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Pesquisa : D12.776.543.750.695.410 [Categoria DeCS]
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[PMID]:29335207
[Au] Autor:Kim SM; Lee M; Lee SY; Lee SM; Kim EJ; Kim JS; Ann J; Lee J; Lee J
[Ad] Endereço:R&D Center, TiumBio Company Ltd., Seongnam-si, Gyeonggi-do, 13493, South Korea.
[Ti] Título:Synthesis and biological evaluation of 3-(2-aminoethyl) uracil derivatives as gonadotropin-releasing hormone (GnRH) receptor antagonists.
[So] Source:Eur J Med Chem;145:413-424, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:We investigated a series of uracil analogues by introducing various substituents on the phenyl ring of the N-3 aminoethyl side chain and evaluated their antagonistic activity against human gonadotropin-releasing hormone (GnRH) receptors. Analogues with substituents at the ortho or meta position demonstrated potent in vitro antagonistic activity. Specifically, the introduction of a 2-OMe group enhanced nuclear factor of activated T-cells (NFAT) inhibition up to 6-fold compared to the unsubstituted analogue. We identified compound 12c as a highly potent GnRH antagonist with moderate CYP inhibition. Compound 12c showed potent and prolonged LH suppression after a single dose was orally administered in castrated monkeys compared to a known antagonist, Elagolix. We believe that our SAR study offers useful insights to design GnRH antagonists as a potential treatment option for endometriosis.
[Mh] Termos MeSH primário: Inibidores do Citocromo P-450 CYP3A/farmacologia
Citocromo P-450 CYP3A/metabolismo
Receptores LHRH/antagonistas & inibidores
Uracila/farmacologia
[Mh] Termos MeSH secundário: Animais
Inibidores do Citocromo P-450 CYP3A/administração & dosagem
Inibidores do Citocromo P-450 CYP3A/química
Relação Dose-Resposta a Droga
Seres Humanos
Hormônio Luteinizante/antagonistas & inibidores
Hormônio Luteinizante/sangue
Macaca fascicularis
Estrutura Molecular
Relação Estrutura-Atividade
Uracila/análogos & derivados
Uracila/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytochrome P-450 CYP3A Inhibitors); 0 (Receptors, LHRH); 56HH86ZVCT (Uracil); 9002-67-9 (Luteinizing Hormone); EC 1.14.13.67 (CYP3A4 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP3A)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


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[PMID]:29228137
[Au] Autor:Odle AK; Benes H; Melgar Castillo A; Akhter N; Syed M; Haney A; Allensworth-James M; Hardy L; Winter B; Manoharan R; Syed R; MacNicol MC; MacNicol AM; Childs GV
[Ad] Endereço:Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
[Ti] Título:Association of Gnrhr mRNA With the Stem Cell Determinant Musashi: A Mechanism for Leptin-Mediated Modulation of GnRHR Expression.
[So] Source:Endocrinology;159(2):883-894, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cyclic expression of pituitary gonadotropin-releasing hormone receptors (GnRHRs) may be an important checkpoint for leptin regulatory signals. Gonadotrope Lepr-null mice have reduced GnRHR levels, suggesting these receptors may be leptin targets. To determine if leptin stimulated GnRHR directly, primary pituitary cultures or pieces were exposed to 1 to 100 nM leptin. Leptin increased GnRHR protein levels and the percentages of gonadotropes that bound biotinylated analogs of gonadotropin-releasing hormone (bio-GnRH) but had no effect on Gnrhr messenger RNA (mRNA). An in silico analysis revealed three consensus Musashi (MSI) binding elements (MBEs) for this translational control protein in the 3' untranslated region (UTR) of Gnrhr mRNA. Several experiments determined that these Gnrhr mRNA MBE were active: (1) RNA electrophoretic mobility shift assay analyses showed that MSI1 specifically bound Gnrhr mRNA 3'-UTR; (2) RNA immunoprecipitation of pituitary fractions with MSI1 antibody pulled down a complex enriched in endogenous MSI protein and endogenous Gnrhr mRNA; and (3) fluorescence reporter assays showed that MSI1 repressed translation of the reporter coupled to the Gnrhr 3'-UTR. In vitro, leptin stimulation of pituitary pieces reduced Msi1 mRNA in female pituitaries, and leptin stimulation of pituitary cultures reduced MSI1 proteins selectively in gonadotropes identified by binding to bio-GnRH. These findings show that leptin's direct stimulatory actions on gonadotrope GnRHR correlate with a direct inhibition of expression of the posttranscriptional regulator MSI1. We also show MSI1 interaction with the 3'-UTR of Gnrhr mRNA. These findings now open the door to future studies of leptin-modulated posttranscriptional pathways.
[Mh] Termos MeSH primário: Leptina/farmacologia
Proteínas do Tecido Nervoso/metabolismo
Proteínas de Ligação a RNA/metabolismo
Receptores LHRH/genética
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula/efeitos dos fármacos
Linhagem da Célula/genética
Células Cultivadas
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Gonadotrofos/efeitos dos fármacos
Gonadotrofos/metabolismo
Masculino
Camundongos
Camundongos Knockout
Regiões Promotoras Genéticas/efeitos dos fármacos
RNA Mensageiro/metabolismo
Receptores LHRH/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Leptin); 0 (Msi1h protein, mouse); 0 (Nerve Tissue Proteins); 0 (RNA, Messenger); 0 (RNA-Binding Proteins); 0 (Receptors, LHRH)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00586


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[PMID]:29197784
[Au] Autor:Banerjee S; Chaturvedi CM
[Ad] Endereço:Department of Zoology, Banaras Hindu University, Varanasi 221005, India.
[Ti] Título:Simulated photoperiod influences testicular activity in quail via modulating local GnRHR-GnIHR, GH-R, Cnx-43 and 14-3-3.
[So] Source:J Photochem Photobiol B;178:412-423, 2018 Jan.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The hypothalamo-hypophyseal-gonadal axis mediated differential photosexual responses in quail kept under different simulated photoperiodic conditions have been studied in details. Local testicular GnRH-GnIH and their receptor system has been hypothesized to be modulated in quail showing different photo-sexual responses and thus influence the testicular activity and steroidogenesis through local (paracrine and autocrine) action. To validate this hypothesis, we studied the expression of gonadotropin releasing hormone receptor (GnRH-R), gonadotropin inhibiting hormone receptor (GnIH-R) mRNA, growth hormone receptor (GH-R), proliferating cell nuclear antigen (PCNA), 14-3-3, Connexin-43 (Cnx-43), steroidogenic factor-1 (SF-1), Steroidogenic Acute Regulatory protein (StAR), steroidogenic enzyme (3ß HSD) in testis as well as androgen receptor (AR) in testis and epididymis of photosensitive (PS), scotorefractory (SR), photorefractory (PR) and scotosensitive (SS) quail. Experimental findings clearly indicate the increased expression of GnIH-R mRNA and suppression of GnRH-R, GH-R, PCNA, 14-3-3, Connexin-43, SF-1, StAR, 3ß HSD in testis as well as AR in testis and epididymis of PR and SS quail, while PS and SR quail exhibited the opposite results i.e., significantly decreased expression of GnIH-R mRNA and increased expression of GnRH-R, GH-R, PCNA, 14-3-3, Cnx-43, SF-1, StAR, 3ß HSD in testis as well as AR in testis and epididymis. The significantly increased intra-testicular testosterone has been observed in the PS and SR quail while, PR and SS quail showed opposite results. Hence, we conclude that PS and SR quail showed significantly increased testicular activity and steroidogenesis while opposite pattern was observed in PR and SS quail.
[Mh] Termos MeSH primário: Proteínas 14-3-3/metabolismo
Conexina 43/metabolismo
Hormônio Liberador de Gonadotropina/metabolismo
Receptores LHRH/metabolismo
Testículo/metabolismo
[Mh] Termos MeSH secundário: Proteínas 14-3-3/genética
Animais
Conexina 43/genética
Epididimo/metabolismo
Epididimo/patologia
Hormônio Liberador de Gonadotropina/genética
Masculino
Microscopia Confocal
Fotoperíodo
Antígeno Nuclear de Célula em Proliferação/genética
Antígeno Nuclear de Célula em Proliferação/metabolismo
Codorniz
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Receptores LHRH/genética
Fator Esteroidogênico 1/genética
Fator Esteroidogênico 1/metabolismo
Testículo/patologia
Testosterona/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (14-3-3 Proteins); 0 (Connexin 43); 0 (Proliferating Cell Nuclear Antigen); 0 (Receptors, Androgen); 0 (Receptors, LHRH); 0 (Steroidogenic Factor 1); 33515-09-2 (Gonadotropin-Releasing Hormone); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE


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[PMID]:29182666
[Au] Autor:Hietamäki J; Hero M; Holopainen E; Känsäkoski J; Vaaralahti K; Iivonen AP; Miettinen PJ; Raivio T
[Ad] Endereço:Pediatric Research Center, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
[Ti] Título:GnRH receptor gene mutations in adolescents and young adults presenting with signs of partial gonadotropin deficiency.
[So] Source:PLoS One;12(11):e0188750, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biallelic, partial loss-of-function mutations in GNRHR cause a wide spectrum of reproductive phenotypes from constitutional delay of growth and puberty to complete congenital hypogonadotropic hypogonadism. We studied the frequency of GNRHR, FGFR1, TAC3, and TACR3 mutations in nine adolescent and young adult females with clinical cues consistent with partial gonadotropin deficiency (stalled puberty, unexplained secondary amenorrhea), and describe phenotypic features and molecular genetic findings of monozygotic twin brothers with stalled puberty. Two girls out of nine (22%, 95%CI 6-55%) carried biallelic mutations in GNRHR. The girl with compound heterozygous c.317A>G p.(Gln106Arg) and c.924_926delCTT p.(Phe309del) GNRHR mutations displayed incomplete puberty and clinical signs of hypoestrogenism. The patient carrying a homozygous c.785G>A p.(Arg262Gln) mutation presented with signs of hypoestrogenism and unexplained secondary amenorrhea. None of the patients exhibited mutations in FGFR1, TAC3, or TACR3. The twin brothers, compound heterozygous for GNRHR mutations c.317A>G p.(Gln106Arg) and c.785G>A p.(Arg262Gln), presented with stalled puberty and were discordant for weight, and the heavier of them had lower testosterone levels. These results suggest that genetic testing of the GNRHR gene should be offered to adolescent females with low-normal gonadotropins and unexplained stalled puberty or menstrual dysfunction. In male patients with partial gonadotropin deficiency, excess adipose tissue may suppress hypothalamic-pituitary-gonadal axis.
[Mh] Termos MeSH primário: Gonadotropinas/deficiência
Mutação
Receptores LHRH/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Feminino
Seres Humanos
Masculino
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gonadotropins); 0 (Receptors, LHRH)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188750


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[PMID]:28502477
[Au] Autor:Kyritsi K; Meng F; Zhou T; Wu N; Venter J; Francis H; Kennedy L; Onori P; Franchitto A; Bernuzzi F; Invernizzi P; McDaniel K; Mancinelli R; Alvaro D; Gaudio E; Alpini G; Glaser S
[Ad] Endereço:Department of Internal Medicine, Texas A&M Health Science Center, College of Medicine, Temple, Texas.
[Ti] Título:Knockdown of Hepatic Gonadotropin-Releasing Hormone by Vivo-Morpholino Decreases Liver Fibrosis in Multidrug Resistance Gene 2 Knockout Mice by Down-Regulation of miR-200b.
[So] Source:Am J Pathol;187(7):1551-1565, 2017 Jul.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatic fibrosis occurs during the progression of primary sclerosing cholangitis (PSC) and is characterized by accumulation of extracellular matrix proteins. Proliferating cholangiocytes and activated hepatic stellate cells (HSCs) participate in the promotion of liver fibrosis during cholestasis. Gonadotropin-releasing hormone (GnRH) is a trophic peptide hormone synthesized by hypothalamic neurons and the biliary epithelium and exerts its biological effects on cholangiocytes by interaction with the receptor subtype (GnRHR ) expressed by cholangiocytes and HSCs. Previously, we demonstrated that administration of GnRH to normal rats increased intrahepatic biliary mass (IBDM) and hepatic fibrosis. Also, miR-200b is associated with the progression of hepatic fibrosis; however, the role of the GnRH/GnRHR /miR-200b axis in the development of hepatic fibrosis in PSC is unknown. Herein, using the mouse model of PSC (multidrug resistance gene 2 knockout), the hepatic knockdown of GnRH decreased IBDM and liver fibrosis. In vivo and in vitro administration of GnRH increased the expression of miR-200b and fibrosis markers. The GnRH/GnRHR axis and miR-200b were up-regulated in human PSC samples. Cetrorelix, a GnRHR antagonist, inhibited the expression of fibrotic genes in vitro and decreased IBDM and hepatic fibrosis in vivo. Inhibition of miR-200b decreased the expression of fibrosis genes in vitro in cholangiocyte and HSC lines. Targeting the GnRH/GnRHR /miR-200b axis may be key for the management of hepatic fibrosis during the progression of PSC.
[Mh] Termos MeSH primário: Subfamília B de Transportador de Cassetes de Ligação de ATP/genética
Regulação da Expressão Gênica
Hormônio Liberador de Gonadotropina/metabolismo
MicroRNAs/metabolismo
Morfolinos/farmacologia
Receptores LHRH/metabolismo
[Mh] Termos MeSH secundário: Subfamília B de Transportador de Cassetes de Ligação de ATP/metabolismo
Animais
Linhagem Celular
Proliferação Celular
Colestase
Modelos Animais de Doenças
Progressão da Doença
Regulação para Baixo
Hormônio Liberador de Gonadotropina/genética
Células Estreladas do Fígado/metabolismo
Seres Humanos
Fígado
Cirrose Hepática
Masculino
Camundongos
Camundongos Knockout
MicroRNAs/genética
Receptores LHRH/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP Binding Cassette Transporter, Sub-Family B); 0 (MicroRNAs); 0 (Mirn200 microRNA, mouse); 0 (Morpholinos); 0 (P-glycoprotein 2); 0 (Receptors, LHRH); 33515-09-2 (Gonadotropin-Releasing Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE


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[PMID]:28432269
[Au] Autor:Oliveira FT; Salvatori R; Marcondes J; Macena LB; Oliveira-Santos AA; Faro ACN; Campos VC; Oliveira CRP; Costa UMM; Aguiar-Oliveira MH
[Ad] Endereço:Federal University of SergipeDivision of Endocrinology, Aracaju, Brazil.
[Ti] Título:Altered sleep patterns in patients with non-functional GHRH receptor.
[So] Source:Eur J Endocrinol;177(1):51-57, 2017 Jul.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: GH-releasing hormone (GHRH) exerts hypnotic actions increasing the non-rapid eye movement (NREM) sleep. Conversely, GH stimulates the REM sleep. GH deficiency (GHD) often leads to sleep problems, daytime fatigue and reduced quality of life (QoL). GHD may be due to lack of hypothalamic GHRH or destruction of somatotroph cells. We have described a cohort with isolated GHD (IGHD) due to GHRH resistance caused by a homozygous mutation (c.57 + 1G > A) in the GHRH receptor gene. They have normal QoL and no obvious complaints of chronic tiredness. The aim of this study was to determine the sleep quality in these subjects. METHODS: A cross-sectional study was carried out in 21 adult IGHD subjects, and 21 age- and gender-matched controls. Objective sleep assessment included polygraphic records of the awake, stages NREM [N1 (drowsiness), N2 and N3 (already sleeping)] and REM (R). Subjective evaluation included the Pittsburgh Sleep Quality Index, the Insomnia Severity Index and the Epworth Sleepiness Scale. RESULTS: IGHD subjects showed a reduction in sleep efficiency ( = 0.007), total sleep time ( = 0.028), duration of N2 and R in minutes ( = 0.026 and 0.046 respectively), but had increased duration and percentage of N1 stage ( = 0.029 and 0.022 respectively), wake ( = 0.007) and wake-time after sleep onset ( = 0.017). There was no difference in N3 or in sleep quality questionnaire scores. CONCLUSION: Patients with IGHD due to GHRH resistance exhibit objective reduction in the sleep quality, with changes in NREM and REM sleep, with no detectable subjective consequences. GHRH resistance seems to have a preponderant role over GHD in the sleep quality of these subjects.
[Mh] Termos MeSH primário: Receptores LHRH/deficiência
Transtornos do Sono-Vigília/fisiopatologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Estudos de Coortes
Estudos Transversais
Feminino
Seres Humanos
Masculino
Meia-Idade
Mutação/genética
Polissonografia
Qualidade de Vida
Receptores LHRH/genética
Índice de Gravidade de Doença
Sono
Distúrbios do Início e da Manutenção do Sono/etiologia
Distúrbios do Início e da Manutenção do Sono/genética
Fases do Sono
Sono REM
Inquéritos e Questionários
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, LHRH)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0145


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[PMID]:28350068
[Au] Autor:Sipos E; Hegyi K; Treszl A; Steiber Z; Mehes G; Dobos N; Fodor K; Olah G; Szekvolgyi L; Schally AV; Halmos G
[Ad] Endereço:Department of Biopharmacy, University of Debrecen, 4032 Debrecen, Hungary.
[Ti] Título:Concurrence of chromosome 3 and 4 aberrations in human uveal melanoma.
[So] Source:Oncol Rep;37(4):1927-1934, 2017 Apr.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Uveal melanoma (UM) is the most common primary intraocular malignancy with a very poor prognosis. The most frequent chromosome aberration in UM is the monosomy of chromosome 3. Previously, we demonstrated that ~50% of UMs express type-I receptor for luteinizing hormone­releasing hormone (LH-RH-R). The gene encoding LH-RH-R is located in chromosome 4 (location: 4q21.2); however, the occurrence of numerical aberrations of chromosome 4 have never been studied in UM. In the present study, we investigated the abnormalities of chromosome 3 and 4, and the possible correlation between them, as well as with LH-RH-R expression. Forty-six specimens of UM were obtained after enucleation. Numerical aberrations of chromosome 3 and 4 were studied by fluorescence in situ hybridization (FISH). Chromosome 4 was detected in normal biparental disomy only in 14 (30%) samples; however, 32 cases (70%) showed more than 2 signals/nucleus. Monosomy of chromosome 3 could be found in 16 (35%) samples. In 6 specimens (13%), more than 2 copies of chromosome 3 were found, while normal biparental disomy was detected in 24 (52%) samples. Statistical analysis indicated a statistically significant (p<0.05) correlation between the copy number of chromosome 3 and 4. Moreover, moderate difference was revealed in the survival rate of the UM patients with various pathological profiles. No correlation was found between chromosome aberrations and LH-RH-R expression. Our results clearly demonstrate abnormalities in chromosome 3 and 4 and the incidence of the monosomy of chromosome 3 in human UM. In summary, our results provide new incite concerning the genetic background of this tumor. Our findings could contribute to a more precise determination of the prognosis of human UM and to the development of new therapeutic approaches to this malignancy.
[Mh] Termos MeSH primário: Aberrações Cromossômicas
Cromossomos Humanos Par 3/genética
Cromossomos Humanos Par 4/genética
Melanoma/genética
Neoplasias Uveais/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Hibridização in Situ Fluorescente
Masculino
Meia-Idade
Prognóstico
Receptores LHRH
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, LHRH)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.3892/or.2017.5496


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[PMID]:28348023
[Au] Autor:Caburet S; Fruchter RB; Legois B; Fellous M; Shalev S; Veitia RA
[Ad] Endereço:Institut Jacques MonodUniversité Paris Diderot, Paris, France Sandrine.caburet@ijm.fr stavit_sh@clalit.org.il.
[Ti] Título:A homozygous mutation of in a familial case diagnosed with polycystic ovary syndrome.
[So] Source:Eur J Endocrinol;176(5):K9-K14, 2017 May.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: PCOS is a heterogeneous condition characterized by hyperandrogenism and chronic anovulation and affects about 10% of women. Its etiology is poorly known, but a dysregulation of gonadotropin secretion is one of its hallmarks. OBJECTIVE: As the etiology of PCOS is unclear, we have performed a genome-wide analysis of a consanguineous family with three sisters diagnosed with PCOS. METHODS: Whole-exome sequencing and Sanger sequencing confirmation. RESULTS: Whole-exome sequencing allowed the detection of the missense variant rs104893836 located in the first coding exon of the gene and leading to the p.Gln106Arg (p.Q106R) substitution. Sanger sequencing of all available individuals of the family confirmed that the variant was homozygous in the three affected sisters and heterozygous in both parents. CONCLUSIONS: This is the first description of a gene mutation in patients diagnosed with PCOS. Although we do not exclude a possible interaction of the identified variant with the genetic background and/or the environment, our result suggests that genetic alterations in the hypothalamo-pituitary axis may play role in the pathogenesis of PCOS.
[Mh] Termos MeSH primário: Consanguinidade
Homozigoto
Mutação
Síndrome do Ovário Policístico/genética
Receptores LHRH/genética
[Mh] Termos MeSH secundário: Feminino
Hormônio Foliculoestimulante/sangue
Seres Humanos
Israel
Hormônio Luteinizante/sangue
Linhagem
Arábia Saudita/etnologia
Análise de Sequência de DNA
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GNRHR protein, human); 0 (Receptors, LHRH); 9002-67-9 (Luteinizing Hormone); 9002-68-0 (Follicle Stimulating Hormone)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-16-0968


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[PMID]:28346489
[Au] Autor:Busby ER; Sherwood NM
[Ad] Endereço:Department of Biology, University of Victoria, Victoria, BC, Canada.
[Ti] Título:Gonadotropin-releasing hormone receptor (Gnrhr) gene knock out: Normal growth and development of sensory, motor and spatial orientation behavior but altered metabolism in neonatal and prepubertal mice.
[So] Source:PLoS One;12(3):e0174452, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gonadotropin-releasing hormone (GnRH) is important in the control of reproduction, but its actions in non-reproductive processes are less well known. In this study we examined the effect of disrupting the GnRH receptor in mice to determine if growth, metabolism or behaviors that are not associated with reproduction were affected. To minimize the effects of other hormones such as FSH, LH and sex steroids, the neonatal-prepubertal period of 2 to 28 days of age was selected. The study shows that regardless of sex or phenotype in the Gnrhr gene knockout line, there was no significant difference in the daily development of motor control, sensory detection or spatial orientation among the wildtype, heterozygous or null mice. This included a series of behavioral tests for touch, vision, hearing, spatial orientation, locomotory behavior and muscle strength. Neither the daily body weight nor the final weight on day 28 of the kidney, liver and thymus relative to body weight varied significantly in any group. However by day 28, metabolic changes in the GnRH null females compared with wildtype females showed a significant reduction in inguinal fat pad weight normalized to body weight; this was accompanied by an increase in glucose compared with wildtype females shown by Student-Newman-Keuls Multiple Comparison test and Student's unpaired t tests. Our studies show that the GnRH-GnRHR system is not essential for growth or motor/sensory/orientation behavior during the first month of life prior to puberty onset. The lack of the GnRH-GnRHR axis, however, did affect females resulting in reduced subcutaneous inguinal fat pad weight and increased glucose with possible insulin resistance; the loss of the normal rise of estradiol at postnatal days 15-28 may account for the altered metabolism in the prepubertal female pups.
[Mh] Termos MeSH primário: Comportamento Animal/fisiologia
Metabolismo Energético/genética
Locomoção/genética
Atividade Motora/genética
Orientação Espacial/fisiologia
Receptores LHRH/genética
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Animais
Feminino
Resistência à Insulina/genética
Masculino
Camundongos
Camundongos Knockout
Receptores LHRH/metabolismo
Reflexo/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, LHRH)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174452


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[PMID]:28215488
[Au] Autor:Dosouto C; Haahr T; Humaidan P
[Ad] Endereço:The Fertility Clinic Skive Regional Hospital, Skive, Denmark; Hospital Universitario Dexeus, Barcelona, Spain. Electronic address: cardos@dexeus.com.
[Ti] Título:Gonadotropin-releasing hormone agonist (GnRHa) trigger - State of the art.
[So] Source:Reprod Biol;17(1):1-8, 2017 Mar.
[Is] ISSN:2300-732X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:GnRH agonist (GnRHa) trigger for final oocyte maturation in GnRH antagonist co-treated IVF/ICSI cycles significantly reduces the risk of ovarian hyperstimulation syndrome (OHSS). GnRHa trigger followed by modifications of the standard luteal phase support (modified luteal phase support) secures fresh transfer in the majority of patients with excellent reproductive outcomes. In freeze all cycles (segmented cycles) GnRHa trigger allows oocyte retrieval with a minimal risk of early onset OHSS and good reproductive outcomes in subsequent frozen thaw cycles. Overall, two different luteal phase support strategies have been proposed when a fresh transfer is performed after GnRHa trigger. These involve either boosting the endogenous steroid production or adding exogenous steroids. The present review discusses the advancement of GnRHa trigger in fresh and segmented cycles and how a modified luteal phase support policy in fresh transfer cycles results in good reproductive outcomes as well as a high safety in terms of OHSS reduction. Finally, the new concept of an individualized luteal phase support policy taking the number of pre-ovulatory follicles into account when planning a fresh transfer in GnRHa triggered IVF/ICSI cycle is discussed.
[Mh] Termos MeSH primário: Manutenção do Corpo Lúteo/efeitos dos fármacos
Fármacos para a Fertilidade Feminina/uso terapêutico
Hormônio Liberador de Gonadotropina/agonistas
Síndrome de Hiperestimulação Ovariana/prevenção & controle
Medicina de Precisão
Receptores LHRH/agonistas
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Fármacos para a Fertilidade Feminina/efeitos adversos
Fertilização In Vitro
Hormônio Liberador de Gonadotropina/antagonistas & inibidores
Hormônio Liberador de Gonadotropina/metabolismo
Seres Humanos
Técnicas de Maturação in Vitro de Oócitos
Infertilidade Feminina/terapia
Nascimento Vivo
Recuperação de Oócitos/efeitos adversos
Síndrome de Hiperestimulação Ovariana/epidemiologia
Reserva Ovariana/efeitos dos fármacos
Indução da Ovulação/efeitos adversos
Gravidez
Taxa de Gravidez
Receptores LHRH/antagonistas & inibidores
Receptores LHRH/metabolismo
Risco
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fertility Agents, Female); 0 (GNRHR protein, human); 0 (Receptors, LHRH); 33515-09-2 (Gonadotropin-Releasing Hormone)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE



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