Spelling suggestions: "subject:"thyrotropin releasing factor."" "subject:"thyrotrophin releasing factor.""
1 |
Discovery of a uridine kinase inhibitory factor (UKIF) in acid extracts of clonal rat pituitary cells whose concentration is modulated by hormone treatment with TRH or VIPRuck, Deborah Ann. January 1983 (has links)
Thesis (M.S.)--University of Wisconsin--Madison, 1983. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 29-33).
|
2 |
Cardiovascular and metabolic responses to central thyrotropin-releasing hormone during caloric restriction in ratsKnight, W. David. Overton, J. Michael. January 2005 (has links)
Thesis (M.S.)--Florida State University, 2005. / Advisor: J. Michael Overton, Florida State University, College of Human Sciences, Dept. of Nutrition, Food, and Exercise Sciences. Title and description from dissertation home page (viewed Jan. 26, 2006). Document formatted into pages; contains vii, 34 pages. Includes bibliographical references.
|
3 |
EFFECTS OF THYROTROPIN RELEASING HORMONE AND ENVIRONMENTAL TEMPERATURE ON THE HYPOPHYSIAL-THYROID AXIS OF HYPOTHYROID, EUTHYROID AND CASTRATED WHITE LEGHORN CHICKENSCarr, Bruce Leslie January 1981 (has links)
Cyclic AMP-dependent protein kinase (cAMP-PK) is an important mediator of hormone action. Its activity ratio is an accurate indicator of cellular activity under various experimental conditions including: (1) age and sex, (2) hormone administration and (3) temperature and photoperiod. Pituitary activity in unstimulated birds is not altered by age, but thyroid activity is much higher in old birds than in young animals. Thyrotropin releasing hormone (TRH) increases pituitary, thyroid and liver activity of prepubescent chickens, but has no effect on aged males and increases only thyroid and liver activities in aged females, suggesting a reduction in pituitary-thyroid function with advancing age. In prepubertal females, TRH increases pituitary and thyroid cAMP-PK activity, plasma T₃ and T₄ levels and liver T₄ monodeiodination. Thyroid activity reaches maximum activity before the pituitary, while plasma T₄ and liver T₄ monodeodinating activity reach their highest levels 20 minutes before plasma T₃. These findings suggest that fluctuations in liver T₄ 5' monodeiodinating activity might be responsible for the cyclic response of plasma T₃ and T₄. Castrated cockerels have larger pituitaries than untreated birds, but contain the same amount of DNA. Methimazole-fed cockerels have pituitaries significantly smaller than controls, while castrated cockerels fed methimazole have pituitaries the same size as untreated birds. Pituitary DNA is less than controls in both groups of methimazole-fed birds. These results are considered to be due to a change in the thyrotroph population, without an increase in total cell numbers, and may indicate a transformation of basophils. Pituitary cAMP-PK activity during cold stress substantiates this conclusion. Thyroid glands of castrated and untreated cockerels are smaller in size, histological appearance and DNA content; however, cAMP-PK activity is much greater in the castrated birds. Methimazole-fed cockerels have enlarged thyroid glands, elevated cAMP-PK activity, increased DNA and cellular hypertrophy; however, these effects may be mitigated by castration. Seven days after removal of testosterone supplements, photostimulated castrates have a higher thyroid cAMP-PK activity ratio than short day castrates; however, both groups are elevated above control, suggesting that long photoperiods enhance the stimulatory effects of castration on thyroid activity. Pituitary activity is elevated in long and short day birds seven days after removal of testosterone, but remains high only in short day castrates. Therefore, a reduction in the sensitivity of the hypothalamic-pituitary axis to testosterone may occur only in long day cockerels.
|
4 |
THE CONTROL OF TSH LEVELS IN THYROTROPHS OF THE CHICKEN PARS DISTALISRadke, William John, 1947- January 1975 (has links)
No description available.
|
5 |
Factors affecting thyrotropin secretion in superfused rat anterior pituitary cellsBartlow, Frederick Scott 01 January 1982 (has links)
The use of static in vitro pituitary cultures has been indispensible for examining the regulation of anterior pituitary hormone secretion. While the static cultures have shown the effects of various chemical stimulators of hormone secretion, the dynamics of such secretion has not been assessed before in vitro. The in vitro superfusion method, which partially stimulates in vivo physiologic conditions, allows for the observation of the dynamics of pituitary hormone secretion.
|
6 |
Neuroprotective Effect Of Thyrotropin-Releasing Hormone (TRH) Against Glutamate Toxicity In VitroYard, Michael 13 November 2009 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / Acute and chronic activation of both ionotropic and metabotropic glutamate (glut) receptors is implicated in many neurodegenerative disorders including AD, dementia, epilepsy, stroke and neurotrauma. TRH and glut receptors (ionotropic & metabotropic) receptors are differentially coexpressed in granule and pyramidal neurons of the hippocampus. The author shows TRH to be protective when added to cultured pituitary adenoma (GH-3) cells and neuron-like pheochromocytoma (PC12) cells either prior to, during, or after glut-induced toxicity (Endo. Soc. Abs. 01), and also shows that the possible neuroprotective mechanism may involve heterologous downregulation of the metabotropic glut receptors, using superfused hippocampal slices and noting a reduction of Gαq/11 (SFN Abs. 02). He has also demonstrated that TRH protected against glut toxicity in fetal cortical cultures (Endo. Soc. Abs. 04). To extend these studies he used 14-day cultured rat fetal hippocampal neurons (Day E17) to determine if TRH is protective against toxicity induced by specific ionotropic and metabotropic glut agonists. Neuronal viability and integrity were assessed by trypan blue exclusion and LDH release after 18 hrs following 30 min exposure to glut agonists. Ten µM dihydroxyphenylglycine (DHPG, a Group 1 receptor agonist) + 30 µM N-methyl-D-aspartate (NMDA)-induced toxicity (42% vs contr. P<0.05); whereas, concurrent and continued treatment with 10 uM but not 1uM 3Me-HTRH resulted in less neuronal death and damage (86% vs contr P<0.05; 53% vs contr. P>0.05) respectively. DHPG treatment alone (10 µM) for 30 min. was non-toxic by both criteria (90% vs contr. P<0.05). The data suggest that TRH may be a selective modulator of glut-induced toxicity.
|
Page generated in 0.0849 seconds