Krishna Banaudha, Jan M. Orenstein, Tamara Korolnek, Georges C. St. Laurent, Takaji Wakita, Ajit Kumar – 23 May 2010 – Analysis of progressive changes in hepatic gene expression that underlie hepatocarcinogenesis following hepatitis C virus (HCV) infection require examination of long‐term cultures of normally differentiating primary human hepatocytes. We report a culture system of primary hepatocytes that support productive replication of infectious HCV.

Julie Lucifora, Isabelle E. Vincent, Pascale Berthillon, Tatiana Dupinay, Maud Michelet, Ulrike Protzer, Fabien Zoulim, David Durantel, Christian Trepo, Isabelle Chemin – 23 May 2010 – The development of new anti–hepatitis B virus (HBV) therapies, especially immunotherapeutic approaches, has been limited by the lack of a primate model more accessible than chimpanzees. We have previously demonstrated that sylvanus and cynomolgus macaques are susceptible to in vivo HBV infection after intrahepatic HBV DNA inoculation.

Ramón Vilana, Alejandro Forner, Luis Bianchi, Ángeles García‐Criado, Jordi Rimola, Carlos Rodríguez de Lope, María Reig, Carmen Ayuso, Concepció Brú, Jordi Bruix – 23 May 2010 – The aim of this study was to describe the imaging features by contrast‐enhanced ultrasound (CEUS) of intrahepatic cholangiocarcinoma (ICC) in cirrhosis patients. We registered the CEUS images of cirrhosis patients with histologically confirmed ICC. In all cases magnetic resonance imaging (MRI) was done to confirm the diagnosis and/or staging purposes.

Josephine H. Li, Xiang Qian Lao, Hans L. Tillmann, Jennifer Rowell, Keyur Patel, Alexander Thompson, Sunil Suchindran, Andrew J. Muir, John R. Guyton, Stephen D. Gardner, John G. McHutchison, Jeanette J. McCarthy – 23 May 2010 – Recently, genetic polymorphisms occurring in the interferon (IFN)‐lambda gene region were associated with response to IFN‐based treatment of hepatitis C infection. Both infection with the hepatitis C virus and IFN therapy are associated with decreased serum cholesterol and high cholesterol has been associated with increased likelihood to respond to IFN.

Andrew K. Burroughs, Ulrich Thalheimer – 23 May 2010

Yoshihiro Ikura, Yoko Iwasa, Makiko Ueda – 23 May 2010

Moreshwar S. Desai, Zainuer Shabier, Michael Taylor, Fong Lam, Sundararajah Thevananther, Astrid Kosters, Saul J. Karpen – 23 May 2010 – Cardiac dysfunction is a major cause of morbidity and mortality in patients with end‐stage liver disease; yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterations in signaling pathways engaged in cardiac energy metabolism and hypertrophy, augmented by direct effects of high circulating levels of bile acids.

Diana B. Douglas, Daniel P. Beiting, John P. Loftus, Judith A. Appleton, Susan K. Bliss – 23 May 2010 – Mice lacking the immunoregulatory cytokine interleukin 10 (IL‐10) develop necrotizing hepatitis after infection with Trichinella spiralis, and inflammation is dependent on the migration of intestinally activated CD4+ T cells into the liver. Hepatic production of IL‐4 is elevated in these mice, and we hypothesized that it plays a role in the development of hepatic pathology.

Vincent Wai‐Sun Wong, Grace Lai‐Hung Wong, Kenneth Kar‐Lung Yan, Angel Mei‐Ling Chim, Hoi‐Yun Chan, Chi‐Hang Tse, Paul Cheung‐Lung Choi, Anthony Wing‐Hung Chan, Joseph Jao‐Yiu Sung, Henry Lik‐Yuen Chan – 23 May 2010 – Approximately 30%‐40% of patients with hepatitis B e antigen (HBeAg)‐positive chronic hepatitis B treated with peginterferon and/or lamivudine achieve HBeAg seroconversion 6 months after the end of treatment. The durability and long‐term effect of treatment are unknown.

Maria Lauda Tomasi, Komal Ramani, Fernando Lopitz‐Otsoa, Manuel S. Rodríguez, Tony W. H. Li, Kwangsuk Ko, Heping Yang, Fawzia Bardag‐Gorce, Ainhoa Iglesias‐Ara, Francesco Feo, Maria Rosa Pascale, José M. Mato, Shelly C. Lu – 23 May 2010 – Increased mitogen‐activated protein kinase (MAPK) activity correlates with a more malignant hepatocellular carcinoma (HCC) phenotype. There is a reciprocal regulation between p44/42 MAPK (extracellular signal‐regulated kinase [ERK]1/2) and the dual‐specificity MAPK phosphatase MKP‐1/DUSP1.