Objective To explore the relationship of the ADAM33 gene Q-1,T2 single nucleotide polymorphism (SNP) and suffering from chronic obstructive pulmonary disease (COPD) in Xinjiang Kazakh and Han population. Methods Peripheral blood samples to extract DNA, and the single nucleotide polymorphisms of Q-1 and T2 in ADAM33 gene were detected by SNaPshot SNP genotyping. Results Case group compared with the control group, frequencies of Q-1 locus genotypes and alleles were significant differences in Kazak (P<0.05). In patient group, there were significant differences in ADAM33 gene Q-1 locus genotypes FEV1% predicted, FEV1/FVC of clinical indicators lung function in Kazak, Han(P < 0.05). Kazak Q-1 locus AA genotype,Han GA genotype than GG genotype were significant difference.Compare Kazak AA genotype,Han GA genotype with GG genotype is more likely to cause COPD in Q-1 locus(P<0.05). In the comparison of the case and control group the two ethnic, there was no significant difference between the frequencies of T2 locus genotypes and the frequencies of Q-1,T2 the alleles (P > 0.05). There were no significant differences in T2 locus genotypes and clinical indicators of lung function FEV1% predicted and FEV1/FVC in patient group (P > 0.05). Conclusion The ADAM33 gene Q-1 locus may be related to the COPD susceptibility in Xinjiang Kazak, Han.

Objective To explore correlation of Xinjiang Kazakh population who suffered from COPD with polymor?phisms of F+1,S2,T1,ST+5 locus of ADAM33 gene. Methods Blood samples (n=193) from healthy controls (Control group, n=193) and COPD patients (Case group, n=197) were detected by SNP SNaP shot. Results Comparing case group with the control group, gene frequency and allele frequency of F+1 locus were of significant differences (P<0.05). In patient group, there were no significant differences in F+1 locus genotype and in clinical indicators include lung function FEV1 predicted and FEV1/FVC (P>0.05). The gene frequencies and allele frequency of S2、T1 and ST+5 locus were not significantly differ?ent between case group and control group (P>0.05). F+1 and S2 locus were analyzed by haplotype analysis which showed that there was significant differences in Hap1 (CC) haplotype between case group and control group (P<0.05), and OR<1 indicated that its haplotype may reduce the risk of COPD . There were significant differences (P<0.05) in Hap3(TC) haplo?type between case group and control group and OR>1 revealed that its haplotype may increase the risk of COPD . The distri?bution of Hap2 (TG) and Hap4 (CG) were not significantly different (P>0.05) between the 2 groups. T1 and ST+5 locus were analyzed by haplotype analysis which showed significant differences in haplotypes between case group and control group (P<0.05). Conclusion The occurrence of COPD may be related to the polymorphism of ADAM33 gene in F+1 locus in Xinjiang Kazakh.

Objective To investigate the relationship between polymorphism of IL-4-590C/T and susceptibility of asthma.Methods The case-control articles reporting the relationship between IL-4-590C/T polymorphism and susceptibility of asthma were collected by China National Knowledge Infrastructure,WanFang data,VIP citation databases,Pubmed,Baidu Scholar,time limits are retrieved from the building a database to January 2016.The Meta-analysis software RevMan5.0 and Stata 12.0 was applied for heterogeneity test and pooled OR calculation.Results Seven case-control studies were selected,including 1 167 cases in the asthma group and 1 101 cases in the control group.Meta-analysis showed that both-590C/T polymorphisms genotypes were significantly associated with asthma,five kinds of senotypes OR(95％ CI) were CT+CC vs.TT[0.7 (0.57-0.85)],CC vs.CT+ TT [0.56(0.43-0.72)],CC vs.TT[0.46(0.33-0.64)],CC vs.CT[0.64(0.48-0.85)],C vs.T[0.45(0.27-0.77)].From subgroup analysis,genotype CC vs.CT+TT[0.50(0.35-0.72)],CC vs.TT[0.50(0.27-0.95)],CT vs.TT[0.61(0.41-0.92)],C vs.T[0.47 (0.23-0.95)] with risk correlated in Asian children asthma(P value is 0.01,0.04,0.02,0.03).Genotype CC vs.CT+TT[0.63(0.44-0.90)],CC vs.TT[0.49(0.25-0.96)],CC vs.CT[0.67(0.45-0.98)] also indicated a significant correlation between-590C/T polymorphisms of IL-4 and asthma in non-Asian children(P value is 0.01,0.04,0.04).Conclusion Current evidence suggests that the-590C/T polymorphism of IL-4 gene is associated with children asthma.

Objective:To investigate the influence of sulforaphane(SFN)on ventricular remodeling in myocardial infarction(MI)rat model by regulating extracellular regulated protein kinase(ERK)/nuclear respiratory factor 1(NRF1)signaling pathway.Methods:Among 48 SD male rats,12 were randomly selected as Sham group.The remaining rats were treated with ligation of left ante-rior descending coronary artery to establish myocardial infarction model.After modeling,36 rats were randomly divided into MI model group,SFN treatment group(10 mg/kg),SFN+SCH772984(ERK inhibitor)group(10 mg/kg+15 mg/kg),with 12 rats in each group.Animal ultrasound was performed to detect cardiac structure and function.Histological analysis was performed to evaluate myo-cardial fibrosis and cell apoptosis.ELISA was used to measure pro-inflammatory factor levels in serum,and Western blot assay was used to observe the expression of ERK/NRF1 pathway related proteins in myocardium of rats in each group.Results:Compared with rats in Sham group,rats in MI model group showed a loss of myocardial compliance and disarray of ventricular myocardial fibers,along with increased myocardial fibrosis and myocardial cell apoptosis.Moreover,rats in MI model group also exhibited overactive inflammatory response and inhibition of the ERK/NRF1 signaling pathway in cardiac tissues(P<0.05).Notably,SFN treatment signifi-cantly not only improved cardiac function,but also ameliorated myocardial fibrosis and cell apoptosis(P<0.05).SFN treatment inhib-ited inflammatory cytokine expression and activated the ERK/NRF1 pathway as well(P<0.05).However,SCH772984 significantly abrogated the protective effect of SFN against myocardial fibrosis and apoptosis in MI rats.Conclusion:SFN may protect against ventricular remodeling in MI rat by activating ERK/NRF1 pathway.

Dihydroflavanol-4-reductase (Dfr) is a key enzyme that regulates the synthesis of anthocyanin and proanthocyanidin in the flavonoid biosynthesis pathway. To investigate the difference of dfr gene in Scutellaria baicalensis Georgi with different colors in the same ecological environment, three complete full-length sequences of dfr gene were cloned from the cDNA of S. baicalensis with white, purple-red and purple colors using homologous cloning and RACE techniques. The three genes were named Sbdfr1, Sbdfr2 and Sbdfr3, respectively, and their corresponding structures were analyzed. The results showed that all three Dfr proteins have highly conserved NADPH binding sites and substrate-specific binding sites. Phylogenetic analysis showed that they are closely related to that of the known S. viscidula (ACV49882.1). Analysis of key structural domains and 3D models revealed differences in the catalytically active regions on the surface of all three Dfr proteins, and their unique structural characteristics may provide favorable conditions for studying the substrate specificity of different Dfr proteins. qRT-PCR analysis shows that dfr was expressed at different level in all tissues except the roots of S. baicalensis in full-bloom. During floral development, the expression level of dfr in white and purple-flowered Scutellaria showed an overall upward trend. In purple-red-flowered Scutellaria, the expression first slowly increased, followed by a decrease, and then rapidly increased to the maximum. This research provides a theoretical basis for further exploring the mechanism and function of Dfr substrate selectivity, and are of great scientific value for elucidating the molecular mechanism of floral color variation in S. baicalensis.
Anthocyanins ; Cloning, Molecular ; Color ; Phylogeny ; Scutellaria baicalensis/genetics*