H Koga, S Sakisaka, M Ohishi, M Sata, K Tanikawa – 30 December 2003 – It is uncertain whether or not apoptosis is involved in the pathogenesis of primary biliary cirrhosis (PBC). The aims of this study were to assess the nuclear DNA fragmentation and expression of Bcl‐2 in the biliary epithelial cells (BECs) and in the hepatocytes of PBC. Additionally, the effects of ursodeoxycholic acid (UDCA) on DNA fragmentation and Bcl‐2 expression in PBC were evaluated.

Timothy Pruett – 30 December 2003

Li Yin, Mingzeng Sun, Zoran Ilic, Hyam L. Leffert, Stewart Sell – 30 December 2003 – Liver progenitor cells (LPCs) cloned from adult rat livers following allyl alcohol injury express hematopoietic stem cell and early hepatic lineage markers when cultured on feeder layers; under these conditions, neither mature hepatocyte nor bile duct, Ito, stellate, Kupffer cell, or macrophage markers are detected. These phenotypes have remained stable without aneuploidy or morphological transformation after more than 100 population doublings.

Michael Frese, Verena Schwärzle, Kerstin Barth, Nicole Krieger, Volker Lohmann, Sabine Mihm, Otto Haller, Ralf Bartenschlager – 30 December 2003 – Persistent infection with hepatitis C virus (HCV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. All treatments known so far rely on the antiviral activity of interferon alfa (IFN‐α) that is given alone or in combination with ribavirin. Unfortunately, only a fraction of the patients clear the virus during therapy and for those who do not respond there is currently no alternative treatment.

Tuvia Gilat, Alicia Leikin‐Frenkel, Ilana Goldiner, Zamir Halpern, Fred M. Konikoff – 30 December 2003 – Gallstones, mostly cholesterol stones, affect some 15% of the population. Oral bile salts dissolve human cholesterol gallstones, but with low efficacy, and surgery remains the main therapeutic option. Fatty acid bile acid conjugates (FABACs) were shown to prevent formation of cholesterol gallstones in experimental animals. The aim of this study was to test whether these compounds could dissolve preexisting cholesterol gallstones via oral administration.

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.

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.

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.

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).

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.