The pathogenesis of nonalcoholic steatohepatitis (NASH) is unclear, despite epidemiological data implicating FFAs. We studied the pathogenesis of NASH using lipoapoptosis models. Palmitic acid (PA) induced classical apoptosis of hepatocytes. PA-induced lipoapoptosis was inhibited by acyl-CoA synthetase inhibitor but not by ceramide synthesis inhibitors, suggesting that conversion products other than ceramide are involved. Phospholipase A 2 (PLA 2 ) inhibitors blocked PA-induced hepatocyte death, suggesting an important role for PLA 2 and its product lysophosphatidylcholine (LPC). Small interfering RNA for Ca 21 -independent phospholipase A 2 (iPLA 2 ) inhibited the lipoapoptosis of hepatocytes. PA increased LPC content, which was reversed by iPLA 2 inhibitors. Pertussis toxin or dominant-negative Ga i mutant inhibited hepatocyte death by PA or LPC acting through G-protein-coupled receptor (GPCR)/Ga i . PA decreased cardiolipin content and induced mitochondrial potential loss and cytochrome c translocation. Oleic acid inhibited PA-induced hepatocyte death by diverting PA to triglyceride and decreasing LPC content, suggesting that FFAs lead to steatosis or lipoapoptosis according to the abundance of saturated/unsaturated FFAs. LPC administration induced hepatitis in vivo. LPC content was increased in the liver specimens from NASH patients. These results demonstrate that LPC is a death effector in the lipoapoptosis of hepatocytes and suggest potential therapeutic values of PLA 2 inhibitors or GPCR/ Ga i inhibitors in

Even after 2 decades of experience in laparoscopic hepatectomy, data on purely laparoscopic approach for donor hepatectomy in adult living donor liver transplantation (LDLT) are limited. We report our initial experience of a purely laparoscopic approach for donor hepatectomy for adult recipients to explore its potential application in the management of donors. We did a retrospective data analysis of 54 consecutive patients operated on between May 2013 and February 2015. There were 41 right, 10 extended right, and 3 left hepatectomies. The median operative time was 436 minutes (range 294-684 minutes), and warm ischemia time was 6 minutes (2-12 minutes). Estimated blood loss was 300 mL (10-850 mL), and none of the patients required intraoperative transfusion. Four cases were converted to open laparotomy. The major complication rate was 16.7%, and biliary complication was the most frequent cause. Patients with normal anatomy had a major complication rate of 9.3% as compared with 45.5% in patients with anatomic variations. All patients recovered, and there was no mortality. In conclusion, a purely laparoscopic donor hepatectomy for adult LDLT recipients seems to be a feasible option; with careful patient selection and when performed by experienced surgeons, it may afford results comparable to the open method.