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)

This review compares the clinical usefulness of immunological methods for the detection of structural components and metabolites of bacteria and fungi. Bacterial antigens (especially those of Mycobacterium, Neisseria, Staphylococcus aureus, Yersinia enterocolitica, Escherichia coli, Salmonella, Chlamydia, and Brucella) are best detected by enzyme-linked immunosorbent assay. Methods involving antibodies are more expensive and are effective only when performed in series. The detection of antibodies that recognize S aureus teichoic acid merely confirms the presence of a metastatic complication. Tissue invasion by Candida albicans is not yet reliably detectable by the presence of a specific antigen. Simple, but not completely reliable methods are available such as the latex test for mannans detection and/or agglutination with liposomes for detecting 48-kDa cytoplasmic protein antigen and an assay for detecting enolase antigen. A latex agglutination test has also been developed for the mannans antigen of Aspergillus and for Cryptococcus neoformans capsular polysaccharide; the latter test is more cost effective. The sensitivity of both tests is improved by serial assays. A negative finding with hemagglutination-based antibody tests rules out C albicans infection, and titers of 1/640 or higher have been associated with disseminated infection by Aspergillus. Concentrations of C albicans blastopore antigen antibodies higher than 400 IU/ml can be seen in disseminated candidiasis. High concentrations of endotoxin are indicative of imminent septic shock. Some biological indicators (C reactive protein, angiotensin converting enzyme, fibronectin, elastase-alpha 1-antitrypsin complex, tumor necrosis factor and interleukin-6) have been used to rule out a bacterial cause of fever.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunological methods for the detection of structural components and metabolites of bacteria and fungi in blood. 821 14

Several studies on disease and treatment effects on neurohormones have been conducted with small numbers of patients, using one blood sample as representative of their states. The aim of this study was to assess the within-patient variability of plasma concentrations of several hormones and cytokines of recent interest, in patients with moderate heart failure and controlled stable background therapy over 3 weeks. Blood for neurohormone and cytokine assays was sampled in duplicate from 18 patients with moderate heart failure. After an initial visit, the patients were kept on stable therapy until the second blood sampling 21 +/- 3 days later. The plasma concentrations of several neurohormones (endothelin, renin, angiotensin II, aldosterone, norepinephrine) and cytokines (interleukin-6 (IL-6), interleukin-13 (IL-13), ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF) and soluble receptor type I of tumour necrosis factor-alpha, (sTNF-RI) were measured with immunochemical methods. Some cytokines (IL-13, CNTF and LIF) were not detected. Despite clinically satisfactory ACE inhibition, circulating angiotensin II and aldosterone levels were still elevated in some patients, suggesting aldosterone escape. The between-visit agreement of plasma concentrations measured in duplicate was less than 35% for all circulating factors, except renin which showed a higher variability throughout the 3-week study period.
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PMID:Within-patient variability of hormone and cytokine concentrations in heart failure. 960 70

During end-stage heart failure, plasma levels of interleukin-6 (IL6) are elevated. This cytokine exerts a negative inotropic influence on the myocardium. The production site of IL6 is unclear. We examined the hypothesis that IL6 in end-stage heart-failure patients is produced in the myocardium itself and is differentially regulated according to etiology. Cardiac tissue was obtained from 27 patients (idiopathic dilated cardiomyopathy, (DCM) 9/6 m/f, age 46 +/- 14 y; ischemic cardiomyopathy (ICM), 11/1 m/f, age 55 +/- 8 y) at the time of transplantation. The tissue was subjected to IL6 Northern-blot analysis. Signals were quantified by densitometric scanning after normalization to G3 PDH mRNA. Data were compared by Mann-Whitney test between DCM and ICM patients, divided by chamber origin. IL6 transcripts were found in all patients. In DCM, left-ventricular IL6 mRNA expression was higher than in ICM (p = 0.006). Median right-ventricular as well as left- and right-atrial IL6 mRNA expression was not significantly different in both groups. In summary, in end-stage heart failure, IL6 mRNA is consistently expressed in the myocardium. Left-ventricular expression is higher in DCM than in ICM. These data support the concept of a potentially reversible inflammatory component in the etiology of DCM which is more pronounced than in patients with ICM of comparable clinical severity.
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PMID:Left-ventricular expression of interleukin-6 messenger-RNA higher in idiopathic dilated than in ischemic cardiomyopathy. 977 95

Heart failure is a common and increasing public problem. Neurohormonal activation plays a role in the pathophysiology of heart failure, but is probably also affected by cytokines. We studied 75 patients with heart failure NYHA functional class II and III-IV, who were treated with angiotensin converting enzyme inhibitor (enarenal), diuretics (furosemide) and digoxine. Their mean age was 63.9 years/range 65-86/, left ventricular ejection fraction in the patients NYHA functional class II and III-IV classes was 68.9% and 47.3% respectively; 12 were females. Significant improvements in NYHA classification were shown. The levels plasma TNF-alpha (tumor necrosis factor-alpha) and interleukin-6 (IL-6) were analysed before and after therapy. The authors showed increased plasma levels TNF-alpha and IL-6 in patients with chronic heart failure. After the treatment the plasma IL-6 levels decreased only in the patients III-IV NYHA functional classes, whereas the treatment had no effect on the plasma TNF-alpha levels.
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PMID:[Do cytokines have any value in the patients with chronic blood circulation insufficiency?]. 1052 13

The in vitro effects on human dermal fibroblasts and the U937 human monocytic cell line of three phases of electrical microcurrents generated by the ACE Stimulator were investigated. The growth and viability of growing and confluent dermal fibroblasts were not directly influenced by the separate microcurrent phases. One form of microcurrent (designated phase 1) stimulated both dermal fibroblasts and U937 cells to secrete transforming growth factor-beta 1 (TGF-beta 1), which is an important regulator of cell-mediated inflammation and tissue regeneration, but none of the three phases stimulated secretion of the pro-inflammatory cytokine interleukin-6 by U937 cells. The stimulation of TGF-beta 1 secretion in these experiments was not dramatic (a median increase over control levels of 20-30%), although it could be biologically significant.
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PMID:Electrical stimulation of transforming growth factor-beta 1 secretion by human dermal fibroblasts and the U937 human monocytic cell line. 1170 43

Angiotensin II (Ang II), the most important component of the renin-angiotensin system, is usually associated with hypertension and renal failure. Through its pro-inflammatory actions, it also plays an important role in each step of the development of atherosclerotic plaques and plaque rupture. Ang II stimulates the expression of nuclear factor-kappaB (NFkappaB), a transcription factor which regulates gene expression of inflammatory cytokines such as interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1). Ang II type 1 receptors (AT1) and angiotensin converting enzyme (ACE) are dramatically increased in atherosclerotic plaques, particularly in monocytes at the fibrous cap. Thus, in multiple ways, Ang II is a critical factor in atherosclerotic plaque formation, inflammation and plaque stability. ACE inhibitors and AT1R inhibitors could therefore be appropriate therapeutic agents in the treatment of atherosclerosis.
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PMID:Angiotensin II as a pro-inflammatory mediator. 1209 Jul 26

Genetics, oxidative stress: superoxide anion (O2*-) and hydrogen peroxide (H2O2), endothelial nitric oxide (eNO), lipid peroxides, anti-oxidants, endothelin, angiotensin converting enzyme (ACE) activity, angiotensinII, transforming growth factor-beta (TGF-beta), insulin, homocysteine, asymmetrical dimethyl arginine, proinflammatory cytokines: interleukin-6 (IL-6), tumor necrosis factor-a (TNF-alpha), C-reactive protein (hs-CRP), and long-chain polyunsaturated fatty acids (LCPUFAs), and activity of NAD(P)H oxidase have a role in human essential hypertension. There is a close interaction between endogenous molecules: eNO, endothelin, cytokines, and nutrients: folic acid, L-arginine, tetrahydrobiopterin (H4B), vitamin B6, vitamin B12, vitamin C, and LCPUFAs. Statins mediate some, if not all, of their actions through LCPUFAs, whereas these fatty acids (especially omega-3 fatty acids) suppress cyclo-oxygenase activity and the synthesis of pro-inflammatory cytokines, and activate parasympathetic nervous system, actions that reduce the risk of major vascular events. Some LCPUFAs form precursors to lipoxins and resolvins that have anti-inflammatory actions. Low-grade systemic inflammation seen in hypertension seems to have its origins in the perinatal period and availability of adequate amounts of LCPUFAs during the critical periods of brain growth prevents the development of hypertension. This indicates that preventive strategies aimed at decreasing the incidence of hypertension and its associated conditions such as atherosclerosis, type 2 diabetes, coronary heart disease (CHD), and cardiac failure in adulthood need to be instituted during the perinatal period if they are to be effective.
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PMID:Hypertension as a low-grade systemic inflammatory condition that has its origins in the perinatal period. 1671 19

We hypothesized that beneficial role of angiotensin converting enzyme inhibitors in stable coronary artery disease (CAD) therapy may involve (among others) their anti-inflammatory effects, which may be reflected by serum interleukin-6 (IL-6) levels. For that reason, we have investigated the influence of short-term administration of quinapril on serum IL-6 concentration. 124 patients suffering from stable CAD and matched for some of CAD risk factors were enrolled in our study. Patients were randomized to treatment with quinapril or control (placebo administration). Blood samples were taken twice: before and after four weeks of quinapril administration. The effect of quinapril administration was assessed under double-blind placebo-controlled conditions. We observed that quinapril reduced serum IL-6 concentration in almost all studied subgroups of patients (p < 0.001). Interestingly, such an effect was not observed in smokers. Additionally, we found that baseline IL-6 levels were higher in: smokers as compared with nonsmokers (p < 0.001), patients with total cholesterol (TC) to high density lipoprotein (HDL)-cholesterol ratio (TC/HDL-ch ratio) above 5 as compared with subjects with TC/HDL-ch < or = 5 (p = 0.001), and in patients who did not report any statin therapy in comparison with patients undergoing statin treatment (p = 0.023). In conclusion, quinapril may interfere with cytokine release by lowering IL-6 levels, which may be of particular importance for secondary prevention of stable CAD.
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PMID:Influence of preventive therapy with quinapril on IL-6 level in patients with chronic stable angina. 1765 34

Diabetes mellitus (DM) may cause an increase in the inflammatory status and oxidative stress as well as sympathetic nervous system overactivity, even in the absence of any other organic heart disease. We investigated the effect of perindopril, an angiotensin-converting enzyme inhibitor (ACE-i), on indexes of systemic inflammation and oxidative stress in normotensive patients with type 2 DM. We also examined the effect of the drug on the disturbances of left ventricular myocardial adrenergic innervation that may be seen in these patients. We studied 62 normotensive patients with type 2 DM, who were randomized to receive perindopril (n=32) or placebo (n=30). At the start of the study and after 6 months' therapy blood samples were taken to evaluate total peroxides (TP), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha), and the patients underwent a (123)I-metaiodobenzylguanidine myocardial scintigraphy study. ACE-i caused a significant reduction in levels of cytokines and TP (P<0.001 for IL-6 and TNF-alpha, P=0.001 for TP). There was also a reduction in total defect score (P<0.001) and the heart to mediastinum ratio at 10 min and 4 h was improved (P<0.001 for both). No significant alterations were observed in the placebo group. Our data indicate that the addition of ACE-i to the medication of normotensive diabetic type 2 patients may improve the disturbed myocardial adrenergic innervation, the systemic inflammatory status and oxidative stress. Our findings indicate the cardioprotective action of ACE-i and suggest that earlier treatment might be appropriate in those patients.
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PMID:Effect of angiotensin-converting enzyme inhibitors on systemic inflammation and myocardial sympathetic innervation in normotensive patients with type 2 diabetes mellitus. 1804 34

Current thinking supports the notion that several inflammatory proteins intervene with endothelium and haemostatic factors leading to plaque formation and rupture. Of these, C-reactive protein (CRP), monocyte/macrophage colony-stimulating factor (MCSF) and interleukin-6 (IL-6) promote atherogenesis by inducing monocyte-macrophage activation, foam cell formation, platelet activation, tissue factor expression, release of other procoagulant cytokines or downregulation of atheroprotective cytokines such as interleukin 10 and transforming growth factor b-1 (TGFb-1). CRP, MSCF and IL-6 are interrelated and have been found in increased blood concentrations in CAD. Increased levels of CRP and IL-6 predict a higher cardiovascular event rate in the general population and in addition to high MCSF or low TGFb-1 predict adverse outcome in CAD patients independently of traditional risk factors. Moreover, in CAD patients, the predictive value of MCSF is additive and beyond that of CRP suggesting the need of a "multimarker approach" in assessing cardiovascular risk. Accumulating evidence supports the utility of non-invasive markers of subclinical atherosclerosis, namely carotid intimal media thickness, flow mediated dilatation of the brachial artery, augmentation index or pulse wave velocity, in the prediction of cardiovascular risk particularly in primary prevention settings. The combination of these non-invasive tests has been shown to improve their prognostic accuracy compared to each other alone. Although several therapeutic strategies like vaccination against antigens promoting atherogenesis, cyclooxygenase inhibitors, statins, and ACE inhibitors may reduce the levels of these inflammatory markers and improve the non-invasive markers of subclinical atherosclerosis, the impact on cardiovascular risk resulting from these changes is unknown. The combination of an established inflammatory marker such as CRP or a vascular marker such as IMT with novel biochemical and vascular markers of cardiovascular disease may offer additive prognostic information for adverse outcome.
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PMID:Inflammatory and non-invasive vascular markers: the multimarker approach for risk stratification in coronary artery disease. 1837 39


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