Pregnancy and the bleeding time.
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Biomedical subjects
Publications and source records attributed to J Pereira.
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Total platelet sialic acid (SA) was measured in three experimental conditions: (1) human and canine platelet density subpopulations obtained by centrifugation in arabinogalactan gradients, (2) circulating canine platelets during recovery from experimental immune and mechanical thrombocytopenias, and (3) platelets obtained from a patient with chronic immune thrombocytopenic purpura before and after splenectomy. The density of human and canine platelets is, in part, determined by their age. We found no significant differences in total SA between high-density (HD) and low-density (LD) platelets (9.32 +/- 2.0 vs. 9.55 +/- 1.3 micrograms/mg of platelet protein in dogs and 9.02 +/- 2.3 vs. 9.10 +/- 2.9 micrograms/mg in humans). In the human and canine thrombocytopenic models, the entrance of new platelets from the bone marrow is followed by their aging in the circulation. In these models, no significant changes in total SA content were detected in sequential measurements during the recovery of the thrombocytopenia. Accordingly, we conclude that total SA in human and canine platelets is unrelated to their age in circulation. These results do not support the notion that the loss of SA from membrane glycoproteins determines the recognition and removal of platelets from the circulation.
To elucidate the pathogenesis of renal dysfunction associated with obstructive jaundice, body water compartments were measured using a multi-isotope dilution technique in ten patients with biliary tract obstruction and in ten control subjects matched for age, sex, weight, height and body surface area. Expressed as a fraction of body-weight, total body water was reduced in jaundiced patients (41.8 versus 46.2 per cent, P less than 0.02). Extracellular water volume was also reduced in patients with jaundice (20.3 versus 24.3 per cent, P less than 0.003) owing to a reduction of the interstitial space (16.1 versus 19.5 per cent, P less than 0.004) and, to a lesser degree, of the plasma volume (4.2 versus 4.8 per cent, P = 0.1). There was a close correlation in jaundiced patients between plasma volume and the creatinine clearance rate (r2 = 0.56, P less than 0.02) and between plasma volume and extracellular volume (r2 = 0.77, P less than 0.0001). Extracellular volume in such patients also correlated with the percentage weight loss (r2 = 0.42, P = 0.04). Obstructive jaundice is associated with a contracted extracellular water compartment, although extracellular water, as a percentage of body-weight, increased in proportion to the body-weight lost. Reduction of the interstitial volume and a marginally reduced plasma volume may be determinant factors in the pathogenesis of the renal and haemodynamic disturbances observed in patients with biliary tract obstruction.
Single Photon Emission Computed Tomography (SPECT) after intravenous administration of Technetium-99m hexamethylpropylene-amine oxime (Tc-99m HM-PAO) makes possible the evaluation of cerebral perfusion. We have been assessing the diagnostic accuracy of SPECT in some groups of head trauma patients: the preliminary results of this study are presented. Fourteen patients have been selected, all of them showing some kind of focal neurological deficit; the Computed Tomography (CT) and Nuclear Magnetic Resonance (NMR) were normal, or showed lesions that could not be responsible for the neurological deficits. In all of the patients Tc-99m HM-PAO SPECT has been performed, showing changes in cerebral perfusion in areas correlated with the abnormalities elicited on clinical examination. These results show that Tc-99m HM-PAO SPECT is a better technique than CT or NMR in demonstrating the organic basis of some neurological deficits observed after head trauma.
Rabbit antibodies to native riboflavin carrier protein (RCP), are to a large extent directed towards conformational epitopes and antibodies to disulphide bond reduced carboxymethylated RCP (RCM-RCP) are towards sequential epitopes. The major cyanogen bromide (CNBr) fragments and tryptic fragments of RCM-RCP interact with both antiserum to RCM-RCP and RCP. Passive immunization of pregnant mice with antibodies to RCM-RCP results in bioneutralization, leading to termination of pregnancy. Recently, a major tryptic fragment of RCM-RCP (24 +/- 2 kd) which could assume conformation at the antibody combining site of native RCP, obtained following mild trypsinization has been identified [Natraj et al. J. Biosci, 15 (1990) 341]. Rabbit antibodies to RCM-RCP treated with trypsin generated antibodies of low titer which interacted with RCM-RCP as well as RCP. The interaction of this antibody with RCP was of high affinity and could be displaced with RCP. The bioneutralizing ability of the antibody was demonstrated by its ability to cause termination of pregnancy in mice.
The phenotype frequency of platelet-specific alloantigens has been reported to vary with the ethnic composition of the population under study and the only two HPA-4a negative individuals found in the United States were of Hispanic origin; therefore, the aim of this work was to define the frequency of expression of these systems in the Chilean population. Using an ELISA with captured antigen by monoclonal antibodies, 604 blood donors were typed for the platelet-specific antigen systems HPA-1 and HPA-4. Eight samples typed negative for HPA-1a (1.32%) and 596 typed positive (98.68%). The calculated gene frequencies were 0.88 for HPA-1a (gene frequency > 0.99). Since these antigens are involved in thrombocytopenic disorders such as neonatal alloimmune thrombocytopenia and post-transfusion purpura, their frequency in a population is of clinical relevance. The gene frequency found for HPA-1a is higher than in Europeans (0.85) and lower than in Mapuche Indians (0.99), which is to be expected from the ethnic origin of our population. The absence of HPA-4a negatives in this study does not support our original hypothesis of a higher polymorphism of this system among hispanics.
Maternal alloimmunization against fetal platelets can cause fetal and neonatal thrombocytopenia. We report our experience in the study of five cases with severe neonatal-thrombocytopenia. Using an ELISA with antigen capture and other serologic tests on platelets, we investigated the sera of the five mothers. Sera from four mothers contained a platelet-specific alloantibody, anti-HPA-1a (PlA1) whereas the platelets typed as HPA-1b/b. In one case despite extensive serological investigation and clinically unequivocal diagnosis of AINT, no antibodies were demonstrated. The use of monoclonal antibodies for antigen immobilization, showed to be a reliable and sensitive test for the detection and identification of platelet antibodies in AINT. These techniques could also be used in the follow-up of patients at risk (e.g. pregnant HPA-1b/b women) and in the screening of blood donors lacking of certain antigens, whose platelets are collected to be transfused in patients with platelet-specific antibodies.
The electrophoretic characterization on SDS-PAGE gels of Paracoccidioides brasiliensis antigens, strains 2511 and 6688; and the additional use of immunoblotting has permitted in this study to identify the immunogenic, sensitive and specific antigen fractions for the diagnosis of Paracoccidioidomycosis. The antigenic preparations showed differences depending on the morphologic form of the fungus and the method utilized. The procedure revealed heterogeneity in the humoral immune response of the patients studied and permitted us to establish indices of activity of Paracoccidioidomycosis by the sequential analysis of sera obtained during different stages of the disease. The high sensitivity of this method makes it useful as an additional technique for the serologic immunodiagnosis of Paracoccidioidomycosis.
Rabbit antibodies to native riboflavin carrier protein (RCP), are to a large extent directed towards the conformational epitopes and antibodies to disulphide bond reduced carboxymethylated riboflavin carrier protein (RCM-RCP) to the sequential epitopes. Taking advantage of this premise and in order to map the epitopes of RCP recognized by the antibodies, enzyme-linked immunosorbent assays were validated for RCP and RCM-RCP using the Avidin-Biotin system. The usefulness of these assays were illustrated when antigenicity of peptides derived from RCM-RCP following trypsinization were examined. Two major (T1,T2) and one minor peptide (T3) fractions were obtained when the tryptic peptides were fractionated on DEAE-cellulose. RCP has a blocked N-terminal. Tryptic peptides (T1 and T2) on microsequencing revealed the absence of an N-terminal amino acid, indicating that these fragments emanate from the N-terminal region of RCP. In support of this observation is the finding that antipeptide antibody to cRCP (10-24) of cRCP interacted with T1 as well as T2 indicating the presence of the sequential epitope (10-24) of cRCP in these fragments. In RCP-ELISA, only T2 displaced RCP and peptides T1 and T2 displaced RCM-RCP in RCM-RCP ELISA. Differences in the ability of these fragments (T1 and T2) to displace RCP and RCM-RCP reflect the subtle changes in the spatial structures of these epitopes in RCP and RCM-RCP.
The health-equity debate has generally given far more attention to empirical rather than conceptual matters. However, empirical work on equity is at its most useful when it can be related to a specific normative framework, such as that provided by public pronouncements. This paper, therefore, aims to extract the precise equity objectives of one health care system, that of Portugal. Three seemingly distinct objectives in Portuguese health policy are identified: (i) access to health promoting commodities; (ii) equal access to NHS care for equal need; and (iii) equal access to both public and private health care. The final section attempts to find common threads running through these definitions and presents suggestions for future research. Though referred specifically to Portugal, the paper should be of interest to researchers in other countries, where a great deal of health-equity investigation continues to put the cart before the horse, by identifying unequal distributions without considering if they are simultaneously inequitable.
Economists have until recently taken a back-seat in the debate on inequality and health, despite various suggestions that economic science has much to contribute to the clarification of issues surrounding that polemic. This article presents a bibliography of English-language sources which explicitly consider the economics of inequality in the health domain or present methods which might suitably inform the debate. Initially, an introductory guide to the literature is presented, followed by the bibliography itself. This second section is divided into four distinct parts in order to facilitate use: works of a general economic nature, including those on the measurement and extent of inequality; discussions of normative aspects of equity in health; positive analyses drawing on models of the demand for health and medical care; and a final sub-section that groups works from other disciplines which are indispensable background for future work by economists.
Serum from patients with paracoccidioidomycosis (PARA) did not block digestive abilities of neutrophils (PMNs) from healthy individuals against Paracoccidioides brasiliensis. Conversely, serum from healthy donors did not enhance digestive capacities of PMNs from patients with PARA vis á vis the causative organism. We conclude that the specific digestive defect present in PMNs from patients with PARA is not mediated by serum factors.
von Willebrand's disease is the most frequent congenital disorder of primary hemostasis; it is transmitted in an autosomal manner and according to type there is an alteration in structure, function and/or synthesis or release of von Willebrand's factor. Patients present with muco-cutaneous hemorrhages of varying severity. Significant advances in the understanding of the molecular defect and laboratory diagnosis of the different subtypes of the disease have been made in the last years, but we still face the emergence of new subtypes and the difficulties posed by the genetic, clinical and laboratory variability of the disorder.
Serial studies were performed in two patients with cyclic thrombocytopenia to investigate the pathogenesis of this disorder. Mean life span of autologous platelets when platelet levels were declining was subnormal (2.4 and 0.8 days), and megakaryocytes were abundant in the bone marrow during thrombocytopenia. Megakaryocyte colony-stimulating activity could not be detected in the serum of either patient at any point of their cycles. In each patient, total platelet-associated IgG varied inversely with platelet levels. Surface platelet-associated IgG was measured only in patient 2 and was significantly elevated (greater than 1,280 IgG molecules per platelet) at all stages of the cycle, even during thrombocytosis. However, the highest values were observed during thrombocytopenia. Platelet-bindable IgG in plasma declined to normal immediately before platelet levels began to rise. IgG eluted from the platelets of this patient reacted strongly with autologous and homologous platelets in contrast to a "mock eluate" prepared from platelets of a normal subject. The eluate from the patient's platelets reacted strongly with immobilized autologous and homologous glycoprotein IIb/IIIa complex and weakly with GPIb but not with isolated GPIIIa alone. In each patient the decline in platelet levels was significantly delayed following administration of intravenous gamma globulin 0.4 g/kg body weight for five days. These findings suggest that platelet-reactive autoantibodies are of pathogenic significance in some patients with cyclic thrombocytopenia.
Peripheral blood neutrophils (PMNs) from a patient with Jorge Lobo's disease (JLD) digested well phagocytosed Paracoccidioides brasiliensis. We found no circulating antibodies against P. brasiliensis in the patient's serum. Such neutrophils showed myeloperoxidase activity and also digested normally phagocytosed Candida albicans. We had previously reported the presence of a specific digestive deficiency of PMNs from patients with paracoccidioidomycosis (PARA) vis à vis P. brasiliensis. Current findings provide new information about leukocyte functions in JLD and bolster the view that JLD, PARA and their respective causative microorganisms are distinct.
An 8-year-old black boy with sickle cell disease and severe hemolytic anemia crisis (95% hemoglobin S) also had mitral incompetence due to rheumatic valve disease. A 27 mm monostrut Björk-Shiley valve prosthesis was implanted after partial exchange transfusions had reduced the hemoglobin S to less than 40%. High-flow normothermic perfusion was used during extracorporeal circulation, with care taken to avoid hypoxia and acidosis. Postoperative recovery was uneventful.
Circulating polymorphonuclear leukocyte (CPMN) functions were studied in patients with widespread psoriasis as well as in persons with chronic alcoholic liver disease (CALD), paracoccidioidomycosis, diverse granulomatous diseases, and normal individuals. We were unable to find stimulation or increase in CPMN functions in patients with psoriasis compared to normal individuals. Leukocytes from individuals with CALD had a lowering of their metabolic activation, chemotaxis, random movement, and adherence. CPMNs from patients with paracoccidioidomycosis showed a significant deficiency in their ability to digest Paracoccidioides brasiliensis. Our results are against the concept that functions of circulating PMNs are stimulated in psoriatics.
Platelet alloantigens and other surface markers were studied in platelet cohorts of different mean density, using monoclonal and polyclonal probes. High density (HD) platelets expressed 12% more P1A1 molecules (46,942) than low density (LD) platelets (41,892). However, LD platelets carried 42% more HLA-A2 molecules (6,267 +/- 184) than HD platelets (4,406 +/- 232) (P less than .01) and 55% more class I HLA antigens (17,034 +/- 2,062 v 11,007 +/- 2,190) (P = .05). The platelet subpopulations did not differ in their content of glycoprotein (GP)IIb/IIIa complex or Baka antigen. The difference in expression of class I HLA antigens on HD and LD platelets is consistent with two possibilities: either class I HLA molecules are acquired from plasma or they are released into plasma as platelets age in circulation. Accordingly, class I HLA molecules may provide a useful marker of platelet age.