Sven Jonas, Wolf O. Bechstein, Thomas Steinmüller, Martin Herrmann, Cornelia Radke, Thomas Berg, Utz Settmacher, Peter Neuhaus – 30 December 2003 – Selection of patients suffering from hepatocellular carcinoma (HCC) in cirrhosis for liver transplantation follows limits of number and diameter of tumor nodules. It has not been investigated whether there is a correlation of these parameters with vascular invasion. From 1989 to 2000, 1,188 liver transplantations were performed in 1,087 patients, including 120 patients (11%) with an HCC in cirrhosis.

Masashi Emoto, Mamiko Miyamoto, Yoshiko Emoto, Jens Zerrahn, Stefan H.E. Kaufmann – 30 December 2003 – Although it is generally assumed that T‐cell receptor (TCR) γ/δ cells participate in protection against intracellular microbial pathogens, their impact remains controversial. In our study, young (14‐day‐old) mice lacking TCRγ/δ cells were far more susceptible to Listeria monocytogenes than wild‐type (WT) mice of the same age.

Jeremy Woodward, James Neuberger – 30 December 2003

François P. Sarasin, Pietro E. Majno, Josep M. Llovet, Jordi Bruix, Gilles Mentha, Antoine Hadengue – 30 December 2003 – Cadaveric liver transplantation (CLT) is an excellent treatment for early hepatocellular carcinoma (HCC). Its use, however, is limited by the shortage of grafts, with up to 30% of patients developing contraindications to the procedure while waiting for a donor. Living donor liver transplantation (LDLT) has emerged as an alternative to overcome this limitation.

Robert A. DeAngelis, Kellen Kovalovich, Drew E. Cressman, Rebecca Taub – 30 December 2003 – Nuclear factor κB (NF‐κB) is rapidly activated during liver regeneration following partial hepatectomy or carbon tetrachloride (CCl4)‐mediated liver injury and is felt to be important in the antiapoptotic and regenerative responses. After partial hepatectomy, livers of mice deficient in the p50 subunit of NF‐κB (p50−/−) showed a loss of NF‐κB and decreased STAT3 transcription factor DNA binding activities.

Cynthia R. L. Webster, M. Sawkat Anwer – 30 December 2003 – We have previously shown that cAMP protects against hydrophobic bile acid‐induced apoptosis in cultured rat hepatocytes through pathways dependent on activation of phosphoinositide 3‐kinase and inhibition of mitogen activated protein kinase. Hepatocyte growth factor protects epithelial cells against apoptosis and activates both of these kinases in hepatocytes.

Leland J. Yee, Jianming Tang, Andrew W. Gibson, Robert Kimberly, Dirk J. van Leeuwen, Richard A. Kaslow – 30 December 2003 – Host genetic factors have been reported to influence the natural history of hepatitis C virus (HCV) infection. We examined whether variation in interleukin 10 (IL‐10) and tumor necrosis factor α (TNF‐α) genes would predict the likelihood of sustained response to antiviral therapy. Single nucleotide polymorphisms (SNPs) and microsatellites at two loci encoding the cytokines IL‐10 and TNF‐α were determined by polymerase chain reaction (PCR)‐based techniques.

Martin Volkmann, Lore Martin, Andrea Bäurle, Hans Heid, Christian P. Strassburg, Christian Trautwein, Walter Fiehn, Michael P. Manns – 30 December 2003 – Autoantibodies to soluble liver antigen (SLA) are considered a specific marker of autoimmune hepatitis. We have performed immunoscreening of a human liver gene expression library with an anti‐SLA—positive serum.

Robert S. Brown, John R. Lake, Nancy L. Ascher, Jean C. Emond, John P. Roberts – 30 December 2003 – Background. Orthotopic liver transplantation (OLT) is a highly effective but costly therapy for end‐stage liver disease. However, there are limited data on the demographic and clinical variables that affect cost. We undertook a preliminary study using multiple regression techniques to analyze factors that influence the cost of OLT.

Birgit Kallinowski, Christine Buhrmann, Stefanie Seipp, Tobias Goeser, Wolfgang Stremmel, Gerd Otto, Lorenz Theilmann – 30 December 2003 – A novel RNA virus of the Flaviviridae family has been discovered recently and designated hepatitis GB‐C virus (GBV‐C). Previous studies have reported that GBV‐C is associated with posttransfusion hepatitis, chronic viral hepatitis, and cryptogenic hepatitis. However, the clinical significance of GBV‐C infection has been questioned increasingly in patients not undergoing transplantation.