OBJECTIVE To study the risk factors of neurosurgical postoperative intracranial infection.METHODS Totally 5405 patients who had a neurosurgical operation from 1996 to 2003 in our department were chosen(172(cases) with intracranial infection).Many risk factors were studied retrospectively,A data-base was set up with EXCEL,and Logistic regression was selected to analyze the factors which might cause infection.RESULTS The(analysis) of 5405 cases revealed that infection rate was closely related to the operation durations,CSF fistulae,(ventricle) drainage,the insertion of tubes,the approach to the post fossa,the complication from diabetes mellitus(DM),and open(craniocerebral) injuries.While had little effect of sex,age,the season,longer application of hormones before the operation,preoperative diseases,and longer application of antibiotics before or after the operation.(CONCLUSIONS) To decrease the infection rate,according the clinical experience,the operation should be finished as soon as possible,the suture should be done completely to prevent CSF fistulae,and the duration of the ventricle drainage should be controlled strictly.

Objective To investigate and compare the actions of vecuronium and atracurium on adult and embryonic-type nicotinic acetylcholine receptors (?-and ?-nAChR) at skeletal muscle cell membrane. Methods The adult and embryonic nAChRs were heterologously expressed in HEK 293 cells. Peak currents induced by actions of vecuronium and atracurium at ?-and ?-nAChR were recorded in HEK 293 cells, using whole cell patch clamp technique. Results Vecuronium and atracurium competitively inhibited ?-and ?-nAChR in HEK 293 cells. The inhibitor concentrations for half-maximal response (IC50) for vecuronium and atracurium ate-nAChR were (8.3 ? 2.6) ?mol/L and (24.2 ? 10.5) ?mol/L respectively; The IC50 values for vecuronium and atracurium at e-nAChR were (55.0 44 28.4) ?mol/L and (183.2 ? 39.2) ?mol/L respectively.Conclusion According to IC50 values for both adult and embryonic type nAChR, vecuronium is more potent than atracurium on e-and 7-nAChR. Embryonic nAChR is less sensitive to vecuronium and atracurium than adult-type nAChR.

Objective To investigate the effects of pancuronium on nicotinic acetylcholine receptors (nAChRs) in pheochromocytoma cells (PC12 cells) and to determine if pancuronium has direct effects on PC cells.Methods PC12 cells (purchased from Institute of Cytology, Chinese Academy of Science) were cultured in DMEM containing penicillin and glutamine. nAChR in PC12 cells were stimulated with different concentrations of Ach ( 10, 30, 100, 300, 1 000 ?mol?L-1 ). Ach-mediated inward currents were recorded using whole-cell patch clamp technique with holding potential set at - 80 mV. To investigate the effects of pancuronium on nAChR in PC cells, the PC12 cells were perfused with different concentrations of pancuronium (0.01,0.1, 1, 10, 100, 1 000 ?mol ? L-1 ) before Ach 1 ?mol?L-1 was added. Results Inward currents were elicited by stimulation of nAChR with Ach in a concentration-dependent manner. 93.7% of nAChRs could be activated by 1 ?mol ? L1 Ach. Pancuronium reversibly suppressed the currents in a concentration-dependent manner compared to the control currents elicited by 1 ?mol?L-1 Ach. 1 ?mol?L-1 pancuronium could almost completely suppressed the currents elicited by 1 ?mol ? L-1 Ach.Conclusion Pancuronium could inhibit nAChR in PC12 cells and reduce catecholamine release.

Objective To study the effect of etomidate on the changes in [Ca2+]i in rat cerebrocortical synaptosomes induced by KCI. Methods Freshly isolated SD rat cerebrocortical synaptosomes were prepared. KCI was used as chemical stimulant. Neurochemical method was employed (Fura-2 was used as calcium indicator) . Etomidate was added (the end concentration was 0.4, 4, 40 and 100 ?mol?L-1 respectively) before and after stimulation with KCI 50 mmol?L-1 to determine the peak and plateau [Ca2+]i in the cerebrocortical synaptomes. Results Before KCI stimulation etomidate inhibited KCl-evoked increase in intra-synaptosomal [Ca2+ ]i in a concentration-dependent manner. The inhibitory ratio of peak calcium concentration was 5%?3% , 11%?6% , 24%?10% and 33%?12% respectively as compared with control. Etomidate at concentration of 40 ?mol?L-1 and above had significant effect on [Ca2+]i. When added immediately after KCI stimulation, 4,40 ?mol?L-1 etomidate significantly increased plateau [Ca2+]i in synaptosomes.Conclusion Etomidate alters KC1-induced calcium dynamics in rat cerebrocortical synaptosomes. Presynaptic calcium channels and calcium removal mechanism are involved in its anesthetic action.

Objective To investigate the effects of rocuronium and vecuronium on the adult-type (?-nAChR) and fetal-type (?-nAChR) muscle nicotinic acetylcholine receptors. Methods HEK293 cells were obtained from Institute of Cytology, Chinese Academy of Sciences.?- and ?-nAChRs were expressed heterologously in HEK293 cells using transfection technique. Whole cell patch clamp technique was used to determine the potencies of the two muscle relaxants alone or in combination in blocking the function of the two types of nAChRs. Results Both rocuronium and vecuronium could competitively inhibit the activation of ?- nAChR and ?-nAChR by Ach. The IC50 of rocuronium and vecuronium for ?-nAChR was 169.2 ? 12.5 and (8.3 ? 2.7) ?mol?L-1 and for ?-nAChR was 8.6 ? 2.7 and (55.0?10.4) ?mol?L-1 respectively. The IC50 of rocuronium in combination with vecuronium was (0.7 ? 0.3) ?mol ? L-1 for ?-nAChR and (36.3 ? 14.2) ?mol ? L-1 for ?-nAChR.Conclusion The two muscle relaxants have different blocking action on the two types of nAChRs. Rocuronium has stronger inhibitory effect on ?-nAChR than on ?-nAChR while vecuronium has stronger inhibitory effect on ?-nAChR than on ?-nAChR. The inhibitory effects of the two muscle relaxants in combination was synergistic on ?-nAChR and additive on ?-nAChR.

Aim Expressing muscle acetylcholin e receptors in mammallian cells using receptor clone technique.Methods The cDNA coding for the ?,?,?, ?,?-subunits of the mouse muscle nAC hR in pSP65, pSP64,pBS SK(-) are subcloned into pcDNA3.1+ by gene recobinant technique and then transfect HEK293 cells using lipofection technique.The ?-n AChR and ?-nAChR are transiently expressed in HEK293 cells membrane. Recording the response of transfected HEK293 cells to acetylcholine by using the whole- cell clamp technique.Results Transfected HEK293 cells may produ ce a inward current as appling acetylcholine.The current values are acctylcholin e-concentration-dependent.Conclusion ?-nAChR or ?-nAChR i s expressed successfully in HEK293 cells.

OBJECTIVE: To evaluate the bioequivalence of domestic and imported Fenofibrate capsules in healthy volunteers. METHODS: In double-period crossover study, 18 healthy volunteers received a single oral dose of domestic Fenofibrate capsule 200 mg (test capsule) and imported capsule 200 mg (reference capsule). The content of fenofibric acid in plasma was measured with HPLC. BECS pharmacokinetics program was used to calculate the pharmacokinetic parameters and bioavailability and to evaluate the bioequivalence of two preparations. RESULTS: The main pharmacokinetic parameters of domestic Fenofibrate capsule vs. imported Fenofibrate capsule were as follows: t1/2(21.34?3.31) h vs.(21.83?4.35) h, Cmax(7.31?2.65) mg?L-1 vs. (7.28?2.66) mg?L-1, tmax(4.72?0.57) h vs.(4.67?0.59) h, AUC0～72(170.09?54.06) mg?h?L-1 vs. (172.2?54.64) mg?h?L-1, AUC0～∞(188.56?55.27) mg?h?L-1 vs. (192.27?56.62) mg?h?L-1. The relative bioavailability F0～72 and F0～∞ of domestic Fenofibrate capsule were(98.87?6.76)% vs.(98.00?6.72)%, respectively. Non-parameter test of tmax and variance analysis and t-test of Cmax and AUC0～72 showed there was no statistical difference between 2 kinds of Fenofibrate capsules. The 90% confidential intervals of AUC0～72 and Cmax of test capsule were 83.3%～116.9% and 81.1%～124.4%, respectively. CONCLUSION: The domestic and imported Fenofibrate capsules are bioequivalent.

To develop a high-performance liquid chromatographic method for the determination of isoguanosine in Semen Crotonis Tiglii.

Objective To explore the impact of puerarin treatment on autophagy in rats with traumatic brain injury (TBⅠ) and the underlying mechanism.Methods Seventy five Sprague-Dawley (SD) rats were randomized into 5 groups:sham group (S group,n =15),traumatic brain injury group (TBⅠ group,n =15),TBⅠ + puerarin treatment group (TBⅠ + Pue group,n =15),TBⅠ + JNK inhibitor group (TBⅠ + SP group,n =15),and TBⅠ + JNK activator + Pue (TBⅠ + An + Pue group,n =15).Feeney method was applied to make rats with TBⅠ model.Mter that,head water content and neurological deficit score (NDS) were measured and recorded at day 1,3 and 7 in each group.Western blot was used to measure the JNK activity and autophagic marker proteins,including LC3B and Beclin1.Results Compared to S group,the head water content and NDS were decreased significantly among the others (P ＜ 0.05).The head water content and NDS in TBⅠ + Pue and TBⅠ + SP groups was decreased remarkably compared with TBⅠ group.Combined with puerarin and animycin treatments failed to reduce head water content and NDS compared to the TBⅠ + Pue group.Activated autophagy could be observed in TBⅠ group compared to S group.Compared to group S,LC3Ⅱ,Beclin1 and P-JNK1 were increased significantly.Pue and SP could reduce their expressions,respectively.Combined with puerarin and animycin treatments failed to reduce LC3Ⅱ,Beclin1 and P-JNK1 compared to TBⅠ + Pue group.Conclusions Puerarin could protect rats with TBⅠ via inhibiting autophagy,JNK signal pathway could involve the process of puerarin regulating autophagy.

Objective:This work aims to detect the levels of miR-200c/141 methylation and miR-200c/141 in gastric cancer tissue and investigate the relationship between miR-200c/141 expression and clinical parameters. Methods:The methylation status of miR-200c/141 CpG island and miR-200c/141 in gastric cancer tissue specimens was evaluated by qRT-PCR or BS-MSP method. We analyzed the relationship among the methylation status of miR-200c/141 CpG island, expression level of miR-200c or miR-141, and clinical parame-ters. Results:The status of miR-200c/141 CpG island methylation in gastric cancer tissue was significantly higher compared with that in paracarcinoma tissue. MiR-200c and miR-141 were markedly decreased in gastric cancer tissue compared with those in adjacent tis-sue. MiR-200c/141 CpG island methylation was negatively related with the expression of miR-200c and miR-141 in gastric cancer speci-mens. Conclusion:The upregulation of miR-200c/141 CpG methylation inhibits miR-200c/141 expression in gastric cancer tissue.