Academic literature on the topic 'Antagonista GnRH'
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Journal articles on the topic "Antagonista GnRH"
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Chianese, Rosanna, Vincenza Ciaramella, Donatella Scarpa, Silvia Fasano, Riccardo Pierantoni, and Rosaria Meccariello. "Anandamide regulates the expression of GnRH1, GnRH2, and GnRH-Rs in frog testis." American Journal of Physiology-Endocrinology and Metabolism 303, no. 4 (2012): E475—E487. http://dx.doi.org/10.1152/ajpendo.00086.2012.
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Gonadotropin-releasing hormone (either GnRH1 or GnRH2) exerts a local activity in vertebrate testis, including human testis. Relationships between endocannabinoid (eCB) and GnRH systems in gonads have never been elucidated in any species so far. To reveal a cross-talk between eCBs and GnRH at testicular level, we characterized the expression of GnRH ( GnRH1 and GnRH2) as well as GnRH receptor ( GnRH-R1, -R2, and -R3) mRNA in the testis of the anuran amphibian Rana esculenta during the annual sexual cycle; furthermore, the corresponding transcripts were localized inside the testis by in situ hybridization. The possible endogenous production of the eCB, anandamide (AEA), was investigated in testis by analyzing the expression of its biosynthetic enzyme, Nape-pld. Incubations of testis pieces with AEA were carried out in the postreproductive period (June) and in February, when a new spermatogenetic wave takes place. In June, AEA treatment significantly decreased GnRH1 and GnRH-R2 mRNA, stimulated the transcription of GnRH2 and GnRH-R1, and did not affect GnRH-R3 expression. In February, AEA treatment upregulated GnRH2 and GnRH-R3 mRNA, downregulated GnRH-R2, and did not affect GnRH1 and GnRH-R1 expression. These effects were mediated by type 1 cannabinoid receptor ( CB1) since they were fully counteracted by SR141716A (Rimonabant), a selective CB1 antagonist. In conclusion, eCB system modulates GnRH activity in frog testis during the annual sexual cycle in a stage-dependent fashion.
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Leaños-Miranda, Alfredo, Alfredo Ulloa-Aguirre, Laura A. Cervini, Jo Ann Janovick, Jean Rivier, and P. Michael Conn. "Identification of new gonadotrophin-releasing hormone partial agonists." Journal of Endocrinology 189, no. 3 (2006): 509–17. http://dx.doi.org/10.1677/joe.1.06724.
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GnRH agonists or antagonists are currently utilized as therapeutic agents in a number of diseases. A side-effect of prolonged treatment with GnRH analogues is hypoestrogenism. In this study, we tested the in vitro potency of different GnRH analogues originally found to be partial agonists (i.e. analogues with decreased efficacy for activating or stimulating their cognate receptor) as well as novel analogues, to identify compounds that might potentially be useful for partial blockade of gonadotrophin release. Cultured COS-7 cells transiently expressing the rat or human GnRH receptor (GnRHR) were exposed to increasing concentrations (10−8 to 10−5 M) of GnRH analogues (c(4–10)[Asp4,DNal6,Dpr10]-GnRH; c(4–10) [Dpr4,DNal6,Asp10]-GnRH; c(4–10)[Cys4,10,DNal6]-GnRH; c[Eaca1,DNal6]-GnRH; c[Gly1,DNal6]-GnRH; c[βAla1,DTrp6]-GnRH; c[Dava1,DNal6]-GnRH; c[Gaba1, DNal6]-GnRH), and the ability of these analogues to provoke or antagonize GnRH-stimulated inositol phosphate production was assessed. With both human and rat GnRHRs, c[Eaca1,DNal6]-GnRH, c[Gly1,DNal6]-GnRH, c[βAla1,DTrp6]-GnRH and c[Dava1,DNal6]-GnRH exhibited partial agonist activity (35–87% of the maximal efficacy shown by 10−6 M GnRH), whereas c[Gaba1,DNal6]-GnRH behaved as a partial agonist with the human GnRHR and as full agonist with the rat GnRHR. c(4–10)[Asp4, DNal6,Dpr10]-GnRH and c(4–10)[Dpr4,DNal6,Asp10]-GnRH exhibited full antagonist activity with both GnRHRs, and c(4–10) [Cys4,10,DNal6]-GnRH was a weak, partial agonist with the human GnRHR and a full antagonist with the rat GnRHR. With the exception of c[Gaba1,DNal6]-GnRH stimulation of the human GnRHR, and c[Dava1,DNal6]-GnRH and c[Gaba1, DNal6]-GnRH stimulation of the rat GnRHR, all partial agonists also exhibited antagonist activity in the presence of the exogenous full agonist. The results demonstrate that structurally similar analogues display variable potencies and efficacies in vitro for a specific GnRHR as well as for the human versus the rat GnRHR. Their ultimate in vivo usefulness to treat clinical conditions in which complete suppression of gonadotroph activity is not required remains to be investigated.
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Tzoupis, Haralambos, Agathi Nteli, Maria-Eleni Androutsou, and Theodore Tselios. "Gonadotropin-Releasing Hormone and GnRH Receptor: Structure, Function and Drug Development." Current Medicinal Chemistry 27, no. 36 (2020): 6136–58. http://dx.doi.org/10.2174/0929867326666190712165444.
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Background: Gonadotropin-Releasing Hormone (GnRH) is a key element in sexual maturation and regulation of the reproductive cycle in the human organism. GnRH interacts with the pituitary cells through the activation of the Gonadotropin Releasing Hormone Receptors (GnRHR). Any impairments/dysfunctions of the GnRH-GnRHR complex lead to the development of various cancer types and disorders. Furthermore, the identification of GnRHR as a potential drug target has led to the development of agonist and antagonist molecules implemented in various treatment protocols. The development of these drugs was based on the information derived from the functional studies of GnRH and GnRHR. Objective: This review aims at shedding light on the versatile function of GnRH and GnRH receptor and offers an apprehensive summary regarding the development of different agonists, antagonists and non-peptide GnRH analogues. Conclusion: The information derived from these studies can enhance our understanding of the GnRH-GnRHR versatile nature and offer valuable insight into the design of new more potent molecules.
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Weng, Shun-Long, Shu-Ling Tzeng, Chun-I. Lee, et al. "Association between GnRH Receptor Polymorphisms and Luteinizing Hormone Levels for Low Ovarian Reserve Infertile Women." International Journal of Environmental Research and Public Health 18, no. 13 (2021): 7006. http://dx.doi.org/10.3390/ijerph18137006.
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The choice of ovarian stimulation protocols in assisted reproduction technology (ART) cycles for low ovarian reserve patients is challenging. Our previous report indicated that the gonadotrophin-releasing (GnRH) agonist (GnRHa) protocol is better than the GnRH antagonist (GnRHant) protocol for young age poor responders. Here, we recruited 269 patients with anti-Müllerian hormone (AMH) < 1.2 ng/mL undergoing their first ART cycles for this nested case-control study. We investigated the genetic variants of the relevant genes, including follicular stimulating hormone receptor (FSHR; rs6166), AMH (rs10407022), GnRH (rs6185), and GnRH receptor (GnRHR; rs3756159) in patients <35 years (n = 86) and patients ≥35 years of age (n = 183). Only the genotype of GnRHR (rs3756159) is distributed differently in young (CC 39.5%, CT/TT 60.5%) versus advanced (CC 24.0%, CT/TT 76.0%) age groups (recessive model, p = 0.0091). Furthermore, the baseline luteinizing hormone (LH) levels (3.60 (2.45 to 5.40) vs. 4.40 (2.91 to 6.48)) are different between CC and CT/TT genotype of GnRHR (rs3756159). In conclusion, the genetic variants of GnRHR (rs3756159) could modulate the release of LH in the pituitary gland and might then affect the outcome of ovarian stimulation by GnRHant or GnRHa protocols for patients with low AMH levels.
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Finch, Ann R., Christopher J. Caunt, Stephen P. Armstrong, and Craig A. McArdle. "Plasma Membrane Expression of Gonadotropin-Releasing Hormone Receptors: Regulation by Peptide and Nonpeptide Antagonists." Molecular Endocrinology 24, no. 2 (2010): 423–35. http://dx.doi.org/10.1210/me.2009-0343.
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Abstract Gonadotropin-releasing hormone acts via cell surface receptors but most human (h) GnRH receptors (GnRHRs) are intracellular. A membrane-permeant nonpeptide antagonist [(2S)-2-[5-[2-(2-axabicyclo[2.2.2]oct-2-yl)-1,1-dimethy-2-oxoethyl]-2-(3,5-dimethylphenyl)-1H-indol-3-yl]-N-(2-pyridin-4-ylethyl)propan-1-amine (IN3)] increases hGnRHR expression at the surface, apparently by facilitating its exit from the endoplasmic reticulum. Here we have quantified GnRHR by automated imaging in HeLa cells transduced with adenovirus expressing hemagglutinin-tagged GnRHR. Consistent with an intracellular site of action, IN3 increases cell surface hGnRHR, and this effect is not blocked or mimicked by membrane-impermeant peptide antagonists [Ac-D2Nal-D4Cpa-D3Pal-Ser-Tyr-d-Cit-Leu-Arg-Pro-d-Ala-NH2 (cetrorelix) and antide]. However, when the C-terminal tail of a Xenopus (X) GnRHR was added (h.XGnRHR) to increase expression, both peptides further increased cell surface GnRHR. Cetrorelix also synergized with IN3 to increase expression of hGnRHR and a G-protein coupling-deficient mutant (A261K-hGnRHR). Cetrorelix also increased cell surface expression of hGnRHR, h.XGnRHR, and mouse GnRHR in gonadotrope-lineage LβT2 cells, and in HeLa cells it slowed h.XGnRHR internalization (measured by receptor-mediated antihemagglutinin uptake). Thus cetrorelix has effects other than GnRHR blockade; it acts as an inverse agonist in internalization assays, supporting the potential importance of ligand-biased efficacy at GnRHR. We also developed an imaging assay for GnRH function based on Ca2+-dependent nuclear translocation of a nuclear factor of activated T cells reporter. Using this in HeLa and LβT2 cells, IN3 and cetrorelix behaved as competitive antagonists when coincubated with GnRH, and long-term pretreatment (16 h) with IN3 reduced its effectiveness as an inhibitor whereas pretreatment with cetrorelix increased its inhibitory effect. This distinction between peptide and nonpeptide antagonists may prove important for therapeutic applications of GnRH antagonists.
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Rosan, Pedro Luís, Gustavo Salata Romão, Rosana Maria dos Reis, Marcos Dias de Moura, and Rui Alberto Ferriani. "Uso de antagonista de GnRH (cetrorelix) em dose única para evitar ovulações prematuras em ciclos de fertilização assistida." Revista Brasileira de Ginecologia e Obstetrícia 25, no. 8 (2003): 563–69. http://dx.doi.org/10.1590/s0100-72032003000800004.
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Sperduti, Samantha, Silvia Limoncella, Clara Lazzaretti, et al. "GnRH Antagonists Produce Differential Modulation of the Signaling Pathways Mediated by GnRH Receptors." International Journal of Molecular Sciences 20, no. 22 (2019): 5548. http://dx.doi.org/10.3390/ijms20225548.
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Commercial gonadotropin-releasing hormone (GnRH) antagonists differ by 1–2 amino acids and are used to inhibit gonadotropin production during assisted reproduction technologies (ART). In this study, potencies of three GnRH antagonists, Cetrorelix, Ganirelix and Teverelix, in inhibiting GnRH-mediated intracellular signaling, were compared in vitro. GnRH receptor (GnRHR)-transfected HEK293 and neuroblastoma-derived SH-SY5Y cell lines, as well as mouse pituitary LβT2 cells endogenously expressing the murine GnRHR, were treated with GnRH in the presence or absence of the antagonist. We evaluated intracellular calcium (Ca2+) and cAMP increases, cAMP-responsive element binding-protein (CREB) and extracellular-regulated kinase 1 and 2 (ERK1/2) phosphorylation, β-catenin activation and mouse luteinizing-hormone β-encoding gene (Lhb) transcription by bioluminescence resonance energy transfer (BRET), Western blotting, immunostaining and real-time PCR as appropriate. The kinetics of GnRH-induced Ca2+ rapid increase revealed dose-response accumulation with potency (EC50) of 23 nM in transfected HEK293 cells, transfected SH-SY5Y and LβT2 cells. Cetrorelix inhibited the 3 × EC50 GnRH-activated calcium signaling at concentrations of 1 nM–1 µM, demonstrating higher potency than Ganirelix and Teverelix, whose inhibitory doses fell within the 100 nM–1 µM range in both transfected HEK293 and SH-SY5Y cells in vitro. In transfected SH-SY5Y, Cetrorelix was also significantly more potent than other antagonists in reducing GnRH-mediated cAMP accumulation. All antagonists inhibited pERK1/2 and pCREB activation at similar doses, in LβT2 and transfected HEK293 cells treated with 100 nM GnRH. Although immunostainings suggested that Teverelix could be less effective than Cetrorelix and Ganirelix in inhibiting 1 µM GnRH-induced β-catenin activation, Lhb gene expression increase occurring upon LβT2 cell treatment by 1 µM GnRH was similarly inhibited by all antagonists. To conclude, this study has demonstrated Cetrorelix-, Ganirelix- and Teverelix-specific biased effects at the intracellular level, not affecting the efficacy of antagonists in inhibiting Lhb gene transcription.
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Schauer, Christian, Tong Tong, Hugues Petitjean, et al. "Hypothalamic gonadotropin-releasing hormone (GnRH) receptor neurons fire in synchrony with the female reproductive cycle." Journal of Neurophysiology 114, no. 2 (2015): 1008–21. http://dx.doi.org/10.1152/jn.00357.2015.
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Gonadotropin-releasing hormone (GnRH) controls mammalian reproduction via the hypothalamic-pituitary-gonadal (hpg) axis, acting on gonadotrope cells in the pituitary gland that express the GnRH receptor (GnRHR). Cells expressing the GnRHR have also been identified in the brain. However, the mechanism by which GnRH acts on these potential target cells remains poorly understood due to the difficulty of visualizing and identifying living GnRHR neurons in the central nervous system. We have developed a mouse strain in which GnRHR neurons express a fluorescent marker, enabling the reliable identification of these cells independent of the hormonal status of the animal. In this study, we analyze the GnRHR neurons of the periventricular hypothalamic nucleus in acute brain slices prepared from adult female mice. Strikingly, we find that the action potential firing pattern of these neurons alternates in synchrony with the estrous cycle, with pronounced burst firing during the preovulatory period. We demonstrate that GnRH stimulation is sufficient to trigger the conversion from tonic to burst firing in GnRHR neurons. Furthermore, we show that this switch in the firing pattern is reversed by a potent GnRHR antagonist. These data suggest that endogenous GnRH acts on GnRHR neurons and triggers burst firing in these cells during late proestrus and estrus. Our data have important clinical implications in that they indicate a novel mode of action for GnRHR agonists and antagonists in neurons of the central nervous system that are not part of the classical hpg axis.
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Chen, Junling, Beum-Soo An, Linan Cheng, Geoffrey L. Hammond та Peter C. K. Leung. "Gonadotropin-Releasing Hormone-Mediated Phosphorylation of Estrogen Receptor-α Contributes to fosB Expression in Mouse Gonadotrophs". Endocrinology 150, № 10 (2009): 4583–93. http://dx.doi.org/10.1210/en.2009-0455.
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Abstract Estrogen receptors (ERs) are activated by their ligands as well as signaling pathways that alter ER phosphorylation in response to peptide hormones and growth factors. In pituitary gonadotrophs, GnRHs act via the type I GnRH receptor (GnRHR). Both GnRH subtypes (GnRH-I and -II) activate an estrogen response element (ERE)-driven luciferase reporter gene in LβT2 mouse pituitary cells, and GnRH-I is most potent in this regard. Moreover, antide (a GnRH antagonist) and a GnRHR small interfering RNA (siRNA) abrogate this effect, whereas an ERα antagonist (ICI 182,780) does not. The ERα in LβT2 cells is phosphorylated at Ser118 in the nucleus and at Ser167 in both nucleus and cytoplasm after GnRH treatments and coincided with increased ERα binding to its coactivator, the p300/cAMP response element-binding protein-associated factor (PCAF). Moreover, siRNA-mediated knockdown of PCAF levels attenuated GnRH-induced ERE-luciferase transactivation in these cells. Most importantly, both GnRH subtypes robustly up-regulated expression of the immediate early response gene, fosB, whereas cotreatment with ERα siRNA or PCAF siRNA attenuated this effect. This appears to occur at the transcriptional level because corecruitment of ERα and PCAF to an ERE within the endogenous fosB promoter was increased by GnRH treatments, as shown by chromatin immunoprecipitation assays. These data demonstrate that GnRH-mediated phosphorylation of ERα in mouse LβT2 pituitary cells results in its rapid association with PCAF and the transcriptional activation of fosB, and we demonstrate that this in turn likely activates other genes in pituitary cells including the FSH β-subunit gene.
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Kawamura, Kazuhiro, Jun Fukuda, Jin Kumagai, et al. "Gonadotropin-Releasing Hormone I Analog Acts as an Antiapoptotic Factor in Mouse Blastocysts." Endocrinology 146, no. 9 (2005): 4105–16. http://dx.doi.org/10.1210/en.2004-1646.
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Abstract Both GnRH-I and its receptor (GnRHR)-I have been shown to be expressed in the mammalian preimplantation embryo. In this study, we investigated the molecular mechanisms of GnRH-I in the regulation of early embryonic development in mouse. We found that GnRH-I and GnRHR-I mRNAs were detectable throughout early embryonic stages and that expression levels of both increased significantly after the early blastocyst stage. In blastocysts, GnRH-I and GnRHR-I expression was detected in both inner cell mass and trophectoderm cells. The pregnant uterus also expressed both genes, suggesting that preimplantation embryos could be affected by GnRH through both paracrine and autocrine signaling. Treatment with GnRH-I agonist, buserelin, promoted development of two-cell-stage embryos to the expanded and hatched blastocyst stages and inhibited apoptosis in a dose-dependent manner. In contrast, treatment with GnRH-I antagonist, ganirelix acetate, inhibited development of preimplantation embryos beyond the expanded blastocyst stage and induced apoptosis; both effects could be reversed by cotreatment with GnRH-I agonist. GnRH-I antagonist-induced cell death was mediated by disruption of mitochondrial function, release of cytochrome c, and activation of caspase-3. Furthermore, treatment with GnRH-I antagonist decreased expression of two antiapoptotic growth factors, epidermal growth factor and IGF-II, in blastocysts. These results indicate that GnRH-I, acting as an antiapoptotic factor, is an important growth factor in development of mouse blastocysts.
Dissertations / Theses on the topic "Antagonista GnRH"
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Cota, Ana Márcia de Miranda [UNESP]. "Agonista versus antagonista do GnRH em ciclos de reprodução assistida: morfologia oocitária." Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/99221.
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Na reprodução assistida, a seleção de gametas com o objetivo de alcançar melhores resultados clínicos é uma tarefa crucial dos embriologistas. A qualidade do oócito é um fator chave na fertilidade feminina, refletindo o potencial intrínseco de desenvolvimento do gameta, além de ter um papel crucial não só na fecundação, mas também no desenvolvimento embrionário subsequente. Após a desnudação, consegue-se definir a maturidade oocitária, com a identificação do primeiro corpúsculo polar, além de permitir a avaliação da morfologia oocitária, analisando as características da zona pelúcida, do espaço perivitelino e do citoplasma. Os dismorfismos oocitários são classificados em 2 tipos: citoplasmáticos, que incluem a presença de granulações e/ou de inclusões citoplasmáticas (vacúolos, corpos refrativos, agregados do retículo endoplasmático) e extracitoplasmáticos (alterações na forma do oócito, alterações na zona pelúcida, no espaço perivitelino e alterações do corpúsculo polar). Essas variações na morfologia oocitária podem ocorrer devido a fatores como idade da mulher, problemas genéticos e alterações no ambiente hormonal a que o oócito é exposto com a hiperestimulação ovariana. A classificação da morfologia oocitária, bem como sua correlação com o desenvolvimento embrionário e taxa de gravidez são bastante controversas na literatura. Vários estudos não demonstram nenhuma associação entre os dismorfismos oocitários e os resultados da fertilização in vitro, enquanto outros relatam uma associação entre a morfologia oocitária e desenvolvimento embrionário. Essas diferenças nos resultados podem ser explicadas devido a utilização de diferentes critérios morfológicos e devido...
The selection of developmentally competent human gametes may increase the efficiency of assisted reproduction. Spermatozoa and oocytes are usually assessed according to morphologic criteria. Oocyte morphology can be affected by the age of the female, genetic aspects, and factors related to controlled ovarian stimulation. However, there is a lack of evidence in the literature concerning the effect of gonadotropin-releasing hormone (GnRH) analogues, either agonists or antagonists, on oocyte morphology. The aim of this randomized study was to investigate if the prevalence of oocyte dysmorphism is influenced by the type of pituitary suppression used in ovarian stimulation. A total of 64 patients at the first intracytoplasmic sperm injection (ICSI) cycle, were prospectively randomized to receive treatment with either a GnRH agonist with a long-term protocol (n: 32) or a GnRH antagonist with a multi-dose protocol (n: 32). Before being subjected to ICSI, the oocytes at metaphase II from both groups were morphologically analyzed under an inverted light microscope at a 400x magnification. The oocytes were classified as follows: normal or with cytoplasmic dysmorphism, extracytoplasmic dysmorphism, or both. The resulting measure was the detection of dysmorphic oocytes among the total number of oocytes analyzed. Out of a total of 681 oocytes, 189 (27.8%) were morphologically normal, 220 (32.3%) showed cytoplasmic dysmorphism, 124 (18.2%) showed extracytoplasmic alterations, and 148 (21.7%) exhibited both types of dysmorphisms. No significant difference was observed in oocyte dysmorphisms between the agonist- and antagonisttreated groups (P>0.05). Analysis for each dysmorphism revealed that the most common conditions were alterations in polar body shape (31.3%) and presence of diffuse cytoplasmic granulations (22.8%), refractile bodies (18.5%) and central cytoplasmic... (Complete abstract click access electronic below)
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Cota, Ana Márcia de Miranda. "Agonista versus antagonista do GnRH em ciclos de reprodução assistida : morfologia oocitária /." Botucatu : [s.n.], 2012. http://hdl.handle.net/11449/99221.
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Orientador: Joao Batista Alcantara OliveiraCoorientador: Claudia Guilhermino Petersen
Banca: Mario Cavagna
Banca: Anice Maria Vieira de Camargo Martins
Resumo: Na reprodução assistida, a seleção de gametas com o objetivo de alcançar melhores resultados clínicos é uma tarefa crucial dos embriologistas. A qualidade do oócito é um fator chave na fertilidade feminina, refletindo o potencial intrínseco de desenvolvimento do gameta, além de ter um papel crucial não só na fecundação, mas também no desenvolvimento embrionário subsequente. Após a desnudação, consegue-se definir a maturidade oocitária, com a identificação do primeiro corpúsculo polar, além de permitir a avaliação da morfologia oocitária, analisando as características da zona pelúcida, do espaço perivitelino e do citoplasma. Os dismorfismos oocitários são classificados em 2 tipos: citoplasmáticos, que incluem a presença de granulações e/ou de inclusões citoplasmáticas (vacúolos, corpos refrativos, agregados do retículo endoplasmático) e extracitoplasmáticos (alterações na forma do oócito, alterações na zona pelúcida, no espaço perivitelino e alterações do corpúsculo polar). Essas variações na morfologia oocitária podem ocorrer devido a fatores como idade da mulher, problemas genéticos e alterações no ambiente hormonal a que o oócito é exposto com a hiperestimulação ovariana. A classificação da morfologia oocitária, bem como sua correlação com o desenvolvimento embrionário e taxa de gravidez são bastante controversas na literatura. Vários estudos não demonstram nenhuma associação entre os dismorfismos oocitários e os resultados da fertilização in vitro, enquanto outros relatam uma associação entre a morfologia oocitária e desenvolvimento embrionário. Essas diferenças nos resultados podem ser explicadas devido a utilização de diferentes critérios morfológicos e devido... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The selection of developmentally competent human gametes may increase the efficiency of assisted reproduction. Spermatozoa and oocytes are usually assessed according to morphologic criteria. Oocyte morphology can be affected by the age of the female, genetic aspects, and factors related to controlled ovarian stimulation. However, there is a lack of evidence in the literature concerning the effect of gonadotropin-releasing hormone (GnRH) analogues, either agonists or antagonists, on oocyte morphology. The aim of this randomized study was to investigate if the prevalence of oocyte dysmorphism is influenced by the type of pituitary suppression used in ovarian stimulation. A total of 64 patients at the first intracytoplasmic sperm injection (ICSI) cycle, were prospectively randomized to receive treatment with either a GnRH agonist with a long-term protocol (n: 32) or a GnRH antagonist with a multi-dose protocol (n: 32). Before being subjected to ICSI, the oocytes at metaphase II from both groups were morphologically analyzed under an inverted light microscope at a 400x magnification. The oocytes were classified as follows: normal or with cytoplasmic dysmorphism, extracytoplasmic dysmorphism, or both. The resulting measure was the detection of dysmorphic oocytes among the total number of oocytes analyzed. Out of a total of 681 oocytes, 189 (27.8%) were morphologically normal, 220 (32.3%) showed cytoplasmic dysmorphism, 124 (18.2%) showed extracytoplasmic alterations, and 148 (21.7%) exhibited both types of dysmorphisms. No significant difference was observed in oocyte dysmorphisms between the agonist- and antagonisttreated groups (P>0.05). Analysis for each dysmorphism revealed that the most common conditions were alterations in polar body shape (31.3%) and presence of diffuse cytoplasmic granulations (22.8%), refractile bodies (18.5%) and central cytoplasmic... (Complete abstract click access electronic below)
Mestre
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Arruda, Jalsi Tacon. "Comparação entre dois protocolos para estimulação ovariana com agonista/antagonista do hormônio liberador de gonadotrofinas (GnRH) em mulheres submetidas ao primeiro ciclo de reprodução assistida." Universidade Federal de Goiás, 2013. http://repositorio.bc.ufg.br/tede/handle/tede/3814.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Infertility affects more couples and assisted reproduction techniques offer a possibility of treatment and the chance of having a child. Thus, the first attempt to ovulation induction is critical to the success of the cycle or even for future attempts is successful. Objective: To compare the protocols using GnRH agonist or antagonist for ovarian stimulation in normo-responders undergoing the first cycle of IVF/ICSI. Methods: we conducted a literature review on the history of ovulation induction controlled by medications. From the data available in the database of electronic medical records SISFERT used in the Laboratory of Human Reproduction (LabRep-HC-FM-UFG) a comparative retrospective observational study was conducted with 50 patients divided into two groups according to protocol: GnRH-agonist (leuprolide acetate 1 mg/day short protocol) or GnRHantagonist (Cetrorelix 0.25 mg/day), which received 150 IU/day of rFSH (follitropin alpha) and 250 µg of rhCG (alpha-coriogonadotrofina) in both groups. Results: Statistically significant differences were observed in the days of stimulation with rFSH, total dose of gonadotropin, days of use of GnRH, GnRH dose and total number of follicles (≥ 16 mm) on the day of the group rhCG GnRH agonist. There was no significant difference in other parameters, however, the number of oocytes retrieved was slightly higher in the GnRH agonist, but fertilization rate was higher in the GnRH-antagonist. Pregnancy rates and clinical chemistry were similar in both groups. Conclusions: although no significant differences in the results analyzed, the use of flexible antagonist protocol facilitates the handling and enables the patient using much lower doses of gonadotropins itself as the antagonist, reducing the cost of treatment when compared to the protocol with GnRH agonist.
A infertilidade afeta cada vez mais casais e as técnicas de reprodução assistida oferecem uma possibilidade de tratamento e a chance de ter um filho. Assim, a primeira tentativa de indução da ovulação é fundamental para o sucesso do ciclo ou, até mesmo, para que tentativas futuras sejam bem sucedidas. Objetivo: comparar os protocolos utilizando agonista ou antagonista do GnRH para estimulação ovariana em pacientes normo-respondedoras submetidas ao primeiro ciclo de FIV/ICSI. Métodos: foi realizada uma revisão da literatura sobre a história da indução da ovulação controlada por medicamentos. A partir dos dados disponíveis no banco de prontuários eletrônicos SISFERT utilizado pelo Laboratório de Reprodução Humana (LabRep–HC–FM–UFG), um estudo observacional retrospectivo comparativo foi conduzido com 50 pacientes distribuídas em dois grupos de acordo com o protocolo: GnRH-agonista (acetato de leuprolide 1 mg/dia protocolo curto) ou GnRH-antagonista (cetrorelix 0,25 mg/dia); e que receberam 150 UI/dia de rFSH (alfa-folitropina) e 250 µg de rhCG (alfa-coriogonadotrofina) em ambos os grupos. Resultados: foram observadas diferenças estatisticamente significativas nos dias de estimulação com rFSH, dose total de gonadotrofina, dias de uso do GnRH, dose total de GnRH e o número de folículos (≥ 16 mm) no dia do rhCG no grupo GnRH-agonista. Não houve diferença significativa nos outros parâmetros, no entanto, o número de oócitos recuperados foi ligeiramente maior no grupo GnRH-agonista, mas a taxa de fertilização foi maior no grupo GnRH-antagonista. As taxas de gravidez química e clínica foram similares nos dois grupos. Conclusões: embora não tenha havido diferenças significativas nos resultados analisados, o uso do protocolo flexível com antagonista facilita a manipulação pela paciente usuária e possibilita doses menores tanto de gonadotrofinas quanto do próprio antagonista, reduzindo o custo do tratamento quando comparado ao protocolo com agonista do GnRH
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Castillo, Farfán Juan Carlos. "Ciclos de fecundación in vitro y maduración final con agonista GNRH: Explorando dosis bajas de HCG para soporte de fase lutea." Doctoral thesis, Universitat de València, 2010. http://hdl.handle.net/10803/52180.
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La hormona gonadotropina coriónica humana (hCG) se emplea de forma rutinaria para inducir la maduración final ovocitaria en ciclos de fecundación in vitro (FIV). Sin embargo, su utilización está relacionada con la aparición del Síndrome de Hiperestimulación Ovárica (SHO), especialmente cuando ciertos factores de riesgo están presentes, principalmente la presencia de un número elevado de folículos. Este riesgo puede ser drásticamente disminuido sustituyendo la hCG por un agonista GnRH como inductor de la maduración final en ciclos FIV con antagonistas GnRH. Aunque, este uso se asocia a una alta tasa de aborto temprano ocasionada por una fase lútea deficiente. La función del cuerpo lúteo se ve seriamente comprometida con el empleo del agonista GnRH (luteólisis), sin embargo, la potente acción luteotrópica de la hCG puede ser beneficiosa empleando dosis pequeñas como suplemento en la fase lútea y sin incrementar el riesgo de SHO.
En un esfuerzo por reducir la tasa de abortos clínicos asociada al empleo de agonista GnRH, la presente tesis estudia la utilización de pequeñas dosis de hCG como suplemento de la fase lútea con el objetivo de rescatar el cuerpo lúteo, normalizar las tasas de embarazo y gestación evolutiva; además de reducir la presentación del SHO en la paciente con alta respuesta a la estimulación ovárica en ciclos FIV.Human gonadotropin chorionic hormone (hCG) is widely used to induce final follicular maturation in in vitro fertilization cycles (IVF). However, its use is closely related to Ovarian Hyperstimulation Syndrome (OHSS) genesis, especially when certain risk factors are present, mainly a high number of recruited follicles. This risk may be drastically reduced, substituting hCG by a GnRH agonist for triggering in GnRH antagonist cycles. Nonetheless, this protocol is linked to high rates of early pregnancy loss due to a deficient luteal phase. Corpus luteum function is seriously compromised when a GnRH agonist is used for triggering (luteolysis), however, the potent luteotrophic action of hCG may be of benefit if low doses are employed for supplementing luteal phase, without increasing OHSS risk. In an effort to reduce early pregnancy losses associated to the use of GnRH agonist for triggering, this PhD. Thesis focuses on the use of low doses of hCG as luteal phase support with the aim of rescue corpus luteum function, normalizing pregnancy and on-going pregnancy rates; and at the same time reducing the frequency of OHSS in high responders to ovarian stimulation in IVF cycles.
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Lavorato, Heloisa Lopes [UNESP]. "Agonista versus antagonista do GnRH em ciclos de reprodução assistida: DNA fragmentação e apoptose das células da granulosa." Universidade Estadual Paulista (UNESP), 2012. http://hdl.handle.net/11449/99222.
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Os agonistas do hormônio liberador de gonadotrofina (Gonadotropin-releasing hormone / GnRH) foram introduzidos na estimulação ovariana para fertilização in-vitro (FIV) com o objetivo de evitar o pico prematuro do hormônio luteinizante (LH). Embora sejam acompanhados de algumas desvantagens, os agonistas do GnRH tornaram-se bem aceitos na prática clínica com sua utilização sendo associada a aumento das taxas de gravidez. O desenvolvimento dos antagonistas do GnRH, capazes de bloqueio imediato da hipófise ofereceu uma nova opção terapêutica. Estudos comparativos entre os dois análogos têm sugerido que o uso de antagonistas está associado a uma menor duração do estímulo ovulatório e uma diminuição da incidência de síndrome de hiperestimulação ovariana, enquanto as taxas de gravidez e de nascidos vivos não parecem sofrer influências significativas do tipo de análogo do GnRH utilizado. Por outro lado, os agonistas do GnRH apresentam outras aplicações em ciclos de reprodução assistida além do bloqueio hipofisário
The expression of the gonadotrophin-releasing hormone (GnRH) receptor has been demonstrated in the human ovary, and it has therefore been suggested that GnRH agonists have different effects on the intraovarian system compared with GnRH antagonists, particularly in the granulosa cell (GC) layer. This study aimed to compare the level of apoptosis and DNA fragmentation in human GCs exposed to agonist or antagonist of GnRH in intracytoplasmic sperm injection (ICSI) cycles supplemented with recombinant LH (r-LH). Patients without ovulatory dysfunction aged ≤ 37 years and in the first ICSI cycle were prospectively randomised to receive either a long GnRH agonist protocol or a multi-dose antagonist protocol. In both groups, the GCs were collected during oocyte denudation and separated from blood cells by centrifugation on a 60% isolate solution. It should be emphasized that the study examined only GCs that had been directly detached from the oocyte cumulus complexes. The GCs were then analyzed for DNA fragmentation by TUNEL assay and for apoptosis using annexin-V. The primary outcome measurements were given as the percentage of GCs with DNA fragmentation and apoptosis out of the total number of GCs analyzed. The comparison of the agonist versus the antagonist group was performed using the Mann-Whitney test
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Lavorato, Heloisa Lopes. "Agonista versus antagonista do GnRH em ciclos de reprodução assistida : DNA fragmentação e apoptose das células da granulosa /." Botucatu : [s.n.], 2012. http://hdl.handle.net/11449/99222.
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Orientador: José Gonçalves Franco Jr.Coorientador: Mario Cavagna
Banca: João Batista Alcantara Oliveira
Banca: Claudia Guilhermino Petersen
Resumo: Os agonistas do hormônio liberador de gonadotrofina (Gonadotropin-releasing hormone / GnRH) foram introduzidos na estimulação ovariana para fertilização in-vitro (FIV) com o objetivo de evitar o pico prematuro do hormônio luteinizante (LH). Embora sejam acompanhados de algumas desvantagens, os agonistas do GnRH tornaram-se bem aceitos na prática clínica com sua utilização sendo associada a aumento das taxas de gravidez. O desenvolvimento dos antagonistas do GnRH, capazes de bloqueio imediato da hipófise ofereceu uma nova opção terapêutica. Estudos comparativos entre os dois análogos têm sugerido que o uso de antagonistas está associado a uma menor duração do estímulo ovulatório e uma diminuição da incidência de síndrome de hiperestimulação ovariana, enquanto as taxas de gravidez e de nascidos vivos não parecem sofrer influências significativas do tipo de análogo do GnRH utilizado. Por outro lado, os agonistas do GnRH apresentam outras aplicações em ciclos de reprodução assistida além do bloqueio hipofisário
Abstract: The expression of the gonadotrophin-releasing hormone (GnRH) receptor has been demonstrated in the human ovary, and it has therefore been suggested that GnRH agonists have different effects on the intraovarian system compared with GnRH antagonists, particularly in the granulosa cell (GC) layer. This study aimed to compare the level of apoptosis and DNA fragmentation in human GCs exposed to agonist or antagonist of GnRH in intracytoplasmic sperm injection (ICSI) cycles supplemented with recombinant LH (r-LH). Patients without ovulatory dysfunction aged ≤ 37 years and in the first ICSI cycle were prospectively randomised to receive either a long GnRH agonist protocol or a multi-dose antagonist protocol. In both groups, the GCs were collected during oocyte denudation and separated from blood cells by centrifugation on a 60% isolate solution. It should be emphasized that the study examined only GCs that had been directly detached from the oocyte cumulus complexes. The GCs were then analyzed for DNA fragmentation by TUNEL assay and for apoptosis using annexin-V. The primary outcome measurements were given as the percentage of GCs with DNA fragmentation and apoptosis out of the total number of GCs analyzed. The comparison of the agonist versus the antagonist group was performed using the Mann-Whitney test
Mestre
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Terres, Letícia Funchal. "Homogenização da coorte folicular pela administração de estradiol em ciclos de estimulação ovariana controlada com antagonista de GnRH protocolo de doses múltiplas." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2005. http://hdl.handle.net/10183/5361.
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Hempelt, Daniela. "Analytische Untersuchungen zur Aggregation von Cetrorelix und weiteren GnRH-Antagonisten." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-99807.
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In der vorliegenden Arbeit werden Beiträge zur Entwicklung neuer qualitativer und quantitativer analytischer Methoden für die Untersuchung von Cetrorelix und anderen GnRH-Antagonisten während des Aggregationsprozesses vorgestellt. Für die qualitative Untersuchung von GnRH-Antagonisten wurden am Modellpeptid Cetrorelix massenspektrometrische Methoden entwickelt und auf weitere GnRH-Antagonisten übertragen. Eingesetzt wurde sowohl die ESI-TOF-MS als auch die MALDI-TOF-MS. Beide massenspektrometrische Verfahren zeigten für die untersuchten GnRH-Antagonisten polydisperse Verteilungen oberhalb der fluoreszenzspektroskopisch bestimmten kritischen Aggregatbildungskonzentration (cac). Bei den ESI-TOF-MS-Messungen konnte ein stark von Cetrorelix abweichendes Aggregationsverhalten für Ozarelix beobachtet werden.
Für die Quantifizierung des Aggregatanteils in Cetrorelix- bzw. Ozarelixproben wurde eine Methode mit der MALDI-TOF-MS etabliert, die Untersuchungen an pharmazeutisch relevanten Peptidhormon-Formulierungen ermöglicht. Systematische Untersuchungen zum Einfluss verschiedener An- und Kationen sowie deren Konzentrationen auf die Cetrorelixaggregation erfolgten mit der Fluoreszenzspektroskopie. Die erhaltenen Ergebnisse ermöglichen eine bessere Charakterisierung der Aggregation und lassen Abschätzungen über das Aggregationsverhalten von Cetrorelix in verschiedenen Medien mit unterschiedlichen Elektrolyten zu. Mit dem Einsatz der Transmissionselektronenmikroskopie war es erstmals möglich, Aggregate von GnRH-Antagonisten visuell darzustellen.
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DUBOURDIEU, SOPHIE. "Effets de l'administration d'un antagoniste de la gnrh chez la femme normale." Nantes, 1989. http://www.theses.fr/1989NANT094M.
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Johansson, Johanna. "GnRH-antagonisten Elagolix effekter och biverkningar vid behandling av endometriosutlöst smärta." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-93676.
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Bakgrund: Endometrios är en kronisk benign östrogenberoende sjukdom som karaktäriseras av tillväxt av endometrioslesioner utanför livmodern. Sjukdomen kännetecknas av smärta. Det finns inget botemedel till sjukdomen, utan syftet med behandlingen är att minska symptom och lindra smärtan. Idag erbjuds drabbade kvinnor bl.a. kombinerade hormonella preventivmedel, gestagen eller gonadotropinfrisättande hormon (GnRH)-agonister, i kombination med icke-steroida antiinflammatoriska läkemedel (NSAID) och paracetamol. En annan tänkbar behandling mot endometrios är GnRH-antagonisten Elagolix. Läkemedlet blockerar GnRH-receptorn vilket leder till hämmad frisättning av luteinisierande hormon (LH) och follikelstimulerande hormon (FSH), och därmed minskas frisättning av könshormonet östrogen. Syfte: Syftet med arbetet var att utvärdera GnRH-antagonisten Elagolix effekter och biverkningar vid behandling mot endometriosutlöst smärta. Metod: Denna litteraturstudie är baserad på fem randomiserade kontrollerade vetenskapliga artiklar (RCT) som hämtats från den medicinska databasen PubMed. De sökord som använts är ”elagolix” och ”endometriosis”. Resultat: Elagolix blockerar omedelbart GnRH-receptorn oberoende av dos. Som svar på detta minskas nivåerna av LH och FSH, och därmed minskas frisättningen av östrogen. FSH-nivåerna minskar långsammare än LH. Högre dosering sänker LH-nivåerna under en längre period. Tiden för maximal plasmakoncentration (Tmax) uppnås inom 0,5-1 timme. Den optimala dosen Elagolix för behandling mot endometriosutlöst smärta är 150 mg en gång dagligen i maximalt tjugofyra månader, eller 200 mg två gånger dagligen i maximalt sex månader. Behandling med Elagolix leder till förlust av benmineraldensiteten (BMD). Ökad dos och behandlingslängd leder till ökad BMD reducering. Biverkningsfrekvensen vid behandling med Elagolix är hög. De låga östrogen-nivåerna resulterar i menopaus-liknande symptom. Slutsats: Denna litteraturstudie tyder på att Elagolix minskar östrogenfrisättningen och där med minskar endometriosutlöst smärta. Behandling med Elagolix bör ske under maximalt tjugofyra månader p.g.a. BMD-förlust. Studierna kring Elagolix är få, och samtliga studier är finansierade av läkemedelsföretag som deltagit i utvecklingen av läkemedlet. Ytterligare studier behövs med objektiv synvinkel.Background: Endometriosis is a chronic benign estrogen-dependent disease characterized by the growth of endometrial tissue outside the uterus. The disease is associated with severe pain. The purpose of all available treatment is to reduce the symptoms and relieve the pain. Today, affected women are offered combined hormonal contraceptives, progestogens or gonadotropin-releasing hormone (GnRH) agonists, in combination with non-steroidal anti-inflammatory drugs (NSAIDs) and paracetamol. Another possible treatment for endometriosis is the GnRH-antagonist Elagolix. The drug blocks the GnRH-receptor, which leads to inhibited release of luteinizing hormone (LH) and folliclestimulating hormone (FSH). Thereby reducing the release of the sex hormone estrogen. Purpose: The aim of this study was to evaluate the effects and side effects of GnRH antagonist Elagolix for treatment of endometriosis-triggered pain. Method: This work is a literature review based on randomized controlled scientific articles (RCTs), which were retrieved from the medical database PubMed.Gov. The article search was performed by using two keywords, namely “endometriosis” and “elagolix”, and resulted in a total of five articles to investigate. Results: The results showed that Elagolix immediately blocks the GnRH receptors regardless of dosage. In response, the levels of LH and FSH are reduced, and thereby reducing estrogen release. FSH levels decrease more slowly than LH. Higher dosage lowers LH levels over a longer period of time. The time to maximum concentration (Tmax) is reached within 0,5-1 hour. The optimal dose of Elagolix for treatment of endometriosis-associated pain is 150 mg once daily for a maximum of twentyfour months, or 200 mg twice a day for a maximum of six months. Treatment with Elagolix leads to bone mineral density (BMD) loss. Increased dosage and duration of treatment lead to increased BMD reduction. Elagolix has a high frequency of adverse events. The adverse events is a result of the low estrogen levels. Conclusion: The conclusion of this study imply that Elagolix reduces estrogen release and thereby reduces endometriosis-associated pain. Elagolix should only be used as treatment for a maxiumum of twenty-four months due to BMD loss. The studies around Elagolix are few, and all studies are funded by pharmaceutical companies that participated in the development of the drug. Further studies are needed with an objective point of view.
Books on the topic "Antagonista GnRH"
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Organon Round Table Conference (3rd 1992 Paris, France). GnRH, GnRH analogs, gonadotropins, and gonadal peptides: The proceedings of the third Organon Round Table Conference, Paris, 1992. Parthenon Pub. Group, 1993.
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Recent progress on GnRH and gonadal peptides. Elsevier, 1990.
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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. Elsevier, 1990.
Book chapters on the topic "Antagonista GnRH"
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Flores, Francisco Javier Ruiz, and Juan Antonio García Velasco. "GnRH Antagonist Protocols." In Textbook of Assisted Reproduction. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-2377-9_10.
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Pavlou, Spyros N. "GnRH Antagonists in Men." In Modes of Action of GnRH and GnRH Analogs. Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_19.
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Gordon, Keith, and Gary D. Hodgen. "Hormone Antagonism for Contraception: GnRH Antagonists and Antiprogestins." In Clinical Perspectives in Obstetrics and Gynecology. Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4612-2730-4_18.
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Gordon, Keith, Douglas R. Danforth, Robert F. Williams, and Gary D. Hodgen. "GnRH Antagonists: Primate Models for Clinical Indications." In Modes of Action of GnRH and GnRH Analogs. Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_22.
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Hall, Janet E., and William F. Crowley. "Use of GnRH Antagonists as Physiologic Probes in the Female." In Modes of Action of GnRH and GnRH Analogs. Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_20.
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Karten, Marvin J. "An Overview of GnRH Antagonist Development: Two Decades of Progress." In Modes of Action of GnRH and GnRH Analogs. Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_18.
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Bremner, William J., Carrie J. Bagatell, and Robert A. Steiner. "Gonadotropin Releasing Hormone Antagonist Plus Testosterone: A Potential Male Contraceptive." In Modes of Action of GnRH and GnRH Analogs. Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_21.
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Hahn, D. W., K. T. Demarest, A. Phillips, et al. "Contraceptive Potential of GnRH Antagonists." In Female Contraception. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73790-9_16.
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Khalaf, Yacoub, and Sesh Kamal Sunkara. "GnRH Antagonist in Ovarian Stimulation." In Principles and Practice of Controlled Ovarian Stimulation in ART. Springer India, 2015. http://dx.doi.org/10.1007/978-81-322-1686-5_10.
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Pavlou, Spyros N., Jean Rivier, Wylie Vale, and Themis Kamilaris. "Clinical Pharmacology of LHRH Antagonists." In GnRH Analogues in Cancer and Human Reproduction. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0725-6_13.
Full textConference papers on the topic "Antagonista GnRH"
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Engel, J., A. Schreiber, S. Seitz, et al. "Triple-Negative Breast Cancers Express Receptors for GnRH and Can Be Effectively Targeted by the Orally Active GnRH-Antagonist AEZS 115." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-6108.
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Engel, JB, M. Ivanisevic, E. Guenther, J. Dietl, U. Kaemmerer, and A. Hoenig. "Orally active gnRH-antagonist AEZS-115 inhibits growth of human ovarian and breast cancers in vitro." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-3065.
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Cucchiara, Vito, Joy C. Yang, Chengfei Liu, et al. "Abstract 1018: GnRH antagonists have direct inhibitory effects on castration-resistant prostate cancer via intracrine androgen and AR-V7 expression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1018.
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Cucchiara, Vito, Joy C. Yang, Chengfei Liu, et al. "Abstract 1018: GnRH antagonists have direct inhibitory effects on castration-resistant prostate cancer via intracrine androgen and AR-V7 expression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1018.
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