Recurrent recessive mutation in deoxyguanosine kinase causes idiopathic noncirrhotic portal hypertension

Sílvia Vilarinho, Sinan Sari, Güldal Yilmaz, Amy L. Stiegler, Titus J. Boggon, Dhanpat Jain, Gulen Akyol, Buket Dalgic, Murat Günel, Richard P. Lifton – 13 February 2016 – Despite advances in the diagnosis and management of idiopathic noncirrhotic portal hypertension, its pathogenesis remains elusive. Insight may be gained from study of early‐onset familial idiopathic noncirrhotic portal hypertension, in which Mendelian mutations may account for disease.

Is increased hepatitis C virus case‐finding combined with current or 8‐week to 12‐week direct‐acting antiviral therapy cost‐effective in UK prisons? A prevention benefit analysis

Natasha K. Martin, Peter Vickerman, Iain F. Brew, Joan Williamson, Alec Miners, William L. Irving, Sushma Saksena, Sharon J. Hutchinson, Sema Mandal, Eamonn O'Moore, Matthew Hickman – 10 February 2016 – Prisoners have a high prevalence of hepatitis C virus (HCV), but case‐finding may not have been cost‐effective because treatment often exceeded average prison stay combined with a lack of continuity of care. We assessed the cost‐effectiveness of increased HCV case‐finding and treatment in UK prisons using short‐course therapies.

FoxO3 inactivation promotes human cholangiocarcinoma tumorigenesis and chemoresistance through Keap1‐Nrf2 signaling

Li Guan, Lei Zhang, Zhicheng Gong, Xiaonan Hou, Yuxiu Xu, Xinhua Feng, Hongyang Wang, Han You – 9 February 2016 – FoxO transcription factors have been reported to play pivotal roles in tumorigenesis and drug resistance. The mechanisms underlying the tumor suppression function of FoxOs in human cancers remain largely unknown. Aberrant expression and activation of Nrf2 often correlate with chemoresistance and poor prognosis. Here, we report that FoxO3 directs the basal transcription of Kelch‐like ECH‐associated protein 1 (Keap1), an adaptor protein that bridges Nrf2 to Cul3 for degradation.

Genome‐wide association study in mice identifies loci affecting liver‐related phenotypes including Sel1l influencing serum bile acids

Wei Wu, Ami Patel, Kaisa Kyöstilä, Hannes Lohi, Nikol Mladkova, Krzysztof Kiryluk, Xiaoyun Sun, Jay H. Lefkowitch, Howard J. Worman, Ali G. Gharavi – 9 February 2016 – Using publicly available data from inbred mouse strains, we conducted a genome‐wide association study to identify loci that accounted for liver‐related phenotypes between C57BL/6J and A/J mice fed a Paigen diet. We confirmed genome‐wide significant associations for hepatic cholesterol (chromosome 10A2) and serum total bile acid concentration (chromosome 12E) and identified a new locus for liver inflammation (chromosome 7C).

Retreatment with sofosbuvir and simeprevir of patients with hepatitis C virus genotype 1 or 4 who previously failed a daclatasvir‐containing regimen

Christophe Hézode, Stéphane Chevaliez, Giovanna Scoazec, Alexandre Soulier, Anne Varaut, Magali Bouvier‐Alias, Isaac Ruiz, Françoise Roudot‐Thoraval, Ariane Mallat, Cyrille Féray, Jean‐Michel Pawlotsky – 8 February 2016 – Failure to achieve sustained virological response (SVR) with hepatitis C virus (HCV) direct‐acting antiviral‐based regimens is commonly associated with emergence of resistance‐associated variants (RAVs).

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