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Journal articles on the topic 'Gonadotropin releasing hormone'

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Published: 4 June 2021

Last updated: 1 August 2024

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1

Schwartz, Neena B. "The 1994 Stevenson Award Lecture. Follicle-stimulating hormone and luteinizing hormone: a tale of two gonadotropins." Canadian Journal of Physiology and Pharmacology 73, no. 6 (June 1, 1995): 675–84. http://dx.doi.org/10.1139/y95-087.

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Although most gonadotropes synthesize both luteinizing hormone and follicle-stimulating hormone, the transcription, content, and secretion rates of the two gonadotropins can be separated. The signals external to the gonadotropic cells that appear to be important in the differential regulation are gonadotropin-releasing hormone pulse frequency (high pulse frequency favors luteinizing hormone), steroid feedback (works on both but induces a more powerful negative feedback on luteinizing hormone), and gonadal peptide feedback (activin increases follicle-stimulating hormone; inhibin and follistatin decrease it). We know very little about the pathways within the gonadotropes that favor one gonadotropin rather than another. It is expected that the cloning of the genes for both gonadotropins and the use of specific cell lines and transfections will lead to elucidation of these pathways.Key words: luteinizing hormone, follicle-stimulating hormone, gonadotropin-releasing hormone, inhibin, anterior pituitary, gonads.

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2

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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3

Braden, Tim D., and P. Michael Conn. "The 1990 James A. F. Stevenson Memorial Lecture. Gonadotropin-releasing hormone and its actions." Canadian Journal of Physiology and Pharmacology 69, no. 4 (April 1, 1991): 445–58. http://dx.doi.org/10.1139/y91-067.

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Gonadotropin-releasing hormone (GnRH) stimulates the release and biosynthesis of gonadotropins, luteinizing hormone, and follicle-stimulating hormone from the pituitary gland. Additionally, GnRH regulates the number of its own receptors on pituitary gonadotropes causing both up- and down-regulation of receptors as well as biosynthesis of GnRH receptors. After exposure to GnRH, gonadotropes become desensitized to further stimulation by GnRH. The mechanisms through which these actions of GnRH are mediated appear to differ. Effects dependent upon extracellular calcium include gonadotropin biosynthesis and release as well as up-regulation of GnRH receptors. Additional actions of GnRH, such as down-regulation of receptors, biosynthesis of receptors, and desensitization, appear to be independent of extracellular calcium. Subsequent studies have ascribed roles for calmodulin and protein kinase C in mediating specific effects of GnRH.Key words: pituitary, gonadotropin-releasing hormone, receptor, protein kinase C, calmodulin.

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4

&NA;. "Gonadotropin releasing hormone." Reactions Weekly &NA;, no. 800 (May 2000): 8. http://dx.doi.org/10.2165/00128415-200008000-00021.

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5

Chow, Billy K. C. "Gonadotropin-releasing hormone." FEBS Journal 275, no. 22 (October 6, 2008): 5457. http://dx.doi.org/10.1111/j.1742-4658.2008.06675.x.

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6

Wiwanitkit, Viroj. "Model of gonadotropin-releasing hormone and gonadotropin-releasing hormone complex." Sexuality and Disability 24, no. 3 (September 2006): 175–78. http://dx.doi.org/10.1007/s11195-006-9018-4.

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7

Burger, L. L., D. J. Haisenleder, A. C. Dalkin, and J. C. Marshall. "Regulation of gonadotropin subunit gene transcription." Journal of Molecular Endocrinology 33, no. 3 (December 2004): 559–84. http://dx.doi.org/10.1677/jme.1.01600.

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Reproductive function in mammals is regulated by the pituitary gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH and FSH are secreted by the gonadotrope cell and act on the gonad in a sequential and synergistic manner to initiate sexual maturation and maintain cyclic reproductive function. The synthesis and secretion of LH and FSH are regulated mainly by the pulsatile release of the hypothalamic decapeptide hormone gonadotropin-releasing hormone (GnRH). The control of differential LH and FSH synthesis and secretion is complex and involves the interplay between the gonads, hypothalamus and pituitary. In this review, the transcriptional regulation of the gonadotropin subunit genes is discussed in a physiologic setting, and we aimed to examine the mechanisms that drive those changes.

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8

TRUDEAU, V., A. PHARAZYN, F. X. AHERNE, and E. BELTRANENA. "NALOXONE ELEVATES PLASMA FOLLICLE STIMULATING HORMONE BUT NOT LUTEINIZING HORMONE LEVELS IN THE IMMATURE MALE PIG." Canadian Journal of Animal Science 69, no. 4 (December 1, 1989): 1095–98. http://dx.doi.org/10.4141/cjas89-126.

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The effects of intraperitoneal injection of gonadotropin-releasing hormone (GnRH) alone, naloxone (NAL) alone, or in combination on plasma levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) was studied in 4- to 5-wk-old male pigs. GnRH (1 μg kg−1) effectively stimulated (P < 0.05) secretion of both gonadotropins whereas NAL (1 and 10 mg kg−1) stimulated only FSH secretion (P < 0.05). There was no interaction between GnRH and NAL on gonadotropin release. These results suggest that endogenous opiates are involved in the regulation of FSH secretion but not LH secretion in the immature male pig. Key words: Follicle-stimulating hormone, luteinizing hormone, naloxone, gonadotropin-releasing hormone, male pig

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9

ALI, A., A. ELTOBGY, H. ELAZIZ, S. ELSHAYEB, M. ELDIN, and A. ELAZEEMSARHAN. "Gonadotropin-releasing hormone mRNA, gonadotropin-releasing hormone peptide, and variants of gonadotropin-releasing hormone receptor in human placenta." Obstetrics & Gynecology 93, no. 4 (April 1999): S5. http://dx.doi.org/10.1016/s0029-7844(99)90007-8.

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10

Sasaki, Kirsten, and Errol R. Norwitz. "Gonadotropin-releasing hormone/gonadotropin-releasing hormone receptor signaling in the placenta." Current Opinion in Endocrinology & Diabetes and Obesity 18, no. 6 (December 2011): 401–8. http://dx.doi.org/10.1097/med.0b013e32834cd3b0.

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11

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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12

ROSER, JANET F., and JOHN P. HUGHES. "Dose‐Response Effects of Gonadotropin‐releasing Hormone on Plasma Concentrations of Gonadotropins and Testosterone in Fertile and Subfertile Stallions." Journal of Andrology 13, no. 6 (November 12, 1992): 543–50. http://dx.doi.org/10.1002/j.1939-4640.1992.tb00350.x.

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ABSTRACT: Five fertile and five subfertile stallions were treated with a single intravenous injection of saline the first week followed by a single intravenous injection of varying doses of gonadotropin‐releasing hormone (5, 10, 25, 100, 500 μg) given in a randomized fashion over the next 5 weeks during the nonbreeding season. Blood samples were collected periodically before and after treatment for analysis of luteinizing hormone, follicle stimulating hormone, and testosterone content by radioimmunoassay. Before treatment, semen samples were collected every other day for 3 weeks for analysis of volume, concentration, motility, pH, and morphology. Basal plasma levels of luteinizing hormone were higher (P < 0.05) in the subfertile group, follicle stimulating hormone levels tended to be higher (P < 0.10) in the subfertile group, and testosterone levels were similar in the two groups. A significant linear‐log dose‐response relationship was observed for plasma luteinizing hormone (P < 0.05) and follicle stimulating hormone (P < 0.05) to exogenous gonadotropin‐releasing hormone in both the fertile and subfertile group. A linear‐log dose‐response relationship was also observed for plasma testosterone (P < 0.05) in the fertile group. The magnitude of the luteinizing hormone and follicle stimulating hormone response to gonadotropin‐releasing hormone across doses was similar in both groups of stallions. A significant testosterone response to gonadotropin‐releasing hormone in the subfertile group of stallions was not observed (P > 0.05). Mean testosterone concentrations after treatment in terms of net increase and percent of baseline were significantly lower (P < 0.05) in the subfertile group compared to the fertile group. Total viable sperm was lower (P < 0.05) in the subfertile group than in the fertile group of stallions. These results demonstrate that, in the nonbreeding season, the pituitary of subfertile stallions, like fertile stallions, has the capacity to respond to exogenous gonadotropin‐releasing hormone in a significant linear‐log dose‐response fashion. However, the capacity of Leydig cells to respond to increasing doses of gonadotropin releasing hormone (via endogenous luteinizing hormone) is significantly reduced in subfertile stallions compared to fertile stallions. The findings that subfertile stallions have high basal levels of gonadotropins, normal basal levels of testosterone, and yet a poor testosterone response to gonadotropin‐releasing hormone suggests that the endocrine dysfunction in stallions with idiopathic subfertility is associated with impaired Leydig/Sertoli cell function and/or alterations in the functional capacity of the hypothalamic‐pituitary axis.

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13

&NA;. "Chorionic gonadotropin/gonadotropin releasing hormone agonists." Reactions Weekly &NA;, no. 1229 (November 2008): 9. http://dx.doi.org/10.2165/00128415-200812290-00023.

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14

Bonnin, M., M. Mondain-Monval, M. C. Audy, and R. Scholler. "Basal and gonadotropin releasing hormone stimulated gonadotropin levels in the female red fox (Vulpes vulpes L.). Negative feedback of ovarian hormones during anoestrus." Canadian Journal of Zoology 67, no. 3 (March 1, 1989): 759–65. http://dx.doi.org/10.1139/z89-107.

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In the red fox, Vulpes vulpes L., an inhibition of gonadotropic function is observed in early anoestrus, particularly during lactation. During this period, secretion of progesterone as a result of the persistent corpora lutea after parturition and episodic releases of estradiol signify ovarian activity, suggesting involvement of these hormones in the modulation of pituitary hormones (luteinizing hormone (LH), follicle-stimulating hormone (FSH)). Effects of ovariectomy and (or) progesterone or estradiol treatments in vivo upon basal and gonadotropin releasing hormone (GnRH)-stimulated LH and FSH were observed. After ovariectomy, a great increase in the basal level of both gonadotropins and in GnRH-stimulated LH release, but not GnRH-stimulated FSH release, were observed. Progesterone treatment induced a decrease in GnRH-stimulated LH and FSH secretions and a decrease in basal LH and FSH levels in ovariectomized females. Estradiol treatment abolished basal secretions and GnRH responses for both hormones. These results suggest a negative feedback of both ovarian steroids at the hypothalamopituitary level on LH and FSH secretions during early anoestrus.

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15

Weiss, Juergen M., Klaus Diedrich, and Michael Ludwig. "Gonadotropin-Releasing Hormone Antagonists." Treatments in Endocrinology 1, no. 5 (2002): 281–91. http://dx.doi.org/10.2165/00024677-200201050-00002.

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16

Winkel, Craig A. "Gonadotropin-releasing hormone agonists." Postgraduate Medicine 95, no. 6 (June 1994): 111–18. http://dx.doi.org/10.1080/00325481.1994.11945846.

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17

Hayes, Frances J., Canine K. Welt, Kathryn A. Martin, and William F. Crowky. "Gonadotropin-Releasing Hormone Deficiency." Endocrinologist 9, no. 1 (January 1999): 36–44. http://dx.doi.org/10.1097/00019616-199901000-00008.

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18

Hodgen, Gary D. "Gonadotropin-releasing hormone agonists." Current Opinion in Obstetrics and Gynecology 3, no. 3 (June 1991): 352–58. http://dx.doi.org/10.1097/00001703-199106000-00007.

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19

Friedman, Yael G., and Nikos Vlahos. "Gonadotropin-Releasing Hormone Antagonists." Postgraduate Obstetrics & Gynecology 19, no. 26 (December 1999): 1–6. http://dx.doi.org/10.1097/00256406-199919260-00001.

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20

Fluker, Margo R. "Gonadotropin-releasing hormone antagonists." Current Opinion in Endocrinology & Diabetes 7, no. 6 (December 2000): 350–56. http://dx.doi.org/10.1097/00060793-200012000-00010.

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21

GORDON, KEITH. "Gonadotropin-Releasing Hormone Antagonists." Annals of the New York Academy of Sciences 943, no. 1 (September 2001): 49–54. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03789.x.

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22

Millar, Robert P., Zhi-Liang Lu, Adam J. Pawson, Colleen A. Flanagan, Kevin Morgan, and Stuart R. Maudsley. "Gonadotropin-Releasing Hormone Receptors." Endocrine Reviews 25, no. 2 (April 1, 2004): 235–75. http://dx.doi.org/10.1210/er.2003-0002.

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23

HERBST, K. "Gonadotropin-releasing hormone antagonists." Current Opinion in Pharmacology 3, no. 6 (December 2003): 660–66. http://dx.doi.org/10.1016/j.coph.2003.06.009.

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24

Sharp, Peter J., and Dominique Blache. "A neuroendocrine model for prolactin as the key mediator of seasonal breeding in birds under long- and short-day photoperiods." Canadian Journal of Physiology and Pharmacology 81, no. 4 (April 1, 2003): 350–58. http://dx.doi.org/10.1139/y03-025.

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Seasonal breeding is associated with sequential increases in plasma luteinizing hormone (LH) and prolactin in the short-day breeding emu, and in long-day breeding birds that terminate breeding by the development of reproductive photorefractoriness. A model of the avian neuroendocrine photoperiodic reproductive response is proposed, incorporating a role for prolactin, to account for neuroendocrine mechanisms controlling both long- and short-day breeding. The breeding season terminates after circulating concentrations of prolactin increase above a critical threshold to depress gonadotropin releasing hormone (GnRH) neuronal and gonadotrope (LH) activity. Subsequently, photorefractoriness develops for prolactin secretion and for LH secretion, independently of high plasma prolactin. The breeding season in the emu is advanced compared with long-day breeders, because after photorefractiness for both LH and prolactin secretion is dissipated, plasma concentrations of both hormones increase to maximum values while days are still short.Key words: seasonal breeding, prolactin, gonadotropin releasing hormone, photorefactoriness.

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25

&NA;. "Chorionic gonadotropin/gonadotropin releasing hormone/recombinant follicle stimulating hormone." Reactions Weekly &NA;, no. 1316 (August 2010): 14. http://dx.doi.org/10.2165/00128415-201013160-00043.

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26

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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27

Ceccatelli, S., A. L. Hulting, X. Zhang, L. Gustafsson, M. Villar, and T. Hökfelt. "Nitric oxide synthase in the rat anterior pituitary gland and the role of nitric oxide in regulation of luteinizing hormone secretion." Proceedings of the National Academy of Sciences 90, no. 23 (December 1, 1993): 11292–96. http://dx.doi.org/10.1073/pnas.90.23.11292.

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By using immunohistochemistry and in situ hybridization, we have demonstrated that the nitric oxide (NO)-synthesizing enzyme NO synthase is present in gonadotrophs and in folliculo-stellate cells of the anterior pituitary gland of male and female rats. A marked increase in levels of NO synthase protein and mRNA was observed after gonadectomy. In vitro studies on dispersed anterior pituitary cells suggest that NO inhibits gonadotropin-releasing-hormone-stimulated luteinizing hormone release. An inhibitory effect of NO has also been shown on growth-hormone-releasing-hormone-stimulated release of growth hormone [Kato, M. (1992) Endocrinology 131, 2133-2138]. Thus these findings support a dual mechanism for NO in the control of anterior pituitary hormone secretion, an autocrine mediation of luteinizing hormone release on gonadotrophs, and a paracrine effect on growth hormone secretion involving folliculo-stellate cells closely related to somatotrophs. We speculate that NO may participate in producing the pulsatile secretion patterns of these two pituitary hormones.

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28

Carriere, Paul D., Riaz Farookhi, and James R. Brawer. "The role of aberrant hypothalamic opiatergc function in generating polycystic ovaries in the rat." Canadian Journal of Physiology and Pharmacology 67, no. 8 (August 1, 1989): 896–901. http://dx.doi.org/10.1139/y89-140.

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Treatment of adult female rats with estradiol valerate produces an intractable hypothalamic impairment that ultimately results in anovulatory acyclicity and polycystic ovaries. Evidence from our laboratory suggests that the hypothalamic impairment compromises regulation of the endogenous opioid system engendering a persistent opiatergic suppression of gonadotropin-releasing hormone secretion, which is subsequently reflected in a chronically low pituitary content of gonadotropin-releasing hormone receptors. If such is the case, inhibition of opiatergic transmission should improve the gonadotropin-releasing hormone pattern resulting in an improvement in the pituitary content of gonadotropin-releasing hormone receptors, and in an amelioration of the polycystic condition. We, therefore, treated rats with the polycystic ovarian condition, with daily injections of naltrexone. Within 1 week, there was a significant increase in the pituitary content of gonadotropin-releasing hormone receptors and a marked improvement in ovarian morphology, indicating that the hypothalamic opiatergic system is chronically active, and contributes significantly to the polycystic ovarian condition.Key words: hypothalamus, opiates, infertility, ovary, polycystic ovaries.

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29

&NA;. "Chorionic gonadotropin/gonadotropin releasing hormone antagonists/urofollitropin." Reactions Weekly &NA;, no. 1138 (February 2007): 12. http://dx.doi.org/10.2165/00128415-200711380-00034.

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30

&NA;. "Chorionic gonadotropin/gonadotropin releasing hormone agonists/menotropin." Reactions Weekly &NA;, no. 1209 (July 2008): 12. http://dx.doi.org/10.2165/00128415-200812090-00040.

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31

Babichev, V. N. "Neuroendocrinology of the reproductive system (state of physiological studies and prospects for their use in clinical practice)." Problems of Endocrinology 44, no. 1 (February 15, 1998): 3–12. http://dx.doi.org/10.14341/probl19984413-12.

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The author analyzes the neuroendocrine relationships between the true adrenergic and cholinergic neuromediators and peptide neuromediators, on the one hand, and neurosecretory neurons regulating gonadotropin and prolactin secretion, on the other. About 30 neuromediators of different origin are characterized with due consideration for their localization in the CNS structures, involvement in the production and secretion of gonadotropin releasing factor, gonadotropins, prolactin, and, hence, the function of the reproductive system in general. The impact of the hormone background of sex steroids in the system of these intricate relationships is analyzed. The author presents his own findings and published data on the time course of catecholamine levels in hypothalamic structures involved in the regulation of the pituitary gonadotropic function and analyzes correlations between changed levels of sex steroids and gonadotropins in the blood and the time course of changes of catecholamines and luteotropin releasing factor in the hypothalamus. Possible mechanisms of coordination of different neuromediators of adrenergic origin and amino neuromediators with different mechanisms of action during the regulation of normal function of the reproductive system are discussed. The author assesses the efficacy of treating disorders of the reproductive system caused by the CNS disorders by combinations of sex hormones and neurotropic agents.

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32

Millar, RP, and JA King. "Evolution of Gonadotropin-Releasing Hormone: Multiple Usage of a Peptide." Physiology 3, no. 2 (April 1, 1988): 49–53. http://dx.doi.org/10.1152/physiologyonline.1988.3.2.49.

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Gonadotropin-releasing hormone was originally isolated as a brain peptide hormone that stimulates the reproductive system by releasing gonadotropins from the anterior pituitary gland. However, it is now clear that during evolution this peptide has been subject to gene duplication and structural changes and has been recruited for diverse regulatory functions: as a neurotransmitter in the central and sympathetic nervous sytems, as a paracrine regulator in the gonads and placenta, and as an autocrine regulator in tumor cells.

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33

Krutova, V. A., and A. A. Baklakova. "Luteal Support and Risk of Ovarian Hyperstimulation in Assisted Reproduction (A Review)." Kuban Scientific Medical Bulletin 27, no. 6 (December 3, 2020): 136–48. http://dx.doi.org/10.25207/1608-6228-2020-27-6-136-148.

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Background. Gonadotropin-releasing hormone agonist as an ovulation trigger effectively reduces the ovarian hyperstimulation risk in in vitro fertilisation protocols, at the same time requiring an effective luteal phase support in embryo transfer cycles.Objectives. A review of modern approaches to luteal support after the ovulation trigger switch in in vitro fertilisation/intracytoplasmic sperm injection protocols; assessment of feasibility and safety of gonadotropin-releasing hormone agonist in the post-transfer period.Methods. Literature sources were mined in the PubMed, eLibrary, Web of Science, Cochrane Library, Cyberleninka databases at a depth of 10 years. The query keywords were: gonadotropin-releasing hormone agonist, luteal phase support, ovulation trigger, in vitro fertilisation, ovarian hyperstimulation syndrome.Results. The review included 35 records selected from the 96 analysed total. The analysis reveals a sensible efﬁciency of gonadotropin-releasing hormone agonist for the luteal phase support, improved success of in vitro fertilisation/intracytoplasmic sperm injection and embryo transfer strategies, improved pregnancy outcomes. Microdosing of chorionic gonadotropin to supplement standard progesterone luteal support also improves the pregnancy outcome rate in assisted reproduction, however, at the risk of late ovarian hyperstimulation syndrome and should be applied with caution.Conclusion. Administration of gonadotropin-releasing hormone agonist for luteal support may improve pregnancy outcomes in in vitro fertilisation/intracytoplasmic sperm injection protocols in patients with the ovarian hyperstimulation risk after the ovulation trigger switch. Nevertheless, further research is necessary into the efﬁcacy and safety of gonadotropin-releasing hormone agonist for luteal support in embryo transfer cycles.

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34

Nakashima, Akira. "The Early Coasting Method during Ovarian Stimulation in Antagonist Protocols with Combined Use of Cabergoline is Useful in Patients with Polycystic Ovary Syndrome." Journal of Reproductive Medicine, Gynaecology & Obstetrics 6, no. 3 (December 8, 2021): 1–6. http://dx.doi.org/10.24966/rmgo-2574/100087.

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Purpose: This study aimed to investigate the efficacy of withholding gonadotropins (coasting) and early administration of cabergoline in a flexible Gonadotropin-Releasing Hormone (GnRH) antagonist protocol for patients with Polycystic Ovarian Syndrome (PCOS).

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35

Armansyah, Teuku, Sara Febria Putri, Oppi Oktaviany, Tongku Nizwan Siregar, Syafruddin Syafruddin, Budianto Panjaitan, and Arman Sayuti. "Pemberian Gonadotropin Releasing Hormone Meningkatkan Konsentrasi Hormon Testosteron pada Domba Waringin." Jurnal Veteriner 22, no. 3 (September 30, 2021): 342–51. http://dx.doi.org/10.19087/jveteriner.22.3.342.

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Salah satu upaya untuk meningkatkan konsentrasi testosteron adalah dengan pemberian gonadotropin releasing hormone (GnRH). Peningkatan testosteron menyebabkan peningkatan kualitas spermatozoa. Penelitian ini bertujuan mengetahui pengaruh pemberian gonadotropin releasing hormone (GnRH) terhadap peningkatan kualitas semen dan level testosteron domba waringin. Dalam penelitian ini digunakan tiga ekor domba waringin dengan rancangan pola bujur sangkar latin 3 x 3 sehingga hewan percobaan menerima suntikan NaCl fisiologis sebagai kontrol (K0), 50 ìg GnRH (K1), dan 100 ìg GnRH (K2). Penampungan semen dilakukan satu kali ejakulasi/minggu, selama tiga minggu. Sampel semen dikoleksi menggunakan elektroejakulator 24 jam setelah perlakuan dan diamati warna, konsistensi, volume, motilitas, konsentrasi, viabilitas, dan abnormalitas spermatozoa. Koleksi darah untuk pemeriksaan konsentrasi hormon testosteron dilakukan 60 menit setelah penyuntikan GnRH. Analisis konsentrasi testosteron dilakukan menggunakan metode enzyme linked immunosorbent assay (ELISA). Data mengenai warna dan konsistensi semen dilaporkan secara deskriptif, sedangkan level testosteron, volume semen, motilitas, konsentrasi, viabilitas dan abnormalitas spermatozoa dianalisis dengan analisis varian. Hasil pengamatan menunjukkan bahwa warna dan konsistensi semen yang dikoleksi pada semua kelompok perlakuan adalah krem dengan konsistensi kental. Hasil analisis statistika menunjukkan bahwa volume semen, konsentrasi spermatozoa, motilitas spermatozoa, viabilitas spermatozoa dan abnormalitas spermatozoa setelah pemberian GnRH menunjukkan perbedaan yang tidak signifikan (P>0,05). Rata-rata (±SD) konsentrasi testosteron pada kelompok K0, K1, dan K2 masing-masing adalah 1,82±1,08; 8,05+2,24; dan 8,81±1,09 ng/mL (P<0,05). Disimpulkan bahwa pemberian GnRH tidak memengaruhi kualitas semen namun dapat meningkatkan konsentrasi hormon testosteron pada domba waringin.

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&NA;. "Gonadotropin-releasing hormone antagonists reviewed." Inpharma Weekly &NA;, no. 1316 (December 2001): 2. http://dx.doi.org/10.2165/00128413-200113160-00002.

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Quintanar, J. Luis. "Neuroimmunomodulation by Gonadotropin Releasing Hormone." Advances in Neuroimmune Biology 1, no. 2 (2011): 125–32. http://dx.doi.org/10.3233/nib-2011-014.

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Lingle, Lisa, and Linda L. Hart. "Gonadotropin-Releasing Hormone in Infertility." DICP 23, no. 3 (March 1989): 246–48. http://dx.doi.org/10.1177/106002808902300313.

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Handelsman, David J., Jim T. Cummins, and Iain J. Clarke. "Pharmacodynamics of Gonadotropin-Releasing Hormone." Neuroendocrinology 48, no. 4 (1988): 432–38. http://dx.doi.org/10.1159/000125045.

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Huirne, Judith AF, and Cornelis B. Lambalk. "Gonadotropin-releasing-hormone-receptor antagonists." Lancet 358, no. 9295 (November 2001): 1793–803. http://dx.doi.org/10.1016/s0140-6736(01)06797-6.

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Talwar, G. P. "Immunobiology of gonadotropin-releasing hormone." Journal of Steroid Biochemistry 23, no. 5 (November 1985): 795–800. http://dx.doi.org/10.1016/s0022-4731(85)80016-9.

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Schwarting, Gerald, Margaret Wierman, and Stuart Tobet. "Gonadotropin-Releasing Hormone Neuronal Migration." Seminars in Reproductive Medicine 25, no. 5 (September 2007): 305–12. http://dx.doi.org/10.1055/s-2007-984736.

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Cornea, Anda, Jo Ann Janovick, Guadalupe Maya-Núñez, and P. Michael Conn. "Gonadotropin-releasing Hormone Receptor Microaggregation." Journal of Biological Chemistry 276, no. 3 (October 16, 2000): 2153–58. http://dx.doi.org/10.1074/jbc.m007850200.

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Beyer, Daniel Alexander, Feriel Amari, Marc Thill, Askan Schultze-Mosgau, Safaa Al-Hasani, Klaus Diedrich, and Georg Griesinger. "Emerging gonadotropin-releasing hormone agonists." Expert Opinion on Emerging Drugs 16, no. 2 (January 19, 2011): 323–40. http://dx.doi.org/10.1517/14728214.2010.547472.

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Ory, S. J. "Gonadotropin-releasing hormone in practice." Archives of Internal Medicine 146, no. 4 (April 1, 1986): 804b—804. http://dx.doi.org/10.1001/archinte.146.4.804b.

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Hammond, Charles B. "Gonadotropin-Releasing Hormone in Practice." Archives of Internal Medicine 146, no. 4 (April 1, 1986): 804. http://dx.doi.org/10.1001/archinte.1986.00360160260037.

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Chesnokova, Vera, and Shlomo Melmed. "Peptide Hormone Regulation of DNA Damage Responses." Endocrine Reviews 41, no. 4 (April 9, 2020): 519–37. http://dx.doi.org/10.1210/endrev/bnaa009.

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Abstract DNA damage response (DDR) and DNA repair pathways determine neoplastic cell transformation and therapeutic responses, as well as the aging process. Altered DDR functioning results in accumulation of unrepaired DNA damage, increased frequency of tumorigenic mutations, and premature aging. Recent evidence suggests that polypeptide hormones play a role in modulating DDR and DNA damage repair, while DNA damage accumulation may also affect hormonal status. We review the available reports elucidating involvement of insulin-like growth factor 1 (IGF1), growth hormone (GH), α-melanocyte stimulating hormone (αMSH), and gonadotropin-releasing hormone (GnRH)/gonadotropins in DDR and DNA repair as well as the current understanding of pathways enabling these actions. We discuss effects of DNA damage pathway mutations, including Fanconi anemia, on endocrine function and consider mechanisms underlying these phenotypes. (Endocrine Reviews 41: 1 – 19, 2020)

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Amšiejienė, Andrė, Audronė Usonienė, and Ieva Šiaudinytė. "Onkologinių pacientų vaisingumo išsaugojimas: klinikinis atvejis." Lietuvos chirurgija 13, no. 1 (January 1, 2014): 46–51. http://dx.doi.org/10.15388/lietchirur.2014.1.2947.

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Onkologinių ligų nuolat daugėja, tačiau tobulėjančios gydymo galimybės labai didina išgyvenamumo rodiklius. Tai rodo vis didėjantį onkologinių pacientų gyvenimo kokybės po sėkmingo gydymo temos aktualumą. Prieš skiriant gonadotoksinį gydymą nuo vėžio, svarbu informuoti kiekvieną vaisingo amžiaus pacientę apie riziką pakenkti vaisingumui. Turėtų būti aptartas ir rekomenduotas vaisingumą išsaugantis gydymas. Kiaušidžių transpozicija, kiaušialąsčių ar embrionų kriokonservacija, kiaušidės audinio užšaldymas ir gonadotropinio hormono agonistų terapija – tai klinikiniais tyrimais pagrįsti vaisingumą išsaugantys gydymo metodai. Svarbu parinkti tinkamiausią ir priimtiniausią metodą, atsižvelgiant į moters amžių, kiaušidžių išteklius, socialinę ekonominę padėtį, religines pažiūras, sveikatos būklę ir gretutines ligas.Reikšminiai žodžiai: onkologiniai pacientai, gydymas nuo vėžio, vaisingumo išsaugojimas, kiaušidžių transpozicija, embrionų užšaldymas, kiaušialąsčių užšaldymas, kiaušidės audinio kriokonservacija ir transplantacija, gonadotropinių hormonų agonistaiFertility preservation in patients with cancer: case report The total number of oncological diseases is constantly growing, but the improvement of treatment options significantly increases the survival rates. It shows the importance of the oncological patients’ quality of life after a succesful treatment. Prior to the prescription of any gonadotoxic medications, every patient of a fertile age should be informed about the risks of damaging fertility and recommended protective treatments. Ovarian transposition, oocyte, embryo or ovarian tissue cryoconservation and gonadotropin releasing hormone agonists’ (GnRHa) therapy these are the clinically tested fertility-protecting treatment methods. For the appropriate method to be selected, it is very important to take into consideration the female’s age, ovarian condition, social-economic situation, religious views, overall health condition, and related diseases.Key words: oncological patients, fertility protection, ovarian transposition, embryo cryoconservation, oocyte cryoconservation, ovarian tissue cryoconservation and transplantation, gonadotropin releasing hormone agonists

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Dolan, Sharron, Neil P. Evans, Trevor A. Richter, and Andrea M. Nolan. "Expression of gonadotropin-releasing hormone and gonadotropin-releasing hormone receptor in sheep spinal cord." Neuroscience Letters 346, no. 1-2 (July 2003): 120–22. http://dx.doi.org/10.1016/s0304-3940(03)00594-9.

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Crowley, WF, and RW Whitcomb. "Gonadotropin-releasing hormone deficiency in men: Diagnosis and treatment with exogenous gonadotropin-releasing hormone." International Journal of Gynecology & Obstetrics 36, no. 1 (September 1991): 85. http://dx.doi.org/10.1016/0020-7292(91)90214-p.

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