Reduced hepatic tumor incidence in cyclin G1‐deficient mice

Michael Rugaard Jensen, Valentina M. Factor, Anna Fantozzi, Kristian Helin, Chang‐Goo Huh, Snorri S. Thorgeirsson – 30 December 2003 – Cyclin G1 is a transcriptional target of the tumor suppressor p53, and its expression is increased after DNA damage. Recent data show that cyclin G1 can regulate the levels of p53 by a mechanism that involves dephosphorylation of Mdm2 by protein phosphatase 2A. To understand the biologic role of cyclin G1, we have generated cyclin G1‐deficient mice.

Endogenous IL‐13 protects hepatocytes and vascular endothelial cells during ischemia/reperfusion injury

Atsushi Kato, Tomohisa Okaya, Alex B. Lentsch – 30 December 2003 – Hepatic ischemia/reperfusion injury involves a complex inflammatory cascade resulting in neutrophil‐mediated injury of hepatocytes. Previous studies from our laboratory have established that exogenous administration of the anti‐inflammatory cytokines interleukin 10 (IL‐10) and IL‐13 can ameliorate the inflammatory response and significantly reduce hepatocellular injury.

Induction of cellular resistance against Kupffer cell–derived oxidant stress: A novel concept of hepatoprotection by ischemic preconditioning

Rolf J. Schauer, Alexander L. Gerbes, Daniel Vonier, Mark op den Winkel, Peter Fraunberger, Manfred Bilzer – 30 December 2003 – Ischemic preconditioning (IP) triggers protection of the liver from prolonged subsequent ischemia. However, the underlying protective mechanisms are largely unknown. We investigated whether and how IP protects the liver against reperfusion injury caused by Kupffer cell (KC)‐derived oxidants.

Increased lipopolysaccharide binding protein in cirrhotic patients with marked immune and hemodynamic derangement

Agustín Albillos, Antonio de la Hera, Mónica González, Jose‐Luis Moya, Jose‐Luis Calleja, Jorge Monserrat, Luis Ruiz‐del‐Arbol, Melchor Alvarez‐Mon – 30 December 2003 – Intestinal bacterial overgrowth and translocation, both common in cirrhosis with ascites, may lead to the activation of monocytes and lymphocytes, increased levels of proinflammatory cytokines, and enhanced synthesis of nitric oxide present in cirrhosis. Bacterial endotoxin promotes the synthesis of lipopolysaccharide (LPS)‐binding protein (LBP), and forms a LPS‐LBP complex that binds to CD14.

Mechanisms of hepatocyte protection against hypoxic injury by atrial natriuretic peptide

Rita Carini, Maria Grazia De Cesaris, Roberta Splendore, Cinzia Domenicotti, Maria Paola Nitti, Maria Adelaide Pronzato, Emanuele Albano – 30 December 2003 – Atrial natriuretic peptide (ANP) reduces ischemia and/or reperfusion damage in several organs, but the mechanisms involved are largely unknown. We used freshly isolated rat hepatocytes to investigate the mechanisms by which ANP enhances hepatocyte resistance to hypoxia.

Hydrogen peroxide overproduction in megamitochondria of troglitazone‐treated human hepatocytes

Shoichiro Shishido, Hironori Koga, Masaru Harada, Hiroto Kumemura, Shinichiro Hanada, Eitaro Taniguchi, Ryukichi Kumashiro, Hiromasa Ohira, Yukio Sato, Masayoshi Namba, Takato Ueno, Michio Sata – 30 December 2003 – Troglitazone has been withdrawn from therapeutic options for diabetes mellitus because of its severe hepatocyte toxicity of unknown pathogenesis. The aim of the present study was to assess both morphologic and functional alterations in the mitochondria of troglitazone‐treated hepatocytes. A polarized human hepatocyte cell line, OUMS‐29, was used in this study.

Clinical profile of autosomal dominant polycystic liver disease

Qi Qian, Airong Li, Bernard F. King, Patrick S. Kamath, Donna J. Lager, John Huston, Clarence Shub, Sonia Davila, Stefan Somlo, Vicente E. Torres – 30 December 2003 – Most reports on the natural history, manifestations, and treatment of polycystic liver disease are based on the disease as it manifests in patients with autosomal dominant polycystic kidney disease (ADPKD). The purpose of this study was to develop a clinical profile of isolated autosomal dominant polycystic liver disease (ADPLD) using nonaffected family members as controls.

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