Background:It is commonly recommended that patients should refrain from driving for 24 hours after sedation for endoscopy,however,this recommendation has been queried recently. Aims:To investigate the effect of sedation on early postoperative cognitive function in patients undergoing endoscopy. Methods:One hundred adult patients undergoing sedative esophagogastroduodenoscopy ( EGD ) were randomly recruited, and another 100 adult patients undergoing conventional EGD were served as controls. All patients had an education level more than 9 years. Cognitive function was assessed by number connection test-A( NCT-A),number cancellation test and digit symbol test( DST)before propofol sedation or the beginning of endoscopic procedure and was reassessed when the discharge criteria were met. If the results obtained were inferior to those before EGD,a third assessment was taken 30 minutes later until the results recovered or being superior to the baseline levels. Results:All patients completed the first and second assessment,and 124 patients had taken the third assessment. When the discharge criteria were met,result of number cancellation test was inferior to that before EGD in sedation group( P =0. 000 ). Furthermore,the results were analyzed by grouping with age,number cancellation test in young patients and NCT-A in elderly patients were inferior to that before EGD,respectively(P=0. 000 and P =0. 025 ). In control group,none of the results were inferior to those before EGD. The results of the third assessment recovered or being superior to the baseline levels. Conclusions:Early postoperative cognitive dysfunction at discharge is common in patients undergoing endoscopy using propofol sedation,but the impairment will recover by a prolonged staying calm before discharge. The optimal time for discharge and resuming driving remains to be further studied.

Objective To evaluate the role of mTOR in spinal cord in the development of diabetic neuropathic pain in rats.Methods Sixty adult male Sprague-Dawley rats,aged 2 months,weighing 180-220 g,were used in the study.Forty-five rats among them were chosen randomly and diabetes mellitus was induced by intraperitoneal streptozotocin (STZ) 60 mg/kg and confirmed by blood glucose ＞ 16.7 mmol/L on day 3 after STZ injection.The left 15 rats received intraperitoneal injection of the equal volume of citric acid-sodium citrate buffer and served as normal control group (group C).Paw withdrawal threshold to von Frey filament stimulation was measured in the right hind paw before STZ injection and on 3,6,9,12,15,18,and 21 days after STZ injection.The diabetic rats with mechanical pain threshold decreasing by more than 50％ of the baseline were allocated to diabetic neuropathic pain group (group DP),and by less than 25 ％ of the baseline were allocated to diabetic non-neuropathic pain group (group NP).The rats were sacrificed at 21 days after STZ injection,and their lumbar enlargements of the spinal cord were removed for determination of the expression of mTOR and phosphorylated mTOR (p-mTOR) by Western blot.Results The expression of mTOR was significantly up-regulated in DP and NP groups when compared with group C (P ＜ 0.05),the expression of p-mTOR was up-regulated in DP group,and no significant change was found in the expression of p-mTOR in group NP (P ＞ 0.05).Compared with group NP,the expression of p-mTOR was significantly up-regulated (P ＜ 0.05),and no significant change was found in the expression of mTOR in group DP (P ＞ 0.05).Conclusion Activation of mTOR in the spinal cord is involved in the development of diabetic neuropathic pain in rats.

Objective To evaluate the effect of intrathecal rapamycin on diabetic neuropathic pain in rats.Methods Thirty adult male Sprague-Dawley rats,weighing 180-220 g,in which IT catheters were successfully implanted,were randomly divided into 5 groups (n =6 each) using a random number table:control group (group C),diabetic neuropathic pain group (group DN),rapamycin 1 μg group (group R1),rapamycin 3 μg group (group R3) and rapamycin 10 μg (group R10).Diabetes mellitus was induced by intraperitoneal streptozotocin (STZ) 60 mg/kg on 5 days after IT catheters were implanted in DN,R1,R3 and R10 groups.Citric acid-sodium citrate buffer 6 ml/kg was injected intraperitoneally in group C.In R1,R3 and R10 groups,rapamycin (dissolved in 10 μl 4％ dimethyl sulfoxide) 1,3 and 10 μg were intrathecally injected,respectively,once a day for 7 consecutive days starting from day 21 after STZ injection,while the equal volume of 4％ dimethyl sulfoxide was given instead in C and DN groups.Paw withdrawal threshold (PWT) to yon Frey filament stimulation was measured before IT catheters were implanted,before STZ injection,on 7,14 and 21 days after STZ injection,and on 1,3,5 and 7 days after rapamycin administration.After measurement of PWT,the rats were sacrificed and L2-5 segments of the spinal cord were removed for determination of the expression of mTOR and phosphorylated mTOR (p-mTOR),S6K and phosphorylated S6K (p-S6K) (by Western blot) and expression of mTOR mRNA and S6K mRNA (by RT-PCR).Results Compared with group C,MWT was significantly decreased at 14 and 21 days after STZ injection in DN,R1,R3 and R10 groups,and the expression of mTOR,p-mTOR,S6K,p-S6K,mTOR mRNA and S6K mRNA was up-regulated in group DN (P ＜ 0.01).Compared with group DN,MWT was significantly increased at 5 and 7 days after rapamycin administration in group R1,at 3,5 and 7 days after rapamycin administration in group R3,and at 1,3,5 and 7 days after rapamycin administration in group R10,and the expression of mTOR,p-mTOR,S6K,p-S6K,mTOR mRNA and S6K mRNA was down-regulated in R1,R3 and R10 groups (P ＜ 0.01).Conclusion Intrathecal rapamycin can alleviate diabetic neuropathic pain in rats.

Objective To evaluate the effects of curcumin preconditioning on the activity of xanthine oxidase (XOD) during intestinal ischemia-reperfusion (I/R) in rats.Methods Thirty female Sprague-Dawley rats,aged 180-220 g,were randomly divided into 3 groups (n =10 each) using a random number table:sham operation group (S group),intestinal I/R group (I/R group),and curcumin preconditioning group (Cur group).Intestinal I/R was induced by clamping the superior mesenteric artery for 75 min followed by reperfusion.Curcumin 200 mg/kg was given everyday for 5 days before intestinal I/R in Cur group and the equal volume of normal saline was given instead of curcumin in S and I/R groups.The rats were sacrificed at 4 h of reperfusion and the intestinal specimens were obtained for microscopic examination of pathologic changes which were graded using Chiu scoring system and for determination of XOD activity,content of malondialdehyde (MDA),and superoxide dismutase (SOD) activity.Results Compared with S group,the Chiu score,activity of XOD and content of MDA were significantly increased,while the activity of SOD was decreased in I/R and Cur groups (P ＜ 0.05).Compared with I/R group,the Chiu score,activity of XOD and content of MDA were significantly decreased,and the activity of SOD was increased in Cur group (P ＜ 0.05).Conclusion Curcumin preconditioning can attenuate intestinal I/R injury in rats,which may be due to inhibition of XOD activity and decreased oxidative stress in intestinal tissues.

Objective To evaluate the effect of curcumin preconditioning on the activation of mast cells during intestinal ischemia/reperfusion (I/R) in rats.Methods Twenty-four female Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (S group),intestinal I/R group (I/R group),and curcumin preconditioning group (Cur group).Intestinal I/R was produced by occlusion of superior mesenteric artery (SMA) for 75 min followed by reperfusion.At 5 days before I/ R,curcumin 200 mg/kg (in 20 mg/ml normal saline) was given through a gastric tube in Cur group,while the equal volume of normal saline was given instead in S and I/R groups.All the rats were sacrificed at 4 h of reperfusion,and the intestinal specimens were obtained for microscopic examination and for determination of tryptase expression and β-hexosaminidase content.Intestinal damage was assessed and scored according to Chiu.Results Compared with S group,Chiu's score and β-hexosaminidase content were significantly increased,and the expression of tryptase was up-regulated in I/R and Cur groups.Compared with I/R group,Chiu' s score and β-hexosaminidase content were significantly decreased,and the expression of tryptase was down-regulated in Cur group.Conclusion The mechanism by which curcumin preconditioning attenuates intestinal I/R injury is related to inhibited activation of mast cells of rats.

Objective To evaluate the effects of curcumin pretreatment on the activity of inducible nitric oxide synthase (iNOS) during lung injury induced by intestinal ischemia-reperfusion (Ⅰ/R) in rats.Methods Twenty-four pathogen-free female Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group Sham);intestinal Ⅰ/R group (group Ⅱ/R);curcumin pretreatment group (group Cur).A rat model of lung injury induced by intestinal Ⅰ/R which was produced by occlusion of superior mesenteric artery for 75 min followed by reperfusion was established.At 5 days before Ⅰ/R,curcumin 200 mg/kg (in 20 mg/ml of normal saline) was given through a gastric tube in group Cur,while the equal volume of normal saline was given instead in Sham and Ⅱ/R groups.The rats were sacrificed at 4 h of reperfusion,and the pulmonary specimens were obtained for determination of wet/dry lung weight ratio (W/D ratio),NO content (by using nitrate reductase method) and iNOS activity (using colorimetric method) and for examination of pathological changes (with light microscope).The pathological changes of the lung were scored.Results Compared with group Sham,the pathological scores,W/D ratio,NO content and iNOS activity were significantly increased in Ⅱ/ R and Cur groups.Compared with Ⅱ/R group,the pathological scores,W/D ratio,NO content and iNOS activity were significantly decreased in group Cur.The pathological changes of lungs were significantly attenuated in group Cur as compared with H/R group.Conclusion The mechanism by which curcumin pretreatment attenuates lung injury induced by intestinal Ⅰ/R is related to decrease in iNOS activity in rats.

ObjectiveTo investigate the correlation between any two of Capsule Endoscopy ScroringIndex (Lewis score),simplified Crohn Disease Activity Index (CDAI) and C-reactive protein (CRP) in small bowel Crohn disease (CD).MethodsA total of 58 consecutive patients with known small bowel CD were enrolled. We evaluated disease activity with Lewis score and simplified CDAI. Correlations among CRP,simplified CDAI and Lewis score were calculated with Spearman's rank order correlation coefficient.The optimal CRP cut-off value was calculated using the ROC curve.ResultsThe Lewis score showed inactive,mild and moderate-severe patients were 13,21 and 24,respectively.CRP of moderate-severe group was significantly higher than that in mild and inactive groups ( P ＜ 0.05 ).The optimal CRP cut-off value that differentiated patients with moderate to severe disease from the others was 13.50 mg/L with sensitivity of 87.5％ and specificity of 82.4％.The area under the ROC curve to analyze the cut-off was 0.849.Lewis score was moderately correlated with CRP (r =0.58,P ＜ 0.01 ),and weakly correlated with the simplified CDAI (r =0.40,P ＜ 0.01 ).ConclusionSerum CRP and the simplified CDAI cannot replace Lewis score for capsule endoscopy in the assessment of disease activity in small bowel CD.However,CRP may be considered as an inflammatory marker for evaluating the moderate to severe capsule endoscopic activity.

Objective To evaluate the role of nitric oxide (NO) in the spinal cord in the maintenance of diabetic neuropathic pain in rats.Methods Male Sprague-Dawley rats,aged 2 months,weighing 180-200 g,were used in the study.Diabetes mellitus was induced by intraperitoneal streptozotocin (STZ) 60 mg/kg and confirmed by blood glucose ＞ 16.7 mmol/L on day 2 after STZ injection.Twenty diabetic rats were randomly allocated into diabetes mellitus group (DM group,n =10) and L-NAME (non-selective NOS inhibitor) group (LN group,n =10).Another 10 age-matched normal rats served as control group (C group).On 21 days after STZ injection,L-NAME 10 mg/kg was injected intraperitoneally once a day for 7 consecutive days in LN group,whereas the equal volume of normal saline 5 ml/kg was given instead of L-NAME in DM group.Paw withdrawal threshold to yon Frey filament stimulation (PWT) was measured before STZ infection and on 7,14,21 and28 days after STZ injection.The rats were sacrificed after the last measurement of PWT and the lumbar segments of spinal cord were removed for determination of NO content and neuronal nitric oxide synthase (nNOS) expression (by Western blot analysis) in spinal cord tissues.Results Compared with C group,PWT was significantly decreased on 14,21 and 28 days after STZ injection,and the NO content and nNOS expression in spinal cord tissues were increased in DM and LN groups (P ＜ 0.05).Compared with DM group,PWT was significantly increased on 28 days after STZ injection,and the NO content and nNOS expression in spinal cord tissues were decreased in LN group (P ＜ 0.05).Conclusion NO in the spinal cord is involved in the maintenance of diabetic neuropathic pain in rats and the mechanism is related to the enhanced function of nNOS.

ObjectiveTo investigate the long-term (＞1 year) rebleeding rate after capsule endoscopy (CE)-guided intervention in patients with obscure gastrointestinal bleeding (OGIB) and to identify the risk factors of rebleeding.MethodsA total of 307 consecutive patients who underwent CE for OGIB in our hospital from June 2002 to October 2010 were enrolled.Follow-up data were obtained by reviewing medical records,CE database and contacting the patients or their relatives by telephone.We evaluated the rebleeding rates and analyzed risk factors predictive of rebleeding by means of COX ratio hazard model.ResultsThe medium follow-up was 52 months (range13-112 months).Significant lesions were found in 202 patients (65.8％).The overall rebleeding rate after interventional therapy induced by CE findings was 28.0％ (86/307).CE positive patients had higher rebleeding rate than CE negative patients (37.6％ vs 9.5％,log-rank test,P=0.000),while specific therapy could prevent rebleeding,compared with nonspecific therapy (32.9％ vs 23.0％,P=0.042).95.3％ (82/86) rebleeding occurred within 24 months after CE.Multivariate analysis performed by using COX proportional hazards model showed that age over 50 years,CE positive findings,lowest hemoglobin (Hb) level 3 months before CE ≤7 g/dl,receiving nonspecific therapy after CE,hypertension,administration of anticoagulants,antiplatelet medicine or NSAIDs after CE were six risk factors associated with rebleeding.Conclusion Clinicians should be aware of these risk factors for OGIB rebleeding,which can reduce the occurrence of rebleeding and improve OGIB patients' prognosis.Those high risk OGIB patients should be followed up for at least 24 months after CE.

Objective To study the long-term effect of argon plasma coagulation (APC) combined with proton pump inhibitor (PPI) on Barrett esophagus (BE). Methods A total of 36 patients, histologically proven as having BE from 2004 to 2007, were enrolled to underwent a therapy of APC plus PPI. The patients were re-examined on endoscopy at 1, 6 and 12 months after first APC and once a year thereafter.Results A total of 48 APC sessions were given to 36 patients with a mean number at 1. 33 per patient. The effective rate of reversal of BE was 100%. The follow-up was accomplished for all patients in 14-51 months with a median of 36months. The total recurrence rate (RR) of BE reached 16. 7% (6/36). The 1-year and 2-year RRs were 2. 8% (1/36) and 11.1% (4/36), respectively. The logistic regression analysis suggested that 2-year and total RRs were related to APC sessions ( P ＜ 0. 01 ). Conclusion The therapy of APC combined with PPI for BE is safe and of long-term effects.