Growth hormone (GH), thyroid-stimulating hormone (TSH), and luteinizing hormone (LH)-like peptides in the rodent brain: non-parallel ontogenetic development with pituitary counterparts

1982 ◽  
Vol 4 (4) ◽  
pp. 427-434 ◽  
Author(s):  
Sally Hojvat ◽  
Nicholas Emanuele ◽  
Georgiann Baker ◽  
Eric Connick ◽  
Lidia Kirsteins ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Thyroid Stimulating Hormone ◽  
Ontogenetic Development ◽  
Rodent Brain ◽  
Stimulating Hormone

A RE-EXAMINATION OF THE TADPOLE IN METAMORPHIC STASIS AS A RECIPIENT IN A BIOASSAY FOR THYROID-STIMULATING HORMONE

1974 ◽  
Vol 61 (1) ◽  
pp. 15-19 ◽  
Author(s):  
MELVIN CHING
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Thyroid Function ◽  
Anterior Pituitary ◽  
Rana Pipiens ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Extract ◽  
Metamorphic Stage ◽  
Stimulating Hormone

SUMMARY The tadpole, in metamorphic stasis, has been used as a bioassay recipient for thyroid-stimulating hormone (TSH). The validity of its use for this purpose, however, has not been tested critically, particularly with respect to the effect of other hormones, most notably, growth hormone (GH) and luteinizing hormone (LH). Growth hormone has been shown to influence thyroid function and LH is a common contaminant of pituitary TSH preparations. Tadpoles of Rana pipiens, arrested at a particular metamorphic stage, received various concentrations of LH alone, a combination of doses of GH and TSH, or GH and rat anterior pituitary extract. Growth hormone was ineffective in re-inducing metamorphosis in 78% of cases, whereas LH stimulated metamorphosis in the tadpoles.

Regarding the validity of the endpoint response of the mouse (McKenzie) bioassay for thyrotrophin (TSH)

1981 ◽  
Vol 96 (3) ◽  
pp. 342-349 ◽  
Author(s):  
Melvin Ching
Keyword(s):  
Growth Hormone ◽  
Chemical Composition ◽  
Thyroid Hormone ◽  
Luteinizing Hormone ◽  
Pituitary Hormones ◽  
Thyroid Stimulating Hormone ◽  
Quantitative Estimates ◽  
Rat Pituitary ◽  
Stimulating Hormone

Abstract. The release of radiolabelled thyroid hormone into the circulation in low iodine fed mice has been used extensively as a bioassay for thyroid stimulating hormone (TSH). However, the specificity of several bioassays of pituitary hormones have been subject to question. Consequently, the validity of the assay endpoint for TSH in the mouse was re-evaluated with respect to the effect of luteinizing hormone (LH) whose chemical composition closely resembles that of TSH. Mice, prepared for bioassay of TSH received injections of purified LH or α or β subunits of LH. Identical doses of LH and LH subunits were quantified by LH and TSH radioimmunoassays and the results compared with those obtained by the bioassay. Microgram quantities of LH and subunits of LH elicited appreciable responses in the TSH bioassay but produced only negligible effects in the TSH radioimmunoassay. The response of the TSH bioassay of LH and α or β subunits of LH was 40–56% that obtained with LH radioimmunoassay. However, the pituitary concentrations obtained by TSH bioassay when compared with those obtained by radioimmunoassays for TSH, LH, or growth hormone (GH) paralleled closely the TSH radioimmunoassay data, although in terms of quantitative estimates, there was a 15-fold discrepancy between the TSH assays. Estimations of pituitary concentrations of LH lead to the conclusion that, at the doses normally employed, most crude rat pituitary extracts do not contain sufficient quantities of LH to alter significantly bioassayable (McKenzie) estimates of TSH.

Monolayer Cultures of Dispersed Cells from Bovine Anterior Pituitary: Responses to Synthetic Hypophysiotropic Peptides

1975 ◽  
Vol 53 (6) ◽  
pp. 1094-1098 ◽  
Author(s):  
G. Queen ◽  
S. Vivian ◽  
F. LaBella
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Control Level ◽  
Thyroid Stimulating Hormone ◽  
Releasing Hormone ◽  
Cell Monolayers ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Stimulating Hormone

Cells were dispersed from bovine anterior pituitary glands, by digestion with collagenase, and cultured. After 4 days the cell monolayers were incubated with fresh medium containing synthetic hypophysiotropic peptides for 2, 6, or 20 h, and hormone released into the medium was estimated by radioimmunoassay. After 2 h, thyroid releasing hormone (TRH) stimulated the release of thyroid-stimulating hormone (TSH) up to eightfold, and of prolactin (PRL) and follicle-stimulating hormone (FSH) about twofold at a minimal effective concentration of 1 ng/ml; enhanced growth hormone (GH) release was not apparent until 20 h, and release of luteinizing hormone (LH) and adrenocorticotrophic hormone (ACTH) was unaffected. Luteinizing hormone releasing hormone (LH-RH) enhanced release of LH maximally (three- to fourfold) during a 2 h incubation and was effective at 0.1 ng/ml; FSH release was significantly enhanced by about 50% above control level. Growth hormone release inhibiting hormone (GH-RIH) (somatostatin) showed significant effects only in the 20 h incubation; GH release was inhibited by 50% and release of PRL was slightly, but significantly, enhanced. Pituitary cell monolayers apparently permit maximal expression of releasing activities inherent in the hypothalamic hormones.

scholarly journals Significance of hyperprolactinemia for cytomorphologic features of breast secretions

2010 ◽  
Vol 67 (1) ◽  
pp. 42-47
Author(s):  
Danijela Radojkovic ◽  
Slobodan Antic ◽  
Milica Pesic ◽  
Milan Radojkovic ◽  
Dijana Basic ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Nipple Discharge ◽  
Thyroid Stimulating Hormone ◽  
Serum Prolactin ◽  
Control Group ◽  
Clinical Group ◽  
Group I ◽  
Stimulating Hormone

Background/Aim. Nipple discharge syndrome is a clinical entity capable of presenting various disorders such is mammary infection (nonpuerperal and puerperal mastitis), intraductal papillomas, fibrodenoma, breast cancer and hyperprolactinemia syndrome. The aim of the study was to determine differencies in cytological features of mammary secretion in patients with hyperprolactinemia and those with normal serum prolactin levels and to define the role of growth hormone, follicle-stimulating hormone, luteinizing hormone and thyroid-stimulating hormone in creating cellular profile of breast secretion. Methods. The study included 50 patients with nipple discharge syndrome. The patients were devided into the clinical group (27 patients with hyperprolactinemia and nipple discharge) and the control group I (23 patients with normal serum prolactin and nipple discharge). The control group II included the patients of the clinical group achiving normalised serum prolactin levels after the treatment of hyperprolactinemia. Serum prolactin, follicle-stimulating hormone and luteinizing hormone levels were assessed by RIA using commercial kits IRMA hPRL, hLH and hFSH, (INEP, Zemun, Serbia) while serum growth hormone and thyroid-stimulating hormone levels were assessed by RIA using commercial kits LKB-wallac. Cytologic evaluation of samples, taken from all the patients with mammary secretion, was done using standard techniques of staining Haemathoxilin-eozine and May- Gr?nwald/Giemsa. Results. Our results showed a significantly higher presence of lipid and protein material in clinical group, in comparison with the control group I (p < 0.01). Also, our data demonstrated significantly higher number of ductal epithelial cells (p < 0.05) and ductal histiocities (p < 0.001) in the clinical group, compared with the control group I. Macrophagies frequency was proportionally higher in clinical group (44.44%) compared the control group I (17.39%). Erythrocites were significantly lower in the clinical group (p < 0.001) than in the control group I. Significantly decreased mammary secretion (p < 0.01), lower lipid (p < 0.01) and protein synthesis (p < 0.01), and less presence of all cellular categories (p < 0.01) were obtained after normalization of serum prolactin levels. Conclusion. Growth hormone, follicle-stimulating hormone, luteinizing hormone and thyroid-stimulating hormone did not show significant influence on creating cytological features of mammary secretion. The most expressive role, hyperprolactinemia demonstrated in the domain of mammary ductal secretory activity, making mammary secretion reach in lipid and protein material and simultaneously increasing number of ductal epithelial cells, ductal histiocytes and 'foam cells'- macrophages. These cytological findings indicate that hyperprolactinemia promote periductal and intraductal steril inflammation which withdraws after serum prolactin normalization.

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