Ramona Nicolau‐Raducu, Thiago Beduschi, Rodrigo Vianna, Christian Diez, Mahmoud Sleem, Bhavna P. Singh, Georgia Vasileiou, Yehuda Raveh – 7 December 2018 – Detrimental consequences of hypofibrinolysis, also known as fibrinolysis shutdown (FS), have recently arisen, and its significance in liver transplantation (LT) remains unknown. To fill this gap, this retrospective study included 166 adults who received transplants between 2016 and 2018 for whom baseline thromboelastography was available.

Franziska Meister, Georg Lurje, Ulf Peter Neumann, Christian Trautwein, Pavel Strnad – 7 December 2018

Paulo S. Pinheiro – 6 December 2018

Joan Clària, Richard Moreau, François Fenaille, Alex Amorós, Christophe Junot, Henning Gronbaek, Minneke J. Coenraad, Alain Pruvost, Aurélie Ghettas, Emeline Chu‐Van, Cristina López‐Vicario, Karl Oettl, Paolo Caraceni, Carlo Alessandria, Jonel Trebicka, Marco Pavesi, Carme Deulofeu, Agustin Albillos, Thierry Gustot, Tania M. Welzel, Javier Fernández, Rudolf E.

Michele Alves‐Bezerra, Yingxia Li, Mariana Acuña, Anna A. Ivanova, Kathleen E. Corey, Eric A. Ortlund, David E. Cohen – 5 December 2018 – In nonalcoholic fatty liver disease (NAFLD), triglycerides accumulate within the liver because the rates of fatty acid accrual by uptake from plasma and de novo synthesis exceed elimination by mitochondrial oxidation and secretion as very low‐density lipoprotein (VLDL) triglycerides. Thioesterase superfamily member 2 (Them2) is an acyl‐coenzyme A (CoA) thioesterase that catalyzes the hydrolysis of fatty acyl‐CoAs into free fatty acids plus CoASH.

Brett McGettigan, Rachel McMahan, David Orlicky, Matthew Burchill, Thomas Danhorn, Prashanth Francis, Lin Ling Cheng, Lucy Golden‐Mason, Claudia V. Jakubzick, Hugo R. Rosen – 5 December 2018 – A crucial component of nonalcoholic fatty liver disease (NAFLD) pathogenesis is lipid stress, which may contribute to hepatic inflammation and activation of innate immunity in the liver. However, little is known regarding how dietary lipids, including fat and cholesterol, may facilitate innate immune activation in vivo.

Douglas A. Simonetto, Laura Piccolo Serafim, Alice Gallo de Moraes, Ognjen Gajic, Patrick S. Kamath – 5 December 2018 – Sepsis in patients with cirrhosis is associated with high mortality. An impaired immune response accounts for the increased infection risk observed in these patients. Hemodynamic and systemic changes suggestive of sepsis may be observed in patients with cirrhosis in the absence of infection; therefore, diagnosis and treatment of sepsis may be delayed.

Michele Alves‐Bezerra, Yingxia Li, Mariana Acuña, Anna A. Ivanova, Kathleen E. Corey, Eric A. Ortlund, David E. Cohen – 5 December 2018 – In nonalcoholic fatty liver disease (NAFLD), triglycerides accumulate within the liver because the rates of fatty acid accrual by uptake from plasma and de novo synthesis exceed elimination by mitochondrial oxidation and secretion as very low‐density lipoprotein (VLDL) triglycerides. Thioesterase superfamily member 2 (Them2) is an acyl‐coenzyme A (CoA) thioesterase that catalyzes the hydrolysis of fatty acyl‐CoAs into free fatty acids plus CoASH.

Ian Huck, Sumedha Gunewardena, Regina Espanol‐Suner, Holger Willenbring, Udayan Apte – 5 December 2018 – Hepatocyte nuclear factor 4 alpha (HNF4α) is critical for hepatic differentiation. Recent studies have highlighted its role in inhibition of hepatocyte proliferation and tumor suppression. However, the role of HNF4α in liver regeneration (LR) is not known. We hypothesized that hepatocytes modulate HNF4α activity when navigating between differentiated and proliferative states during LR.

Brett McGettigan, Rachel McMahan, David Orlicky, Matthew Burchill, Thomas Danhorn, Prashanth Francis, Lin Ling Cheng, Lucy Golden‐Mason, Claudia V. Jakubzick, Hugo R. Rosen – 5 December 2018 – A crucial component of nonalcoholic fatty liver disease (NAFLD) pathogenesis is lipid stress, which may contribute to hepatic inflammation and activation of innate immunity in the liver. However, little is known regarding how dietary lipids, including fat and cholesterol, may facilitate innate immune activation in vivo.