Cyclooxygenase‐2 promotes hepatocellular carcinoma cell growth through AKT activation: Evidence for AKT inhibition in celecoxib‐induced apoptosis

Jing Leng, Chang Han, A. Jake Demetris, George K. Michalopoulos, Tong Wu – 30 December 2003 – Cyclooxygenase‐2 (COX‐2)‐controlled prostaglandin (PG) metabolism recently has been implicated in the pathogenesis of hepatocellular carcinoma (HCC). However, the biologic role and molecular mechanism of COX‐2‐mediated PGs in the control of liver cancer growth have not been established. This study was designed to examine the direct effect of COX‐2 and its inhibitor celecoxib on the growth control of liver cancer cells.

Modulation of the outcome and severity of hepadnaviral hepatitis in woodchucks by antibodies to hepatic asialoglycoprotein receptor

Jingyu Diao, Darlene M. Slaney, Tomasz I. Michalak – 30 December 2003 – Viral hepatitis is frequently accompanied by humoral autoimmune responses toward both organ‐nonspecific and liver‐specific antigens, but contribution of these reactivities to liver injury remains unrecognized. Infection with woodchuck hepatitis virus (WHV) has been identified as a potent inducer of autoantibodies against asialoglycoprotein receptor (anti‐ASGPR), a molecule essentially unique to hepatocytes that mediates clearance of desialylated serum proteins.

A simple noninvasive index can predict both significant fibrosis and cirrhosis in patients with chronic hepatitis C

Chun‐Tao Wai, Joel K. Greenson, Robert J. Fontana, John D. Kalbfleisch, Jorge A. Marrero, Hari S. Conjeevaram, Anna S.‐F. Lok – 30 December 2003 – Information on the stage of liver fibrosis is essential in managing chronic hepatitis C (CHC) patients. However, most models for predicting liver fibrosis are complicated and separate formulas are needed to predict significant fibrosis and cirrhosis. The aim of our study was to construct one simple model consisting of routine laboratory data to predict both significant fibrosis and cirrhosis among patients with CHC.

Neutrophils aggravate acute liver injury during obstructive cholestasis in bile duct–ligated mice

Jaspreet S. Gujral, Anwar Farhood, Mary Lynn Bajt, Hartmut Jaeschke – 30 December 2003 – Obstruction of the common bile duct in a variety of clinical settings leads to cholestatic liver injury. An important aspect of this injury is hepatic inflammation, with neutrophils as the prominent cell type involved. However, the pathophysiologic role of the infiltrating neutrophils during cholestatic liver injury remains unclear.

Regulation of Ca2+ signaling in rat bile duct epithelia by inositol 1,4,5‐trisphosphate receptor isoforms

Keiji Hirata, Jean‐François Dufour, Kazunori Shibao, Roy Knickelbein, Allison F. O'Neill, Hans‐Peter Bode, Doris Cassio, Marie V. St‐Pierre, Nicholas F. LaRusso, M. Fatima Leite, Michael H. Nathanson – 30 December 2003 – Cytosolic Ca2+ (Cai2+) regulates secretion of bicarbonate and other ions in the cholangiocyte. In other cell types, this second messenger acts through Ca2+ waves, Ca2+ oscillations, and other subcellular Ca2+ signaling patterns, but little is known about the subcellular organization of Ca2+ signaling in cholangiocytes.

Predictors of HBeAg loss after lamivudine treatment for chronic hepatitis B

Robert P. Perrillo, Ching‐Lung Lai, Yun‐Fan Liaw, Jules L. Dienstag, Eugene R. Schiff, Solko W. Schalm, E. Jenny Heathcote, Nathaniel A. Brown, Mark Atkins, Mary Woessner, Stephen D. Gardner – 30 December 2003 – Elevated alanine transaminase (ALT) levels and low serum hepatitis B virus (HBV) DNA predict a higher likelihood of hepatitis B e antigen (HBeAg) loss in patients with chronic hepatitis B treated with interferon. Predictors of HBeAg loss in patients treated with lamivudine are not known.

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