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Shalimar, Mohammed Faisal Sheikh, Rajeshwar P. Mookerjee, Banwari Agarwal, Subrat Kumar Acharya, Rajiv Jalan – 11 May 2019
Shalimar, Mohammed Faisal Sheikh, Rajeshwar P. Mookerjee, Banwari Agarwal, Subrat Kumar Acharya, Rajiv Jalan – 11 May 2019
Shaojun Shi, Monique M. A. Verstegen, Laura Mezzanotte, Jeroen Jonge, Clemens W. G. M. Löwik, Luc J. W. Laan – 11 May 2019 – Cell death is a natural process for the turnover of aged cells, but it can also arise as a result of pathological conditions. Cell death is recognized as a key feature in both acute and chronic hepatobiliary diseases caused by drug, alcohol, and fat uptake; by viral infection; or after surgical intervention. In the case of chronic disease, cell death can lead to (chronic) secondary inflammation, cirrhosis, and the progression to liver cancer.
Siavash Raigani, James F. Markmann, Heidi Yeh – 11 May 2019
David Stephen Prince, Ken Liu, Geoffrey William McCaughan, James Kench, Simone Irene Strasser – 11 May 2019
Lu Bai, Hui Peng, Xiaolei Hao, Ling Tang, Cheng Sun, Meijuan Zheng, Fubao Liu, Zhexiong Lian, Li Bai, Haiming Wei, Rui Sun, Zhigang Tian – 11 May 2019 – Liver‐resident natural killer (LrNK) cells are a unique subset of NK cells that are distinct from conventional NK cells. However, little is known about the mechanisms by which LrNK cells mature. In this study, we discovered that LrNK cells exhibit a relatively immature phenotype and impaired cytotoxic capacity in the absence of CD8+ T cells.
Alexandra S. Reynolds, Benjamin Brush, Thomas D. Schiano, Kaitlin J. Reilly, Neha S. Dangayach – 11 May 2019
Michael A. Dunn – 11 May 2019
Nigel Sutherland, Christopher Foong Dhin Li Wai Suen, Christopher Mills, Julie Lokan, Marie Sinclair – 11 May 2019
Nigel Sutherland, Christopher Foong Dhin Li Wai Suen, Christopher Mills, Julie Lokan, Marie Sinclair – 11 May 2019
Zhen‐Zhen Yan, Yong‐Ping Huang, Xin Wang, Hai‐Ping Wang, Fei Ren, Rui‐Feng Tian, Xu Cheng, Jie Cai, Yan Zhang, Xue‐Yong Zhu, Zhi‐Gang She, Xiao‐Jing Zhang, Zan Huang, Hongliang Li – 11 May 2019 – Hepatic ischemia‐reperfusion (IR) injury is the leading cause of liver dysfunction and failure after liver resection or transplantation and lacks effective therapeutic strategies. Here, we applied a systematic proteomic analysis to identify the prominent contributors to IR‐induced liver damage and promising therapeutic targets for this condition.