Objective To investigate the incidence of the aspirin resistance in secondary prevention of cerebral infarction, and the relationship between the aspirin resistance and the cerebral infarction recurrence or other vascular events during the follow-up periods.Methods Aspirin were taken from the first day of admission in 600 patients with cerebral infarction.The platelet aggregation rate was measured after 7-10 days to screen the patients with aspirin resistance or aspirin sensitivity.All patients were followed up for 6 to 24 months and the cerebral infarction recurrence and other vascular events were recorded.Logistic regression model was used to estimate the risk factors of aspirin resistance, vascular events and prognosis.Results Of 600 patients, 150 (25.0% ) patients were resistant to aspirin and 450 (75.0% ) patients were sensitive to aspirin.The proportion of female and diabetes patients, and the level of low density lipoproteins (LDL) in the aspirin resistance group were higher than those in the aspirin sensitivity group.Diabetes (OR = 2.58, 95% CI 1.37-4.85, P=0.003) and high LDL level (OR = 1.89, 95% CI 1.21-2.93, P = 0.005 ) were independent risk factors of aspirin resistance.The incidence of cerebral infarction recurrence and myocardial infarction and all-cause mortality in the aspirin resistance group were all higher than those in the aspirin sensitivity group.Diabetes ( OR = 2.47, 95% CI 1.36-4.65, P = 0.003 ) , atherothrombosis cerebral infarction (OR = 2.13, 95% CI 1.24-3.95, P = 0.023) and aspirin resistance (OR = 3.86,95% CI 1.79-5.87, P = 0.002) were independent risk factors of vascular events during the following-up period.In the patients with aspirin resistance, the risk of the recurrence of vascular events increased 3.86 times.Conclusions The incidence of aspirin resistance is high in secondary prevention of cerebral infarction.Aspirin resistance is closely correlated with cerebral infarction recurrence and other vascular events.

Objective To investigate the interrelations of ALOX5AP SG13S114A/T , COX-2 765G/C , COX-1-50C/T polymorphisms and cerebral infarction. Methods The ALOX5AP SG13S114A/T, COX-2 765G/C and COX-1 50C/T polymorphisms in 411 cases with cerebral infarction and 411 controls were measured by Polymerase Chain Reaction-Restriction Fragment Length Polymorphism method. The generalized multifactor dimensionality reduction (GMDR) method was employed to detect gene-gene interactions. Results Single-gene analysis showed that there were no significant differences in the genotype and allele frequency distributions of ALOX5AP SG13S114A/T, COX-2 765G/C and COX-1 50C/T between two groups. However, in those cases carrying ALOX5AP SG13S114AA as well as COX-2 765CC , the risk of cerebral infarction increased significantly by 2.842 times. Conclusions The combinational analysis among genes used in this study may be helpful in the elucidation of genetic risk factors for common and complex diseases.

ObjectiveTo study the effect of angiotensin Ⅱ type 1 receptor antagonist (ARB) losartan on reducing the incidence of stroke in patients which suffer from hypertension and atrial fibrillation(AF).MethodsProspective randomized analysis was used to divide one hundred and eighty hypertemion patients with atrial fibrillation into two groups.ARB treatment group was treated with losartan (n =90) and beta-blockers treatment group was treated with metoprolol ( n =90),all patients were treated for three years and followed up.Blood pressure,pulse pressure,incidence of stroke and myocardial infarction and mortality of cardiovascular events were evaluated.ResultsAfter antihypertensive treatment,blood pressure was reduced in two groups,the pulse pressure in losartan group was reduced obviously( all P ＜0.01 ).The incidence of stroke and myocardial infarction and mortality of cardiovascular events in losartan group were 22.2％,10.0％ and 13.3％,respectively,lower than that in metoprolol group 70.0％,40.0％ and 44.4％ ( all P ＜0.01 ).ConclusionLosartan reduced the incidence of stroke in the hypertension patients with AF.

Objective To investigate the correlation between two single nucleotide polymorphisms of the leukotriene A4 hydrolase (LTA4H) gene (rs2660845 and rs2540493) and risk of ischemic stroke in population of southern Zhejiang Province.Methods A total of 300 ischemic stroke patients and 300 healthy controls,recruited from the Department of Neurology,Third Affiliated Hospital of Wenzhou Medical University between September 2010 and June 2013,were enrolled in this study.Two single nucleotide polymorphisms of the LTA4H gene (rs2660845 and rs2540493) were analyzed by polymerase chain reaction and matrix-assisted laser desorption/ionization time of flight,respectively.Sixty-seven patients and thirty controls were randomly selected (complete randomization) and detected the serum leukotriene B4 (LTB4)concentration by ELISA method.Results There was no evidence of association between the two variants of LTA4H gene and the risk of ischemic stroke or its TOAST (Trial of Org 10 172 in acute stroke treatment)subtypes (P ＞ 0.05).Analysis of LTB4 levels revealed that there was no statistically significant difference in serum LTB4 concentration between patients (n =67) and controls (n =30; 0.991 ± 0.305 vs 1.035 ± 0.498 ; P =0.692),and no statistically significant difference in LTB4 concentration was found among the three genotypes of rs2660845 as well (AG genotype vs AA genotype vs GG genotype:0.938 ± 0.269 vs 1.038 ± 0.268 vs 1.043 ± 0.383 ; P =0.401).Conclusion The present study suggests that there is no association between the two polymorphisms in the LTA4H gene and risk of ischemic stroke in population of southern Zhejiang Province.

Objective To investigate 4 variants single nucleotide polymorphisms (SNPs) of 5-lipoxygenase-activating protein(ALOX5AP) in lipoxygenase pathway and in cytochrome P450 pathway as susceptibility genes for stroke in a southeastern Chinese population,and evaluate the associations between susceptibility genes and cerebral infarction,to find whether gene-gene interactions increase the risk of cerebral infarction.Methods By case-control study,two hundred and ninety-two patients with cerebral infarction and 259 healthy control subjects were included.Eight variants in 5 candidate genes were examined for stroke risk,including the SG13S32 (rs9551963),SG13S42 (rs4769060),SG13S89 (rs4769874),and SG13Sl14 (rs10507391) variants of the ALOX5AP gene,the G860A (rs751141) variant of the soluble epoxide hydrolase (EPHX2) gene,the A1075C (rs1057910) variant of the CYP2C9 *2 gene,the C430T (rs1799853) variant of the CYP2C9* 3 gene,and the A6986G (rs776746) variant of the CYP3A5 gene.Gene-gene interactions were explored using generalized multifactor dimensionality reduction (GMDR)methods.Results There were no statistically significant differences in the frequencies of the genotypes of the 8 candidate genes.The GMDR analysis showed a significant gene-gene interaction between SG13S114 and A6986G,with scores of 10 for cross-validation consistency and 9 for the sign test (P =0.011).These genegene interactions predicted a significantly higher risk of cerebral infarction (adjusted for age,hypertension,and diabetes mellitus;OR =1.804,95％ CI 1.180-2.759,P =0.006).Conclusions A two-loci gene interaction confers significantly higher risk for cerebral infarction.The combinational analysis used in this study may be helpful in the elucidation of genetic risk factors for common and complex diseases.

Objective To investigate whether metabolic pathway-related gene polymorphisms are associated with arterial plaque stability and their gene-gene interactions increase the risk of cerebral infarctions.Methods Totally 294 patients with atherothrombosis stroke admitted to the Department of Neurology, the Third Affiliated Hospital of Wenzhou Medical University from September 2010 to December 2012 were divided into a carotid vulnerable plaque group ( n=69 ) and a stable plaque group ( n=225 ) according to the results of carotid B-mode ultrasonography.A total of 282 healthy volunteers excluded carotid plaque and stroke were enrolled as well.Genetic polymorphisms of ALOX5AP and CYP3A5, CYP2C9*2, CYP2C9*3 and EPHX2 were genotyped using polymerase chain reaction and mass spectrometry analysis.The SPSS16.0 software was used to compare genotype frequencies and the generalized multifactor dimensionality reduction ( GMDR ) method was applied for gene-gene interaction analyses.Results The results showed that EPHX2 GG genotype might protect against stroke ( OR =0.520, 95% CI 0.288 -0.940, P=0.030).The distribution of CYP3A5 genotypes showed statistically significant differences (χ2 =7.284, P=0.026) between the vulnerable plaque ( AA: 5 cases, AG: 36 cases, GG: 28 cases) and stable plaque ( AA: 26 cases, AG: 77 cases, GG: 122 cases ) groups.Multivariate Logistic regression analysis showed that the GG genotype of CYP3A5 was protective factor for unstable plaques ( OR=0.405, 95%CI 0.178 -0.920, P =0.031 ).Differences in other SNPs did not reach statistical significance between the two groups.The GMDR analysis showed a significant gene-gene interaction between SG13S114 and A6986G, with scores of 10 for cross-validation consistency and 9 for the sign test (P=0.011).The best model for ischemic stroke was found to be SG13S114 AA and A6986G AA.Adjusting for age, hypertension and diabetes, the certain gene-gene interaction predicted a significantly higher risk of cerebral infarction (OR=1.804, 95%CI 1.180-2.759, P=0.006).Conclusions The EPHX2 G860A gene might be linked with the incidence of cerebral infarctions.Only a CYP3A5 gene polymorphism might be associated with carotid plaque instability in patients with stroke.The gene-gene interaction predicts a significantly higher risk of cerebral infarction.There is a 1.804-fold increased risk for ischemic stroke in individuals with these combined genetic factors.

Objective: To explore the clinical benefits and risks of intravenous thrombolysis combined with urinary kallidinogenase in the treatment of minor stroke. Methods: The clinical data of 86 patients with minor stroke were retrospectively analyzed. Patients who received intravenous thrombolysis combined with urinary kallidinogenase were included in observation group (n=48), and those who received intravenous thrombolysis alone were included in control group (n=38). Before treatment and after 2 weeks of treatment, the imaging blood flow perfusion parameters [cerebral blood flow (CBF), mean transit time (MTT), time to peak (TTP)], and breath holding test indexes [cerebral vascular reactivity (CVR), breath holding index (BHI)] and serum biochemical indicators [vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF)] were compared between the two groups. The occurrence of adverse drug reactions during course of treatment and rehabilitation effects at 3 months after treatment [US National Institutes of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS)] were analyzed in the two groups. Results: After 2 weeks of treatment, the CBF, CVR, BHI and serum levels of VEGF and bFGF in the two groups were significantly higher than those before treatment, and the indexes in observation group were significantly higher than those in control group (P<0.05). The MTT and TTP levels in the two groups were significantly higher than those before treatment, and the levels in observation group were significantly higher than those in control group (P<0.05). There was no significant difference in the incidence rate of adverse drug reactions between the two groups during course of treatment (P>0.05). At 3 months after treatment, there was no statistically significant difference in the effective rate of rehabilitation between the two groups (P>0.05), but the Mann-Whitney U rank sum test between-groups showed that the overall rehabilitation effects in observation group were significantly better than those in control group (P<0.05). Conclusions Intravenous thrombolysis has certain treatment effects in patients with minor stroke, and its safety is within the clinical controllable range. Combined with urinary kallidinogenase can obtain ideal long-term prognosis, and it is beneficial to the recovery of neurological function.

Objective:To explore the effect of dual antiplatelet combined with calf serum deproteinized injection in the treatment of mild ischemic stroke after intravenous thrombolysis.Methods:From October 2017 to December 2018, 82 patients with mild ischemic stroke who were diagnosed in the People's Hospital of Ruian were selected.The patients were divided into control group (41 cases) and observation group (41 cases) according to random number table method.The control group was treated with aspirin after intravenous thrombolysis.On this basis, the observation group was treated with dual antiplatelet combined with calf serum deproteinized injection.The course of treatment was 3 months in both two groups.The total effective rate, the changes of hemorheological indicators, the improvement of neurological deficit, the ability of daily living and the ability of returning to society were compared between the two groups before and after treatment.The complications and prognosis were recorded.Results:The total effective rate of the observation group was 95.12% (39/41), which was higher than 78.05% (32/41) of the control group (&chi; 2=5.145, P<0.05). After treatment, the National Institutes of Health Stroke Score Scale (NIHSS) score, Modified Rankin Score (mRS), Barthel index (BI) score of the observation group were (0.34±0.18)points, (92.15±6.73)points, (0.87±0.36)points, respectively, which of the control group were (0.92±0.35)points, (76.05±4.86)points, (1.64±0.52)points, respectively, there were statistically significant differences between the two groups ( t=8.592, 11.308, 7.099, all P<0.05). The whole blood viscosity, plasma viscosity and platelet aggregation rate of the observation group were (4.13±0.36)mPa/s, (1.39±0.31)mPa/s, (32.35±2.61)%, respectively, which were lower than those of the control group [(8.65±0.72)mPa/s, (1.62±0.47)mPa/s, (39.07±3.25)%] ( t=32.740, 2.382, 9.400, all P<0.05). There were no cases of cerebral hemorrhage and death in the two groups, and there was no statistically significant difference in recurrence rate between the two groups (&chi; 2=2.565, P>0.05). Conclusion:After intravenous thrombolytic therapy for patients with mild ischemic stroke, dual antiplatelet therapy combined with calf serum deproteinized injection can improve the neurological function, life ability and hemorheological indicators of patients, with good prognosis, it is safe and effective.

Objective To discuss the relationship between topographic location and neurological deterioration (ND) in patients with acute isolated pontine infarction.Methods Two hundred and fifty-nine patients with acute isolated pontine infarction,collected in our hospital from January 2010 to August 2013 and identified by diffusion weighted imaging (DWI),were included for retrospective review.Patients were divided into two groups according to their clinical symptoms:patients with ND and patients without ND.According to neuroimaging of DWI,the topographic location of pontine infarction was divided into three types:the upper,middle and lower ones;and the correlations of ND with risk factors,laboratory examination results,clinical manifestations and different topographic locations were explored by statistical tests.Results Of 259 patients,27.4％ (71) were diagnosed with ND;72.6％ (188) were diagnosed without ND.Univariate analysis showed that there were no differences in laboratory test results,NIHSS scores and medications between the two groups (P＞0.05);there were differences in female ratio (41 [57.7％] vs.82[43.6％]),smoking ratio (10[14.2％] vs.49[26.2％]),mean length of hospital stay ([22.72±7.01] d vs.[19.42±7.76] d),ratio of worse short-term clinical outcomes (56[78.87％] vs.64[34.04％]) and ratio of lower pontine infarction (31 [43.7％] vs.57[30.3％]) between the two groups (P＜0.05).Logistic regression analysis showed that lower pontine infarction was the independent risk factor of ND (odds ratio=1.952,95％ confidence interval=l.081-3.524,P=0.027).Conclusion Topographic location of lower pons lesions may be reliable predictor of ND in acute isolated pontine infarction.