Hormones and immunological capacity. II. Reconstitution of antibody production in hormonally deficient mice by somatotropic hormone, thyrotropic hormone and thyroxin.
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Test carried out in 96 women aged between 43 to 55 years (50.46 +/- 4.7), who did not take any drugs during the last 3 months. The women were divided into two groups: premenopausal and early postmenopausal. Each group was subdivided according to blood pressure: with normal pressure and with arterial hypertension. The concentration of T4, T3 and TSH were measured using a radioimmunologic method. The saturation of carrier proteins was established with the T3/test, the result of which was used to divide T4 and T3 and to obtain FT4I and FT3I respectively. It was found that women with arterial hypertension have significantly higher (p < 0.001) TSH concentration. The concentration T3 and FT3I were significantly higher (p < 0.01) in women with arterial hypertension in the postmenopausal period.
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Osthol and total coumarins of Fructus Cnidii were given to the model of Kidney-Yang Deficiency rats induced by hydrocortison acetate injection, the changes of serum concentration of thyroxine T3, reverse T3 (rT3), T4 and thyroid stimulating hormone (TSH) were observed. Results showed that in comparison with normal rats, all of the criteria mentioned above were lowered significantly (P < 0.01) in model rats. After treatment, the criteria observed were all increased significantly (P < 0.01 or P < 0.05). It was suggested that the osthol and total coumarins of Fructus Cnidii could elevate the pituitary-thyroid axis function of Kidney-Yang Deficiency rats.
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Cells of the adenohypophysis in the primary 5--8 day monolayer culture responded to the administration of the thyrotropin-releasing-hormone (TRH) by a rapid dose-dependent release of thyrotropic hormone (TTH) and prolactin into the culture medium. This effect is independent of the serum content in the nutrient medium. Thyroxin, the thyroid gland hormone, blocks the stimulating action of TRH with respect to the TTH secretion, but not to prolactin. The blocking effect of thyroxin is apparently expressed not on the cell membranes, but in the cytoplasm, distal to cAMP, by way of the hormonal signal transmission.
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We have studied the effects of thyroid hormone deficiency and excess on GH and TSH economy in the rat fetus near term. Pregnant rats were either left untreated (C group) or treated with methimazole to block thyroid function and infused with placebo, T4, T3, or both, until 21 days of gestation. Two experiments were performed: the doses (per 100 g body wt/day) of T4 ranging from 2.4-21.6 micrograms, those of T3 from 1.5-13.5 micrograms, with groups on 2.4 micrograms T4 + 1.5 micrograms T3. Fetal plasma T4 levels varied between 6-160% of C values and T3 values between 52-770%. Both plasma and pituitary GH decreased in hypothyroid fetuses from methimazole dams, and their plasma TSH was elevated. When T4 and/or T3 were infused, plasma and pituitary GH increased as a function of fetal plasma T4 and T3, reaching normal values when plasma T3 levels became normal, then increasing further. The effects on GH economy were related to the plasma T3 level, with no appreciable difference if T3 had been infused or derived from T4. In contrast, the elevated plasma TSH of the hypothyroid fetus decreased toward normal values when fetal plasma levels of T4, and of T3 derived from T4, became normal, but was not affected by normal fetal plasma T3 when T3 was infused. In the absence of T4, T3 decreased plasma TSH only when infused in doses that increased fetal plasma T3 3-fold above C values or more. Thus, both GH and TSH economy are under thyroid hormone control in rat fetuses near term. Similarities and differences with respect to regulation in adult rats cannot, however, be attributed exclusively to differences in fetal somatotrophs and thyrotrophs, because of the possibility that control is exerted at regulatory sites which are unique to the fetus.
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