Andreas Geier, Gernot Zollner, Christoph G. Dietrich, Martin Wagner, Peter Fickert, Helmut Denk, Nico van Rooijen, Siegfried Matern, Carsten Gartung, Michael Trauner – 22 February 2005 – Cholestatic liver injury is associated not only with accumulation of bile acids but also with activation of proinflammatory cytokines. Common bile duct ligation (CBDL) induces sustained downregulation of the Na+/taurocholate cotransporter (Ntcp) in rodent liver.

Chiemi Noguchi, Hiromi Ishino, Masataka Tsuge, Yoshifumi Fujimoto, Michio Imamura, Shoichi Takahashi, Kazuaki Chayama – 22 February 2005 – G to A hypermutation of the human immunodeficiency virus type 1 (HIV‐1) is induced by a deaminase APOBEC3G and is related to host antiviral defense. APOBEC3G has also been found to reduce the replication of HIV‐1 by an unknown mechanism. This enzyme also reduces the production of hepatitis B virus, although the mechanism for this action has not been clearly elucidated.

Rafael Bañares, Oscar Núñez, María Escudero, Cristina Fernández, Javier Vaquero, Inmaculada Beceiro, Antonio Echenagusía, Gerardo Clemente, Leandro Santos – 22 February 2005 – A trend toward a higher incidence of hepatocelullar carcinoma (HCC) in patients with cirrhosis treated with bare‐stent transjugular intrahepatic portosystemic shunt (TIPS) has been observed in previous studies. To assess the influence of TIPS as a risk factor for developing HCC, we have compared the incidence of HCC in two retrospective cohorts of patients.

Jaime Bosch, Juan Carlos Reverter – 22 February 2005

Yoshitaka Kamegaya, Yoichi Hiasa, Lawrence Zukerberg, Nina Fowler, Jason T. Blackard, Wenyu Lin, Won H. Choe, Emmett V. Schmidt, Raymond T. Chung – 22 February 2005 – We developed hepatitis C virus (HCV) core‐E1‐E2 and HCV core transgenic mice on a common genetic background to assess the contribution of HCV structural proteins to hepatocarcinogenesis. Eight‐week‐old core‐E1‐E2, core, and nontransgenic mice inbred on the FVB×C57Bl/6 background were treated with diethylnitrosamine (DEN) and sacrificed at 32 weeks old. Proliferation and apoptosis were assessed by immunohistochemistry.

Joan Clària, Jeffrey D. Kent, Marta López‐Parra, Ginés Escolar, Luís Ruiz‐del‐Arbol, Pere Ginès, Wladimiro Jiménez, Boris Vucelic, Vicente Arroyo – 22 February 2005 – Nonselective inhibition of cyclooxygenase (COX) by nonsteroidal anti‐inflammatory drugs frequently induces renal failure in decompensated cirrhosis. Studies in experimental cirrhosis suggest that selective inhibitors of the inducible isoform COX‐2 do not adversely affect renal function. However, very limited information is available on the effects of these compounds on renal function in human cirrhosis.

Adrien Croquelois, Alex Blindenbacher, Luigi Terracciano, Xueya Wang, Igor Langer, Freddy Radtke, Markus H. Heim – 22 February 2005 – The discovery that the human Jagged1 gene (JAG1) is the Alagille syndrome disease gene indicated that Notch signaling has an important role in bile duct homeostasis. The functional study of this signaling pathway has been difficult because mice with targeted mutations in Jagged1, Notch1, or Notch2 have an embryonic lethal phenotype.

Stefan G. Hübscher, Alastair J. Strain – 22 February 2005

Naiara Beraza, Juan Martín Marqués, Eduardo Martínez‐Ansó, María Iñiguez, Jesús Prieto, Matilde Bustos – 22 February 2005 – Prostaglandins are hepatoprotective molecules generated in liver regeneration by the rapid induction of cyclooxygenase‐2 (COX‐2). Cardiotrophin‐1 (CT‐1) and vascular endothelial growth factor (VEGF) are other hepatoprotective mediators upregulated at 24 hours after partial hepatectomy. The interactions among these molecules during liver regeneration have not yet been defined.

Qin Zhou, Xuhuai Ji, Lixin Chen, Harry B. Greenberg, Shelly C. Lu, M. Bishr Omary – 22 February 2005 – Mutation of the cytoskeletal intermediate filament proteins keratin 8 and keratin 18 (K8/K18) is associated with cirrhosis in humans, whereas transgenic mice that overexpress K18 Arg89→Cys (R89C) have significant predisposition to liver injury. To study the mechanism of keratin‐associated predisposition to liver injury, we used mouse microarrays to examine genetic changes associated with hepatocyte keratin mutation and assessed the consequences of such changes.