Relevant bibliographies by topics / Gonadotrophic hormone

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Gonadotrophic hormone'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Gonadotrophic hormone"

1

Gracia-Navarro, F., and P. Licht. "Subcellular localization of gonadotrophic hormones LH and FSH in frog adenohypophysis using double-staining immunocytochemistry." Journal of Histochemistry & Cytochemistry 35, no. 7 (1987): 763–69. http://dx.doi.org/10.1177/35.7.3108366.

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We applied double post-embedding immunocytochemical methods using specific antibodies against bullfrog (Rana catesbeiana) luteinizing hormone (LH) and follicle-stimulating hormone (FSH) with immunogold staining (5- and 20-nm particles) to determine the subcellular localization of both gonadotropins and to observe their immunostaining patterns in anterior pituitary of the frog Rana pipiens. Results showed that individual gonadotrophs may store either one or both gonadotropins in a given secretory granule and in large globules (lysosomes?). Most gonadotrophs (50-88%) contain both hormones; 12-50% contain only FSH, and only a few (0-7%) contain LH alone. Individual secretory granules, even in cells that contain both hormones, may contain only one or both gonadotropin molecules. Evaluation of the percentage of monohormonal and multihormonal secretory granules revealed that multihormonal secretory granules were the most numerous and that LH monohormonal secretory granules were the least numerous. These results indicate that cellular storage of gonadotropin in amphibian pituitary is similar to that described for mammals, where a single cell type containing both gonadotropins predominates. Variability in hormone content both of cells and of granules in all individuals is consistent with the hypothesis that frog pituitary possesses a single multipotential gonadotroph.
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Chopineau, M., N. Martinat, H. Marichatou, et al. "Evidence that the alpha-subunit influences the specificity of receptor binding of the equine gonadotrophins." Journal of Endocrinology 155, no. 2 (1997): 241–45. http://dx.doi.org/10.1677/joe.0.1550241.

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Horse LH/chorionic gonadotrophin (eLH/CG) exhibits, in addition to its normal LH activity, a high FSH activity in all other species tested. Donkey LH/CG (dkLH/CG) also exhibits FSH activity in other species, but about ten times less than the horse hormone. In order to understand the molecular basis of these dual gonadotrophic activities of eLH/CG and dkLH/CG better, we expressed, in COS-7 cells, hybrids between horse and donkey subunits, between horse or donkey alpha-subunit and human CG beta (hCG beta), and also between the porcine alpha-subunit and horse or donkey LH/CG beta. The resultant recombinant hybrid hormones were measured using specific FSH and LH in vitro bioassays which give an accurate measure of receptor binding specificity and activation. Results showed that it is the beta-subunit that determines the level of FSH activity, in agreement with the belief that it is the beta-subunit which determines the specificity of action of the gonadotrophins. However, donkey LH/CG beta combined with a porcine alpha-subunit exhibited no FSH activity although it showed full LH activity. Moreover, the hybrid between horse or donkey alpha-subunit and hCG beta also exhibited only LH activity. Thus, the low FSH activity of dkLH/CG requires an equine (donkey or horse) alpha-subunit combined with dkLH/CG beta. These results provide the first evidence that an alpha-subunit can influence the specificity of action of a gonadotrophic hormone.
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Charlton, Harry. "Neural transplantation in hypogonadal (hpg) mice – physiology and neurobiology." Reproduction 127, no. 1 (2004): 3–12. http://dx.doi.org/10.1530/rep.1.00066.

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The hypogonadal (hpg) mouse mutant has a deletion in the region encoding the hypothalamic gonadotrophic hormone-releasing hormone decapeptide. As a consequence pituitary gonadotrophic hormone synthesis and release is severely curtailed and there is little or no post-natal gonadal development. Grafts of late fetal/early neonatal brain tissue containing the decapeptide-producing neurones into the third ventricle of hpg mice result, in a majority of animals, in a near normalisation of pituitary function with full spermatogenesis in male mice and full follicular and uterine development in females. The vast majority of positive responding females with vaginal opening and uterus growth show no evidence of spontaneous oestrous cycles, ovulation or corpora lutea. These female mice mate with normal males with many of them demonstrating reflex ovulation. In both male and female mutants with successful grafts there is an absence of gonadal steroid negative feedback upon the synthesis and secretion of pituitary gonadotrophic hormones. The releasing factor axon terminals from grafts within the third ventricle identified by immunohistochemical methods are targeted specifically to the median eminence. There is evidence for host innervation of grafts, but how specific this is for the control of gonadotrophic hormone-releasing hormone cell bodies remains to be elucidated.
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Reznikov, A. G., N. D. Nosenko, E. N. Boris, L. I. Poliakova, P. V. Sinitsyn, and L. V. Tarasenko. "Evaluation of the efficacy of gonadotrophic inductors of ovulation in rats with hyperandrogenemia given flutamide." Problems of Endocrinology 57, no. 4 (2011): 28–31. http://dx.doi.org/10.14341/probl201157428-31.

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The objective of the present work was to study the influence of antiandrogen flutamide (flutapharm) at a dose of 1.0 mg/kg b.w., human chorionic gonadotropin (choragon, 5 IU), and folliculostimulating hormone (menopur, 0.01 IU) on the morphofunctional characteristics of ovaries. These products were administered either alone or sequentially to sexually mature female rats after the implantation of testosterone-containing polymeric capsules. The presence of hyperandogenism was confirmed by the five-fold rise in the blood testosterone levels. Analysis of the oestrus cycle, the weight and histological structure of the ovaries gave evidence of disturbed folliculogensis, degenerative changes in follicular epithelium, the development of ovarian polycystosis and anovulatory state in the hyperandrogenic animals. It is concluded neither flutamide nor gonadotrophic hormones administered at the above doses promoted normalization of the generative function of rat ovaries. At the same time, stimulation with gonadotropins following glutamide administration restored folliculogenesis, ovulation, an formation of luteal bodies. The results of this study indicate that flutamide can be used to enhance the stimulating action of gonadotropic hormones on the ovaries in hyperandrogenic individuals.
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Das, Nandana, and T. Rajendra Kumar. "Molecular regulation of follicle-stimulating hormone synthesis, secretion and action." Journal of Molecular Endocrinology 60, no. 3 (2018): R131—R155. http://dx.doi.org/10.1530/jme-17-0308.

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Follicle-stimulating hormone (FSH) plays fundamental roles in male and female fertility. FSH is a heterodimeric glycoprotein expressed by gonadotrophs in the anterior pituitary. The hormone-specific FSHβ-subunit is non-covalently associated with the common α-subunit that is also present in the luteinizing hormone (LH), another gonadotrophic hormone secreted by gonadotrophs and thyroid-stimulating hormone (TSH) secreted by thyrotrophs. Several decades of research led to the purification, structural characterization and physiological regulation of FSH in a variety of species including humans. With the advent of molecular tools, availability of immortalized gonadotroph cell lines and genetically modified mouse models, our knowledge on molecular mechanisms of FSH regulation has tremendously expanded. Several key players that regulate FSH synthesis, sorting, secretion and action in gonads and extragonadal tissues have been identified in a physiological setting. Novel post-transcriptional and post-translational regulatory mechanisms have also been identified that provide additional layers of regulation mediating FSH homeostasis. Recombinant human FSH analogs hold promise for a variety of clinical applications, whereas blocking antibodies against FSH may prove efficacious for preventing age-dependent bone loss and adiposity. It is anticipated that several exciting new discoveries uncovering all aspects of FSH biology will soon be forthcoming.
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McDonald, William C., Nilanjana Banerji, Kelsey N. McDonald, Bridget Ho, Virgilia Macias, and Andre Kajdacsy-Balla. "Steroidogenic Factor 1, Pit-1, and Adrenocorticotropic Hormone: A Rational Starting Place for the Immunohistochemical Characterization of Pituitary Adenoma." Archives of Pathology & Laboratory Medicine 141, no. 1 (2016): 104–12. http://dx.doi.org/10.5858/arpa.2016-0082-oa.

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Context.—Pituitary adenoma classification is complex, and diagnostic strategies vary greatly from laboratory to laboratory. No optimal diagnostic algorithm has been defined. Objective.—To develop a panel of immunohistochemical (IHC) stains that provides the optimal combination of cost, accuracy, and ease of use. Design.—We examined 136 pituitary adenomas with stains of steroidogenic factor 1 (SF-1), Pit-1, anterior pituitary hormones, cytokeratin CAM5.2, and α subunit of human chorionic gonadotropin. Immunohistochemical staining was scored using the Allred system. Adenomas were assigned to a gold standard class based on IHC results and available clinical and serologic information. Correlation and cluster analyses were used to develop an algorithm for parsimoniously classifying adenomas. Results.—The algorithm entailed a 1- or 2-step process: (1) a screening step consisting of IHC stains for SF-1, Pit-1, and adrenocorticotropic hormone; and (2) when screening IHC pattern and clinical history were not clearly gonadotrophic (SF-1 positive only), corticotrophic (adrenocorticotropic hormone positive only), or IHC null cell (negative-screening IHC), we subsequently used IHC for prolactin, growth hormone, thyroid-stimulating hormone, and cytokeratin CAM5.2. Conclusions.—Comparison between diagnoses generated by our algorithm and the gold standard diagnoses showed excellent agreement. When compared with a commonly used panel using 6 IHC for anterior pituitary hormones plus IHC for a low-molecular-weight cytokeratin in certain tumors, our algorithm uses approximately one-third fewer IHC stains and detects gonadotroph adenomas with greater sensitivity.
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Matson, Christine, and B. T. Donovan. "Acute effects of GnRF-induced gonadotrophin secretion upon ovarian steroid secretion in the ferret." Acta Endocrinologica 111, no. 3 (1986): 373–77. http://dx.doi.org/10.1530/acta.0.1110373.

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Abstract. The effects of an increase in endogenous gonadotrophin secretion on the production of oestradiol, progesterone, androstenedione and testosterone by the ovaries of anaesthetized anoestrous and oestrous ferrets were followed. Gonadotrophin secretion was enhanced by the injection of gonadotrophin releasing factor (GnRF), and serial blood samples were collected over 9 h for hormone assay. Thyrotrophic hormone releasing factor (TRF) or acetic acid were injected for control purposes. The plasma content of oestradiol in oestrous females was significantly higher than during anoestrus, but secretion of this steroid was not increased by any means. The plasma concentration of progesterone in anoestrous females was significantly higher than during oestrus. It was increased by GnRF in anoestrous ferrets and less markedly in oestrous females. The plasma concentration of androstenedione was raised by GnRF to a greater extent during anoestrus than during oestrus. Testosterone was present in higher concentration in the plasma during anoestrus than during oestrus, and the level was increased by GnRF administration. These findings indicate that the ovaries of the anoestrous ferret secrete significant quantities of steroid hormones, and that they respond readily to gonadotrophic hormone.
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Kanayama, K., H. Osada, and T. Endo. "Cleavage of Unfertilized Eggs after Repeated Administration of Human Chorionic Gonadotrophin to Hamsters." Journal of International Medical Research 25, no. 4 (1997): 202–5. http://dx.doi.org/10.1177/030006059702500405.

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The proportions of unfertilized eggs in the oviducts, showing abnormal cleavage, were examined in hamsters given single or repeated doses of 30 IU human gonadotrophic hormone for the induction of ovulation. In control animals ( n = 7), 1.7% of the total ovulated eggs were morphologically abnormal unfertilized eggs showing cleavage. The proportions of unfertilized eggs that were abnormal in the groups of seven hamsters treated with one, two or three doses of the gonadotrophin were 20.4%, 19.4%, and 30.4%, respectively. The proportion of unfertilized eggs showing abnormal cleavage thus appeared to increase with repeated administrations of gonadotrophin.
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Tortonese, Domingo J., Susan J. Gregory, Rebecca C. Eagle, Carolyne L. Sneddon, Claire L. Young, and Julie Townsend. "The equine hypophysis: a gland for all seasons." Reproduction, Fertility and Development 13, no. 8 (2001): 591. http://dx.doi.org/10.1071/rd01066.

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The intrahypophysial mechanisms involved in the control of gonadotrophin secretion remain unclear. In the horse, a divergent pattern of gonadotrophins is observed at different stages of the reproductive cycle in response to a single secretagogue (gonadotrophin-releasing hormone), and dramatic changes in fertility take place throughout the year in response to photoperiod. This species thus provides a useful model to investigate the regulation of fertility directly at the level of the hypophysis. A series of studies were undertaken to examine the cytological arrangements and heterogeneity of gonadotrophin storage in the pars distalis (PD) and pars tuberalis (PT) of the hypophysis of male and female horses. Specifically, the seasonal and gonadal effects on distribution, density and hormonal identity of gonadotrophs, the existence of gonadotroph–lactotroph associations and the expression of prolactin receptors (PRL-R) as possible morphological bases for the differential control of gonadotrophin secretion were investigated. It became apparent that both isolated and clustered gonadotrophs are normally distributed around the pars intermedia and surrounding capillaries in the PD, and in the caudal ventral region of the PT. In the PD, no effects of season or of reproductive state on the density or number of gonadotrophs could be detected in either male or female animals. In contrast, a fivefold increase in gonadotroph density was observed in the PT during the sexually active stage. In males, robust gonadal effects were detected on the gonadotroph population; orchidectomy significantly reduced both the number and proportion of gonadotrophs, in relation to other hypophysial cell types, in both the PD and PT regions. Luteinizing hormone (LH) monohormonal, follicle-stimulating hormone (FSH) monohormonal and bihormonal gonadotrophs were identified in the PD and PT of male and female horses. Interestingly, in males, the relative proportions of gonadotroph subtypes and the LH/FSH monohormonal gonadotroph ratio were not affected by either season or the presence of the gonads. In contrast, a larger proportion of monohormonal gonadotrophs was clearly observed in sexually active females. Specific gonadotroph–lactotroph associations and expression of PRL-R in cells other than gonadotrophs were detected in the PD throughout the annual reproductive cycle. In addition to a stimulatory gonadal effect on lactotroph density, a substantial gonadal-independent effect of season was apparent on this variable. The findings have revealed important seasonal and gonadal effects on the cytological configuration of the equine hypophysis, which may provide the morphological basis for the intrahypophysial control of fertility.
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Gründker, Carsten, and Günter Emons. "Role of Gonadotropin-Releasing Hormone (GnRH) in Ovarian Cancer." Cells 10, no. 2 (2021): 437. http://dx.doi.org/10.3390/cells10020437.

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The hypothalamus–pituitary–gonadal (HPG) axis is the endocrine regulation system that controls the woman’s cycle. The gonadotropin-releasing hormone (GnRH) plays the central role. In addition to the gonadotrophic cells of the pituitary, GnRH receptors are expressed in other reproductive organs, such as the ovary and in tumors originating from the ovary. In ovarian cancer, GnRH is involved in the regulation of proliferation and metastasis. The effects on ovarian tumors can be indirect or direct. GnRH acts indirectly via the HPG axis and directly via GnRH receptors on the surface of ovarian cancer cells. In this systematic review, we will give an overview of the role of GnRH in ovarian cancer development, progression and therapy.
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Dissertations / Theses on the topic "Gonadotrophic hormone"

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Gaudron, Sylvie-Marylène. "Environment endocrine pheromone relationships in the control of reproduction in the scale worm Harmothoë imbricata (Polychaeta: Polynoidae) (L.)". Thesis, University of Newcastle Upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289277.

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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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Kirkpatrick, Bridgette Lee 1966. "Hormonal regulation of gonadotropin releasing hormone receptor expression in the ewe." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282660.

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Endocrine regulation of expression of GnRH receptors is an important step in the control of reproduction. During the early follicular phase of the estrous cycle in the ewe, GnRH receptor expression increases in preparation for the preovulatory surge of LH. The studies described herein were designed to further elucidate the hormonal interactions controlling GnRH receptor expression. In long-term ovariectomized ewes, neither removal of progesterone, nor the presence of estradiol affected the expression of GnRH receptors. However, in ewes ovariectomized during the luteal phase of the estrous cycle and immediately implanted with progesterone and estradiol for 48 hours, low levels of estradiol for 24 hours were required to increase GnRH receptor mRNA following the removal of progesterone. In ovariectomized ewes following hypothalamic-pituitary disconnection, low levels of estradiol and pulsatile GnRH were required to increase GnRH receptor expression within 24 hours of treatment initiation. These results suggest an interaction between estradiol and GnRH is involved in increasing GnRH receptor expression during the periovulatory period. How progesterone, estradiol and, GnRH interact to increase GnRH receptors is unknown, but a possible candidate involved in mediating these interactions may be the cell specific transcription factor, steroidogenic factor-1 (SF-1). SF-1 mRNA increased within 24 hours of treatment of ewes with prostaglandin F₂(α) compared to ewes in the luteal phase of the estrous cycle. This suggests that progesterone may have an inhibitory effect on SF-1 mRNA. SF-1 mRNA was similar between ovariectomized ewes and ovariectomized ewes following hypothalamic-pituitary disconnection treated with estradiol and GnRH. Treatment with estradiol or GnRH alone did not increase SF-1 mRNA. The results of these experiments suggest that progesterone removal as well as the presence of estradiol and GnRH are required to increase GnRH receptor expression during the early follicular phase in the ewe. Further, the transcription factor, SF-1 may be involved in mediating the effects of these hormones on GnRH receptor expression.
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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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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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Armstrong, Stephen Paul. "Pulsatile Gonadotrophin-releasing Hormone Receptor Signalling." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526055.

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李繼仁 and Kai-yan Lee. "Regulation of gonadotropin-releasing hormone and gonadotropin in goldfish, carassius auratus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31214332.

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Lee, Kai-yan. "Regulation of gonadotropin-releasing hormone and gonadotropin in goldfish, carassius auratus /." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18038165.

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Flanagan, Colleen A. "Gonadotropin releasing hormone receptor ligand interactions." Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27029.

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The decapeptide, gonadotropin releasing hormone (GnRH), is the central regulator of reproductive function. It binds to receptors on the gonadotrope cells of the pituitary and stimulates release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). Eleven different structural forms of GnRH have now been identified in various animal species. Chimaeric analogues of some of the variant forms of GnRH were synthesized in order to study the functional significance of the most common amino acid substitutions, which occur in positions 5, 7 and 8. Peptide binding affinities for sheep and rat GnRH receptors and potencies in stimulating LH and FSH release from cultured sheep pituitary cells and LH release from cultured chicken pituitary cells were measured. Histidine in position 5 decreased LH releasing potency in chicken cells, but slightly increased receptor binding affinity in rat and sheep membranes. Tryptophan in position 7 had minimal effect on GnRH activity in mammals, but increased LH release in chicken cells. Although differences in the structural requirements of mammalian and chicken GnRH receptors were anticipated, it was also found that rat GnRH receptors exhibited higher affinity for analogues with Tryptophan in position 7, than did sheep GnRH receptors. Substitutions in position 8 revealed the most marked differences in the structural requirements of mammalian and chicken GnRH receptors. Arginine was required for high GnRH activity in mammalian systems, but analogues with neutral substitutions in position 8 were more potent in chicken pituitary cells. The tolerance of position 8 substitutions, combined with the relatively small effects, in chicken cells, of incorporating a D-amino acid in position 6, indicate that the chicken GnRH receptor is less stringent than mammalian receptors in its recognition of peptide conformation. To examine how changes in ligand structure cause changes in receptor binding affinity and receptor activation, it was necessary to know the structures of the GnRH receptors. A protocol was developed for the purification of GnRH binding proteins from detergent-solubilized pituitary membranes, by affinity chromatography. This procedure yielded a protein which migrated as a single band on sodium dodecyl sulfate polyacrylamide gel electrophoresis, but was different from the recently cloned GnRH receptor. To test the proposal that the arginine residue in mammalian GnRH interacts with an acidic receptor residue, eight conserved acidic residues of the cloned mouse GnRH receptor were mutated to asparagine or glutamine. Mutant receptors were transiently expressed in COS-1 cells and tested for decreased preference for Arg⁸-containing ligands by ligand binding and inositol phosphate production. One mutant receptor, in which the glutamate residue in position 301 was mutated, exhibited decreased affinity for mammalian GnRH. The mutant receptor also exhibited decreased affinity for [Lys⁸]-GnRH, but unchanged affinity for [Gln⁸]-GnRH compared with the wildtype receptor, and increased affinity for the acidic analogue, [Glu⁸]-GnRH. This loss of affinity was specific for the residue in position 8, because the mutant receptor retained hiszh affinity for analogues with favourable substitutions in positions 5, 6 and 7. Thus, the Glu³⁰¹ residue of the GnRH receptor plays a role in receptor recognition of Arg⁸ in the ligand, consistent with an electrostatic interaction between these two residues. The Glu³⁰¹ and Arg⁸ residues were not required for the high affinity interactions of conformationally constrained peptides. This indicates that an interaction which involves these two residues may induce changes in the conformation of GnRH after it has bound to the receptor.
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Gardner, Samantha. "Gonadotropin-releasing hormone targets Wnt signalling." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29112.

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This thesis describes a potential mechanism by which GnRH promotes the nuclear accumulation of β-catenin, activation of TCF-dependent transcription and up-regulation of Wnt target genes, c-Jun, Fra-1, Cyclin D1 and c-Mye. GnRH-induced nuclear accumulation of β-catenin and activation of β-catenin/TCF-dependent transcription was found to be dependent on a pathway utilising G<sub>q</sub>-Phospholipase C (PLC)-Diacylglycerol (DAG)/Protein kinase C (PKC), and was found to be specifically dependent on the PKC δ isoform. GnRH was found to mediate the inactivation of Glycogen Synthase Kinase-3 (GSK-3), a protein serine/threonine kinase that regulates β-catenin degradation within the canonical Wnt signalling pathway. These results were observed in HEK293/GnRH receptor expressing cells and have been recapitulated in LβT2 and αT3-1 mouse gonadotrope cells, and then extended to various peripheral cell lines, sub-cultured prostate cells and whole prostate organ cultures. A potential mechanism of non-canonical Wnt/Ca<sup>2+ </sup>pathway activation by GnRH is described. GnRH was found to activate NFAT, a potential effecter of the non-canonical Wnt/Ca<sup>2+</sup> pathway. GnRH-induced NFAT activation was found to be dependent on important mediators of the non-classical Wnt/Ca<sup>2+</sup> pathway, including G<sub>q</sub>, Ca<sup>2+</sup>, Calcineurin and PKC δ.  Intriguingly, by expression of a dominant negative TCF construct, GnRH-induced NFAT activation was found to be TCF-dependent, thereby implicating TCF in targeting both Wnt/β-catenin and Wnt/Ca<sup>2+</sup> signalling. This novel finding suggests that a TCF-NFAT interaction may exist that functions either, to inhibit β-catenin/TCF-dependent transcription through competition for nuclear TCF, or to synergistically regulate TCF- and NFAT-target gene expression.
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Books on the topic "Gonadotrophic hormone"

1

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

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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. Parthenon Pub. Group, 1993.

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Saade, Georges. The regulation of luteinizing hormone and prolactin gene expression by gonadotrophin-releasing hormone and gonadal steroids in mice. University of Birmingham, 1988.

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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. Parthenon Pub. Group, 1996.

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

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

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

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Elgendy, Manal. Minimising the dose of gonadotrophin releasing hormone agonist [GnRHa] and recombinant follicle stimulating hormone [FSH] used for controlled ovarian hyperstimulation in in-vitro fertilisation. University of Birmingham, 2001.

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Gillespie, Julia M. A. Melatonin mediated regulation of gonadotropin-releasing hormone (GnRH): Role of melatonin receptors and circadian rhythms. National Library of Canada, 2002.

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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-. Ferring, 1985.

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Book chapters on the topic "Gonadotrophic hormone"

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Seth, John. "Gonadotrophin Releasing Hormone." In The Immunoassay Kit Directory. Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1414-1_24.

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

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Manji, Husseini K., Jorge Quiroz, R. Andrew Chambers, et al. "Gonadotropin-Releasing Hormone." In Encyclopedia of Psychopharmacology. 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. 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. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_2477.

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de Roux, Nicolas, Beate Doeker, and Edwin Milgrom. "Gonadotropin and TSH Receptors." In Hormone Signaling. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_10.

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Latronico, Ana Claudia, and Ivo Jorge Prado Arnhold. "Gonadotropin Resistance." In Hormone Resistance and Hypersensitivity. S. KARGER AG, 2013. http://dx.doi.org/10.1159/000342496.

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Helvacioglu, A. "Gonadotropin Releasing Hormone Treatment." In New Trends in Reproductive Medicine. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60961-9_17.

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

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

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Conference papers on the topic "Gonadotrophic hormone"

1

Liang, Zhe-Hao, and Wei Lu. "Prediction of the basic gonadotrophic hormone levels in girls with precocious puberty using ultrasonic union artificial neural network." In 2011 Seventh International Conference on Natural Computation (ICNC). IEEE, 2011. http://dx.doi.org/10.1109/icnc.2011.6022283.

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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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Hamad, Eyad M., Ghadeer Hawamdeh, Noor Abu Jarrad, Omar Yasin, Samer I. Al-Gharabli, and Raed Shadfan. "Detection of Human Chorionic Gonadotropin (hCG) Hormone using Digital Lateral Flow Immunoassay." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8513355.

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Sand, Sharon R., Catherine Klifa, Michael F. Press, 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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Pacucci, VA, F. Ceccarelli, G. Perrone, 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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Asman, Aulia, Debby Sinthania, and Linda Marni. "The Effect of Epinephrine Administration on the Level of Gonadotropin Hormones of Japan Strain Female Mice (Mus Musculus)." In The Health Science International Conference. SCITEPRESS - Science and Technology Publications, 2019. http://dx.doi.org/10.5220/0009124301190123.

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Kim, HJ, MH Lee, JE 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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Stepochkina, Anna, Andrey Bakhtyukov, Kira Derkach, Viktor Sorokoumov, Dmitry Dar’in, and Alexander Shpakov. "POTENTIAL EFFECT OF PRETREATMENT OF MALE RATS WITH TP03, AN ALLOSTERIC AGONIST OF LUTEINIZING HORMONE RECEPTOR, ON THE STEROIDOGENIC EFFECT OF GONADOTROPIN." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2338.sudak.ns2021-17/359-360.

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Yoon, TI, HJ Kim, JH Yu, et al. "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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