Management of patients with hepatitis C virus genotype 2 or 3: Comments on updated american association for the study of liver diseases practice guidelines
Olav Dalgard, Alessandra Mangia – 23 June 2009
Olav Dalgard, Alessandra Mangia – 23 June 2009
Kinji Asahina, Hidekazu Tsukamoto – 23 June 2009
Melania Manco, Valerio Nobili – 23 June 2009
Lars Marius Ytrebø, Rune Gangsøy Kristiansen, Hanne Mæhre, Ole Martin Fuskevåg, Trine Kalstad, Arthur Revhaug, María Jover Cobos, Rajiv Jalan, Christopher F. Rose – 23 June 2009 – Hyperammonemia is a feature of acute liver failure (ALF), which is associated with increased intracranial pressure (ICP) and brain herniation.
Leilei Chen, Liang Hu, Tim Hon Man Chan, George Sai‐Wah Tsao, Dan Xie, Ke‐Ke Huo, Li Fu, Stephanie Ma, Bo‐Jian Zheng, Xin‐Yuan Guan – 23 June 2009 – Amplification of 1q21 has been detected in 58% to 78% of primary hepatocellular carcinoma cases, suggesting that one or more oncogenes within the amplicon play a critical role in the development of this disease. The chromodomain helicase/adenosine triphosphatase DNA binding protein 1–like gene (CHD1L) is a recently identified oncogene localized at 1q21.
Fin Stolze Larsen, Julia Wendon – 23 June 2009
Gregory J. Anderson – 23 June 2009
Keith D. Lindor, M. Eric Gershwin, Raoul Poupon, Marshall Kaplan, Nora V. Bergasa, E. Jenny Heathcote – 23 June 2009
Hongmei Zhao, Malgorzata Przybylska, I‐Huan Wu, Jinhua Zhang, Panagiotis Maniatis, Joshua Pacheco, Peter Piepenhagen, Diane Copeland, Cynthia Arbeeny, James A. Shayman, Johannes M. Aerts, Canwen Jiang, Seng H. Cheng, Nelson S. Yew – 23 June 2009 – Steatosis in the liver is a common feature of obesity and type 2 diabetes and the precursor to the development of nonalcoholic steatohepatitis (NASH), cirrhosis, and liver failure. It has been shown previously that inhibiting glycosphingolipid (GSL) synthesis increases insulin sensitivity and lowers glucose levels in diabetic rodent models.
Elina Zorde‐Khvalevsky, Rinat Abramovitch, Hila Barash, Irit Spivak‐Pohis, Ludmila Rivkin, Jacob Rachmilewitz, Eithan Galun, Hilla Giladi – 23 June 2009 – The current model for liver regeneration suggests that cell damage triggers Toll‐like receptor (TLR) signaling via MyD88, leading to the induction of nuclear factor κB (NF‐κB) and secretion of inflammatory cytokines that in turn prime liver regeneration.