Hui Yang, Qi Zhan, Yu‐Jui Yvonne Wan – 7 December 2010 – The synthetic retinoid fenretinide is one of the most promising clinically tested retinoids. Previously, we have shown that fenretinide induces apoptosis of Huh7 cells, but HepG2 cells are relatively resistant to fenretinide‐induced apoptosis. This study examines the interactive role of fenretinide and histone deacetylase inhibitors (HDACi) in inducing apoptosis of human hepatocellular carcinoma (HCC) cells and the underlying mechanism.

Soo Han Bae, Su Haeng Sung, Eun Jung Cho, Se Kyoung Lee, Hye Eun Lee, Hyun Ae Woo, Dae‐Yeul Yu, In Sup Kil, Sue Goo Rhee – 7 December 2010 – Peroxiredoxins (Prxs) are peroxidases that catalyze the reduction of reactive oxygen species (ROS). The active site cysteine residue of members of the 2‐Cys Prx subgroup (Prx I to IV) of Prxs is hyperoxidized to cysteine sulfinic acid (Cys‐SO2) during catalysis with concomitant loss of peroxidase activity. Reactivation of the hyperoxidized Prx is catalyzed by sulfiredoxin (Srx).

Isabel Gómez‐Hurtado, Pedro Zapater, Pablo Bellot, Sonia Pascual, Miguel Pérez‐Mateo, José Such, Rubén Francés – 7 December 2010 – Patients with cirrhosis receiving norfloxacin show a restored inflammatory balance that likely prevents clinical complications derived from an excessive proinflammatory response to bacterial product challenges. This study sought to investigate associated inflammatory control mechanisms established in patients with cirrhosis receiving norfloxacin. A total of 62 patients with cirrhosis and ascites in different clinical conditions were considered.

Tim O. Lankisch, Jochen Metzger, Ahmed A. Negm, Katja Voβkuhl, Eric Schiffer, Justyna Siwy, Tobias J. Weismüller, Andrea S. Schneider, Kathrin Thedieck, Ralf Baumeister, Petra Zürbig, Eva M. Weissinger, Michael P. Manns, Harald Mischak, Jochen Wedemeyer – 7 December 2010 – Early detection of malignant biliary tract diseases, especially cholangiocarcinoma (CC) in patients with primary sclerosing cholangitis (PSC), is very difficult and often comes too late to give the patient a therapeutic benefit. We hypothesize that bile proteomic analysis distinguishes CC from nonmalignant lesions.

Marco Senzolo, Maria T. Sartori, Kryssia Rodriguez‐Castro, Paolo Simioni, Valeria Rossetto – 6 December 2010

Catherine Rongey, Hal F. Yee – 6 December 2010

Marie‐Luise Berres, Christian Trautwein, Maximilian Schmeding, Dennis Eurich, Frank Tacke, Marcus Bahra, Peter Neuhaus, Ulf P. Neumann, Hermann E. Wasmuth – 6 December 2010 – The recurrence of liver fibrosis after liver transplantation (LT) for hepatitis C virus (HCV) infection is responsible for graft loss and patient mortality. Although the contribution of the immune system to fibrosis recurrence is anticipated, systematic studies evaluating immune parameters as predictive markers of allograft fibrosis are lacking.

Oyekoya T. Ayonrinde, John K. Olynyk, Lawrence J. Beilin, Trevor A. Mori, Craig E. Pennell, Nicholas de Klerk, Wendy H. Oddy, Peter Shipman, Leon A. Adams – 6 December 2010 – Nonalcoholic fatty liver disease (NAFLD) is a predominantly adult‐diagnosed disorder. Knowledge regarding the epidemiology, phenotype, and metabolic risk factors, during adolescence is limited.

Dennis Eurich, Sabine Boas‐Knoop, Martin Ruehl, Maria Schulz, Esperanza D. Carrillo, Thomas Berg, Ruth Neuhaus, Peter Neuhaus, Ulf Peter Neumann, Marcus Bahra – 6 December 2010 – Up to 30% of liver transplants will develop graft cirrhosis within 5 years after liver transplantation (LT) due to recurrent HCV‐infection forwarding accelerated graft damage. Genetic variants of cytokines involved in the immune response may contribute to the degree of graft inflammation, fibrosis progression, and antiviral therapy outcome.

Christine Gauglhofer, Sandra Sagmeister, Waltraud Schrottmaier, Carina Fischer, Chantal Rodgarkia‐Dara, Thomas Mohr, Stefan Stättner, Christoph Bichler, Daniela Kandioler, Fritz Wrba, Rolf Schulte‐Hermann, Klaus Holzmann, Michael Grusch, Brigitte Marian, Walter Berger, Bettina Grasl‐Kraupp – 6 December 2010 – Fibroblast growth factors (FGFs) and their high‐affinity receptors [fibroblast growth factor receptors (FGFRs)] contribute to autocrine and paracrine growth stimulation in several nonliver cancer entities.