Objective:To investigate the effect of flurbiprofen axetil on the pain after artifical abortion and its mechanism. Methods: A total of 120 ASAⅠ~Ⅱ induced abortion patients were randomly divided into 4 groups(n=30 each). Group F50 was treated with flurbiprofen axetil(50 mg) combined with propofol,Group F75 with flurbiprofen axetil(75 mg) combined with propofol,Group C with blank emulsion combined with propofol and Group K with ketamine combined with propofol.All patients took Misoprostol tablet by mouth 2 hours before artifical abortion, patients of group F50,group F75 and group C were intravenousely injected flurbiprofen axetil or blank emulsion five minutes before propofol, and patients of group K were administered mixed solution of ketamine and propofol. HR, BP, side effect,and pain of VAS score after artifical abortion were recorded. Reslts: Pain of VAS score after artifical abortion in group C and group K were higer than those of group F50 and group F75 at the same time(P

PONV (Postoperation nausea and vomiting) is one of the most possible problems after operation, and it has been a barraier to recovery of patients who had been orperationed, This review will focus on risk factors and prophylactic antiemetic therapy for PONV.

Objective To investigate the etiology and novel treatment of plasma cell mastitis (PCM).Methods 145 cases of PCM undergoing massage dredge,ductal lavage and local amalgesic injection from Jan.2011 to Dec.2012 were retrospectively analyzed.Results 145 cases of PCM underwent conservative treatment for 2 to 8 weeks,among whom 128 cases were cured and the other 17 cases underwent surgical treatment for poor outcome.Among the 128 cases undergoing conservative treatment,9 cases had relapse during the follow-up of 12 to 36 months.Conclusions The combined treatment of massage dredge,ductal lavage and partial closed treatment is effective for patients with PCM,and it can keep patients from having mastectomy and reduce the recurrent rate.

Objective To investigate the effect of parecoxib pretreatment on focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Sixty-four male SD rats weighing 250-300 g were randomly divided into 4 groups ( n= 16 each): sham operation group (group S); focal cerebral I/R group; focal cerebral I/R + parecoxib 5 mg/kg group (group P5); focal cerebral I/R + parecoxib 10 mg/kg group (group P10). Focal cerebral I/R was produced by occlusion of middle cerebral artery for 2 h followed by 24 h of reperfusion. Parecoxib 5 and 10 mg/kg were injected intravenously through the internal jugular vein 30 min before ischemia in group P5 and P10 respectively. The neurologic deficit scores (NDSs) were measured at 24 h of reperfusion and then the rats were decapitated.Brains were rapidly removed for determination of the infarct volume, apoptosis rate and expression of Bcl-2 and Bax. The ratio of Bcl-2 to Bax (Bcl-2/Bax) was calculated. Results The NDSs, apoptosis rate and expression of Bcl-2 and Bax were significantly higher, Bcl-2/Bax was significantly lower, and the infarct volume was significantly larger in group I/R than in group S ( P ＜ 0.01 ). The NDSs were significantly lower in group P10, and the apoptosis rate and Bax expression were significantly lower, the infarct volume was significantly smaller, Bcl-2 expression and Bcl-2/Bax were significantly higher in group P5 and P10 than in group I/R (P ＜0.05 or 0.01). The infarct volume was significantly smaller, the apoptosis rate and Bax expression were significantly lower, and Bcl-2 expression and Bcl-2/Bax were significantly higher in group P10 than in group P5 ( P ＜ 0.05 or 0.01 ). Conclusion Pretreatment with parecoxib can attenuate focal cerebral I/R injury in a dose-dependent manner through inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation of Bax expression in rats.

The optimum convolution spectra of β-galactosidase and the linear equation of Qj=1.906×10-2＋4.946×10-3 C＋1.909×10-4 C2,r=1.0000 under the best condition were established by the convolution spectrum method.Based on the chromogenic substrate o-nitrophenyl-β-galactoside,a method for the determination ofβ-galactosidase activity in the COS-1 extraction sample which had been transfected transiently expression vector of β-galactosidase was determined by using the convolution curve transformation technology.The convolution spectrum method was compared with the absorption method and the result was satisfactory.The method was simple,convenient,fast and valuable to the biochemical analysis.

Objective: To qualitatively identify 5 chlorin metal complexes which had similar structures. Methods: The compounds were identified by the convolution curve transformation technology and computer information process technology. Results: The results were demonstrated by match comparison and three dimensional differential diagram of convolution spectra. Five chlorin metal complexes were identified satisfactorily and 10 nonidentity identification results were acquired. Conclusion: The convolution spectrum method is simple and feasible for the identification of the compounds which have similar structures. [

Objective To investigate the effects of simvastatin pretreatment on ischemia-reperfusion (I/R)injury to the spinal cord in rats. Methods Ninety-six healthy male SD rats weighing 220-280 g were randomly divided into 3 groups (n=32 each): Ⅰ group sham operation (group S); Ⅱ group I/R and Ⅲ group simvastatin pretreatment (group Si). The animals were anesthetized with 10% chloral hydrate 0.4 ml/100g. I/R to the spinal cord was induced by cross-clamping the aorta below renal artery for 45 min followed by reperfusion according to Zivin in group Ⅱ and Ⅲ. In group Ⅲ simvastatin 20 mg/kg was administered via gastric tube in the morning for 3 days before operation. Neurological function was assessed and scored (0 = no spontaneous movement of the hindlimbs, 7 = normal gait) at 2, 6, 12 and 24 h (n = 8 at each time point). The animals were then sacrificed and the lumbar segment (L2-5) of the spinal cord was removed for microscopic examination and determination of expression of TLR4 mRNA, NF-κB protein activity and TNF-α and ICAM-1 contents in the spinal cord. Results I/R to the spinal cord significantly increased TLR4 mRNA expression, NF-κB protein activity and TNF-α and ICAM-1 content in the spinal cord and decreased neurological scores in group Ⅱ compared with group C. Simvastatin pretreatment significantly attenuated the I/R-induced increase in the above-mentioned variables and ameliorated I/R-induced neurological dificit and histopathological damage. Conclusion Simvastatin pretreatment has neuroprotective effects on the spinal cord against I/R injury by attenuating inflammatory response.

Objective To investigate the effects of flurbiprofen pretreatment on the permeability of bloodbrain barrier in a rat model of global cerbral ischemia-reperfusion (I/R) injury. Methods Forty-five male SD rats weighing 300-350 g were randomly divided into 3 groups (n = 15 each): sham operation group (group S); global cerebral I/R group (group I/R); flurbiprofen 10 mg/kg + global cerebral I/R group (group F). Global cerebral ischemia was induced by 20 min occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg). In group F, flurbiprofen 10 mg/kg was injected iv at 15 min before ischemia. Evans blue 3 ml/kg was injectcd iv at 24 h of reperfusion, then the rats were sacrificed and their brains were immediately removed for determination of the apoptosis rate, brain water content, Evans blue content, TNF-α, IL-1β and IL-10 content, and microscopic examination. Results The apoptosis rate, brain water content, Evans blue content, and TNF-α, IL-1β and IL-10 content were significantly higher in group I/R and F than in group S (P ＜ 0.05 or 0.01).The apoptosis rate, brain water content, and Evans blue content and TNF-α and IL-1β content were significantly lower, while IL-10 content was higher in group F than in group I/R (P ＜ 0.01). Global cerbral I/R-induced changes were significantly attenuated in group F. Conclusion Pretreatment with flurbiprofen can protect bloodbrain barrier against cerebral I/R injury by inhibition of the inflammatory reaction.

ObjectiveTo investigate the learning curve of total thoracoscopicy cardiac surgery.MethodsClinical data of a succession of 125 patients undering total thoracoscopicy ASD and VSD repair between October 2004 to January 2010 were collected and reviewed.The procedure was perfomed by the same surgeon.The patients were divided equally into 5 groups (groupA,B,C,D and E,n =25 in each group ) according to the sequence of the operation.The operative time,extracorporeal circulation time,aortic cross-clamped time,the rate of conversion rate to thoracotomy and postoperative complications were compared between the 5 groups.ResultsThere were no statistically significant differences between the 5 groups with respect to age,gender,weight,dieases and surgical approach(P ＞ 0.05).The operative time,extracorporeal circulation time and aortic clump time in group A and group B significant longer then that in group C,group D and group E(P ＜0.05).Group A and group B was no statistically significant difference each other( P ＞ 0.05 ).Group C,D and E have no statistically significant differences between(P ＞0.05 ).The rate of conversion rate to thoracotomy and postoperative complications in 5 groups have no statistically significant differences comparative( P ＞ 0.05 ).ConclusionThe learning curve of total thoracoscopicy surgery is approximalely 50 cases.

Objective To evaluate the effects of dexmedetomidine on the permeability of blood-brain barrier in rats subjected to global cerebral ischemia-reperfusion (I/R).Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP was maintained at 35-45 mm Hg) in anesthetized rats.In group D,dexmedetomidine was infused at a rate of 3μg· kg-1 · h-1 until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was injected intravenously immediately after onset of I/R.The rats were sacrificed at 24 h of reperfusion and their brains were immediately removed for microscopic examination of hippocampal CA1 region and for determination of the cell apoptosis,brain water content,Evans blue content and aquaporin 4 (AQP4) expression.Results The number of apoptotic cells was significantly larger,and brain water content,Evans blue content and AQP4 expression were higher in groups I/R and D than in group S (P ＜ 0.05 or 0.01).The number of apoptotic cells was significantly smaller,and brain water content,and Evans blue content and AQP4 expression were lower in group D than in group I/R (P ＜ 0.05 or 0.01).Global cerebral I/R-induced pathological changes were significantly attenuated in group D.Conclusion Dexmedetomidine can decrease the permeability of blood-brain barrier and attenuate global cerebral I/R injury in rats,and down-regulation of AQP4 expression may be involved in the mechanism.