Liu Rong, Li Jiazeng, Mu Hong, Jiang Yan, Wang Yuliang, Dang Qun, Cui Xianwei, Ji Miao, Huang Fanqiang
Tianjin First Central Hospital, Tianjin Institute of Thrombosis and Hemostasis, Tianjin 300192, China.
Zhonghua Xue Ye Xue Za Zhi. 2002 Sep;23(9):453-6.
To analyze the frequency of beta-fibrinogen (beta-Fg) gene -455G/A, -148C/T and 448G/A polymorphism, fibrinogen molecular reactivity and their association with plasma fibrinogen levels in health adults, myocardial infarction and cerebral infarction disease.
The beta-Fg gene -455G/A, -148C/T and 448G/A polymorphisms were analyzed by restriction fragment length polymorphism (RFLP). Fibrinogen molecular reactivity was analyzed for the conversion kinetics of fibrinogen into fibrin by a computer assistant procedure. Plasma fibrinogen levels were determined by Clauss method.
The frequencies of -455A, -148T, 448A allele in health adults were 0.185, 0.194 and 0.192, in myocardial infarction disease 0.295, 0.318 and 0.307, in cerebral infarction disease 0.177, 0.193 and 0.182, respectively. The frequencies of -455A, -148T, 448A alleles in myocardial infarction disease were apparently higher than that of health adults. There were close linkage between -455G, -148C and 448G or -455A, -148T and 448A, the correspondence was over 98%. There are no differences in the plasma fibrinogen levels of the three polymorphisms in two genotype groups. The fibrinogen molecular reactivity was significantly increased in cardiocerebral vascular disease and related with plasma fibrinogen level.
The three polymorphisms loci are strong linkage disequilibrium. There are no significant differences in the plasma fibrinogen levels of the three polymorphisms in two genotype groups. The frequencies of -455A, -148T, 448A alleles in myocardial infarction disease were apparently higher than that of health adults. It suggest that there was no association between beta-Fg gene -455G/A, -148C/T and 448G/A polymorphisms and plasma fibrinogen levels, but did in myocardial infarction disease. The fibrinogen molecular reactivity was significantly increased in cardiocerebral vascular disease and related with plasma fibrinogen level.
分析健康成年人、心肌梗死和脑梗死患者中β-纤维蛋白原(β-Fg)基因-455G/A、-148C/T和448G/A多态性、纤维蛋白原分子反应性及其与血浆纤维蛋白原水平的相关性。
采用限制性片段长度多态性(RFLP)分析β-Fg基因-455G/A、-148C/T和448G/A多态性。通过计算机辅助程序分析纤维蛋白原转化为纤维蛋白的动力学过程来分析纤维蛋白原分子反应性。采用Clauss法测定血浆纤维蛋白原水平。
健康成年人中-455A、-148T、448A等位基因频率分别为0.185、0.194和0.192,心肌梗死患者中分别为0.295、0.318和0.307,脑梗死患者中分别为0.177、0.193和0.182。心肌梗死患者中-455A、-148T、448A等位基因频率明显高于健康成年人。-455G、-148C与448G或-455A、-148T与448A之间存在紧密连锁,符合率超过98%。两个基因型组中三种多态性的血浆纤维蛋白原水平无差异。心脑血管疾病中纤维蛋白原分子反应性显著增加,且与血浆纤维蛋白原水平相关。
三个多态性位点存在强连锁不平衡。两个基因型组中三种多态性的血浆纤维蛋白原水平无显著差异。心肌梗死患者中-455A、-148T、448A等位基因频率明显高于健康成年人。提示β-Fg基因-455G/A、-148C/T和448G/A多态性与血浆纤维蛋白原水平无关联,但在心肌梗死疾病中有关联。心脑血管疾病中纤维蛋白原分子反应性显著增加,且与血浆纤维蛋白原水平相关。