Comparison of thyrotrophin receptors in membranes prepared from fat and thyroid tissue.
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Biomedical subjects
Publications and source records attributed to R Hall.
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The hypothalamic tetradecapeptide growth hormone release inhibiting hormone (GH-RIH) blocked the thyrotrophin response to thyrotrophin-releasing hormone (TRH) in normal people and in patients with primary hypothyroidism. This inhibition was dose related. The TRH-induced prolactin release was not affected by GH-RIH. This dissociation of the thyrotrophin and prolactin responses to TRH by GH-RIH suggests that there are different mechanisms for release of thyrotrophin and prolactin and that only the former is affected by GH-RIH.
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Growth-hormone release-inhibiting hormone (G.H.-R.I.H.) inhibited gastric acid and pepsin secretion in response to pentagastrin and food stimulation in cats. This effect is mediated by a direct action on the parietal and peptic cells. No evidence of a post-inhibitory acid or pepsin secretory rebound was obtained. Thus a compound of hypothalamic origin can exert a direct effect on exocrine secretion. In view of its widespread actions and its presence in relatively high concentrations in various organs apart from the hypothalamus, G.H.-R.I.H. might also be regarded as a factor responsible for local coordination of endocrine and exocrine secretion.
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Thyroid-stimulating immunoglobulins (T.S.I.) have been detected in the serum of all patients with untreated Graves' disease, and in these patients the levels of T.S.I. correlated significantly with the early uptake of 131I by the thyroid. The frequency of T.S.I. in patients treated solely by antithyroid drugs, by radioiodine, or by partial thyroidectomy was 53 per cent, 50 per cent, and 17 per cent, respectively. The reduced frequency of T.S.I. in the serum of patients treated by drugs or radioiodine was probably due to spontaneous remission, but in the case of partial thyroidectomy the operation itself clearly had a dramatic effect on the serum-T.S;I. These results accorded well with the reported frequency of thyroid autonomy in similar groups of patients and suggested that thyroid-stimulating immunoglobulins were responsible for hyperthyroidism in Graves' disease.
Effusions into body cavities secondary to hypothyroidism, though rare, are well recognised. They may precede the more specific and typical manifestations of the disease, thereby misleading the clinician.
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Thyroid function in health is largely controlled by thyroid-stimulating hormone (TSH) produced by the thyrotroph cells of the anterior pituitary. Alterations of intrathyroidal iodine content may also be involved in autoregulation by the thyroid, particularly in states of iodine deficiency and excess (Ingbar, 1972). During pregnancy placental thyroid-stimulating agents-human chorionic thyrotrophin (HCT) and human molar thyrotrophin (HMT)-are produced. In the common variety of hyperthyroidism, Graves' disease, thyroid function appears to be regulated by thyroid-stimulating immunoglobulins (TSI) (Smith & Hall, 1974a). Human molar thyrotrophin can be produced by trophoblastic tumours in both sexes and thyroid-stimulating factors have been reported to be released by malignant tumours of the gut and by bronchogenic carcinomas, although this is one of the rarest of the ectopic hormone syndromes.
The growth hormone response to the administration of the currently available synthetic hypothalamic hormones was assessed in eleven patients with acromegaly. Eight of them showed a positive GH response to thyrotrophin releasing hormone and three showed no response. The GH response to TRH was shown to be unrelated to the thyrotrophin response to TRH. The GH response to TRH was inhibited by the administration of growth hormone release inhibiting hormone. Luteinizing hormone/follicle stimulating hormone releasing hormone (LHRH) caused a positive GH response in four patients, but this was trivial in three. The TRH mediated GH release in acromegaly is not mediated via TSH and appears to be attributable to loss of specificity of the receptor sites on the somatotroph to the hypothalamic hormones.
A study has been made of the effects of changing [Ca]O and [Mg]O on the binomial statistic parameters p and n which control the average quantal content (m) of the synaptic potential due to acetylcholine release. 2. When [Ca]O was varied in the range 0-1 to 1-0 mM, p increased as the first power of [Ca]O whereas n increased as the third power of [Ca]O. 3. Increasing [Mg]O depressed both p and n, however variations of [Ca]O in the presence of high [Mg]O did not significantly change the power relationship between either p and [Ca]O or between n and [Ca]O. 4. The facilitated increase in m during a short train was due to an increase in n, whereas the post-tetanic increase in m during a tetanus was due to an increase in p. These results are considered in terms of the role of Ca ions in facilitation and post-tetanic potentiation.
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In a double-blind trial 600 mug. of thyrotrophin-releasing hormone (TRH) was compared with placebo given daily for four days to two groups of ten patients. There was no significant difference between the antidepressant effects of TRH and placebo.
The cytochemical bioassay is able to detect minute amounts of thyroteopin and thyroid stimulating immunoglobulins. Estimations of serum TSH by the cytochemical bioassay are in good agreement with values obtain by radioimmunoassay. In untreated hyperthyroid patients with Graves' disease the TSH levels are significantly lower than in control subjects. Thyroid stimulating immunoglobulins showed a delayed time corse of action in the bioassy and this provided a voncenient method of distinguishing between the two thyroid stimulators.