Addition of adult‐to‐adult living donation to liver transplant programs improves survival but at an increased cost

Patrick G. Northup, Michael M. Abecassis, Michael J. Englesbe, Jean C. Emond, Vanessa D. Lee, George J. Stukenborg, Lan Tong, Carl L. Berg, Adult‐to‐Adult Living Donor Liver Transplantation Cohort Study Group – 28 January 2009 – Using outcomes data from the Adult‐to‐Adult Living Donor Liver Transplantation Cohort Study, we performed a cost‐effectiveness analysis exploring the costs and benefits of living donor liver transplantation (LDLT).

In vitro–targeted gene identification in patients with hepatitis C using a genome‐wide microarray technology

Susanne Hagist, Holger Sültmann, Gunda Millonig, Ulrike Hebling, Dörthe Kieslich, Rupert Kuner, Sabrina Balaguer, Helmut‐Karl Seitz, Annemarie Poustka, Sebastian Mueller – 28 January 2009 – Iron in association with reactive oxygen species (ROS) is highly toxic, aggravating oxidative stress reactions. Increased iron not only plays an important role in the progression of hereditary hemochromatosis (HH) but also in common liver diseases such as chronic hepatitis C. The underlying mechanisms of hepatitis C virus (HCV)‐mediated iron accumulation, however, are poorly understood.

Liver damage underlying unexplained transaminase elevation in human immunodeficiency virus‐1 mono‐infected patients on antiretroviral therapy

Patrick Ingiliz, Marc‐Antoine Valantin, Claudine Duvivier, Fadia Medja, Stephanie Dominguez, Frédéric Charlotte, Roland Tubiana, Thierry Poynard, Christine Katlama, Anne Lombès, Yves Benhamou – 28 January 2009 – Liver damage associated with chronic unexplained high serum transaminases in human immunodeficiency virus (HIV)‐infected patients under combined antiretroviral therapy is unknown.

Hepatitis delta virus inhibits alpha interferon signaling

Paolo Pugnale, Valerio Pazienza, Kévin Guilloux, Francesco Negro – 28 January 2009 – Hepatitis delta virus (HDV) can cause severe acute and chronic liver disease in patients infected with hepatitis B virus. Interferon‐α (IFN‐α) is the only treatment reported to be effective in chronic hepatitis delta, albeit in a minority of patients. The molecular mechanisms underlying resistance to therapy are unclear. IFN‐α–induced activation of the Janus kinase‐signal transducer and activator of transcription (JAK‐STAT) signaling cascade is essential for the induction of an antiviral state.

Treatment of hepatitis C in liver transplant recipients

Fredric D. Gordon, Paul Kwo, Hugo E. Vargas – 28 January 2009 – Recurrent hepatitis C after liver transplantation is a universal phenomenon. Graft reinfection occurs rapidly; once it is established, allograft cirrhosis and decompensation rapidly ensue in many patients. Treatment with pegylated interferon plus ribavirin is the standard of care among nontransplant patients with hepatitis C; however, the applicability of these therapies in liver transplant patients is severely limited.

Architectural changes during regenerative and ontogenic liver growth in the rat

Veronika Papp, Katalin Dezsö, Viktória László, Peter Nagy, Sándor Paku – 28 January 2009 – Although liver architecture has a major impact on function, morphological aspects of liver growth are relatively neglected. In our recent experiments, the architectural changes of the rat liver were compared during 2 basic processes: ontogeny and regenerative liver growth. The hepatic tissue is constructed as structural/functional units, and probably the most established and well‐defined such unit is the classic lobule.

Allelic imbalances and homozygous deletion on 8p23.2 for stepwise progression of hepatocarcinogenesis

Yutaka Midorikawa, Shogo Yamamoto, Shingo Tsuji, Naoko Kamimura, Shumpei Ishikawa, Hisaki Igarashi, Masatoshi Makuuchi, Norihiro Kokudo, Haruhiko Sugimura, Hiroyuki Aburatani – 28 January 2009 – Early hepatocellular carcinoma (eHCC) originates from the hepatocytes of chronic liver disease and develops into classical hepatocellular carcinoma (HCC). To identify sequential genetic changes in multistep hepatocarcinogenesis, we analyzed molecular karyotypes using oligonucleotide genotyping 50K arrays.

Human inhibitor of growth 1 inhibits hepatoma cell growth and influences p53 stability in a variant‐dependent manner

Zhi Zhu, Zhigang Luo, Yongmei Li, Canrong Ni, Honghua Li, Minghua Zhu – 28 January 2009 – Inhibitor of growth 1 (ING1) is a type II tumor suppressor that affects cell function by altering chromatin structure and regulating transcription. Recently, three ING1 splice variants have been cloned, but their roles in apoptosis and p53 regulation in human hepatocellular carcinoma (HCC) have not been fully elucidated.

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