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Heat–alkali treatment of synthetic α- and β-melanocyte-stimulating hormones (MSH), known to cause racemization of amino acids within the peptides, results in prolongation of the darkening (melanophore dispersion) effect of these hormones on frog and lizard skins in vitro. Skins remain darkened for hours or even days if supramaximal concentrations of the racemized hormones are used. This response can be partially reversed by melatonin or noradrenaline. Heat–alkali treatment of α-MSH at either 60 or 97 °C results in a retardation of the response of the skins to the racemized peptides. In contrast, the response of frog skins to heat–alkali-treated β-MSH is immediately enhanced and potentiated. Heat–alkali treatment also prolongs and potentiates the activity of synthetic [des-acetyl]-α-MSH (in contrast to the retardation effect on the natural acetylated peptide). These data suggest a role for the N-acetyl group in the retardation phenomenon. The activity of synthetic [2-d-tyrosine]-α-MSH is much lower than that of α-MSH itself, indicating that heat–alkali treatment of the hormone may produce either potentiation or partial inactivation of the peptide, depending on the site of racemization.
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SUMMARY
The significance of a positive thyroid complement-fixation (c.f.) test in thyrotoxicosis has been investigated by studying the correlation between various features of the disease in 468 patients. A significant correlation was found between the positivity of the c.f. test and (1) the degree of lymphocytic infiltration in the gland; (2) incidence of postoperative hypothyroidism; (3) size of the goitre; (4) previous treatment with radioiodine, and (5) a family history of thyroid disease. No correlation was found between the results of the test and the incidence of reactions to antithyroid drugs. The results suggest that thyrotoxic patients with positive c.f. tests should be treated initially with antithyroid drugs unless there is a definite indication for surgery.
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Endogenous glucocorticoid action is important in the structural and functional maturation of the fetal heart. In fetal mice, although glucocorticoid concentrations are extremely low before E14.5, glucocorticoid receptor (GR) is expressed in the heart from E10.5. To investigate whether activation of cardiac GR prior to E14.5 induces precocious fetal heart maturation, we administered dexamethasone in the drinking water of pregnant dams from E12.5 to E15.5. To test the direct effects of glucocorticoids upon the cardiovascular system we used SMGRKO mice, with Sm22-Cre-mediated disruption of GR in cardiomyocytes and vascular smooth muscle. Contrary to expectations, echocardiography showed no advancement of functional maturation of the fetal heart. Moreover, litter size was decreased 2 days following cessation of antenatal glucocorticoid exposure, irrespective of fetal genotype. The myocardial performance index and E/A wave ratio, markers of fetal heart maturation, were not significantly affected by dexamethasone treatment in either genotype. Dexamethasone treatment transiently decreased the myocardial deceleration index (MDI; a marker of diastolic function), in control fetuses at E15.5, with recovery by E17.5, 2 days after cessation of treatment. MDI was lower in SMGRKO than in control fetuses and was unaffected by dexamethasone. The transient decrease in MDI was associated with repression of cardiac GR in control fetuses following dexamethasone treatment. Measurement of glucocorticoid levels in fetal tissue and hypothalamic corticotropin-releasing hormone (Crh) mRNA levels suggest complex and differential effects of dexamethasone treatment upon the hypothalamic–pituitary–adrenal axis between genotypes. These data suggest potentially detrimental and direct effects of antenatal glucocorticoid treatment upon fetal heart function.