Patricia Stiedl, Robert McMahon, Leander Blaas, Victoria Stanek, Jasmin Svinka, Beatrice Grabner, Gernot Zollner, Sonja M. Kessler, Thierry Claudel, Mathias Müller, Wolfgang Mikulits, Martin Bilban, Harald Esterbauer, Robert Eferl, Johannes Haybaeck, Michael Trauner, Emilio Casanova – 1 September 2014
Chao Wang, Yuanlin Zhao, Xing Gao, Le Li, Yuan Yuan, Fang Liu, Lijun Zhang, Jie Wu, Peizhen Hu, Xiumin Zhang, Yu Gu, Yuqiao Xu, Zhe Wang, Zengshan Li, Huizhong Zhang, Jing Ye – 1 September 2014 – Abnormal metabolism of nonesterified fatty acids (NEFAs) and their derivatives has been reported to be the main cause of intracellular lipotoxic injury. Normally, NEFAs are stored in lipid droplets (LDs) in the form of triglyceride (TG), which could reduce the lipotoxicity of cytosolic NEFAs.
James W. Galbraith, Ricardo A. Franco, John P. Donnelly, Joel B. Rodgers, Jordan M. Morgan, Andres F. Viles, Edgar T. Overton, Michael S. Saag, Henry E. Wang – 1 September 2014
Deepak Joshi, George J. Webster – 1 September 2014
Quirino Lai, Jan Lerut – 1 September 2014
David D. Lee, Amandeep Singh, Justin M. Burns, Dana K. Perry, Justin H. Nguyen, C. Burcin Taner – 1 September 2014 – Donation after cardiac death (DCD) liver allografts have been associated with increased morbidity from primary nonfunction, biliary complications, early allograft failure, cost, and mortality. Early allograft dysfunction (EAD) after liver transplantation has been found to be associated with inferior patient and graft survival.
Patrick McKiernan – 1 September 2014
Amy S. Lee, Wan‐Ting Chen – 30 August 2014
Na Shang, Maribel Arteaga, Ali Zaidi, Jimmy Stauffer, Scott J. Cotler, Nancy J. Zeleznik‐Le, Jiwang Zhang, Wei Qiu – 28 August 2014 – Hepatocellular carcinoma (HCC) is the third most common cause of cancer death worldwide and most patients with HCC have limited treatment options. Focal adhesion kinase (FAK) is overexpressed in many HCC specimens, offering a potential target for HCC treatment. However, the role of FAK in hepatocarcinogenesis remains elusive.
James E. Heubi, Kenneth D.R. Setchell, Pinky Jha, Donna Buckley, Wujuan Zhang, Philip Rosenthal, Carol Potter, Simon Horslen, David Suskind – 28 August 2014 – Bile acid amidation defects were predicted to present with fat/fat soluble vitamin malabsorption with minimal cholestasis. We identified and treated five patients (one male, four females) from four families with defective bile acid amidation due to a genetically confirmed deficiency in bile acid CoA:amino acid N‐acyl transferase (BAAT) with the conjugated bile acid, glycocholic acid (GCA).