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.

Lifeng Huang, Jie Cai, Han Guo, Jinyang Gu, Ying Tong, Bijun Qiu, Chenchen Wang, Meng Li, Lei Xia, Jianjun Zhang, Hailong Wu, Xiaoni Kong, Qiang Xia – 5 December 2018 – Cancer stem cells contribute to a high rate of recurrence and chemotherapeutic resistance in many types of cancer, including intrahepatic cholangiocarcinoma (ICC). Inhibitor of differentiation 3 (ID3) has been reported to promote cancer stem cells, but its role in ICC is obscure.

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.

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.

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.

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.

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.

4 December 2018

4 December 2018