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Biomedical subjects

L Valdes

Publications and source records attributed to L Valdes.

At least 19 recordsLinked to original sources
PubMed2006

Towards active community participation in dengue vector control: results from action research in Santiago de Cuba, Cuba.

Community participation is advocated as essential for attaining effective dengue prevention, but knowledge of how to foster this is limited. In Santiago de Cuba, multiple small task forces were created at the neighbourhood level that included all stakeholders in the control of Aedes aegypti. The task forces assessed the perceived needs and elaborated action plans to promote specific behavioural change and to reduce environmental risks through social communication strategies and intersectoral local government activities. We monitored five dimensions of the participation process and assessed behavioural and environmental results and entomological outcomes. Participation was weak to good. At the household level, uncovered water storage containers decreased from 49.3% to 2.6% between 2000 and 2002, and removing larvicide from them dropped from 45.5% to 1%. There was a reduction of 75% in the absolute number of positive containers and a significant decrease from 1.23% to 0.35% in the house index. Local task forces, in which the interests of householders as well as vector control workers are directly represented, can lead to effective government-community partnerships that resolve problems of mutual concern.

Animals↗
PubMed2000

Epidemiologic studies on Dengue in Santiago de Cuba, 1997.

A small, isolated outbreak of dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) due to dengue virus type 2 (DEN-2) was documented in Santiago de Cuba on the island of Cuba beginning in January 1997. There were 205 DHF/DSS cases, all in persons older than age 15 years. All but three had evidence of a prior dengue infection, with the only known opportunity being the islandwide dengue virus type 1 (DEN-1) epidemic of 1977-1979. Virtually complete clinical and laboratory surveillance of overt disease was achieved. From December 1997 to January 1998, a random, age-stratified serum sample was obtained from 1,151 persons in 40 residential clusters in Santiago. Sera were tested for DEN-1 and DEN-2 neutralizing antibodies. The prevalence of DEN-2 antibodies in children age 15 years and under, born after the 1981 DEN-2 epidemic, was taken as the 1997 DEN-2 infection rate. This was adjusted slightly to accommodate observed cases, resulting in an estimated infection rate of 4.3%. Dengue fever and DHF/DSS attack rates were calculated from estimated total primary and secondary DEN-2 infections. Only 3% of 13,116 primary infections were overt. The DHF/DSS attack rate for adults of all ages was 420 per 10,000 secondary DEN-2 infections.

Adolescent↗
PubMed2000

Comparison of the effects of felodipine and cilazapril on exercise performance in patients with mild to moderate hypertension. A crossover study.

This double-blind crossover study was designed to compare the effects of felodipine and cilazapril on exercise performance in hypertensive patients. After a 2-week placebo run-in period, 40 patients with mild to moderate hypertension were randomized into two parallel groups to receive either felodipine (10 mg) or cilazapril (5 mg) for 4 weeks. After another 2-week washout period, treatments were then crossed over for a further 4-week study period. All patients were given an extensive rest and exercise evaluation at the end of the placebo period. Extensive rest and exercise evaluations were repeated after a 4-week treatment period and again after the second washout period and after the second 4-week treatment period. Before each exercise test, epinephrine, norepinephrine and dopamine plasma levels and plasma renin activity were measured. Two groups were similar at baseline for systolic and diastolic blood pressure and heart rate as well as for laboratory and hormonal variables and duration of exercise test. At the end of treatment diastolic blood pressure was significantly reduced in the felodipine group (p = 0.019). Duration of exercise test was longer than at baseline (p = 0.031) in the felodipine group. Plasma dopamine levels were significantly increased in the cilazapril group. Plasma renin activity significantly increased in the felodipine group. In conclusion, our data show that the two drugs have the same effectiveness in resting conditions but that felodipine is more effective in lowering maximum exercise diastolic blood pressure and in improving exercise time with an double product increase (not significant); it has no statistically significant effect on maximal exercise systolic blood pressure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Maintenance of blood pressure control and left ventricular performance with small doses of enalapril.

Enalopril treatment (20 mg every 12 hours) of 24 patients with essential hypertension and left ventricular (LV) hypertrophy established normal blood pressure (BP) after 8 weeks, and after 7 years had reduced LV mass index by 39% from 148 +/- 34 to 90 +/- 16 g/m2, and had normalized LV structure and function and QT dispersion. Stepwise reduction of the enalapril dosage from 40 to 30, 20, 10, and 5 mg/day during the eighth year caused no significant changes in BP, LV structure, LV systolic function, or QT dispersion, which all likewise remained unaltered during a further year of the 5-mg/day regimen. We conclude that for hypertensive patients in whom prolonged treatment with standard doses of enalapril has normalized BP, LV structure and function, and QT dispersion, significantly smaller doses are sufficient to maintain these cardiovascular achievements.

Adult↗
PubMed1999

[Severe lactic acidosis disease disclosing milk-protein intolerance to cows' milk].

UNLABELLED: The age of discovery and initial symptoms of cow milk allergy can vary. Lactic acidosis is exceptionally associated to this allergy. CASE REPORT: A 32-day-old girl was admitted for a severe malaise with metabolic acidosis and hyperlactacidemia. There were no neonatal or family problems; breastfeeding was stopped on the 25th day. Fever was noted on the 29th day and her mother reported behavior anomalies followed by a severe malaise with unconsciousness between the 29th and 32nd day. At admission, the infant showed a severe neurological distress, hypotonia and lethargy. Infection and neurological imaging were normal. A compensated metabolic acidosis with hyperlactacidemia (5.96 mmol/L) was noted. There was no argument for esophageal reflux nor vagal hypertony; mitochondrial cytopathy was also excluded. After a 24 hours fast, the clinical state gradually improved and normalized at h48. The infant was discharged with a milk protein hydrolysate formula. Her mother attempted to reintroduce cow milk on the 59th and 64th day, but this was immediately followed by allergic manifestations which supported the diagnosis of cow milk allergy. CONCLUSION: Neurological distress and hyperlactacidemia exceptionally reveal this type of intolerance. The mechanism of hyperlactacidemia remains unclear; it is possibly the consequence of severe changes of the intestinal mucosa, an exclusive glycolytic tissue.

Acidosis, Lactic↗
PubMed1999

Step-down of enalapril treatment for arterial hypertension.

Enalapril treatment (20 mg every 12 hours) of 24 patients with essential hypertension and left ventricular (LV) hypertrophy established normal blood pressures after 8 weeks, and after 5 years, it had reduced LV mass index by 39% (from 148+/-34 to 90+/-16 g/m(2)) and had normalized LV structure and function and QT dispersion. Stepwise reduction of the enalapril dosage from 40 to 30, 20, 10, and 5 mg/d during the eighth year caused no significant change in blood pressure, LV structure, LV systolic function, or QT dispersion, which all likewise remained unaltered during an additional 2-year period of the 5-mg/d regimen. We conclude that for hypertensive patients in whom prolonged treatment with high doses of enalapril has normalized blood pressure, LV structure, LV function, and QT dispersion, the dose may be reduced as much as 8-fold without detriment to cardiovascular control. The use of smaller doses is evidently advantageous from the point of view of health costs.

Adult↗
PubMed1997

Utility of tumour markers in the diagnosis of neoplastic pleural effusion.

Approximately 20% of pleural effusions are caused by neoplastic processes. Although cytology is the most specific routine diagnostic procedure, its sensitivity of 50-60% is insufficient, and thus diagnosis is usually carried out by more invasive techniques such as pleural biopsy, thoracoscopy or thoracotomy. The object of this study is to evaluate the use of determining some tumour markers in pleural fluid obtained by thoracocentesis for diagnosis of neoplastic pleural effusion. Patients (271) with pleural effusions were classified in five groups: I: neoplasms n = 88; II: tuberculosis n = 63; III: parapneumonics n = 53; IV: miscellaneous exudates n = 39 and V: transudates n = 28. The tumour markers studied were: carcinoembryonic antigen (CEA), CA 125, squamous cell carcinoma antigen (SCC), and neuron specific enolase (NSE). The tumour makers had the following diagnostic efficiencies for neoplastic origin of the pleural effusion: CEA 76% (sensitivity 31%, specificity 93%); CA 125 66% (70% and 61%); SCC 65% (48% and 80%) and NSE 53% (30% and 89%). The diagnostic efficiencies for pulmonary neoplastic origins were 68% for NSE (sensitivity 83%, specificity 53%); 65% for SCC (54% and 75%); 63% for CEA (80% and 48%) and 61% for CA 125 (79% and 42%). We believe that the routine testing of tumour markers in pleural fluid obtained by thoracocentesis would greatly increase diagnostic effectiveness and could avoid the practice of more aggressive diagnostic techniques on the patient.

Antigens, Neoplasm↗
PubMed1997

[Syncope with long QT interval in a 39 day-old infant treated with cisapride].

UNLABELLED: Cardiotoxicity of cisapride may increase when this drug is associated with ranitidine. CASE REPORT: A 37-day old term infant, treated with cisapride (1.2 mg/kg/d) and ranitidine for regurgitations, was hospitalized for malaise. A prolonged QT interval (with isolate ventricular extrasystoles), noted at admission, disappeared rapidly after cisapride withdrawal. Linkage to cisapride was probable, promoted by high dosage and cisapride metabolism inhibition by ranitidine, but its plasma concentration was not measured. CONCLUSION: This case report stresses the problem of cisapride dosage in infants and the question of an interaction between cisapride and ranitidine.

Anti-Ulcer Agents↗
PubMed1997

Early captopril treatment reduces plasma endothelin concentrations in the acute and subacute phases of myocardial infarction: a pilot study.

It has been reported that endothelin-1 (ET-1) increases in acute myocardial infarction (AMI). Experimental studies showed that captopril administration reduces ET-1 secretion. In addition, it was reported that the increased ET-1 levels are a negative prognostic index. The study sought to verify whether captopril can reduce plasma ET levels in the acute and subacute phases of reperfused anterior AMI. Forty-five patients, hospitalized for suspected anterior AMI within 4 h from the onset of symptoms, suitable for thrombolysis (first episode), Killip class I-2, were randomized (double blind) into two groups: group A (23; seven women/16 men) received captopril (as first dose) 2-4 h after starting thrombolysis (the dose was then increased up to 25 mg every 8 h). Group B (22; five women/17 men) received placebo after thrombolysis. All the patients met the reperfusion criteria. The two groups were similar with regard to age, sex, CK peak, ejection fraction, end-systolic volume and risk factors. Plasma ET levels were measured at entry, and 2, 12, 24, 48, and 72 h after starting thrombolysis. Mean concentrations of ET +/- SD: Group A basal, 1.50 +/- 0.67; at 2h, 2.31 +/- 1.24; 12 h, 1.84 +/- 1.45; 24 h, 1.30 +/- 0.72; 48 h, o.95 +/- 0.50; 72 h, 0.60 +/- 0.15 fmol/ml; p < 0.001. Group B basal, 1.58 +/- 0.83; at 2 h, 2.38 +/- 1.35; 12 h, 2.33 +/- 1.71; 24 h, 1.80 +/- 1.41; 48h, 1.46 +/- 0.88; 72 h, 0.93 +/- 0.44 fmol/ml; p < 0.001. Difference between the two groups was significant at the beginning of the test (between 2 and 12 h, p[=]0.002). After that, the values of the plasma endothelin decreased in parallel, p < 0.001. Our data suggest that captopril affects plasma ET levels in the acute and subacute phases of AMI. Moreover, these results provide additional evidence for a beneficial effect of early captopril treatment.

Adult↗
PubMed1996

Muscle length changes during swimming in scup: sonomicrometry verifies the anatomical high-speed cine technique.

Recent attempts to determine how fish muscles are used to power swimming have employed the work loop technique (driving isolated muscles using their in vivo strain and stimulation pattern). These muscle strains have in turn been determined from the anatomical high-speed cine technique. In this study, we used an independent technique, sonomicrometry, to attempt to verify these strain measurements and the conclusions based on them. We found that the strain records measured from sonomicrometry and the anatomical-cine techniques were very similar. The ratio of the strain measured from sonomicrometry to that from the anatomical-cine technique was remarkably close to unity (1.046 +/- 0.013, mean +/- S.E.M., N = 15, for transducers placed on the muscle surface and corrected for muscle depth, and 0.921 +/- 0.028, N = 8, in cases where the transducers were inserted to the average depth of the red muscle). These measurements also showed that red muscle shortening occurs simultaneously with local backbone curvature, unlike previous results which suggested that white muscle shortening during the escape response occurs prior to the change in local backbone curvature.

Animals↗
PubMed1993

Effects of captopril on myocardial protection during cardioplegia.

UNLABELLED: The study aimed at checking effects exerted by captopril (C) on human myocardial ACE system as well as the role played by tissue ACE inhibition in reducing reperfusion damage. A human experimental model was used during cardioplegia due to aorto-coronary-by-pass (CABG). Fifty-four patients with coronary artery disease affecting 3 vessels having suffered from acute myocardial infarction anterior (AMI-ant), homogeneous as far as ejection fraction (35-55%), number of grafts (3), clamping time, age and sex, were randomised in a double blind experiment, and were given captopril or placebo (P). A total of 4 mg/l Captopril was mixed into the cardioplegic solution with blood according to the method of Buckberg (Buckberg GD. J Thorac Cardiovasc Surg 1987; 93: 127-139). Eight samples (blood/perfusate) were obtained from each patients and norepinephrine (NE), epinephrine (E) were assayed using an HPLC technique. Angiotensin I was assayed by RIA. CK was also assayed (units/ml). Blood/perfusate samples were taken during CABG: (1) pre-pump; (2) pump sample; (3) pump preclamping; (4) coronary sinus; (5) coronary sinus sample during reperfusion; (6) coronary sinus during warm reperfusion; (7) after clamping sample; (8) after decanulation; RESULTS: Captopril group (29 patients): angiotensin I: (1) 8.15; (2) 7.0; (3) 7.31; (4) 8.45; (5) 8.93; (6) 8.73; (7) 9.07; (8) 9.40; versus placebo: (1) 7.09, (2) 7.43; (3) 7.80; (4) 9.31; (5) 9.01; (6) 8.35; (7) 8.85; (8) 8.07 ng/ml, probability, not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1992

Captopril and glutathione before thrombolysis in acute myocardial infarction: a pilot study.

This study is aimed at checking whether treatment with glutathione (GL) and captopril (CA) before thrombolysis can further improve the protective effects of ACE-inhibitors in cases with anterior acute myocardial infarction (AMI). Ninety-eight double blind randomized patients (86 men and 12 women) showing symptoms of AMI anterior and undergoing thrombolytic treatment were admitted to our study and subdivided into 4 groups. Group A (25 pts) received thrombolytic treatment only, Group B (23 pts) received 3 g GL intravenously 15 min before thrombolysis and for 2 h thereafter, Group C (26 pts) received 6.25 mg CA orally 15 min before starting thrombolytic treatment, Group D (24 pts) received 3 g GL intravenously before thrombolysis and for 2 h thereafter, and captopril as well like group C. On the third day after AMI onset groups A and B received CA also. In all groups, the doses of CA were gradually increased according to blood pressure values. The following features were considered: a) the occurrence of early (within the first 2 h after thrombolysis) ventricular hyperkinetic arrhythmias; b) CK peak; c) the normalization time of CK peak (NT); d) the occurrence of late ventricular hyperkinetic arrhythmias (VHA) in the predischarge Holter test (Lown's class 2); e) ejection fraction (EF) being measured in 60 pts undergoing haemodynamic test. The results were an follows: Group A: VHA early 13/25, CK peak 1982 +/- 282; NT 71 +/- 2 h; Late VHA 8/25; EF 53.5 +/- 2.5% (16 pts). Group B: VHA early 11/23; CK peak 1917 +/- 242 U/l; NT 69 +/- 3 h; late VHA 7/23; EF 54.5 +/- 5.4% (14 pts). Group C: VHA early 4/26; CK peak 1671 +/- 266 U/l; NT 58 +/- 3 h; late VHA 5/26; EF 55.5 +/- 3% (16 pts). Group D: VHA early 3/24; CK peak 1463 +/- 201; NT 56 +/- 4 h; late VHA 5/24; EF 57.6 +/- 4% (14 pts).

Aged↗
PubMed1992

[Effect of captopril on human myocardial ACE-inhibition: neurohumoral variations during coronary sinus cardioplegia. Cardioprotective effect during aortocoronary bypass].

UNLABELLED: The present study is aimed at checking effects exerted by captopril on human myocardial ACE system (ACE-T) as well as the role played by tissue ACE-inhibition in reducing reperfusion damage. A human experimental model was used during cardioplegia due to aortocoronary bypass graft (CABG): 54 patients with coronary artery disease affecting 3 vessels having suffered from acute anterior myocardial infarction, homogeneous as far as ejection fraction (35-55%), number of grafts (3), clamping time, age and sex, were randomised in a double blind experiment, and were given captopril or placebo: 4 mg/l captopril were mixed into the cardioplegic solution with blood according to Buckberg, 8 blood samples were obtained from each patient and norepinephrine, epinephrine were assayed using an HPLC technique. Angiotensin 1 was assayed by RIA. CK was assayed as well (U/L). Blood samples were taken during CABG: pre-pump sample; pump sample; pump preclamping sample; coronary sinus sample; warm reperfusion sample; coronary sinus during warm reperfusion; after clamping sample; after cannulation. RESULTS: captopril group (29 patients): angiotensin 1:8.15; 6.9; 7.45; 8.66; 8.93; 8.70; 9.07; 9.40 versus placebo: 7.09; 7.43; 7.80; 9.31; 9.01; 8.35; 8.85; 8.07 mcg (all NS). Noradrenaline: captopril group: 359; 404; 329; 282; 263; 216; 310; 337 versus placebo: 439; 520; 499; 469; 526; 566; 501; 443 pg (p < 0.001). CK, captopril group: 79.9; 95.1; 100.8; 94.3; 104.2; 94.7; 108.4; 108 versus placebo: 76.2; 120.2; 135.5; 203; 225; 272; 247; 228.7 U/L (p < 0.01). Epinephrine values showed no significant difference between the 2 groups. Norepinephrine and CK decrease as well as angiotensin I increase in treated patients as compared to controls suggest some effect exerted by captopril ACE-T and its capability of reducing reperfusion damage and recommend its use for heart protection during CABG.

Aged↗