC). Microarrays containing 6,720 sequence‐verified human cDNAs were used in this study.

Liang Qiao, Adly Yacoub, Elaine Studer, Seema Gupta, Xin Yan Pei, Steven Grant, Philip B. Hylemon, Paul Dent – 30 December 2003 – The mechanisms by which bile acids induce apoptosis in hepatocytes and the signaling pathways involved in the control of cell death are not understood fully. Here, we examined the impact of mitogen‐activated protein kinase (MAPK) and phosphatidyl inositol 3‐kinase (PI3K) signaling on the survival of primary hepatocytes exposed to bile acids.

Michael Charlton, Raghavakaimal Sreekumar, Deborah Rasmussen, Keith Lindor, K. Sreekumaran Nair – 30 December 2003 – The pathophysiology of hepatic steatosis, a prerequisite of nonalcoholic fatty liver disease, is poorly understood. Because very‐low–density lipoprotein (VLDL) formation is the chief route of hepatic lipid export, we hypothesized that the synthesis of apoB‐100, a rate‐determining step in hepatic VLDL formation, may be altered in patients with nonalcoholic steatohepatitis (NASH).

Raleigh D. Kladney, Xiaoyen Cui, Gary A. Bulla, Elizabeth M. Brunt, Claus J. Fimmel – 30 December 2003 – GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant‐cell hepatitis (Gene 2000;249:53‐65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied.

Yun Ma, Manabu Okamoto, Mark G. Thomas, Dimitrios P. Bogdanos, Agnel R. Lopes, Bernard Portmann, James Underhill, Ralf Dürr, Giorgina Mieli‐Vergani, Diego Vergani – 30 December 2003 – Prevalence and clinical relevance of antibodies to soluble liver antigen (tRNP(Ser)Sec/SLA) in autoimmune hepatitis (AIH) have been investigated using partially purified or prokaryotically expressed antigen.

György Baffy, Chen‐Yu Zhang, Jonathan N. Glickman, Bradford B. Lowell – 30 December 2003 – Nonalcoholic fatty liver disease (NAFLD), a prevalent condition associated with obesity, has the potential of evolving into end‐stage liver disease. The biochemical mechanisms that define the progression of NAFLD are not well known, but reactive oxygen species (ROS) have been implicated in this process. Uncoupling protein (UCP) 2 is a mitochondrial inner‐membrane protein that mediates proton leak, uncouples adenosine triphosphate (ATP) synthesis, and negatively regulates ROS production.