Echocardiographic diagnosis of cardiac tumors in symptomatic tuberous sclerosis patients.
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Biomedical subjects
Publications and source records attributed to S Diamant.
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The immune functions were evaluated in 30 children, aged one year to 9 8/12 years, who had suffered during their early infancy from protein-calorie malnutrition (PCM) as the result of intractable diarrhea. Twelve healthy children matched for age and sex served as controls. All 42 children responded normally to intradermal injections of tuberculin and candida antigens. The reduction of nitrous blue tetrazolium (NBT) by the polymorphonuclear leucocytes (PMN) was normal. Apart from the lower concentrations of IgM in the post-PCM group--145 +/- 67 mg % as compared to 212.8 +/- 46 mg % (p less than 0.005)--no differences were noted in the other serum immunoglobulin and complement levels. The response to phytohaemagglutinins (PHA) in two different concentrations was significantly enhanced in the post-PCM group (p less than 0.05). The per cent of T cells in both groups was normal. The results of this study indicate that most immunologic parameters return to normal after a healthy nutritional status has been achieved, with the exception of some abnormalities in IgM production and lymphocyte reactivity to PHA. These need further investigation.
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A case of an IgA deficient child who developed several autoimmune diseases namely, celiac disease, pernicious anemia, autoimmune thyroiditis and autoimmune thrombocytopenic purpura is reported; the possible connections and etiology of these phenomena is briefly discussed. Individuals with selective IgA deficiency should no longer be considered "normal".
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Phorbol myrystate acetate (PMA) activates nitroblue tetrazolium reduction in human polymorphs. The activation is inhibited by dibutyryl cyclic AMP, theophylline and phenylbutazone, but is not influenced by hydrocortisone in vitro, nor is it inhibited by leukocytes from patients treated with prednisone. Peptide analogues of Tuftsin also had no effect on this stimulatory activity. We conclude that the action of PMA on the nitroblue tetrazolium reduction is mediated through cyclic nucleotides.
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Serum tuftsin concentrations were measured, using a radioimmunoassay developed in Israel, in normal subjects and in patients who had undergone splenectomy. Concentrations in those who had undergone traumatic and elective splenectomy were much lower. The tuftsin concentration in 38 patients with Hodgkin's disease who had undergone splenectomy during staging laparotomy was not significantly different from the mean concentration in other patients who had had elective splenectomy. In four patients who underwent splenectomy for non-malignant haematological disorders measurements made before and after operation showed that tuftsin concentrations fell significantly in the days after operation. The increased susceptibility to overwhelming infections of patients with Hodgkin's disease and others who have undergone splenectomy may be related to the low tuftsin concentrations. As pre-splenectomy tuftsin concentrations in patients with Hodgkin's disease were normal, the practice of performing staging laparotomy and splenectomy in patients with Hodgkin's disease should perhaps be reconsidered.
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Administration of triamcinolone or dexamethasone to rats led to a prompt, marked and persistent rise in liver acetyl-CoA carboxylase activity. The activity of fatty acid synthetase increased to a lesser extent and after a more prolonged glucocorticoid treatment, whereas the changes in that of NADP-malate dehydrogenase and ATP-citrate lyase were not appreciable. The overall channeling of [1-14-C]acetyl-CoA to fatty acids was enhanced. The triamcinolone effect on acetyl-CoA carboxylase activity appeared to be dependent on the coincident hyperinsulinemia since it was not obtained in alloxan-diabetic rats, whereas the alanine-aminotransferase-inducing effect of this hormone was additive to that of insulin deficiency. In adipose tissue triamcinolone treatment caused a reduction in the activity of all lipogenesis enzymes and blunted their response to insulin administration. The antagonism of glucocorticoids toward insulin, selectively modulating the responses of the insulin-sensitive enzymes in liver and adipose tissue is discussed. The rise in hepatic lipogenic capacity, through the retention of the ability of insulin to induce acetyl-CoA carboxylase, may be physiologically important in restraining the ketogenesis from acetyl-CoA despite the increased fat utilization during glucocorticoid excess.
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