美托洛尔对慢型克山病患者血浆B型利钠肽及心功能的影响

目的 探讨美托洛尔对慢型克山病患者血浆B型利钠肽(BNP)水平及心功能的影响.方法 7l例慢型克山病患者随机分为美托洛尔组和对照组,对照组给予地高辛、螺内酯和双氢克尿噻口服治疗,美托洛尔组在对照组治疗的基础上加用美托洛尔,疗程12周.观察两组治疗前后BNP水平变化及心功能改善情况.结果 美托洛尔组与对照组的临床总有效率分别为80.0%和58.3%(P<0.05),两组治疗后血浆BNP水平和Tei指数比较差异均有统计学意义(P<0.05),而两组左室射血数差异无统计学意义(P>0.05).结论 美托洛尔能明显降低慢型克山病患者BNP水平和Tei指数,改善患者心功能.     

克山病发病与谷胱甘肽过氧化物酶-1基因多态性的关系研究

Objective To assess the association of blood selenium and polymorphism of glutathione peroxidase-1 (GPx-1) genes in patients with Keshan Disease (KD) and provide genetic evidence for KD susceptibility.Methods The levels of whole blood selenium and the activity of GPx-1 were measured with spectrophotometric and enzymatic method among 71 KD patients and 290 controls (including 78 internal controls and 212 external controls).The genotype of GPx-1 at 198 site was analyzed by sequencing and PCRRFLP.The functions of two GPx-1 variants were studied by rat neonatal cardiomyocytes transfection and expression pLamid.Results Blood level of selenium in KD patients was (0.8 ±0.2) μmol/L,the internal controls' was (0.9 ±0.2) μmoL/L,and the external controls' was ( 1.2 ±0.2) μmol/L (F=4.888,P＜0.001 ).GPx-1 activity of KD patients was (73.0 ± 12.6) × 10-10 U/RBC, internal controls' was ( 80.9 ±9.2) × 10-10U/RBC,and external controls' was ( 115.8 ±21.1 ) × 10 -10U/RBC ( F =5.324,P ＜0.001 ).Those of KD patients were significantly lower than controls.The polymorphism (Pro198Leu) of GPx-1 were identified; the frequency of Pro198Leu of KD patients was 21.1% , the frequency of controls was 10.7%(χ2 =5.588 ,P =0.018).The level of blood selenium in variant subgroup( Pro198Leu or Leu198Leu) was(0.9 ± 0.2) μmoL/L, and its in non-variant subgroup was ( 1.1 ± 0.3 ) μmol/L ( t = 3.183, P ＜ 0.01 );The GPx-1 activity in variant subgroup was (86.1 ± 23.0 ) × 10-10U/RBC, and its in non-variant subgroup was ( 101.8 ± 25.9 ) × 10-10 U/RBC ( t = 5.784, P＜ 0.01 ) .Further analysis revealed a synergisticmultiplicative interaction between presence of GPx-1 codon198 alleles and low blood selenium level Overexpression of GPx-1 (198Leu) in rat cardiomyocytes caused 30% lower enzyme activity and less response to increasing concentrations of selenium than with over-expression of GPx-1 (198Pro).Conclusion Low blood selenium in carriers with the 198Leu-susceptible genotype of GPx-1 is associated with low GPx-1 activity,synergistic-multiplicative interaction was found between these two factors.And these two factors may increase the risk of KD.     

硒、谷胱甘肽过氧化物酶-1与地方性扩张型心肌病的交互关系

克山病是我国缺硒地区特有的地方性扩张型心肌病,病因至今未明.硒缺乏是主要的条件致病因子,但并不是惟一的致病因子.同样处在低硒环境下个体的克山病患病风险存在很大差异,提示病区个体可能存在遗传背景差异.本研究旨在筛选与克山病相关的GPx-1基因单核苷酸多态性位点,针对相关的基因位点进行深入的功能研究,以最终明确GPx-1基因多态性位点在克山病发病机制中的作用.     

134例有症状患者中64层螺旋CT检出冠心病的准确性:钙化的影响

背景:新型64层螺旋CT扫描下的血管造影可以在屏气时间较短和心率较快的情况下检出有症状患者的冠心病。作者旨在确定64层扫描是否可以克服轻至中度钙化的限制作用。方法:拟行常规冠状动脉造影的134例患者在3个月内施行多层螺旋CT下的血管造影。依照改良的Agatson公式将患者分为     

卵母细胞固定、染色及压片方法研究

目的:建立卵母细胞(单细胞)固定、染色及压片方法。方法:应用显微操作技术,在体视显微镜下通过液滴法移动、洗涤和抗体孵育卵母细胞。结果:通过点柱法压片的方法成功建立了卵母细胞(单细胞)固定、染色及压片方法。共固定卵母细胞58枚,其中1枚丢失,1枚破损,成功率96.55%。结论:此制片方法解决了卵母细胞在固定、染色及压片中容易丢失和碎裂的问题,从而使卵母细胞和胚胎的实验室研究变得较为简单有效。     

克山病发病与谷胱甘肽过氧化物酶-1基因多态性的关系研究

Objective To assess the association of blood selenium and polymorphism of glutathione peroxidase-1 (GPx-1) genes in patients with Keshan Disease (KD) and provide genetic evidence for KD susceptibility.Methods The levels of whole blood selenium and the activity of GPx-1 were measured with spectrophotometric and enzymatic method among 71 KD patients and 290 controls (including 78 internal controls and 212 external controls).The genotype of GPx-1 at 198 site was analyzed by sequencing and PCRRFLP.The functions of two GPx-1 variants were studied by rat neonatal cardiomyocytes transfection and expression pLamid.Results Blood level of selenium in KD patients was (0.8 ±0.2) μmol/L,the internal controls' was (0.9 ±0.2) μmoL/L,and the external controls' was ( 1.2 ±0.2) μmol/L (F=4.888,P＜0.001 ).GPx-1 activity of KD patients was (73.0 ± 12.6) × 10-10 U/RBC, internal controls' was ( 80.9 ±9.2) × 10-10U/RBC,and external controls' was ( 115.8 ±21.1 ) × 10 -10U/RBC ( F =5.324,P ＜0.001 ).Those of KD patients were significantly lower than controls.The polymorphism (Pro198Leu) of GPx-1 were identified; the frequency of Pro198Leu of KD patients was 21.1% , the frequency of controls was 10.7%(χ2 =5.588 ,P =0.018).The level of blood selenium in variant subgroup( Pro198Leu or Leu198Leu) was(0.9 ± 0.2) μmoL/L, and its in non-variant subgroup was ( 1.1 ± 0.3 ) μmol/L ( t = 3.183, P ＜ 0.01 );The GPx-1 activity in variant subgroup was (86.1 ± 23.0 ) × 10-10U/RBC, and its in non-variant subgroup was ( 101.8 ± 25.9 ) × 10-10 U/RBC ( t = 5.784, P＜ 0.01 ) .Further analysis revealed a synergisticmultiplicative interaction between presence of GPx-1 codon198 alleles and low blood selenium level Overexpression of GPx-1 (198Leu) in rat cardiomyocytes caused 30% lower enzyme activity and less response to increasing concentrations of selenium than with over-expression of GPx-1 (198Pro).Conclusion Low blood selenium in carriers with the 198Leu-susceptible genotype of GPx-1 is associated with low GPx-1 activity,synergistic-multiplicative interaction was found between these two factors.And these two factors may increase the risk of KD.     

试用临界慢化原理探讨常见未病状态——血糖失稳态

中医学使用阴平阳秘的相对平衡状态界定人的健康，即健康是人体这个开放复杂巨系统整体动态平衡的稳态。稳态失衡则进入狭义的未病状态，邪正相争，存在向愈与向疾的两种演化趋势，一旦扰动过强或干预不力，则系统持续失稳，突变形成疾病稳态。治未病理论作为一种重要的实践原则，贯穿中医预防、诊断、治疗、康复的临床过程始终，对于多种疾病未病人群的筛查与早期干预具有重要的指导意义。本文围绕生理意义巨大、病理影响广泛的血糖失稳态，详述其防治意义、筛查现状与干预方式，系统分析其作为多种重大疾病未病状态的临界慢化原理，阐释中医治未病方法论所蕴含的基于系统整体性与开放性的藏-象映射模型思维、基于系统动态发展的临界慢化模型思维，探讨基于中医四诊合参的未病状态识别与干预路径，以期为复杂性科学视域下的中医诊疗模式研究提供参考。