B7‐H4 mediates inhibition of T cell responses by activated murine hepatic stellate cells

Raghavan Chinnadurai, Arash Grakoui – 1 September 2010 – Liver fibrosis is mediated by the transformation of hepatic stellate cells (HSC) from a quiescent to an activated state. To understand the role of HSC in liver immunity, we investigated the effect of this transition on T cell stimulation in vitro. Unlike quiescent HSC, activated HSC did not induce proliferation of antigen‐specific T cells. Phenotypic analysis of quiescent and activated HSC revealed that activated HSC expressed the coinhibitory molecule B7‐H4.

Unconjugated bile salts shuttle through hepatocyte peroxisomes for taurine conjugation

Krzysztof P. Rembacz, Jannes Woudenberg, Mark Hoekstra, Elles Z. Jonkers, Fiona A.J. van den Heuvel, Manon Buist‐Homan, Titia E. Woudenberg‐Vrenken, Jana Rohacova, M. Luisa Marin, Miguel A. Miranda, Han Moshage, Frans Stellaard, Klaas Nico Faber – 1 September 2010 – Bile acid‐CoA:amino acid N‐acyltransferase (BAAT) conjugates bile salts to glycine or taurine, which is the final step in bile salt biosynthesis. In addition, BAAT is required for reconjugation of bile salts in the enterohepatic circulation.

Association of host pharmacodynamic effects with virologic response to pegylated interferon alfa‐2a/ribavirin in chronic hepatitis C

Raymond T. Chung, Fred F. Poordad, Tarek Hassanein, Xiaolei Zhou, Ellen Lentz, Avinash Prabhakar, Adrian M. Di Bisceglie – 31 August 2010 – Patients receiving therapy for chronic hepatitis C virus (HCV) infection frequently experience cytopenias and weight loss. We retrospectively assessed the pharmacodynamic effects of pegylated interferon (PEG‐IFN) alfa‐2a and ribavirin by evaluating the relationship between changes in hematologic parameters, body weight, and virologic response.

Incidental intracardiac thromboemboli during liver transplantation: Incidence, risk factors, and management

Victor W. Xia, Jonathan K. Ho, Hamid Nourmand, Christopher Wray, Ronald W. Busuttil, Randolph H. Steadman – 31 August 2010 – Even though numerous cases of massive thromboemboli have been reported in the literature, intracardiac thromboemboli (ICTs) incidentally found during orthotopic liver transplantation (OLT) have not been examined. In this study, we retrospectively examined the incidence, risk factors, and management of incidental ICTs during OLT.

Alemtuzumab induction in non‐hepatitis C positive liver transplant recipients

Josh Levitsky, Kavitha Thudi, Michael G. Ison, Edward Wang, Michael Abecassis – 31 August 2010 – Limited data exist for the use of alemtuzumab (AL) induction in liver transplantation (LT) recipients. We compared the outcomes of hepatitis C virus–negative LT recipients who received AL induction followed by tacrolimus and mycophenolate mofetil without steroids to cohort who received no AL induction, tacrolimus, and a steroid taper. Fifty‐five AL‐induced recipients were compared to 85 non–AL‐induced recipients with similar characteristics.

Down‐regulation of tumor suppressor a kinase anchor protein 12 in human hepatocarcinogenesis by epigenetic mechanisms

Benjamin Goeppert, Peter Schmezer, Céline Dutruel, Christopher Oakes, Marcus Renner, Marco Breinig, Arne Warth, Monika Nadja Vogel, Michel Mittelbronn, Arianeb Mehrabi, Georg Gdynia, Roland Penzel, Thomas Longerich, Kai Breuhahn, Odilia Popanda, Christoph Plass, Peter Schirmacher, Michael André Kern – 31 August 2010 – The A kinase anchor protein 12 (AKAP12) is a central mediator of protein kinase A and protein kinase C signaling.

Thrombin is a therapeutic target for metastatic osteopontin‐positive hepatocellular carcinoma

Yu‐Hua Xue, Xiao‐Fei Zhang, Qiong‐Zhu Dong, Jian Sun, Chun Dai, Hai‐Jun Zhou, Ning Ren, Hu‐Liang Jia, Qin‐Hai Ye, Lun‐Xiu Qin – 31 August 2010 – We previously identified osteopontin (OPN) as a promoter and thus a potential therapeutic target for hepatocellular carcinoma (HCC) metastasis. The serine protease thrombin interacts with OPN and can modify its biological activity.

Rosiglitazone attenuates age‐ and diet‐associated nonalcoholic steatohepatitis in male low‐density lipoprotein receptor knockout mice

Anisha A. Gupte, Joey Z. Liu, Yuelan Ren, Laurie J. Minze, Jessica R. Wiles, Alan R. Collins, Christopher J. Lyon, Domenico Pratico, Milton J. Finegold, Stephen T. Wong, Paul Webb, John D. Baxter, David D. Moore, Willa A. Hsueh – 31 August 2010 – Nonalcoholic fatty liver disease (NAFLD) is a common complication of obesity that can progress to nonalcoholic steatohepatitis (NASH), a serious liver pathology that can advance to cirrhosis. The mechanisms responsible for NAFLD progression to NASH remain unclear.

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