Relevant bibliographies by topics / Luteinizing hormone releasing hormone

Academic literature on the topic 'Luteinizing hormone releasing hormone'

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Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "Luteinizing hormone releasing hormone"

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Glass, A. R. "Luteinizing hormone-releasing hormone." Archives of Internal Medicine 146, no. 3 (March 1, 1986): 603b—603. http://dx.doi.org/10.1001/archinte.146.3.603b.

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Glass, Allan R. "Luteinizing Hormone-Releasing Hormone." Archives of Internal Medicine 146, no. 3 (March 1, 1986): 603. http://dx.doi.org/10.1001/archinte.1986.00360150257038.

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Mező, Gábor, and Marilena Manea. "Luteinizing hormone-releasing hormone antagonists." Expert Opinion on Therapeutic Patents 19, no. 12 (November 26, 2009): 1771–85. http://dx.doi.org/10.1517/13543770903410237.

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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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Della Manna, Thais, Nuvarte Setian, Durval Damiani, Hilton Kuperman, and Vaê Dichtchekenian. "Premature thelarche: identification of clinical and laboratory data for the diagnosis of precocious puberty." Revista do Hospital das Clínicas 57, no. 2 (2002): 49–54. http://dx.doi.org/10.1590/s0041-87812002000200001.

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PURPOSE: Two groups of girls with premature breast development were studied retrospectively. We tried to identify clinical, radiological, and hormonal parameters that could distinguish between a benign, nonprogressive premature thelarche and a true precocious puberty. METHODS: The clinical outcome of 88 girls with breast enlargement before 6.1 years of age was analyzed. Taking into account the progression of their sexual maturation, we allocated the children into 2 groups: "Isolated Premature Thelarche" (n = 63) and "Precocious Puberty" (n = 25) groups. Chronological and bone ages, height and growth velocity centiles, computerized tomography of hypothalamus-pituitary area, pelvic ultrasonography, gonadotropin response to luteinizing hormone-releasing hormone stimulation as well as basal levels of luteinizing hormone, follicle-stimulating hormone, estradiol, and prolactin were studied in both groups. Statistical analysis were performed using the Student t test to compare the sample means. Fisher's exact test and chi² test were used to analyze the nonparametric variables. RESULTS: Isolated premature thelarche most frequently affected girls younger than 2 years who presented exaggerated follicle-stimulating hormone response to luteinizing hormone-releasing hormone stimulation test. The precocious puberty group had higher initial stature, accelerated growth rate and bone age, increased uterine and ovarian volumes, high spontaneous luteinizing hormone levels by immunofluorimetric assay, as well as a high luteinizing hormone response and peak luteinizing hormone/follicle-stimulating hormone ratio after luteinizing hormone-releasing hormone stimulation. CONCLUSION: At initial presentation, girls who undergo true precocious puberty present advanced bone age, increased uterine and ovarian volumes in addition to breast enlargement, as well as an luteinizing hormone-predominant response after a luteinizing hormone-releasing hormone stimulation test.
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McCann, Samuel, and Valeria Rettori. "Physiology of Luteinizing Hormone - Releasing Hormone." Seminars in Reproductive Medicine 5, no. 04 (November 1987): 333–43. http://dx.doi.org/10.1055/s-2007-1021880.

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Meakin, Janice L., Edward J. Keogh, and Clayton E. Martin. "Human anti-luteinizing hormone-releasing hormone antibodies in patients treated with synthetic luteinizing hormone-releasing hormone *." Fertility and Sterility 43, no. 5 (May 1985): 811–13. http://dx.doi.org/10.1016/s0015-0282(16)48572-9.

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Mukhopadhyay, Banibrata, and Rakhi Bhattacharyya. "A delayed mathematical model for testosterone secretion with feedback control mechanism." International Journal of Mathematics and Mathematical Sciences 2004, no. 3 (2004): 105–15. http://dx.doi.org/10.1155/s0161171204307271.

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A mathematical model describing the biochemical interactions of the luteinizing hormone (LH), luteinizing hormone–releasing hormone (LHRH), and testosterone (T) is presented. The model structure consists of a negative feedback mechanism with transportation and secretion delays of different hormones. A comparison of stability and bifurcation analysis in the presence and absence of delays has been performed. Mathematical implications of castration and testosterone infusion are also studied.
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Bulatov, A. A., E. E. Makarovskaya, N. B. Smirnova, V. G. Shlykova, and S. Yu Kasumova. "Multigormonal secretory activity of cells of clinically non-functioning pituitary tumors in vitro and the effect of tyroliberin on it." Problems of Endocrinology 45, no. 1 (October 6, 2019): 40–43. http://dx.doi.org/10.14341/probl11705.

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Experiments on cell cultures demonstrated that isolated cells of clinically inert pituitary tumors release several hormones in small amounts into the medium: luteinizing and follicle-stimulating hormones, alpha-subunit of glycoprotein hormones, prolactin, and growth hormone. Multihormonal secretion of these cells indicates their poor morphofunctional differentiation. In contrast to normal pituitary cells, cells of clinically inert pituitary tumors respond nonspeciflcally to hypothalamic thyrotropin releasing hormone: by increased secretion of prolactin, gonadotropins, glycoprotein hormone alpha-subunit, and growth hormone. This capacity of tumor cells detected in vitro agrees with the probability of increased levels of gonadotropins and glycoprotein hormone alpha-subunit in the serum of patients with clinically inert pituitary tumors during pharmacodynamic thyrotropin releasing hormone test.
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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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Dissertations / Theses on the topic "Luteinizing hormone releasing hormone"

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Sheward, William John. "Thyrotrophin releasing hormone, somatostatin and luteinizing hormone releasing hormone : aspects of their synthesis, release and actions." Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/20183.

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Stevens, Jeffrey David. "LHRH fusion protein vaccines in beef heifers and bovine ectopic ovarian xenografting." Online access for everyone, 2004. http://www.dissertations.wsu.edu/Dissertations/Fall2004/J%5FStevens%5F092204.pdf.

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CASTEL, VINCENT. "Les analogues de la luteinizing hormone-releasing hormone en pathologie uterine." Angers, 1990. http://www.theses.fr/1990ANGE1046.

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Wang, Jian. "Action of luteinizing hormone-releasing hormone in rat ovarian cells : hormone production and signal transduction." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/29313.

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The present study was conducted to investigate the hypothesis that membrane phosphoinositide breakdown may participate in the actions of luteinizing hormone-releasing hormone (LHRH) on hormone production in the rat ovary. In granulosa cells prelabeled with [³H]-arachidonic acid or [³H]-inositol, treatment with LHRH increased the accumulation of radiolabeled inositol lipids, diacylglycerol and free arachidonic acid, but luteinizing hormone (LH) or cholera toxin did not exert the same effect. Activation of protein kinase C by the phorbol ester, 12-0-tetradecanoyl phorbol-13-acetate (TPA) had a stimulatory action on membrane phosphoinositide breakdown. In addition, TPA did not alter arachidonic acid release but potentiated the A23187 stimulated liberation of arachidonic acid. Changes in the cytosolic free calcium ion concentrations, [Ca²⁺]i, induced by LHRH were studied in individual cells using fura-2 microspectrofluorimetry. The resting [Ca²⁺]i was 96.7 ± 2.9 nM (n= 115). The alterations in [Ca²⁺]i induced by LHRH were transient and returned to resting levels within 84±3 second (n=64). A potent LHRH antagonist completely blocked the effect of LHRH on [Ca²⁺]i. Some cells responded to LHRH alone, whereas others responded to angiotensin II, suggesting that there are different subpopulations of granulosa cells. Sustained perifusion of LHRH resulted in a desensitization of the [Ca²⁺]i response to LHRH but not to the calcium ionophore A23187. LHRH treatment accelerated [Ca²⁺]i depletion in granulosa cells perifused with Ca²⁺ free medium, indicating the involvement of intracellular Ca²⁺ pool(s) in [Ca²⁺]i changes induced by LHRH. The complex interactions between the signal transduction pathways involved in the regulation of progesterone and prostaglandin E₂ were also examined. LHRH increased basal progesterone level (5 and 24h culture) and attenuated progesterone production induced by follicle-stimulating hormone (FSH) or cholera toxin (24h). On the other hand, both basal and FSH or cholera toxin stimulated prostaglandin E₂ formation were increased by LHRH (5 and 24h) . A23187, TPA and melittin (an activator of phospholipase A₂) were used to examine the roles of Ca²⁺, protein kinase C and free arachidonic acid, respectively, in LHRH action. Melittin stimulated basal progesterone and prostaglandin E₂ production, and enhanced the stimulation of prostaglandin E₂ by LHRH, A23187 and TPA, indicating that LHRH alters cyclooxygenase activity. A23187 or TPA attenuated the formation of progesterone induced by FSH or cholera toxin (5 and 24h). In contrast, A23187 and TPA augmented cholera toxin or FSH induced prostaglandin E₂ formation. The stimulatory effects of A23187 and TPA on prostaglandin E₂ were synergistic, whether or not FSH or cholera toxin was present during the incubation. The role of arachidonic acid in the action of LHRH was further investigated. Arachidonic acid enhanced progesterone production in a dose dependent manner and potentiated TPA induced progesterone production. The stimulatory effect of arachidonic acid was blocked by nordihydroguaiaretic acid, whereas monohydroxyeicosatetraenoic acids and hydroperoxyeicosatetraenoic acid mimicked the effect of arachidonic acid, suggesting the involvement of lipoxygenase metabolites in LHRH action. In addition, arachidonic acid partially reversed the inhibitory action of LHRH and TPA on FSH induced progesterone production. Although arachidonic acid, TPA and LHRH stimulated progesterone production, arachidonic acid only slightly elevated 20-alpha-hydroxy- progesterone production as compared to that induced by LHRH and TPA. These results suggest that arachidonic acid or its metabolites have a stimulatory role in the action of LHRH on the de novo synthesis of ovarian steroid hormones. Collectively, these findings support the hypothesis that the actions of LHRH or LHRH like peptides on ovarian hormone production are mediated by multiple second messengers involving Ca²⁺, protein kinase C and arachidonic acid metabolites.
Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
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Kallmeier, Robert Charles. "Molecular studies of luteinizing hormone-releasing hormones in the brain of domestic fowl." Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306719.

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顔秀慧 and S. W. Ngan. "Transcriptional regulation of the human gonadotropin releasing hormonereceptor gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31240847.

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Albertson, Asher J. "Extra-pituitary functions for GnRH." Laramie, Wyo. : University of Wyoming, 2007. http://proquest.umi.com/pqdweb?did=1313910061&sid=1&Fmt=2&clientId=18949&RQT=309&VName=PQD.

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Ngan, S. W. "Transcriptional regulation of the human gonadotropin releasing hormone receptor gene /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21687584.

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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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Wibullaksanakul, Sunee. "Regulation of gonadotropin releasing hormone (GnRH) secretion : in-vitro studies in the male rat." Thesis, The University of Sydney, 1992. https://hdl.handle.net/2123/26487.

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The study described in this thesis was carried out between 1986—1990 while the author was a postgraduate candidate at The University of Sydney, and in receipt of a scholarship from the Australian International Development Assistance Bureau (AIDAB), Department of Foreign Affairs and Trade. The author would like to thank AIDAB for its financial support. During this time, all experimental work and data analysis was carried out by the author, with excellent technical assistance from Mrs Jennifer Spaliviero and Miss Elsa Kidston. Experimental work involving animals was approved by the University of Sydney Animal Ethics Review Committee. Matters of design and interpretation were closely supervised by Associate Professor David J Handelsman, whose invaluable advice the author wishes to acknowledge. This thesis has been arranged into six related chapters. The first section is a literature review. This section outlines the current state of knowledge concerning general~ aspects of gonadotropin—releasing hormone (GnRH) function, regulatory mechanisms of hypothalamic GnRH secretion, and the methodology suitable for investigation of the regulatory mechanisms of GnRH secretion from the medial basal hypothalamus (MBH) of adult male rats. Both systems are compared for features of methodological integrity, including stability of baseline GnRH release and technical limitations or artefacts. In the third part of this work, these in-vitro methods are applied to examine the effect of castration on GnRH secretion, the results of which are discussed in chapter three. The fourth section of this project concerns the effects of steroids, opioids and noradrenergic signals on GnRH secretion from MBH of adult male rats. In the fifth section of this project, the effect of experimental uremia as a model disease on GnRH secretion is addressed. The last chapter of this project is a summary and discussion. Since each chapter is discussed in detail, the final section is an overview of the content of previous chapters.
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Books on the topic "Luteinizing hormone releasing hormone"

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P, Bouchard, Ipsen-Biotech, and International Symposium on GnRH, GnRH Analogs, and Gonadal Peptides (1989 : Paris, France), eds. Recent progress on GnRH and gonadal peptides: Proceedings of the international symposium, Paris, 16-17 September 1989. Amsterdam: Elsevier, 1990.

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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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International Symposium on GnRH Analogues in Cancer and Human Reproduction (4th 1996 Geneva, Switzerland). GnRH analogues the state of the art 1996: A summary of the 4th International Symposium on GnRH Analogues in Cancer and Human Reproduction, Geneva, February 1996. New York: Parthenon Pub. Group, 1996.

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

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D, Klingmüller, and Wildt L, eds. GnRH analogues in therapy. Stuttgart: G. Thieme, 1994.

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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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International Symposium on GnRH Analogues in Cancer and Human Reproduction (8th 2005 Salzburg, Austria). GnRH analogs in human reproduction. London: Taylor & Francis, 2005.

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1941-, Vickery Brian H., and Lunenfeld Bruno, eds. GnRH analogues in cancer and human reproduction. Dordrecht: Kluwer Academic Publishers, 1989.

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W, Shaw Robert, ed. The Control and stimulation of follicular growth. Carnforth, Lancs., UK: Parthenon Pub. Group, 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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Book chapters on the topic "Luteinizing hormone releasing hormone"

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Jan, Yuh Nung, and Lily Yeh Jan. "Luteinizing Hormone-Releasing Hormone." In Neurotransmitter Actions in the Vertebrate Nervous System, 459–78. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4961-7_16.

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Denis, L. "Luteinizing Hormone Releasing Hormone Agonists." In The Medical Management of Prostate Cancer, 49–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73238-6_7.

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Engel, J. B., and K. Diedrich. "Luteinizing Hormone-releasing Hormone Antagonists in Gynecology." In Peptides and Non Peptides of Oncologic and Neuroendocrine Relevance, 29–38. Milano: Springer Milan, 2003. http://dx.doi.org/10.1007/978-88-470-2085-6_3.

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Kolb, Vera M. "Luteinizing hormone regulators: Luteinizing hormone releasing hormone analogs, estrogens, opiates, and estrogen-opiate hybrids." In Progress in Drug Research / Fortschritte der Arzneimittelforschung / Progrès des recherches pharmaceutiques, 39–52. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7153-2_3.

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Haviv, Fortuna, Timothy D. Fitzpatrick, Charles J. Nichols, Eugene N. Bush, Gilbert Diaz, Hugh N. Nellans, Daniel J. Hoffman, et al. "Metabolically stabilized agonists of luteinizing hormone-releasing hormone (LHRH)." In Peptides, 54–56. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2264-1_15.

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Lascelles, P. T., and D. Donaldson. "Gonadotrophin-Releasing Hormone (Gn-RH, luteinizing hormone/follicle-stimulating hormone-releasing hormone, LH/FSH-RH) Stimulation Test." In Diagnostic Function Tests in Chemical Pathology, 77–78. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1846-7_40.

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Haviv, F., T. D. Fitzpatrick, C. J. Nichols, E. N. Bush, G. Diaz, G. Bammert, A. T. Nguyen, et al. "Active reduced size octapeptide analogues of luteinizing hormone-releasing hormone." In Peptides, 400–402. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0683-2_130.

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Crawford, E. David, and Marilyn A. Davis. "Luteinizing Hormone-Releasing Hormone Analogues in the Treatment of Prostate Cancer." In Cancer Treatment and Research, 25–38. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1731-9_2.

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Harvey, Harold A. "Luteinizing Hormone-Releasing Hormone Agonists in the Treatment of Breast Cancer." In Cancer Treatment and Research, 39–49. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1731-9_3.

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Schwanzel-Fukuda, Marlene, and Donald W. Pfaff. "Theories of Luteinizing Hormone Releasing Hormone Neuronal Migration: Mechanisms and Biological Importance." In Modes of Action of GnRH and GnRH Analogs, 131–43. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_9.

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Conference papers on the topic "Luteinizing hormone releasing hormone"

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Olivos, David J., Mary R. Saunders, Yuanpei Li, Nasir Al Awwad, and Kit S. Lam. "Abstract A37: Discovery of novel luteinizing hormone releasing hormone (LHRH) peptides as a nanotherapeutic targeting drug delivery system for prostate, ovarian, breast, and cervical cancers." In Abstracts: Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Oct 27–30, 2012; San Diego, CA. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1055-9965.disp12-a37.

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Lee, Irene, Swathi Prabhu, Meenakshi Singhal, Alice Tor, and Gert Cauwenberghs. "Luteinizing Hormone Dynamics in Menstruation." In 2022 44th Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2022. http://dx.doi.org/10.1109/embc48229.2022.9871940.

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Lucas, Rudolf, Supruya Sridhar, Boris Gorshkov, Richard White, Nagavedi S. Umapathy, Evgeny Zemskov, Guang Yang, et al. "Growth Hormone Releasing Hormone Agonist Protects From Pneumolysin-Induced Pulmonary Permeability." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3664.

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Wang, Qin. "Analysis of Luteinizing Hormone Beta-Subunit Gene in Mammal." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.68.

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Catanuto, P., X. Xia, S. Pereira-Simon, A. Schally, S. Elliot, and M. K. Glassberg Csete. "MIA602 Downregulates Bleomycin-Induced Fibrosis Mediated by Growth Hormone-Releasing Hormone Receptor Activation." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2225.

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Jackson, R. M., T. Cui, M. Wangpaichitr, W. Sha, and A. V. Schally. "Growth Hormone Releasing Hormone Receptor (GHRH-R) Mediates Alveolar Epithelial Type 2 Cell Inflammation." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4379.

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Liu, Juntao, Zhuang Kong, Yang Wang, Yan Fan, Jinping Luo, Shengwei Xu, Hongyan Jin, and Xinxia Cai. "A rapid quantitative determination method of Luteinizing hormone with gold immunochromatographic strip." In 2017 39th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2017. http://dx.doi.org/10.1109/embc.2017.8036752.

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Jackson, R. M., T. Cui, M. Wangpaichitr, and A. V. Schally. "Alveolar Type 2 Cell Growth Hormone Releasing Hormone Receptor (GHRH-R) Modulates Inflammatory and Fibrotic Signaling." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5665.

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Jackson, Robert M., Lin Ai, Chongxu Zhang, Gaetan Delcroix, Tengjiao Cui, Xianyang Zhang, Mehdi Mirsaeidi, Aaron Lazerson, and Andrew Schally. "Growth hormone-releasing hormone receptor antagonist MIA-602 modulates mouse lung inflammation and fibrosis due to bleomycin." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa5349.

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"The Correlation between Luteinizing hormone, Follicle stimulating hormone, Testosterone, and Prolactin Level at Different Depression Level in Polycystic Ovary Syndrome Patients." In 5th International Conference on Applied Science Energy and Environment. Ishik University, 2018. http://dx.doi.org/10.23918/icasee2018.12.

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Reports on the topic "Luteinizing hormone releasing hormone"

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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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Zeitler, Philip S. The Physiology of Growth Hormone-Releasing Hormone (GHRH) in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada396677.

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Zeitler, Philip S. The Physiology of Growth Hormone-Releasing Hormone (GHRH) in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada407126.

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Zeitler, Philip S. The Physiology of Growth Hormone-Releasing Hormone (GHRH) in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada418139.

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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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El Halawani, Mohamed, and Israel Rozenboim. Environmental factors affecting the decline in reproductive efficiency of turkey hens: Mediation by vasoactive intestinal peptide. United States Department of Agriculture, January 2007. http://dx.doi.org/10.32747/2007.7696508.bard.

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Reproductive failure associated with heat stress is a well known phenomenon in avian species. Increased prolactin (PRL) levels in response to heat stress have been suggested as a mechanism involved in this reproductive malfunction. To test this hypothesis, laying female turkeys were subjected to 40°C for 12 h during the photo-phase daily or maintained at 24–26°C. Birds in each group received oral treatment with parachlorophenyalanine (PCPA; 50 mg/kg BW/day for 3 days), an inhibitor of serotonin (5-HT) biosynthesis; or immunized against vasoactive intestinal peptide (VIP). Both treatments are known to reduce circulating PRL levels. Non treated birds were included as controls. In the control group, high ambient temperature terminated egg laying, induced ovarian regression, reduced plasma luteinizing hormone (LH) and ovarian steroids (progesterone, testosterone, estradiol) levels, and increased plasma PRL levels and the incidence of incubation behavior. Pretreatment with PCPA reduced (P< 0.05) heat stress-induced decline in egg production, increase in PRL levels, and expression of incubation behavior. Plasma LH and ovarian steroid levels of heat stressed birds were restored to that of controls by PCPA treatment. As in PCPA-treated birds, VIP immunoneutralization of heat-stressed turkeys reduced (P< 0.05) circulating PRL levels and prevented the expression of incubation behavior. But it did not restore the decline in LH, ovarian steroids, and egg production (P> 0.05). The present findings indicate that the detrimental effect of high temperature on reproductive performance may not be related to the elevated PRL levels in heat-stressed birds but to mechanism(s) that involve 5-HT neurotransmission and the induction of hyperthermia.
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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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A hormone-releasing coil is best for relieving heavy periods. National Institute for Health Research, September 2015. http://dx.doi.org/10.3310/signal-000127.

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