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)

The authors restate their personal researches about several antigen systems, viz. ACE, neurospecific antigens. They point out the complementarity of immunochemistry and immunohistochemistry which implicates a very precise methodology and utilization of rigorously monospecific immune serums with regard to the studied antigen. This conduces to reproducible, responsive and reliable techniques in optic microscopy but much less easily so in electron microscopy. These techniques are still partly experimental; but their application to the study of pathological tissues and especially of tumors may however be considered. The identification of histological types and the correlated evolution is suggested on hand of concrete examples.
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PMID:[Methods for study of soluble antigens in pathological anatomy]. 102 84

The activity of LDG, ACE and CE was determined in the lumbar CSF and blood serum of patients with sustained mild concussion of the brain. As compared to healthy persons the diseased demonstrated a significant rise of the LDG activity in the CSF while the mounting activity of 2 other enzymes, observed in individual instances in the CSF, lacked statistical significance. It was found that in functional upsets without any marked morphological lesions there may be encountered changes in the enzymatic activity that should be considered as a consequence of deranged metabolism.
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PMID:[Activity of the enzymes of cerebrospinal fluid and blood serum in patients with the concussion syndrome]. 116 37

In 30 patients affected by testicular non-seminomatous cancer we evaluated pulmonary function tests before and after bleomycin-including combination chemotherapy. We paid particular attention to changes in diffusing lung capacity (DCO) and its two components, namely diffusing capacity of the alveolar-capillary membrane (Dm) and pulmonary capillary blood volume (Vc). In the same patients we also evaluated the behaviour of serum procollagen III aminopeptide (sP-III-P), assumed to be a biochemical equivalent to Dm, and of serum angiotensin converting enzyme (S-ACE), assumed to be a biochemical equivalent to Vc. We found that, after chemotherapy, patients showed a significant decline in several pulmonary function parameters, namely VC, TLC, and FEV1 (P < 0.0001, P = 0.0351, P = 0.0004, respectively), when compared to pre-treatment values. DCO was significantly impaired after chemotherapy (P < 0.0001), but with regard to its components, Vc values showed a significant decline (P = 0.0002), whereas Dm values were unchanged. Values of sP-III-P raised significantly after chemotherapy (P = 0.003), whereas S-ACE activity did not show any significant variation. When we looked at relationships between functional and biochemical parameter variations, the only significant correlation we found was between DCO and S-ACE (r2 = 0.112; P < 0.02). We conclude that in asymptomatic patients treated by bleomycin-including combination chemotherapy, DCO impairment is likely to occur because of a subclinical injury to pulmonary vessels, as suggested by Vc decline. Although the occurrence of pulmonary interstitial fibrosis after chemotherapy was excluded by chest X-ray examination and by stable values of Dm, sP-III-P elevation would suggest an accelerated type III collagen turnover in interstitial fibroblasts activated by bleomycin.
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PMID:Study of functional and biochemical indicators of subclinical lung damage in bleomycin-treated patients. 128 Mar 68

Protein sequencing and molecular cloning of human endothelial angiotensin I-converting enzyme (ACE; kininase II), have led to a description of the structure of the enzyme and to several questions concerning the intracellular maturation of ACE and the mechanisms of enzyme action. With the help of recombinant ACE expression in mammalian cells and site-directed mutagenesis, a model for the maturation of ACE in endothelial cells has been proposed. This model comprises transmembrane anchoring of the membrane-bound ACE near its carboxyterminal extremity, and post-translational cleavage of the anchor in the secreted form. The endothelial ACE displays a high degree of internal homology between two large peptidic domains that each bears a consensus sequence for zinc binding and therefore a putative active site. The testicular ACE, however, encoded from the same gene by a shorter mRNA, contains only the carboxyterminal half of endothelial ACE and therefore a single active site. Expression of ACE mutants with only one intact homologous domain, however, indicates that in endothelial ACE both domains are enzymatically active. Further characterization of these two active sites of endothelial ACE is in progress. In humans, population studies have indicated that the large interindividual variability in plasma ACE levels is partly genetically determined and under the influence of a major gene effect. This was later confirmed and extended by the observation of an insertion-deletion polymorphism of the ACE gene that is associated with the level of ACE in plasma. The clinical implications of these observations are discussed.
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PMID:The angiotensin I-converting enzyme (kininase II): molecular organization and regulation of its expression in humans. 128 23

The cardiovascular effects of bradykinin require additional vasoactive mediators for a fully balanced response. This includes arachidonic acid (eicosatetraenoic acid) and its metabolites, the eicosanoids (prostaglandins, leukotrienes, thromboxanes, and others). Eicosanoid generation by bradykinin is started by binding of the peptide to specific B2 receptors at the plasma membrane. This initiates G-protein coupled stimulation of phospholipase C, IP3-induced increases in cytosolic Ca2+, and stimulation of protein kinase C. Arachidonic acid is liberated from membrane phospholipids primarily via Ca(2+)-induced stimulation of phospholipase A2 and converted into tissue-specific eicosanoids by enzymes in the vicinity. In vascular tissue, most of the available arachidonic acid is converted into vasodilator prostaglandins, i.e., prostacyclin (PGI2) and prostaglandin E2 (PGE2). These prostaglandins are involved in vasodilator actions of the kinins. There is also some evidence for generation of vasoconstrictor eicosanoids, such as thromboxane A2, under certain conditions. The biological significance of kinin-related prostaglandin formation becomes apparent after inhibition of kinin breakdown by ACE inhibitors. These compounds prevent generation of vasoconstrictor angiotensin II and stimulate endothelial eicosanoid formation via local kinin accumulation. There is evidence suggesting that kinin-induced prostaglandin generation contributes to anti-ischemic, inotropic, and blood pressure-lowering effects of the compounds. This also includes inhibition of polymorphonuclear leukocyte (PMN) accumulation in injured myocardial tissue, which is antagonized by PGI2-related pathways, stimulated by ACE inhibition and/or bradykinin.
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PMID:Role of prostaglandins in the cardiovascular effects of bradykinin and angiotensin-converting enzyme inhibitors. 128 33

With the availability of a wide selection of antihypertensive drugs acting by different mechanisms, it should be possible to match the requirement of individual patients with the pharmacological and clinical properties of an appropriate agent. Although the concept of stepped-care therapy is now largely outdated, therapy must be initiated with one agent. Diuretics remain a first-choice option in the elderly and in Black patients, as do calcium antagonists. In patients with ischaemic heart disease or enhanced adrenergic drive, beta-blockers are preferred. Calcium antagonists or ACE inhibitors are finding increasing use as initial therapy when quality of life is important and metabolic neutrality is required. The choice of antihypertensive agent may be limited by adverse effects, e.g. pedal oedema with nifedipine, constipation with verapamil, and cough with ACE inhibitors. Certain advantages are evident for both calcium antagonists and ACE inhibitors. Calcium antagonists are more likely to be effective first-line therapy than ACE inhibitors in Black patients, in those with a high salt intake, in patients with Raynaud's disease, and when angina pectoris is present. ACE inhibitors are preferred for use in combination with diuretic agents, and in the presence of congestive heart failure or low salt intake. Combination therapy between these 2 drug classes is finding increasing acceptance because of its many theoretical advantages, and may provide a means of maximising benefit.
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PMID:Choosing the correct drug for the individual hypertensive patient. 128 79

Blood serum activity of ACE, alfa2-macroglobulin as well as triglycerides concentration was determined in 90 patients with diabetes and in 40 healthy persons. Taking into account criteria established by WHO the patients with diabetes were divided into two groups. The first group consisted of 32 patients with diabetes of type I (juvenile one); the second group consisted of 58 patients with diabetes of type II (adult one). It was found that blood serum level of all tested parameters is statistically increased (p < or = 0.001) in comparison with control group. In patients with diabetes of type I the level of alfa2-macroglobulin and ACE was higher than in those with diabetes of type II. The serum contents of triglycerides in both groups of patients was comparable. No correlation between parameters determined in patients with diabetes was found.
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PMID:Blood serum angiotensin-converting enzyme, alfa2-macroglobulin and triglycerides in patients with diabetes. 128 70

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10

24 hour blood pressure monitoring is a well established method in the field of antihypertensive research. Patients self recorded blood pressure values are an additional option to overcome the disadvantages of casual office readings--however they are not frequently used within intervention trials. To prove the usefulness of selfrecordings in clinical trials we investigated both selfrecordings taken twice a day and casual readings within intervals of 1 to 3 weeks, in this study on the efficacy and tolerability of the ACE-inhibitor Accupro. 108 hypertensive patients (grade WHO I to II) were included in this trial for ten weeks. Although blood pressures were measured by the patients using sphygmomanometers of the same type and the physicians, decisions to treat or to increase dosage were based on the patients' recordings only. Accupro was dispensed according to the package leaflet at a daily dosage of 5 mg up to 40 mg. In case of failing response to monotherapy, Accupro was combined with Diltiazem or with a diuretic. 7 patients discontinued the treatment due to mild adverse events, one did not cooperate. 82 of the remaining patients were treated effectively with Accupro monotherapy--60 (73%) got one dose daily, 22 (27%) 2 doses per day,--and in 18 patients a drug combination was required. Therapeutic response (RRd < or = 90 mm Hg) was gained within 86 of the 100 evaluable patients according to the doctors' and 83 according to the patients' records. In this respect the two methods used gave comparable overall results. This somewhat surprising fact is due to the design of the study, because treatment decisions were based on the selfrecordings only. Clinical trials based on selfrecordings are in some points preferable to casual office readings: As patients being normotensive at home should not be included into an interventional study, a change of dosage within this group is avoided. Additionally the compliance of a cooperative patient taking his blood pressure twice daily is at a high level. Measurements of each single patient may be evaluated statistically by time series-analysis regarding longterm distribution of blood pressure-values. Taking the means of selfrecordings over adequate time-intervals eliminates the influence of "outliers" (occasionally extremely high or low values) and also reduces the standard deviation compared to that of the casual readings. Research work based on self recordings provides more information and therefore more security for treatment decisions.
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PMID:[Comparison of results of daily blood pressure self-monitoring and general practice monitoring within the scope of a study assessing treatment of hypertension with quinapril]. 783 92

Arterial hypertension is the most frequent cause of a disturbance of coronary microcirculation. Inspite of having normal epicardial coronary arteries, patients with arterial hypertension often have symptoms of angina pectoris and a positive exercise tolerance test. The angina pectoris symptoms in patients with arterial hypertension are due to functional and structural alterations of the coronary microcirculation. Consequently, an antihypertensive therapy should not only aim at lowering blood pressure and reversing myocardial hypertrophy, but also to improve coronary microcirculation in order to avoid the consequences of chronic ischemia on the myocardium. Until now, only experimental studies have indicated that antihypertensive therapy can improve coronary flow reserve. To determine (also under clinical conditions) if coronary flow reserve can be improved, in 30 hypertensive patients maximal coronary blood flow, minimal coronary resistance, and coronary reserve (dipyridamol) were studied before and after a long-term antihypertensive treatment (9-12 months) with an ACE-inhibitor (enalapril 10-20 mg/d), a calcium channel blocker (diltiazem 120-180 mg/d) and a beta 1-selective beta-receptor-blocker (bisoprolol 5-10 mg/d). To assess the chronic effects rather than the acute effects of the antihypertensive pharmacon, coronary microcirculation was studied after intermission of medical therapy for a period of 1 week. Along with a comparable decrease in LV muscle mass, coronary reserve was improved after enalapril by 48%, after diltiazem by 48%, and after bisoprolol by 22%. It is possible that the observed increase in coronary reserve is related to the reversal of structural vascular abnormalities on the level of the coronary microcirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevention with vasoactive drugs]. 129 Feb 99


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