Gene/Protein Disease Symptom Drug Enzyme Compound
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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have shown that serum activity of angiotensin-converting enzyme (ACE; EC 3.4.15.1) significantly decreases in patients with carcinoma of different localizations. There is no information in literature about measuring this enzyme in primary liver carcinoma patients. The serum activity of ACE has been examined on 15 primary liver carcinoma patients, 10 patients with cirrhosis, and 26 healthy subjects. Serum activity has been determined by spectrophotometric method using synthetic substrate Hip-His-Leu. The results were given in units which correspond to one nmol of hippuric acid released by enzymatic hydrolyze of Hip-His-Leu substrate in one minute on serum milliliter. The results have shown that serum activity of ACE increased in patients with cirrhosis (37.06 +/- 2.9; X +/- SEM; p < 0.05), and decreased in primary liver carcinoma patients (23.44 +/- 1.87; p < 0.01), what was statistically significant in comparison with the activity of the same enzyme in healthy subjects (29.90 +/- 2.72). These results point out the possibility of clinical application of measuring serum ACE activity as one of primary liver carcinoma marker in differential diagnosis of the disease.
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PMID:[Serum angiotensin converting enzyme in patients with primary liver carcinoma]. 1038 37

ACE inhibitors block B(2) receptor desensitization, thereby potentiating bradykinin beyond blocking its hydrolysis. Angiotensin (Ang)-(1-7) also acts as an ACE inhibitor and, in addition, may stimulate bradykinin release via angiotensin II type 2 receptors. In this study we compared the bradykinin-potentiating effects of Ang-(1-7), quinaprilat, and captopril. Porcine coronary arteries, obtained from 32 pigs, were mounted in organ baths, preconstricted with prostaglandin F(2alpha), and exposed to quinaprilat, captopril, Ang-(1-7), and/or bradykinin. Bradykinin induced complete relaxation (pEC(50)=8.11+/-0.07, mean+/-SEM), whereas quinaprilat, captopril, and Ang-(1-7) alone were without effect. Quinaprilat shifted the bradykinin curve to the left in a biphasic manner: a 5-fold shift at concentrations that specifically block the C-domain (0.1 to 1 nmol/L) and a 10-fold shift at concentrations that block both domains. Captopril and Ang-(1-7) monophasically shifted the bradykinin curve to the left, by a factor of 10 and 5, respectively. A 5-fold shift was also observed when Ang-(1-7) was combined with 0.1 nmol/L quinaprilat. Repeated exposure of porcine coronary arteries to 0.1 micromol/L bradykinin induced B(2) receptor desensitization. The addition of 10 micromol/L quinaprilat or Ang-(1-7) to the bath, at a time when bradykinin alone was no longer able to induce relaxation, fully restored the relaxant effects of bradykinin. Angiotensin II type 1 or 2 receptor blockade did not affect any of the observed effects of Ang-(1-7). In conclusion, Ang-(1-7), like quinaprilat and captopril, potentiates bradykinin by acting as an ACE inhibitor. Bradykinin potentiation is maximal when both the ACE C- and N-terminal domains are inhibited. The inhibitory effects of Ang-(1-7) are limited to the ACE C-domain, raising the possibility that Ang-(1-7) synergistically increases the blood pressure-lowering effects of N-domain-specific ACE inhibitors.
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PMID:Bradykinin potentiation by angiotensin-(1-7) and ACE inhibitors correlates with ACE C- and N-domain blockade. 1146 67

The Dex/CRH test is one of the most reliable neuroendocrine function tests for hypothalamic-pituitary-adrenocortical (HPA) system dysregulation in depression. Persistent overdrive of HPA system activity after successful antidepressant treatment predicts an enhanced risk for relapse of a depressive episode. As the renin-angiotensin system has been shown to play a role in HPA system activity, we investigated the impact of the angiotensin converting enzyme (ACE) gene insertion (I)/deletion (D) polymorphism, which determines ACE plasma concentrations, on HPA system dysregulation. We performed repeated combined Dex/CRH tests in 115 patients suffering from major depression. Dex/CRH test results were related to the I/D polymorphism within the ACE gene, which was assessed by PCR. Genotype frequencies were comparable to those in the general population (I/I 16.8%, I/D 59.3%, D/D 23.9%). D/D genotypes showed a higher cortisol stimulation during the first Dex/CRH test after admission than homozygous I-allele carriers (repeated measurement ANOVA: P=0.034). Cortisol area under the curve values were highest in those with the D/D genotype (mean+/-SEM [nmol/l*75 min]: 12700+/-2220), intermediate in those with the I/D genotype (9570+/-1000), and lowest in those with the I/I genotype (5160+/-1000; ANOVA: P=0.04). After successful antidepressive treatment and attenuation of HPA system overdrive these differences were no more detectable. The HPA axis stimulating properties of higher ACE and consecutively higher AT-II and/or lower substance P concentrations may be crucial factors for the HPA system hyperactivity during major depressive episodes.
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PMID:Hypothalamic-pituitary-adrenocortical axis dysregulation in patients with major depression is influenced by the insertion/deletion polymorphism in the angiotensin I-converting enzyme gene. 1214 30

Insulin is known to upregulate apolipoprotein A-I (apoA-I) promoter activity and to increase apoA1 gene expression in vivo. To determine if enhancement of insulin action with insulin sensitizers can also increase the apoA-I expression, we studied the in vivo effect of troglitazone, a potent insulin sensitizer, on the expression of rat hepatic and intestinal apoA-I mRNA using Northern blot analysis. The plasma, hepatic, and intestinal apoA-I content was also measured with immunoblot analysis using a specific anti-rat apoA-I antiserum. Troglitazone, given mixed with rat chow (0.2%) for 18 days, did not increase either plasma or tissue apoA-I mRNA or protein content. Intestinal apoA-I mRNA content relative to glyceraldehyde-3 phosphate dehydrogenase (G(3)PDH) mRNA was significantly lower compared with hepatic tissue content in both control and troglitazone-treated rats. The effect of troglitazone on the rat apoA-I promoter was examined using transient transfection analysis in HepG2 cells transfected with the apoA-I-chloramphenicol acetyl transferase (CAT) reporter plasmid (pAI.474.CAT). CAT activity (percentage acetylation of chloramphenicol as means +/- SEM) was not significantly different in ethanol (vehicle)-treated cells compared with cells treated with troglitazone (50.5% +/- 2.5% in control cells vs 57.7% +/- 8.2% and 53.5% +/- 4.2% in cells treated with 10 and 100 mM troglitazone, respectively). It is concluded that troglitazone doses known to achieve insulin sensitization did not enhance rat apoA-I promoter activity sufficiently to result in an increased apoA-I mRNA or protein expression in the intact rat. However, peroxisome proliferator activator receptor (PPAR) agonists that have significant PPAR alpha activity in addition to their PPAR gamma effects, may well be able to induce apoA-I expression.
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PMID:Apolipoprotein A-I expression in rats is not altered by troglitazone. 1248 10

Nitric oxide (NO) derived from neuronal NO synthase (nNOS) in the macula densa is a modulator of tubuloglomerular feedback. However, little is known about the regulation of the afferent arteriolar diameter by NO from the macula densa in salt-sensitive hypertension. We investigated the relationship between nNOS in the macula densa and the afferent arteriolar diameter in deoxycorticosterone acetate (DOCA)-salt hypertensive rats treated with angiotensin converting enzyme (ACE) inhibitor or thiazide for 5 weeks. DOCA rats had reduced nNOS expression in the macula densa compared to controls and reduction of NO production evaluated with 4,5-diaminofluorescein diacetate in the juxtaglomerular apparatus (JGA). Treatment with ACE inhibitor and thiazide increased nNOS and NO production in the JGA. The diameter of the afferent arteriole observed by SEM using microvascular casts was smaller in DOCA rats compared to control rats, and ACE inhibitor or thiazide dilated the afferent arteriole with a positive correlation to nNOS immunoreactivity in the macula densa. In conclusion, the afferent arteriolar diameter might be regulated by NO derived from nNOS in the macula densa in DOCA-salt hypertensive rats.
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PMID:Nitric oxide generated by nNOS in the macula densa regulates the afferent arteriolar diameter in rat kidney. 1561 48

This study was performed to determine whether adult male patients with Fabry disease who demonstrate a continuing decline in renal function despite 2 to 4 yr of conventionally dosed agalsidase alfa therapy (0.2 mg/kg every other week [EOW]) show an improved slope of decline with weekly administration using the same dosage. Eleven (27%) of 41 adult male patients with Fabry disease who participated in long-term agalsidase alfa clinical trials and who had demonstrated a slope of decline in estimated GFR (eGFR) of > or =5 ml/min per 1.73 m(2)/yr while receiving long-term treatment with agalsidase alfa at the currently recommended dosage of 0.2 mg/kg, infused EOW, were enrolled in this open-label, prospective study. Patients were switched from EOW to weekly infusions and followed for an additional 24 mo. Before switching to weekly dosing, eGFR was 53.7 +/- 6.3 ml/min per 1.73 m(2) (mean +/- SEM), and mean rate of change in eGFR was -8.0 +/- 0.8 ml/min per 1.73 m(2)/yr. During the 24-mo follow-up period after switching to weekly dosing, the mean rate of change in eGFR was observed to slow to -3.3 +/- 1.4 ml/min/1.73 m(2)/yr (P = 0.01 versus EOW). After switching to weekly dosing, three patients demonstrated an improvement in eGFR and six patients demonstrated a slowing in the rate of eGFR decline; only two patients failed to improve their eGFR slope. A multiple regression model confirmed that the weekly infusion regimen was the strongest explanatory variable for the change in eGFR (P = 0.0008), with a weaker contribution from the concomitant use of angiotensin converting enzyme inhibitors/angiotensin receptor blockers (P = 0.02). These results suggest that weekly infusions of agalsidase alfa at a dosage of 0.2 mg/kg may be beneficial in the subgroup of patients who have Fabry disease and whose kidney function continues to decline after 2 to 4 yr or more of standard EOW dosing.
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PMID:Weekly enzyme replacement therapy may slow decline of renal function in patients with Fabry disease who are on long-term biweekly dosing. 1742 46

The Second Australian National Blood Pressure Trial reported better prognosis for hypertensive subjects randomly assigned to an angiotensin-converting enzyme inhibitor (ACE-I) compared with a diuretic-based regimen despite no difference in brachial blood pressure control. A possible explanation is that there was a difference in central aortic pressures despite similar brachial pressure reductions. We examined this hypothesis in a subset of the Second Australian National Blood Pressure Trial cohort evaluated both before and after 4 years of treatment. The average age of the 479 subjects was 71.6+/-4.7 years (mean+/-SD), and 56% were women. Brachial systolic and pulse pressures after treatment were 145+/-1 (mean+/-SEM), 143+/-1, 72+/-1, and 70+/-1 mm Hg for diuretic and ACE-I groups, respectively. The respective changes from pretreatment values were -17+/-2, -16+/-2, -9+/-1, and -7+/-1 mm Hg. None of the differences between diuretic and ACE-I groups were significant. Central arterial pressure waveforms were acquired from carotid tonometry and calibrated from brachial pressures. Central systolic and pulse pressures posttreatment were 144+/-2, 144+/-2, 71+/-2, and 72+/-2 mm Hg for diuretic and ACE-I groups, respectively. The respective changes from pretreatment values were -15+/-2, -17+/-2, -6+/-2, and -8+/-2 mm Hg. None of the differences between diuretic and ACE-I groups were significant. The similarity of central and brachial pressures in this cohort of older hypertensive subjects is most likely because of the influences of age and hypertension in increasing arterial stiffness. There is no evidence that the better prognosis for patients randomly assigned to ACE-I in Second Australian National Blood Pressure Trial resulted from a disproportionate lowering of central blood pressure.
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PMID:Similar effects of treatment on central and brachial blood pressures in older hypertensive subjects in the Second Australian National Blood Pressure Trial. 1763 48

We assessed the possible association between variants of the genes encoding for the angiotensin-converting enzyme ( ACE) and alpha-actinin-3 ( ACTN3) (both individually and combined) and several endurance phenotypic traits, e.g., peak power output (PPO), ventilatory (VT) and respiratory compensation threshold (RCT), among others, in professional road cyclists and sedentary controls (n = 46 each). We applied an ANCOVA test using the aforementioned phenotype traits as dependent variables, ACE and/or ACTN3 genotype as the fixed (independent) factor and age and body mass as covariates. We only found a significant genotype effect with no concomitant covariate effect for ACTN3, with cyclists who were not alpha-actinin-3 deficient (RR + RX genotypes) having higher PPO and VT values than their XX counterparts (mean [SEM]: 7.4 (0.1) vs. 7.1 (0.1) W/kg, p = 0.035; and 4.5 (0.1) vs. 4.3 (0.1) W/kg, p = 0.029, respectively). Cyclists with an "extreme" ACTN3 and ACE genotype combination, i.e., most strength/power oriented (DD + RR/RX), had higher RCT values than those with the "intermediate" combinations (II + RX/RR, p = 0.036; and DD + XX, p = .0004) but similar to those with the most endurance oriented genotype (II + XX). No significant differences (p > 0.05) were found in controls. In summary, in world-class cyclists, we only found an association between ACTN3 genotypes and VT and PPO, and between ACTN3/ACE genotype combinations and RCT.
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PMID:Endurance performance: genes or gene combinations? 1865 73

Microcrystalline cellulose (MCC), calcium phosphate (DCP)/MCC (4:1, w/w) and lactose (Lac)/MCC (4:1) pellets with different intragranular porosity were prepared in an extrusion-spheronizator and three volume ratios of ethanol/water were used as binder agents to prepare pellets. The compression behaviors of these pellets with different intragranular pore volume were evaluated with the parameters of Kawakita model. The results showed that high pore volume of pellets made up of MCC had the best compressibility and low pore volume of pellets had a poor compactibility. However, the compressibility of different porosity of pellets made up of DCP/MCC (4:1) or Lac/MCC (4:1) was good, but they were not significantly different. The reason might be the main compression mechanism of high porosity of MCC pellets was plastic deformation and that of DCP/MCC pellets or Lac/MCC pellets was not plastic deformation but fragmentation. These results can be observed directly by the SEM photographs. According to these results, the conclusion could be drawn that high porosity MCC pellets and different porosity DCP/MCC pellets and Lac/MCC pellets can be used as cushion granules to maintain the original shape and release characteristics of drug pellets when pellets were tabletted.
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PMID:[Evaluation with compression equations of compression behavior of pellets with different intragranular pore volumes]. 1954 61

The anaerobic degradation of 2,4-dichlorophenol (2,4-DCP) in upflow anaerobic sludge blanket (UASB) and expanded granular sludge bed (EGSB) reactors using glucose as main carbon source was studied. The performance of both systems was compared in terms of 2,4-DCP and COD removal efficiencies, methane production, stability, granular sludge adaptability as well as reversion of the bacterial inhibition. Both organic and 2,4-DCP loading rates were incrementally varied through the experiments. With loading rates of 1.9 gCODL(-1)d(-1) and 100mg 2,4-DCP L(-1)d(-1), 75% and 84% removal efficiencies of this compound, accompanied by COD consumption efficiencies of 61% and 80% were achieved in the UASB and EGSB reactors, respectively. In these conditions, methane production reached 0.088 L CH(4)g(-1) COD in the EGSB reactor whereas in the UASB reactor was almost negligible. Decreasing the 2,4-DCP loading rate to 30 mgL(-1)d(-1) an improvement in the methane production was observed in both reactors (methanogenic activity of 0.148 and 0.192 L CH(4)g(-1) COD in UASB and EGSB reactors, respectively). Efficiency of dechlorination was improved in both reactors from around 30% to 80% by reducing to one-half the COD due to a decreasing of the 4-chlorophenol concentration accumulated in the effluents of both reactors. The dechlorination efficiency of the UASB reactor was dramatically inhibited at a 2,4-DCP feed concentration above around 210 mgL(-1) because of 2,4-DCP accumulation in the effluent. SEM studies revealed no significant morphological changes in the sludge granules.
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PMID:Comparison of UASB and EGSB performance on the anaerobic biodegradation of 2,4-dichlorophenol. 1957 92


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