Phenotypic characterization of idiosyncratic drug‐induced liver injury: The influence of age and sex

M. Isabel Lucena, Raúl J. Andrade, Neil Kaplowitz, Miren García‐Cortes, M. Carmen Fernández, Manuel Romero‐Gomez, Miguel Bruguera, Hacibe Hallal, Mercedes Robles‐Diaz, Jose F. Rodriguez‐González, Jose Maria Navarro, Javier Salmeron, Pedro Martinez‐Odriozola, Ramón Pérez‐Alvarez, Yolanda Borraz, Ramón Hidalgo, Spanish Group for the Study of Drug‐Induced Liver Disease – 28 May 2009 – Increased age and female sex are suggested risk factors for drug‐induced hepatotoxicity (DILI).

Nonstructural 3/4A protease of hepatitis C virus activates epithelial growth factor–induced signal transduction by cleavage of the T‐cell protein tyrosine phosphatase

Erwin Daniel Brenndörfer, Juliane Karthe, Lars Frelin, Patricia Cebula, Andreas Erhardt, Jan Schulte am Esch, Hartmut Hengel, Ralf Bartenschlager, Matti Sällberg, Dieter Häussinger, Johannes Georg Bode – 28 May 2009 – The hepatitis C virus (HCV) is a worldwide major cause of chronic liver disease with a high tendency to establish a persistent infection.

Indirect action of tumor necrosis factor‐alpha in liver injury during the CD8+ T cell response to an adeno‐associated virus vector in mice

Matthew Giannandrea, Robert H. Pierce, Ian Nicholas Crispe – 28 May 2009 – CD8+ T cells can cause hepatocellular injury by two distinct mechanisms. In addition to their direct cytotoxic effect, there is also collateral liver injury, which occurs when cells are killed in an antigen‐independent manner. Whereas immune effector cytokines interferon‐gamma (IFNγ) and tumor necrosis factor‐alpha (TNFα) have both been implicated in various forms of hepatitis, their respective roles in direct and/or collateral liver damage remains unclear.

Variants in interferon‐alpha pathway genes and response to pegylated interferon‐Alpha2a plus ribavirin for treatment of chronic hepatitis C virus infection in the hepatitis C antiviral long‐term treatment against cirrhosis trial

Tania Mara Welzel, Timothy R. Morgan, Herbert L. Bonkovsky, Deepa Naishadham, Ruth M. Pfeiffer, Elizabeth C. Wright, Amy A. Hutchinson, Andrew T. Crenshaw, Arman Bashirova, Mary Carrington, Myhanh Dotrang, Richard K. Sterling, Karen L. Lindsay, Robert J. Fontana, William M. Lee, Adrian M. Di Bisceglie, Marc G. Ghany, David R. Gretch, Stephen J. Chanock, Raymond T. Chung, Thomas R.

Extracellular matrix modulates sensitivity of hepatocytes to fibroblastoid dedifferentiation and transforming growth factor β–induced apoptosis

Patricio Godoy, Jan G. Hengstler, Iryna Ilkavets, Christoph Meyer, Anastasia Bachmann, Alexandra Müller, Gregor Tuschl, Stefan O. Mueller, Steven Dooley – 28 May 2009 – Hepatocytes in culture are a valuable tool to investigate mechanisms involved in the response of the liver to cytokines. However, it is well established that hepatocytes cultured on monolayers of dried stiff collagen dedifferentiate, losing specialized liver functions.

Role of adenosine monophosphate‐activated protein kinase–p70 ribosomal S6 kinase‐1 pathway in repression of liver X receptor‐alpha–dependent lipogenic gene induction and hepatic steatosis by a novel class of dithiolethiones

Seong Hwan Hwahng, Sung Hwan Ki, Eun Ju Bae, Hyun Eun Kim, Sang Geon Kim – 28 May 2009 – Dithiolethiones, a novel class of adenosine monophosphate‐activated protein kinase (AMPK) activators, prevent insulin resistance through AMPK‐dependent p70 ribosomal S6 kinase‐1 (S6K1) inhibition. There is no known effect of S6K1 for liver X receptor‐alpha (LXRα)‐mediated lipogenic gene expression and steatosis, a cause of chronic liver disease.

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