Yuki Imaoka, Masahiro Ohira, Ryosuke Nakano, Seiichi Shimizu, Shintaro Kuroda, Hiroyuki Tahara, Kentaro Ide, Tsuyoshi Kobayashi, Hideki Ohdan – 18 July 2018 – Abdominal aortic calcification (AAC) is known as a risk factor of coronary artery disease, stroke, hyperphosphatemia, chronic inflammation, diabetes, and decreased estimated glomerular filtration rate. However, the clinical implications of incidental AAC findings in liver transplantation (LT) have not been evaluated in terms of posttransplantation survival and complications.

Michael J. Vinikoor, Edford Sinkala, Belinda Chihota, Annie Kanunga, Gilles Wandeler – 18 July 2018

Yoosoo Chang, Yong Kyun Cho, Yejin Kim, Eunju Sung, Jiin Ahn, Hyun‐Suk Jung, Kyung Eun Yun, Hocheol Shin, Seungho Ryu – 17 July 2018 – The effect of modest alcohol consumption on fibrosis progression in the general population with nonalcoholic fatty liver disease (NAFLD) remains unclear. We examined the association of nonheavy alcohol consumption with worsening of noninvasive fibrosis indices in a large‐scale, low‐risk population with NAFLD. A cohort study was performed in 58,927 Korean adults with NAFLD and low fibrosis scores who were followed for a median of 4.9 years.

Eva Román, Cristina Gely, Montse Flavià, Maria Poca, Edilmar Alvarado, Víctor Vargas, Carlos Guarner, Germán Soriano – 17 July 2018

Raj Vuppalanchi, Karan Mathur, Maximillian Pyko, Niharika Samala, Naga Chalasani – 17 July 2018 – Noncirrhotic portal hypertension (NCPH) is often a diagnostic challenge due to signs and symptoms of portal hypertension that overlap with cirrhosis. The etiology of NCPH is broadly classified as prehepatic, hepatic (presinusoidal and sinusoidal) and posthepatic. Some common etiologies of NCPH encountered in clinical practice include portal vein thrombosis (prehepatic) and nodular regenerative hyperplasia (hepatic).

Raj Vuppalanchi, Karan Mathur, Maximillian Pyko, Niharika Samala, Naga Chalasani – 17 July 2018 – Noncirrhotic portal hypertension (NCPH) is often a diagnostic challenge due to signs and symptoms of portal hypertension that overlap with cirrhosis. The etiology of NCPH is broadly classified as prehepatic, hepatic (presinusoidal and sinusoidal) and posthepatic. Some common etiologies of NCPH encountered in clinical practice include portal vein thrombosis (prehepatic) and nodular regenerative hyperplasia (hepatic).

Patrick J. Navin, Moira B. Hilscher, Christopher L. Welle, Taofic Mounajjed, Michael S. Torbenson, Patrick S. Kamath, Sudhakar K. Venkatesh – 17 July 2018

Mamta K. Jain, Mae Thamer, George Therapondos, Mitchell L. Shiffman, Onkar Kshirsagar, Christopher Clark, Robert J. Wong – 17 July 2018 – Direct‐acting antivirals (DAA) for hepatitis C virus (HCV) became available in 2014, but the role of mental health or substance use disorders (MH/SUD) on access to treatment is unknown. The objective of this study was to examine the extent and predictors of HCV treatment in the pre‐DAA and post‐DAA periods in four large, diverse health care settings in the United States.

Daniel M. Green, Mingjuan Wang, Matthew J. Krasin, DeoKumar Srivastava, Mary V. Relling, Carrie R. Howell, Kirsten K. Ness, Sue C. Kaste, William Greene, Dennis W. Jay, Israel Fernandez‐Pineda, Ching‐Hon Pui, Sima Jeha, Michael W. Bishop, Wayne L. Furman, Leslie L. Robison, Melissa M. Hudson – 17 July 2018 – The purpose of this study was to define the prevalence of and risk factors for elevated serum alanine aminotransferase (ALT) level among adult childhood cancer survivors (CCS). The study cohort comprised 2,751 CCS from the St.

Xiangdong Wang, Ana C. Maretti‐Mira, Lei Wang, Laurie D. DeLeve – 17 July 2018 – Recruitment of liver sinusoidal endothelial cell progenitor cells (sprocs) from the bone marrow by vascular endothelial growth factor‐stromal cell‐derived factor‐1 (VEGF‐sdf‐1) signaling promotes recovery from injury and drives liver regeneration. Matrix metalloproteinases (MMPs) can proteolytically cleave VEGF, which might inhibit progenitor cell recruitment, but systemic matrix metalloproteinase inhibition might prevent efflux of progenitors from the bone marrow.