Oxidative stress induces anti‐hepatitis C virus status via the activation of extracellular signal‐regulated kinase

Masahiko Yano, Masanori Ikeda, Ken‐ichi Abe, Yoshinari Kawai, Misao Kuroki, Kyoko Mori, Hiromichi Dansako, Yasuo Ariumi, Shougo Ohkoshi, Yutaka Aoyagi, Nobuyuki Kato – 27 August 2009 – Recently, we reported that β‐carotene, vitamin D2, and linoleic acid inhibited hepatitis C virus (HCV) RNA replication in hepatoma cells. Interestingly, in the course of the study, we found that the antioxidant vitamin E negated the anti‐HCV activities of these nutrients. These results suggest that the oxidative stress caused by the three nutrients is involved in their anti‐HCV activities.

Long‐term reduction of jaundice in Gunn rats by nonviral liver‐targeted delivery of Sleeping Beauty transposon

Xia Wang, Debi P. Sarkar, Prashant Mani, Clifford J. Steer, Yong Chen, Chandan Guha, Voshavar Chandrasekhar, Arabinda Chaudhuri, Namita Roy‐Chowdhury, Betsy T. Kren, Jayanta Roy‐Chowdhury – 27 August 2009 – Asialoglycoprotein receptor (ASGPR)‐mediated endocytosis has been used to target genes to hepatocytes in vivo. However, the level and duration of transgene expression have been low because of lysosomal translocation and degradation of the DNA and lack of its integration into the host genome.

CD24 polymorphisms affect risk and progression of chronic hepatitis B virus infection

Dongling Li, Linghua Zheng, Lei Jin, Yuesu Zhou, Haiying Li, Junliang Fu, Ming Shi, Peishuang Du, Lizhong Wang, Hao Wu, Guo‐Yun Chen, Pan Zheng, Yang Liu, Fu‐Sheng Wang, Shengdian Wang – 27 August 2009 – T‐cell immunity to hepatitis B virus (HBV) is involved in both viral clearance and the pathogenesis of cirrhosis and hepatocellular carcinoma following chronic HBV infection. It is therefore of great interest to analyze whether genetic polymorphism of genes involved in the immune response may determine the outcomes of chronic HBV infection.

Microenvironmental regulation of the sinusoidal endothelial cell phenotype in vitro

Sandra March, Elliot E. Hui, Gregory H. Underhill, Salman Khetani, Sangeeta N. Bhatia – 27 August 2009 – Liver sinusoidal endothelial cells (LSECs) differ, both structurally and functionally, from endothelial cells (ECs) lining blood vessels of other tissues. For example, in contrast to other ECs, LSECs possess fenestrations, have low detectable levels of platelet endothelial cell adhesion molecule 1 expression, and in rat tissue, they distinctively express a cell surface marker recognized by the SE‐1 antibody.

Myeloid derived suppressor cells inhibit natural killer cells in patients with hepatocellular carcinoma via the NKp30 receptor

Bastian Hoechst, Torsten Voigtlaender, Lars Ormandy, Jaba Gamrekelashvili, Fei Zhao, Heiner Wedemeyer, Frank Lehner, Michael P. Manns, Tim F. Greten, Firouzeh Korangy – 27 August 2009 – Several immune suppressive mechanisms that evade the host immune response have been described in patients with hepatocellular carcinoma (HCC); one of these mechanisms is expansion of myeloid‐derived suppressor cells (MDSCs). MDSCs have been shown to inhibit T cell responses in tumor‐bearing mice, but little is known about these cells in humans.

Less Smad2 is good for you! A scientific update on coffee's liver benefits

Olav A. Gressner – 27 August 2009 – Scientists at the National Institutes of Health have reported that increased coffee consumption is associated with a slower progression of fibrogenesis in patients with chronic and particularly alcoholic liver disease and a reduced incidence of heptocellular carcinoma. However, a causal mechanistic explanation was pending.

Aggravation by prostaglandin E2 of interleukin‐6‐dependent insulin resistance in hepatocytes

Janin Henkel, Frank Neuschäfer‐Rube, Andrea Pathe‐Neuschäfer‐Rube, Gerhard P. Püschel – 27 August 2009 – Hepatic insulin resistance is a major contributor to fasting hyperglycemia in patients with metabolic syndrome and type 2 diabetes. Circumstantial evidence suggests that cyclooxygenase products in addition to cytokines might contribute to insulin resistance. However, direct evidence for a role of prostaglandins in the development of hepatic insulin resistance is lacking.

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