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.

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.

Bilateral frontal polymicrogyria is a recently recognized syndrome characterized by symmetric polymicrogyria of both frontal lobes that presents with delayed motor and language development, spastic quadriparesis, and variable mental retardation. However, the postmortem findings of this syndrome are not fully elaborated. Here we describe an autopsy case of bilateral frontal polymicrogyria in a male fetus delivered at 22 weeks gestation due to extensive chorioamnionitis. The microscopic findings included a thinned cortical plate with fair neuronal maturation. There were no signs of neuronal damage and the white matter was unremarkable.
Autopsy ; Chorioamnionitis ; European Continental Ancestry Group ; Female ; Fetus ; Frontal Lobe ; Humans ; Intellectual Disability ; Language Development ; Male ; Malformations of Cortical Development ; Muscle Spasticity ; Neuronal Migration Disorders ; Neurons ; Pregnancy ; Quadriplegia

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 observe the changes of left atrial dimension and f unction before and after cardioversion for atrial fibrillation (AF) and the rela tion between dimension and function.Methods Among 94 cases,34 ca ses who had spontaneous cardioversion converted to sinus rhythm,60 cases were ra ndomly grouped into 31 cases with drug cardioversion and 29 cases with direct-c urrent shock.Left atrial diameter,volume and A-wave velocity were measured to e valuate left atrial dimension and function using Dopplor echocardiogram in all c ases before and after cardioversion.Results After conversion,Lef t atrial diameter and volume decreased remarkably (P

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 explore the value of biomechanics parameter of rabbit abdominal aortic atheroma using velocity vector imaging(VVI).Methods Ten of 45 male New Zealand rabbits were chosen as normal control group randomly,the rest experimental rabbits were made atheromatous plaque model.The rabbits were examined by two-dimensional ultrasound and VVI respectively.The intima-media thickness(IMT) or thickness of plaques of abdominal aorta 1 cm from right renal artery branch were recorded.Maximum tangential velocity,strain and strain rate of IMT or plaques were measured using VVI.Then the rabbits were killed for pathological and immuno-histochemical examination.Results Based on pathology,the rabbites were divided into 4 groups:control group(group A,n=10),group of pathological endometrial thickening(group B,n=9),group of thick fibrous cap atheromatous plaques (group C,n=15) and group of thin fibrous cap atheromatous plaques (group D,n=11).The difference of plaques thickness and biochemical indicators had no statistically significant between group B and C(P>0.05),both bigger than group A and B (P<0.05).The difference of Vmax,Smax and SRmax had statistically significant each group(P<0.05).With Vmax>0.46×10-2 cm/s,Smax>0.37%,SRmax>1.415×10-2 s-1 to find the vulnerable plaques,the sensitivity were 75.0%,84.4%,84.4% respectively,specificity were 70.8%,91.7%,83.3% respectively.Conclusions VVI can identify plaque biomechanics parameter of different progression periods,which is expected to be a reliable method to find vulnerable plaques earlier in clinic.

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.

No abstract available.
Finite Element Analysis* ; Plastics* ; Titanium*

Objective To investigate the effects of celastrol on the cell growth and apoptosis of human gallbladder cancer NOZ cells,and explore its potential molecular mechanism.Methods NOZ cell were cultured in vitro.And CCK-8 assay,Annexin V-FITC/PI staining method,cell cycle analysis were conducted to investigate the effects of celastrol on the growth and apoptosis of NOZ cells after being treated with drugs.The mitochondrial membrane potential and Bax and Bcl-2 protein expression level were determined by Rhodamine 123 and Western blot,respectively.Results Celastrol could inhibit NOZ cell growth,and the IC50 value was 5.3 μmol/L.Annexin-V/PI staining showed that cell apoptosis of NOZ cells were induced as the celastrol concentration increased,and the apoptosis ratio of control group was 4.4％,while the apoptosis rates of the test groups (2,5,10 p mol/L) were 7.4％,27.1％ and 43.4％,respectively.In addition,cell cycle analysis revealed that celastrol could induce G1-phase arrest.The G1-phase rate of control group was 25.6％,while the G1-phase rates of the test groups (2,5,10 μmol/L) were 36.5％,45.7％ and 92.5％,respectively.The mitochondrial membrane potential was measured after treatment with celastrol and the results indicated that the mitochondrial membrane potential was significantly decreased.Western Blot showed that the protein expression of Bax increased and Bcl-2 decreased in a time-dependent manner after treatment with celastrol.Conclusions Celastrol may inhibit cell proliferation of human gallbladder cancer NOZ cells and induce cell apoptosis partly by inducing the loss of mitochondrial membrane potential.