Objective To explore the mutation in corel β3-galactosyl-transferase specific molecular chaperone(Cosmc、no-coding region and it's effects on the transcription level of Cosmc in Tn antigen positive tumor cells.Methods The Tn antigen positive(Tn+)and negative(Tn-)cells were separated from tumor tissues by immune magnetic bead,then the genomic DNA(gDNA),total RNA were prepared by Qiagen AllPrep DNA/RNA mini kit. In these cells.the transcription levels of T-synthase and Cosmc mRNA were tested by RT-PCR.the DNA of Cosmc non-coding region was amplified by PCR,the mutation in Cosmc non-coding region were further detected by sequencing.Results There are no mutation appearing in Tn-cells,one or more mosaic sequence allele appearing in portion of patient's Tn-cells.Almost of the Tn+cells which separated from tumor tissues and Jurkat T cell exists mutation.but the mutation style and mutation point were not saine in different tumor.Thtee patient's Tn+cells have loss of hetemzygosity(LOH),four patient's Tn+cells and Jurkat T cell have point mutation.Although no difference of transcription level of T-synthase mRNA in Tn+ and Tn-cells.but the transcription level of Cosmc mRNA in Tn+ cell was much lower than that in Tn-cell.The ratio of T-synthase/Cosmc mRNA in Tn+ tumor cells was hiigher than that in Tn-cell.Conclusion The tumor Tn antigen arise from mutation in Cosmc non-coding region maybe result from transcription level decreased of Cosmc mRNA.

Objective To investigate the genotype and drug resistance of extended-spectrum beta-lac-tamases(ESBLs) -producing Shigella in pediatric patients.Methods A total of 59 strains of Shigella were isolated from stool specimens of hospitalized children with shigellosis in Beijing Children's Hospital from January 2004 to December 2008.Phenotypic confirmatory test,which is based on Clinical and Laboratory Standards Institute(CLSI),was used to detect the ESBLs-producing strains.Agar dilution method was used to determine the minimal inhibitory concentration (MIC).PCR amplification was performed for ESBLs producers to determine the genotype.PCR product was sequenced and then analyzed to confirm the subtype of ESBLs.Results Of the 59 isolates,21 (35.6%) strains were identified as ESBLs producers.The 21 strains of ESBLs-producing Shigella all carried the genes of CTX-M as shown by PCR,and CTX-M-1,CTX-M-9 accounted for 6,15,respectively.Among the 21 CTX-M producers,there were 4 strains accompanied by TEM-type and 6 strains accompanied by OXA-type.Nucleotide sequence analysis showed that there were CTX-M-3 (n = 1),CTX-M-15 (n = 2),CTX-M-57(n =3) of the 6 CTX-M-1-producing isolates.The subtypes of CTX-M-9,TEM,OXA were all CTX-M-14,TEM-1,OXA-1,respectively.The sensitive drugs to ESBLs producers were imipenem,meropenem,piperacillin/tazobactam,cefoperazone/sulbactam and cefoxitin,with resistance rate all less than 15%.The resistance to ceftazidime was remarkably variable among different CTX-M producers.Conclusion The prevalence of ESBLsproducing Shigella is in a high level in pediatric patients in this area.The genotypes of ESBLs are all CTX-M.Most of them are CTX-M-14,but some are CTX-M-3,CTX-M-15 and CTX-M-57.Most ESBLs-producing strains are multidrug resistant.Carbopenems should be the first choice for ESBLs producers.

Objective To explore the diagnosis and management of ruptured abdominal aortic aneurysm(RAAA).Methods Twelve patients with RAAA treated in past 7 years were revienled retrospectively.The main clinical manifestations were abdominal pain and / or back pain,low blood pressure or shock,and pulsating abdominal mass.All cases were accurately diagnosed with CT and 7 were treated by conventional operation,one by EVAR,and the other 4 did not receive surgical treatment.Results Perioperative death occurred in 5 cases(mortality rate was 62.5%) in 8 surgical treated patients,including circulatory failure in 2 cases,renal failure in 1 case,and multiple organ failure in 2 cases.All the 4 patients treated with nonoperative method were dead.Conclusions Surgical operation in RAAA cases still carried a high mortality.Early dignosis,appropriate resuscitation,urgent surgical repair,reduction of operative time,and infrarenal clamping are measures conducive to lowering the mortality rate of RAAA.EVAR has the potential to reduce the mortality rate from RAAA.

Objective To study the effect of sevoflurane and propofol anesthetic techniques on interleukin (IL)-6 and IL-10 in patients with laparoscopic hysterectomy.Methods Fifty elective laparoscopic hysterectomy patients were randomly divided into sevoflurane group (25 patients) and propofol group (25 patients) who received either sevoflurane or propofol for their anesthesia.After induction,adjusted the sevoflurane inhalation concentration in sevoflurane group and propofol pumping speed in propofol group.Maintained the Bispectral index (BIS) value at 50 +5.Recorded heart rate (HR),mean arterial blood pressure (MAP),BIS,IL-6,IL-10 on 5 min before anesthesia (T1),10 min after pneumoperitoneum (T2),40 min after pneumoperitoneum (T3) and 5 ain before the end of the operation (T4),and compared.Results The level of BIS,HR,MAP in two groups and between two groups had no significant difference (P ＞ 0.05).The level of IL-6,IL-10 on T2-T4 were significantly higher than those on T1 [sevoflurane group:(31.0 ± 9.0),(33.0 ± 11.0),(34.0 ± 16.0) ng/L vs.(29.0 ± 8.0) ng/L and (19.3 ± 1.7),(24.0 ± 2.8),(27.0 ± 8.0) ng/L vs.(2.0 + 0.4) ng/L; propofol group:(38.0 ± 9.0),(40.0 + 12.0),(45.0 ± 18.0) ng/L vs.(29.0 + 11.0) ng/L and (8.2 ± 2.3),(11.0 ± 4.2),(18.0 ± 7.0) ng/L vs.(2.0 ± 0.3) ng/L] (P ＜ 0.05).The level of IL-6,IL-10 on T1 between two groups had no significant difference (P ＞ 0.05).The level of IL-6 on T2-T4 in sevoflurane group was significantly lower than that in propofol group and the level of IL-10 on T2-T4 in sevoflurane group was significantly higher than that in propofol group (P＜ 0.05).Conclusions At maintaining the balance of cytokines in laparoscopic hysterectomy,the effect of sevoflurane is better than propofol.Sevoflurane is more suitable for maintenance of anesthesia for laparoscopic gynecologic operation.

Objective To evaluate the clinical anesthetic efficacy of a combination of propofol and remifentanil for ultrasound-guided transvaginal oocyte retrieval.Pharmacodynamic (PD) model was established and its characteristics were analyzed based on the simulated concentrations of propofol and remifentanil in respective pharmacokinetic models, so as to guide further study.Methods Forty-two female patients undergoing transvaginal oocyte retrieval were divided into groups PR15 (n=24) and PR10 (n=18), who were received intravenous bolus of remifentanil 1.5 μg/kg + propofol 1.5 mg/kg and remifentanil 1.0 μg/kg+propofol 1.0 mg/kg, respectively.The anesthesia quality evaluation was based on the following indicators: onset time (loss of eyelash reflex), recovery time of orientation, the incidence of hypoxemia (SpO2 < 92%) and adverse reactions.Nonlinear mixed-effects model was used to evaluate the time courses of the simulated propofol and remifentanil concentrations-effect and to establish the PD model with NONMEM software.Results The time of recovering orientation in the patients of group PR10 was significantly faster compared with the patients in group PR15;the time of loss of eyelash reflex , incidence of hypoxemia (12.5% vs 16.7%) and cough (16.7% vs 11.1%) had no significant differences between the both groups.With the final PD model, the estimated parameters as following: EC50 of propofol and remifentanil for effective sedation and analgesia were 1.71 μg/ml and 2.57 ng/ml, respectively.EC95 of propofol and remifentanil for effective sedation and analgesia were 4.30 g/ml and 4.57 ng/ml, respectively.The effect site concentration of propofol 1 mg/kg was lower than EC50, but the effect site concentration of 1.5 mg/kg was higher than EC50.The peak effect site of 1.0 μg/kg and 1.5 μg/kg remifentanil was higher than EC50, and 1.5 μg/kg concentration was close to EC95.Conclusion Based on patients' recovery time, propofol 1.0 mg/kg combined with fentanyl 1.0 μg/kg is appropriate in patients undergoing transvaginal oocyte retrieval.

Objective To evaluate the effect of ropivacaine combined with low-dose naloxone or sufentanilropivacaine mixture on brachial plexus block carried under the guidance of ultrasound.Methods A total of 100 patients of our hospital undergoing upper limb surgery was randomly divided into four groups with 25 patients in each group.Four groups are patients receiving 20 mL of 0.375％ mesylate ropivacaine (Group D),20 mL of 0.375％ mesylate ropivacaine + 10 μg sufentanil (Group S),20 mL of 0.375％ mesylate ropivacaine + 100 ng naloxone (Group N) and 20 mL of 0.375％ mesylate ropivacaine + 10 μg sufentanil +100 ng naloxone (Group N+S).All patients underwent interscalene brachial plexus block under ultrasound guidance.The sensory block,motor block and other adverse reactions were observed and recorded at 5min,6,12,18,24 h.Results The sensory and motor block time of group D was (435.5 ± 77.9) min and (350.2 ± 69.8) min,group S (831.7 ± 52.0)min and (675.8 ± 48.1)min,group N (933.0 ± 117.1) min and (499.0 ± 40.5) min,group N+S (919.3 ± 59.0) min and (534.8 ± 56.6)min.The sensory block time of group N and group N + S were significantly longer than that of group D and S (P ＜0.05).The sensory and motor block time of group D were obviously shorter than that of other groups (P ＜ 0.05).There were no significant difference in the onset time of sensory and motor block in all groups.Conclusion Low dose of naloxone combined with ropivacaine or sufentanil-ropivacaine mixture can increase the duration of sensory block on brachial plexus.

Objective To detect the protective effect of sufentanil preconditioning on hepatic ischemia-reperfusion injury in rats and the role of c-Jun N-terminal kinase signal pathway in the mech-enism.Methods One hundred and sixty-two SD rats(in either gender,weighing 250-300 g)were ran-domly divided into seven groups:Sham-operated group (group S,n = 30 ),ischemia-reperfusion group (group IR,n =30),sufentanil preconditioning group (group SF1:1 μg/kg,n =30;group SF5:5 μg/kg,n =30;group SF10:10 μg/kg,n =30),SP600125 group (group SP,n =30),and dimethyl sulphoxide control group (group DMSO,n =6),different doses of sufentanil was administered 30 min before hepatic ischemia in group SF1,SF5 and SF10.Blood and liver samples were collected from each group at 0(T1 ),1 (T2 ),2 (T3 ),4 (T4 ),and 6 (T5 )hours after reperfusion.Serum alanine amin-otransferase (ALT)and aspartate aminotransferase (AST)were measured by an automatic biochemi-cal analyzer.Malondialdehyde (MDA)and superoxide dismutase (SOD)in liver tissue was measured. Liver sample was stained with HE to observe the hepatic pathological changes.Immunohistochemical method was used to determine the expression of JNK and western blotting was used to detect the ex-pression of P-JNK.Results Compared with group S,levels of AST,ALT increased significantly in group IR,SF1,SF5,SF10 at T1-T5 and in group SP,DMSO at T3 (P <0.05 ).Compared with group IR,levels of AST,ALT decreased significantly in group SF1,SF5,SF10 at T1-T5 and in group SP at T3 (P <0.05).Compared with group S,levels of MDA,SOD increased significantly in group IR,SF1, SF5,SF10 at T1-T5 and in group SP,DMSO at T3 (P < 0.05 ).Compared with group IR,levels of MDA,SOD decreased significantly in group SF1,SF5,SF10 at T1-T5 and in group SP at T3 (P <0.05).Compared with group SF1 and SF5,levels of MDA,SOD decreased significantly in SF10 at T4 . Compared with T1 ,the expression of p-JNK in group IR increased significantly at T3 (P < 0.05 ). Compared with group S,the expression of p-JNK in groups IR,SF1,SF5,SF10,SP,DMSO increased significantly at T3 (P < 0.05 ).Compared with group IR,the expression of p-JNK in groups SF1, SF5,SF10,SP decreased significantly and that in groups SF5,SF10 were less than that in group SF1 (P <0.05 ).The expression of p-JNK in group SF10 was less than that in group SF5 (P < 0.05 ). Conclusion Sufentanil preconditioning can reduce the hepatic ischemia-reperfusion injury and the dos-age of 10 μg/kg was the most effective.The protective mechanisms may inhibit JNK pathway and re-duce the expression of JNK.

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) signaling pathway in the protective effect of isoflurane preconditioning and sevoflurane preconditioning against oxygen-glucose deprivation (OGD) injury in rat hippocampal slices. Methods Male adult SD rats weighing 270-290 g were anesthetized with ether and decapitated. The hippocampi were removed and sagittally sliced (400 μm thick) and placed in artificial cerebral spinal fluid aerated with 95% O2-5% CO2 . Ninety-six hippocampal slices were randomly divided into 8 groups (n = 12 each): control group (group C), OGD group, isoflurane preconditioning group (group Iso),sevoflurane preconditioning group (group Sevo) , SP600125 + isoflurane preconditioning group (group SP + Iso),SP600125 +sevoflurane preconditioning group (group SP + Sevo), DMSO + isoflurane preconditioning group (group DMSO + Iso) and DMSO + sevoflurane preconditioning group (group DMSO + Sevo). Electrophysiological technique was used to record the amplitude of population spike ( PS) in the stratum pyramidale of CA1 region and the degree of recovery of PS was calculated. The cell viability was determined by propidium iodide staining. Results Compared with group C, the degree of recovery of PS and cell viability were significantly decreased in the other groups ( P ＜ 0.01) . Compared with group OGD, the degree of recovery of PS and cell viability were significantly increased in groups Iso, Sevo, SP+Iso, SP+Sevo, DMSO+ Iso and DMSO + Sevo (P＜ 0.01). Compared with group Iso, the degree of recovery of PS and cell viability were significantly increased in group SP+Iso ( P ＜ 0.01) , while no significant change was found in group DMSO + Iso ( P ＞ 0.05) . Compared with group Sevo, the degree of recovery of PS and cell viability were significantly increased in group SP + Sevo ( P ＜ 0.01) , while no significant change was found in group DMSO + Sevo ( P ＞ 0.05). Conclusion Isoflurane preconditioning and sevoflurane preconditioning can attenuate the OGD injury to rat hippocampal slices through inhibiting JNK signaling pathway.

Objective To study the protective effect of sufentanil preconditioning on hepatic ischemia-reperfusion injury in rats and to investigate the mechanisms whether may be by activating p38 MAPK signal pathway to promote p38 MAPK phosphoryla-tion .Methods Thirty SD rats(in either gender ,weighing 220-270 g) were randomly divided into five groups :Sham-operated group (Ⅰ) ,ischemia-reperfusion group(Ⅱ);sufentanil preconditioning group(5 μg/kg ,Ⅲ) ,SB203580(an inhibitor of p38 MAPK) group (Ⅳ) ,and dimethyl sulphoxide (DMSO) control group(Ⅴ) .Sample specimens were collected from each group at 240 minutes after reperfusion .Serum alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were measured by an automatic biochem-ical analyzer .Malondialdehyde(MDA) and superoxide dismutase(SOD) in liver tissue was measured .HE staining was used to ob-serve the hepatic pathological changes ,and to examine the expression of phosphor-p38 mitogen-activated protein kinases (p-p38 MAPK)of hepatic tissues by western blotting .Results Compared with group Ⅰ ,levels of AST ,ALT and MDA showed signifi-cantly increased in group Ⅱ-Ⅴ ,but levels of SOD decreased ,and obvious pathological changes were observed in the liver .In GroupⅢ significantly decreased the elevated levels of ASL ,ALT and MDA but increased levels of SOD ,and lessened hepatic pathological changes ,caused promoted p38 MAPK phosphorylation at 240 minutes after reperfusion .The protective effects of sufentanil precon-ditioning were abolished by SB203580 pretreatment .There were no significant differences between group Ⅴ and group Ⅱ .Conclu-sion Sufentanil preconditioning can reduce the hepatic ischemia-reperfusion injury .The protective mechanisms may be by activating p38 MAPK signal pathway to promote p38 MAPK phosphorylation .

acts was much lower than that in Tn-cell.Conclusion The expression of Tn,STn,T and ST antigen in gastric carcinoma tissues of different TNM stages is different.Tn antigen expression in tumor cells may be caused by the decrease of T-Synthase activity.