Disease relevance of Rifathyroin

• Very high intravenous doses (2-19 mg/min) of thyrotropin-releasing hormone (TRH, L-pyroglutamyl-L-histidyl-L-prolinamide) given to 12 patients with amyotrophic lateral sclerosis (ALS) produced a moderate to marked improvement of functions caused by deficiency of lower motor neurons (weakness) and upper motor neurons (spasticity) [1].
• Polyadenylate-rich mRNA extracted from an established line of functional rat pituitary tumor cells (GH3) which respond to the addition of thyrotropin-releasing factor with the synthesis and secretion of prolactin directed cell-free synthesis using a cell-free protein-synthesizing system derived from wheat embryos [2].
• Serum levels of thyroid-stimulating hormone (TSH), before and after thyrotropin-releasing factor (TRF) administration, were in the range generally considered to be indicative of primary, rather than secondary, hypothyroidism [3].
• Plasma ACTH and cortisol responses to TRF, vasopressin or hypoglycemia in cushing's disease and nelson's syndrome [4].
• Hyperprolactinemia: comparison of thyrotropic-releasing hormone and tomography [5].

High impact information on Rifathyroin

• Base-line gonadotropin levels and thyrotropin-releasing-factor-stimulated prolactin were the most reliable measures of residual pituitary function [6].
• Injection of somatostatin into the third ventricle also decreased plasma concentrations of luteinizing hormone, follicle-stimulating hormone, and thyroid-stimulating hormone, probably by inhibiting the release of luteinizing hormone-releasing factor and thyrotropin-releasing factor [7].
• The addition of fibroblast growth factor (FGF) to primary cultures of rat anterior pituitary cells modifies their response to thyrotropin-releasing factor in a dose-dependent manner [8].
• Somatostatin inhibits release of thyrotropin releasing factor from organ cultures of rat hypothalamus [9].
• Thyrotropin-releasing factor-induced adrenocorticotropin secretion is mediated by corticotropin-releasing factor [10].

Chemical compound and disease context of Rifathyroin

• The diagnosis of prolactinoma was made in three of the 16 patients by the absence of PRL response to thyrotropin-releasing factor (TRF) and a dopamine receptor antagonist, metoclopramide, without radiologic evidence of an adenoma [11].
• Thus, neither TRH nor thyroxine is involved in the etiology of hypothalamic obesity [12].

Biological context of Rifathyroin

• The respiratory activity in newborn preterm (29 days gestation) rabbits was studied after administration of thyrotropic releasing hormone [13].
• No hydrolysis of thyrotropin-releasing factor or bradykinin potentiating nonapeptide from B. jararaca is observed [14].
• Levels of estrogen and progesterone in milk of animals induced into lactation by reproductive steroids and thyrotropic releasing hormone [15].

Anatomical context of Rifathyroin

• Thyrotropin-releasing factor (TRF) activity was higher after 2 and 24 h of cold exposure in the median eminence and after 8 h in the anterior hypothalamus-preoptic area, but lower after 8 and 24 h in the dorsomedial hypothalamus [16].
• These results suggest that most, if not all of the thyrotropin-releasing factor (TRF) necessary for normal TSH secretion in resting conditions or during the hypothyroid state, is produced and released in the median eminence-arcuate nucleus area, the adequate activity of which, in turn, depends on intact connections with the anterior hypothalamus [17].
• An increase in the TI/TTOT ratio but (unaffected) VT/TI ratio indicates that thyrotropic releasing hormone affects "respiratory timing" mechanisms rather than "inspiratory drive." The changes in respiratory parameters are most probably due to an effect on the central respiratory controlling centers in the brain stem [13].
• In non-mammalian vertebrates, CRH not only acts as a neurotransmitter and hypophysiotropin, it also acts as a potent thyrotropin-releasing factor, allowing CRH to regulate both the adrenal and thyroid axes, especially in development [18].
• Metabolism of thyrotropin releasing factor in two clonal cell lines of nervous system origin [19].

Associations of Rifathyroin with other chemical compounds

• In addition, activation of metabotropic receptors by achetylcholine, glutamate, noradrenaline, serotonin, substance P and thyrotropin releasing factor (TRH) can alter the properties of various voltage- and calcium-sensitive channels and thereby affect synaptic current delivery and input resistance [20].
• The response of plasma ACTH and/or cortisol concentrations to thyrotropin-releasing-factor (TRF), vasopressin, and insulin administration was determined in 5 patients with Nelson's syndrome and 12 patients with untreated Cushing's disease [4].
• Recent studies from this laboratory have suggested a similarity, if not identity, of thyrotropin releasing factor (TRF) deamidase and post-proline cleaving enzyme [21].
• Baclofen (BACL: 1 x 10(-5) M) significantly inhibited basal and thyrotropic releasing hormone (TRH)-stimulated (1 x 10(-7) M) PRL secretion in anterior pituitary cells from proestrous rats [22].
• With Cu2+ the hormone has been shown to behave similarly to the thyrotropin releasing factor, forming a very stable [CuH-1L] complex involving coordination of three nitrogen donors: the Nim atom of the imidazole side chain and the two amido-N atoms of the pyroglutamylhistidyl unit [23].

Gene context of Rifathyroin

• In two anencephalic infants, thyrotropin releasing factor (TRF) (200 mug IV) evoked a rise in serum hPRL in one patient from 43 to 156 ng/ml at 30 min, and in the other from 65 to 404 ng/ml at 120 min [24].
• Role of corticotropin-releasing hormone as a thyrotropin-releasing factor in non-mammalian vertebrates [25].
• Effect of human growth hormone-releasing factor and(or) thyrotropin-releasing factor on hormone concentrations in dairy calves [26].
• Prolactin responses to provocative thyrotropin-releasing factor (TRH) stimulation were evaluated in 43 chronic alcoholic men were divided into groups for analysis based on the presence or absence of gynecomastia and the histologic appearance of their livers as determined by percutaneous liver biopsy [27].
• Psychopharmacological activities of L-6-ketopiperidine-2-carbonyl-L-leucyl-L-proline amide (RGH-2202) were compared with those of the parent peptide, thyrotropin releasing hormone (TRH, L-pyroglutamyl-L-histidyl-L-prolinamide, Pyr-His-Pro amide) in rodents [28].

Analytical, diagnostic and therapeutic context of Rifathyroin

• Sensitive immunoradiometric assay (IRMA) for serum thyrotropin may be insufficient to make the thyrotropin-releasing-factor test unnecessary [29].
• Thyrotropin releasing factor: radioimmunoassay and distribution in biological fluids and tissues [30].

References