Amino acid substitution in hepatitis C virus core region and genetic variation near the interleukin 28B gene predict viral response to telaprevir with peginterferon and ribavirin

Norio Akuta, Fumitaka Suzuki, Miharu Hirakawa, Yusuke Kawamura, Hiromi Yatsuji, Hitomi Sezaki, Yoshiyuki Suzuki, Tetsuya Hosaka, Masahiro Kobayashi, Mariko Kobayashi, Satoshi Saitoh, Yasuji Arase, Kenji Ikeda, Kazuaki Chayama, Yusuke Nakamura, Hiromitsu Kumada – 23 July 2010 – Genetic variation near the IL28B gene and substitution of amino acid (aa) 70 and 91 in the core region of hepatitis C virus (HCV) genotype 1b can predict the response to pegylated interferon (PEG‐IFN)/ribavirin combination therapy, but its impact on triple therapy of telaprevir/PEG‐IFN/ribavirin is not clear.

Hepatic iron loading in mice increases cholesterol biosynthesis

Ross M. Graham, Anita C. G. Chua, Kim W. Carter, Roheeth D. Delima, Daniel Johnstone, Carly E. Herbison, Martin J. Firth, Rebecca O'Leary, Elizabeth A. Milward, John K. Olynyk, Debbie Trinder – 23 July 2010 – Iron and cholesterol are both essential metabolites in mammalian systems, and too much or too little of either can have serious clinical consequences. In addition, both have been associated with steatosis and its progression, contributing, inter alia, to an increase in hepatic oxidative stress.

Carbonyl reductase 1 as a novel target of (−)‐epigallocatechin gallate against hepatocellular carcinoma

Weixue Huang, Liya Ding, Qiang Huang, Hairong Hu, Shan Liu, Xianmei Yang, Xiaohui Hu, Yongjun Dang, Suqin Shen, Jie Li, Xiaona Ji, Songmin Jiang, Jun O. Liu, Long Yu – 23 July 2010 – Human carbonyl reductase 1 (CBR1) converts the antitumor drug and anthracycline daunorubicin (DNR) into the alcohol metabolite daunorubicinol (DNROL) with significantly reduced antitumor activity and cardiotoxicity, and this limits the clinical use of DNR. Inhibition of CBR1 can thus increase the efficacy and decrease the toxicity of DNR.

Transcriptome sequencing, microarray, and proteomic analyses reveal cellular and metabolic impact of hepatitis C virus infection in vitro

Stephen D. Woodhouse, Ramamurthy Narayan, Sally Latham, Sheena Lee, Robin Antrobus, Bevin Gangadharan, Shujun Luo, Gary P. Schroth, Paul Klenerman, Nicole Zitzmann – 23 July 2010 – Hepatitis C virus (HCV) is a major cause of liver disease but the full impact of HCV infection on the hepatocyte is poorly understood. RNA sequencing (RNA‐Seq) is a novel method to analyze the full transcriptional activity of a cell or tissue, thus allowing new insight into the impact of HCV infection.

Evaluation of depression as a risk factor for treatment failure in chronic hepatitis C

Peter Derek Christian Leutscher, Martin Lagging, Mads Rauning Buhl, Court Pedersen, Gunnar Norkrans, Nina Langeland, Kristine Mørch, Martti Färkkilä, Simon Hjerrild, Kristoffer Hellstrand, Per Bech, for the NORDynamIC Group – 23 July 2010 – The Major Depression Inventory (MDI) was used to estimate the value of routine medical interviews in diagnosing major depression among patients receiving peginterferon alfa‐2a and ribavirin therapy for chronic hepatitis C virus (HCV) infection (n = 325).

Molecular characterization of the vascular features of focal nodular hyperplasia and hepatocellular adenoma: A role for angiopoietin‐1

Annette S. H. Gouw, Wenjiao Zeng, Marijke Buiskool, Inge Platteel, Marius C. van den Heuvel, Sibrand Poppema, Koert P. de Jong, Grietje Molema – 23 July 2010 – Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are two hepatic nodular lesions of different etiologies. FNH, a polyclonal lesion, is assumed to be a regenerative reaction following a vascular injury, whereas HCA is a monoclonal, benign neoplastic lesion.

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