Relevant bibliographies by topics / Gonadotropin-Releasing hormones

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Academic literature on the topic 'Gonadotropin-Releasing hormones'

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Published: 7 December 2024

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Journal articles on the topic "Gonadotropin-Releasing hormones"

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Podhorec, P., and J. Kouril. "Induction of final oocyte maturation in Cyprinidae fish by hypothalamic factors: a review." Veterinární Medicína 54, No. 3 (April 8, 2009): 97–110. http://dx.doi.org/10.17221/50/2009-vetmed.

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Gonadotropin-releasing hormone in Cyprinidae as in other Vertebrates functions as a brain signal which stimulates the secretion of luteinizing hormone from the pituitary gland. Two forms of gonadotropin-releasing hormone have been identified in cyprinids, chicken gonadotropin-releasing hormone II and salmon gonadotropin-releasing hormone. Hypohysiotropic functions are fulfilled mainly by salmon gonadotropin-releasing hormone. The only known factor having an inhibitory effect on LH secretion in the family Cyprinidae is dopamine. Most cyprinids reared under controlled conditions exhibit signs of reproductive dysfunction, which is manifested in the failure to undergo final oocyte maturation and ovulation. In captivity a disruption of endogenous gonadotropin-releasing hormone stimulation occurs and sequentially that of luteinizing hormone, which is indispensible for the final phases of gametogenesis. In addition to methods based on the application of exogenous gonadotropins, the usage of a method functioning on the basis of hypothalamic control of final oocyte maturation and ovulation has become popular recently. The replacement of natural gonadotropin-releasing hormones with chemically synthesized gonadotropin-releasing hormone analogues characterized by amino acid substitutions at positions sensitive to enzymatic degradation has resulted in a centuple increase in the effectiveness of luteinizing hormone secretion induction. Combining gonadotropin-releasing hormone analogues with Dopamine inhibitory factors have made it possible to develop an extremely effective agent, which is necessary for the successful artificial reproduction of cyprinids.
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Saleh, Ahmed A., Nada N. A. M. Hassanine, Taha K. Taha, Amr M. A. Rashad, and Mahmoud A. Sharaby. "Molecular regulation and genetic basis of gonadotropin-releasing hormone genes: A review." Applied Veterinary Research 2, no. 4 (October 10, 2023): 2023017. http://dx.doi.org/10.31893/avr.2023017.

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This review systematically introduces basic information on the hypothalamic pituitary-gonad axis and provides knowledge on the regulation, location, function, reproduction, gene mutations, disorders, sexual behavior, life cycle, and effect of environmental factors on the gonadotropin-releasing hormone gene. On the other hand, this review focused on the GnRH gene, regulations, receptor structures, and their signaling pathways, in addition to its related genes and its effect on crucial hormones such as follicle-stimulating hormone, luteinizing hormone, testosterone, estradiol, and progesterone. Additionally, gonadotropin-inhibiting hormone and its related peptides, such as R-Famide peptides, were found to decrease hormone secretion by working on the hypothalamic pituitary gonads axis to inhibit the biosynthesis process of gonadotropin alpha and beta subunits. Additionally, the roles of crucial hormones in reproduction and fertility, as well as the disruption, resulted from mutations. Special characteristics of several hormones and pulsatile secretion of gonadotropin-releasing hormone were also summarized.
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Crowley, W. R. "Toward Multifactorial Hypothalamic Regulation of Anterior Pituitary Hormone Secretion." Physiology 14, no. 2 (April 1999): 54–58. http://dx.doi.org/10.1152/physiologyonline.1999.14.2.54.

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The hypothalamus regulates the secretion of anterior pituitary hormones via release of releasing hormones into the hypophysial portal vasculature. Additional neuromessengers act at the pituitary to modulate responses to the hypothalamic hormones. For example, neuropeptide Y enhances the effect of gonadotropin-releasing hormone and the response to the prolactin-inhibiting hormone dopamine.
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King, Judy A., and Robert P. Millar. "Evolution of gonadotropin-releasing hormones." Trends in Endocrinology & Metabolism 3, no. 9 (November 1992): 339–46. http://dx.doi.org/10.1016/1043-2760(92)90113-f.

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SHERWOOD, NANCY M., DAVID A. LOVEJOY, and IMOGEN R. COE. "Origin of Mammalian Gonadotropin-Releasing Hormones." Endocrine Reviews 14, no. 2 (April 1993): 241–54. http://dx.doi.org/10.1210/edrv-14-2-241.

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Pehlivan, Erkan, Hüseyin Polat, and Gürsel Dellal. "Annual Change of Reproductive Hormones in Female Angora Goats." Turkish Journal of Agriculture - Food Science and Technology 5, no. 4 (April 6, 2017): 343. http://dx.doi.org/10.24925/turjaf.v5i4.343-348.1220.

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In this research, annual changes of melatonin, gonadotropin-releasing hormone, follicle stimulating hormone, luteinizing hormone, estrogen, testosterone and progesterone were studied on 6 heads of 1.5 years old female Angora goat. To determine hormones concentrations, blood samples were taken from jugular vein of each goat in every month for a year. The blood samples were centrifuged at 4000xg for 5 min. and serum was stored at -20°C until analyses time. Hormones analyses in the serum were performed by enzyme immunoassay (EIA) method. Monthly climatic values and photoperiod were obtained from the Turkish State Meteorological Service and temperature-humidity index was calculated with climatic values. In the study, in order to determine any possible differences in the observed hormones concentrations with respect to months, repeated measures ANOVA analysis was performed. As a result of statistical analysis, there were no significant differences among the months for gonadotropin-releasing hormone, follicle stimulating hormone and testosterone concentration, while significant differences were found among the months for melatonin, luteinizing hormone and progesterone, and estrogen concentration in female Angora goats. According the results of this study, could be concluded that the releases of reproductive hormones examined in female Angora goats was seasonally dependent.
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Kotlyar, Alexander M., Lubna Pal, and Hugh S. Taylor. "Eliminating Hormones With Orally Active Gonadotropin-releasing Hormone Antagonists." Clinical Obstetrics & Gynecology 64, no. 4 (October 21, 2021): 837–49. http://dx.doi.org/10.1097/grf.0000000000000664.

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Richalet, Jean-Paul, Murielle Letournel, and Jean-Claude Souberbielle. "Effects of high-altitude hypoxia on the hormonal response to hypothalamic factors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 6 (December 2010): R1685—R1692. http://dx.doi.org/10.1152/ajpregu.00484.2010.

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Acute and chronic exposure to high altitude induces various physiological changes, including activation or inhibition of various hormonal systems. In response to activation processes, a desensitization of several pathways has been described, especially in the adrenergic system. In the present study, we aimed to assess whether the hypophyseal hormones are also subjected to a hypoxia-induced decrease in their response to hypothalamic factors. Basal levels of hormones and the responses of TSH, thyroid hormones, prolactin, sex hormones, and growth hormone to the injection of TRH, gonadotropin-releasing hormone, and growth hormone-releasing hormone (GHRH) were studied in eight men in normoxia and on prolonged exposure (3–4 days) to an altitude of 4,350 m. Thyroid hormones were elevated at altitude (+16 to +21%), while TSH levels were unchanged, and follicle-stimulating hormone and prolactin decreased, while leutinizing hormone was unchanged. Norepinephrine and cortisol levels were elevated, while no change was observed in levels of epinephrine, dopamine, growth hormone (GH), IGF-1, and IGFBP-3. The mean response to hypothalamic factors was similar in both altitudes for all studied hormones, although total T4 was lower in hypoxia during 45 to 60 min after injection. The effect of hypoxia on the hypophyseal response to hypothalamic factors was similar among subjects, except for the GH response to GHRH administration. We conclude that prolonged exposure to high-altitude hypoxia induces contrasted changes in hormonal levels, but the hypophyseal response to hypothalamic factors does not appear to be blunted.
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Muñoz-Cueto, José A., Nilli Zmora, José A. Paullada-Salmerón, Miranda Marvel, Evaristo Mañanos, and Yonathan Zohar. "The gonadotropin-releasing hormones: Lessons from fish." General and Comparative Endocrinology 291 (May 2020): 113422. http://dx.doi.org/10.1016/j.ygcen.2020.113422.

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Chen, Huiqin, Baoliang Bi, Lingfu Kong, Hua Rong, Yanhua Su, and Qing Hu. "Seasonal Changes in Plasma Hormones, Sex-Related Genes Transcription in Brain, Liver and Ovary during Gonadal Development in Female Rainbow Trout (Oncorhynchus mykiss)." Fishes 6, no. 4 (November 12, 2021): 62. http://dx.doi.org/10.3390/fishes6040062.

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The purpose of this study was to investigate the periodic seasonal changes in endocrine activity and gonadal development of female rainbow trout (Oncorhynchus mykiss) in a high-altitude cold-water environment. The fish were sampled monthly from January to November and the levels of plasma hormones (estradiol (E2), cortisol and thyroid hormones (THS)) and vitellogenin (VTG) were measured by ELISA. Moreover, the transcriptions of sex-related genes in the ovary, brain, and liver were detected by qRT-PCR. The results showed a seasonal fluctuation of plasma hormones and VTG together with the development of the ovary, which reached a peak from August to October. Similarly, the transcription of hypothalamic gonadotropin-releasing hormone-2 (cgnrh-2), hypothalamic gonadotropin-releasing hormone receptors (gnrhr) and follicle-stimulating hormone (fsh) in the brain varied from January to September, but the highest level was detected in September to November. In addition, the transcription of sex-related genes located in the ovary and liver increased significantly during August to October, accompanied by a continuous increase in the gonadosomatic index (GSI) and a decrease in the hepatosomatic index (HSI). Therefore, plasma hormones and sex-related genes regulate the development and maturation of O. mykiss oocytes with the change in seasons and peaked in November. The results of this study provide a reference for improving the efficiency of the artificial reproduction of O. mykiss.
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Dissertations / Theses on the topic "Gonadotropin-Releasing hormones"

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Powell, R. C. "Evolution of the structure and function of vertebrate brain gonadotropin-releasing hormone." Master's thesis, University of Cape Town, 1986. http://hdl.handle.net/11427/27201.

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In this study, the structure and function of gonadotropin-releasing hormone (GnRH) in different vertebrate species, in the classes Aves, Reptilia and Pisces was investigated. Acetic acid extracts were subjected to gel filtration chromatography and semipreparative high performance liquid chromatography (HPLC) to partially purify the GnRHs. The GnRH immunoreactivity was then characterized by analytical HPLC, and by assaying HPLC fractions by radioimmunoassay with region-specific antisera generated against mammalian GnRH, Gln⁸-GnRH and Trp⁷,Leu⁸-GnRH and assessing luteinizing hormone (LH)-releasing activity of fractions in a chicken dispersed anterior pituitary cell bioassay. Five GnRH molecular forms have thusfar been structurally characterized in vertebrate brain. In mammals a GnRH with the structure pGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH₂ has been demonstrated in the hypothalamus (Matsuo et al., 1971; Burgus et al., 1972). Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were present in chicken hypothalamus (King and Millar, 1982a, 1982c; Miyamoto et al., 1983, 1984), Trp⁷,Leu⁸-GnRH in salmon brain (Sherwood et al., 1983) and Tyr³,Leu⁵,Glu⁶,Trp⁷,Lys⁸-GnRH in lamprey brain (Sherwood et al., 1986). In ostrich (Struthio camelus) hypothalamus two GnRHs with identical properties to Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH have been demonstrated, as well as four other LR-releasing factors with different chromatographic and immunological properties to any of the known naturally-occurring GnRHs. Since Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were also present in chicken hypothalamus it appears likely that these two GnRHs occur in all birds. In alligator (Alligator mississippiensis) brain only two GnRHs were detected. These forms co-eluted with Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH in two HPLC systems. They cross-reacted similarly to the two synthetic peptides with antisera directed against mammalian GnRH and Gln⁸-GnRH and released LH from chicken dispersed anterior pituitary cells in a similar manner to the synthetic peptides. The Archosaurs (alligators and crocodiles) are believed to be closely related to birds and therefore it seems likely that they should have identical GnRHs. In skink (Calcides ocellatus tiligugu) brain one GnRH, which co-eluted with His⁵,Trp⁷,Tyr⁸-GnRH, was demonstrated. Two other lizards (Cordylis nigra and Pordarcis s. sicula) have been studied (Powell et al., 1985; R.C. Powell, G. Ciarcia, V. Lance, R.P. Millar and J.A. King, submitted). In c. nigra four immunoreactive GnRHs were detected, two of which co-eluted released chicken LH similarly to, Trp⁷,Leu⁸-GnRH and with, and His⁵,Trp⁷,Tyr⁸-GnRH. In P. s. sicula a GnRH molecular form similar to Trp⁷,Leu⁸-GnRH occurred as well as two novel GnRHs. It thus appears that Gln⁸-GnRH does not occur in lower reptiles, but His⁵,Trp⁷,Tyr⁸-GnRH and/or Trp⁷,Leu⁸-GnRH do. His⁵,Trp⁷,Tyr⁸-GnRH appears to he a widespread GnRH, occurring in vertebrates as diverse as birds and elasmobranch fish. In dogfish (Poroderma africanum) brain seven factors, which stimulated release of LH from chicken dispersed anterior pituitary cells, were separated on analytical HPLC. Two of these factors were partially characterized as Trp⁷,Leu⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH. Three of the other forms cross-reacted with GnRH antisera, but appear to be novel GnRHs. In teleost (Coris julis) brain two GnRHs similar to Trp⁷,Leu⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were present. These two GnRHs therefore appear to occur in both fish species studied. Trp⁷,Leu⁸-GnRH is widespread amongst teleost fish (Jackson and Pan, 1983; Sherwood et al., 1983; Breton et al., 1984; Sherwood et al., 1984; King and Millar, 1985). From these data it seems evident that the mammalian GnRH molecular form occurs only in mammals and amphibians, Gln⁸-GnRH in birds and higher reptiles, and Trp⁷,Leu⁸-GnRH in gnathostomes. His⁵,Trp⁷, Tyr⁸-GnRH appears to he present in numerous different vertebrates. Tyr³,Leu⁵,Glu⁶,Trp⁷,Lys⁸-GnRH has thus far only been detected in lamprey brain. A number of novel GnRHs, whose structures have not been elucidated are present.
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Von, Schalburg Kristian Robert. "The gonadotropin-releasing hormone gene : characterization, regulation and expression in two salmonids." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ36651.pdf.

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Von, Boetticher S. "Investigating the mechanism of transcriptional regulation of the gonadotropin-releasing hormone receptor (GnRHR) gene by dexamethasone." Thesis, Link to the online version, 2008. http://hdl.handle.net/10019/1796.

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An, Beum-Soo. "Cross-talk between gonadotropin-releasing hormones and progesterone receptor in neuroendocrine cells." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/30705.

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Hypothalamic gonadotropin-releasing hormone (GnRH) is a decapeptide that plays a pivotal role in mammalian reproduction. It is hypothesized that progesterone (P4) may regulate GnRH I, GnRH II (a second form of GnRH) and GnRH I receptor (GnRH I R) at the transcriptional level. Alternatively, GnRHs may stimulate transactivation of the progesterone receptor (PR), thereby, modulating gonadotropin subunit gene expression. Treatment of human neuronal cells with P4 suppressed GnRH I R promoter activity. This P4-stimulated inhibition was enhanced when PR A was over-expressed. With respect to the two GnRHs, P4 increased GnRH I mRNA levels, but did not significantly affect GnRH II gene expression. Regulation of gonadotropin production involves interplay between steroids and neuropeptides, thus we have examined the effects of GnRHs on PR activation in pituitary cells. Treatment with GnRHs increased a progesterone response element (PRE)-luciferase reporter gene activity. PR was phosphorylated at Ser294 and translocated into nucleus after GnRH treatment in the absence of P4. Interactions between the PR and several coactivators were examined, and treatment with GnRHs specifically induced PR: Steroid Receptor Coactivator-3 (SRC-3) interaction. In chromatin immunoprecipitation assays, recruitment of PR and SRC-3 to the PRE reporter gene was also increased by GnRHs. The knockdown of GnRH I R and SRC-3 levels by siRNA treatment reduced GnRH-induced PR transactivation. Gonadotropin subunit gene expression was evaluated following treatment with GnRHs, and common α-subunit and FSHβ transcription were upregulated by GnRHs. We used siRNA for PR to examine the involvement of PR in GnRH I-induced FSHβ gene expression. The effect of GnRH I on FSHβ, but not α -subunit gene expression was reduced when siRNA targeting PR was introduced. In summary, these results indicate that P4 is a potent regulator of GnRH I R and GnRH I at the transcriptional level, and this distinct effect of P4 on the GnRH system may be derived from the differential action of PR A or PR B . Conversely, GnRHs can activate PR-mediated transcription in the absence of P4, and this ligand-independent mechanism of PR additionally regulates FSHβ subunit gene expression.
Medicine, Faculty of
Obstetrics and Gynaecology, Department of
Graduate
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Styger, Gustav. "The role of steroidogenic factor-1 (SF-1) in transcriptional regulation of the gonadotropin-releasing hormone (GnRH) receptor gene." Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52572.

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Thesis (MSc)--Stellenbosch University, 2001.
ENGLISH ABSTRACT: The GnRH receptor is a G-protein-coupled receptor in pituitary gonadotrope cells. Binding of its ligand, GnRH, results in synthesis and release of gonadotropin hormones luteinizing hormone (LH) and follicle stimulating hormone (FSH). Steroidogenic factor 1 (SF-1), a transcription factor, binds to specific sites in the promoter region of gonadotropin genes, and thus regulates transcription of these genes. The promoter region of the GnRHreceptor gene contains two SF-1-like binding sites, one at -14 to -8 (site 1) and another at -247 to -239 (site 2), relative to the methionine start codon. The role played by these two SF-1-like sites in basal transcription of the mouse GnRH receptor (mGnRH-R) gene in a pituitary precursor gonadotrope cell line, aT3 cells, was the first area of investigation during this study. Luciferase reporter constructs containing 580 bp of mGnRH-R gene promoter were prepared, where SF-1-like sites were either wildtype or mutated. Four such constructs were made, i.e. wildtype (LG), site 1 mutant (LGM1), site 2 mutant (LGM2) and mutated site 1 plus site 2 (LGM1/2). These constructs were transfected into aT3 cells to determine the effect of mutations of sites 1 and/or 2 on the basal expression of the mGnRH-R gene. Mutation of either site 1 or site 2 had no effect on basal expression of the mGnRH-R gene. It was found that only upon simultaneous mutation of both sites 1 and 2, a 50% reduction in basal transcription took place. The implications of this is that SF-1 protein seems to only require one intact DNA-binding site, to mediate basal transcription of the mGnRH-R gene, suggesting that these two sites lie in close proximity during basal transcription. The effect of the protein kinase A (PKA) pathway on the endogenous mGnRH-R gene was also investigated by incubating non- , transfected aT3 cells with the PKA activators, forskolin and 8-Br-cAMP. Similar incubations were also performed on the wild type and mutated site 1 constructs transfected into pituitary gonadotrope aT3 cells. It was found that forskolin and 8-Br-cAMP were able to increase endogenous mGnRH-R mRNA levels in a concentration-dependent fashion, showing that endogenous GnRH receptor gene expression is stimulated via a protein kinase A pathway. Similar results were obtained with the wildtype promoter construct, showing that the protein kinase A pathway stimulates transcription of the promoter. This effect was only seen with wild type and not with the mutated site 1. These results are consistent with a role for a SF-1-like transcription factor in mediating the protein kinase A effect via binding to the site 1 at position -14 in the GnRH receptor gene. A separate investigation was performed to determine whether 25-hydroxycholesterol (25-0HC) is a ligand for SF-1, by incubating aT3 cells transfected with the various constructs with 25-0HC. Results show a dose-dependant response, with an increase in gene expression at 1 μM and a decrease at higher concentrations, for both mutant and wild type constructs. This suggests that, if SF-1 is indeed the protein binding to sites 1 and 2, then 25-0HC is not a ligand for SF-1 protein in aT3 cells and that the effect of 25-0HC on the mGnRH-R gene is not mediated via site 1. The results indicate that these decreases of expression at the higher concentrations may be due to cytotoxic effects. Towards the end of the study the laboratory obtained a luminoskan instrument with automatic dispensing features. Optimisation studies on the luciferase and β-Gal assays were performed on the luminoskan in a bid to decrease experimental error. It was found that automation of these assays resulted in a decrease in experimental error, showing that future researchers could benefit substantially from these optimisation studies.
AFRIKAANSE OPSOMMING: Die GnRH reseptor is 'n G proteïen-gekoppelde reseptor in pituitêre gonadotroopselle. Binding van die ligand, GnRH, lei tot die sintese en vrystelling van die gonadotropien hormone, luteïniserende hormoon (LH) en follikel stimulerende hormoon (FSH). Steroidogeniese faktor-t (SF-1) is 'n transkripsie faktor wat aan spesifieke areas in die promotergebied van die gonadotropien hormone bind, en dus transkripsie van hierdie gene reguleer. Die promotergebied van die GnRH reseptor geen bevat twee SF-1 bindings areas, een by -14 to -8 (area 1) asook by -247 to -239 (area 2), relatief to die metionien beginkodon. Die rol wat hierdie twee SF-1 areas speel in basale transkripsie van die muis GnRH reseptor (mGnRH-R) geen in 'n pituïtêre voorloper gonadotroop sellyn, aT3 selle, was die eerste gebied van ondersoek gedurende hierdie studie. Plasmiede bestaande uit die 580 basispaar mGnRH-R promoter verbind aan 'n lusiferase geen is vervaardig, waar SF-1-soortige areas enersyds onveranderd gelaat is, of gemuteer is. Vier sulke plasmiede is vervaardig, nl. onveranderd (LG), area 1 mutant (LGM1), area 2 mutant (LGM2) en gemuteerde area 1 plus area 2 (LGM1/2). Hierdie plasmiede is gebruik om aT3 selle te transfekteer om die effek van mutasies van areas 1 en/of 2 op die basale ekspressie van die mGnRH-R geen te ondersoek. Daar is gevind dat mutasies van areas 1 of 2 geen effek op basale ekspressie op die bogenoemde geen gehad het nie. Slegs tydens gelyktydige mutasie van areas 1 en 2 het 'n 50% vermindering in basale transkripsie plaasgevind. Die implikasies hiervan is dat die SF-1 proteïen blykbaar slegs een volledige DNA-bindingsarea benodig om basale transkripsie van die mGnRH-R geen te reguleer. Dit wil dus voorkom of hierdie twee areas baie na aan mekaar geposisioneer is tydens basale transkripsie. Die effek van die proteïen kinase A (PKA) roete op die natuurlike mGnRH-R geen is ook ondersoek tydens inkubasie van nie-getransfekteerde aT3 selle met die PKA akiveerders, forskolin en 8-Br-cAMP. Soortgelyke inkubasie is ook gedoen op die onveranderde en gemuteerde area 1 plasmiede wat in aT3 selle getransfekteer is. Daar is gevind dat forskolin en 8-Br-cAMP daarin geslaag het om die natuurlike mGnRH-R geen mRNA vlakke op 'n konsentrasie-afhanklike wyse te vermeerder. Hierdie resultaat dui daarop aan dat die natuurlike mGnRH-R geen se ekspressie gestimuleer kan word via 'n proteïen kinase A roete. Soortgelyke resultate is verkry met die onveranderde promoter plasmied en dit wys ook daarop dat proteïen kinase A transkripsie deur die promoter kan stimuleer. Hierdie effek was slegs aanwesig met die onveranderde en nie met die gemuteerde area 1 plasmied nie. Die resultate stem ooreen met 'n rol vir SF-1 transkripsie faktor in die regulering van proteren kinase A effek deur middel van binding aan die area 1 by posisie -14 in die GnRH-R geen. 'n Afsonderlike ondersoek is gedoen om vas te stel of 25-hidroksiecholesterol (25-0HC) 'n ligand vir SF-1 is deur getransfekteerde aT3 selle met 25-0HC te inkubeer. Resultate toon 'n dosis-afhanklike respons met 'n verhoging in geen ekspressie by 1 μM en 'n verlaging met hoër konsentrasies vir beide onveranderde en gemuteerde plasmiede. Dit impliseer dat, indien SF-1 wel die faktor is wat aan areas 1 en 2 bind, 25-0HC nie die ligand vir SF-1 proteren in aT3 selle is nie en dat die effek van 25-0HC op die mGnRH-R geen nie gereguleer word via area 1 nie. Die verlaging in ekspressie gevind by die hoër konsentrasies is dalk die gevolg van sitotoksiese effekte. Teen die einde van die studie het die laboratorium luminoskan toerusting met outomatiese pipettering verkry. Optimiseringstudies van die lusifirase en β-Galtoetse is met die luminoskan gedoen in 'n poging om eksperimentele foute te minimaliseer. Daar is gevind dat outomatisering van hierdie toetse wel gelei het tot 'n verlaging in eksperimentele foute. Toekomstige navorsers kan dus grootliks voordeel trek uit hierdie optimiseringstudies.
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Wormald, Patricia J. "GnRH and neuropeptide regulation of gonadotropin secretion from cultured human pituitary cells." Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27168.

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Gonadotropin-releasing hormone (GnRH) and its superactive analogues are currently being used in the treatment of a number of endocrine disorders, such as endometriosis, precocious puberty, infertility and prostatic cancer. Selection of these analogues for clinical use have been previously based on their activities in animal models. This thesis has therefore investigated the binding characteristics of the human GnRH receptor, in comparison to those of the rat receptor, as well as the activities of a number of GnRH analogues for stimulating luteinising hormone (LH) and follicle stimulating hormone (FSH) secretion from cultured human pituitary cells. The establishment of a human pituitary bioassay system has further made possible the investigation of the direct regulatory roles of GnRH and other neuropeptides in man. To date, such studies in man have been performed in vivo and are thus complicated by the simultaneous interactions of numerous modulators.
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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.

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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.
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Kaplan, Hilton. "The control of prolactin secretion and the role of gonadotrophin releasing hormone in the production of concordant secretory spikes of luteinizing hormone and prolactin in the luteal phase of the menstrual cycle." Master's thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27203.

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The control of prolactin secretion is a complex interaction of peptides and neurotransmitters acting either in an inhibitory or stimulating way to effect final secretion of this hormone from the lactotrope cell in the anterior hypothalamus. These factors may act either directly on the lactotrope cell or indirectly by changing either dopamine restraint of prolactin secretion or by modulating peptide substances or neurotransmitters higher up in the hypothalamus. Gonadal steroids may also modulate the effect of peptides or dopamine at the level of the lactotrope. Prolactin's major role in the female rat is one of milk production post - partum, nurturing the young. It probably also has other physiological functions and may play a part in the menstrual cycle although this is controversial. Certainly, pulsatile secretion of prolactin during the menstrual cycle is well established and in the luteal phase this is concomitant with the secretion of luteinizing hormone. Theories explaining the synchronous surges seen during this phase of the menstrual cycle have been proposed and GnRH has been implicated in the genesis of the concordance of these secretory spikes. Using a potent GnRH antagonist an experiment was undertaken to establish the role of GnRH by blocking this hypothalamic peptide and observing the effect that this had on luteinizing hormone, prolactin and follicle stimulating hormone. In the first part of the thesis the control of prolactin secretion is reviewed. In the following section, an experiment was performed using a potent GnRH antagonist. A dose response curve was established for the antagonist action on LH. Then a twice maximum dose of this peptide was administered to three subjects in the midluteal phase of the menstrual cycle and the response of LH, prolactin and FSH was measured. The results indicate that although the GnRH antagonist significantly blocked LH secretory peaks, this action was not observed for either prolactin or FSH. This result is perhaps at variance with previous data which suggested that GnRH was responsible for concordant secretory spikes of LH and prolactin in the midluteal phase of the menstrual cycle.
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De, Villiers Charon. "The effect of gonadotropin-releasing hormones (GnRH) I & II on sperm motility and acrosome status of the Vervet monkey (Chlorocebus aethiops) in vitro." Thesis, University of the Western Cape, 2006. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_9134_1253841818.

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Gonadotropin Releasing Hormone (GnRH) is a hypothalmic decapeptide, which regulates mammalian gonadotropin secretions by binding to specific, high affinity receptors in the pituitary. Two forms of GnRH (GnRH I and GnRH II) are expressed in the brain of human and some primates. Even though primates have been used extensively in a variety of investigations in relation to the role of GnRH in reproduction, there is no evidence of any research to investigate the direct effect of GnRH on primate sperm.

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Jeanne, Fabian. "Evοlutiοns des systèmes GΝRΗ et des hοrmοnes glycοprοtéiques dans les cοntrôles endοcrine et paracrine de la spermatοgénèse chez la rοussette, Scyliοrhinus canicula." Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMC225.

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La spermatogenèse est un processus hautement spécialisé de prolifération et de différenciation cellulaire conduisant à la production de spermatozoïdes haploïdes à partir de cellules souches spermatogoniales diploïdes. Chez les Gnathostomes, les fonctions testiculaires sont principalement contrôlées de façon endocrine par l’axe hypothalamo-hypophyso-gonadique (HHG) impliquant notamment les GnRHs hypothalamiques et les hormones gonadotropes, FSH et LH, dont l’émergence s’est produite à la racine des Vertébrés cartilagineux. De plus, des fonctions paracrines des GnRHs et de la thyrostimuline ont été explorées au niveau gonadique chez des Vertébrés osseux. L’objet de cette thèse était de caractériser les régulations endocrines et paracrines de la spermatogenèse médiées par les GnRHs et les hormones gonadotropes chez un modèle Élasmobranche, la roussette Scyliorhinus canicula. Ce travail a été étendu à la caractérisation de GPA2 et GPB5, constituant la thyrostimuline, qui correspondent aux orthologues des ancêtres moléculaires des sous-unités des hormones glycoprotéiques. Dans ce travail, l’évolution du protéome testiculaire au cours de la spermatogenèse de S. canicula a été décrite, les neuropeptides GnRHs, les hormones glycoprotéiques FSH, LH, TSH, GPA2 et GPB5, et leurs récepteurs associés ont fait l’objet d’analyses in silico et d’expressions dans différents tissus avec un focus au cours de la spermatogenèse. Il a été observé une expression à tous les stades de la spermatogenèse de fshr, lhr et des récepteurs aux GnRHs au niveau germinale et sertolien, de tshr et gpb5 au niveau sertolien et de gpa2 au niveau germinal, avec des abondances plus importantes associées aux stades spermatides. Ce travail a été complété par des tests fonctionnels in vitro qui ont montré que FSHR pouvait être activé par FSH et LH, LHR uniquement par LH, et que GPB5-GPA2 pouvait activer les trois récepteurs FSHR, LHR et TSHR, suggérant ainsi un rôle paracrine de la thyrostimuline au niveau testiculaire. L’ensemble de ce travail permet de proposer un modèle de régulation de la spermatogenèse chez les Élasmobranches qui associe des hormones endocrines, avec les GnRHs et gonadotropines circulantes, et des hormones paracrines, avec GPA2, GPB5 et les stéroïdes. Ce modèle apparaît cohérent et intermédiaire dans l’évolution des systèmes régulateurs de la spermatogenèse qui seraient passés d’une régulation paracrine prépondérante chez les Bilatériens non-Vertébrés à une régulation endocrine prépondérante chez les Vertébrés osseux avec la mise en place de l’axe hypothalamo-hypophyso-gonadique
Spermatogenesis is a highly specialized process of cell proliferation and differentiation leading to the production of haploid spermatozoa from diploid spermatogonial stem cells. In Gnathostomes, testicular functions are mainly controlled by the endocrine hypothalamic-pituitary-gonadal (HHG) axis, involving hypothalamic GnRHs and the gonadotropic hormones FSH and LH, which emerged at the root of cartilaginous vertebrates. In addition, paracrine functions of GnRHs and thyrostimulin have been explored at the gonadic level in bony vertebrates. The aim of this thesis was to characterize the endocrine and paracrine regulation of spermatogenesis exerted by GnRHs and gonadotropic hormones in an Elasmobranch model, the catshark Scyliorhinus canicula. This work has been extended to the characterization of GPA2 and GPB5, constituting thyrostimulin, which correspond to orthologs of the molecular ancestors of glycoprotein hormone subunits. In this work, the evolution of the testicular proteome during spermatogenesis in S. canicula was described, and the neuropeptides GnRHs, the glycoprotein hormones FSH, LH, TSH, GPA2 and GPB5, as well as their associated receptors were studied by in silico and expression analyses in different tissues, with a focus on spermatogenesis. Expressions were observed at all stages of spermatogenesis for fshr, lhr and GnRH receptors associated at germinal and sertolian levels, for tshr and gpb5 at sertolian level and for gpa2 at germinal level, with higher abundances associated with spermatid stages. This work was complemented by in vitro functional tests which showed that FSHR could be activated by FSH and LH, LHR only by LH, and that GPB5-GPA2 could activate all three receptors FSHR, LHR and TSHR, suggesting a paracrine role for thyrostimulin at the testicular level. Taken together, this work proposes a model for the regulation of spermatogenesis in Elasmobranchs that combines endocrine hormones, with circulating GnRHs and gonadotropins, and paracrine hormones, with GPA2, GPB5 and steroids. This model appears consistent and intermediate in the evolution of spermatogenesis regulating systems, which has shift from predominantly paracrine regulation in non-vertebrate bilaterians to predominantly endocrine regulation in bony vertebrates, with the establishment of the hypothalamic-pituitary-gonadal axis
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Books on the topic "Gonadotropin-Releasing hormones"

1

L, Barbieri Robert, and Friedman Andrew J, eds. Gonadotropin releasing hormone analogs: Applications in gynecology. New York: Elsevier, 1991.

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Organon Round Table Conference (3rd 1992 Paris, France). GnRH, GnRH analogs, gonadotropins, and gonadal peptides: The proceedings of the third Organon Round Table Conference, Paris, 1992. London: Parthenon Pub. Group, 1993.

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Ferring Symposium on Brain and Pituitary Peptides (3rd 1985 Noordwijk, Netherlands). Pulsatile GnRH 1985: Proceedings of the 3rd Ferring Symposium, Noordwijk, September 11-13, 1985. Edited by Coelingh Bennink, Herman Jan Tymen, 1943-. Haarlem: Ferring, 1985.

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Jan, Horský. Gonadotropin-releasing hormone and ovarian function. Prague: Avicenum, Czechoslovak Medical Press, 1986.

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1958-, Parhar Ishwar S., ed. Gonadotropin-releasing hormone: Molecules and receptors. Amsterdam: Elsevier, 2002.

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Goodman, Stephanie Robin. Effects of gonadotrophin releasing hormone on growth hormone release in the rat. [New Haven, Conn: s.n.], 1993.

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World, Congress on Fertility and Sterility (15th 1995 Bologna Italy). Treatment with GnRH analogs: Controversies and perspectives : the proceedings of a satellite symposium of the 15th World Congress on Fertility and Sterility held in Bologna, Italy, 15-16 September 1995. New York: Parthenon Pub. Group, 1996.

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Nyean, Lee Chin, ed. Using gonadotropin-releasing hormone (GnRH) to improve dairy cattle conception rates in the tropics. [Honolulu]: HITAHR, College of Tropical Agriculture and Human Resources, University of Hawaii, 1989.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Book chapters on the topic "Gonadotropin-Releasing hormones"

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Sherwood, Nancy. "Gonadotropin-Releasing Hormones in Fishes." In Hormones and Reproduction in Fishes, Amphibians, and Reptiles, 31–60. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1869-9_2.

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Moghissi, Kamran S. "Gonadotropin Releasing Hormones: Physiopathology and Clinical Applications." In The Brain as an Endocrine Organ, 1–13. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3480-7_1.

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Licht, Paul, and David A. Porter. "Role of Gonadotropin-Releasing Hormone in Regulation of Gonadotropin Secretion from Amphibian and Reptilian Pituitaries." In Hormones and Reproduction in Fishes, Amphibians, and Reptiles, 61–85. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1869-9_3.

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Manji, Husseini K., Jorge Quiroz, R. Andrew Chambers, Anthony Absalom, David Menon, Patrizia Porcu, A. Leslie Morrow, et al. "Gonadotropin-Releasing Hormone." In Encyclopedia of Psychopharmacology, 561. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1886.

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Naor, Zvi, and Rony Seger. "Gonadotropin-Releasing Hormone." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2477-2.

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Naor, Zvi, and Rony Seger. "Gonadotropin-Releasing Hormone." In Encyclopedia of Cancer, 1938–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_2477.

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Naor, Zvi, and Rony Seger. "Gonadotropin-Releasing Hormone." In Encyclopedia of Cancer, 1577–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2477.

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Bidlingmaier, M. "Gonadotropin-Releasing-Hormon." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1312-1.

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Bidlingmaier, M. "Gonadotropin-Releasing-Hormon." In Springer Reference Medizin, 1014. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1312.

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Colao, Annamaria, and Claudia Pivonello. "Gonadotropin Releasing Hormone (GnRH)." In Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5110-1.

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Conference papers on the topic "Gonadotropin-Releasing hormones"

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Ohlsson, M., A. J. W. Hsueh, and T. Ny. "HORMONE REGULATION OF THE FIBRINOLYTIC SYSTEM IN THE OVARY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644389.

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In the ovary, the release of oocytes from graafian follicles during hormone-induced ovulation has been found to be associated with substantial increases in follicular plasminogen activator (PA) activity. Most of the PA activity comes from the granulosa cells that have been shown to produce tPA, uPA as well as the type-1 PA-inhibitor,(PAI-1).We have studied the molecular mechanism of follicle stimulating hormone (FSH) and gonadotropin releasing hormone (GnRH) on the synthesis of tPA in primary cultures of rat granulosa cells. FSH and GnRH were both found to induce tPA in granulosa cells in a time and dose dependent manner. The effect of FSH and GnRH on the levels of tPA mRNA was also studied by northern and slot blot hybridizations. FSH and GnRH were both found to increase the level of tPA mRNA. The stimulation was up to 18 -fold compared to untreated cells.The induction of tPA mRNA by FSH and GnRH was additive and the time courses of the stimulation by the hormones differed, suggesting that different cellular mechanisms are involved. Consistent with the ability of FSH to activate the cAMP dependent protein kinase A pathway, the phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine further enhanced the FSH induction of tPA mRNA.GnRH is known to activate the phospholipid-dependent protein kinase C pathway. Likewise the effect of GnRH can be mimicked by the kinase C activator, phorbol myristate acetate.It is concluded that FSH and GnRH regulates tPA production by differnt molecular mechanisms, and that the increase in tPA activity is mediated via an increase in the levels tPA mRNA. Since both gonadotropins and GnRH cause ovulation in hyposectomized animals, similar stimulatory actions of these hormones on the tPA activity suggest a correlative relationship between this enzyme and the ovulatory process.
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Sand, Sharon R., Catherine Klifa, Michael F. Press, Malcolm Pike, Giske Ursin, Darcy Spicer, Lalit Vora, et al. "Abstract 3557: Reduced ovarian hormones & reduced mammographic & MRI determined breast density inBRCAcarriers following a hormonal chemo-prevention regimen of gonadotropin releasing hormone agonist (GnRHA) & low-dose add-back estrogen & testosterone." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3557.

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"TOWARDS A NEW HOMOGENEOUS IMMUNOASSAY FOR GONADOTROPIN-RELEASING HORMONE BASED ON TIME-RESOLVED FLUORESCENCE ANISOTROPY." In International Conference on Biomedical Electronics and Devices. SciTePress - Science and and Technology Publications, 2011. http://dx.doi.org/10.5220/0003152001840188.

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Bibiari, Georgia, Agathi Nteli, Carmen Simal, Christos Markatos, Vlasios Karageorgos, Alexios Vlamis-Gardikas, George Liapakis, and Theodore Tselios. "Design and Synthesis of Gonadotropin Releasing Hormone (GnRH) Peptide Analogues Conjugated with Anthraquinone for Selective Immunosuppression." In 36th European Peptide Symposium. The European Peptide Society, 2022. http://dx.doi.org/10.17952/36eps.2022.065.

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Biniari, Georgia, Agathi Nteli, Carmen Simal, Christos Markatos, Vlasios Karageorgos, Alexios Vlamis-Gardikas, George Liapakis, and Theodore Tselios. "Design and Synthesis of Gonadotropin Releasing Hormone (GnRH) Peptide Analogues Conjugated with Anthraquinone for Selective Immunosuppression." In 36th European Peptide Symposium. The European Peptide Society, 2022. http://dx.doi.org/10.17952/36eps/36eps.2022.065.

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Biniari, Georgia, Agathi Nteli, Christos Markatos, Vlasios Karageorgos, Alexios Vlamis-Gardikas, George Liapakis, Maria Venihaki, Theodore Tselios, and Carmen Simal. "Rational design, synthesis and evaluation of mitoxantrone conjugated with mutated Gonadotropin Releasing Hormone (GnRH) for the treatment of hormone-dependent cancer." In 37th European Peptide Symposium, 1216. The European Peptide Society, 2024. http://dx.doi.org/10.17952/37eps.2024.p1216.

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Pacucci, VA, F. Ceccarelli, G. Perrone, I. Zannini, M. Candelieri, I. Leccese, C. Perricone, et al. "SAT0260 Ovarian function preservation with gonadotropin-releasing hormone analogues in patients with systemic lupus erythematosus treated with cyclophosphamide." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6381.

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Kim, HJ, MH Lee, JE Lee, SH Park, ES Lee, Y.-J. Kang, JH Lee, et al. "Abstract P1-12-09: The oncologic effect of a gonadotropin releasing hormone (GnRH) agonist for ovarian protection during breast cancer chemotherapy." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p1-12-09.

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Xue, Yu, Youting Dong, and Xiaojun Chen. "PR001/#476 Gonadotropin-releasing hormone agonist (GnRH-a) plus letrozole in young women with early endometrial cancer: a prospective randomized controlled trial." In IGCS 2024 Annual Meeting Abstracts, A37.1—A37. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/ijgc-2024-igcs.43.

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Yoon, TI, HJ Kim, JH Yu, G. Sohn, BS Ko, JW Lee, BH Son, and SH Ahn. "Abstract P5-13-06: Concurrent gonadotropin-releasing hormone (GnRH) agonist administration with chemotherapy improves neoadjuvant chemotherapy responses in young premenopausal breast cancer patients." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p5-13-06.

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Reports on the topic "Gonadotropin-Releasing hormones"

1

Zohar, Yonathan, Robert Langer, Shimon Hassin, Walton Dickhoff, Abigail Elizur, and Yoav Gothilf. A Novel Technology for the Manipulation of Fish Reproductive Cycles: Controlled Release of Gonadotropin Releasing Hormones. United States Department of Agriculture, March 1993. http://dx.doi.org/10.32747/1993.7603811.bard.

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Xu, Dan, Xueying Zhou, Junfei Wang, Xi Cao, and Tao Liu. The Value of Urinary Gonadotropins in the Diagnosis of Central Precocious Puberty: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0076.

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Review question / Objective: Precocious puberty is defined as the onset of secondary sexual characteristics before the age of 8 years in girls and 9 years in boys. It can be differentiated into central precocious puberty (CPP) and peripheral precocious puberty, and it is more common in girls than in boys. CPP may result in a decreased final adult height, an early age at menarche, and psychological and health problems in adulthood. Gonadotropin-releasing hormone (GnRH) GnRH stimulation test has been indispensable in the diagnosis of CPP. GnRH stimulation test is not only invasive, time-consuming and expensive, but also sometimes difficult to have patients cooperate. Nocturnal urinary LH and FSH can represent gonadotropin excretion in children with normal and early puberty. And urinary sample collection and evaluation are more convenient, more acceptable, cheaper, and noninvasive. This meta-analysis aims to assess the value of first-voided urinary luteinizing hormone (LH) and the ratio of urinary luteinizing hormone and follicle-stimulating hormone (FSH) in the diagnosis of female CPP and to compare the accuracy between urinary gonadotropins and serum GnRH-stimulated gonadotropins.
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Gu, Li, Xurui Li, and Wentao Liu. Adverse cardiovascular effect following Gonadotropin-releasing Hormone (GnRH) antagonist versus GnRH agonist for Prostate Cancer Treatment: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0009.

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Yaron, Zvi, Abigail Elizur, Martin Schreibman, and Yonathan Zohar. Advancing Puberty in the Black Carp (Mylopharyngodon piceus) and the Striped Bass (Morone saxatilis). United States Department of Agriculture, January 2000. http://dx.doi.org/10.32747/2000.7695841.bard.

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Both the genes and cDNA sequences encoding the b-subunits of black carp LH and FSH were isolated, cloned and sequenced. Sequence analysis of the bcFSHb and LHb5'flanking regions revealed that the promoter region of both genes contains canonical TATA sequences, 30 bp and 17 bp upstream of the transcription start site of FSHb and LHb genes, respectively. In addition, they include several sequences of cis-acting motifs, required for inducible and tissue-specific transcriptional regulation: the gonadotropin-specific element (GSE), GnRH responsive element (GRE), half sites of estrogen and androgen response elements, cAMP response element, and AP1. Several methods have been employed by the Israeli team to purify the recombinant b subunits (EtOH precipitation, gel filtration and lentil lectin). While the final objective to produce pure recombinantGtH subunits has not yet been achieved, we have covered much ground towards this goal. The black carp ovary showed a gradual increase in both mass and oocyte diameter. First postvitellogenic oocytes were found in 5 yr old fish. At this age, the testes already contained spermatozoa. The circulating LH levels increased from 0.5 ng/ml in 4 yr old fish to >5ng/ml in 5 yr old fish. In vivo challenge experiments in black carp showed the initial LH response of the pituitary to GnRH in 4 yr old fish. The response was further augmented in 5 yr old fish. The increase in estradiol level in response to gonadotropic stimulation was first noted in 4 yr old fish but this response was much stronger in the following year. In vivo experiments on the FSHb and LHb mRNA levels in response to GnRH were carried out on common carp as a model for synchronom spawning cyprinids. These experiments showed the prevalence of FSHP in maturing fish while LHP mRNA was prevalent in mature fish, especially in females. The gonadal fat-pad was found to originate from the retroperitoneal mesoderm and not from the genital ridge, thus differing from that reported in certain amphibians This tissue possibly serves as the major source of sex steroids in the immature black carp. However, such a function is taken over by the developing gonads in 4 yr old fish. In the striped bass, we described the ontogeny of the neuro-endocrine parameters along the brain-pituitary-gonadal axis during the first four years of life, throughout gonadal development and the onset of puberty. We also described the responsiveness of the reproductive axis to long-term hormonal manipulations at various stages of gonadal development. Most males reached complete sexual maturity during the first year of life. Puberty was initiated during the third year of life in most females, but this first reproductive cycle did not lead to the acquisition of full sexual maturity. This finding indicates that more than one reproductive cycle may be required before adulthood is reached. Out of the three native GnRHs present in striped bass, only sbGnRH and cGnRH II increased concomitantly with the progress of gonadal development and the onset of puberty. This finding, together with data on GtH synthesis and release, suggests that while sbGnRH and cGnRH II may be involved in the regulation of puberty in striped bass, these neuropeptides are not limiting factors to the onset of puberty. Plasma LH levels remained low in all fish, suggesting that LH plays only a minor role in early gonadal development. This hypothesis was further supported by the finding that experimentally elevated plasma LH levels did not result in the induction of complete ovarian and testicular development. The acquisition of complete puberty in 4 yr old females was associated with a rise in the mRNA levels of all GtH subunit genes, including a 218-fold increase in the mRNA levels of bFSH. mRNA levels of the a and PLH subunits increased only 11- and 8-fold, respectively. Although data on plasma FSH levels are unavailable, the dramatic increase in bFSH mRNA suggests a pivotal role for this hormone in regulating the onset and completion of puberty in striped bass. The hormonal regulation of the onset of puberty and of GtH synthesis and release was studied by chronic administration of testosterone (T) and/or an analog of gonadotropin-releasing hormone (G). Sustained administration of T+G increased the mRNA levels of the PLH subunit to the values characteristic of sexually mature fish, and also increased the plasma levels of LH. However, these changes did not result in the acceleration of sexual maturation. The mRNA levels of the bFSH subunit were slightly stimulated, but remained about 1/10 of the values characteristic of sexually mature fish. It is concluded that the stimulation of FSH gene expression and release does not lead to the acceleration of sexual maturity, and that the failure to sufficiently stimulate the bFSH subunit gene expression may underlie the inability of the treatments to advance sexual maturity. Consequently, FSH is suggested to be the key hormone to the initiation and completion of puberty in striped bass. Future efforts to induce precocious puberty in striped bass should focus on understanding the regulation of FSH synthesis and release and on developing technologies to induce these processes. Definite formulation of hormonal manipulation to advance puberty in the striped bass and the black carp seems to be premature at this stage. However, the project has already yielded a great number of experimental tools of DNA technology, slow-release systems and endocrine information on the process of puberty. These systems and certain protocols have been already utilized successfully to advance maturation in other fish (e.g. grey mullet) and will form a base for further study on fish puberty.
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