Suppressor of cytokine signaling 3 (SOCS3) expression and hepatitis C virus–related chronic hepatitis: Insulin resistance and response to antiviral therapy

Marcello Persico, Mario Capasso, Eliana Persico, Monica Svelto, Roberta Russo, Daniela Spano, Lori Crocè, Vincenzo La Mura, Francesco Moschella, Flora Masutti, Roberto Torella, Claudio Tiribelli, Achille Iolascon – 1 August 2007 – The response to antiviral therapy is lower in hepatitis C virus (HCV) patients with genotype 1 than in those with genotype 2. Overexpression of the suppressor of cytokine signaling 3 (SOCS3) gene in liver tissue is associated with a poorer treatment outcome in patients with chronic hepatitis C viral genotype 1.

Features associated with treatment failure in type 1 autoimmune hepatitis and predictive value of the model of end‐stage liver disease

Aldo J. Montano‐Loza, Herschel A. Carpenter, Albert J. Czaja – 1 August 2007 – Autoimmune hepatitis may fail to respond to corticosteroid therapy, but the frequency and bases for this outcome are uncertain. We aimed to determine the frequency and nature of treatment failure in patients with type 1 autoimmune hepatitis, define features associated with its occurrence, and assess if the model for end‐stage liver disease can predict this outcome. Patients failing conventional corticosteroid regimens were compared to patients who responded to similar regimens.

Lack of response to exogenous interferon‐α in the liver of chimpanzees chronically infected with hepatitis C virus

Robert E. Lanford, Bernadette Guerra, Catherine B. Bigger, Helen Lee, Deborah Chavez, Kathleen M. Brasky – 1 August 2007 – The mechanism of the interferon‐alpha (IFNα)–induced antiviral response is not completely understood. We recently examined the transcriptional response to IFNα in uninfected chimpanzees. The transcriptional response to IFNα in the liver and peripheral blood mononuclear cells (PBMCs) was rapidly induced but was also rapidly down‐regulated, with most interferon‐alpha–stimulated genes (ISGs) returning to the baseline within 24 hours.

Aging in rat causes hepatic hyperresposiveness to interleukin‐1β which is mediated by neutral sphingomyelinase‐2

Kristina Rutkute, Alexander A. Karakashian, Natalia V. Giltiay, Aneta Dobierzewska, Mariana N. Nikolova‐Karakashian – 1 August 2007 – The process of aging has recently been shown to substantially affect the ability of cells to respond to inflammatory challenges. We demonstrate that aging leads to hepatic hyperresponsiveness to interleukin 1β (IL‐1β), and we examine the factors that could be responsible for this phenomenon. IL‐1β‐induced phosphorylation of c‐jun N‐terminal kinase (JNK) in hepatocytes isolated from aged rats was 3 times more potent than that in hepatocytes from young rats.

Effect of the interleukin‐6 C174G gene polymorphism on treatment of acute and chronic hepatitis C in human immunodeficiency virus coinfected patients

Jacob Nattermann, Martin Vogel, Thomas Berg, Mark Danta, Baumgarten Axel, Christoph Mayr, Raffaele Bruno, Christina Tural, Gerd Klausen, Bonaventura Clotet, Thomas Lutz, Frank Grünhage, Michael Rausch, Hans Dieter Nischalke, Knud Schewe, Bernhard Bienek, Georg Haerter, Tilman Sauerbruch, Juergen K. Rockstroh, Ulrich Spengler – 1 August 2007 – Hepatitis C virus (HCV)/human immunodeficirency virus (HIV) coinfection poses a difficult therapeutic problem. Response to HCV‐specific therapy is variable but might be influenced by host genetic factors, including polymorphisms of cytokine genes.

Fibroblast growth factor 10 is critical for liver growth during embryogenesis and controls hepatoblast survival via β‐catenin activation

Tove Berg, C. Bart Rountree, Lily Lee, Joaquin Estrada, Fréderic G. Sala, Andrea Choe, Jacqueline M. Veltmaat, Stijn De Langhe, Rene Lee, Hide Tsukamoto, Gay M. Crooks, Saverio Bellusci, Kasper S. Wang – 1 August 2007 – Fibroblast growth factor (FGF) signaling and β‐catenin activation have been shown to be crucial for early embryonic liver development. This study determined the significance of FGF10‐mediated signaling in a murine embryonic liver progenitor cell population as well as its relation to β‐catenin activation.

Presence of intrahepatic (total and ccc) HBV DNA is not predictive of HBV recurrence after liver transplantation

Munira Hussain, Consuelo Soldevila‐Pico, Sukru Emre, Velimir Luketic, Anna S.F. Lok – 30 July 2007 – Previous studies reported that hepatitis B virus (HBV) deoxyribonucleic acid (DNA) can be detected in livers of patients who received transplants for hepatitis B despite the absence of serological markers of HBV recurrence. Quantification of HBV DNA was not performed and presence of covalently closed circular (ccc) DNA was not analyzed in most studies.

Graft vs. host disease after liver transplantation: A new approach is needed

Roman Perri, Maha Assi, Jayant Talwalkar, Julie Heimbach, William Hogan, S. Breanndan Moore, Charles B. Rosen – 30 July 2007 – Graft‐vs.‐host disease (GVHD) is a rare, serious complication of orthotopic liver transplantation (OLT). We have treated 5 patients to date with GVHD after OLT. A total of 78 patients worldwide have been reported to have experienced this complication. The means by which GVHD after OLT has been managed is guided by experience with the more common GVHD that occurs after stem cell transplantation.

Death of a living liver donor from illicit drugs

Burckhardt Ringe, Ralph J. Petrucci, Humberto E. Soriano, James C. Reynolds, William C. Meyers – 30 July 2007 – In children with acute hepatic failure, it has been suggested to offer living donor transplantation to all parents when a deceased donor organ can not be provided. Ethically, living related donation is coercive by its very nature, especially in emergencies. We report a 36‐year‐old woman who died from a drug overdose 57 days after living donor liver resection. The recipient was her 3‐year‐old son, who experienced acute hepatic failure as a result of acetaminophen intoxication.

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