Robert Thimme, Michaela Neagu, Tobias Boettler, Christoph Neumann‐Haefelin, Nadine Kersting, Michael Geissler, Frank Makowiec, Robert Obermaier, Ulrich T. Hopt, Hubert E. Blum, Hans Christian Spangenberg – 24 November 2008 – Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide, with a poor prognosis and limited therapeutic options. Therefore, the development of novel therapeutic strategies is of high priority. α‐Fetoprotein (AFP) is overexpressed in the majority of HCCs.

Matthew J. Ryan, Christina Bales, Anthony Nelson, Dorian M. Gonzalez, Lara Underkoffler, Michelle Segalov, Jeanne Wilson‐Rawls, Susan E. Cole, Jennifer L. Moran, Pierre Russo, Nancy B. Spinner, Kenro Kusumi, Kathleen M. Loomes – 24 November 2008 – Alagille syndrome (AGS) is a heterogeneous developmental disorder associated with bile duct paucity and various organ anomalies. The syndrome is caused by mutations in JAG1, which encodes a ligand in the Notch signaling pathway, in the majority of cases and mutations in the NOTCH2 receptor gene in less than 1% of patients.

Jennifer Altomonte, Rickmer Braren, Stephan Schulz, Sabrina Marozin, Ernst J. Rummeny, Roland M. Schmid, Oliver Ebert – 24 November 2008 – Oncolytic virotherapy is a promising strategy for safe and effective treatment of malignancy. We have reported previously that recombinant vesicular stomatitis virus (VSV) vectors are effective oncolytic agents that can be safely administered via the hepatic artery in immunocompetent rats to treat multifocal hepatocellular carcinoma (HCC), resulting in tumor necrosis and prolonged survival.

Samuele De Minicis, Ekihiro Seki, Christoph Oesterreicher, Bernd Schnabl, Robert F. Schwabe, David A. Brenner – 24 November 2008 – Although leptin induces fibrotic activity in hepatic stellate cells (HSCs), the mechanisms are not entirely understood. To investigate the potential role of reduced nicotinamide adenine dinucleotide phosphate oxidase (NADPH) and reactive oxygen species (ROS) in leptin signaling in HSCs, we analyzed leptin‐induced intracellular signaling pathways in primary wild‐type (WT), p47, and signal transducer and activator of transcription protein 3 (STAT3)‐deleted HSCs.

Melania Manco, Anna Alisi, Valerio Nobili – 24 November 2008

24 November 2008

Russell H. Wiesner – 24 November 2008

Fernando A. Crocenzi, Enrique J. Sánchez Pozzi, María Laura Ruiz, Andrés E. Zucchetti, Marcelo G. Roma, Aldo D. Mottino, Mary Vore – 24 November 2008 – The endogenous estradiol metabolite estradiol 17β‐D‐glucuronide (E217G) induces an acute cholestasis in rat liver coincident with retrieval of the canalicular transporters bile salt export pump (Bsep, Abcc11) and multidrug resistance‐associated protein 2 (Mrp2, Abcc2) and their associated loss of function.

Haruaki Shirakawa, Akihiro Matsumoto, Satoru Joshita, Michiharu Komatsu, Naoki Tanaka, Takeji Umemura, Tetsuya Ichijo, Kaname Yoshizawa, Kendo Kiyosawa, Eiji Tanaka, Nagano Interferon Treatment Research Group – 24 November 2008 – The interferon sensitivity determining region (ISDR) of the hepatitis C virus (HCV) and T‐helper type 1 and type 2 (Th1/Th2) ratio were analyzed along with other host and viral factors for their ability to predict the response of patients with chronic hepatitis C to pegylated interferon alpha‐2b (Peg‐IFN) and ribavirin (RBV) combination therapy.

Hiroyuki Nakashima, Manabu Kinoshita, Masahiro Nakashima, Yoshiko Habu, Satoshi Shono, Takefumi Uchida, Nariyoshi Shinomiya, Shuhji Seki – 24 November 2008 – Although concanavalin A (Con‐A)‐induced experimental hepatitis is thought to be induced by activated T cells, natural killer T (NKT) cells, and cytokines, precise mechanisms are still unknown. In the current study, we investigated the roles of Kupffer cells, NKT cells, FasL, tumor necrosis factor (TNF), and superoxide in Con‐A hepatitis in C57BL/6 mice.