目的:系统评价内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)基因G894T多态性与糖尿病肾病(diabetic nephropathy,DN)易感性之间的关系。方法:全面检索建库以来至2019年6月与eNOS基因G894T多态性及DN易感性相关的文献,...目的:系统评价内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)基因G894T多态性与糖尿病肾病(diabetic nephropathy,DN)易感性之间的关系。方法:全面检索建库以来至2019年6月与eNOS基因G894T多态性及DN易感性相关的文献,通过纽卡斯尔渥太华(Newcastle-Ottawa Scale,NOS)标准对纳入文献进行质量评价。采用Stata 15.0进行统计学分析,通过计算发病风险比值比(odds ratio,OR)及95%置信区间(confidence interval,CI)来评估eNOS基因G894T多态性与DN易感性之间的关系。结果:共纳入29项病例对照研究,包含实验组5345例,对照组4827例。分析结果显示eNOS基因G894T多态性可显著增加DN发病风险[等位基因模型T vs G:OR=1.39(95%CI:1.19~1.64),P<0.001;纯合子模型TT vs GG:OR=1.34(95%CI:1.02~1.77),P=0.038;显性遗传模型TT+GT vs GG:OR=1.48(95%CI:1.21~1.81),P<0.001;隐性遗传模型TT vs GG+GT:OR=1.30(95%CI:1.04~1.63),P=0.022;杂合子模型TG vs GG:OR=1.43(95%CI:1.17~1.75),P=0.001]。结论:eNOS基因G894T多态性可明显增加DN易感性。展开更多
目的探讨内皮型一氧化氮合酶(NOS3或eNOS)G894T基因多态性与肿瘤易感性的关系。方法通过计算机检索和手工检索,收集有关NOS3G894T基因多态性与肿瘤易感性的文献,筛选出符合纳入和排除标准的文献,应用Meta分析软件对各项研究进行异质性检...目的探讨内皮型一氧化氮合酶(NOS3或eNOS)G894T基因多态性与肿瘤易感性的关系。方法通过计算机检索和手工检索,收集有关NOS3G894T基因多态性与肿瘤易感性的文献,筛选出符合纳入和排除标准的文献,应用Meta分析软件对各项研究进行异质性检验,计算合并OR值及其95%CI,并行敏感性分析和发表偏倚的评估。结果 19篇文献纳入本研究,共计有7 679例肿瘤患者和8 180例对照人群。总体来说,NOS3G894T基因多态性与肿瘤无明显易感性(T versus G:OR=1.030,95%CI0.964-1.101;TT versus GG:OR=1.056,95%CI 0.895-1.245;TG versus GG:OR=1.045,95%CI 0.977-1.119;TT/TG versus GG:OR=1.047,95%CI0.981-1.117;TT versus TG/GG:OR=1.005,95%CI0.900-1.123)。根据种族、肿瘤类型及对照组来源进行分层分析,没有发现有明显易感性。结论 NOS3G894T基因多态性与肿瘤不存在明显易感性。展开更多
The intracellular free calcium concentration plays a key role as the second messenger in the regulation of cellular reaction.The changes of cytoplasmic free calcium concentration([Ca^(2+)]_i) in human platelets loaded...The intracellular free calcium concentration plays a key role as the second messenger in the regulation of cellular reaction.The changes of cytoplasmic free calcium concentration([Ca^(2+)]_i) in human platelets loaded with the fluorescent calcium indicator quin-2 were measured in this study. The result showed that thrombin(0.3 U/ml)raised the[Ca^(2+)]_i of platelets four to five times in the presence of 1 mmol/L external calcium.but there was a much smaller increase in[Ca^(2+)]_i in the absence of external calcium.It seems that thrombin increased[Ca^(2+)]_i partly by release of internal Ca^(2+),but mainly by stimulating influx.J-894 markedly inhibited the rise of[Ca^(2+)]_i in platelets induced by thrombin in a dose dependent manner through decreasing both calcium influx and calcium release.This suggests that J-894 may be a calcium channel blocker.展开更多
文摘目的:系统评价内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)基因G894T多态性与糖尿病肾病(diabetic nephropathy,DN)易感性之间的关系。方法:全面检索建库以来至2019年6月与eNOS基因G894T多态性及DN易感性相关的文献,通过纽卡斯尔渥太华(Newcastle-Ottawa Scale,NOS)标准对纳入文献进行质量评价。采用Stata 15.0进行统计学分析,通过计算发病风险比值比(odds ratio,OR)及95%置信区间(confidence interval,CI)来评估eNOS基因G894T多态性与DN易感性之间的关系。结果:共纳入29项病例对照研究,包含实验组5345例,对照组4827例。分析结果显示eNOS基因G894T多态性可显著增加DN发病风险[等位基因模型T vs G:OR=1.39(95%CI:1.19~1.64),P<0.001;纯合子模型TT vs GG:OR=1.34(95%CI:1.02~1.77),P=0.038;显性遗传模型TT+GT vs GG:OR=1.48(95%CI:1.21~1.81),P<0.001;隐性遗传模型TT vs GG+GT:OR=1.30(95%CI:1.04~1.63),P=0.022;杂合子模型TG vs GG:OR=1.43(95%CI:1.17~1.75),P=0.001]。结论:eNOS基因G894T多态性可明显增加DN易感性。
文摘目的探讨内皮型一氧化氮合酶(NOS3或eNOS)G894T基因多态性与肿瘤易感性的关系。方法通过计算机检索和手工检索,收集有关NOS3G894T基因多态性与肿瘤易感性的文献,筛选出符合纳入和排除标准的文献,应用Meta分析软件对各项研究进行异质性检验,计算合并OR值及其95%CI,并行敏感性分析和发表偏倚的评估。结果 19篇文献纳入本研究,共计有7 679例肿瘤患者和8 180例对照人群。总体来说,NOS3G894T基因多态性与肿瘤无明显易感性(T versus G:OR=1.030,95%CI0.964-1.101;TT versus GG:OR=1.056,95%CI 0.895-1.245;TG versus GG:OR=1.045,95%CI 0.977-1.119;TT/TG versus GG:OR=1.047,95%CI0.981-1.117;TT versus TG/GG:OR=1.005,95%CI0.900-1.123)。根据种族、肿瘤类型及对照组来源进行分层分析,没有发现有明显易感性。结论 NOS3G894T基因多态性与肿瘤不存在明显易感性。
文摘The intracellular free calcium concentration plays a key role as the second messenger in the regulation of cellular reaction.The changes of cytoplasmic free calcium concentration([Ca^(2+)]_i) in human platelets loaded with the fluorescent calcium indicator quin-2 were measured in this study. The result showed that thrombin(0.3 U/ml)raised the[Ca^(2+)]_i of platelets four to five times in the presence of 1 mmol/L external calcium.but there was a much smaller increase in[Ca^(2+)]_i in the absence of external calcium.It seems that thrombin increased[Ca^(2+)]_i partly by release of internal Ca^(2+),but mainly by stimulating influx.J-894 markedly inhibited the rise of[Ca^(2+)]_i in platelets induced by thrombin in a dose dependent manner through decreasing both calcium influx and calcium release.This suggests that J-894 may be a calcium channel blocker.
