Minimum graft size calculated from preoperative recipient status in living donor liver transplantation

Shigeru Marubashi, Hiroaki Nagano, Hidetoshi Eguchi, Hiroshi Wada, Tadafumi Asaoka, Yoshito Tomimaru, Akira Tomokuni, Koji Umeshita, Yuichiro Doki, Masaki Mori – 19 December 2015 – Small‐for‐size graft syndrome is an inevitable complication in living donor liver transplantation (LDLT). We hypothesized that graft weight (GW) measured after graft procurement is one of the variables predicting postoperative graft function. A total of 138 consecutive recipients of adult‐to‐adult LDLT between March 1999 and October 2014 were included in this study.

Activation of liver X receptor/retinoid X receptor pathway ameliorates liver disease in Atp7B−/− (Wilson disease) mice

James P. Hamilton, Lahari Koganti, Abigael Muchenditsi, Venkata S. Pendyala, David Huso, Joseph Hankin, Robert C. Murphy, Dominik Huster, Uta Merle, Christopher Mangels, Nan Yang, James J. Potter, Esteban Mezey, Svetlana Lutsenko – 17 December 2015 – Wilson disease (WD) is a hepatoneurological disorder caused by mutations in the copper‐transporter, ATP7B. Copper accumulation in the liver is a hallmark of WD. Current therapy is based on copper chelation, which decreases the manifestations of liver disease, but often worsens neurological symptoms.

Activation of liver X receptor/retinoid X receptor pathway ameliorates liver disease in Atp7B−/− (Wilson disease) mice

James P. Hamilton, Lahari Koganti, Abigael Muchenditsi, Venkata S. Pendyala, David Huso, Joseph Hankin, Robert C. Murphy, Dominik Huster, Uta Merle, Christopher Mangels, Nan Yang, James J. Potter, Esteban Mezey, Svetlana Lutsenko – 17 December 2015 – Wilson disease (WD) is a hepatoneurological disorder caused by mutations in the copper‐transporter, ATP7B. Copper accumulation in the liver is a hallmark of WD. Current therapy is based on copper chelation, which decreases the manifestations of liver disease, but often worsens neurological symptoms.

Gab1 adaptor protein acts as a gatekeeper to balance hepatocyte death and proliferation during acetaminophen‐induced liver injury in mice

Kunimaro Furuta, Yuichi Yoshida, Satoshi Ogura, Tomohide Kurahashi, Takashi Kizu, Shinichiro Maeda, Mayumi Egawa, Norihiro Chatani, Keigo Nishida, Yoshikazu Nakaoka, Shinichi Kiso, Yoshihiro Kamada, Tetsuo Takehara – 17 December 2015 – Acetaminophen (APAP) overdose is the leading cause of drug‐induced acute liver failure. In APAP‐induced acute liver failure, hepatocyte death and subsequent liver regeneration determines the prognosis of patients, making it necessary to identify suitable therapeutic targets based on detailed molecular mechanisms.

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