Mirko Moreno Zaldivar, Katrin Pauels, Philipp von Hundelshausen, Marie‐Luise Berres, Petra Schmitz, Jörg Bornemann, M. Anna Kowalska, Nikolaus Gassler, Konrad L. Streetz, Ralf Weiskirchen, Christian Trautwein, Christian Weber, Hermann E. Wasmuth – 26 March 2010 – Liver fibrosis is a major cause of morbidity and mortality worldwide. Platelets are involved in liver damage, but the underlying molecular mechanisms remain elusive. Here, we investigate the platelet‐derived chemokine (C‐X‐C motif) ligand 4 (CXCL4) as a molecular mediator of fibrotic liver damage.

Luca Valenti, Ahmad Al‐Serri, Ann K. Daly, Enrico Galmozzi, Raffaela Rametta, Paola Dongiovanni, Valerio Nobili, Enrico Mozzi, Giancarlo Roviaro, Ester Vanni, Elisabetta Bugianesi, Marco Maggioni, Anna Ludovica Fracanzani, Silvia Fargion, Christopher P.

Ian N. Hines – 26 March 2010

Pietro E. Majno, Gilles Mentha, Vincenzo Mazzaferro – 26 March 2010

Paul Feuerstadt, Ari L. Bunim, Heriberto Garcia, Jordan J. Karlitz, Hatef Massoumi, Amar J. Thosani, Andrew Pellecchia, Allan W. Wolkoff, Paul J. Gaglio, John F. Reinus – 26 March 2010 – Randomized controlled trials of hepatitis C virus (HCV) therapy with pegylated interferon and ribavirin have demonstrated sustained viral response rates (SVRs) of 54%‐63% (efficacy). Treatment results in clinical practice (effectiveness) may not be equivalent.

Heping Yang, Kwangsuk Ko, Meng Xia, Tony W.H. Li, Pilsoo Oh, Jiaping Li, Shelly C. Lu – 26 March 2010 – We previously showed that hepatic expression of glutathione (GSH) synthetic enzymes and GSH levels fell 2 weeks after bile duct ligation (BDL) in mice. This correlated with a switch in nuclear anti‐oxidant response element (ARE) binding activity from nuclear factor erythroid 2–related factor 2 (Nrf2) to c–avian musculoaponeurotic fibrosarcoma (c‐Maf)/V‐maf musculoaponeurotic fibrosarcoma oncogene homolog G (MafG).

Nicole K. Paulk, Karsten Wursthorn, Zhongya Wang, Milton J. Finegold, Mark A. Kay, Markus Grompe – 26 March 2010 – Adeno‐associated virus (AAV) vectors are ideal for performing gene repair due to their ability to target multiple different genomic loci, low immunogenicity, capability to achieve targeted and stable expression through integration, and low mutagenic and oncogenic potential. However, many handicaps to gene repair therapy remain. Most notable is the low frequency of correction in vivo. To date, this frequency is too low to be of therapeutic value for any disease.

Anna S. Lok – 26 March 2010

Silvia Fargion, Luca Valenti, Anna Ludovica Fracanzani – 26 March 2010

Jesper B. Andersen, Roberto Loi, Andrea Perra, Valentina M. Factor, Giovanna M. Ledda‐Columbano, Amedeo Columbano, Snorri S. Thorgeirsson – 26 March 2010 – Human hepatocellular carcinoma (HCC) is a heterogeneous disease of distinct clinical subgroups. A principal source of tumor heterogeneity may be cell type of origin, which in liver includes hepatocyte or adult stem/progenitor cells. To address this issue, we investigated the molecular mechanisms underlying the fate of the enzyme‐altered preneoplastic lesions in the resistant hepatocyte (RH) model.