Alexandra Milona, Bryn M. Owen, Jeremy F. L. Cobbold, Ellen C. L. Willemsen, Isobel J. Cox, Mohamed Boudjelal, William Cairns, Kristina Schoonjans, Simon D. Taylor‐Robinson, Leo W. J. Klomp, Malcolm G. Parker, Roger White, Saskia W. C. van Mil, Catherine Williamson – 29 July 2010 – Pregnancy alters bile acid homeostasis and can unmask cholestatic disease in genetically predisposed but otherwise asymptomatic individuals. In this report, we show that normal pregnant mice have raised hepatic bile acid levels in the presence of procholestatic gene expression.

Le‐Xing Yu, He‐Xin Yan, Qiong Liu, Wen Yang, Hong‐Ping Wu, Wei Dong, Liang Tang, Yan Lin, Ya‐Qin He, Shan‐Shan Zou, Chao Wang, Hui‐Lu Zhang, Guang‐Wen Cao, Meng‐Chao Wu, Hong‐Yang Wang – 29 July 2010 – Increasing evidence suggests that the presence of endotoxemia is of substantial clinical relevance to patients with cirrhosis, but it is unclear whether and how gut‐derived LPS amplifies the tumorigenic response of the liver. We found that the circulating levels of LPS were elevated in animal models of carcinogen‐induced hepatocarcinogenesis.

Mrzljak Anna, Peric Zinaida, Kovacevic Visnja, Gustin Denis, Vrhovac Radovan, Andrasevic Arjana Tambic – 29 July 2010

Albert J. Czaja – 29 July 2010 – Autoimmune hepatitis emerged during an era when concepts of neonatal immune tolerance, clonal selection of lymphocytes, and “forbidden clones” of activated immune cells were forming. The diagnosis had to be deduced from circumstantial evidence and by exclusion of other conditions. The goals of this review are to demonstrate how a clinician nonscientist can contribute to the maturation of autoimmune hepatitis and to illustrate the principles of clinical investigation that can be applied broadly to other projects.

Robert Roomer, Bettina E. Hansen, Harry L. A. Janssen, Robert J. de Knegt – 29 July 2010 – Neutropenia during treatment with peginterferon alfa and ribavirin for chronic hepatitis C virus (HCV) infection is a common cause of dose reductions of peginterferon alfa. These reductions are performed to prevent bacterial and fungal infections, which are common during HCV treatment and can be attributed to neutropenia. The aims of this study were to investigate the occurrence of infections and their relation to neutropenia and to identify potential risk factors for infections during HCV treatment.

Giorgia Ghittoni, Eugenio Caturelli, Sandro Rossi – 29 July 2010

Jason Grebely, Kathy Petoumenos, Margaret Hellard, Gail V. Matthews, Vijayaprakash Suppiah, Tanya Applegate, Barbara Yeung, Phillipa Marks, William Rawlinson, Andrew R. Lloyd, David Booth, John M. Kaldor, Jacob George, Gregory J. Dore, for the ATAHC Study Group – 29 July 2010 – Polymorphisms in the IL28B (interleukin‐28B) gene region are important in predicting outcome following therapy for chronic hepatitis C virus (HCV) infection. We evaluated the role of IL28B in spontaneous and treatment‐induced clearance following recent HCV infection.

Milan J. Sonneveld, Vincent Rijckborst, Charles A. B. Boucher, Bettina E. Hansen, Harry L. A. Janssen – 29 July 2010 – Serum hepatitis B surface antigen (HBsAg) levels may reflect the immunomodulatory efficacy of pegylated interferon (PEG‐IFN). We investigated within a large randomized trial whether quantitative HBsAg levels predict response to PEG‐IFN in patients with hepatitis B e antigen (HBeAg)‐positive chronic hepatitis B.

Haofeng Ji, Xiuda Shen, Feng Gao, Bibo Ke, Maria Cecilia S. Freitas, Yoichiro Uchida, Ronald W. Busuttil, Yuan Zhai, Jerzy W. Kupiec‐Weglinski – 29 July 2010 – Programmed death‐1 (PD‐1)/B7‐H1 costimulation acts as a negative regulator of host alloimmune responses. Although CD4 T cells mediate innate immunity‐dominated ischemia and reperfusion injury (IRI) in the liver, the underlying mechanisms remain to be elucidated. This study focused on the role of PD‐1/B7‐H1 negative signaling in liver IRI.

James G. Cripps, Jing Wang, Ann Maria, Ian Blumenthal, James D. Gorham – 29 July 2010 – Immune‐mediated liver injury in hepatitis is due to activated T cells producing interferon‐γ (IFN‐γ). It is important to identify negative feedback immune mechanisms that can regulate T cell activity.