Background The present study was undertaken to replicate the associations of representative polymorphisms in three genes （complement factor H （CFH）, complement factor B （BF） and HtrA serine peptidase 1 （HTRA1）...Background The present study was undertaken to replicate the associations of representative polymorphisms in three genes （complement factor H （CFH）, complement factor B （BF） and HtrA serine peptidase 1 （HTRA1）） with exudative age-related macular degeneration （AMD） in a Han Chinese population, and to test if the modifiable environmental factors affect AMD susceptibility associated with different type of genotype in these genes. Methods An age, gender and ethnicity matched case-control study was conducted to genotype the representative single neucleotide polymorphisms （SNPs） loci including rs1061170 and rs1410996 in CFH, rs641153 and rs4151667 in BF and rs11200638 in HTRA1 gene in 144 exudative AMD patients and 126 normal controls using PCR-RFLP and direct resequencing. The demographic characteristics and behavioral risk factors were also recorded. Allelic and genotypic associations for individual SNP and joint associations with two loci were performed. The gene-gene and gene-environment interactions were analyzed using multivariate non-conditional Logistic regression analysis. Results The C risk allele frequencies for CFH Y402H （rs1061170） in cases and controls were 12.5% and 5.4% respectively, which were much lower than those in Caucasians （P 〈0.001）. Compared with TT homozygous genotype, the CT heterozygous genotype was positively associated with AMD with odds ratio （OR） of 3.23 （1.36-5.07）. However, the population attributable risk （PAR） of C allele was only 3.3% （1.4%-4.3%）. rs1410996 was also associated with AMD independent of Y402H. The ORs of exudative AMD for individuals carrying one copy risk allele and two copy risk alleles were 2.57 （1.21-5.45） and 4.76 （2.15-10.55） respectively, with correspondent PARs of 28.3% （2.0%-40.5%） and 38.2% （21.8%-45.4%）. rs11200636 in HTRA1 was another susceptible locus for AMD and the risk homozygotes were significantly susceptible for exudutive AMD （OR=3.98, 1.88-8.43） with PAR of 38.9% （24.3%-45.8%）展开更多
Objective To evaluate the effects of environmental factors and microRNAs （miRNAs） （miR-126, miR-143, and miR-145） on the risk of coronary heart disease （CHD）. Methods A frequency-matched case-control study （450...Objective To evaluate the effects of environmental factors and microRNAs （miRNAs） （miR-126, miR-143, and miR-145） on the risk of coronary heart disease （CHD）. Methods A frequency-matched case-control study （450 patients, 450 controls） was conducted from April 2014 to December 2016 in Fuzhou City, China. Environmental factors were investigated using a self-administered questionnaire, and the expression levels of miR-126, rniR-143, and miR-145 were determined by quantitative real-time Polymerase Chain Reaction （PCR） in pe- ripheral blood mononuclear cells. Unconditional logistic regression models were used for statistical evaluation. Results Alcohol consumption, high-salt diets, high-intensity work, and lack of physical activity were significantly associated with increased CHD risk, whereas light diet was significantly associated with decreased risk. MiR-126, miR-143, and miR-145 were highly expressed in the CHD group compared with the control group. After adjustment for other environmental factors, unconditional logistic regression results revealed that miR-126, miR-143, and depression were the independent risk factors of CHD, and light diet was the independent protective factor of CHD. Conclusions Our data suggest that a family history of CHD, anxiety, and alcohol consumption was significantly associated with increased CHD risk, whereas light diet was significantly associated with decreased risk. Furthermore, miR-126 and miR-143 in combination with several risk factors, could play a joint role in the development of CHD. Therefore, it is necessary to manage patients with CHD in all directions and multiple level.展开更多
Inflammation plays a significant role in the etiology of type 2 diabetes mellitus(T2DM).The rise in the pro-inflammatory cytokines is the essential step in glucotoxicity and lipotoxicity induced mitochondrial injury,o...Inflammation plays a significant role in the etiology of type 2 diabetes mellitus(T2DM).The rise in the pro-inflammatory cytokines is the essential step in glucotoxicity and lipotoxicity induced mitochondrial injury,oxidative stress and beta cell apoptosis in T2 DM.Among the recognized markers are interleukin(IL)-6,IL-1,IL-10,IL-18,tissue necrosis factor-alpha(TNF-α),C-reactive protein,resistin,adiponectin,tissue plasminogen activator,fibrinogen and heptoglobins.Diabetes mellitus has firm genetic and very strong environmental influence; exhibiting a polygenic mode of inheritance.Many single nucleotide polymorphisms(SNPs) in various genes including those of pro and antiinflammatory cytokines have been reported as a risk for T2 DM.Not all the SNPs have been confirmed by unifying results in different studies and wide variations have been reported in various ethnic groups.The inter-ethnic variations can be explained by the fact that gene expression may be regulated by gene-gene,gene-environment and gene-nutrient interactions.This review highlights the impact of these interactions on determining the role of single nucleotide polymorphism of IL-6,TNF-α,resistin and adiponectin in pathogenesis of T2 DM.展开更多
文摘Background The present study was undertaken to replicate the associations of representative polymorphisms in three genes （complement factor H （CFH）, complement factor B （BF） and HtrA serine peptidase 1 （HTRA1）） with exudative age-related macular degeneration （AMD） in a Han Chinese population, and to test if the modifiable environmental factors affect AMD susceptibility associated with different type of genotype in these genes. Methods An age, gender and ethnicity matched case-control study was conducted to genotype the representative single neucleotide polymorphisms （SNPs） loci including rs1061170 and rs1410996 in CFH, rs641153 and rs4151667 in BF and rs11200638 in HTRA1 gene in 144 exudative AMD patients and 126 normal controls using PCR-RFLP and direct resequencing. The demographic characteristics and behavioral risk factors were also recorded. Allelic and genotypic associations for individual SNP and joint associations with two loci were performed. The gene-gene and gene-environment interactions were analyzed using multivariate non-conditional Logistic regression analysis. Results The C risk allele frequencies for CFH Y402H （rs1061170） in cases and controls were 12.5% and 5.4% respectively, which were much lower than those in Caucasians （P 〈0.001）. Compared with TT homozygous genotype, the CT heterozygous genotype was positively associated with AMD with odds ratio （OR） of 3.23 （1.36-5.07）. However, the population attributable risk （PAR） of C allele was only 3.3% （1.4%-4.3%）. rs1410996 was also associated with AMD independent of Y402H. The ORs of exudative AMD for individuals carrying one copy risk allele and two copy risk alleles were 2.57 （1.21-5.45） and 4.76 （2.15-10.55） respectively, with correspondent PARs of 28.3% （2.0%-40.5%） and 38.2% （21.8%-45.4%）. rs11200636 in HTRA1 was another susceptible locus for AMD and the risk homozygotes were significantly susceptible for exudutive AMD （OR=3.98, 1.88-8.43） with PAR of 38.9% （24.3%-45.8%）
文摘Objective To evaluate the effects of environmental factors and microRNAs （miRNAs） （miR-126, miR-143, and miR-145） on the risk of coronary heart disease （CHD）. Methods A frequency-matched case-control study （450 patients, 450 controls） was conducted from April 2014 to December 2016 in Fuzhou City, China. Environmental factors were investigated using a self-administered questionnaire, and the expression levels of miR-126, rniR-143, and miR-145 were determined by quantitative real-time Polymerase Chain Reaction （PCR） in pe- ripheral blood mononuclear cells. Unconditional logistic regression models were used for statistical evaluation. Results Alcohol consumption, high-salt diets, high-intensity work, and lack of physical activity were significantly associated with increased CHD risk, whereas light diet was significantly associated with decreased risk. MiR-126, miR-143, and miR-145 were highly expressed in the CHD group compared with the control group. After adjustment for other environmental factors, unconditional logistic regression results revealed that miR-126, miR-143, and depression were the independent risk factors of CHD, and light diet was the independent protective factor of CHD. Conclusions Our data suggest that a family history of CHD, anxiety, and alcohol consumption was significantly associated with increased CHD risk, whereas light diet was significantly associated with decreased risk. Furthermore, miR-126 and miR-143 in combination with several risk factors, could play a joint role in the development of CHD. Therefore, it is necessary to manage patients with CHD in all directions and multiple level.
文摘Inflammation plays a significant role in the etiology of type 2 diabetes mellitus(T2DM).The rise in the pro-inflammatory cytokines is the essential step in glucotoxicity and lipotoxicity induced mitochondrial injury,oxidative stress and beta cell apoptosis in T2 DM.Among the recognized markers are interleukin(IL)-6,IL-1,IL-10,IL-18,tissue necrosis factor-alpha(TNF-α),C-reactive protein,resistin,adiponectin,tissue plasminogen activator,fibrinogen and heptoglobins.Diabetes mellitus has firm genetic and very strong environmental influence; exhibiting a polygenic mode of inheritance.Many single nucleotide polymorphisms(SNPs) in various genes including those of pro and antiinflammatory cytokines have been reported as a risk for T2 DM.Not all the SNPs have been confirmed by unifying results in different studies and wide variations have been reported in various ethnic groups.The inter-ethnic variations can be explained by the fact that gene expression may be regulated by gene-gene,gene-environment and gene-nutrient interactions.This review highlights the impact of these interactions on determining the role of single nucleotide polymorphism of IL-6,TNF-α,resistin and adiponectin in pathogenesis of T2 DM.
