Maureen M. Jonas, William Balistreri, Regino P. Gonzalez‐Peralta, Barbara Haber, Steven Lobritto, Parvathi Mohan, Jean P. Molleston, Karen F. Murray, Michael R. Narkewicz, Philip Rosenthal, Kathleen B. Schwarz, Bruce A. Barton, John A. Shepherd, Paul D. Mitchell, Christopher Duggan – 2 March 2012 – Weight loss and changes in growth are noted in children treated with interferon alpha (IFN‐α). The aim of this study was to prospectively determine changes in weight, height, body mass index (BMI), and body composition during and after treatment of children with hepatitis C virus (HCV).

Jesús M. Banales, Elena Sáez, Miriam Úriz, Sarai Sarvide, Aura D. Urribarri, Patrick Splinter, Pamela S. Tietz Bogert, Luis Bujanda, Jesús Prieto, Juan F. Medina, Nicholas F. LaRusso – 2 March 2012 – Cl−/HCO anion exchanger 2 (AE2) participates in intracellular pH homeostasis and secretin‐stimulated biliary bicarbonate secretion. AE2/SLC4A2 gene expression is reduced in liver and blood mononuclear cells from patients with primary biliary cirrhosis (PBC).

Roheeth D. Delima, Anita C.G. Chua, Janina E.E. Tirnitz‐Parker, Eng K. Gan, Kevin D. Croft, Ross M. Graham, John K. Olynyk, Debbie Trinder – 2 March 2012 – Mutations in hemochromatosis protein (HFE) or transferrin receptor 2 (TFR2) cause hereditary hemochromatosis (HH) by impeding production of the liver iron‐regulatory hormone, hepcidin (HAMP). This study examined the effects of disruption of Hfe or Tfr2, either alone or together, on liver iron loading and injury in mouse models of HH.

Yao‐Chun Hsu, Jaw‐Town Lin, Tzu‐Ting Chen, Ming‐Shiang Wu, Chun‐Ying Wu – 1 March 2012 – Peptic ulcer bleeding leads to substantial morbidity and mortality in patients with liver cirrhosis, but their long‐term risk of recurrent bleeding remains elusive. This nationwide cohort study aimed to elucidate the association between cirrhosis and recurrent peptic ulcer bleeding by analyzing the Taiwan National Health Insurance Research Database.

Jimmy K. Stauffer, Anthony J. Scarzello, Qun Jiang, Robert H. Wiltrout – 1 March 2012 – Sustained hepatic inflammation, driven by alcohol consumption, nonalcoholic fatty liver disease, and/or chronic viral hepatitis (hepatitis B and C), results in damage to parenchyma, oxidative stress, and compensatory regeneration/proliferation. There is substantial evidence linking these inflammation‐associated events with the increased incidence of hepatocellular carcinogenesis.

David Y. Zhang, Scott L. Friedman – 1 March 2012 – Hepatocellular carcinoma (HCC) is a rising worldwide cause of cancer mortality, making the elucidation of its underlying mechanisms an urgent priority. The liver is unique in its response to injury, simultaneously undergoing regeneration and fibrosis. HCC occurs in the context of these two divergent responses, leading to distinctive pathways of carcinogenesis. In this review we highlight pathways of liver tumorigenesis that depend on, or are enhanced by, fibrosis.

Salvador Augustin, Antonio González, Laia Badia, Laura Millán, Aranzazu Gelabert, Alejandro Romero, Antoni Segarra, María Martell, Rafael Esteban, Jaime Guardia, Joan Genescà – 1 March 2012 – Although it is assumed that hemodynamic responders to pharmacological therapy after a variceal hemorrhage are adequately protected from rebleeding, there is no evidence that either this response or its protective effect extend beyond the usual 2‐year follow‐up featured in available studies.

Youhui Si, Shufeng Liu, Xiuying Liu, Jana L. Jacobs, Min Cheng, Yuqiang Niu, Qi Jin, Tianyi Wang, Wei Yang – 1 March 2012 – Hepatitis C virus (HCV) entry is a complicated process that requires multiple host factors, such as CD81, scavenger receptor BI, claudin‐1 (CLDN1), and occludin. The interaction of virus and cellular entry factors represents a promising target for novel anti‐HCV drug development. In this study, we sought to identify peptide inhibitors for HCV entry by screening a library of overlapping peptides covering the four above‐mentioned entry factors.

Ananya Pongpaibul, Robert S. Venick, Sue V. McDiarmid, Charles R. Lassman – 29 February 2012 – De novo autoimmune hepatitis (DAIH) is a well‐recognized complication of pediatric liver transplantation (LT). The diagnosis is largely based on elevated liver function test results and the development of autoimmune antibodies. The histology of DAIH was first described in 1998. We present detailed histological data from the largest series to date of pretreatment and posttreatment biopsy samples from pediatric LT patients with DAIH.

David A. Axelrod, Alan Reed – 29 February 2012