Gin‐Ho Lo, Wen‐Chi Chen, Huay‐Min Wang, Ching‐Chang Lee – 23 June 2010 – Both nadolol and ligation have proved to be effective in the prophylaxis of first variceal bleeding. This study was conducted to evaluate the effects and safety of combining nadolol with ligation. Cirrhotic patients with high‐risk esophageal varices but without a bleeding history were considered for enrolment. Eligible patients were randomized to receive band ligation plus nadolol (Combined group, 70 patients) or nadolol alone (Nadolol group, 70 patients). In the Combined group multiligators were applied.

Marco Antonio Montes‐Cano, José Raúl García‐Lozano, Cristina Abad‐Molina, Manuel Romero‐Gómez, Natalia Barroso, José Aguilar‐Reina, Antonio Núñez‐Roldán, María Francisca González‐Escribano – 23 June 2010 – Genetic host factors may modify the course of the hepatitis C virus (HCV) infection. Very recently, a genome‐wide scan that reported association of the IL28B locus with response to treatment in HCV infection was published.

Guo‐Ming Shi, Ai‐Wu Ke, Jian Zhou, Xiao‐Ying Wang, Yang Xu, Zhen‐Bin Ding, Ranjan Prasad Devbhandari, Xiao‐Yong Huang, Shuang‐Jian Qiu, Ying‐Hong Shi, Zhi Dai, Xin‐Rong Yang, Guo‐Huan Yang, Jia Fan – 23 June 2010 – Tetraspanin CD151 is involved in several pathological activities associated with tumor progression, including neoangiogenesis. However, the role and molecular mechanism of CD151 in the neoangiogenesis of hepatocellular carcinoma (HCC) remain enigmatic.

Janina E. E. Tirnitz‐Parker, Cornelia S. Viebahn, Aniela Jakubowski, Borut R. S. Klopcic, John K. Olynyk, George C. T. Yeoh, Belinda Knight – 23 June 2010 – Liver progenitor cells (LPCs) represent the cell compartment facilitating hepatic regeneration during chronic injury while hepatocyte‐mediated repair mechanisms are compromised. LPC proliferation is frequently observed in human chronic liver diseases such as hereditary hemochromatosis, fatty liver disease, and chronic hepatitis.

Nabora Soledad Reyes de Mochel, Scott Seronello, Shelley Hsiuying Wang, Chieri Ito, Jasper Xi Zheng, T. Jake Liang, J. David Lambeth, Jinah Choi – 23 June 2010 – Oxidative stress has been identified as a key mechanism of hepatitis C virus (HCV)–induced pathogenesis. Studies have suggested that HCV increases the generation of hydroxyl radical and peroxynitrite close to the cell nucleus, inflicting DNA damage, but the source of reactive oxygen species (ROS) remains incompletely characterized.

Thomas Touboul, Nicholas R. F. Hannan, Sébastien Corbineau, Amélie Martinez, Clémence Martinet, Sophie Branchereau, Sylvie Mainot, Hélène Strick‐Marchand, Roger Pedersen, James Di Santo, Anne Weber, Ludovic Vallier – 23 June 2010

Philippe Halfon, Michelle Martinot‐Peignoux, Hacène Khiri, Patrick Marcellin – 23 June 2010

Mariana Verdelho Machado, António Gouveia Oliveira, Helena Cortez‐Pinto – 23 June 2010 – Hepatic steatosis (HS) is frequent in patients with hepatitis C virus (HCV) infection, occurring in 40%‐80%, associating with metabolic and virus‐related factors, namely, genotype 3 and viral load. Human immunodeficiency virus (HIV) infection and antiretroviral treatment seem to be risk factors for HS. Several studies addressed this issue in coinfected patients, with discrepant results. A meta‐analysis was performed on the HS risk factors in coinfected patients.

Emmanouil Sinakos, Hanns‐Ulrich Marschall, Kris V. Kowdley, Alex Befeler, Jill Keach, Keith Lindor – 23 June 2010 – High‐dose (28‐30 mg/kg/day) ursodeoxycholic acid (UDCA) treatment improves serum liver tests in patients with primary sclerosing cholangitis (PSC) but does not improve survival and is associated with increased rates of serious adverse events. The mechanism for the latter undesired effect remains unclear.

Steve S. Choi, Rafal P. Witek, Liu Yang, Alessia Omenetti, Wing‐Kin Syn, Cynthia A. Moylan, Youngmi Jung, Gamze F. Karaca, Vanessa S. Teaberry, Thiago A. Pereira, Jiangbo Wang, Xiu‐Rong Ren, Anna Mae Diehl – 23 June 2010 – Hepatic accumulation of myofibroblastic hepatic stellate cells (MF‐HSCs) is pivotal in the pathogenesis of cirrhosis. Two events are necessary for MF‐HSCs to accumulate in damaged livers: transition of resident, quiescent hepatic stellate cells (Q‐HSCs) to MF‐HSCs and expansion of MF‐HSC numbers through increased proliferation and/or reduced apoptosis.