Effect of the prokinetic agent, erythromycin, in the richardson ground squirrel model of cholesterol gallstone disease

Qi‐Wei Xu, R. Brent Scott, Daimen T. M. Tan, Eldon A. Shaffer – 30 December 2003 – Impaired gallbladder motility and delayed intestinal transit contribute to cholesterol gallstone formation by impeding the enterohepatic circulation of bile salts and causing gallbladder stasis. The therapeutic value of erythromycin, a prokinetic motilin analog, was evaluated in an animal model of gallstone formation. Eighty ground squirrels were fed either a trace‐ (control) or a high‐ (1%) cholesterol diet.

Parenchymal cell apoptosis as a signal for sinusoidal sequestration and transendothelial migration of neutrophils in murine models of endotoxin and fas‐antibody–induced liver injury

Judy A. Lawson, Michael A. Fisher, Carol A. Simmons, Anwar Farhood, Hartmut Jaeschke – 30 December 2003 – Endotoxin (ET) induces neutrophil sequestration in hepatic sinusoids, the activation of proinflammatory transcription factors (nuclear factor κB [NF‐κB]) with up‐regulation of adhesion molecules on sinusoidal endothelial cells and hepatocytes. However, if galactosamine (Gal) is co‐administered with ET, neutrophils transmigrate and attack parenchymal cells. This suggests that a signal from parenchymal cells triggers neutrophil transmigration.

The hepatitis B virus X protein up‐regulates tumor necrosis factor α gene expression in hepatocytes

Enrique Lara‐Pezzi, Pedro L. Majano, Marta Gómez‐Gonzalo, Carmelo García‐Monzón, Ricardo Moreno‐Otero, Massimo Levrero, Manuel López‐Cabrera – 30 December 2003 – Human hepatocytes infected by hepatitis B virus (HBV) produce the proinflammatory cytokine, tumor necrosis factor α (TNF‐α). In this study, we explored the mechanism of induction of TNF‐α synthesis by HBV. We found that the stable HBV‐transfected hepatoma cell line, 2.2.15, expressed high‐molecular‐weight (HMW) TNF‐α mRNAs, which were absent in the parent HepG2 cells.

Tumor necrosis factor primes hepatocytes for DNA replication in the rat

Eric M. Webber, Jordi Bruix, Robert H. Pierce, Nelson Fausto – 30 December 2003 – Signaling through tumor necrosis factor receptor type 1 (TNFR‐1) using a pathway that involves nuclear factor κB (NF‐κB), interleukin‐6 (IL‐6), and STAT3 is required for the initiation of liver regeneration. We have proposed that TNF primes hepatocytes to respond to the mitogenic effect of growth factors, but so far, there has been no experimental demonstration that TNF enhances growth factor responses of hepatocytes.

Interleukin‐6, hepatocyte growth factor, and their receptors in biliary epithelial cells during a type i ductular reaction in mice: Interactions between the periductal inflammatory and stromal cells and the biliary epithelium

Zejin Liu, Toshiki Sakamoto, Tsukasa Ezure, Shigeki Yokomuro, Noriko Murase, George Michalopoulos, Anthony J. Demetris – 30 December 2003 – The interleukin‐6 (IL‐6)/gp‐80 and hepatocyte growth factor (HGF)/met ligand/receptor systems have been shown to stimulate biliary epithelial cell (BEC) DNA synthesis in vitro. The mRNA and protein production of these two in vitro mitogens were mapped in vivo during the first week after bile duct ligation (BDL) when peak BEC DNA synthesis is seen.

Release of osmolytes from perfused rat liver on perivascular nerve stimulation: α‐adrenergic control of osmolyte efflux from parenchymal and nonparenchymal liver cells

Stephan Vom Dahl, Johannes Georg Bode, Roland Michael Reinehr, Irmhild Mönnighoff, Ralf Kubitz, Dieter Häussinger – 30 December 2003 – The effects of perivascular nerve stimulation and phenylephrine on osmolyte release were studied in the intact perfused rat liver and isolated liver parenchymal cells (PC) and nonparenchymal cells.

Kinetics of hepatitis B surface antigen–specific immune responses in acute and chronic hepatitis B or After HBs vaccination: Stimulation of the in vitro antibody response by interferon gamma

Wulf Otto Böcher, Sabine Herzog‐Hauff, Jörg Schlaak, Karl‐Hermann Meyer zum Büschenfelde, Hanns Friedrich Löhr – 30 December 2003 – Because cellular and humoral immune responses against the hepatitis B virus (HBV) surface antigen (HBs) might be crucial to overcome HBV infection, HBs‐specific B‐ and T‐cell responses of HBV patients and HBs vaccine recipients were analyzed quantitatively and functionally.

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