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[PMID]:29220789
[Au] Autor:Kuznetsov YV; Levina IS; Scherbakov AM; Andreeva OE; Fedyushkina IV; Dmitrenok AS; Shashkov AS; Zavarzin IV
[Ad] Endereço:N.D. Zelinsky Institute of Organic Chemistry, Russian Academy of Sciences, Leninsky Prospect 47, Moscow 119991, Russia. Electronic address: yukuv@mail.ru.
[Ti] Título:New estrogen receptor antagonists. 3,20-Dihydroxy-19-norpregna-1,3,5(10)-trienes: Synthesis, molecular modeling, and biological evaluation.
[So] Source:Eur J Med Chem;143:670-682, 2018 Jan 01.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:New estrogen receptor α (ERα) antagonists - 3,20-dihydroxy-19-norpregna-1,3,5(10)-trienes containing an additional carbocyclic ring D' at the 16α,17α positions - were synthesized. The effects of the new compounds on the MCF-7 breast cancer cells and ERα activation were investigated. All the steroids studied were synthesized starting from estrone methyl ether. The scaffold of compounds containing the six-membered ring D' was constructed via the Diels-Alder reaction of butadiene with 3-methoxy-19-norpregna-1,3,5(10),16-tetraen-20-one 5. The hydrogenation of primary 16α,17α-cyclohexeno-adduct 7 followed by 3-demethylation (by HBr-AcOH) and reduction of 20-oxo group (by LiAlH ) or in one step by DIBAH gave target mono- and dihydroxy steroids 9-11. The Corey-Chaykovsky reaction of the same 3-methoxy-19-norpregna-1,3,5(10),16-tetraen-20-one 5 gave 16α,17α-methylene-substituted compound. The reaction of the latter with DIBAH immediately yielded 3,20-dihydroxy-16α,17α-methyleno-19-norpregna-1,3,5(10)-triene 13. The same procedures using 3-methoxy-19-norpregna-1,3,5(10),16-tetraen-20-one 5 produced corresponding 3,20-dihydroxy-16,17-19-norpregna-1,3,5(10)-triene 16 and 3,20-dihydroxy-19-norpregna-1,3,5(10),16-tetraene 17. All compounds were fully characterized by 1D and 2D NMR, HRMS, and X-ray diffraction. The molecular docking showed that the target compounds can bind to ER, their binding mode being similar to that of natural estradiol. 16α,17α-Methylene- or unsubstituted compounds exhibit the highest cytotoxicity against MCF-7 cells, being simultaneously relatively weak ERα inhibitors. 3,20-Dihydroxy steroids containing the six-membered ring D' proved to be the most effective ERα inhibitors. These compounds displayed moderate cytotoxicity comparable of that of tamoxifen and showed no toxic effect on MCF-10A normal, nontumorigenic epithelial cells. The new ER antagonists were found to be good candidates for further testing as agents for the treatment and prevention of ERα-positive breast cancers.
[Mh] Termos MeSH primário: Antagonistas do Receptor de Estrogênio/farmacologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Norpregnatrienos/farmacologia
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Relação Dose-Resposta a Droga
Antagonistas do Receptor de Estrogênio/síntese química
Antagonistas do Receptor de Estrogênio/química
Seres Humanos
Células MCF-7
Modelos Moleculares
Estrutura Molecular
Norpregnatrienos/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor Antagonists); 0 (Estrogen Receptor alpha); 0 (Norpregnatrienes); 0 (estrogen receptor alpha, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


  2 / 120 MEDLINE  
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[PMID]:28745321
[Au] Autor:Andò S; Malivindi R; Catalano S; Rizza P; Barone I; Panza S; Rovito D; Emprou C; Bornert JM; Laverny G; Metzger D
[Ad] Endereço:Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Arcavacata di Rende (CS), Italy.
[Ti] Título:Conditional expression of Ki-Ras in the mammary epithelium of transgenic mice induces estrogen receptor alpha (ERα)-positive adenocarcinoma.
[So] Source:Oncogene;36(46):6420-6431, 2017 Nov 16.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Appropriate 'in vivo' models are crucial for studying breast cancer biology and evaluating the efficacy of therapeutic agents. Thus we engineered a novel transgenic mouse line expressing the human Ki-Ras bearing an activating mutation (Ki-Ras ) selectively in the mammary epithelium after lactation. These mice develop invasive ductal adenocarcinomas with 100% incidence within 3-9 months after Ki-Ras induction. Immunophenotyping revealed that the mammary tumors express luminal markers, are positive for estrogen and progesterone receptors, negative for HER2 and have a low proliferation index. Moreover, cell lines derived from such tumors are estrogen-responsive and, when transplanted into nude mice, form tumors that respond to the antiestrogen ICI 182780. In conclusion, the mammary tumors of these transgenic mice and the derived cell lines exhibit key features of the major form of human breast cancer, that is, luminal A subtype and thus have a high potential for breast cancer research and treatment.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Epitélio/metabolismo
Receptor alfa de Estrogênio/genética
Genes ras/genética
Glândulas Mamárias Animais/metabolismo
Neoplasias Mamárias Experimentais/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Animais
Estradiol/análogos & derivados
Estradiol/farmacologia
Antagonistas do Receptor de Estrogênio/farmacologia
Receptor alfa de Estrogênio/metabolismo
Feminino
Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células MCF-7
Neoplasias Mamárias Experimentais/tratamento farmacológico
Neoplasias Mamárias Experimentais/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Nus
Camundongos Transgênicos
Mutação de Sentido Incorreto
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor Antagonists); 0 (Estrogen Receptor alpha); 22X328QOC4 (fulvestrant); 4TI98Z838E (Estradiol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.252


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[PMID]:28969348
[Au] Autor:Van der Weijden-Van Doornik EM; Slot DE; Burtin C; van der Weijden GA
[Ad] Endereço:Fysiotherapeuten Maatschap Woerden, Woerden, the Netherlands.
[Ti] Título:Grip Strength in Women Being Treated for Breast Cancer and Receiving Adjuvant Endocrine Therapy: Systematic Review.
[So] Source:Phys Ther;97(9):904-914, 2017 Sep 01.
[Is] ISSN:1538-6724
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Adjuvant endocrine therapy in breast cancer has increased survival rates; however, it is not without musculoskeletal side effects. Purpose: The purpose of this review was to systematically and critically appraise the available scientific evidence concerning the effect of adjuvant endocrine treatment on grip strength in women being treated for breast cancer. Data sources and study selection: The National Library of Medicine (MEDLINE-PubMed), Cochrane Central Register of Controlled Trials (CENTRAL), Excerpta Medical Database by Elsevier (EMBASE), Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Physiotherapy Evidence Database (PEDro) were searched from inception to February 2017 for appropriate papers that could answer the focused question. The searches were independently screened by 2 reviewers. The data from 7 papers that met the eligibility criteria were processed for further analysis. Data extraction and synthesis: The collective data and the statistical analysis of all included studies were summarized and presented in a descriptive manner. If not provided, based on data from the individual included studies, a mean percent change in grip strength was calculated. The included studies evaluating aromatase inhibitors had inconclusive outcomes, and studies with a follow-up of 6 or 12 months showed a percent reduction in grip strength varying from 0.1% to 9.7%. None of the included studies showed a significant decrease in grip strength in tamoxifen users, with a percent reduction in grip strength varying from 1.4% to 2.2%. Limitations: The 7 studies included cohort studies lacking a control group. Conclusions: There is inconclusive evidence for a small decrease in grip strength in women treated for breast cancer who are also receiving aromatase inhibitors. In those that use tamoxifen, grip strength did not change significantly.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/uso terapêutico
Inibidores da Aromatase/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Antagonistas do Receptor de Estrogênio/uso terapêutico
Força da Mão/fisiologia
Tamoxifeno/uso terapêutico
[Mh] Termos MeSH secundário: Neoplasias da Mama/mortalidade
Quimioterapia Adjuvante
Feminino
Seres Humanos
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Aromatase Inhibitors); 0 (Estrogen Receptor Antagonists); 094ZI81Y45 (Tamoxifen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1093/ptj/pzx069


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[PMID]:28582470
[Au] Autor:Bi RY; Meng Z; Zhang P; Wang XD; Ding Y; Gan YH
[Ad] Endereço:The Third Dental Center, Peking University School and Hospital of Stomatology, Haidian District, Beijing, China.
[Ti] Título:Estradiol upregulates voltage-gated sodium channel 1.7 in trigeminal ganglion contributing to hyperalgesia of inflamed TMJ.
[So] Source:PLoS One;12(6):e0178589, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Temporomandibular disorders (TMDs) have the highest prevalence in women of reproductive age. The role of estrogen in TMDs and especially in TMDs related pain is not fully elucidated. Voltage-gated sodium channel 1.7 (Nav1.7) plays a prominent role in pain perception and Nav1.7 in trigeminal ganglion (TG) is involved in the hyperalgesia of inflamed Temporomandibular joint (TMJ). Whether estrogen could upregulate trigeminal ganglionic Nav1.7 expression to enhance hyperalgesia of inflamed TMJ remains to be explored. METHODS: Estrous cycle and plasma levels of 17ß-estradiol in female rats were evaluated with vaginal smear and enzyme linked immunosorbent assay, respectively. Female rats were ovariectomized and treated with 17ß-estradiol at 0 µg, 20 µg and 80 µg, respectively, for 10 days. TMJ inflammation was induced using complete Freund's adjuvant. Head withdrawal thresholds and food intake were measured to evaluate the TMJ nociceptive responses. The expression of Nav1.7 in TG was examined using real-time PCR and western blot. The activity of Nav1.7 promoter was examined using luciferase reporter assay. The locations of estrogen receptors (ERα and ERß), the G protein coupled estrogen receptor (GPR30), and Nav1.7 in TG were examined using immunohistofluorescence. RESULTS: Upregulation of Nav1.7 in TG and decrease in head withdrawal threshold were observed with the highest plasma 17ß-estradiol in the proestrus of female rats. Ovariectomized rats treated with 80 µg 17ß-estradiol showed upregulation of Nav1.7 in TG and decrease in head withdrawal threshold as compared with that of the control or ovariectomized rats treated with 0 µg or 20 µg. Moreover, 17ß-estradiol dose-dependently potentiated TMJ inflammation-induced upregulation of Nav1.7 in TG and also enhanced TMJ inflammation-induced decrease of head withdrawal threshold in ovariectomized rats. In addition, the estrogen receptor antagonist, ICI 182,780, partially blocked the 17ß-estradiol effect on Nav1.7 expression and head withdrawal threshold in ovariectomized rats. ERα and ERß, but not GPR30, were mostly co-localized with Nav1.7 in neurons in TG. In the nerve growth factor-induced and ERα-transfected PC12 cells, 17ß-estradiol dose-dependently enhanced Nav1.7 promoter activity, whereas mutations of the estrogen response element at -1269/-1282 and -1214/-1227 in the promoter completely abolished its effect on the promoter activity. CONCLUSION: Estradiol could upregulate trigeminal ganglionic Nav1.7 expression to contribute to hyperalgesia of inflamed TMJ.
[Mh] Termos MeSH primário: Estradiol/farmacologia
Hiperalgesia/genética
Canal de Sódio Disparado por Voltagem NAV1.7/genética
Síndrome da Disfunção da Articulação Temporomandibular/genética
Articulação Temporomandibular/efeitos dos fármacos
Gânglio Trigeminal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Estradiol/análogos & derivados
Estradiol/metabolismo
Antagonistas do Receptor de Estrogênio/farmacologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor alfa de Estrogênio/genética
Receptor alfa de Estrogênio/metabolismo
Receptor beta de Estrogênio/antagonistas & inibidores
Receptor beta de Estrogênio/genética
Receptor beta de Estrogênio/metabolismo
Ciclo Estral/fisiologia
Feminino
Adjuvante de Freund
Regulação da Expressão Gênica
Genes Reporter
Hiperalgesia/metabolismo
Hiperalgesia/patologia
Luciferases/genética
Luciferases/metabolismo
Canal de Sódio Disparado por Voltagem NAV1.7/metabolismo
Nociceptividade/efeitos dos fármacos
Ovariectomia
Regiões Promotoras Genéticas
Ratos
Ratos Sprague-Dawley
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/metabolismo
Articulação Temporomandibular/inervação
Articulação Temporomandibular/metabolismo
Articulação Temporomandibular/patologia
Síndrome da Disfunção da Articulação Temporomandibular/induzido quimicamente
Síndrome da Disfunção da Articulação Temporomandibular/metabolismo
Síndrome da Disfunção da Articulação Temporomandibular/patologia
Gânglio Trigeminal/metabolismo
Gânglio Trigeminal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor Antagonists); 0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (GPR30 protein, rat); 0 (NAV1.7 Voltage-Gated Sodium Channel); 0 (Receptors, G-Protein-Coupled); 0 (Scn9a protein, rat); 22X328QOC4 (fulvestrant); 4TI98Z838E (Estradiol); 9007-81-2 (Freund's Adjuvant); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178589


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[PMID]:28473445
[Au] Autor:McRobb LS; McGrath KCY; Tsatralis T; Liong EC; Tan JTM; Hughes G; Handelsman DJ; Heather AK
[Ad] Endereço:From the Heart Research Institute, Sydney, New South Wales, Australia (L.S.M., K.C.Y.M., T.T., E.C.L., J.T.M.T.); Department of Clinical Medicine, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, New South Wales, Australia (L.S.M.); School of Life Sciences, Faculty of Science,
[Ti] Título:Estrogen Receptor Control of Atherosclerotic Calcification and Smooth Muscle Cell Osteogenic Differentiation.
[So] Source:Arterioscler Thromb Vasc Biol;37(6):1127-1137, 2017 Jun.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Vascular calcification is associated with increased risk of myocardial infarction and stroke. The objective of this work was to examine the ability of 17ß-estradiol (E2) to stimulate calcification of vascular smooth muscle cells (VSMC) in vivo, using aged apolipoprotein E-null mice with advanced atherosclerotic lesions, and subsequently to explore underlying mechanisms in vitro. APPROACH AND RESULTS: Silastic E2 capsules were implanted into male and female apolipoprotein E-null mice aged 34 weeks. Plaque and calcified area were measured in the aortic sinus and innominate artery after 8 weeks. Immunohistochemical analysis examined expression of the estrogen receptors (estrogen receptor alpha and estrogen receptor beta [ERß]). VSMC expression of osteogenic markers was examined using digital polymerase chain reaction. Advanced atherosclerotic lesions were present in all mice at the end of 8 weeks. In both male and female mice, E2 increased calcified area in a site-specific manner in the aortic sinus independently of plaque growth or lipid levels and occurred in association with a site-specific decrease in the proportion of ERß-positive intimal cells. Calcified lesions expressed collagen I and bone sialoprotein, with decreased matrix Gla protein. In vitro, E2 suppressed ERß expression and increased VSMC mineralization, demonstrating increased collagen I and II, osteocalcin and bone sialoprotein, and reduced matrix Gla protein and osteopontin. Antagonism or RNA silencing of estrogen receptor alpha, ERß, or both further increased VSMC mineralization. CONCLUSIONS: We have demonstrated that E2 can drive calcification in advanced atherosclerotic lesions by promoting the differentiation of VSMC to osteoblast-like cells, a process which is augmented by inhibition of estrogen receptor alpha or ERß activity.
[Mh] Termos MeSH primário: Aterosclerose/induzido quimicamente
Diferenciação Celular/efeitos dos fármacos
Estradiol/toxicidade
Receptor alfa de Estrogênio/agonistas
Receptor beta de Estrogênio/agonistas
Músculo Liso Vascular/efeitos dos fármacos
Miócitos de Músculo Liso/efeitos dos fármacos
Osteogênese/efeitos dos fármacos
Calcificação Vascular/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Aterosclerose/genética
Aterosclerose/metabolismo
Aterosclerose/patologia
Proteínas de Ligação ao Cálcio/metabolismo
Bovinos
Células Cultivadas
Colágeno/metabolismo
Modelos Animais de Doenças
Implantes de Medicamento
Estradiol/administração & dosagem
Antagonistas do Receptor de Estrogênio/farmacologia
Receptor alfa de Estrogênio/genética
Receptor alfa de Estrogênio/metabolismo
Receptor beta de Estrogênio/genética
Receptor beta de Estrogênio/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Feminino
Predisposição Genética para Doença
Seres Humanos
Sialoproteína de Ligação à Integrina/metabolismo
Masculino
Camundongos Knockout
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/patologia
Neointima
Osteocalcina/metabolismo
Osteopontina/metabolismo
Fenótipo
Placa Aterosclerótica
Interferência de RNA
Transdução de Sinais/efeitos dos fármacos
Transfecção
Calcificação Vascular/genética
Calcificação Vascular/metabolismo
Calcificação Vascular/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Calcium-Binding Proteins); 0 (Drug Implants); 0 (ESR2 protein, human); 0 (Estrogen Receptor Antagonists); 0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Extracellular Matrix Proteins); 0 (Integrin-Binding Sialoprotein); 0 (Spp1 protein, mouse); 0 (estrogen receptor alpha, human); 0 (matrix Gla protein); 104982-03-8 (Osteocalcin); 106441-73-0 (Osteopontin); 4TI98Z838E (Estradiol); 9007-34-5 (Collagen)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309054


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[PMID]:28373583
[Au] Autor:Channappanavar R; Fett C; Mack M; Ten Eyck PP; Meyerholz DK; Perlman S
[Ad] Endereço:Department of Microbiology, University of Iowa, Iowa City, IA 52242.
[Ti] Título:Sex-Based Differences in Susceptibility to Severe Acute Respiratory Syndrome Coronavirus Infection.
[So] Source:J Immunol;198(10):4046-4053, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pathogenic human coronaviruses (CoVs), such as the severe acute respiratory syndrome (SARS)-CoV and the Middle East respiratory syndrome-CoV, cause acute respiratory illness. Epidemiological data from the 2002-2003 SARS epidemic and recent Middle East respiratory syndrome outbreak indicate that there may be sex-dependent differences in disease outcomes. To investigate these differences, we infected male and female mice of different age groups with SARS-CoV and analyzed their susceptibility to the infection. Our results showed that male mice were more susceptible to SARS-CoV infection compared with age-matched females. The degree of sex bias to SARS-CoV infection increased with advancing age, such that middle-aged mice showed much more pronounced differences compared with young mice. Enhanced susceptibility of male mice to SARS-CoV was associated with elevated virus titers, enhanced vascular leakage, and alveolar edema. These changes were accompanied by increased accumulation of inflammatory monocyte macrophages and neutrophils in the lungs of male mice, and depletion of inflammatory monocyte macrophages partially protected these mice from lethal SARS. Moreover, the sex-specific differences were independent of T and B cell responses. Furthermore, ovariectomy or treating female mice with an estrogen receptor antagonist increased mortality, indicating a protective effect for estrogen receptor signaling in mice infected with SARS-CoV. Together, these data suggest that sex differences in the susceptibility to SARS-CoV in mice parallel those observed in patients and also identify estrogen receptor signaling as critical for protection in females.
[Mh] Termos MeSH primário: Suscetibilidade a Doenças
Síndrome Respiratória Aguda Grave/fisiopatologia
Caracteres Sexuais
[Mh] Termos MeSH secundário: Animais
Antagonistas do Receptor de Estrogênio/farmacologia
Feminino
Pulmão/imunologia
Pulmão/patologia
Pulmão/virologia
Masculino
Camundongos
Monócitos/imunologia
Ovariectomia
Receptores Estrogênicos/metabolismo
Vírus da SARS/isolamento & purificação
Vírus da SARS/patogenicidade
Síndrome Respiratória Aguda Grave/patologia
Síndrome Respiratória Aguda Grave/virologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor Antagonists); 0 (Receptors, Estrogen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601896


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[PMID]:28320163
[Au] Autor:Zhang Y; Huang Y; Wang G; Wang X; Wang Y
[Ad] Endereço:Institutes of Brain Science, State Key Laboratory for Medical Neurobiology, Collaborative Innovation Center for Brain Science, Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
[Ti] Título:Inhibition of 17-beta-estradiol on neuronal excitability via enhancing GIRK1-mediated inwardly rectifying potassium currents and GIRK1 expression.
[So] Source:J Neurol Sci;375:335-341, 2017 Apr 15.
[Is] ISSN:1878-5883
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Catamenial epilepsy is a common central nervous system disease in female, which is influenced by the 17-ß-estradiol (estrogen) level during the menstrual cycle. Low level (<0.05ng/ml) of estrogen normally accompanies with the perimenstrual classification of catamenial epilepsy, however, without clear mechanism. In previous studies, estrogen has been demonstrated to possess widely regulatory effects on potassium channels. Here, the effect of 17-ß-estradiol on modulating inwardly rectifying K (Kir) currents was investigated in cultured hippocampal neurons. The underlying mechanism was also detected. METHODS: In this research, null-estrogen cultures and spaying animals were used to mimicked the low level estrogen condition in menstrual period. Patch clamp recordings, western blotting and pharmacological experiments were performed to detect the effects of estrogen receptors and the underlying mechanisms. RESULTS: Compared to those neurons in normal medium (with 0.1ng/ml estrogen), null-estrogen cultures or neurons treated by estrogen receptor blocker (ICI 182,780) both had significant suppressed Kir currents. The expression level of G protein-gated inwardly rectifying K channel subunit 1 (GIRK1) was significantly decreased in spaying animals. Furthermore, a GIRK channel inhibitor (TPQ) similarly suppressed the Kir currents. Lastly, estrogen deficiency, estrogen receptor blocker and GIRK channel inhibitor all promoted the epileptiform bursting activities in neurons, as a result of Kir current suppression. CONCLUSION: Taken together, 17-ß-estradiol, by the activation of estrogen receptors, is essential for the maintenance of Kir currents, and thus has an inhibitory effect on the epileptiform bursting activities in cultured hippocampal neurons, whereas GIRK1 is the major intermedial mediator. This research provides a new mechanism for the pathogenesis of catamenial epilepsy, particularly in the menstrual period and the early section of follicular phase.
[Mh] Termos MeSH primário: Estradiol/farmacologia
Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
[Mh] Termos MeSH secundário: Animais
Venenos de Abelha/farmacologia
Células Cultivadas
Modelos Animais de Doenças
Embrião de Mamíferos
Epilepsia/induzido quimicamente
Epilepsia/tratamento farmacológico
Epilepsia/metabolismo
Estradiol/análogos & derivados
Antagonistas do Receptor de Estrogênio/farmacologia
Feminino
Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G/metabolismo
Hipocampo/citologia
Ovariectomia
Bloqueadores dos Canais de Potássio/farmacologia
Gravidez
Ratos
Ratos Sprague-Dawley
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bee Venoms); 0 (Estrogen Receptor Antagonists); 0 (G Protein-Coupled Inwardly-Rectifying Potassium Channels); 0 (Potassium Channel Blockers); 0 (Potassium Channels, Inwardly Rectifying); 0 (Sodium Channel Blockers); 22X328QOC4 (fulvestrant); 3A7MX9B7E8 (tertiapin); 4368-28-9 (Tetrodotoxin); 4TI98Z838E (Estradiol)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


  8 / 120 MEDLINE  
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[PMID]:28255459
[Au] Autor:Chen X; Wang Y; Xu F; Wei X; Zhang J; Wang C; Wei H; Xu S; Yan P; Zhou W; Mody I; Xu X; Wang Q
[Ad] Endereço:Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo 315211, China.
[Ti] Título:The Rapid Effect of Bisphenol-A on Long-Term Potentiation in Hippocampus Involves Estrogen Receptors and ERK Activation.
[So] Source:Neural Plast;2017:5196958, 2017.
[Is] ISSN:1687-5443
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bisphenol-A (BPA), a widely used synthetic compound in plastics, disrupts endocrine function and interferes with physiological actions of endogenous gonadal hormones. Chronic effects of BPA on reproductive function, learning and memory, brain structure, and social behavior have been intensively investigated. However, less is known about the influence of BPA on long-term potentiation (LTP), one of the major cellular mechanisms that underlie learning and memory. In the present study, for the first time we investigated the effect of different doses of BPA on hippocampal LTP in rat brain slices. We found a biphasic effect of BPA on LTP in the dentate gyrus: exposure to BPA at a low dose (100 nM) enhanced LTP and exposure to BPA at a high dose (1000 nM) inhibited LTP compared with vehicle controls. The rapid facilitatory effect of low-dose BPA on hippocampal LTP required membrane-associated estrogen receptor (ER) and involved activation of the extracellular signal-regulated kinase (ERK) signaling pathway. Coadministration of 17 -estradiol (E , the primary estrogen hormone) and BPA (100 nM) abolished both the BPA-induced enhancement of LTP and the E -induced enhancement of baseline fEPSP, suggesting a complex interaction between BPA- and E -mediated signaling pathways. Our investigation implies that even nanomolar levels of endocrine disrupters (e.g., BPA) can induce significant effects on hippocampal LTP.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/farmacologia
Hipocampo/efeitos dos fármacos
Hipocampo/fisiologia
Potenciação de Longa Duração/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Fenóis/farmacologia
Receptores Estrogênicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Compostos Benzidrílicos/administração & dosagem
Giro Denteado/efeitos dos fármacos
Giro Denteado/fisiologia
Relação Dose-Resposta a Droga
Estradiol/análogos & derivados
Estradiol/farmacologia
Antagonistas do Receptor de Estrogênio/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Masculino
Fenóis/administração & dosagem
Ratos
Ratos Wistar
Receptores Estrogênicos/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Estrogen Receptor Antagonists); 0 (Phenols); 0 (Receptors, Estrogen); 22X328QOC4 (fulvestrant); 4TI98Z838E (Estradiol); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.1155/2017/5196958


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[PMID]:28215489
[Au] Autor:Takahashi M; Ichimura R; Inoue K; Morikawa T; Kuwata K; Watanabe G; Yoshida M
[Ad] Endereço:Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan.
[Ti] Título:The role of estrogen receptor subtypes for induction of delayed effects on the estrous cycle and female reproductive organs in rats.
[So] Source:Reprod Biol;17(1):111-119, 2017 Mar.
[Is] ISSN:2300-732X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:It has been reported that neonatal exposure to estrogens at relatively low doses can induce early onset anovulation as a delayed effect in female rats. Dysfunction of kisspeptin neurons in the anteroventral periventricular nucleus (AVPV) was proposed to be a trigger for this effect. To determine the roles of estrogen receptor (ER) subtypes in the induction of delayed effects, we conducted a series of experiments using Donryu rats to examine whether neonatal injection of an ERα agonist (PPT), an ERß agonist (DPN) or an ERα antagonist (ICI) could induce delayed effects. Also, involvement of the kisspeptin neurons in the AVPV for induction of delayed effect by PPT and DPN was investigated. We observed that neonatal exposure to PPT, DPN and ICI induced the early onset of abnormal estrous cyclicity after sexual maturation, suggesting that the compounds capable of inducing delayed effects are not limited to ERα agonists. On the other hand, the data suggested the possibility that DPN and ICI functioned partially as ERα agonists in the neonatal brain. Regardless of the agents used, there is a possibility that dysfunction of kisspeptin neurons in the AVPV might contribute to induction of early onset anovulation.
[Mh] Termos MeSH primário: Receptor alfa de Estrogênio/agonistas
Receptor beta de Estrogênio/agonistas
Estrogênios não Esteroides/toxicidade
Hipotálamo Anterior/efeitos dos fármacos
Distúrbios Menstruais/induzido quimicamente
Ovário/efeitos dos fármacos
Útero/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Anovulação/induzido quimicamente
Anovulação/metabolismo
Anovulação/patologia
Relação Dose-Resposta a Droga
Antagonistas do Receptor de Estrogênio/administração & dosagem
Antagonistas do Receptor de Estrogênio/metabolismo
Antagonistas do Receptor de Estrogênio/toxicidade
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor alfa de Estrogênio/metabolismo
Receptor beta de Estrogênio/metabolismo
Estrogênios não Esteroides/administração & dosagem
Estrogênios não Esteroides/metabolismo
Feminino
Hipotálamo Anterior/metabolismo
Hipotálamo Anterior/patologia
Kisspeptinas/metabolismo
Distúrbios Menstruais/metabolismo
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Neurônios/patologia
Tamanho do Órgão/efeitos dos fármacos
Ovário/metabolismo
Ovário/patologia
Gravidez
Distribuição Aleatória
Ratos
Distribuição Tecidual
Toxicocinética
Útero/metabolismo
Útero/patologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor Antagonists); 0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Estrogens, Non-Steroidal); 0 (Kiss1 protein, rat); 0 (Kisspeptins)
[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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[PMID]:28000875
[Au] Autor:Huang Y; Jiang D; Sui M; Wang X; Fan W
[Ad] Endereço:Department of Chemotherapy, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China.
[Ti] Título:Fulvestrant reverses doxorubicin resistance in multidrug-resistant breast cell lines independent of estrogen receptor expression.
[So] Source:Oncol Rep;37(2):705-712, 2017 Feb.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Drug resistance, a major obstacle to successful cancer chemotherapy, frequently occurs in recurrent or metastatic breast cancer and results in poor clinical response. Fulvestrant is a new type of selective estrogen receptor (ER) downregulator and a promising endocrine therapy for breast cancer. In this study, we evaluated the combination treatment of fulvestrant and doxorubicin in ER-negative multidrug-resistant (MDR) breast cancer cell lines Bads­200 and Bats­72. Fulvestrant potentiated doxorubicin-induced cytotoxicity, apoptosis and G2/M arrest with upregulation of cyclin B1. It functioned as a substrate for P-glycoprotein (P-gp) without affecting its expression. Furthermore, fulvestrant not only restored the intracellular accumulation of doxorubicin but also relocalized it to the nuclei in Bats­72 and Bads­200 cells, which may be another potential mechanism of reversal of P-gp mediated doxorubicin resistance. These results indicated that the combination of fulvestrant and doxorubicin-based chemotherapy may be feasible and effective for patients with advanced breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/tratamento farmacológico
Doxorrubicina/farmacologia
Resistência a Múltiplos Medicamentos/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Estradiol/análogos & derivados
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Antibióticos Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Western Blotting
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Estradiol/farmacologia
Antagonistas do Receptor de Estrogênio/farmacologia
Feminino
Seres Humanos
Receptores Estrogênicos/antagonistas & inibidores
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Estrogen Receptor Antagonists); 0 (Receptors, Estrogen); 22X328QOC4 (fulvestrant); 4TI98Z838E (Estradiol); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170404
[Lr] Data última revisão:
170404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161222
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.5315



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