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 replacement value of undecorticated sunflower meal (SFM) in the diets of dairy animals was assessed on-station and on-farm. Eighteen primiparous crossbred (Bos taurus x Bos indicus) cows (350.4 +/- 8.84 kg), randomly allocated to three groups, were used in the on-station study. The animals were fed on either a conventional concentrate supplement (control) or on an experimental concentrate, in which SFM replaced 25% (SFM-25) or 50% (SFM-50) of the CP in the control supplement. Green oats (Avena sativa) were supplied ad libitum. A metabolism trial conducted following 60 days of experimental feeding revealed that the intakes of DM, DCP and TDN were similar among the groups. The digestibilities of OM, CP, EE, NDF and ADF were also without significant differences. All the groups were in positive nitrogen balance. Inclusion of SFM at either level had no effect on the intake, excretion or retention of nitrogen. The daily milk yield and its composition did not differ among the dietary treatments. Moreover, the efficiency of utilization of DOM and TDN for FCM production tended to reflect, although non-significantly, increasing levels of SFM inclusion. In the on-farm study, seven multiparous milking buffaloes belonging to six farmers were used to assess the effect of replacing 20% of the CP of the conventional supplement with SFM, in a predominantly crop residue-based diet. The study continued for 4 months and revealed that the average daily feed intake and milk production was similar in the control and SFM-fed groups. It was concluded that SFM can be effectively utilized as a cheaper replacement for costly oil cakes and wheat bran for economic milk production by smallholder farmers.
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PMID:Replacement value of undecorticated sunflower meal as a supplement for milk production by crossbred cows and buffaloes in the northern plains of India. 1273 4

It is not known whether angiotensin II type 1 receptor antagonists can influence the function and morphology of small arteries in renal failure. We investigated the effect of 8-week losartan therapy (20 mg/kg per day) on isolated mesenteric resistance arteries by wire and pressure myographs in 5/6 nephrectomized rats. Plasma urea nitrogen was elevated 1.6-fold after nephrectomy, and ventricular synthesis of atrial and B-type natriuretic peptides was increased 2.2-fold and 1.7-fold, respectively, whereas blood pressure was not affected. Losartan did not influence these variables. The endothelium-mediated relaxation to acetylcholine was impaired in nephrectomized rats in the absence and presence of nitric oxide synthase and cyclooxygenase inhibition. Blockade of calcium-activated potassium channels by charybdotoxin and apamin reduced the remaining acetylcholine response, and this effect was less marked in nephrectomized than in sham-operated rats. Relaxation to levcromakalim, a vasodilator acting through adenosine triphosphate-sensitive potassium channels, was also impaired after nephrectomy. The arteries of nephrectomized rats showed eutrophic inward remodeling: Wall-to-lumen ratio was increased without change in wall cross-sectional area. All changes in arterial relaxation and morphology were normalized by losartan therapy. Aortic ACE content, measured by autoradiography, directly correlated to the plasma level of urea nitrogen, suggesting that renal failure has an enhancing influence on the vascular renin-angiotensin system. Losartan normalized relaxation and morphology of resistance arteries in experimental renal failure, independent of its influence on blood pressure, impaired kidney function, or volume overload. The mechanism of improved vasodilation by losartan may include enhanced relaxation through potassium channels.
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PMID:AT1 receptor blockade improves vasorelaxation in experimental renal failure. 1274 14

The pharmacokinetics of enalapril (0.5 mg/kg i.v.) and the pharmacodynamics of enalapril (0.5 mg/kg PO) in 5 mares were investigated. After single i.v. dosing, concentrations of enalapril and enalaprilat, its active metabolite, were measured. Two weeks later, enalapril was administered by nasogastric tube. Potassium, creatinine, blood urea nitrogen (BUN), enalapril, and enalaprilat concentrations and angiotensin converting enzyme (ACE) activity were measured in serum. In addition, heart rate, blood pressure, digital venous blood gases, and lactate were measured. Two weeks later, enalapril was again administered by nasogastric tube. To mimic activation of the renin-angiotensin-aldosterone system, angiotensin I (0.5 microg/kg) was administered at fixed intervals, followed by blood-pressure and heart-rate measurement. The elimination half lives of enalapril and enalaprilat were 0.59 and 1.25 hours, respectively, after i.v. administration. After PO administration, enalapril and enalaprilat were not detectable in serum. There was a tendency (P = .0625) toward a decrease in ACE activity 45-120 minutes after enalapril administration, but ACE activity suppression was never > 16%. There was a tendency (P = .0625) toward a decrease in mean arterial pressure (MAP) 6-8 hours after enalapril administration. Serum concentrations of potassium, creatinine, and BUN and digital venous blood gases and lactate concentrations did not change. In response to angiotensin I, there was a tendency (P = .0625) toward a decrease in the MAP response 4-24 hours after enalapril administration. Single-dose enalapril at 0.5 mg/kg PO did not demonstrate significant availability, pharmacodynamic effect, or substantial suppression of ACE activity.
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PMID:Characterization of the pharmacokinetic and pharmacodynamic properties of the angiotensin-converting enzyme inhibitor, enalapril, in horses. 1505 76

75% of patients systematically taking over the period of 6 weeks nonsteroidal anti-inflammatory drugs have their mucous of gastrointestinal tract pathologically changed. This process is called induced NSAID gastropathy. Inhibitors of angiotensin converting enzyme (I-ACE) seems to have gastroprotective effect by enhancing level of endogenous prostaglandins. Besides, an application of I-ACE reduces angiotensin II formation and activates renin-kallicrein-kinin system resulting in nitrogen oxide formation that is in its turn an important component of reparative process of mucous of gastrointestinal tract.
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PMID:[Prophylactic use of angiotensin-converting enzyme inhibitors in indomethacin-induced ulcer and erosion lesions of the stomach]. 1520 73

Diabetes mellitus is one of the most common chronic diseases affecting millions of people worldwide. Cardiovascular complication including myocardial infarction is one of the major causes of death in diabetic patients. Diabetes mellitus induces abnormal pathological findings including cell hypertrophy, neuropathy, interstitial fibrosis, myocytolysis and apoptosis and lipid deposits in the heart. In addition, the cytoplasmic organelles of cardiomyocytes including the plasma membrane, mitochondrion and sarcoplasmic reticulum are also impaired in both type I and type II diabetes. Hyperglycaemia is a major aetiological factor in the development of diabetic cardiomyopathy in patients suffering from diabetes. Hyperglycaemia promotes the production of reactive oxygen (ROS) and nitrogen species (RNS). The release of ROS and RNS induces oxidative stress leading to abnormal gene expression, faulty signal transduction and apoptosis of cardiomyocytes. Hyperglycaemia also induces apoptosis by p53 and the activation of the cytochrome c-activated caspase-3 pathway. Stimulation of connective tissue growth factor and the formation of advanced glycation end products in extracellular matrix proteins induces collagen cross-linking and contribute to the fibrosis observed in the interstitium of the heart of diabetic subjects. In terms of signal transduction, defects in intracellular Ca2+ signalling due to alteration of expression and function of proteins that regulate intracellular Ca2+ also occur in diabetes. All of these abnormalities result in gross dysfunction of the heart. Beta-adrenoreceptor antagonists, ACE inhibitors, endothelin-receptor antagonist (Bonestan), adrenomedullin, hormones (insulin, IGF-1) and antioxidants (magniferin, metallothionein, vitamins C and E) reduce interstitial fibrosis and improve cardiac function in diabetic cardiomyopathy.
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PMID:Molecular and cellular basis of the aetiology and management of diabetic cardiomyopathy: a short review. 1536 3

Near-infrared reflectance spectroscopy (NIRS) was used to predict the chemical composition, apparent digestibility and digestible nutrients and energy content of commercial extruded compound foods for dogs. Fifty-six foods of known chemical composition and in vivo apparent digestibility were analysed overall and 51 foods were used to predict gross energy digestibility and digestible energy content. Modified partial least square calibration models were developed for organic matter (OM), crude protein (CP), ether extract (EE), crude fibre (CF), nitrogen free extracts (NFE) and gross energy (GE) content, the apparent digestibility (OMD, CPD, EED, NFED and GED) and the digestible nutrient and energy content (DOM, DCP, DEE, DNFE and DE) of foods. The calibration equations obtained were evaluated by the standard error and the determination coefficient of cross-validation. The cross-validation coefficients of determination (R) were 0.61, 0.99, 0.91, 0.96, 0.94 and 0.92 for OM, CP, EE, CF, NFE and GE, the corresponding standard error of cross-validation (SECV) being 5.80, 3.51, 13.35, 3.64 and 16.95 g/kg dry matter (DM) and 0.29 MJ/kg DM respectively. The prediction of apparent digestibility was slightly less accurate, but NIRS prediction of digestible nutrient (g/kg DM) and DE (MJ/kg DM) gave satisfactory results, with high R (0.93, 0.97, 0.93, 0.83 and 0.93 for DOM, DCP, DEE, DNFE and DE respectively) and relatively low SECV (11.55, 6.85, 12.14 and 22.98 g/kg DM and 0.47 MJ/kg DM). It is concluded that the precision of NIRS in predicting the energy value of compound extruded foods for dogs is similar or better than by proximate analysis, as well as being faster and more accurate.
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PMID:Energy evaluation of extruded compound foods for dogs by near-infrared spectroscopy. 1578 94

Positron emission tomography (PET) is perfectly suited for quantitative imaging of the kidneys, and the recent improvements in detector technology, computer hardware, and image processing software add to its appeal. Multiple positron emitting radioisotopes can be used for renal imaging. Some, including carbon-11, nitrogen-13, and oxygen-15, can be used at institutions with an on-site cyclotron. Other radioisotopes that may be even more useful in a clinical setting are those that either can be obtained from radionuclide generators (rubidium-82, copper-62) or have a sufficiently long half-life for transportation (fluorine-18). The clinical use of functional renal PET studies (blood flow, glomerular filtration rate) has been slow, in part because of the success of concurrent technologies, including single-photon emission computed tomography (SPECT) and planar gamma camera imaging. Renal blood flow studies can be performed with O-15-labeled water, N-13-labeled ammonia, rubidium-82, and copper-labeled PTSM. With these tracers, renal blood flow can be quantified using a modified microsphere kinetic model. Glomerular filtration can be imaged and quantified with gallium-68 EDTA or cobalt-55 EDTA. Measurements of renal blood flow with PET have potential applications in renovascular disease, in transplant rejection or acute tubular necrosis, in drug-induced nephropathies, ureteral obstruction, before and after revascularization, and before and after the placement of ureteral stents. The most important clinical application for imaging glomerular function with PET would be renovascular hypertension. Molecular imaging of the kidneys with PET is rather limited. At present, research is focused on the investigation of metabolism (acetate), membrane transporters (organic cation and anion transporters, pepT1 and pepT2, GLUT, SGLT), enzymes (ACE), and receptors (AT1R). Because many nephrological and urological disorders are initiated at the molecular and organelle levels and may remain localized at their origin for an extended period of time, new disease-specific molecular probes for PET studies of the kidneys need to be developed. Future applications of molecular renal imaging are likely to involve studies of tissue hypoxia and apoptosis in renovascular renal disease, renal cancer, and obstructive nephropathy, monitoring the molecular signatures of atherosclerotic plaques, measuring endothelial dysfunction and response to balloon revascularization and restenosis, molecular assessment of the nephrotoxic effects of cyclosporine, anticancer drugs, and radiation therapy. New radioligands will enhance the staging and follow-up of renal and prostate cancer. Methods will be developed for investigation of the kinetics of drug-delivery systems and delivery and deposition of prodrugs, reporter gene technology, delivery of gene therapy (nuclear and mitochondrial), assessment of the delivery of cellular, viral, and nonviral vectors (liposomes, polycations, fusion proteins, electroporation, hematopoietic stems cells). Of particular importance will be investigations of stem cell kinetics, including local presence, bloodborne migration, activation, seeding, and its role in renal remodeling (psychological, pathological, and therapy induced). Methods also could be established for investigating the role of receptors and oncoproteins in cellular proliferation, apoptosis, tubular atrophy, and interstitial fibrosis; monitoring ras gene targeting in kidney diseases, assessing cell therapy devices (bioartificial filters, renal tubule assist devices, and bioarticial kidneys), and targeting of signal transduction moleculas with growth factors and cytokines. These potential new approaches are, at best, in an experimental stage, and more research will be needed for their implementation.
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PMID:Future direction of renal positron emission tomography. 1635 95

The state of lipid transport function of the blood, blood contents of stable nitrogen metabolites, and proinflammatory cytokines (TNF-a and IL-1b) during therapy with simvastatin were studied in 29 patients receiving combination antihypertensive therapy with angiotensin converting enzyme inhibitors (ACEI) and verapamil. Lipid lowering action of simvastatin was realized just in 1 month of treatment and remained sustained for half a year (average duration). 6 months after addition of simvastatin to antihypertensive therapy substantial (58.4%, p=0.044) rise of plasma content of stable nitrogen metabolites took place. At the same time therapy with metoprolol in a similar group of patients exerted no considerable effect on blood plasma concentration of nitrate and nitrite anions. Lowering of median values of TNF-alpha from 20.13 (12.67-52.80) to 11.34 (3.31-31.29) pg/ml (p<0.0038) was also noted at the background of combination antihypertensive therapy. This happened without distinct affair with degree of lipid lowering action of simvastatin. The results of the study document positive effect of half year treatment of patients with concomitant hypertension and diabetes with simvastatin (10-20 mg/day) in combination with ACEI and verapamil on metabolism of nitric oxide and plasma content of TNF-alpha which realizes independently from degree of hypolipidemic action of simvastatin.
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PMID:[Effect of 6-month therapy with simvastatin on lipid transport function of the blood and the state of endothelium in patients with diabetes and hypertension]. 1647 6

The objective of the present study was to verify whether the generic reference levels (GRL) for soils contaminated with 2,4-dichlorophenol (2,4 DCP), established by Spanish legislation and published in the Real Decreto 9/2005, are accurate for Galician soils. For this, the surface horizons of seven soils under different types of land use were experimentally contaminated with different doses (between 0 and 10,000 times the GRL) of 2,4 DCP, and were then were subject to OECD toxicity test numbers 208 (root emergence and elongation) and 216 (soil nitrogen mineralization). The results obtained for the nitrogen mineralization test were difficult to interpret because they varied among soils, whereas the results of the root germination and elongation test were more coherent -- the values decreased with increasing doses of contaminant added to the soil. The results suggest that the root elongation test reflects the effect of this contaminant more clearly than the soil nitrogen mineralization test. Nevertheless, considering that in the lowest quality soils (i.e. agricultural soils containing a very low level of organic matter) contaminant doses of up to 1000 times the GRL did not affect root germination and elongation, it is clear that the GRL indicated in the relevant legislation are very low for the soils under study and that the threshold should be established taking into account the soil characteristics.
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PMID:Suitability of the OCDE tests to estimate contamination with 2,4-dichlorophenol of soils from Galicia (NW Spain). 1730 60

Insulin Resistance along with endothelial dysfunction give rise to a constellation of syndromes designated as IRS/MBS metabolic syndrome. Endothelial dysfunction starts early in life much before the development of structural atherosclerosis. Recent insights into vascular biology enable us to understand the molecular mechanisms underlying endothelial dysfunction, and the scope and need for prevention of "pre-clinical" coronary atherosclerosis through lifestyle modification; diet, exercise and stress management. Diminished production of nitric oxide (NO) and/or increased inactivation of NO through oxidative stress (reactive oxygen species ROS and reactive nitrogen species (RNS) are the basis of endothelial dysfunction hence increasing the bioavailability of NO and decreasing its inactivation is the aim of prevention and reversal of endothelial dysfunction. Insulin regulates constitutive NOS gene expression in endothelial cells in vivo; vasodilation is an important component of Insulin-stimulated whole body glucose uptake. Successful strategies are: PPAR alpha and gamma agonists which increase NO production in endothelium; anti-oxidants such as vit. E and C; supplementation with L-arginine, tetrahydrobiopterin-BH4 or sepiapterin (precursor of BH4), SOD mimetic tempol, statins which apart from lowering cholesterol improve NO production, selective beta1 adrenoreceptor antagonists such as nebivolol; suppression of angiotensin-mediated endothelin production by ACE inhibitors and ATR blockers; CB1 receptor blockers, PKCb inhibitors, nitric oxide donors (glyceryl trinitrate and isosorbide dinitrate), dietary supplements of EPA/DHA and regular physical exercise and control of mental stress.
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PMID:Causation, prevention and reversal of vascular endothelial dysfunction. 1805 38


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