Objective To study the effect of He-Ne laser at lower power on proliferation and differentiation of embryo midbrain nerve cell.Methods The embryo midbrain nerve cell of rat embryo were randomly divided into one control group and three experimental groups.The cells in experimental groups were respectively irradiated at different time:3 min(A组),6 min(B组),10min(C组),each day.After ten days,we counted the concentration rate and determined the content of protein and the amount of superoxide dismutase(SOD)and malonyldialolehyde(MDA).Results The concentration rate of group A and of group B significantly increased than that of the control group(P

Objective To measure the dynamic and static frictional resistances between different self-ligating orthodontic brackets and different combination of tandem archwires.Methods On standard model the upper right quadrant Damon Q self-ligating brackets was pasted as team A,3M Smart clip self-ligating brackets as team B and Forestadent Quick 3.0 self-ligating brackets as team C respectively.Nickel-titanium archwires of 0.012 inch and 0.016 inch and two nickel-titanium archwires of 0.014 inch were applied to simulate sliding in the brackets and measure the friction changes in brackets and archwires,so as to explore the frictional resistance between different combination of the tandem archwires and different self-ligating brackets.Results When using the combination of two 0.014-inch nickel-titanium tandem archwires,the static frictional resistances was significantly different (P＜ 0.05):team A ＜team B ＜team C while the kinetic frictional resistance was also significantly different (P＜0.05):team A ＜team B ＜team C,When using the combination of 0.012-inch and 0.016-inch nickel-titanium tandem archwires,the static frictional resistances was significantly different (P＜0.05):team A＜team B＜team C,while the kinetic frictional resistance was also significantly different (P＜0.05):team A＜team B＜team C.Gonclusion There are different frictional resistance in different kind of self-ligating brackets and different combination of the tandem archwires.The combination of two 0.014-inch nickel-titanium tandem archwire applied to Forestadent Quick 3.0 self-ligating brackets has the biggest frictional resistance while the combination of 0.012-inch and 0.016-inch nickel-titanium tandem archwire applied to the Damon Q self-ligating brackets has the lowest frictional resistance,which enables the teeth to move at the fastest speed and facilitates the following use of the edgewires.

AIM To study the antitumor activity of astragalosides(AST) and its mechanism of action. METHODS By using two experimental models of hepatoma(HepA) and Sarcoma 180 in mice, the rate of inhibition of tumor weight AST on the growth of HepA and S180 tumor cells were tested. The growth inhibition of AST on Hela cells was detected by MTT assay. The effect of AST on cell cycle and apoptosis was analyzed by flow cytometry and TUNEL. RESULTS AST inhibited the growth of tumor cells of HepA and S180 in mice. AST inhibited the growth of Hela cell in concentration dependent manner with IC 50 of 80 4 mg?L -1 . Flow cytomety analgsis showed that G 0/G 1 phase rate was increased but S phase rate was decreased. The apoptosis rate of Hela cells treated with AST( 80 and 160 mg?L -1 ) was significantly higher than that of control. CONCLUSION AST can inhibit the growth of tumor cells of HepA and S180 in mice and the growth of HeLa cells in vitro . Causing cell cycle arrest and apoptosis is probably one of the mechanisms of antitumor effect by AST.

This paper summarizes the experiences of observation and nursing of postoperative complications in 28 patients underwent orthopedic surgery for correction of severe kyphoscoliosis,the Cobb's angle was(150.0±25.3)°. Postoperative nursing focused on monitoring of patients' vital signs,observation of the feeling and motor function of lower limbs and wound drainage,nursing care of gastrointestinal reaction and respiratory complications. The postoperative complications were controlled effectively after timely treatment. There was no any severe complications of spine-cord injury after stage-II surgery.

Aim Toinvestigatetheroleofbrain-de-rived neurotrophic factor(BDNF)-tyrosine receptor ki-nase B (trkB ) signaling pathway in the therapeutic effects of ketamine on diabetic neuropathic pain.Meth-ods Forty-eightWistarrats,aged3months,weighing 200~250 g,were equally randomized into 4 groups(n=12 ):control group (C group ), saline group (S group),ketamine group (K group)and ketamine +ANA-12 group (KA group ).Rats in S,K and KA groups were intraperitoneally injected with a single of streptozotocin(STZ)65 mg·kg-1 to construct diabetic neuropathic pain model.After twenty-eight days,rats in S,K and KA groups were intraperitoneally injected with saline, ketamine 10 mg·kg-1 and ketamine 10 mg·kg-1 +ANA-12 0. 5 mg·kg-1 for consecutive 7 days, respectively. On the 8th day, mechanical withdrawal threshold(MWT)of rats was measured.Af-ter that,the rats were immediately sacrificed,and dor-sal ganglion of lumbar spine and prefrontal cortex (PFC)were harvested for measuring BDNF,p-trkB/trkB,synaptophysin and spine density by Western blot andglogistaining.Results ComparedwithCgroup, rats in S group significantly decreased MWT,BDNF, p-trkB/trkB,synaptophysin and spine density in dorsal ganglion and PFC (P <0. 05 ).Compared with S group,rats in K group showed a significant increase of MWT,BDNF,p-trkB/trkB,synaptophysin and spine density in the all observed regions(P<0. 05 ).On the contrary,rats in KA group showed a significant de-crease of MWT and BDNF,p-trkB/trkB,synaptophys-in and spine density as compared with K group in all regions(P<0. 05 ).Furthermore,BDNF was positive-ly correlated with spine density in all regions (P <0.05).Conclusion BDNF-trkBsignalingpathway mediates ketamine-induced therapeutic effects in dia-betic neuropathic pain.

Aim To investigate the effect of zacopride ( Zac) on cardiac arrhythmia in isoproterenol ( ISO)-in-duced myocardial hypertrophic rats and the underlying electrophysiological mechanisms .Methods ① Fifty-one rats were randomly divided into control group ( n=17 ) , ISO group ( n=17 ) and ISO +Zac group ( n =17 ) .Rat model with cardiac arrhythmia and hypertro-phy was established by intraperitoneal ISO ( 5 mg?kg -1 ) injection.②ECGs were recorded to observe the effects of Zac on arrhythmia in model rats .③ Whole-cell patch clamp was applied to record inwardly rectifi-er potassium current(IK1), resting membrane potential ( RMP ) and amplicated delayed afterdepolarizations (DADs).Results ① Echocardiographic examination showed that , left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) significantly decreased in rats in ISO group compared with control group , whereas left ventricular posterior wall end-diastolic thickness ( LVPWd) and in-terventricular septum end-diastolic thickness ( IVSd ) increased ( P<0.05 ) , suggesting rat model of isoprot-erenol-induced myocardial hypertrophy was successfully established .② ECGs showed that 88.89% of rats in ISO group had ventricular premature beats ( VPBs ) , which significantly decreased to 11.11% after the ap-plication of Zac ( P <0.05 ) .③ Values of RMP de-creased from ( -71.05 ±1.27 ) mV in control group to (-69.38 ±1.21 ) mV in ISO group ( P<0.05 ) . After Zac administration , RMP significantly increased to ( -73.86 ±1.33 ) mV compared with control and ISO group(P<0.05).④DADs and TA incidence sig-nificantly decreased from 88.24% in ISO group to 11.76%in ISO+Zac group ( P<0.05 ) .⑤ Compared with control group , IK1 density was markedly reduced in ISO group, whereas Zac could effectively rescue IK1 suppression to normal level .Conclusions Zac, as a selective IK1 channel agonist , can significantly inhibit cardiac arrhythmia in isoproterenol-induced myocardial hypertrophic rats , which is mainly attributed to in-creased RMP by enhancing IK1 and subsequent suppres-sion of DADs.

Objective To evaluate effect of intensive insulin treatment(IIT)on healthcare-associated infection (HAI)rate in patients with acute stroke and stress hyperglycemia.Methods Databases,including PubMed,Em-base,Cochrane Library,WanFang,and China National Knowledge Infrastructure(CNKI)Data,were electronically searched,relevant journals and references of the included literatures were also searched manually,literatures were selected according to the uniform inclusion and exclusion criteria,incidence of HAI and mean blood glucose in patients who received IIT for acute stroke were assessed systematically.Results A total of 13 randomized controlled trials (RCT)involving 1 032 patients were included in this systematic review.Meta-analysis results showed that 10 studies involving 832 patients were finally enrolled for comparing HAI rate, HAI rates in IIT group and conventional insulin treatment group were 28.3% and 56.1 %,respectively(Z =4.50 ),difference between two groups was statistically significant (RR=0.53 [95 %CI :0.40 to 0.70],P <0.001 );A total of 328 patients in 5 studies were finally included in the comparison of blood glucose,difference in mean blood glucose between two groups was statistically significant(MD =-2.52 [95% CI :-4.30 to -0.74],P =0.006).Funnel plot of HAI rate revealed that there was publication bias.Conclusion IIT is used for the regulation of stress hyperglycemia in acute stroke,it can reduce the incidence of HAI and blood glucose in patients.

Aim To explore the role of AMPK/ PGC-1α pathway in cardioprotection of hydrogen sulfide ( H2 S ) against ischemia/reperfusion ( I/R ) injury. Methods Langendorff perfusion apparatus was used to build an isolated rat myocardial I/R model. Seventy-two male SD rats were randomly divided into 6 groups (n=12):control group (Control), ischemia/reperfu-sion group ( I/R ) , DMSO group ( DMSO ) , inhibitor Compound C group ( CC) , H2 S postconditioning group ( NP) , and H2 S with Compound C group ( N +C ) . The heart rate ( HR ) , the left ventricular developed pressure ( LVDP ) , the maximum rate of increase or decrease of left ventricular pressure ( ± dp/dtmax ) and the left ventricular diastolic pressure ( LVEDP ) were registered at 20 min of baseline and 60 min of reperfu-sion separately. Triphenyl tetrazolium chloride ( TTC) staining and HE staining were used to determine the myocardial infarct size and the myocardial tissue mor-phological change of each group was observed respec-tively. Immunohistochemistry was used to determine the expression of PGC-1α. The expressions of total AMPK ( tAMPKα ) , phosphorylated AMPK ( pAMPKα) and PGC-1α were detected with Western blot anaylsis. Results There were no differences in e-quilibrium hemodyamics observed between the experi-mental groups(P>0. 05). At the end of reperfusion, compared with I/R group, NP group had obviously a-meliorated functional recovery and significantly de-creased myocardial infarct size [ ( 23. 9 ± 3. 4 )% vs (60. 9 ± 3. 8 )%, ( P <0. 05 ) ] . HE staining showed that in NP group, the myocardial injury was reduced. Meanwhile, the expression of pAMPKα and PGC-1αincreased significantly. However, Compound C re-versed the cardioprotection effects provided by hydro-gen sulfide postconditioning and reduced the expression of pAMPKαand PGC-1α. Conclusion AMPK/ PGC-1α pathway is involved in the role of hydrogen sulfide against ischemia/reperfusion injury.

Aim To observe the effect of antibody NCX-3F10 on the main ion current of rat ventricular myocytes and its effect on arrhythmias induced by ischemia/reperfusion(I/R).Methods ① The whole-cell patch clamp technique was employed to record the Na+/Ca2+ exchange current(INa/Ca) and other major ion currents in rat ventricular myocytes.② The rat models of arrhythmia induced by ischemia/reperfusion were established by ligating the left coronary artery to in vivo and in vitro.Then the effects of antibody on the arrhythmia were observed.③ The IonOptix ion imaging system was used to observe the effect of antibody on calcium transients in single ventricular myocytes.Results ① The antibody NCX-3F10 dose-dependently inhibited INa/Ca from 5 to 40 mg·L-1.The IC50 for outward and inward currents was 11.15 and 11.69 mg·L-1, and the maximum inhibitory rates were 61% and 62%, respectively.The antibody also had an inhibitory effect on calcium current(ICa-L), and had no significant effect on inward rectifier potassium current(IK1), transient outward potassium current(Ito) and sodium current(INa).② In the isolated rat heart group I/R, 100% rats showed ventricular tachycardia, and 88.89% rats had ventricular fibrillation.After administration of antibody NCX-3F10(10 mg·L-1) 5 min before reperfusion, the incidence of ventricular tachycardia decreased to 44.43%(P<0.05), and the duration of ventricular tachycardia and ventricular fibrillation was also shortened remarkably(P<0.05).③ In the anesthetized rats after administration of antibody NCX-3F10(50 μg·kg-1) 5 min before reperfusion, the incidence and duration of ventricular tachycardia,the incidence and duration of ventricular fibrillation, and total number of ventricular premature beats were significantly decreased(P<0.05).④ From 5 to 40 mg·L-1, NCX-3F10 antibody decreased calcium transient amplitude in rat single ventricular myocytes dose-dependently(P<0.05).Conclusions The NCX-3F10 antibody shows significant arrhythmic effects on ischemia-reperfusion induced arrhythmia in rats both in vitro and in vivo, the underlying mechanism of which is related to NCX and L-type calcium current inhibition and calcium overload reduction by the NCX antibody.

AIM: To investigate the effect of zacopride, an inward rectifier potassium channel agonist, on ouabain-induced arrhythmias in adult rats, and to explore the underlying electrophysiological mechanism.METHODS: Using ouabain to establish in vitro and in vivo arrhythmic rat models, the effects of zacopride on ouabain-induced arrhythmias were observed.The technique of whole-cell patch clamp was used to observe the effects of zacopride on inward rectifier potassium current (IK1), resting membrane potential (RMP) and delayed afterdepolarizations (DADs) in single rat ventricular myocyte.RESULTS: Zacopride at 1 μmol/L significantly reduced total number of premature ventricular beats, and the duration and incidence of ventricular tachycardia and ventricular fibrillation induced by ouabain in rat hearts in vitro (P<0.05).In anesthetized rats, zacopride at 15 μg/kg significantly reduced total number of premature ventricular beats, and the duration and incidence of ventricular tachycardia and ventricular fibrillation induced by ouabain (P<0.05).IK1 was significantly inhibited by ouabain (P<0.05), which was partially and even completely reversed by zacopride at 0.1~10 μmol/L.RMP value was significantly reduced by ouabain (P<0.05), and then increased to different levels after treatment with zacopride (0.1~10 μmol/L).Zacopride at 1 μmol/L showed its maximal effect and RMP was restored to normal level.Moreover, zacopride at 1 μmol/L markedly suppressed ouabain-induced DADs in single rat ventricular myocyte.The incidence of DADs decreased from 91.67% to 12.50% after zacopride was applied (P<0.05), and this effect was abolished by 1 μmol/L BaCl2.CONCLUSION: Inward rectifier potassium channel agonist zacopride significantly inhibits ouabain-induced ventricular arrhythmias in adult rats.The mechanism is related to increased RMP level and inhibition of DADs by activation of IK1 channel.