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Biomedical subjects

A M Acosta

Publications and source records attributed to A M Acosta.

At least 37 records · Page 2Linked to original sources
PubMed1990

[The effect of anti-insulin antibodies and of peptide C residual secretion on the metabolic control of diabetes type 1].

In 20 type I diabetic patients treated with conventional insulin preparations, we measured insulin antibodies and peptide C secretion. Peptide C levels 90 and 120 min after a standard breakfast correlated well with glucosylated Hb levels (r = -0.48 and -0.52, respectively). No correlation with free insulin levels was observed, in spite of a good correlation of the latter with blood glucose levels (r = -0.50 and -0.73, respectively). There was no relation between insulin antibody levels and peptide C or free insulin. Metabolic control was not affected by insulin antibodies. Insulin dose decreased in relation to the duration of the disease and reduction of body weight index and was not correlated to glycosylated Hb levels.

Adult↗
PubMed1990

[Cholestyramine in the treatment of hypercholesterolemia. Our experience in 11 cases].

Bile acid sequestrant resins are considered agents of choice in the therapy of hypercholesterolemia non responsive to diet treatment. We evaluated the effects of cholestyramine, 12 g per day during 4 weeks, in 11 adult patients with severe hypercholesterolemia. Total cholesterol decreased from 414 +/- 112 to 302 +/- 140 mg/dl (28%), LDL cholesterol from 330 +/- 122 to 226 +/- 143 (33%) and Apo B lipoprotein from 141 +/- 31 to 115 +/- 34 mg/dl (18%), p < 0.01. HDL cholesterol including fractions HDL2 and HDL3, Apo A1 and Triglyceride levels were not modified. No significant side effects on gastrointestinal function were observed. Thus, we confirm that cholestyramine is an effective therapy for severe hypercholesterolemia.

Adolescent↗
PubMed1990

[Alcohol and the risk factors of coronary cardiopathy. A study in 571 men].

In 571 healthy professional males we correlated alcohol consumption with serum total cholesterol (C), HDL-C, triglycerides, blood sugar, cigarette consumption, body mass index and arterial blood pressure. An outstanding finding was a positive independent, correlation of alcohol consumption and serum HDL-C levels (r 0.22, p < 0.0001). Univariate analysis showed correlation of alcohol consumption with body mass index, blood pressure and total serum C, however this was dependent on age and/or body mass. No correlation was found between alcohol consumption and blood sugar or TG levels. Alcohol consumption did not identify a group of subjects with high risk factors. Consumption of more than 10 cigarettes per day decreased the strength of the association between elevated HDL levels and alcohol consumption. We conclude that a moderate intake of alcohol is associated to increased serum HDL levels with no significant change of other coronary risk factors.

Adult↗
PubMed1989

[Serum lipids, HDL2 and HDL3 cholesterol and apolipoproteins A1 and B as predictors of coronary artery disease diagnosed by coronarography].

Serum levels of total, HDL2 and HDL3 cholesterol, triglycerides and apolipoproteins A1 and B were compared in 100 Chilean males with (n = 80) or without (n = 20) coronary artery disease (CAD). The presence and severity of CAD was determined by an angiographic score. Discriminating power, sensitivity, specificity and positive predictive value for CAD were calculated for all variables. As an isolated factor, total cholesterol had the greatest discriminating power (p less than 0.002): 21% of patients with CAD had cholesterol levels below 200 mg/dl while no patient with cholesterol over 275 mg/dl was free of disease. Even though all cases with HDL cholesterol below 25 mg/dl belonged in the CAD group, this factor had no overall discriminating power. Total cholesterol/HDL cholesterol ratio had the greatest discriminating power (p less than 0.001) while total/HDL2 cholesterol had the best positive predictive value.

Adult↗
PubMed1989

[Parenteral nutrition: stability of lipid emulsions in different preparations].

We studied the stability of fat emulsions kept in plastic bags and mixed with different proportions of amino acids, glucose and divalent cations. The quantity of fat, vitamins and other electrolytes was kept constant. Visual examination, pH determination, and measurement of particle diameter in Coulter Counter was performed at 0, 24 and 84 h. Particles greater than 5 microns were detected only in mixtures with Ca++, Mg++ and Zn++ concentrations at or above 7.7, 13.3 and 23.4 mEq/l, respectively. We conclude that fat emulsions for parenteral nutrition remain stable in mixtures when the concentration of divalent cations is not unduly raised.

Drug Stability↗
PubMed1985

Primary muscle disease: definition of a 25-kDa polypeptide myopathic specific chagas antigen.

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 +/- 10.4% (N = 101) (P less than 0.001 when compared to normal subjects). Two of twelve (16.7%) patients with acute T. cruzi infection and parasitemia developed elevated antisarcolemma titers, and 9/46 (19.6%) patients with chronic T. cruzi infection without evidence of cardiomyopathy yielded high antisarcolemma titers. On the other hand, patients with chronic T. cruzi infection with advanced cardiomyopathy yielded high antisarcolemma titers in 35/74 (47.3%) (P less than 0.001 when compared to normal subjects). Radioimmunoprecipitation showed a circulating antibody to a 25-kDa T. cruzi polypeptide (P25) in 16/17 (94.1%) patients with advanced cardiomyopathy and T. cruzi infection. No such antibody was shown in 12 asymptomatic subjects with chronic T. cruzi infection.

Antibodies↗
PubMed1985

Autoimmune myocarditis induced by Trypanosoma cruzi.

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. No antiheart antibody or antibody-directed cellular cytotoxicity was observed, nor was there an increase in natural killer cell activity. Hearts from mice studied at 150 days after infection showed mononuclear cell myocarditis with myocytolysis in the absence of intracellular T. cruzi forms. Hearts from the other mice did not exhibit any histologic changes. Other reports from our laboratory have identified a cross-reacting antigen (SRA) shared by T. cruzi and striated muscle. Immunization of BALB/c mice with SRA produced immunopathogenic dynamics similar to those seen with long-term T. cruzi infection. Collectively these data indicate that the cardiac lesions seen in patients with Chagas' disease may be attributed to autoimmune reactions elicited by cross-reacting antigens of T. cruzi and striated muscle.

Animals↗
PubMed1984

Reversible defect in antigen-induced lymphokine and gamma-interferon generation in cutaneous leishmaniasis.

Peripheral blood mononuclear cells from a patient with progressive Leishmania mexicana (LM) infection were examined for responses to mitogen and antigen before, during, and after successful treatment. Before therapy, his cells proliferated normally and secreted effective macrophage-activating lymphokines in response to concanavalin A (Con A) and Toxoplasma gondii antigen, but failed to show any response to LM antigen. At this time, suppressive humoral factors were not present, the intracellular antimicrobial activity of the patient's monocytes was intact, and once stimulated with normal lymphokines, his monocyte-derived macrophages readily killed his own infecting LM strain. One month after initial treatment, the patient's T cells showed variable but measurable responses to LM antigen, and by 6 mo, these responses were fully developed in proliferative and lymphokine-generating assays. The patient's lymphokines were examined for gamma-interferon (IFN-gamma) because a) a monoclonal anti-human IFN-gamma antibody abolished the capacity of lymphokines to activate normal macrophages to kill LM, and b) partially purified and recombinant IFN-gamma alone could induce macrophage leishmanicidal activity. The patient's pretreatment Con A- and T. gondii antigen-stimulated lymphocyte supernatants (which activated macrophages to kill LM) contained 2000 to 3000 U/ml of IFN-gamma, whereas his LM antigen lymphokine was devoid of activity (less than 10 U/ml). At 1 and 6 mo after therapy, however, the latter lymphokine showed 20 and 600 U/ml of IFN-gamma, respectively, paralleling the development of antigen-specific proliferation and active lymphokine generation and the clinical status of his infection. These results appear to support previous suggestions that the ability of T cells to secrete antigen-induced macrophage-activating lymphokines (particularly IFN-gamma) is a key cellular immune response to intracellular Leishmania infections.

Antibody Formation↗
PubMed1983

Reversible acquisition of a host cell surface membrane antigen by Trypanosoma cruzi.

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. This type of reversible acquisition of host surface antigen has not been previously described in T. cruzi or other intracellular protozoan parasites.

Animals↗
PubMed1983

Anti-striated muscle antibody activity produced by Trypanosoma cruzi.

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. cruzi or to a tryptic fragment of striated muscle SRA, it was shown that SRA is present in the striated muscle of animals representative of the evolutionary scale ranging from nonhuman primate to fish. The small membranes of nine different T. cruzi strains isolated from widely divergent areas of the American continents also reacted with the reference antisera. This indicates that SRA is present in these T. cruzi strains and may be prevalent among all T. cruzi strains. The shared T. cruzi-striated muscle antigen, SRA, may be a heteroantigen present in all T. cruzi strains and in the striated muscle of all classes of animals. Immunization of rabbits (three of five) or chickens (five pairs of five pairs) with striated muscle membrane preparations of different classes of animals, particularly those of nonhuman primate, chicken, and turtle, gave rise to IgG anti-allogeneic striated muscle antibody activity. Immunization of rabbits (four of nine) and chickens (five pairs of six pairs) with the small membranes of different T. cruzi strains also produced IgG anti-allogeneic striated muscle. These data indicate that T. cruzi shares cross-immunogenicity with striated muscle SRA. Since SRA is apparently present on the sarcolemma of cardiac myofibers, it may be implicated in the immunopathogenesis of Chagas' disease.

Animals↗
PubMed1982

Muscle sarcoplasmic reticulum antigen shared by a Trypanosoma cruzi clone.

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. No surface cross-reaction was detected with intact, freely swimming flagellates. Indeed, the degree of cross-reactivity was increased when T. cruzi microsomes were trypsinized, probably resulting in further exposure of the normally internal cross-reactive epitope.

Animals↗