Ghazaleh Aram, James J. Potter, Xiaopu Liu, Lan Wang, Michael S. Torbenson, Esteban Mezey – 24 February 2009 – Reactive oxygen species (ROS) activate hepatic stellate cells and enhance fibrogenesis. This study determined the role of nicotinamide adenine dinucleotide phosphate, reduced form (NADPH) oxidase deficiency in the development of hepatocellular necrosis, inflammation, and apoptosis in relation to fibrosis produced by chronic carbon tetrachloride (CCl4) administration.

Li Ye, Xu Wang, Shihong Wang, Yanjian Wang, Li Song, Wei Hou, Lin Zhou, He Li, Wenzhe Ho – 24 February 2009 – CD56+ T cells are abundant in liver and play an important role in defense against viral infections. However, the role of CD56+ T cells in control of hepatitis C virus (HCV) infection remains to be determined. We investigated the noncytolytic anti‐HCV activity of primary CD56+ T cells in human hepatocytes.

Christophe Frémin, Anne Bessard, Frédéric Ezan, Luc Gailhouste, Morgane Régeard, Jacques Le Seyec, David Gilot, Gilles Pagès, Jacques Pouysségur, Sophie Langouët, Georges Baffet – 24 February 2009 – We investigated the specific role of the mitogen‐activated protein kinase (MAPK) extracellular signal‐regulated kinase 1 (ERK1)/ERK2 pathway in the regulation of multiple cell cycles and long‐term survival of normal hepatocytes. An early and sustained epidermal growth factor (EGF)‐dependent MAPK activation greatly improved the potential of cell proliferation.

Teoman Dogru, Cemal Nuri Ercin, Gokhan Erdem, Guldem Kilciler, Serkan Tapan – 24 February 2009

Yasuji Arase, Fumitaka Suzuki, Yoshiyuki Suzuki, Norio Akuta, Masahiro Kobayashi, Yusuke Kawamura, Hiromi Yatsuji, Hitomi Sezaki, Tetsuya Hosaka, Miharu Hirakawa, Kenji Ikeda, Hiromitsu Kumada – 24 February 2009 – Diabetes is present in patients with chronic hepatitis C virus infection. The aim of this retrospective cohort study was to assess the cumulative development incidence and predictive factors for type 2 diabetes after the termination of interferon therapy in Japanese patients positive for hepatitis C virus (HCV).

Richard G. Ruddell, Diem Hoang‐Le, Joanne M. Barwood, Paul S. Rutherford, Terrance J. Piva, Dianne J. Watters, Paolo Santambrogio, Paolo Arosio, Grant A. Ramm – 24 February 2009 – Circulating ferritin levels reflect body iron stores and are elevated with inflammation in chronic liver injury. H‐ferritin exhibits a number of extrahepatic immunomodulatory properties, although its role in hepatic inflammation and fibrogenesis is unknown. Hepatic stellate cells respond to liver injury through production of proinflammatory mediators that drive fibrogenesis.

Richard Guerrero, Gloria L. Vega, Scott M. Grundy, Jeffrey D. Browning – 24 February 2009 – Nonalcoholic fatty liver disease is a burgeoning problem. We have previously shown that Hispanics were at greater risk for nonalcoholic fatty liver disease than were African‐Americans despite a similar prevalence of risk factors between these groups.

Christian Toso, Sonal Asthana, David L. Bigam, A. M. James Shapiro, Norman M. Kneteman – 24 February 2009 – The current model of liver graft allocation in place in the United States favors transplantation of patients with small hepatocellular carcinomas (HCCs) within the Milan criteria (a single tumor up to 5 cm in diameter or up to three lesions, none larger than 3 cm). Although several reports have suggested that these criteria could be extended, there is currently no agreement on new selection tools.

Sarah L. George, Bruce R. Bacon, Elizabeth M. Brunt, Kusal L. Mihindukulasuriya, Joyce Hoffmann, Adrian M. Di Bisceglie – 24 February 2009 – One hundred fifty patients with sustained virologic response (SVR) after treatment of chronic hepatitis C were enrolled in a long‐term clinical follow‐up study; patients were followed for 5 years for liver‐related outcomes and evidence of biochemical or virologic relapse. Patients with stage 2 or greater fibrosis on pretreatment biopsy were invited to undergo a long‐term follow‐up biopsy after their fourth year of follow‐up.

Timothy J. Kendall, Selina Hennedige, Rebecca L. Aucott, Stephen N. Hartland, Madeleine A. Vernon, R. Christopher Benyon, John P. Iredale – 24 February 2009 – Hepatic myofibroblast apoptosis is critical to resolution of liver fibrosis. We show that human hepatic myofibroblasts co‐express p75NTR (p75 neurotrophin receptor) and sortilin, thus facilitating differential responses to mature and pro nerve growth factor (proNGF). Although mature NGF is proapoptotic, proNGF protects human hepatic myofibroblasts from apoptosis.