血管紧张素转换酶固相化方法的选择

分别采用琼脂包埋法、卵清包埋法、海藻酸钙包埋法、明胶-戊二醛包埋法、溴化氰活化连接法和苯甲磺酰氯结合方法对血管紧张素转换酶进行固相化研究,发现苯甲磺酰氯结合法用于血管紧张素转换酶固相化效果最好。此实验是在低水活度条件下,利用苯甲磺酰氯在丙酮和吡啶存在的条件下活化Sepharose CL-4B凝胶侧链基团上的羟基,形成具有高反应活性的苯甲磺酰基团,在pH7.8的0.2mol/L HEPES-HCl缓冲系统中,4℃反应12h,将酶与凝胶连接在一起。25mg ACE与5g活化琼脂糖凝胶在这种条件下反应,所得固相酶活力为10.86U/mg,蛋白固相率达到66%,酶活力固相率为53.3%。固相酶4℃保存3个月,活力剩余80%,20℃保存1个月酶活残留61%。同样条件下,溶液酶活力分别只剩余62%和19%,由此可见血管紧张素转换酶经固相化后稳定性明显提高。     

血管紧张素转移酶紫外分光光度法的方法学评价

目的初步评价血管紧张素转移酶检测试剂盒性能。方法依据临床和实验室标准协会颁布的《定量临床检验方法的初步评价,批准指南第2版（EP10-A2）》提供的方法,按特定的顺序连续测定低、中、高浓度的质控品5d,对该试剂盒检测方法的性能进行初步评价。结果血管紧张素转移酶低、中、高浓度的质控血清的靶值分别为49、89.5、130U/L时,按特定的顺序连续测定5d,没有离群值。线性回归方程为y=0.879x＋8.45,相关系数为0.9964;绝对偏差分别是0.64、1.26、-9.6U/L;总不精密度（CV%）分别为4.39%、2.26%、1.39%。结论血管紧张素转移酶检测试剂盒检测方法的线性、总变异和抗交叉污染能力均达到EP10-A2文件的标准,符合临床应用要求。高值的偏差提示超出可接受范围,需要进一步进行评估。     

西藏藏族人群血管紧张素转换酶基因多态性分布

目的:探讨西藏拉萨、那曲地区藏族健康人群血管紧张素转换酶(ACE)基因第16内含子287bpAlu顺序插入/缺失(I/D)多态性分布。方法:采用聚合酶链反应(PCR)方法检测ACE基因型。结果:76例拉萨藏族人ACE基因型频率分别为Ⅱ=0．395,ID=0．316,DD=0．289,等位基因频率分别为Ⅰ=0．553,D=0．447。81例那曲藏族人ACE基因型频率分别为Ⅱ=0．346,ID=0．444,DD=0．210,等位基因频率分别为Ⅰ=0．568,D=0．432。结论:拉萨、那曲地区藏族人ACE基因型及等位基因频率分布无显著差异;西藏藏族与英国白人和美国黑人相比基因型及等位基因频率均存在显著性差异,但与韩国人及日本人相似。     

血管紧张素转换酶基因多态性与慢性阻塞性肺病易感性的关系

探讨ACE基因插入 (insertion ,I)与缺失 (deletion ,D)多态性对COPD易感性、气道重构和肺功能损害程度的影响。从外周血白细胞中提取人类基因组DNA ,应用血管紧张素转换酶 (ACE)基因第 16内含子多态区两侧序列作为引物 ,采用PCR方法测定 12 2例COPD患者、15 9例健康人的ACE基因型。用多元线性逐步回归分析纠正性别、年龄等影响因素后确定独立危险因子。COPD组中DD基因型的分布频率显著高于正常对照组 (分别为 0 4 7、0 16 ,P<0 0 5 ) ;D等位基因频率也高 (分别为 0 6 2、0 4 3,P <0 0 5 ) ;DD型COPD患者肺通气功能损害较II型者为重 (P <0 0 5 )。ACE基因D型纯合子可能与COPD的遗传易感性相关 ,DD型基因可能是COPD发病新的独立危险因素。     

血管紧张素原及血管紧张素转化酶基因多态性与高血压之间的关系

目的 研究血管紧张素原基因（ａｎｇｉｏｔｅｎｓｉｎｏｇｅｎ,ＡＧＴ）第２外显子Ｍ２３５Ｔ等位基因的变异及血管紧张素转换酶（ａｎｇｉｏｔｅｎｓｉｎ ｃｏｎｖｅｒｔｉｎｇ ｅｎｚｙｍｅ,ＡＣＥ）基因多态性、在中国正常人群及原发性高血压（ｅｓｓｅｎｔｉａｌ ｈｙｐｅｒｔｅｎｓｉｏｎ,ＥＨ）患者中的频率分布,分析基因在ＥＨ中的发病作用。方法 应用多聚酶链反应结合限制性酶切方法,对９５例健康体检者和８７例Ｅ     

放免法同时测定糜酶转基因小鼠心脏中血管紧张素转换酶及糜酶样活性

为研究糜酶的功能,本文利用蛋白酶抑制剂Lisinopril、Aprotinin及EDTA结合放射免疫分析的方法同时测定了糜酶转基因小鼠心脏组织中血管紧张素转换酶（angiotensinconvertingenzyme,ACE）及糜酶样活性。结果显示转基因小鼠心脏组织中康酶比活力（0．274±0．071U／mg蛋白）较对照（0.152±0.021U／mg蛋白）显著升高,而ACE比活力不变（分别为0.172±0．029U／mg蛋白和0．177±0．019U／mg蛋白）。同时测定出转基因小鼠心脏局部血管紧张素Ⅱ（angiotensinⅡ,AngⅡ）含量（1984±184pg／g心脏组织）为对照（568±88pg／g心脏组织）的3倍。表明糜酶转基因小鼠心脏中可表达糜酶且糜酶能催化AngⅡ的生成,而蛋白酶抑制剂结合放免分析是一种快速、灵敏的检测ACE及糜酶样活性的方法。     

Monoclonal antibodies to small-cell carcinoma of the human lung

Laboratory of Immunochemistry, Research Institute of Carcinogenesis, All-Union Oncologic Scientific Center, Academy of Medical Sciences of the USSR. Cellular Immunology Group, Institute of Experimental Cardiology, All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. N. Smirnov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 9, pp. 282–285, September, 1991.     

非小细胞肺癌合并肺部感染患者组织中血管紧张素转换酶2的表达及机制

目的:探讨血管紧张素转换酶2(ACE2)在非小细胞肺癌(NSCLC)合并肺部感染的表达及作用.方法:2017年12月至2019年12月来宁夏医科大学总医院就诊的NSCLC患者纳入此次研究.患者分为NSCLC组(病理诊断为NSCLC,临床和影像学诊断不合并肺部感染)和合并感染组(病理诊断为NSCLC,临床和影像学诊断合并...     

血管紧张素转换酶基因插入/缺失多态性在人群中的分布及其与原发性高血压的关系

目的　研究血管紧张素转换酶 (angiotensin converting enzyme,ACE)基因 I/ D多态性在人群中的分布特征及其与原发性高血压的关系。方法　应用 PCR方法对 2 966名开滦矿务局职工进行 ACEI/ D基因型检测 ,并分析比较。结果　研究人群中 II、ID、DD基因型分布频率分别为 41.5%、3 8.4%、2 0 .1% ,I、D等位基因分布频率分别为 60 .7%和 3 9.3 %。ACE DD基因型在高血压组 (13 0 8例 )和对照组(1658名 )的频率分别为 18.9%和 2 1.0 % ,差异无显著性 (P>0 .0 5) ,按年龄及性别分层后差异也无显著性(P>0 .0 5)。DD基因型及 D等位基因分布频率有随年龄的增长而下降的趋势 (P<0 .0 0 1)。结论　 ACE I/D多态性与原发性高血压无关 ,基因型及等位基因的分布因年龄不同而不同 ,并提示具有 DD基因型特征的人群早期死亡危险的增加     

血管紧张素转换酶2研究进展

肾素-血管紧张素系统(renin-angiotensin sys-em,RAS)是一个非常古老而复杂的调节系统,低等生物如酵母菌即有完整的RAS。在哺乳类动物,RAS不仅对水盐代谢、维持血压稳定起重要作用,而且还是心血管、泌尿、生殖等系统发育和功能调节的一个重要系统;在炎症反应、损伤的修复、愈合及造血等病理生理过程中亦起重要作用。血管紧张素转换酶(angiotensin convertingenzyme,ACE)是血管紧张素合成主要的限速酶,是RAS的枢纽。随研究的不断深入,发现RAS的复杂程度远远超出人们的想象,尽管对它的研究已超过了100年,但对RAS的认识才刚刚开始。20…     

Association of angiotensin I‐converting enzyme gene polymorphisms with aspirin intolerance in asthmatics

Background Aspirin‐intolerant asthma (AIA) refers to the development of bronchoconstriction in asthmatic individuals following the ingestion of aspirin or other non‐steroidal anti‐inflammatory drugs (NSAIDs). Angiotensin I‐converting enzyme (ACE), a membrane‐bound peptidase present in the lung, plays a pivotal role in the metabolism of the endogenous peptides involved in the pathogenesis of asthma. Methods We screened a Korean asthma cohort (581 asthmatics including 81 aspirin‐intolerant asthmatics and 231 aspirin‐tolerant asthmatics, and 181 normal controls) for four single nucleotide polymorphisms (SNPs; ?262 A>T and ?115 T>C in the 5′‐flanking region and +5467 T>C [Pro450Pro] and+11860 A>G [Thr776Thr] in the coding region) and one ins/del (+21288 CT) in the ACE gene. Results None of the SNPs or haplotypes showed any association with the development of asthma, but they were significantly associated with the risk of AIA. Logistic regression indicated that the frequency of the rare alleles of ?262 A>T and ?115 T>C was higher in subjects with AIA than in subjects with aspirin‐tolerant asthma (ATA) (P=0.003–0.01, P ^corr=0.015–0.05). Subjects homozygous for the rare alleles of ?262 A>T and ?115 T>C showed a greater decline in forced expiratory volume in 1 s (FEV₁) after aspirin provocation than those homozygous for the common alleles (P<0.05). A luciferase reporter assay indicated that ACE promoters containing the rare ?262 A>T allele possessed lower activity than did those containing the common allele (P=0.009). In addition, ACE promoters bearing the rare ?115 T>C allele had no luciferase activity. DNA–protein binding assays revealed a band containing the ACE promoter region (including ?262 A) and a protein complex. Conclusion The ?262 A>T polymorphism in the promoter of the ACE gene is associated with AIA, and the rare allele of ?262 A>T may confer aspirin hypersensitivity via the down‐regulation of ACE expression.     

新疆哈萨克族隔离群血管紧张素转换酶基因I/D多态性与高血压病的关系

目的 探讨哈萨克族人群血管紧张素转换酶(angiotensin converting enzyme,ACE)基因第16内含子中的插入／缺失(insertion／deletion，I／D)多态性是否为高血压病(essential hypertension，EH)的遗传易患因素。方法 应用聚合酶链反应检测了新疆巴里坤县201例哈萨克族高血压病患者和151名正常人的ACE基因16内含子I／D多态性。结果 哈萨克族正常人群及高血压患者的ACE基因I／D多态性DD、ID、Ⅱ基因型频率分布分别为0．17、0．43、0．40和0．18、0．52、0．30，D和I等位基因分布频率分别为0．39和0．61和0．44、0．56，符合Hardy-Weinberg平衡。群体相关分析结果表明，ACE基因的D及I等位基因分布在高血压病组及正常血压组的差异无显著性(x^2＝1．98，P＝0.16)；基因型频率之间差异也无显著性(x^2＝4．0，P＝0．14)。结论 ACE基因16内含子I／D多态性可能与新疆巴里坤哈萨克族高血压病无关。     

α-内收蛋白基因、血管紧张素转换酶基因多态性与盐敏感性高血压及其早期肾损害的相关性

目的 探讨α-内收蛋白(α-adducin)基因G460T和血管紧张素转换酶(angiotensin converting enzyme,AcE)基因插入或缺失(insertion/detetion,I/D)多态性与汉族盐敏感性高血压(salt-sensitive hypertension,SSHT)及早期肾损害的关系.方法 用改良的Sullivan's法(急性口服盐水负荷试验)将200例原发性高血压(essential hypertension,EH)患者分为盐敏感109例和非盐敏感91例,用PCR检测ACE基因I/D多态性基因型,聚合酶链反应-限制性片段长度多态性方法检测α-adducin基因型,用放射免疫法检测晨尿微量白蛋白.结果 (1)EH组的α-adducin基因TT型频率显著高于健康对照组(200名)(P＜0.05),而EH组和对照组ACE I/D基因型分布差异无统计学意义(P＞0.05);盐敏感组的α-adducin基因TT型、α-adducin基因TT+ACE Ⅱ型频率显著高于非盐敏感组(P＜0.05).(2)盐敏感组尿微量白蛋白/尿肌酐显著高于非盐敏感组(P＜0.05);盐敏感组的ACE Ⅱ型尿微量白蛋白/尿肌酐显著高于ID、DD型(P＜0.05),α-adducin基因TT型尿微量白蛋白/尿肌酐显著高于GT、GG型(P＜0.05),α-adduein基因TT+ACE基因Ⅱ型尿微量自蛋白/尿肌酐显著高于其它基因组合型(P＜0.05).结论 α-adducin基因TT基因型或与ACE基因Ⅱ型协同可能是SSHT的遗传标志之一,可能是SSHT早期肾损害的遗传易感因素.     

Effect of angiotensin converting enzyme gene I/D polymorphism in South Indian children with nephrotic syndrome

Nephrotic syndrome is one of the most common childhood kidney diseases. It is mostly found in the age group of 2 to 8 years. Around 10%–15% of nephrotic syndrome cases are non-responders of steroid treatment (SRNS). Angiotensin converting enzyme (ACE) (I/D) gene association studies are important for detecting kidney disease and herein we assessed the association of ACE (I/D) polymorphism with nephrotic syndrome in South Indian children. We recruited 260 nephrotic syndrome (162 boys and 98 girls) and 218 (140 boys and 78 girls) control subjects. ACE I/D polymorphism was analyzed by PCR using genotype allele specific primers. In ACE (I/D), we did not find significant association for the ungrouped data of nephrotic syndrome children and the control subjects. Kidney biopsies were done in 86 nephrotic syndrome cases (minimal change disease, n = 51; focal segmental glomerulosclerosis, n = 27; diffuse mesangial proliferation, n = 8). We segregated them into the minimal change disease / focal segmental glomerulosclerosis groups and observed that the ACE 'D' allele was identified with borderline significance in cases of focal segmental glomerulosclerosis and the 'Ⅰ' allele was assessed as having very weak association in cases of minimal change disease. 'Ⅱ' genotype was weakly associated with minimal change disease. Gender specific analysis revealed weak association of 'ID' genotype with female nephrotic syndrome in females. Dominant expression of DD genotype was observed in males with nephrotic syndrome. Our finding indicated that ACE (I/D) has moderate association with focal segmental glomerulosclerosis. However, due to the limited number of biopsy proven focal segmental glomerulosclerosis subjects enrolled, further studies are required to confirm these results.     

Renal hypertension following aortic constriction is abolished by angiotensin II converting enzyme inhibitor,but not by low-salt diet

This study evaluates the role of different sodium intakes and the role of angiotensin II in the development and the maintenance of renovascular hypertension in rats with constriction of the aorta proximal to the renal arteries. The rats were studied 3 weeks after surgery when the hypertension was well established. Glomerular filtration rate was decreased and filtration fraction was increased in rats with proximal aortic constriction. Low and high salt intakes had no effect on glomerular filtration and filtration fraction. Treatment with angiotensin II converting enzyme inhibitor increased the glomerular filtration rate and reduced the filtration fraction in rats with proximal aortic constriction to the same levels as in control rats. Serum levels of angiotensin II were about the same in rats with proximal aortic constriction as in control rats.     

Monoclonal antibodies to the β-subunit of human chorionic gonadotrophin

Research Institute of Human Morphology, Academy of Medical Sciences of the USSR. Research Institute of Clinical Oncology, All-Union Oncologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. P. Avtsyn.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 106, No. 12, pp. 693–695, December, 1988.