Publications by authors named "Santos-Buch C"

Chagas disease is the clinical condition triggered by infection with the protozoan Trypanosoma cruzi. The infection is transmitted by triatomine insects while blood feeding on a human host. Field studies predict that one third of an estimated 18 million T cruzi-infected humans in Latin America will die of Chagas disease.

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Between November 1993 and March 1994, a cluster 6 pediatric patients with acute febrile illnesses associated with rashes was identified in Jujuy Province, Argentina. Immunohistochemical staining of tissues confirmed spotted fever group rickettsial infection in a patient with fatal disease, and testing of serum of a patient convalescing from the illness by using an indirect immunofluorescence assay (IFA) demonstrated antibodies reactive with spotted fever group rickettsiae. A serosurvey was conducted among 16 households in proximity to the index case.

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Background: Subsequent to the publication of a report in 1984 entitled "Poorly Differentiated ("Insular") Carcinoma: A Reinterpretation of Langhans "wuchernde Struma," poorly differentiated insular thyroid carcinoma (PDITC) has become recognized as a distinct thyroid neoplasm. It is classified morphologically and biologically as an intermediate entity between well-differentiated (papillary and follicular) and undifferentiated (anaplastic) thyroid carcinomas. Only a few publications have addressed the findings with fine needle aspiration biopsy (FNAB).

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Trypanosoma cruzi has a plasma membrane ATP transport system that may consist of an exterior receptor domain (ATP-R) and an interior domain regulated by tyrosine and serine/threonine kinases. The addition of exogenous ATP to freely swimming trypomastigotes resulted in a receptor-mediated inward movement of the nucleotide, and the system obeyed mass action law (Km, 9.42 microM and Vmax, 77.

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Trypomastigotes of Trypanosoma cruzi were impermeable to exogenous radiolabeled ATP for up to 2 h at 4 degrees C. Radioligand binding assays in the cold showed that trypomastigotes had two populations of saturable ATP receptors (ATP-Rs) and the radioligand interaction was reversed by nonlabeled ATP in concentration-dependent assays. The Kds of high- and low-affinity ATP-Rs were 7.

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Monolayers of L6 rat skeletal myoblast cells formed surface binding isotherms with the purified tobacco leaf glycoprotein TGP1 and the enriched cigarette tar glycoprotein TGP2. Scatchard analysis showed that the binding in the range of the limited concentrations tested was to a single class molecule and the calculated affinity constant (Kd) for TGP1 and TGP2 showed similar values (9.78 x 10(-13) M and 3.

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Previous investigations have shown that the adhesion of T. cruzi plasma membrane vesicles (PMV) to monolayers of host cell myoblasts and to immobilized heart muscle sarcolemma membranes (PAM) on polyacrylamide beads is mediated by the interaction of T. cruzi attachment sites with the muscarinic cholinergic and beta-adrenergic receptors of the host cell membrane.

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The accuracy of fine-needle aspiration (FNA) cytologic diagnosis of nonpalpable breast lesions and the prevalence of neoplasm occurring in areas unrelated to the radiologic abnormality were studied. Template-guided FNA cytologic examination was performed in 101 surgically excised breast specimens. The exact area of the mammographic abnormality was aspirated with radiographic control.

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Plasma membrane vesicles of Trypanosoma cruzi (PMVs) formed saturation binding isotherms with naive murine T lymphocytes. Parasite membrane attachment to the muscarinic cholinergic receptors of Lyt 2.2+T cells (suppressor cells) resulted in the synthesis of cGMP, attenuation of cAMP levels and in the secretion of prostaglandin E2, an immunoregulator effector substance.

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Antibody F(ab')2 fragments derived from the sera of four patients with histology-proven chronic Chagas myocarditis [cF(ab')2]-complexed antibody F(ab')2 fragments of children with acute Trypanosoma cruzi infection [aF(ab')2] in significantly higher molar ratios than those measured with F(ab')2 antibody fragments of normal subjects [nF(ab')2] from nonendemic areas (p less than 0.05). Anti-idiotype [cF(ab')2 X aF(ab')2] immune-complex formation was significantly blunted by preabsorption of cF(ab')2 with porcine heart atria sarcolemma (PAMs) immobilized on sepharose beads (inhibition, mean, 78.

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Plasma membrane vesicles (PMVs) of Trypanosoma cruzi adhered to L6 myoblast host cells as a function of time and concentration in saturation phenomena in a similar fashion to that reported in a previous publication. The initial adhesion rate (A0) of T. cruzi PMVs to L6 myoblasts in tissue culture was inhibited by acetylcholine (10(-5) M), isoproterenol (10(-5) M) and norepinephrine (10(-8) M) (range 29.

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A simple method to prepare a high yield of Trypanosoma cruzi plasma membrane vesicles (PMV) from epimastigotes and metacyclic trypomastigotes is described. The method may be applicable to other protozoa. Solid-phase immunoassay to bind surface T.

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Plasma membranes with complementary surface epitopes and with essentially the same orientation as tissue infective metacyclic trypomastigotes and epimastigotes of Trypanosoma cruzi adhere to L6 myoblast host cells preferentially to smooth muscle and epithelial cells as a function of time, surface area and concentration in saturation phenomena at 4 and 37 degrees C. The initial adhesion rates are partially calcium ion dependent and, at saturation, they are also dependent on high energy phosphorylated intermediates, exerting an active grip on adherent parasite membranes. These phenomena are consistent with the existence of parasite attachment molecules on the external surface of the plasma membrane and complementary host cell receptor structures with the capacity to bind them.

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The pathogenic mechanisms related to the development of idiopathic inflammatory skeletal muscle disease are unknown. The myotropic protozoa Trypanosoma cruzi and Toxoplasma gondii are implicated in the induction of myositis in experimental animals (1) and humans (2). In the experiments reported here, a model of pathoimmune myositis is described in C3H/HeJ T.

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The sera from patients with primary heart and skeletal muscle diseases, hospitalized patients without intrinsic muscle disease from an area endemic for Trypanosoma cruzi infections, and normal subjects (N = 693) were studied for the presence of immunoglobulin G (IgG) antisarcolemma activity using serologic methods. The prevalence of elevated serum IgG antisarcolemma activity from patients with chronic Chagas' cardiomyopathy, idiopathic cardiomyopathy, polymyositis, and Duchenne muscular dystrophy was 58.9 +/- 10.

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Antiheart immune reactions have been reported in patients with Chagas' disease, and we have postulated that the observed cardiac lesions are mediated by autoimmune antiheart reactions elicited by the etiologic agent Trypanosoma cruzi. In this report, BALB/c mice infected with a low inoculum of T. cruzi developed splenic lymphocyte cytotoxicity against normal syngeneic neonatal cardiac myofibers in vitro 150 days after infection, whereas splenic lymphocytes obtained from mice at 15, 45, 90, or 120 days after infection or from matched controls did not.

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The ability of Trypanosoma cruzi, the etiological agent of Chagas' disease to acquire host cell surface antigen was tested. Parasites emerging after intracellular replication in WOS sarcoma monolayers expressed a sarcoma-associated surface antigen. This antigen was deleted from these parasites after replication in the MNS control monolayer, which does not express WOS sarcoma-associated surface antigen, or by replication in cell-free medium.

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We have previously shown that Trypanosoma cruzi shares antigenic determinants with preparations of the calcium-sequestering adenosine triphosphatase of sarcoplasmic reticulum. The cross-reacting antigen (SRA) is also apparently present on the sarcolemma of cardiac myofibers. Using highly specific reference antisera to either the small membranes of T.

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The results reported here show that a clone of a South American Trypanosoma cruzi human isolate has an epitope antigenically related to sarcoplasmic reticulum adenosine triphosphatase preparations (SRA), an enzyme implicated in the contraction-relaxation cycle of striated muscle. The antigenic determinant of T. cruzi, which is cross-reactive with SRA, is located in the interior of the parasite.

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Two strains of Trypanosoma cruzi, isolated from humans and assayed for their biological capacity to kill outbred white Swiss mice (HaM/CR-CD) following reticuloendothelial system blockade with thorium dioxide, were used in these experiments: the Maria Cristina strain, which killed all blocked mice at a rate following a rectangular dose-response curve, and the José Cardoso strain, which did not kill blocked mice at comparable dosages. When inoculated into pregnant HaM/CR-CD mice, the non-pathogenic José Cardoso strain did not cross the placental barrier, in either blocked or unblocked mice, to cause fetal parasitosis. The pathogenic Maria Cristina strain did not cross the barrier in non-blocked mice, but in thorium-dioxide blocked mice it produced an incidence of fetal parasitosis of 8.

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Cerebral and ocular microaneurysms were produced in rabbits made hypertensive by surgically induced silk-turpentine perinephritis combined with contralateral nephrectomy 7 days later. The aneurysms distributed throughout the brain and iris were studied by microradiography; a few representative aneurysms selected from the microradiographs were studied histologically. The microradiographic findings and histological sections correlated well.

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The development of miliary aneurysms of the iris is associated with the high risk of cerebral hemorrhage in rabbits with renal hypertension. The high-risk group of hypertensive rabbits in this series was characterized by the formation of iris aneurysms, and this group developed a striking proportion of hemorrhagic strokes (42.5%).

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