Requirement for interleukin‐12 in the pathogenesis of warm hepatic ischemia/reperfusion injury in mice

Alex B. Lentsch, Hiroyuki Yoshidome, Atsushi Kato, Roscoe L. Warner, William G. Cheadle, Peter A. Ward, Michael J. Edwards – 30 December 2003 – Hepatic ischemia and reperfusion causes neutrophil‐dependent liver injury. Although the mechanisms of ischemia/reperfusion‐induced liver neutrophil recruitment are somewhat understood, less is known regarding the early events that initiate the inflammatory injury. Using a murine model of partial hepatic ischemia and reperfusion, we evaluated the role of endogenous interleukin (IL)‐12 in this inflammatory response.

Hypoxic stimulation of vascular endothelial growth factor expression in activated rat hepatic stellate cells

Victor Ankoma‐Sey, Yun Wang, Zhihao Dai – 30 December 2003 – The tissue repair response to hypoxic stimuli during wound healing includes enhanced production of angiogenic factors, such as vascular endothelial growth factor (VEGF). Hepatic stellate cells are oxygen‐sensing cells, capable of producing VEGF. We hypothesized that hypoxia‐stimulated signaling in activated stellate cells mediate VEGF secretion during liver injury.

In vitro evaluation of hepatitis B virus polymerase mutations associated with famciclovir resistance

Xiaofeng Xiong, Huiling Yang, Christopher E. Westland, Ruiming Zou, Craig S. Gibbs – 30 December 2003 – Several mutations (V521L, P525L, L528M, T532S, and V555I) in the gene for hepatitis B virus (HBV) polymerase have been identified in HBV isolated from patients that displayed break‐through viremia during famciclovir treatment.

Ischemic preconditioning protects the mouse liver by inhibition of apoptosis through a caspase‐dependent pathway

Surinder S. Yadav, David Sindram, David K. Perry, Pierre‐Alain Clavien – 30 December 2003 – A short period of ischemia and reperfusion, called ischemic preconditioning, protects various tissues against subsequent sustained ischemic insults. We previously showed that apoptosis of hepatocytes and sinusoidal endothelial cells is a critical mechanism of injury in the ischemic liver.

The transforming growth factor β1–inducible transcription factor, TIEG1, mediates apoptosis through oxidative stress

Afonso Ribeiro, Steven F. Bronk, Patricia J. Roberts, Raul Urrutia, Gregory J. Gores – 30 December 2003 – Transforming growth factor β1(TGF‐β1)–inducible transcription factors have recently elicited interest because of their critical role in the regulation of cell proliferation, differentiation, and apoptosis. We have previously reported that the TGF‐β1 –inducible transcription factor, TIEG1, induces apoptosis in a pancreas‐derived cell line. However, the mechanisms underlying the apoptotic effects of this transcription factor remain to be defined.

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