Min Suk Chae, Kwang Uck Moon, Joon‐Yong Jung, Ho Joong Choi, Hyun Sik Chung, Chul Soo Park, Jaemin Lee, Jong Ho Choi, Sang Hyun Hong – 24 January 2018 – Patients with end‐stage liver disease show sarcopenia, and preoperative sarcopenia is independently associated with patient mortality after liver transplantation. However, few studies have examined the relationship between perioperative loss of core muscle and patient mortality in living donor liver transplantation (LDLT).

Enis Kostallari, Petra Hirsova, Alena Prasnicka, Vikas K. Verma, Usman Yaqoob, Nicha Wongjarupong, Lewis R. Roberts, Vijay H. Shah – 23 January 2018 – Liver fibrosis is characterized by the activation and migration of hepatic stellate cells (HSCs), followed by matrix deposition. Recently, several studies have shown the importance of extracellular vesicles (EVs) derived from liver cells, such as hepatocytes and endothelial cells, in liver pathobiology.

Elizabeth Brunt, Shinichi Aishima, Pierre‐Alain Clavien, Kathryn Fowler, Zachary Goodman, Gregory Gores, Annette Gouw, Alex Kagen, David Klimstra, Mina Komuta, Fukuo Kondo, Rebecca Miksad, Masayuki Nakano, Yasuni Nakanuma, Irene Ng, Valerie Paradis, Young Nyun Park, Alberto Quaglia, Massimo Roncalli, Tania Roskams, Michiie Sakamoto, Romil Saxena, Christine Sempoux, Claude Sirlin, Ashley Stueck, Swan Thung, W.M.S.

Qin Li, Amal Dutta, Charles Kresge, Abhijit Bugde, Andrew P. Feranchak – 23 January 2018 – Bile acids stimulate a bicarbonate‐rich choleresis, in part, through effects on cholangiocytes. Because Cl− channels in the apical membrane of cholangiocytes provide the driving force for secretion and transmembrane member 16A (TMEM16A) has been identified as the Ca2+‐activated Cl− channel in the apical membrane of cholangiocytes, the aim of the present study was to determine whether TMEM16A is the target of bile‐acid–stimulated Cl− secretion and to identify the regulatory pathway involved.

Amritpal Dhaliwal, Jenny Towey, Geoffrey Haydon, Ahmed M. Elsharkawy, Matthew J. Armstrong – 22 January 2018

Jacob E. Friedman, Evgenia Dobrinskikh, Alba Alfonso‐Garcia, Alexander Fast, Rachel C. Janssen, Taylor K. Soderborg, Aimee L. Anderson, Julie A. Reisz, Angelo D'Alessandro, Daniel N. Frank, Charles E. Robertson, Becky A. de la Houssaye, Linda K. Johnson, David J. Orlicky, Xiaoxin X. Wang, Moshe Levi, Eric O. Potma, Karim C. El Kasmi, Karen R.

Annalisa Berzigotti, Jaime Bosch, on behalf of the Spordiet Study Investigators – 22 January 2018

Rachel J. Church, Gerd A. Kullak‐Ublick, Jiri Aubrecht, Herbert L. Bonkovsky, Naga Chalasani, Robert J. Fontana, Jens C. Goepfert, Frances Hackman, Nicholas M. P. King, Simon Kirby, Patrick Kirby, John Marcinak, Sif Ormarsdottir, Shelli J. Schomaker, Ina Schuppe‐Koistinen, Francis Wolenski, Nadir Arber, Michael Merz, John‐Michael Sauer, Raul J. Andrade, Florian van Bömmel, Thierry Poynard, Paul B. Watkins – 22 January 2018 – Current blood biomarkers are suboptimal in detecting drug‐induced liver injury (DILI) and predicting its outcome.

Xiaolei Wang, Heng Du, Shanshan Shao, Tao Bo, Chunxiao Yu, Wenbin Chen, Lifang Zhao, Qiu Li, Li Wang, Xiaojing Liu, Xiaohui Su, Mingqi Sun, Yongfeng Song, Ling Gao, Jiajun Zhao – 21 January 2018 – Physiological opening of the mitochondrial permeability transition pore (mPTP) is indispensable for maintaining mitochondrial function and cell homeostasis, but the role of the mPTP and its initial factor, cyclophilin D (CypD), in hepatic steatosis is unclear. Here, we demonstrate that excess mPTP opening is mediated by an increase of CypD expression induced hepatic mitochondrial dysfunction.

Xin Wang, Minmin Zhang, Fangfang Ping, Hongchun Liu, Jingya Sun, Yueqin Wang, Aijun Shen, Jian Ding, Meiyu Geng – 21 January 2018 – Though kinase inhibitors have been heavily investigated in the clinic to combat advanced hepatocellular carcinoma (HCC), clinical outcomes have been disappointing overall, which may be due to the absence of kinase‐addicted subsets in HCC patients. Recently, strategies that simultaneously inhibit multiple kinases are increasingly appreciated in HCC treatment, yet they are challenged by the dynamic nature of the kinase networks.