Electric foot shock stress‐induced exacerbation of α‐galactosylceramide–triggered apoptosis in mouse liver

Yoichi Chida, Nobuyuki Sudo, Junko Sonoda, Hiroshi Sogawa, Chiharu Kubo – 25 March 2004 – Recently, liver natural killer T (NKT) cells, which are specifically stimulated by α‐galactosylceramide (α‐GalCer), were found to play a critical role in intrahepatic immunity to several infections and certain hepatic disorders. However, the role of psychophysical stress on NKT cell–dependent liver injury induced by α‐GalCer still remains to be elucidated.

Sinusoidal endothelial cell and hepatocyte death following cold ischemia‐warm reperfusion of the rat liver

Pierre‐Michel Huet, Marcia R. Nagaoka, Geneviève Desbiens, Esther Tarrab, Antoine Brault, Marie‐Pierre Bralet, Marc Bilodeau – 25 March 2004 – Cold ischemia‐warm reperfusion (CI‐WR) injury of the liver is characterized by marked alterations of sinusoidal endothelial cells (SECs), whereas hepatocytes appear to be relatively unscathed. However, the time course and mechanism of cell death remain controversial: early versus late phenomenon, necrosis versus apoptosis?

Variation of hepatic glucuronidation: Novel functional polymorphisms of the UDP‐glucuronosyltransferase UGT1A4

Ursula Ehmer, Arndt Vogel, Jan Karl Schütte, Britta Krone, Michael P. Manns, Christian P. Strassburg – 25 March 2004 – UDP‐glucuronosyltransferases are a family of drug metabolizing enzymes contributing to hepatic drug metabolism and protection against environmental toxins. The aim of this study was to identify polymorphisms at the human UGT1A gene locus and to characterize their function and potential association with hepatocellular carcinoma (HCC).

Abnormal hepatocystin caused by truncating PRKCSH mutations leads to autosomal dominant polycystic liver disease

Joost P. H. Drenth, Esa Tahvanainen, Rene H. M. te Morsche, Pia Tahvanainen, Helena Kääriäinen, Krister Höckerstedt, Jiddeke M. van de Kamp, Martijn H. Breuning, Jan B. M. J. Jansen – 25 March 2004 – Mutations in protein kinase C substrate 80K‐H (PRKCSH), encoding for the protein hepatocystin, cause autosomal dominant polycystic liver disease (PCLD), which is clinically characterized by the presence of multiple liver cysts. PCLD has been documented in families from Europe (Netherlands, Belgium, Finland) as well as from the United States.

Treatment of chronic hepatitis C in HIV/HCV‐coinfection with interferon α‐2b+ full‐course vs. 16‐week delayed ribavirin

Norbert Bräu, Maribel Rodriguez‐Torres, Dale Prokupek, Maurizio Bonacini, Carol A. Giffen, Jeffery J. Smith, Kevin R. Frost, Jay R. Kostman – 25 March 2004 – Human immunodeficiency virus (HIV)‐infected patients increasingly experience the consequences of chronic hepatitis C virus (HCV) coinfection. This trial randomized 107 patients coinfected with HIV and HCV to receive 48 weeks of interferon alfa‐2b (IFN) 3 million units three times weekly plus either a full course of ribavirin (RBV) at 800 mg/day (group A; n = 53) or 16 weeks of placebo, followed by RBV (group B; n = 54).

Progression of HCC in mice is associated with a downregulation in the expression of hepatocyte nuclear factors

Natalia L. Lazarevich, Oksana A. Cheremnova, Ekaterina V. Varga, Dmitry A. Ovchinnikov, Elena I. Kudrjavtseva, Olga V. Morozova, Daria I. Fleishman, Natalia V. Engelhardt, Stephen A. Duncan – 25 March 2004 – Hepatocyte nuclear factors (HNF) play a critical role in development of the liver. Their roles during liver tumorigenesis and progression of hepatocellular carcinomas (HCC) are, however, poorly understood.

Coordinate expression of regulatory genes differentiates embryonic and perinatal forms of biliary atresia

Dong‐Yi Zhang, Gregg Sabla, Pranavkumar Shivakumar, Greg Tiao, Ronald J. Sokol, Cara Mack, Benjamin L. Shneider, Bruce Aronow, Jorge A. Bezerra – 25 March 2004 – The molecular basis for the embryonic and perinatal clinical forms of biliary atresia is largely undefined. In this study, we aimed to: 1) determine if the clinical forms can be differentiated at the transcriptional level, and 2) search for molecular mechanisms underlying phenotypic differences.

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