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Kaur, Baljit. "The conformational analysis of thyrotropin releasing hormone and its analogues". Thesis, Manchester Metropolitan University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284878.
Pełny tekst źródłaOuafik, L'Houcine. "Etude sur la biosynthèse de la Thyrotropin-Releasing Hormone (TRH) pancréatique". Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb37608585w.
Pełny tekst źródłaOuafik, L'Houcine. "Etude sur la biosynthèse de la thyrotropin-releasing hormone (TRH) pancréatique". Aix-Marseille 2, 1987. http://www.theses.fr/1987AIX22004.
Pełny tekst źródłaXiang, Shi Zhan. "Central control of the rat thyroid axis". Thesis, Brunel University, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320216.
Pełny tekst źródłaEbiou, Jean-Claude. "Le rôle biologique de la thyrotropin-releasing hormone (TRH) dans le pancréas endocrine". Paris 7, 1992. http://www.theses.fr/1992PA077056.
Pełny tekst źródłaHart, G. R. "Mechanism of control of growth hormone release from the anterior pituitary : A role for thyrotropin-releasing hormone". Thesis, University of Sussex, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305765.
Pełny tekst źródłaNguyen, Kim Thoa Thi [Verfasser]. "Thyrotropin releasing hormone (TRH) selectively stimulates human hair follicle pigmentation / Kim Thoa Thi Nguyen". Lübeck : Zentrale Hochschulbibliothek Lübeck, 2017. http://d-nb.info/114120309X/34.
Pełny tekst źródłaCarter, Rebecca Ann. "Thyroid Status in Exercising Horses and Laminitic Ponies". Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/35454.
Pełny tekst źródłaMaster of Science
Dromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.
Pełny tekst źródłaSun, Yuh-Man. "Cloning and charaterisation of the Thyrotrophin-releasing hormone receptor and Gonadotrophin-relasing hormone receptor from chicken pituitary gland". Doctoral thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26973.
Pełny tekst źródłaBertacchini, Eleonora. "Molecular study of stress system in the European sea bass (Dicentrarchus labrax): cloning of different components and effects of essential oil of Lippia alba during stress situation". Master's thesis, Alma Mater Studiorum - Università di Bologna, 2018.
Znajdź pełny tekst źródłaShortridge, Emily. "The Cryptic Peptides, Prepro-Thyrotropin Releasing Hormone 186-199 and 194-199, Suppress Anterior Pituitary Prolactin Secretion in vivo and in vitro". Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/221632.
Pełny tekst źródłaPrepro-thyrotropin releasing hormone (ppTRH)-176-199 is one of several peptide fragments cleaved during TRH synthesis and has been implicated as a regulator of neuroendocrine function. ppTRH 176-199 has been shown to acutely inhibit the stress-induced rise in ACTH, corticosterone (CORT), and prolactin (PRL) in the rat. The receptor for ppTRH 176-199 currently remains unknown. In this study we sought to characterize the active domain of ppTRH 176-199 and, using in vivo and in vitro approaches, determine its role in regulating anterior pituitary secretion of PRL. The 186-199, 194-199, and 186-191 amino acid fragments of ppTRH were administered I.P. to adult male Sprague-Dawley rats 15 min. prior to a 20 min restraint stress to determine the peptide’s active moiety in regulating prolactin secretion. Animals were euthanized and plasma was saved for assay of circulating PRL using enzyme immunoassay (EIA). ppTRH 186-199 significantly attenuated the stress-induced rise in prolactin in male rats in a dose-responsive fashion. This effect was mimicked by ppTRH 194-199 but not by ppTRH 186-191. At the highest dose (10 mg/kg BW), ppTRH 194-199 also reduced the stress-induced rise in plasma CORT. Additionally, in vitro studies were performed using the rat growth hormone (GH)/PRL –secreting MMQ cell line. MMQ cells were treated with ppTRH 186-199 and media was assayed for PRL levels. Cells were harvested and examined for changes in PRL mRNA. Within 30 minutes following treatment of estradiol-stimulated MMQ cells with ppTRH 186-199 there was a decrease in media levels of PRL compared to vehicle. Furthermore, in MMQ cells that were primed with 10nM estradiol for 48 hours there was an increase in media PRL levels, which was reduced following ppTRH 186-199 treatment. After 4 hrs of treatment, the inhibitory effect of ppTRH 186-199 on PRL secretion from MMQ cells was only seen on estradiol-stimulated cells. There were no effects of ppTRH 186-199 when examined after 24 hrs of treatment. There were no effects of ppTRH 186-199 or 194-199 of PRL mRNA levels. These data suggest that the carboxy terminal fragment of preproTRH 178-199 contains all the activity of this ppTRH cryptic peptide for regulation of PRL and corticosterone secretion. This suggests a potential moiety responsible for interaction with the peptide’s receptor. The inhibitory effect of ppTRH 186-199 and 194-199 on media PRL levels and not on mRNA synthesis implicates it as an effector of hormone secretion rather than protein synthesis. The short-lived duration of its effects supports a role as 6 an acute effector of the PRL system. The target receptor of the ppTRH 178-199 fragment remains uncertain. However the use of ppTRH 194-199 as a peptide bait may prove useful in identifying the receptor.
Yamamoto, Akane. "Response of preterm infants with transient hypothyroxinaemia of prematurity to the thyrotropin-releasing hormone stimulation test is characterized by a delayed decrease in thyroid-stimulating hormone after the peak". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263539.
Pełny tekst źródłaEymin, Cécile. "Étude des récepteurs de la sérotonine et de la thyrotropin-releasing hormone dans l'hippocampe humain normal et pathologique : mort subite du nourrisson et suicide". Lyon 1, 1993. http://www.theses.fr/1993LYO1T108.
Pełny tekst źródłaTrouslard, Jérôme. "Etude electrophysiologique du couplage excitation-secretion des cellules endocrines du lobe intermediaire de l'hypophyse : mise en evidence d'un effet excitateur medie par la thyrotropin-releasing hormone". Université Louis Pasteur (Strasbourg) (1971-2008), 1990. http://www.theses.fr/1990STR13072.
Pełny tekst źródłaSheward, William John. "Thyrotrophin releasing hormone, somatostatin and luteinizing hormone releasing hormone : aspects of their synthesis, release and actions". Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/20183.
Pełny tekst źródłaGarnier, Marianne. "Contribution à l'étude du contrôle multifactoriel de l'activité sécrétoire des cellules mélanotropes : mécanisme d'action de l'acétylcholine, de la TRH et des agonistes adrénergiques". Rouen, 1998. http://www.theses.fr/1998ROUES025.
Pełny tekst źródłaCoggins, P. J. "Histidylproline : biochemical and behavioural studies on a thyrotrophin releasing hormone metabolite". Thesis, University of Newcastle Upon Tyne, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356142.
Pełny tekst źródłaWatson, Christopher David. "The role of thyrotrophin-releasing hormone in cognitive function in the rat". Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262166.
Pełny tekst źródłaBristow, L. J. "A functional role for histamine in brain : Interactions with thyrotrophin releasing hormone (TRH)". Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384327.
Pełny tekst źródłaLighton, C. "Interactions between thyrotrophin-releasing hormone and 5-hydroxytryptamine in the rat central nervous system". Thesis, University of Nottingham, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355293.
Pełny tekst źródłaMabrouk, Mabrouk Mohamed. "Behavioural effects and neurochemical studies of a novel thyrotrophin-releasing hormone (TRH)-like peptide (FPP)". Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339688.
Pełny tekst źródłaRojas, Asheebo. "KIR Channels in CO2 Central Chemoreception: Analysis with a Functional Genomics Approach". unrestricted, 2007. http://etd.gsu.edu/theses/available/etd-08032007-163450/.
Pełny tekst źródłaTitle from file title page. Chun Jiang, committee chair; Delon Barfuss, Deborah Baro, Teryl Frey, committee members. Electronic text (226 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Nov. 1, 2007. Includes bibliographical references (p. 210-226).
Waterfall, Alan H. "The development of in vivo methods to measure the neuropeptide thyrotrophin releasing hormone in the central nervous system". Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358269.
Pełny tekst źródłaDrust, Debra Sue. "Thyrotropin-releasing hormone stimulated protein phosphorylation in GH₃ cells". 1985. http://catalog.hathitrust.org/api/volumes/oclc/13037265.html.
Pełny tekst źródłaMarrero, Diana. "Enhanced peptide transdermal diffusion of thyrotropin releasing hormone by iontophoresis". 1985. http://catalog.hathitrust.org/api/volumes/oclc/12717461.html.
Pełny tekst źródłaTypescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 77-90).
Dowty, Martin E. "Permeability of thyrotropin releasing hormone in rabbit buccal mucosa in-vitro". 1988. http://catalog.hathitrust.org/api/volumes/oclc/19054754.html.
Pełny tekst źródłaTypescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 84-89).
Dowty, Martin E. "Transport of thyrotropin releasing hormone in rabbit buccal mucosa in-vitro". 1991. http://catalog.hathitrust.org/api/volumes/oclc/25270907.html.
Pełny tekst źródłaTypescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 174-193).
Yard, Michael. "NEUROPROTECTIVE EFFECT OF THYROTROPIN-RELEASING HORMONE (TRH) AGAINST GLUTAMATE TOXICITY IN VITRO". Thesis, 2009. http://hdl.handle.net/1805/2005.
Pełny tekst źródłaAcute 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.
Liu, Shy-Rong, i 劉詩蓉. "Interaction between triiodothyronine and ovarian steroids on the regulation of the release of thyrotropin and thyrotropin-releasing hormone". Thesis, 1994. http://ndltd.ncl.edu.tw/handle/94753419535004024562.
Pełny tekst źródłaTSAI, SHIOW-CHWEN, i 蔡秀純. "Effects of thyroid hormones on the release of thyrotropin-releasing hormone (TRH) and the response of thyrotropin and prolactin to TRH in rats". Thesis, 1992. http://ndltd.ncl.edu.tw/handle/97647378333674655421.
Pełny tekst źródłaChen, Li-Min, i 陳利旻. "Comparison of Thyrotropin-Releasing Hormone Test and Thyroid-Stimulating Hormone Assay alone in Children with Neonatal Hyperthyrotropinemia". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/95621025628898946496.
Pełny tekst źródła高雄醫學大學
醫學研究所
101
Background: Thyrotropin-releasing hormone (TRH) test is useful for differentiating central and primary hypothyroidism, and is also valuable for diagnosing sub-biochemical hypothyroidism, an earlier stage than subclinical hypothyroidism, and usually the threshold of TRH test was set at 10~40 mIU/L. However, some experts are of the opinion that TRH test has a limited role in evaluating the early stage of hypothyroidism after the new generation of the thyroid-stimulating hormone (TSH) assay was applied to clinical use. The aim of this study was to investigate whether TRH test detects subclinical hypothyroidism earlier than TSH assay alone. Methods: This is a retrospective case analysis. Totally 228 children with thyroid eutopia who had neonatal hyperthyrotropinemia (HT) under levothyroxine supplement were collected between 1989 and 2008. Basal TSH level and TRH test were performed at the age of three to evaluate whether hypothyroidism developed after levothyroxine discontinued, and statistic analysis was performed. All the patients received follow-up visits for cognitive development and thyroid function after the TRH test to avoid over- or under-treatment. Results: In patients with thyroid eutopia and neonatal HT, 31.6% of them were still in status of hypothyroidism after the age of three if without supplement of levothyroxine. The basal TSH has good specificity (100%) for diagnosing euthyroidism, but with only 40.38% of sensitivity. When the basal TSH level was near the upper limit of normal range (4.5~8.5 mIU/L), the TRH test result correlated with hypothyroidism better (p = 0.033). The threshold of the TRH test set at 60 mIU/L had greater area under the curve compared with the previous threshold. Conclusions: Neonatal HT is a risk factor of hypothyroidism. We suggest the TRH test be administered in children with a basal TSH value near the upper limit of the normal range; the threshold of the TRH test may be set at 60 mIU/L. When the peak TSH level is above 60 mIU/L, the child is in hypothyroidism and usually needs levothyroxine supplement.
Knight, W. David Overton J. Michael. "Cardiovascular and metabolic responses to central thyrotropin-releasing hormone during caloric restriction in rats". Diss., 2005. http://etd.lib.fsu.edu/theses/available/etd-11092005-145251.
Pełny tekst źródłaAdvisor: 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.
ZHANG, GING-ZHONG, i 張慶忠. "Serum thyrotropin (TSH) and prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) in patients with thyroid, adrenal and pituitary diseases". Thesis, 1986. http://ndltd.ncl.edu.tw/handle/79665522155501982441.
Pełny tekst źródłaHuang, Sheng-Wang, i 黃生旺. "Regulation of Ovarian Steroid Hormones and Thyroxine on the Secretion of Hypothalamic Thyrotropin-Releasing Hormone and Dopamine in Rats". Thesis, 1996. http://ndltd.ncl.edu.tw/handle/08347174788625148217.
Pełny tekst źródłaMO, FAN-YI, i 莫凡毅. "The interaction between acetylcholine and thyrotropin-releasing hormone on the secretion and gene expression of prolactin". Thesis, 1990. http://ndltd.ncl.edu.tw/handle/28166163504260496129.
Pełny tekst źródłaHUANG, SHENG-WANG, i 黃生旺. "Interaction between estradiol and thyroxine on the release of thyrotropin-releasing hormone into hypophysial portal blood". Thesis, 1990. http://ndltd.ncl.edu.tw/handle/17263751716442504131.
Pełny tekst źródłaLIU, ZHE-YU, i 劉哲育. "Effects of aging on the release of rat prolactin in response to thyrotropin-releasing hormone in vitro". Thesis, 1987. http://ndltd.ncl.edu.tw/handle/09388256591553296749.
Pełny tekst źródłaLin, Feng-Ping, i 林豐平. "Mechanism of the potentiation effect of acetylcholine (ACh) on the thyrotropin releasing hormone (TRH)-induced c-fos mRNA expression". Thesis, 1995. http://ndltd.ncl.edu.tw/handle/03276673446680222249.
Pełny tekst źródła國立陽明大學
生物化學研究所
83
GH3腦下腺垂體癌細胞株,經acetylcholine (ACh)24小時前處理後,會增強thyrotropin-releasinghormone(TRH)引發prolactin及C-fos基因表現。本篇進一步探討ACh對TRH刺激C-fos基因表現促進作用機轉。 我們發現以TMB-8(細胞內鈣離子流動抑制劑),thapsigargin(calcium/ATPase抑制劑,可以枯竭細胞內貯藏的鈣離子),verapamil或nifedipine(specific L-type calcium channel blockeL),EGTA(可螯合鈣離子)或Co2+(non-specificcalcium channel blocke),與TRH共同處理細胞,結果ACh對TRH刺激c-fos基因表現仍有促進作用。KC1(增加鈣離子內流)可以刺激c-fos基因表現,且此作用被Ach促進。以高濃度PMA長期處理細胞以去除protein kinase C,發現ACh促進作用仍然存在,而低濃度PMA所刺激的c-fos基因表現,則可以被ACh所促進。進一步以HA1004為Ser/Thr kinase抑制劑處理細胞,發現無法去除ACh的促進作用,而cAMPanalog 8-Br-cAMP刺激c-fos基因表現,可以被ACh所促進。而在transfection實驗中ACh可以促進TRH刺激FC2 plasmid(c-fos promoter-CAT constructplasmid) CAT活性的表現。 所以根據我們的結果,ACh的促進作用,可能發生在TRH刺激c-fos基因表現的下游蛋白,這個蛋白參與calcium、protein kinase C及cAMP對c-fos基因表現的調控。 We have previously showed acetylcholine (ACh) pretreatment potentiated thyrotropin-releasing hormone (TRH) induced c-fos gene expression in GH3 pituitary tumor cells. In the present study, we investigated the mechanisms underlying this potentiation effect. In the presence of TMB-8 to inhibit the intracellular calcium mobilization or thapsigargin to deplete intracellular calcium pool, the augmentation on TRH-stimulated c-fos mRNA expression by ACh persisted. Moreover, neither L-type channel blocker verapamil or nifedipine nor EGTA or Co2+ was able to inhibit the potentiation effect of ACh. KC1 increased c-fos mRNA expression, and this effect was potentiated by ACh. These results indicate that calcium is possibly not involved in the potentiation of ACh, but calcium stimulates c-fos mRNA expression were potentiated by ACh. Depleting cellular PKC by high dosage phorbol myristic acetate (PMA) have no effect on the potentiation of ACh. However, the PMA stimulated c-fos expression was potentiated by ACh. In addition, 8-Br-cAMP stimulated c-fos mRNA expression was potentiated in the ACh conditioned cells. The possibility that the augmentation by ACh was exerted at the transcriptional levels was examined with fusion gene construct composed of chloramphenicol-acetyl transferase (CAT) reporter gene driven by c- fos promoter (FC2 plasmid). Transfection of FC2 plasmid into GH3 cells show that TRH stimulated-CAT activity was increased by ACh pretreatment. Our results suggest that the signaling pathway downstream of calcium, PKC and cAMP appear to be responsible for the potentiation effect that eventually leads to accelerated c-fos gene transcription in the ACh conditioned cells.
Chien-Hung, Pan, i 潘建宏. "Part 1 Subpopulation of the thyrotropin-releasing hormone- response anterior pituitary cells changed by aging Part 2 Effect of hypoxia on the expression of protein kinase C in rat brain". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/88387306684698064762.
Pełny tekst źródła中山醫學大學
生物化學研究所
91
Part 1 The anterior pituitary cell subpopulations of young and old Wistar male rat were tested by an experimental model of thyrotropin-releasing hormone (TRH)-induced increase in intracellular Ca2+ and were divided into five types: Type A, the cells with the reponse to TRH in low, media and high doses; type B, the cells response to either low or high doses TRH; type C, the cells only response to TRH low dose TRH; type D,the cells response to both media and high doses TRH; and type E,the cells response to only high dose TRH. Both young and old groups with high percentage of type A cells .The highly type A and type B were exist in young group(73.6 ±1.6% and 12.9±1.2%,respectively) compared with old group (68.3±1.1% and 4.4±1.0%,respectively).However, the percentages of type D and type E were significantly higher in old group(13.2±0.8% and 14.0±1.9% ;respectively) than in young group (7.6±1.2%and 4.7±0.8 %;respectively). These data indicated that the anterior pituitary cells in response to thyrotropin-releasing hormone may be partly shifted to low -sensitive cell types in aging. Part 2 To study the differential expressions of PKC isoforms in brain under hypoxia in conscious rats, the mRNAs were measured by RT-PCR. The male Sprague-Dawley rats were exposed in a simulated hypobaric chamber at 12 % O2 and 88% N2 for 8 h per day for 1 day or 4 days. The result showed that after hypoxia exposure the mRNA levels of some PKC isoforms were significantly decreased on day 1 and day 4: a (50% and 21%, respectively), d (40% and 17%, respectively), e (81% and 23%, respectively), q (64% and 12%, respectively) and l (88% and 28%, respectively), except PKC z was also significantly decreased but only on day 4 (74%), whereas PKC b and h were significantly increased on day 1 and day 4 (309% and 277% for b, respectively; and 241% 和 221% for h, respectively). Besides the PKC g was increased on day 1 (153%) and then decreased on day 4 (79%). All these findings suggested that the various expressions of PKC isoforms may be involved in the modulation of rat brain damage during hypoxia by different manner.
Merta, Ladislav. "Organizace a mobilita receptorů spřažených s G proteiny v plasmatické membráně". Master's thesis, 2014. http://www.nusl.cz/ntk/nusl-332195.
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