Objective To study the effect of acupuncturing at Jiaji points plus cervical traction in treating unsteady lower cervical vertebrae.Methods The 90 outpatients willing to accept our treatment were randomized into 3 groups with 30 in each.Acupuncture group:acupuncture at the cervical Jiaji points.Traction group:traction at the cervical vertebrae.Acupuncture + traction group:acupuncture at the cervical Jiaji points plus cervical traction.Total effect,symptom scoring and X-ray examination were evaluated after 3 course of treatment.Results The total effective rate of acupuncture group,traction group and acupuncture + traction group was 47.67%,73.33% and 90.00% respectively.In total effect,symptoms of unsteady lower cervical vertebrae and the changes of X-ray examination,acupuncture + traction group was better than that of acupuncture group(P

Objective To characterize angular dependency of MatfiXX and develop a method for its calibration in order to verify treatment plan with original gantry angles.Methods Absolute dose calibration was carried with thimble ionization chamber on the linear accelerator.so as to make sure 1 MU=1 cGy at the depth of maximum dose(dmax).A MatriXX was put into a Mutlicube phantom,and the ionization chamber matrix was calibrated with absolute dose.In order to determine a correction factor CF as a function of gantry angle θ.open beam fields of 10 cm×10 cm size were irradiated for gantry angles θ=0°-180°(every 5°)and every 1°for lateral angles θ in the range of 85°-95°.CF was defined as the ratio of the dose measured with ionization chamber and the dose from MatriXX.Results Relatively large discrepancies in response to posterior VS.anterior fields for MatriXX detectors(up to 10%)were found during the experiment and relatively large variability of response as a function of gantry angle.The pass rate of treatment plan in lateral beams was lower than that of other beams.The isodose distribution of corrected MatriXX matched well with the outcome from the treatment planning system. Conclusions The angular dose dependency of MatriXX must be considered when it is used to verify the treatment plan with original gantry angles.

Objective To evaluate the effects of different concentrations of remifentanil on the expression and distribution of gap junction protein connexin 43 (Cx43) in the cardiomyocytes of rabbits.Methods Healthy adult rabbits of both sexes,weighing 2.0-2.5 kg,were anesthetized with pentobarbital sodium.Their hearts were rapidly excised and retrogradely perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃.After 15 min of stabilization with K-H solution,the 24 isolated hearts were randomly divided into 4 groups (n =6 each) using a random number table:control group (group C),and low,medium and high concentrations of remifentanil groups (R1-3 groups).The hearts were continuously perfused with K-H solution at 37 ℃ in group C.The hearts were perfused for 60 min with K-H solution containing remifentanil 12,25 and 50 ng/ml in R1-3 groups,respectively.The myocardial specimens were then obtained from the anterior wall of the left ventricle for detection of the expression and distribution of Cx43 by Western blot and immunohistochemistry,respectively.Results The expression of Cx43 was gradually down-regulated in C and R1-3 groups in turn (P＜0.05).Compared with group C,there was a tendency for the proteins localized at end-to-end contact sites of ventricular cardiomyocytes to localize at side-to-side contact sites in R1-3 groups,and the distribution was messy in R1-3 groups.Conclusion Remifentanil dose-dependently down-regulates the expression of Cx43 and changes the distribution of Cx43,which may be one of the mechanisms of remifentanil-induced arrhythmia in rabbits.

AIM:To study the effect of remifentanil on monophasic action potential and transmural dispersion of repolarization (TDR) in the 3-layer myocardium of isolated rabbit hearts .METHODS:Adult rabbits (n=18, 2.0 ~2.5 kg) were used to isolate the hearts for preparing Langendorff perfusion model .The hearts were randomly divided into 3 groups after perfusion with K-H solution for 15 min: the perfusion in control group ( C group ) continued for 60 min; the hearts in remifentanil group ( R group ) were perfused with 12 μg/L remifentanil K-H solution for 60 min; the hearts in remifentanil+aminophylline group ( RA group ) were given 60-min perfusion of 12 μg/L K-H remifentanil +30 mg/L aminophylline .The HR and 3 layers of myocardial monophasic action potential ( MAP) in the left ventricular anterior wall were recorded at time points after balanced infusion for 15 min ( T0 ) , and continued perfusion for 15 min ( T1 ) , 30 min ( T2 ) and 60 min ( T3 ) .The monophasic action potential duration of repolarization at 90%( MAPD90 ) and the transmural dispersion of repolarization (TDR) were calculated.The early afterdepolarization, delay afterdepolarization and arrhythmia were also observed.RESULTS:In R group, slower HR and prolonger MAPD90 and TDR at T1 ~T3 were observed as com-pared with those at T0(P<0.05).R group showed slower HR and longer MAPD 90 and TDR than C group and RA group (P<0.05).CONCLUSION:Remifentanil slows the HR, extends the MAPD90 and increases the TDR, thus being prone to induce reentry.Aminophylline makes HR faster and MAPD90 shorter, thereby reducing the TDR.

OBJECTIVETo study the effect of excessive fluoride on calcium overload and apoptosis in cultured rat ameloblasts in vitro.

METHODSLogarithmic-phase ameloblasts (HAT-7) were treated with 0, 0.4, 0.8, 1.6, 3.2, and 6.4 mmol · L(-1) sodium fluoride (NaF) solution. Cell activities were detected by using a Cell Counting Kit 8 (CCK-8) assay after 48 h of treatment. The effect of fluoride on cell apoptosis was analyzed by using flow cytometry. Excessive fluoride-induced calcium concentration and calreticulin expression changes in ameloblasts were detected by using laser scanning confocal microscopy, Western blot analysis, and real-time quantitative polymerase chain reaction.

RESULTSNaF inhibited ameloblast activity at 1.6, 3.2, and 6.4 mmol · L(-1) (dose-dependent) after 48 h of induction. The Ca2+ fluorescence intensity of HAT-7 cells incubated with 1.6 and 3.2 mmol · L(-1) NaF was higher than that in the control group. The fluoride-induced early-stage apoptosis of ameloblasts after 48 h of induction and the early-stage apoptosis rate was positively correlated with fluoride concentration. Calreticulin mRNA expression in HAT-7 cells was higher than that in the control group after 48 h of incubation with 0.8, 1.2, and 1.6 mmol · L(-1) NaF.

CONCLUSIONExcessive fluoride-induced calcium overload in ameloblasts and further caused endoplasmic reticulum stress-mediated apoptosis.

Objective To investigate the effects of target-controlled confusion of propofol with different concentrations on ventricular repolarization after prophylactic infusion of cefuroxime sodium. Methods Sixty ASA physical status Ⅰ or Ⅱ female patients,aged 18-65 years,undergoing elective gynecological surgery were randomly divided into three groups:group P2 (n =20)with TCI 2 μg/ml, group P3 (n =1 9)with TCI 3 μg/ml and group P4 (n =20)with TCI 4 μg/ml.Firstly,they were re-hydrated;secondly,the patients in groups P2,P3 and P4 were intravenous infused with cefuroxime sodium 2.5 g (in 100 ml normal saline)and then target-controlled infused of propofol 2 μg/ml,3μg/ml and 4 μg/ml in target plasma concentration,respectively.At three pionts of time:after rehy-dration before intravenous antibiotics (T0 ),after intravenous antibiotics before TCI of propofol (T1 ), after TCI of propofol (T2 ),QT interval,QTc interval,Tp-e interval were measured and recorded, respectively.Results Compared with T0 ,QTc [(469.9 ± 34.0)ms vs.(451.2 ± 24.9)ms],Tp-e [(107±25)ms vs.(94±20)ms]and Tp-e/QT (0.260±0.058 vs.0.236±0.043)in group P4 were sig-nificantly prolonged at T1 (P < 0.05 ).Compared with T1 ,QTc of groups P2 [(437.4 ± 24.4)ms vs. (453.3±28.0)ms]and P4 [(438.8±29.9)ms vs.(469.9±34.0)ms]were shortened significantly at T2 (P <0.05).Conclusion Propofol could improve ventricular reporlarization heterogeneity caused by cefu-roxime sodium.

Objective To investigate the role of potassium channel in remifentanil-induced prolongation of monophasic action potential duration (MAPD) in the myocardium of rabbits.Methods Eighteen adult rabbit hearts successfully perfused in a Langendorff apparatus were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C),remifentanil group (group R),and K+ channel blocker tetraethylammonium group (group T).After 15 min stabilization with K-H solution,group C was continuously perfused with K-H solution for 60 min,and R and T groups were perfused with KH solution containing 12 ng/ml remifentanil and 10 ng/ml tetraethylammonium,respectively,for 60 min.At 15 min of stabilization,and 15,30 and 60 min of perfusion,heart rate,MAPD of all the three layers of the myocardium in the anterior wall of the left ventricular was recorded.MAPD at 50％ and 90％ repolarization (MAPD50,MAPD90) were calculated.Results Compared with group C,heart rate was significantly decreased,MAPD50 and MAPD90 were prolonged in R and T groups (P ＜0.05).Conclusion The mechanism by which remifentanil prolongs MAPD in the myocardium of rabbits is associated with blockade of the potassium channels.

Objective To study the effects of dexmedetomidine on the monophasic action po-tential duration and the transmural dispersion of repolarization during ischemia-reperfusion of isolated rabbit hearts and thus explore its effect on myocardial ischemia-reperfusion electrophysiological char-acteristics.Methods Eighteen healthy adult rabbits,weighing (2.0±0.5)kg,were randomly divided into 3 groups after successful preparation of Langendorff isolated heart perfusion model and 1 5 min perfusion and balance of K-H fluid.In the control group (group C),37 ℃ K-H fluid was continuously perfused and balanced for 1 50 min.In the ischemia/reperfusion group (group IR),K-H fluid was stopped after continuous perfusion and balance for 1 5 min and cardiac arrest was induced for 60 min with the injection of Thomas solution (4 ℃,10 ml/kg)while the heart was protected by the low tem-perature Thomas solution (4 ℃)around it.Reperfusion of Thomas solution (4 ℃,5 ml/kg)was performed for 30 min and the heart was resuscitated by the perfusion of K-H fluid for 60 min.In dexmedetomidine group (group DEX),dexmedetomidine (25 ng/ml)was added in the K-H fluid and the Thomas solution.Other procedures were same as in group IR.Heart rate(HR),monophasic ac-tion potential amplitude (MAPA)of the three layers of heart [endocardium (Endo),myocardium (Mid)and epicardium (Epi)],0 phase maximal increase rate (Vmax),90% monophasic action po-tential duration (MAPD90 )and transmural dispersion of repolarization (TDR)were recorded at the time of continuous balance perfusion 1 5 min(T0 ),continuous perfusion 1 5 min/balance 30 min(T1 ), reperfusion 30 min/balance 120 min(T2 )and reperfusion 60 min/balance 1 50 min(T3 ).Cardiac ar-rhythmia and resuscitation time at cardiac reperfusion were observed,without using drugs to restore normal cardiac rhythm.Results In group DEX,cardiac resuscitation time was significantly shorter (1 6.67±3.78)s than that in group IR (46.33±7.29)s (P <0.05);At T2 ,in group IR,arrhythmia was seen in 6 rabbits and normal cardiac rhythm was restored within 2 min in two rabbits,while in group DEX,arrhythmia was seen in 2 rabbits and normal cardiac rhythm was restored within 2 min in one rabbit,without the use of any drugs.When compared with T0 ,HR was slower at T2 and T3 in group IR and at T1-T3 in group DEX (P <0.05);Compared with T1 ,HR was slower at T2 and T3 in group DEX (P <0.05);Compared with T2 and group C,HR was slower at T3 in group DEX;At T1-T3 ,HR in group DEX were significantly slower than that in group IR (P <0.05).Compared with T0 ,MAPD90 of Mid at T1 and Epi,Mid,Endo at T2 and T3 in group DEX were significantly extend-ed (P <0.05);Compared with T1 ,MAPD90 of Epi,Mid,Endo in group DEX were significantly ex-tended at T3 ;MAPD90 of Mid in group DEX was significantly longer than that in group C at T3 (P <0.05);At T2 and T3 ,MAPD90 of Epi,Mid,Endo in group DEX were longer than that in group IR (P <0.05).Compared with T0 and group C,TDR at T2 and T3 in group IR and at T1-T3 in group DEX significantly increased (P <0.05),while TDR in group DEX were less than that in group IR at T2 and T3 (P <0.05).Conclusion Dexmedetomidine appeared to prolong MAPD and restrain the dis-proportion of resuscitation of myocardial ischemia-reperfusion injury.Dexmedetomidine could have the effect of stabilizing myocardial ischemia-reperfusion electrophysiological characteristics.

Objective To evaluate efficacy of rotigaptide ZP123 on prevention of negative chronotropic effect caused by dexmedetomidine lengthening repolarization duration of the isolated rat hearts.Methods Eighteen healthy adult SD rats of either gender,weighing (300±30) g,were prepared isolated heart perfusion model by Langendorff.After 15 min perfusion and balance of K-H fluid,the isolated hearts were randomly divided into 3 groups (n=6 each): The hearts were continuously pefused for 30 min with 37℃ K-H solution in control group (group C),with dexmedetomidine 50 ng/ml in dexmedetomidine group (group D),or with rotigaptide 80 nmol/L combined with dexmedetomidine 50 ng/ml in rotigaptide combined with dexmedetomidine group (group ZD).In the whole Langendorff-perfused hearts,at the end of balanced infusion for 15 min (T0) and at 15(T1),30(T2) min of continued perfusion with K-H solution,the monophasic action potential (MAP) and heart rate (HR) were recorded from left anterior free wall,MAP duration at 50% repolarization (MAPD50) and at 90% repolarization (MAPD90),monophasic action potential amplitude (MAPA) and maximal velocity (Vmax) were calculated.Results Compared with T0,HR in group D was significantly declined at T1,T2;MAPD90 and MAPD50 in group D were significantly increased at T1,T2 (P<0.05).Compared with groups C and ZD,HR in group D was significantly declined at T1,T2;MAPD90 and MAPD50 in group D were significantly increased at T1,T2 (P<0.05).There was no significant difference in MAPA and Vmax between the three groups.Conclusion Rotigaptide antagonizes negative chronotropic effect induced by dexmedetomidine through shortening monophasic action potential duration in the myocardium of left ventricle of the isolated rat hearts.

Objective To evaluate the effects of different concentrations of remifentanil on myocardial monophasic action potential (MAP) in isolated rabbit hearts.Methods Adult rabbits of both sexes,weighing 2.0-2.5 kg,were used in the study.Their hearts were excised,and retrogradely perfused with oxygenated K-H solution saturated with 95％O2-5％CO2 at 37 ℃ in a Langendorff apparatus.Twenty-four isolated hearts were randomly divided into 4 groups (n =6 each) using a random number table:control group (group C) and 3 different concentrations of remifentanil groups (group R1-3).After 15 min of stabilization,K-H solution was continuously perfused for 60 min in group C,and K-H solution containing 12,25 and 50 ng/ml remifentanil was continuously perfused for 60 min in R1,R2 and R3 groups,respectively.At 15 min of stabilization,and 15,30 and 60 min of perfusion with K-H solution,the heart rate,and the maximal velocity and amplitude of the MAP in the three layers of the left ventricular anterior wall were recorded,and the action potential duration at 90％ repolarization and transmural dispersion of repolarization (TDR) were calculated.Results Compared with group C,the heart rate was significantly decreased,and the action potential duration at 90％ repolarization and TDR were significantly prolonged at 15,30 and 60 min of perfusion in R1-3 groups (P＜0.05).Compared with C and R1 groups,the maximal velocity and amplitude of MAP were significantly decreased at 15,30 and 60 min of perfusion in R2 and R3 groups (P＜0.05).Conclusion Low-concentration remifentanil induces heart block through increasing TDR,however,high-concentration remifentanil induces heart block through inhibiting myocardial MAP depolarization and increasing TDR in the isolated rabbit hearts.