Fatty acid synthase is up‐regulated during hepatitis C virus infection and regulates hepatitis C virus entry and production

Wei Yang, Brian L. Hood, Sara L. Chadwick, Shufeng Liu, Simon C. Watkins, Guangxiang Luo, Thomas P. Conrads, Tianyi Wang – 28 October 2008 – Hepatitis C virus (HCV) is a major human pathogen that causes serious illness, including acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma.

Treating hepatitis C in the prison population is cost‐saving

Jennifer A. Tan, Tom A. Joseph, Sammy Saab – 28 October 2008 – The prevalence of chronic hepatitis C infection in U.S. prisons is 12% to 31%. Treatment of this substantial portion of the population has been subject to much controversy, both medically and legally. Studies have demonstrated that treatment of chronic hepatitis C with pegylated interferon (PEG IFN) and ribavirin is a cost‐effective measure in the general population; however, no study has addressed whether the same is true of the prison population.

Using controlled clinical trials to learn more about acute drug‐induced liver injury

Paul B. Watkins, Paul J. Seligman, John S. Pears, Mark I. Avigan, John R. Senior – 28 October 2008 – Drug‐induced liver injury (DILI) is of major interest to hepatologists and clinicians in general, patients, government regulators, and the pharmaceutical industry. Understanding why this form of injury occurs only in certain individuals has major implications for the development and availability of drug therapies and in the prevention of these events.

Suppressor of cytokine signaling‐3 (SOCS‐3) and a deficit of serine/threonine (Ser/Thr) phosphoproteins involved in leptin transduction mediate the effect of fructose on rat liver lipid metabolism

Laia Vilà, Núria Roglans, Marta Alegret, Rosa María Sánchez, Manuel Vázquez‐Carrera, Juan Carlos Laguna – 28 October 2008 – There is controversy regarding whether fructose in liquid beverages constitutes another dietary ingredient of high caloric density or introduces qualitative changes in energy metabolism that further facilitate the appearance of metabolic diseases. Central to this issue is the elucidation of the molecular mechanism responsible for the metabolic alterations induced by fructose ingestion.

Alterations in hepatic glucose and energy metabolism as a result of calorie and carbohydrate restriction

Jeffrey D. Browning, Brian Weis, Jeannie Davis, Santhosh Satapati, Matthew Merritt, Craig R. Malloy, Shawn C. Burgess – 28 October 2008 – Carbohydrate restriction is a common weight‐loss approach that modifies hepatic metabolism by increasing gluconeogenesis (GNG) and ketosis.

The stem cell niche of human livers: Symmetry between development and regeneration

Lili Zhang, Neil Theise, Michael Chua, Lola M. Reid – 28 October 2008 – Human livers contain two pluripotent progenitors: hepatic stem cells and hepatoblasts. The hepatic stem cells uniquely express the combination of epithelial cell adhesion molecule (EpCAM), neural cell adhesion molecule (NCAM), cytokeratin (CK) 19, albumin ±, and are negative for α‐fetoprotein (AFP). They are precursors to hepatoblasts, which differ from hepatic stem cells in size, morphology, and in expressing the combination of EpCAM, intercellular cell adhesion molecule (ICAM‐1), CK19, albumin++, and AFP++.

Treatment of chronic hepatitis C in hemodialysis patients

Marina Berenguer – 28 October 2008 – Hepatitis C virus (HCV) infection is especially problematic in patients with end‐stage renal disease (ESRD) who are undergoing hemodialysis. Rates of HCV infection are higher among hemodialysis patients than in the general population, and several routes of transmission are thought to stem from the dialysis unit. Management of chronic hepatitis C is also more complicated in hemodialysis patients because of altered pharmacokinetics and a predisposition for drug‐related toxicity, particularly ribavirin‐induced anemia.

Hepatitis C virus–induced oxidative stress suppresses hepcidin expression through increased histone deacetylase activity

Kouichi Miura, Kojiro Taura, Yuzo Kodama, Bernd Schnabl, David A. Brenner – 28 October 2008 – Chronic hepatitis C is characterized by iron accumulation in the liver, and excessive iron is hepatotoxic. However, the mechanism by which hepatitis C virus (HCV) regulates iron metabolism is poorly understood. Hepcidin plays a pivotal role as a negative regulator of iron absorption. The aim of the current study was to elucidate the mechanisms that govern hepcidin expression by HCV.

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