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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Acta Med Scand. 1979;206(6):459-61.
The role of endogenous cortisol in patients with non-thyroidal illness and decreased T3 levels.

Kallner G, Ljunggren JG.

The aim of the study was to elucidate if endogenous cortisol, as previously suggested, could be involved in the mechanism behind the reduced serum T3 levels seen in euthyroid patients with various non-thyroidal illnesses. The correlation between the serum levels of T3 and cortisol was investigated in 41 hospitalized patients with non-thyroidal illness during hyperpyrexia. The results showed a correlation coefficient of -0.94, indicating a close reciprocal association between the two hormones. Cortisol may thus be one factor associated with the decreased T3 levels seen in euthyroid patients with non-thyroidal illness. The results also indicate a close parallelism between the total and free T3 levels during hyperpyrexia.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119429&dopt=Abstract

Arch Dis Child. 1979 Dec;54(12):937-41.
TSH and PRL response to thyrotrophin-releasing hormone in children with chronic renal failure undergoing haemodialysis.

Ijaiya K.

Eight children (aged between 8 1/2 and 15 1/2 years) with chronic renal failure receiving intermittent haemodialysis, and 2 children with renal transplants were studied. The response of TSH and prolactin (PRL), and basal T4 and T3 values was measured. Basal TSH was normal, and rose only slightly after TRH stimulation. Plasma T4 and T3 were below normal levels in 6 children. Mean basal PRL was raised and could not be stimulated by TRH. This study demonstrates the involvement of the hypothalamus and pituitary in chronic renal disease. The cause of the abnormal secretion of TSH and PRL in chronic renal failure is discussed in the light of clinical importance.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119489&dopt=Abstract

Clin Endocrinol (Oxf). 1979 Dec;11(6):645-56.
Interaction between the thyrotrophin-releasing hormone-induced growth hormone rise and dopaminergic drugs: studies in pathologic conditions of the animal and man.

Muller EE, Salerno F, Cocchi D, Locatelli V, Panerai AE.

A rise in plasma growth hormone (GH) after thyrotrophin-releasing hormone (TRH) and a striking reduction after dopaminergic drugs is present in acromegalic ('responder') patients. We have investigated the GH response to dopaminergic stimuli in two conditions of animals and man, which, like acromegaly, are characterized by a TRH-induced GH rise, i.e. rats with electrolytic lesions of the median eminence (ME) and patients with hepatic cirrhosis. In addition, we have studied the TRH-induced GH rise in rats with ME lesions, in the cirrhotic patients and in a group of 'responder' acromegalics before and after administration of dopaminergic drugs. In rats with ME lesions an infusion of dopamine (DA) neither modified baseline GH levels nor the TRH-induced GH rise. In five out of six cirrhotic patients oral administration of L-Dopa was followed by the usual rise in plasma GH. infusion of DA increased plasma GH levels in three out of seven cirrhotic patients and in four out of five subjects an earlier GH rise after TRH was seen. However, in the 'responder' acromegalics, the infusion of DA, besides lowering baseline plasma GH, was capable of reducing the TRH-induced GH rise. Collectively these data indicate that the TRH-induced GH rise emphasizes defects in the neurohormonal links between the central nervous system and the anterior pituitary. Instead, the paradoxical fall of GH after dopaminergic drugs appears to be a prerequisite of acromegaly and may be attributable to receptors for DA located on the tumorous tissue.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119594&dopt=Abstract

Contraception. 1979 Dec;20(6):559-67.
Treatment of rhesus monkeys (Macaca mulatta) with intravaginal rings loaded with levonorgestrel.

Wadsworth PF, Heywood R, Allen DG, Hossack DJ, Sortwell RJ, Walton RM.

The effects of levonorgestrel-releasing intravaginal rings were investigated in 15 rhesus monkeys for 52 weeks. The intravaginal rings were designed to provide a sustained release of either three or ten times the human dose level of the hormone. Untreated placebo rings were used as a control. The devices were well retained. After insertion of the vaginal rings, a dose-related decrease in vaginal bleeding was observed. The vaginal microbial flora were assessed qualitatively and semi-quantitatively and although all groups including controls showed some changes in microbial populations, by the end of the study nearly all animals returned to a normal balanced microflora. Terminal studies showed that, at the high dose level, ovulation was suppressed and widespread atrophy of the uterine mucosal and glandular epithelium had occurred. A dose-related increase in mucus within the lumen of the endocervical canal was observed. Focal or diffuse atrophy of the vaginal mucosal epithelium was seen in the majority of levonorgestrel-treated animals.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119606&dopt=Abstract

Nippon Yakurigaku Zasshi. 1979 Apr 20;75(3):239-50.
[Thyrotropin-releasing hormone (TRH): action mechanism of an enhanced dopamine release from rat striatal slices (author's transl)]

[Article in Japanese]

Narumi S, Nagai Y, Nagawa Y.

The enhancing effect of TRH on dopamine(DA) release from rat striatal slices was investigated in relation to Ca2+ and cholinergic mechanisms. TRH(10(-5)--10(-3) M) facilitated concentration dependently the uptake of 14C-DA by rat striatal slices, while methamphetamine (10(-6)--10(-4)M) exhibited a considerable inhibitory effect. TRH (10(-7)--10(--3)M) alone did not increase the DA release into the incubation medium, but it clearly enhanced the DA release in the concomitant presence of desipramine (5 x 10(-5)M). In the superfusion study, TRH (10(-5)--10(-3)M), methamphetamine (10(-6)--10(-4)M) and KCl (2.5--5.0 x 10(-2)M) enhanced the DA release into the perfusion fluid. The DA releasing effect of TRH was completely blocked by cholinergic blockers (scopolamine, hexamethonium and hemicholinium), Ca2+ chelator(EGTA), Ca2+ antagonist(CoCl2) and Ca2+ influx blocker(D-600) or by the removal of Ca2+ from the medium. The methamphetamine-enhanced DA release, however, was not modified by the above treatments except for a partial decline produced by EGTA coupled with the removal of Ca2+. TRH(10(-4)M) also facilitated the uptake of norepinephrine (NE) by rat cerebral cortex slices, but methamphetamine (10-(6)--10(-4)M) exhibited a considerable inhibitory effect. In the superfusion study, TRH (10(-5)--10(-4)M) and methamphetamine (10(-7)--10(-4)M) enhanced the NE release into the perfusion fluid. Therefore, it can be concluded that TRH facilitated the DA release from rat striatal slices by mediating through a cholinergic mechanism and enhancing the influx of Ca2+.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=119692&dopt=Abstract

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