Christopher Goldring, Daniel J. Antoine, Frank Bonner, Jonathan Crozier, Chris Denning, Robert J. Fontana, Neil A. Hanley, David C. Hay, Magnus Ingelman‐Sundberg, Satu Juhila, Neil Kitteringham, Beatriz Silva‐Lima, Alan Norris, Chris Pridgeon, James A. Ross, Rowena Sison Young, Danilo Tagle, Belen Tornesi, Bob van de Water, Richard J. Weaver, Fang Zhang, B. Kevin Park – 24 October 2016 – Current preclinical drug testing does not predict some forms of adverse drug reactions in humans.

Barbara Rehermann – 24 October 2016

Hongli Hu, Wenwei Zhu, Jun Qin, Min Chen, Liyan Gong, Long Li, Xiangyuan Liu, Yongzhen Tao, Huiyong Yin, Hu Zhou, Lisha Zhou, Dan Ye, Qinghai Ye, Daming Gao – 24 October 2016 – Phosphoglycerate kinase 1 (PGK1) is an important enzyme in the metabolic glycolysis pathway. In this study, we observed a significant overexpression of PGK1 in liver cancer tissues and a negative correlation between PGK1 expression and liver cancer patient survival.

Dana Tedesco, Manoj Thapa, Sanjeev Gumber, Elizabeth J. Elrod, Khalidur Rahman, Chris C. Ibegbu, Joseph F. Magliocca, Andrew B. Adams, Frank Anania, Arash Grakoui – 24 October 2016 – Persistent hepatotropic viral infections are a common etiologic agent of chronic liver disease. Unresolved infection can be attributed to nonfunctional intrahepatic CD8+ T‐cell responses. In light of dampened CD8+ T‐cell responses, liver disease often manifests systemically as immunoglobulin (Ig)‐related syndromes due to aberrant B‐cell functions.

Jin‐zhao Ma, Fu Yang, Chuan‐chuan Zhou, Feng Liu, Ji‐hang Yuan, Fang Wang, Tian‐tian Wang, Qing‐guo Xu, Wei‐ping Zhou, Shu‐han Sun – 24 October 2016 – N6‐Methyladenosine (m6A) modification has been implicated in many biological processes. However, its role in cancer has not been well studied. Here, we demonstrate that m6A modifications are decreased in hepatocellular carcinoma, especially in metastatic hepatocellular carcinoma, and that methyltransferase‐like 14 (METTL14) is the main factor involved in aberrant m6A modification.

Pavel Sumazin, Yidong Chen, Lisa R. Treviño, Stephen F. Sarabia, Oliver A. Hampton, Kayuri Patel, Toni‐Ann Mistretta, Barry Zorman, Patrick Thompson, Andras Heczey, Sarah Comerford, David A. Wheeler, Murali Chintagumpala, Rebecka Meyers, Dinesh Rakheja, Milton J. Finegold, Gail Tomlinson, D. Williams Parsons, Dolores López‐Terrada – 24 October 2016 – Despite being the most common liver cancer in children, hepatoblastoma (HB) is a rare neoplasm.

Sukanta Das, Jaswinder Singh Maras, Md. Shabir Hussain, Shvetank Sharma, Paul David, Sukriti Sukriti, Saggere Muralikrishna Shasthry, Rakhi Maiwall, Nirupama Trehanpati, Tej P. Singh, Shiv Kumar Sarin – 24 October 2016 – Albumin is a potent scavenger of reactive oxygen species (ROS). However, modifications in albumin structure may reduce its antioxidant properties and modulate its immune‐regulatory functions.

Jari E. Kaikkonen, Peter Würtz, Emmi Suomela, Miia Lehtovirta, Antti J. Kangas, Antti Jula, Vera Mikkilä, Jorma S.A. Viikari, Markus Juonala, Tapani Rönnemaa, Nina Hutri‐Kähönen, Mika Kähönen, Terho Lehtimäki, Pasi Soininen, Mika Ala‐Korpela, Olli T. Raitakari – 24 October 2016 – Nonalcoholic fatty liver is associated with obesity‐related metabolic disturbances, but little is known about the metabolic perturbations preceding fatty liver disease.

Feng Su, Pamela K. Green, Kristin Berry, George N. Ioannou – 24 October 2016 – Black race and Hispanic ethnicity were associated with lower rates of sustained virologic response (SVR) to interferon‐based treatments for chronic hepatitis C virus infection, whereas Asian race was associated with higher SVR rates compared to white patients. We aimed to describe the association between race/ethnicity and effectiveness of new direct‐acting antiviral regimens in the Veterans Affairs health care system nationally.

Moreshwar S. Desai, Bhoomika Mathur, Zeena Eblimit, Hernan Vasquez, Heinrich Taegtmeyer, Saul J. Karpen, Daniel J. Penny, David D. Moore, Sayeepriyadarshini Anakk – 24 October 2016 – Cardiac dysfunction in patients with liver cirrhosis is strongly associated with increased serum bile acid concentrations. Here we show that excess bile acids decrease fatty acid oxidation in cardiomyocytes and can cause heart dysfunction, a cardiac syndrome that we term cholecardia.