Journal articles on the topic 'Luteinizing hormone releasing hormone'

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Puger, I. Gusti Ngurah. "HORMON YANG BERPERAN DALAM PEMBENTUKAN SPERMATOZOA DAN OVUM." Daiwi Widya 9, no. 2 (January 17, 2023): 1–17. http://dx.doi.org/10.37637/dw.v9i2.1181.

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AbstractNormal men after stepping into the adolescent phase, they must produce sperm. Likewise, normal women after reaching the adolescent phase, they must produce ovum. However, there are still many men and women who have produced sperm or ovum and do not know about the hormones that affect on producing sperm or ovum. In males, the hypothalamus secretes releasing factors and stimulates the anterior pituitary gland to produce follicle stimulating hormone (FSH) and interstitial cell stimulating hormone (ICSH). The combination of FSH and ICSH will stimulate the testes to produce the hormone testosterone. The hormone testosterone is responsible for sperm production, penis growth, facial hair, and widening of the shoulders. In women, the hypothalamus secretes releasing factors and stimulates the anterior pituitary gland to produce follicle stimulating hormone (FSH) and luteinizing hormone (LH). FSH stimulates young follicles until they become mature follicles. Mature follicles due to the influence of luteinizing hormone will rupture, so that the ovum is released from the follicle. Follicles that no longer contain ovum will turn into a corpus luteum. The corpus luteum then produces the hormones progesterone and estrogen to keep the corpus luteum from being damaged.Keywords: Hormones, sperm formation, and ovum formation.
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12

Rasgon, Natalie L., Lara Pumphrey, Paolo Prolo, Shana Elman, Andre B. Negrao, Julio Licinio, and Alan Garfinkel. "Emergent Oscillations in Mathematical Model of the Human Menstrual Cycle." CNS Spectrums 8, no. 11 (November 2003): 805–14. http://dx.doi.org/10.1017/s1092852900019246.

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ABSTRACTBackground:The aim of this study was to develop a mathematical model of the hypothalamo-pituitary-gonadal axis that would reflect available data in humans.Methods:A model of hormonal relationships at the early follicular and midluteal phases of the human menstrual cycle is proposed.Findings:Two distinct temporal patterns of oscillatory behavior have been demonstrated for both pituitary and gonadal steroids in the early follicular phase: first, rapid oscillations in gonadotropin releasing hormone, follicle stimulating hormone, and luteinizing hormone (Q∼1 hour) that were an immediate consequence of the programmed equations. Second, there were slower, undulating, emergent rhythms in luteinizing hormone and follicle stimulating hormone, and also in estrogen, having oscillatory periods of 2–12 hours. There was also a longer-period (Q2–3 days) emergent rhythm in progesterone. In the mid-luteal phase, estrogen and progesterone rhythms were correlated, and all hormones showed an ∼6-hour periodicity.Conclusion:To our knowledge, the oscillatory behavior of peripheral sex steroids in the follicular phase has not been previously noted.
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13

MacDonald, R. D., and R. D. Page. "Luteinizing Hormone Response to Pulsatile Luteinizing Hormone-Releasing Hormone in Prepubertal Heifers." Journal of Dairy Science 69, no. 7 (July 1986): 1922–31. http://dx.doi.org/10.3168/jds.s0022-0302(86)80619-1.

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14

Leshin, L. S., R. R. Kraeling, C. R. Barb, and G. B. Rampacek. "Associated luteinizing hormone-releasing hormone and luteinizing hormone secretion in ovariectomized gilts." Domestic Animal Endocrinology 9, no. 1 (January 1992): 77–88. http://dx.doi.org/10.1016/0739-7240(92)90011-l.

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15

Schwanzel-Fukuda, Marlene, and Donald W. Pfaff. "Origin of luteinizing hormone-releasing hormone neurons." Nature 338, no. 6211 (March 1989): 161–64. http://dx.doi.org/10.1038/338161a0.

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16

Balmaceda, Jose, Claudia Borrero, and Ricardo Asch. "Luteinizing Hormone - Releasing Hormone Analogs: Female Contraception." Seminars in Reproductive Medicine 5, no. 04 (November 1987): 371–80. http://dx.doi.org/10.1055/s-2007-1021883.

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17

de Boer, Hans, Petri van Gastel, and Adriaan van Sorge. "Luteinizing Hormone–Releasing Hormone and Postmenopausal Flushing." New England Journal of Medicine 361, no. 12 (September 17, 2009): 1218–19. http://dx.doi.org/10.1056/nejmc0905923.

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18

McDonough, Paul G., Andrew V. Schally, Gabor Halmos, and Jacek Pinski. "Terminology for Luteinizing Hormone-Releasing Hormone Antagonists." Fertility and Sterility 64, no. 1 (July 1995): 226. http://dx.doi.org/10.1016/s0015-0282(16)57696-1.

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19

Wray, S. "Development of Luteinizing Hormone Releasing Hormone Neurones." Journal of Neuroendocrinology 13, no. 1 (January 2001): 3–11. http://dx.doi.org/10.1111/j.1365-2826.2001.00609.x.

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20

Simerska, Pavla, Hoi Lai, and Istvan Toth. "Luteinizing Hormone Releasing Hormone/Galactose Core/Lipopeptide." Molbank 2015, no. 4 (December 16, 2015): M881. http://dx.doi.org/10.3390/m881.

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21

Wray, S. "Development of Luteinizing Hormone Releasing Hormone Neurones." Journal of Neuroendocrinology 13, no. 1 (January 2001): 3–11. http://dx.doi.org/10.1046/j.1365-2826.2001.00609.x.

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22

Silversides, D. W., A. F. Allen, V. Misra, L. Qualtiere, R. J. Mapletoft, and B. D. Murphy. "A synthetic luteinizing hormone releasing hormone vaccine." Journal of Reproductive Immunology 13, no. 3 (August 1988): 249–61. http://dx.doi.org/10.1016/0165-0378(88)90005-8.

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23

TIWARY, CHANDRA M. "Luteinizing Hormone Releasing Hormone and Human Behavior." Archives of Pediatrics & Adolescent Medicine 142, no. 7 (July 1, 1988): 699. http://dx.doi.org/10.1001/archpedi.1988.02150070013005.

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24

Oerter, KE, PK Manasco, KM Barnes, J. Jones, S. Hill, and GB Cutler Jr. "Effects of luteinizing hormone-releasing hormone agonists on final height in luteinizing hormone-releasing hormone-dependent precocious puberty." Acta Paediatrica 82 (January 21, 2008): 62–68. http://dx.doi.org/10.1111/j.1651-2227.1993.tb12846.x.

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25

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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26

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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27

Walker, Greg F., Robin Ledger, and Ian G. Tucker. "Activity of pancreatic endopeptidases towards luteinizing hormone-releasing hormones." International Journal of Pharmaceutics 216, no. 1-2 (March 23, 2001): 77–82. http://dx.doi.org/10.1016/s0378-5173(01)00571-3.

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28

AMARANT, Tanchum, Mati FRIDKIN, and Yitzhak KOCH. "Luteinizing Hormone-Releasing Hormone and Thyrotropin-Releasing Hormone in Human and Bovine Milk." European Journal of Biochemistry 127, no. 3 (March 3, 2005): 647–50. http://dx.doi.org/10.1111/j.1432-1033.1982.tb06921.x.

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29

Bhasin, Shalender, and Ron Swerdloff. "Contraceptive Studies with Luteinizing Hormone - Releasing Hormone Agonists." Seminars in Reproductive Medicine 5, no. 04 (November 1987): 381–87. http://dx.doi.org/10.1055/s-2007-1021884.

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30

Moretto, M., F. J. López, and A. Negro-Vilar. "Nitric oxide regulates luteinizing hormone-releasing hormone secretion." Endocrinology 133, no. 5 (November 1993): 2399–402. http://dx.doi.org/10.1210/endo.133.5.8104781.

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31

Nabors, W., and E. D. Crawford. "Luteinizing Hormone Releasing Hormone Agonists: The US Experience." Journal of International Medical Research 18, no. 1_suppl (January 1990): 31–34. http://dx.doi.org/10.1177/03000605900180s106.

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32

Stricker, Hans J. "Luteinizing hormone–releasing hormone antagonists in prostate cancer." Urology 58, no. 2 (August 2001): 24–27. http://dx.doi.org/10.1016/s0090-4295(01)01238-9.

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33

MacLeod, Tara L., Abraham Eisen, and Gordon L. Sussman. "Anaphylactic reaction to synthetic luteinizing hormone-releasing hormone." Fertility and Sterility 48, no. 3 (September 1987): 500–502. http://dx.doi.org/10.1016/s0015-0282(16)59428-x.

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34

Tucker, S. "Cost Savings and Luteinizing Hormone-Releasing Hormone Agonist." Journal of Oncology Practice 2, no. 3 (May 1, 2006): 103. http://dx.doi.org/10.1200/jop.2.3.103.

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35

Tucker, Steven. "Cost Savings and Luteinizing Hormone–Releasing Hormone Agonist." Journal of Oncology Practice 2, no. 3 (May 2006): 103. http://dx.doi.org/10.1200/jop.2006.2.3.103.

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36

MAHEUX, RODOLPHE, CHANTAL GUILLOTEAU, ANDRÉ LEMAY, ADRIEN BASTIDE, and ATILLA T. A. FAZEKAS. "Luteinizing Hormone-releasing Hormone Agonist and Uterine Leiomyoma." Obstetrical & Gynecological Survey 41, no. 3 (March 1986): 167–68. http://dx.doi.org/10.1097/00006254-198603000-00013.

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37

Mayagoitia, S. B., C. Hernández-Morales, A. M. T. Macías, and R. R. Vega. "Luteinizing hormone releasing hormone agonist for postpartum contraception." Advances in Contraception 12, no. 1 (March 1996): 27–41. http://dx.doi.org/10.1007/bf01849544.

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38

Brown, D., A. E. Herbison, J. E. Robinson, R. W. Marrs, and G. Leng. "Modelling the luteinizing hormone-releasing hormone pulse generator." Neuroscience 63, no. 3 (December 1994): 869–79. http://dx.doi.org/10.1016/0306-4522(94)90531-2.

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39

Keller, Gunhild, Andrew V. Schally, Timo Gaiser, Attila Nagy, Benjamin Baker, Gabriela Westphal, Gabor Halmos, and Jörg B. Engel. "Human Malignant Melanomas Express Receptors for Luteinizing Hormone Releasing Hormone Allowing Targeted Therapy with Cytotoxic Luteinizing Hormone Releasing Hormone Analogue." Cancer Research 65, no. 13 (July 1, 2005): 5857–63. http://dx.doi.org/10.1158/0008-5472.can-04-3816.

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40

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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41

SOLOMON, ABBY L., and ROBERT A. SHALWITZ. "Elevated Cord Human Chorionic Gonadotropin in Leprechaunism." Pediatrics 90, no. 3 (September 1, 1992): 466–68. http://dx.doi.org/10.1542/peds.90.3.466.

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Many of the distinguishing features of leprechaunism (Donohue's syndrome) suggest abnormalities of endocrine regulation. Prominent genitalia, rugation of the labioscrotal folds, polycystic ovaries, and precocious puberty are associated with leprechaunism,1 and these characteristics indicate possible pathology in the hypothalamic-pituitary-gonadal axis. In the few reported cases of leprechaunism in which this area has been evaluated, no consistent biochemical abnormalities have emerged. A review by Elders et al1 describes three cases in which baseline gonadotropin levels were normal, and gonadotropin-releasing hormone response in the one patient tested was normal.1 Szilagyi et al, however, reported a single case in which baseline luteinizing hormone was extremely elevated (385 mIU/mL) and did not respond to luteinizing hormone-releasing hormone, whereas baseline follicle-stimulating hormone was slightly elevated (13.0 mIU/mL) and had an exaggerated response to luteinizing hormone-releasing hormone.2
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42

Tena-Sempere, Manuel, and Ilpo Huhtaniemi. "Sex in the brain: How the brain regulates reproductive function." Biochemist 31, no. 2 (April 1, 2009): 4–7. http://dx.doi.org/10.1042/bio03102004.

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Reproductive functions are maintained by a complex hormonal regulatory network called the hypothalamic–pituitary–gonadal (HPG) axis, which is under the hierarchical control of a network of neurohormones that ultimately modulate the synthesis and pulsatile release of the decapeptide gonadotropin-releasing hormone (GnRH) by specialized neural cells distributed along the mediobasal hypothalamus. This neuropeptide drives the production of the two gonadotropic hormones of the anterior pituitary gland, luteinizing hormone (LH) and folliclestimulating hormone (FSH), which are released into the circulation and regulate specific functions of the ovary and testis. In turn, hormones produced by the gonads feed back to the hypothalamic– pituitary level to maintain functional balance of the HPG axis, through negative and positive (only in females) regulatory loops. In this article, we review the main hormonal regulatory systems that are operative in the HPG axis with special emphasis on recent developments in our knowledge of the neuroendocrine pathways governing GnRH secretion, including the identification of kisspeptins and G-protein-coupled receptor 54 (GPR54) as major gatekeepers of puberty onset and fertility.
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43

Schillo, K. K., L. S. Leshin, D. Kuehl, and G. L. Jackson. "Simultaneous Measurement of Luteinizing Hormone-releasing Hormone and Luteinizing Hormone during Estradiol-induced Luteinizing Hormone Surges in the Ovariectomized Ewe1." Biology of Reproduction 33, no. 3 (October 1, 1985): 644–52. http://dx.doi.org/10.1095/biolreprod33.3.644.

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44

Ciocca, Daniel R., Libertad A. Puy, Liliana C. Fasoli, Olga Tello, Juan C. Aznar, Francisco E. Gago, Sara I. Papa, and Roberto Sonego. "Corticotropin-releasing hormone, luteinizing hormone-releasing hormone, growth hormone-releasing hormone, and somatostatin-like immunoreactivities in biopsies from breast cancer patients." Breast Cancer Research and Treatment 15, no. 3 (May 1990): 175–84. http://dx.doi.org/10.1007/bf01806354.

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Lee, W. S., M. S. Smith, and G. E. Hoffman. "Luteinizing hormone-releasing hormone neurons express Fos protein during the proestrous surge of luteinizing hormone." Proceedings of the National Academy of Sciences 87, no. 13 (July 1, 1990): 5163–67. http://dx.doi.org/10.1073/pnas.87.13.5163.

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Won, Ho-Shik. "NMR Studies of Metal-binding Luteinizing Hormone Releasing Hormone." Bulletin of the Korean Chemical Society 32, no. 11 (November 20, 2011): 4021–26. http://dx.doi.org/10.5012/bkcs.2011.32.11.4021.

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HO, TERESA L., JOHN J. NESTOR, GEORGIA I. McCRAE, and BRIAN H. VICKERY. "Hydrophobic, aza-glycine analogues of luteinizing hormone-releasing hormone." International Journal of Peptide and Protein Research 24, no. 1 (January 12, 2009): 79–84. http://dx.doi.org/10.1111/j.1399-3011.1984.tb00931.x.

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Rick, Ferenc G., Norman L. Block, and Andrew V. Schally. "Agonists of luteinizing hormone-releasing hormone in prostate cancer." Expert Opinion on Pharmacotherapy 14, no. 16 (August 28, 2013): 2237–47. http://dx.doi.org/10.1517/14656566.2013.834328.

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Wong, P. C., and Ricardo Asch. "Induction of Follicular Development with Luteinizing Hormone - Releasing Hormone." Seminars in Reproductive Medicine 5, no. 04 (November 1987): 399–409. http://dx.doi.org/10.1055/s-2007-1021886.

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Archer, David. "Use of Luteinizing Hormone-Releasing Hormone for Ovulation Induction." Seminars in Reproductive Medicine 4, no. 03 (August 1986): 285–91. http://dx.doi.org/10.1055/s-2007-1022507.

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