Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Do extremely old persons have a genetically favourable profile which has protected them from cardiovascular death? We have tried to answer this question by measuring DNA polymorphisms of selected cardiovascular risk indicators [factor VII, FVII (R/Q353, intron 7 (37bp)n, and -323ins10), beta fibrinogen (-455G/A), plasminogen activator inhibitor type 1, PAI-1 (-675(4G/5G)), tissue plasminogen activator, t-PA (intron 8 ins311), platelet receptor glycoprotein IIb/IIIa, GPIIb/IIIa (L/P33), prothrombin (20210G/A), methylene tetrahydrofolate reductase, MTHFR (A/V114), angiotensin converting enzyme, ACE (intron 16 ins287), and angiotensinogen (M/T235)]. Blood was collected from 187 unselected Danish centenarians, and 201 healthy Danish blood donors, aged 20-64 years (mean age 42 years). Genomic DNA was amplified using PCR and the genotype was determined by RFLP methods or allele-specific amplification followed by agarose gel electrophoresis. The frequencies of the high-risk alleles in centenarians were: for FVII R/Q353 0.91; for FVII intron 7 (37bp)n 0.67; for FVII-323 ins10 0.90; for fibrinogen 0.16; for PAI-1 0.52; for t-PA 0.59; for GPIIb/IIIa 0.16; for prothrombin 0.008; for MTHFR 0.33; for ACE 0.52; and for angiotensinogen 0.36. Comparable frequencies were observed in the blood donors. Subgroup analysis of men and women separately gave similar results. The genotype frequencies in the centenarians and the blood donors were similar for all polymorphisms, and this study suggests that common variations in genes associated with cardiovascular risk do not contribute significantly to longevity.
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PMID:Longevity is independent of common variations in genes associated with cardiovascular risk. 1049 71

Complications of pregnancy have been found to be related with thrombophilic polymorphisms that explain about 30% of obstetric complications. We evaluated the angiotensin converting enzyme (ACE) and the angiotensin type 1 receptor (AT1R) gene polymorphisms in the renin-angiotensin system (RAS) as possible risk factors for fetal loss. Fifty-nine women with a history of three or more first-trimester fetal losses and 70 healthy women with a history of normal pregnancies were enrolled in this study. Thrombophilic factors, ACE insertion/deletion (I/D) and AT1R A1166C polymorphisms, prothrombin G20210A and factor V Leiden mutations were analyzed. At univariate and multivariate analysis, a significant association between ACE DD and AT1R CC genotype and fetal loss was observed. The effect of the ACE DD genotype on the risk of fetal loss was higher in AT1R C allele carriers. The prevalence of hyperhomocysteinemia (Hcy) (defined as baseline plasma levels higher than the 95% percentile; cut-off, 10.5 micromol/l per l) was significantly higher in women with fetal loss, and an association between Hcy and fetal loss was detected. All patients showed normal antithrombin, protein C, protein S, and plasminogen activator inhibitor-1 (PAI-1) values. The presence of one risk factor not associated with others was found in 33 out of 59 patients (56%); ACE DD genotype was the most prevalent risk factor. Our results identify new possible predictive markers for fetal loss in RAS polymorphisms and Hcy. Large-scale studies are warranted to attribute clinical relevance to these polymorphisms as risk factors for complicated pregnancies.
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PMID:Angiotensin-converting enzyme DD genotype, angiotensin type 1 receptor CC genotype, and hyperhomocysteinemia increase first-trimester fetal-loss susceptibility. 1108 86

In June, 1997, we initiated a prospective study to analyze the effect of granulocyte colony-stimulating factor (G-CSF) on coagulation system in peripheral blood stem cells (PBSC) donors following G-CSF administration. Since, 25 consecutively healthy donors received G-CSF (filgrastim) to mobilize and collect PBSC and 20 donors were finally included in the study. Blood samples were collected immediately before starting G-CSF and prior to PBSC collection to analyze the following parameters: prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen, hypercoagulability markers (D-dimer, TAT complex, F1 + 2), natural anticoagulants (antithrombin, protein C, protein S), endothelial activation markers [von Willebrand factor antigen (vWF:Ag) and angiotensin converting enzyme (ACE)], and resistance to activated protein C. We found a significant increase in F1 + 2 and D-dimer while a significant decrease of antithrombin and protein C activity was evidenced. Regarding endothelial cell activation markers, a significant increase of vWF:Ag with a slightly significant decrease of ACE were also observed. Therefore, in PBSC donors receiving G-CSF our results reveal activation of both coagulation and endothelial cells that could favor the developing of thrombotic events. In consequence, a careful monitoring should be considered in those cases with risk factors for thrombosis.
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PMID:Induction of a hypercoagulability state and endothelial cell activation by granulocyte colony-stimulating factor in peripheral blood stem cell donors. 1220 56

Hepatocellular carcinoma (HCC) is one of the most important medical problems facing the Asian-Pacific region, where the prevalence of chronic hepatitis B and C is so high. Every year, we have approximately 500 admissions to our department due to this malignancy. It is of utmost importance that we have efficient screening, diagnosis and treatment. Over the past several years, there has been steady improvement in elucidating the super-high risk group for HCC, and in the management of these patients. I discuss how effectively we can screen patients by using three tests, conventional AFP, AFP-L3 (lectin fraction) and DCP (des-gamma-carboxy-prothrombin). With these tests we can detect HCC as small as 10 mm. In addition, imaging technology including CT-angiography can effectively pick up small cancer nodules. However, they are not always readily available in all Asian countries. Thus, diagnostic procedures and treatment methods can be modified in each country depending on the situation. One such treatment modality is the percutaneous therapy. The recent introduction of radiofrequency ablation (RFA) has dramatically changed our daily clinical practice. The time needed to treat cancer nodules of 2 to 3 cm in size has been reduced from 1 month or longer with ethanol injection to less than a week with RFA. However, the most important issue is to prevent infection and progression from chronic hepatitis to HCC. The recent introduction of improved antiviral therapy makes us feel optimistically that we might eventually have a comprehensive strategy for HCC in the region where it is most needed.
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PMID:Resolution of liver cirrhosis and prevention of hepatocellular carcinoma by interferon therapy against chronic hepatitis C. 1279 82

The deletion/deletion (D/D) genotype of the angiotensin converting enzyme (ACE) has been purported to be a risk for post-operative thrombosis.This D/D genotype has not been evaluated as a risk factor for idiopathic venous thromboembolism (VTE). The primary objective of the present study was to determine whether the D/D genotype of ACE is independently associated with the occurrence of idiopathic venous thromboembolic disease. We prospectively enrolled consecutive patients with at least one objectively confirmed idiopathic VTE. Friends of cases were recruited as controls and matched to cases by sex, ethnicity, and age. Patients were tested for the ACE I/D polymorphism in addition to factor V Leiden, prothrombin G20210A, and factor VIII levels. Three hundred cases and 300 controls were enrolled; 97% were Caucasian. There were 148 females and 152 males in each group with a mean age of 56.21 years (SD = 15.33). The ACE D/D genotype was present in 25.3% of cases and 32.4% of controls for an adjusted odds ratio of 0.66 (95% CI = 0.433 to 0.997). We can conclude that the ACE D/D genotype is protective against idiopathic venous thromboembolism.
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PMID:The ACE D/D genotype is protective against the development of idiopathic deep vein thrombosis and pulmonary embolism. 1459 66

Whether hormone replacement therapy (HRT) is beneficial for coronary heart disease (CHD) is controversial. We hypothesized that continuous combined transdermal HRT may have benefits on CHD risk markers without the potential adverse effects seen with certain other HRT regimens. Sixty apparently healthy postmenopausal women, aged 40-65 years, entered a prospective, double-blind, randomized, placebo-controlled clinical trial; 55 women completed the 6-month study. Women received either transdermal oestradiol 17beta 0.05 mg and norethisterone acetate 0.125 mg daily, or identical placebo. Circulating markers of vascular function and remodelling, forearm blood flow, lipids and lipoproteins, glucose and insulin, and haemostatic safety parameters were measured at baseline and after treatment. Compared with placebo after 6 months, HRT administration resulted in decreased E-selectin (P < 0.01), and angiotensin-converting-enzyme (ACE; P = 0.05). Cholesterol (P < 0.05), low-density lipoproteins (LDL; P < 0.05), high-density lipoprotein3 (HDL3; P < 0.05) and apolipoproteins AII (P < 0.05) and B (P < 0.05), and fasting insulin (P < 0.05) also decreased in the HRT group. Factor VII coagulation activity decreased (P < 0.01) and plasminogen activator inhibitor-1 and fibrin D-dimer increased (P < 0.05) in the HRT group, whilst prothrombin fragment 1 + 2 (P < 0.05) decreased, more so in the placebo group. There were no changes in matrix metalloproteinase (MMP)-2, or in LDL particle size. This transdermal HRT had beneficial effects on vascular function and CHD risk markers.
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PMID:Randomized trial of effect of transdermal continuous combined hormone replacement therapy on cardiovascular risk markers. 1500 73

The aim of this study was to evaluate prognostic factors after the recurrence of hepatocellular carcinoma (HCC) in patients who had undergone hepatic resection. We used univariate and multivariate retrospective analyses of 29 clinicopathologic factors in 143 patients with recurrent HCC. Patients were classified into four groups according to the positivity of tumor markers at the time of recurrence. Survival rates and prognostic factors were then compared among the four groups. Multivariate analysis revealed four independent prognostic factors at recurrence: albumin level < 3.5 g/dl ( p = 0.0003), period until recurrence </= 1 year ( p = 0.0004), positive status of alpha-fetoprotein and des-gamma-carboxy prothrombin (AFP+/DCP+) ( p < 0.0001), and portal vein invasion ( p < 0.0001). Among groups with varying status of AFP/DCP, the survival rate in patients with AFP+/DCP+ at recurrence was significantly lower than those in the other three groups (+/+ 15.9% vs. +/- 47.2%, -/+ 44.8%, or -/- 61.1% at 3 years: p < 0.05). The AFP+/DCP+ group also had significantly higher rates of the recurrence appearing </= 1 year after operation (+/+ 68.3% vs. +/- 45.2%, -/+ 41.9%, or -/- 32.5%: p = 0.0108), extrahepatic recurrence (29.3% vs. 6.5%, 9.7%, or 5.0%: p = 0.0026), and no treatment at recurrence (29.3% vs. 9.7%, 9.7%, or 5.0%: p = 0.0115). These results indicate that the tumor markers AFP and DCP are significant prognostic factors for recurrent HCC, and their monitoring is essential for improving the prognosis after recurrence.
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PMID:Positive status of alpha-fetoprotein and des-gamma-carboxy prothrombin: important prognostic factor for recurrent hepatocellular carcinoma. 1518

During the last years several genetic markers have appeared which were extensively studied for their clinical consequences and impact. Therefore, we developed 14 new genetic tests using the TaqMan technology. The new test systems detect the alpha1-antitrypsin, ACE, apolipoprotein B-100, apolipoprotein E, factor V Leiden, prothrombin, HFE, MTHFR, COL1A1, VDR and HLA-B27 mutations. These new kits were compared to the established endonuclease restriction digestion and flow cytometry, respectively. The results showed, that the allelic discrimination assays (TaqMan method) were in 100% concordance with the formerly used digestion method. Flow cytometry revealed a lower specificity in contrast to the TaqMan PCR system. Thus, it could be demonstrated that the new TaqMan assays are robust, rapid and automated methods for high throughput applications which avoid time consuming (and therefore expensive) and difficult post-PCR steps.
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PMID:A highly reproducible and economically competitive SNP analysis of several well characterized human mutations. 1520 39

Acute thrombotic complications remain a constant, proportionally increasing complication before and after renal transplantation. We sought to investigate predictors for a prothrombotic state that increased the risk of vascular access thrombosis, among chronic renal failure patients during the waiting period prior to cadaveric renal transplantation. Chronic renal failure patients awaiting cadaveric renal transplantation and followed between January 2002 and January 2005 were included in this study. The 109 subjects including, 61 females and 48 males of mean age: 47.4 +/- 12.9 years; There were 36 continuous ambulatory peritoneal dialysis and 73 hemodialysis patients. Serum albumin, prealbumin, CRP, d-dimer, fibrinogen, antithrombin III, anticardiolipin antibodies (immunoglobulins G and M), homocystein, vitamin B12, folic acid, total cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and total platelet count were measured in each patient. Factor V Leiden, prothrombin 20210, ACE and MTHFR gene mutations were studied in all patients. Vascular Access thrombosis was detected in 62 patients. During follow-up 31 of 109 patients died. Vascular access thrombosis occurred in 78 patients who survived and 31 who died. The patients who died showed a significantly higher rate of thrombosis than those who survived (P = .003, OR: 4.61, CI: 1.70 to 12.50). Among the above biochemical risk factors, multiple regression analysis and backward logistic analysis revealed that d-dimer was the strongest biochemical predictor of thrombosis (P = .013, RR: 17.8). Upon evaluation of genetic risk factors, only factor V Leiden mutation was related to vascular access thrombosis (P = .001). In conclusion, the presence of vascular access thrombosis is a risk factor for mortality during the waiting period for cadaveric renal transplantation. As patients with factor V Leiden mutation or high serum d-dimer levels are at high risk for vascular access thrombosis, we recommend close monitorizing of these patients and use of anticoagulant therapy during the waiting period prior to renal transplantation.
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PMID:Predictors of vascular access thrombosis among patients on the cadaveric renal transplantation waiting list. 1654 34

This study compared the antithrombotic effect of plasma angiotensin converting enzyme inhibitors (ACE-Is): captopril (CAP), enalapril (ENA) and tissue ACE-Is: perindopril (PER), quinapril (QUIN) in experimental venous and arterial thrombosis. Normotensive Wistar rats were treated p.o. with CAP (75 mg/kg), ENA (20 mg/kg), PER (2 mg/kg) and QUIN (3 mg/kg) for 10 days. The influence of ACE-Is on coagulation and fibrinolytic systems as well as platelet function was evaluated. The hypotensive effect of ACE-Is was equal in all groups. QUIN maintained the final carotid blood flow at the highest value in comparison to PER and plasma ACE-Is. The arterial thrombus weight was reduced in PER and QUIN groups while venous thrombus weight was also reduced after CAP. Tissue and plasma ACE-Is caused the inhibition of platelet adhesion and aggregation. A reduction of fibrin generation, prolongation of prothrombin time (PT), activated partial thromboplastin time (APTT) and shortening of euglobulin clot lysis time (ECLT) were observed after PER and QUIN treatment. In conclusion, given in equipotent hypotensive doses, tissue ACE-Is exerted more pronounced antithrombotic effect than plasma ACE-Is in experimental thrombosis. The differences between tissue and plasma ACE-Is in terms of their more pronounced inhibition of experimental thrombosis may be related to the intensified activation of fibrinolysis and inhibition of coagulation.
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PMID:Antithrombotic effect of tissue and plasma type angiotensin converting enzyme inhibitors in experimental thrombosis in rats. 1684 28


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