目的:探讨肿瘤坏死因子-α(TNFα)基因多态性与糖尿病性牙周炎(DP)易感性的相关性。方法:电子检索MEDLINE、Web of Science、CNKI、万方以及中国生物医学文摘数据库自建库至2016-04收录的所有文献,从中收集TNFα-(308G/A)位点基因多态性...目的:探讨肿瘤坏死因子-α(TNFα)基因多态性与糖尿病性牙周炎(DP)易感性的相关性。方法:电子检索MEDLINE、Web of Science、CNKI、万方以及中国生物医学文摘数据库自建库至2016-04收录的所有文献,从中收集TNFα-(308G/A)位点基因多态性与DP易感性的相关研究并进行meta分析。同时采用病例对照研究进行验证:分别收集慢性牙周炎(CP)患者(60例)、健康对照者(N)(56例)、2型糖尿病(T2DM)患者(58例)、DP患者(60例)的血液样本并采用DNA测序法检测其TNFα-(308G/A)位点的基因型。随后采用χ~2检验分析基因型和等位基因频率在各组间分布的差异,并应用非条件Logistic回归分析计算风险比(OR)及95%可信区间(95%CI),以评估各基因型与DP发病风险的相关性。结果:meta分析结果显示,TNFα-(308G/A)位点多态性可能是汉族人群DP易感性的相关因素。病例对照研究结果显示,TNFα-(308G/A)位点的3种基因型(GG、GA、AA)及等位基因(G、A)频率在各组间的分布均有统计学差异(P<0.05);携带A等位基因的人群患DP的风险明显增加(OR=5.074,95%CI:1.857~13.868,P=0.002),而且携带GA基因型的人群患DP的风险显著高于携带GG基因型的人群(OR=5.637,95%CI:1.949~16.301,P=0.001)。结论:汉族人群中TNFα-(308G/A)位点基因多态性可能是DP易感性的相关因素。展开更多
目的探讨雌激素受体α(ER-α)基因XbaⅠ、PvuⅡ位点多态性与女性膝骨关节炎(KOA)易感性的关系。方法通过计算机检索Pubmed、EMBASE、CENTRAL、Web of science、Ovid、知网、维普和万方数据库,收集有关ER-α基因XbaⅠ (A/G)或PvuⅡ (T/C...目的探讨雌激素受体α(ER-α)基因XbaⅠ、PvuⅡ位点多态性与女性膝骨关节炎(KOA)易感性的关系。方法通过计算机检索Pubmed、EMBASE、CENTRAL、Web of science、Ovid、知网、维普和万方数据库,收集有关ER-α基因XbaⅠ (A/G)或PvuⅡ (T/C)位点多态性与女性KOA易感性的研究。提取相关数据,计算OR值及95%CI,利用STATA 11软件行Meta分析。结果共纳入7篇文献,9个病例-对照或队列研究,试验组2 194例,对照组2 959例。总体结果显示,XbaⅠ、PvuⅡ位点多态性与女性KOA易感性均无显著相关(P>0.05)。亚组分析结果显示,XbaⅠ位点多态性(G vs A; GG vs AA; GG+AG vs AA; GG vs AG+AA)可显著降低亚洲女性KOA的发病风险(P<0.01);PvuⅡ位点多态性(C vs T; CC vs TT; CC vs CT+TT)可显著增加亚洲女性KOA的发病风险(P<0.01)。结论本研究提示ER-α基因XbaⅠ、PvuⅡ位点多态性与女性KOA易感性存在种族差异,但本实验纳入样本量较少,结论仍需更多研究予以证实。展开更多
Background： Many studies have suggested that cigarette smoking and polymorphisms of resi stin and glutathione peroxidase-1 （GPx-1） genes are closely correlated with tile pathogenesis of nonalcoholic lhtty liver dis...Background： Many studies have suggested that cigarette smoking and polymorphisms of resi stin and glutathione peroxidase-1 （GPx-1） genes are closely correlated with tile pathogenesis of nonalcoholic lhtty liver disease （NAFLD）. However, few reports have investigated these associations with respect to NAFLD susceptibility. We, therefore, exalnined the distribution of polymorphisms in GPx-l and resistin genes in NAFLD patients and healthy controls and analyzed the relationship between these polymorphisms and smoking status. Methods： Nine hundred NAFLD patients and 900 healthy controls were selected, and the genetic polymorphisms of resistin gene promoter- 420C/G and GPx- 1 gene Pro 198Leu were analyzed by polymorphism-polymerase chain reaction （PCR） in DNA extracted from peripheral blood leukocytes. Interactions between tile two mutants and the gene-environment interaction with cigarette smoking were also analyzed. Results： Genotype frequencies of 420C/G （GG） and Pro198Leu （LL） were significantly higher in NAFLD cases （49.56% and 50.11%, respectively） compared with healthy controls （23.67% and 24.22%, respectively） （P = 0.0069： P= 0.0072）. Moreover, the risk of NAFLD with 420C/G （GGJ was significantly higher than in controls （odds ratio [OR] =3.1685, 95% confidence interval （（7） 1.9366-5.2073）. Individuals carrying Pro198Leu （LL） had a high risk of NAFLD （OR - 3.1424, 95% C/= 1.7951 5.2367）. Combined analysis of the polymorphisms showed that the -420C/G （GG）/Pro198Leu （LL） genotype was significantly more common in the NAFLD group than in the control group （39.44% vs. 12.78%, respectively, P 0.0054）, while individuals with -420C/G （GG）/Pro198Leu （LL） had a high risk of NAFLD （OR = 5.（1357, 95% CI= 3.1852 7.8106）. Moreover, the cigarette smoking rate in the NAFLD group was significantly higher than in tile control group （OR = 1.8990, P = 0.0083 in the smoking index （SI） _〈400 subgroup： OR = 5.0937, P = 0.0051 in the SI 〉400 subgroup）, and statistical analysis suggested a positive interaction between cigarette smoking and 420C/G （GG） （y = 5.6018 in tile SI≤400 subgroup; γ - 4.4770 in the SI 〉400 subgroup） and Pro198Leu （LL） （y = 5.7715 in the SI ≤400 subgroup： γ 4.5985 in the SI 〉400 subgroup） in increasing the risk of NAFLD. Conclusion： NAFLD risk factors include -420C/G （GG）, Pro198Leu （LL） and cigarette smoking, and these three factors have a significant additive effect on NAFLD risk.展开更多
文摘目的:探讨肿瘤坏死因子-α(TNFα)基因多态性与糖尿病性牙周炎(DP)易感性的相关性。方法:电子检索MEDLINE、Web of Science、CNKI、万方以及中国生物医学文摘数据库自建库至2016-04收录的所有文献,从中收集TNFα-(308G/A)位点基因多态性与DP易感性的相关研究并进行meta分析。同时采用病例对照研究进行验证:分别收集慢性牙周炎(CP)患者(60例)、健康对照者(N)(56例)、2型糖尿病(T2DM)患者(58例)、DP患者(60例)的血液样本并采用DNA测序法检测其TNFα-(308G/A)位点的基因型。随后采用χ~2检验分析基因型和等位基因频率在各组间分布的差异,并应用非条件Logistic回归分析计算风险比(OR)及95%可信区间(95%CI),以评估各基因型与DP发病风险的相关性。结果:meta分析结果显示,TNFα-(308G/A)位点多态性可能是汉族人群DP易感性的相关因素。病例对照研究结果显示,TNFα-(308G/A)位点的3种基因型(GG、GA、AA)及等位基因(G、A)频率在各组间的分布均有统计学差异(P<0.05);携带A等位基因的人群患DP的风险明显增加(OR=5.074,95%CI:1.857~13.868,P=0.002),而且携带GA基因型的人群患DP的风险显著高于携带GG基因型的人群(OR=5.637,95%CI:1.949~16.301,P=0.001)。结论:汉族人群中TNFα-(308G/A)位点基因多态性可能是DP易感性的相关因素。
文摘目的探讨雌激素受体α(ER-α)基因XbaⅠ、PvuⅡ位点多态性与女性膝骨关节炎(KOA)易感性的关系。方法通过计算机检索Pubmed、EMBASE、CENTRAL、Web of science、Ovid、知网、维普和万方数据库,收集有关ER-α基因XbaⅠ (A/G)或PvuⅡ (T/C)位点多态性与女性KOA易感性的研究。提取相关数据,计算OR值及95%CI,利用STATA 11软件行Meta分析。结果共纳入7篇文献,9个病例-对照或队列研究,试验组2 194例,对照组2 959例。总体结果显示,XbaⅠ、PvuⅡ位点多态性与女性KOA易感性均无显著相关(P>0.05)。亚组分析结果显示,XbaⅠ位点多态性(G vs A; GG vs AA; GG+AG vs AA; GG vs AG+AA)可显著降低亚洲女性KOA的发病风险(P<0.01);PvuⅡ位点多态性(C vs T; CC vs TT; CC vs CT+TT)可显著增加亚洲女性KOA的发病风险(P<0.01)。结论本研究提示ER-α基因XbaⅠ、PvuⅡ位点多态性与女性KOA易感性存在种族差异,但本实验纳入样本量较少,结论仍需更多研究予以证实。
文摘Background： Many studies have suggested that cigarette smoking and polymorphisms of resi stin and glutathione peroxidase-1 （GPx-1） genes are closely correlated with tile pathogenesis of nonalcoholic lhtty liver disease （NAFLD）. However, few reports have investigated these associations with respect to NAFLD susceptibility. We, therefore, exalnined the distribution of polymorphisms in GPx-l and resistin genes in NAFLD patients and healthy controls and analyzed the relationship between these polymorphisms and smoking status. Methods： Nine hundred NAFLD patients and 900 healthy controls were selected, and the genetic polymorphisms of resistin gene promoter- 420C/G and GPx- 1 gene Pro 198Leu were analyzed by polymorphism-polymerase chain reaction （PCR） in DNA extracted from peripheral blood leukocytes. Interactions between tile two mutants and the gene-environment interaction with cigarette smoking were also analyzed. Results： Genotype frequencies of 420C/G （GG） and Pro198Leu （LL） were significantly higher in NAFLD cases （49.56% and 50.11%, respectively） compared with healthy controls （23.67% and 24.22%, respectively） （P = 0.0069： P= 0.0072）. Moreover, the risk of NAFLD with 420C/G （GGJ was significantly higher than in controls （odds ratio [OR] =3.1685, 95% confidence interval （（7） 1.9366-5.2073）. Individuals carrying Pro198Leu （LL） had a high risk of NAFLD （OR - 3.1424, 95% C/= 1.7951 5.2367）. Combined analysis of the polymorphisms showed that the -420C/G （GG）/Pro198Leu （LL） genotype was significantly more common in the NAFLD group than in the control group （39.44% vs. 12.78%, respectively, P 0.0054）, while individuals with -420C/G （GG）/Pro198Leu （LL） had a high risk of NAFLD （OR = 5.（1357, 95% CI= 3.1852 7.8106）. Moreover, the cigarette smoking rate in the NAFLD group was significantly higher than in tile control group （OR = 1.8990, P = 0.0083 in the smoking index （SI） _〈400 subgroup： OR = 5.0937, P = 0.0051 in the SI 〉400 subgroup）, and statistical analysis suggested a positive interaction between cigarette smoking and 420C/G （GG） （y = 5.6018 in tile SI≤400 subgroup; γ - 4.4770 in the SI 〉400 subgroup） and Pro198Leu （LL） （y = 5.7715 in the SI ≤400 subgroup： γ 4.5985 in the SI 〉400 subgroup） in increasing the risk of NAFLD. Conclusion： NAFLD risk factors include -420C/G （GG）, Pro198Leu （LL） and cigarette smoking, and these three factors have a significant additive effect on NAFLD risk.
