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)

Numerous factors causing the disturbances of pressure natriuresis mechanism may be involved in the development of arterial hypertension in kidney diseases. In particular patients with parenchymatous kidney disease, the relative effect of the impaired renal sodium excretion causing extracellular fluid volume expansion and the disequilibrium of vasoconstricting and vasorelaxating factors may differ, and in addition, these effects are influenced by the type of kidney disease, the degree of the kidney function impairment and sodium intake. In our studies on the hypertension in kidney disease we have choosen the evaluation of incidence of hypertension in the early stage of primary glomerulonephritis (GN) and the comparison of distribution of genotypes and alleles depending on insertion/deletion polymorphism of angiotensin converting enzyme (ACE) gene in patients with early stage of GN and healthy subjects. Arterial hypertension was diagnosed according to actual criteria in 46% out of 74 patients with early stage of GN. It was also found that hypertension was more common in patients with nephrotic syndrome (63%) than in patients with lower proteinuria (36% of patients). Among 50 patients with early stage of GN the distribution of genotypes and alleles depending on the polymorphism ACE gene was significantly different from 100 healthy controls. These results indicate that hypertension is often present in early stage of GN, particularly in patients with nephrotic syndrome and depends on the morphological type of glomerular disease. Further studies are needed for verification of the role of ACE gene polymorphism in the predisposition to development of GN and associated arterial hypertension.
Pol Merkur Lekarski 2003 Oct
PMID:[Arterial hypertension in glomerulonephritis]. 1497 62

Essential hypertension accounts for 95% of all cases of hypertension. A small number of patients (between 2% and 5%) have a reversible disease as the cause for raised blood pressure. Unilateral and bilateral renal artery stenosis may be responsible for secondary hypertension. Diagnosis and treatment of renal artery stenosis are of a great importance. Revascularization of ischemic kidney may correct blood pressure control and preserve renal function. Much data suggest close pathophysiological relation between renal artery stenosis, ischemic nephropathy and development of hypertension. However, it should be stressed that not every renal artery stenosis leads to hypertension and ischemic nephropathy. Therefore diagnosis of renal artery stenosis in hypertensive patient is not always equivalent with renovascular hypertension. The true prevalence of renal artery stenosis is unknown. In unselected population it accounts for less than 1% of hypertensive patients. Renovascular etiology of hypertension may be suggested by abrupt onset of hypertension, resistant and malignant hypertension or recurrent pulmonary edema of unknown etiology. Physical examination may reveal bruits over major vessels, including the abdominal aorta and renal arteries. The principle aim of the renal artery stenosis investigation is to confirm presence and size of vessel obstruction and its association with hypertension. Typical evaluation is based on imaging techniques and physiological studies. Former include: doppler duplex ultrasonography, conventional angiography, intraarterial and intravenous digital subtraction angiography, computed axial tomography, magnetic resonance angiography and intravascular ultrasonography. Functional studies are occasionally used. These are renal scintigraphy, evaluation of plasma renin activity in renal veins and evaluation of plasma rennin activity after ACE inhibition. Treatment of patients with renal artery stenosis and hypertension should restore vessel patency and inhibit its occlusion. Revascularization should elicit an improvement in or normalization of blood pressure control and renal function. Therapeutic approach include percutaneous renal artery angioplasty (PTRA), with or without stenting, revascularization by surgery and pharmacotherapy. PTRA is currently the first choice option. In general, it is simpler and similarly effective as surgical reconstruction. In some cases PTRA is completed with stent placement. It prevents immediate recoil but does not completely eliminate restenosis of revascularized artery. Surgical bypass is currently reserved for patients in whom PTRA and stenting fail and in patients with extensive atherosclerotic lesions. Patients with renal artery stenosis and hypertension should be provided with pharmacological treatment according to current recommendations. Specific procedures to limit associated risk factors of atherosclerosis should also be introduced.
Pol Merkur Lekarski 2003 Oct
PMID:[Renovascular hypertension: is it only the top of the iceberg?]. 1497 69

The most investigated novel risk factors of atherosclerosis are: fibrinogen (Fb), homocysteine (Hcy), lipoprotein (a) (Lp(a)), plasminogen activator inhibitor (PAI-1), markers of inflammation and infectious factors. Atherosclerotic renal artery stenosis (RAS) is a manifestation of generalized atherosclerosis and often coexist with hypertension and renal failure. The aim of the study was to assess plasma concentration of Hcy, von Willebrand factor (VWF), (Lp(a), Fb, PAI-1, and assessment of ACE gene polymorphism in pts with RAS and hypertension. The study included 15 patients with RAS (mean age 51.4 +/- 16.5 yrs) and 27 healthy volunteers (C) (mean age 42.9 +/- 9.5 yrs). Plasma concentrations of Hcy were significantly higher in RAS (11.0 +/- 3.9 mumol/L) than in C (6.8 +/- 1.3 mumol/L). Plasma concentration of VWF was also significantly higher in RAS than C (104.7 +/- 40 vs 73.6 +/- 20%) as was FB concentration (325.9 +/- 70.0 vs 256.2 +/- 54.7 mg%). DD genotype was present in 45% of RAS pts and in 12% of controls. In patients with atherosclerotic RAS novel markers of atherosclerosis may be an additional risk factor in the development and progression of atherosclerotic lesions.
Pol Merkur Lekarski 2003 Oct
PMID:[Non-traditional atherosclerosis risk factors in patients with renal artery stenosis and hypertension]. 1497 71

Cathepsin B is a lysosomal cysteine protease exhibiting mainly dipeptidyl carboxypeptidase activity, which decreases dramatically above pH 5.5, when the enzyme starts acting as an endopeptidase. Since the common cathepsin B assays are performed at pH 6 and do not distinguish between these activities, we synthesized a series of peptide substrates specifically designed for the carboxydipeptidase activity of cathepsin B. The amino-acid sequences of the P(5)-P(1) part of these substrates were based on the binding fragments of cystatin C and cystatin SA, the natural reversible inhibitors of papain-like cysteine protease. The sequences of the P'(1)-P'(2) dipeptide fragments of the substrates were chosen on the basis of the specificity of the S'(1)-S'(2) sites of the cathepsin B catalytic cleft. The rates of hydrolysis by cathepsin B and papain, the archetypal cysteine protease, were monitored by a continuous fluorescence assay based on internal resonance energy transfer from an Edans to a Dabcyl group. The fluorescence energy donor and acceptor were attached to the C- and the N-terminal amino-acid residues, respectively. The kinetics of hydrolysis followed the Michaelis-Menten model. Out of all the examined peptides Dabcyl-R-L-V-G-F- E(Edans) turned out to be a very good substrate for both papain and cathepsin B at both pH 6 and pH 5. The replacement of Glu by Asp turned this peptide into an exclusive substrate for cathepsin B not hydrolyzed by papain. The substitution of Phe by Nal in the original substrate caused an increase of the specificity constant for cathepsin B at pH 5, and a significant decrease at pH 6. The results of kinetic studies also suggest that Arg in position P(4) is not important for the exopeptidase activity of cathepsin B, and that introducing Glu in place of Val in position P(2) causes an increase of the substrate preference towards this activity.
Acta Biochim Pol 2004
PMID:Fluorogenic peptide substrates for carboxydipeptidase activity of cathepsin B. 1509 28

Chronic heart failure affects between 1-5% of the population and rise steeply with age. Most patients with chronic heart failure should be routinely managed with a combination of 4 types of drugs: a diuretic, an angiotensin converting enzyme inhibitors (ACE-I), beta-blocker and usually digitalis. Diuretics are essential for symptomatic treatment when fluid overload is present, and should always be administrated in combination with ACE-I if possible. ACE-I improves survival and symptoms and reduces hospitalization in patients with moderate to severe ventricular systolic dysfunction, and in the absence of fluid retention should be given first. Angiotensin II receptor antagonist could be considered in patients who not tolerate ACE-I. beta-blocking agents are recommended for treatment of patients with stable, mild, moderate and severe heart failure unless there is a contraindication. Bisoprolol, metoprolol and carvedilol have been associated with reduction in total mortality, cardiovascular mortality and sudden death. Cardiac glycosides are indicated in atrial fibrillation and any degree of symptomatic heart failure in order slow ventricular rate. Indications for antiarrhythmic drug therapy include atrial fibrillation, non-sustained or sustained ventricular tachycardia. Oral anticoagulation reduces the risk of stroke in patients with atrial fibrillation, and there is a lack of evidence to support the use of antithrombotic therapy in patients in sinus rhythm.
Pol Merkur Lekarski 2004 Apr
PMID:[Pharmacotherapy of chronic heart failure in clinical practice]. 1551 21

Cardiovascular diseases and strokes are the main reasons of premature deaths in 70% patients with non insulin-dependent and also insulin-dependent diabetes mellitus. Hypertension is 2 to 3 times more frequent in diabetic patients than in the rest of population. In the guidelines for management of hypertension in diabetes published this year beta-blockers are proposed together with the ACE-inhibitors as the first-choice drugs. The latest studies did not confirm the risk of higher and prolonged hypoglycemia during cardioselective beta-adrenergic blocade, but the insulin-treated diabetics with hypoglycemia episodes in the past should be watched very carefully when given beta-blockers. It is emphasized, that beta-blockers are very useful especially in patients with diabetes mellitus, hypertension and coronary artery disease. In patients after myocardial infarction the advantages with treatment with beta-blockers dominate over the potential risk of adverse drug reactions.
Pol Merkur Lekarski 2004 Apr
PMID:[beta-blockers in the treatment of hypertension in diabetic patients]. 1551 41

Hepatocyte growth factor (HGF) takes part in tissue regeneration after injury. It is a potent survival and regeneration factor after severe tissue damage. It promotes cell growth and protection from apoptosis, regulates the cell migration and differentiation. HGF is a subject of intensive investigations in order to apply it in the future in gene therapy to improve treatment of angina pectoris or intermittent claudication. The aim of this review is discussion about the role of HGF in pathogenesis and treatment of atherosclerosis. Angiogenetic activity of HGF was proven in vivo as well as in vitro. In patients with collaterals increased HGF plasma concentration was revealed. It is possible to determine with high probability the risk of cardiovascular event on the basis of HGF concentration. Plasma concentration of this factor increases dramatically after heparin injection, particularly after unfractionated heparin. Also other drugs (ACE-inhibitors) may take part in regulation of HGF synthesis.
Pol Merkur Lekarski 2004 Jul
PMID:[Hepatocyte growth factor (HGF) and atherosclerosis]. 1555 22

Progression of a variety of chronic renal diseases may be largely due to secondary hemodynamic and metabolic factors, rather than the activity of the underlying disorder. Some of these factors can be treated, possibly preventing or minimizing further glomerular injury. An important component of this approach is antihypertensive therapy, particularly with angiotensin converting enzyme (ACE) inhibitors and, at least in patients with type 2 diabetes, angiotensin II receptor blockers. The clinical studies supporting importance of blood pressure control in diabetic and nondiabetic chronic renal diseases and recommended treatment goals will be presented here.
Pol Arch Med Wewn 2004 Oct
PMID:[New therapeutic options in renal diseases--hypotensive therapy]. 1566 2

In Europe, 20% of the populations is over 65 years of age. About 5% of the older adults have heart failure. Heart failure (HF) in the elderly is an increasing public health problem, leading cause of hospitalization in older patients and a major cause of morbidity and mortality. Prognosis has improved only slightly during the past decade. Typically, heart failure occurs when ventricles do not fill (diastolic heart failure - DHF) or empty blood (systolic heart failure - SHF) properly. Transthoracic echocardiography is the key investigation to confirm the underlying structural and functional abnormalities of the heart. Patients with heart failure due to left ventricular systolic dysfunction should be treated with a diuretic, an angiotensin converting enzyme inhibitor, and a beta-blocker (unless contraindicated). Several epidemiologic studies have recently shown that more than 50% of older patients who present with symptoms of HF have DHF. While numerous large trials have established specific therapies for SHF, such trials are lacking for DHF. The finding of similar key pathophysiologic abnormalities in DHF and SHF suggests the possibility that therapies that have been successful for SHF may have a role in therapy for DHF. A recent survey showed that despite physicians' awareness of the benefits of beta-blocker therapy, only minority of patients with heart failure are treated with beta-blocker or combination of ACE inhibitors and beta-blocker.
Pol Arch Med Wewn 2004 Oct
PMID:[Heart failure in advanced age]. 1566 9

Single nucleotide incorporation assays have been used to probe the kinetic parameters of many DNA and RNA polymerases. Traditionally, oligonucleotide primers are 5'-(32)P labeled using T4 kinase and annealed to a complementary template with a 5' overhang. To quantify the reaction kinetics, the products of the primer extension reactions are usually separated using denaturing polyacrylamide gel electrophoresis and quantified using a phosphorimager or other method to measure radioactivity. We have developed a method using a 5' fluorescently labeled oligonucleotide to examine the kinetics of single nucleotide incorporation catalyzed by recombinant human mitochondrial polymerase gamma (Pol gamma) holoenzyme. Using laser-induced fluorescence detection in the P/ACE MDQ instrument, primers 5' labeled with fluorescent probes such as 6-carboxyfluorescein can be rapidly separated and quantified. However, we also show that only select probes can be used, presumably due to unfavorable interactions between Pol gamma and certain 5' labels.
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PMID:Analysis of single nucleotide incorporation reactions by capillary electrophoresis. 1580 27


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