China has huge amount of population and have a lot of literatures on IBS in Chinese publications. The aim of this article was to review the reported investigations on IBS in China and discuss the difference between China and other country. Methods:  Literatures pertaining IBS epidemiology, pathogenesis and pathophysiology, which published in the high level journals in china and SCI journals after 1998 were reviewed. Result:  In the general health population, 5–6% meets the Rome II IBS criteria. Intestinal infection, food intolerance,

genetic factor and psychological disturbance were responsible for the pathogenesis of IBS. In IBS patients, the impaired Ganetespib molecular weight reaction to rectal distension, abnormal gastrointestinal motility, impaired autonomic nerve function, weakened colon epithelium connection, altered cerebral neuclei activation were the main pthophysiological findings. PI3K inhibitor Conclusion:  Comparing to the findings from other area, literatures from China provided more evidences on epidemiological data of IBS in China, post-infection IBS, visceral hypertension and gastrointestinal motility abnormalities in IBS. This detailed literature review may help the understanding and promoting the

future studies on IBS. “
“Didier Y.R. Stainier: Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany Nonalcoholic fatty liver disease is the 上海皓元 most common liver disease in both adults and children. The earliest stage of this disease is hepatic steatosis, in which triglycerides are deposited as cytoplasmic lipid droplets in hepatocytes. Through a forward genetic approach in zebrafish, we found that guanosine monophosphate (GMP) synthetase

mutant larvae develop hepatic steatosis. We further demonstrate that activity of the small GTPase Rac1 and Rac1-mediated production of reactive oxygen species (ROS) are down-regulated in GMP synthetase mutant larvae. Inhibition of Rac1 activity or ROS production in wild-type larvae by small molecule inhibitors was sufficient to induce hepatic steatosis. More conclusively, treating larvae with hydrogen peroxide, a diffusible ROS that has been implicated as a signaling molecule, alleviated hepatic steatosis in both GMP synthetase mutant and Rac1 inhibitor-treated larvae, indicating that homeostatic production of ROS is required to prevent hepatic steatosis. We further found that ROS positively regulate the expression of the triglyceride hydrolase gene, which is responsible for the mobilization of stored triglycerides in hepatocytes. Consistently, inhibition of triglyceride hydrolase activity in wild-type larvae by a small molecule inhibitor was sufficient to induce hepatic steatosis.