AIM: To compare the therapeutic effects and adverse reactions of nicardipine and labetalol injection in treating acute and severe hypertensions. 　METHODS: Sixty-seven patients in nicardipine group (M 46, F 21; age 52 a± s 11 a) were given nicardipine 2 mg in 0.9 % sodium chloride or 5 % glucose injection 10 mL within 2 min iv, first, and then given 30 mg nicardipine in 0.9 % sodium chlocide or 5 % glucose injection 250 mL by continual intravenous infusion for 6 h. Sixty-one patients in labetalol group (M 41, F 20; age 53 a±9 a) received 50 mg labetalol in 5 % glucose injection 20 mL by intravenous once. The treatment could be repeated every 15 min, in case it was less effective, but the total dose should be no more than 200 mg.　RESULTS: The treatment for the nicardipine group and the labetalol group, reached the marked effect within 5 min. The total marked effective rate was all 100 % (P>0.05). Severe adverse reactions occured in the two patients (one occured significantly lowering of blood pressure, and the other aggravated asthma) in the labetalol group. 　CONCLUSION: Intravenous nicardipine and labetalol are fast and smooth in reducing the blood pressure of the patients with acute and severe hypertension, but the safety of nicardipine is superior to that of labetalol

Objective To investigate the relationship between body mass index(BMI)and cardiac structure and function of adult men living in Hebei province.Methods A total of 160 adults were assigned to 4 groups by BMI:normal body weight group(group A,BMI 18.5 to 23.9 kg/m2),overweight group (group B,BMI 24.0 to 27.9 kg/m2),mild obese group(group C,BMI 28.0 to 29.9 kg/m2),and severe obese group(group D,BMI ≥ 30 kg/m2).Left ventricular end-diastolic diameter(EDD),end-systolic diameter(ESD),inter ventricular septal thickness(IVS),left ventricular posterior wall thickness (LVPW),left ventricular mass(LVM),and left ventricular mass index(LVMI)were examined by echocardiography.Early(E)peak diastolic and late(A)diastolic mitral inflow velocity and E/A ratio were measured by Doppler echocardiography.Pulsed wave Doppler tissue image(PW-DTI)of the lateral mitral annulus was performed to evaluate early peak diastolic velocity(Em),late peak diastolic velocity(Am)and Em/Am ratio.Results Compared with group A,EDD,ESD,LNM,LVMI,Am,IVS and LVPW were increased in the other 3 groups(all P ＜ 0.05).E,E/A ratio,Em,and Em/Am ratio were decreased in group B,C,and D(all P ＜ 0.05).Compared with group B,Sm was decreased in group C and D(both P ＜ 0.05).Conclusion Overweight and obesity could contribute to ventricular hypertrophy and deteriorate diastolic function in a BMI dependent manner.Obesity may be also related to decreased Sm.

T is the etiologic mutation in this family.Screening of female carrier state and follow-up study of the confirmed carriers are important for X-liked DCM family.

[Objective]To construct the recombinant adenovirus vector co-expressing human vascular endothelial growth factor 165(VEGF165) and angiogenin-1(Ang-1),and to observe the expression of target gene after transfection.[Method]Molecular biologic techniques were used to clone the genes of VEGF165 and Ang-1,and PCR was used to amplify the DNA sequence of IRES(internal ribozyme entry site) from pIRES2-EGFP.The genes of VEGF165,IRES and Ang-1 were subcloned to pTrack-CMV one by one to get the plasmid named pTrack-CMV-VIA,which contained all the three genes.The linearized shuttle plasmid was cotransformed into BJ5183 bacteria with backbone vector AdEasy-1.Further the recombinant plasmid was packaged and amplified in QBI-293A cells after Pac I digestion to get adenovirus vector pAd-VIA.The expression of the gene of interests was evaluated by fluorescence microscopic analysis of GFP expression and enzyme linked immunosorbent assay(ELISA).[Result]The recombinant adenovirus plasmid was consistent with that shown by sequencing and restriction endonucleases digestion.The recombinant pAd-VIA vector was packaged and amplified successfully in QBI-293A cells.The titer was 2?1010 PFU/ml after amplifying.High positive GFP was expressed in the field through fluorescence microscopy after being transfected by recombinant pAd-VIA.ELISA indicated the expression of the target genes.The difference between the tansfected and non-transfected group was significant(P

85%).From the in vitro release experiment,the rhBMP-2 was controlled to release from the chitosan microsphere over 30 days.[Conclusion]The rhBMP-2 loaded chitosan microsphere prepared by emulsion cross-linking method shows a good controlled release property.Such a novel type of controlled release system has the potential of being applied for controlled cytokine delivery and the bone tissue engineering.

Objective To study the influence of different intensities of treadmill exercise training on bone biomechanical properties and the bone healing in type 2 diabetic model rats.Methods Fifty-two healthy 8-month-old male Sprague-Dawley rats were randomly divided into a control group (n =10) and a type 2 diabetic model group (n =42).Type 2 diabetes was modeled in rats of the model group by feeding feedstuff containing high glucose,fat and energy food for 4weeks,followed by a single intra-abdominal injection of streptozotocin.Thirty model rats were then randomized into 3 subgroups:type 2 diabetes group,a mild exercise group and a moderate exercise group.Different intensities of treadmill training protocols was administered accordingly for 8 weeks.The biomechanical indices of the femur bone including maximum load and stress,module and energy was measured with mechanical testing instrument.Results Compared with the control group,both maximum load and energy were decreased significantly in type2 diabetes group [(148.5±17.8)N vs (192.3±43.4)N] for maximum load,and (51.38 ±13.7)mJ vs (82.0 ± 30.8) mJ for maximum stress] (P ＜ 0.05,P ＜ 0.01).Compared with the type 2 diabetes group,maximum load and stress were increased significantly in the mild and moderate exercise groups(P ＜ 0.05,P ＜ 0.01).Maximum load and energy were improved more in the moderate exercise group than in the mild exercise group [(184.1 ± 26.6)N vs (165.4±21.5)N for maximum load and (83.59 ±29.96)mJ vs (62.33 ±14.32)mJ for maximum stress] (P ＜ 0.05).Conclusions A significant decrease of the bone biomechanical properties was observed in rats with experimental type 2 diabetes,which could be alleviated by treadmill exercise training.

Objective To determine the influence of aerobic exercise on advanced glycation end products (AGEs)in plasma using a rat model of type 2 diabetes,and to provide an experimental basis for explaining the rehabilitative mechanism of aerobic exercise in type 2 diabetes.Methods Fifty-two healthy 8-week-old male SpragueDawley rats were allocated at random into a normal control group(n=10)and a type 2 diabetes model group(n=42).The latter were overfed with a high-sugar,high-fat and high-energy diet for 4 weeks,then 30ms/kg of streptozotocin was injected intraperitoneally to create a model of type 2 diabetes.Thirty diabetic rats were then allocated at random into a diabetes control group,a low intensity exercise group and a moderate intensity exercise group with 10 in each group.The treadmill exercise was administered to the animals in the low and moderate exercise groups accordingly.Results Compared with the normal control group,plasma AGEs increased significantly in the diabetes control and moderate intensity exercise groups.Compared with the diabetes control group,AGEs in the lower intensity exercise group were significantly lower.Compared with the moderate intensity exercise group,plasma AGEs in the low intensity exercise group were somewhat lower,but not significantly.Conclusion Aerobic exercise can reduce plasma AGE levels in rats with a model of type 2 diabetes.The effect is probably related to decreasing excessive blood glncose and the exercise intensity.

Objective To analyze the association between interleukin-23 receptor (IL23R) gene single nucleotide polymorphisms (SNPs) and multiple sclerosis (MS) in a Southern Han Chinese population.Methods Three SNPs (rs2201841,rs10889677,rs7517847) within the IL23R gene were detected in 178 MS patients and 221 controls using polymerase chain reaction and restriction fragment length polymorphism method (PCR-RFLP).Haplotypes of the IL23R gene were constructed with SHEsis software.Results The frequencies of the genotype or allele in the IL23R gene SNPs(rs2201841:TT,TC,CC in MS patients:5.7％ (10/175),45.7％ (80/175),48.6％ (85/175),in controls:7.4％ (16/217),41.0％ (89/217),51.6％ (112/217),x2 =1.08,P =0.58 ; rs10889677:AA,AC,CC in MS patients:52.0％ (89/171),42.7％ (73/171),5.3％ (9/171),in controls:57.7％ (123/213),36.2％ (77/213),6.1％ (13/213),x2 =1.71,P =0.43 ; rs7517847:GG,GT,TT in MS patients:16.9％ (29/172),51.7％(89/172),31.4％ (54/172),in controls:14.4％ (31/215),49.3％ (106/215),36.3％(78/215),x2=1.15,P =0.56)showed no significant difference between MS patients and controls.The genotype did not influence the age of onset,the duration or disease severity in MS patients.The SNPs rs2201841 and rs10889677 had strong linkage disequlibrium (D' =0.614,r2 =0.327).The haplotype frequencies showed no significant difference between the MS patients and controls.Conclusion There is no evidence in our study to support the association between IL23R SNPs and MS in a Southern Han Chinese population.

Objective To investigate the relationship between metabolic syndrome (MS) and female subclinical carotid atherosclerosis. Methods A total of 835 female subjects were enrolled in this study. MS was defined based on the ATP Ⅲ criteria. Age groups were ＜45,45 to 65,and ≥65 years. The participants were evaluated by the number of components of MS and clusters of MS components. Measurement of carotid arteries with B-mode ultrasound imaging was performed. Intima-media thickness and plague of the carotid arteries were regarded as the indicators of subclinical carotid atherosclerosis. Results The prevalence of carotid atherosclerosis, MS components and MS was significantly increased with the increased age. After age was adjusted, multiple logistic regression analysis showed that every component of MS was independently associated with carotid atherosclerosis; the increased waist circumstance and blood pressure and reduced HLD showed stronger effect. The prevalence of carotid atherosclerosis was increased with increasing number of components of MS. When compared to the 0 MS component group,the odds ratio (OR)of carotid atherosclerosis of the groups with 1, 2,3,4, or 5 components were 1.4,2. 0,3.4,5. 7 and 7. 1,respectively. The altered cluster components of MS impacted differently on carotid atherosclerosis. The clusters of components of MS with increased waist circumstance were more frequent than without ones. Conclusion Every component of MS may be an independent risk factor of carotid atherosclerosis;increased components of MS could contribute higher odd risk to carotid atherosclerosis; clusters of MS components might show different impacts on carotid atherosclerosis.

Objective: Overexpression of the HER2/neu oncogene is a frequent molecular event in multiple human cancers. Being a cancer antigen, p185 erbB2 is an ideal target for immunotherapy. In order to decrease the immunogenicity of mouse anti-p185 erbB2 monoclonal antibody in human cancer therapy, we constructed the eukaryotic expression vector of anti-p185 erbB2 chimeric monoclonal antibody and verified expression of the chimeric antibody in CHO-dhfr - cell. Methods: The variable regions of light chain and heavy chain were amplified with RT-PCR and inserted into the chimeric antibody vector pWSD2. After CHO-dhfr - cells were transfected with recombination plasmid by lipofectAMINE, the chimeric antibody expressing level was identified with RT-PCR, indirect-ELISA, and Western blot. The specificity of the anti-p185 erbB2 chimeric antibody was testified with ELISA assay and immunoprecipitation. Moreover, the effects of chimeric antibody on the proliferation of breast cancer cell line SKBR3, which is overexpressing p185 erbB2 , were measured with MTT assay in vitro. Results: The anti-p185 erbB2 chimeric antibody eukaryotic expression vector was constructed successfully and the expression of the chimeric antibody in CHO-dhfr - was verified by RT-PCR, indirect-ELISA, and Western blot. ELISA assay showed that chimeric antibody reacted with cells overexpressing p185 erbB2 specifically, but did not react with that non-overexpressing p185 erbB2 . Immunoprecipitation test confirmed that the chimeric antibody could bind to p185 erbB2 specifically. The MTT assay demonstrated that the chimeric antibody could inhibit the growth of SKBR3 cells overexpressing p185 erbB2 . Conclusion: The anti-p185 erbB2 mouse/human chimeric antibody that was expressed in CHO-dhfr - cells can bind to p185 erbB2 specifically and inhibit proliferation of SKBR3 cells overexpressing p185 erbB2 . It has a potential application in biotherapy of cancer.