TGR5 contributes to hepatic cystogenesis in rodents with polycystic liver diseases through cyclic adenosine monophosphate/Gαs signaling

Tatyana V. Masyuk, Anatoliy I. Masyuk, Maria Lorenzo Pisarello, Brynn N. Howard, Bing Q. Huang, Pui‐Yuen Lee, Xavier Fung, Eduard Sergienko, Robert J. Ardecky, Thomas D.Y. Chung, Anthony B. Pinkerton, Nicholas F. LaRusso – 23 May 2017 – Hepatic cystogenesis in polycystic liver disease is associated with increased levels of cyclic adenosine monophosphate (cAMP) in cholangiocytes lining liver cysts. Takeda G protein receptor 5 (TGR5), a G protein–coupled bile acid receptor, is linked to cAMP and expressed in cholangiocytes.

Sofosbuvir and ribavirin in adolescents 12‐17 years old with hepatitis C virus genotype 2 or 3 infection

Stefan Wirth, Philip Rosenthal, Regino P. Gonzalez‐Peralta, Maureen M. Jonas, William F. Balistreri, Chuan‐Hao Lin, Winita Hardikar, Kathryn Kersey, Benedetta Massetto, Bittoo Kanwar, Diana M. Brainard, Jiang Shao, Evguenia Svarovskaia, Brian Kirby, Ronen Arnon, Karen F. Murray, Kathleen B. Schwarz – 22 May 2017 – Children with chronic hepatitis C virus infection have limited treatment options. We evaluated the all‐oral combination of sofosbuvir and ribavirin in adolescents aged 12‐17 with hepatitis C virus genotype 2 or 3 (ClinicalTrials.gov NCT02175758).

Model for end‐stage liver disease Na Score predicts incident major cardiovascular events in patients with nonalcoholic fatty liver disease

Tracey G. Simon, Uri Kartoun, Hui Zheng, Andrew T. Chan, Raymond T. Chung, Stanley Shaw, Kathleen E. Corey – 22 May 2017 – Cardiovascular disease (CVD) is the leading cause of mortality among adults with nonalcoholic fatty liver disease (NAFLD); however, accurate tools for identifying NAFLD patients at highest CVD risk are lacking. Using a validated algorithm, we identified a retrospective cohort of 914 NAFLD patients without known CVD. Fibrosis severity was estimated using the fibrosis‐4 index.

Syndecan‐1 limits the progression of liver injury and promotes liver repair in acetaminophen‐induced liver injury in mice

Eon Jeong Nam, Kazutaka Hayashida, Rafael S. Aquino, John R. Couchman, Rosemary A. Kozar, Jian Liu, Pyong Woo Park – 22 May 2017 – Accidental or intentional misuse of acetaminophen (APAP) is the leading cause of acute liver failure in the Western world. Although mechanisms that trigger APAP‐induced liver injury (AILI) are well known, those that halt the progression of APAP liver disease and facilitate liver recovery are less understood.

Sequencing of hepatitis C virus for detection of resistance to direct‐acting antiviral therapy: A systematic review

Sofia R. Bartlett, Jason Grebely, Auda A. Eltahla, Jacqueline D. Reeves, Anita Y.M. Howe, Veronica Miller, Francesca Ceccherini‐Silberstein, Rowena A. Bull, Mark W. Douglas, Gregory J. Dore, Patrick Harrington, Andrew R. Lloyd, Brendan Jacka, Gail V. Matthews, Gary P. Wang, Jean‐Michel Pawlotsky, Jordan J. Feld, Janke Schinkel, Federico Garcia, Johan Lennerstrand, Tanya L. Applegate – 22 May 2017 – The significance of the clinical impact of direct‐acting antiviral (DAA) resistance‐associated substitutions (RASs) in hepatitis C virus (HCV) on treatment failure is unclear.

Dropout rate from the liver transplant waiting list because of hepatocellular carcinoma progression in hepatitis C virus–infected patients treated with direct‐acting antivirals

Alberto Zanetto, Sarah Shalaby, Alessandro Vitale, Claudia Mescoli, Alberto Ferrarese, Martina Gambato, Enrica Franceschet, Giacomo Germani, Marco Senzolo, Antonietta Romano, Paolo Angeli, Massimo Rugge, Fabio Farinati, Daniel M. Forton, Umberto Cillo, Patrizia Burra, Francesco Paolo Russo – 22 May 2017 – Concerns about an increased hepatocellular carcinoma (HCC) recurrence rate following direct‐acting antiviral (DAA) therapy in patients with cirrhosis with a prior complete oncological response have been raised.

Loss of L‐selectin‐guided CD8+, but not CD4+, cells protects against ischemia reperfusion injury in a steatotic liver

Vasantha L. Kolachala, Sirish Palle, Ming Shen, Alayna Feng, Dmitry Shayakhmetov, Nitika A. Gupta – 20 May 2017 – Steatotic liver responds with increased hepatocellular injury when exposed to an ischemic‐reperfusion insult. Increasing evidence supports the role of immune cells as key mediators of this injury in a normal (lean) state, but data about their role in a steatotic liver are practically nonexistent. The objective of the current study was to delineate the contribution of specific phenotypes of T cells and adhesion molecules in exacerbated cell death in steatotic liver injury.

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