Determination of angiotensin I-converting enzyme activity in equine blood: lack of agreement between methods of analysis

Angiotensin-I converting enzyme (ACE) is a key regulator of blood pressure, electrolytes and fluid homeostasis through conversion of angiotensin I into angiotensin II. Recently, a genetic polymorphism of the ACE gene, which accounts for 47% of the variation of ACE activity in blood, has been advocated as a biomarker of athletic aptitude. Different methods of analysis and determination of ACE activity in plasma have been used in human and equine research without a consensus of a "gold standard" method. Different methods have often been used interchangeably or cited as being comparable in the existing literature; however, the actual agreement between assays has not been investigated. Therefore, in this study, we evaluated the level of agreement between three different assays using equine plasma obtained from 29 horses. Two spectrophotometric assays using Furylacryloyl-phenylalanyl-glycyl-glycine as substrate and one fluorimetric assay utilizing o-aminobenzoic acid-FRK-(Dnp)P-OH were employed. The results revealed that the measurements from the different assays were not in agreement, indicating that the methods should not be used interchangeably for measurement of equine ACE activity. Rather, a single method of analysis should be adopted to achieve comparable results and critical appraisal of the literature is needed when attempting to compare results obtained from different assays

Angiotensin-Converting Enzyme Gene Polymorphism in Patients with Coronary Artery Disease

Several genetic investigations have been attempted to elucidate the association of gene polymorphism of angiotensin-converting enzyme (ACE) in coronary artery disease. This study was conducted to investigate the role of gene polymorphism of ACE in patients with coronary artery disease. The study included fifty-six numbers of patients with atherosclerotic coronary artery disease where proven angiographically and fifty-six numbers of healthy individuals of sex matched as a control group. The patients and control group were subjected to routine investigations, assays like, serum cholesterol, triglycerides, high-density Lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C). Genomic DNA was extracted and analyzed for angiotensin-converting enzyme insertion/deletion polymorphism using polymerase chain reaction (PCR). When we compared the genotypes of patients with coronary artery disease and controls, it was observed that all three genotypes were not statistically different also no significant difference of alleles in ACE gene genotypes was found. Inpatient serum cholesterol, triglyceride and HDL-C (P <0.001, P <0.001 and P <0.001: respectively) showed a significant increase than the control group. In patients, LDL-C level was not more significant than controls. In the evaluated population, we conclude that the gene I/D polymorphism for ACE are not risk associated and may not be a useful marker for coronary artery disease

Angiotensin-converting enzyme gene insertion/deletion polymorphism in migraine patients

<p>Abstract</p> <p>Background</p> <p>The main objective of this study was to investigate the angiotensin converting enzyme (<it>ACE</it>) genotype as a possible risk factor for migraine (both with and without aura) compared to controls. We also wanted to examine whether a clinical response to an ACE inhibitor, lisinopril, or an angiotensin II receptor blocker, candesartan, in migraine prophylaxis was related to <it>ACE </it>genotype.</p> <p>Methods</p> <p>347 migraine patients aged 18–68 (155 migraine without aura (MoA), 187 migraine with aura (MwA) and 5 missing aura subgroup data) and 403 healthy non-migrainous controls > 40 years of age were included in the study. A polymerase chain reaction (PCR) was performed on the genomic DNA samples to obtain the <it>ACE </it>insertion (I)/deletion(D) polymorphisms.</p> <p>Results</p> <p>No significant differences between migraine patients and controls were found with regard to <it>ACE </it>genotype and allele distributions. Furthermore, there was no significant difference between the controls and the MwA or MoA subgroups.</p> <p>Conclusion</p> <p>In our sample there is no association between <it>ACE </it>genotype or allele frequency and migraine. In addition, <it>ACE </it>genotype in our experience did not predict the clinical response to lisinopril or candesartan used as migraine prophylactics.</p

Associations of insertion-deletion polymorphism of angiotensin-converting enzyme with the risk of preeclampsia development among pregnant women in Central Russia

The associations of the insertion-deletion angiotensin-converting enzyme (I/D ACE) genetic polymorphism with the risk of preeclampsia development were studie

Genetic determinants of survival

The human genome comprises some 20,000 genes, or 3 billion base pairs. Variation in this genetic sequence is common and some of these variants affect gene function or the protein transcribed from it. Human characteristics are determined by the interaction of the genome with environmental challenges, and differences between us thus result from variation in those challenges and in the genome itself. This is true of human susceptibility to disease, and survival from it. Genetic variation influences human behaviours which may predispose to health or disease; the risk of contracting an infectious disease, or of suffering diseases such as cancer or myocardial infarction; the development of complications; the response to any treatment administered; and thus the outcome of the disease state. Genetic studies can help shed light on the mechanisms which underpin disease processes, whilst perhaps suggesting ways in which treatment might be ‘personalised’, and novel therapeutic targets for drug development. More sophisticated approaches to such endeavours are required, given the failure to identify the bulk of gene variants of influence using conventional strategies

DNA sequences of Alu elements indicate a recent replacement of the human autosomal genetic complement

DNA sequences of neutral nuclear autosomal loci, compared across diverse human populations, provide a previously untapped perspective into the mode and tempo of the emergence of modern humans and a critical comparison with published clonally inherited mitochondrial DNA and Y chromosome measurements of human diversity. We obtained over 55 kilobases of sequence from three autosomal loci encompassing Alu repeats for representatives of diverse human populations as well as orthologous sequences for other hominoid species at one of these loci. Nucleotide diversity was exceedingly low. Most individuals and populations were identical. Only a single nucleotide difference distinguished presumed ancestral alleles from descendants. These results differ from those expected if alleles from divergent archaic populations were maintained through multiregional continuity. The observed virtual lack of sequence polymorphism is the signature of a recent single origin for modern humans, with general replacement of archaic populations

Impact of Angiotensin-Converting Enzyme Gene Polymorphism on Proteinuria and Arterial Hypertension

Proteinuria is the hallmark of renal disease. In essential hypertension the onset of de novo proteinuria is associated with faster rate of progression of disase. Some authors have suggested that the DD genotype of the angiotensin-convert- ing enzyme (ACE) gene would be an adverse renal prognosis factor. It may also have different effects on the reduction of proteinuria by ACE inhibitors in patients with proteinuria. Observations on the association between the ACE gene poly- morphism and hypertension have been inconsistent, which might be due to ethnic and geographical variations. In this study was to investigated the relationship between ACE gene polymorphism and antiproteinuric effect of ACE inhibitors (ramipril) and to evaluate the possible association between I/D polymorphism and hypertension. We recruited 66 hyper- tensive patients (male 42, female 24) with overt proteinuria (urinary protein excretion over 500 mg/day). Patients were classified into three groups in accordance with ACE genotypes (17 DD; 35 ID; 14 II). They were treated with ramipril and prospectively followed up for one year. Various clinical parameters including age, body mass index (BMI), 24-h urine protein, creatinine, creatinine clearance (Ccr), systolic and diastolic blood pressure (SBP and DBP), mean arterial pres- sure (MAP) were measured in the pre- and post-treatment periods. The ACE gene insertion/deletion(I/D) polymorphisms in intron 16 were determined by PCR. Results showed that there were no significant differences in the clinical parame- ters such as age, gender, serum creatinine, Ccr, SBP , DBP , MAP , and daily urinary excretion of protein among three groups (P>0.05). ID genotype patients were found to have lower BMI (p=0.031). ACE inhibition significantly reduced proteinuria in all genotype groups (p<0.05). The percentage reductions of 24-h urinary excretion of protein were signifi- cantly different between the genotype groups (p=0.042) and for DD genotype were significantly greater than in ID (79.2± 28.9% vs 49.2±64.8%, P=0.015). The slope of SBP was the main factor related to the slope of the percentage reduction of proteinuria, however, a significant negative correlation coefficient between these parameters was found (rs=–0.382, p= 0.002). We failed to find significant difference in outcomes of treatments with ACE inhibitor between male and female ac- cording the I/D polymorphism of the ACE gene. D allele in the ACE genotype could be a useful genetic marker with im- portant clinical, therapeutic and prognostic implications in recognizing patients with proteinuria that are at greater risk of renal damage