Projected future increase in aging hepatitis C virus–infected liver transplant candidates: A potential effect of hepatocellular carcinoma

Scott W. Biggins, Kiran M. Bambha, Norah A. Terrault, John Inadomi, Stephen Shiboski, Jennifer L. Dodge, Jane Gralla, Hugo R. Rosen, John P. Roberts – 24 September 2012 – In the United States, the peak hepatitis C virus (HCV) antibody prevalence of 4% occurred in persons born in the calendar years 1940‐1965. The goal of this study was to examine observed and projected age‐specific trends in the demand for liver transplantation (LT) among patients with HCV‐associated liver disease stratified by concurrent hepatocellular carcinoma (HCC).

Morbidity and mortality following transarterial liver chemoembolization in patients with hepatocellular carcinoma and synthetic hepatic dysfunction

Elisabeth R. Garwood, Nicholas Fidelman, Sarah E. Hoch, Robert K. Kerlan, Francis Y. Yao – 24 September 2012 – The purpose of this study was to determine the rate and risk factors for the development of irreversible hepatotoxicity after transarterial chemoembolization (TACE) in patients with hepatocellular carcinoma (HCC) and synthetic hepatic dysfunction. Two hundred fifty‐one consecutive patients with HCC and hepatic dysfunction who underwent 443 TACE procedures from 2005 to 2010 were retrospectively reviewed.

Impact of estimated liver volume and liver weight on gender disparity in liver transplantation

Ayse L. Mindikoglu, Sukru H. Emre, Laurence S. Magder – 24 September 2012 – Although lower Model for End‐Stage Liver Disease (MELD) scores due to lower levels of serum creatinine in women might account for some of the gender disparity in liver transplantation (LT) rates, even within MELD scores, women undergo transplantation at lower rates than men. It is unclear what causes this disparity, but transplant candidate/donor liver size mismatch may be a factor. We analyzed Organ Procurement and Transplantation Network data for patients with end‐stage liver disease on the waiting list.

Hepatitis B virus polymerase impairs interferon‐α–induced STA T activation through inhibition of importin‐α5 and protein kinase C‐δ

Jieliang Chen, Min Wu, Xiaonan Zhang, Wen Zhang, Zhanqing Zhang, Lixiang Chen, Jing He, Ye Zheng, Cuncun Chen, Fan Wang, Yunwen Hu, Xiaohui Zhou, Cong Wang, Yang Xu, Mengji Lu, Zhenghong Yuan – 19 September 2012 – Treatment with exogenous interferon (IFN)‐α is not effective in the majority of patients with chronic hepatitis B virus (HBV) infection. Recent evidence suggests that HBV has evolved strategies to block the nuclear translocation of signal transducer and activator of transcription (STAT) 1 to limit IFN‐α–induced cellular antiviral responses.

Hepatic fat loss in advanced nonalcoholic steatohepatitis: Are alterations in serum adiponectin the cause?

David van der Poorten, Caroline F. Samer, Mehdi Ramezani‐Moghadam, Sally Coulter, Marina Kacevska, Dennis Schrijnders, Lindsay E. Wu, Duncan McLeod, Elisabetta Bugianesi, Mina Komuta, Tania Roskams, Christopher Liddle, Lionel Hebbard, Jacob George – 19 September 2012 – Advanced liver fibrosis in nonalcoholic steatohepatitis (NASH) is often accompanied by a reduction in hepatic fat to the point of complete fat loss (burnt‐out NASH), but the mechanisms behind this phenomenon have not been elucidated. Adiponectin is raised in cirrhosis of any cause and has potent antisteatotic activity.

Successful transplantation of human hepatic stem cells with restricted localization to liver using hyaluronan grafts†

Rachael A. Turner, Eliane Wauthier, Oswaldo Lozoya, Randall McClelland, James E. Bowsher, Claire Barbier, Glenn Prestwich, Edward Hsu, David A. Gerber, Lola M. Reid – 19 September 2012 – Cell therapies are potential alternatives to organ transplantation for liver failure or dysfunction but are compromised by inefficient engraftment, cell dispersal to ectopic sites, and emboli formation.

Inhibition of RelA‐Ser536 phosphorylation by a competing peptide reduces mouse liver fibrosis without blocking the innate immune response

Anna Moles, Ana M. Sanchez, Paul S. Banks, Lindsay B. Murphy, Saimir Luli, Lee Borthwick, Andrew Fisher, Steven O'Reilly, Jacob M. van Laar, Steven A. White, Neil D. Perkins, Alastair D. Burt, Derek A. Mann, Fiona Oakley – 19 September 2012 – Phosphorylation of the RelA subunit at serine 536 (RelA‐P‐Ser536) is important for hepatic myofibroblast survival and is mechanistically implicated in liver fibrosis.

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