Snorri S. Thorgeirsson – 7 March 2007 – Hepatocellular carcinoma (HCC) is a leading cause of cancerrelated deaths worldwide. Here, we provide evidence that the Forkhead Box (Fox) m1b (Foxm1b or Foxm1) transcription factor is essential for the development of HCC. Conditionally deleted Foxm1b mouse hepatocytes fail to proliferate and are highly resistant to developing HCC in response to a Diethylnitrosamine (DEN)/Phenobarbital (PB) liver tumor‐induction protocol.

Marcin T. Kortylewski, Andreas Barthel – 7 March 2007 – The transcription factor, signal transducer and activator of transcription‐3 (STAT‐3) contributes to various physiological processes. Here we show that mice with liver‐specific deficiency in STAT‐3, achieved using the Cre‐loxP system, show insulin resistance associated with increased hepatic expression of gluconeogenic genes. Restoration of hepatic STAT‐3 expression in these mice, using adenovirus‐mediated gene transfer, corrected the metabolic abnormalities and the alterations in hepatic expression of gluconeogenic genes.

Young‐Soo Kim, Robert F. Schwabe, Ting Qian, John J. Lemasters, David A. Brenner – 7 March 2007 – Tumor necrosis factor (TNF)‐related apoptosis‐inducing ligand (TRAIL) induces apoptosis in a wide range of malignant cells. However, several cancers, including human hepatoma, are resistant to TRAIL. In this study, we analyzed TRAIL‐induced pro‐ and antiapoptotic signaling pathways in human hepatoma cells. Nuclear factor k B (NF‐kB) was found to be a critical TRAIL‐induced antiapoptotic factor in the PLC/PRF/5, HepG2, and Hep3B cell lines.

Hauke Rensing, Inge Bauer, Jian X. Zhang, Markus Paxian, Benedikt H. J. Pannen, Yukihiro Yokoyama, Mark G. Clemens, Michael Bauer – 7 March 2007 – Heme oxygenase (HO)‐1 is up‐regulated after ischemia/reperfusion and contributes to maintenance of hepatic perfusion and integrity. Blockade of HO‐1 leads to an increased portal pressor response in the stress‐exposed liver. We tested whether the increase in portal pressure reflects unmasking of a concomitant up‐regulation of the vasoconstrictor endothelin (ET)‐1.

Timothy J. Davern, Steven Galson – 7 March 2007

Florian Kuchenbauer, Christian P. Strassburg, Arndt Vogel, Wolfgang Hiddemann, Ulrich Beuers – 7 March 2007

Feng Hong, Svetlana Radaeva, Hong‐Na Pan, Zhigang Tian, Richard Veech, Bin Gao – 7 March 2007 – Fatty liver, formerly associated predominantly with excessive alcohol intake, is now also recognized as a complication of obesity and an important precursor state to more severe forms of liver pathology indluding ischemia/reperfusion injury. No standard protocol for treating fatty liver exists at this time. We therefore examined the effects of 10 days of interleukin 6 (IL‐6) injection in 3 murine models of fatty liver: leptin deficient ob/ob mice, ethanol‐fed mice, and mice fed a high‐fat diet.

Stephen D. Zucker, Paul S. Horn, Kenneth E. Sherman – 7 March 2007 – Bilirubin, the primary end product of heme catabolism, is a key marker of liver and hematological disorders, and important cytoprotective properties have been ascribed to this bile pigment. The Third National Health and Nutrition Examination Survey, a comprehensive assessment of health and nutrition in the United States, was analyzed to determine the demographics and correlates of serum bilirubin levels in the general population.

Victor J. Navarro, Thomas St. Louis, Beth Z. Bell, André N. Sofair – 7 March 2007

Milan Dodig, Kevin D. Mullen – 7 March 2007 – Background & Aims: Hepatic stellate cells play an important role in liver fibrogenesis, and hepatic stellate cell death may be involved in the termination of this response. Methods: Molecular mechanisms of hepatic stellate cell killing were studied in hepatic stellate cell/Kupffer cell cocultures. Results: Lipopolysaccharide stimulation of hepatic stellate cell/Kupffer cell cocultures, but not of hepatic stellate cell monocultures, induced profound alterations of hepatic stellate cell morphology and hepatic stellate cell death.