Objective: To establish an ultra performance liquid chromatography-tandem quadrupole mass spectrometry ( UPLC-MS/MS) method to determine the concentration of carbamazepine and phenobarbital in human plasma, and apply in the clinical moni-toring. Methods:Diazepam was used as the internal standard, and the samples were precipitated by acetonitrile. An ACQUITY UPL-C? BEH C18 (50 mm × 2. 1 mm, 1. 7 μm) column was used as the stationary phase at 40℃ with a Waters XEVO TQD. The mobile phase consisted of acetonitrile (containing 10 mmol·L-1 ammonium formate) and water (containing 10 mmol·L-1 ammonium for-mate and 0. 1% formic acid) with gradient elution pumped at a flow rate of 0. 4 ml·min-1 . ESI was applied and the samples were scanning analyzed by positive ion multi-reaction monitoring mode. The plasma was precipitated by 200 μl acetonitrile and centrifugated at 12 000 × g for 10 min and tranfer it into an Ep tube. The sample size was 20 μl. Results:The retention time of carbamazepine was 1. 23 min. Excellent linear calibration curves of carbamazepine were obtained within the concentration range of 0. 25-25μg·ml-1(r=0. 999 7). The lower limit of quantification of carbamazepine was 0. 01 μg·ml-1. The retention time of phenobarbital was 1. 11 min. Excellent linear calibration curves of carbamazepine were obtained within the concentration range of 0. 5-50 μg·ml-1(r=0. 999 6). The lower limit of quantification of carbamazepine was 0. 05 μg·ml-1. The recovery of three concentrations of carbamazepine was (82. 1 ± 6. 83)%, (82. 91 ± 4. 3)% and (84. 35 ± 3. 09)%, and the recovery of three concentrations of phenobarbital was (84. 27 ± 6. 91)%, (84. 32 ± 7. 74)% and (89. 07 ± 6. 24)%, respectively. The intra- and inter-day RSDs were all less than 10%. There were no endogenous substances existing in the incubation system, therefore, there was no interference with the determination. Conclu-sion:The simple, accurate and rapid method is suitable for the determination of carbamazepine and phenobarbital in human plasma, which can contribute greatly to the therapeutic drug monitoring service for patients.

Objective To study the effect of CsA in a therapeutic dose on the hepatic ultrastructure in rats.Methods Twenty-four SD rats were divided into 3 groups.The control group was orally administered olive oil,and the other 2 groups were orally given CsA 25 mg/kg and 50 mg/kg daily respectively.After 2 weeks.the liver samples were taken for ultrathin sections.The stereological method was used to quantify some hepatic ultrastructural parameters including volume density (Vv),surface density(Sv),numerical density(Nv) and specific surface(δ).Results CsA caused an increases of Vv and Sv and a decrease of δ in endoplasmic reticulum;a decreases of Vv and Nv in microbody;decreases of Vv in Golgi complex and glycogen inclusions;an increases of Vv and Nv in lipid inclusions.Conclusion CsA in a therapeutic dose could cause the change of hepatic ultrastructure of rat.

Objective To evaluate the effect of gastroesophageal reflux disease(GERD)on exacerbations of chronic obstructive pulmonary disease(COPD).Methods All of 74 patients with COPD accomplishing the reflux diagnostic questionnaire(RDQ)were.divided into GERD group(n=38)and non-GERD group(n=36)according the scores of RDQ.The clinical data including the frequency of exacerbations of COPD were compared between the two groups.Results The frequency of exacerbations of COPD was significantly higher in GERD group compared with that in non-GERD group[(2.68±0.77)times/year vs (1.38±0.49)times/year,t=8.74,P＜0.05].The mean FEV;percentage was similar in the two groups [(39.82 4-10.95)%vs(37.11±12.24)%,t=1.00,P＞0.05].The score of RDQ was probably as a factor of predicting the frequency of exacerbations of COPD(R2a=o.39,t=6.98,P＜0.05).Conclusion The presence of GERD appears to be associated with increased exacerbations of COPD.

Objective To explore the value of electronic colonoscope,MSCT and MRI in the etiological diagnosis of intestinal obstruction.Methods The clinical data of 140 ileus patients were retrospectively studied.Results 140 cases of ileus included 60 cases of colon ileus,70 cases of small intestines ileus and 7 indefinite cases.67 cases were checked with colonoscopy,among them,41 cases with colon tumors,6 cases with colon polypi,6 cases with colon set folds,2 cases with sigmoid colon turned round,2 cases with ileum tumor and 10 cases with unknown reason.80 cases were checked by MSCT checks,among them,26 cases with small intestines tumor 24 cases with small intestines muck piece,23 cases with unknown reasons,2 cases with muck stone 2,4 cases with bowel chamber outside lymphoid lump,1 case with bowel fastens film blood to bolt.30 cases were kept to cure.2 cases were turn round to reset under the eolonoscopy,3 cases were set folds air to infuse bowel to reset,6 cases with inside the mirror descend colon polyp were resected with hish frequency electricity resection.99 cases were cured by surgical operation.5 cases were dead and 135 cases were recovered from illness.Conclusion Electronic colonoscopy,MSCT and MRI checking are accurate methods to diagnose why and where of ileus,and which establish importance basts for clinical treatment.

Objective To evaluate the protective effects of oral administration of D-methionine tablets on noise-induced hearing loss.Methods A total of 203 volunteers were recruited and randomly divided into two groups:experimental group (n=113)and control group (n=90).The subjects in the experimental group received oral administration of D-methionine tablets(1 500 mg/day)and those in the control group received placebo for 3 days before impulse noise exposure.The routine audiometric evaluation and ABR testing were performed and recor-ded 1 day and 7 days post- noise exposure.The statistical analysis was carried out with SPSS 11.0.ResuIts The changes of hearing in all participators were observed after noise exposure.The results were as follow:The hearing thresh-olds at three time points were 40.5±9.3,51.7±12.3,44.1±11.4 dB nHL in experimental group and 41.5±8.9,62.4± 13.7,47.6±12.5 dB nHL in control group,respectlvely;the ABR I-V IPLs at three time points were 3.72±0.21 ms, 3.99±0.36 ms,3.82±0.25 ms in experimental group,while 3.71±0.22 ms,4.45±0.37 ms,3.85±0.34 ms in control group,respectively.There were statistically significant differences between the two groups.ConcIusion The oral adminis-tration of D-methionine tablets pre noise exposure can protect against noise-induced hearing loss.

Objective To observe the effect of wound specialist group on preventing and managing pressure ulcer in operation. Methods The knowledge about pressure ulcer and ability of risk assessment for pressure ulcer of operating room nurses were tested and the incidenc-es of pressure ulcer were compared before and after the intervention of the wound specialist group. Results After the intervention of the wound specialist group, the passing rate of nurses in operating room increased from 58.23%to 94.11%in pressure ulcer theory (χ2=29.63, P<0.001) and from 56.96%to 95.29%in new type of dressings paste (χ2=33.80, P<0.001), and the rate of pressure ulcer risk factor assessment increased from 56.38%to 93.35%(χ2=5828.07, P<0.001), accuracy of assessment increased from 56.23%to 96.78%(χ2=4674.89, P<0.001). The incidence of intraoperative acute pressure ulcer decreased from 1.5‰to 0.22‰(χ2=17.59, P<0.001). Conclusion The intervention of wound specialist group may improve the awareness of assessing risk factors of pressure ulcer in the operation room and standardize the oper-ation to prevent pressure ulcer, and reduce the incidence of pressure ulcer in operation.

Objective To explore the morbidity and risk factors of postoperative delirium in the patients undergoing coronary artery bypass grafting (CABG).Methods A total of 286 patients were continuously enrolled for CABG surgery from January to December 2013 in cardiac surgery ward in Beijing Anzhen Hospital.Delirium Rating Scale-Revised-98 was used as the diagnostic tool for the analysis of the morbidity and risk factors of postoperative delirium.Results (1) Delirium occurred in 24 patients of 286 patients and morbidity of postoperative delirium was 8.4％.Sixteen of 24 patients (66.7％) suffered from transient delirium (＜24 h).Eight of 24 patients (33.3％) suffered from continuous delirium (≥48 h).(2) The common clinical presentation of postoperative delirium included increased psychomotor activity, a disordered sleep-wake cycle and a reduced level of consciousness.(3) Univariate Logistic regression analysis results showed that delirium was associated with advanced age over 70 years old (OR =3.05, 95％ CI 2.55-72.94, P =0.023), previous cerebral infarction(OR =1.78, 95％ CI 1.07-2.96, P =0.026), previous brain heamorrhage (OR =1.99, 95 ％ CI 1.20-3.31, P =0.003), surgery time (OR =1.05, 95％ CI0.05-2.04, P =0.047), intensive care unit (ICU) staying time (OR =2.87, 95％ CI 1.43-5.72, P=0.003), use offentanyl (OR=2.78, 95％ CI 1.02-7.57, P=0.045).(4) The multiple Logistic stepwise regression analysis indicated that the perioperative risk factors of delirium included advanced age over 70 years old (OR =3.196, 95％ CI 1.574-6.488, P =0.001), cerebrovascular accident history(OR =2.610, 95％ CI 1.538-4.431, P =0.000) and ICU duration time(OR =1.480, 95 ％ CI 1.070-2.046, P =0.018).Conclusions The morbidity of postoperative delirium after CABG is 8.4％.Many predisposing and precipitating factors contribute to postoperative delirium.These factors include age ＞ 70 years, cerebral infarction and ICU staying time.Assessment and preventive strategies should be considered to reduce the incidence of delirium, particularly among those patients with high risks.

Objective To study the expression and regulation of pro‐inflammatory cytokinesTNF‐α,IL‐1 ,IL‐6 in mononucle‐ar macrophages stimulated with staphylococcal protein A (SpA) .Methods THP‐1 was incubated with PMA and induced into mononuclear macrophages .Then the macrophages were incubated with varying concentrations of SpA under different time points . The effect of SpA on macrophage proliferation was measured by MTT method .The levels of inflammatory cytokines ,TNF‐α,IL‐1 and IL‐6 from the cultured cell media were measured by ELISA respectively .The levels of mRNA expression corresponding to TNF‐α,IL‐1 and IL‐6 were detected by RT‐PCR from the macrophages stimulated with SpA .All statistical analyses were performed by SPSS17 .0 software .Results The MTT result indicated that SpA had a positive effect on the proliferation of THP‐1 cells in a dosage depended manner .The addition of SpA could enhance the mRNA expression of TNF‐α,IL‐1 and IL‐6 in the stimulated mac‐rophages .It also showed a specific dose‐effect and time‐effect correlation .The macrophages secreted inflammatory cytokines and its corresponding mRNA reached its peak levels at 12 h post stimulation .Compared with the control group ,the expression and release of TNF‐α,IL‐1 and IL‐6 in macrophages from the experimental group was increased with statistical significance(P<0 .01) .Conclu‐sion SpA can promote the secretion and expression of early pro‐inflammatory cytokines ,such as TNF‐α,IL‐1 and IL‐6 in macro‐phages .Therefore ,SpA plays a very important role in the initiation and development of the staphylococcus aureus sepsis .

Objective:To investigate the effects of 5-aza-2′deoxycytidine(5-aza-dC),a DNA methyltransferase (DNMT)inhibitor, on the methylation status of the RECK gene and the invasion of salivary adenoid cystic carcinoma cell lines.Methods:Methylation-specific PCR,Western blot analysis and quantitative real-time PCR were used to investigate the methylation status of RECK gene and the expression of RECK mRNA and protein in SACC cell lines.The invasive ability of SACC cells was examined by transwell assay. Results:Promoter methylation was only found in ACC-Mcell line and not in ACC-2 cell line.Treatment of ACC-Mcells with 5-aza-dC partially reversed the hypermethylation status of the RECK gene and significantly enhanced the expression level of mRNA and pro-tein of RECK,suppressed ACC-Mcell invasive ability.Conclusion:5-aza-dC can inhibit ACC-Mcell invasion by reversal of hyperm-ethylation status of RECK gene.