Transcriptome sequencing, microarray, and proteomic analyses reveal cellular and metabolic impact of hepatitis C virus infection in vitro

Stephen D. Woodhouse, Ramamurthy Narayan, Sally Latham, Sheena Lee, Robin Antrobus, Bevin Gangadharan, Shujun Luo, Gary P. Schroth, Paul Klenerman, Nicole Zitzmann – 23 July 2010 – Hepatitis C virus (HCV) is a major cause of liver disease but the full impact of HCV infection on the hepatocyte is poorly understood. RNA sequencing (RNA‐Seq) is a novel method to analyze the full transcriptional activity of a cell or tissue, thus allowing new insight into the impact of HCV infection.

Evaluation of depression as a risk factor for treatment failure in chronic hepatitis C

Peter Derek Christian Leutscher, Martin Lagging, Mads Rauning Buhl, Court Pedersen, Gunnar Norkrans, Nina Langeland, Kristine Mørch, Martti Färkkilä, Simon Hjerrild, Kristoffer Hellstrand, Per Bech, for the NORDynamIC Group – 23 July 2010 – The Major Depression Inventory (MDI) was used to estimate the value of routine medical interviews in diagnosing major depression among patients receiving peginterferon alfa‐2a and ribavirin therapy for chronic hepatitis C virus (HCV) infection (n = 325).

Molecular characterization of the vascular features of focal nodular hyperplasia and hepatocellular adenoma: A role for angiopoietin‐1

Annette S. H. Gouw, Wenjiao Zeng, Marijke Buiskool, Inge Platteel, Marius C. van den Heuvel, Sibrand Poppema, Koert P. de Jong, Grietje Molema – 23 July 2010 – Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are two hepatic nodular lesions of different etiologies. FNH, a polyclonal lesion, is assumed to be a regenerative reaction following a vascular injury, whereas HCA is a monoclonal, benign neoplastic lesion.

CXC receptor‐2 knockout genotype increases X‐linked inhibitor of apoptosis protein and protects mice from acetaminophen hepatotoxicity

Bin Hu, Lisa M. Colletti – 23 July 2010 – Although acetaminophen is a commonly used analgesic, it can be highly hepatotoxic. This study seeks to further investigate the mechanisms involved in acetaminophen‐induced hepatotoxicity and the role of chemokine (C‐X‐C motif) receptor 2 (CXCR2) receptor/ligand interactions in the liver's response to and recovery from acetaminophen toxicity. The CXC chemokines and their receptor, CXCR2, are important inflammatory mediators and are involved in the control of some types of cellular proliferation.

Subscribe to