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作 者:汤珂珂[1] 高祖华[1] 邱夏桑[1] 颜勤明[1]
出 处:《心脑血管病防治》2015年第1期18-20,共3页CARDIO-CEREBROVASCULAR DISEASE PREVENTION AND TREATMENT
基 金:浙江省医药卫生科技计划项目(编号:2011KYA160);浙江省台州市科技计划项目(编号:11KY03)
摘 要:目的探讨CD4+CD28nullT细胞亚群在2型糖尿病动脉粥样硬化发生发展中的作用。方法根据彩色多普勒超声检查结果,将92例2型糖尿病患者分为颈动脉粥样硬化组与对照组,采用流式细胞仪检测分析颈动脉粥样硬化组和对照组外周血CD4+CD28nullT细胞亚群的表达情况,并分析其与年龄、C反应蛋白(CRP)、血糖、血脂、体质指数(BMI)、腰围、臀围、舒张压、收缩压的关系。结果颈动脉粥样硬化组CD4+CD28nullT细胞亚群的表达明显高于对照组,分别为(4.40±2.95)%和(3.04±2.20)%,差异有统计学意义(P<0.05)。CD4+CD28nullT细胞亚群的表达与年龄、CRP、糖化血红蛋白(Hb A1c)相关(r=0.20~0.25,P<0.05)。控制年龄和Hb A1c因素后,CD4+CD28nullT细胞亚群的表达与CRP仍相关(r=0.24,P<0.05)。结论 2型糖尿病动脉粥样硬化患者具有更高的CD4+CD28null T细胞表达。CD4+CD28nullT细胞亚群可能通过介导炎症反应影响2型糖尿病患者动脉粥样硬化的发生和发展。Objective To investigate the effect of CD4^+CD28^nullT cell subset on occurrence and progress of atherosclerosis in patients with type 2 diabetes. Methods 92 patients with type 2 diabetes were divided into the carotid atherosclerosis group and control group according to the detecting results by color doppler ultrasound. The expressions of CD4^+CD28^nullT cell subset in peripheral blood of the carotid atherosclerosis and control groups were detected by a flow cytometry. The relationships between the expression of CD4^+CD28^nullT cell subset and age,C react protein( CRP),blood glucose,blood lipid,body mass index( BMI),waist circumference,hip circumference,diastolic blood pressure,systolic blood pressure were also analyzed. Results The expression of CD4^+CD28^nullT cell subset of the carotid atherosclerosis group is significantly higher than that of the control group( 4. 40 ± 2. 95% vs. 3. 04 ± 2. 20%,P〈0. 05). The expressions of CD4^+CD28^nullT cell subset were correlated with age,CRP,Hemoglobin A1C( Hb A1c)( r- 0. 20 - 0. 25,P〈0. 05). After controlling the factors of age and Hb A1 c,the expression of CD4^+CD28^nullT cell subset was still relevant with CRP( r = 0. 24,P〈0. 05). Conclusions The type 2 diabetes patients with atherosclerosis have a higher expression of CD4^+CD28^nullT lymphocyte. CD4^+CD28^nullT cell subset may affect the occurrence and process of atherosclerosis via mediated inflammatory response in the patients with type 2 diabetes.
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