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Biomedical subjects

A Carvalho

Publications and source records attributed to A Carvalho.

At least 37 records · Page 2Linked to original sources
PubMed1993

No evidence of genetic heterogeneity in Brazilian facioscapulohumeral muscular dystrophy families (FSHD) with 4q markers.

The gene responsible for facioscapulohumeral muscular dystrophy (FSHD), an autosomal dominant neuromuscular condition, has been mapped to chromosome 4. Until recently, the two closest available markers were D4S139 and D4S163 but a new marker (p13E-11) which recognizes de novo rearrangements in isolated cases of FSHD characterized by shorter EcoRI fragments has been now identified. Linkage analysis in FSHD families with p13E-11 shows that usually a smaller fragment segregates with the disease gene among the affected individuals from each genealogy. In the present paper, we report the results from linkage analysis with the marker loci D4S163 and D4S139 in 6 FSHD families and with p13E-11 in these and in 6 other additional Brazilian families (total of 12). The results from such analysis do not suggest genetic heterogeneity for FSHD in our population. In 11 out of the 12 families studied with p13E-11, a shorter specific EcoRI band was found to segregate in all affected patients from each genealogy. In one family, the normal individuals had a smaller EcoRI fragment than the affected ones. The size of the EcoRI fragments detected with p13E-11 varied from 13.5 to 29 kb but was constant within each genealogy. Our results suggest that the use of the marker p13E-11 for preclinical and prenatal diagnosis should be done only in families in which it is possible to identify the fragments segregating among the affected individuals.

Adolescent↗
PubMed1993

[Hepatitis C epidemiology in the central area of Portugal. Prevalence of anti-HCV in the population of the district of Coimbra].

Anti-hepatitis C virus antibody (anti-HCV) screening was performed in a sample of the adult population of the Coimbra District. 657 persons were included (267 male and 390 female, mean age of 42.7 +/- 13.1 years), aleatorily chosen from four characteristic councils. Anti-HCV was detected using an ELISA-2 test and all positive sera were also tested with RIBA-2. General prevalence of anti-HCV was 0.46%. All positive patients live in urban areas and presented risk factors for HCV infection. Anti-HCV was found in 33.3% of intravenous drug abusers, in 1.8% of transfused individuals, in 1.33% of alcoholics (higher than 80 g/d alcohol ingestion), in 1% of cases with history of surgical operations, and in 0.65% of persons who lived in risk regions for hepatitis B. We conclude that anti-HCV prevalence is low in our region. We think it is important to perform other studies in larger samples of general population and to study risk groups.

Adult↗
PubMed1993

[Cefoxitin: its role in the therapy of anaerobic infections].

Cefoxitin is a second generation cephalosporin commonly used to treat anaerobic and mixed infections. The authors reviewed the recently published data about the efficacy of cefoxitin; its utility in different clinical entities, patterns of resistance and resistance mechanisms, indications and reliability of in vitro susceptibility testing. These data indicate the need for determining susceptibility patterns of anaerobics at each hospital and point out to the essential close communication between the microbiologist and clinician to the rational treatment of anaerobic infections.

Bacteria, Anaerobic↗
PubMed1993

["Severe" congestive heart failure at a medical center].

UNLABELLED: Heart failure (HF) is a dynamic clinical syndrome depending on multiple hemodynamic and neurohormonal factors. This syndrome concerns not only left ventricular systolic dysfunction but also left ventricular diastolic dysfunction and right ventricular dysfunction. Clinical features and therapeutic approaches are different for each of them. NYHA class IV is just one of the various prognostic factors of heart failure; consequently, severe heart failure is not synonymous of NYHA class IV. OBJECTIVE: To study hospitalised patients with heart failure in NYHA class IV, in order to characterise the predominant dysfunction, and analyze evolution and mortality. DESIGN: A retrospective analysis of a prospective study. SETTING: Hundred and eight hospitalised patients (1985-89). Patients with chronic obstructive pulmonary disease and acute myocardial infarction were excluded. PATIENTS: Sixty nine patients: 29 female and 40 male, aged 18 to 81 years old (m = 59 +/- 15.5). METHODS: Patients were clinically examined and had chest radiographs, electrocardiogram and M + 2D mode echocardiogram. Three groups were identified: Group I-patients with predominant left ventricular systolic dysfunction; Group II-patients with predominant left ventricular diastolic dysfunction; Group III-patients with predominant right ventricular dysfunction. RESULTS: 41% of the patients had coronary artery disease; 44%, valvular heart disease; 11.8% dilated cardiomyopathy; 8.7% hypertrophic cardiomyopathy; 8.7% hypertensive cardiomyopathy. Fifty five percent of the patients were in group I and the major aetiology were coronary artery disease and valvular heart disease; 25% of the patients were in group II and the major aetiology were coronary artery disease and hypertrophic cardiomyopathy; 20% of the patients were in group III, all had valvular heart disease. The global mortality during the hospitalisation period was 15.9%, mostly group III (29%) and II (17%). CONCLUSIONS: Heart failure patients in NYHA class IV formed an heterogeneous group, requiring individualised therapeutic approaches. Left ventricular systolic dysfunction was the major pathophysiological mechanism, however, diastolic dysfunction and right ventricular dysfunction were frequent. Coronary artery disease presented as a frequent aetiology of heart failure, resulting in diastolic and/or systolic dysfunction. Valvular heart disease can be present as left ventricular systolic or diastolic dysfunction or as a right ventricular dysfunction, depending on the valvulopathy and the time of evolution. Echocardiography, in association with clinical features, has been very useful for each patient approach, allowing HF aetiology and pathophysiological mechanisms characterisation. The low mortality observed in this study was related certainly to the correction of precipitating factors, together with early etiologic diagnosis and pathophysiological characterisation, and adequate individualised treatment.

Adolescent↗
PubMed1993

Purification of superoxide dismutase from placental haemolisate blood: a simple and efficient method.

Superoxide dismutase functions as a scavenger of superoxide radical protecting living organisms. This enzyme has potential use as anti-inflammatory or anti-reperfusion injury drug. Here we present a simple and efficient SOD purification method from human placental blood. Superoxide dismutase from clarified haemolysed placental blood after chloroform and ethanol treatment was purified by DEAE-Sepharose, Phenyl-Sepharose chromatographies and cross flow ultrafiltration. The purified product is 98% pure by SDS-PAGE with 71% yield and specific activity of 2.8 x 10(5) U/mg protein.

Blotting, Western↗
PubMed1990

Neutralization of low molecular weight heparin by polybrene prevents thromboxane release and severe pulmonary hypertension in awake sheep.

Protamine reversal of heparin anticoagulation in patients is occasionally associated with life-threatening acute pulmonary hypertension. In a sheep model, we evaluated the effect on this adverse cardiopulmonary reaction of modifying the type of heparin (low molecular weight heparin compared with unfractionated heparin) and the type of heparin antagonist (polybrene compared with protamine). Protamine reversal of low molecular weight heparin (LMWH) and polybrene reversal of unfractionated heparin induced more than a 10-fold increase of plasma thromboxane B2 levels, a threefold increase of pulmonary vascular resistance and pulmonary artery pressure, and a 25% decrease of PaO2. A similar adverse reaction followed protamine reversal of conventional unfractionated heparin. However, with polybrene (1 mg/kg) reversal of LMWH (1 mg/kg), we measured neither pulmonary hypertension (pulmonary artery pressure was 22.6 +/- 3.6 mm Hg at 1 minute after polybrene reversal of LMWH compared with 47.9 +/- 4.2 mm Hg after protamine reversal of unfractionated heparin, p less than 0.005 groups differ), hypoxemia (PaO2 was unchanged 2 minutes after polybrene compared with a decrease of 26 mm Hg 2 minutes after protamine, p less than 0.05), nor acute release of thromboxane into arterial plasma (thromboxane B2 was 0.2 +/- 0.1 at 1 minute after polybrene compared with 3.7 +/- 1.7 ng/ml at 1 minute after protamine, p less than 0.005). The hemodynamic effects and mediator release were also benign after neutralization of larger doses of LMWH (3 mg/kg) by polybrene (3 mg/kg). The increases of activated clotting time and activated partial thromboplastin time due to both types of heparin were completely reversed with polybrene. Anti-Xa activity increased to more than 3 IU/ml 4 minutes after LMWH anticoagulation (p less than 0.01) but was only partially neutralized by polybrene. Various polyanion-polycation complexes that are formed when heparin anticoagulation is reversed induce thromboxane release and acute pulmonary vasoconstriction in awake sheep. Reversal of LMWH anticoagulation with polybrene does not elicit this adverse reaction.

Animals↗
PubMed1989

Effect of platelet depletion on lung vasoconstriction in heparin-protamine reactions.

In six awake sheep the control heparin-protamine reaction was associated with a 150-fold rise in arterial plasma thromboxane B2 (TxB2) levels, a 4.5-fold increase in pulmonary vascular resistance, a 20% decrease in cardiac output, a 30% decrease in arterial PO2, and a 30% reduction in arterial white blood cell concentrations. Depletion of 99% of circulating platelets by antibodies did not prevent either acute and severe pulmonary hypertension or increased plasma TxB2 levels induced by heparin-protamine administration. We produced sheep platelet aggregation in vitro with bovine thrombin and measured marked TxB2 release (36.3 +/- 16.3 ng/10(9) platelets). In contrast, neither heparin, protamine, nor heparin-protamine complexes over a 10,000-fold range of concentrations induced platelet aggregation and release of thromboxane in vitro. Therefore sheep platelets are not the source of thromboxane production associated with acute pulmonary hypertension during the heparin-protamine reaction, and other cells must produce the thromboxane.

Animals↗
PubMed1987

Pulmonary vascular obstruction in severe ARDS: angiographic alterations after i.v. fibrinolytic therapy.

IV streptokinase was infused to test the potential reversibility of adult respiratory distress syndrome (ARDS) associated pulmonary vascular thrombosis in five patients suffering from severe ARDS with elevated mean pulmonary artery pressure, increased pulmonary vascular resistance, and angiographically documented pulmonary vascular thrombosis. At 48 hr there was clearance of obstructions in arteries larger than 1 mm in diameter in all patients, increased filling of the microvasculature and small arteries less than 1 mm in diameter in four patients, a fall in pulmonary vascular resistance in all patients, a rise in cardiac output in four patients, improved oxygenation (PAO2/FlO2) in three patients, and variable changes in shunt fraction and ventilator pressures. Expressed as a mean fraction of the preinfusion controls, the postinfusion physiologic values were pulmonary artery pressure = 0.89 mm Hg, pulmonary vascular resistance = 0.68 mm Hg X min/L, cardiac output = 1.36 L/min, central venous pressure = 0.77 cm H2O, pulmonary capillary wedge pressure = 0.92 mm Hg, PAO2/FlO2 = 1.08, and shunt fraction = 0.95. Follow-up angiography showed no evidence of reocclusion. Postmortem studies of the three nonsurvivors confirmed recanalization of thrombosed pulmonary arteries. One documented bleeding episode occurred. We conclude that fibrinolytic infusion can lyse thrombi and possibly improve hemodynamics and oxygenation in ARDS-associated pulmonary vascular thrombosis.

Angiography↗
PubMed1987

Effects of granulocytopenia on the hemodynamic responses of dogs during E. coli bacteremia.

In both neutropenic and normal dogs a significant and sustained fall in mean arterial pressure (MAP) occurred within 2 h (P less than .01) of the onset of E. coli bacteremia. The MAP remained depressed (P less than .001) in the neutropenic dogs while it increased to normal by 4 h in the control dogs. The fall in MAP was primarily related to a fall in total peripheral resistance (TPR). Although myocardial performance curves declined in both groups over the 4-h period, cardiac index (CI) and left ventricular stroke work index (LVSWI) were not significantly different from baseline in either group; nor was LV filling as assessed by the pulmonary artery wedge pressure (PAWP). No significant differences between groups were demonstrated between the mean pulmonary vascular resistance (PVR), dead space, shunt, or oncotic pressure for either group. A significant (P less than .01) percent reduction of arterial PO2 (PaO2) occurred in the neutropenic dogs. The pH of both groups fell during the course of the experiment and was significantly lower (P less than .02) in the neutropenic dogs at the termination of the study. A similar percent fall in platelet count, factor VIII, and fibrinogen levels was observed in both groups. Circulating endotoxin levels were paradoxically higher in normal animals and did not correlate with any hemodynamic alteration in either group--except that the earlier, higher endotoxin levels in the normal animals were associated with a more rapid decline in myocardial performance. However, the vasodilation of the neutropenic group was clearly related to the higher level of E. coli circulating since the concentration of E. coli in both groups at 4 h was significantly inversely correlated with the MAP (P less than .001).

Agranulocytosis↗
PubMed1986

Massive hemolysis following inhalation of volatile nitrites.

Volatile nitrites are drugs which have become widely used for their mood-altering and aphrodisiac effects. Their use has been associated with methemoglobinemia and mild hemolysis; more significant hemolysis has been noted in a patient with G6PD deficiency. We report here a case of massive hemolysis following inhalation of volatile nitrites in the absence of an apparent intrinsic red cell defect. It is important that health care workers are aware of side effects from these commonly abused substances.

Adult↗
PubMed1985

Left ventricular thrombi diagnosed by echocardiography in patients with acute myocardial infarction treated with intracoronary streptokinase followed by intravenous heparin.

Thirty patients with acute myocardial infarction (AMI) treated with intracoronary streptokinase (7 X 10(5) +/- 3 X 10(5) IU) followed by 10 days of intravenous heparin (800 to 1,500 IU/hour) therapy were prospectively studied by serial 2-dimensional echocardiography for left ventricular (LV) thrombus. Within the first 24 hours, evidence of a thrombolytic state appeared as indicated by fibrin and fibrinogen degradation products (123 +/- 45 mg/dl at 24 hours). Throughout the course of this study partial thromboplastin times were maintained within therapeutic range (40 to 100 seconds). Apical LV thrombus developed in 8 of 30 patients (27%). Apical thrombus developed within 24 hours in 3 patients with anterior AMI and persisted through day 10. By day 10, apical thrombus developed in 3 additional patients with anterior AMI and 2 patients with inferior AMI. In these patients, anterior AMI and apical dysfunction were significant (p less than 0.01 for both) determinants of LV thrombus formation. Hence, the incidence of LV thrombus in patients treated with streptokinase/heparin is similar to that reported earlier in comparable patients not receiving thrombolytic therapy.

Aged↗
PubMed1982

Technetium-99m labeling of antibodies to cardiac myosin Fab and to human fibrinogen.

We have developed a method of labeling biologically active labile macromolecules, such as human fibrinogen (HF) and anticardiac-myosin Fab (AM-Fab), with Tc-99m at neutral pH. This method uses dithionite reduction of pertechnetate and subsequent labeling, to test the method with acid-labile macromolecules. Complexes of diethylene triamine pentaacetic acid with macromolecules such as human fibrinogen (D-HF) and anticardiac-myosin Fab (D-AM-Fab) were labeled and utilized in in vitro and in vivo studies. In biodistribution studies, the Tc-99m D-HF had a two-component blood clearance (half-times 1 hr and 15 hr) and was 80--88% coagulable. The Tc-99m AM-Fab retained its immunoreactivity as tested by affinity chromatography; also during in vivo localization in experimental myocardial infarction. This labeling technique provides an easy and efficient approach to the Tc-99m labeling of other biologically active and acid-labile macromolecules.

Animals↗
PubMed1981

Antiperinuclear factor and keratin antibodies in rheumatoid arthritis.

Tests for antiperinuclear factor (APF) demonstrable by indirect immunofluorescence (IF) on smears of human buccal mucosal cells and for antibodies to keratin (AKA) detected on cryostat sections of rat oesophagus were performed on serum from 102 cases of rheumatoid arthritis (RA) and 117 controls. APF was detected in 92% of the cases of RA; positive tests obtained with non-RA sera were generally weaker than those given by the RA group, and the antibody in both RA and non-RA serum was predominantly IgG class. The difficulty in obtaining suitable substrate material previously reported was confirmed, and only 2 satisfactory donors were identified among 27 individuals tested. The incidence of keratin antibodies detected was found to be related to the site from which the tissue was taken; low oesophagus provided the best discrimination between RA and controls (51% and 5% positive respectively), and cardia of the stomach gave the highest incidence of staining in all groups. A laminar staining pattern was seen with most positive sera, but occasionally the keratinised layer was diffusely stained. The presence of AKA showed a marked correlation with both IgM rheumatoid factor and increased Clq binding in RA, but APF did not.

Antibodies↗
PubMed1981

Urokinase or heparin in the management of patients with deep vein thrombosis?

Twenty patients with clinical signs of deep vein thrombosis of a duration not exceeding 72 hours, and with the condition confirmed phlebographically, were randomly allocated to one of two groups in a double-blind study. In group 1 the patients received urokinase in a low-dose regimen of 200 000 Ploug units during the first 24 hours, followed by infusion of heparin, 40 000 units daily during the next 5 days. Patients in group 2 received heparin only, 40 000 units daily for 6 days. The clinical course was assessed daily. When the infusion period was completed, the phlebography was repeated, and the results of the two examinations were compared with respect to extent of filling defects and the degree of non-filling of the deep veins. We found no superiority in the regimen consisting of urokinase preceding heparin infusion, compared with that of heparin infusion alone. Most of the patients improved clinically during the 6-day infusion period, but the degree of thrombosis, evaluated phlebographically, was unaltered or even deteriorated during the period in all patients except two. Overt bleeding was noted in 6 patients.

Clinical Trials as Topic↗