Chengbin Wang, Jianming Tang, Wei Song, Elena Lobashevsky, Craig M. Wilson, Richard A. Kaslow – 25 March 2004 – Variable immune responses to hepatitis B virus (HBV) infection and recombinant HBV vaccines have been associated with polymorphisms in several genes within the human leukocyte antigen (HLA) complex.
Pietro Invernizzi, Domenico Alvaro, Andrea Crosignani, Eugenio Gaudio, Mauro Podda – 25 March 2004
Raffaele Iorio, Mariangela D'Ambrosi, Matilde Marcellini, Christiana Barbera, Giuseppe Maggiore, Lucia Zancan, Raffaella Giacchino, Pietro Vajro, Maria Grazia Marazzi, Ruggiero Francavilla, Fabio Michielutti, Massimo Resti, Tullio Frediani, Maria Pastore, Angela Vegnente – 25 March 2004
Pascal Lapierre, Idriss Djilali‐Saiah, Susana Vitozzi, Fernando Alvarez – 25 March 2004 – Autoimmune hepatitis (AIH) is characterized by an immune‐mediated injury of the hepatic parenchyma of unknown pathogenesis. Type 2 AIH is identified by the presence of anti‐liver‐kidney microsomes type 1 (anti‐LKM1) and anti‐liver cytosol type 1 (anti‐LC1) autoantibodies. The current study shows that a murine model of AIH can be generated by DNA immunization against type 2 AIH self‐antigens (P450 2D6 and formiminotransferase‐cyclodeaminase).
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.
Armelle Poujol‐Robert, Pierre‐Yves Boëlle, Raoul Poupon, Annie Robert – 25 March 2004
Robert J. Fontana, Ziad Kronfol – 25 March 2004
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.
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.