ObjectiveTo explore the effects of transmembrane protein 16B （TMEM16B） on brain edema and blood-brain barrier after cerebral ischemia-reperfusion injury in rats. MethodsTMEM16B overexpression and knockdown was performed by adeno-associated virus （AAV）， and then adult male Sprague-Dawley rats were subjected to middle cerebral artery occlusion （MCAO）. Rats were randomly divided into Sham group， MCAO group， AAV no-load group， TMEM16B overexpression group and TMEM16B knockdown group. Modified neurological severity scores， adhesive removal test and cylinder test were used to evaluate neurologic function. The ultrastructure of ischemic brain tissue was observed by transmission electron microscope. Brain water content was reflected by dry wet weight ratio of brain tissue. The expressions of TMEM16B， aquaporin4 （AQP4）， Claudin5 and zonula occludens-1 （ZO-1） were investigated by immunofluorescence and Western blot. ResultsCompared with the AAV no-load group， the sensory and motor functions of rats in TMEM16B overexpression group were significantly impaired. Mitochondria were swollen； mitochondrial cristae and tight junctions disappeared. The brain water content was higher in overexpression group. The expression of TMEM16B and AQP4 increased while the expression of Claudin5 and ZO-1 decreased （all P<0.05）. Compared with the AAV no-load group， the rats in TMEM16B knockdown group showed some recovery in motor function. The mitochondrial cristae and structure were clear， and the basement membrane was partially blurred. The brain water content was lower in knockdown group. The protein levels of TMEM16B and AQP4 were lower while the levels of Claudin5 and ZO-1 were higher in TMEM16B knockdown group than in AAV no-load group （all P<0.05）. ConclusionAn increase in TMEM16B expression aggravates brain edema and blood-brain barrier damage in rats after cerebral ischemia-reperfusion injury， while a decrease in TMEM16B expression alleviates brain edema and protects the blood-brain barrier.

Objective To discuss the pathogeny,treatment and prophylactic measures of postcholecystectomy syndrome (PCS).Methods The clinical data of 150 patients with laparoscopic PCS in our department from October 2000 to March 2009 were analyzed.Results Etiological factors were found in 131 patients:one hundred and twelve cases were due to the reasons of biliary system,including bile duct residual stones after cystic resection,the injury bile duct stenosis,a long residual cystic canal,nipple benign stricture,bile duct tumor etc;Nineteen examples were due to other reasons,including gallbladder stone merger reflux gastritis,gastroduodenal ulcer,diverticulum beside duodenal nipple,and so on,which resulted in the symptoms un-release after cystic resection.Nineteen cases were not found organic lesion.In ones whose etiological factors were definite,117 cases were treated with different surgeries according to different etiological factors;another 33 cases were treated with conservative treatment.Total 145 cases were followed up,and 139 cases in them were cured or relieved at different degrees.Conclusion Careful preoperative examination,normalized operation avoiding damaging bile duct and leaving behind bile duct stones can effectively prevent laparoscopic PCS.