Jinghong Wan, Merieme Benkdane, Fatima Teixeira‐Clerc, Stéphanie Bonnafous, Alexandre Louvet, Fouad Lafdil, Françoise Pecker, Albert Tran, Philippe Gual, Ariane Mallat, Sophie Lotersztajn, Catherine Pavoine – 6 July 2013 – Alcoholic and nonalcoholic fatty liver disease (ALD and NAFLD) are the predominant causes of liver‐related mortality in Western countries. We have shown that limiting classical (M1) Kupffer cell (KC) polarization reduces alcohol‐induced liver injury. Herein, we investigated whether favoring alternatively activated M2 KCs may protect against ALD and NAFLD.

Mohamed Rela – 3 July 2013

C. Kristian Enestvedt, Saloni Malik, Peter P. Reese, Alexander Maskin, Peter S. Yoo, Sameh A. Fayek, Peter Abt, Kim M. Olthoff, Abraham Shaked – 2 July 2013 – Inferior outcomes are consistently observed for recipients of liver retransplantation (re‐LT) versus recipients of primary transplants. Few studies have examined the incidence and impact of biliary complications (BCs) on outcomes after re‐LT. The aim of this study was to compare patient and graft survival for re‐LT recipients with BCs (BC+) and re‐LT recipients without BCs (BC−).

Stefan Mauss, Dietrich Hueppe, Ulrich Alshuth – 28 June 2013 – In clinical trials with telaprevir (TLV) and boceprevir (BOC) renal impairment was not reported as a relevant adverse event. The PAN study is a noninterventional study enrolling patients treated with peginterferon alfa‐2a/ribavirin (PEG/RBV) with or without TVL or BOC. Here we restrict the analysis to hepatitis C virus genotype 1 patients having completed 12 (n = 895) or 24 weeks (n = 591) of treatment.

Peter Fickert, Elisabeth Krones, Marion J. Pollheimer, Andrea Thueringer, Tarek Moustafa, Dagmar Silbert, Emina Halilbasic, Min Yang, Hartmut Jaeschke, Geurt Stokman, Rebecca G. Wells, Kathrin Eller, Alexander R. Rosenkranz, Gosta Eggertsen, Carsten A. Wagner, Cord Langner, Helmut Denk, Michael Trauner – 28 June 2013 – Tubular epithelial injury represents an underestimated but important cause of renal dysfunction in patients with cholestasis and advanced liver disease, but the underlying mechanisms are unclear.

Helen S. Te – 28 June 2013

Shiv Kumar Sarin, Chandan Kumar – 28 June 2013

Alexander Wree, Akiko Eguchi, Matthew D. McGeough, Carla A. Pena, Casey D. Johnson, Ali Canbay, Hal M. Hoffman, Ariel E. Feldstein – 28 June 2013 – Inflammasome activation plays a central role in the development of drug‐induced and obesity‐associated liver disease. However, the sources and mechanisms of inflammasome‐mediated liver damage remain poorly understood. Our aim was to investigate the effect of NLRP3 inflammasome activation on the liver using novel mouse models.

Tao Lin, Wessam Ibrahim, Cheng‐Yuan Peng, Milton J. Finegold, Robert Y.L. Tsai – 28 June 2013 – During liver development and regeneration, hepatocytes undergo rapid cell division and face an increased risk of DNA damage associated with active DNA replication. The mechanism that protects proliferating hepatocytes from replication‐induced DNA damage remains unclear. Nucleostemin (NS) is known to be up‐regulated during liver regeneration, and loss of NS is associated with increased DNA damage in cancer cells.

Esther Bertran, Eva Crosas‐Molist, Patricia Sancho, Laia Caja, Judit Lopez‐Luque, Estanislao Navarro, Gustavo Egea, Raquel Lastra, Teresa Serrano, Emilio Ramos, Isabel Fabregat – 28 June 2013 – Transforming growth factor‐beta (TGF‐β) is an important regulatory suppressor factor in hepatocytes. However, liver tumor cells develop mechanisms to overcome its suppressor effects and respond to this cytokine by inducing other processes, such as the epithelial‐mesenchymal transition (EMT), which contributes to tumor progression and dissemination.