Heme oxygenase‐1 suppresses hepatitis C virus replication and increases resistance of hepatocytes to oxidant injury

Zhaowen Zhu, Anne T. Wilson, M. Meleah Mathahs, Feng Wen, Kyle E. Brown, Bruce A. Luxon, Warren N. Schmidt – 28 October 2008 – Oxidative injury to hepatocytes occurs as a result of hepatitis C virus (HCV) infection and replication. Modulation of host cell antioxidant enzymes such as heme oxygenase‐1 (HO‐1) may be useful therapeutically to minimize cellular injury, reduce viral replication, and attenuate liver disease. In this report, we evaluated the effects of HO‐1 overexpression on HCV replication and hepatocellular injury.

Functional alterations of liver innate immunity of mice with aging in response to CpG‐oligodeoxynucleotide

Toshinobu Kawabata, Manabu Kinoshita, Akihito Inatsu, Yoshiko Habu, Hiroyuki Nakashima, Nariyoshi Shinomiya, Shuhji Seki – 28 October 2008 – Immune functions of liver natural killer T (NKT) cells induced by the synthetic ligand α‐galactosylceramide enhanced age‐dependently; hepatic injury and multiorgan dysfunction syndrome (MODS) induced by ligand‐activated NKT cells were also enhanced. This study investigated how aging affects liver innate immunity after common bacteria DNA stimulation.

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.

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.

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++.

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.

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.

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.

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