Itsuki Ajioka, Toshihiro Akaike, Yoshifumi Watanabe – 30 December 2003 – A complex vascular network forms an important component of the liver architecture. This network is essential for the supply of oxygen and nutrients to cells and delivery of molecules for metabolic exchange. In this study, we attempted to construct a vascular network in transplanted hepatic tissues and examined the effect of such network on tissue formation.

Andrew L. Mason, Johnson Y. Lau, Nicole Hoang, KePing Qian, Graeme J. Alexander, Lizhe Xu, Linsheng Guo, Sheraj Jacob, Fredric G. Regenstein, Robert Zimmerman, James E. Everhart, Clive Wasserfall, Noel K. Maclaren, Robert P. Perrillo – 30 December 2003 – While patients with liver disease are known to have a higher prevalence of glucose intolerance, preliminary studies suggest that hepatitis C virus (HCV) infection may be an additional risk factor for the development of diabetes mellitus.

Tsutomu Masaki, Masato Okada, Masaki Tokuda, Yasushi Shiratori, Osamu Hatase, Mutsunori Shirai, Mikio Nishioka, Masao Omata – 30 December 2003 – The proto‐oncogene product pp60c‐src is the cellular homologue of the Rous sarcoma transforming gene, and it is a non–receptor‐linked and membrane‐associated tyrosine kinase. There is a close correlation between elevated pp60c‐src activity and cell transformation. We have recently reported that pp60c‐src was activated in hepatocellular carcinoma (HCC) of human and Long‐Evans cinnamon (LEC) rats.

Michael Friedt, Patrick Gerner, Ekkehart Lausch, Hubert Trübel, Bernhard Zabel, Stefan Wirth – 30 December 2003 – The involvement of precore stop codon 1896‐A and base exchanges in the AT‐rich region at positions 1762 and 1764 of the hepatitis B core promotor has been controversely discussed in adults with fulminant hepatitis B. Because no data are currently available on children, we analyzed the basic core promotor (BCP) and precore region in children with chronic and fulminant hepatitis B. The BCP and precore region were sequenced directly and after cloning from mothers and infants.

Andrea Galli, Donna Price, David Crabb – 30 December 2003 – The mechanisms by which ethanol causes fatty liver are complex. Reducing equivalents generated during ethanol oxidation inhibit tricarboxylic acid cycle activity and fatty acid oxidation. In addition, ethanol inhibits lipoprotein export and increases fatty acid uptake and lipid peroxidation. To test the role that alcohol metabolism by alcohol dehydrogenase (ADH) has on cellular lipid metabolism, a cell line expressing rat ADH was generated by transducing HeLa cells with an ADH‐expressing retrovirus.

Adam F. Steinlauf, Guadalupe Garcia‐Tsao, Maram F. Zakko, Kevin Dickey, Tarun Gupta, Roberto J. Groszmann – 30 December 2003 – The hepatic venous pressure gradient (HVPG) is becoming increasingly used clinically. It is useful in the differential diagnosis of portal hypertension and provides a prognostic index in cirrhotic patients. Performance of serial measurements has been shown to be useful in guiding pharmacological therapy of portal hypertension and variceal hemorrhage. The technique is safe to perform; however, many patients are anxious and reluctant to undergo serial measurements.

Stephen J. Polyak, Denise M. Paschal, Susan McArdle, Michael J. Jr., Darius Moradpour, David R. Gretch – 30 December 2003 – The hepatitis C virus (HCV) nonstructural 5A (NS5A) protein has been implicated in the inherent resistance of HCV to interferon (IFN) antiviral therapy in clinical studies. Biochemical studies have demonstrated that NS5A interacts in vitro with and inhibits the IFN‐induced, RNA‐dependent protein kinase, PKR, and that NS5A interacts with at least one other cellular kinase.

Margaret James Koziel – 30 December 2003

James Neuberger, Bridget Gunson, Piyawat Komolmit, Mervyn H. Davies, Erik Christensen – 30 December 2003 – Liver transplantation remains the only treatment for patients with end‐stage primary sclerosing cholangitis (PSC); however, selection criteria for the procedure and its timing remains uncertain. The aim of this study was to identify pretransplant variables associated with survival after transplantation and to devise a Cox regression model for prediction of post‐transplant survival.

R. Brian Doctor, Rolf H. Dahl, Kelli D. Salter, J. Gregory Fitz – 30 December 2003 – Cholangiocytes contribute significantly to bile formation through the vectorial secretion of water and electrolytes and are a focal site of injury in a number of diseases including liver ischemia and post‐transplantation liver failure. Using ischemia in intact liver and adenosine triphosphate (ATP) depletion in cultured cells to model cholangiocyte injury, these studies examined the effects of metabolic inhibition on cholangiocyte viability and structure.