AIM: To observe the mechanism of intracellu la r signal transduction that fraction F of naja naja atra venom inhibits plate let aggregation. METHODS: Tests were divided into six groups: (1) blank group; (2 ) control group and (3)-(6) ADP plus fraction F group (doses of fraction F were 100, 30, 10, 3 mg/L, respectively). Protein tyrosine phosphorylation in platelet s was assayed by Western blotting and platelet aggregation was assayed by nephel omete r. RESULTS: Fraction F significantly inhibited molecular masses (MW ) 76, 66 and 37.5 kD protein tyrosine phosphorylation in platelet that induced by ADP in a dose-dependent manner, in which 30 and 100 mg/L dose group showed ob viously different effects when compared to control group (P

Objective To investigate the effects of propefol on β-amyloid protein(β-AP)-induced injury to cultured rat cortical neurons.Methods Eighteen days pregnant SD rats were anesthetized with ether.The fetal rats were obtained under sterile condition and decapitated. Cortices were then dissected under dissecting microscope.Cortical neurons were isolated according to the method described by Velly LJ et al and cultured for 7 days.There were 5×104 neurons in each well (200 μl).The experiment included 2 parts.In part T 15 wells of neurons were randomly divided into 5 groups(n=3 each ) : group I control(C);group II β-AP 25 μmol/L; group III and IV 2 propofol pretreatment groups (PP1,PP2) and greup V propofol treatment (PT).In group PPt propofol 50 μmol/L was added to the culture medium 24 h before the addition of β-AP 25 μmol/L and the neurons were incubated for another 24 h.In group PP2 propofol 50 μmol/L and μ-AP 25 μmol/L were added to the culture medium simultaneously and the neurons were then incubated for 24 h.In group PT propefol 50 μmol/L was added to the culture medium at 6 h after the addition of β-AP 25 μmol/L and the neurons were incubated for another 18 h.In part Ⅱ 18 wells of neurons were randomly divided into 6 groups(n=3 each):group I control (C) ; group IIβ-AP 25 μmol/L; group III intralipid; group IV,V,and VI 3 prepofol treatment groups (P1,P10,P50).In intralipid group equal volume of 10% intralipid was added to the culture medium at 6 h after β-AP 25 μmol/L and the neurons were then incubated for another 18 h.In group IV- VI propofol 1,10 and 50 μmol/L were added at 6 h alter β-AP 25 μmol/L respectively and the neurons were incubated for another 18 h.The amount of lactic dehydrogenase (LDH) released was measured.Neuronal viability was assessed by MTT assay.The neuronal apoptosis was detected using Hoechst33342 staining and TUNEL technique,and the.apoptosis rate was calculated.Results In part Ⅰ there was no significant difference in the amount of LDH released between group Ⅱ(β-AP) and the 2 propofol pretreatment groups(Ⅲ,Ⅳ).The amount of LDH released was significantly lower in group Ⅴ (propofol treatment) than in group β-AP(Ⅱ).In part Ⅱ the amount of LDH released was significantly lower,neuronal viability higher and the apoptosis rate was lower in group P50 than in group Ⅱ(β-AP).Conclusion Propofol 50 μmol/L given after β-AP can attenuate β-AP induced injury to cultured rat cortical neurons while prophylactic administration of propofol can't.

Dexmedetomidine( DEX) is a pure potent, highly se-lective and highly specific agonist ofα2-adrenergic receptors with sedative, analgesic and sympatholytic properties. The sedative effect mimics natural sleep of“arousable” and“cooperative” se-dation without respiratory depression. Due to the above properties and advantages, DEX has received adequate attention in clinical practice and its spectrum of application is also expanding. In re-cent years, it is proved that DEX is neuroprotective not only in animal researches but also in clinical studies. The neuroprotec-tion of DEX and its related mechanism will be briefly reviewed in this paper.

Objective To investigate the effectiveness of entropy in measuring the level of sedation during target controlled infusion (TCI) of propofol in patients of different ages. Methods Twenty-nine ASA Ⅰ-Ⅱ patients undergoing elective surgery under general anesthesia were divided into two age groups: Ⅰ adult group (20-64 yr) (n = 16) and Ⅱ the aged group (65-85 yr) ( n = 13). The patients were unpremedicated. The level of sedation was assessed using OAA/S scale. Propofol was given by TCI. The effect-site concentration (Ce) of propofol was set first at 1 ?g?ml-1 and then increased step by step by 0.5 ?g?ml-1 every 60 seconds until Ce reached 6 ?g?ml-1. Response entropy ( RE), state entropy ( SE), BP, HR, SpO2 were monitored and recorded at each Ce, before intubation, and immediately and 1, 2, 3, 4, 5, 10 min after intubation. The predictive performance of entropy was evaluated by prediction probability (Pk) .Results The two groups were comparable with respect to sex (M/F ratio), body weight and body weight index (kg?m-2). The RE and SE values decreased as Ce increased. The difference between RE and SE was also reduced. In adult group when Ce reached 2.0 ?g?ml-1, the RE and SE values were lower than the baseline values ( P

Aim To investigate the effects of propofol on focal cerebral ischemia and the changes of protein kinase C isoform ?(PKC?) expression in rats brain. Methods Male SD rats were randomly allocated into five groups: Ⅰ: sham group, Ⅱ: injury group, Ⅲ: propofol (25 mg?kg-1) plus injury group, Ⅳ: propofol (50 mg?kg-1) plus injury group, Ⅴ: intralipid plus injury group. The focal cerebral ischemia was induced by 3 h of middle cerebral artery occlusion (MCAO) and 24 h of reperfusion. 30 min before reperfusion, propofol and intralipid were infused intraperitoneal of the rats in groups Ⅲ, Ⅳ, Ⅴ, respectively. After 24 h of reperfusion, rats were weighted and the neurological deficit was assessed by 5-point scale. Brain pathologic changes were observed by HE staining, the method of terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) was carried out for the assessment of neural apoptosis, and immunocytochemistry was used to investigate the changes of PKC?.Results After 3 h of MCAO and 24 h of reperfusion, the weight of rats in group Ⅱ, Ⅲ, Ⅳ, Ⅴ decreased and their neurological deficits scores increased. Compared to the rats of sham group, the numbers of apoptosis neurons in striatum were marked-ly increased, and the expression of PKC? were significantly decreased in rats of injury group (P

Objective To evaluate the desflurane-induced sympathetic activation with finger tip perfusion index (FTPl). Methods Forty-eight ASA ⅠorⅡ patients aged 25-60 yr undergoing elective surgery under general anesthesia were randomly divided into 3 groups (n=16 each): groupⅠsevoflurane; group Ⅱ desflurane and groupⅢ desthrane + propofol. Anesthesia was induced with midazolam 0.03 mg/kg, propofol 2 mg/kg and fentanyl 2 μg/kg. Tracheal intubatian was facilitated with vecuronium 0.1 mg/kg. The patients were mechanically ventilated (VT 8-10 ml/kg, RR 12 bpm). PETCO2 was maintained at 35-40 mm Hg. In group ⅠandⅡanesthesia was maintained with sevoflurane and desflurane respectively. The end-tidal concentration of sevoflurane and desflurane were rapidly increased to 0.5 MAC, 1.0 MAC and 1.5 MAC and maintained at each level for 5 rain. In group Ⅲanesthesia was maintained with TCI of propofol and destlurane. The target plasma prepofol concentration was set at 1 μg/ml and the end-tidal concentration was rapidly increased to 0.5 MAC and 1.0 MAC and maintained at each level for 5 mitt. MAP, HR, FTPI and BIS were continuously monitored and recorded at 5 rain after midazolam (T0), 3 rain after induction of anesthesia (T1), immediately after tracheal intubation (T2), as soon as the end-tidal concentration of sevoflurane and desflurane reached 0.5 MAC(T3), 1.0 MAC(T5) and 1.5 MAC(T7) and after being maintained at 0.5 MAC (T4), 1.0 MAC (T6) and 1.5 MAC (T8) for5 rain. The plasma renin activity and the levels of angintonin Ⅱwere determined at T0, T1, T2, T5 and T7 by using radioimmuno-ssay. Results FTPI was significantly lower at T5 than at T4 in group Ⅱ HR and MAP were significantly lower at T4-6 and T8 and FTPI were significantly lower at T3～6 and T0 than at T7 in group Ⅱ. HR and MAP were significantlyhigher while FTPI was lower at T7 in groupⅡthan in group Ⅰ The changes in MAP and FTPI between T4 and T5 were significantly less in group Ⅲthan in group Ⅱ. The time when the highest value of FTPI was maintain was significantly shorter than the time when the highest values of HR and MAP were maintained at T5 and T7 in group ⅡΔFTPI was negatively correlated with ΔHR and ΔMAP (r=-0.593, P<0.05;r=-0.591, P<0.05). Conclusion FTPI can reflect the desflurane-induced sympathetic activation promptly and sensitively.

BACKGROUND:MicroRNAs (miRNAs) are widely involved in regulation of physiological processes, such as human development, cel proliferation, differentiation, and apoptosis, angiogenesis and lipid metabolism. MiRNAs also play an important regulating role in the pathological process of femoral head necrosis. At present, the research about the effect of icarin on miRNA expression in glucocorticoid- induced avascular necrosis is stil in the exploratory stage, and the specific targets, possible regulation mechanism and signaling pathway remain unclear.
OBJECTIVE:To explore the effect of icarin on miRNA expression of bone microvascular endothelial cels in steroids-induced human femoral head lesionsin vitro.
METHODS: Bone microvascular endothelial cels in cancelous bone of the femoral head were isolated and harvested in vitro. Icarin preconditioning preceded establishment of models of glucocorticoid-induced bone microvascular endothelial cel injury. Differential expression profiles and transcriptomes in glucocorticoid and normal groups were tested by miRNA microarrays. The most differentialy expressed miR-23b and miR-339 in microarray analysis were further confirmed by real-time quantitative PCR, Meanwhile the effects of icarin on the expression of miR-23b-5p and miR-339-5p were detected.
RESULTS AND CONCLUSION:According to the microarray analysis, one miRNA was up-regulated and four mi RNAs were down-regulated in the glucocorticoid group (fold > 2,P < 0.05). Results of RT-qPCR revealed that miR-23b was down-regulated and miR-339 up-regulated in the glucocorticoid group, which were in agreement with the microarray analysis (P < 0.05). Icarin pretreatment effectively prevented the imbalances of miR-23b expression induced by glucocorticoid (P < 0.01). These findings indicate that Icarin may participate in the pathological process of steroid-induced femoral head necrosis through regulating the expression of miR-23b.

Objective To evaluate the efficacy and safety of bilateral transversus abdominis plane block (TAPB)combined with bilateral rectus sheath block (RSB)in abdominal surgery. Methods Ninety ASA Ⅰ or Ⅱ patients,35 males,55 females,aged 19-79 years,with body mass index 18-30 kg/m2 ,scheduled for elective laparoscopic cholecystectomy were randomly divided into three groups(n=30):ultrasound-guided bilateral TAPB combined with bilateral RSB group (group TR),ultrasound-guided bilateral TAPB group (group T),patient-controlled intravenous analgesia (PCIA)group (group P).In group TR,ultrasound-guided bilateral TAPB were performed with 20 ml of 0.22% ropivacaine mesylate injection in each side and ultrasound-guided bilateral RSB were per-formed with 10 ml of 0.22% ropivacaine mesylate injection in each side before surgery.In group T, ultrasound-guided bilateral TAPB were performed with 20 ml of 0.22% ropivacaine mesylate injection in each side and ultrasound-guided bilateral RSB were performed with 10 ml of NS in each side before surgery.In group P,ultrasound-guided bilateral TAPB were performed with 20 ml of NS in each side and ultrasound-guided bilateral RSB were performed with 10 ml of NS in each side before surgery, and PCIA was applied in group P.BP,HR,SpO2 were observed when patients were sent into the op-erating room, 2 minutes before trocar puncture, and 2 minutes after trocar puncture, the consumption of propofol and remifentanil used during the surgery were recorded.The score of visual analogue scale (VAS)during rest and movement were recorded at 2,6,12,24 h after surgery.The patient analgesia satisfaction and the adverse reactions were recorded.Results Compared with group T and group P,group TR had less change of BP before and after trocar puncture(P <0.05).The VAS score was significantly lower in group TR after operation(P <0.05).There were no statistical significant differences of VAS score at 24 h after operation among the three groups.The patient anal-gesia satisfaction was significantly better in group TR than other two groups (P < 0.05 ). Conclusion Ultrasound-guided bilateral transversus abdominis plane block combined with bilateral rectus sheath block is of safety and much efficacy of postoperative analgesia in patients undergoing laparoscopic cholecystectomy.

Objective To observe the effect of pigplacenta ins tead of Ziheche (P lacenta Hominis) for the treatment of senile dementia. Methods Seventy Kunming mice were divided into blank group, model group, pos itive control group, Zih eche low and high dosage groups, and pigplacenta low and high dosage grou ps, wi th 10 in each. The senile dementia models were established with the D-Galactose subcutaneous injection. The blank group was not administered any medicines. The model group was prescribed normal saline instead of the tested medicine; the pos itive control group was given Naofukang by gavage; the Zih eche low and high dosage groups were given 2g/kg and 4g/kg Ziheche respectivel y by gavage; while the pigplacenta low and high dosage groups were treated wi th p igplacenta 4g/kg and 8g/kg respectively by gavage. After treatment for 6 week s, the behavior experimental dark-avoiding test and step-down test were applied to test the effect of the medicines on the learning memory of mice, and acetylchol inesterase and monoamine levels in brain tissues. Results There was no s ignificant difference between the effect of pigplacenta and Ziheche in resi stin g senile dementia. In the latency of dark-avoiding test, the effect of high d osa ge of pigplacenta was significantly better than that of Ziheche (P

Aim To develop King cobra antivenom from the egg yolks of immunized hens,and study dynamic expression of IgY in egg yolks.Methods chickens(white Leghorn) were immunized with detoxicated King cobra venom by formaldehyde ,Egg yolk antibody (IgY) was isotated by thiophilic interaction chromatography and identified by SDS-PAGE. Activity of IgY was evaluated by enzyme-linked immunoserbent assay(ELISA) and Double immuodiffusion. Protein was measured using folin-lowry method. Results Specific antivenom could be detected in the yolk laid by the hens 9 d after immunization, At the 60th day after primary immunization ,ELISA titers reached 1∶ 100 000,and 97.5 mg IgY?ml -1 yolk was obtained from thiophilic interaction chromatography. IgY was highly specific, No cross reactivity was observed among IgY and agkistrodon acutus venom and vipera venom ;Little cross reactivity was shown with cobra genus venoms.Conclusion King cobra IgY was obtained and purified from the egg yolks of immunized hens,The dynamic expression of IgY was manitered during the course of immunization,Further investigation is needed.