Yung‐Chang Chen, Pere Ginès, Jianhui Yang, Sandra N. Summer, Sandor Falk, Nash S. Russell, Robert W. Schrier – 25 March 2004 – Vascular heme oxygenase (HO) regulates vascular tone in normal conditions and in some pathologic circumstances (e.g., sepsis). However, its possible role in the pathogenesis of arterial vasodilation in cirrhosis is unknown. To address this question, the expression and activity of HO in arterial vessels was studied in rats at 1, 2, and 4 weeks after bile duct ligation (BDL) or sham operation.

Leon A. Adams, Ariel Feldstein, Keith D. Lindor, Paul Angulo – 25 March 2004 – Patients with hypopituitarism develop a phenotype similar to metabolic syndrome with central obesity and diabetes. Similarly, patients with hypothalamic damage may develop central obesity, insulin resistance, and hyperphagia. We sought to examine the clinical associations between hypopituitarism, hypothalamic dysfunction, and nonalcoholic fatty liver disease (NAFLD).

Vlad Ratziu, Françoise Imbert‐Bismut, Djamila Messous, Thierry Poynard – 25 March 2004

Simon C.H. Yu, Simon S.M. Ho, Wan Y. Lau, Deacons T.K. Yeung, Edmund H.Y. Yuen, Paul S.F. Lee, Constantine Metreweli – 25 March 2004 – This study aims to compare the therapeutic effectiveness of continuous catheter drainage versus intermittent needle aspiration in the percutaneous treatment of pyogenic liver abscesses.

David A. Rudnick, Yunjun Liao, Jae‐Koo An, Louis J. Muglia, David H. Perlmutter, Jeffrey H. Teckman – 25 March 2004 – α‐1‐Antitrypsin (α1‐AT) deficiency is the most common cause of metabolic pediatric liver disease. Hepatocellular injury is caused by toxicity of the mutant α‐1‐antitrypsin Z (α1‐ATZ) molecule retained within hepatocytes. In these studies, we used the PiZ transgenic mouse model of α1‐AT deficiency to examine hepatocellular proliferation in response to chronic liver injury resulting from this metabolic disease.

Marshall M. Kaplan, Steven Cheng, Lori Lyn Price, Peter A. L. Bonis – 25 March 2004 – Primary biliary cirrhosis frequently progresses despite treatment with ursodeoxycholic acid (UDCA), the only approved therapy. Previous studies suggested that colchicine and methotrexate may improve biochemical tests of liver function, symptoms, and liver histology. The aim of the present study was to determine if the addition of colchicine or methotrexate to UDCA would improve survival free of liver transplantation.

25 March 2004

Robert J. Fontana, Ziad Kronfol – 25 March 2004

Armelle Poujol‐Robert, Pierre‐Yves Boëlle, Raoul Poupon, Annie Robert – 25 March 2004

Zichen Zhang, Guan‐Hua Lai, Alphonse E. Sirica – 25 March 2004 – Recently, we demonstrated that the cyclooxygenase‐2 (COX‐2) inhibitor celecoxib acts to significantly suppress the growth of rat C611B cholangiocarcinoma (ChC) cells in vitro. To establish a molecular mechanism for this growth suppression, we investigated the effects of celecoxib on apoptotic signaling pathways in cultured rat C611B ChC cells.