Chronic kidney disease after liver transplantation in human immunodeficiency virus/hepatitis C virus–coinfected recipients versus human immunodeficiency virus–infected recipients without hepatitis C virus: Results from the national institutes of health mu

Ranjeeta Bahirwani, Burc Barin, Kim Olthoff, Peter Stock, Barbara Murphy, K. Rajender Reddy, for the Solid Organ Transplantation in HIV: Multi‐Site Study Investigators – 20 March 2013 – Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) are both associated with chronic kidney disease (CKD), a major complication after orthotopic liver transplantation (OLT). The aim of this study was to assess predictors of post‐OLT CKD in HIV/HCV‐coinfected recipients versus HIV‐infected recipients without HCV (HIV/non‐HCV recipients).

Epidermal growth factor receptor signaling impairs the antiviral activity of interferon‐alpha

Joachim Lupberger, François H.T. Duong, Isabel Fofana, Laetitia Zona, Fei Xiao, Christine Thumann, Sarah C. Durand, Patrick Pessaux, Mirjam B. Zeisel, Markus H. Heim, Thomas F. Baumert – 20 March 2013 – Interferon‐alpha (IFN‐α) exhibits its antiviral activity through signal transducer and activator of transcription protein (STAT) signaling and the expression of IFN response genes (IRGs). Viral infection has been shown to result in activation of epidermal growth factor receptor (EGFR)—a host cell entry factor used by several viruses, including hepatitis C virus.

Hepatocyte divalent metal‐ion transporter‐1 is dispensable for hepatic iron accumulation and non‐transferrin‐bound iron uptake in mice

Chia‐Yu Wang, Mitchell D. Knutson – 19 March 2013 – Divalent metal‐ion transporter‐1 (DMT1) is required for iron uptake by the intestine and developing erythroid cells. DMT1 is also present in the liver, where it has been implicated in the uptake of transferrin‐bound iron (TBI) and non‐transferrin‐bound iron (NTBI), which appears in the plasma during iron overload. To test the hypothesis that DMT1 is required for hepatic iron uptake, we examined mice with the Dmt1 gene selectively inactivated in hepatocytes (Dmt1liv/liv).

Genomic landscape of copy number aberrations enables the identification of oncogenic drivers in hepatocellular carcinoma

Kai Wang, Ho Yeong Lim, Stephanie Shi, Jeeyun Lee, Shibing Deng, Tao Xie, Zhou Zhu, Yuli Wang, David Pocalyko, Wei Jennifer Yang, Paul A. Rejto, Mao Mao, Cheol‐Keun Park, Jiangchun Xu – 18 March 2013 – Cancer is a genetic disease with frequent somatic DNA alterations. Studying recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the prioritization of candidate oncogenic drivers with causal roles in oncogenesis.

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