Craig Lammert, Stefan Einarsson, Chandan Saha, Anna Niklasson, Einar Bjornsson, Naga Chalasani – 7 February 2008 – Idiosyncratic drug‐induced liver injury (DILI) is traditionally thought not to be dose‐related. However, it has been pointed out that most medicines that were withdrawn from marketing or received a black‐box warning because of hepatotoxicity were prescribed at daily doses greater than 50 mg/day. To examine the relationship between daily dose of medications and idiosyncratic DILI, we conducted a study with two aims.

Guadalupe Garcia‐Tsao, Jaime Bosch, Roberto J. Groszmann – 7 February 2008

Muhammad Y. Sheikh, Jinah Choi, Ishtiaq Qadri, Jacob E. Friedman, Arun J. Sanyal – 7 February 2008 – Chronic infection with hepatitis C virus (HCV) can induce insulin resistance (IR) in a genotype‐dependent fashion, thus contributing to steatosis, progression of fibrosis and resistance to interferon therapy. The molecular mechanisms in genotype 1 patients that lead to metabolic syndrome are still ambiguous. Based on our current understanding, HCV proteins associate with mitochondria and endoplasmic reticulum and promote oxidative stress.

Beate Katharina Straub, Pamela Stoeffel, Hans Heid, Ralf Zimbelmann, Peter Schirmacher – 7 February 2008 – Fatty change (steatosis) is the most frequent liver pathology in western countries and is caused by a broad range of disorders such as alcohol abuse and metabolic syndrome. The surface layer of lipid droplets (LDs) contains members of a protein family that share homologous sequences and domains, the so‐called PAT proteins, named after their constituents, perilipin, adipophilin, and TIP47.

Eve A. Roberts, Michael L. Schilsky – 4 February 2008

Yann Malato, Leif E. Sander, Christian Liedtke, Malika Al‐Masaoudi, Frank Tacke, Christian Trautwein, Naiara Beraza – 4 February 2008 – Nuclear factor κB (NF‐κB) is one of the main transcription factors involved in liver regeneration after partial hepatectomy (PH). It is activated upon IκB phosphorylation by the IκB kinase (IKK) complex comprising inhibitor of kappaB kinase 1 (IKK1), inhibitor of kappaB kinase 2 (IKK2), and nuclear factor‐B essential modifier (NEMO). We studied the impact of hepatocyte‐specific IKK2 deletion during liver regeneration.

Charbel El Boustany, Gabriel Bidaux, Antoine Enfissi, Philippe Delcourt, Natalia Prevarskaya, Thierry Capiod – 4 February 2008 – Store‐operated calcium entry (SOCE) is the main Ca2+ influx pathway involved in controlling proliferation of the human hepatoma cell lines Huh‐7 and HepG2. However, the molecular nature of the calcium channels involved in this process remains unknown. Huh‐7 and HepG2 cells express transient receptor potential canonical 1 (TRPC1) and TRPC6, as well as STIM1 and Orai1, and these 4 channels are the most likely candidates to account for the SOCE in these cells.

Peter Ferenci, Harald Brunner, Hermann Laferl, Thomas‐Matthias Scherzer, Andreas Maieron, Michael Strasser, Gabriele Fischer, Harald Hofer, Martin Bischof, Rudolf Stauber, Michael Gschwantler, Petra Steindl‐Munda, Katharina Staufer, Karin Löschenberger – 4 February 2008 – We compared the efficacy and tolerability of 24 weeks of treatment with ribavirin 800 mg/day (group A) or 400 mg/day (group B) plus peginterferon alfa‐2a 180 μg/week in treatment‐naive patients infected with hepatitis C virus (HCV) genotype 2 or 3.

Samuel Martín‐Vílchez, Paloma Sanz‐Cameno, Yolanda Rodríguez‐Muñoz, Pedro L. Majano, Francisca Molina‐Jiménez, Manuel López‐Cabrera, Ricardo Moreno‐Otero, Enrique Lara‐Pezzi – 4 February 2008 – Chronic hepatitis B virus (HBV) infection is a major cause of liver fibrosis, eventually leading to cirrhosis and hepatocellular carcinoma. Although the involvement of the X protein of HBV (HBx) in viral replication and tumor development has been extensively studied, little is known about its possible role in the development of fibrosis.

Yannick Ladeiro, Gabrielle Couchy, Charles Balabaud, Paulette Bioulac‐Sage, Laura Pelletier, Sandra Rebouissou, Jessica Zucman‐Rossi – 1 February 2008 – Molecular classifications defining new tumor subtypes have been recently refined with genetic and transcriptomic analyses of benign and malignant hepatocellular tumors. Here, we performed microRNA (miRNA) profiling in two series of fully annotated liver tumors to uncover associations between oncogene/tumor suppressor mutations and clinical and pathological features.