James E. Nelson, Elizabeth M. Brunt, Kris V. Kowdley, for the Nonalcoholic Steatohepatitis Clinical Research Network – 21 May 2012 – Hepcidin regulation is linked to both iron and inflammatory signals and may influence iron loading in nonalcoholic steatohepatitis (NASH). The aim of this study was to examine the relationships among HFE genotype, serum hepcidin level, hepatic iron deposition, and histology in nonalcoholic fatty liver disease (NAFLD).

Yun Shin Chun, Julien Calderaro, Jessica Zucman‐Rossi – 21 May 2012

Leticia Muñoz, María José Borrero, María Ubeda, Margaret Lario, David Díaz, Rubén Francés, Jorge Monserrat, Óscar Pastor, Elia Aguado‐Fraile, José Such, Melchor Álvarez‐Mon, Agustín Albillos – 21 May 2012 – Cirrhosis with ascites is associated with a high rate of gut bacterial translocation (GBT) and spontaneous bacterial infections of enteric origin. We addressed the activation state and role of intestinal dendritic cells (DCs) in experimental ascitic cirrhosis and their relationship with GBT. Cirrhosis with ascites was CCl4 induced in rats.

Yun Shin Chun, Julien Calderaro, Jessica Zucman‐Rossi – 21 May 2012

Lisa B. VanWagner, Manali Bhave, Helen S. Te, Joe Feinglass, Lisa Alvarez, Mary E. Rinella – 21 May 2012 – Nonalcoholic steatohepatitis (NASH) is an independent predictor of coronary artery disease (CAD). Our aim was to compare the incidence of cardiovascular (CV) events between patients transplanted for NASH and alcohol (ETOH)‐induced cirrhosis. This is a retrospective cohort study (August 1993 to March 2010) of 242 patients (115 NASH and 127 ETOH) with ≥12 months follow‐up after liver transplantation (LT). Those with hepatocellular carcinoma or coexisting liver diseases were excluded.

Bastian Höchst, Frank A. Schildberg, Jan Böttcher, Christina Metzger, Sebastian Huss, Andreas Türler, Markus Overhaus, Andreas Knoblich, Berthold Schneider, Dimitrios Pantelis, Christian Kurts, Jörg C. Kalff, Percy Knolle, Linda Diehl – 18 May 2012 – Immunity against cancer is impeded by local mechanisms promoting development of tumor‐specific T cell tolerance, such as regulatory T cells, myeloid‐derived suppressor cells, or immunosuppressive factors in the tumor microenvironment.

Edmondo Falleti, Davide Bitetto, Carlo Fabris, Giovanna Fattovich, Annarosa Cussigh, Sara Cmet, Elisa Ceriani, Ezio Fornasiere, Michela Pasino, Donatella Ieluzzi, Mario Pirisi, Pierluigi Toniutto – 18 May 2012 – Vitamin D deficiency seems to predict the unsuccessful achievement of sustained viral response (SVR) after antiviral treatment in hepatitis C virus (HCV) difficult‐to‐treat genotypes. Vitamin D binding protein (GC) gene polymorphisms are known to influence vitamin D levels.

Jeffry Florian, Pravin R. Jadhav, Shashi Amur, Ruben Ayala, Patrick Harrington, Poonam Mishra, Jules O'Rear, Michael Pacanowski, Sarah Robertson, Mary Singer, Greg Soon, Wen Zeng, Jeffrey Murray – 18 May 2012

Yiliang Zhang, Wei Wei, Na Cheng, Kaihui Wang, Bin Li, Xiaoqing Jiang, Shuhan Sun – 18 May 2012 – Hepatitis C virus (HCV) infection usually induces chronic hepatic inflammation, which favors the initiation and progression of hepatocellular carcinoma (HCC). Moreover, microRNA‐155 (miR‐155) plays an important role in regulating both inflammation and tumorigenesis. However, little is known about whether and how miR‐155 provides the link between inflammation and cancer. In this study we found that miR‐155 levels were markedly increased in patients infected with HCV.

Stuart C. Gordon, Paul J. Pockros, Norah A. Terrault, Robert S. Hoop, Ami Buikema, David Nerenz, Fayez M. Hamzeh – 18 May 2012 – Hepatitis C virus (HCV) infection increases total healthcare costs but the effect of the severity of liver disease associated with chronic hepatitis C (CHC) on healthcare costs has not been well studied. We analyzed the demographics, healthcare utilization, and healthcare costs of CHC patients in a large U.S. private insurance database (January, 2002 to August, 2010), with at least 1 year of baseline enrollment and 30 days of continuous follow‐up.