Inflammation‐associated interleukin‐6/signal transducer and activator of transcription 3 activation ameliorates alcoholic and nonalcoholic fatty liver diseases in interleukin‐10–deficient mice

Andrew M. Miller, Hua Wang, Adeline Bertola, Ogyi Park, Norio Horiguchi, Sung Hwan Ki, Shi Yin, Fouad Lafdil, Bin Gao – 2 July 2011 – Alcoholic and nonalcoholic steatohepatitis are characterized by fatty liver plus inflammation. It is generally believed that steatosis promotes inflammation, whereas inflammation in turn aggregates steatosis.

Reversal of hepatitis B virus‐induced immune tolerance by an immunostimulatory 3p‐HBx‐siRNAs in a retinoic acid inducible gene I–dependent manner

Qiuju Han, Cai Zhang, Jian Zhang, Zhigang Tian – 30 June 2011 – It is extensively accepted that hepatitis B virus (HBV) escapes from innate immunity by inhibiting type I interferon (IFN) production, but efficient intervention to reverse the immune tolerance is still not achieved.

Novel poly (ADP‐ribose) polymerase 1 binding motif in hepatitis B virus core promoter impairs DNA damage repair

Hui‐Ling Ko, Ee‐Chee Ren – 30 June 2011 – It is well‐established that hepatitis B virus (HBV) infection is associated with the development of hepatocellular carcinoma (HCC), but patients with high viral DNA load have significantly higher risk. As host factors are required for efficient viral replication and may, therefore, contribute to high viral DNA load, we screened for host factors that can transcriptionally activate the HBV core promoter (HBVCP).

Endogenous histones function as alarmins in sterile inflammatory liver injury through Toll‐like receptor 9 in mice

Hai Huang, John Evankovich, Wei Yan, Gary Nace, Lemeng Zhang, Mark Ross, Xinghua Liao, Timothy Billiar, Jun Xu, Charles T. Esmon, Allan Tsung – 30 June 2011 – Sterile inflammatory insults are known to activate innate immunity and propagate organ damage through the recognition of extracellular damage‐associated molecular pattern (DAMP) molecules. Although DAMPs such as endogenous DNA and nuclear high‐mobility group box 1 have been shown to be critical in sterile inflammation, the role of nuclear histone proteins has not yet been investigated.

Cross‐presentation of antigen by diverse subsets of murine liver cells

Mohammad R. Ebrahimkhani, Isaac Mohar, Ian N. Crispe – 30 June 2011 – Antigen cross‐presentation is a principal function of specialized antigen‐presenting cells of bone marrow origin such as dendritic cells. Although these cells are sometimes known as “professional” antigen‐presenting cells, nonbone marrow‐derived cells may also act as antigen‐presenting cells.

Fighting against viral hepatitis: Lessons from Taiwan

Ding‐Shinn Chen – 30 June 2011 – Viral hepatitis and its sequelae are important health problems worldwide, including Taiwan. For the last 40 years, Taiwan's scientists and health care providers have worked hard to control these sequelae, and the results have been excellent. The author, Ding‐Shinn Chen, had a key role in planning and establishing the control program in Taiwan, and participated in the endeavors from the very beginning.

Spontaneous repopulation of β‐catenin null livers with β‐catenin‐positive hepatocytes after chronic murine liver injury

Michael D. Thompson, Emily D. Wickline, William B. Bowen, Amy Lu, Sucha Singh, Amalea Misse, Satdarshan P.S. Monga – 30 June 2011 – Prolonged exposure of mice to diet containing 0.1% 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine (DDC) results in hepatobiliary injury, atypical ductular proliferation, oval cell appearance, and limited fibrosis. Previously, we reported that short‐term ingestion of DDC diet by hepatocyte‐specific β‐catenin conditional knockout (KO) mice led to fewer A6‐positive oval cells than wildtype (WT) littermates.

Intercellular nanovesicle‐mediated microRNA transfer: A mechanism of environmental modulation of hepatocellular cancer cell growth

Takayuki Kogure, Wen‐Lang Lin, Irene K. Yan, Chiara Braconi, Tushar Patel – 30 June 2011 – Hepatocellular carcinoma (HCC) is characterized by a propensity for multifocality, growth by local spread, and dysregulation of multiple signaling pathways. These features may be determined by the tumoral microenvironment. The potential of tumor cells to modulate HCC growth and behavior by secreted proteins has been extensively studied. In contrast, the potential for genetic modulation is poorly understood.

Genetic variation in the interleukin‐28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection

Francesco Marabita, Alessio Aghemo, Stella De Nicola, Maria G. Rumi, Cristina Cheroni, Rossana Scavelli, Marco Crimi, Roberta Soffredini, Sergio Abrignani, Raffaele De Francesco, Massimo Colombo – 30 June 2011 – Polymorphisms in the interleukin‐28B (IL28B) region are associated with spontaneous and treatment‐induced viral clearance in hepatitis C virus (HCV) infection. Nevertheless, it is unknown whether genetic variation at the IL28B locus influences the natural history of chronic HCV infection.

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